Kenya Medical Training College

Faculty of Public Health Sciences

Department of Nutrition and Dietetics

Training Manual
For
Diet Therapy III
ACKNOWLEDGEMENT
The exercise of manual development would not have been successful without the contribution
of the following persons. This list is not intended to be exclusive as there may be several other
individuals whose indirect contribution influenced its success. We greatly appreciate all their
contributions.
We acknowledge the main sponsor in this process KMTC for authority, technical team support
and financial support in developing the training manual. We particularly wish to recognize and
sincerely thank the Director, Kenya Medical Training College, Professor Michael Kiptoo for
authorizing the development of the training Manuals, Deputy director academics (Mrs Nancy
Michire), the registrar, Dr. Lucy Waweru, Dr. Solomon Kilaha (Deputy registrar curriculum)
and all Principals.
We also wish to acknowledge the manual development working team that comprised of
Purity Njoki Chege (HoD Nutrition and Dietetics), Jane Nyabuti (D/P/A- Karen), Jacob Omare
(HoD Lodwar), Florence Oloo (HoD Karen), Bonaya Komora (HoD Homabay), Beatrice Tanui
(HoD Kabarnet), Catherine Syombua (HoD Nyandarua), Rebecca Kurui (Kapenguria),
Florence Cherop (Rera), Margaret Mburu (Thika), Janeverlyne Onyango ( Homabay),
Christine Okute (Lodwar), Susan Jelagat (Nakuru), Esther Mbogo (Nairobi), Adelaide
Muraguri (Karen), Emily Wasike (Nairobi), Evalyne Kamau (Karen) and Stella Makau
(Nairobi).

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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
MS Multiple Sclerosis
MSD Musculoskeletal Diseases

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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

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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.

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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
4. 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).

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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 ................................................................................................................. 10
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; ........................................................ 29
UNIT 4: BURNS...................................................................................................................... 35
3.6 Assessment of burns .................................................................................................. 35
3.7 Consequences/implication of burns; ......................................................................... 37
3.8 Nutrition management of burns................................................................................. 38
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

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 5.4 Treatment of cancer;.................................................................................................. 48
5.5 Nutritional care for cancer; ....................................................................................... 51
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 ..................................................................................................... 81
7.8 Guillain-barre syndrome (GBS) ................................................................................ 83
7.9 Myasthenia gravis ..................................................................................................... 83
7.10 Multiple sclerosis (MS) ......................................................................................... 84
7.11 Parkinson’s disease ................................................................................................ 85
7.12 Alzheimers’s disease ............................................................................................. 86
7.13 Spina bifida ............................................................................................................ 87
7.14 Dysphagia as a complication of interest in neurologic disorders .......................... 88
REFERENCES ....................................................................................................................... 90

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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.

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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-

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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.

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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

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 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;

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 • Increased response of trachea and • Excess mucus
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)

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 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.

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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

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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.

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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

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 ✓ 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.

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Page 12
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

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 • 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.
2.1 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

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 • 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.

Page 15
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.
2.2 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.

Page 16
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.
2.3 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;

Page 17
• 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.

Page 18
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.

Page 19
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.

Page 20
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
3.1 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;

Page 21
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

Page 22
 • 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.

Page 23
 • 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.

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Conditions associated with metabolic stress include surgery, cancer and burns.
3.2 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;

Page 25
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.

Page 26
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.
3.3 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

Page 27
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.

Page 28
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.
3.4 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.
3.5 Post-operative complications and implications;
i. Anorexia which leads to low nutrient intake
ii. Immobilization which leads to loss of nutrients e.g. proteins

Page 29
 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.

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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)
• Dumping syndrome occurs in some patients due to removal of > 2/3 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

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 ✓ 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.

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 • 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.

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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.

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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. sulphuric • Cold
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.
3.6 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;

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 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%)

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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’

3.7 Consequences/implication of burns;

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• Hypermetabolism –increased • Loss of fluids ad electrolytes especially in
requirements for energy 2nd to 3rd degree burns or <15 TBSA. In
• Exaggerated protein catabolism and children and the old >10%TBSA.
increased urinary nitrogen loss and • Heat loss
nitrogen loss through Immobilization and • Development of ileus (loss of intestinal
through burnt exudates peristalsis or lack of effective coordinated
• Wasting and weight loss peristalsis)which may be due to reduced
• Anorexia blood flow to the GIT to supply nutrients
• Failure to feed and oxygen
• Generalized discomfort and depression • Infections due to open wounds
• Anaemia
• Malnutrition
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.
3.8 Nutrition management of burns
Aims of nutrition management

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• 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;

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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.

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 • 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

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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

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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
5.1 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)

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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.
5.2 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;

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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

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 • 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.
5.3 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

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 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,

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 • 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.
5.4 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;

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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

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 • 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

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 • 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.

5.5 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

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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.

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• 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.

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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.

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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
6.1 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

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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

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 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.

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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.

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 • 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

6.2 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;

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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

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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.
6.3 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.

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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 jobs
• Joint injury 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;

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• 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

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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.

6.4 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;

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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 in
ii. Feeling weak the morning
iii. Swollen joints vi. Low fever
iv. Lumps under the skin especially on vii. Weight loss
the hands or elbows viii. Fatigue due to anaemia that
accompanies RA

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ix. Loss of energy xi. Loss of appetite
x. Over time decreased range of motion 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 mouth
ii. Bone loss and dry eyes and other eye problems)
iii. Anemia vi. Inflections
iv. Rheumatoid nodules under the 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.

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 • 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.

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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
7.1 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.

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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

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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 e.g. • Certain drugs and poisons
epilepsy, Parkinson’s disease • Secondary to other complex disease
• Viral infection conditions e.g. diabetes, stroke,
• Autoimmune disorder with no known obesity
cause • Mechanical injury e.g. traumatic
• Hormonal disorder brain injury
• Metabolic disorder • Advanced age e.g. Alzheimer’s
• Simple deficiencies or excesses of disease
nutrient e.g. neuropathy associated • Lifestyle factors e.g. alcoholism,
with thiamin deficiency, Wernicke- physical inactivity, diet
Korsakoff syndrome, beriberi, spina • Unknown factors.
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 • Muscle pain
• Muscle wastage • Breathing difficulties
• Muscular cramps • Swallowing difficulties.
• Muscle spasticity (stiffness), which
later causes joint or skeletal
deformities
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 ▪ Inadequate energy intake related to
▪ Chewing difficulty inability to obtain and present food to
the mouth may also occur

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 ▪ Increased energy expenditure ▪ Difficulty with independent eating
▪ Inadequate fluid intake ▪ Underweight
▪ Physical inactivity ▪ Elimination problems
▪ Poor nutritional quality ▪ Inadequate access to food or 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;

7.2 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

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 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

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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.

7.3 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

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 • 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.

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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.

7.4 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

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 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

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 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 words • Change in personality; emotional
• difficulty communicating problems
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 • Pulmonary infections

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• Disability • Institutional care
• Increased length of hospital stay
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.

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7.5 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 • Neonatal jaundice
• Blood-type incompatibility • Anoxia at birth – absence or deficiency of
• Placental insufficiency oxygen reaching the tissues.
• Maternal infection that includes German • Bacterial infections of the mother, fetus,
measles or infant that affect the central nervous
• Viral diseases e.g. German measles system.
(Rubella) • LBW babies
Nutrition implications of CP

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• 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.

7.6 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

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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.

7.7 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 • Overweight
• Mental retardation • Dental problems

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• Thyroid disease • Small oral cavity
• Decreased muscle tone • Short, broad hands with the single palmar
• Hyperflexibility of joints crease
• Speckling of the iris • A wide gap between the first and second
• Upward slant of the eyes toes
• Epicanthal folds

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.

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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.

7.8 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.

7.9 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

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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.

7.10 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

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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.

7.11 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 transmission
• Resting tremor
Medical Nutrition Therapy
Goals of MNT
i) To optimize dietary intake particularly to maintain muscle mass for strength and
mobility.

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 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.

7.12 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.

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Risk factors for AD
• Advanced age • Down’s syndrome
• A positive family history of AD. • Low educational level
• Suboptimal folate intake or metabolism • Diabetes mellitus - Hyper-
• The presence of APOE-4 alleles andhypoglycemia as well as unchecked
• Female gender insulin resistance can causedamage to
• Cardiovascular disease brain structures. Medically managing

• Head injury diabetes and insulin resistance is

• Free radicals and oxidative stress which criticalto delaying progression of

results in damage to DNA, cell dementia of any type.

membranes and proteins.

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.

7.13 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.

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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.
7.14 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

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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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