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Bloc E - GI & Metabolism > Feb15 M2-Gastric Physiology > Flashcards

Feb15 M2-Gastric Physiology Flashcards

1
Q

receptive relaxation: what does that and what variable changes

A

PROXIMAL stomach. accomodate for food. pressure stays 5 mmHg. volume increases

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2
Q

receptive relaxation done how

A

vago-vagal reflex ends up activating ENS NANC neurons (VIP, NO)

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3
Q

ENS in proximal stomach

A

MOSTLY inhibitory innervation

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4
Q

vagus cut to proximal stomach consequence

A

no receptive relaxation (discomfort)

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5
Q

predominant activity of proximal stomach + RMP charact

A

variation in its tone to accomodate for food.

RMP of 50 and partial contraction at RMP

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6
Q

length vs tension proximal vs distal stomach

A

prox: length can change a lot with no tension increase
distal: length increase = tension increase

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7
Q

3 rules of gastrointestinal peristalsis (trigger, amplitude and charact)

A

trigger: local distension, enteric reflexes
amplitude: determined by stimulus magnitude
charact: determined by SM frequency, direction, velocity

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8
Q

innervation necessary for gastrointestinal peristalsis

A

none. ENS alone

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9
Q

BER (electrical control activity) (basal electrical rhythm) def

A

slow waves depol-repol (upstroke, plateau, repol) of muscle cells. propagating (not same time in all stomach)
NOT ASSOCIATED WITH CONTRACTION

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10
Q

BER: how does it lead to contraction

A

ONLY IF spikes on plateau (ERA: electrical response activity or SES second electrical signal)

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11
Q

cells making BER name + charact

A

ICC. processes that touch other ICCs, myocytes and neurons (are between circular and longitudinal muscle layers)

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12
Q

how ICCs communicate

A

gap junctions (so are not really neurons)

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13
Q

ICCs 3 roles

A
  • origin and propagation of BER
  • comm between muscles and nerves
  • coordination of groups of muscle cells
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14
Q

ERA 2 important charact

A
  1. stimulus = Ach or stretch (Ca dependent)

2. spikes frequency proportional to stimulus magnitude

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15
Q

max frequency of ERA

A

is max frequency of BER (are phase-locked)

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16
Q

pyloric sphincter when open and when closed + why

A
  • open AT REST

- closes when antrum contracts (so food bounces back and mixes)

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17
Q

principles of gastric emptying

A
  • emptying proportional to P gradient over resistance (PROXIMAL stomach vs duodenum)
  • solid empties slower than liquid
  • fat empties slower
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18
Q

vagotomy effect on stomach emptying

A

liquids empty MUCH FASTER (bc no receptive relaxation in proximal so has higher pressure)

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19
Q

what influences solid emptying of meals from stomach

A

amplitude of contractions, duodenal resistance, how quickly the meal is ground up

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20
Q

function of vagus in antral peristalsis

A

vago-vagal reflex triggered by stretch of muscle will increase intensity of peristalsis (independent of BER and ERA)

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21
Q

2 things that regulate (inhibit) antra peristalsis AND increase sphincter tone

A

enterogastric neural reflex: factors inhibit antral peristalsis through vago-vagal and SS
enterogastrone hormone complex: hormones circulating

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22
Q

enterogastric neural reflex components

A
  • distension
  • pH below 3.5
  • osmolarity
  • chemical composition
  • fat > prot > carbs
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23
Q

enterogastrone hormonal complex components

A
  • secretin
  • CCK
  • GIP
  • VIP
  • neurotensin
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24
Q

distal stomach vagotomy effect on antral persitalsis and solid emptying

A

sluggish solid emptying. pyloric sphincter OPENING (remember it is closed when antrum contracts. less antrum contraction, but still existant, with vagotomy)

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25
Q

4 disorders of gastric emptying

A
  • high P (faster solid emptying)
  • decreased P (neuropathies, patho)
  • increased R (duodenal obstruction like mass, pyloric obstruction)
  • central (emotional, drugs)
26
Q

3 important stomach secretions

A

pepsinogen
intrinsic factor
mucin

27
Q

fundus and body main gastric glands important cells

A

parietal cells for IF and HCl

28
Q

cardiac and pylorus glands important secretion

A

alkaline mucin rich fluid

29
Q

pepsinogen, mucin, HCl: cells and where

A 
main gastric glands neck: 
1. mucous neck cells = mucin
2. chief cells = pepsinogen
3. parietal cells = HCl and IF
surface epithelial cell of the glands: bicarb and mucous
30
Q

parietal cell charact

A

canaliculi where HCl secreted

31
Q

chief cell charact

A

zymogen granules

32
Q

2 phases of acid secretion

A 
low rate (low secretion) = parietal cells (that make the large volume acidic) not active: more neutral pH
high rate: parietal cells very active: low pH
33
Q

parietal cell how secretes HCl + target

A
  1. HK ATPase luminal
  2. Cl channel luminal
  3. bicarb secreted in blood (postprandial alkaline tide)
    TARGET: PPI = omaprozol
34
Q

pepsin and HCl fcts

A

pepsin autocatalyzes more pepsinogen into pepsin. low pH (HCl) needed for that AND low HCl needed for proteolysis by pepsin

35
Q

other stomach secretions

A

gelatinase and lipase

36
Q

B12 abso: stomach steps

A
  1. B12 broken down into free B12 by acid
  2. free B12 binds R protein from saliva
  3. stomach makes IF (free for now)
37
Q

B12 abso: intestine steps

A

duodenum: trypsin frees B12. IF binds B12
ileum: IF-B12 abso

38
Q

ways of B12 deficiency

A

pancreatic deficiency, ileum problem, parietal cell deficiency, abso problem, R protein problem

39
Q

protective factors of stomach

A
  • mucin-bicarb layer
  • gastric mucosal barrier (GMB)=tight junctions of epith cells
  • rapid turnover
  • effective blood flow
40
Q

ulcerations how

A

if acid leaks below GMB (between tight junctions)

41
Q

3 effects of endogenous PGs on stomach

A
  • more mucin and bicarb secretion
  • more blood flow (vasodilate)
  • less acid production
42
Q

2 mechanisms of stomach damage by ASA and NSAIDs

A

-direct GMB damage
-PG inhibition
leads to ULCERATIONS

43
Q

4 phases of gastric secretion and importance

A
  1. basal (fasting) …

2. postprandial (cephalic 30% gastric 60% intestinal 10%)

44
Q

cephalic phase works how

A

psychic or gustatory stimulus = vagus stims parietal, chief and mucous cells + G cells for gastrin prod for more HCl (antrum). **Ach (N) on ENS neurons. ENS neurons Ach (M) on cells

45
Q

3 components of gastric phase

A
  1. local ENS reflex
  2. vago-vagal reflex
  3. FOOD PARTICLES ARE SECRETAGOGUES: stim G cells to make gastrin: parietal cells make more HCl
46
Q

stimuli of G cells

A
  1. vagus (cephalic phase)
  2. vago-vagal
  3. secretagogues (aa, small peptides), ..
47
Q

potentiation definition

A

response of a cell to 2 substances together is greater than the maximum response of each alone

48
Q

gastrin effect

A
  1. parietal cells increase in number (trophic effect) + 2. HCl
49
Q

max output of acid when

A

parietal cells activated by both GASTRIN and ACH

50
Q

why gastrin self-regulating

A 
positive feedback initially (more secretagogues so stims itselfs)
neg feedback (below pH 2: gastrin release reduced)
51
Q

histamine in stomach

A

present a lot in mucosa. always there as paracrine tone to parietal cells (permissive tone) for HCl secretion in resp to Ach and gastrin

52
Q

why gastrin said to allow itself to work

A

stimulates also enterochromafin cells to produce histamine (are histamine forming cells)

53
Q

cells inhibiting G cells

A

D cells (produce somatostatin)

54
Q

H pylori consequences

A

ulcer disease and gastric cancer

55
Q

H pylori infects what layer

A

only mucosa

56
Q

H pylori 2 types of infection

A

antral predominant

pangastritis (whole stomach)

57
Q

H pylori effect on duodenum

A

bc kills D cells. no more sts, more gastrin. more stomach acid. duodenum acid = metaplasia + duodenal ulcers**

58
Q

gastric rx to h pylori

A

gastric metaplasia (and ulcers form)

59
Q

H pylori effect on proximal stomach

A

parietal cells destroyed so less acid so more susceptible to bug infection (and gastric cancer)

60
Q

inhibition of gastric secretion in duodenum

A

enterogastrone hormone complex and enterogastric reflex (SECRETAGOGUES therefore don’t only inhibit peristalsis but also acid secretion)

61
Q

minor excitatory component of duodenum on stomach acid secretion but overriden by inhibitory component

A

secretagogues lead to entero oxyntin or gastrin (stims HCl) = very minor

Bloc E - GI & Metabolism (58 decks)

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