Nutritional Disorders Flashcards

1
Q

State the two protein compartments of the body and give a brief description of each.

A

(1) Somatic protein compartment
☛ Primarily found in skeletal muscles.
☛ Provides structural support and is involved in movement and physical activity.
☛ This compartment is relatively homogenous, meaning it consists mostly of similar types of proteins.

(2) Visceral protein compartment
☛ Found within the organs (such as the liver, pancreas, and kidneys), as well as in blood cells (like granulocytes and lymphocytes) and serum proteins.
☛ Plays a crucial role in metabolic processes, immune function, and maintaining homeostasis.
☛ This compartment is more heterogeneous, containing a wide variety of proteins that serve different structural and functional roles.

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2
Q

Briefly discuss primary and secondary causes of malnutrition.

A

Primary causes are related to diet. Secondary causes are due to nutrient malabsorption, impaired nutrient utilization or storage, excess nutrient losses and increased need for nutrients.

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3
Q

What are two main clinical syndromes brought about by protein-energy malnutrition?

A

Marasmus, Kwashiokor

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4
Q

clinical features of marasmus

A

✓ weight is less than 60% of normal
✓ loss of muscle mass and subcutaneous fat resulting in emaciation of extremeties
✓ head appears too large for the body
✓ serum protein is normal
✓ no edema
✓ associated with anemia, multivitamin deficiencies and immune deficiency
[Image 1] [Image 2]

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5
Q

clinical presentation of Kwashiokor

A

Edema: Swelling with fluid, especially in the ankles and feet
Ascites: build-up of fluid in the abdominal cavity
Hair changes: Dry, brittle hair, hair loss, and loss of pigment in hair
Dermatitis: Dry, peeling skin, scaly patches, or red patches
Enlarged liver: Often a symptom of fatty liver disease
Depleted muscle mass: Despite retaining subcutaneous fat (under the skin)
Dehydration: Due to poor intake and loss of fluids
[Image 1] [Image 2]

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6
Q

Discuss protein-energy malnutrition in the developed world. [vulnerable populations, signs]

A

✓ This type of PEM develops in chronically ill, older and bed-ridden patients and people with eating disorders.
✓ Obvious signs of secondary PEM include:
☛ depletion of subcutaneous fat in arms, chest wall, shoulders or metacarpal regions.
☛ wasting of quadriceps and deltoid muscles
☛ ankle or sacral edema

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7
Q

discuss cachexia

A

✓ This is a type of PEM in patients with chronic diseases such as AIDS, advanced cancer, congestive heart failure, chronic obstruction pulmonary disease (COPD) and chronic kidney disease.
✓ It is characterized by extreme weight loss, fatigue, muscle atrophy, anemia, anorexia and edema.

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8
Q

discuss anorexia nervosa

A

🍔 Self induced starvation resulting in marked weight loss.
🍔 Clinical features are similar to severe PEM and they include:
✓ extreme weight loss and thin appearance
✓ fatigue and insomnia
✓ amenorrhea (GnRH secretion decreases)
✓ symptoms of hypothyroidism
✓ bone density decreases [osteoporosis]
✓ dehydration and electrolyte abnormalities
✓ cardiac arrhythmias and hypokalemia

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9
Q

Discuss bulimia nervosa.

A

📝 Bulimia nervosa is an eating disorder characterized by episodes of binge eating followed by compensatory behaviors such as vomiting, excessive exercise, or the use of laxatives to prevent weight gain.

📝Clinical features:
- recurrent episodes of binge eating
- self-induced vomiting, misuse of laxatives
- preoccupation with body shape and weight
- normal or slightly above normal body weight

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10
Q

What is obesity?

A

Obesity is defined as an accumulation of adipose tissue that is of sufficient magnitude to impair health.

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11
Q

Define:
(a) orexigenic factors
(b) anorexigenic factors

A

(a) orexigenic factors: Factors which increase appetite and stimulate food intake.
(b) anorexigenic factors: Factors that decrease appetite and reduce food intake.

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12
Q

Pathophysiology of Obesity, Afferent system of energy homeostasis

Briefly explain the role of each of the following in energy homeostasis [also state where they are produced]:
(a) leptin
(b) ghrelin

A

(a) leptin
Leptin is a hormone produced by adipose (fat) tissue. It plays a crucial role in regulating energy balance by inhibiting hunger, which in turn reduces food intake and promotes energy expenditure. Leptin signals the hypothalamus in the brain about the amount of energy stored in fat cells. When fat stores are sufficient, leptin levels increase, signaling the brain to reduce appetite and increase energy expenditure.
[Diagram 1] [Diagram 2] [Diagram 3]

(b) ghrelin
Ghrelin is known as the “hunger hormone” because it stimulates appetite. It is produced mainly in the stomach and signals the hypothalamus to increase food intake. Ghrelin levels rise before meals and fall after eating. It also promotes the release of growth hormone and plays a role in regulating energy balance by increasing food intake and reducing energy expenditure.
[Diagram 4] [Diagram 5] [Diagram 6] [Diagram 7]

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13
Q

Pathophysiology of Obesity, Afferent system of energy homeostasis

Briefly explain the role of each of the following in energy homeostasis:
(a) peptide YY
(b) glucagon-like peptide
(c) insulin

A

(a) Peptide YY
Peptide YY is a hormone released by the cells in the ileum and colon in response to eating. It helps to reduce appetite and inhibit gastric motility. PYY acts on the hypothalamus to decrease food intake and increase satiety. It is part of the body’s mechanism to signal fullness and reduce further food intake after a meal.

(b) Glucagon-Like Peptide-1 (GLP-1)
GLP-1 is an incretin hormone produced in the gut in response to food intake. It enhances insulin secretion, inhibits glucagon release, and slows gastric emptying, which helps to regulate blood glucose levels. GLP-1 also acts on the brain to promote satiety and reduce food intake, playing a significant role in energy homeostasis.

(c) Insulin
Insulin is a hormone produced by the pancreas that regulates blood glucose levels. It facilitates the uptake of glucose into cells for energy production and storage as glycogen in the liver and muscle. Insulin also inhibits the breakdown of fat and protein. In the brain, insulin signals the hypothalamus to reduce food intake and increase energy expenditure, thus playing a key role in maintaining energy balance.

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14
Q

Pathophysiology of Obesity, CPS of Energy Homeostasis

Where is the central processing system for energy homeostasis located?

A

The central processing system for energy homeostasis is located in the arcuate nucleus of the hypothalamus.

Hypothalamic nuclei recap:
[Diagram 1] [Diagram 2] [Diagram 3]

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15
Q

Pathophysiology of Obesity, CPS of Energy Homeostasis

What is the function of the central processing system in energy homeostasis?

A

The central processing system integrates neurohumoral signals from the periphery to generate efferent signals that regulate food intake and energy expenditure.

Further notes:
Neurohumoral refers to the interaction between the nervous system and the endocrine system, particularly involving the release of hormones or neurotransmitters.

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16
Q

Pathophysiology of Obesity, CPS of Energy Homeostasis

What are the two types of first-order neurons involved in central processing?

A

The two types of first-order neurons are Pro-Opiomelanocortin (POMC) and Cocaine and Amphetamine-Regulated Transcript (CART) neurons, and Neuropeptide Y (NPY) and Agouti-Related Peptide (AgRP) neurons.
[Diagram 1] [Diagram 2] [Diagram 3]

Further notes:
🍔 POMC is a precursor polypeptide that is cleaved into several active peptides, including:
➤ Melanocyte-Stimulating Hormones (MSHs)
➤ Adrenocorticotropic Hormone (ACTH)
➤ β-Endorphin
These peptides play various roles in the body, such as regulating skin pigmentation, stress response, and pain modulation. In the brain, POMC neurons are primarily located in the arcuate nucleus of the hypothalamus and are involved in reducing appetite and increasing energy expenditure.

🍔 CART is another neuropeptide that is co-expressed with POMC in certain neurons. It is involved in:
➤ Inhibiting appetite
➤ Regulating reward and stress responses
CART neurons are also found in the arcuate nucleus and work alongside POMC neurons to help maintain energy homeostasis.

17
Q

Pathophysiology of Obesity, CPS of Energy Homeostasis

What are the two types of second-order neurons involved in central processing?

A

The two types of second-order neurons are neurons with Melanocortin Receptors 3 and 4 (MC3/4R) [Melanocortin Receptor Expressing Neurons] and neurons with Y1 and Y5 receptors [Neuropeptide Y (NPY) and Agouti-Related Peptide (AgRP) Receptor-Expressing Neurons].

[Diagram 1] [Diagram 2] [Diagram 3]

18
Q

Pathophysiology of Obesity, CPS of Energy Homeostasis

How do POMC/CART neurons promote satiety and energy expenditure?

A

When activated, POMC/CART neurons release alpha-melanocyte-stimulating hormone (α-MSH), which acts on melanocortin receptors (MC3/4R) on second-order neurons to promote satiety and energy expenditure.

[Diagram 1] [Diagram 2] [Diagram 3]

19
Q

Pathophysiology of Obesity, CPS of Energy Homeostasis

What is the function of NPY [Neuropeptide Y] / AgRP [Agouti-related Peptide] neurons?

A

NPY/AgRP neurons stimulate food intake and reduce energy expenditure.

[Diagram 1] [Diagram 2] [Diagram 3]

20
Q

Pathophysiology of Obesity, CPS of Energy Homeostasis

How do NPY/AgRP neurons increase appetite and decrease energy expenditure?

A

NPY/AgRP neurons release NPY and AgRP, which act on Y1 and Y5 receptors on second-order neurons to increase appetite and decrease energy expenditure. AgRP also antagonizes the effects of α-MSH on MC3/4R, further promoting food intake.

[Diagram 1] [Diagram 2] [Diagram 3]

21
Q

Pathophysiology of Obesity, CPS of Energy Homeostasis

What is the function of neurons with Melanocortin Receptors 3 and 4 (MC3/4R)?

A

These neurons receive signals from POMC/CART neurons and are involved in reducing food intake and increasing energy expenditure, contributing to the catabolic pathway.

[Diagram 1] [Diagram 2] [Diagram 3]

22
Q

Pathophysiology of Obesity, CPS of Energy Homeostasis

What is the function of neurons with Y1 and Y5 receptors?

A

These neurons receive signals from NPY/AgRP neurons and are involved in increasing food intake and reducing energy expenditure, contributing to the anabolic pathway.

23
Q

Pathophysiology of Obesity, CPS of Energy Homeostasis

How does Agouti-Related Peptide (AgRP) affect energy homeostasis?

A

AgRP, released by NPY/AgRP neurons, antagonizes the effects of α-MSH on MC3/4R, promoting food intake and reducing energy expenditure.

[Diagram 1] [Diagram 2] [Diagram 3]

24
Q

How are POMC/CART neurons and NPY/AgRP neurons stimulated respectively?

A

POMC/CART neurons are stimulated by signals that indicated energy sufficiency/satiety e.g. leptin, insulin and serotonin.

NPY/AgRP neurons are stimulated by signals indicating energy deficiency or hunger e.g. ghrelin, low leptin levels and low insulin levels.

25
Q

What are some clinical consequences of obesity?

A

🍔 Obesity is associated with insulin resistance and hyperinsulinemia
🍔 Obese persons generally have hypertriglyceridemia and low HDL cholesteral levels.
🍔 Non-alcoholic fatty liver
🍔 Cholelithiasis (gallstones) [is six times more common in obese than in lean subjects. The obesity associated increase in total body cholesterol and cholesterol turnover leads to elevated biliary excretion of cholesterol in the bile, which in turn predisposes affected persons to the formation of cholesterol-rich gallstones.]
🍔 Obstructive sleep apnea
🍔 Right-sided heart failure
🍔 Osteoarthritis

26
Q

Briefly discuss effects of Vitamin A deficiency.

A

🥕 Night blindness
🥕 Xerophthalmia due to corneal epithelial metaplasia [the normal lacrimal and mucus-secreting epithelium is replaced by keratinized epithelium]
🥕 Bitot spots and Keratomalacia
🥕 Complete blindess
🥕 Metaplasia of epithelium of upper respiratory passages, and hence loss of mucociliary epithelium, predisposes to secondary pulmonary infections
🥕 Immune deficiency

27
Q

Briefly discuss chronic and acute effects of Vitamin A toxicity.

A

Acute Vitamin A toxicity: headache, dizziness, vomiting, stupor, blurred vision
Chronic Vitamin A toxicity: weight loss, anorexia, nausea, vomiting, bone and joint pain