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Flashcards in metabolic and nutritional mechanisms Deck (31)
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1
Q

protein energy metabolism (PEM)

A
  • lead to malnutrition
  • increase susceptibility to infectious diseases
  • determined by body mass index - malnutrition below 16
2
Q

marasmus

A

PEM syndrome

  • somatic protein –> proteins in skeletal muscle
  • prevent loss of visceral protein, but depleted carbs
  • growth retardation, emaciation, large head, immune deficiency, anemia
3
Q

kwashiorkor

A

PEM syndrome

  • visceral protein –> proteins in visceral organs (ex. liver)
  • loss of visceral protein, but have plenty of carbs
  • edema, swollen abdomen due to hypoalbuminemia and fatty liver, hypovolemic shock, heart failure
4
Q

cachexia

A

occur with tumors and chronic inflammatory rxns
-proteolysis inducing factor (PIF) and pro inflammatory cytokines (TNF, IL-6) –> skeletal muscle breakdown via NFkB activation of proteasome

5
Q

anorexia nervosa

A

self induced starvation

  • severe PEM with effects on endocrine system
  • amenorrhea from low GnRH, LH, FSH
  • decreased thyroid hormone and bond density
  • cardiac arrhythmia and sudden death
6
Q

bulimia

A

binging on food and induced vomiting

-menstrual irregularities, electrolyte imbalances, pulmonary aspiration, esophageal and gastric rupture

7
Q

fat soluble vitamins

A
  • stored in adipose and liver

- not excreted –> vit. A, D can build up and become toxic

8
Q

folic acid (vitamin B9)

A
  • needed for maturation of hematopoietic cells
  • deficiency common in alcoholics and pregnancy
  • can make RNA, but not DNA –> megaloblastic anemia
  • can become deficient quickly
9
Q

vit. B12 (cobalamin)

A
  • associated with folate
  • convert homocysteine to methionine
  • degrades FAs –> accumulation of FAs (neurologic conditions) if deficient
  • important for neurological function
  • long stores in body - not deficient quickly
  • pernicious anemia w/ no parietal cells or IF
10
Q

microcytic vs. macrocytic anemia

A

microcytic –> vit. B6 deficiency

macrocytic –> vit. B9 deficiency

11
Q

pyridoxine deficiency (vit. B6)

A
  • coenzyme for amino acid metabolism
  • deficiency –> microcytic anemia
  • toxicity –> sensory neuropathy
12
Q

thiamine (vit. B1)

A
  • decarboxylation rxns and energy metabolism in nervous system
  • wernicke Korsakoff –> memory loss, loss of balance
  • beriberi (sever) –> wet (cardiovascular) or dry (nervous system); tachycardia, convulsions, confusion, paralysis
13
Q

niacin (vit. B3)

A
  • coenzymes in oxidation/reduction rxns (OXPHOS, ETC)
  • deficiency –> pellagra
  • supplementation lowers VLDL, LDL and increase HDL
14
Q

riboflavin (B2)

A
  • active forms of FMN and FAD

- coenzymes for oxidation/reduction rxns

15
Q

biotin (B7)

A
  • coenzyme for carboxylation rxns (carry CO2)

- supplied by intestinal bacteria

16
Q

pantothenic acid (B5)

A

-CoA –> transfer acyl groups

17
Q

vitamin A (retinol)

A

vision, reproduction, growth, epithelial tissues

  • stored in liver, bound to retinol binding protein
  • absorbed by bile and pancreatic enzymes –> chylomicrons and apolipoprotein E
18
Q

major functions of Vitamin A

A
  1. maintain normal vision
    - rhodopsin for night vision
    - photopsins for color vision
  2. cell growth and differentiation
    - epithelial growth and differentiation
    - retinoids used for acne, psoriasis, and acute promyelocytic leukemia
19
Q

deficiency and toxicity of vitamin A

A
  1. deficiency
    - night blindness, epith. metaplasia and keratinization, xerophthalmia, bitot spots, keratomalacia, respiratory and urinary tract infections
  2. overdose
    - liver cirrhosis, teratogen
20
Q

vitamin D

A
  • 1,25 dihydroxycholecalciferol (active)
  • ergocalciferol in plants, D2
  • cholecalciferol in animals, D3
  • most formed from UV exposure
  • PTH dependent to convert to final active form in kidney
21
Q

metabolism of vit. D

A
  • can get D3 from diet or UV light
  • bind to vit. D binding protein to transport to liver
  • increase Ca++ and phosphate absorption in small intestine
  • increase RANKL in osteoblasts –> activate osteoclasts and produce osteocalcin
  • regulate in kidney by 1alpha-hydroxylase
  • maintain plasma Ca++
  • prevent hypocalcemia tetany etc.
22
Q

deficiency and toxicity of vit. D

A
  1. deficiency - osteomalacia and rickets

2. toxicity - renal stones

23
Q

vitamin C (ascorbic acid)

A

antioxidant and hydroxylation of collagen

  • need collagen for stable helical configuration
  • deficiency –> scurvy and hemorrhage
  • toxicities –> Fe overload, hemolytic anemia, kidney stones
24
Q

vitamin K

A

blood clotting factors

-antibiotics can inhibit gut bacteria production of vit. K leading to malnourishment and bleeding

25
Q

vitamin E

A

tocopherols

  • antioxidants
  • deficiency –> susceptible to oxidative stress
  • does not help with CV disease
26
Q

3 hormones for regulating satiety and appetite

A
  1. ghrerlin - secreted by stomach, stimulates appetite
  2. leptin - secreted by adipocytes, decrease appetite
  3. insulin, CCK, peptide YY - produce satiety
27
Q

leptin

A
  • increase sensitivity to brain for satiety signals
  • deficiency –> overeat
  • stimulated when fat stores are abundant
28
Q

adiponectin

A

fat burning molecule

-injections can stimulate fatty acid oxidation causing a decrease in muscle mass

29
Q

ghrelin

A
  • produced in stomach and hypothalamus
  • only one that increases food intake
  • suppression of ghrelin in obese –> overeating
  • PYY and amylin inhibit neurons decreasing food consumption
30
Q

adipocytes

A

produce cytokines that produce pro-inflammatory states leading to atherosclerosis

31
Q

consequences of obesity

A
  • metabolic syndrome - increase risk for cardiovascular disease and diabetes
  • high risk for gallstones, hypoventilation, osteoarthritis
  • increased IGF-1 leading to proliferation and inhibit apoptosis leading to tumor
  • hypercholesterolemia –> atherosclerosis