UNITED REPUBLIC OF TANZANIA

Ministry of Health, Community

Development, Gender, Elderly and
Children

PST 06106
Basic Pharmacotherapy

NTA Level 6 Semester 1

Facilitator Guide

March 2019
PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator Guide i
 Copyright © Ministry of Health, Community Development, Gender, Elderly and Children – 2019

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator Guide i

 Table of Contents
Background ...............................................................................................................................iii
Acknowledgment ...................................................................................................................... iv
Introduction ............................................................................................................................... iv
Abbreviations ............................................................................................................................ ix
Session 1: Introduction to Pharmacotherapy ............................................................................. 1
Session 2: Therapeutic Drug Monitoring (TDM) ...................................................................... 8
Session 3: Pharmacotherapy of Malaria .................................................................................. 14
Session 4: Pharmacotherapy of HIV/AIDS ............................................................................. 23
Session 5: Pharmacotherapy of Tuberculosis .......................................................................... 34
Session 6: Pharmacotherapy of Leprosy .................................................................................. 42
Session 7: Pharmacotherapy of Pharyngitis, Sinusitis, and Otitis Media ................................ 50
Session 8: Pharmacotherapy of Pneumonia ............................................................................. 61
Session 9: Pharmacotherapy of Bronchitis .............................................................................. 70
Session 10: Pharmacotherapy of Typhoid Fever ..................................................................... 77
Session 11: Pharmacotherapy of Amebiasis ............................................................................ 83
Session 12: Pharmacotherapy of Trypanosomiasis.................................................................. 89
Session 13: Pharmacotherapy of Schistosomiasis ................................................................... 96
Session 14: Pharmacotherapy of Gonorrhoea ........................................................................ 102
Session 15: Pharmacotherapy of Syphilis .............................................................................. 108
Session 16: Pharmacotherapy of Chlamydial Genital Tract Infections ................................. 116
Session 17: Pharmacotherapy of Genital Herpes ................................................................... 122
Session 18: Pharmacotherapy of Urinary Tract Infections .................................................... 129
Session 19: Pharmacotherapy of Folliculitis, Furunculosis ................................................... 137
and Carbuncles ....................................................................................................................... 137
Session 20: Pharmacotherapy of Vulvovaginal Candidiasis ................................................. 143
Session 21: Pharmacotherapy of Asthma .............................................................................. 151
Session 22: Pharmacotherapy of Diabetes Mellitus............................................................... 162
Session 23: Pharmacotherapy of Peptic Ulcers Disease ........................................................ 175
Session 25: Pharmacotherapy of Heart Failure ...................................................................... 192
Session 26: Pharmacotherapy of Schizophrenia .................................................................... 203
Session 27: Pharmacotherapy of Epilepsy ............................................................................. 212
Session 28: Pharmacotherapy of Hepatitis B ......................................................................... 220
Session 29: Pharmacotherapy of Cholera .............................................................................. 226
Session 30: Pharmacotherapy of Shigellosis ......................................................................... 232
Session 31: Pharmacotherapy of Breast Cancer .................................................................... 237
Session 32: Pharmacotherapy of Prostate Cancer .................................................................. 244
Session 33: Pharmacotherapy of Oropharyngeal Candidiasis ............................................... 251

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide ii
Background
There is currently an ever increasing demand for pharmaceutical personnel in Tanzania. This
is due to expanding investment in public and private pharmaceutical sector. Shortage of
trained pharmaceutical human resource contributes to poor quality of pharmaceutical services
and low access to medicines in the country (GIZ, 2012).
Through Public-Private-Partnership (PPP) the Pharmacy Council (PC) together with
Development Partners (DPs) in Germany and Pharmaceutical Training Institutions (PTIs)
worked together to address the shortage of human resource for pharmacy by designing a project
named “Supporting Training Institutions for Improved Pharmaceutical Services in Tanzania”
in order to improve quality and capacity of PTIs in training, particularly of lower cadre
pharmaceutical personnel.
The Pharmacy Council formed a Steering committee that conducted a stakeholders workshop
from18th to 22ndAugust 2014 in Morogoro to initiate the implementation of the project.

Key activities in the implementation of this project included carrying out situational analysis,
curriculum review and harmonization, development of training manual/facilitators guide,
development of assessment plan, training of trainers and supportive supervision.
After the curricula were reviewed and harmonized, the process of developing standardized
training materials was started in August 2015 through Writer’s Workshop (WW) approach.

The approach included two workshops (of two weeks each) for developing draft documents
and a one-week workshop for reviewing, editing and formatting the sessions of the modules.

The goals of Writers Workshops were to build capacity of tutors in the development of training
materials and to develop high-quality, standardized teaching materials.

The training package for pharmacy cadres includes a Facilitator Guide, Assessment plan and
Practicum. There are 12 modules for NTA level 6 making 12 Facilitator guides and one
Practicum guide.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide iii
Acknowledgment
The development of standardized training materials of a competence-based curriculum for
pharmaceutical sciences has been accomplished through involvement of different
stakeholders.
Special thanks go to the Pharmacy Council for spearheading the harmonization of training
materials in the pharmacy after noticing that training institutions in Tanzania were using
different curricula and train their students differently.
I would also like to extend my gratitude to Christian Social Service Commission (CSSC) for
their tireless efforts to mobilize funds from development partners (German Ministry of Industry
and action medeor). It is through the implementation of the Multi-Actors Partnership (MAP)
project, CSSC has been able to provide the financial and technical support needed during the
development of this training material.
Many thanks go to the Centre for Educational Development in Health Arusha (CEDHA)
experts on health material development and training who coordinated the development of
these module sessions particularly Ms. Diana H. Gamuya for her commitment in coordinating
and facilitating the planning and development to its completion.
Particular acknowledgements are sent to Mr. Dickson Mtalitinya and Members from the
secretariat of National Council for Technical Education (NACTE) for facilitating and
providing their expertise to the success of this work.
It will be unfair if I will not recognize the efforts and contributions of all CEDHA supportive
staff that made this process a success; accountant, secretary, drivers and printers

Finally, I very much appreciate the contributions of the tutors and content experts
representing PTIs, hospitals, and other health training institutions. Their participation in
meetings and workshops, and their input in the development of this training
manual/facilitators guide have been invaluable.

These participants are listed with our gratitude below:

Ms. Elizabeth Shekalaghe Registrar, Pharmacy Council of Tanzania

Dr. Fadhili Lyimo Assistant Director Allied Health, MoHCDGEC
Mr. Dennis Busuguli MoHCDGEC
Dr. Jacqueline Uriyo Acting Principal, CEDHA
Dr. Sungwa N. Kabissi Project Manager - MAP, CSSC
Dr. Loishooki S. Laizer CEDHA
Ms. Diana H. Gamuya CEDHA
Mr. Dickson Mtalitinya SIBS
Ms. Grace Mallange PC
Mr. Wensaa Muro KSP
Mr. John Mmassy CSSC
Ms. Emily Mwakibolwa Pharmacy Council
PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator
Guide iv
Mr. Samwel M. Zakayo Pharmacy Council
Mr. Godfrey Komba NACTE
Mr. Samweli Mdallingwa NACTE
Mr. Daniel Muhochi CEDHA
Dr. Byera Shwekerela CEDHA
Dr. Johannes Lukumay CEDHA
Dr. Mwandu Jiyenze CEDHA
Dr. Peter Sala CEDHA
Mr. Stephano Kiberiti CEDHA
Mr. Amani Phillip HKMU
Mr. John M. Bitoro CUHAS
Mr. Omary Mejjah CUHAS
Mr. Karol Marwa CUHAS
Mr. Raphael Matinde CUHAS
Mr. Rajabu I. Amiri MUHAS
Mr. Peter Njalale MUHAS
Ms. Tumaini H. Lyombe MUHAS
Ms. Dilisi J. Makawia KSP
Mr. Richard P. Mmassy KSP
Mr. Nemes Uisso RAS-KLM
Mr. Gaspar Baltazary RuCU
Mr. Goodluck Mdugi RuCU
Mr. Godfrey A. Pharaoh SIBS
Mr. Joel M.Selestine SIBS
Mr. Jimmy M. Mulee SIBS
Mr. Evalist Shileki DECOHAS
Mr. Eliabu Mshashi KIUT

Dr. Loishooki S. Laizer

Director of Human Resources Development
Ministry of Health, Community Development, Gender, Elderly and Children

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide v
Introduction
Module Overview

This module content is a guide for tutors of Pharmaceutical schools for training of students.
The session contents are based on sub-enabling outcomes and their related tasks of the
curriculum for Basic Technician Course in Pharmaceutical Sciences. The module sub-enabling
outcomes and their related tasks are as indicated in the in the Ordinary Diploma Course in
Pharmaceutical Sciences (NTA Level 6) Curriculum

Target Audience

This module is intended for use primarily by tutors of pharmaceutical schools. The module’s
sessions give guidance on the time, activities and provide information on how to teach the
session. The sessions include different activities which focus on increasing students’
knowledge, skills and attitudes.

Organization of the Module

The module consists of thirty three (33) sessions; each session is divided into several parts as
indicated below:

• Session Title: The name of the session

• Total Session Time: The estimated time for teaching the session, indicated in minutes

• Pre-requisites: A module or session which needs to be covered before teaching the

session.

• Learning Tasks: Statements which indicate what the student is expected to learn by the
end of the session

• Resources Needed: All resources needed for the session are listed including handouts
and worksheets

• Session Overview: The session overview box lists the steps, time for each step, the
activity or method used in each step and the step title

• Session Content: All the session contents are divided into steps. Each step has a heading
and an estimated time to teach that step as shown in the overview box. Also, this section
includes instructions for the tutor and activities with their instructions to be done during
teaching of the contents

• Key Points: Key messages for concluding the session contents at the end of a session
This step summarizes the main points and ideas from the session, based on the learning
tasks of the session

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide vi
• Evaluation: The last section of the session consists of short questions based on the
learning tasks to check the understanding of students.

• Handouts: Additional information which can be used in the classroom while teaching or
later for students’ further learning. Handouts are used to provide extra information related
to the session topic that cannot fit into the session time. Handouts can be used by the
students to study material on their own and to refer to them after the session. Sometimes, a
handout will have questions or an exercise for the participants including the answers to the
questions.

Instructions for Use and Facilitators Preparation

• Tutors are expected to use the module as a guide to train students in the classroom and
skills laboratory
• The contents of the modules are the basis for teaching and learning dispensing.
• Use the session contents as a guide
• The tutors are therefore advised to read each session and the relevant handouts and
worksheets as preparation before facilitating the session
• Tutors need to prepare all the resources, as indicated in the resource section or any other
item, for an effective teaching and learning process
• Plan a schedule (timetable) of the training activities
• Facilitators are expected to be innovative to make the teaching and learning process
effective
• Read the sessions before facilitation; make sure you understand the contents in order to
clarify points during facilitation
• Time allocated is estimated, but you are advised to follow the time as much as possible,
and adjust as needed
• Use session activities and exercises suggested in the sessions as a guide
• Always involve students in their own learning. When students are involved, they learn more
effectively
• Facilitators are encouraged to use real life examples to make learning more realistic
• Make use of appropriate reference materials and teaching resources available locally

Preparation with Handouts and Worksheets

• Go through the session and identify handouts and worksheets needed for the session
• Reproduce pages of these handouts and worksheets for student use while teaching the
session. This will enable students to refer to handouts and worksheets during the session
in the class. You can reproduce enough copies for students or for sharing
• Give clear instructions to students on the student activity in order for the students to
follow the instructions of the activity
• Refer students to the specific page in the student manual as instructed in the facilitator
guide

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide vii
Using Students Manual When Teaching
• The student manual is a document which has the same content as the facilitator guide, which
excludes facilitator instructions and answersfor exercises.
• The student manual is for assisting students to learn effectively and acts as a reference
document during and after teaching the session
• Some of the activities included in facilitator guide are in the student manual without
facilitator instructions

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide viii
Abbreviations
ARV Anti-Retroviral
CNS Central Nervous System
COCs Combined Oral Contraceptives
COPD Chronic Obstructive Pulmonary Diseases
CUHAS C atholic University of Heal and Allied sciences
E.L.C.T Evangelical Lutheran Church in Tanzania
HKMU Hurbert Kairuki Memorial University
ICP Increased Intra Cranial Pressure
IGs Immunoglobulins
ITP Idiopathic Thrombocytopenic Purpura
JSI John Snow Inc
KCMC Kilimanjaro College of Medical Sciences
LZHRC Lake zone Health Recourse Centre
MAO Mono Amine Oxidase
MMR Measles, Mumps and Rubella
MoHCGC Ministry of Health, Community development, Gender, Elderly and
children
MUHAS Muhimbili University of Health and Allied Sciences
NACTE National Council For Technical Education
NSAIDS Non-steroidal anti-inflammatory drugs
POPs Progestogen Only Pills
RuCU Ruaha Catholic University
SIBS Spring Institute of Business and Science
SLF Saint Luke Foundation
USP United States Pharmacopoeia

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide ix
Session 1: Introduction to Pharmacotherapy

Total Session Time: 120 minutes

Prerequisites
• None

Learning Tasks
• By the end of this session students are expected to be able to:
• Define terminologies used in Pharmacotherapy
• Describe principles and concepts applied in Pharmacotherapy
• Explain importance of Pharmacotherapy in the management of common diseases

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Computer and projector

SESSION OVERVIEW

Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning tasks
Presentation Definition of Terminologies Used in
2 20 minutes
Pharmacotherapy
Principle and Concepts Applied in
3 60 minutes Presentation
Pharmacotherapy
Presentation/
4 25 minutes Small Group Importance of Pharmacotherapy
Discussion
5 05 minutes Presentation Key Points

6 05 minutes Presentation Evaluation

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator Guide 1

SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning tasks (5 minutes)

READ or ASK students to read the learning tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of Common Terminologies used in Pharmacotherapy

(20 minutes)
• Pharmacotherapy is application of knowledge in making therapeutic decisions that are
most likely to have maximum positive benefit for a specific patient.
• Pharmacotherapy specialist: is an individual who is specialized in administering and
prescribing medication, and requires extensive academic knowledge in pharmacotherapy.
o Pharmaceutical personel are experts in pharmacotherapy and are responsible for
ensuring the safe, appropriate, and economical use of pharmaceutical drugs.
• Pathophysiology is the physiology of abnormal states; specifically: the functional changes
that accompany a particular syndrome or disease.
o Also is the study of changes in the way the body works that result from disease or
injury
• Pharmaceutical care involves the process through which a pharmacist/ other
pharmaceutical personel cooperates with a patient and other professionals in designing,
implementing, and monitoring a therapeutic plan that will produce specific therapeutic
outcomes for the patient.

STEP 3: Principles and Concepts applied in pharmacotherapy (60 minutes)

There are three steps that are involved in the Pharmacotherapy process which are;
• Patient assessment
• Development of the pharmacotherapy care plan
• Evaluation of the impact or results of the care plan.
Fig 1.1 Patient Care Process in the Pharmacotherapy

Souce: DiPiro JT, et al (2008): Pharmacotherapy: A Pathophysiologic Approach (7th ed)

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator
Guide 2
Patient Assessment
• In this step, the focus is on drug therapy problems in which case it is important to assess if
the patient’s problem(s) is/are be caused by drug therapy and can be managed by a change
in drug therapy
• The following is the list of drug therapy problems that should be identified;
o Inappropriate drug selection
o Need for additional drug therapy
o Unnecessary drug therapy
o Incorrect drug regimen
o Therapeutic duplication
o Drug allergy/adverse drug event
o Drug Interactions
o Medication adherence issues
• Once a drug therapy problem is identified and categorized, it is then necessary to identify
the cause of the problem, thereby leading to potential solutions.
• The process of drug therapy problem identification is to assessing the patient’s drug therapy
needs and ensuaring appropriateness, effectiveness and safety of medications, and
the patient’s adherence

Pharmacotherapy Care Plan

• The pharmacotherapy care plan is important in order to achieve improved pharmacotherapy
outcomes.
• It is the action plan developed from assessment of patient described above
• Each item in the patient’s problem list must be addressed in the care plan, and the care plan
should be prioritized in the same way as the problem list.
• The pharmacotherapy care plan has several key components for each problem:
o Current drug regimen
o Drug therapy problems
o Therapy goals, desired endpoints
▪ The goals of therapy must be achievable and realistic for the patient.
▪ Drug therapy may aim to
• cure a disease;
• reduce or eliminate signs and/or symptoms
• slow or halt the progression of a disease
• prevent a disease
• normalize laboratory values and/or
• assist in the diagnostic process
• Therapeutic recommendations
• Rationale
• Therapeutic alternatives
• Monitoring

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 3
 o Monitoring helps in determining whether treatment goals and endpoints (achieving
positive goals and avoiding negative endpoints) are being reached.
o An effective monitoring plan must be realistic for the patient setting and include
▪ specific monitoring parameters (clinical and laboratory/diagnostic test)
▪ frequency of monitoring, and
▪ When the patient needs to be seen again for follow-up.
• Patient education

Evaluation
• The patient care process involves continuous follow-up.
• As the pharmacotherapy care plan is implemented, the patient’s response to therapy
is monitored, and changes in therapy may be necessary.
• Changes in previous problems or the development of new signs and symptoms will require
the assessment process and changes in the pharmacotherapy care plan
• During the Pharmacotherapy process, it is important to consider/review the following
factors for optimal therapeutic outcome;
o Patient Dermographics—name, age, etc.
o Chief Complaint—why the patient is seeking help, in the patient’s own words
o History of Present Illness (HPI)—the patient’s story about why they are seeking help
o Past Medical History (PMH)—including all significant illnesses, surgical procedures,
injuries
o Family History—age and health of immediate family (parents, siblings, children); for
deceased relatives, the age and cause of death are included; any hereditary diseases
should be noted
o Social History—may include where the patient is from or lives, ethnicity/race, marital
status, number of children, educational background, occupation, diet
o Tobacco/Alcohol/Substance Use
o Allergy/Intolerances/Adverse Drug Events (ADEs)—a common area where
information from the patient is missing or incomplete
o Medication History—should include current (or medications prior to admission if
hospitalized) and previous medications; the list should include what the patient actually
is taking, not just what is prescribed, and must include OTC drugs and dietary
supplements (including herbal and complementary/alternative products).
o Signs and symptoms
o Laboratory and Other Diagnostic Tests
o Diagnosis.
o Treatment (Drug) plan
o Follow-up plan

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 4
STEP 4: Importance of Pharmacotherapy (25 minutes)

Activity: Small Group Discussion ( 20 minutes)

DIVIDE students into small manageable groups

ASK students to discuss on the following question

• What is the importance of Pharmacotherapy?

ALLOW students to discuss for 15 minutes

ALLOW few groups to present and the rest to add points not mentioned

CLARIFY and SUMMARIZE by using the contents below:

The following are the importance of Pharmacotherapy;

• Helps in optimization of drug treatment in complex pharmacotherapy patients such as;
o Patients with multiple medications
o Patients with multiple disease states or conditions
o Patients on narrow therapeutic index medications
o Patients on medications requiring laboratory monitoring
o Helps in optimization of drug therapy in patients with high risk for loss of continuity
of care such as;
o Patients with multiple prescribers
o Patients with recent transitions of care (e.g., hospital discharge, rehabilitation, skilled
nursing facility discharge)
• Helps in reduction of medication nonadherence especially in patients with;
o Irregular refill history
o History of failure to pick up new prescriptions
o Stockpiling or incorrect pill counts
o Financial burden (e.g., uninsured or underinsured)
o Low health literacy
o Patient’s beliefs indicate resistance to treatment
o High-cost regimens
o Noticeable decline in the health or functionality
• Improves patients-pharmaceutical personnel relationship which is important for better
therapeutic outcome

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 5
STEP 5: Key Points (5 minutes)
• Pharmacotherapy is the therapy that is provided using pharmaceutical
• Pharmacotherapy comprises the safe, applicable, and cost-effective use of pharmaceutical
drugs.
• Steps that are involved in the Pharmacotherapy process which are Patient assessment,
Development of the pharmacotherapy care plan and Evaluation of the impact or results of
the care plan.
• Pharmacotherapy helps in improving quality of patient care through optimal medication
management based on sound pharmacotherapeutic principles.

STEP 6: Evaluation (5 minutes)

• What is pharmacotherapy?
• What are the steps involved in the pharmacotherapy process?
• What is importance of pharmacotherapy?

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 6
References

Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 7
Session 2: Therapeutic Drug Monitoring (TDM)
Total Session Time: 120 minutes

Prerequisites
• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define therapeutic drug monitoring
• List principles and outline concepts of therapeutic drug monitoring
• Outline criteria for therapeutic drug monitoring
• List drugs that qualify for therapeutic drug monotoring
• Explain clinical significance of therapeutic drug monitoring
• List limitations of therapeutic drug monitoring

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Computer and LCD projector

SESSION OVERVIEW

Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Tasks
Principles And Concepts of Therapeutic
2 35 minutes Presentation
Drug Monitoring
Presentation/
3 20 minutes Criteria for Therapeutic Drug Monitoring
Brainstorming
Drugs that Qualify for Therapeutic Drug
4 15 minutes Presentation
Monitoring
Presentation/ Clinical Significance of Therapeutic Drug
5 15 minutes
Buzzing Monitoring
6 20 minutes Presentation Limitations of Therapeutic Drug Monitoring

7 05 minutes Presentation Key Points

8 05 minutes Presentation Evaluation

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 8
SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning tasks (5 minutes)

READ or ASK students to read the learning tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Principles and Concepts of Therapeutic Drug Monitoring

(35 minutes)
• Therapeutic drug monitoring (TDM) is defined as the use of drug concentration
measurements in plasma as an aid to the management of drug therapy for the cure,
alleviation or prevention of disease.
• TDM enables the assessment of the efficacy and safety of a particular medication in a
variety of clinical settings.
• Therapeutic Drug Monitoring aims to individualize therapeutic regimens for optimal
patient benefit and avoid both subtherapeutic and toxic plasma drug concentrations.
o Specifi cally, TDM is a practice applied to a small group of drugs in which there is a
direct relation between plasma drug concentration and pharmacological response
o Therefore, close relationship between the plasma level of the drug and its clinical
effect is essential.
o If such a relationship does not exit TDM is of little value.
o The measurement of plasma level is justified only when the information provided is
of potential therapeutic benefit.
• In summary, TDM process involves the following;
o Administration of a predetermined dose of drug
o Collection of blood samples
o Determination/measurements of blood samples using analytical procedures
o Evaluation of Clinical effect of drug
o Development/Adjustment of dosage regimen
STEP 3: Criteria for Therapeutic Drug Monitoring (20Minutes)
Activity: Brainstorming (5 minutes)

Ask students to brainstorm on the following question:

• What are the criteria for therapeutic drug monitoring?

ALLOW few students to respond

WRITE their responses on the flip chart/ board

CLARIFY and SUMMARISE by using the content below

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator
Guide 9
• The drug in question has a narrow therapeutic range, eg: Lithium, phenytoin, and digoxin
• A direct relationship exists between the drug or drug metabolite levels in plasma and the
pharmacological or toxic effects,
• The therapeutic effect can not be readily assessed by the clinical observation,
• Large individual variability in steady state plasma concentration exits at any given dose
• Appropriate analytic techniques are available to determine the drug and metabolite levels
• Drugs for which relationship between dose and plasma concentration is unpredictable, e.g
Phenytoin
• Non compliance
• Therapeutic failure
• Major organ failure
• Prevention of adverse drug effects

STEP 4: Drugs that qualify for Therapeutic Drug Monitoring (15 Minutes)
The following are drugs that qualifies for TDM
• Cardio active drugs
o amiodarone,
o digoxin,
o digitoxin
o disopyramide,
o lignocaine,
o procainamide,
o propranolol and
o quinidine
• Aminoglycoside
o gentamycin,
o amikacin
o tobramycin

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 10
 Fig 2.1:
Summary of
TDM Process
o

• Antidepressants:
o lithium
o tricyclic antidepressants
• Antiepileptic drugs
o Phenytoin,
o phenobarbitone
o benzodiazepines,
o carbamazepine,
o Valproic acid and
o ethosuximide
• Bronchodilators :
o theophylline
• Anti Cancer
o methotrexate

STEP 5:Clinical Significance of Therapeutic Drug Monitoring (15 minutes)

Activity: Buzzing (5 minutes)

ASK students to pair up and buzz on the following question for 2 minutes

• What is Clinical Significance of therapeutic drug monitoring?

ALLOW few pairs to respond and let other pairs add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZE by using the content below

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator
Guide 11
• Drug levels from TDM are used in conjunction with other clinical data to assist
practitioners in determining how a patient is responding.
• Drug levels provide a basis for individualizing patient dosage regimens.
• Drug levels assist in determining if a change in patient-specific pharmacokinetics has
occurred during a course of treatment, whether as a result of a change in physiological
state, a change in diet, or addition of other drugs.
• Maximizes drug efficacy
• Helps in avoidance of drug toxicity
• Identifies therapeutic failure due to subtherapeutic level
• May help to identifies patients who are non compliant

STEP 6: Limitation of Therapeutic Drug Monitoring (20Minutes)

• There may be some factors that may lead to incorrect interpretation of plasma drug levels
such as;
o Non-compliance of patient leading to low plasma drug levels
o Low dose administered which leads to subtharapapeutic concentrations
o Patient suffer from mal-absorption
o Drug with low bioavailability may also lead to subtherapeutic concentrations
o Concomitant drugs that could affect the plasma levels of the drug in question
o Hepatic or renal dysfunction
o Diseases related to genetic factors affecting drug metabolism
o .Time of administration of the drug is not accurate.
o Dose administration error.
o Inaccurate time of sampling, or timing was before steady-state is reached
o Wrong site of sampling.
o Lab assay error.

• Effect of age
o There is a great variability in response to drugs at extremes of age.
o As an example, elderly patients are more sensitive to the CNS depressant effect of drugs
but are less sensitive to cardiovascular effects of Propranolol.
o It is well known that children are more sensitive to morphine.

• Pregnancy
o Many drugs can be affected by pregnancy state.
o As an example, drug levels of phenytoin and phenobarbitone are lower during
pregnancy

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 12
STEP 7: Key Points (5 minutes)
• TDM is a very important and widely used technique throughout the treatment process.
• TDM is used when there is a sufficient relationship between the plasma level of the drug
and its clinical effect

STEP 8: Evaluation (5 minutes)

• What is therapeutic drug monitoring?
• What are steps involved during therapeutic drug monitoring?
• What are criteria for therapeutic drug monitoring
• What the clinical significance of therapeutic drug monitoring?

References

Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.

DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 13
Session 3: Pharmacotherapy of Malaria
Total Session Time: 120 minutes

Prerequisites
• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define malaria
• Explain pathophysiology of malaria
• Explain the clinical presentation of malaria
• Outline diagnosis of malaria
• Describe pharmacological treatment of malaria
• Describe monitoring malaria therapy

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Computer/LCD projector

SESSION OVERVIEW

Activity/
Step Time Content
Method

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 14
 1 05 minutes Presentation Introduction, Learning Tasks
15 minutes Presentation Disease status of Malaria
2
Buzzing
3 20 minutes Presentation Pathophysiology of Malaria

15 minutes Presentation Clinical Presentation of Malaria

4

5 05 minutes Presentation Diagnosis of Malaria

30 minutes Presentation Pharmacological Treatment

6 Small Group
Discussion
20 minutes Presentation Monitoring of Malaria Therapy
7

8 05 minutes Presentation Key Points

9 05 minutes Presentation Evaluation

SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)

READ or ASK students to read the learning Tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of Malaria (15 minutes)

Activity: Buzzing (5 minutes)

ASK students to pair up and buzz on the following question for 2 minutes

• What is the disease status of a patient with malaria?

ALLOW few pairs to respond and let other pairs to add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZE by using the content below

• Uncomplicated malaria: defined as symptomatic malaria without signs of severity or

evidence (clinical or laboratory) of vital organ dysfunction.

o It has the following features; fever, headache, joint pains, malaise, vomiting,
diarrhoea, body ache, body weakness, poor appetite, pallor, enlarged spleen
PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator
Guide 15
• Severe malaria: In a patient with P. falciparum asexual parasitaemia and no other
obvious cause of symptoms the presence of one or more of features listed below classify
the patient as suffering from severe malaria

o It has the following features; prostration/extreme weakness, impaired consciousness,

change of behaviour, convulsions, respiratory distress (due to lactic acidosis and/or
pulmonary oedema), bleeding tendency, jaundice, circulatory collapse, vomiting
everything, inability to drink or breast feed

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 16
STEP 3: Pathophysiology of Malaria (20 minutes)

• The Plasmodium species that infect humans are P. falciparum, P. vivax, P. ovale, P.
malariae and P. knowlesi (rarely). The basic elements of the life cycle are the same for all
Plasmodium sp

• Transmission begins when a female Anopheles mosquito feeds on a person with malaria
and ingests blood containing gametocytes.

• During the following 1 to 2 wk, gametocytes inside the mosquito reproduce sexually and
produce infective sporozoites. When the mosquito feeds on another human, sporozoites
are inoculated and quickly reach the liver and infect hepatocytes.

• The parasites mature into tissue schizonts within hepatocytes. Each schizont produces
10,000 to 30,000 merozoites, which are released into the bloodstream 1 to 3 wk later
when the hepatocyte ruptures.

o Each merozoite can invade an RBC and there transform into a trophozoite

• Trophozoites grow, and most develop into erythrocyte schizonts; schizonts produce
further merozoites, which 48 to 72 h later rupture the RBC and are released in plasma.
• These merozoites then rapidly invade new RBCs, repeating the cycle
• Some trophozoites develop into gametocytes, which are ingested by an Anopheles
mosquito
• They undergo sexual union in the gut of the mosquito, develop into oocysts, and release
infective sporozoites, which migrate to the salivary glands

Fig: 3.1. Plasmodium life cycle

Source: DiPiro JT, et al (2008): Pharmacotherapy: A Pathophysiologic Approach (7th ed)

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 17
STEP 4: Clinical Presentation of Malaria (15 minutes)
Signs and symptoms of uncomplicated Malaria
• Fever
• Headache
• Malaise
• Joint pains
• Vomiting /diarrhoea
• Body ache
• Poor appetite
• Body weakness
• Pallor
• Enlarged spleen

Signs and symptoms of Severe Malaria

• Extreme weakness
• Impaired consciousness
• Change of behaviour ( hallucinations, delusions, agitation, and acute state of confusion)
• Respiratory distress
• Bleeding tendency
• Jaundice
• Circulatory collapse/ shock
• Vomiting everything
• Inability to drink or breastfeed

STEP 5: Diagnosis of Malaria (5 minutes)

• Parasite-based diagnosis is recommended for all patients presenting with signs and
symptoms of malaria.
• The recommended investigations are: malaria microscopy and malaria rapid diagnostic
tests (mRDTs)
• In severe malaria, blood slide (BS) is a recommended malaria test as it quantifies
parasitemia.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 18
STEP 6: Pharmacological Treatment of Malaria (50 minutes)

Activity: Small Group Discussion (15 minutes)

DIVIDE students into small manageable groups

ASK students to discuss on the following question

• What is pharmacological treatment of malaria?

ALLOW students to discuss for 15 minutes

ALLOW few groups to present and the rest to add points not mentioned

CLARIFY and SUMMARIZE by using the contents below

Management of uncomplicated Malaria:

Drug of choice for treatment of uncomplicated malaria is Artemether-Lumefantrine (AL),
which is a fixed formulation of artemether 20mg and lumefantrine 120mg or dispersible
tablets for paediatric use

Dosage regimen of ALU

Source: Tanzania Standard Treatment Guideline-2017

Use of Artemether-lumefantrine (ALu) in Pregnancy

• Presently, Artemisinin compounds cannot be recommended for treatment of malaria in
the first trimester of pregnancy.
• In the first trimester of pregnancy quinine should be used as first line treatment.
• After the first trimester ALu tablets is first line medicine.

Use of Artemether-lumefantrine (ALu) in Lactation

• Due to the long elimination half-life of Lumefantrine (up to 10 days), it is not
recommended in mothers breast-feeding children below 5kgs.
• In this case quinine should be used.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 19
Management of Severe Malaria:
• Parenteral artesunate Dosage: 2.4 mg/kg in body weight. IV or IM given on admission
(time = 0 hour), then at 12 hours and 24 hours for a minimum of 3 injections in 24 hours
regardless of patient’s recovery

• Alternatively; Injectable Artemether should be administered in a dose of 3.2mg/kg body

weight loading dose IM stat then 1.6mg/kg bwt (time= 0 hrs, then 24hrs then 48 hrs)

Table 3.2. Major Antimalarial drugs

Source: Applied Therapeutics: Clinical Use of Drugs by Kode-Kimble (10th Ed)

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 20
STEP 7: Monitoring of Malaria Therapy (50 minutes)

• It is important to monitor Malaria therapy in order to evaluate if it is effective

• Patients can be monitored clinically and/or by using laboratory test to confirm for
absence/presence of malaria parasite in their blood
• A follow-up period after the completion of the Malaria therapy varies according to the
drugs used.
• Follow-up periods longer than 14 days are appropriate for amodiaquine, chloroquine and
SP which is 28 days
• For lumefantrine+artemether is 42 days,
• For mefloquine is 63 days
• This allows drug levels in the blood to fall below the minimum therapeutic threshold.
• Any recrudescence of parasites before this threshold is reached would be due to drug
resistance
• Recrudescence after this threshold is reached is not necessarily related to resistance (even
sensitive parasites could recrudesce if blood drug levels are subtherapeutic).
• Shorter follow-up (i.e. <14 days) will underestimate overall treatment failure rates
• It is also important for patient to report any adverse reaction of the drugs that may occurs
during Malaria therapy.

STEP 8: Key Points (10 minutes)

• P. falciparum causes microvascular obstruction and tissue ischemia, particularly in the

brain, kidneys, lungs, and GI tract of nonimmune infants and adults; patients may die
within days of their initial symptoms.
• P. vivax, P. ovale, and P. malariae typically do not compromise vital organs; mortality is
rare.
• Clinical maanifestations include recurrent fever and rigor, headache, myalgia, and nausea;
hemolytic anemia and splenomegaly are common.
• Treatment with antimalarial drugs is based on the species (if known) and drug resistance
patterns in the area in which infection was acquired
• Artemisinin-based combination therapy (eg, artemether/lumefantrine) is the most rapidly
active therapy and is available worldwide

STEP 9: Evaluation (10 minutes)

• What is the disease status of a patient with Malaria?
• What is the pathophysiology of malaria?
• What is the diagnosis of malaria?
• What parameters can be used to monitor malaria therapy?

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 21
References
Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 22
Session 4: Pharmacotherapy of HIV/AIDS
Total Session Time: 120 minutes

Prerequisites

• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define HIV/AIDS
• Explain pathophysiology of HIV/AIDS
• Explain the clinical presentation of HIV/AIDS
• Outline diagnosis of HIV/AIDS
• Describe pharmacological treatment of HIV/AIDS
• Describe the monitoring of HIV/AIDS Therapy

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Computer and LCD Projector

SESSION OVERVIEW

Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Tasks
10 minutes Presentation Definition of HIV/AIDS
2
Buzzing
3 20 minutes Presentation Pathophysiology of HIV/AIDS

15 minutes Presentation Clinical Presentation of HIV/AIDS

4

5 10 minutes Presentation Diagnosis of HIV/AIDS

30 minutes Presentation Pharmacological Treatment of HIV/AIDS

6 Small Group
Discussion
20 minutes Presentation Monitoring of HIV/AIDS Therapy
7

8 05 minutes Presentation Key Points

9 05 minutes Presentation Evaluation

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 23
SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)

READ or ASK students to read the learning Tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of HIV/AIDS (10 minutes)

Activity: Buzzing (5 minutes)

ASK students to pair up and buzz on the following question for 2 minutes

• What is HIV/AIDS?
ALLOW few pairs to respond and let other pairs to add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZEby using the content below

• AIDs is a set of symptoms (or syndrome) caused by Human Immunodeficiency Virus

(HIV). The clinical features may be due to HIV per se or as a result of immune system
destruction.
• It has the following features:
o Fever, diarrhoea, weight loss, skin rashes, sores, generalized pruritis, altered mental
status, persistent severe headache, oral thrush or Kaposi’s sarcoma may be found in
patients with advanced disease

o Most patients, however, present with symptoms due to opportunistic infections such
as tuberculosis, candidiasis and pyogenic infections
Fig 4.1 Human Immunodeficiency Virus

Source: DiPiro JT, et al (2008): Pharmacotherapy: A Pathophysiologic Approach (7th ed)

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 24
STEP 3: Pathophysiology of HIV/AIDS (20 minutes)

• The virus through its envelope proteins attaches to the CD4 receptor and co-receptors
found on the surface of T lymphocytes and macrophage to gain entry to the host cells.
• Following entry of the HIV into a susceptible host cell using the enzyme reverse
transcriptase, the viral genome copies itself from RNA to DNA genetic material.
• The viral DNA copy enters the nucleus of the host cell and becomes intimately
incorporated into the host cell’s own DNA using the enzyme integrase.
• The virus thus becomes a permanent part of an infected person’s nuclear proteins.
• There follows a latent period during which the provirus in the infected nucleus waits for
an external stimulus to start reproducing.
• CD4+ T lymphocytes, when stimulated by new HIV, other infections and infestations
which would normally result in the CD4+ T lymphocyte reproducing itself, now responds
to these stimuli by manufacturing HIV.
• As more and more viruses are produced and leave the host cell, the cell membrane
weakens leading eventually to the death of the infected CD4+ T lymphocytes

• The multiple steps in replication of HIV provide multiple opportunities for intervention.
• Therapeutic regimens may be directed at one or several of the following stages essential
for viral replication:
o Attachment of HIV to the host cell;
o Reverse transcription of viral RNA to DNA;
o Integration of the pro-viral DNA into the host cells’ DNA; or
o Expression of the viral gene after it has been integrated into host cell DNA, including
the transcription of more viral RNA and the translation of viral proteins.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 25
STEP 4: Clinical Presentation of HIV/AIDS (15 minutes)
• In the absence of ART, disease progression goes through the following clinical stages

o Primary Infection or becoming HIV Infected

▪ Most primary infection, i.e. new infection with HIV, usually is not immediately
noticed.
▪ It presents with short illnesses and flu-like symptoms such as fever, malaise,
enlarged lymph nodes, sore throat, skin rash, and/or joint pain soon after being
infected.
▪ It may last for a few weeks.
▪ This acute febrile illness is accompanied by widespread dissemination of the virus
to different tissues, especially the lymphoid system. This is called sero-conversion
illness.

o Clinically Asymptomatic Stage

▪ This stage is free of symptoms, except for the possibility of swollen glands:
persistent generalized lymphadenopathy - Persistent Generalized
Lymphadenopathy (PGL).
▪ However, this is the stage where there is ongoing extensive immunologic
fighting/changes and rapid viral replication begins.
▪ This may last for an average of eight to ten years.
▪ However, disease progression in children and elderly is faster due to high set
point.
▪ This is WHO Stage1

o Symptomatic HIV

▪ Over time, the immune system loses the struggle to contain HIV, resulting in
extensive destruction of CD4 cells
▪ This is characterised by the occurrence of opportunistic infections (OIs), which is
when) symptoms develop
▪ The most common symptoms include fever, respiratory infections, cough, TB
tuberculosis, weight loss, skin diseases, viral infections, oral thrush, pain, and
lymphadenopathy
▪ This is WHO Stage 2 or 3, depending on the particular OI seen

o Acquired Immune Deficiency Syndrome (AIDS)

▪ AIDS is defined as a point when a person with HIV develops severe

immunosuppression, OIs, or malignancies/cancers.
▪ Such conditions are: severe weight loss, Kaposi’s sarcoma, Cryptococcus
meningitis, PCP, toxoplasmosis, CMV (Cytomegalovirus) retinitis, etc.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 26
 ▪ This is WHO Stage 4

STEP 5: Diagnosis of HIV/AIDS (10 minutes)

• The common tests for diagnosing HIV/AIDs include:
o ELISA Test — ELISA, which stands for enzyme-linked immunosorbent assay, is
used to detect HIV infection (detects antibodies against HIV-1)and is both highly
sensitive and specific
▪ If an ELISA test is positive, the Western blot test is usually administered to
confirm the diagnosis. If an ELISA test is negative, but you think you may have
HIV, you should be tested again in one to three months
▪ ELISA is quite sensitive in chronic HIV infection, but because antibodies aren't
produced immediately upon infection, you may test negative during a window of a
few weeks to a few months after being infected.
o Viral Load Test — This test measures the amount of HIV in your blood. It quantifies
viremia by measuring the amount of viral RNA. Generally, it's used to monitor
treatment progress or detect early HIV infection. Three technologies measure HIV
viral load in the blood: reverse transcription polymerase chain reaction (RT-PCR),
branched DNA (bDNA) and nucleic acid sequence-based amplification assay
(NASBA). The basic principles of these tests are similar. HIV is detected using DNA
sequences that bind specifically to those in the virus
o Western Blot — This is a very sensitive blood test used to confirm a positive ELISA
test result

Fig: 4.2 Tanzania National HIV Rapid Testing Algorithm for Adults and Children over 18 Months

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 27
Source: National Guideline for the Management of HIV and AIDS 2015

STEP 5: Pharmacological Treatment of HIV/AIDS (30 minutes)

Activity: Small Group Discussion ( 15 minutes)

DIVIDE students into small manageable groups

ASK students to discuss on the following question

• What explanations can you give on monitoring therapy for HIV/AIDS?

ALLOW students to discuss for 15 minutes

ALLOW few groups to present and the rest to add points not mentioned

CLARIFY and SUMMARIZE by using the contents below

• Early initiation of combination treatment (ART) is associated with health benefits in

terms of reduced morbidity and mortality in all age groups.
• In addition, ART is effective for preventing HIV transmission.
• It also helps to drastically reduce TB incidences.
• Therefore, all patients diagnosed with HIV should be initiated ART regardless of CD4
cell count and clinical stage
• The most effective means to accomplish durable suppression of HIV replication is the
simultaneous initiation of combinations of effective anti HIV drugs with which the patient
has not been previously treated and that are not cross resistant with antiretroviral agents
with which the patient has been treated previously
• Each of the antiretroviral drugs used in combination therapy regimens should always be
used according to optimum schedules and dosages

Antiretroviral Agents
• The recommended antiretroviral drugs to be used fall into the following main categories:
o Nucleotide reverse transcriptase inhibitors (NRTIs)
o Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
o Protease inhibitors (Pls)
o Integrase strand transfer inhibitors (INSTI)/ Integrase inhibitors
o Fusion inhibitors
o Chemokine receptor inhibitors/CCR5 inhibitors

First Line ART

Triple therapy consisting of 2 NRTI + 1 NNRTI

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 28
Recommended first-line regimens for adults and adolescents

Source: National Guideline for the Management of HIV and AIDS 2015

NOTE:
• Clients on TDF/3TC/EFV600 can be switched to TDF/3TC/ EFV400 (when available) to
reduce CNS related toxicity with exception of Pregnant women and TB-HIV Co-infected
patients
• TDF 300mg based regimens should not be initiated on patients with weight less than
35kg.
• EFV400 based regimens should not be initiated on patients with weight below 20Kg

Second-line Antiretroviral Therapy in Adults and Adolescents

• Treatment failure will be based on virological criteria of more than 1000copies /ml after
two successive tests, at least three months apart with assurance of good adherence, in
areas where there is access to routine viral load monitoring.
• Drugs used as the second line in Tanzania include

• NRTIs/NtRIs
o Zidovudine (AZT)
o Tenofovir (TDF)
o Abacavir (ABC)
o Lamivudine (3TC)
o Emtricitabine (FTC)

• PIs
o Atazanavir boosted by Ritonavir (ATV/r)
o Lopinavir boosted by Ritonavir (LPV/r)

• INSTIs
o Dolutegravir (DTG)

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 29
Source: National Guideline for the Management of HIV and AIDS 2015

• The second line NRTI choice for adults and adolescents depends on the first line regimen
• For patients on TDF based regimens in first line, the preferred second line option is AZT
plus 3TC combined with a ritonavir-boosted PI, preferably ATV/r because it is dosed
once daily and has fewer metabolic complications and side effects

Third-Line Art Treatment

• Patients failing 2nd line regimens may have extensive NRTI and NNRTIs associated
resistance mutations (RAMS) which preclude/minimise their use in third-line regimens.
• Therefore, 3rd line regimens, in order to have at least two or preferably three effective
drugs, need to be constructed using other new classes of drugs or second generation
formulations of previous drugs
• These second generation drugs usually have a higher genetic barrier to resistance and
their efficacy is not compromised by RAMs associated with the first generation
formulations. Therefore, the following are used:
o Integrase Inhibitors: Dolutegravir 50mg (DTG) and Raltegravir 400mg (RAL),
o Second generation PIs: Darunavir 800mg /Ritonavir 100mg (DRV/r)
o Second generation NNRTI: Etravirine 200g (ETV)

STEP 6: Monitoring of Antiretroviral Therapy (20 minutes)

• Tests for Monitoring responses to Antiretroviral treatment and diagnosis of treatment
failure/toxicity are important
• Clinical assessment and laboratory tests play a key role in assessing individuals before ART
is initiated, monitoring treatment response and possible toxicity of ARV drugs.
• The following laboratory tests are recommended:
o HIV Viral Load test is a preferred monitoring approach to diagnose and confirm early
treatment failure.
▪ HVL for adults and adolescents should be done 6 months after initiation of ART
▪ Successful antiretroviral therapy result in decrease of HIV viral load, immune
recovery and therefore increase in number of CD4 cells.

o CD4 T lymphocytes count should also be done at baseline for all clients.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 30
 ▪ CD4 cells progressively decrease as HIV advances and immune status
deteriorates. Measurements of CD4 cells counts are important immunological
markers of the disease progression.
▪ CD4 cells counts are reported in percentage (%).
▪ CD4 testing will be measured as a baseline test and for suspected treatment failure
for those clients on ART

Fig 4.3 Monitoring of CD4 Count

Source: National Guideline for the Management of HIV and AIDS 2015

o A complete blood count (If not available, conduct hemoglobin test for patients on
AZT based regimens)
o Urinalysis to exclude proteinuria (HIV associated nephropathy or HIVAN) and
glycosuria (Diabetes Mellitus).
o Tests to rule out active TB (sputum AFB, GeneXpert, CXR) in cases where there is
suspected TB from the screening tool
o Urine pregnancy test (to women of reproductive age) in order to identify PLHIV
requiring EFV 600mg.
o Liver function tests (serum alanine aminotransferase, ALT) if on anti-TB drugs or
requiring NVP based treatment
o Renal function tests (serum creatinine, blood urea nitrogen (BUN)) for patients
requiring TDF based regimens
o Lipids test (for clients requiring PIs)

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 31
STEP 6: Key Points (5 minutes)
• HIV/AIDs is a set of symptoms (or syndrome) caused by Human Immunodeficiency
Virus (HIV)
• HIV is commonly transmitted via unprotected sexual activity, blood transfusions,
hypodermic needles, and from mother to child.
• Upon acquisition of the virus, the virus replicates inside and kills T helper cells, which
are required for almost all adaptive immune responses.
• Diagnosis of HIV/AIDS is commonly done by ELISA, Viral load and Western blot tests
• Treatment of HIV/AIDS is initiated regarless of CD4 count
• Varieties of tests are done in order to monitor ART therapy

STEP 7: Evaluation (5 minutes)

• What is the disease status of a patient with HIV/AIDS?
• What is the pathophysiology of HIV/AIDS?
• What is the diagnosis of HIV/AIDS?
• What are the first line treatment regimes for HIV/AIDS?
• What laboratory tests are used to monitor ART?

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 32
References
Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 33
Session 5: Pharmacotherapy of Tuberculosis
Total Session Time: 120 minutes

Prerequisites

• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define tuberculosis
• Explain pathophysiology of tuberculosis
• Explain the clinical presentation of tuberculosis
• Outline diagnosis of tuberculosis
• Describe pharmacological treatment of tuberculosis
• Describe monitoring of tuberculosis therapy

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Computer and LCD Projector

SESSION OVERVIEW

Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Tasks
10 minutes Presentation Definition of Tuberculosis
2
Buzzing
3 20 minutes Presentation Pathophysiology of Tuberculosis

4 20 minutes Presentation Diagnosis of Tuberculosis

30 minutes Presentation Pharmacological Treatment of Tuberculosis

5 Small Group
Discussion
25 minutes Presentation Monitoring of Tuberculosis Therapy
6

7 05 minutes Presentation Key Points

8 05 minutes Presentation Evaluation

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 34
SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)

READ or ASK students to read the learning Tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of Tuberculosis (10 minutes)

• Tuberculosis (TB) is a chronic infectious disease caused mainly by Mycobacterium
tuberculosis (M. tuberculosis) and occasionally by Mycobacterium bovis or
Mycobacterium africanum
• These micro-organisms are also known as acid-fast bacilli (AFB) because of their staining
characteristics
• TB is transmitted from one person to another through inhalation of droplets during;
o Coughing which is the most common means of transmission
o Laughing
o talking,
o Sneezing, and singing
• Untreated smear-positive patients who are in the community are the potential source of
infection.
• The concentration of infected droplets in the air and the length of time a person breathes
that air determines an individual’s risk of exposure.
• TB can be grouped into two main types: pulmonary and extra-pulmonary.
• The most common form is pulmonary tuberculosis (PTB), which accounts for 80% of all
cases of TB.
o PTB is infectious, and affects the lungs.
• Extra-pulmonary tuberculosis (EPTB) affects organs other than the lungs, and is non-
infectious.
o EPTB accounts for 20% of all cases of TB.

STEP 3: Pathophysiology of Tuberculosis (20 minutes)

Activity: Buzzing (5 minutes)

ASK students to pair up and buzz on the following question for 2 minutes

• What is the pathophysiology of Tuberculosis?

ALLOW few pairs to respond and let other pairs to add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZEby using the content below

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 35
• Infection occurs when a person inhales droplet nuclei containing tubercle bacilli that
reach the alveoli of the lungs.
• These tubercle bacilli are ingested by alveolar macrophages; the majority of these bacilli
are destroyed or inhibited.
• A small number may multiply intracellularly and are released when the macrophages die.
• If alive, these bacilli may spread by way of lymphatic channels or through the
bloodstream to more distant tissues and organs (including areas of the body in which TB
disease is most likely to develop: regional lymph nodes, apex of the lung, kidneys, brain,
and bone)
• This process of dissemination primes the immune system for a systemic response
• Within 2 to 8 weeks, special immune cells called macrophages ingest and surround the
tubercle bacilli. The cells form a barrier shell, called a granuloma, that keeps the bacilli
contained and under control
• If the immune system cannot keep the tubercle bacilli under control, the bacilli begin to
multiply rapidly (TB disease).
• This process can occur in different areas in the body, such as the lungs, kidneys, brain, or
bone

STEP 4: Diagnosis of Tuberculosis (20 minutes)

Clinical Diagnosis
Clinical diagnosis of TB involves a careful and extensive history-taking, which includes
asking the patient questions relative to symptoms suggestive of TB disease:
• Prolonged fever, cough (with or without haemoptysis),
• Anorexia,
• Weight loss
• Haemoptysis - Cough out blood (once or recurrent)
• Cough (dry/productive sputum)
• Fatigue
• Night sweats

Laboratory diagnosis
• Early identification of TB cases and putting them on effective treatment is important in
TB care and control.
• Diagnosis of PTB depends on the identification of tubercle bacilli either by sputum smear
microscopy or culture and identification of bacterial DNA using molecular techniques
• There are two common methods for the detection of AFB in clinical specimens:
o The Ziehl-Neelsen (ZN) technique using bright field microscopes, and
o The Auramine O technique using light-emitting diode fluorescence microscope (LED
FM)
• Chest x-ray may be very useful as a screening tool for PTB.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 36
STEP 5: Pharmacological Treatment of Pulmonary Tuberculosis (30
minutes)

Activity: Small Group Discussion ( 15 minutes)

DIVIDE students into small manageable groups

ASK students to discuss on the following question

• What is the first line treatment of Pulmonary Tuberculosis?

ALLOW students to discuss for 15 minutes

ALLOW few groups to present and the rest to add points not mentioned

CLARIFY and SUMMARIZE by using the contents below

Specifically, TB treatment aims to:

• Cure the patient and restore quality of life and productivity.
• Prevent relapse of TB.
• Reduce transmission of TB to others.
• Prevent the development and transmission of drug-resistant tubercle bacilli.
• Prevent death from active TB or its late effects.

Recommended daily doses of first-line anti-TB drugs

New
Initial phase; Rifampicin + Isoniazid + Pyrazinamide and Ethambutol in fixed dose (RHZE)
for 2 months
Continuation phase; Rifampicin + Isoniazid (RH) for 4 months

Retreatments
Initial phase; Streptomycin+ Rifampicin + Isoniazid + Pyrazinamide and Ethambutol for
2months then RHZE for 1months
Continuation phase; Rifampicin + Isoniazid+ Ethambutol (RHE) for 5 months

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 37
Table 5.1 Recommended Anti-TB daily doses in Adults

Source: Manual for the Management of Tuberculosis and Leprosy (6th ed) National Tuberculosis and Lepros y
Programme, Ministry of Health and Social Welfare

The following shall be considered in treatment of TB patients:

• The most serious problem with TB therapy is nonadherence to the prescribed regimen.
The most effective way to ensure adherence is with directly observed therapy (DOT)
• The oral drugs should preferably be given on an empty stomach in a fixed dose
combination

Treatment of Tuberculosis in Special Cases

Consideration is needed when handling a patient with TB/HIV co-infection;
• Start ART for all TB patients living with HIV irrespective of CD4 counts; Treat TB first
and start ART as soon as possible, preferably within two weeks of initiating treatment
• If CD4 count is less than 50 cells/mm3; Treat TB first and start ART within the first two
weeks of initiating TB treatment
• Already on ART at TB diagnosis; Treat TB and replace nevirapine with efavirenz

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 38
Table 5.2. Adverse drug rections of Anti-TB drugs and their Management

Source: Manual for the Management of Tuberculosis and Leprosy (6th ed) National Tuberculosis and Lepros y
Programme, Ministry of Health and Social Welfare

STEP 6: Monitoring of Anti-tuberculosis Therapy (25 minutes)

• For each patient with newly diagnosed TB disease, a specific treatment and monitoring
plan should be developed in collaboration with the local TB control program within 1
week of the presumptive diagnosis.
• This plan should include:
o Description of the TB treatment regimen
o Methods of assessing and ensuring adherence to the TB treatment regimen;
o Methods to monitor for adverse reactions; and
o Methods for evaluating treatment response.
• A number of measures are monitored to determine response to treatment.
• These can broadly be divided into clinical and microbiological markers.
• Physical signs of tuberculosis treatment success include:
o A reduction in symptoms, such as less coughing
o Overall improvement in the way one feels
o Weight gain
o Increased appetite
o Improvement in strength and stamina

• Laboratory Tests to Monitor Tuberculosis Treatment

o Lab tests including Sputum tests are performed during tuberculosis treatment to
determine if any TB bacteria are left in the TB patient.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

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STEP 7: Key Points (5 minutes)
• Tuberculosis is one of the world’s most widespread and deadly illnesses
• Mycobacteria tuberculosis is the organism that causes tuberculosis infection and disease
• The patient with pulmonary tuberculosis typically presents with slowly progressive
constitutional symptoms of malaise, anorexia, weight loss, fever, and night sweats
• Diagnosis is done by Sputum- smears microscopy, Culture and sensitivity tests and Chest
x-ray
• Main medicines that are used for treatment are Steptomycin, Rifampicin, Isoniazid,
Pyrazinamide and Ethambutol (SRHZE respectively)

STEP 7: Evaluation (5 minutes)

• What is Tuberculosis?
• What is the pathophysiology of TB?
• How is TB diagnosed?
• How is the first line treatment of Tuberculosis?

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 40
References

Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 41
Session 6: Pharmacotherapy of Leprosy
Total Session Time: 120 minutes

Prerequisites

• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define leprosy
• Explain pathophysiology of leprosy
• Explain the clinical presentation of leprosy
• Outline diagnosis of leprosy
• Describe pharmacological treatment of leprosy
• Describe monitoring of leprosy therapy

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Computer and LCD Projector

SESSION OVERVIEW

Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Tasks
10 minutes Presentation Definition of Leprosy
2
Buzzing
3 20 minutes Presentation Pathophysiology of Leprosy

20 minutes Presentation Clinical Presenation and Diagnosis of

4
Leprosy
35 minutes Presentation Pharmacological Treatment of Leprosy
5 Small Group
Discussion
20 minutes Presentation Monitoring of Leprosy
6

7 05 minutes Presentation Key Points

8 05 minutes Presentation Evaluation

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 42
SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)

READ or ASK students to read the learning Tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of Leprosy (10 minutes)

Activity: Buzzing (2 minutes)

ASK students to pair up and buzz on the following question for 2 minutes

• What is Leprosy?
ALLOW few pairs to respond and let other pairs to add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZEby using the content below

Definition
• Leprosy is a chronic infectious disease caused by Mycobacterium leprae (M. leprae).
• It mainly affects the skin, peripheral nerves, and mucous membranes.
• It is a disease mainly of human beings, which affects people of all races, all ages, and both
sexes.
• Similar to TB, leprosy bacilli are mainly transmitted through infectious droplets that are
spread by an infectious individual through coughing and sneezing.
• Patients carrying many leprosy bacilli are called multibacillary (MB) patients.
• They are the main source of infection.
• People may carry the bacilli but not develop the disease.
• These people, called healthy carriers, are also probably able to transmit the bacilli to
others.
• Individuals with few bacilli in their body are called paucibacillary (PB).
• Like healthy carriers, they are not a significant source of infection.

STEP 3: Pathophysiology of Leprosy (20 minutes)

• Onset of leprosy is insidious.
• The disease affects nerves, skin and eyes.
o It may also affect mucosa (mouth, nose, pharynx), testes, kidney, voluntary/smooth
muscles, reticulo-endothelial system, and vascular endothelium.
• Bacilli enter the body usually through respiratory system.
PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator
Guide 43
• It has low pathogencity, only a small proportion of infected people develop signs of the
disease.
• Though infected, majority of the population do not develop the disease.
• After entering the body, bacilli migrate towards the neural tissue and enter the Schwann
cells. Bacteria can also be found in, macrophages, muscle cells and endothelial cells of
blood vessels. After entering the Schwann cells /macrophage; fate of the bacterium depends
on the resistance of the infected individual towards the infecting organism.
• Bacilli start multiplying slowly (about 12-14 days for one bacterium to divide into two)
within the cells, get liberated from the destroyed cells and enter other unaffected cells.
• Till this stage person remains free from signs and symptoms of leprosy.
• As the bacilli multiply, bacterial load increases in the body and infection is recognized by
the immunological system.
• Lymphocytes and histiocytes (macrophages) invade the infected tissue.
• At this stage clinical manifestation may appear as involvement of nerves with impairment
of sensation &/ or skin patch.
• If it is not diagnosed and treated in the early stages, further progress of the diseases is
determined by the strength of the patient’s immune response
• Specific and effective cell mediated immunity (CMI) provides protection to a person
against leprosy.
• When specific CMI is effective in eliminating/ controlling the infection in the body, lesions
heal spontaneously or it produces pauci-bacillary (PB) type of leprosy.
• If CMI is deficient; the disease spreads uncontrolled and produces multi bacillary (MB)
leprosy with multiple system involvement.
• Some times, the immune response is abruptly altered, either following treatment (MDT) or
due to improvement of immunological status, which results in - 12 - the inflammation of
skin or / and nerves and even others tissue, called as leprosy reaction

STEP 4: Clinical Presentation and Diagnosis of Leprosy (20 minutes)

The diagnosis of leprosy
The diagnosis of leprosy relies on both passive and active case-finding.
Clinical diagnosis.
This is achieved through observation of signs or symptoms of leprosy which includes;
• One or more pale or reddish, hypo-pigmented patch(es) on the skin with diminished or loss
of sensation.
• Painless swelling or lumps in the face and/or earlobes.
• Enlarged and/or tender nerves.
• Burning sensation of the skin.
• Numbness or tingling of hands and/or feet.
• Weakness of eyelids, hands, and/or feet.
• Painless wounds or burns on the hands and/or feet.
Examination of other organs:

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 44
• Leprosy can affect a few organs other than skin and peripheral nerves.
• Depending on the duration of the disease and the spread of leprosy through the body,
various other organs may show signs typical for leprosy
STEP 5: Pharmacological Treatment of Leprosy (35 minutes)

Activity: Small Group Discussion ( 20 minutes)

DIVIDE students into small manageable groups

ASK students to discuss on the following question

• What is the first line treatment of Leprosy?

ALLOW students to discuss for 15 minutes

ALLOW few groups to present and the rest to add points not mentioned

CLARIFY and SUMMARIZE by using the contents below

Treatment regimens
The drugs and dosages for PB and MB for both adults and children are shown below:

Adults (MB)
Monthly treatment: Day 1
Rifampicin 600 mg (2 x 300 mg)
Clofazimine 300 mg (3 x 100 mg)
Dapsone 100 mg
Daily treatment: Days 2–28
Clofazimine 50 mg
Dapsone 100 mg

Duration of treatment
12 blister packs (Figure 13) to be taken within a period of 12-18 months.

Children 10-14 years (MB)

Monthly treatment: Day 1
Rifampicin 450 mg (3 x 150 mg)
Clofazimine 150 mg (3 x 50 mg)
Dapsone 50 mg
Daily treatment: Days 2–28
Clofazimine 50 mg every other day
Dapsone 50 mg daily
Duration of treatment
PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator
Guide 45
12 blister packs to be taken within a period of 12-18 months.
Adults (PB)
Monthly treatment: Day 1
Rifampicin 600 mg (2 x 300 mg)
Dapsone 100 mg
Daily treatment: Days 2–28
Dapsone 100 mg
Duration of treatment
Six blister packs (Figure 14) to be taken within a period of 6–9 months.

Children 10-14 years (PB)

Monthly treatment: Day 1
Rifampicin 450 mg (3 x 150 mg)
Dapsone 50 mg
Daily Treatment: Days 2–28
Dapsone 50 mg
Duration of treatment
Six blister packs to be taken within a period of 6–9 months.
Note: Adjust the dose appropriately for a child (PB) younger than 10 years. For example,
dapsone 25 mg daily and rifampicin 300 mg given once a month under supervision.

Source: Manual for the Management of Tuberculosis and Leprosy (6th ed) National Tuberculosis and Lepros y
Programme, Ministry of Health and Social Welfare

STEP 6: Monitoring of Leprosy Therapy (20 minutes)

Treatment monitoring
• MDT should be provided to the patient as close to the patient’s home as possible
PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator
Guide 46
• Based on the geographic distribution of health facilities, the availability of trained staff,
and the patient’s wish, the health worker and/or DTLC decides where MDT should be
delivered. In principle, every health facility should be able to provide MDT
• Staff need to be trained on leprosy management as described in the NTLP training manual
for health workers
• Patients should have access to treatment on any day immediately after finishing the blister
pack, but they should be given an appointment to attend a fixed clinic day in order to be
reviewed and assessed by a trained health worker or DTLC
• The trained health worker or DTLC should arrange leprosy clinics everythree months
• The DTLC, in collaboration with the district pharmacist, is responsible for the supply of
MDT drugs and drugs for treating reactions
• There should always be a minimum of three blister packs in stock for every patient
attending the clinic at any given time
• Under normal circumstances patients should not be given more than a one-month drug
supply (one blister pack)
• Those patients who cannot come on monthly basis to a health facility due to problems such
as long distance, impassable roads during the rainy season, nomadic lifestyle, etc., may be
given drugs for more than one month, sufficient to cover the expected period of absence
• Under exceptional circumstances, a full course supply can be given
• When patients are given more than a one-month supply, it is better to involve a formal or
informal community leader or relative who will then be oriented to support the patient to
complete the full course of treatment (accompanied MDT)
• Each time a patient comes to a health facility to collect an MDT blister pack, a health
worker should ask the patient about new complaints regarding nerve function impairment.
• If there are any complaints, the health worker should conduct nerve function tests to assess
for damage
• If there are indications of nerve damage, the patient should be managed appropriately
• In case of uncertainty, the health worker should refer the patient to the DTLC
• The health staff is also responsible for tracing a patient who does not attend for two
consecutive months
• When the patient is found, s/he should be persuaded to continue with treatment (see
defaulter management)

STEP 7: Key Points (5 minutes)

• Leprosy is caused by a slow-growing type of bacteria called Mycobacterium leprae (M.
leprae)
• The disease mainly affects the skin, the peripheral nerves, mucosal surfaces of the upper
respiratory tract and the eyes.
• The main symptom of leprosy is disfiguring skin sores, lumps, or bumps that do not go away
after several weeks or months. The skin sores are pale-colored.
• The disease was transmitted by contact between cases of leprosy and healthy persons.
• Leprosy is curable with a combination of drugs known as multidrug therapy (MDT)
PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator
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STEP 7: Evaluation (5 minutes)
• What is Leprosy?
• What are the signs and symptoms of Leprosy?
• What is the pathophysiology of Leprosy?
• What is the treatment of leprosy?

References
PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator
Guide 48
Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 49
Session 7: Pharmacotherapy of Pharyngitis, Sinusitis, and
Otitis Media

Total Session Time: 120 minutes

Prerequisites

• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define pharyngitis, sinusitis, and otitis media
• Explain pathophysiology of pharyngitis, sinusitis, and otitis media
• Explain the clinical presentation of pharyngitis, sinusitis, and otitis media
• Outline diagnosis of pharyngitis, sinusitis, and otitis media
• Describe pharmacological treatment of pharyngitis, sinusitis, and otitis media
• Describe monitoring of pharyngitis, sinusitis, and otitis media therapy

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Computer and LCD Projector

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 50
SESSION OVERVIEW

Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Tasks
10 minutes Presentation Definition of Pharyngitis, Sinusitis, and
2
Buzzing Otitis Media
20 minutes Pathophysiology of Pharyngitis, Sinusitis,
3 Presentation
and Otitis Media
20 minutes Presentation Clinical Presentation and Diagnosis of
4
Pharyngitis, Laryngitis, and Otitis Media
35 minutes Presentation Pharmacological Treatment of Pharyngitis,
5 Small Group Sinusitis, and Otitis Media
Discussion
20 minutes Presentation Monitoring of Pharyngitis, Sinusitis, and
6
Otitis Media Therapy
7 05 minutes Presentation Key Points

8 05 minutes Presentation Evaluation

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 51
SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)

READ or ASK students to read the learning Tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of Pharyngitis, Sinusitis, and Otitis Media (10 minutes)

Activity: Buzzing (5 minutes)

ASK students to pair up and buzz on the following question for 2 minutes

• What is pharyngitis?
ALLOW few pairs to respond and let other pairs to add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZEby using the content below

Pharyngitis
• Pharyngitis is an acute infection of the oropharynx or nasopharynx.
• It is caused by virus and bacteria
• Viruses cause the majority of acute pharyngitis cases
o Specific etiologies include rhinovirus, coronavirus, adenovirus, herpes simplex virus,
influenza virus, parainfluenza virus, and Epstein-Barr virus
• Group A β –hemolytic streptococci (GAS; also known as S. pyogenes ), is the primary
bacterial cause.
o Other, less-common causes of acute pharyngitis are groups C and G Streptococcus,
Corynebacterium diphtheriae, Neisseria gonorrhoeae, Mycoplasma pneumoniae,
Arcanobacterium haemolyticum, Yersinia enterocolitica, and Chlamydia pneumonia

REFER Students to Handout 7.1: Pharmacotherapy of Sinusitis

REFER Students to Handout 7.2: Pharmacotherapy of Otitis Media

STEP 3: Pathophysiology of Pharyngitis (10 minutes)

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator
Guide 52
• The mechanism by which GAS causes pharyngitis is not well defined
• Asymptomatic pharyngeal carriers of the organism may have an alteration in host
immunity (e.g., a breach in the pharyngeal mucosa) and the bacteria of the oropharynx,
allowing colonization to become an infection
• Pathogenic factors associated with the organism itself may also play a role
• These include pyrogenic toxins, hemolysins, streptokinase, and proteinase

STEP 4: Clinical Presentation and Diagnosis of Pharyngitis (20 minutes)

General
• A sore throat of sudden onset that is mostly self-limited
• Fever and constitutional symptoms resolving in about 3 to 5 days
• Clinical signs and symptoms are similar for viral causes and nonstreptococcal bacterial
causes

Signs and Symptoms

• Sore throat
• Pain on swallowing
• Fever
• Headache, nausea, vomiting, and abdominal pain (especially children)
• Erythema/inflammation of the tonsils and pharynx with or without patchy exudates
• Enlarged, tender lymph nodes
• Red swollen uvula, petechiae on the soft palate, and a scarlatiniform rash
• Several symptoms that are not suggestive of group A streptococci are cough,
conjunctivitis, coryza, and diarrhea

Signs Suggestive of Viral Origin for Pharyngitis

• Conjunctivitis
• Coryza
• Cough
• Diarrhea

Laboratory Tests
• Throat swab and culture
• Rapid antigen detection testing (RADT)

STEP 5: Pharmacological Treatment of Pharyngitis (35 minutes)

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator
Guide 53
Activity: Small Group Discussion ( 20 minutes)

DIVIDE students into small manageable groups

ASK students to discuss on the following question

• What is the first line treatment of Pharyngitis?

ALLOW students to discuss for 15 minutes

ALLOW few groups to present and the rest to add points not mentioned

CLARIFY and SUMMARIZE by using the contents below

The goals of treatment for pharyngitis are to;

• Improve clinical signs and symptoms,
• minimize adverse drug reactions,
• prevent transmission to close contacts, and
• prevent acute rheumatic fever and suppurative complications, such as peritonsillar
abscess, cervical lymphadenitis, and mastoiditis

Source: DiPiro JT, et al (2008): Pharmacotherapy: A Pathophysiologic Approach (7th ed)

For recurrent pharyngitis

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 54
Source: DiPiro JT, et al (2008): Pharmacotherapy: A Pathophysiologic Approach (7th ed)

STEP 6: Monitoring of Pharyngitis Therapy (20 minutes)

• Most pharyngitis cases are self-limited; however, antibiotics hasten resolution when given
early for proven cases of GAS pharyngitis.
• Generally, fever and other symptoms resolve within 3 or 4 days of onset without
antibiotics; however, symptoms will improve 16 hours to 2 days earlier with antibiotic
therapy.
• Follow-up testing is generally not necessary for index cases or in asymptomatic contacts
of the index patient.
• However, for patients who remain symptomatic or when symptoms recur despite
completion of treatment, posttreatment throat cultures 2 to 7 days after completion of
antibiotics should be done.

STEP 7: Key Points (5 minutes)

• Acute pharyngitis is characterized by the rapid onset of sore throat and pharyngeal
inflammation (with or without exudate). .
• It can be caused by a variety of viral and bacterial pathogens, including group
A Streptococcus (GAS),
• Diagnosis can be done clinically especially and by using lab test
• Most of the time the condition is self limiting, but antibiotics may be needed

STEP 7: Evaluation (5 minutes)

• What is pharyngitis?
• What are the signs and symptoms of pharyngitis?
• How is pharyngitis diagnosed?
• How is the treatment of pharyngitis?

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 55
References
Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 56
 Handout 7.1: Pharmacotherapy of Acute Sinusitis

Sinusitis is an inflammation and/or infection of the paranasal sinuses, or membrane-lined air

spaces, around the nose.
The term rhinosinusitis is used by some specialists because sinusitis typically also involves
the nasal mucosa.
Even though the majority of these infections are viral in origin, antibiotics are prescribed
frequently.
It is thus important to differentiate between viral and bacterial sinusitis to aid in optimizing
treatment decisions.
Viruses are responsible for most cases of acute sinusitis; however, when symptoms persist for
7 days or more or become severe, bacteria may be a primary or secondary cause of infection.
Acute bacterial sinusitis is caused most often by the same bacteria implicated in acute otitis
media: S. pneumoniae and H. influenzae.

Pathophysiology
• Similar to acute otitis media, acute bacterial sinusitis usually is preceded by a viral
respiratory tract infection that causes mucosal inflammation.
• This can lead to obstruction of the sinus ostia—the pathways that drain the sinuses.
• Mucosal secretions become trapped, local defenses are impaired, and bacteria from
adjacent surfaces begin to proliferate.
• The maxillary and ethmoid sinuses are the ones most frequently involved.
• The pathogenesis of chronic sinusitis has not been well studied.
• Whether it is caused by more persistent pathogens or there is a subtle defect in the host’s
immune function, some patients develop chronic symptoms after their acute infection

Clinical Presentation and Diagnsosis of Acute sinusitis

General
A nonspecific upper respiratory tract infection that persists beyond 7 to 14 days

Signs and Symptoms

Acute Sinusitis
Adults
• Nasal discharge/congestion
• Maxillary tooth pain, facial or sinus pain that may radiate (unilateral in particular), as well
as deterioration after initial improvement
• Severe or persistent (>7 days) signs and symptoms are most likely bacterial and should be
treated with antibiotics

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 57
Children
Nasal discharge and cough for longer than 10 to 14 days or severe signs and symptoms such
as temperature above 39°C (102°F) or facial swelling or pain are indications for antibiotic
therapy

Chronic
• Symptoms are similar to acute sinusitis but more nonspecific
• Rhinorrhea is associated with acute exacerbations
• Chronic unproductive cough, laryngitis, and headache may occur
• Chronic/recurrent infections occur three or four times per year and are unresponsive to
steam and decongestants

Laboratory Tests
Gram stain, culture, and sensitivities of draining fluid or aspirated fluid if sinus puncture is
performed

Pharmacological Management

Source: DiPiro JT, et al (2008): Pharmacotherapy: A Pathophysiologic Approach (7th ed)

Monitoring of the therapy

• Persistent or worsening symptoms 72 hours after initiating antibiotic therapy should be
considered treatment failure.
• Referral to a specialist should be considered for patients who have not responded to first-
or second-line therapy; for those with severe, recurrent, and chronic disease; and for
patients who are at risk for complications.
• Patients who experience changes in visual acuity or mental status should be referred
immediately.
• Acute bacterial sinusitis lasts less than 30 days with complete resolution of symptoms,
• whereas chronic sinusitis is defined as episodes of inflammation lasting more than 3
months with persistence of respiratory symptoms

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 Handout 7.2: Pharmacotherapy of Acute Otitis Media

• The term otitis media is an inflammation of the middle ear.

• There are three subtypes of otitis media:
o acute otitis media,
o otitis media with effusion, and
o Chronic otitis media.
• The three are differentiated by onset, signs and symptoms of infection, and the presence
of fluid in the middle ear.
• Most of acute otitis media cases are causedby viral pathogens.
• Some cases are caused by bacteria and common bacterial pathogens include
Streptococcus pneumoniae, nontypeable Haemophilus influenzae, and Moraxella
catarrhalis

Pathophysiology
Acute bacterial otitis media usually follows a viral upper respiratory tract infection that
causes eustachian tube dysfunction and mucosal swelling in the middle ear.
The middle ear is the space behind the tympanic membrane, or eardrum.
A noninfected ear has a thin, clear tympanic membrane.
In otitis media, this space becomes blocked with fluid, resulting in a bulging and
erythematous tympanic membrane.
Bacteria that colonize the nasopharynx enter the middle ear and are not cleared properly by
the mucociliary system.
The bacteria proliferate and cause infection.
Children tend to be more susceptible to otitis media than adults because the anatomy of their
eustachian tube is shorter and more horizontal, facilitating bacterial entry into the middle ear

Clinical Presentation and Diagnosis of Acute Otitis Media

General
Acute onset of signs and symptoms of middle ear infection following cold symptoms of
runny nose, nasal congestion, or cough

Signs and Symptoms

Ear pain that can be severe (>75% of patients)
Children may be irritable, tug on the involved ear, and have difficulty sleeping
Fever is present in less than 25% of patients and, when present, occurs more often in younger
children
Examination shows a discolored (gray), thickened, bulging eardrum
Pneumatic otoscopy or tympanometry demonstrates an immobile eardrum

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Guide 59
Draining middle ear fluid occurs in less than 3% of patients and usually has a bacterial
etiology

Laboratory Tests
Gram stain, culture, and sensitivities of draining fluid or aspirated fluid if tympanocentesis is
performed

General Approach to Treatment

• The first step in the treatment of otitis media is to differentiate acute otitis media from
otitis media with effusion or chronic otitis media, as the latter two types do not benefit
substantially from antibiotic therapy.
• The second step is to address pain with oral analgesics.
• Acetaminophen or a nonsteroidal antiinflammatory drug (NSAID), such as ibuprofen,
• should be offered early to relieve pain in acute otitis media
• In addition, eardrops with a local anesthetic, such as ametocaine, benzocaine, or
lidocaine, provide pain relief when administered with oral pain medication to children
ages 3 to 18 years
• The third step is to consider if a brief observation period is warranted or if the disease
severity or patient characteristics require immediate antibiotic therapy

Antibiotics therapy may include the following;

Source: DiPiro JT, et al (2008): Pharmacotherapy: A Pathophysiologic Approach (7th ed)

Monitoring of the therapy

• Pain and fever tend to resolve after 2 or 3 days, with most children becoming
asymptomatic at 7 days.
• Treatment failure is a lack of clinical improvement in the signs and symptoms of
infection,
• Including pain, fever, and erythema/bulging of the tympanic membrane, after 3 days.
• If antibiotics were withheld initially, they should be instituted now.
• If the patient initially received an antibiotic, then the antibiotic should be changed

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

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Session 8: Pharmacotherapy of Pneumonia
Total Session Time: 120 minutes

Prerequisites
• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define pneumonia
• Explain pathophysiology of pneumonia
• Explain the clinical presentation of bronchitis and pneumonia
• Outline diagnosis of bronchitis and pneumonia
• Describe pharmacological treatment of bronchitis and pneumonia
• Describe monitoring of bronchitis and pneumonia therapy

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Computer and LCD Projector

SESSION OVERVIEW

Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Tasks
10 minutes Presentation Definition of Pneumonia
2
Buzzing
3 15 minutes Presentation Pathophysiology of Pneumonia

20 minutes Presentation Clinical Presentation and Diagnosis of

4
Pneumonia
40 minutes Presentation Pharmacological Treatment of Pneumonia
5 Small Group
Discussion
20 minutes Presentation Monitoring of Pneumonia Therapy
6

7 05 minutes Presentation Key Points

8 05 minutes Presentation Evaluation

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 61
SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)

READ or ASK students to read the learning Tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of Pneumonia (10 minutes)

Activity: Buzzing (2 minutes)

ASK students to pair up and buzz on the following question for 2 minutes

• What is Pneumonia?
ALLOW few pairs to respond and let other pairs to add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZEby using the content below

Pneumonia
• Pneumonia is the inflammation of the lung tissue.
• Pneumonia can either be primary (to the causing organism) or secondary to pathological
damage in the respiratory system
• It occurs in persons of all ages, although the clinical manifestations are most severe in the
very young, the elderly, and the chronically ill.
• The most prominent pathogen causing community-acquired pneumonia (CAP) in
otherwise healthy adults is S. pneumonia and accounts for up to 75% of all acute cases.
• Other common pathogens include M. pneumoniae, Legionella species, C. pneumoniae, H.
influenzae, and a variety of viruses including influenza.

REFER Students to Handout 8.1: Classification of Pneumonia and Risk Factors

STEP 3: Pathophysiology of Pneumonia (15 minutes)

• Microorganisms gain access to the lower respiratory tract by three routes.
o Through inhalation as aerosolized particles, or
o via the bloodstream from an extrapulmonary site of infection;
o Aspiration of oropharyngeal contents which is a common occurrence in both healthy
and ill persons during sleep is the major mechanism by which pulmonary pathogens
gain access to the normally sterile lower airways and alveoli.
• When pulmonary defense mechanisms are functioning optimally, aspirated
microorganisms are cleared from the region before infection can become established;

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 62
 o However, aspiration of potential pathogens from the oropharynx can result in
pneumonia if lung defenses are impaired.
• Factors that promote aspiration, such as altered sensorium and neuromuscular disease,
may result in an increase in the size of the inoculum delivered to the lower respiratory
tract, thereby overwhelming local defense mechanisms.
• Lung infections with viruses suppress the antibacterial activity of the lung by impairing
alveolar macrophage function and mucociliary clearance, thus setting the stage for
secondary bacterial pneumonia.
• Mucociliary transport is also depressed by ethanol and narcotics and by obstruction of a
bronchus by mucus, tumor, or extrinsic compression.
• All these factors can severely impair pulmonary clearance of aspirated bacteria hence
causing infection in the lung

STEP 4: Clinical Presentation and Diagnosis of Pneumonia (20 minutes)

Signs and symptoms
• Abrupt onset of fever, chills, dyspnea, and productive cough
• Rust-colored sputum or hemoptysis
• Pleuritic chest pain

Physical examination
• Tachypnea and tachycardia
• Dullness to percussion
• Increased tactile fremitus, whisper pectoriloquy, and egophony
• Chest wall retractions and grunting respirations
• Diminished breath sounds over affected area
• Inspiratory crackles during lung expansion

Chest radiograph
Dense lobar or segmental infiltrate

Laboratory tests
• Leukocytosis with predominance of polymorphonuclear cells
• Low oxygen saturation on arterial blood gas or pulse oximetry

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 63
 Signs and symptoms of Pneumonia in Children under-fives

Source: Standard Treatment Guidelines & National Essential Medicines List Tanzania Mainland (2017)
The Ministry of Health, Community Development, Gender, Elderly and Children

STEP 5: Pharmacological Treatment of Pneumonia (40 minutes)

Activity: Small Group Discussion ( 20 minutes)

DIVIDE students into small manageable groups

ASK students to discuss on the following question

• What is the first line treatment of Pneumonia?

ALLOW students to discuss for 15 minutes

ALLOW few groups to present and the rest to add points not mentioned

CLARIFY and SUMMARIZE by using the contents below

Treatment goasl for bacterial Pneumonia are;

• Eradication of the offending organism through selection of the appropriate antibiotic and
complete clinical cure
• Therapy should minimize associated morbidity, including reversible or irreversible
disease and drug-induced organ toxicity (e.g., renal, lung, or hepatic dysfunction).
• Most cases of viral pneumonia are self-limiting, although therapy of influenza pneumonia
with specific antiviral agents (oseltamivir and zanamivir) may hasten recovery.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

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Treatment of Pneumonia in Adults
First- line

Source: Standard Treatment Guidelines & National Essential Medicines List Tanzania Mainland (2017)
The Ministry of Health, Community Development, Gender, Elderly and Children

Treatment of Atypical Community Acquired Pneumonias

Source: Standard Treatment Guidelines & National Essential Medicines List Tanzania Mainland (2017)
The Ministry of Health, Community Development, Gender, Elderly and Children

Treatment of Pneumonia in Children

Non-severe pneumonia
A: Amoxicillin 25 mg/kg 8 hourly for 5 days
Plus A: Paracetamol suppositories 10–15mg/kg (if there is fever)
OR
B: Ibuprofen 15mg/kg 12 hourly for 5 days
• Give the first dose at the clinic and teach the mother how to give the other doses at home.
• Encourage breasting and feeding.

Severe Pneumonia
A: Benzyl Penicillin 50000 units/kg IV or IM every 6 hours for at least 3 days
THEN A: Amoxicillin 40 mg/kg 8 hourly for 7 days.
OR
A: Ampicillin 50 mg/kg IV/IM every 6 hourly
AND
A: Gentamicin (7.5 mg/kg IV/IM once a day) for 5 days;
PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator
Guide 65
then, If child responds well, complete treatment at home or in hospital with
A: Amoxicillin 30 mg/kg 8 hourly for 7 days.

Very severe Pneumonia:

A: Ampicillin 50 mg/kg IV/IM every 6 hours AND
A: Gentamicin (7.5 mg/kg IV/IM once a day) for 5 days; then, If child responds well,
complete treatment at home or in hospital with
A: Amoxicillin (40 mg/kg12 hourly 10 days
Alternatively,
A: Ceftriaxone 80 mg/kg IV or IM once daily for 10 days.

STEP 6: Monitoring of Pneumonia Therapy (20 minutes)

• After therapy has been instituted, appropriate clinical parameters such as signs and
symptoms and other laboratory markers should be monitored to ensure the efficacy and
safety of the therapeutic regimen.
• For patients with CAP or pneumonia from any source of mild to moderate clinical
severity, the time to resolution of cough, decreasing sputum production, and fever, as well
as other constitutional symptoms of malaise, nausea, vomiting, and lethargy, should be
noted.
• Initial resolution should be observed within the first 2 days and progression to complete
resolution within 5 to 7 days but usually no more than 10 days.
• For patients with HAP, substantial underlying diseases, or both, additional parameters can
be followed, including the magnitude and character of the peripheral blood WBC count,
chest radiograph, and blood gas determinations.
• Similar to patients with less severe disease, some resolution of symptoms should be
observed within 2 days of instituting antibiotic therapy.
• If no resolution of symptoms is observed within 2 days of starting seemingly appropriate
antibiotic therapy or if the patient’s clinical status is deteriorating, the appropriateness of
initial antibiotic therapy should be critically reassessed.
• The patient should be evaluated carefully for deterioration of underlying concurrent
disease(s).
• Additionally, the caregiver should consider the possibility of changing the initial
antibiotic therapy to expand antimicrobial coverage not included in the original regimen
(e.g. Mycoplasma, Legionella, and anaerobes).
• Furthermore, the need for antifungal therapy (lipid-based amphotericin B) should be
considered.
• Some resolution of symptoms should be observed within 2 days of starting proper
antibiotic therapy, with complete resolution expected within 10 to 14 days

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STEP 7: Key Points (5 minutes)
• Pneumonia is an infection of the lung tissue whereby the air sacs in the lungs become
infected with microorganisms, fluid and inflammatory cells and hence they lungs fail to
work properly.
• Diagnosis of pneumonia is based on symptoms and signs of an acute lower respiratory
tract infection, and can be confirmed by a chest X-ray showing new shadowing that is not
due to any other cause
• Penicillins as well as other antibiotics can be used for treatment of Pneumonia as
indicated
STEP 8: Evaluation (5 minutes)
• What is pneumonia?
• What are the signs and symptoms of pneumonia?
• How is pneumonia diagnosed?
• How is the treatment of pneumonia in adult and children?
• Which clinical parameters can be used to monitor pneumonia therapy?

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Guide 67
References

Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 68
 Handout 8.1: Classification of Pneumonia and Risk Factors

Source: DiPiro JT, et al (2008): Pharmacotherapy: A Pathophysiologic Approach (7 th ed)

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Guide 69
Session 9: Pharmacotherapy of Bronchitis
Total Session Time: 120 minutes
Prerequisites
• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define bronchitis
• Explain pathophysiology of bronchitis
• Explain the clinical presentation of bronchitis
• Outline diagnosis of bronchitis
• Describe pharmacological treatment of bronchitis
• Describe the monitoring of bronchitis therapy

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Computer and LCD Projector

SESSION OVERVIEW

Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Tasks
20 minutes Presentation Definition of Bronchitis
2
Buzzing
3 20 minutes Presentation Pathophysiology of Bronchitis

4 20 minutes Presentation Diagnosis of Bronchitis

40 minutes Presentation Pharmacological Treatment of Bronchitis

5 Small Group
Discussion
05 minutes Presentation Monitoring of Bronchitis Therapy
6

7 05 minutes Presentation Key Points

8 05 minutes Presentation Evaluation

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

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SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)

READ or ASK students to read the learning Tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of Bronchitis (20 minutes)

Activity: Buzzing (2 minutes)

ASK students to pair up and buzz on the following question for 2 minutes

• What is Chronic Bronchitis?

ALLOW few pairs to respond and let other pairs to add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZEby using the content below

• Bronchitis is an infection resulting from the inflammation of the lining of the

lungs/bronchioles
• It is subdivided into two types
o Acute Bronchitis
o Chronic Bronchitis

REFER Students to Handout 9.1: Pharmacotherapy of Acute Bronchitis

Chronic Bronchitis
• It defined by a chronic productive cough for three months in each of two successive years
in a patient in whom other causes of chronic cough have been excluded.
• Patients may get secondary bacterial infection with development of fever and production
of thick smelly sputum.
• The disease is a result of several contributing factors; the most prominent include;
o cigarette smoking,
o exposure to occupational dusts, fumes, and environmental pollution; and
o Host factors [e.g., genetic factors and bacterial (and possibly viral) infections].

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 71
STEP 3: Pathophysiology of Chronic Bronchitis (20 minutes)
• Microorganisms gain access to the lower respiratory tract by three routes.
o Through inhalation as aerosolized particles, or
o via the bloodstream from an extrapulmonary site of infection;
o Aspiration of oropharyngeal contents which is a common occurrence in both healthy
and ill persons during sleep is the major mechanism by which pulmonary pathogens
gain access to the normally sterile lower airways and alveoli.
• When pulmonary defense mechanisms are functioning optimally, aspirated
microorganisms are cleared from the region before infection can become established;
o However, aspiration of potential pathogens from the oropharynx can result in
pneumonia if lung defenses are impaired.
• Factors that promote aspiration, such as altered sensorium and neuromuscular disease,
may result in an increase in the size of the inoculum delivered to the lower respiratory
tract, thereby overwhelming local defense mechanisms.
• Lung infections with viruses suppress the antibacterial activity of the lung by impairing
alveolar macrophage function and mucociliary clearance, thus setting the stage for
secondary bacterial pneumonia.
• Mucociliary transport is also depressed by ethanol and narcotics and by obstruction of a
bronchus by mucus, tumor, or extrinsic compression.
• All these factors can severely impair pulmonary clearance of aspirated bacteria hence
causing infection in the lung

STEP 4: Clinical Presentation and Diagnosis of Chronic Bronchitis (20

minutes)
Signs and symptoms
• Excessive sputum expectoration
• Cyanosis (advanced disease)
• Obesity

Physical examination
• Chest auscultation usually reveals inspiratory and expiratory rales, rhonchi, and mild
wheezing with an expiratory phase that is frequently prolonged;
• hyperresonance on percussion with obliteration of the area of cardiac dullness
• Normal vesicular breathing sounds are diminished
• Clubbing of digits (advanced disease)

Chest radiograph
• Increase in anteroposterior diameter of the thoracic cage (observed as a barrel chest)
• Depressed diaphragm with limited mobility

Laboratory tests
Erythrocytosis (advanced disease)

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 72
Pulmonary function tests
• Decreased vital capacity
• Prolonged expiratory flow

STEP 5: Pharmacological Treatment of Chronic Bronchitis (40 minutes)

Activity: Small Group Discussion ( 20 minutes)

DIVIDE students into small manageable groups

ASK students to discuss on the following question

• What is the first line treatment of Pneumonia?

ALLOW students to discuss for 15 minutes

ALLOW few groups to present and the rest to add points not mentioned

CLARIFY and SUMMARIZE by using the contents below

The goals of therapy for chronic bronchitis are:

• to reduce the severity of chronic symptoms and
• to ameliorate acute exacerbations and achieve prolonged infection-free intervals

Non-Pharmacological Treatment
• Stop smoking and/or remove from hazardous environment
• Prompt treatment of infective exacerbations
o Antibiotics as above in case of secondary bacterial infection
• Controlled oxygen therapy
• Physiotherapy

Pharmacological Treatment
Inhaler Salbutamol (PO) 100 μg two puff 6 hourly
OR
Salbutamol (PO) 4mg 8 hourly
OR
Ipratropium bromide aerosol 20–80mg, 6–8 hourly
Trial of steroids if there is possibility of reversible airways obstructions
Prednisolone (PO) 20mg once daily for 5 days

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• Antibiotics are probably helpful only in acute exacerbations of chronic bronchitis
• Common current clinical practice is to promptly use antibiotics empirically in patients
who demonstrate a fever or a change in sputum character.
• Such therapy should be directed against streptococcal species, Haemophilus species
and Moraxella catarrhalis.

Source: DiPiro JT, et al (2008): Pharmacotherapy: A Pathophysiologic Approach (7 th ed)

STEP 6: Monitoring of Chronic Bronchitis Therapy (5 minutes)

• After therapy has been instituted, appropriate clinical parameters such as signs and
symptoms and other laboratory markers such as lung function tests should be monitored
to ensure the efficacy and safety of the therapeutic regimen.

STEP 7: Key Points (5 minutes)

• Pneumonia is an infection of the lung tissue whereby the air sacs in the lungs become
infected with microorganisms, fluid and inflammatory cells and hence they lungs fail to
work properly.
• Diagnosis of pneumonia is based on symptoms and signs of an acute lower respiratory
tract infection, and can be confirmed by a chest X-ray showing new shadowing that is not
due to any other cause
• Penicillins as well as other antibiotics can be used for treatment of Pneumonia as
indicated

STEP 8: Evaluation (5 minutes)

• What is Chronic Bronchitis?
• What are the signs and symptoms of Chronic Bronchitis?
• How is Chronic Bronchitis diagnosed?
PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator
Guide 74
• How is the treatment of Chronic Bronchitis?
References

Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 75
 Handout 9.1: Pharmacotherapy of Acute Bronchitis

Acute bronchitis is one of the most common conditions associated with antibiotic misuse.
Respiratory viruses are by far the most common infectious agents associated with acute
bronchitis
The common cold viruses (rhinovirus and coronavirus) and lower respiratory tract pathogens
(influenza virus and adenovirus) account for the majority of cases.
M. pneumoniae appears to be a frequent cause of acute bronchitis.
Additionally, C. pneumoniae (also referred to as Chlamydophila) and B. pertussis (agent
responsible for whooping cough) have been associated with acute respiratory tract infections.

Pathophysiology
• In general, infection of the trachea and bronchi yields hyperemic and edematous mucous
membranes with an increase in bronchial secretions.
• Destruction of respiratory epithelium can range from mild to extensive and may affect
bronchial mucociliary function.
• In addition, the increase in desquamated epithelial cells and bronchial secretions, which
can become thick and tenacious, further impairs mucociliary activity.
• The probability of permanent damage to the airways as a result of acute bronchitis
remains unclear but appears very unlikely.
• However, epidemiologic evaluations support the belief that recurrent acute respiratory
infections may be associated with increased airway hyperreactivity and possibly the
pathogenesis of asthma or chronic obstructive pulmonary disease (COPD)

Diagnostic Criteria
• Acute bronchitis usually begins as an upper respiratory infection with nonspecific
complaints.
• Cough is the hallmark of acute bronchitis and occurs early.
• The onset of cough may be insidious or abrupt, and the symptoms persist despite
resolution of nasal or nasopharyngeal complaints; cough may persist for up to 3 or more
weeks.
• Frequently, the cough initially is nonproductive but then progresses, yielding
mucopurulent sputum. In older children and adults, the sputum is raised and expectorated;
o In the young child, sputum often is swallowed and can result in gagging and vomiting.

Symptomatic Treatment
• With non-steroidal anti-inflammatory drugs:
• paracetamol, aspirin
• Cough suppressant syrups
• There is NO benefit from antibiotic use
PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator
Guide 76
Session 10: Pharmacotherapy of Typhoid Fever
Total Session Time: 120 minutes

Prerequisites
• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define typhoid fever
• Explain pathophysiology of typhoid fever
• Explain the clinical presentation of typhoid fever
• Outline diagnosis of typhoid fever
• Describe pharmacological treatment of typhoid fever
• Describe monitoring of typhoid fever therapy

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Computer and LCD Projector

SESSION OVERVIEW
Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Tasks
15 minutes Presentation Definition of Typhoid Fever
2
Buzzing
3 10 minutes Presentation Pathophysiology of Typhoid Fever

4 30 minutes Presentation Diagnosis of Typhoid Fever

40 minutes Presentation Pharmacological Treatment of Typhoid

5 Small Group Fever
Discussion
10 minutes Presentation Monitoring of Typhoid Fever Therapy
6

7 05 minutes Presentation Key Points

8 05 minutes Presentation Evaluation

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 77
SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)

READ or ASK students to read the learning Tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of Typhoid Fever (15 minutes)

Activity: Buzzing (5 minutes)

ASK students to pair up and buzz on the following question for 2 minutes

• What is typhoid fever?

ALLOW few pairs to respond and let other pairs to add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZEby using the content below

Typhoid Fever
• Typhoid fever, also called enteric fever, is caused by a bacterial infection with Salmonella
enterica subspecies enterica serotype Typhi or serotypes Paratyphi A, B or C.
• Infection is acquired through ingestion of contaminated food and water.
• Humans are the only known hosts of Salmonella Typhi.
• Bacteria are shed in the faeces of an infected person and transmitted from person to
person via ingestion of food or water contaminated by these faeces (faecaloral route).
• Large outbreaks of typhoid fever are often associated with contamination of a drinking
water.
• The organism can survive for several days in fresh water (e.g. ground water, pond-water)
and seawater.
• Furthermore, the organism can survive for prolonged periods (up to several months) in
contaminated foods

STEP 3: Pathophysiology of Typhoid Fever (10 minutes)

• Once ingested and successfully beyond host defense mechanisms such as low gastric pH
and bile salts, organisms can attach and invade the distal ileum and proximal colon.
• Gastroenteritis often is characterized by massive neutrophil infiltration followed by
lymphocytes and macrophages.
• The serotypes that are responsible for human illness cause intestinal epithelial cells
to secrete interleukin 8, a potent neutrophil chemo-tactic factor.

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• Degranulation and release of toxic substances by neutrophils may contribute to
inflammation and result in tissue damage, fluid secretion, or leakage across the intestinal
mucosa

STEP 4: Clinical Presentation and Diagnosis of Typhoid Fever (30 minutes)

Few clinical features reliably distinguish typhoid fever from other causes of febrile illnesses.
Infection in the absence of treatment manifests after an average incubation period of 10-14
days (range 5-21 days) as a multistage febrile illness.

Acute typhoid fever:

• Systemic illness characterised by:
• Fever: remittent during the first week, rising in a stepwise fashion and becomes sustained
(lasting > 48 hours) after the first week.
• Headache
• Gastrointestinal symptoms including:
o Abdominal pain/cramps
o Nausea and vomiting (usually not severe), and/or
o Constipation or diarrhoea (diarrhoea is more frequent in children and HIVinfected
adults).
• Relative bradycardia (
• Hepatosplenomegaly (23-65%).
• Leukopenia (16-46%).
• Nonspecific symptoms, such as chills, diaphoresis, anorexia, cough, weakness, sore
throat,
• Dizziness, and muscle pains, are frequent before the onset of fever.
• Severe illness and extra-intestinal complications may include;
o gastrointestinal bleeding ,
o intestinal perforation,
o Septic shock or acidosis.
• Blood culture is the diagnostic test of choice

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 79
STEP 5: Pharmacological Treatment of Typhoid Fever (40 minutes)

Activity: Small Group Discussion ( 20 minutes)

DIVIDE students into small manageable groups

ASK students to discuss on the following question

• What is the first line treatment of Typhoid Fever?

ALLOW students to discuss for 15 minutes

ALLOW few groups to present and the rest to add points not mentioned

CLARIFY and SUMMARIZE by using the contents below

Source: Guidelines for the Management of Typhoid Fever (2011) WHO Zimbabwe

STEP 6: Monitoring of Typhoid Fever Therapy (10 minutes)

• After therapy has been instituted, appropriate clinical parameters such as signs and
symptoms and other laboratory markers should be monitored to ensure the efficacy and
safety of the therapeutic regimen.

STEP 7: Key Points (5 minutes)

• It is an acute systemic disease resulting from infection by Salmonella typhi and
S.paratyphi, serovar group A and B respectively.
• Infection is acquired through ingestion of contaminated food and water.

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Guide 80
• Patients may complain of nausea and vomiting followed by abdominal cramps, headache,
fever, and diarrhea
• Ciprofloxacin (PO) 500mg 12 hourly for 10 days OR Azithromycin (PO) Adult 500mg
for 7 days can be used for treatment

STEP 8: Evaluation (5 minutes)

• What is typhoid fever?
• What is the pathophysiology of typhoid fever?
• What are the signs and symptoms of acute typhoid fever?
• How is the treatment of typhoid fever?

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 81
References

Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 82
Session 11: Pharmacotherapy of Amebiasis

Total Session Time: 120 minutes

Prerequisites
• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define of amebiasis and ameobic liver abscess
• Explain pathophysiology of amebiasis and ameobic liver abscess
• Explain the clinical presentation of amebiasis and ameobic liver abscess
• Outline diagnosis of amebiasis and ameobic liver abscess
• Describe pharmacological treatment of amebiasis and ameobic liver abscess
• Describe the monitoring of amebiasis and ameobic liver abscess therapy

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Computer and LCD Projector

SESSION OVERVIEW

Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Tasks
10 minutes Presentation Definition of Amebiasis and Ameobic Liver
2
Buzzing Abscess
15 minutes Pathophysiology of Amebiasis and Ameobic
3 Presentation Liver Abscess

30 minutes Presentation Diagnosis of Amebiasis and Ameobic Liver

4
Abscess
40 minutes Presentation Pharmacological Treatment of Amebiasis
5 Small Group and Ameobic Liver Abscess
Discussion
10 minutes Presentation Monitoring of Amebiasis and Ameobic Liver
6
Abscess Therapy
7 05 minutes Presentation Key Points

8 05 minutes Presentation Evaluation

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Guide 83
SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)

READ or ASK students to read the learning Tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of Amebiasis (10 minutes)

Activity: Buzzing (2 minutes)

ASK students to pair up and buzz on the following question for 2 minutes

• What is Amebiasis?
ALLOW few pairs to respond and let other pairs to add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZEby using the content below

Amebiasis
• Amoebiasis is an infection caused by the protozoa organism Entamoeba histolytica,
which can cause colitis and other extra-intestinal manifestations.
• The infection is primarily acquired through ingestion of contaminated food and water and
occasionally can be acquired through oral-anal sexual practices.

Amoebic Liver Abscess

It is the most frequent extra-intestinal manifestation of Entamoeba histolytica infection which
results from the invasion of the portal venous system from the colon leading to inflammation
and subsequently abscess formation particularly involving the right lobe of the liver.

STEP 3: Pathophysiology of Amebiasis (15 minutes)

• E histolytica invades mucosal cells of colonic epithelium, producing the classic flask-
shaped ulcer in the submucosa.
• The trophozoite has a cytolethal effect on cells through a toxin.
• If the trophozoite gets into the portal circulation, it will be carried to the liver, where it
produces abscess and periportal fibrosis.
• Amebic ulcerations can affect the colon, perineum, and genitalia, and abscesses may
occur in the lung and brain.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

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STEP 4: Clinical Presentation and Diagnosis of Amebiasis (30 minutes)
Intestinal disease
• Vague abdominal discomfort, malaise to severe abdominal cramps, flatulence,
• bloody diarrhea (heme-positive in 100% of cases) with mucus
• Eosinophilia is usually absent, although moderate leukocytosis is not unusual
• Evidence of motile trophozoites or cysts on saline wet mount from a stool specimen

Amebic liver abscess

• High fever, rigors and profuse sweating,
• significant leukocytosis with left shift,
• elevated alkaline phosphatase, and liver tenderness on palpation
• Right-upper-quadrant pain, hepatomegaly, and liver tenderness, with referred pain
• to the left or right shoulder
• Erosion of liver abscesses may also present as peritonitis
• Positive imaging evidence of liver abscess AND Serological evidence of E. histolytica
antibodies or antigens.

STEP 5: Pharmacological Treatment of Amebiasis (40 minutes)

Activity: Small Group Discussion ( 20 minutes)

DIVIDE students into small manageable groups

ASK students to discuss on the following question

• What is the treatement of amebiasis?

ALLOW students to discuss for 15 minutes

ALLOW few groups to present and the rest to add points not mentioned

CLARIFY and SUMMARIZE by using the contents below

In amebiasis, the goals of therapy are initially to eradicate the parasite by use of specific
amebicides and then to render supportive therapy.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

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 Table 11:1 Treatment of Amebiasis

Source: Ritter JM, et al: A Textbook of Clinical Pharmacology and Therapeutics (5th ed)

STEP 6: Monitoring of Amebiasis Therapy (10 minutes)

• Follow up in patients with amebiasis should include;
o repeat stool examination, serology, colonoscopy (for colitis), or
o Computed tomography (CT) (for liver abscess) between days 5 and 7, at the end of
the course of therapy, and a month after the end of therapy.
• Most patients with either intestinal amebiasis or colitis will respond in 3 to 5 days with
amelioration of symptoms.
• Patients with liver abscesses may take from 7 to 10 days to respond;
• Patients not responding during this period may require aspiration of abscesses or
exploratory laparotomy.
• Serial liver scans have demonstrated healing of liver abscesses over 4 to 8 months after
adequate therapy.

STEP 7: Key Points (5 minutes)

• Amebiasis is a parasitic infection of the intestines caused by the protozoan Entamoeba
histolytica, or E. histolytica.
• Infection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally
contaminated food, water, or hands
• The symptoms of amebiasis include loose stool, abdominal cramping, and stomach pain.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

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• Treatment for uncomplicated cases of amebiasis generally consists of a course
of metronidazole or tinidazole

STEP 8: Evaluation (5 minutes)

• What is Amebiasis?
• What is the pathophysiology of amebiasis?
• What are the signs and symptoms of Amebiasis?
• How is the treatment of Amebiasis?

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References

Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

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Session 12: Pharmacotherapy of Trypanosomiasis
Total Session Time: 120 minutes
Prerequisites
• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define trypanosomiasis
• Explain the clinical presentation of trypanosomiasis
• Outline diagnosis of trypanosomiasis
• Describe pharmacological treatment of trypanosomiasis
• Describe monitoring of trypanosomiasis therapy

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Computer and LCD Projector

SESSION OVERVIEW

Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Tasks
15 minutes Presentation Definition of Trypanosomiasis
2
Buzzing
20 minutes Clinical Presentation of Trypanosomiasis
3 Presentation

4 20 minutes Presentation Diagnosis of Trypanosomiasis

40 minutes Presentation Pharmacological Treatment of

5 Small Group Trypanosomiasis
Discussion
10 minutes Presentation Monitoring of Trypanosomiasis Therapy
6

7 05 minutes Presentation Key Points

8 05 minutes Presentation Evaluation

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

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SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)

READ or ASK students to read the learning Tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of Trypanosomiasis (15 minutes)

Activity: Buzzing (5 minutes)

ASK students to pair up and buzz on the following question for 2 minutes

• What is Trypanosomiasis?
ALLOW few pairs to respond and let other pairs to add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZEby using the content below

Trypanosomiasis
• Two distinct forms of the genus Trypanosoma occur in humans.
o One is associated with African trypanosomiasis (sleeping sickness) and the other with
American trypanosomiasis (Chagas disease)
• Human African trypanosomiasis, also known as sleeping sickness, is a vector-borne
parasitic disease.
• The parasites concerned are protozoa belonging to the Trypanosoma genus.
• They are transmitted to humans by tsetse fly (Glossina genus) bites which have acquired
their infection from human beings or from animals harbouring the human pathogenic
parasites
• Two forms of the disease exist.
o The slow-progressing form, caused by Trypanosoma brucei gambiense, is found in
Western and Central Africa.
o The faster progressing form, caused by T. b. rhodesiense, is found in Eastern and
Southern Africa
• Mother-to-child infection: the trypanosome can cross the placenta and infect the fetus.
o Mechanical transmission through other blood sucking insects is possible.
o Accidental infections have occurred in laboratories due to pricks from contaminated
needles.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

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STEP 3: Clinical Presentation of Trypanosomiasis (20 minutes)
• In the first stage, the trypanosomes multiply in subcutaneous tissues, blood and lymph.
• This is known as a haemolymphatic phase, which entails bouts of fever, headaches, joint
pains and itching.
o After their inoculation, parasites proliferate at the site of infection, leading to an
inflammatory nodule or ulcer.
o This trypanosomal chancre arises in about 50% of all rhodesiense—but rarely in
gambiense—infections.
o After 3–4 weeks, the chancre usually heals with overlying desquamation, sometimes
with altered pigmentation.
o Parasites spread to the draining lymph node and reach the bloodstream, initiating the
haemolymphatic stage of the disease.
o This stage is characterised by general malaise, headache, and fever of an undulating
type.
o In rhodesiense infection, with its more acute course, pancarditis with congestive
heart failure, pericardial effusion, and pulmonary oedema can cause fatalities at this
early stage, whereas gambiense infection shows a more insidious development that is
frequently unrecognised or misdiagnosed.
o A typical sign of gambiense human African trypanosomiasis is generalised
lymphadenopathy that develops after several weeks, frequently in the posterior
triangle of the neck
• In the second stage the parasites cross the blood-brain barrier to infect the central nervous
system.
• This is known as the neurological phase.
• In general this is when more obvious signs and symptoms of the disease appear: changes
of behaviour, confusion, sensory disturbances and poor coordination.
• Disturbance of the sleep cycle, which gives the disease its name, is an important feature
of the second stage of the disease.

STEP 4: Diagnosis of Trypanosomiasis (20 minutes)

• The diagnosis of African Trypanosomiasis is made through laboratory methods, because
the clinical features of infection are not sufficiently specific.
• The diagnosis rests on finding the parasite in body fluid or tissue by microscopy.
• The parasite load in T. b. rhodesiense infection is substantially higher than the level in T.
b. gambiense infection.
• T. b. rhodesiense parasites can easily be found in blood.
• They can also be found in lymph node fluid or in fluid or biopsy of a chancre.
• The classic method for diagnosing T. b. gambiense infection is by microscopic
examination of lymph node aspirate, usually from a posterior cervical node.
• It is often difficult to detect T. b. gambiense in blood. Concentration techniques and serial
examinations are frequently needed.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

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• Serologic testing is available outside the U.S. for T. b. gambiense; however, it normally is
used for screening purposes only and the definitive diagnosis rests on microscopic
observation of the parasite.
• All patients diagnosed with African trypanosomiasis must have their cerebrospinal fluid
examined to determine whether there is involvement of the central nervous system, since
the choice of treatment drug(s) will depend on the disease stage.
• The World Health Organization criteria for central nervous system involvement include
increased protein in cerebrospinal fluid and a white cell count of more than 5.
• Trypanosomes can often be observed in cerebrospinal fluid in persons with second stage
infection.

STEP 5: Pharmacological Treatment of Trypanosomiasis (40 minutes)

Activity: Small Group Discussion ( 20 minutes)

DIVIDE students into small manageable groups

ASK students to discuss on the following question

• What is the treatement of Trypanosomiasis?

ALLOW students to discuss for 15 minutes

ALLOW few groups to present and the rest to add points not mentioned

CLARIFY and SUMMARIZE by using the contents below

• The type of treatment depends on the stage of the disease.

• The drugs used in the first stage of the disease are of lower toxicity and easier to
administer.
• The earlier the disease is identified, the better the prospect of a cure.
• Treatment success in the second stage depends on a drug that can cross the blood-brain
barrier to reach the parasite.
• Such drugs are toxic and complicated to administer.

Table 12;1 Treatment of Trypanosomiasis According to stage of the disease

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

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 .
Barrett MP, et al: The trypanosomiases; THE LANCET • Vol 362;www.thelancet.com

STEP 6: Monitoring of Trypanosomiasis Therapy (10 minutes)

• Monitor clinically and by using laboratory test
• In both early- and late-stage trypanosomiasis, symptoms usually resolve after treatment,
and the parasitemia clears on repeat blood smears.
• Patients who have recovered from late-stage East African trypanosomiasis should
undergo lumbar punctures every 3 months for the first year.
• Patients who have recovered from West African trypanosomiasis should undergo lumbar
punctures every 6 months for 2 years.
• If symptoms return, the CSF WBC count is higher than 20/µL, CSF pleocytosis occurs, or
trypanosomes are still present in blood or CSF, a relapse is suggested.
• However, a persistently elevated CSF WBC count may also be observed in recovering
patients; thus, the change (increase or decrease) in the WBC count is more diagnostically
helpful than the count by itself.
• If a relapse is noted, repeat treatment with melarsoprol or eflornithine may be considered.

STEP 7: Key Points (5 minutes)

• Human African trypanosomiasis, also known as sleeping sickness, is a vector-borne
parasitic disease.
• It is caused by infection with protozoan parasites belonging to the genus Trypanosoma.
• They are transmitted to humans by tsetse fly (Glossina genus) bites which have acquired
their infection from human beings or from animals harbouring human pathogenic
parasites.
• The type of treatment depends on the disease stage whereby drugs used in the first stage
are safer and easier to administer than those for second stage.
• Also, the earlier the disease is identified, the better the prospect of a cure.

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STEP 8: Evaluation (5 minutes)
• What is trypanosomiasis?
• What is the pathophysiology of trypanosomiasis?
• What are the signs and symptoms of trypanosomiasis?
• How is the treatment of trypanosomiasis?

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References

Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 95
Session 13: Pharmacotherapy of Schistosomiasis
Total Session Time: 120 minutes
Prerequisites
• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define schistosomiasis
• Explain pathophysiology of schistosomiasis
• Explain the clinical presentation of schistosomiasis
• Outline diagnosis of schistosomiasis
• Describe pharmacological treatment of schistosomiasis
• Describe monitoring of schistosomiasis therapy

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Computer and LCD Projector

SESSION OVERVIEW

Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Tasks
15 minutes Presentation Definition of Schistosomiasis
2
Buzzing
20 minutes Pathophysiology of Schistosomiasis
3 Presentation

4 20 Minutes Presentation Clinical Presentation of schistosomiasis

5 20 minutes Presentation Diagnosis of Schistosomiasis

20 minutes Presentation Pharmacological Treatment of

6 Small Group Schistosomiasis
Discussion
10 minutes Presentation Monitoring of Schistosomiasis Therapy
7

8 05 minutes Presentation Key Points

9 05 minutes Presentation Evaluation

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

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SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)

READ or ASK students to read the learning Tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of Schistosomiasis (15 minutes)

Activity: Buzzing (2 minutes)

ASK students to pair up and buzz on the following question for 2 minutes

• What is Schistosomiasis?
ALLOW few pairs to respond and let other pairs to add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZEby using the content below

Schistosomiasis
• Schistosomiasis is an acute and chronic parasitic disease caused by blood flukes
(trematode worms) of the genus Schistosoma.
• There are 2 major forms of schistosomiasis which are intestinal and urogenital caused by
5 main species of blood fluke as follows;
Habitation Species
Intestinal Schistosoma mansoni
schistosomiasis Schistosoma japonicum
Schistosoma mekongi
Schistosoma guineensis and
related S. intercalatum
Urogenital Schistosoma haematobium
schistosomiasis
• Infection happens when larval forms of the parasite released by freshwater snails
penetrate the skin during contact with infested water.
• Transmission occurs when infected individual from schistosomiasis contaminate
freshwater sources with their excreta containing parasite eggs, which hatch in water.
• In the body, the larvae develop into adult schistosomes.
• Adult worms live in the blood vessels where the females release eggs.
• Some of the eggs are passed out of the body in the faeces or urine to continue the
parasite’s lifecycle.
• Others become trapped in body tissues, causing immune reactions and progressive
damage to organs.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

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STEP 3: Pathophysiology and Symptoms of Schistosomiasis (20 minutes)
• In schistosomiasis, adult worms reside in the mesenteric and pelvic venules in various
sites where they lay eggs
• These sites tend to be specific for each species (e.g. S. japonicum prefers the superior
mesenteric veins draining to the small intestine, while S. mansoni prefers the superior
mesenteric veins of the large intestine)
o Many eggs are carried upstream where they get lodged in various organs, especially in
the liver, bowel, and genitourinary tract
o Acute disease may trigger a cell-driven inflammatory response (involving tumour
necrosis factor, interleukin-1, and interleukin-6 cytokines) and cause febrile illness
o As mature female worms lay eggs, products of worm and egg metabolism induce
formation of immune complexes resulting to a serum like-sickness called Katayama
syndrome
o In chronic disease, eggs are the cause of pathology; they evoke a Thelper type 2 (Th2)
cell-driven granulomatous reaction (involving interleukin-4, interleukin-5, and
interleukin-13 cytokines) resulting in tissue fibrosis and chronic morbidity
o Gastrointestinal schistosomiasis due to S. mansoni, S. japonicum and S. mekongi can
cause bowel lesions such as ulceration, pseudopolyps, and microabcesses.
o These manifest clinically as abdominal pain, altered bowel habits, and blood in stools
• The classic sign of urogenital schistosomiasis is haematuria and is specifically noted with
S. haematobium
o Bladder, ureter fibrosis and kidney damage are sometimes seen in advanced cases
o The urogenital form may present with genital lesions (e.g. vulvar nodules), vaginal
bleeding, dyspareunia, and fallopian tube damage (in the late stages) in females
o Genital infection in males may resultin damage to seminal vesicles, prostate and other
related organs; this may lead to irreversible infertility

STEP 4: Clinical Presentation of Schistosomiasis (20 minutes)

• Symptoms of schistosomiasis are caused by the body’s reaction to the worms' eggs.
• Intestinal schistosomiasis can result in abdominal pain, diarrhoea, and blood in the stool.
• Liver enlargement is common in advanced cases, and is frequently associated with an
accumulation of fluid in the peritoneal cavity and hypertension of the abdominal blood
vessels.
o In such cases there may also be enlargement of the spleen.
• The classic sign of urogenital schistosomiasis is haematuria (blood in urine).
• Fibrosis of the bladder and ureter, and kidney damage are sometimes diagnosed in
advanced cases.
• Bladder cancer is another possible complication in the later stages. In women, urogenital
schistosomiasis may present with genital lesions, vaginal bleeding, pain during sexual
intercourse, and nodules in the vulva.
• In men, urogenital schistosomiasis can induce pathology of the seminal vesicles, prostate,
and other organs.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

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• This disease may also have other long-term irreversible consequences, including
infertility.

STEP 5: Diagnosis of Schistosomiasis (20 minutes)

• Schistosomiasis is diagnosed through the detection of parasite eggs in stool or urine
specimens
• Antibodies and/or antigens detected in blood or urine samples are also indications of
infection
• For urogenital schistosomiasis, a filtration technique using nylon, paper or polycarbonate
filters is the standard diagnostic technique
• Children with S. haematobium almost always have microscopic blood in their urine which
can be detected by chemical reagent strips
• The eggs of intestinal schistosomiasis can be detected in faecal specimens through a
technique using methylene blue-stained cellophane soaked in glycerine or glass slides,
known as the Kato-Katz technique
• For people living in non-endemic or low-transmission areas, serological and
immunological tests may be useful in showing exposure to infection and the need for
thorough examination, treatment and follow-up

STEP 6: Pharmacological Treatment of Schistosomiasis (20 minutes)

Activity: Small Group Discussion ( 15 minutes)

DIVIDE students into small manageable groups

ASK students to discuss on the following question

• What is the treatement of Schistosomiasis?

ALLOW students to discuss for 15 minutes

ALLOW few groups to present and the rest to add points not mentioned

CLARIFY and SUMMARIZE by using the contents below

• Praziquantel (PO) 40mg/kg as a single dose or in 2 divided doses

• The control of schistosomiasis is based on large-scale treatment of at-risk population
groups, access to safe water, improved sanitation, hygiene education, and snail control.
• The WHO strategy for schistosomiasis control focuses on reducing disease through
periodic, targeted treatment with praziquantel through the large-scale treatment
(preventive chemotherapy) of affected populations.
• It involves regular treatment of all at-risk groups.
• Groups targeted for treatment are:
o School-aged children in endemic areas.
PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator
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 o Adults considered to be at risk in endemic areas, and people with occupations
involving contact with infested water, such as fishermen, farmers, irrigation workers,
and women whose domestic tasks bring them in contact with infested water.
o Entire communities living in highly endemic areas.
• In high-transmission areas, treatment may have to be repeated every year for a number of
years.
• Monitoring is essential to determine the impact of control interventions.

STEP 7: Monitoring of Schistosomiasis Therapy (10 minutes)

• Follow-up of treatment response in schistosomiasis needs to be guided by active disease

parameters, such as suggestive symptoms, raised eosinophil count, or
parasitological/histological evidence of viable eggs
• If symptoms such as hematuria or bloody diarrhea persist for weeks after treatment, urine
or stool samples should be tested for parasite eggs and appropriate action should be taken
depending on the results
• Serological assays of the levels of anti-schistosome-egg antibodies can also be used in the
post-treatment monitoring to confirm for treatement success or failure for praziquentel.

STEP 8: Key Points (5 minutes)

• Schistosomiasis is an acute and chronic parasitic disease caused by blood flukes
(trematode worms) of the genus Schistosoma.
• People become infected when larval forms of the parasite are released by freshwater
snails and then penetrate the skin during contact with infested water.
• Transmission occurs when people suffering from schistosomiasis contaminate freshwater
sources with their excreta containing parasite eggs, which hatch in water.
• The classic sign of urogenital schistosomiasis is haematuria (blood in urine
• Praziquantel is the recommended treatment against all forms of schistosomiasis.

STEP 9: Evaluation (5 minutes)

• What is Schistosomiasis?
• What is the pathophysiology of Schistosomiasis?
• What are the signs and symptoms of Schistosomiasis?
• How is the treatment of Schistosomiasis?

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References

Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

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Session 14: Pharmacotherapy of Gonorrhoea

Total Session Time: 120 minutes

Prerequisites
• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define gonorrhoea
• Explain pathophysiology of gonorrhoea
• Explain the clinical presentation of gonorrhoea
• Outline diagnosis of gonorrhoea
• Describe pharmacological treatment of gonorrhoea
• Describe monitoring of gonorrhoea therapy

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Computer and LCD Projector

SESSION OVERVIEW

Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Tasks
15 minutes Presentation Definition of Gonorrhoea
2
Buzzing
10 minutes Pathophysiology of Gonorrhoea
3 Presentation

4 20 minutes Presentation Clinical Presentation of Gonorrhoea

5 20 minutes Presentation Diagnosis of Gonorrhoea

30 minutes Presentation Pharmacological Treatment of Gonorrhoea

6 Small Group
Discussion
10 minutes Presentation Monitoring of Gonorrhoea Therapy
7

8 05 minutes Presentation Key Points

9 05 minutes Presentation Evaluation

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 102
SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)

READ or ASK students to read the learning Tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of Gonorrhoea (15 minutes)

Activity: Buzzing (5 minutes)

ASK students to pair up and buzz on the following question for 2 minutes

• What is Gonorrhoea?
ALLOW few pairs to respond and let other pairs to add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZEby using the content below

Gonorrhoea
• Gonorrhea is a sexually transmitted disease (STD) caused by infection with the
bacterium Neisseria gonorrhoeae.
• It tends to infect warm, moist areas of the body, including the:
o urethra (the tube that drains urine from the urinary bladder)
o eyes
o throat
o vagina
o anus
o female reproductive tract (the fallopian tubes, cervix, and uterus)
• Gonorrhea is transmitted from person to person through unprotected oral, anal, or vaginal
sex.
• People with numerous sexual partners or those who don’t use a condom are at greatest
risk of infection.

STEP 3: Pathophysiology of Gonorrhoea (10 minutes)

• On contact with a mucosal surface lined by columnar, cuboidal, or noncornified
squamous epithelial cells, the gonococci attach to cell membranes by means of surface
pili and are then pinocytosed.
• The virulence of the organism is mediated primarily by the presence of pili and other
outer membrane proteins.
• After mucosal damage is established, polymorphonuclear (PMN) leukocytes invade the
tissue, submucosal abscesses form, and purulent exudates are secreted.

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STEP 4: Clinical Presentation of Gonorrhoea (20 minutes)
• Individuals infected with gonorrhea can be;
o symptomatic or asymptomatic,
o have complicated or uncomplicated infections, and
o Have infections involving several anatomic sites.
• The most common clinical features of gonococcal infections are presented in Table 14.1
• Complications associated with untreated gonorrhea appear more pronounced in women,
because most of them are asymptomatic
o As a result, most of these patients develop serious complications, such as;
o pelvic inflammatory disease (PID),
o Infertility and ectopic pregnancies.
o In other patients the gonococci invade the bloodstream and produce disseminated
disease
Table 14.1: Clinical Presentation of Gonorrhoea

Source: DiPiro JT, et al(2008): Pharmacotherapy: A Pathophysiologic Approach (7th ed)

STEP 5: Diagnosis of Gonorrhoea (20 minutes)

• Diagnosis of gonococcal infections can be made by ;
o gram-stained smears,
o culture, or
• Methods based on the detection of cellular components of the gonococcus such as
Enzyme immunoassay, DNA probe techniques, and nucleic acid amplification techniques
(NAATs) are also used in clinical specimens.
• Various stains have been used to identify gonococci microscopically, with the Gram stain
the most widely used in clinical practice.
o Gram-stained smears are positive for gonococci when gram-negative diplococci of
typical kidney bean morphology are identified within PMN leukocytes.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

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STEP 6: Pharmacological Treatment of Gonorrhoea (30 minutes)

Activity: Small Group Discussion ( 20 minutes)

DIVIDE students into small manageable groups

ASK students to discuss on the following question

• What is the treatement of Gonorrhoea?

ALLOW students to discuss for 15 minutes

ALLOW few groups to present and the rest to add points not mentioned

CLARIFY and SUMMARIZE by using the contents below

Table 14:2, .Treatment for Uncomplicated Gonococcal Infections of the Cervix, Urethra, and
Rectum

Source: Sexually Transmitted DiseasesTreatment Guidelines, 2015: Center for Disease Control (USA)

Treatment of various forms of Gonorrhoea Infection

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Source: DiPiro JT, et al(2008): Pharmacotherapy: A Pathophysiologic Approach (7th ed)

STEP 7: Monitoring of Gonorrhoea Therapy (10 minutes)

• It is recommended to obtain follow-up cultures at least 3 days after treatment
o However the combination gonorrhea and chlamydial therapy rarely results in
treatment failures, and routine follow-up of patients treated with a regimen is not
necessary.
• Persistence of symptoms following any treatment requires culture of the site(s) of
gonorrheal infection, as well as susceptibility testing if gonococci are isolated.
• In most cases, the presence of gonococci indicates reinfection rather than treatment
failure and reflects the need for improved patient education and sex partner referral.
• Persistence of symptoms also can be caused by other infectious causes, such as
C. trachomatis

STEP 8: Key Points (5 minutes)

• Gonorrhea is a sexually transmitted disease (STD).
• It’s caused by infection with the bacterium Neisseria gonorrhoeae
• Gonorrhea passes from person to person through unprotected oral, anal, or vaginal sex.
• First line drug treatment with Cetriaxone and Azithromycin is recommended

STEP 9: Evaluation (5 minutes)

• What is Gonorrhoea?
• What is the pathophysiology of Gonorrhoea?
• What are the signs and symptoms of Gonorrhoea?
• How is the treatment of Gonorrhoea?

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References

Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

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Session 15: Pharmacotherapy of Syphilis
Total Session Time: 120 minutes
Prerequisites
• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define syphilis
• Explain the clinical presentation of syphilis
• Outline diagnosis of syphilis
• Describe pharmacological treatment of syphilis
• Describe the monitoring of syphilis therapy

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Computer and LCD Projector

SESSION OVERVIEW

Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Tasks
10 minutes Presentation Definition of Syphilis
2
Buzzing
3 25 Minutes Presentation Clinical Presentation of Syphilis

4 20 minutes Presentation Diagnosis of Syphilis

40 minutes Presentation Pharmacological Treatment of Syphilis

5 Small Group
Discussion
10 minutes Presentation Monitoring of Syphilis Therapy
6

7 05 minutes Presentation Key Points

8 05 minutes Presentation Evaluation

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SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)

READ or ASK students to read the learning Tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of Syphilis (15 minutes)

Activity: Buzzing (2 minutes)

ASK students to pair up and buzz on the following question for 2 minutes

• What is syphilis?
ALLOW few pairs to respond and let other pairs to add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZEby using the content below

Syphilis
• Syphilis is an infectious venereal disease caused by the spirochete Treponema pallidum.
• Syphilis is transmissible by sexual contact with infectious lesions, from mother to fetus in
utero, via blood product transfusion, and occasionally through breaks in the skin that
come into contact with infectious lesions.
• If untreated, it progresses through 4 stages: primary, secondary, latent, and tertiary

STEP 3: Clinical Presentation of Syphilis (25 minutes)

Primary Syphilis
• The primary stage, characterized by the appearance of a chancre on cutaneous or
mucocutaneous tissue exposed to the organism, is highly infectious.
• Even without treatment, chancres persist only for 1 to 8 weeks before healing
spontaneously. Because syphilitic chancres can be confused with other infectious
etiologies, appropriate diagnostic testing is important.
Secondary Syphilis
• The secondary stage of syphilis is characterized by a variety of mucocutaneous eruptions
resulting from widespread hematogenous and lymphatic spread of T. pallidum .
• Skin lesions can be either generalized or localized to a small portion of the body and, with
the exception of follicular lesions, are nonpruritic.

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• Generalized lymphadenopathy also is seen in the majority of patients, as are nonspecific
symptoms such as mild and transitory malaise, fever, pharyngitis, headache, anorexia, and
arthralgia.
• If untreated, secondarysyphilis disappears in 4 to 10 weeks; however, lesions can recur at
any time within 4 years.
Latent Syphilis
• These are persons with a positive serologic test for syphilis but with no other evidence of
disease.
• Latent syphilis is further divided into early and late latency.
• During early latency, the patient is considered potentially infectious.
• Eearly latencyis defined as 1 year from the onset of infection, up to 2 to 4 years.
• Late latency is considered noninfectious, although the patient remains a host.
• Most untreated patients with late latent syphilis have no further sequelae; however,
approximately 25% to 30% progress either to neurosyphilis or to late syphilis with
clinical manifestations other than neurosyphilis.
• Treatment of all patients with latent syphilis is essential because there is no way to predict
which patients will have progression of their disease .

Tertiary Syphilis and Neurosyphilis

• If left untreated, syphilis can slowly produce an inflammatory reaction in virtually any
organ in the body.
• Manifestations of this disease progression are referred to as tertiary syphilis.
• These clinical manifestations are differentiated into two subgroups based on the presence
or absence of central nervous system (CNS) involvement which are neurosyphilis or
tertiary syphilis (i.e., gumma and cardiovascular syphilis).
• B2wThe gumma, a nonspecific granulomatous lesion, is the classic lesion of late syphilis
and develops in 50% of patients with disease progression.
• These chronic, destructive lesions characteristically infiltrate the skin, bone, soft tissue,
and liver but can be found in any organ or tissue.
• Gummas of critical organs, such as the heart or brain, can be fatal

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Table 15.1: Clinical Presentation of Syphilis

Source: DiPiro JT, et al(2008): Pharmacotherapy: A Pathophysiologic Approach (7th ed)

STEP 4: Diagnosis of Syphilis (20 minutes)

• Syphilis diagnosis is based on the;
o patient’s history,
o physical examination,
o laboratory testing and
o Radiology
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• The available laboratory tests for diagnosis of syphilis include
o direct detection methods (i.e. darkfield microscopy, direct fluorescent antibody test
and nucleic acid amplification test),
o serology tests such as;
▪ Treponemal tests which include the Treponema pallidum haemagglutination
assay (TPHA), the Treponema pallidum particle agglutination assay (TPPA) and
the fluorescent treponemal antibody absorbed (FTA-ABS) tests
▪ Non-treponemal tests (the microscopic Venereal Diseases Research Laboratory -
VDRL and the macroscopic rapid plasma reagin –RPR tests),
o Examination of cerebrospinal fluids
o Rapid diagnostic tests (RDTs) for treponemal antibodies in syphilis infection

STEP 6: Pharmacological Treatment of Syphilis (40 minutes)

Activity: Small Group Discussion ( 20 minutes)

DIVIDE students into small manageable groups

ASK students to discuss on the following question

• What is the treatement of Gonorrhoea?

ALLOW students to discuss for 15 minutes

ALLOW few groups to present and the rest to add points not mentioned

CLARIFY and SUMMARIZE by using the contents below

• Parenteral penicillin G is the treatment of choice for all stages of syphilis.

• Because T. pallidum multiplies slowly, single doses of short- or intermediate-acting
penicillins do not provide the prolonged, low-level exposure to penicillin required for
eradication of the treponeme.
o A result, benzathine penicillin G is the only penicillin effective for single-dose
therapy.
• The recommended treatment for syphilis of less than 1 year’s duration is benzathine
penicillin G 2.4 million units as a single dose.
o Units can be administered once a week for 2 consecutive weeks.
• In patients with syphilis of longer than 1 year’s duration and normal CSF examination,
benzathine penicillin G is administered weekly for three successive doses
• Treatment is summarized in the table below;

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Table 15.2 Treatment of various forms of Gonorrhoea Infection

Source: DiPiro JT, et al(2008): Pharmacotherapy: A Pathophysiologic Approach (7th ed)

STEP 7: Monitoring of Syphilis Therapy (10 minutes)

• Non treponemal tests should be performed at 6 and 12 months in all patients treated
for primary and secondary syphilis and at 6, 12, and 24 months for early and late latent
disease.
• More frequent monitoring of HIV-infected individuals (i.e., 3, 6, 9, 12, and 24 months
after therapy) should be done
• In general, the time to reach seronegativity is proportional to the duration of the disease.
Table 15–1 also includes specific testing recommendations for other stages of syphilis.
• Despite adequate therapy, some patients can remain seropositive based on nontreponemal
test results.
• In these cases, stabilization of low antibody titers is indicative of adequate therapy.
• For women treated during pregnancy, monthly quantitative nontreponemal tests are
recommended in those at high risk of reinfection.

STEP 8: Key Points (5 minutes)

• Syphilis is a systemic disease from the outset and is caused by the spirochaete,
Treponema pallidum (T. pallidum)
• The infection can be classified as congenital (transmitted from mother to child in utero) or
acquired (through sex or blood transfusion)
• Acquired syphilis is divided into early and late syphilis
• Early syphilis comprises the primary, secondary and early latent stages while late syphilis
refers to late latent syphilis, gummatous, neurological and cardiovascular syphilis
• Long-acting benzathine benzylpenicillin provides optimal treponemicidal penicillinaemia
and is recommended for syphilis treatment

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STEP 9: Evaluation (5 minutes)
• What is Syphilis?
• What are the signs and symptoms of syphilis?
• What is the treatment of Syphilis?
• How will you monitor patient on syphilis therapy?

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References

Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

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Session 16: Pharmacotherapy of Chlamydial Genital Tract
Infections
Total Session Time: 120 minutes
Prerequisites
• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define chlamydial genital tract infections
• Explain pathophysiology of chlamydial genital tract infections
• Explain the clinical presentation of chlamydial genital tract infections
• Outline diagnosis of chlamydial genital tract infections
• Describe pharmacological treatment of chlamydial genital tract infections
• Describe the monitoring of chlamydial genital tract infections therapy

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers

SESSION OVERVIEW

Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Tasks
10 minutes Presentation Definition of Chlamydial Genital Tract
2
Buzzing Infections
15 minutes Pathophysiology of Chlamydial Genital
3 Presentation
Tract Infections
20 Minutes Clinical Presentation of Chlamydial Genital
4 Presentation
Tract Infections
10 minutes Presentation Diagnosis of Chlamydial Genital Tract
5
Infections
40 minutes Presentation Pharmacological Treatment of Chlamydial
6 Small Group Genital Tract Infections
Discussion
10 minutes Presentation Monitoring of Chlamydial Genital Tract
7 InfectionsTherapy

8 05 minutes Presentation Key Points

9 05 minutes Presentation Evaluation

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SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)

READ or ASK students to read the learning Tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of Chlamydial Genital Tract Infections (10 minutes)

Activity: Buzzing (2 minutes)

ASK students to pair up and buzz on the following question for 2 minutes

• What is Chlamydial Genital Tract Infections?

ALLOW few pairs to respond and let other pairs to add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZEby using the content below

Chlamydial Genital Tract Infections

• Chlamydial Genital Tract Infections is a sexually transmissible infection caused by
bacterium Clamydia Trachomatis
• Persons infected with the bacterium may not have symptoms of infection but can still
transmit the bacterium.
• Chlamydia can affect the urethra (the urine passage), cervix (the neck of the womb),
rectum and anus, throat, and eyes.

STEP 3: Pathophysiology of Chlamydial Genital Tract Infections

(15 minutes)
• C. trachomatis is an obligate intracellular parasite that shares properties of both viruses
and bacteria.
• Like viruses, chlamydiae require cellular material from host cells for replication;
however, unlike viruses, chlamydiae maintain their cellular identity throughout
development.
• Although C. trachomatis lacks a cell-wall peptidoglycan, its major outer membrane is
similar to gram-negative bacteria.
• At least 18 serovars (subspecies) of C. trachomatis exist, of which only the
lymphogranuloma venereum strains produce potentially invasive infections.
• The remaining serovars are involved primarily with superficial infection of epithelial
cells.
• Chlamydiae have the ability to establish long-term associations with host cells.

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• When an infected host cell is starved for various nutrients such as amino acids (for
example, tryptophan), iron, or vitamins, this has a negative consequence for Chlamydiae
since the organism is dependent on the host cell for these nutrients.
• The starved chlamydiae enter a persistent growth state wherein they stop cell division and
become morphologically aberrant by increasing in size.
• Persistent organisms remain viable as they are capable of returning to a normal growth
state once conditions in the host cell improve and causing chronic chlamydial diseases.

STEP 4: Clinical Presentation of Chlamydial Genital Tract Infections

(20 minutes)
• In comparison with gonorrhea, chlamydial genital tract infections are more frequently
asymptomatic, and when present, symptoms tend to be less noticeable.
• Urethral discharge usually is less profuse and more mucoid or watery than the urethral
discharge associated with gonorrhea.
• Table 16–1 summarizes the usual clinical presentation of chlamydial infections.

Table 16.1: Clinical Presentation of Chlamydial Genital Tract Infections

Source: DiPiro JT, et al(2008): Pharmacotherapy: A Pathophysiologic Approach (7th ed)

STEP 5: Diagnosis of Chlamydial Genital Tract Infections (10 minutes)

• A sample of urine can be collected and analyzed in the laboratory to investigate the
presence of this infection.
• A swab of the discharge can be collected for culture or antigen testing for chlamydia.

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• Nucleic acid amplification tests (NAAT), such as polymerase chain reaction (PCR),
transcription mediated amplification (TMA), and the DNA strand displacement
amplification (SDA) now are the mainstays.
• NAAT for chlamydia may be performed on swab specimens sampled from the cervix
(women) or urethra (men), on self-collected vaginal swabs, or on voided urine

STEP 6: Pharmacological Treatment of Chlamydial Genital Tract

Infections (40 minutes)

Activity: Small Group Discussion ( 20 minutes)

DIVIDE students into small manageable groups

ASK students to discuss on the following question

• What is the treatment of Chlamydial Genital Tract Infections?

ALLOW students to discuss for 10 minutes

ALLOW few groups to present and the rest to add points not mentioned

CLARIFY and SUMMARIZE by using the contents below

Table 16.2 Treatment of Chlamydial Genital Tract Infections

Source: DiPiro JT, et al(2008): Pharmacotherapy: A Pathophysiologic Approach (7th ed)

STEP 7: Monitoring of Chlamydial Genital Tract Infections Therapy

(10 minutes)
• Treatment of chlamydial infections with the recommended regimens is highly effective;
therefore, post-treatment laboratory testing is not recommended routinely unless
symptoms persist or there are other specific concerns (e.g., pregnancy).
• Post-treatment tests should not be performed for at least 3 weeks following completion
of therapy.
• When post-treatment tests are positive, they usually represent noncompliance, failure to
treat sexual partners, or laboratory error rather than inadequate therapy or resistance to
therapy.
PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator
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• Infants with pneumonitis should receive follow-up testing because erythromycin is only
80% effective, and a second course of therapy can be necessary

STEP 8: Key Points (5 minutes)

• Chlamydia is a sexually transmissible infection caused by bacterium Clamydia
Trachomatis
• Persons infected with the bacterium may not have symptoms of infection but can still
transmit the bacterium.
• Azithromycin is drug of choice for the treatment of chlamydia infection

STEP 9: Evaluation (5 minutes)

• What is Clamydia infection?
• What is the pathophysiology of Clamydial infection?
• What are the signs and symptoms of Clamydia infection?
• How is the treatment of Clamydia Infection?

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References

Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

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Session 17: Pharmacotherapy of Genital Herpes

Total Session Time: 120 minutes

Prerequisites
• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define genital herpes
• Explain pathophysiology of genital herpes
• Explain the clinical presentation of genital herpes
• Outline diagnosis of genital herpes
• Describe pharmacological treatment of genital herpes
• Describe the monitoring of genital herpes therapy

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Computer and LCD Projector

SESSION OVERVIEW

Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Tasks
15 minutes Presentation Definition of Genital Herpes
2
Buzzing
20 minutes Pathophysiology of Genital Herpes
3 Presentation

4 10 minutes Presentation Clinical Presentation of Genital Herpes

5 10 minutes Presentation Diagnosis of Genital Herpes

40 minutes Presentation Pharmacological Treatment of Genital

6 Small Group Herpes
Discussion
10 minutes Presentation Monitoring of Genital Herpes Therapy
7

8 05 minutes Presentation Key Points

9 05 minutes Presentation Evaluation

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SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)

READ or ASK students to read the learning Tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of Genital Herpes (15 minutes)

Activity: Buzzing (5 minutes)

ASK students to pair up and buzz on the following question for 2 minutes

• What is Genital Herpes?

ALLOW few pairs to respond and let other pairs to add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZEby using the content below

Genital Herpes
• Genital herpes is a common sexually transmitted infection caused by the herpes simplex
virus (HSV).
• Sexual contact is the primary way that the virus spreads.
• There are two types of Herpes Simplex viruses; herpes simplex virus type 1 (HSV-1) and
herpes simplex virus type 2 (HSV-2).
• HSV-1 is associated most commonly with oropharyngeal disease, and HSV-2 is
associated most closely with genital disease;
o However, each virus is capable of causing clinically indistinguishable infections in
both anatomic areas.
• Humans are the sole known reservoir for HSV.
• Infection is transmitted via inoculation of virus from infected secretions onto mucosal
surfaces (e.g., urethra, oropharynx, cervix, and conjunctivae) or through abraded skin.
• The cycle of HSV infection occurs in five stages: primary muco-cutaneous infection,
infection of the ganglia, establishment of latency, reactivation, and recurrent infection.

STEP 3: Pathophysiology of Genital herpes (20 minutes)

• After viral inoculation, HSV infection is associated with cytoplasmic granulation,
ballooning degeneration of cells, and production of mononucleated giant cells.

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• Initially, the cellular response is predominantly polymorphonuclear, followed by a
lymphocytic response.
• Replication occurs with viral spread to contiguous cells and peripheral sensory nerves.
Latency then is established in sensory or autonomic nerve root ganglia.
• Latency appears to be lifelong, interrupted only by reactivation of the viral infection.
• It is unclear what factors are important in maintaining latency, but immune responses and
emotional and physical stresses appear important in reactivating latent virus.

STEP 4: Clinical Presentation of Genital herpes (10 minutes)

• The signs and symptoms of genital herpes infection are influencedby many factors,
including previous exposure to HSV, viral type, and host factors such as age and site of
infection.
• High percentage of initial and recurrent infections are asymptomatic,
• Viral shedding can occur in the absence of apparent lesions or symptoms
• A summary of the clinical presentation of genital herpes is provided in Table 17–1 .

Table 17.1: Clinical Presentation of Genital Herpes Infection

Source: DiPiro JT, et al(2008): Pharmacotherapy: A Pathophysiologic Approach (7th ed)

STEP 5: Diagnosis of Genital herpes (10 minutes)

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• A presumptive diagnosis of genital herpes commonly is made based on the presence of
dark-fieldnegative, vesicular, or ulcerative genital lesions.
o A prior history of similar lesions or recent sexual contact with an individual with
similar lesions also is useful in making the diagnosis
• Viral culture. This test involves taking a tissue sample or scraping of the sores for
examination in the laboratory.
• Polymerase chain reaction (PCR) test. PCR is used to copy patient DNA from a blood
sample, tissue from a sore or spinal fluid.
o The DNA can then be tested to establish the presence of HSV and determine which
type of HSV you have.
• Blood test. This test analyzes a sample of blood for the presence of HSV antibodies to
detect a past herpes infection.
• Several serologic tests capable of distinguishing HSV-1 and HSV-2 antibodies are
available.
o These tests detect antibodies to type-specific HSV-1 and HSV-2 proteins gG-1 and
gG-2, respectively

STEP 6: Pharmacological Treatment of Genital Herpes (40 minutes)

Activity: Small Group Discussion ( 10 minutes)

DIVIDE students into small manageable groups

ASK students to discuss on the following question

• What is the treatment of Genital Herpes?

ALLOW students to discuss for 15 minutes

ALLOW few groups to present and the rest to add points not mentioned

CLARIFY and SUMMARIZE by using the contents below

• The most achievable goals in the management of genital herpes are to relieve symptoms
and to shorten the clinical course, to prevent complications and recurrences, and to
decrease disease transmission.
• Although research has focused primarily on the treatment of active infection and
suppression of recurrences, increasing emphasis is being placed on various approaches,
including immunotherapy that might provide protection from disease transmission or
possibly eliminate established latency.
• Oral formulations of acyclovir, famciclovir, and valacyclovir have demonstrated efficacy
in reducing viral shedding, duration of symptoms, and time to healing of first-episode
genital herpes infections, with maximal benefits seen when therapy is initiated at the
earliest stages of infection.

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• Table 17.2 below summarizes the treatment of genital herpes as follows;

Table 17.2 Treatment of Genital herpes

Source: DiPiro JT, et al(2008): Pharmacotherapy: A Pathophysiologic Approach (7th ed)

STEP 7: Monitoring of Genital Herpes Therapy (10 minutes)

• Available antiviral compounds are of greatest benefit in patients experiencing first-
episode primary infections, immunocompromised patients, and patients with frequent or
severe recurrent infections.
• Antivirals, however, are palliative and not curative, and patients receiving these agents
should be monitored closely for adverse drug effects.
• Discontinuation of suppressive therapy after 1 year should be considered to assess for
possible changes in the patient’s intrinsic pattern of recurrence.
• In many patients, decreases in recurrence rates and the severity of symptoms occur over
time. However, it is also prefered to continue suppressive therapy indefinitely because it
significantly reduces asymptomatic viral shedding, a potential benefit in reducing the risk
of disease transmission to uninfected sexual partners

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STEP 8: Key Points (5 minutes)
• Genital herpes is a common sexually transmitted infection caused by the herpes simplex
virus (HSV).
• Infection is transmitted via inoculation of virus from infected secretions onto mucosal
surfaces (e.g., urethra, oropharynx, cervix, and conjunctivae) or through abraded skin
• The signs and symptoms of genital herpes infection are influencedby many factors,
including previous exposure to HSV, viral type, and host factors such as age and site of
infection
• Oral formulations of acyclovir, famciclovir, and valacyclovir have demonstrated efficacy
in the treatment of genital herpes

STEP 9: Evaluation (5 minutes)

• What is genital herpes?
• What is the pathophysiology of genital herpes?
• What are the signs and symptoms of genital herpes?
• How is the treatment of genital herpes?

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References

Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

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Session 18: Pharmacotherapy of Urinary Tract Infections
Total Session Time: 120 minutes
Prerequisites
• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define urinary tract infections
• Explain pathophysiology of urinary tract infections
• Explain the clinical presentation of urinary tract infections
• Outline diagnosis of urinary tract infections
• Describe pharmacological treatment of urinary tract infections
• Describe the monitoring of urinary tract infections therapy

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Computer and LCD Projector

SESSION OVERVIEW

Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Tasks
20 minutes Presentation Definition of Urinary Tract Infections
2
Buzzing
20 minutes Pathophysiology of Urinary Tract Infections
3 Presentation

10 minutes Clinical Presentation of Urinary Tract

4 Presentation
Infections
5 10 minutes Presentation Diagnosis of Urinary Tract Infections

35 minutes Presentation Pharmacological Treatment of Urinary Tract

6 Small Group Infections
Discussion
10 minutes Presentation Monitoring of Urinary Tract Infections
7
Therapy
8 05 minutes Presentation Key Points

9 05 minutes Presentation Evaluation

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SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)

READ or ASK students to read the learning Tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of Urinary Tract Infections (20 minutes)

Activity: Buzzing (5 minutes)

ASK students to pair up and buzz on the following question for 2 minutes

• What is Urinary Tract Infections?

ALLOW few pairs to respond and let other pairs to add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZEby using the content below

Urinary Tract Infections (UTI)

• UTI is defined as the presence of microorganisms in the urinary tract that cannot be
accounted for by contamination.
• The organisms present have the potential to invade the tissues of the urinary tract and
adjacent structures.
• Infection may be limited to the growth of bacteria in the urine, which frequently may not
produce symptoms.
• A UTI can present as several syndromes associated with an inflammatory response to
microbial invasion and can range from asymptomatic bacteriuria to pyelonephritis with
bacteremia or sepsis.
• UTIs are classified by lower and upper urinary tract infections.
• Upper tract infection include pyelonephritis (an infection involving the kidneys)
represents
• Lower tract infections correspond to cystitis (bladder),
• Also, UTIs are designated as uncomplicated or complicated.
• Uncomplicated infections occur in individuals who lack structural or functional
abnormalities of the urinary tract that interfere with the normal flow of urine or voiding
mechanism.
• These infections occur in females of child-bearing age (15 to 45 years) who are otherwise
normal healthy individuals.

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• Complicated UTIs are the result of a predisposing lesion of the urinary tract, such as a
congenital abnormality or distortion of the urinary tract, a stone, indwelling catheter,
prostatic hypertrophy, obstruction, or neurologic deficit that interferes with the normal

Table18.1 Classification of UTIs

STEP 3: Pathophysiology of Urinary Tract Infections (20 minutes)

• The bacteria causing UTIs usually originate from bowel flora of the host.
• Although virtually every organism is associated with UTIs, certain organisms
predominate as a result of specific virulence factors.
• The most common cause of UTIs is Escherichia coli , which accounts for 80% to 90% of
community-acquired infections.
• Additional causative organisms in uncomplicated infections include Staphylococcus
saprophyticus , Klebsiella pneumoniae, Proteus spp., Pseudomonas aeruginosa , and
Enterococcus spp.
• Pathogenic organisms have differing degrees of pathogenicity (virulence), which play a
role in the development and severity of infection.
• Bacteria that adhere to the epithelium of the urinary tract are associated with colonization
and infection
• The mechanism of adhesion of gram-negative bacteria, particularly E. coli, is related to
bacterial fimbriae that are rigid, hair-like appendages of the cell wall
• These fimbriae adhere to specific glycolipid components on epithelial cells
• The most common type of fimbriae is type 1, which binds to mannose residues present in
glycoproteins
• Glycosaminoglycan and Tamm-Horsfall protein are rich in mannose residues that readily
trap those organisms that contain type 1 fimbriae, which are then washed out of the
bladder.
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• Other fimbriae are mannose resistant and are associated more frequently with
pyelonephritis, such as P fimbriae, which bind avidly to specific glycolipid receptors on
uroepithelial cells
• These bacteria are resistant to washout or removal by glycosaminoglycan and are able to
multiply and invade tissue, and causing infection

STEP 4: Clinical Presentation of UTIs (10 minutes)

Signs and symptoms
• Lower UTI: dysuria, urgency, frequency, nocturia, suprapubic heaviness
• Gross hematuria
• Upper UTI: flank pain, fever, nausea, vomiting, malaise

Physical examination
Upper UTI: costovertebral tenderness

Laboratory tests
• Bacteriuria
• Pyuria (white blood cell count >10/mm 3 )
• Nitrite-positive urine (with nitrite reducers)
• Leukocyte esterase-positive urine
• Antibody-coated bacteria (upper UTI)

STEP 5: Diagnosis of UTIs (10 minutes)

• Symptoms alone are unreliable for the diagnosis of bacterial UTIs.
• The key to the diagnosis of UTI is the ability to demonstrate significant numbers of
microorganisms in an appropriate urine specimen to distinguish contamination from
infection.
• Urine testing
o The gold standard for a urine test is to perform a bacteriological urine culture, with
identification of the pathogen, with quantification and sensitivity testing.
o To test whether the patient has a UTI at all, orientating indirect methods are often
used in practice to detect the bacteria or inflammation (dip sticks).
o The bacterial count may be assessed by urine microscopy and immersion culture
media.
o Midstream urine is normally collected

• Dip sticks
o Urine dip sticks are one of the most frequently used instruments for diagnostic testing
if there is clinical evidence that a patient is suffering from UTI.
o Multistix are most often used, which may be able to detect nitrite (a metabolic product
of typical pathogens of the urinary tract), leukocyte esterase, protein and blood (as a
marker of inflammation).
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 o If nitrite is detected, this increases the probability of a urinary tract infection, with a
likelihood ratio [LR] of 2.6 to 10.6.
o However, the sensitivity is relatively low.
o In contrast, the detection of leukocyte esterase increases the probability to a lesser
degree (LR 1.0 to 2.6). The detection of blood is admittedly highly sensitive, but the
specificity is low.

• Urine microscopy
o Due to methodological limitations the sensitivity in detecting UTI with <105 cfu/mL
by gram stained microscopy is low.

• Immersion culture media

o These immersion tests use a plastic rod coated with culture medium—mostly a
combination of CLED agar and MacConkey agar.
o They require 24 h culture.

STEP 6: Pharmacological Treatment of UTIs (35 minutes)

Activity: Small Group Discussion ( 20 minutes)

DIVIDE students into small manageable groups

ASK students to discuss on the following question

• What is the treatment of UTI?

ALLOW students to discuss for 15 minutes

ALLOW few groups to present and the rest to add points not mentioned

CLARIFY and SUMMARIZE by using the contents below

• The management of a patient with a UTI includes;

o Initial evaluation,
o Selection of an antibacterial agent and duration of therapy, and
o Followup evaluation.
• The initial selection of an antimicrobial agent for the treatment of UTI is based primarily
on;
o The severity of the presenting signs and symptoms,
o The site of infection, and
o Whether the infection is determined to be uncomplicated or complicated.
• Other considerations include antibiotic susceptibility, side-effect potential, cost, and the
comparative inconvenience of different therapies.

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Table 18.2 Emprical Treatment of UTIs

Source: DiPiro JT, et al(2008): Pharmacotherapy: A Pathophysiologic Approach (7th ed)

Table 18:3 Treatement of UTI according to Pathogen

Source: DiPiro JT, et al(2008): Pharmacotherapy: A Pathophysiologic Approach (7th ed)

STEP 7: Monitoring of UTI Therapy (10 minutes)

• In asymptomatic post-treatment patients routine urinalysis and/or urine culture is not
recommended
• In patients with persistent symptoms, microbiological screening is recommended.
• In women whose symptoms do not resolve by end of treatment, and in those whose
symptoms resolve but recur within two weeks, urine culture and antimicrobial
susceptibility testing should be performed

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• For therapy in this situation, one should assume that the infecting organism is not
susceptible to the agent originally used.
• Retreatment with a seven day regimen using another agent should be considered
• Antibiotic treatments may be repeated with a more prolonged course, higher dosage
and/or different compounds for patients with recurrent infections

STEP 8: Key Points (5 minutes)

• UTI is defined as the presence of microorganisms in the urinary tract that cannot be
accounted for by contamination.
• UTIs are classified by lower and upper urinary tract infections.
• The most common cause of UTIs is Escherichia coli , which accounts for 80% to 90% of
community-acquired infections
• Signs and Symptoms of UTI include dysuria, urgency, frequency, nocturia, suprapubic
heaviness
• Variety of antibiotics can be used for the treatment of UTI

STEP 9: Evaluation (5 minutes)

• What is UTIs?
• What is the pathophysiology of UTIs?
• What are the signs and symptoms of uncomplicated UTI?
• How is the treatment of Uncomplicated UTI?

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References

Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

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Session 19: Pharmacotherapy of Folliculitis, Furunculosis
and Carbuncles
Total Session Time: 60 minutes
Prerequisites
• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define folliculitis, furunculosis and carbuncles
• Explain pathophysiology of folliculitis, furunculosis and carbuncles
• Explain the clinical presentation of folliculitis, furunculosis and carbuncles
• Outline diagnosis of folliculitis, furunculosis and carbuncles
• Describe pharmacological treatment of folliculitis, furunculosis and carbuncles
• Describe the monitoring of folliculitis, furunculosis and carbuncles therapy

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Computer and LCD Projector

SESSION OVERVIEW

Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Tasks
05 minutes Presentation Definitions of Folliculitis, Furunculosis and
2
Buzzing Carbuncles
10 minutes Pathophysiology of Folliculitis,
3 Presentation
Furunculosis and Carbuncles
05 Minutes Clinical Presentation of Folliculitis,
4 Presentation
Furunculosis and Carbuncles
05 minutes Presentation Diagnosis of Folliculitis, Furunculosis and
5
Carbuncles
15 minutes Presentation Pharmacological Treatment of Folliculitis,
6 Small Group Furunculosis and Carbuncles
Discussion

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 05 minutes Presentation Monitoring of Folliculitis, Furunculosis and
7 Carbuncles Therapy

8 05 minutes Presentation Key Points

9 05 minutes Presentation Evaluation

SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)

READ or ASK students to read the learning Tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of Folliculitis, Furunculosis and Carbuncles

(5 minutes)
Activity: Buzzing (2 minutes)

ASK students to pair up and buzz on the following question for 2 minutes

• What are Folliculitis, Furunculosis and Carbuncles?

ALLOW few pairs to respond and let other pairs to add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZEby using the content below

Folliculitis, Furunculosis and Carbuncles

• Folliculitis is inflammation of the hair follicle and is caused by physical injury, chemical
irritation, or infection.
o Infection occurring at the base of the eyelid is referred to as a stye.
o Folliculitis is a superficial infection with pus present only in the dermis,
• Furuncles and carbuncles occur when a follicular infection extends from around the hair
shaft to involve deeper areas of the skin.
o A furuncle, commonly known as an abscess or boil, is a walled-off mass of purulent
material arising from a hair follicle.
• The lesions are called carbuncles when they coalesce and extend to the subcutaneous
tissue.
o This aggregate of infected hair follicles forms deep masses that generally open and
drain through multiple sinus tracts.
• S. aureus is the most common cause of folliculitis, furuncles, and carbuncles.
• Inadequate chlorine levels in whirlpools, hot tubs, and swimming pools have been
responsible for outbreaks of folliculitis caused by P. aeruginosa .

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STEP 3: Pathophysiology of Folliculitis, Furunculosis and Carbuncles
(10 minutes)
• The skin and subcutaneous tissues normally are extremely resistant to infection but may
become susceptible under certain conditions.
• Even when high concentrations of bacteria are applied topically or injected into the soft
tissue, resulting infections are rare.
• Several host factors act together to confer protection against skin infections.
• Because the surface of the skin is relatively dry and has a pH of approximately 5.6, it is
not conducive to bacterial growth.
• Continuous renewal of the epidermal layer results in the shedding of keratocytes, as well
as skin bacteria.
• In addition, sebaceous secretions are hydrolyzed to form free fatty acids that strongly
inhibit the growth of many bacteria and fungi.
• Conditions that may predispose a patient to the development of skin infections include
o high concentrations of bacteria (>10 5 microorganisms),
o excessive moisture of the skin,
o inadequate blood supply,
o availability of bacterial nutrients, and
o Damage to the corneal layer allowing for bacterial penetration.
• The majority of Skin and Soft Tissue Infections result from the disruption of normal host
defenses by processes such as skin puncture, abrasion, or underlying diseases (e.g.,
diabetes).
• The nature and severity of the infection depend on both the type of microorganism
present and the site of innoculation.

STEP 4: Clinical Presentation and Diagnosis of Folliculitis, Furunculosis

and Carbuncles (10 minutes)
Folliculitis
• Pruritic, erythematous papules typically appear within 48 hours (range: 6 to 72 hours) of
exposure to large numbers of organisms.
• Papules evolve into pustules that generally heal in several days.
• Systemic signs such as fever and malaise are uncommon, although they have been
reported in cases caused by P. aeruginosa.

Furuncles/ Furunculosis
• Furuncles can occur anywhere on hairy skin but generally develop in areas subject to
friction and perspiration.
• Furuncles are discrete lesions, whether occurring as singular or multiple nodules.
• The lesion starts as a firm, tender, red nodule that becomes painful and fluctuant.
• Lesions often drain spontaneously.

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• Lesions caused by CA-MRSA often have necrotic centers characteristic of “spider bites.”
• Culture of lesion for laboratory investigation to conform the prensence and the type of the
pathogen

Carbuncles
• Carbuncles are broad, swollen, erythematous, deep, and painful follicular masses.
• Carbuncles commonly develop on the back of the neck and are more likely to occur in
patients with diabetes.
• Unlike folliculitis and furuncles, carbuncles are commonly associated with fever, chills,
and malaise.
• Bacteremia with secondary spread to other tissues is common
• Culture of lesion for laboratory investigation to conform the prensence and the type of the
pathogen

STEP 5: Pharmacological Treatment of Folliculitis, Furunculosis and

Carbuncles (15 minutes)

Activity: Small Group Discussion ( 10 minutes)

DIVIDE students into small manageable groups

ASK students to discuss on the following question

• What is the treatment of Folliculitis, Furunculosis and Carbuncles?

ALLOW students to discuss for 10 minutes

ALLOW few groups to present and the rest to add points not mentioned

CLARIFY and SUMMARIZE by using the contents below

• Treatment of folliculitis generally requires only local measures, such as warm moist
compresses or topical therapy (e.g., clindamycin, erythromycin, mupirocin,
or benzoyl peroxide).
o Topical agents generally are applied two to four times daily for 7 days.
• Small furuncles generally can be treated with moist heat, which promotes localization and
drainage of pus.
• Large and/or multiple furuncles and carbuncles require incision and drainage.
• Systemic antibiotics are usually not necessary unless accompanied by fever or extensive
cellulitis.
• Treatment of more severe infections generally consists of a penicillinase-resistant
penicillin (such as dicloxacillin) or a first-generation cephalosporin (such as cephalexin)
for 5 to 10 days
• Treatment is summarized in the table 19:1

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Table 19.1 treatment of Folliculitis, Furuncles and Cubancles

Source: DiPiro JT, et al(2008): Pharmacotherapy: A Pathophysiologic Approach (7th ed)

STEP 6: Monitoring of Folliculitis, Furuncles and Carbuncles Therapy (5

minutes)
• Many follicular infections resolve spontaneously without medical or surgical intervention.
• Lesions should be incised if they do not respond to a few days of moist heat and
nonprescription topical agents.
• Following drainage, most lesions begin to heal within several days without antimicrobial
therapy.
• Any patient who is unresponsive to several days of therapy with a penicillinase-resistant
penicillin or first-generation cephalosporin should have a culture and sensitivity
Performed because of the increasing frequency of MRSA.

STEP 7: Key Points (5 minutes)

• Folliculitis is inflammation of the hair follicle and is caused by physical injury, chemical
irritation, or infection
• Symptoms of Folliculitis include Pruritic, erythematous papules typically appear within
48 hours (range: 6 to 72 hours) of exposure to large numbers of organisms
• Treatment of folliculitis generally requires only local measures, such as warm moist
compresses or topical therapy

STEP 8: Evaluation (5 minutes)

• What are Folliculitis, Furuncles and Carbuncles?
• What is the pathophysiology of Folliculitis, Furuncles and Carbuncles?
• What are the signs and symptoms of Folliculitis, Furuncles and Carbuncles?
• How is the treatment of Folliculitis, Furuncles and Carbuncles?

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References

Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

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Session 20: Pharmacotherapy of Vulvovaginal Candidiasis
Total Session Time: 120 minutes
Prerequisites
• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define vulvovaginal candidiasis
• Explain pathophysiology of vulvovaginal candidiasis
• Explain the clinical presentation of vulvovaginal candidiasis
• Outline diagnosis of vulvovaginal candidiasis
• Describe pharmacological treatment of vulvovaginal candidiasis
• Describe the monitoring of vulvovaginal candidiasis therapy

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Computer and LCD Projector

SESSION OVERVIEW

Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Tasks
15 minutes Presentation Definition of Vulvovaginal Candidiasis
2
Buzzing
20 minutes Pathophysiology of Vulvovaginal
3 Presentation Candidiasis

10 Minutes Clinical Presentation of Vulvovaginal

4 Presentation
Candidiasis
5 10 minutes Presentation Diagnosis of Vulvovaginal Candidiasis

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 30 minutes Presentation Pharmacological Treatment of Vulvovaginal
6 Small Group Candidiasis
Discussion
20 minutes Presentation Monitoring of Vulvovaginal Candidiasis
7
Therapy
8 05 minutes Presentation Key Points

9 05 minutes Presentation Evaluation

SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)

READ or ASK students to read the learning Tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of Vulvovaginal Candidiasis (15 minutes)

Activity: Buzzing (2 minutes)

ASK students to pair up and buzz on the following question for 2 minutes

• What is Vulvovaginal Candidiasis?

ALLOW few pairs to respond and let other pairs to add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZEby using the content below

Vulvovaginal Candidiasis
• Vulvovaginal candidiasis (VVC) refers to infections in individuals with or without
symptoms who have positive vaginal cultures for Candida species.
• Depending on episodic frequency, VVC can be classified as either;
o Sporadic or
o Recurrent.
• This classification is essential to understanding the pathophysiology, as well as the
Pharmacotherapy, of VVC.
• VVC may also be classified as;
o uncomplicated, which refers to sporadic infections that are susceptible to all forms of
antifungal therapy regardless of the duration of treatment, or
o Complicated, in which consideration of factors affecting the host, microorganism, and
pharmacotherapy all have an essential role in successful treatment.

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• Complicated VVC includes recurrent VVC, severe disease, non– Candida albicans
candidiasis, and host factors, including diabetes mellitus, immunosuppression,
and pregnancy

STEP 3: Pathophysiology of Vulvovaginal Candidiasis (20 minutes)

• Candida albicans is the major pathogen responsible for VVC, accounting for 80% to 92%
of symptomatic episodes.
• The remainders are caused by non– C. albicans species, with Candida glabrata
dominating.
• The number of cases of non– C. albicans candidiasis appears to be increasing, possibly
related to the use of nonprescription vaginal antifungal preparations and short-course
therapy and/ or the increased use of long-term maintenance therapy in preventing
recurrent infections.
• Candida species can act as commensal members of the vaginal flora.
• Asymptomatic colonization with Candida species has been found in 10% to 20% of
women of reproductive age.
• Candida organisms are dimorphic;
o blastospores are believed to be responsible for colonization (transmission and spread),
whereas
o Germinated Candida forms are associated with tissue invasion and symptomatic
infections.
• To colonize the vagina, Candida species must be able to attach to the mucosa. The
attachment process is complex.
• Not only are candidal surface structures important for attachment, but appropriate
receptors for attachment must be present in the epithelial tissue.
• Not all women have the same range of receptors, which may explain variation in
colonization.
• Changes in the host’s vaginal environment or response are necessary to induce a
symptomatic infection.
• Unfortunately, in most cases of symptomatic VVC, no precipitating factor can be
identified.

STEP 4: Clinical Presentation and Diagnosis of Vulvovaginal Candidiasis

(20 minutes)
General
Often involves both the vulva and the vagina

Symptoms
Intense vulvar itching, soreness, irritation, burning on urination, and dyspareunia

Signs
Erythema, fissuring, curdy “cheese”-like discharge, satellite lesions, edema
PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator
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Laboratory tests
Vaginal pH—normal, saline and 10% KOH microscopy— blastospores or pseudohyphae
Other diagnostic tests
Candida cultures not recommended unless classic signs and symptoms with normal vaginal
pH and microscopy are inconclusive or recurrence is suspected

STEP 5: Pharmacological Treatment of Vulvovaginal Candidiasis

(30 minutes)
Activity: Small Group Discussion ( 20 minutes)

DIVIDE students into small manageable groups

ASK students to discuss on the following question

• What is the treatment of Vulvovaginal Candidiasis?

ALLOW students to discuss for 15 minutes

ALLOW few groups to present and the rest to add points not mentioned

CLARIFY and SUMMARIZE by using the contents below

• The management of a patient with a UTI includes;

o initial evaluation,
o selection of an antibacterial agent and duration of therapy, and
o Followup evaluation.
• The initial selection of an antimicrobial agent for the treatment of UTI is based primarily
on;
o the severity of the presenting signs and symptoms,
o the site of infection, and
o Whether the infection is determined to be uncomplicated or complicated.
• Other considerations include antibiotic susceptibility, side-effect potential, cost, and the
comparative inconvenience of different therapies.

Table 20.1 Treatment of Uncomplicated Vulvoviginal candidiasis

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Source: DiPiro JT, et al(2008): Pharmacotherapy: A Pathophysiologic Approach (7th ed)

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Complicated Vulvovaginal Candidiasis
• Complicated VVC occurs in patients who are immunocompromised or have uncontrolled
diabetes mellitus and pregnant.
• These individualsneed a more aggressive treatment plan.
• Current recommendations are to lengthen therapy to 10 to 14 days regardless of the route
of administration.
• Therapeutic options include those listed in Table 20–1 above; however, regimens should
be continued for 10 to 14 days.
• It is also recommended to repeat 150 mg dose of fluconazole 72 hours after the initial
dose for better therapeutic outcomes

Antifungal-Resistant Vulvovaginal Candidiasis

• Resistance to azole antifungals should be considered in individuals who have persistently
positive yeast cultures and fail to respond to therapy despite adherence to prescribed
regimens.
• These infections can be treated with;
o Boric acid Boric acid administered as a 600 mg intravaginal capsule daily for 14 days
of induction therapy, followed by a maintenance regimen of one capsule
intravaginally twice weekly.
▪ Boric acid should not be administered orally, as it is toxic.
or
o 5-Flucytosine cream is administered vaginally, 1,000 mg inserted nightly for 7 days.

STEP 6: Monitoring of Vulvovaginal Candidiasis Therapy (20 minutes)

• Efficacy of the antifungal agent is partly influenced by patient adherence to the
medication regimen.
• Patients must be counseled on proper administration and dosing
• Safety end points include monitoring for occurrence of the relevant drug side effects and
drug interactions
• It is still prudent to monitor for hypersensitivity reactions and side effects that
might occur with any medication.
• GI intolerance is more associated with the oral azoles.
• Hepatotoxicity can occur when azole therapy is prolonged beyond 7 to 10 days or high
doses are used.
• Periodic monitoring of liver enzymes (alanine transaminase and aspartate amino-
transferase) should be considered, especially if prolonged therapy (longer than 21 days) is
anticipated.
• Patients who are receiving IV amphotericin B require daily monitoring by the pharmacist.

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STEP 7: Key Points (5 minutes)
• Vulvovaginal candidiasis (VVC) refers to infections in individuals with or without
symptoms who have positive vaginal cultures for Candida species
• Symptoms include intense vulvar itching, soreness, irritation, burning on urination, and
dyspareunia
• Azole antifungals and other topical antifungals are drug of choice for culvovaginal
candidiasis

STEP 8: Evaluation (5 minutes)

• What is Vulvovaginal Candidiasis?
• What is the pathophysiology of Vulvovaginal Candidiasis?
• What are the signs and symptoms of Vulvovaginal Candidiasis?
• How is the treatment of Vulvovaginal Candidiasis?

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Guide 149
References

Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

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Guide 150
Session 21: Pharmacotherapy of Asthma
Total Session Time: 120 minutes
Prerequisites
• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define asthma
• Explain pathophysiology of asthma
• Explain the clinical presentation of asthma
• Outline diagnosis asthma
• Describe pharmacological treatment of asthma
• Describe the monitoring of asthma

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Computer and LCD Projector

SESSION OVERVIEW

Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Tasks
15 minutes Presentation Definition of Asthma
2
Buzzing
20 minutes Pathophysiology of Asthma
3 Presentation

4 10 minutes Presentation Clinical Presentation of Asthma

5 10 minutes Presentation Diagnosis of Asthma

30 minutes Presentation Pharmacological Treatment of Asthma

6 Small Group
Discussion
20 minutes Presentation Monitoring of Asthma Therapy
7

8 05 minutes Presentation Key Points

9 05 minutes Presentation Evaluation

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SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)

READ or ASK students to read the learning Tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of Asthma (15 minutes)

Activity: Buzzing (2 minutes)

ASK students to pair up and buzz on the following question for 2 minutes

• What is Asthma?
ALLOW few pairs to respond and let other pairs to add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZEby using the content below

Asthma
• Asthma is a common, chronic respiratory disease of the airways of the lung characterized
by either the intermittent or persistent presence of highly variable degrees of airflow
obstruction from airway wall inflammation and bronchial smooth muscle constriction.
• People with asthma experience episodes of wheezing, breathlessness and chest tightness
due to widespread narrowing of the airways.
• The cause of Asthama is unkown but the risk if associated with genetics and
envoromental factors.
• Genetic factors account for 60% to 80% of the susceptibility.
o Asthma represents a complex genetic disorder in that the asthma phenotype is likely a
result of polygenic inheritance or different combinations of genes.
• Environmental risk factors for the development of asthma include;
o socioeconomic status,
o family size,
o exposure to secondhand tobacco smoke in infancy and in utero,
o allergen exposure
o urbanization,
o respiratory syncytial virus infection, and
o decreased
o exposure to common childhood infectious agents

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Table 21:1 List of Agents and Events Triggering Asthma

Source: DiPiro JT, et al(2008): Pharmacotherapy: A Pathophysiologic Approach (7th ed)

STEP 3: Pathophysiology of Asthma (20 minutes)

• The major characteristics of asthma include a variable degree of airflow obstruction
(related to bronchospasm, edema, and mucus hypersecretion) and airways inflammation
• To understand the pathogenetic mechanisms that underlies the many phenotypes of
asthma, it is critical to identify factors that initiate, intensify, and modulate the
inflammatory response of the airways and to determine how these processes produce the
characteristic airway abnormalities.

• The immunohistopathologic features of asthma include inflammatory cell infiltration:

o Neutrophils (especially in sudden-onset, fatal asthma exacerbations; occupational
asthma, and patients who smoke)
o Eosinophils
o Lymphocytes
o Mast cell activation
o Epithelial cell injury
• Airway inflammation contributes to airway hyperresponsiveness, airflow limitation,
respiratory symptoms, and disease chronicity.
• In some patients, persistent changes in airway structure occur, including sub-basement
fibrosis, mucus hypersecretion, injury to epithelial cells, smooth muscle hypertrophy, and
angiogenesis.
• Gene-by-environment interactions are important to the expression of asthma.

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• Atopy, the genetic predisposition for the development of an immunoglobulin E (IgE)-
mediated response to common aeroallergens, is the strongest identifiable predisposing
factor for developing asthma.
• Viral respiratory infections are one of the most important causes of asthma exacerbation
and may also contribute to the development of asthma.

STEP 4: Clinical Presentation and Diagnosis of Asthma (20 minutes)

Clinical Presentation is divided into
• Acute Asthma
• Chronic asthma

Acute asthma
General
An episode can progress over several days or hours (usual scenario) or progresses rapidly
over 1 to 2 hours.
Symptoms
• The patient is anxious in acute distress and complains of severe dyspnea , shortness of
breath, chest tightness, or burning and wheezing sound
• The patient is only able to say a few words with each breath.
• Symptoms are unresponsive to usual measures (shortacting inhaled β 2 –agonist
administration).
Signs
• Signs include expiratory and inspiratory wheezing on auscultation (breath sounds may be
diminished with very severe obstruction),
• dry hacking cough,
• tachypnea,
• tachycardia,
• pale or cyanotic skin,
• hyperinflated chest with intercostal and supraclavicular retractions, and
• Hypoxic seizures if very severe.
Laboratory
• PEF and/or FEV 1 less than 40% of normal predicted values.
• Decreased arterial oxygen (PaO 2 ), and O 2 saturations by pulse oximetry (SaO 2 less
than 90% on room air is severe).
• Decreased arterial or capillary CO 2 if mild, but in the normal range or increased in
moderate to severe obstruction.
Other Diagnostic Tests
• Blood gases to assess metabolic acidosis (lactic acidosis) in severe obstruction.
• Complete blood count if there are signs of infection (fever and purulent sputum).
• Serum electrolytes as therapy with β 2 -agonist and corticosteroids can lower serum
potassium, magnesium, and phosphate, and increase glucose.
• Chest radiograph if signs of consolidation on auscultation
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Chronic Asthma
General
Asthma is a disease of exacerbation and remission, so the patient may not have any signs or
symptoms at the time of exam.
Symptoms
• The patient may complain of episodes of dyspnea, chest tightness, coughing (particularly
at night), wheezing, or a whistling sound when breathing.
• These often occur in association with exercise, but also occur spontaneously or in
association with known allergens.
Signs
Expiratory wheezing on auscultation, dry hacking cough, or signs of atopy (allergic rhinitis
and/or eczema) may occur.
Laboratory
Spirometry demonstrates obstruction (reduced FEV 1 /FVC) with reversibility following
inhaled β 2 -agonist administration (at least a 12% improvement in FEV 1).
Other Diagnostic Tests
• A fall in FEV 1 of at least 15% following 6 minutes of near maximal exercise.
• Elevated eosinophil count and IgE concentration in blood.
• Positive methacholine challenge (PC 20 FEV 1 less than 12.5 mg/mL) or mannitol
challenge (FEV 1 decrease of at least 15% from baseline after 635 mg or less).

STEP 5: Pharmacological Treatment of Asthma (30 minutes)

Activity: Small Group Discussion ( 20 minutes)

DIVIDE students into small manageable groups

ASK students to discuss on the following question

• What is the treatment of Asthma?

ALLOW students to discuss for 15 minutes

ALLOW few groups to present and the rest to add points not mentioned

CLARIFY and SUMMARIZE by using the contents below

Acute Severe Asthma

• The primary goal is prevention of life-threatening asthma by early recognition of signs of
deterioration and early intervention.
• The principal goals of treatment include:
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 o Correction of significant hypoxemia
o Rapid reversal of airflow obstruction
o Reduction of the likelihood of relapse of the exacerbation or future recurrence of
severe airflow obstruction
Table 21:2 Treatment of Acute Asthma according Severity

Source: Standard Treatment Guidelines & National Essential Medicines List Tanzania Mainland (2017)

Chronic Asthma in Adults

• The assessment of the frequency of daytime and nighttime symptoms and limitation of
physical activity determines whether asthma is intermittent or persistent.
• There are 4 categories.
o Therapy is step-wise (Step 1–4) based on the category of asthma and consists of:
o Preventing the inflammation leading to bronchospasm (controllers)
o Relieving bronchospasm (relievers)
• Controller medicines in asthma
o Inhaled corticosteroids e.g. Beclomethasone
• Reliever medicines in asthma
o β2 agonists e.g. Salbutamol (short-acting)

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21:2Treatment of Chronic Asthma According to Severity

Source: Standard Treatment Guidelines & National Essential Medicines List Tanzania Mainland (2017)

STEP 6: Monitoring of AsthmaTherapy (20 minutes)

• Figures 21.1 below provide the monitoring parameters for acute severe asthma.
• Lung function, either spirometric or peak flow measurements, should be monitored 5 to
10 minutes after each treatment.
• Oxygen saturations can be easily monitored continuously with pulse oximetry.
• For young children and infants, pulse oximetry, lung auscultation, and observation of the
presence of supraclavicular retractions are useful.
• The majority of patients will respond within the first hour of initial inhaled β 2 -agonists
regardless of history of home administration of drug.
• Patients not achieving an initial response should be monitored every half hour to 1 hour.
• Depending on whether there is a standard ED or a special unit for acute severe asthma,
the decision to admit to the hospital should be made within 4 to 6 hours of entry to the
emergency department

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Figure 21.1 Monitoring of Asthma Therapy

Source: DiPiro JT, et al (2008): Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY:
McGraw-Hill. Pg 452

STEP 7: Key Points (5 minutes)

• Asthma is a common, chronic respiratory disease of the airways of the lung characterized
by either the intermittent or persistent presence of highly variable degrees of airflow
obstruction from airway wall inflammation and bronchial smooth muscle constriction.

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• Symptoms of Asthma include severe dyspnea, shortness of breath, chest tightness, or
burning and wheezing sound
• The principal goals of treatment of Asthma include correction of significant hypoxemia
and rapid reversal of airflow obstruction by using pharmacological and non
pharmacological therapy
STEP 8: Evaluation (5 minutes)
• What is Asthma?
• What is the pathophysiology of Asthma?
• What are the signs and symptoms of Asthma?
• How is the treatment of asthma?

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PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator
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References

Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

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Session 22: Pharmacotherapy of Diabetes Mellitus
Total Session Time: 120 minutes
Prerequisites
• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define diabetes mellitus
• Explain pathophysiology of diabetes mellitus
• Explain the clinical presentation of diabetes mellitus
• Outline diagnosis of diabetes mellitus
• Describe pharmacological treatment of diabetes mellitus
• Describe the monitoring of diabetes mellitus therapy

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Computer and LCD Projector

SESSION OVERVIEW

Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Tasks
15 minutes Presentation Definition of Diabetes Mellitus
2
Buzzing
20 minutes Pathophysiology of Diabetes Mellitus
3 Presentation

4 10 Minutes Presentation Clinical Presentation of Diabetes Mellitus

5 10 minutes Presentation Diagnosis of Diabetes Mellitus

30 minutes Presentation Pharmacological Treatment of Diabetes

6 Small Group Mellitus
Discussion
10 minutes Presentation Monitoring of Diabetes Mellitus Therapy
7

8 05 minutes Presentation Key Points

9 05 minutes Presentation Evaluation

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SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)

READ or ASK students to read the learning Tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of Diabetes Mellitus (15 minutes)

Activity: Buzzing (2 minutes)

ASK students to pair up and buzz on the following question for 2 minutes

• What is Diabetes Mellitus?

ALLOW few pairs to respond and let other pairs to add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZEby using the content below

Diabetes Mellitus
• Diabetes mellitus (DM) is a group of metabolic disorders of fat, carbohydrate, and protein
metabolism characterized by hyperglycemia that results from defects in insulin secretion,
insulin action (sensitivity), or both.
Or
• Diabetes mellitus is a chronic disease caused by inherited and/or acquired deficiency in
production of insulin by the pancreas, or by the ineffectiveness of the insulin produced
which results in increased concentrations of glucose in the blood, which in turn damage
many of the body's systems, in particular the blood vessels and nerves.
• There are two types of DM
o Type 1 diabetes (formerly known as insulin-dependent) in which the pancreas fails
to produce the insulin which is essential for survival. This form develops most
frequently in children and adolescents, but is being increasingly noted later in life.
o Type 2 diabetes (formerly named non-insulin-dependent) which results from the
body's inability to respond properly to the action of insulin produced by the
pancreas.
• Type 2 diabetes is much more common and accounts for around 90% of all diabetes
cases worldwide.
o It occurs most frequently in adults, but is being noted increasingly in adolescents
as well.
• Certain genetic markers have been shown to increase the risk of developing Type 1
diabetes.

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• Type 2 diabetes is strongly familial, but it is only recently that some genes have been
consistently associated with increased risk for Type 2 diabetes in certain populations.
• Both types of diabetes are complex diseases caused by mutations in more than one
gene, as well as by environmental factors.
• DM if not well managed can resultinto complications including;
o Microvascular complications such as retinopathy, neuropathy, and nephropathy
o Macrovascular complications such as coronary heart disease, stroke, and peripheral
vascular disease.

Gestational Diabetes
• It is a condition in which a woman without diabetes develops high blood sugar levels
during pregnanc
• Diabetes in pregnancy may give rise to several adverse outcomes, including congenital
malformations, increased birth weight and an elevated risk of perinatal mortality.
• Strict metabolic control may reduce these risks to the level of those of non-diabetic
expectant mothers.

STEP 3: Pathophysiology of Urinary Tract Infections (20 minutes)

Type 1 DM
• Type 1 DM is the result of a combination of genetic and environmental influences.
• Type 1 DM is characterized by an absolute deficiency of pancreatic β -cell function.
• Most often this is the result of an immunemediated destruction of pancreatic β cells, but
rare unknown or idiopathic processes may contribute.
• It most commonly results from autoimmune destruction of insulin-producing β-cells in
the pancreas.
• One or more environmental factors, such as enteroviruses, dietary factors or toxins, might
trigger the development of T-cell dependent autoimmunity in genetically susceptible
individuals
• Autoimmunity is manifested by detectable antibodies to ICA512/IA-2, insulin
autoantibody (IAA) and glutamic acid decarboxylase (GAD).
• Insulitis with gradual β-cell destruction leads to pre-diabetes and finally to overt DM.

Type 2 DM
Type 2 diabetic individuals are characterized by
• defects in insulin secretion; and
• Insulin resistance involving muscle, liver, and the adipocyte.

Impaired insulin secretion

• Impaired insulin secretion is a decrease in glucose responsiveness, which is observed
before the clinical onset of disease.

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• More specifically, impaired glucose tolerance (IGT) is induced by a decrease in glucose-
responsive early-phase insulin secretion, and a decrease in additional insulin secretion
after meals causes postprandial hyperglycemia
• In the type 2 diabetic patient, decreased postprandial insulin secretion is due to both
impaired pancreatic beta cell function and a reduced stimulus for insulin secretion from
gut hormones
• Normally there is an increased insulin secretion in response to an oral glucose stimulus
and which is referred to as “the incretin effect”
• The incretin effect is the result that gut-derived hormones (,glucagon-like peptide 1
(GLP-1) and glucose-dependent insulinotropic polypeptide (GIP)) when stimulated by
glucose.
• In type 2 diabetic patients, this “incretin effect” is very minimal
• The two gut hormones, glucagon-like peptide 1 (GLP-1) and glucose-dependent
insulinotropic polypeptide (GIP), are responsible for over 90% of the increased insulin
secretion seen in response to an oral glucose load.
• Patients with type 2 diabetes remain sensitive to GLP-1 while they are often resistant to
GIP.

Insulin resistance
• Insulin resistance is a condition in which insulin in the body does not exert sufficient
action proportional to its blood concentration.
• The impairment of insulin action in major target organs such as liver and muscles is a
common pathophysiological feature of type 2 diabetes.
• Insulin resistance develops and expands prior to disease onset.
• Insulin resistance is related to genetic factors and environmental factors (hyperglycemia,
free fatty acids, inflammatory mechanism, etc.).
o Known genetic factors, such as change in the shape of insulin receptors that directly
affect insulin signalling mechanisms is associated with visceral obesity and promote
insulin resistance.
• Glucolipotoxicity and inflammatory mediators are also important as the mechanisms for
impaired insulin secretion and insulin signaling impairment

STEP 4: Clinical Presentation of Diabetes Mellitus (10 minutes)

The clinical presentations of type 1 DM and type 2 DM are very different.
• Autoimmune type 1 DM can occur at any age.
• Individuals with type 1 DM are often thin and are prone to develop diabetic ketoacidosis
if insulin is withheld, or under conditions of severe stress
• polyuria,
• polydipsia,
• polyphagia
• Weight loss.
• Blurred vision
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• Slow-healing sores
• Frequent infections

• Signs and symptoms of type 2 diabetes often develop slowly.

• The following are the signs and symptoms;
o Patients with type 2 DM often present without symptoms,
o Even though complications tell us that they may have been hyperglycemic
o For several years.
o Often these patients are diagnosed secondary to unrelated blood testing.
o Lethargy,
o polyuria,
o nocturia, and
o polydipsia
o Blurred vision
o Slow-healing sores
o Frequent infections
o Patients can have normal to grossly abnormal insulin sensitivity.

Table22.1 Clinical Presentation of DM

Source: DiPiro JT, et al(2008): Pharmacotherapy: A Pathophysiologic Approach (7th ed)

STEP 5: Diagnosis of Diabetes Mellitus (10 minutes)

• DM is diagnosed by both clicall using signs and symptoms together with blood tests
• The following are blood test for diagnosis of DM

Glycated hemoglobin (A1C) test.

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• This blood test, which doesn't require fasting, indicates your average blood sugar level for
the past two to three months.
• It measures the percentage of blood sugar attached to hemoglobin, the oxygen-carrying
protein in red blood cells.
• An A1C level of 6.5 percent or higher on two separate tests indicates DM.
• An A1C between 5.7 and 6.4 percent indicates prediabetes.
• Below 5.7 is considered normal.

Random blood glucose test.

• A blood sample will be taken at a random time.
• Normal blood glucose is 11 millimoles/L
• Reading of 11.1 millimoles per liter (mmol/L) — or higher suggests diabetes.

Fasting blood glucose test.

• A blood sample will be taken after an overnight fast.
• A fasting blood glucose level less than 5.6 mmol/L is normal.
• A fasting blood glucose level from 5.6 to 6.9 mmol/L is considered prediabetes.
• A fasting blood glucose of 7 mmol/L) or higher on two separate tests, you have diabetes.

Oral glucose tolerance test.

• For this test, fasting blood glucose level is measured after overnight fast.
• Then a patient drink sugary liquid and blood glucose levels are measured periodically for
the next two hours.
• A blood sugar level less tha 7.8 mmol/L is normal.
• More than 11.1 mmol/L after two hours indicates diabetes.
• A reading between 7.8 mmol/L and 11.0 mmol/L indicates prediabetes.

Urinalysis
If type 1diabetes is suspected, Urinalysis will be done to investigate for the presence of
ketones bodies

Table 22.2 Diagnostic criteria for DM

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Source: DiPiro JT, et al(2008): Pharmacotherapy: A Pathophysiologic Approach (7th ed)
STEP 6: Pharmacological Treatment of Diabetes Mellitus (40 minutes)

Activity: Small Group Discussion ( 20 minutes)

DIVIDE students into small manageable groups

ASK students to discuss on the following question

• What is the treatment of Diabetes Mellitus?

ALLOW students to discuss for 15 minutes

ALLOW few groups to present and the rest to add points not mentioned

CLARIFY and SUMMARIZE by using the contents below

• The primary goals of DM management are to;

o reduce the risk for microvascular and macrovascular disease complications,
o ameliorate symptoms,
o reduce mortality,
o Improve quality of life.
• Near-normal glycemia will reduce the risk for development of microvascular disease
complications,
• Aggressive management of traditional cardiovascular risk factors (i.e., smoking cessation,
treatment of dyslipidemia, intensive blood pressure control, and antiplatelet therapy) are
needed to reduce the likelihood of development of macrovascular disease.
• Pharmacological treatement of DM depends on the type and the severity of the disease

Treatment of Type 1 DM
Insulins are the mainstay for the treatment of type 1 DM

Table22.3. Types of Insulin

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Source:
https://www.google.com/search?q=types+of+insulin&source=lnms&tbm=isch&sa=X&ved=0ahUKEwizs4nKt
9vgAhUVA2MBHSKsAPwQ_AUIDigB&biw=1366&bih=657#imgrc=1GmofkSm-YXANM:
Fig 22.1 Insulin regimes

Treatment of Type 2 DM

Oral Antihyperglycemic Drugs

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Biguanide:
Metformin
• Metformin is considered the agent of first line for treatment of T2DM, in the absence of
contraindications
• It decreases fasting blood glucose by approximately 20% and HbA1c by 1.5%.
• It can be given in combination with sulfonylureas, glinides, alpha-glucosidase inhibitors,
insulin, thiazolidinediones (TZD), glucagon-like peptide-1 receptor agonist (RA-GLP1),
dipeptidylpeptidase 4 inhibitors (iDPP4), and sodium-glucose co-transporter 2 inhibitors
(iSGLT2).
• Metformin is contraindicated in patients with factors that predispose to lactic acidosis.
• The predisposing factors are: A renal function damaged, concomitant liver disease or
excessive alcohol intake, unstable or acute heart failure and personal history of lactic
acidosis

Table 22.4 Antihyperglycemic drugs

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Source: DiPiro JT, et al(2008): Pharmacotherapy: A Pathophysiologic Approach (7th ed)

Fig 22.2 Global Guidelines for managing Adults with type 2 diabetes

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Source: International Diabetes Federation (IDF) for Managing Older People Withg Type 2 DIABETES
GLOBAL GUIDELINE (2013)

STEP 7: Monitoring of Diabetes Mellitus Therapy (10 minutes)

• A comprehensive pharmaceutical care plan for the patient with DM is needed in order to
reach treatment goals
• Parameteres to monitor include
o Glycemic control (tested minimally yearly; HbA lc <8% is good control and
HbA lc >9% is poor control),
▪ Minimally, HbA lc should be measured twice a year in patients meeting treatment
goals on a stable therapeutic regimen.
▪ Quarterly assessments are recommended for those whose therapy has changed or
who are not meeting glycemic goals.
▪ Glycemic control requires frequent assessment and adjustment in diet, exercise,
and pharmacologic therapies
o lipid (percentage of patients with LDL <100 mg/dL)

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 ▪ Fasting lipid profiles should be obtained as part of an initial assessment and
thereafter at each
▪ Follow-up visit, annually, or every 2 years if the lipid profile suggests low risk.
• Documenting regular frequency of foot exams (each visit), urine albumin assessment
(annually), dilated ophthalmologic exams (yearly or more frequently with identified
abnormalities), and office visits for follow-up are also important.
• Management of other cardiovascular risks (e.g., smoking and antiplatelet therapy) are
components of preventive medicine strategies.

STEP 8: Key Points (5 minutes)

• Diabetes mellitus (DM) is a group of metabolic disorders of fat, carbohydrate, and protein
metabolism characterized by hyperglycemia that results from defects in insulin secretion,
insulin action (sensitivity), or both
• Symptoms of Diabetes Mellitus are variable and depends on the type of the disease
wheather is type 1 or 2 DM.
• Insulin is the mainstay pharmacological treatment for type 1 DM while Metformin is first
line pharmacological treatment for type 2 DM obese patient

STEP 9: Evaluation (5 minutes)

• What is Diabetes Mellitus?
• What is the pathophysiology of Diabetes Mellitus?
• What are the signs and symptoms of Diabetes Mellitus?
• How is the treatment of Diabetes Mellitus?

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References

Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

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Session 23: Pharmacotherapy of Peptic Ulcers Disease

Total Session Time: 120 minutes

Prerequisites
• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define peptic ulcers disease
• Explain pathophysiology of peptic ulcers disease
• Explain the clinical presentation of peptic ulcers disease
• Outline diagnosis of peptic ulcers disease
• Describe pharmacological treatment of peptic ulcers disease
• Describe the monitoring of peptic ulcers disease therapy

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Computer and LCD Projector

SESSION OVERVIEW

Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Tasks
15 minutes Presentation Definition of Peptic Ulcers Disease
2
Buzzing
20 minutes Pathophysiology of Peptic Ulcers Disease
3 Presentation

10 minutes Clinical Presentation of Peptic Ulcers

4 Presentation
Disease
5 10 minutes Presentation Diagnosis of Peptic Ulcers Disease

35 minutes Presentation Pharmacological Peptic Ulcers Disease

6 Small Group Infections
Discussion
15 minutes Presentation Monitoring of Peptic Ulcers Disease Therapy
7

8 05 minutes Presentation Key Points

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 9 05 minutes Presentation Evaluation
SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)

READ or ASK students to read the learning Tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of Peptic Ulcers Disease (15 minutes)

Activity: Buzzing (5 minutes)

ASK students to pair up and buzz on the following question for 2 minutes

• What is Peptic ulcer Disease?

ALLOW few pairs to respond and let other pairs to add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZEby using the content below

Peptic Ulcers Disease

• Peptic ulcer disease refers to painful sores or ulcers in the lining of the stomach or first
part of the small intestine, called the duodenum.
• Peptic ulcer disease (PUD), also known as a peptic ulcer or stomach ulcer, is a break in
the lining of the stomach, first part of the small intestine, or occasionally the lower
esophagus
• An ulcer in the stomach is known as a gastric ulcer while that in the first part of the
intestines is known as a duodenal ulcer.
• Most ulcers are caused by an infection with a type of bacteria called Helicobacter pylori
(H. pylori).
• Factors that can increase your risk for ulcers include:
o Use of nonsteroidal anti-inflammatory drugs (NSAIDs), such as;
▪ Aspirin, even safety-coated aspirin and aspirin in powered form can frequently
cause ulcers.
▪ naproxen,
▪ ibuprofen
o Many other prescription drugs such;
▪ Concomitant use of oral bisphosphonates (e.g., alendronate)
▪ Concomitant use of corticosteroids
▪ Concomitant use of anticoagulant or coagulopathy
▪ Concomitant use of antiplatelet drugs (e.g., clopidogrel)
▪ Concomitant use of selective serotonin reuptake inhibitor
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 o Excess acid production from Zollinger-Ellison syndrome, (ZES)gastrinomas, tumors
of the acid producing cells of the stomach that increases acid output
o Excessive drinking of alcohol
o Smoking or chewing tobacco
o Peptic ulcers are also associated with radiation, chemotherapy, vascular insufficiency,
and other chronic diseases

STEP 3: Pathophysiology of Peptic Ulcers Disease (20 minutes)

• A physiologic imbalance between aggressive (gastric acid and pepsin) and protective
factors (mucosal defense and repair) remain important issues in the pathophysiology of
gastric and duodenalulcers.
• Gastric acid is secreted by the parietal cells, which contain receptors for histamine,
gastrin, and acetylcholine.
• Acid (as well as H. pylori infection and NSAID use) is an independent factor that
contributes to the disruption of mucosal integrity.
• Increased acid secretion has been observed for patients with duodenal with Zollinger-
Ellison syndrome (ZES) (described in the section
• Zollinger-Ellison Syndrome) have profound gastric acid hypersecretion resulting from a
gastrin-producing tumor
• H. pylori produce large amounts of urease, which hydrolyzes urea in the gastric juice and
converts it to ammonia and carbon dioxide.
• The local buffering effect of ammonia creates a neutral microenvironment within and
surrounding the bacterium, which protects it from the lethal effect of gastric acid.
• H. pylori also produces acid inhibitory proteins, which allows it to adapt to the low-pH
environment of the stomach
• Mucosal injury is produced by
o elaborating bacterial enzymes (urease, lipases, and proteases),
▪ Lipases and proteases degrade gastric mucus, ammonia produced by urease may
be toxic to gastric epithelial cells,
o Adherence
▪ bacterial adherence enhances the uptake of toxins into gastric epithelial cells
o H. pylori virulence factors.
▪ H. pylori induces gastric inflammation by altering the host inflammatory response
and damaging epithelial cells directly by cell-mediated immune mechanisms or
indirectly by activated neutrophils or macrophages attempting to phagocytose
bacteria or bacterial products

STEP 4: Clinical Presentation and Diagnosis of Peptic Ulcers Disease (20

minutes)
• The clinical presentation of PUD varies depending on the severity of epigastric pain and
the presence of complications

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• Ulcer-related pain in duodenal ulcer often occurs 1 to 3 hours after meals and is usually
relieved by food, but this is variable

General
Mild epigastric pain or acute life-threatening upper gastrointestinal complications

Symptoms
• Abdominal pain that is often epigastric and described as burning but may present as
vague discomfort, abdominal fullness, or cramping
• A typical nocturnal pain that awakens the patient from sleep (especially between 12 AM
and 3 AM)
• The severity of ulcer pain varies from patient to patient and may be seasonal,
• episodes of discomfort usually occur in clusters, lasting up to a few weeks and followed
• by a pain-free period or remission lasting from weeks to years
• Changes in the character of the pain may suggest the presence of complications
• Heartburn, belching, and bloating often accompany the pain
• Nausea, vomiting, and anorexia are more common for patients with gastric ulcer than
with duodenal ulcer but may also be signs of an ulcer-related complication

Signs
• Weight loss associated with nausea, vomiting, and anorexia
• Complications including ulcer bleeding, perforation, penetration, or obstruction

Laboratory tests
• Gastric acid secretory studies
• The hematocrit and hemoglobin are low with bleeding, and stool hemoccult tests are
positive.
• Tests for Helicobacter pylori.

Diagnostic tests
• Fiberoptic upper endoscopy (esophagogastroduodenoscopy) detects more than 90% of
peptic ulcers and permits direct inspection, biopsy, visualization of superficial erosions,
and sites of active bleeding.
• Upper gastrointestinal radiography with barium and upper endoscopy are also the
diagnostic procedures for suspected peptic ulcer.

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 Table 23;1 Tests for Detection of Helicobacter Pylori

Source: DiPiro JT, et al(2008): Pharmacotherapy: A Pathophysiologic Approach (7th ed)

STEP 5: Pharmacological Treatment of Peptic Ulcers Disease (35 minutes)

Activity: Small Group Discussion ( 20 minutes)

DIVIDE students into small manageable groups

ASK students to discuss on the following question

• What is the treatment of Peptic Ulcers Disease?

ALLOW students to discuss for 15 minutes

ALLOW few groups to present and the rest to add points not mentioned

CLARIFY and SUMMARIZE by using the contents below

• The treatment of chronic PUD varies depending on the etiology of the ulcer ( H. pylori or
NSAID), whether the ulcer is initial or recurrent, and whether complications have
occurred
• Overall treatment is aimed at relieving ulcer pain, healing the ulcer, preventing ulcer
recurrence, and reducing ulcer-related complications.
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• The goal of therapy for H. pylori positive patients with an active ulcer, a previously
documented ulcer, or a history of an ulcer-related complication, is to eradicate H. pylori,
heal the ulcer, and cure the disease.
• Successful eradication heals ulcers and reduces the risk of recurrence for most patients.

Table 23.2 Drug Regimens Used to Eradicate Helicobacter pylori

Source: DiPiro JT, et al(2008): Pharmacotherapy: A Pathophysiologic Approach (7th ed)

• Other options for Triple therapy for eradication of the H. pylori include;
Omeprazole (PO) 20mg twice daily Plus amoxycillin (PO) 1000mg twice daily
AND
Metronidazole (PO) 400mg twice daily for 10–14 days
OR
Lansoprazole (PO) 30mg twice daily
AND
Clarithromycin (PO) 500mg twice
AND
B: Tinidazole (PO) 500mg twice daily for 10–14 days
OR
Any combination of PPI + 2 antibiotics active for H. pylori

• Other drugs as indicated in the table below can also be used in the treatment of peptic
ulcer disease

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Table 23.2 Oral Drug Regimens Used to Heal PepticUlcers and Maintain Ulcer Healing

Source: DiPiro JT, et al(2008): Pharmacotherapy: A Pathophysiologic Approach (7th ed)

STEP 6: Monitoring of Peptic Ulcers Disease Therapy (15 minutes)

Treatment of Helicobacter pylori -associated ulcer
• Assess patient allergies to determine if allergic to penicillin (or other antibiotics) so that
drug regimens that contain penicillin (or other antibiotics) can be avoided.
• Assess patient use of alcohol or alcohol-containing products with metronidazole and oral
birth control medications with antibiotics and counsel appropriately.
• Assess likelihood of nonadherence to the drug regimen as a cause of treatment failure.
• Recommend a different antibiotic combination if H . pylori eradication fails.
• Inform the patient of change in stool color when bismuth salicylate is included in an H.
pylori eradication regimen.
• Assess and monitor patients for potential adverse effects, especially those associated with
metronidazole, clarithromycin, and amoxicillin.
• Assess and monitor patients for potential drug interactions, especially those receiving
metronidazole, clarithromycin, or cimetidine.
• Monitor patients for persistent or recurrent symptoms within 14 days after completion of
a course of H. pylori eradication therapy.
• Provide patient education to patients who are receiving H . pylori eradication therapy and
include why antibiotic and antiulcer combinations are used;
o when and how to take medications;
o adverse effects;
o alarm symptoms;

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 o the importance of adherence to the entire course of drug treatment; and
o Contact their healthcare provider if alarm symptoms develop (e.g., blood in the stools,
black tarry stools, vomiting, severe abdominal pain), or if symptoms persist or return
after H. pylori eradication.

Treatment of NSAID-induced ulcer

• Monitor patients for signs and symptoms of NSAID-related upper GI complications.
• Assess and monitor patients for potential drug interactions and adverse effects (especially
misoprostol).
• Provide patient education to patients who are at risk of NSAID-induced ulcers or GI-
related complications and include why cotherapy is used with nonselective NSAIDs;
o when and how to take medications;
o adverse effects;
o alarm symptoms;
o when to contact their healthcare provider; and
o The importance of adherence to drug treatment.

STEP 7: Key Points (5 minutes)

• Peptic ulcer disease refers to painful sores or ulcers in the lining of the stomach or first
part of the small intestine, called the duodenum
• A physiologic imbalance between aggressive (gastric acid and pepsin) and protective
factors (mucosal defense and repair) and H. pylori infection remain important issues in
the pathophysiology of gastric and duodenal ulcers.
• Symptoms of PUD include abdominal pain that is often epigastric and described as
burning but may present as vague discomfort, abdominal fullness, or cramping
• The treatment of chronic PUD varies depending on the etiology of the ulcer ( H. pylori or
NSAID), whether the ulcer is initial or recurrent, and whether complications have
occurred

STEP 8: Evaluation (5 minutes)

• What is Peptic Ulcers Disease?
• What is the pathophysiology of Peptic Ulcers Disease?
• What are the signs and symptoms of Peptic Ulcers Disease?
• How is the treatment of Peptic Ulcers Disease?

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References

Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

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Session 24: Pharmacotherapy of Hypertension
Total Session Time: 120 minutes

Prerequisites
• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define hypertension
• Explain pathophysiology of hypertension
• Explain the clinical presentation of hypertension
• Outline diagnosis of hypertension
• Describe pharmacological treatment of hypertension
• Describe the monitoring of hypertension therapy

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Computer and LCD Projector

SESSION OVERVIEW

Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Tasks
15 minutes Presentation Definition of Hypertension
2
Buzzing
20 minutes Pathophysiology of Hypertension
3 Presentation

4 10 minutes Presentation Clinical Presentation of Hypertension

5 10 minutes Presentation Diagnosis of Hypertension

35 minutes Presentation Pharmacological Treatment of Hypertension

6 Small Group
Discussion

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 15 minutes Presentation Monitoring of Hypertension Therapy
7

8 05 minutes Presentation Key Points

9 05 minutes Presentation Evaluation

SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)

READ or ASK students to read the learning Tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of Hypertension (5 minutes)

Activity: Buzzing (2 minutes)

ASK students to pair up and buzz on the following question for 2 minutes

• What is Hypertension?
ALLOW few pairs to respond and let other pairs to add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZEby using the content below

Hypertension
• Hypertension is defined as a systolic blood pressure (SBP) of higher than 140mmHg or a
diastolic blood pressure (DPB) higher than 90mmHg
• The classification of BP is as been follows:
o Normal: Systolic lower than 120 mm Hg, diastolic lower than 80 mm Hg
o Prehypertension: Systolic 120-139 mm Hg, diastolic 80-89 mm Hg
o Stage 1: Systolic 140-159 mm Hg, diastolic 90-99 mm Hg
o Stage 2: Systolic 160 mm Hg or greater, diastolic 100 mm Hg or greater
• Hypertension may be;
o Primary, which may develop as a result of environmental or genetic causes, or
o Secondary, which has multiple etiologies, including renal, vascular, and endocrine
causes.
• Primary or essential hypertension accounts for 90-95% of adult cases, and secondary
hypertension accounts for 2-10% of cases.

STEP 3: Pathophysiology of Hypertension (20 minutes)

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• Multiple factors that control BP are potential contributing components in the development
of essential hypertension.
• These include;
o Malfunctions in either humoral [i.e., the renin-angiotensin- aldosterone system
(RAAS)] or vasodepressor mechanisms,
o Abnormal neuronal mechanisms,
o Defects in peripheral autoregulation, and
o Disturbances in sodium, calcium, and natriuretic hormone.
• Many of these factors are cumulatively affected by the multifaceted RAAS, which
ultimately regulates arterial BP.
• It is probable that no one factor is solely responsible for essential hypertension.

STEP 4: Clinical Presentation and Diagnosis of Hypertension (20 minutes)

General:
• The patient may appear healthy or may have the presence of additional CV risk factors:
• Age (greater than or equal to 55 for men, greater than or equal to 65 for women)
• Diabetes mellitus
• Dyslipidemia
• Microalbuminuria
• Family history of premature CV disease
• Obesity (body mass index greater than or equal to 30 kg/m2)
• Physical inactivity
• Tobacco use

Symptoms:
Usually none related to elevated BP.
Signs:
Previous BP values in either the prehypertension or the hypertension category.
Laboratory Tests:
• BUN/serum creatinine,
• fasting lipid panel,
• fasting blood glucose,
• serum electrolytes (sodium, potassium),
• Spot urine albumin-to-creatinine ratio.
• The patient may have normal values and still have hypertension.
o However, some may have abnormal values that are consistent with either additional
CV risk factors or hypertension-related damage.

Other Diagnostic Tests:

• 12-lead electrocardiogram,
• Estimated glomerular filtration rate [using modification of diet in renal disease (MDRD)
equation].
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Hypertension-Related Target-Organ Damage:
• The patient may have a previous medical history or diagnostic findings that indicate
• the presence of hypertension-related target-organ damage:
• Brain (stroke, transient ischemic attack, dementia)
• Eyes (retinopathy)
• Heart (left ventricular hypertrophy, angina, prior MI, prior coronary revascularization,
heart failure)
• Kidney (chronic kidney disease)
• Peripheral vasculature (peripheral arterial disease)

STEP 5: Pharmacological Treatment of Hypertension (35 minutes)

Activity: Small Group Discussion ( 20 minutes)

DIVIDE students into small manageable groups

ASK students to discuss on the following question

• What is the treatment of Hypertension?

ALLOW students to discuss for 15 minutes

ALLOW few groups to present and the rest to add points not mentioned

CLARIFY and SUMMARIZE by using the contents below

• The overall goal of treating hypertension is to reduce hypertension- associated morbidity

and mortality.
• This morbidity and mortality is related to hypertension-associated target-organ damage
(e.g.CV events, cerebrovascular events, heart failure, and kidney disease).
• Reducing CV risk remains the primary purpose of hypertension therapy and the specific
choice of drug therapy is significantly influenced by evidence demonstrating such CV
risk reduction.
• Treating patients with hypertension to achieve a desired target BP value is simply a
surrogate goal of therapy
o In most cases the target BP should be: systolic below 140 mmHg and diastolic below
90 mmHg.
o In diabetic patients and patients with cardiac or renal impairment, target BP should be
below 130/80mmHg;
• The choice of initial drug therapy depends on the degree of BP elevation and presence of
compelling indications (e.g coexisting conditions such as diabetes and other
cardiovascular conditions)
• Most patients with stage 1 hypertension should be initially treated with a first-line
antihypertensive drug, or the combination of two agents.

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• Combination drug therapy is recommended for patients with more severe BP elevation
(stage 2 hypertension), using preferably two first-line antihypertensive drugs.

Fig24.1 Approach of Pharmacological Treatment of hypertension

Recommended
initial
medication
doses for
hypertension
treatment.
Thiazide
diuretics

Hydrochlothiazide 12.5mg/daily
OR
Bendroflumethiazide 5mg/daily
OR
Indapamide 5mg/daily preferred for patient with previous stroke/TIA

Loop diuretics
Furosemide initial dose 40mg twice a day
OR
Torsemide 5mg/daily Dose can be up scaled depending on congestive status to maximum
dose

Mineralocorticoid (Aldosterone) Receptor antagonist

Spironolactone 25mg/daily
OR
Eplerenone 25mg/daily

Angiotensin-Converting Enzyme Inhibitor (ACEI)

Captopril 6.125mg, 12.5mg or 25mg three times daily
OR

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Enalapril 10mg twice a day
OR
Perindopril 8mg/daily orally

Angiotensin Receptor Blocker–ARB

(*Don’t combine with ACEI contraindications, indicated in patient sensitive to ACEIs)

Losartan 50mg/daily*

Beta–blocker
Atenolol 50mg/daily
OR
Metoprolol 50mg/daily

Calcium Channel Blocker (Dihydropyridines):

Nifedipine (Slow Release/Long Acting) 20mg/30mg/ 60mg/90mg/daily
OR
Amlodipine 5mg or 10mg/daily

Non–dihydropyridine
Verapamil 30mg twice–three times a daily
OR
Diltiazem 30mg twice–three times a day

STEP 6: Monitoring of Hypertension Therapy (15 minutes)

• Routine ongoing monitoring to assess disease progression, the desired effects of
antihypertensive therapy
• The monitoring parameters include;
o Signs and symptoms of Disease Progression
o Efficacy of antihypertensives and BP goal attainment, and
o Undesired adverse side effects (toxicity)

Disease Progression
• Patients should be monitored for signs and symptoms of progressive hypertension-
associated target-organ disease.
• A careful history for ischemic chest pain (or pressure), palpitations, dizziness, dyspnea,
orthopnea, headache, sudden change in vision, one-sided weakness, slurred speech, and
loss of balance should be taken to assess the presence of CV and cerebrovascular
hypertensive complications.
Efficacy
• The most important strategy to prevent CV morbidity and mortality in hypertension is BP
control to goal values
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• Clinic-based BP monitoring remains the standard for managing hypertension.
• BP response should be evaluated 2 to 4 weeks after initiating or making changes in
therapy.
• Once goal BP values are attained, assuming no signs or symptoms of acute target-organ
disease are present, BP monitoring can be done every 3 to 6 months.
• More frequent evaluations are required for patients with a history of poor control,
nonadherence, progressive target-organ damage, or symptoms of adverse drug effects.
• Self-measurements of BP or automated ambulatory BP monitoring can be useful
clinically to establish effective 24-hour control

Toxicity
• Patients should be monitored routinely for symptoms of adverse drug reactions.
• Laboratory monitoring should typically occur 2 to 4 weeks after starting a new agent or
dose increase, and then every 6 to 12 months in stable patients.

STEP 8: Key Points (5 minutes)

• Hypertension is defined as a systolic blood pressure (SBP) of higher than 140mmHg or a
diastolic blood pressure (DPB) higher than 90mmHg
• The overall goal of treating hypertension is to reduce hypertension- associated morbidity
and mortality.
• This morbidity and mortality is related to hypertension-associated target-organ damage
• The choice of initial drug therapy depends on the degree of BP elevation and presence of
compelling indications (e.g coexisting conditions such as diabetes and other
cardiovascular conditions)

STEP 9: Evaluation (5 minutes)

• What is Hypertension?
• What is the pathophysiology of Hypertension?
• What are the signs and symptoms of Hypertension?
• How is the treatment of Hypertension?

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References

Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

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Session 25: Pharmacotherapy of Heart Failure

Total Session Time: 120 minutes

Prerequisites
• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define heart failure
• Explain pathophysiology of heart failure
• Explain the clinical presentation of heart failure
• Outline diagnosis of heart failure
• Describe pharmacological treatment of heart failure
• Describe the monitoring of heart failure therapy

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers

SESSION OVERVIEW

Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Tasks
15 minutes Presentation Definition of Heart Failure
2
Buzzing
20 minutes Pathophysiology of Heart Failure
3 Presentation

4 10 minutes Presentation Clinical Presentation of Heart Failure

5 10 minutes Presentation Diagnosis of Heart Failure

35 minutes Presentation Pharmacological Treatment of Heart Failure

6 Small Group
Discussion
15 minutes Presentation Monitoring of Heart Failure Therapy
7

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 8 05 minutes Presentation Key Points

9 05 minutes Presentation Evaluation

SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)

READ or ASK students to read the learning Tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of Heart Failure (15 minutes)

Activity: Buzzing (5 minutes)

ASK students to pair up and buzz on the following question for 5 minutes

• What is Heart Failure?

ALLOW few pairs to respond and let other pairs to add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZEby using the content below

Heart Failure
• Heart failure is a progressive clinical syndrome that can result from any abnormality in
cardiac structure or function that impairs the ability of the ventricle to fill with or eject
blood, thus rendering the heart unable to pump blood at a rate sufficient to meet the
metabolic demands of the body.
• It is the final common pathway for numerous cardiac disorders, including those affecting
the pericardium, heart valves, and myocardium.
• Diseases that adversely affect ventricular diastole (filling), ventricular systole
(Contraction), or both can lead to heart failure
• Heart Failure is characterized by typical symptoms (e.g. breathlessness, ankle swelling
and fatigue) that may be accompanied by signs (e.g. elevated jugular venous pressure,
pulmonary crackles and peripheral oedema) caused by a structural and/or functional
cardiac abnormality, resulting in a reduced cardiac output and/or elevated intracardiac
pressures at rest or during stress
• Heart failure can result from any disorder that affects the ability of the heart to contract
(systolic function) and/or relax (diastolic dysfunction)
o Therefore, Heart Failure can be;
▪ Systolic Heart Failure or/and

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 ▪ Diastolic Heart Failure
• Heart failure with impaired systolic function (i.e., reduced LVEF) is the classic, more
familiar form of the disorder

Table 25.1 Common Causes of Heart Failure

Source: DiPiro JT, et al(2008): Pharmacotherapy: A Pathophysiologic Approach (7th ed)

STEP 3: Pathophysiology of Heart Failure (20 minutes)

Key components of the pathophysiology of cardiac remodeling are.
• Myocardial injury (e.g., myocardial infarction) results in the activation of a number of
hemodynamic and neurohormonal compensatory responses in an attempt to maintain
circulatory homeostasis.
• Chronic activation of the neurohormonal systems results in a cascade of events that affect
the myocardium at the molecular and cellular levels.
• These events lead to the changes in ventricular size, shape, structure, and function known
as ventricular remodeling.
• The alterations in ventricular function result in further deterioration in cardiac systolic
and diastolic function, which further promotes the remodeling process. (LV left
ventricular)

Fig 25.1 Pathophysiology of Heart Failure

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Source: DiPiro JT, et al(2008): Pharmacotherapy: A Pathophysiologic Approach (7th ed)
STEP 4: Clinical Presentation and Diagnosis of Heart Failure (20 minutes)
General
Patient presentation may range from asymptomatic to cardiogenic shock.
Symptoms
• Dyspnea, particularly on exertion
• Orthopnea
• Paroxysmal nocturnal dyspnea
• Exercise intolerance
• Tachypnea
• Cough
• Fatigue
• Nocturia
• Hemoptysis
• Abdominal pain
• Anorexia
• Nausea
• Bloating
• Poor appetite, early satiety
• Ascites
• Mental status changes
Signs
• Pulmonary rales
• Pulmonary edema
• Cool extremities
• Pleural effusion
• Tachycardia
• Narrow pulse pressure
• Cardiomegaly
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• Peripheral edema
• Hepatojugular reflux
• Hepatomegaly
Laboratory Tests
• Electrocardiogram may be normal, or it could show numerous abnormalities, including
acute ST-T wave changes from myocardial ischemia, atrial fibrillation, bradycardia, and
left ventricular hypertrophy.
• Serum creatinine may be increased due to hypoperfusion.
• Preexisting renal dysfunction can contribute to volume overload.
• Complete blood count (CBC) can be useful in determining if heart failure is due to a
reduced oxygen-carrying capacity.
• Chest x-ray: useful for detecting cardiac enlargement, pulmonary edema, and pleural
effusions
• Echocardiogram: used to assess the size of the left ventricle, valve function, pericardial
effusion, wall motion abnormalities, and ejection fraction
• Hyponatremia: serum sodium <130 mEq/L is associated with reduced survival and may
indicate worsening volume overload and/or disease progression.

STEP 5: Pharmacological Treatment of Heart Failure (35 minutes)

Activity: Small Group Discussion ( 10 minutes)

DIVIDE students into small manageable groups

ASK students to discuss on the following question

• What is the treatment of Heart Failure?

ALLOW students to discuss for 15 minutes

ALLOW few groups to present and the rest to add points not mentioned

CLARIFY and SUMMARIZE by using the contents below

• Treatment of Heart Failure of depends on the stage of the Disease

• There are four identified stages of heart failure, and their treatment recommendations.
• The Functinal stages are indicated in the table below;

Table 25.2 Functional Classification of Heart Failure

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Source: DiPiro JT, et al(2008): Pharmacotherapy: A Pathophysiologic Approach (7th ed)

• Unless contraindicated, all patients with HF-REF should be started on an ACE inhibitor
and a beta blocker (and a diuretic, in most cases).
• No patient should receive three drugs which block the renin-angiotensin-aldosterone
system as hyperkalaemia and renal dysfunction will be common.
• The safety and efficacy of combining an ACE inhibitor, an ARB and MRA is uncertain
and the use of these three drugs together is not recommended.

Fig 25.2 Treatment allogarism of Heart Failure according to the functional stages of Heart Failure

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Beta Blockers
• A meta-analysis confirms that beta blockers also reduce mortality in patients with
diabetes and HF
• All patients with heart failure with reduced ejection fraction,class II-IV, should be started
on beta blocker therapy as soon as their condition is stable.
• Bisoprolol, carvedilol or nebivolol should be the first choice of beta blocker for the
treatment of patients with heart failure with reduced ejection fraction.
• If beta blockers are contraindicated consider using ivabradine

Angiotensin-Converting Enzyme Inhibitors

• Patients with heart failure with reduced ejection fraction of all NYHA functional classes,
should be given angiotensin-converting enzyme inhibitors.
• Important adverse effects are cough, hypotension, renal impairment and hyperkalaemia.
• A key but rare adverse effect, which can be life threatening (due to laryngeal
involvement), is angioedema.
• Any patient who experiences angioedema should have the ACE inhibitor withdrawn
immediately and be prescribed an alternative agent.

Angiotensin Receptor Blockers

• Angiotensin II type 1 receptor blockers (ARBs) block the biological effect of angiotensin
II.
• Unlike ACE inhibitors they do not produce cough as a side effect and should be used in
patients who cannot tolerate an ACE inhibitor due to cough.
• Patients with heart failure with reduced ejection fraction, NYHA class II-IV, who are
intolerant of angiotensin-converting enzyme inhibitors should be given an angiotensin
receptor blocker.
• An angiotensin receptor blocker in addition to an angiotensin-converting enzyme
inhibitor should be considered in patients with heart failure with reduced ejection fraction
NYHA class II-IV, who are unable to tolerate a mineralocorticoid receptor antagonist.

Mineralocorticoid Receptor Antagonists

• Patients with heart failure with reduced ejection fraction who have ongoing symptoms of
heart failure, NYHA class II-IV, LVEF ≤35%, despite optimal treatment, should be
given mineralocorticoid receptor anatgonists unless contraindicated by the presence of
renal impairment (chronic kidney disease stage ≥4–5) and/or elevated serum potassium
concentration (K+ >5.0 mmol/l).
• Eplerenone can be substituted for spironolactone in patients who develop gynaecomastia.

Angiotensin Receptor/Neprilysin Inhibitors

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• Patients with heart failure with reduced ejection fraction who have ongoing symptoms of
heart failure, NYHA class II-III, LVEF ≤40% despite optimal treatment should be given
sacubitril/valsartan instead of their ACE inhibitor or ARB, unless contraindicated.
• It may be considered in patients with NYHA class IV symptoms.
• If the patient is already on an ACE inhibitor, the ACE inhibitor should be stopped for 36
hours before initiating sacubitril/valsartan to minimise the risk of angioedema.
• Patients should be seen by a heart failure specialist with access to a multidisciplinary
heart failure team before starting treatment with sacubitril/valsartan

Diuretics/ Loop Diuretics

• In the majority of patients with heart failure fluid retention occurs, causing ankle oedema,
pulmonary oedema or both, contributing to the symptom of dyspnoea.
• Diuretic treatment relieves oedema and dyspnoea.
• Patients with heart failure and clinical signs or symptoms of fluid overload or congestion
should be considered for diuretic therapy.
• Care should be taken to select the dose of the loop diuretic on an individual basis, so that
the dose chosen or reached should eliminate ankle or pulmonary oedema without
dehydrating the patient and placing them at risk of renal dysfunction or hypotension.
• The tendency of loop diuretics to cause hypokalaemia is offset by ACE inhibitors, ARBs
and spironolactone.
• Serum potassium should be monitored to maintain its concentration in the range 4–5
mmol/l and adjustments in therapy should be made to prevent both hypokalaemia and
hyperkalaemia.
• The dose of diuretic should be individualised to reduce fluid retention without
overtreating which may cause dehydration or renal dysfunction.

Digoxin
• Digoxin is usually only reserved for patients with severe HF who have not responded to
other treatment
• In patients with HF and sinus rhythm, digoxin may reduce symptoms and hospital
admission
• Digoxin should be considered as an add-on therapy for patients with heart failure in sinus
rhythm who are still symptomatic after optimum therapy.
• If excessive bradycardia occurs with concurrent beta blockade and digoxin therapy,
digoxin should be stopped.

Hydralazine and Isosorbide Dinitrate

• The combination of hydralazine and isosorbide dinitrate (H-ISDN) was shown to reduce
mortality in patients with HF before ACE inhibitors were introduced

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• Patients who are intolerant of an angiotensin-converting enzyme inhibitor and an
angiotensin II receptor blocker due to renal dysfunction or hyperkalaemia should be
considered for treatment with a combination of hydralazine and isosorbide dinitrate.
• Patients with heart failure with reduced ejection fraction, NYHA class III or IV, should be
given hydralazine and isosorbide dinitrate in addition to standard therapy

STEP 6: Monitoring of Heart Failure Therapy (15 minutes)

• Monitoring parameters for patients with Heart Failure focuses on three general areas:
o evaluation of functional capacity,
o evaluation of volume status, and
o Laboratory evaluation.
• Assessment of volume status is a vital component of the ongoing care of patients with
heart failure.
• This evaluation provides the clinician important information about the adequacy of
diuretic therapy.
• Because the cardinal signs and symptoms of heart failure are caused by excess fluid
retention, the efficacy of diuretic treatment is readily evaluated by the disappearance of
these signs and symptoms.
• The physical examination is the primary method for the evaluation of fluid retention, and
specific attention should be focused on;
o the patient’s body weight,
o extent of jugular vein distention (JVD),
o presence and severity of pulmonary congestion and,
o Peripheral edema.
• Specifically, in a patient with pulmonary congestion, monitoring is indicated for
resolution of; rales and pulmonary edema and improvement or resolution of dyspnea on
exertion, orthopnea, and Paroxysmal Nocturnal Dyspnea (PND).
• Other therapeutic outcomes include an improvement in exercise tolerance and fatigue and
a decrease in nocturia and heart rate.
• It should be noted that, particularly with β -blocker therapy, symptoms may worsen
initially and that it may take weeks to months of treatment before patients notice
improvement in symptoms.
• Routine monitoring of serum electrolytes and renal function is required in patients with
heart failure.
• Assessment of serum potassium is especially important because hypokalemia is a
common adverse effect of diuretic therapy and is associated with an increased risk of
arrhythmias and digoxin toxicity.
• Serum potassium monitoring is also required because of the risk of hyperkalemia
associated with ACE inhibitors, ARBs, and aldosterone antagonists.
• A serum potassium ≥4 mEq/L should be maintained, with some evidence suggesting it
should be ≥4.5 mEq/L.

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• Assessment of renal function (BUN and serum creatinine) is also an important end point
for monitoring diuretic and ACE inhibitor therapy.

STEP 7: Key Points (5 minutes)

• Heart Failure is characterized by typical symptoms (e.g. breathlessness, ankle swelling
and fatigue)
• Other signs of Heat Failure include elevated jugular venous pressure, pulmonary crackles
and peripheral oedema which are caused by a structural and/or functional cardiac
abnormality, resulting in a reduced cardiac output and/or elevated intracardiac pressures
at rest or during stress
• Treatment of Heart Failure of depends on the stage of the Disease
• Monitoring parameters for patients with Heart Failure focuses on three general areas
which are evaluation of functional capacity, evaluation of volume status, and Laboratory
evaluation

STEP 8: Evaluation (5 minutes)

• What is Heart Failure?
• What is the pathophysiology of Heart Failure?
• What are the signs and symptoms of Heart Failure?
• How is the treatment of Heart Failure?

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References

Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

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Session 26: Pharmacotherapy of Schizophrenia

Total Session Time: 120 minutes

Prerequisites
• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define schizophrenia
• Explain pathophysiology of schizophrenia
• Explain the clinical presentation of schizophrenia
• Outline diagnosis of schizophrenia
• Describe pharmacological treatment of schizophrenia
• Describe the monitoring of schizophrenia therapy

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Computer and LCD Projector

SESSION OVERVIEW

Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Tasks
10 minutes Presentation Definition of Schizophrenia
2
Buzzing
25 minutes Pathophysiology of Schizophrenia
3 Presentation

4 15 minutes Presentation Clinical Presentation of Schizophrenia

5 15 minutes Presentation Diagnosis of Schizophrenia

30 minutes Presentation Pharmacological Treatment of Schizophrenia

6 Small Group
Discussion
10 minutes Presentation Monitoring of Schizophrenia Therapy
7

8 05 minutes Presentation Key Points

9 05 minutes Presentation Evaluation

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SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)

READ or ASK students to read the learning Tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of Schizophrenia (10 minutes)

Activity: Buzzing (5 minutes)

ASK students to pair up and buzz on the following question for 2 minutes

• What is Schizophrenia?
ALLOW few pairs to respond and let other pairs to add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZEby using the content below

Schizophrenia
Schizophrenia is a chronic and severe mental disorder characterised by disorganized and
bizarre thoughts, delusions, hallucinations, inappropriate affect, and impaired psychosocial
functioning

STEP 3: Pathophysiology of Schizophrenia (25 minutes)

• The pathophysiology of schizophrenia is complex.
• A number of theories attempt to explain the link between altered brain function
and schizophrenia, including;
o the dopamine hypothesis and
o the glutamate hypothesis
o Neurodevelopmental model
The dopamine hypothesis
• The first formulations of the dopamine hypothesis of schizophrenia came from post-
mortem studies finding increased striatal availability of D2/D3 receptors in the striatum, as
well as studies finding elevated CSF levels of dopamine metabolites.
• Psychotic symptoms are related to dopaminergic hyperactivity in the brain. Hyperactivity
of dopaminergic systems during schizophrenia is result of increased sensitivity and
density of dopamine D2 receptors in the different parts of the brain.

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The glutamate hypothesis
• In humans, NMDA receptor antagonists such as phencyclidine, ketamine and dizocilpine
can produce both positive and negative psychotic symptoms-in contrast to amphetamine
which produces only positive symptoms.
• It has therefore been postulated that schizophrenia may result from disruption of
glutamatergic neurotransmission, evident as a reduction in the function of NMDA
receptors

Neurodevelopmental model
• Neurodevelopmental model supposes in schizophrenia the presence of “silent lesion” in
the brain, mostly in the parts, important for the development of integration (frontal,
parietal and temporal), which is caused by different factors (genetic, inborn, infection,
trauma) during very early development of the brain in prenatal or early postnatal period of
life.
• It does not interfere too much with the basic brain functioning in early years, but
expresses itself in the time, when the subject is stressed by demands of growing needs for
integration, during formative years in adolescence and young adulthood

STEP 4: Clinical Presentation of Schizophrenia (15 minutes)

The symptoms of schizophrenia fall into three categories:
• positive,
• negative, and
• Cognitive.

Positive symptoms:
• “Positive” symptoms are psychotic behaviors not generally seen in healthy people.
• People with positive symptoms may “lose touch” with some aspects of reality.
• Symptoms include:
o Hallucinations
o Delusions
o Thought disorders (unusual or dysfunctional ways of thinking)
o Movement disorders (agitated body movements)

Negative symptoms:
• “Negative” symptoms are associated with disruptions to normal emotions and behaviors.
• Symptoms include:
o “Flat affect” (reduced expression of emotions via facial expression or voice tone)
o Reduced feelings of pleasure in everyday life
o Difficulty beginning and sustaining activities
o Reduced speaking

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Cognitive symptoms:
• For some patients, the cognitive symptoms of schizophrenia are subtle, but for others,
they are more severe and patients may notice changes in their memory or other aspects of
thinking.
• Symptoms include:
o Poor “executive functioning” (the ability to understand information and use it to make
decisions)
o Trouble focusing or paying attention
o Problems with “working memory” (the ability to use information immediately after
learning it)

STEP 5: Diagnosis of Schizophrenia (15 minutes)

The Diagnostic and Statistical Manual of the American Psychiatric Association, text revision
(DSM-IV-TR), is the guide for diagnosing and classifying schizophrenia and other
psychiatric disorders

Source: Koda-Kimble et al: Applied Therapeutics; Clinical Use of drugs (10th ed)

• Many patients demonstrate both positive and negative symptoms.

• Patients with negative symptoms frequently have more antecedent cognitive dysfunction,
poor premorbid adjustment, low level of educational achievement, and a poorer overall
prognosis.
• Differential diagnosis has to be made in order to exclude other psychiatric conditions that
resembles schizophrenia as indicated in the table below;

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Table 26.1 Differential diagnosis of Schizophrenia

Source: Koda-Kimble et al: Applied Therapeutics; Clinical Use of drugs (10th ed)

STEP 6: Pharmacological Treatment of Schizophrenia (30 minutes)

Activity: Small Group Discussion ( 20 minutes)

DIVIDE students into small manageable groups

ASK students to discuss on the following question

• What is the treatment of Schizophrenia?

ALLOW students to discuss for 15 minutes

ALLOW few groups to present and the rest to add points not mentioned

CLARIFY and SUMMARIZE by using the contents below

The treatment falls under Acute Phase and Maintainance Phase

Acute Phase
• Haloperidol 5 mg (IM) repeat in 30–60 minutes, if required. (Max dose: 20 mg within 24
hours)
AND
• Diazepam 10 mg (IV), stat. Repeat after 30–60 minutes if needed.
OR
• Promethazine 25–50 mg (deep IM). Repeat after 30–60 minutes if needed.
OR
• Lorazepam 4 mg (IM), stat. Repeat after 30–60 minutes if needed

If haloperidol is unavailable give;

• Chlorpromazine 25–50 mg (deep IM). May be repeated as necessary 4 times in 24 hours.

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If patient is known to suffer from schizophrenia and is not neuroleptic naïve give:
• Zuclopenthixol acetate 50–150 mg (IM) Repeat after 2–3 days, if necessary

If patient develops acute dystonia give:

• Promethazine deep IM 25–50 mg. In the elderly 25 mg.
OR
• Anticholinergic agent, e.g.Biperiden, IM/IV, 2 mg. Repeat as necessary.

For maintenance:
• Haloperidol 3-4.5 mg (PO) 12hourly
OR
• Chlorpromazine 100–600 mg (PO) daily in divided doses
OR
• Olanzepine 5–10mg (PO). Maximum dose 25mg/day
OR
• Risperidone 1mg (PO) 12 hourly then increase by 1mg every 2–3 days to 2–3mg 12
hourly. Maximum dose 16mg/day 7

STEP 6: Monitoring of Schizophrenia Therapy (10 minutes)

• Monitoring parameters for patients with Schizophrenia focuses on three general areas:
o Improvement of four positive symptoms which are suspiciousness, hallucinations,
unusual thought contents and conceptual disorganization
o Improvement of negative symptoms such as prolonged time to respond, emotion
including unchanging facial expression, blank, expressionless face, reduced social
drive, poor grooming and hygiene
o Cognition
• Pharmacotherapeutic plan should include specific monitoring parameters for side effects.
• Given the risk of weight gain, diabetes, and lipid abnormalities associated with many of
the Antipsychotics,baseline parameters should be taken before beginning antipsychotics:
o family history,
o weight,
o height,
o body mass index,
o waist circumference,
o blood pressure,
o fasting plasma glucose, and
o Fasting lipid profile.
o Then follow-up monitoring of these parameters should be done after beginning or
changing antipsychotics.

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STEP 7: Key Points (5 minutes)
• Schizophrenia is a chronic and severe mental disorder characterised by disorganized and
bizarre thoughts, delusions, hallucinations, inappropriate affect, and impaired
psychosocial functioning
• The symptoms of schizophrenia fall into three categories which are positive, negative,
and cognitive
• The treatment of Schizophrenia falls under Acute Phase and Maintainance Phase of the
disease using typical or atypical antipsychotics.

STEP 8: Evaluation (5 minutes)

• What is Schizophrenia?
• What is the pathophysiology of Schizophrenia?
• What are the signs and symptoms of Schizophrenia?
• How is the treatment of Schizophrenia?

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References

Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

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Session 27: Pharmacotherapy of Epilepsy

Total Session Time: 120 minutes

Prerequisites
• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define epilepsy
• Explain pathophysiology of epilepsy
• Explain the clinical presentation of epilepsy
• Outline diagnosis of epilepsy
• Describe pharmacological treatment of epilepsy
• Describe the monitoring of epilepsy therapy

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Computer and LCD Projector

SESSION OVERVIEW

Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Tasks
15 minutes Presentation Definition of Epilepsy
2
Buzzing
20 minutes Pathophysiology of Epilepsy
3 Presentation

4 10 minutes Presentation Clinical Presentation of Epilepsy

5 10 minutes Presentation Diagnosis of Epilepsy

40 minutes Presentation Pharmacological Treatment of Epilepsy

6 Small Group
Discussion
10 minutes Presentation Monitoring of Epilepsy Therapy
7

8 05 minutes Presentation Key Points

9 05 minutes Presentation Evaluation

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SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)

READ or ASK students to read the learning Tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of Epilepsy (15 minutes)

Activity: Buzzing (5 minutes)

ASK students to pair up and buzz on the following question for 5 minutes

• What is Epilepsy?
ALLOW few pairs to respond and let other pairs to add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZEby using the content below

Epilepsy
• The term 'epilepsy' is used to define a group of neurological disorders all of which exhibit
periodic seizures.
• Seizures are associated with episodic high-frequency discharge of impulses by a group of
neurons (sometimes referred to as the focus) in the brain.
• Epilepsy implies a periodic recurrence of seizures with or without convulsions.
• A seizure results from an excessive discharge of cortical neurons and is characterized by
changes in electrical activity as measured by the electroencephalogram (EEG).
• A convulsion implies violent, involuntary contraction(s) of the voluntary muscles
• The site of the primary discharge and the extent of its spread determine the symptoms that
are produced, which range from a brief lapse of attention to a full convulsive fit lasting
for several minutes, as well as odd sensations or behaviours

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Table 27.1 Classification of Epilepsy

Source: Koda-Kimble et al: Applied Therapeutics; Clinical Use of drugs (10th ed)

STEP 3: Pathophysiology of Epilepsy (20 minutes)

• Seizures result from excessive excitation, or in the case of absence seizures, from
disordered inhibition of a large population of cortical neurons.
• Initially, a small number of neurons fire abnormally.
o Normal membrane conductances and inhibitory synaptic currents break down, and
excess excitability spreads, either locally to produce a focal seizure or more widely to
produce a generalized seizure.
o This onset propagates by physiologic pathways to involve adjacent or remote areas.
• The clinical manifestations depend on the site of the focus, the degree of irritability of the
surrounding area of the brain, and the intensity of the impulse.
• There are multiple mechanisms that might contribute to synchronous hyperexcitability,
including:
o alterations in the distribution, number, type, and biophysical properties of ion
channels in the neuronal membranes;
o biochemical modifications of receptors;
o modulation of second messaging systems and gene expression;
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 o changes in extracellular ion concentrations;
o alterations in neurotransmitter uptake and metabolism in glial cells
o Modifications in the ratio and function of inhibitory circuits.
o Local neurotransmitter imbalances between the main neurotransmitters, glutamate
(excitatory) and γ -aminobutyric-acid (GABA) (inhibitory), and neuromodulators
(e.g., acetylcholine, norepinephrine, and serotonin) might play a role in precipitating
seizures in susceptible patients.

STEP 4: Clinical Presentation and Diagnosis of Epilepsy (20 minutes)

General
• In most cases, the healthcare provider will not be in a position to witness a seizure.
• Many patients (particularly those with complex partial (CP) or generalized tonic clonic
(GTC) seizures are amnestic to the actual seizure event.
• Obtaining an adequate history and description of the actual event (including time course)
from a witness is critically important.

Symptoms
• Symptoms of a specific seizure will depend on seizure type.
• Although seizures can vary between patients, they tend to be stereotyped within an
individual.
• CP seizures can include somatosensory or focal motor features.
• CP seizures are associated with altered consciousness.
• Absence seizures can be almost nondetectable with only very brief (seconds) periods of
altered consciousness.
• GTC seizures are major convulsive episodes and are always associated with a loss of
consciousness.
Signs
Interictally (between seizure episodes), there are typically no objective or pathognomonic
signs.

Laboratory Tests
• There are currently no diagnostic laboratory tests for epilepsy.
• Laboratory tests can be done to rule out treatable causes of seizures (e.g., hypoglycemia,
altered electrolyte concentrations, infections, etc.) that do not represent epilepsy.

Other Diagnostic Tests

• EEG is very useful in the diagnosis of various seizure disorders.
• A prolactin serum level obtained within 10 to 20 minutes of a tonic-clonic seizure can be
useful in differentiating seizure activity from pseudoseizure activity but not from
syncope.
• Magnetic resonance imaging (MRI) is very useful especially imaging of the temporal
lobes

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STEP 6: Pharmacological Treatment of Epilepsy (40 minutes)

Activity: Small Group Discussion ( 20 minutes)

DIVIDE students into small manageable groups

ASK students to discuss on the following question

• What is the treatment of Epilepsy?

ALLOW students to discuss for 15 minutes

ALLOW few groups to present and the rest to add points not mentioned

CLARIFY and SUMMARIZE by using the contents below

• The general approach to treatment involves assessment of seizure type and frequency,
identification of treatment goals, development of a care plan, and a plan for follow-up
evaluation.
• During the assessment phase, it is critical to establish an accurate diagnosis of the seizure
type and classification in order to select the appropriate initial AEDs .

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Source: Rang & Dale Pharmacology (7th Ed)

Source: Rang & Dale Pharmacology (7th Ed)

STEP 6: Monitoring of Epilepsy Therapy (10 minutes)

• Patients should be monitored long term for seizure control, comorbid conditions, social
adjustment, drug interactions, compliance, and adverse effects.
• Periodic screening for comorbid neuropsychiatric disorders such as depression and
anxiety is also important.
• Clinical monitoring involves identifying the number and type of seizures.
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• Patients should record the severity and the frequency of seizures in a seizure diary. ‘
• There should be a decrease in the number and/or severity of seizures.
• Patients and family should be questioned regularly to determine whether they are truly
seizure free.

STEP 7: Key Points (5 minutes)

• The term 'epilepsy' is used to define a group of neurological disorders all of which exhibit
periodic seizures.
• Seizures are associated with episodic high-frequency discharge of impulses by a group of
neurons (sometimes referred to as the focus) in the brain.
• Seizures result from excessive excitation, or in the case of absence seizures, from
disordered inhibition of a large population of cortical neurons
• The general approach to treatment involves assessment of seizure type and frequency,
identification of treatment goals, development of a care plan, and a plan for follow-up
evaluation

STEP 8: Evaluation (5 minutes)

• What is Epilepsy?
• What is the pathophysiology of Epilepsy?
• What are the signs and symptoms of Epilepsy?
• How is the treatment of Epilepsy?

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References

Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

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Session 28: Pharmacotherapy of Hepatitis B

Total Session Time: 60 minutes

Prerequisites
• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define hepatitis B
• Explain pathophysiology of hepatitis B
• Explain the clinical presentation of hepatitis B
• Outline diagnosis of hepatitis B
• Describe pharmacological treatment of hepatitis B
• Describe the monitoring of hepatitis b therapy

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Computer and LCD Projector

SESSION OVERVIEW

Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Tasks
05 minutes Presentation Definition Hepatitis B
2
Buzzing
10 minutes Pathophysiology of Hepatitis B
3 Presentation

4 10 minutes Presentation Clinical Presentation of Hepatitis B

5 05 minutes Presentation Diagnosis of Hepatitis B

10 minutes Presentation Pharmacological Treatment of Hepatitis B

6 Small Group
Discussion
05 minutes Presentation Monitoring of Hepatitis B Therapy
7

8 05 minutes Presentation Key Points

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 9 05 minutes Presentation Evaluation

SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)

READ or ASK students to read the learning Tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of Schizophrenia (5 minutes)

Activity: Buzzing (2 minutes)

ASK students to pair up and buzz on the following question for 2 minutes

• What is Hepatitis B?
ALLOW few pairs to respond and let other pairs to add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZEby using the content below

Hepatitis B
• Hepatitis B is a potentially life-threatening liver infection caused by the hepatitis B virus
(HBV).
• It can cause chronic infection and puts people at high risk of death from cirrhosis and
liver cancer.
• HBV is transmitted sexually, parenterally, and perinatally.
• In areas of high HBV prevalence, perinatal transmission from mother to infant is most
common, whereas in areas of intermediate prevalence, horizontal transmission from child
to child is most common.
• Sexual contact, both homosexual and heterosexual, and injection drug use are the
predominant forms of transmission in low-endemic countries

STEP 3: Pathophysiology of Hepatitis B (10 minutes)

• The life cycle of HBV is complex but, essentially, it acts as a stealth virus by evading the
immune system.
• During the first stage of infection, the HBV virion (virus particle) attaches to a liver cell
(hepatocyte) then penetrates the hepatocyte’s cytoplasm

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• The HBV virion is uncoated, which means that nucleocapsids can move into the
hepatocyte’s nucleus and convert the DNA to covalently closed circular DNA (cccDNA)
- a double-stranded DNA structure
• The cccDNA is very stable and can stay in the host nucleus for many months in chronic
disease
• The virus makes copies of itself in a process that lacks “proof reading ability”, which
allows the virus to mutate
• The newly formed HBV virions are released into the bloodstream, from where they
invade other hepatocytes and repeat the replication process.
• It is thought that HBV causes inflammation and progressive fibrosis in the infected liver
by triggering the immune system to attack the hepatocytes

STEP 4: Clinical Presentation and Diagnosis of Hepatitis B (10 minutes)

The majority of acute HBV infections are also asymptomatic but around 30% of adults will
present with the following symptoms;
Signs and symptoms
• Easy fatigability, anxiety, anorexia, and malaise
• Ascites, jaundice, variceal bleeding, and hepatic encephalopathy can manifest with liver
decompensation
• Hepatic encephalopathy is associated with hyperexcitability, impaired mentation,
confusion, obtundation, and eventually coma
• Vomiting and seizures

Laboratory tests
• Presence of hepatitis B surface antigen >6 mo
• Intermittent elevations of hepatic transaminase (alanine transaminase
and aspartate transaminase) and hepatitis B virus DNA >20,000 IU/mL (105 copies/mL)
• Liver biopsies for pathologic classification as chronic persistent hepatitis, chronic active
hepatitis, or cirrhosis

STEP 5: Pharmacological Treatment of Hepatitis B (10 minutes)

Activity: Brainstorming (5 minutes)

Ask students to brainstorm on the following question:

• What is the treatment of Hepatitis B infection?

ALLOW few students to respond

WRITE their responses on the flip chart/ board

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CLARIFY and SUMMARISE by using the content below

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HBV infections are not curable; rather, the goals of therapy are to increase the chances for
seroclearance, prevent disease progression to cirrhosis and HCC, and to minimize further
injury in patients with ongoing liver damage.

Pharmacological treatment includes;

Tenofovir (PO) 300mg once daily for life

OR
Entecavir (PO) 0.5mg–1mg once daily for life
OR
Lamuvidine (PO) 100mg once daily for life

• Prophylaxis against HBV can be achieved by vaccination or by passive immunity in

postexposure cases with hepatitis B immunoglobulin.
• Vaccination is the most effective strategy to prevent infection

STEP 6: Monitoring of Hepatitis B Therapy (5 minutes)

• Response to therapy is monitored by;
o Biochemical (normalization of ALT levels),
o Histologic examination of liver cells from biopsy (a minimum 2-point decrease in
histology activity compared with baseline biopsy), and
o Virologic response (undetectable serum HBV DNA levels and loss of HBeAg in
HBeAg-positive patients).
• Maintenance of viral suppression is defined as durability of response.
• In HBeAg-positive patients, successful therapy includes loss of HBeAg status and
seroconversion to anti-HBeAg.

STEP 7: Key Points (5 minutes)

• Hepatitis B is a potentially life-threatening liver infection caused by the hepatitis B virus
(HBV).
• It can cause chronic infection and puts people at high risk of death from cirrhosis and
liver cancer
• HBV infections are not curable; rather, the goals of therapy are to increase the chances for
seroclearance, prevent disease progression to cirrhosis and HCC, and to minimize further
injury in patients with ongoing liver damage.

STEP 8: Evaluation (5 minutes)

• What is Hepatitis B?
• What is the pathophysiology of Hepatitis B?
• What are the signs and symptoms of Hepatitis B?
• How is the treatment of Hepatiti
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References

Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 225
Session 29: Pharmacotherapy of Cholera

Total Session Time: 60 minutes

Prerequisites
• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define cholera
• Explain pathophysiology of cholera
• Explain the clinical presentation of cholera
• Outline diagnosis of cholera
• Describe pharmacological treatment of cholera
• Describe the monitoring of cholera therapy

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Computer and LCD Projector

SESSION OVERVIEW

Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Tasks
05 minutes Presentation Definition of Cholera
2
Buzzing
05 minutes Pathophysiology of Cholera
3 Presentation

4 05 minutes Presentation Clinical Presentation of Cholera

5 05 minutes Presentation Diagnosis of Cholera

15 minutes Presentation Pharmacological Treatment of Cholera

6 Small Group
Discussion
05 minutes Presentation Monitoring of Cholera Therapy
7

8 05 minutes Presentation Key Points

9 05 minutes Presentation Evaluation

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

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SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)

READ or ASK students to read the learning Tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of Cholera (5 minutes)

Activity: Buzzing (2 minutes)

ASK students to pair up and buzz on the following question for 2 minutes

• What is Cholera?
ALLOW few pairs to respond and let other pairs to add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZEby using the content below

Cholera
• Cholera is an acute gastrointestinal infection caused by Vibrio cholerae.
• Infection occurs through ingestion of contaminated water or food by human faeces
leading to severe diarrhoea and emesis associated with body fluid and electrolyte
depletion.

STEP 3: Pathophysiology of Cholera (5 minutes)

• V. cholerae is a gram-negative bacillus sharing similar characteristics with the family
Enterobacteriaceae.
• Most pathology of cholera results from an enterotoxin (cholera toxin) produced by the
bacteria.
• Conditions that reduce gastric acidity, such as the use of antacids, histamine receptor
blockers, or proton pump inhibitors, or infections with Helicobacter pylori, increase the
risk for clinical disease.
• Cholera toxin stimulates adenylate cyclase,which increases intracellular cyclic adenosine
monophosphate (cAMP) and results in inhibition of sodium and chloride absorption
by microvilli and promotes the secretion of chloride and water by crypt cells.
• The toxin likely acts along the entire intestinal tract, but most fluid loss occur in the
duodenum.
• The net effect of the cholera toxin is isotonic fluid secretion (primarily in the small
intestine) that exceeds the absorptive capacity of the intestinal tract (primarily the colon).
• This results in the production of watery diarrhea with electrolyte concentrations similar to
that of plasma

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

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STEP 4: Clinical Presentation and Diagnosis of Cholera (10 minutes)
• A sudden onset of painless watery diarrhoea that may quickly become severe with
profuse watery stools, vomiting, severe dehydration and muscular cramps, leading to
hypovolemic shock and death
• The stool has a characteristic “rice water” appearance (non-bilious, grey, slightly cloudy
fluid with flecks of mucus, no blood and inoffensive odour)
• Laboratory evidence of dark field microscopic isolation of motile curved bacillus on a
wet mount of fresh stool specimen OR
• Isolation of bacteria through stool culture on TCBS agar.

STEP 5: Pharmacological Treatment of Cholera (15 minutes)

Activity: Brainstorming (5 minutes)

Ask students to brainstorm on the following question:

• What is the treatment of cholera?

ALLOW few students to respond

WRITE their responses on the flip chart/ board

CLARIFY and SUMMARISE by using the content below

Treat according to Plan as indicated in the Standard Treatment Guideline (Tanzania)

Plan A: No dehydration,
Plan B: Moderate dehydration and
Plan C: Severe dehydration.
• When a case of cholera is suspected at home, advise to rehydrate the patient using ORS if
available while preparing to take a patient to the nearest health facility or Cholera
Treatment Centre
• Manage a suspected cholera case in an isolation ward or in an established Cholera
Treatment Centre
• Assess the patient's level of dehydration as per National Guidelines for Prevention and
Control of Cholera. It is of paramount importance to make correct diagnosis and
administer the right treatment according to the Treatment

For severe Rehydration

• Administer intravenous (IV) fluid immediately to replace fluid deficit; Use Ringer
Lactate solution or, if that is not available, 0.9% sodium chloride solution. Give 100
ml/kg IV in 3 hours, 30 ml/kg as rapidly as possible (within 30 min) then 70 ml/kg in the
next 2.5 hours

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

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• After the initial 30 ml/kg has been administered, the radial pulse should be strong and
blood pressure should be normal. If the pulse is not yet strong, continue to give IV fluid
rapidly. Administer ORS solution (about 5 ml/kg/hour) as soon as the patient can drink, in
addition to IV fluid
• If the patient can drink, begin giving A: oral rehydration salt solution (ORS) by mouth
while the drip is being set up; ORS can provide the potassium, bicarbonate, and glucose
that saline solution lacks.
• Give an oral antibiotic to patients with severe dehydration as follows:
o Adults (Not for pregnant women) :
Doxycycline (PO) 300 mg as a single dose or 5mg/kg single dose OR
Ciprofloxacin (PO) 1g stat or 15mg/kg 12 hourly for 3 days AND
Folic acid (PO) 5mg once daily for the duration of the treatment.
o Expectant mothers: Erythromycin (PO) 500mg 8 hourly for 5 days
o Children: A: Erythromycin syrup (PO) 12.5mg/kg 6 hourly for 3 days OR
A: Co-trimoxazole 48mg/kg once a day for 3 days AND
Folic acid AND Zinc.
o For adolescents: Ciprofloxacin (PO) 12mg/kg 2 times for 3 days OR
Doxycycline (PO) 300mg as single dose or 5mg/kg single dose AND
Folic acid AND Zinc
▪ Start feeding 3-4 hours after oral rehydration begins. Preferably, give antibiotics
with food to minimize vomiting
• Give ORS for rehydration; they have to be taken frequently

For moderate Dehydration

• Give oral rehydration, approximately 75-100ml/kg in the first four hours
• Reassess after four hours; if improved, continue giving WHO based ORS, in quantity
corresponding to losses (eg. after each stool) or 10 to 20ml/kg.
• If not improved, treat as severe If no signs of dehydration
• Patients who have no signs of dehydration when first observed can be treated at home
• Give these patients ORS packets to take home, enough for 2 days
• Demonstrate how to prepare and give the solution
• Instruct the patient or the caretaker to return if any of the following signs develop;
increased number of watery stools repeated vomiting or any signs indicating other
problems (eg, fever, blood in stool)

STEP 6: Monitoring of Cholera Therapy (5 minutes)

• It is important to monitor for resolution of the symtoms, adherence to medicines and
adverse drug reactions and severe side effects; in case of any they should be reported and
addressed accordingly

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

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STEP 7: Key Points (5 minutes)
• Cholera is an infection of the small intestine by some strains of the bacterium Vibrio
cholerae.
• Symptoms may range from none, to mild, to severe and the classic symptom is large
amounts of watery diarrhea that lasts a few days.
• Diarrhea can be so severe that it leads within hours to severe dehydration and electrolyte
imbalance
• It is spread mostly by unsafe water and unsafe food that has been contaminated
with human feces containing the bacteria
• Cholera can be successfully treated with oral rehydration therapy (ORT) and
chemotherapy

STEP 8: Evaluation (5 minutes)

• What is Cholera?
• What is the pathophysiology of Cholera?
• What are the signs and symptoms of Cholera?
• How is the treatment of Cholera?

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

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References

Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 231
Session 30: Pharmacotherapy of Shigellosis
Total Session Time: 60 minutes

Prerequisites
• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define shigellosis
• Explain pathophysiology of shigellosis
• Explain the clinical presentation of shigellosis
• Outline diagnosis of shigellosis
• Describe pharmacological treatment of shigellosis
• Describe the monitoring of shigellosis therapy

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Computer and LCD Projector

SESSION OVERVIEW

Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Tasks
05 minutes Presentation Definition of Shigellosis
2
Buzzing
10 minutes Pathophysiology of Shigellosis
3 Presentation

4 05 minutes Presentation Clinical Presentation of Shigellosis

5 05 minutes Presentation Diagnosis of Shigellosis

10 minutes Presentation Pharmacological Treatment of Shigellosis

6 Small Group
Discussion
05 minutes Presentation Monitoring of Shigellosis Therapy
7

8 05 minutes Presentation Key Points

9 05 minutes Presentation Evaluation

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

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SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)

READ or ASK students to read the learning Tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of Shigellosis (5 minutes)

Activity: Buzzing (2 minutes)

ASK students to pair up and buzz on the following question for 2 minutes

• What is Shigellosis?
ALLOW few pairs to respond and let other pairs to add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZEby using the content below

Shigellosis
• Shigellosis is spread by means of fecal-oral, by ingestion of contaminated food and water
and it leads to bacillary dysentery.

STEP 3: Pathophysiology of Shigellosis (10 minutes)

• The source of infection is the feces of infected people or convalescent carriers; humans
are the only natural reservoir for Shigella.
• Direct spread is by the fecal-oral route. Indirect spread is by contaminated food and
fomites.
• Flies serve as vectors.
• Because Shigella is relatively resistant to gastric acid, ingestion of as few as 10 to 100
organisms can cause disease.
• Shigella organisms penetrate the mucosa of the colon, causing mucus secretion,
hyperemia, leukocytic infiltration, edema, and often superficial mucosal ulcerations.
• Shigella dysenteriae type 1 (commonly present in travelers returning from endemic areas)
produces Shiga toxin, which causes marked watery diarrhea and sometimes hemolytic-
uremic syndrome(HUS)

STEP 4: Clinical Presentation and Diagnosis of Shigellosis (10 minutes)

Signs and Symptoms
• Acute abdominal cramping, high-grade fever, emesis and large-volume watery diarrhea,
• Tenesmus, urgency, fecal incontinence, mucoid bloody diarrhea,
• Severe headache, lethargy, meningismus, delirium and convulsions,
PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator
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• Hemolytic uremic syndrome (HUS),
• microangiopathic hemolytic anemia, thrombocytopenia, and renal failure,
• Profound dehydration and hypoglycemia .

Diagnosis
• Laboratory evidence of microscopic isolation of the bacteria from stool or rectal swabs
specimens OR
• Stool culture for suspected cases in early course of infection OR
• An enzyme immunoassay (ELISA) for shiga toxin detection in stool for S. dysenteriae
type-1.

STEP 5: Pharmacological Treatment of Cholera (10 minutes)

Activity: Small Group Discussion ( 10 minutes)

DIVIDE students into small manageable groups

ASK students to discuss on the following question

• What is the treatment of Shigellosis?

ALLOW students to discuss for 15 minutes

ALLOW few groups to present and the rest to add points not mentioned

CLARIFY and SUMMARIZE by using the contents below

Treatment
• Ciprofloxacin (PO) 500mg 12 hourly for 5 days OR
• Nalidixic acid (PO) 1000mg 6 hourly for 7 days OR
• Erythromycin (PO) 250mg 6 hourly for 5 days

STEP 6: Monitoring of Shigellosis Therapy (5 minutes)

• It is important to monitor for resolution of the symtoms, adherence to medicines and
adverse drug reactions and severe side effects; in case of any they should be reported and
addressed accordingly

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

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STEP 7: Key Points (5 minutes)
• Shigella infection (shigellosis) is an intestinal disease caused by a family of bacteria
known as shigella.
• The main sign of shigella infection is diarrhea, which often is bloody.
• Shigella can be passed through direct contact with the bacteria in the stool.
• Shigella infection usually clears up without complications, although chemotherapy may
be needed to some patients
• It may take weeks or months before the bowel habits return to normal.

STEP 8: Evaluation (5 minutes)

• What is Shigellosis?
• What is the pathophysiology of Shigellosis?
• What are the signs and symptoms of Shigellosis?
• How is the treatment of Shigellosis?

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 235
References

Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 236
Session 31: Pharmacotherapy of Breast Cancer

Total Session Time: 120 minutes

Prerequisites

• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define breast cancer
• Explain pathophysiology of breast cancer
• Explain the clinical presentation of breast cancer
• Outline diagnosis of breast cancer
• Describe pharmacological treatment of breast cancer
• Describe the monitoring of breast cancer therapy

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Computer and LCD Projector

SESSION OVERVIEW

Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Tasks
15 minutes Presentation Definition of Breast Cancer
2

20 minutes Presentation Pathophysiology of Breast Cancer

3
Buzzing
4 10 minutes Presentation Clinical Presentation of Breast Cancer

5 10 minutes Presentation Diagnosis of Breast Cancer

35 minutes Presentation Small Pharmacological Treatment of Breast

6
Group Discussion Cancer
15 minutes Presentation Monitoring of Breast Cancer Therapy
7

8 05 minutes Presentation Key Points

9 05 minutes Presentation Evaluation

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 237
SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)

READ or ASK students to read the learning Tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of Breast Cancer (15 minutes)

• Breast cancer is a malignancy originating from breast tissue.
• Disease confined to a localized breast lesion is referred to as early, primary, localized, or
curable
• Disease detected clinically or radiologically in sites distant from the breast is referred to
as advanced or metastatic breast cancer (MBC), which is usually incurable.
• Breast cancer cells often spread undetected by contiguity, lymph channels, and through
the blood early in the course of the disease, resulting in metastatic disease after local
therapy.
• The most common metastatic sites are lymph nodes, skin, bone, liver, lungs, and brain.

STEP 3: Pathophysiology of Breast Cancer (20 minutes)

Activity: Buzzing (5 minutes)

ASK students to pair up and buzz on the following question for 2 minutes

• What is the pathophysiology of breast cancer?

ALLOW few pairs to respond and let other pairs to add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZE by using the content below

• Breast cancer is a malignant tumor that starts in the cells of the breast
• Like other cancers, there are several factors that can raise the risk of getting breast cancer:
o Female gender
o Age
o Previous breast cancer
o Benign breast disease
o Hereditary factors (family history of breast cancer)
o Early age at menarche
o Late age at menopause
o Late age at first full-term pregnancy
PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator
Guide 238
 o Obesity (postmenopausal)
o Low physical activity
o High-dose exposure to ionizing radiation early in life
• Damage to the DNA and genetic mutations can lead to breast cancer; have been
experimentally linked to estrogen exposure. Some individuals inherit defects in the DNA
and genes like the BRCA1, BRCA2 and P53 among others. Those with a family history
of ovarian or breast cancer thus are at an increased risk of breast cancer.
• The immune system normally seeks out cancer cells and cells with damaged DNA and
destroys them. Breast cancer may be a result of failure of such an effective immune
defence and surveillance.
• These are several signalling systems of growth factors and other mediators that interact
between stromal cells and epithelial cells. Disrupting these may lead to breast cancer as
well.

STEP 4: Clinical Presentation and Diagnosis of Breast Cancer (20 minutes)

The patient may not have any symptoms, as breast cancer may be detected in asymptomatic
patients though routine screening mammography.
• The initial sign in more than 90% of women with breast cancer is a painless lump that is
typically solitary, unilateral, solid, hard, irregular, and nonmobile.
• Less common initial signs are pain and nipple changes.
• More advanced cases present with prominent skin edema, redness, warmth, and
induration.
• Symptoms of MBC depend on the site of metastases, but may include bone pain,
difficulty breathing, abdominal pain or enlargement, jaundice, and mental status changes.
• Many women first detect some breast abnormalities themselves, but it is increasingly
common for breast cancer to be detected during routine screening mammography in
asymptomatic women.
Staging
• Stage is based on the size of the primary tumor, presence and extent of lymph node
involvement, and presence or absence of distant metastases. Simplistically stated, these
stages may be represented as follows:
o Early Breast Cancer
▪ Stage 0: Carcinoma in situ or disease that has not invaded the basement
membrane.
▪ Stage I: Small primary tumor without lymph node involvement.
▪ Stage II: Involvement of regional lymph nodes.
o Locally Advanced Breast Cancer
▪ Stage III: Usually a large tumor with extensive nodal involvement in which node
or tumor is fixed to the chest wall; also includes inflammatory breast cancer,
which is rapidly progressive.
o Advanced or Metastatic Breast Cancer
▪ Stage IV: Metastases in organs distant from the primary tumor.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 239
Clinical presentation:
• Local Signs and Symptoms
o A painless, palpable lump is most common.
o Less common: pain; nipple discharge, retraction or dimpling;
o Skin edema, redness or warmth.
o Palpable local–regional lymph nodes may also be present.

• Signs and Symptoms of Systemic Metastases

o Depends on the site of metastases, but may include bone pain, difficulty breathing,
abdominal pain or enlargement, jaundice, mental status changes
Diagnosis
• Initial workup for a woman presenting with a localized lesion or suggestive symptoms
should include a careful history, physical examination of the breast, three-dimensional
mammography, and, possibly, other breast imaging techniques such as ultrasound.
• Breast biopsy is indicated for a mammographic abnormality that suggests malignancy or a
mass that is palpable on physical examination.

Laboratory Tests
• Tumor markers such as cancer antigen (CA) or carcinoembryonic antigen (CEA) may be
elevated.
• Alkaline phosphatase or liver function tests may be elevated in metastatic disease.

Other Diagnostic Tests

• Mammogram (with or without ultrasound, breast MRI, or both)
• Biopsy for pathology review and determination of tumor estrogen/progesterone receptor
(ER/PR) status and HER2 status.
• Systemic staging tests may include: chest x-ray, chest CT, bone scan, abdominal CT or
ultrasound, or MRI.

STEP 5: Pharmacological Treatment of Breast Cancer (35 minutes)

Activity: Small Group Discussion (15 minutes)

DIVIDE students into small manageable groups

ASK students to discuss on the following question

• What is the pharmacological treatment of breast cancer?

ALLOW students to discuss for 15 minutes

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 240
 ALLOW few groups to present and the rest to add points not mentioned

CLARIFY and SUMMARIZE by using the contents below

• Chemotherapy is indicated for almost all patients as neo-adjuvant, adjuvant or palliative.

Patients, who are planned for surgery and have ≥ T3 tumors, should receive neo-adjuvant
chemotherapy before operation

• Several regimens are available. Few of them include:

▪ Dosing schedules for combinations for HER 2 negative disease:
▪ Doxorubicin 60 mg/m2 IV day 1 + Cyclophosphamide 600 mg/m2 IV day 1 given
every 2 weeks for 4 cycles THEN Paclitaxel 175 mg/m2 by 3hr IV infusion day 1,
given every 14 days for 4 cycles.
▪ Doxorubicin 60 mg/m2 IV day 1 + Cyclophosphamide 600 mg/m2 IV day 1 given
every 14 days for 4 cycles followed by Paclitaxel 80 mg/m2 by 1 h IV infusion
weekly for 12 weeks.
▪ Doxorubicin 60 mg/m2 IV on day1 + Cyclophosphamide 600 mg/m2 IV day 1 given
every 21 days for 4 cycles then followed by Paclitaxel 175 mg/m2 by 3 h IV infusion
day 1, given every 21 days for 4 cycles OR Docetaxel 100 mg/m2 IV day 1 Cycled
every 21 days for 4 cycles.

NOTE: FBC, RFT, LFT before each cycle

o Dosing schedule for combinations for HER2-Positive disease:

Doxorubicin 60 mg/m2 IV day1 AND Cyclophosphamide 600 mg/m2 IV day 1 given
every 21 days for 4 cycles followed by Paclitaxel 80 mg/m2 by 1 h IV weekly for 12 wks

AND
Trastuzumab 4 mg/kg IV with first dose of paclitaxel followed by Trastuzumab 2 mg/kg
IV weekly to complete 1 y of treatment

As an alternative, Trastuzumab 6 mg/kg IV every 21 days may be used following the

completion of Paclitaxel, and given to complete 1 year of Trastuzumab treatment.

• Endocrine therapy
o Premenopausal ER/PR Positive: Tamoxifen 20 mg (PO) daily for 5 years
o Post-menopausal ER/ PR Positive: Anastrazole 1 mg daily for 5 years OR Tamoxifen 20
mg daily for 2 years followed Anastrazole 1 mg daily for 3 years.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

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STEP 6: Monitoring of Breast Cancer Therapy (15 minutes)
• Monitoring response to treatment is a key element in the management of breast cancer
that involves several different viewpoints from surgery, radiology, and medical oncology
• After completion of adjuvant therapy, follow up care focuses on detecting recurrent
disease with the intention of improving long term survival
• Monitor patient adherence to the treatment as maintaining dose intensity has been
demonstrated to be important in the cure of disease
• Tumor response to a particular treatment regimen may be measured by clinical chemistry
such as liver enzyme elevation in a patient with hepatic metastases or tumor markers, or
imaging techniques such as bone scans or chest radiographs.
• However, assessment of the patient’s clinical status and symptom control is often
adequate to evaluate response to the therapy administered.
• In the patient with metastatic breast cancer, it is common to initiate hormonal therapy or
chemotherapy and continue administration until signs and symptoms of disease
progression or new signs and symptoms present
• Monitor the adverse effects of drugs and manage them accordingly

STEP 7: Key Points (5 minutes)

• Breast cancer is a malignancy originating from breast tissue. Disease confined to a
localized breast lesion is referred to as early, primary, localized, or curable
• Disease detected clinically or radiologically in sites distant from the breast is referred to
as advanced or metastatic breast cancer (MBC), which is usually incurable
• Damage to the DNA and genetic mutations can lead to breast cancer; have been
experimentally linked to estrogen exposure. Some individuals inherit defects in the DNA
and genes like the BRCA1, BRCA2 and P53 among others. Those with a family history
of ovarian or breast cancer thus are at an increased risk of breast cancer.
• Chemotherapy is indicated for almost all patients as neo-adjuvant, adjuvant or palliative.
Patients, who are planned for surgery and have ≥ T3 tumors, should receive neo-adjuvant
chemotherapy before operation

STEP 8: Evaluation (5 minutes)

• What is Breast Cancer?
• What is the pathophysiology of Breast Cancer?
• How is Breast Cancer diagnosed?
• How is monitoring of Breast Cancer therapy done?

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 242
References

Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy (2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 243
Session 32: Pharmacotherapy of Prostate Cancer

Total Session Time: 120 minutes

Prerequisites

• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define prostate cancer
• Explain pathophysiology of prostate cancer
• Explain the clinical presentation of prostate cancer
• Outline diagnosis of prostate cancer
• Describe pharmacological treatment of prostate cancer
• Describe the monitoring of prostate cancer therapy

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Computer and LCD Projector

SESSION OVERVIEW
Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Tasks
15 minutes Presentation Definition of Prostate Cancer
2

20 minutes Presentation Pathophysiology of Prostate Cancer

3
Buzzing
10 minutes Clinical Presentation of Oropharyngeal
4 Presentation
Candidiasis
5 10 minutes Presentation Diagnosis of Prostate Cancer

40 minutes Presentation Pharmacological Treatment of Prostate

6 Small Group Cancer
Discussion
10 minutes Presentation Monitoring of Prostate Cancer Therapy
7

8 05 minutes Presentation Key Points

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

Guide 244
 9 05 minutes Presentation Evaluation

SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)

READ or ASK students to read the learning Tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of Prostate Cancer (15 minutes)

• Prostate cancer is a malignant neoplasm that arises from the prostate gland.
• Prostate cancer has an indolent course; localized prostate cancer is curable by surgery or
radiation therapy, but advanced prostate cancer is not yet curable.
• The most common type of prostate cancer is adenocarcinoma (95 %)
• Tumours are stratified by T stage, Gleason score (GS), and PSA into three prognostic
groups of low, intermediate and high risk.
o Low risk: T1–T2a and PSA < 10 ng/ml and GS ≤ 6
o Intermediate risk: T2b or PSA 10 – 20 ng/ml or GS 7
o High risk: T2c–T4 or PSA > 20ng/ml or GS 8–10
• Patient can be offered appropriate treatment options according to stage of disease,
prognostic risk group and estimated survival taking into account performance status and
comorbidity.

STEP 3: Pathophysiology of Prostate Cancer (20 minutes)

Activity: Buzzing (5 minutes)

ASK students to pair up and buzz on the following question for 2 minutes

• What is the pathophysiology of prostate cancer?

ALLOW few pairs to respond and let other pairs to add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZE by using the content below

• The prostate gland is a part of the male reproductive system that helps to make and store
seminal fluid.
• Because of its location, prostate disease often affects urination, ejaculation, and rarely
defecation.

PST 06106 Basic Pharmacotherapy NTA Level 6 Semester 1 Facilitator

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• Prostate cancer begins when normal semenscreening prostate gland cells mutate into
cancer cells.
• The region of prostate gland where the adenocarcinoma is most common is the peripheral
zone.
• Initially, small clumps of cancer cells remain confined to otherwise normal prostate
glands, a condition known as carcinoma in situ or prostate intraepithelial neoplasia(PIN).
• Overtime, these cancer cells begin to multiply and spread to the surrounding prostate
tissue (the stroma) forming a tumor.
• Eventually, the tumor may grow large enough to invade nearby organs such as the
seminal vesicles, or the rectum, or the tumor cells may develop the ability to travel in the
blood stream and lymphatic system.
• The invasion of other organs is called metastasis.
• Prostate cancer most commonly metastasizes to the bones, lymph nodes, and may invade
rectum, bladder and lower ureters after local progression.

STEP 4:Clinical Presentation and Diagnosis of Prostate Cancer

(20 minutes)
Localized Disease
Asymptomatic
Locally Invasive Disease
• Impotence
• Prostatic symptoms are associated with advanced stages of the disease, which include:
reduced potency, urinary frequency and nocturnal, poor stream, hesitancy and terminal
dribbling

Advanced Disease
• Back pain
• Cord compression
• Lower extremity edema
• Anemia
• Weight loss
• Very often patients may present with bone pain including backache or pathological
fracture

Table32.1 Diagnostic and Staging Workup for Prostate Cancer

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Source: DiPiro JT, et al (2008): Pharmacotherapy: A Pathophysiologic Approach (7 th ed)

STEP 5: Pharmacological Treatment of Prostate Cancer (40 minutes)

Activity: Small Group Discussion (20 minutes)

DIVIDE students into small manageable groups

ASK students to discuss on the following question

• What are the drugs treatments for prostate cancer?

ALLOW students to discuss for 15 minutes

ALLOW few groups to present and the rest to add points not mentioned

CLARIFY and SUMMARIZE by using the contents below

• Luteinizing Hormone–Releasing Hormone Agonists

o LHRH agonists are a reversible method of androgen ablation and are as effective as
orchiectomy.
o Leuprolide acetate, leuprolide depot, leuprolide implant, triptorelin depot,
triptorelin implant, and goserelin acetate implant are currently available.
▪ Dosing intervals range from once monthly to every 16 weeks.
o Leuprolide implant is a miniosmotic pump that delivers daily doses for 1 year.
▪ The most common adverse effects of LHRH agonists include disease flare-up
during the first week of therapy (eg, increased bone pain or urinary symptoms),
hot flashes, erectile impotence, decreased libido, and injection-site reactions.
▪ Use of an antiandrogen (eg, flutamide, bicalutamide, or nilutamide) prior to
initiation of LHRH therapy and for 2 to 4 weeks after is a strategy to minimize
initial tumor flare.
▪ Decreases in bone mineral density complicate androgen deprivation therapy
(ADT), resulting in increased risk of osteoporosis, osteopenia, and skeletal
fractures.

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 ▪ Calcium and vitamin D supplements and a baseline bone mineral density are
recommended.

• Gonadotropin-Releasing Hormone Antagonists

o Degarelix binds reversibly to GnRH receptors in the pituitary gland, reducing the
production of testosterone to castrate levels in 7 days or less
o A major advantage of degarelix over LHRH agonists the lack of tumor flares.
o Degarelix is administered as a subcutaneous injection every 28 days
o Injection site reactions are the most frequently reported adverse effects and include
pain, erythema, swelling, induration, and nodules.

• Antiandrogens
o Monotherapy with flutamide, bicalutamide, and nilutamide is no longer recommended
due to decreased efficacy as compared with patients treated with LHRH agonist
therapy
o Antiandrogens are indicated for advanced prostate cancer only when
combined with an LHRH agonist (flutamide and bicalutamide]) or orchiectomy
(nilutamide). In combination, antiandrogens can reduce the LHRH agonist–induced
flare.
o Enzalutamide is approved as a single agent in metastatic hormone-resistant prostate
cancer patients who have previously received docetaxel.

• Chemotherapy
o Docetaxel, 75 mg/m2 every 3 weeks up to 6 cycles, combined with prednisone, 5 mg
twice daily, improves survival in castrate-refractory prostate cancer.
o It is mainly reserved for hormonal-refractory prostate cancer. The most common
adverse events include nausea, alopecia, and myelosuppression.
o Cabazitaxel 25 mg/m2 every 3 weeks with prednisone 10 mg daily significantly
improves progression-free and overall survival.
o Neutropenia, febrile neutropenia, neuropathy, and diarrhea are the most significant
toxicities.
o For Bone metastases/osteolytic/tumour induced hypercalcemia: Zolendronic acid IV
4mg over 15min given 4 Weekly

STEP 6: Monitoring of Prostate Cancer Therapy (10 minutes)

• Monitor primary tumor size, involved lymph nodes, and tumor marker response such as
PSA with definitive, curative therapy
• PSA level is checked every 6 months for the first 5 years, then annually.
• With metastatic disease, clinical benefit can be documented by evaluating performance
status, weight, quality of life, analgesic requirements, and PSA or DRE at 3-month
intervals.
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STEP 7: Key Points (5 minutes)
• Prostate cancer is a malignant neoplasm that arises from the prostate gland. Prostate
cancer has an indolent course; localized prostate cancer is curable by surgery or
radiation therapy, but advanced prostate cancer is not yet curable
• There are different stages of Prostate Cancer according to Glearson score
• Metastatic spread can occur by local extension, lymphatic drainage, or hematogenous
dissemination
• The diagnosis is based on various diagnostic criteria and various diagnostic tests such as
abdominal and pelvic USS and or CT Scan, Pelvic MRI in early stage disease,Bone scan
etc
• The common drugs used for the treatment of Prostate Cancer are LHRH agonists and
GnRH antagonists
• Monitoring therapy should be done by checking primary tumor size, involved lymph
nodes, and tumor marker response such as PSA with definitive, curative therapy. PSA
level should checked every 6 months for the first 5 years, then annually.

STEP 7: Evaluation (5 minutes)

• What is Prostate Cancer?
• What is the pathophysiology of Prostate Cancer?
• How is Prostate Cancer diagnosed?
• What is the first line treatment of Prostate Cancer?

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References

Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

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Session 33: Pharmacotherapy of Oropharyngeal
Candidiasis

Total Session Time: 120 minutes

Prerequisites

• None

Learning Tasks
By the end of this session students are expected to be able to:
• Define oropharyngeal candidiasis
• Explain pathophysiology of oropharyngeal candidiasis
• Explain the clinical presentation of oropharyngeal candidiasis
• Outline diagnosis of oropharyngeal candidiasis
• Describe pharmacological treatment of oropharyngeal candidiasis
• Describe the monitoring of oropharyngeal candidiasis therapy

Resources Needed:
• Flip charts, marker pens, and masking tape
• Black/white board and chalk/whiteboard markers
• Computer and LCD Projector

SESSION OVERVIEW

Activity/
Step Time Content
Method
1 05 minutes Presentation Introduction, Learning Tasks
15 minutes Presentation Definition of Oropharyngeal Candidiasis
2
20 minutes Presentation Pathophysiology of Oropharyngeal
3
Buzzing Candidiasis
10 minutes Clinical Presentation of Oropharyngeal
4 Presentation
Candidiasis
5 10 minutes Presentation Diagnosis of Oropharyngeal Candidiasis

40 minutes Presentation Pharmacological Treatment of

6 Small Group Oropharyngeal Candidiasis
Discussion
10 minutes Presentation Monitoring of Oropharyngeal
7 CandidiasisTherapy

8 05 minutes Presentation Key Points

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 9 05 minutes Presentation Evaluation
SESSION CONTENTS

STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)

READ or ASK students to read the learning Tasks and clarify

ASK students if they have any questions before continuing.

STEP 2: Definition of Oropharyngeal Candidiasis (10 minutes)

• Oropharyngeal candidiasis (OPC), or thrush, refers to an infection of the oral mucosa.
• Candida is responsible for the majority of oralfungal infections, and C. albicans is the
principal species causing the infection, commonly referred to as candidiasis
• The infection may extend into the esophagus, causing esophageal candidiasis.

STEP 3: Pathophysiology of Oropharyngeal Candidiasis (20 minutes)

Activity: Buzzing (5 minutes)

ASK students to pair up and buzz on the following question for 2 minutes

• What is the pathophysiology of oropharyngeal candidiasis?

ALLOW few pairs to respond and let other pairs to add on points not mentioned

WRITE their response on the flip chart/board

CLARIFY and SUMMARIZE by using the content below

• The pathogenesis of OPC is most clearly elucidated in the setting of HIV infection.
• There appear to be several levels of immune defense against the development of OPC in
HIV-infected persons, and they involve both systemic and local immunity.
• The primary line of host defense against C. albicans is cell-mediated immunity (CMI) at
the mucosal surfaces, which is mediated by CD4 T cells.
• The efficacy of the CD4 T cells is reduced when the number of cells drops below a
protective threshold, and protection against infection becomes dependent on secondary or
local immune mechanisms.
• When the number of CD4 T cells drops too low, recruitment of these cells to the oral
cavity is impaired.
• The CD4 T-cell count has been considered as the hallmark predictor for development of
OPC.
• The changeover of the role of Candida species from commensal to pathogenic in the
human host usually occurs when breakdown in these host defenses occurs.

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• Other virulence factors are the adhesive ability of C. albicans to epithelial cells and
proteins and its ability to invade host cells by means of phospholipase and proteinase
enzymes.
o This may be one of the factors leading to OPC in non-HIV-infected individuals.
• Other components of the pathogenesis in the absence of HIV that have been postulated
are the ability of the Candida species to adhere to buccal epithelial cells including those
patients receiving broad-spectrum antimicrobial therapy.

REFER Students to Handout 33.1: Risk Factors for the Development of Oropharyngeal
and/or Esophageal Candidiasis

STEP 4:Clinical Presentation and Diagnosis of Oropharyngeal Candidiasis

(20 minutes)
General
The clinical features can be quite diverse
Symptoms
Symptoms are diverse and range from none to sore, painful mouth, burning tongue, metallic
taste, and dysphagia and odynophagia with involvement of the hypopharynx
Signs
Signs are variable and can include diffuse erythema and white patches on the surfaces of the
buccal mucosa, throat, tongue, or gums; constitutional signs are absent
Laboratory tests
• Scraping of an active lesion for microscopic examination can help confirm the diagnosis
(presence of pseudohyphae and budding yeast) but is usually not necessary
• Cultures are not necessary because isolation of Candida species does not distinguish
between colonization and true infection; cultures can be taken in patients responding
poorly to therapy to determine the infecting species and to predict likely drug resistance

STEP 5: Pharmacological Treatment of Prostate Cancer (45 minutes)

Activity: Small Group Discussion (15 minutes)

DIVIDE students into small manageable groups

ASK students to discuss on the following question

• What are the drugs treatments for oropharyngeal candidiasis?

ALLOW students to discuss for 15 minutes

ALLOW few groups to present and the rest to add points not mentioned

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CLARIFY and SUMMARIZE by using the contents below

• The management of OPC should be individualized for each patient, taking into
consideration the underlying immune status, other concurrent mucosal and medical
diseases, concomitant medications, and exogenous infectious sources.
• In HIV-infected patients with inadequately controlled disease, antifungal treatment
produces only a transient clinical response, and the relapse rates are higher than in other
patient populations.
• Topical therapies should be the first choice for milder forms of infections.

Table1: Therapeutic Options for Mucosal Candidiasis

Source: DiPiro JT, et al (2008): Pharmacotherapy: A Pathophysiologic Approach (7 th ed)

STEP 6: Monitoring of Oropharyngeal Candidiasis Therapy (10 minutes)

• Efficacy end points for oropharyngeal and esophageal candidiasis include rapid relief of
symptoms and prevention of complications without early relapse after completion of the
course of therapy.
• Symptomatic relief of presenting signs and symptoms generally occurs within 48 to 72
hours of starting therapy, with complete resolution by 7 to 10 days.
• Patients should be advised about the time course and told to return for reassessment when
signs and symptoms recur.

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• It is usually unnecessary for the patient to be reassessed soon after finishing the treatment
course.
• However, HIV patients should be questioned and examined for the occurrence of mucosal
candidiasis as part of their regular follow-up.
• The frequency of monitoring can be more often in neutropenic patients because
of concern for dissemination of candidiasis.
• During the period of neutropenia, temperature should be monitored daily, as well as
signs of dissemination.
• Efficacy of the antifungal agent is partly influenced by patient adherence to the
medication regimen.
• Patients must be counseled on proper administration and dosing, in particular for topical
agents
• Safety end points include monitoring for occurrence of the relevant drug side effects and
drug interactions
• Hepatotoxicity can occur when azole therapy is prolonged beyond 7 to 10 days or high
doses are used.
• Periodic monitoring of liver enzymes (alanine transaminase and aspartate amino-
transferase) should be considered, especially if prolonged therapy (longer than 21 days) is
anticipated.

STEP 7: Key Points (5 minutes)

• Oropharyngeal candidiasis (OPC), or thrush, refers to an infection of the oral mucosa.
• Symptoms are diverse and range from none to sore, painful mouth, burning tongue,
metallic taste, and dysphagia and odynophagia with involvement of the hypopharynx
• The management of OPC should be individualized for each patient, taking into
consideration the underlying immune status, other concurrent mucosal and medical
diseases, concomitant medications, and exogenous infectious sources

STEP 7: Evaluation (5 minutes)

• What is Oropharyngeal Candidiasis?
• What is the pathophysiology of Oropharyngeal Candidiasis?
• How is Oropharyngeal Candidiasis?
• What is the first line treatment of Oropharyngeal Candidiasis?

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References

Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6th Ed). New
York, NY: McGraw-Hill.
DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008):
Pharmacotherapy: A Pathophysiologic Approach (7th ed): New York, NY: McGraw-
Hill.
Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles &
Practice Study Guide: A Case-Based Care Plan Approach: New York, NY: McGraw-
Hill.
Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused
Approach (7th ed): New York, NY: McGraw-Hill.

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 Handout 33.1 Risk Factors for the Development of
Oropharyngeal and/or Esophageal Candidiasis;

Source: DiPiro JT, et al (2008): Pharmacotherapy: A Pathophysiologic Approach (7 th ed)

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