Nutritional Diseases Flashcards

1
Q

Kwashiorkor’s

A

Depletes the visceral protein compartment

Serum albumin levels are very low - hypoalbuminemia - which causes generalized edema

Occurs when protein sufficiency is relatively more severe than total caloric deficit; occurs in first-born child when second child is born because first is weaned too early and fed a purely carbohydrate diet.

Weight loss masked by edema, so wasting is not as evident; other symptoms include hyper- pigmentation, areas of desquamation, flaky dermatosis, severe anemia, and hair changes.
LOSS OF APPETITE; MENTAL CHANGES; FATTY INFILTRATION OF LIVER.

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2
Q

Marasmus

A

Starvation with deprivation of all nutrients in proportion.

Depletes the somatic protein compartment because muscle proteins are used for fuel; fat is also used, rendering subcutaneous fat absent.

Serum albumin levels are either normal or only slightly reduced.

Extremities are emaciated, anemia, vitamin deficiencies, and possible immune deficiency, leading to concurrent infections. Wasting is quite evident.

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3
Q

Anorexia nervosa

A

Psychiatric disease with self-induced starvation due to obsession with thinness.

Highest death rate of any psychiatric disorder

Signs: amenorrhea, cold intolerance, bradycardia, constipation, and changes in skin and hair.

Major complication: increased susceptibility to cardiac arrhythmia and sudden death, resulting from hypokalemia.

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4
Q

Cachexia

A

A state of profound loss of lean body mass and fat due to cytokines, especially TNF.

Cancer is the most common cause, occurring in 50% of cases. Seen mostly in GI, pancreatic, and lung cancers.

Signs: extreme weight loss, fatigue, muscle atrophy, anemia, anorexia, and edema.

Major complication: Wasting eventually affects diaphragm and other respiratory muscles, leading to death.

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5
Q

Proteolysis-inducing factor

A

A mediator secreted by a tumor that tends the body toward cachexia. Causes skeletal muscle breakdown through the NF-kB-induced activation of the ubiquitin proteasome pathway, which breaks down myofibrils.

A glycosylated peptide excreted in the urine of weight-losing patients with pancreatic, breast, colon, and other cancers

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6
Q

Lipid-mobilizing factor

A

A mediator secreted by a tumor that tends the body toward cachexia. Causes skeletal muscle breakdown through the NF-kB-induced activation of the ubiquitin proteasome pathway, which breaks down myofibrils.

Increases fatty acid oxidation, TNF, and IL-6.

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7
Q

Vitamin A

A

Fat-soluble vitamin stored in liver

Functions: maintenance of normal vision, regulation of cell growth and differentiation, and regulation of lipid metabolism.

Deficiency => order of symptoms: 1) Xerophthalmia (dry eye); 2) Impaired vision, particularly at night; 3) Corneal ulceration; 4) Bitot spots, which are a buildup of keratin debris in small opaque plaques; 5) destruction of the cornea (keratomalacia) and blindness.
Secondary: Squamous metaplasia of mucous-secreting epithelium into a keratinized epithelium as well as loss of mucociliary epithelium of the airways

Healing affects: acne, psoriasis, acute promyelocytic leukemia, and neuroblastoma.

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8
Q

Bitot spots

A

Small opaque plaques that form on the eye due to a build-up of keratin debris that occurs with vitamin A deficiency.

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9
Q

Vitamin D

A

Fat soluble vitamin

Function: Maintains adequate plasma levels of calcium and phosphorous to support metabolic functions, bone mineralization, and neuromuscular transmission.
It also stimulates osteoblasts to synthesize the calcium-binding protein osteocalcin, involved in deposition of calcium during bone development. Vit. D is required to prevent rickets in children and osteomalacia in adults.

Process of metabolism: Vitamin D taken in from food or made endogenously with help of sun. DBP binds and takes it to liver. Vitamin D ==» 25-OH-D in liver, then most active form produced in kidney with conversion of
25-OH-D ==» 1, 25-dihydroxyvitamin D by 1-alpha-hydroxylase.

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10
Q

Regulation of 1,25-dihydroxyvitamin D in kidney

A

Hypocalcemia causes secretion of PTH, which activates 1-alpha-hydroxylase

Hypophosphatemia directly activates 1-alpha-hydroxylase

Negative feedback of 1, 25-dihydroxyvitamin D by itself - inhibits 1-alpha-hydroxylase

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11
Q

1, 25-dihydroxyvitamin D and calcium

A

Vitamin D stimulates intestinal absorption of calcium

Vitamin D encourages calcium reabsorption in the kidney

Vitamin D maintains saturated levels of calcium and phosphorous in the plasma. It works with PTH to induce osteoclasts to dissolve bone and release calcium and phosphorous into the circulation.

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12
Q

Who can make 1,25-dihydroxyvitamin D?

A

Macrophages, keratinocytes, and tissues such as breast, prostate, and colon.

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13
Q

Vitamin D and infections

A

Pathogen-induced activation of TLRs in macrophages causes increased expression of vitamin D receptor and CYP27B (vitamin D synthesizer in mitochondria), leading to vitamin D synthesis. Studies show that vitamin D can increase lymphocyte counts and enhance clearance of Mycobacterium tuberculosis.

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14
Q

Result of hypervitaminosis D

A

Children: metastatic calcification of soft tissues (kidney)

Adults: bone pain and hypercalcemia

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15
Q

POMC/CART neurons

A

provide the anorexigenic signal - the one that tells you you’re full.

Stimulated by leptin

These guys enhance energy expenditure and weight loss through the production of anorexigenic alpha-melanocyte-stimulating hormone (MSH), and the activation of melanocortin receptors 3, and 4. MSH and MC3/4R then produce TSH and CRH, which increase metabolic basal rate and anabolic metabolism, thus favoring weight loss.

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16
Q

Leptin

A

Secreted in response to abundant adipose tissue; travels to hypothalamus and stimulates the POMC/CART neurons while inhibiting the NPY/AgRP neurons.

Increases energy expenditure by stimulating physical activity, energy expenditure, and thermogenesis.

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17
Q

NPY/AgRP

A

provide orexigenic signals (the ones that tell you you’re hungry) and promote weight gain

Inhibited by leptin

These guys activate Y1/5 receptors in secondary neurons, which in turn release facts such as melanin-concentrating hormone (MCH) and orexin, which stimulate appetite.

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18
Q

Stable weight vs. inadequate weight ==> relationship to leptin

A

stable weight: POMC/CART and NPY/AgRP pathways are balanced

Inadequate stores of body fat: leptin secretion is diminished and food intake is increased.

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19
Q

PYY (Peptide YY)

A

Satiety signal

Released post-prandially by endocrine cells in the ileum and colon

20
Q

Ghrelin

A

Meal-initiating signal/Stimulates appetite

Produced in the stomach

21
Q

Normal weight BMI

A

18.5 - 24.9 kg/m2

22
Q

Over-weight BMI

A

25 - 29.9 kg/m2

Asians: 23-24.9

23
Q

Obesity BMI

A

30 - 39.9 kg/m2

Asians: greater than 25

24
Q

Morbid Obesity BMI

A

40 or greater kg/m2

25
Q

How to assess abdominal obesity

A

Measure BMI and waist circumference

26
Q

Patients with abdominal obesity are at increased risk for:

A

heart disease, diabetes, hypertension, and dyslipidemia

27
Q

Atherosclerosis

How are obesity and atherosclerosis linked?

A

Microscopic: look for thickening of artery with cholesterol clefts and a fibrous cap.

28
Q

Metabolic Syndrome: definition and prevalence

A

Diabetes mellitus, hypertension, dyslipidemia, and abdominal (male pattern) obesity (AKA: trancal or central). Need at least two of these criteria to have metabolic syndrome.

It is pro-inflammatory and pro-thrombotic.

Highest in native Americans, then Hispanics, African-Americans, and whites.

29
Q

Elevated levels of which cytokines persist in metabolic syndrome?

A

CRP, IL-1, IL-6, IL-18, TNF, and plasminogen activator inhibitor-1

30
Q

Adiponectin

AKA: “fat-burning molecule”

A

An anti-inflammatory cytokine produced exclusively by adipocytes. It enhances insulin sensitivity, inhibits steps in the inflammatory process, and directs fatty acids to muscle for their oxidation.

Reduced levels in metabolic syndrome.

31
Q

Possible to get rid of metabolic syndrome?

A

Yes! Diet and exercise!

32
Q

Non-alcoholic fatty liver disease

A

Consistently associated with insulin resistance and the metabolic syndrome.

Microscopic: Look for adipoctyes in liver.

33
Q

How do triglycerides accumulate in hepatocytes?

A

1) Impaired oxidation of fatty acids
2) Increased synthesis and uptake of fatty acids
3) Decreased hepatic secretion of very-low-density-lipoprotein cholesterol

34
Q

Gallstones

A

Two types: 1) most common => cholesterol stones (as bile formation is the only significant pathway for elimination of excess cholesterol from the body) and 2) pigment stones.

Qualifications: female, 40s, fertile, and fat.

35
Q

Raynaud phenomenon

A

Abnormal vasoconstriction of digital arteries that cuts off arterial blood inflow, resulting in pallor. Deoxygenation of residual blood in fingertips causes cyanosis. Reperfusion causes hyperemia.

Benign, unless you’ve got scleroderma with it.

36
Q

Anti-dsDNA

A

Systemic lupus erythematosus

37
Q

Anti-Sm

A

Systemic lupus erythematosus

38
Q

Anti-RNP U1

A

Systemic lupus erythematosus

39
Q

Anti-SS-A (Ro)

A

Sjorgren syndrome and systemic lupus erythematosus

40
Q

Anti-SS-B (La)

A

Sjogren Syndrome and systemic lupus erythematosus

41
Q

Anti-Scl-70

A

Systemic sclerosis

42
Q

Anti-centromere

A

Limited scleroderma and systemic sclerosis

43
Q

Osteoarthritis

A

The continually increased pressure on the cartilage in weight-bearing joints causes pressure atrophy, progressing to injury and necrosis.

44
Q

Breast cancer

A

Gross pathology: A stellate tan-white lesion surrounded by yellow fat.

Microscopic: Adipose cells next to tumor cells

Possible causes for its development in obese people:

1) Fat tissue produces excess estrogen, which is associated with the risk of breast, endometrial, and some other cancers
2) Obese people have increased levels of insulin and insulin-like growth factor-1 (IGF-1) in their blood
3) Fat cells produce adipokines that stimulate cell growth
4) Leptin, more prevalent in obese people, promotes cell proliferation
5) Fat cells may have effects on mTOR
6) Obese people have chronic, low-level inflammation

45
Q

Amylin

A

A peptide secreted from pancreatic beta cells that stimulates POMC/CART neurons in the hypothalamus, causing a decrease in food intake.

May be used to help obese people lose weight in the future.