Feb5 M2-Appetite and Obesity Flashcards

1
Q

mouth main secretion

A

amylase by salivary glands

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2
Q

stomach main secretion + other

A
  • pepsinogen by chief cells (zymogen). becomes pepsin bc of low pH
  • lipases too to make monoglycerides and FFAs
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3
Q

pancreas main secretions

A

lipases, proteolytic enzymes, amylase

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4
Q

gallbladder main secretion

A

bile

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5
Q

2 detergents in bile and what they do

A

lecithin and bile salts. convert fat globules into very small droplets called micelles (emulsification) so that lipases can act on the fat

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6
Q

main proteolytic enzymes fro mthe pancreas

A

trypsin, chymotrypsin, carboxypolypeptidase

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7
Q

large intestine function

A

absorb water and NaCl and store feces

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8
Q

what’s responsible for the preparation to digestion when you smell something or feel hungry

A

molecules called secretagogues. signaling peptides

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9
Q

what cells secrete HCl in the stomach

A

parietal cells

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10
Q

what controls HCl release by parietal cells in the stomach

A
  • gastrin (secretagogue) from G cells of the end of the stomach
  • vagus may stimulate gastric mucosa to make GRP (gastrin releasing peptide) to act on G cells and make gastrin
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11
Q

how stomach can expand

A

stretch and pressure trigger vagus to brainstem to vagus reflex to accomodate

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12
Q

2 secretagogues secreted upon entry of gastric chyme in duodenum and why

A
  • secretin bc of low pH

- cholecystokin (CCK) bc of fat and aa content

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13
Q

CCK and secretin function

A
  • CCK + secretin: make pancreas secrete more

- CCK stimulates GB bile secretion

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14
Q

where proteolytic enzymes of the small intestine (enteropeptidases, etc.) are located

A

on surface of epithelial cell

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15
Q

first brake discovered and what it is (brake = signal regulating chyme propulsion in SI)

A

ileal brake. strong inhibition of SI peristaltis bc of fat

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16
Q

why people with distal SI obstruction or high volume diarrhea (ex. caused by cholera) are vulnerable to hyovolemia and death

A

bc of large amounts of fluid secreted by GI tract and that is normally reabsorbed (and reabso is impaired)

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17
Q

appetite vs hunger

A
hunger = uncomfortable feeling + interest in eating food
appetite = conscious desire to eat specific food
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18
Q

what do we call eating triggered by anticipated pleasure

A

hedonic feeding behavior

19
Q

feeding and satiety centers in the hypothalamus

A

feeding centers = lateral nuclei

satiety centers = ventromedial nuclei, inhibit feeding centers

20
Q

leptin comes from where and what it does

A

from adipocytes. inhibits feeding centers

21
Q

ghrelin comes from where and what it does

A

peptide hormone from stomach. stimulates hunger (feeding center) and increases appetite

22
Q

CCK does what on hypothalamus

A

inhibits hunger (feeding, lateral center)

23
Q

name of hormones that increase feeding vs those that decrease feeding

A

increase feeding = orexigenic hormones

decrease feeding = anorexigenic hormones

24
Q

anorexia nervosa def

A

reduced food intake bc of fear of gaining weight, will to lose weight

25
Q

how hunger and satiety intensity may vary between people

A

hunger: may start eating as soon as feel hungry or only when feel very hungry
satiety: may stop eating as soon as they fill full or only after a while

26
Q

how obesity diagnosed

A

measure BMI (kg over height in m2)

27
Q

how risk varies with BMI

A

health risks increases proportionally with BMI and increases greatly over BMI of 30

28
Q

how important is fat distribution

A

greater health risk if central and abd fat but not as much if hips and rear end fat deposition

29
Q

waist definition

A

narrowest abd circumference (or halfway between iliac crest and costal margin)

30
Q

hip circumference def

A

widest part of the gluteal region

31
Q

central fat distribution def

A

WH ratio over 1 in men

WH ratio over 0.85 in women

32
Q

obesity strong risk factor for what other disease

A

type 2 diabetes

33
Q

metabolic syndrome def

A

combination of insulin resistance (doesn’t have to type 2 DM), high BP, CV disease promoting lipid profile and high uric acid

34
Q

why epidemic of obesity

A
  • more sendentarity

- more use of processed foods and sugar-sweetened beverages

35
Q

who becomes obese

A

people living in obesity-promoting environment (obesogenic) and with obesity predisposition

36
Q

obesity and genetic

A

moderately strong genetic link (noticed strong familial links but no genes identified except a few rare). multifactorial and polygenic

37
Q

thrifty gene hypothesis

A

notion of a certain genetic profile suitable for food scarce environment but not that predisposes to obesity in the modern environment

38
Q

in who does obesity NOT occur

A

doesn’t occur in people who are genetically or metabolically predisposed to a resistance to excessive fat gain

39
Q

proof that a regulated and modifiable fat ‘‘set point’’ may exist

A

pregnant women gain 15-20 kg, 25% of which is fat

40
Q

steps to go about obesity as a physician

A
  1. no negative bias
  2. measure it + risks
  3. how did it come
  4. formulate a plan
  5. exercise
  6. diet
41
Q

how to measure obesity

A

BMI, WH ratio and check for risk factors (BP, diabetes, lipids, liver fat, sleep apnea)

42
Q

when are risk factors more important

A

when obesity is more severe and when there are other risk factors (like family history, high BP,..)

43
Q

when to consider gastric bypass surgery

A

severe and life long obesity with family history + unlikely to change + very bad risk factors with it (lipids, fatty liver) or comobordities

44
Q

2 types of exercise that work

A
  • formal

- non-exercise associated thermogenesis