NUTRITIONAL DISEASES

Question 1

Definition of malnutrition?

Answer 1

Defined by WHO as the cellular imbalance between supply of nutrients and energy and the body’s demand for them to ensure growth , maintenance and specific functions.

Question 2

Forms of Protein energy malnutrition?

Answer 2

• Marasmus
• Kwashiorkor
• caused by inadequate intake of proteins and calories in the body.

Question 3

What is the major difference between Marasmus and Kwashiorkor?

Answer 3

• Marasmus involves starvation with overall deficiency of calories while in Kwashiorkor, the protein deprivation is more severe than deficit in calories.
• Marasmus affects the somatic protein compartment ( skeletal muscles) , while Kwashiorkor affects the visceral compartment.

Question 4

Outline the major clinical features seen in Marasmus patients.

Answer 4

• Wasting of muscle and fat tissue ( skin and bone ) - underweight body.
• Loss of muscle mass and subcutaneous fat leading to emaciation of extremities - the head may appear too large for the body.
• Multivitamin and immune deficiencies leading to concurrent infections.
• Hair appears normal .
• Old man or wizened appearance.
• Thin limbs with little muscle or fat.

Question 5

Outline the major clinical features seen in Kwashiorkor patients.

Answer 5

• Hypoalbuminemia and generalized or dependent edema.
• Loss of weight masked by edema - usually between 60-80% of the normal - usually sparing of muscle and subcutaneous fat.
• Flaky paint appearance of the skin ( alternating zones of hyperpigmentation, desquamation and hypo pigmentation).
• Apathy and listlessness.
• Loss of appetite.
• Vitamin and immune deficiencies .
• Periorbital edema - mat also affect the limbs .
• Flag sign - alternating bands of pale and dark hair.
• Distended abdomen.
• Skin appears shiny and stretched.
• Enlarged fatty liver.
• Atrophy and loss of small intestinal villi leading to concurrent loss of small intestinal enzymes - disaccharidase deficiency.
• Sparse hair.
• Moon face
• Flaky appearance of the skin .
• Little interest in surroundings.

Question 6

Outline some of the features that are similar between Marasmus and Kwashiorkor patients.

Answer 6

• In both , growth failure is evident.
• In both , anaemia may occur.
• In both , the bone marrow appears hypoplastic.
• In both , there is cerebral atrophy.
• In both , there is thymic and lymphoid atrophy, though less marked in Marasmus .

Question 7

State the major signs of Secondary Protein Energy Malnutrition in humans.

Answer 7

• Depletion of subcutaneous fat in arms, chest wall, shoulders or metacarpal regions .
• Wasting of quadriceps and deltoid muscles.
• Ankle or sacral edema .

Question 8

Outline the distinguishing features between manifestations of Marasmus and Kwashiorkor.

Answer 8

• Kwashiorkor occurs in children between 6months - 3 years while Marasmus is common in infants under 1 year of age.
• Kwashiorkor results in muscle wasting with sparing of adipose tissue while in Marasmus all tissues including AT are involved.
• Kwashiorkor causes localized or generalized edema which is absent in Marasmus.
• Enlarged fatty liver seen in Kwashiorkor is absent in Marasmus.
• Kwashiorkor causes atrophy of small bowel and loss of villi and microvilli which is rarely seen in Marasmus.

Question 9

What are the major signs of Cachexia in patients with AIDS and advanced cancer?

Answer 9

• Extreme weight loss.
• Fatigue.
• Muscle atrophy.
• Anemia .
• Anorexia.
• Edema .

Question 10

List down the major chemical mediators produced by tumors which may be implicated in the aetiology of Cachexia.

Answer 10

1. Pro- inflammatory cytokines e.g
   - Tumor Necrosis Factor
   - Interleukin-1 and 6
   - Interferon gamma
2. Proteolysis Inducing Factor
3. Lipid Mobilizing Factor
4. Myostatin
5. Angiotensin II
6. Leptin
7. Glucocorticoids

Question 11

Distinguish between Anorexia Nervosa and Bulimia Nervosa.

Answer 11

Anorexia Nervosa refers to self induced starvation resulting in significant weight loss while Bulimia Nervosa refers to a condition where a patient binges on food and then induces vomiting.

Question 12

Outline the major clinical complications associated with Anorexia Nervosa.

Answer 12

• Endocrine system dysfunction
  – Amenorrhea due to reduced GnRH production.
  – Symptoms of hypothyroidism.
  – Reduced bone density.
  – Dehydration and electrolyte abnormalities.
• Cardiac arrhythmia
• Sudden death dye to hypokalemia.

Question 13

What are the major clinical complications associated with Bulimia Nervosa?

Answer 13

• Mainly occur due to frequent vomiting and chronic use of laxatives and diuretics.
• Electrolyte imbalance.
• Cardiac arrhythmia may occur due to hypokalemia.
• Pulmonary aspiration of gastric content .
• Esophageal and gastric rupture.

Question 14

State the genetic factors that may predispose individuals to obesity.

Answer 14

• Loss of function mutation in leptin.
• Mutation of melanocortin receptor 4 ( MC4R).
• Haplo insufficiency of Braun Derived Neutrophic factor , associated with obesity in WAGR syndrome.

Question 15

Cardinal signs of WAGR syndrome ?

Answer 15

• Wilms Tumor
• Aniridia
• Genitourinary defects
• Mental retardation

Question 16

Distinguish between central and visceral obesity.

Answer 16

Central Obesity (Abdominal Obesity):refers to excess fat accumulation around the abdomen or waist and is often measured by waist circumference or waist-to-hip ratio while Visceral obesity refers to the accumulation of fat around the internal organs, such as the liver, pancreas, and intestines. This type of fat is not as visible as subcutaneous fat, making it more dangerous as it surrounds vital organs.

Question 17

Distinguish between Lifelong Obesity and Adult - Onset Obesity.

Answer 17

• Life long obesity/ hyperplastic obesity begins in childhood and is characterized by increased adipocytes in peripheral parts of the body .
• Adult onset obesity/ hypertrophic obesity is characterized by increased size of fat cells and central obesity. ( Fat accumulates in the trunk )

Question 18

What are the 3 major components of the Neurohormonal mechanisms regulating Energy balance?

Answer 18

• Peripheral/ afferent system
• Arcuate. Nucleus of the Hypothalamus
• Efferent system

Question 19

What are the 2 major subsets of first order neurons in the Arcuate nucleus of the Hypothalamus?

Answer 19

• Pro-opiomelanocortin and CART ( Cocaine and Amphetamine Regulated Transcript) neurons
• Neuropeptide Y and Agouti - Related Peptide neurons

Question 20

Discuss the mechanisms by which POMC & CART neurons promote weight loss .

Answer 20

• Produce the anorexigenic α- MSH , which leads to activation of Melanocortin receptor 3 & 4 in second order neurons.
• 2nd order neurons produce factors such as TRH & CRH which increase BMR and anabolic metabolism, thus favoring weight loss.

Question 21

Describe the mechanism by which Neuropeptide Y and Agouti Related Peptide neurons promote food intake.

Answer 21

• Thet activate Y1/5 receptors in the 2nd order neurons. These neurons then release factors like Melanin Concentrating Hormone and Orexin which stimulate appetite.
• Overall effect - promote food intake and weight gain .

Question 22

State the major roles of Leptin in the body.

Answer 22

• Bind to Leptin receptors in the Hypothalamus to increase energy consumption.
• Stimulates POMC/ CART neurons to produce the anorexigenic Neuropeptide ( MSH) .
• Inhibits NPY/ AGRP neurons , hence reduced food intake.
• Overall effect - suppresses food intake and increases expenditure of calories.
• Functions as a pro - inflammatory cytokine and participates in regulation of hematopoiesis and lymphopoiesis.

Question 23

Mechanisms by which Adiponectin protects against Obesity?

Answer 23

• Directs fatty acids to muscles for their oxidation.
• Decreases influx of fatty acids to the liver and total hepatic triglyceride content .
• Decreases glucose production in the liver causing and increase in insulin sensitivity n
  ( Fat burning molecule/ guardian against Obesity)

Question 24

State the major gut hormones that have a role in obesity.

Answer 24

• Ghrelin - produced in the stomach and Arcuate Hypothalamic nucleus. Increases food intake by stimulating NPY/ AgRP neurons.
• Pancreatic Peptide YY - from endocrine L cells of the ileum and colon . Reduces food intake.
• Amylun - from pancreatic B cells - reduced food intake and weight gain .

Question 25

What is the genetic basis of Hyperphagia and obesity in Prader Eilli Syndrome ?

Answer 25

• Syndrome is caused by loss of imprinted genes in Chromosome 15q11- q13. Hyperphagia and obesity occur due to reduced plasma levels of Pancreatic Peptide YY in individuals with the syndrome.

Question 26

Outline the major adverse consequences of Obesity .

Answer 26

• Hyperinsulinemia and insulin resistance resulting in Type 2 DM.
• Hypertension .
• Hyper triglyceridemia and low HDL&raquo_space; atherosclerosis&raquo_space; coronary heart disease.
• Cholelithiasis.
• Cancer
• Osteoarthritis
• Hypoventilation Syndrome ( Pickwickian Syndrome )

Question 27

Cardinal signs of Hypoventilation ( Pickwickian Syndrome ) ?

Answer 27

• Hypersomnolence ( both at night and during the day )
• Sleep apnea.
• Polycythemia.
• Right sided heart failure ( Cor pulmonale) .

Question 28

Major classification of Vitamins ?

Answer 28

• Fat soluble vitamins - A, D, E , K
• Water soluble vitamins - Vitamin B complex , Ascorbic acid