obesity Flashcards

1
Q

fuel storage
liver + muscles: glycogen
adipocytes: fat

A

obesity

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2
Q

fuel storage
liver + muscles: glycogen
adipocytes: fat

A

obesity

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3
Q

BMI

A

weight (kg)/

(height (m))^2

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4
Q

underweight BMI

A
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5
Q

normal BMI

A

18.5-24.9

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6
Q

overweight BMI

A

25.0-29.9

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7
Q

obese BMI

A

equal or > 30

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8
Q

hypothalamic nuclei involved in regulation of hunger

A

paraventricular nuclei
dorsal medial nuclei
arcuate nucleus
involve LEPTIN:
lateral hypothalamus (“lateral likes lunch - but lesion/leptin lateral you get little”: stimulation → hunger, INHIBITED by LEPTIN from adipocytes→ anorexia
ventromedial nuclei: STIMULATED by LEPTIN → satiety, lesion → hyperphagia

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9
Q

hypothalamic nuclei involved in regulation of hunger

A

paraventricular nuclei
dorsal medial nuclei
arcuate nucleus
involve LEPTIN:
lateral hypothalamus (“lateral likes lunch - but lesion/leptin lateral you get little”: stimulation → hunger, INHIBITED by LEPTIN from adipocytes→ anorexia
ventromedial nuclei: STIMULATED by LEPTIN → satiety, lesion → hyperphagia

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10
Q

BMI

A

weight (kg)/

(height (m))^2

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11
Q

underweight BMI

A
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12
Q

normal BMI

A

18.5-24.9

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13
Q

overweight BMI

A

25.0-29.9

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14
Q

obese BMI

A

equal or > 30

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15
Q

function of adipocytes

A

store TG’s from blood (greater capacity than liver cells)
synthesize FA/TG from carbs
break down stored fats → release FA for energy
produce LEPTIN: when adipocytes are full, tell hypothalamus that they have enough energy stored as fat (stop eating!)

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16
Q

hypothalamic nuclei involved in regulation of hunger

A

paraventricular nuclei
dorsal medial nuclei
arcuate nucleus
involve LEPTIN:
lateral hypothalamus (“lateral likes lunch - but lesion/leptin lateral you get little”: stimulation → hunger, INHIBITED by LEPTIN from adipocytes→ anorexia
ventromedial nuclei: STIMULATED by LEPTIN → satiety, lesion → hyperphagia

17
Q

leptin control of hypothalamic nuclei: ↓ APPETITE

A

lateral hypothalamus: INHIBITED by LEPTIN

ventromedial nuclei: STIMULATED by LEPTIN

18
Q

2 signals for fat utilization of adipocytes

A

↑ sympathetic tone in both states→↑ NE, epi released from adrenal medulla → epi activates hormone-sensitive TG lipase in fat cells → breakdown TG, mobilization of FA to be used by muscles as energy

1) heavy exercise
2) stress: also stimulates ↑ACTH →↑ cortisol → cortisol ALSO activates TG lipase in fat cells

19
Q

local atrophy of adipocytes or hyperplasia of adipocytes + abnormal fatty deposits
abdominal obesity with no fat on extremities
associated with cushing syndrome: cortisol triggers mobilization + redistribution of fat = buffalo hump = type of lipodystrophy

A

lipodystrophy

20
Q

causes of lipodystrophy

A
leptin deficiency
HIV meds (protease inihbitors)
cushing syndrome: buffalo hump
21
Q

medications that can ↑ weight gain

A

atypical antipsychotics
mirtazapine (antidepressant)
insulin, TZD, sulfonylurea
some progestins

22
Q

complications of obesity

A

gout
gall stones: female, fat, fertile, fourty
fatty liver
osteoarthritis (hips, knees)
candidal infection in skin folds
↑cancer: esophageal, colon, liver, gallbladder, pancreatic, breast/ovarian/uterine, prostate, non-hodgkin lymphoma, MM
PCOS

23
Q

cause: obesity, type 2 DM, hyperlipidemia, insulin resistance
insulin resistance at liver → excess lipid accumulation in liver
NAFL → NASH → cirrhosis (↑ risk HCC)
can worsen hep C progression
CHRONICALLY elevated ALT/AST + alk phos

A

nonalcoholic steatohepatitis (NASH)

fat accumulation in hepatocytes causes with inflammation (neutrophils, collagen) of liver + elevated LFTs

looks like early changes seen in heavy drinker (alcoholic fatty liver→alcoholic hepatitis →cirrhosis)

24
Q

diagnosis of nonalcoholic steatohepatitis (NASH)

A

liver US, CT scan, MRI MRS: (gold standard)

liver bx