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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
4 disorders of gastric emptying
- high P (faster solid emptying) - decreased P (neuropathies, patho) - increased R (duodenal obstruction like mass, pyloric obstruction) - central (emotional, drugs)
26
3 important stomach secretions
pepsinogen intrinsic factor mucin
27
fundus and body main gastric glands important cells
parietal cells for IF and HCl
28
cardiac and pylorus glands important secretion
alkaline mucin rich fluid
29
pepsinogen, mucin, HCl: cells and where
``` 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
parietal cell charact
canaliculi where HCl secreted
31
chief cell charact
zymogen granules
32
2 phases of acid secretion
``` 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
parietal cell how secretes HCl + target
1. HK ATPase luminal 2. Cl channel luminal 3. bicarb secreted in blood (postprandial alkaline tide) TARGET: PPI = omaprozol
34
pepsin and HCl fcts
pepsin autocatalyzes more pepsinogen into pepsin. low pH (HCl) needed for that AND low HCl needed for proteolysis by pepsin
35
other stomach secretions
gelatinase and lipase
36
B12 abso: stomach steps
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
B12 abso: intestine steps
duodenum: trypsin frees B12. IF binds B12 ileum: IF-B12 abso
38
ways of B12 deficiency
pancreatic deficiency, ileum problem, parietal cell deficiency, abso problem, R protein problem
39
protective factors of stomach
- mucin-bicarb layer - gastric mucosal barrier (GMB)=tight junctions of epith cells - rapid turnover - effective blood flow
40
ulcerations how
if acid leaks below GMB (between tight junctions)
41
3 effects of endogenous PGs on stomach
- more mucin and bicarb secretion - more blood flow (vasodilate) - less acid production
42
2 mechanisms of stomach damage by ASA and NSAIDs
-direct GMB damage -PG inhibition leads to ULCERATIONS
43
4 phases of gastric secretion and importance
1. basal (fasting) ... | 2. postprandial (cephalic 30% gastric 60% intestinal 10%)
44
cephalic phase works how
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
3 components of gastric phase
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
stimuli of G cells
1. vagus (cephalic phase) 2. vago-vagal 3. secretagogues (aa, small peptides), ..
47
potentiation definition
response of a cell to 2 substances together is greater than the maximum response of each alone
48
gastrin effect
1. parietal cells increase in number (trophic effect) + 2. HCl
49
max output of acid when
parietal cells activated by both GASTRIN and ACH
50
why gastrin self-regulating
``` positive feedback initially (more secretagogues so stims itselfs) neg feedback (below pH 2: gastrin release reduced) ```
51
histamine in stomach
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
why gastrin said to allow itself to work
stimulates also enterochromafin cells to produce histamine (are histamine forming cells)
53
cells inhibiting G cells
D cells (produce somatostatin)
54
H pylori consequences
ulcer disease and gastric cancer
55
H pylori infects what layer
only mucosa
56
H pylori 2 types of infection
antral predominant | pangastritis (whole stomach)
57
H pylori effect on duodenum
bc kills D cells. no more sts, more gastrin. more stomach acid. duodenum acid = metaplasia + duodenal ulcers**
58
gastric rx to h pylori
gastric metaplasia (and ulcers form)
59
H pylori effect on proximal stomach
parietal cells destroyed so less acid so more susceptible to bug infection (and gastric cancer)
60
inhibition of gastric secretion in duodenum
enterogastrone hormone complex and enterogastric reflex (SECRETAGOGUES therefore don't only inhibit peristalsis but also acid secretion)
61
minor excitatory component of duodenum on stomach acid secretion but overriden by inhibitory component
secretagogues lead to entero oxyntin or gastrin (stims HCl) = very minor

Bloc E - GI & Metabolism (58 decks)

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