Nutritional Disorders

Chapter 7 Nutritional Disorders



I. Nutrient and Energy Requirements in Humans

A. Recommended dietary allowance (RDA)

1. Optimal dietary intake of nutrients that under ordinary conditions will keep the general population in good health

2. Varies with sex, age, body weight, diet, and physiologic status


B. Daily energy expenditure (DEE)

1. Factors influencing DEE

a. Basal metabolic rate (BMR)

b. Thermic effect of food

c. Physical activity

2. BMR


BMR: most important factor in determining daily energy expenditure


a. Accounts for ∼︀60% of DEE

b. Energy consumption involved in normal body functions

• Examples—cardiac function, maintaining ion pumps

c. Body weight is the most important factor determining BMR.

d. Thyroid function alters the BMR.

• BMR is increased or decreased in hyperthyroidism and hypothyroidism, respectively.


BMR: ↓ hypothyroidism, ↑ hyperthyroidisim


3. Thermic effect of foods

• Energy used in digestion, absorption, and distribution of nutrients

4. Degree of physical activity

II. Dietary Fuels

A. Carbohydrates

1. Glucose

a. Stored primarily as glycogen in liver and muscle

b. RBCs use only glucose for energy.

c. Complete oxidation produces 4 kcal/g.

2. Enzymatic digestion


Carbohydrate digestion: begins in the mouth; 4 kcal/g


a. Begins in the mouth (amylase)

b. Pancreatic amylase

• In chronic pancreatitis, carbohydrates are not malabsorbed due to predigestion by salivary amylase.


Disaccharidases: lactase, maltase, Sucrase


c. Brush border intestinal enzymes (disaccharidases)

(1) Hydrolyze lactose (galactose + glucose), maltose (glucose + glucose), and sucrose (fructose + glucose)

(2) Disaccharidases produce glucose, galactose, and fructose.


Disaccharidases: produce glucose, galactose, fructose


B. Proteins

1. Amino acids are substrates for gluconeogenesis.


Amino acids: substrates for gluconeogenesis


a. Transaminases remove amine groups to form corresponding α-ketoacid.

b. Examples—alanine becomes pyruvate, aspartate becomes oxaloacetic acid

2. Digestion

a. Begins in the stomach (pepsin and acid)


Protein digestion: begins in the stomach; pepsin and acid


b. Pancreatic proteases (e.g., trypsin) and peptidases release amino acids.

3. Complete oxidation produces 4 kcal/g.

C. Fats

1. Triglycerides

a. Major dietary lipids

b. Major source of energy for cells except RBCs and brain

2. Essential fatty acids (FAs)

a. Linolenic acid (ω-3) is cardioprotective.

b. Linoleic acid (ω-6) is required for synthesis of arachidonic acid.


Essential FAs: linolenic, linoleic acids


c. Deficiency of essential fatty acids

(1) Scaly dermatitis, hair loss

(2) Poor wound healing

3. Digestion of dietary triglyceride (TG)


Fat digestion: begins in the small intestine


a. Occurs primarily in the small intestine

(1) Hydrolyzed by pancreatic lipase

• Produces monoglycerides (MGs) and FAs

(2) Bile salts/acid produce micelles to enhance reabsorption by villi.


Fat digestion: pancreas → bile salts/acids → intestinal cells


• Contain MGs, FAs, fat-soluble vitamins, and cholesterol esters

(3) Intestinal cells resynthesize TG and package it into chylomicrons, which enter the blood.

• Formation and secretion of chylomicrons requires apolipoprotein B48.

b. Complete oxidation produces 9 kcal/g.

III. Protein-Energy Malnutrition (PEM)

A. Kwashiorkor

1. Pathogenesis

a. Inadequate protein intake


Kwashiorkor: inadequate protein intake


b. Adequate caloric intake consisting mainly of carbohydrates

c. Protein in liver and other organs (i.e., visceral protein) is decreased.

d. Muscle protein (i.e., somatic protein) is relatively unchanged.

• Carbohydrates are protein sparing (source of energy)

2. Clinical findings (Fig. 7-1, left)

a. Pitting edema and ascites

image

7-1: Kwashiorkor and marasmus. Left, Child with kwashiorkor, showing dependent pitting edema involving the lower legs. Right, Child with marasmus, showing “broomstick” extremities with loss of muscle mass and subcutaneous tissue.


(From Forbes C, Jackson W: Color Atlas and Text of Clinical Medicine, 2nd ed. St. Louis, Mosby, 2003, p 343, Fig. 7-138.)



Pitting edema is characteristic of kwashiorkor


• Caused by hypoalbuminemia and loss of plasma oncotic pressure

b. Fatty liver


Kwashiorkor: fatty liver– ↓ apoB synthesis; ↑ VLDL synthesis


(1) Decreased synthesis of apolipoproteins

• Apolipoprotein B-100 is required for assembly and secretion of very low density lipoproteins (VLDLs) in the liver.

(2) Increased synthesis of VLDL from glycerol 3-phosphate

c. Diarrhea

• Caused by loss of the brush border enzymes and parasitic infections

d. Anemia and defects in cell-mediated immunity (CMI)

B. Marasmus

1. Pathogenesis


Marasmus: total calorie deprivation


a. Dietary deficiency of both protein and carbohydrates

b. Decrease in somatic protein (muscle protein)

2. Clinical findings (see Fig. 7-1, right)

a. Extreme muscle wasting (“broomstick extremities”)


Extreme muscle wasting is common in marasmus.


(1) Breakdown of muscle protein for energy

(2) Loss of subcutaneous fat

b. Growth retardation; anemia; defects in CMI

IV. Eating Disorders and Obesity

A. Anorexia nervosa

1. Pathogenesis

a. Self-induced starvation leading to PEM (Fig. 7-2)

b. Distorted body image

image

7-2: Anorexia nervosa. Note the loss of muscle and subcutaneous tissue consistent with total calorie deprivation.


(From Forbes C, Jackson W: Color Atlas and Text of Clinical Medicine, 2nd ed. St. Louis, Mosby, 2003, p 344, Fig. 7-141.)



Anorexia nervosa: distorted body image


2. Clinical findings

a. Secondary amenorrhea

(1) Decreased gonadotropin-releasing hormone

• Caused by excessive loss of body fat and weight

(2) Decreased serum gonadotropins produces hypoestrinism.

b. Osteoporosis


Anorexia nervosa: secondary amenorrhea; osteoporosis


(1) Caused by hypoestrinism

• Estrogen normally enhances osteoblastic activity and inhibits osteoclastic activity.

(2) Lack of estrogen leads to decreased osteoblastic activity and increased osteoclastic activity.

c. Increased lanugo (fine, downy hair)

d. Increased hormones associated with stress (e.g., cortisol, growth hormone)


Most common cause of death in anorexia nervosa: ventricular arrhythmia


e. Most common cause of death is ventricular arrhythmia

B. Bulimia nervosa

1. Pathogenesis

• Bingeing with self-induced vomiting

2. Clinical findings

a. Possible complications of vomiting

(1) Acid injury to tooth enamel

(2) Hypokalemia and metabolic alkalosis


Vomiting in bulimia nervosa: produces hypokalemic metabolic alkalosis


b. Ventricular arrhythmia is the most common cause of death.

C. Obesity

1. Body mass index (BMI) ≥ 30 kg/m2 (normal, 18.5–24.9 kg/m2)

a. BMI = weight (kg)/height (m2)


BMI: weight (kg)/height (m2)


b. Other factors than body weight

(1) Excess fat in the waist and flanks is more important than an excess in the thighs and buttocks.

(2) Excess visceral fat in the abdominal cavity has greater significance than excess subcutaneous fat.


Obesity: abdominal visceral fat most important


• Magnetic resonance imaging is used to access the amount of visceral fat.

2. Pathogenesis

a. Genetic factors account for 50% to 80% of cases.

• Examples—defects in the leptin gene, syndrome X (obesity, hypertension, diabetes)

b. Acquired causes

(1) Endocrine disorders—hypothyroidism, Cushing syndrome

(2) Hypothalamic lesions, menopause

c. Leptin


Leptin: hormone; maintains energy balance (intake and output)


(1) Leptin is a hormone.

(a) Secreted by adipose tissue

(b) Maintains energy balance (intake and output)

(2) Leptin secretion increases when adipose stores are increased.


3500 calorie excess = 1 pound


(a) Decreases food intake (via hypothalamus)

(b) Increases energy expenditure (e.g., ↑ β-oxidation of fatty acids)

(3) Leptin secretion decreases when adipose stores are decreased.

(a) Increases food intake (via hypothalamus)

(b) Decreases energy expenditure (e.g., ↓ β-oxidation of fatty acids)

(4) Obesity related to leptin dysfunction may be caused by the following:

Leptin gene: often defective in obesity


(a) Resistance to leptin effects

(b) Mutations resulting in inhibition of leptin release

3. Clinical findings (Table 7-1)


Table 7-1 Clinical Findings Associated with Obesity

image


Obesity: ↑ adipose causes ↓ synthesis insulin receptors


V. Fat-Soluble Vitamins

• Vitamins A, D, E, and K are fat soluble.

A. Vitamin A

Related posts:

  1. White Blood Cell Disorders
  2. Vascular Disorders
  3. Genetic and Developmental Disorders
  4. Red Blood Cell Disorders

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Jun 25, 2017 | Posted by in PATHOLOGY & LABORATORY MEDICINE | Comments Off on Nutritional Disorders

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