Environmental and Nutritional Disorders: Part IV Flashcards

1
Q

What is primary malnutrition?

A

when something is missing from the diet

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2
Q

what is secondary malnutrition?

A

malabsorption, impaired utilization or storage, or increased need

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3
Q

What is severe acute malnutrition (SAM)?

A

previously known as PEM; it is the consequence of inadequate intake of proteins and calories or deficiencies in the digestion or absorption of proteins

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4
Q

what are the signs of secondary PEM?

A

depletion of subcutaneous fat in the arms, chest wall, shoulders, and metacarpal regions; wasting of the quadriceps and deltoid muscles; ankle or sacral edema

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5
Q

what are the two protein components of PEM?

A

somatic (proteins in skeletal muscles; marasmus) or visceral (organs, primarily liver; kwashiorkor)

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6
Q

what is marasmus?

A

a severe lack of calories; weight is less 60% than the normal limit, growth retardation and muscle loss

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7
Q

what are patients with marasmus at risk for? and what are their albumin levels like?

A

albumin levels are within normal limits; they are anemic and immuno deficient, which leads to infections; the muscle proteins and subQ fat is used as fuel–> so they have emaciated extremities (“large head”)

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8
Q

what is kwashiorkor?

A

decreased protein intake (much more severe)

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9
Q

what does kwashiorkor lead to?

A

hypoalbuminemia–> generalized or dependent edema; immuno deficient and secondary infections

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10
Q

what is the classical presentation of a patient with kwashiorkor?

A

apathy, listless, and loss of appetite; depletion of visceral protein compartment–> fatty liver but sparing of the subQ fat and muscle (normal looking extremities)

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11
Q

what could lead to kwashiorkor in the US? (6)

A

chronic diarrhea, protein losing enteropathies, nephrotic syndrome, extensive burns, fad diets, or replacement of milk with rice-based beverages

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12
Q

what is the dermatological sign of “flaky paint” associated with and what is this?

A

associated with kwashiorkor; alternating zones of hypopigmentation, desquamation, and hyperpigmentation

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13
Q

what is pathognomonic of anorexia?

A

gelatinous transformation of the bone matrix (there will be fat in the bone marrow, and a mucinous matrix material

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14
Q

what are anorexic and bulimic patients more susceptibly to? (complication of both)

A

susceptibility to cardiac arrhythmia and sudden death due to hypokalemia

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15
Q

what are the functions of vitamin A? (3)

A

a component of visual pigment; maintenance of specialized epithelia; maintenance of resistance to infection

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16
Q

what are the syndromes associated with deficiency of vitamin a?

A

night blindness, xerophthalmia, blindness; squamous metaplasia; vulnerability to infection-particularly measles

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17
Q

what is the function of vitamin D? (2 things)

A

facilitates intestinal absorption of calcium and phosphorus and mineralization of bone

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18
Q

what are the deficiency syndromes associated with vitamin d?

A

rickets in children; osteomalacia in adults

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19
Q

what is the function of vitamin K?

A

it is a cofactor in hepatic carboxylation of procoagulants

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20
Q

what are the deficiency syndromes associated with vitamin k?

A

bleeding diathesis

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21
Q

what is the function of vitamin B1 (thiamine)

A

a coenzyme in decarboxylation reactions

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22
Q

what are the syndromes associated with deficiency of vitamin B 1 (thiamine)

A

dry and wet beriberi; wernicke syndrome; korsakoff syndrome

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23
Q

what are the functions of Niacin?

A

it is incorporated into NAD and NADP, which are involved in redox reactions

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24
Q

what are the syndromes associated with deficiency of Niacin?

A

Pellagra- three Ds: dementia, dermatitis, and diarrhea

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25
Q

what is the function of vitamin B 6 (pyridoxine)?

A

its derivatives serve as coenzymes in many reactions

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26
Q

what is associated with a deficiency of vitamin B6 (pyridoxine)?

A

cheilosis, glossitis, dermatitis, peripheral neuropathy, maintenance of myelinization of spinal cord tracts

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27
Q

what is the function of vitamin c?

A

serves in many oxidation-reduction reactions and hydroxylation of collagen

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28
Q

what is the syndrome associated with deficiency of vitamin c?

A

scurvy

29
Q

when might you get a secondary deficiency of vitamin a? (5)

A

with fat malabsorption (diseases such as CYSTIC FIBROSIS, celiac disease, crohn disease, bariatric surgery, or mineral oil laxative)

30
Q

when might a child have a vitamin a deficiency?

A

when they have infections their stores are depleted

31
Q

what is one of the earliest signs of a vitamin a deficiency?

A

night blindness

32
Q

what type of metaplasia occurs with vitamin a deficiency?

A

epithelial to squamous metaplasia and keratinization

33
Q

what is xerophthalmia?

A

dry eye

34
Q

what are bitot spots?

A

build up of keratin

35
Q

what type of metaplasia occurs in the respiratory epithelium with vitamin a deficiency?

A

squamous metaplasia of the respiratory epithelium (this leads to increased pulmonary infections

36
Q

where can metaplasia occur with vitamin a deficiencies?

A

in the eye, in the respiratory tract, and in the urinary tract

37
Q

what type of metaplasia occurs in the urinary tract with vitamin a deficiencies?

A

squamous metaplasia (the desquamation of keratin predisposes to urinary bladder stones)

38
Q

vitamin a deficiency leads to an immune deficiency. What are they more susceptible to dying from? (3)

A

measles, PNA, infectious diarrhea

39
Q

what is acute vitamin a toxicity, what are the symptoms (5) and who might have it?

A

too much vitamin a; headache, dizziness, stupor, blurred vision, confused with psedotumor cerebri; almost always the patient will be from alaska, canada, or Arctic region

40
Q

What are the signs and symptoms of chronic vitamin A toxicity? (5)

A

weight loss, anorexia, n/v, bone and joint pain (because retinoic acid increases osteoclast production and activity)

41
Q

what sign is seen in patients with a vitamin d deficiency?

A

hypocalcemic tetany (a convulsive state caused by insufficient extracellular concentration of ionized calcium, which is required for relaxation of muscles)

42
Q

what are the signs of rickets? (6)

A

frontal bossing, squared head, rachitic rosary, pigeon breast deformity, lumbar lordosis, bowing of the legs

43
Q

what does hypervitaminosis d in kids cause? in adults?

A

metastatic calcifications of soft tissues; bone pain and hypercalcemia; it is considered to be a potent rodenticide in large doses

44
Q

what form of vitamin d do you need?

A

the active form- 1,25(OH)2-D3

45
Q

what are the effects of vitamin C (ascorbic acid) deficiency? (3 things)

A

scurvy, hemorrhages, and healing defects in both children and adults

46
Q

how do we get vitamin c?

A

it is not synthesized endogenously, so we are entirely dependent on the diet for vitamin c; milk, some animal products, fruits and vegetables

47
Q

who is at risk for a secondary deficiency of vitamin c? (3)

A

older individuals who live alone and chronic alcoholics and those who have erratic and inadequate eating patterns

48
Q

when might scurvy occur in a specific population of patients?

A

patients undergoing peritoneal dialysis and hemodialysis

49
Q

what is the function of iron?

A

it is an essential component of hemoglobin as well several different enzymes

50
Q

what is the basis of iron deficiency and what are the clinical features of this?

A

inadequate diet or chronic blood loss; hypochromic microcytic anemia

51
Q

what is the normal BMI range?

A

18.5-25

52
Q

what BMI is considered obese?

A

> 30

53
Q

what BMI is considered overweight?

A

25-30

54
Q

in the energy balance regulatory circuits, what are the effects of the anabolic circuits?

A

to increase food intake and to reduce energy expenditure

55
Q

in the energy balance regulatory circuits, what are the effects of the catabolic circuits?

A

reduce food intake and increase energy expenditure

56
Q

what are the different energy sufficient signals and where do they each come from? (4)

A

leptin (adipocytes in fat), ghrelin (parietal cells in stomach), insulin (beta cells in pancreas), PYY (L cells in intestines)

57
Q

what is the only known gut hormone that increases food intake?

A

ghrelin

58
Q

what is metabolic syndrome? (3 things)

A

abnormalities of glucose and lipid metabolism, HTN, and systemic proinflammatory state

59
Q

Obese persons generally have what? both of which increase the risk of coronary artery disease. (2 things)

A

hypertriglyceridemia and low HDL

60
Q

obesity is associated with what? that could progress to cirrhosis

A

nonalcoholic fatty liver disease (NASH)

61
Q

what is pickwickian syndrome? and what is it associated with? (3 things)

A

hypoventilation syndrome- hypersomnolence, both at night and during the day, often associated with sleep apnea, polycythemia, and eventual right-sided heart failure (cor pulmonale)

62
Q

obese men are at risk for what cancers? (4)

A

esophagus, thyroid, colon, and kidney

63
Q

obese women are at risk for what cancers?

A

esophagus, endometrium, gallbladder, and kidney

64
Q

what does hyperinsulinemia lead to?

A

increased free insulin-like growth factor-1 (IGF-1); the IGF-1 receptor is highly expressed in many human cancers

65
Q

how does IGF-1 contribute to tumor development?

A

it can stimulate cell proliferation and inhibit apoptosis

66
Q

what toxin is produces by fungi that is found on agricultural crops, maize, peanuts, and tree nuts that can lead to what cancer?

A

aflatoxin; can lead to hepatocellular carcinoma

67
Q

nitrosamines and nitrosamides (preservatives) can lead to what cancer?

A

gastric carcinomas

68
Q

high animal fat and low fiber can lead to what cancer?

A

colon cancer

69
Q

what vitamins seem to have an anticarcinogenic effect due to their antioxidant properties? (4)

A

vitamin C, and E, and beta-carotenes and selenium