LIST OF ABBREVIATIONS

ACE Angiotensin Converter Enzyme

Ach Acetylcholine
AchR Acetylcholine Receptors
AD Alzheimer’s Disease
Anti-CCP Anti-cyclic Citrullinated Peptide
BMI Body Mass Index
BMR Basal Metabolic Rate
CF Cystic Fibrosis
CNS Central Nervous System
COPD Chronic Obstructive Pulmonary Disease
CP Cerebral Palsy
CSF Cerebral-Spinal Fluid
CT-scan Computerized Topography scan
CVA Cerebrovascular Accident
DMARDs Disease Modifying Anti-rheumatic Drugs
DNA Deoxyribonucleic Acid
DS Down’s Syndrome
EN Enteral Nutriton
ESR Erythrocyte Sedimentation Rate
GBS Guillaine-Barre Syndrom
GERD Gastroesophageal Reflux Disease
GIT Gastrointestinal Tract
HCl Hydrochloric Acid
HIV Human Immunodeficiency Virus
HPV Human Papilloma Virus
IC Indirect Calorimetry
ICP Intracranial Pressure
MG Myasthenia Gravis
MNT Medical Nutrition Therapy
MRI Magnetic Resonance Imaging
i
MS Multiple Sclerosis
MSD Musculoskeletal Diseases
NSAIDs Non-Steroidal Anti-inflammatory Drugs
OA Osteoarthritis
OA Osteoarthritis
PD Parkinson’s Disease
PEM Protein Energy Malnutrition
PN Parenteral Nutrition
PUFA Polyunsaturated fatty acids
RA Rheumatoid Arthritis
RA Rheumatoid Arthritis
SCI Spinal Cord Injury
TB Tuberculosis
TBI Traumatic Brain Injury
TBSA Total Body Surface Area
TIA Transient Ischemic Attack
URT Upper Respiratory Tract
VAP Ventilator Associated Pneumonia
WBc White Blood cells
WHO World Health Organization
MODULE INTRODUCTION
Diet Therapy II module is designed to equip the learner with knowledge, skills and
attitude to enable them plan and execute nutrition care to patients.
The prerequisite modules include; Human anatomy and physiology, Principles of
human nutrition, Introduction to Microbiology and Communicable & non
communicable diseases, nutrition assessment and surveillance and basic critical
reasoning and patient documentation skills.
The module takes 60 contact hours: 33 hours for theory and 27 hours for practicals.
Learners undertaking this module will have both theory and practical assessments.
The formative assessment will be in the form of continuous assessment tests,
assignments, clinical and field assessments and promotional/end of semester
examination whereas summative assessment will be done in form of final qualifying
examination.
Module competences
To enable the learner plan and execute nutrition care to patients
Module outcomes
1. Discuss the basic concepts of diet therapy
2. Discuss the need and role of special diet in management of diseases and
disorders
3. Apply diet planning in management of diseases and disorders
. Discuss drug and nutrient interaction in management of diseases and disorders
5. Prepare therapeutic diets for various conditions
Module learning strategies
Lectures, individual and group assignments and presentation, practicals, clinical
exposure, demonstrations, case studies, role playing etc.
Module learning logistics/resources
LCDS, white boards, laptops, markers, diet therapy textbooks, flip charts, student
notebooks, food items for practicals, hospital facilities
Module assessment
Formative Assessment (continuous assessment tests, individual assignments and
group assignments) - 40% and Summative Assessment (end of semester
examination) - 60% and final qualifying practical examination).
TABLE OF CONTENTS
ACKNOWLEDGEMENT i
LIST OF ABBREVIATIONS ii
MODULE INTRODUCTION iv
Module competences v
Module outcomes v
Module learning strategies v
Module learning logistics/resources v
Module assessment v
UNIT 1: RESPIRATORY DISEASES 1
1.1 Cold and Flu 2
1.2 Bronchitis 4
1.3 Asthma; 5
1.4 Chronic obstructive pulmonary disease (COPD) 7
1.5 Pneumonia 11
UNIT 2: FEBRILE CONDITIONS 13
2.1 Typhoid 14
2.2 Malaria 16
2.3 Tuberculosis (TB) 17
UNIT 3: NUTRITION IN SURGERY 21
3.1 Introduction to stress response 21
3.2 Introduction to Surgery 25
3.3 Pre-surgery nutrition care 27
3.4 Post-operative nutritional care 29
3.5 Post-operative complications and implications; 30
UNIT 4: BURNS 35
3.6 Assessment of burns 35
3.7 Consequences/implication of burns; 38
3.8 Nutrition management of burns 39
UNIT 5: CANCER 43
5.1 Introduction to cancer 43
5.2 Cancer development process; 44
 5.3 Nutritional effects or consequences of cancer; 46
5.4 Treatment of cancer; 48
5.5 Nutritional care for cancer; 52
UNIT 6: MUSCULOSKELETAL DISORDERS (MSDs) 55
6.1 Gout 55
6.2 Osteoporosis 59
6.3 Osteoarthritis (OA) 61
6.4 Rheumatoid arthritis (RA) 64
UNIT 7: NEUROMUSCULAR DISEASES 68
7.1 Introduction to neuromuscular disorders 68
7.2 Traumatic brain injury 71
7.3 Spinal cord injury 73
7.4 Cerebrovascular accident (CVA)/stroke 75
7.5 Cerebral palsy 79
7.6 Epilepsy 80
7.7 Down’s syndrome 82
7.8 Guillain-barre syndrome (GBS) 83
7.9 Myasthenia gravis 84
7.10 Multiple sclerosis (MS) 85
7.11 Parkinson’s disease 86
7.12 Alzheimers’s disease 87
7.13 Spina bifida 88
7.14 Dysphagia as a complication of interest in neurologic disorders 89
REFERENCES 91
UNIT 1: RESPIRATORY DISEASES
Unit Objectives
By the end of the unit the learner should be able to:
a) Describe types, causes and management of respiratory diseases
b) Plan and prepare meals for respiratory diseases
c) Visit a health facility to learn more about management of respiratory diseases
Functions of the respiratory system
i) Gaseous exchange - The lungs enable the body to obtain the oxygen needed to
meet its cellular metabolic demands and to remove the carbon dioxide (CO2)
produced. Healthy nerves, blood, and lymph are needed to supply oxygen and
nutrients to all tissues.
ii) The lungs also filter, warm, and humidify inspired air.
iii) Defense against air borne pathogens e.g. the epithelial surface of the alveoli
contains macrophages. By the process of phagocytosis, these alveolar
macrophages engulf inhaled inert materials and microorganisms and digest
them.
iv) Other metabolic functions e.g. they help regulate the body’s acid-base balance.
The body’s pH is maintained partially by the proper balance of CO2 and O2.
The lungs also synthesize arachidonic acid that ultimately may be converted to
prostaglandins or leukotrienes. These appear to play a role in
bronchoconstriction seen in asthma. The lungs convert angiotension I to
angiotensin II by the angiotension-converting enzyme (ACE) found mainly in the
numerous capillary beds of the lungs. Angiotensin II increases blood pressure.
Because of the ultrastructure and the fact that they receive the total cardiac
output, lungs are well suited to function as a chemical filter.
Introduction to Respiratory diseases
It is a term that encompasses pathological conditions affecting the organs and tissues
that make gaseous exchange possible in higher organisms. They are conventionally
classified into upper and lower respiratory tract infections.
Upper respiratory tract infections include:
 Common cold (most common URT  Otitis media
infection)  Pharyngitis
 Sinusitis  Laryngitis
 Tonsillitis
Lower respiratory tract infections include:
Pneumonia is the most common. It is caused by an infection of the lungs which is
usually caused by bacteria, particularly Streptococcus pneumoniae. Tuberculosis is an
important cause of pneumonia. There are clinical studies that have linked pneumonia
with poor oral health. Additionally, dental treatment and improvements in oral health
have been associated with significant reductions in respiratory diseases in
institutionalized elderly adults.
Others lower respiratory tract infections include those infections affecting the trachea,
bronchi, bronchioles, alveoli, pleura and pleural cavity, and the nerves and muscles of
breathing.
Pulmonary system disorders may also be categorized as primary, such as tuberculosis
(TB), bronchial asthma, and cancer of the lung; or secondary when associated with
cardiovascular disease, obesity, human immunodeficiency virus (HIV) infection or sickle
cell disease.
Furthermore conditions may also be acute or chronic. Examples of acute conditions
include aspiration pneumonia, airway obstruction from foods such as peanuts, and
allergic anaphylaxis from consumption of shellfish. Examples of chronic conditions
include cystic fibrosis (CF) and chronic obstructive pulmonary disease (COPD), asthma,
lung cancer.
1.1 Cold and Flu
Cold and flu (or Influenza) are both respiratory illnesses and the terms are used
interchangeably. However, they are both caused by different viruses. The cold (also
known as nasopharyngitis, acute viral rhinopharyngitis, acute coryza, or a common
cold) is a viral infectious disease of the upper respiratory system. Cold is caused
primarily by rhinoviruses and corona viruses.
Influenza is a contagious respiratory tract infection caused by one of three influenza
viruses: A, B and C. Influenza C causes mild infections in infants and young children,
which may confer life-long immunity, in adult cases are rare and usually asymptomatic.
Influenza A & B viruses cause seasonal epidemics in people of all ages. Influenza B & C
viruses are virtually restricted to humans and both have been isolated from other
mammals, there are no natural animal reservoir of infection. Although, both A & B
viruses can be responsible for the annual winter epidemics (widespread) of influenza
(‘seasonal flu’) that occur around the world, only influenza A has the potential to give
rise to global pandemic/outbreak disease.
Exposure to cold, damp, wind and rapid temperature change can make people more
susceptible. During cold, virus particles penetrate the mucous layer of the nose and
throat and attach themselves to cells there. The viruses punch holes in the cell
membranes, allowing viral genetic material to enter the cells. Within a short time, the
virus takes over and forces the cells to produce thousands of new virus particles. In
response to this viral invasion, the body marshals its defenses. The nose and throat
release chemicals that spark the immune system; injured cells produce chemicals
called prostaglandins, which trigger inflammation and attract infection-fighting white
blood cells; tiny blood vessels stretch, opening up space to allow blood fluid (plasma)
and specialized white cells to enter the infected area; the body temperature rises,
enhancing the immune response; and histamine is released, increasing the production
of nasal mucus in an effort to trap viral particles and remove them from the body. As
the battle against the cold virus rages on, the body counterattacks with its specialized
white blood cells called monocytes and lymphocytes. The symptoms experienced as a
cold are actually the body’s natural immune response.
Colds manifest slowly with cough, nasal congestion and sore throat, usually without
fever.
Flu comes on more suddenly with fever, sore muscles, fatigue and cough. These
ailments can last from a few days to about a week, but can progress into bronchitis,
strep throat or asthma if not properly treated. Mucus production is an act to wash
viruses out of cells and coughing clears the mucus and viruses out of the body. Fever
causes the body to heat up and destroy infection
Medical management
1. Vaccination - Both inactivated and live, attenuated influenza vaccines are used
worldwide according to WHO recommendations.
2. Antibiotics- they do not kill viruses and they should not be used for colds or flu.
They can however treat bacterial complications such as sinus or ear infections.
The overuse of antibiotics has become a very serious problem, which leads to a
resistance in disease-causing bacteria that may decrease the effectiveness of
antibiotics when really needed.
3. Antivirals - There are several antiviral medications that can limit the course and
duration of these infections and are specific to the viruses. They work by
inhibiting viral replication rather than directly killing the viruses. They are
generally avoided because of resistance problem.
4. Anti-histamines - Antihistamines can be used for symptoms such as runny nose,
sneezing and itching. There are many formulas containing different drugs like
diphenhydramine, loratidine etc. Precautions are necessary as most of these
drugs cause drowsiness.
Nutritional considerations
 Vitamin C - Stimulates antibody response. Regular use can prevent colds before they
happen. Eating plenty of fruits and vegetables that are loaded with vitamin C, such
as citrus fruits, melons, berries, parsley, and bell peppers is helpful. Vitamin C acts
as a mild natural antihistamine and supporting the function of white blood cells.
Antihistamines reduce mucus secretion and inflammation in airways and sinuses,
making it easier to breathe.
 Vitamin A and/or beta carotene strengthen the mucus membranes making them
 more resistant to infection. Vitamin A is a nutrient vital to the mucous membranes
throughout the respiratory system during a cold or flu. It can be taken in the form of
beta carotene, a precursor of vitamin A, in higher dosages.
 Zinc especially in the form of lozenges helps prevent viral replication in the throat by
stimulating T-cell response. The lozenges should not be used for more than one
week. Zinc can suppress the immune system if used for an extended period of time.

1.2 Bronchitis
This is the inflammation of the mucosa lining the bronchial passages. Bronchitis is
caused by infections and is exacerbated by inhalation of irritant fumes such as tobacco
smoke.
Symptoms;
i. Cough
ii. Expulsion of excess mucous
iii. Inflamed airway
iv. Difficulty in breathing out
Aims of treatment of bronchitis;
i. To aid in expulsion of mucus
ii. To relieve cough
Nutrition management of bronchitis;
i. Use of mucoltyics e.g. onions, leeks and radishes
ii. Provide emollients e.g. dates, okra and figs as they soften and reduce
inflammation in the respiratory system
iii. Use of foods with antibiotic and antiseptic properties e.g. garlic as it combats
bacteria and viruses that cause or aggravate bronchitis
iv. Encourage intake of lemon juice with honey which is a traditional remedy for
coughs
v. Provide foods which are rich in vitamin A as it is vital for healthy bronchial
mucosa and helps relieve coughs.
1.3 Asthma;
This is a chronic condition that manifest with attacks of dyspnea (difficulty in breathing)
accompanied by wheezing, cough, expectoration and chest pain. Asthma is caused by
allergic reactions. It is the result of a complex interaction between environmental
exposures and genetics. When people are genetically susceptible, environmental
factors exacerbate airway hyper-responsiveness, airway inflammation, and atopy
(tendency to develop allergic reaction) that eventually leads to asthma.

Environmental risk factors for the development of asthma

 Indoor allergies (dust mites, animal allergies)
 Outdoor allergies (pollen and fungi)
 Air pollution
 Tobacco smoke exposure
 Small size at birth
 Respiratory infection
 Lower socioeconomic status.
 A higher than desirable BMI during childhood

Symptoms of asthma;
 Increased response of trachea  Excess mucus
and bronchi stimuli  Coughing
 Breathlessness  Wheezing
 Reduced airway  Chest pressure
 Swelling of airway  Expectoration
 chest tightness  Difficulty in breathing
Medical management
 Routine monitoring of symptoms and lung functions
 Patient education
 Control of environmental triggers
 Pharmacotherapy – stepwise and tailored to meet individual patient needs. Quick
 relief (short-acting beta agonists – bronchodilators and steroids) and long term
controller medication (inhaled long acting beta agonists and leukotriene
modifiers) are used as therapy for asthma.
Medical nutrition therapy
Goals of nutrition therapy
 Correct energy and nutrient deficiencies and excesses in the diet.
 Address dietary triggers. GERD (Gastroesophageal reflux disease), food allergens
and some specific food additives are the two most common dietary triggers.
 Monitoring food-drug interactions.

The nutrition care involves;

i. Provide antioxidants e.g. vitamin A, C and E because they enhance bronchial
tubes’ ability to withstand free radicals coming from the environment
ii. Provide honey as it contains some pollen which can desensitize the body
against environmental pollens.
iii. Encourage the consumption of onions as it is a bronchial dilator and
antispasmodic which can relieve and prevent asthma attack.
iv. Reduce intake of food additives e.g. salt, wine, beer and fish. Fish contains
histamines which provoke all allergic reactions. N/B- asthma and bronchitis
are conditions that are collectively called chronic obstructive pulmonary
disease (COPD)
v. Provide omega-3 polyunsaturated fatty acid (PUFA) fish oil supplements
throughout childhood to reduce wheezing.
vi. Supplementation of zinc to improve asthma symptoms and lung function
vii. Provide diet free of known irritants such as spicy foods, caffeine, chocolate,
and acidic foods.
viii. Limit the intake of high fat foods and control portions to prevent gastric
secretions, which exacerbate GERD.
ix. Food allergens e.g. an immunoglobulin E-mediated reaction to a food protein
can lead to bronchoconstriction. Completely avoiding the allergenic food
 protein is the only dietary treatment currently available for food allergies.
x. Some food additives used in the processing of foods such as potassium
metasulfite and sodium sulfide, have been found to be a trigger for
asthmatics. Therefore they should be avoided.
xi. Some asthma patients need maintenance oral steroids, and these patients
are prone to develop drug-nutrient interaction problems and should be
managed as appropriate.

1.4 Chronic obstructive pulmonary disease (COPD)

This refers to a group of conditions characterized by the persistent obstruction of
airflow through the lungs particularly in the main airways (bronchi and bronchioles) and
air sacs (alveoli) of the normal respiratory system and reduced expiratory flow.
As COPD progresses, the work of breathing increases to 10 to 20 times that of a person
with normal lung function. The two main types of COPD are chronic bronchitis and
emphysema, and in many patients, these conditions may co-exist in varying degrees
and are generally irreversible.
Chronic bronchitis is characterized by persistent inflammation and excessive
secretions of mucus in the airways of the lungs, which may ultimately thicken and
become too narrow for adequate mucus clearance. Chronic bronchitis is diagnosed
when a chronic, productive cough persists for at least 3 months of the year for
2consecutive years.
Emphysema is characterized by the breakdown of the lungs’ elastic structure and
destruction of the walls of the bronchioles and alveoli, changes that significantly reduce
the surface area available for respiration. Emphysema is diagnosed on the basis of
clinical signs and the results of lung function tests.
Both chronic bronchitis and emphysema are associated with:
 Abnormal levels of
oxygen and carbon dioxide in the blood
 Shortness of breath
(dyspnea)
 COPD may eventually lead
 to respiratory or heart failure
 Dramatic reductions in
physical activity
 Reduced quality of life
 Weight loss and wasting
are common in the advanced stages of disease resulting from hypermetabolism,
poor food intake, and the actions of various inflammatory proteins
Causes of COPD
 Smoke from cigarettes is
a major risk factor, along with that from biomass fuel used for cooking and heating
in rural areas, occupational exposure as well as other forms of air pollution may also
predispose an individual to COPD.
 Genetic factors - Alpha-1-
antitrypsin deficiency. Individuals with this defect have inadequate blood levels of a
plasma protein (alpha-1-antitrypsin) that normally inhibits the enzymatic breakdown
of lung tissue.
Medical treatment of COPD
The primary objectives of COPD treatment are
 To prevent the disease
from progressing and relieve major symptoms (dyspnea and coughing).
 Individuals with COPD are
also encouraged to quit smoking to prevent disease progression and to get
vaccinated against influenza and pneumonia to avoid complications
 For people with severe
COPD, supplemental oxygen therapy (12 hours daily) can maintain normal oxygen
levels in the blood and reduce mortality risk.
 Improve the quality of life
Nutrition therapy for COPD
Goals of MNT
 To correct malnutrition
(which affects up to 60% of COPD patients) resulting from poor food intake and
poor appetite.
 To promote the
maintenance of a healthy body weight
 To prevent muscle
wasting resulting from hyper-metabolism.
General nutrition care plan
Energy needs of COPD patients are usually raised due to hyper-metabolism (about 20
percent above normal), which results from chronic inflammation and the increased
workload of respiratory muscles. The energy requirements of most adult COPD patients
range from 25 to 35kcal/kg body weight.
In addition, it has been proposed that patients with COPD may benefit from a high fat,
moderate carbohydrate diet distributed as protein (15% to 20% of total calories), fat
(30% to 45% of total calories) and carbohydrate (40% to 55% of total calories) so as to
preserve a satisfactory respiratory quotient (volume of CO2 expired/volume of O2
consumed) from substrate metabolism use.
Weight management – for underweight COPD patients a high-kcalorie, high-protein diet
may be helpful, but excessive energy intakes increase the amount of carbon dioxide
produced and can increase respiratory stress.
Excess body weight places an additional strain on the respiratory system, and so
overweight or obese COPD patients may benefit from energy restriction and gradual
weight reduction.
Decreased food intake - Food intake often declines as COPD progresses.
Causes of decreased food intake in COPD patients
 Dyspnea may interfere
with chewing or swallowing.
  Physical changes in the
lungs and diaphragm which may reduce abdominal volume, leading to early
satiety.
 Medications which may
reduce appetite
 Depression
 Altered taste perception
(which may be due to the use of bronchodilators or the mouth dryness caused by
chronic mouth breathing)
 Disability in some patients
hence they are unable to shop or prepare food or may lack adequate support at
home.
Provide small, energy dense and frequent meals spaced throughout the day rather than
two or three large ones. The lower energy content of small meals reduces the carbon
dioxide load, and the smaller meals may produce less abdominal discomfort and
dyspnea.
Some individuals may eat better if they receive supplemental oxygen at mealtimes.
Fluids - Consuming adequate fluids should be encouraged to help prevent the secretion
of overly thick mucus; however, some patients should consume liquids between meals
so as not to interfere with food intake.
Cigarette smoking – a combination of nutritional counselling and nicotine replacement
may optimize success.
Oral supplements may be recommended as between-meal snacks to improve weight
gain or endurance, but patients should be cautioned not to consume amounts that
reduce energy intake at mealtime.
Pulmonary Formulas- Enteral formulas designed for use in COPD provide more
kcalories from fat and fewer from carbohydrate than standard formulas. The ratio of
carbon dioxide production to oxygen consumption is lower when fat is consumed.
Incorporating an exercise Program - Loss of muscle can be more readily prevented or
reversed if the treatment plan includes an effective exercise program. With exercise,
patients are likely to see improvements in their strength, endurance, and ability to
perform activities of daily living. Both aerobic training and resistance exercise can be
beneficial.
Protein - Sufficient protein of 1.2 to 1.5 g/kg of dry body weight is necessary to maintain
or restore lung and muscle strength, as well as to promote immune function.
Vitamins and Minerals - the requirements for individuals with stable COPD depend on
the underlying pathologic conditions of the lung, other concurrent diseases, medical
treatments, weight status, and bone mineral density. For people continuing to smoke
tobacco, additional vitamin C is necessary. The role of minerals such as magnesium
and calcium in muscle contraction and relaxation may be important for people with
COPD. Other minerals of importance include vitamin D and K depending on the
comorbidities and the drugs administered.

1.5 Pneumonia
It is an inflammation and consolidation of lung tissue in response to an infectious agent.
Several organisms and disease conditions have been identified to infect or inflame the
lungs.
In the clinical setting there are various kinds of pneumonias, such as
 Community-acquired pneumonia, which may be viral or bacterial
 Hospital-acquired pneumonia
 Pneumonia in an immune compromised host
 Ventilator associated pneumonia(VAP)
 Aspiration pneumonia – which occurs when solid or liquid food passes into the
lungs, causing infection.
Approximately 50% of pneumonia cases are caused by viruses and tend to be less
severe than those of bacterial origin. Pneumococcus (Streptococcus pneumoniae) is
the most common cause of bacterial pneumonia. Aspiration pneumonia Prevention of
pneumonia primarily includes maintenance of immune status and pneumococcal
vaccination.
Treatment of pneumonia involves a combination of pharmacologic therapy (e.g.,
antibiotics), pulmonary rehabilitation, and maintenance of nutritional status. Protein
energy malnutrition (PEM) is associated within voluntary weight loss, functional
impairment and impaired immunity. Adequate nutritional status plays a critical role in
the modulation of immune function.
Medical Nutrition Therapy in management of pneumonia
i) To preserve lean body mass and immune function
ii) Prevent unintentional weight loss
iii) Maintain nutrition status
Energy: Provide enough energy to maintain reasonable body weight. Increased energy
may be needed for patients with infection, fever, or weight loss.
Protein: Provide enough protein to maintain visceral protein status and meet the
demands of infection.
Fluid: Fluids are encouraged, unless contraindicated. From 3 to 3.5 L of fluid per day has
been recommended to liquefy secretions and help lower temperature in febrile
patients (to be discussed in a later section of this module).
Specific nutrients and the immune system: several nutrients have been linked to the
preservation and maintenance of immune function. Nutrients that have been
identified include vitamins A, E, and B6, zinc, copper, selenium, the amino acids
glutamine and arginine, and omega-3 fatty acids. These nutrients may play a key
role in the immune function, leading to less of a risk of developing pneumonia.
Supplementation is not warranted since there are no studies demonstrating a
direct cause and effect relationship with the incidence of pneumonia. However, it
is recommended to increase consumption of foods that are rich in these
nutrients.
UNIT 2: FEBRILE CONDITIONS
Unit Objectives
By the end of the unit the learner should be able to:
a) Explain the nutrition and metabolic implications of febrile conditions
b) Describe types, causes and management of febrile conditions
c) Plan and prepare meals for various hypothetical febrile condition patients
d) Visit a health facility to learn more about management of febrile conditions.
Febrile (fever) is a condition that is associated with having a high body temperature.
During fever, the body temperature rise above the normal of 37oc. the invasion of the
body by a pathogen results infections, fever, lung and other diseases. Fever often
accompanies infection; the patient may have chills and may complain of feeling cold.
N/B: all fevers are not as a result of infection, and elevation in body temperature is not
fever e.g. elevation in body temperature in heat stroke as the body is unable to eliminate
heat.
Fever may be acute or chronic.
i) Acute fever; is fever of short duration and the body temperature may rise very
high as in;
 Typhoid
 Influenza
 Malaria
 Pneumonia
 Asthma
 Tonsillitis
ii) Chronic fever; this is fever of long duration. The temperatures may remain low
although the fever continues for a long time. It can take several months as in
tuberculosis. The fever has a gradual start and is also low in severity.
The nutritional needs of the body are increased to resist the pathogens, to recoup
(recover) the losses incurred metabolically and rebuild the cells damaged by the invader.
Hence a higher protein diet is indicated.
The elevated body temperature results in several metabolic changes inside the body
that are proportional to the increase in temperatures.

Some of the metabolic changes that occur in fever include

 A 13% increase in Basal Metabolic rate (BMR) with every 1oc increase in body
temperature.
 Decrease in adipose and glycogen stores normally due to increase in energy
expenditure
 There is reduced absorption of minerals, vitamins and proteins and increased
breakdown of proteins.
 There is increase in loss of body fluids due to excessive sweating and urination.
 Increase in urine volume so as to remove excess nitrogenous wastes
 There is electrolytes imbalance due to high loss of minerals through sweat, urine
and sometimes vomiting. The common minerals lost are sodium, chloride and
potassium.
1.6 Typhoid
This is an infectious disease caused by Salmonella typhii. The infection is transmitted
through feacal-oral route i.e. by consuming water, food or milk contaminated with
intestinal contents. It may affect all age groups but commonly occur in children.
Symptoms;
 Nausea  Sweating
 Vomiting  Headache
 Anorexia  Weight loss
 Diarrhoea
Effects of typhoid on the body;
i. There is loss of tissue protein which may amount to as much as 250mg-500g
of muscle tissue a day
ii. Body stores of glycogen are quickly depleted and the water and electrolyte
balance is disturbed
iii. The intestinal tract is inflamed and irritable. Diarrhoea is therefore a frequent
 complication which interferes with absorption of nutrients
iv. Ulceration of the intestines is so severe that even hemorrhage and
perforation of the intestines may occur.

Nutrition management of typhoid;

Objectives of nutrition management;
 To maintain adequate nutrition
 To restore positive nitrogen balance
 To provide relief from symptoms
 To correct and maintain water and electrolyte balance
 To avoid irritation of the intestinal tract.
Nutrition management involves;
 Keep the patient warm
 Encourage bed rest
 Give antibiotics
 Modify the diet.
During high fever, there is an aversion towards food in the form of anorexia, nausea and
vomiting.
To attain the nutrition management objectives, the following are the nutrient
requirements;
i) Energy; the BMR may increase as high as 50% due to increase in body
temperature and also restlessness which increase energy expenditure.
Increase energy by 10%-20%. Initially during the acute stage, 600-1200kcals may
be consumed per day, this energy intake should be increased gradually with
recovery and improved tolerance.
ii) Proteins; requirements of proteins are related the severity and duration of
infection rather than on the height of the fever.
There is an excessive destruction of tissues, protein intake should be increased
to between 1.5 to2g/ideal body weight/day. Proteins of high biological value
should be used e.g. soya beans, milk, fish, meat and chicken. Meals should be
 supplemented with high protein beverages e.g. milk shakes.
iii) Carbohydrates; provide liberal carbohydrates to replenish glycogen stores. Well-
cooked and easily digestible starches should be given e.g. simple starches,
glucose, honey and sugar cane.
iv) Dietary fibre; as the symptoms of fever include diarrhoea and lesions in the
intestinal tract, all forms of irritants have to be eliminated from the diet as it is a
mechanical irritant.
v) Fats; fats are required mainly to increase energy intake. However, due to
presence of diarrhoea, fats only in the emulsified form should be included in the
diet as they are easily digested and well tolerated by patients. Limit fats as they
may aggravate nausea; avoid fried foods.
vi) Minerals; there is excessive loss of electrolytes like sodium, potassium and
chloride due to increased perspiration. Salty soups, broths, fruit juices, milk etc
should be included to compensate for loss of electrolytes.
vii) Vitamins; there is need to increase vitamin A and C as fever increases their
requirements. The need for B vitamins is also increased. The use of antibiotics
and drugs interfere with intestinal bacteria synthesis of some B vitamins so
vitamins B supplementation may have to be given for sometime.
viii) Fluids; a liberal fluid intake is very essential. A fluid intake of 2.5-5litres per day is
recommended.
1.7 Malaria
It is a vector borne disease caused by a parasite known as plasmodium malarie from an
infected Anopheles mosquito.
Common symptoms of malaria
In the early stages, malaria symptoms are sometimes similar to those of many other
infections caused by bacteria, viruses, or parasites. Symptoms may include:
 Fever.  Nausea and vomiting.
 Chills.  Dry (nonproductive) cough.
 Headache.  Muscle and/or back pain.
 Sweats.  Enlarged spleen.
 Fatigue.
Nutritional implication of malaria
 Dehydration
 Loss of electrolytes
 Among pregnant mother it can lead to low birth weight
 Development of malnutrition,
 Pathogenesis of anemia- malaria experience diminished absorption of orally
administered iron
Recommended diet for an individual infected with malaria
Fluids: Maintaining good hydration status during malarial fever is very important since it
can help bring down the body temperature. Also, frequent vomiting in malarial fever
causes dehydration.
Vitamin A: It is important to incorporate rich sources of this vitamin such as liver, milk,
fruits (mangoes, papaya) and vegetables (carrots, tomatoes, drumstick, amaranth,
spinach, pumpkin) in the daily diet to boost the body’s immune system.
Zinc: Zinc deficient individuals are also more likely to get malarial infection. Foods rich
in zinc are oysters, meat, poultry, beans, nuts, certain types of seafood (such as crab
and lobster), whole grains, fortified breakfast cereals, and dairy products.
1.8 Tuberculosis (TB)
TB is an infectious disease caused by bacteria known as Mycobatceria tuberclii. It is
transmitted through cough or sneeze of an infected person when it gets sprayed into
the air. Most people who breathe in the bacteria do not get infected. In those who do
not get infected even after inhaling the bacteria, the microorganism may remain
dormant as their immune system triggers activation of macrophages which engulf the
bacteria. About 10% of those infected develop TB some time in their life when the
natural immunity is lowered.
TB is accompanied by coughs, sneezing, and fever and tissue wastage. In acute forms,
the fever is high and the symptoms are similar to pneumonia. The chronic form is
associated with low grade fever. TB can affect several parts of the body including the
lungs, spine, and the bones among others. Lungs are the most frequently affected parts
of the body.
Nutrition is the principal determinant of morbidity and mortality from tuberculosis.
There is evidence that malnutrition contributes for up to 60% of both incidence and
severity of TB. It increases as one passes from well-to-do to poor populations.
Together with poverty, overcrowding and HIV, malnutrition has contributed to a global
problem of TB referred to as “Triple Trouble” i.e. malnutrition, TB and HIV.

Symptoms of TB;
i) Cough lasting for more than two v) Blood in sputum
weeks vi) Oozing matted lymph nodes or
ii) Fever/high sweat enlargement of lymph nodes
iii) Loss of appetite vii) Breathlessness and fatigue.
iv) Weight loss
Consequences of TB in the body;
 Reduced ability to utilize fats hence increased protein losses
 Increased calorie requirements due to excessive sweating associated with high
body temperature
 Nutrient deficiency including of proteins due to their breakdown to be used in the
synthesis of immune bodies resulting in protein wasting and weight loss
 Loss of iron through bloody sputum can cause anemia.
 Frequent prolonged and severe infection due to reduced immunity
 Reduced food intake due to loss of appetite
 Increased nutrient requirements due to loss of nutrients e.g. through blood in
sputum and the increased energy needs due to increase in body temperature i.e.
10% increase in energy needs for every 1oc increase in body temperature.
Increased micronutrients
Nutrition implications of TB
a) Active TB is associated with weight loss, cachexia (wasting syndrome), and low
serum concentration of leptin (a hormone for mediating long-term regulation of
energy balance, suppressing food intake and thereby inducing hormones. It is
 antagonistic to ghrelin).
b) Food-nutrient interactions with anti-TBs
i) Isoniazid (Nydrazid) Drug may cause pyridoxine (vitamin B6) and niacin
(vitamin B3) deficiency resulting in peripheral neuropathy and pellagra. Drug
may affect vitamin D metabolism and decreased calcium and phosphate
absorption.
Avoid in malnourished individuals and others at increased risk for peripheral
neuropathy. Supplement with 25-50 mg of pyridoxine and possibly B-complex
if skin changes occur. Maintain adequate calcium and vitamin D intake. In
addition, it can also result to hepatitis, nausea, abdominal pain and vomiting.
ii) Rifampin (Rifadin) Drug may increase metabolism of vitamin D. Rare cases of
osteomalacia have been reported. May need vitamin D supplement with long-
term use.
iii) Ethabutol (Myambutol)
Myambutol: may decrease copper and zinc. Therefore increase foods high in
Cu and Zn; daily multivitamin with may be necessary for long term use
Myambutol:
iv) Pyrazinamide (Rifater) Drug may decrease the excretion of uric acid, leading
to
hyperuricemia and gout. Maintain adequate hydration and purine-restricted
diet.
c) Micronutrient deficiencies - At the time of diagnosis, patients with active TB may
have low levels of several micronutrients most notably vitamins C and E, retinol, zinc,
iron and selenium. As mentioned above, the drug therapy initiated may also have
adverse effects on the levels of micronutrients in the patient’s body particularly
vitamin D, vitamin B6.
d) Reduced food intake the excessive coughing associated with tuberculosis may lead
to reduced food intake
Nutrition management of TB;
Objectives of nutrition management of TB;
i. To maintain good nutritional status
 ii. To prevent and control body wasting and weakness
iii. To correct nutrient deficiencies which may have occurred during the disease
iv. To modify diets based on the body’s ability to metabolize nutrients during the
disease.
v. To manage anemia
vi. To accelerate the healing process.
vii. Maintain adequate hydration status
viii. Alleviate nutrient-drug interactions
Dietary management of TB;
It requires the use of a high protein high calorie diet.
i. Energy; most patients with TB are malnourished and energy needs are
increased. In order to minimize weight loss and achieve desirable weight 35-
40kcal/ideal body weight/day is recommended (app. 2500-3000Kcals/day).
This will help in protein sparing.
ii. Proteins; an intake of 1.2-1.5g/ideal body weight/day (app. 75-100g/day) is
required to generate serum albumin levels due to tissue wasting and repair of
worn out tissues.
iii. Fats; these should provide between 25-30% of the total kilocalories
requirements of an individual.
iv. Vitamins and minerals; if there has been lung hemorrhage, iron supplements
with large intake of vitamin C are needed.
Additional amounts of vitamin C to the diet is recommended to facilitate healing of
lesions.
Other antioxidants e.g. vitamin A and E, folic acids, zinc and selenium are recommended
so as to neutralize free radicals and prevent the production of peroxides from lipids.
In TB conversion of Beta carotene to retinol is affected in the intestinal mucosa, the
patient should be supplemented with vitamin a (as per the National vitamin a
supplementation schedule) and encouraged to eat vitamin A rich foods. The patient
should eat foods mainly rich in preformed vitamin A.
In patients on Isoniazid drug for treating TB which is a vitamin B6 antagonist; vitamin B6
supplements must be given to avoid its deficiency.
 v. Water; the patients should take atleast 8 glasses (each measuring 250ml) of
safe drinking water or more per day.
N/B- education of patients on the need for prolonged treatment and monitoring until
complete recovery is an important part of the control of TB since most patients tend to
neglect medications as soon as they feel a little better. This leads to its recurrence.
It is important for the patient to take the drug and diet treatment consistently until the
patient is fully back to normal health. Failure to do so results in the recurrence of the
disease; the resistant bacteria which causes the second attack is a very hardy and hard
to treat.
UNIT 3: NUTRITION IN SURGERY
Unit Objectives
By the end of the unit the learner should be able to:
a) Describe types, causes and management of conditions leading to metabolic
stress
b) Discuss the physiological changes during surgery
c) Explain nutrition implications of pre and postsurgery its nutrition care and
rehabilitation
d) Describe types and management of surgeries of the GIT
e) Plan and prepare meals for various hypothetical surgical cases
1.9 Introduction to stress response
Metabolic stress is a disruption in the body’s internal chemical environment which can
result from uncontrolled infection or extensive tissue damage.
Stress can be mental, emotional or physical. It disturbs the normal homeostasis of the
body. Emotional and mental stress is caused by anxiety, worries and tension due to a
variety of situations real and sometimes imaginary.
Some of the common emotional stress situations include sudden death of a near
relative (e.g. a child, mate or parent), losing a job, divorce, financial problems, loss of a
limb in an accident and even inability to cope with change e.g. job, location, new family
member etc.
Emotional stress is one of the factors which is found to cause some serious conditions
e.g. peptic ulcers, hypertension, cardiovascular diseases and even cancer. Physical
stress includes; burns, thermal injury and surgery.
The ability of an individual to handle stress varies. The body’s response to sever stress
can alter metabolism enough to threaten survival. Stress also raises nutritional needs
considerably increasing the risk of malnutrition even in previously healthy individuals.
In the body, stress can have both beneficial and harmful effects in an attempt to restore
balance. Metabolic stress can result in;
 Hypermetabolism i.e. above normal metabolic rate,
 Wasting, loss i.e. loss of muscle tissue
 In severe circumstances life threatening consequences.

How the body responds to stress;

Stress response is the body’s non-specific response to a variety of stressors e.g.
infection, fractures, surgery and burns.
During stress, metabolic processes that support immediate survival are given priority
while those of lesser consequence are delayed. Energy is of primary importance;
therefore energy nutrients are mobilized from storage and made available in the blood.
Heart rate and respiratory rate (breathing) increases to deliver oxygen and nutrients to
cells more quickly and blood pressure rises. Energy is diverted from processes that are
not life sustaining e.g. growth, reproduction and long-term immunity. If stress continues
for a long period, interference with these processes may begin to cause damage or
illness.
There are two types of response to stress;
1. Hormonal responses;
Stress is mediated by several hormones which are released into the blood soon after
the onset of injury. They include;
i. Catecholamines (adrenalin/epinephrine and noradrenalin/norepinehrine) often
called fight and flight hormones. Which have the following metablic effects;
 Stimulate heart muscle contraction
 Raise blood pressure
 Increase metabolic rate
 Promote secretion of glucagon which prompts the release of nutrients from
storage e.g. glycogen from the liver and muscles.
 Increase the production of glucose from amino acids
 Increase the release of fatty acids from the adipose tissues.
ii. Glucagon;
 this prompts the release of glycogen from the liver
  increase the release of fatty acids from adipose tissues
 increase the production of glucose from amino acids

iii. Steroid hormones (cortisol);

 enhance protein degradation to increase amino acids levels used in the
production of glucose
 it enhances glucagon’s action on the liver glycogen
 increases glucose production from amino acids
iv. Aldosterone results in sodium reabsorption in the kidneys to help in maintaining
blood volume
v. Antidiuretic hormone results in water reabsorption in the kidneys
N/B- all the hormones have similar effects on glucose and fat metabolism causing the
breakdown of glycogen, production of glucose from amino and the breakdown of
triglycerides in adipose tissues. These hormones combine contributing to
hyperglycemia which often accompanies critical illness.
Cortisol’s effects can be detrimental when stress is prolonged; in excess, it causes the
depletion of protein in muscles, bones, connective tissues and skin. This impairs wound
healing, so high levels of cortisol may be especially dangerous for a patient with severe
injuries; it also leads to insulin resistance contributing to hyperglycemia. Cortisol also
suppresses immune response, increasing susceptibility to infection.
2. Inflammatory response to stress;
Cells of the immune system mount a quick non-specific response to infection or tissue
injury. This is known as inflammatory response which helps to contain and destroy
infectious agents and their products and prevent further tissue damage.
Inflammatory response begins with dilation of arterioles and capillaries at the site of
injury which increases blood flow to the affected area. The capillaries within the
damaged tissue become more permeable allowing some blood plasma to escape into
the tissue and cause local oedema.
The various changes in blood vessels also encourage the entry of immune cells that can
destroy foreign agents. These cells include phagocytes which slip through gaps
between the endothelial cells that form the vessel walls. These phagocytes engulf the
microorganisms and destroy them with hydrolytic enzymes and reactive forms of
oxygen. When inflammation becomes chronic, these normally useful products
phagocytes can damage healthy tissues.
Numerous chemical substances control the inflammatory process which are known as
mediators that are released from damaged tissues, blood vessel cells and activated
immune cells. Many of them help to regulate more than one step in the process. E.g.
 Histamines; is released by granules within the mast cells causing vasodilation
and capillary permeability.
 Cytokines; produced by white blood cells
 Eicosanoids derived from dietary fatty acids (major precursor is arachidonic acid
an omega 6 fatty acid from vegetable oil). Some omega 3 fatty acids compete
with arachidonic acid so as to inhibit the most powerful inflammatory mediator.
Replacing vegetable oils with fish oils rich in omega 3 fatty acids will help to
suppress inflammation.
Systemic effects of stress;
Within hours of inflammation, infection or severe injury, the liver steps up its production
of certain proteins in an effort known as the acute-phase of response. These proteins
are known as C-reactive proteins or complement blood clotting proteins e.g. fibrinogen
and prothrombin etc.
During this phase of stress response the following occur;
i. Protein catabolism to make amino acids available for glucose production,
tissue repair and immune protein synthesis resulting in negative nitrogen
balance.
ii. There is hypermetabolism
iii. Increased blood neutrophil levels
iv. Lethargy
v. Anorexia
vi. Fever
If inflammation doesn’t resolve the continued production of pro-inflammatory cytokines,
it may lead to the systemic inflammatory response syndrome (SIRS) which is diagnosed
when the patient’s symptoms include;
 High heart rate
 High respiratory rate
 Abnormally high levels of white blood cell count
 And/or elevated body temperature
If these symptoms are due to severe infection, the condition is called, Sepsis with
complications such as;
 Fluid retention and tissue oedema
 Low blood pressure
 Impaired blood flow
If the blood flow is so severe enough to deprive body tissues of oxygen and nutrients a
condition known as shock occur and multiple organs may fail.
Conditions associated with metabolic stress include surgery, cancer and burns.
1.10 Introduction to Surgery
Surgery is the removal of all or a section of a human organ or tissue. Nutrition plays an
important role in a person’s ability to recover from surgery.
Purposes of good nutrition before and after surgery
It ensures;
i. Fewer post-operative complications
ii. Effective wound healing
iii. Increased resistance to infection
iv. Reduced mortality rate
v. Shortened convalesce period or shortened recovery.
Poor nutrition prior to recovery results in;
i. Excessive weight loss
ii. Poor wound healing
iii. Oedema or dehydration
iv. Reduced serum proteins, haemoglobin and electrolyte levels.
A malnourished patient is at a higher risk than a patient with a better nutritional status
during and following surgery. The surgical procedure may directly influence intake,
digestion and absorption. A patient who develops complications after surgery is more
likely to become malnourished.
After surgery the need do nutrients is increased because;
i. There is loss of blood or plasma
ii. Haemorrhage
iii. Loss of nutrients e.g. protein accelerated due to immobilization(the patient is
confined to bed)

Metabolism following surgery

Both catabolism and anabolism are the normal reactions in surgery and trauma from
accidents, hemorrhage or burns.
a) Catabolic phase
This phase usually lasts for few days. In this phase, there is increased secretion of
pituitary and adrenal hormones which results in;
i. Sodium and water retention (oedema).
ii. There is loss of body cells and consequently an increase in excertion of nitrogen
and potassoium
iii. Peristalsis is reduced or even absent
iv. The acid-base balance may be disturbed
b) Anabolic phase
This phase represents wound healing. In this phase, there is;
i. Tissue cell replacement leading to positive nitrogen and potassium balance
ii. Sodium and water losses return to normal and the body returns to its normal
state of hydration
iii. Peristalsis gradually returns to normal
N/B- this phase occurs despite the initial poor intake of food and only emphasizes the
importance of good nutrition prior to surgery.
Principles of nutrition care in surgery;
Energy proteins and ascorbic acid are major needs for rapid wound healing and
convalescence from surgery.
1. Energy; if the calorie intake is inadequate, proteins will be used to supply energy
rather than for wound repair and tissue building. Even very small amounts of glucose
in a parenteral feeding can have some protein-sparing effects.
2. Proteins; this is important for normal wound healing to protect the liver against
possible injury and to increase the resistance to infection. For well-nourished
individuals, a normal protein intake is adequate, where there has been malabsorption,
the protein need may be over 100g/day.
3. Fluid-electrolyte balance; each day a significant amount of fluid is lost from the
body. In surgical procedures the losses are further increased through exudates,
hemorrhage and vomiting. Ordinarily, the fluids and electrolytes are replaced by
taking both beverages and food although the intake is usually decreased because of
inability to eat in surgically procedures.
There is a need for the correct of fluid and electrolyte imbalance prior to surgery so as
to reduce the risks that accompany dehydration and acidosis.
The fluids are given orally and parenterally as indicated. Subsequent to surgery,
parenteral fluids are given until the patient can take satisfactory amounts of fluids and
food by mouth. The total fluid intake and excretion should be noted.
4. Vitamins; ascorbic acid is especially important for wound healing. The surgeon
sometimes prescribes a supplement in addition to vitamin C provided by the diet.
There is also a need for vitamin K supplements because there could be a failure for
synthesis of the vitamin by the intestines which may occur when antibiotics are
given or the liver may be unable to convert vitamin K to prothrombin. Deficiency of
the two vitamins (C and K) increases the likelihood of abnormal bleeding.
N/B: When the calorie requirements are greatly increased there is corresponding
increase in the need for vitamin B complex.
1.11 Pre-surgery nutrition care
Ideally the nutritional status should be optimal before surgery. It may be difficult to
maintain optimal nutritional status prior to surgery especially if;
i. The illness has interfered with food intake and nutrient utilization
ii. Due to investigation procedures which require nil by mouth
Evaluation of nutritional status should be a routine part of the pre-operative assessment
so as to help identify those at risk of malnutrition and complications. It is done through;
i. Anthropometric measurements e.g. weight and height status
ii. Diet history (brief accounts of eating problems, appetite, past and current
dietary intake)
iii. Biochemical assessment e.g. albumin levels
iv. Clinical observations
v. Observation of fluid and food intake.
N/B: weight loss of over 10% compromises the patient’s ability to combat infection or
heal wounds. For well-nourished patients with uncomplicated surgery, a regular diet is
generally adequate. They can withstand short-term starvation and some degree of
protein catabolism without serious consequences.
Sometimes it is possible to improve the state of nutrition prior to surgery. Obesity
presents an hazard to surgery. Whenever possible, the obese patient should lose some
weight before surgery is attempted. There are patients who are malnourished prior to
surgery because of lack of appetite, pain, digestive discomfort or fear of eating.
If surgery can be delayed for sometimes, a high calorie, high protein diet is of value
even for a week or two. Such diet may provide 1000kcals more than the regular diet
and 1-1.5g of proteins/kg body weight/day. For those with inadequate oral intake,
enteral feeding may be necessary. If the GIT is to be bypassed, parenteral nutrition is
necessary.
When surgery is delayed to improve nutritional status, each day’s intake should
represent such improvement innutrition such that the delay is justified. Encourage the
patient that the intake is necessary through offering a variety, preference foods and
small frequent meals. Foods that provide dense nutrients in a minimum volume are
necessary.
Diet modification;
 For additional proteins, milk beverages may be enriched with dry milk powder and
commercial supplements
 Strained meats may be used if the patient is unable to eat meat
  Butter, margarine and oil may be incorporated to increase energy intake
 Adequate vitamins and minerals should be provided. A patient with iron
deficiency anemia should be provided with iron supplements or blood
transfusion be done if surgery is immediate.
Zinc and vitamin C are required for wound healing while vitamin K is for blood clotting.
The B complex increases in requirement because the energy and protein intake are high.
These vitamins continue to be important even after surgery.
Usually no food is allowed after the evening meal on the day before surgery because the
stomach should be empty of food during the operation to avoid dangerous vomitus
aspirations (vomit entering t\he respiratory tr upon awakening. However if surgery is
planned for late afternoon or if a local anesthesia is to be used, a light breakfast is
sometimes ordered. In elective surgery, fluid and food are withheld 6-8hours before
surgery.
Fluids are generally permitted until midnight preceding the day of operation. In
emergency a procedure called gastric lavage is advisable to remove gastric contents.
Before abdominal surgery the colon should be free of residue to prevent post-operative
infection. Colonic bacteria are increased when lots of food residue is present.
A low fibre diet or a liquid diet is give 2-3 days prior to the surgery then an enema a few
hours before surgery.
N/B synthetic low residue diets or elemental diets or chemically defined diets are used
to replace the low residue diet in many hospitals. These diets contain simple
carbohydrates (glucose), amino acids, essential fatty acids, minerals and vitamins. They
are easily absorbed and leave no residue in the GIT. They are available in several
flavours. They are more acceptable if served cold and should be sipped slowly.
1.12 Post-operative nutritional care
The resumption of the oral food intake depends on the nature of the surgery. On an
individual;
 Oral feeding is delayed for the first 24-48hours following surgery to await return of
bowel sounds or passage of flatus which is an indication of GIT motility.
 After a general anesthesia, gastric motility is reduced and emptying delayed. If GIT
 surgery or a major surgery has been undertaken, the normal GIT function may be
slowed and this may delay intake for a few days.
 After minor surgery, liquids are often tolerated after a few hours, initially sips of
water 15-30mls hourly, the volume is then increased gradually.
 The immediate concern after surgery is maintenance of fluids and electrolyte
balance. Fluids and electrolytes are replaced by intravenous fluids (IV) infusion
(parenteral feeding). Once the patient is taking fluids freely orally, the IV ones can be
reduced or discontinued.
 They then progress to clear liquids e.g. strained clear fruit juice, black tea, clear
soups.
 They can proceed to full liquids, soft or light diets then to the regular diets in
accordance to the patient’s tolerance.
 If the patient’s oral feeding is not possible, or there is an extended nil by mouth
period, enteral feeding may be indicated.
 After an uncomplicated surgery, a well-nourished patient tolerating regular diet well
will do well on a standard nutritionally adequate diet.
 Patients with depleted nutrient stores and those with complications or those with
major surgery need a high protein, high calorie diet.
1.13 Post-operative complications and implications;
i. Anorexia which leads to low nutrient intake
ii. Immobilization which leads to loss of nutrients e.g. proteins
iii. Infection which increases the nutrient requirements which can lead to
hospital malnutrition
Ways of preventing hospital malnutrition;
i. Provide small frequent meals that are attractively presented at the correct
temperature and patient’s preferences
ii. Nutrient and energy dense meals and snacks
iii. Avoiding low nutrient and energy drinks and meals.
iv. Encouraging mobilization or movement- getting out of bed and walking as soon
as they are medically safe
v. There is need of monitoring fluid intake and output, body weight and other
biochemistry (albumin and haemoglobin levels) which will indicate nutritional
status and also monitor food intake.
Some conditions that need surgery and their dietary management;
Surgery of the alimentary tract;
1. Teeth;
i. Full extraction of the teeth;
ii. Adjusting and fitting with dentures (artificial teeth)
 One to two days after surgery, it may be necessary to restrict diets to liquids taken
by a straw or a tube.
 Proceed to soft foods requiring little chewing for about three weeks.
2. Surgery in the mouth;
 Initial mouth surgery –after the surgery use a full fluid diet or pureed foods then
proceed to soft foods.
3. Removal of tonsils (post tonsilectomy)
 First day, provide cold fluids e.g. milk and bland fruit juices, soft foods e.g. eggs,
warm cereals, mashed potatoes, fruit and vegetable purees.
 After a few days, progress to regular diet.
4. Surgery of the stomach;
i. Gastric surgery in morbid obese patients with BMI >40;
This is gastric restrictions which reduces the reservoir capacity of the stomach by
closing off part of the stomach.
ii. Gastrectomy; this is a partial or total removal of the stomach due to peptic ulcers,
gastric cancer, damage after a trauma e.g. accident or a gun shot. E.g. of
gastrectomy include;
 Partial gastrectomy- removal of part of the stomach
 Gastroduodenostomy- removal of part of the stomach and joining it directly to the
duodenum
 Gastrojejunostomy- removal of part of the stomach and bypassing the duodenum to
join it directly to the jejunum
 Total gastrectomy- removal of whole the stomach
Some of the problems of gastrectomy include;
 Weight loss
 Loss of food reservoir which leads to early satiety and stomach distention
 Absence of pepsin and HCl
 Impaired fat utilization because of inadequate mixing of food with digestive juices or
inadequate pancreatic secretions when the duodenum is by-passed.
 There is increased intestinal motility (i.e. the stomach acts as a reservoir which
reduces the movement of food) which decreases digestion and absorption of the
nutrients.
 When there is total gastrectomy, iron absorption is decreased due to inadequate
HCL which can lead to anemia
 There is a decrease or absence of intrinsic factor which means a decrease in the
absorption of Vitamin B12 which can lead to pernicious anemia.
 There is malabsorption of vitamin D and calcium due to bacterial overgrowth (as a
result of lack of HCL which inhibits growth of bacteria)
2
 Dumping syndrome occurs in some patients due to removal of > /3 of the stomach.
It is a physiological response to the presence of undigested food in the jejunum that
occurs when a full diet regimen is started.
Food is “dumped” into the jejunum 10-15 minutes after ingestion instead of being
released gradually in small amounts this is called early dumping.
Symptoms of early dumping;
 Weakness
 Dizziness
 Rapid heart beat
 Perspiration
 After a while diarrhoea
Mechanisms leading to dumping syndrome;
Due gastric surgery, food doesn’t empty into the intestines in a controlled rate and
therefore it is “dumped” into the jejunum due to the reduced distance even if the
duodenum was not bypassed.
It includes;
Ingestion of large amounts of easily hydrolyzed carbohydrates which introduces
hyperosmolar mixture into the proximal intestines (jejunum) or due to the rapid and
subsequent hydrolysis of nutrients which leads to hyperosmolar mixture.
Fluid is withdrawn from the extracellular spaces to dilute the mixture and this leads to
distention and a decrease in blood volume which causes; dizziness, rapid heartbeat,
sweating and weakness.
The large fluid load in the jejunum causes hyperperistalsis followed by diarrhoea.
Presence of large fluids can also cause one to feel pain.
Late dumping
This is a condition that occur 1-2hrs after ingestion of food in this syndrome,
hypoglycemia is observed. Rapid digestion and absorption of food into the duodenum
especially carbohydrates leads to a rapid glucose entrance into the blood. This leads to
hyperglycemia and a resultant effect in increased insulin production which leads to
hypoglycemia. Some of the symptoms experienced include;
 Dizziness,
 Fainting,
 Sweating
 Nausea.
Dietary management
Objectives of dietary management in gastrectomy include
 To restore nutritional status
 Improve the quality of life.
 The dietary progression depends on individual patients but the general one is
progression from; water, then clear liquid followed by full liquid (on the third day).
 4th- 5th day they can proceed to soft or light diet and should be usually low in
connective tissue, easy to chew and the fibre should be low e.g. custard, soft
eggs and other soft foods, purees, mashed potatoes, soft foods can be given.
 Give small frequent foods and should be high in proteins and energy (1-
 2g/kgbwt/day).
 They should be avoid or limit concentrated sugars or simple or refined
carbohydrates because these are hydrolyzed rapidly and can cause the problems
of dumping.
 Complex carbohydrates are preferred initially 100-120g/day to avoid distention at
the beginning.
 Have a liberal (high) protein and fat intake (30-40%) of the total energy from fat,
20% from proteins (1-2g/kgbwt/day).
 Proteins and fats are hydrolyzed more slowly and do not increase the osmolar
load rapidly.
 Fluids should not be taken with meals but should be taken in between meals (30-
60min after meals) because liquids enter the jejunum rapidly.
 They should be provided with small frequent meals to fit reduced stomach
capacity.
N/B- milk is often tolerated. Initially it should be withheld and gradually introduced as
tolerated.
5. Intestinal surgery;
Among the reasons for the removal of the intestines include;
 Diverticulitis,
 Cancer,
 Obstruction
 Inflammation.
If you remove a section of the ileum it is called ilectomy (opening into the ileum through
the abdomen to allow wastes elimination, this is done when the colon, rectum and the
anus are to be removed), if you remove a section of the colon it is called coleoctomy
(this is an opening into the colon to remove wastes when the rectum and the anus are
to be removed).
Upto 50% of the small intestines can be removed without serious consequences. When
a large segment is removed, the person may experience;
 Diarrhoea,
 Weight loss,
 Protein and fat malabsorption,
 Hypocalcemia and hypomagnesia in the blood (there is the formation of soaps of
calcium and magnesium with fats)
 Anemia due to reduced absorptive surface.
The syndrome of the symptoms above is known as short bowel syndrome i.e. reduced
absorptive surfaces.
Loss of the terminal ileum which is involved in vitamin B12 and bile salt absorption leads
to a reduction in the bile salt pool and thus decrease the hydrolysis of fats. Reduced
vitamin B12 absorption mean that injections will be required. Fat soluble vitamins will
also be poorly absorbed.
Dietary management of surgery of the intestines;
Progression in the diet is like for other surgical patients. Initially the diet should be low
in residue.
N/B- ileostomy patients usually do not tolerate nuts, seeds or gas forming foods e.g.
peas, cabbages, sweet corn etc.
There is usually weight loss therefore a high protein diet, high energy diet may be
required.
UNIT 4: BURNS
Unit Objectives
By the end of the unit the learner should be able to:
a) Define terms used in the unit
b) Explain the causes and classification of burns
c) Explain the nutrition implication of burns
d) Describe nutrition management of burns
e) Plan and prepare meals for hypothetical burn patients
f) Visit a health facility to learn more about management of burns
Definition of terms
A burn is the destruction of body tissues by thermo extremes (temperatures) causing a
bodily shock reaction.
Introduction to burns
Extensive burns represent the most extreme state of stress that a person can
experience. A burn is the destruction of body tissues by thermo extremes
(temperatures) causing a bodily shock reaction.
Causes of burns
 Fire i.e. dry heat  Friction with another
 Corrosive chemicals e.g.  Cold
sulphuric acid  Sun burn
 Moist heat e.g. boiling water  Prolonged exposure to hot liquids
 Electricity  Flammable liquids
 Lightning
Major burns result in severe trauma. When a patient suffer from burns injuries, the
energy requirements can sometimes increase as much as 100% above the BMR
depending on the extend of the burn and the depth of the injury.
1.14 Assessment of burns
i. It can be assessed by size i.e. the percentage skin burn compared to the total
body surface area (%TBSA)
ii. It can be assess by depth of the burn which include;
a) Superficial burns where only the epidermis is affected thus referred to as first
degree burn. The skin is red, painful and very sensitive to touch. The
damaged skin may be slightly moist from leakage of the fluid in the deeper
layers of skin.
b) Partial burns where the epidermis plus part of t he dermis is affected. It is
known as second degree burn. The damage is deeper and blisters usually
appear on the skin. The skin is still painful and sensitive.
c) Full thickness burns. This is where the epidermis, all the dermis and the fat
layer are destroyed. It is also referred to as third degree burn. The tissues in
all skin are dead. Usually there are no blisters. The burnt surface can appear
normal, white, black (charred) or bright red from blood in the bottom of the
wound. Damage to the skin nerves can mean it is quite painless. The burnt
skin lacks sensation to touch.
Most burns heal without any problem but complete healing in terms of cosmetic
outcome is often dependent on appropriate care, especially within the first few days
after the burn. Most simple burns can be managed in primary care but most complex
burns and all major burns warrant a specialist and skilled multidisciplinary approach for
a successful clinical outcome.
If a burn is superficial; there is no need for grafting, if its partial, it may need some
grafting while the full thickness burns usually need grafting.
The amount of body area burnt;
In addition to the depth of the burn, the total area of the burn is significant. Burns are
measured as a % of the total body area affected.
The ‘rule of nines’ is often used though this measurement is adjusted for infants and
children. The calculation is based upon the fact that the surface area of the following
body parts of an adult body each corresponds to approximately 9% of the total (the total
body area of 100% is achieved). i.e;
i. Head= 9%
ii. Chest (front)= 9%
iii. Abdomen (front)=9%
iv. Each arm=9%
v. Upper/mid/low back and buttocks=18%
vi. Each palm=1%
vii. Groin=1%
viii. Each leg total = 18% (front=9% and back=9%)
Example= if both legs, the groin and the front chest and abdomen were burnt, this would
involve=55% of the body. I.e. both legs=18% x 2=36%, groin=1%, front chest=9% and
front abdomen=9%. (36 + 1 + 9 + 9=55%)
NB: - as the % burnt surface area increases, the risk of death increases as well.
Patients with burns involving less than 20% of their body should do well but those with
burns greater than 50% have a significant death risk depending upon a variety of factors
including underlying medical conditions and age. The figure below illustrates the rule of
nines.

Figure 1‘Rule of nines’

1.15 Consequences/implication of burns;
 Hypermetabolism –increased or <15 TBSA. In children and the old
requirements for energy >10%TBSA.
 Exaggerated protein catabolism and  Heat loss
increased urinary nitrogen loss and  Development of ileus (loss of
nitrogen loss through Immobilization intestinal peristalsis or lack of
and through burnt exudates effective coordinated
 Wasting and weight loss peristalsis)which may be due to
 Anorexia reduced blood flow to the GIT to

 Failure to feed supply nutrients and oxygen

 Generalized discomfort and  Infections due to open wounds

depression  Anaemia

 Loss of fluids ad electrolytes  Malnutrition

especially in 2nd to 3rd degree burns

Special concerns for burn patients;
 Burn patients have all typical characteristics of hypermetabolic state and
nitrogen losses, that exceed any other type of stress or trauma
  Hypermetabolism increases with size of the burnt area peaking up to 2-2.5 times
above the normal metabolic rate for burns as much as 40%TBSA.
 When the skin surface is destroyed, the body’s first line of defense against
infection is lost.
 Loss of skin also results in increased water and heat loss. The larger the burnt
surface a rare, the greater the loss of water vapour and heat. Approximately 2.5-
4l/day of water vapour may be lost from a major burnt wound.
 The burnt surface allows leakage of protein rich fluids containing approximately
1
/3 as much proteins as plasma.
 Burn patients do not feed well because of pain, generalized discomfort and
depression
 Many are anorexic and unable to consume a sufficient amount of kilocalories to
satisfy energy requirements.
 Large amounts of waste products e.g.nitrogen and potassium must be excreted
by the kidneys-fluids are required to keep these in solution.
 Acute ulceration of the stomach or duodenum.
1.16 Nutrition management of burns
Aims of nutrition management
 Achieving and maintaining good nutrition status
 Minimize nutrient and rapid weight loss
 Replacement of fluids and electrolytes to maintain circulatory volume and prevent
renal failure
 Preserve lean body mass; promote wound healing and ‘taking’ of skin graft at
maximal rates
 Achieving immunocompetence and prevention of infection
 Attain normal hydration status and electrolyte balance.
The nutrition care of burn patients requires the use of high protein and high calories in
the diet. It is done in stages which include;
N/B- aggressive nutritional therapy should be undertaken if;
i. There is over 20% TBSA
ii. Pre-injury malnutrition existed
iii. There is a threat of over 10% weight loss associated with the injury
-People who are well nourished and with less than 20% TBSA can do well on a regular
diet.
Stage I;
This stage is also known as Ebb phase. It is also known as the shock period and it
occurs between 48-72hours.
At this stage there is;
 Loss of fluids and electrolytes due to the skin loss and exposure of tissues.
 Movement of fluids into the burnt site leading to oedema resulting in decreased
blood volume and blood pressure and can lead to shock.
 There is cell dehydration as water is drawn out to balance water loss.
 Cell potassium is withdrawn from the damaged cells to the blood increasing the
circulating potassium levels (hyperkalemia).
 Plasma protein mainly albumin and sodium leak through the capillaries to the burnt
area and they are lost therefore metabolic acid condition can result due to loss of
bicarbonate with sodium.
 The peak of hypermetabolism occur 5-10days after the burn.
During this stage, the major concern is fluid and electrolyte repletion to prevent
irreversible shock and renal failure. Usually IV solutions are provided; usually glucose
free electrolytes solutions are administered to prevent hyperglycemia. Antibiotics are
also given to prevent infection.
Stage II;
This is after 48-72hours. It occurs after stabilization of fluids and electrolytes when
there is tissue perfusion and increased dieresis indicating replacement therapy has
been effective.
N/B- it is important to check fluid intake and output for signs of under or over nutrition.
Tissue wasting is reversed thus catabolism is expected to be reversed and oral feeding
can begin. Nutrition support is necessary for wound healing and closure and to prevent
complications including infections.
Generally the requirements for energy and nutrients are increased due to;
 Hypermetabolism
 Tissue destruction
 Loss of electrolytes, proteins, zinc and potassium.

Specific nutrients;
i. Energy; this is increased due to hypermetabolism which is the rate of increase in
metabolism which depends on the body temperature and also the %TBSA. There
is loss of energy as heat in the absence of the skin.
ii. Proteins; their requirements increase due to;
 Increased gluconeogenesis,
 Increased urinary loss of proteins,
 Loss through burn exudates(i.e. discharge from wounds),
 Breakdown of body proteins
 Increased requirements for protein for wound healing
 Maintenance of the host defense.

iii. Vitamins and minerals;

 Vitamin C is required for wound healing for it is needed for collagen synthesis
and promotion of capillary strength.
 Vitamin A is required for epithelial repair (i.e. integrity of the epithelium)
 Vitamin B complex (1,2,3) needed for metabolism of extra carbohydrates and
proteins
 Iron because of blood loss.
 Zinc requirements increases because of increased loss in burn exudates,
from muscle breakdown and also via urine. It is also very important in the
immune function
 Potassium requirements may also increase because of protein utilization
Estimation of nutrient requirements in burn patients;
For burn patients, a high protein high calorie diet is vital for faster recovery.
In adults TBSA of more than 10%, protein should comprise 20% of the total calorie
requirements; TBSA 1%-10%, protein provides 15% of the total calorie requirements. For
children younger than 1 year of age, a conservative recommendation of 3-4g/kg can be
given.
The daily energy and protein needs of both adults and children burn patients can be
determined using the Curreri et. al formula (1979);
Adults;
Energy= (25kcals x pre-burnt body weight (kgs)) + (40kcals x TBSA (%burn))
Protein needs= (1g x pre-burnt body weight (kgs)) + (3g x TBSA (%burn))

Children;
Energy= (60kcals x pre-burnt body weight (kgs)) + (35kcals x TBSA (%burn))
Protein needs= (3g x pre-burnt body weight (kgs)) + (1g x TBSA (%burn))

Estimation of fluid requirements = (3-4ml x pre-burnt body weight (kg) x %TBSA)mls

Example;
Determine the daily energy, protein and fluid requirements of a woman with a usual
weight of 50kgs and 40% TBSA.
For patients with less than 20% TBSA, a regular high calorie high protein diet would be
sufficient. Patients with severe burns have extra protein and energy needs and may
require other forms of nutrition support e.g. tube feeding and parenteral feeding.
Enteral nutrition is preferred unless contraindicated.
Nutrition assessment;
i. Anthropometric- weight, height, fat stores and physical look (wasting or gaining
weight).
ii. Visceral proteins or organ proteins e.g. serum albumin and transferrin
iii. Nitrogen balance studies (e.g. urea in urine)
N/B- small frequent meals which are nutrient or energy dense should be provided as the
patients are usually anorexic or depressed.
Stage 2 continues until the burnt surface is covered with new tissue or until skin
grafting begins.

Stage III;
This is called the follow up period of reconstructive surgery and rehabilitation. It is
characterized by reconstruction with grafting and plastic surgery. Optimal nutrition is
important for success of these procedures but the diet doesn’t usually have to contain
high levels of nutrients as for stage 2.
Problems encountered in burns;
 Hypothermia
 Oedema at the sites of injury
 Failure to obtain skin growth
 Weight loss
UNIT 5: CANCER
Unit Objectives
By the end of the unit the learner should be able to:
a) Describe types, causes and management of cancer
b) Discuss the complications of cancer
c) Plan and prepare meals for various hypothetical cancer patients
d) Visit a health facility to learn more about management of cancer
1.17 Introduction to cancer
It is a disease that results from abnormal and uncontrollable proliferation of cells at a
particular site. The cells grow without control. Cancer develops from mutation of genes
that regulates cell division. The mutation silences the genes that ordinarily monitor
replication of DNA for chemical errors.
The development of cancer is called carcinogenesis which often proceeds slowly and
continues for several decades. The affected cells rapidly divide in an uncontrolled way
but do not differentiate to specialized cells but form an abnormal mass called a tumour
or neoplasm. A tumour is a new growth of tissue which form an abnormal mass with
no function. Blood vessels form to supply the tumor with nutrients, the tumor may
invade healthy tissues and spread.
Malignant tumours are tumours that threaten health and requires treatment. They
usually invade surrounding structures and can spread or metastasize to distant sites
via the blood or lymph.
Benign tumours are tumours that stop growing without intervention or those which can
be removed surgically and pose no threat to health. They are usually enclosed in
membranes that prevent penetration to other tissues.
N/B- cancer does not cause death but the mortality rate of cancer patients is high due
to malnutrition caused by the disease as well as the treatment means used.
Signs and symptoms of cancer that warranty attention;
i. C-change in bowel/bladder habits
ii. A-a sore throat that doesnot heal
iii. U—unusual bleeding or discharge
iv. T-thickening or lump in the breast or elsewhere in the body
v. I- indigestion or difficulty in swallowing
vi. O- obvious change in the whole skin (mole or wart)
vii. N-a nagging cough or hoarsness of voice
viii. U-unexplained weight loss
Classification of cancer;
This is based on the tissue or cells from which they develop e.g.
i) Carcinomas which arise from the lining of epithelial tissues e.g. lining of the GIT,
skin, breast, prostate glands etc.
ii) Glicomas these are from the glial cells or tissue s of the CNS
iii) Adenomas from glandular tissues
iv) Leukemia of white blood cells. These do not produce a mass therefore not
classified as tumours.
v) Lymphoma from the lymph tissues.
vi) Melanoma from pigmented skin cells
vii) Myeloma which arise from the bone marrow
viii) Sarcoma arises from muscle, bone or connection tissue.
1.18 Cancer development process;
Carcinogenesis to thought to occur in three phases i.e. initiation, promotion and
progression.
i. Initiation; this may be due to chemical carcinogens such as aflatoxin,
benzo(a)pyrene (in smoked foods), virus, radiation from the sun or replication
errors which lead to permanent alteration in DNA of a cell.
ii. Promotion; this is speeding up the cancer development. An environmental agent
increases the chances of expression. This include; alcohol, dietary fat etc. which
encourage cell division.
iii. Progression; this is where cells undergo uncontrolled proliferation and
metastasize (i.e. spreading)
Both genetics and lifestyle are potent forces that influence the risk of development of
cancers. Genetics have been shown to be important in colon and some types of breast
cancer.

Cancer initiators;
80%-90% of cancer is related to the environment including 30%-35% that are diet related.
Generally cancers of the lungs, breasts and large bowel and skin cancer are more
common in developed countries but those of the cervix, stomach and mouth in
developing countries.
Dietary factors and cancer initiators;
i. Diet;
 Heavily smoked, pickled and salt cured foods produce nitrosamines which are
carcinogenic e.g. Smoked ham, sausages, fish, bacon these foods are also high
in fats and contains benzo (a) pyrene which may cause stomach cancer and
oesophageal cancer.
 Nitritites used in preservation of some processed foods are beneficial but they
also form nitrosamines which are cancer initiators.
 Excessive intake of protein and fats which may be involved in cancer
development this is because fats may stimulate excessive production of bile
which may be carcinogenic unless diluted by fibre
 Some lipids e.g. Sterols in the body are broken down to carcinogenic substances
 High intake polyunsaturated fatty acids (PUFA), especially linoleic acid has
shown involvement in the development of cancer of the breasts, colon, pancreas
and prostate gland because of lipolysis.

ii. Environmental factors;

 Excess alcohol increases the risk of cancer of the mouth, throat, liver, urinary
bladder and breast cancer.
 Cigarette smoking also enhances initiate cancer of the lungs, nasal cavity,
mouth, pharynx, larynx, oesophagus, stomach, colon, rectum, liver, pancreas,
 kidneys, renal pelvis and urinary bladder.
 Grilling and roasting of foods also causes GIT cancer because of tar
formation.
 Domestic and occupational sooths and smoke e.g. burnt foods which can
form substances which are carcinogenic.
 Mycotoxins e.g. aflatoxin which is associated with liver cancer.
 Chromium compounds causes nasal cavity and lung cancer
 Oestrogen-progesteron replacement therapy cause breast cancer
 Asbestos causes lung, pleural and peritoneum cancer
 Immunosuppressive medication which cause lymphoid tissue and liver
cancer
 Helicobacter pylori associated with peptic ulcer infection causes cancer of
the stomach
 Hepatitis B and Hepatitis C virus infections cause cancer of the liver
 Human papillomavirus (HPV) infections causes cancer of the cervix
N/B-The above viruses are referred to as oncogenic viruses
 Ionization radiation e.g. X-rays etc. causes cancer of white blood cells
(leukemia), oesophagus, stomach, colon, thyroid, lung, bladder and the breast.
 Ultraviolet radiation (sun exposure) causes cancer of the skin.
N/B-only prolonged exposure to these carcinogens leads to cancer not an occasional
exposure.
iii. Heredity; this is the inherited gene defect that can give a potential cancerous cell
a head start. This makes families to have more predisposition for cancer when
exposed to environmental factors and thus the need for regular checkup.
Cancer promoters;
High fat diet accelerates initiation of cancer e.g. breast, colon, prostate and pancreatic
cancers. It is believed that high fat diet may stimulate excessive production of bile
which may be carcinogenic unless diluted by fibre.
Obesity is related to all forms of cancer except lung cancer because of adiposity i.e. a
lot of fatty tissues and thus high levels of oestrogen thus are thought to be promote
cancer.
1.19 Nutritional effects or consequences of cancer;
This depends on the severity, location and the treatment undertaken.
Pancreatic and GIT cancer severely affect nutritional status as this impairs digestion
and absorption.
a) Local effects of cancer
i) Tumors growing in the GIT can cause obstruction, nausea and vomiting,
impaired digestion, delayed transit and malabsorption.
ii) Ascites related to ovarian and genitourinary cancer may lead to early feeling
of satiety, progressive protein malnutrition, and fluid and electrolyte
imbalance.
iii) Pain related to tumours or location may cause severe anorexia and poor oral
intake.
iv) Tumours of the central nervous system that cause confusion, somnolence
may lead to poor intake related to poor attention as well as dysphagia.
v) Head and neck cancer leads to difficulty in swallowing
vi) Oesophageal cancer leads to dysphagia related to obstruction
vii) Liver cancer leads to watery diarrhoea related to increase in serotonin,
histamines and other substances, malabsorption as well as diabetes.
viii) The fast growing malignant tissue extracts maximum nutrients from the
available nutrients and thus starving the body.
b) Systemic effects of cancer;
i) Abnormalities in metabolism which include increased energy expenditure,
increased protein catabolism and whole protein turn over (i.e. reuse of amino
acid that are generated by protein metabolism) and potential use of fats as an
energy source.
ii) Tumours can also produce hormones like substances that alter nutrient
absorption and metabolism
iii) Other substances produced by cancer cells may alter sense of taste, promote
anorexia or contribute to cancer cachexia.
iv) The patient also has imbalance in the physiological, psychological and emotional
 state thus the patient needs careful handling.
v) Anorexia accompanied by depression or discomfort from normal eating. This
results in cancer cachexia brought about by reduced food intake, a high energy
demand or both compounded by impaired digestion and absorption.
vi) Malabsorption which can occur due to a condition known as blind loop
syndrome which is a syndrome that occur when part of the small intestines
becomes by-passed due to cancer. The blind loop formed by the by passed
intestines means food cannot move normally through the digestive tract.
The slow moving food and waste products become a breeding ground for bacteria
which can lead to a condition known as bacterial overgrowth which affect nutrients
absorption especially of vitamin B12 and diarrhoea which can cause weight loss and
malnutrition. It is also called stasis syndrome or stagnant loop syndrome.
The major problems observed in cancer are;
i. Anorexia
ii. Cancer cachexia
i. Anorexia precedes cachexia and its contributory factors include;
 Early satiety,
 Nausea,
 Fatigue,
 Pain,
 Psychological stress,
 GIT problems which interfere with chewing, swallowing, cause vomiting or
nausea.
ii. Cancer Cachexia; is a wasting syndrome associated with cancer. It is severe
emaciation as a result of hypermetabolism i.e. increased energy expenditure due
to rapid dividing malignant cells. It is also referred to as protein energy
malnutrition (PEM) of cancer which is characterized;
 By weight loss (i.e. unintentional weight loss of 10% or more within 6 months),
 Anorexia,
 Depletion of lean body mass (muscle wasting),
  Serum albumin abnormalities,
 Fatigue,
 Anemia
 Loss of immunocompetence
 Abnormalities in carbohydrate, protein and fat metabolism.
Cancer cachexia diminishes the quality of life and increases the risk of mortality.
1.20 Treatment of cancer;
These include;
i. Radiation therapy
ii. Chemotherapy (drugs)
iii. Surgery
iv. A combination of the three above.
v. Bone marrow transplant for leukemia
All the above treatments have nutritional consequences because of side effects. The
side effects can cause;
a) Reduced food intake and accelerated nutrient loss
b) Skin damage, hair loss and fatigue.

Consequences/side effects of the treatments and the dietary management;

1. Anorexia-this is caused by radiotherapy to the head, neck or upper abdomen or
chemotherapy. Surgery can also cause it.
Dietary management;
 Give small frequent meals, high energy, high protein snacks and meals.
 Give appetizing and well preserved meals.
 Provide a pleasant eating atmosphere
 Encourage favorite foods and discourage intake of low energy fluids which are
filling e.g. water
2. Dysphagia; this is difficulty or pain when swallowing. It can be caused by
radiotherapy to the head and neck or surgery to the mouth and throat.
Dietary management;
  Alter the consistency of foods i.e. provide soft non-chew or pureed foods or
fluid diet.
 Avoid dry, rough and irritating foods avoid extreme temperature.
3. Mucosilitis/oesophagitis; which is the inflammation of the membranes of the mouth
and eosophagus. Caused by radiotherapy of the mouth and oesophagus and
chemotherapy.
Dietary Management;
 Soft bland and cool diets
 Sometimes pureed food may be necessary
 Extreme temperature and irritants should be avoided
 Foods like fruits, grains and raw vegetables should be avoided
4. Dysgeusia; this is altered taste e.g. there can be decreased taste sensitivity for
sugar and salts and poor taste for meals and mouth blindness (not able to taste
whether good or bad). Causes include radiotherapy of the neck region and also
chemotherapy.
Dietary management;
 Increase the use of spices
 Improve the odour, eye appeal and texture by including variety
 Use strong flavoured foods which are non-irritant
 Use alternatives of red meats thus use white meat e.g. chicken, fish, eggs,
milk or cheese.
 Marinate the meat with wine or vinegar
 Add a pinch of salt to sweet foods and a little sugar to salty or acidic foods.
 Avoid highly salted foods or very sugary foods.
5. Xerostomia; dry mouth due to decreased saliva flow. It is caused by head and neck.
Dietary management;
 Increase the liquid content of foods e.g. include soups or sauces
 Deeping foods in beverages
 Increasing fluid intake throughout the day and night
  Decreasing the use of very hot drinks and alcohol because they have a drying
effect.
 Having good dental habits e.g. cleaning the mouth
 Including energy dense beverages
6. Thick viscous saliva; this is caused by radiotherapy to the head and the neck.
Dietary management;
 Use of fluidy diet
 Taking black tea with lemon
 Rinsing the mouth with soda water
7. Loss of smell; this is due to radiotherapy of the head and neck.
Dietary management;
 Improve the food eye appeal, texture and taste.
8. Nausea and vomiting; it is caused by radiotherapy to the throat and upper abdomen.
It can also be caused by chemotherapy.
Dietary management;
 Sipping dry gingerale or lemonade
 Eating dry starchy foods
 Avoiding fatty foods, overly spicy and sweet foods e.g. fatty foods which delay
the emptying of the stomach
 Taking fluids separately from solids
 Small frequent meals
 Plenty of fluids
 Avoid odourous or strong smelling foods
 Eating in a pleasant environment
 Eating while relaxed and after meals
 Use nutrient rich supplements and also cool foods which are less odourous.
9. Cramping and gas production; this is caused by radiotherapy to the lower abdomen
and pelvis.
Dietary management;
  Avoid gas forming foods e.g. cabbages, onions, garlic, lettuce.
10. Diarrhoea; this is caused by radiotherapy to the lower abdomen and pelvis,
chemotherapy and surgery to the GIT.
Dietary management;
 Use Low residue diet
 Avoid fatty foods
 Increasing fluid intake
 Having small frequent meals.
11. Constipation and paralytic ileus; this is caused by chemotherapy.
Dietary management;
 Give high fibre diet
 If soft diet is necessary, bran and raw vegetables can be used.
12. Oral thrush; this is caused by chemotherapy. Its remedy involves use of cool moist
foods.
13. Radiation enteritis (inflammation of the intestines); caused by radiotherapy to lower
abdomen leading to loss of enzymes and malabsorption.
Dietary management;
Give low residue and lactose free diet.
14. Malabsorption ad water and electrolyte loss; this is due surgery to various sides of
the GIT.

1.21 Nutritional care for cancer;

N/B- Nutrition in the management of cancer is mainly supportive not therapeutic. It is
normally used as an adjunct to cancer treatment. The most important aspect to
remember is maintaining weight.
Aims of dietary management;
i. To maintain optimal nutritional status
ii. To prevent or correct nutrient deficiencies
iii. To avoid progression by treating a particular cancer that nutritional status of the
patient
iv. To prevent poor nutritional state from significantly influencing a patient’s ability
to withstand treatment
v. To improve immunocompetency
vi. To enhance the quality of life through good nutritional status.
vii. To promote wound healing
In case where nutrition therapy cannot achieve weight gain, nutrition therapy may help
to;
 Lessen side effects
 Reduce risk of infection
 Improve the sense of wellbeing.

Dietary management of cancer;

 There is no standard cancer diet this is because the nutrient needs are highly
individualized and less static.
 Diet plan in the management of cancer requires specific attention. They need to be
made in consultation with the patient and taking care to include favourite foods
prepared in familiar ways and served attractively.
 Cancer causes hypermetabolic state which increases energy demands. There is
need to rebuild damaged tissues and replace nutrients lost to cancer. Patients on
high calorie high protein diets tolerate the side effects of the therapy and high doses
of drugs better than those who cannot eat normally. Patients who can maintain or
minimize weight loss have a greater chance of responding to treatment and thus
recovery.
 Chemotherapy results in anorexia i.e. dislike of food though there is high nutritional
needs therefore chemotherapy needs to be scheduled 2-3hours before or after
meals.
 Though energy needs vary from one patient to the other, 25-35kcals/kg
bodyweight/day may be recommended for weight maintenance and 40-50kcals/kg
body weight/day to replenish body stores. Carbohydrates and fats must provide the
energy and spare proteins for tissue building and immune system.
 Protein needs vary from 1.0-1.2g/kg body weight/day for those with good nutritional
status and 1.3-2g/kg body weight/day for malnourished patients i.e. use of protein
rich foods e.g. meat, eggs, fish, poultry, milk etc.
 The patient should also consume high protein high calorie nutritional supplements.
These supplements may be consumed between meals and as replacements if
necessary.
 Sufficient fluids need to be ingested to help the kidneys eliminate the metabolic
waste and the toxins from the drugs.
 Give small frequent meals than 3 large ones
 Parenteral and enteral support is required for patients with increased needs for
energy and protein that cannot be met by oral intake
 The product taste, osmolality, digestibility and specific disease effects determines
the use of the formula.
 In parenteral feedings;
 Calorie intake must be 40-45kcals/kg body weight/day
 Protein intake 1.5g/kg body weight/day to achieve a positive nitrogen balance
 Fat emulsions which give 1.1kcals/ml and essential fatty acids
 Long term TPN requires an intake of vitamin K, B12, folic acid, iron via another
route.
N/B-avoid abrupt change in the modalities of route if feeding must be done, it must be
gradual progressing from parenteral to parenteral + enteral then to enteral + oral
feeding and to oral feeding.
Anticancer promoters/anticarcinogens/protectors;
There are some substances which have been shown to protect against cancer. They
include;
i) High fibre diet; mechanism involved seems to be by speeding up the transit time
of feacal materials in the colon that may contain carcinogens or by binding
carcinogens in stool. Thus no contact time with the GIT lining. This reduces the
incidence of colon and rectal cancer.
ii) Antioxidants e.g. vitamin A, C and E and β carotene these seem to lower the risk
 of many cancers by acting as scavengers of oxygen derived free radicals thereby
preventing damage of cells and tissues that can lead to cancer.
iii) Phytochemicals; these are substances found in cabbage family, kales,
cauliflower, onions, garlic, citrus etc. which activate enzymes that destroy
carcinogens.
iv) Calcium and vitamin D; these have been postulated to be antipromoters
v) Omega-3 fatty acids
vi) Drinking more than five glasses of water per day.
Guidelines for preventing cancer or reducing the risk of cancer;
For healthy living;
i. Controlling weight and preventing overweight an dobesity
ii. Reducing fat intake to less than 30% of the total energy
iii. Increasing fibre intake
iv. Consuming a variety of fruits and vegetables
v. Minimizing consumption of salt, cured and smoked foods.
vi. Discourage alcohol and cigarette smoking.
vii. Avoid sun burns
viii. Take up offers of cancer screening test
ix. Observe safety rules in jobs where exposure to chemicals, radiation and other
factors increase the risk.
UNIT 6: MUSCULOSKELETAL DISORDERS (MSDs)
Unit Objectives
By the end of the unit the learner should be able to:
a) Define terms used in the unit
b) Describe types, causes and management of musculoskeletal diseases
c) Plan and prepare meals for various hypothetical musculoskeletal disease
patients
These are injuries and disorders that affect the human body’s movement or
musculoskeletal system (i.e. muscles, tendons, ligaments, nerves, discs, blood vessels,
etc.).
Other common names for MSDs are “repetitive motion injury”, “repetitive stress injury”
and “overuse injury”, the reason for use is because repetitive stress is implicated as the
singular cause of these disorders to cause damage to the musculoskeletal system.
Types of musculoskeletal disorders include;
i. Gout
ii. Osteoporosis
iii. Osteoarthritis
iv. Rheumatoid arthritis
1.22 Gout
Gout is a disease of wealth and disappears in times of need. It is a disorder of purine
metabolism which occurs when its final metabolite uric acid crystallize in the form of
monosodium urate due to loss of uricase digestive enzyme which breaks down uric
acid. Gout is known as podagra when it involves the big toe.
It is a chronic and progressive disease with the depositions of hard lumps of uric acid in
tissues particularly in joints and it may cause damage to the joint and tendons and
destruction and decreased kidney stones (nephrolithiasis).
Gout is a medical condition usually characterized by recurrence of painful attacks of
acute inflammatory arthritis which is a red tender hot swollen joint due to inherent
abnormality in the body’s ability to process uric acid.
It is a disease observed in middle age and older men and post menopause women and
has a unique distinction of being one of the most frequently recorded illness throughout
history. Gout has been known since 1200aD and is referred to as “the King’s disease
and diseases of Kings” or “rich man’s disease”. In ancient times, more wise men than
fools were victims e.g. Dr. Livingnstone, Franklin etc.
Gout is a disease that results from uric acid in the body. The overload of uric acid leads
to the formation of tiny crystals of urate that deposits in tissues of the body especially
the points around joints. They take on the shapes like that of needles that jabs its way
into the joints.
When these crystals form in the joints, they accumulate causing recurrent attacks of
joint inflammation. Overload of uric acid on the other hand leads to elevated blood uric
acid levels a condition called hyperuricemia. This condition has no symptoms of
arthritis or kidney problems and is known as asymptomatic hyperuricemia. It is a
condition that is a precursor stage to the development of gout.
Gout is thus a clinical condition and hyperuricemia is its biochemical basis. Gouty
arthritis is typically an extremely painful attack with a rapid onset of joint inflammation.
These inflammations are precipitated by the deposits of uric acid crystals in the joint
fluids (synovial fluids) and synovial lining of the joint.
Intense joint inflammation occurs as the immune system reacts causing white blood
cells to engulf the uric acid crystals and chemical messengers of inflammation to be
released leading to pain, hotness and redness of the joint tissues without treatment
episodes of acute gout may develop into chronic gout with destruction of joint surface,
joint deformities and painless tophi (tophus -singular is a deposit of monosodium urate
crystals in people with high levels of uric acid in blood. It forms in joints, cartilages,
bones, kidneys and nasal cartilages and other places throughout the body). These may
develop about 10 years after the onset of the gout. These tophi can also occur in the
helix of the ear, at the knees and the big toe (which are the most affected areas of the
body).
Diagnosis of gout is confirmed clinically by visualization.
Signs and symptoms of gout;
i. Slight redness of the skin overlying the metartarsal-phalangeal joint.
 ii. Recurrent attacks of acute inflammatory arthritis (red tender, hot and swollen
joint) at the big toe joint, heels, wrists and fingers which usually begin over 2-
4hours and during the night due to lower temperatures at night.
iii. Hyperuricemia related symptoms like hard painless deposits of uric acid
crystals known as tophi.
iv. Fatigue due to high fever
v. Elevated levels of uric acid may also lead to crystals precipitating in the
kidneys leading to stone formation and subsequent urate nephropathy.
Causes of gout;
Hyperuricemia is the underlying cause which results from;
i. Diet
ii. Genetic predisposition
iii. Under excretion of urate (salts of uric acid)
iv. Over production of uric acid
v. Certain drugs
vi. Physical trauma and surgery
Renal underexcretion of urate is the primary cause of hyperuricemia in about 90% of
cases.
N/B- those with uric acid levels in blood about or >9mg/dl are at greater risk of
developing gout.
 Dietary causes account for 12% of gout which has a strong association with the
consumption of alcohol, fructose- sweetened drinks, meat and sea food.
 Physical trauma and surgery can as well contribute to the development of gout due
to changes in fluid balance.
 Genetic predisposition- it partly contributes to gout in about 60% of the population.
This is because there are people who have an inherited abnormality in handling uric
acid.
 Certain drugs e.g. thiazide diuretic, low doses of aspirin and niacin causes elevated
uric acid in the blood.
Risk factors associated with gout;
i. Certain diseases that causes production of high levels of uric acid in the body e.g.
levels of uric acid e.g. leukemia, lymphomas and haemoglobin disorders.
ii. Obesity and excessive weight gain as well as their management that involves
total starvation due to fats breakdown.
iii. Moderate to heavy alcohol intake this leads to high levels of purine production
which in turn leads to high serum uric acid levels and a decrease in urine uric acid
levels. This condition results due to elevated levels of serum lactate due to
alcohol breakdown
iv. High blood pressure
v. Insulin resistance in diabetes mellitus.
vi. Abnormal lipid levels which decreases uric acid excretion through urine.
vii. Starvation which leads to ketoacidosis which in turn causes hyperuricemia that
coincides with it because it reduces renal excretion of uric acid
viii. Abnormal kidney function
ix. Dehydration
Treatment of gout;
Treatment of gout involves;
i) Drug therapy-gout treatment involves the use of uricosuric drugs which are urate
lowering drugs which help in increasing renal clearance of urate e.g. sulfurin
pyrazone or probenecid and Allopurinol which inhibits the synthesis of uric acid.

ii) Ice application for 20-30minutes several times a day to decrease pain.

iii) Nutritional management of gout; the dietary advice for a patient who has had one or
more attacks of gout should be based on the following principles.

 If the patient is overweight, he/she should be advised to bring its weight down by
a gentle dietary regime so as to produce a moderate reduction of serum urate.
N/B- fasting even for a short period should be avoided because it may induce an
attack of gout due to ketoacidosis.
 Feasting should be equally avoided. Heavy rich meals high in purine or fat are
likely to raise the serum urate which may be followed by an acute attack by gout.
  Alcoholic drinks should be restricted since excessive intake is the underlying
stress which precipitates gout (men who take two drinks a day have serum urate
concentration higher than normal).
 Patients with severe gout who respond poorly or are intolerant to uricosuric
drugs need to stick to a strict low purine diet. Patients who respond to the drugs
can be placed on modified diet of purine wher they will be required to avoid food
srich in purine e.g. liver, kidneys, sweet-breads, sardines, anchories, fish rolls and
meat extracts.
 Patients with increased risk of uric acid stones in the urinary tract should
maintain a good intake of non-alcoholic fluids and take a drink of water before
going to bed. Coffee and tea can be drunk because caffeine is not converted to
uric acid easily.
 The patient should be advised to check fasting plasma lipids and treat
hyperlipidemia if present.
 High sucrose or high fructose diet should be avoided because fructose can
accelerate the rates of uric acid production. The patient therefore need to
consume a diet with low simple sugars and high in complex carbohydrates.
 Consume adequate vitamin C
 Use a low calorie diet for obese and overweight patients.
Dietary recommendations for gout patients;
i. Achieve an ideal body weight by gradual weight reduction
ii. Avoid excessive alcohol consumption particularly beer
iii. Avoid excessive intake of purine foods
iv. Consume a moderate amount of protein approximately 1g/kg body
weight/day.
v. Consume a moderate amounts of fat (less than 40% of total kilocalorie), limit
saturated fats
vi. Reduce simple sugars and increase complex carbohydrates in the diet.
vii. Consume a liberal amount of non-alcoholic fluids.
Assignment: List foods high in purine and those low in purine
1.23 Osteoporosis
Osteoporosis is a condition where there is loss of bone mass i.e. where the bone
becomes fragile and brittle causing them to break more easily. Bone mineral density
reduce after significant decline of sex hormones especially oestrogen in women that
the bone cannot sustain ordinary strain.
It is in two forms;
i. Osteopenic osteoporosis- (osteopenia) means too little bone mass during any
stage of life.
ii. Osteoporotic osteoporosis- (fragility) fractures due to weak bones it occurs in
old age.

Types of osteoporosis;
It can be classified based on;
i. Sex
ii. Age at which fractures occur
iii. Kind of bones involved
Osteoporosis is of two types;
i. Type I (post menopause or oestrogen/androgen deficient osteoporosis)-
This type occurs in women within a few years after menopause and is rare in men (>50
years). It is involved in cessation of ovarian production of oestrogen.
N/B- men may also develop it due to a decline in androgen production (though it is rare).
It is an osteoporosis characterized by fractures of the distal radius (“colles fractures”
and “crush fractures”) of the lumbar vertebrae that are often painful and deforming.
ii. Type 2 (age related osteoporosis)-
This type occurs at around age 70 and beyond. It affects both sexes (older men are
increasingly at risk of hip fracture). Bone tissues affected are mainly the trabecular and
cortical. It is characterized by fractures of the hips and verterbral fractures (wedge)
with symptoms of;
 Pain
 Loss of height
 Spinal deformities
 Kyphosis or “dowager’s hump”
N/B- loss of menses at any age is major determinant of osteoporosis risk in women.
Women with “female athlete triad” of disordered eating, amenorrhea and anorexia
nervosa have an increasingly low bone mass, density and increased risk of having
fractures while involved in athletics.
Lactating mother especially for 6 months or longer have a bone loss especially from the
femoral neck and lumbar spine.
Risk factors for development of osteoporosis;
i. Family history of osteoporosis
ii. Female gender
iii. White or Asian ethnicity
iv. Sarcopenia or slight body build
v. Estrogen depletion in menopause or early oophorectomy in women.
vi. Andogen depletion with hypogonadism in men
vii. Amenorrhea in women due to excessive exercise and in anorexia nervosa.
viii. Lack of exercise due to lack of exposure of bones to weight bearing pressure
especially within 10-20 years and stress from muscle contraction and
maintenance of body in an upright position against the pull of gravity so as to
stimulate osteoblast function
ix. Age especially >60years
x. Low body weight because the higher the body weight the greater the bone mass
due to the load that has to be borne by the bones.
xi. Confinement to bed
xii. Astronauts not exposed leads to bone mass loss.
Management of osteoporosis;
i. Intake of adequate calcium through diet and supplements
ii. Adequate vitamin D from supplements and sun exposure
iii. Avoidance of excess phosphorus intake
 iv. Use of a balanced diet that provides adequate proteins, energy and
micronutrients.
v. Exercise.
Medical management;
 Estrogen replacement e.g. use of oral contraceptive agents
 Calcitonin
 Education about prevention of falls.
1.24 Osteoarthritis (OA)
Osteoarthritis is a degenerative cartilage disease resulting in stiffness and loss of
motion most commonly affecting the spine, knee and hips which may lead to bone
spurs in and around the joint. It is a condition that comes due to over use of the joint. It
is also known as “wear and tear” type of arthritis.
It is associated with factors such as aging, injury or obesity. It mainly affects the elderly
and adults. It is a joint disease that mostly affects cartilages (the slippery tissue that
covers bones in a joint). Healthy cartilage allows bones to glide over each other and
helps absorb shock of movement. In OA, the top layer of cartilage breaks down and
wears away. This causes bones under it to rub together. The rubbing causes pain,
swelling and loss of motion of the joint over time.
The joint may lose its normal shape. Also bone spurs may grow on the edges of joint.
Bits of bone or cartilage may break off and float inside the joint space which causes
more pain and damage. People with OA often have joint pain and reduced motion.
Unlike other arthritis OA only affects the joints but not internal organs.
It is a clinical syndrome of joint pain accompanied by varying degree of functional
limitation and reduced quality of life. It is the most common form of arthritis and one of
the leading causes of pain and disability worldwide.
OA is a condition that is characterized by localized loss of cartilage, remodeling of
adjacent bone and associated inflammation. It may be triggered by trauma which
triggers the need for a joint to repair itself.
OA can occur in any joint but most often it affects peripheral joints such as the knees,
hips, hand joints as well as the spine. OA occurs most often in older people, younger
people get OA primarily from joint injuries. It usually occurs gradually over time.
Risk factors that might lead to OA;
 Overweight and obesity  A genetic defect in joint cartilage
 Getting older  Stresses on the joints from certain
 Joint injury jobs and playing sports.
 Joints that are not properly formed
Causes of OA;
 Knee- being overweight, having a previous knee injury, jobs involving kneeling,
climbing and squatting
 Hips- being overweight, having a previous injury, jobs involving lifting heavy loads e.g.
farming and a family history of osteoarthritis
 Hands; a family history of OA, repetitive use or previous injury to the hands and
being overweight.
Warning signs (symptoms) of OA;
 Stiffness in a joint after getting out of bed or sitting for a long time
 Swelling or tenderness in one or more joints
 A crunching feeling (clicking noise) or the sound of bone rubbing on bone to loss of
flexibility of joint.
 Pain
 Decreased range of motion
These symptoms may affect the ability to do normal daily activities e.g. walking,
climbing the stairs and opening a jar. The symptoms tend to get worse with activity
throughout the day.
Diagnosis of OA;
 Medical history
 Physical examination
 X-rays
 MRI scan
 Other tests e.g. blood tests or fluid in the joints
 Athroscopy
Treatment of OA;
N/B-OA has no cure. Treatment can effectively control its symptoms.
The treatment depends on which joint is affected and the severity of the conditions.
Aims of treatment;
i. To improve joint function
ii. To keep healthy body weight
iii. To control pain
iv. To achieve a healthy lifestyle.
The treatment involves;
i. Stay active by exercising the joints and muscles to keep them healthy and
flexible and to prevent other health problems. The exercise programme should be
tailored to the condition and ability of the patient.
ii. Weight control which involves weight loss for those who are overweight
iii. Rest and joint care
iv. Balance between rest and activity
v. Non-drug relief techniques to control pain
vi. Pain management using medicine e.g. Non-steroidal anti-inflammatory drugs
(NSAIDs), paracetamol, intra-articular hyaluronate injections, intra-articular
corticosteroid injections etc.
vii. Joint replacement surgery if symptoms are no longer controlled with other
therapies.
viii. Use of devices such as braces, walking sticks and shoe insoles
ix. Use a diet that is aimed at maintaining an ideal body weight
x. Learning to change the way you think about and react to pain.
Important consequences of OA;
i. Pain
ii. Reduced function
iii. Effects on a person’s ability to carry out their day to day activities
iv. It can cause severe disability because of poor repair of cartilage
v. In itself it is a biopsychosocial issue that is associated with changes in mood,
sleep and coping abilities because it can affect a person’s belief in his ability to
complete tasks and reach goals.

1.25 Rheumatoid arthritis (RA)

RA is a chronic autoimmune (i.e. idiopathic) disease that affects young people that
causes swelling of joints. It involves the inflammation of the synovium lining the joint. It
is the most common autoimmune inflammatory arthritis. It is a condition in which the
body’s immune system attacks the body’s own tissues of joints leading to pain,
inflammation and eventually joint damage.
RA causes the joints to swell and can result in pain, stiffness and progressive loss of
function. In addition to joint pain and swelling, people with RA may also have symptoms
such as weight loss, low grade fever and fatigue.
RA often affect pairs of joint e.g. both hands and feet etc. and can affect more than one
joint including small joints in the wrist and hands and over time other joints can be
affected e.g. shoulders, elbows, knees, feet and ankles. Over time inflammation of RA
can cause damage to the joints. In some patients this may lead to permanent joint
damage. As this joint damage progress, in severe case, it can cause deformity of the
joint and loss of function. It may it may begin to interfere with daily activities making
them more difficult and painful to do.
RA affects people worldwide at similar rate. It often in middle age but can start at any
age. Women are 2-3 times more likely to be diagnosed with RA than men. RA is a
condition that progress over time.
People with RA may feel sick and tired and they sometimes get fevers. Some people
with have mild or moderate forms of the disease with times when the symptoms get
worse and times when they get better. Others have severe forms of the disease that can
last for many years or a life time. This form of the disease can cause serious joint
damage.
Causes of RA;
RA has no known cause. Research has found that it is a condition that occurs due to
autoimmunity where a person’s immune system attacks his/her own body tissues. The
causes of this autoimmunity are due to the following possible causes;
i. Genetics- people with family members who have RA may be more likely to
get it.
ii. Hormones- female hormones may play a role in the disease.
iii. Viruses or bacteria- RA may be related to viruses or bacteria that come in
contact with during one’s life.
Diagnosis of RA;
It involves;
i. Use of medical history- whether there is a family member who has had RA
ii. Physical examination- to check for reflexes, muscle strength and general health,
ability to walk, bend and carry out activities of daily living and evidence of
inflammation in the lungs
iii. Laboratory test- to check for R-factor (RF), anticyclic citrullinated peptide (anti-
CCP) antibody test and other tests e.g. white blood cell count, anemia test
erythrocyte sedimentation rate (ESR) and C-reactive protein.
iv. X-rays- to determine the degree of joint damage
N/B-Early diagnosis is important to an accurate and appropriate treatment as early as
possible.
Symptoms of RA;
RA affects people in different ways. Symptoms may slowly develop over several years
or the disease may progress quickly. The symptoms may be mild or very severe. The
patient may go through phrases called “flares” or “flare up” (period where RA symptoms
appear or worsen) when symptoms are severe. At times it may go through phases
called “remission” if the disease and its symptoms have gone away. Joint pain and
swelling may happen slowly and may occur over weeks or months.
The symptoms include;
i. Painful joints v. Stiffness in the joints particularly
ii. Feeling weak in the morning
iii. Swollen joints vi. Low fever
iv. Lumps under the skin especially vii. Weight loss
on the hands or elbows viii. Fatigue due to anaemia that
 accompanies RA motion
ix. Loss of energy xi. Loss of appetite
x. Over time decreased range of xii. Dry eyes and mouth
N/B: the effects generally worsen in the morning or after long rest and lack of activity.
Effects/consequences of RA;
It results in stiffness in the morning and pain and swelling of joints often in the same
joint on both sides of the body. When RA progress, it may lead to joint damage. It can
cause surrounding muscles, ligaments and tendons to become weak and unable to
work normally.
Patients with RA apart from them having joint conditions may also have other
conditions due to RA and medications used or treat it e.g.;
i. Heart disease v. Sjogrens syndrome (i.e. dry
ii. Bone loss mouth and dry eyes and other eye
iii. Anemia problems)
iv. Rheumatoid nodules under the vi. Inflections
skin vii. Lung disease.
Treatment of RA;
Goals of RA;
i. To reduce pain and swelling
ii. To decrease or stop further joint damage
iii. To improve physical function by helping people feel better and stay active.
The treatment of RA depends on the progress of the disease.
The treatment options include;
i. Lifestyle changes that can help in the management of RA such as education on;
 Rest and exercise
 Stress reduction
 Joint care
 Healthy diet
ii. Medications that can help to decrease pain and or swelling such as;
 Pain relievers
  Non-steroidal anti-inflammatory drugs (NSAIDs)
 Corticosteroids
iii. Medications that can help reduce inflammation and may also slow the rate of
joint damage e.g.
 Non-biologic disease modifying antirheumatic drugs (DMARDs)
 Biologic DMARDs for patients with moderate to severe RA
 Other oral agents used in moderate to severe Ra alone or in combination with
methotrexate or similar drugs (DMARDs)
iv. Surgery for severe RA.
UNIT 7: NEUROMUSCULAR DISEASES
Unit Objectives
By the end of the unit the learner should be able to:
a) Define terms used in the unit
b) Describe types, causes and management of neuromuscular diseases
c) Plan and prepare meals for various hypothetical neuromuscular disease patients
d) Visit a health facility to learn more about management of neuromuscular
diseases
1.26 Introduction to neuromuscular disorders
Neuromuscular system is a combination of nervous system and muscles working
together to permit movement. The brain controls the movements of skeletal (voluntary)
muscles via specialized nerves. These movements include both voluntary e.g. walking
and talking and involuntary e.g. breathing and digestion. For any movement of any part
of the body, a message is sent to particular neurons (nerve cells), called upper motor
neurons which have long tails (axons) that go into and through the brain, and into the
spinal cord, where they connect with lower motor neurons. At the spinal cord, the lower
motor neurons in the spinal cord send their axons via nerves in the arms and legs
directly to the muscle they control.
Definition of Terms
Aneurysm – it is the bulging of an artery or cardiac chamber walls or a blood-filled
pouch ballooned out from an artery. Can be caused by high blood pressure,
atherosclerosis, trauma, heredity and abnormal blood flow at the junction where arteries
come together.
Embolus – a blood clot that occurs in another part of the body away from the brain e.g.
the neck or lining of the heart.
Thrombus – a blood clot that forms in a blood vessel the brain.
CT scan (computerized topography) – provides doctors with more detailed about
spinal cord of brain damage than X-rays can.
Hemorrhage – internal or external bleeding caused by damage to a blood vessel.
Motor function – ability to control muscles voluntarily and their resultant use.
MRI (Magnetic Resonance Imaging) - Uses a strong magnetic field and radio waves to
produce computer-generated images. It can help identify blood clots, swelling or skull
fractures that may be compressing the brain and/or the spinal cord.
Paraplegia– Paralysis, or loss of motion. It typically affects the trunk (the body apart
from limbs and head) and both legs, but not the arms. This is usually a result of injuries
at the thoracic and lumbar levels.
Tetraplegia (also quadriplegia) – Paralysis from approximately the neck down. It results
from injury to the spinal cord in the neck and is associated with total or partial loss of
function in both arms and legs.
Neurology is the branch of medicine that deals with the diagnosis and treatment and/or
management of conditions and diseases affecting the central nervous system
Hemiparesis is weakness on one side of the body that causes the body to slump
toward the affected side; it may increase a patient’s risk of aspiration.
Hemianopsia is blindness for one half of the field of vision. The patient must learn to
recognize that he or she no longer has a normal field of vision and must compensate by
turning the head.
Neglect is inattention to a weakened or paralyzed side of the body; this occurs when the
non- dominant (right) parietal side of the brain is affected. The patient ignores the
affected body part, and his or her perception of the body’s midline is shifted.
Dysphagia refers to difficulty in swallowing.
Intracranial pressure (ICP)–this refers to the pressure within the skull and thus in the
brain tissue and cerebrospinal fluid (CSF).
Trauma – can refer to either physical or psychological trauma.
Physical trauma is injury caused by an external force.
Psychological trauma on the other hand refers to damage to the psyche as a result of
an extremely distressing event.
Neutrophilia higher than normal number of circulating neutrophils i.e. the primary white
blood cells (WBCs) responding to infection.
Functions of nervous system
i) Control of body’s internal environment to maintain homeostasis e.g. maintaining
core body temperature
ii) Memory and learning
iii) Programming of spinal cord reflexes
iv) Voluntary control of movement e.g. walking, writing, running, chewing, initiating
swallowing, presentation of food to the mouth
Causes of neuromuscular diseases
There are many diseases that are classified as neuromuscular disorders. They may
result from:
 Hereditary and genetic mutation  Certain drugs and poisons
e.g. epilepsy, Parkinson’s disease  Secondary to other complex
 Viral infection disease conditions e.g. diabetes,
 Autoimmune disorder with no stroke, obesity
known cause  Mechanical injury e.g. traumatic
 Hormonal disorder brain injury
 Metabolic disorder  Advanced age e.g. Alzheimer’s
 Simple deficiencies or excesses disease
of nutrient e.g. neuropathy  Lifestyle factors e.g. alcoholism,
associated with thiamin physical inactivity, diet
deficiency, Wernicke-Korsakoff  Unknown factors.
syndrome, beriberi, spina bifida
Symptoms of neuromuscular diseases
The symptoms of neuromuscular disease vary according to the condition and may be
mild, moderate or life threatening. They include:
 Muscular weakness skeletal deformities
 Muscle wastage  Muscle pain
 Muscular cramps  Breathing difficulties
 Muscle spasticity (stiffness),  Swallowing difficulties.
which later causes joint or
Issues complicating nutrition therapy in neuromuscular diseases
Severe neurologic impairments often compromise the mechanisms and cognitive
abilities needed for adequate nourishment. Common nutritional diagnoses common in
neurologic patients include
 Dysphagia  Physical inactivity
 Chewing difficulty  Poor nutritional quality
 Inadequate energy intake related  Difficulty with independent eating
to inability to obtain and present  Underweight
food to the mouth may also occur  Elimination problems
 Increased energy expenditure  Inadequate access to food or
 Inadequate fluid intake fluid
Types of neuromuscular diseases
Neuromuscular diseases encompasses many different medical conditions that impair
functioning of the muscles. It makes muscles weak and waste away. Neurology is the
branch of medicine that deals with the diagnosis and treatment and/or management of
conditions and diseases affecting the central nervous system and peripheral nervous
system.
The diseases of neuromuscular system include;

1.27 Traumatic brain injury

The brain is the functional regulator for metabolic activities. Traumatic brain injury (TBI)
is also known as acquired brain injury, head injury, or brain injury. It occurs when sudden
trauma damages the brain disrupting normal brain function resulting in substantial
disability and mortality. TBI can be categorized into three types i.e. Concussion,
contusion and diffuse axonal injury. In TBI, a complex scene of metabolic alterations
may occur which consists of hormonal changes, abnormal cellular metabolism, and
inflammatory ‘force’.
These abnormal metabolic processes, mainly include
 Hypermetabolism
 Fever
 Neutrophilia
  Altered amino acid metabolism
 Production of hepatic acute-phase proteins
 Hypercatabolism
 Glucose intolerance
These abnormalities complicate the initial period of hospitalization and stabilization and
negatively impact rehabilitative treatments.
Injury resulting in TBI can be classified into:
i) Primary injury – this is induced by mechanical force and occurs at the
moment of injury; the 2 main mechanisms that cause primary injury are
contact (e.g. an object striking the head or the brain striking the inside of the
skull) and acceleration-deceleration forces (commonly referred to, or
associated with whiplash. Whiplash involves transfer of
acceleration and deceleration forces; usually this is caused by car accidents
which cause the body to be thrust forward and then backwards in quick
succession).
ii) Secondary injury –this is not mechanically induced; it may be delayed from
the moment of impact. It follows primary injury through a combination of
systemic disorders such as;
 Hypoxia-deficiency in the amount of oxygen reaching the tissues
 Hypotension-abnormally low blood pressure
 Hypercarbia/hypercapnia-abnormally elevated carbon dioxide levels in
the blood and other local events.
Medical Nutrition Therapy (MNT)
Goals of MNT
 To maintain adequate nutrition status
 To oppose the hypercatabolism and hypermetabolism associated with inflammation
Nutrition support in TBI
Hypercatabolism is manifested by protein degradation, evidenced by profound urinary
urea nitrogen excretion. Nitrogen catabolism in a fasting normal human is only 3 to 5 g
of nitrogen per day, whereas nitrogen excretion is 14 to 25 g of nitrogen per day in the
fasting patient with severe head injury. In the absence of nutritional intake, this degree
of nitrogen loss can result in a 10% decrease in lean mass within 7 days. A 30% weight
loss increases mortality rate.
Nutrition support is particularly important in TBI because of the gastrointestinal
complications that arise. The most frequent GI complications are;
 Stress ulcers
 Dysphagia
 Bowel incontinence (inability to control bowel movements)
 Elevated levels on liver function tests
 Increased gastric residuals
 Reflux/vomiting
Nutritional support is an important additional therapy for metabolic disorders following
TBI. Early initiation of nutritional support for TBI patients, can decrease mortality, reduce
complications and facilitate recovery.
PN appears to be superior to EN in reducing mortality and improving outcome in the
acute gut-intolerant phase of TBI. Immune-modulating formulae seem to be superior to
standard formulae in reducing infectious complications.
Immune enhancing nutrition formulas are available for critically ill head-injured patients
that are enhanced with glutamine, arginine and omega-3 fatty acids.

1.28 Spinal cord injury

While the brain is the command center for the body, the spinal cord acts as the nerve
pathway that allows the brain and the brain to communicate. Spinal cord injury occurs
after any damage to the spinal cord that blocks communication between the brain and
the body. After a spinal cord injury, a person’s sensory, motor and reflex messages are
affected and may not be able to get past the damage in the spinal cord. The location of
the SCI and the disruption of the descending axon determines the extent of paralysis.
The higher on the spinal cord the injury occurs, the more dysfunction the person will
experience.
Spinal cord injuries are referred to as complete or incomplete, based on whether any
movement and sensation occurs at or below the level of injury. Complete SCI is defined
as a defect in which there is of motor or sensory function below the level of injury
whereas incomplete SCI refers to a defect in which some degree of motor or sensory
function is retained below the level of injury.
Causes of SCI
i) Traumatic injuries- e.g. motor vehicle accidents, falls, violence, football,
gymnastics and diving into shallow water.
ii) Non-traumatic injuries/illnesses- e.g. cancer, multiple sclerosis, arthritis,
osteoporosis, inflammation of the spinal cord
Consequences of spinal cord injury
 Loss of movement/paralysis
 Loss of sensation
 Loss of bowel and/or bladder control
 Exaggerated reflex actions or spasms
 Changes in sexual function, sexual sensitivity and fertility
 Pain or intense stinging sensation
 Loss of muscle tone caused by skeletal muscle paralysis below the level of injury
contributes to decreased metabolic activity, initial weight loss, and predisposition
to osteoporosis. The greater the injury, the lower the metabolic rate.
Medical nutrition therapy
Goals of MNT
1. To provide the most appropriate form of nutrition support e.g. enteral or
parenteral nutrition depending on the patient’s characteristics.
2. To provide high-fiber diet, adequate hydration to minimize constipation.
3. To provide dietary intake to maintain nutrition health and adequate weight
Key guidelines for managing SCI
If the patient with SCI is in the acute phase, energy needs should be assessed by
indirect calorimetry (IC).
Initial weight loss during the acute phase of injury may lead to weight gain in the chronic
phase because of body mass redistribution.
Patients with SCI have reduced metabolic activity because of denervated muscle in part
due to loss of motor function. Actual energy needs are at least 10% below predicted
needs. Because of decreased energy expenditure and caloric needs, secondary to lower
levels of spontaneous physical activity and a lower thermic effect of food, adults in the
chronic phase of SCI are often overweight or obese and therefore at risk for diabetes
and cardiovascular disease. Persons of all ages with SCI appear to be at high risk for
cardiovascular disease, atherogenesis, and undesirable blood lipid values. The
modifiable risk factors such as obesity, inactivity, dietary factors, and smoking must be
addressed.
Physical activity, including sports, swimming, electrically stimulated exercise, and body-
weight supported treadmill training, may result in improvements in blood lipid
parameters. Dietary intervention using the current evidence-based guide for lipid
disorders should be provided.
Cranberry juice may be beneficial for prevention of urinary tract infections. One cup (250
ml) three times daily can be recommended, unless the patient has diabetes. A minimum
of 1.5 L of fluid is recommended per day.
Provide therapeutic diets of high fiber (15 g) and adequate water intake for the
treatment of constipation with a routine bowel preparation program.
Maintenance of nutritional health is important because poor nutrition is a risk factor for
infection and pressure ulcer development. Regular assessment of nutritional status, the
provision of adequate nutritional intake, and the implementation of aggressive
nutritional support measures are indicated. Reduced pressure ulcer development
occurs in patients who maintain a normal weight, higher activity levels, and better serum
levels of total protein, albumin, prealbumin, zinc, vitamin D, and vitamin A. Thus
sufficient intake of calories, protein, zinc, and vitamins C, A, and B-complex is warranted.
When pressure ulcers are present, provide 30 to 40 kcal/kg of body weight/day and 1.2
g to 1.5 g of protein/kg body weight/day. Fluid requirements should be at least 1 ml
fluid per kcal provided.

1.29 Cerebrovascular accident (CVA)/stroke

The brain does not store oxygen and therefore relies on the network of blood vessels to
provide it with oxygen rich blood. A stroke occurs when blood flow to a section of the
brain is cut off as a result of blocked or busted blood vessel. When tissue is cut off from
its supply of oxygen for more than 3 to 4 minutes, it begins to die. This results in
inability of the nerve cells to communicate with other cells and bodily functions e.g.
speech, movement and memory, are therefore impaired. When a stroke occurs on the
right side of the brain, the left side of the body is affected and vice versa.
Risk factors for stroke
Risk factors are behaviors or traits that make an individual more likely to develop a
disease or condition. They can be categorized into modifiable and non-modifiable risk
factors.
Modifiable risk factors
 Diet–Cholesterol elevation which is a risk factor for atherosclerosis.
 Diabetes mellitus - increases stroke risk, especially for strokes due to damage of
small blood vessels.
 Existing carotid and/or coronary artery disease -The carotid arteries in your neck
supply most of the blood to your brain. A carotid artery that has been damaged
by fatty build-up of plaque inside the artery wall may become blocked by a blood
clot, causing a stroke.
 Drug and substance abuse e.g. Smoking and use of street drugs, such as crack,
cocaine, and marijuana have been shown to increase the risk of stroke. Some of
these drugs directly affect the blood vessels in the brain causing a stroke. Others
cause damage to the heart, which can lead to stroke.
 Hypertension
 Overweight and obesity.
Non-modifiable risk factors
 Age: People of all ages, including children, have strokes. However, the risk of
stroke increases as age increases.
 Gender: Stroke is more common in men than in women. In most age groups,
more men than women will have a stroke in a given year. However, women
account for more than half of all stroke deaths. Women who are pregnant have a
 higher stroke risk. Also at higher risk are women who take birth control pills and
who also smoke or have risk factors such as high blood pressure.
 Race: The risk of stroke varies with race and ethnicity. African Americans and
Hispanics are more likely to have strokes than Caucasians. The risk of stroke is
also high among Native Americans and Alaskan Natives.
 Family history: Your stroke risk is greater if a parent, grandparent, sister, or
brother has had a stroke.
 Prior stroke or heart attack: A person who has already had a stroke or heart
attack is at much higher risk of having a second stroke
Types of stroke
Stokes can present as hemorrhagic, ischemic or transient ischemic attacks.
i) Hemorrhagic stroke – as the name suggests, this occurs as a result of ruptured
blood vessel in the brain. Bleeding from the blood vessel occurs suddenly and
the force of this blood can damage the surrounding brain tissue. It is the most
serious kind of stroke.
There are two types of hemorrhagic stroke i.e. intracerebral and subarachnoid.
 Intracerebral hemorrhages occur when a blood vessel in the deep tissue of the
brain ruptures.
 Subarachnoid hemorrhages occur when an aneurysm ruptures and bleeds into
the space between the brain and the skull. Usually as a result of high blood
pressure.
ii) Ischemic stroke – occurs when a blood vessel in the brain develops a clot and
cuts off the blood supply to the brain. This can result from a thrombus or an
embolus. Blood clots are usually as a result of atherosclerosis (build-up of
plaque with fatty deposits within blood vessel walls).Embolic stroke occurs when
a cholesterol plaque is dislodged from a proximal vessel, travels to the brain, and
blocks an artery. Thrombotic stroke occurs when a cholesterol plaque within an
artery ruptures, and platelets subsequently aggregate to clog an already
narrowed artery.
iii) Transient ischemic attack (TIA) - has the same symptoms as stroke. However,
 they only last several minutes or up to 24 hours. It differs from stroke in that, it
does not result in death of brain cells. However, it is to be taken as a warning
sign of stroke. 1 in 3 people who have TIA end up developing stroke.

Consequences of stroke
 Inability to move part of the body  Difficulty swallowing
(paralysis)  Vision loss
 Weakness in part of the body  Memory loss, confusion or poor
 Numbness in part of the body judgment
 Inability to speak or understand  Change in personality; emotional
words problems
 difficulty communicating
Medical nutrition therapy
Goals of MNT
i) To maintain adequate nutrition
ii) To assess and manage dysphagia
iii) To provide vitamin and mineral supplementation as needed
iv) To provide enteral nutrition support may be necessary
Medical nutrition therapy in stroke
Lifestyle and behavior changes that include diet are key components to primary
prevention of stroke. A diet high in omega-3 fatty acids provides protective benefits
against stroke.
N/B: Omega-3 fat supplements should be avoided by patients taking blood thinners
such as warfarin or aspirin.
Eating difficulties and resulting behavioral problems are determined by the extent of the
stroke and the area of the brain affected. Dysphagia accompanies most stroke cases
and contributes to;
 Malnutrition  Increased length of hospital stay
 Pulmonary infections  Institutional care
 Disability
In some instances nutrition support is required to maintain nutritional health until oral
alimentation can be resumed.
As motor functions improve, eating and other activities of daily living are part of the
patient’s rehabilitation process and necessary for resuming independence. Malnutrition
predicts a poor outcome and should be prevented.
1.30 Cerebral palsy
Cerebral Palsy (CP) is a group of disorders of muscle control or coordination resulting
from injury to the brain during its early (fetal, perinatal, and early childhood)
development; there may be associated problems within intellectual, visual, or other
functions.
The problem in CP lies in the inability of the brain to control the muscles, even though
the muscles themselves and the nerves connecting them to the spinal cord are normal.
The extent and location of the brain injury determine the type and distribution of CP.
There are various types of CP, which are classified according to the neurologic signs
involving muscle tone and abnormal motor patterns and postures. The diagnosis of CP
is generally made between 9 to 12 months of age and as late as 2 years with some
types.
Types of CP
1. Spastic CP: Increased muscle tone, persistent infant reflexes, increased deep
tendon reflexes in one of three patterns: hemiplegia(arm and leg on one side of
the body), diplegia (involving the lower extremities), and quadriplegia (all four
extremities and may include the trunk, head, and neck)
2. Dyskinetic CP: Abnormalities in muscle tone that affect the entire body; includes
athetoid CP, which includes uncontrolled and continuous involuntary movements
3. Mixed CP: A condition in which both athetosis (a condition in which abnormal
muscle contraction causes involuntary movement) and spasticity are present
4. Ataxic CP: Abnormalities of voluntary movement and balance such as unsteady
gait
5. Athetoid dyskinetic CP: Normal intelligence but difficulty walking, sitting,
speaking clearly
Causative agents for CP
 Prematurity German measles
 Blood-type incompatibility  Viral diseases e.g. German measles
 Placental insufficiency (Rubella)

 Maternal infection that includes  Neonatal jaundice

 Anoxia at birth – absence or fetus, or infant that affect the central
deficiency of oxygen reaching the nervous system.
tissues.  LBW babies
 Bacterial infections of the mother,
Nutrition implications of CP
 Bone mineral density of children and adolescents with moderate to severe CP is
reduced in those with gross motor function and feeding difficulties
 Constipation, usually caused by inactivity and lack of fiber and fluids, often
connected to feeding problems.
 Feeding problems - As infants they have difficulty swallowing and coordinating
swallowing and chewing, so the normal progression to solid foods is later than usual.
 Dental problems occur and often are related to malocclusion, dental irregularities,
and fractured teeth. Lengthy and prolonged bottle-feedings of milk and juice
promote the decay of the primary upper front teeth and molars.
 Hearing problems and especially visual impairments, mental retardation, respiratory
problems, and seizures affect nutrition status.
 Drug-nutrient interactions particularly with anticonvulsants used to control seizures.
Nutrition assessment for CP
Indirect methods of anthropometric assessment, including knee-height measurements,
arm span, or recumbent length using a tape measure, may be options for clients with
CP as they cannot stand or stand straight or they cannot be stretched out straight. In
addition, it is important to note that children with CP are often shorter than their
healthier counterparts.
Mid–upper arm circumference and triceps skinfold measures are recommended reliable
ways to
screen for fat stores in children with CP.

1.31 Epilepsy
It is a chronic condition characterized by unprovoked, recurring seizures. Seizures are
caused by abnormal electrical activity of a group of neurons. This can create
uncontrolled muscle movements or loss of consciousness. Seizures before age 2 are
usually caused by fever, developmental defects, birth injuries, or a metabolic disease.
Epilepsy however, is more than just seizures as it can result in memory problems,
learning disabilities and behavioral problems.
Medical nutrition therapy
The ketogenic diet
This is an individualized and structured diet that provides specific meal plans. Foods are
weighed and meals should be consumed in their entirety for best results. The ratio of
this diet can be adjusted to effect better seizure-control and also liberalized for better
tolerance. This diet is also considered allow glycemic therapy and results in steady
glucose levels.
The ketogenic diet has been in existence since 1920s and can be used for treatment of
all types of seizures. Originally designed using ratios of 4:1 or 3:1 (grams of fat to
nonfat), meaning that there are 3 or 4 g of fat for every 1 g of protein and carbohydrate
combined in the diet. With a 4:1 ratio, the diet is calculated so that at least 90% of the
kilocalories are from fat. Protein is calculated to provide appropriate intake for growth
(approximately 1 g/kg/day). Carbohydrates are added to make up the remaining small
portion of calories.
This helps to achieve strong and consistent ketosis, less restrictive versions are now
available that can also be effective. Ketones provided by ketogenic diet therapy offer an
alternative fuel source which improves symptoms, preserves neurons, and can prevent
further decline.
The beneficial effect of ketosis in epilepsy may be caused by a change in neuronal
metabolism; ketones may inhibit neurotransmitters, thus producing an anticonvulsant
and neuroprotective effect in the brain.
Antiepileptic drugs are not stopped but may be reduced before initiation, if medication
toxicity occurs, or after it has been established that the diet therapy is effective.
The ketogenic diet has minimal side effects, and risks of the diet are low blood sugar,
upset stomach at first caused by the high amounts of fat, and constipation. The long-
term risk of kidney stones is rare; elevated serum cholesterol is usually temporary and
disappears with discontinuation of the diet; and growth, which is sometimes slowed
while on the diet, resumes at the child’s normal rate. Ketosis is monitored by regular
measurements of urine ketones or serum betahydroxybutyrate.

1.32 Down’s syndrome

Down’s syndrome is a genetic disorder that results from the presence of an extra
chromosome in each cell of the body. Normally every cell of the human body except for
the gametes (sperm or ova) contains 46 chromosomes, which are arranged impairs.
With DS there is one extra chromosome for a total of 47.
This anomaly causes physical and developmental implications e.g.
 Congenital heart disease  Upward slant of the eyes
 Mental retardation  Epicanthal folds
 Overweight  Small oral cavity
 Dental problems  Short, broad hands with the single
 Thyroid disease palmar crease
 Decreased muscle tone  A wide gap between the first and
 Hyperflexibility of joints second toes

 Speckling of the iris

General nutrition assessment parameters for Down’s syndrome

Feeding problems
• Decreased nutritional intake • Weight changes
• Decreased fluid intake • Dysphagia
• BMI compared with Down’s syndrome • Hemoglobin concentration
standards
Intervention strategies for Down’s syndrome
1. Overweight -The most effective intervention for the overweight child with DS is to
design a calorie-controlled eating plan based on kilocalories per centimeter of
height i.e. 14.3 kcal/cmhgt (girls) and 16.1 kcal/cmhgt (boys).
Environmental changes to manage overweight should include:
Following a regular eating schedule that includes three meals at regular times with the
child sitting either in a high chair or at the table.
Planned snacks should be low in fat and sugar. Soft drinks should be eliminated, and
milk should be low fat (after age 2).
Physical activity should be encouraged.
A prescription for a special meal at school can be obtained by using the school food
service prescription.
Parent training in behavioral intervention as they play an active role in determining food
preparation, decreasing number of times meals are purchased in fast food restaurants
and serving sizes.
2. Eating skills - During intervention programs the feeding team can guide the parent in
positioning the child and working toward attainable feeding skills related to the
developmental level of the child.
3. Constipation - This is a frequent problem for the child with DS because of overall
low tone followed by lack of fiber and fluid in the diet. Its treatment should involve
increasing fiber and fluid, with water consumption emphasized. Fiber content of the
diet for children after age 3, is 5 to 6 g per year of age per day. For adults the
recommendation is for 25 to 30 g of dietary fiber daily.

1.33 Guillain-barre syndrome (GBS)

GBS falls under a class of immune-mediated inflammatory disorder of the peripheral
nervous system. It results in loss of function in affected nerves due to demyelination,
which results from an attack on myelin (specialized fatty insulation that envelops the
axon) by the immune system. GBS reveals itself in a matter of days. The most common
sequence of symptoms;
1. Areflexia (absence of reflexes)
2. Proximal limb weakness
3. Cranial nerve weakness
4. Respiratory insufficiency
In most cases of GBS (approx.60%), the disorder follows an infection, surgery or an
immunization. Because of the swift progression of the disorder, vital capacity and
swallowing function may rapidly deteriorate such that intensive care is sometimes
necessary.
Medical nutrition therapy
Gluten sensitivity has been reported in some cases of GBS. For these patients, gluten
rich foods may need to be eliminated from the diet e.g. wheat.
Guillain-Barré syndrome evolves quickly; during the acute stage, the metabolic response
of GBS is similar to the stress response that occurs in neurotrauma.
Energy needs assessed by indirect calorimetry may be as high as 40 to 45 kcal/kg and
protein needs twice the usual amount.
For a small portion of the patients, dysphagia may arise, therefore, supportive nutritional
care should be offered to decrease muscle wasting.

1.34 Myasthenia gravis

MG is caused by an error in the transmission of nerve impulses to muscles. In MG the
body unwittingly makes antibodies to acetylcholine receptors (AchR). These antibodies
bind to AchR and make them unresponsive to acetylcholine (Ach) (the molecule that
carries nerve impulses to muscle membranes).
MG is characterized by;
 Weakness  Facial muscle weakness
 Fatigue  Dysphagia
 Double vision  Severe diaphragmatic
 Weakness which can result in respiratory difficulty
N/B: There is no disorder of nerve conduction and no intrinsic disorder of muscle.
Patients with MG commonly have an overactive thymus gland. This gland plays a role in
the maturation of B-lymphocytes, the cells that are charged with synthesizing antibodies.

Medical nutrition therapy for MG

Chewing and swallowing often are compromised in MG. Because this compromise
occurs with fatigue, it is important to provide nutritionally dense foods at the beginning
of meals before the patient tires. Small, frequent meals that are easy to chew and
swallow are helpful. Difficulties holding a bolus on the tongue also have been observed,
suggesting that foods that do not fall apart easily may be better tolerated.
For patients treated with anticholinesterase drugs (they inhibit acetylcholinesterase
therefore increasing amount of Ach in the neuromuscular junction), it is crucial to time
medication with feeding to facilitate optimal swallowing.
Physical activity should be limited before mealtime to ensure maximum strength to eat
a meal. It is also important not to encourage food consumption once the patient begins
to fatigue because this may contribute to aspiration.

1.35 Multiple sclerosis (MS)

It is a chronic inflammatory disorder of the central nervous system (CNS) and is one of
the most common causes of non-traumatic disability among young and middle-aged
adults. MS affects the CNS and is characterized by destruction of the myelin sheath,
the function of which is transmission of electrical nerve impulses. Multiple areas of
optic nerves, spinal cord, and brain undergo “sclerosis,” whereby myelin is replaced with
sclera or scar tissue.
Risk factors of MS
Genetics - A familial predisposition to MS has been noted in a minority of cases.
Geographic latitude i.e. prevalence of MS has shown to generally increase the further
one travels from the equator in either hemisphere. This may in part be related to the
various diet people conform to.
Sunshine exposure due to its implication on vitamin D production in the skin. The
degree of sunlight exposure catalyzes the production of vitamin D in the skin. Vitamin D
produced by the skin is eventually metabolized to vitamin D3 which is a selective
immune system regulator and may inhibit MS progression.
Smoking - evidence shows that there is increased risk of development and progression
of MS for smokers.
Medical Nutrition Therapy
Vitamin D status should be assessed by measuring 25-hydroxy vitamin D, and
supplementation may be warranted.
Diet consistency may have to be modified from solids to mechanically soft or pureed
items, even progressing to thick liquids to prevent aspiration due to the neurologic
deficits that occur as the disease progresses.
A diet that is high in fiber with adequate fluid can moderate either diarrhea or
constipation that tends to occur in MS.

1.36 Parkinson’s disease

It is caused by the progressive impairment or deterioration of neurons (nerve cells) in an
area of the brain where dopamine (neurotransmitter that controls the body’s reward and
pleasure centers, it also regulates movement and emotional responses) is produced.
It is characterized by
 Slow and decreased movement  Postural instability
 Muscular rigidity  Decreased dopamine
 Resting tremor transmission
Medical Nutrition Therapy
Goals of MNT
i) To optimize dietary intake particularly to maintain muscle mass for strength
and mobility.
ii) To minimize drug nutrient interactions e.g. anorexia, nausea, reduced sense
of smell, constipation, and dry mouth.
iii) To manage dysphagia that occurs in the late stages of PD
Specific interventions
Fiber and fluid adequacy lessen constipation, a common concern for persons with PD.
Assisted eating may be recommended for patients experiencing tremors, extreme
muscle rigidity.
Sufficient intake of vitamin D3 andomega-3 fatty acids should be recommended.
Anti-inflammatory and neuroprotective effects come from phenolic compounds e.g.
green tea, grapes, turmeric etc.
Vitamin preparations containing pyridoxine should not be taken with doses of L-dopa
(precursor to dopamine used in management of PD).
Manganese should be carefully monitored to avoid excesses above DRI levels as it
reproduces PD symptoms after long and chronic exposure.
1.37 Alzheimers’s disease
It is a progressive, degenerative disease that attacks the brain and impairs thinking,
behavior, and memory. It is associated with loss of neurons, characterized by
microscopic changes in the brain. It is the most prevalent form of dementia resulting
from death of brain cells which are responsible for coordinating memory and cognition.
Diagnosis of Alzheimer’s depends on its characteristic symptoms: the victim gradually
loses memory, reasoning ability, the ability to communicate, physical capabilities, and,
eventually, life itself.
NB: AD is not when one keeps forgetting where one left the keys. It’s when one forgets
how to USE the keys. The “4 As” of AD point to the sequential changes in brain function,
behavior, and performance that impair the individual and ultimately can make adequate
nutritional intake difficult to maintain. The “4 As” of AD are;
i) Amnesia - The inability to use or retain memory, including short-term and long-
term memory.
ii) Aphasia - The inability to use or understand a language.
iii) Apraxia - The inability to use or coordinate purposeful muscle movement or
coordination.
iv) Agnosia - The inability to recognize people, or use common objects.
Risk factors for AD
 Advanced age membranes and proteins.
 A positive family history of AD.  Down’s syndrome
 Suboptimal folate intake or  Low educational level
metabolism  Diabetes mellitus - Hyper-
 The presence of APOE-4 alleles andhypoglycemia as well as
 Female gender unchecked insulin resistance can

 Cardiovascular disease causedamage to brain structures.

 Head injury Medically managing diabetes and

insulin resistance is criticalto
 Free radicals and oxidative stress
delaying progression of dementia of
which results in damage to DNA, cell
 any type.
Nutrition interventions for AD
Caregiver should supervise food planning and mealtimes. Provide well-liked and well-
balanced meals and snacks in a cheerful atmosphere encourages food consumption.
To avoid mealtime disruptions, control distractions such as music, television, children,
and the telephone.
Eating a low-fat diet high in antioxidants, maintaining a normal weight, exercising
regularly, not smoking, and not drinking excessively during adulthood have been shown
to delay or prevent Alzheimer’s disease.
Maintaining social connections and keeping the brain active with lifetime learning will
also help to protect against Alzheimer’s disease. Nearly half of those that live past the
age of 85 will develop this devastating disease. Protection and prevention are essential.
Diets designed to support a healthy heart, which include the omega-3 fatty acids of oily
fish, may benefit brain health as well. Similarly, physical activity supports heart health
and slows the cognitive decline of Alzheimer’s disease.
Depression and forgetfulness can lead to changes in eating behaviors and poor food
intake.

1.38 Spina bifida

It is a neural tube defect that occurs due to the derangement in the formation of the
spinal cord and usually occurs between 26 to 30 days of gestation i.e. the tube fails to
close properly.
The membranes covering the spinal cord and sometimes the cord itself may protrude
from the spine as a sac. Spina bifida often produces paralysis in varying degrees,
depending on the extent of spinal cord damage.
Mild cases may not be noticed. Moderate cases may involve curvature of the spine,
muscle weakness, mental handicaps, and other ills, while severe cases can lead to
death.
The lesion may occur in the thoracic, lumbar, or sacral area and influences the amount
of paralysis. The higher the lesion, the greater is the paralysis. Manifestations range
from weakness in the lower extremities to complete paralysis and loss of sensation.
Other manifestations include: incontinence and hydrocephalus.
Occurrence of spina bifida can be prevented through supplementation of women of
child bearing age with folic acid (400 micrograms) plus multivitamins before conception.
Nutrition implications of spina bifida include;
 Obesity resulting from limited physical activity and refusal of the patients to accept a
wide variety of foods.
 Feeding problems
 Constipation
 Drug nutrient interaction problems.
1.39 Dysphagia as a complication of interest in neurologic disorders
Dysphagia refers to difficulty in swallowing. It is generally caused by either a problem
affecting the muscles involved with swallowing or a physical obstruction between the
mouth and stomach.
Symptoms of dysphagia include;
 Drooling during or following meals
 Choking during or following meals
 Coughing during or following meals
 Inability to suck from a straw
 A gurgly voice quality
 Holding pockets of food in the buccal recesses (of which the patient may be
unaware)
 Absent gag reflex
 Chronic upper respiratory infections
Patients with neurologic disorders are likely to have dysphagia which results from
increased intracranial pressure or intracranial nerve damage leading to poorly
coordinated tongue movements.
There are three phases of swallowing i.e. voluntary/oral phase, pharyngeal phase and
esophageal phase.
Nutrition interventions for dysphagia
Proper positioning for effective swallowing should be encouraged.
Patient should also be encouraged to concentrate on the swallowing process as it
reduces choking.
Diet consistency should also be modified while maintaining the nutritional adequacy
and diet palatability. E.g. a soft, blended or pureed consistency. Generally, foods
included in dysphagia diets should have easy-to-manage textures and consistencies.
To avoid monotony of consuming foods that have a similar consistency, a variety of
flavors and colors can make a meal more appealing should be include.
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