Feb15 M2-Gastric Physiology Flashcards
receptive relaxation: what does that and what variable changes
PROXIMAL stomach. accomodate for food. pressure stays 5 mmHg. volume increases
receptive relaxation done how
vago-vagal reflex ends up activating ENS NANC neurons (VIP, NO)
ENS in proximal stomach
MOSTLY inhibitory innervation
vagus cut to proximal stomach consequence
no receptive relaxation (discomfort)
predominant activity of proximal stomach + RMP charact
variation in its tone to accomodate for food.
RMP of 50 and partial contraction at RMP
length vs tension proximal vs distal stomach
prox: length can change a lot with no tension increase
distal: length increase = tension increase
3 rules of gastrointestinal peristalsis (trigger, amplitude and charact)
trigger: local distension, enteric reflexes
amplitude: determined by stimulus magnitude
charact: determined by SM frequency, direction, velocity
innervation necessary for gastrointestinal peristalsis
none. ENS alone
BER (electrical control activity) (basal electrical rhythm) def
slow waves depol-repol (upstroke, plateau, repol) of muscle cells. propagating (not same time in all stomach)
NOT ASSOCIATED WITH CONTRACTION
BER: how does it lead to contraction
ONLY IF spikes on plateau (ERA: electrical response activity or SES second electrical signal)
cells making BER name + charact
ICC. processes that touch other ICCs, myocytes and neurons (are between circular and longitudinal muscle layers)
how ICCs communicate
gap junctions (so are not really neurons)
ICCs 3 roles
- origin and propagation of BER
- comm between muscles and nerves
- coordination of groups of muscle cells
ERA 2 important charact
- stimulus = Ach or stretch (Ca dependent)
2. spikes frequency proportional to stimulus magnitude
max frequency of ERA
is max frequency of BER (are phase-locked)
pyloric sphincter when open and when closed + why
- open AT REST
- closes when antrum contracts (so food bounces back and mixes)
principles of gastric emptying
- emptying proportional to P gradient over resistance (PROXIMAL stomach vs duodenum)
- solid empties slower than liquid
- fat empties slower
vagotomy effect on stomach emptying
liquids empty MUCH FASTER (bc no receptive relaxation in proximal so has higher pressure)
what influences solid emptying of meals from stomach
amplitude of contractions, duodenal resistance, how quickly the meal is ground up
function of vagus in antral peristalsis
vago-vagal reflex triggered by stretch of muscle will increase intensity of peristalsis (independent of BER and ERA)
2 things that regulate (inhibit) antra peristalsis AND increase sphincter tone
enterogastric neural reflex: factors inhibit antral peristalsis through vago-vagal and SS
enterogastrone hormone complex: hormones circulating
enterogastric neural reflex components
- distension
- pH below 3.5
- osmolarity
- chemical composition
- fat > prot > carbs
enterogastrone hormonal complex components
- secretin
- CCK
- GIP
- VIP
- neurotensin
distal stomach vagotomy effect on antral persitalsis and solid emptying
sluggish solid emptying. pyloric sphincter OPENING (remember it is closed when antrum contracts. less antrum contraction, but still existant, with vagotomy)
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)
3 important stomach secretions
pepsinogen
intrinsic factor
mucin
fundus and body main gastric glands important cells
parietal cells for IF and HCl
cardiac and pylorus glands important secretion
alkaline mucin rich fluid
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
parietal cell charact
canaliculi where HCl secreted
chief cell charact
zymogen granules
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
parietal cell how secretes HCl + target
- HK ATPase luminal
- Cl channel luminal
- bicarb secreted in blood (postprandial alkaline tide)
TARGET: PPI = omaprozol
pepsin and HCl fcts
pepsin autocatalyzes more pepsinogen into pepsin. low pH (HCl) needed for that AND low HCl needed for proteolysis by pepsin
other stomach secretions
gelatinase and lipase
B12 abso: stomach steps
- B12 broken down into free B12 by acid
- free B12 binds R protein from saliva
- stomach makes IF (free for now)
B12 abso: intestine steps
duodenum: trypsin frees B12. IF binds B12
ileum: IF-B12 abso
ways of B12 deficiency
pancreatic deficiency, ileum problem, parietal cell deficiency, abso problem, R protein problem
protective factors of stomach
- mucin-bicarb layer
- gastric mucosal barrier (GMB)=tight junctions of epith cells
- rapid turnover
- effective blood flow
ulcerations how
if acid leaks below GMB (between tight junctions)
3 effects of endogenous PGs on stomach
- more mucin and bicarb secretion
- more blood flow (vasodilate)
- less acid production
2 mechanisms of stomach damage by ASA and NSAIDs
-direct GMB damage
-PG inhibition
leads to ULCERATIONS
4 phases of gastric secretion and importance
- basal (fasting) …
2. postprandial (cephalic 30% gastric 60% intestinal 10%)
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
3 components of gastric phase
- local ENS reflex
- vago-vagal reflex
- FOOD PARTICLES ARE SECRETAGOGUES: stim G cells to make gastrin: parietal cells make more HCl
stimuli of G cells
- vagus (cephalic phase)
- vago-vagal
- secretagogues (aa, small peptides), ..
potentiation definition
response of a cell to 2 substances together is greater than the maximum response of each alone
gastrin effect
- parietal cells increase in number (trophic effect) + 2. HCl
max output of acid when
parietal cells activated by both GASTRIN and ACH
why gastrin self-regulating
positive feedback initially (more secretagogues so stims itselfs) neg feedback (below pH 2: gastrin release reduced)
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
why gastrin said to allow itself to work
stimulates also enterochromafin cells to produce histamine (are histamine forming cells)
cells inhibiting G cells
D cells (produce somatostatin)
H pylori consequences
ulcer disease and gastric cancer
H pylori infects what layer
only mucosa
H pylori 2 types of infection
antral predominant
pangastritis (whole stomach)
H pylori effect on duodenum
bc kills D cells. no more sts, more gastrin. more stomach acid. duodenum acid = metaplasia + duodenal ulcers**
gastric rx to h pylori
gastric metaplasia (and ulcers form)
H pylori effect on proximal stomach
parietal cells destroyed so less acid so more susceptible to bug infection (and gastric cancer)
inhibition of gastric secretion in duodenum
enterogastrone hormone complex and enterogastric reflex (SECRETAGOGUES therefore don’t only inhibit peristalsis but also acid secretion)
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
