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151 Cards in this Set

  • Front
  • Back
describe the extrinsic innervation: 2 components
autonomic: PSNS and SNS
describe the components of PSNS innervation
vagus n.
pelvic n.
synapse with cells in enteric NS
vagovagal reflex
describe vagus innervation of GI
innervates esophagus, stomach, SI, upper colon
pelvic n.
innervates descending colon, sigmoid colon, rectum, and anal canal
describe the vagovagal reflex of the GI tract
info from receptors in mucosa and smooth m. relayed to CNS via vagus afferents
response carried back to GI via vagus efferents
describe the SNS of GI
most preganglionic synapse outside GI in prevertebral ganglia
some innervate smooth m, blood vessels and secretory cells directly
postganglionic innervate cells in enteric NS
where do sympathetic postganglionic fibers synapse?
innervate enteric NS cells
what forms the intrinsic NS?
(enteric NS)
formed by myenteric and submucosal plexuses
how does the intrinsic NS relay info to/from the gut?
via the enteric NS
how does the intrinsic NS promote communication within the GI tract?
stimulus in one part of GI can prod a resp in another part w/o the entrinsic NS via the intrinsic
what stim the rel of gastrin?
rel in resp to meal, peptides and aa, stomach distention, vagus stim (GRP)
what cells rel gastrin?
G cells of stomach
what inhibits the rel of gastrin?
ph < 3 in stomach
action of gastrin
stim HCl rel by parietal cells of stomach
what is zollinger-ellison syndrome?
pt with a gastrinoma
rel xs gastrin and gastric acid
dev duodenal ulcers, diarrhea, steatorrhea
what stim rel of CCK?
small peptides, aa, FFA and monoglycerides
where is CCK rel?
rel from I cells of proximal SI
action of CCK?
stim gallbladder contraction, pancreatic enzyme secretion
potentiates pancreatic bicarb rel stim by secretin
inhibits gastric emptying
why do fatty meals take longer to digest?
fatty meals stim CCK rel which inhibits gastric emptying
what stim the rel of secretin? from where?
rel by S cells of prox SI in resp to acid
actions of secretin
overall: reduce acid in SI lumen
bicarb and water secretion in pancreas, liver
incr bile prod
inhibit gastric acid secretion by parietal cells
what stim GIP rel? from where?
rel from prox SI in resp to fat, protein, CHO
what is special abt GIP?
only hormone rel in resp to all 3 foodstuffs
actions of GIP
stim insulin rel
why does oral glucose stim insulin rel more than IV glucose?
b/c GIP is only rel in resp to oral glucose load-> insulin
what stim motilin rel? from where? what inhibits its rel?
rel every 90 min from prox SI when fasting
rel inhibited by eating
action of motilin?
stim migrating myoelectric complex in stomach, SI
helps to clear remaining food
what are 2 paracrines?
somatostatin and histamine
when/from where is somatostatin rel?
rel by cells throughout GI in resp to acid in lumen
action of somatostatin
inhibits rel of gastrin and gastric acid
inhibits rel of all GI hormones
from where is histamine rel?
rel from gastric enterochromaffin-like cells
action of histamine? where is it found in high concentrations?
incr gastric acid secretion directly and indirectly- potentiating effects of gastrin and ACh
found in high conc in acid-rel portions of stomach
what are the 3 neurcrines?
vasoactive intestinal peptide (VIP)
gastrin-rel peptide (GRP)/ bombesin
from where is VIP rel?
rel from nn in mucosa and smooth m of GI
action of VIP
relax GI smooth mm
stim intestinal and pancreatic secretion (can mediate cholera syndromes)
from where and when is GRP rel? action?
rel from nn of gastric mucosa in resp to vagal stimulation
stim gastrin rel
from where are enkephalins rel?
nn in mucosa and smooth m of GI
actions of enkephalins
stim contraction of GI smooth m- esp sphincters (lower esophageal, pyloric, ileocecal)
inhibits intestinal secretion of fluid, electrolytes
why are opiates used to tx diarrhea?
opiates act as enkephalins- inhibit secretion of fluid and electrolytes
what is the basic electrical rhythm?
periodic changes in resting mbr potential of smooth m cells in GI
what are the pacemakers of the slow wave?
interstitial cells of cajal
what makes up a slow wave?

consist of upstroke/depolariztion and plateau
what has to occur for contraction to occur?
plateau phase must reach threshold
are slow waves action potentials?
NO- but they determine the pattern of APs
what happens once threshold is reached?
VG Ca channels open-> APs/spike potentials
how do the APs contribute to the contraction/?
incr strength and duration

greater # of APs-> greater F of contraction
can contractions occur without APs?
yes, but only in stomach (not in rest of GI tract)
how do neural and hormonal inputs affect freq of slow waves and APs?
have little effect on freq of slow waves;
greatly affect APs-> det strength of contractions
what det the max frequency of contractions?
freq of SLOW WAVES
3 fxns of salivation
digestion of starches, fats
facilitates swallowing
order of contribution of 3 salivary glands
submaxillary> parotid> sublingual
structure of gland
acinus- blind end with cells secreting saliva
intercalated duct- conn acinus and striated duct
striated duct- modifies composition of saliva
where are myoepithelial cells located in the gland?
acinus and intercalated duct
in which part of the gland is saliva modified?
striated duct
what controls saliva prod? what doesnt?
under ANS control (PSNS and SNS)
NOT under hormonal control
how does PSNS lead to salivation?
incr transport in acinus and ductal cells
vasodilation of vessels prov water for saliva prod
stim gland metabolism
how does SNS contribute to saliva prod?
transiently incr prod of saliva
contraction of myoepithelial cells
constriction of bld vessels
what induces salivation?
food in mouth
smells, reflexes (pavlov)
what inhibits salvation?
sleep, fatigue, dehydration, fear, anticholinergics (block PSNS)
composition of saliva
pH 5.5-6
water, electrolytes, organic cmpds
bacteriocidal subst
what proteins does saliva contain?
alpha amylase to digest starches
lingual lipase to digest fats
mucin for lubrication
how does the ionic composition of saliva compare to plasma?
ALWAYS HYPOTONIC to plasma b/c is an ultrafiltrate
how do striated ducts modify ionic composition of saliva?
reabsorb Na, Cl
secrete K and HCO3
relatively impermeable to water
how does flow rate affect saliva ion concentrations?
higher flow rate -> more isotonic saliva b/c less time for Na reabsorption (Cl also incr)
HCO3 also incr in saliva with incr flow rate (eventually plateaus)
K decr then plateaus
what is xerostomia?
dry mouth
due to lack of salivary secretion
assoc with chronic infections of buccal mucosa and dental cavities
what is xerostomia most commonly due to?
antidepressants (which are anticholinergic and inhibit PSNS)
also, beta blockers and antihistamines
radiation damage
describe the oral phase of swallowing
pharyngeal phase of swallowing
breathing inhibited
nasopharynx closed by soft palate
peristalsis begins in pharynx
laryngeal mm contract, close glottis
upper esophageal sphincter relaxes
what triggers the swallowing reflex?
initiated voluntarily but req something to trigger reflex
swallowing center in medulla
lesions in swallowing center leads to...?
loss of pharyngeal phase of swallowing
basic structure of esophagus mm
upper 1/3 striated
lower 1/2 smooth
what makes up the UES? fxn?
cricopharyngeal mm
sep esophagus from oral cavity
prevents entry of air
LES? fxn?
sep esophagus from stomach
prevents reflux of gastric acid
primary peristaltic contraction in esophagus
initiated by swallowing
creates zone of incr pressure behind bolus
what happens as bolus reaches LES?
LES relaxes to let bolus pass, then constricts to prevent reflux
describe smooth m of esophagus when quiescent
LES tonically contracted
remainder flaccid
secondary peristaltic contraction
initiated by presence of food in esophagus
cont until all material removed from esophagus
decr tone of LES
-> heartburn, esophagitis
tx with lifestyle changes: lose weight, stop smoking
what can longterm exposure to acid reflux lead to?
barrett's esophagus
metaplasia and esophageal cancer
what is achalasia?
n/m disorder of lower 2/3 esophagus
peristalsis absent
LES cant relax
what are s/s of achalasia?
food accumulated in esophagus
takes hrs to digest meals
dysphagia, regurgitation of food, wt loss
what is eructation?
swallowed air etc forms bubbles in stomach
air enters esophagus when LES relaxes
what are the 2 functional regions of stomach?
orad-proximal; receives meal
caudad-distal; contracts to mix food and propels it into duodenum
describe the thickness of the smooth m layers in the stomach
thickness incr distally towards pylorus
stronger contractions in caudad
what is receptive relaxation?
orad relaxes to accept meal (up to 1.5 L) without incr pressure
mediated by vagovagal reflex which is stim by stretch of stomach
what abolishes receptive relaxation?
what causes the caudad to contract?
presence of food
produces chyme
where do peristalsis contractions begin in the stomach?
midstomach (near fundal-corpus border)
move caudally; incr force and velocity
where is the pacemaker in the stomach and what does it initiate?
near border of orad/caudad
prod slow waves
what is retropulsion?
wave of contraction closes pyloric sphincter before chyme reaches there and forces chyme to be propelled back into stomach
incr time allowed to break down food
what is the migrating myoelectric complex? when is it active?
contractions that occur every 90 min when fasting
clear stomach of residual food
abolished with eating
what det rate of gastric emptying?
food ingested (liq vs solid)
(CHO > protein > fat)
rate inversely proportional to pressure in orad stomach (eat big meal, takes longer to empty)
what is gastric emptying mainly controlled by?
signals from duodenum
prevents flow of chyme from exceeding ability of SI to handle it
what inhibits gastric emptying?
low pH, high fat, protein products; non-isotonic solutions
incr distention or orad
incr pressure in prox SI
decr freq and force of contractions on caudad
what is gastroparesis? (s/s, causes)
impaired or delayed emptying
sx include fullness, nausea, vomiting
caused by diabetes (neuropathy), anticholinergics, peptic ulcers that obstruct gastroduodenal canal
how do duodenal ulcers cause diarrhea?
stomach acid damages duodenal lining and impairs reabsorption
what is dumping syndrome? who is it freq seen in?
lower SI fills too fast with undigested food from stomach
right after meal or 1-3 hrs later
stomach surgery/gastric bypass
what are the 2 regions of the stomach based on secretory fxn?
oxyntic gland mucosa- prox 80%; rel acid, pepsinogen, intrinsic factor, mucus

pyloric gland mucosa- distal 20%; rel mainly gastrin; some mucus, pepsinogen
where are the stem cells located in the oxyntic gland?
stem cells in mucous neck cell area give rise to parietal or epithelial surface cells
what do parietal cells secrete?
intrinsic factor and acid
what do chief cells secrete?
what is the order of cells in the oxyntic gland from lumen out?
chief cells-> parietal cell-> mucous neck cells-> surface epithelial cells-> goblet cells
what do the surface epithelial cells in the oxyntic gland secrete?
bicarb and mucous
what are the 4 components of gastric juice?
intrinsic factor
fxn of HCl in gastric juice
rel by parietal cells
begins protein digestion
activates pepsinogen-> pepsin
kills bacteria
fxn of pepsin in gastric juice
stored/rel as pepsinogen; converted by HCl and pepsin to pepsin
begins protein digestion
rel due to vagal stimulation
what are the 2 forms of mucus?
soluble and insoluble
when is soluble mucus secreted?
rel by mucous neck cells after vagal stimulation
lubricates chyme
not present in resting stomach
when is insoluble mucus secreted?
rel by surface epithelial cells
secreted by resting stomach with irritation
secreted as gel; forms unstirred layer over mucosa
traps HCO3 to maintain more neutral pH at surface of stomach
what happens when the insoluble mucus contacts acid?
precipitates into clumps and moves into duodenum with chyme
fxn of intrinsic factor in gastric juice
rel by parietal cells
binds B12 and allows reabsorption in ileum
absence leads to pernicious anemia
mxn of HCl secretion
parietal cells rel HCl into the lumen of stomach and rel HCO3 into the blood when stimulated
how is H+ formed in the parietal cell and how is it secreted?
dissoc of H20-> H+ + OH-
H+ secreted into lumen in exchange for K+ via H/K ATPase
how is HCO3 rel into blood from parietal cell?
exchanged for Cl-; Cl- then moves through channel into lumen
how does HCl form in the lumen of the stomach?
H+ and Cl- secreted separately from the parietal cell; forms HCl in the lumen
what is the alkaline tide?
in venous blood of actively secreting stomach
created by HCO3 being rel into blood
how does gastric juice composition change with rate of secretion?
at basal rates: primarily NaCl from nonparietal secretion
high rates: primarily HCl from parietal secretion
how does the conc of K in gastric juice compare to that in plasma?
more K in gastric juice than plasma
chronic vomiting-> hypokalemia from loss of K
what are 3 stimulants of acid secretion in the stomach?
how does ACh incr acid secretion?
binds muscarinic R on parietal cells
activated PLC---> Ca
how does histamine incr acid secretion?
binds H2 R on parietal cells
activates adenylate cyclase-->cAMP
how does gastrin incr acid secretion?
binds gastrin/CCK-B R on parietal cells
activates PLC--> Ca
which stimulants of acid secretion in the stomach work via PLC?
ACh and gastrin
when does potentiation occur in the stomach?
histamine potentiates actions of ACh and gastrin in acid secretion
what is the best MOA to block acid secretion in the stomach?
H2-R blocker because also blocks potentiating effects of histamine on ACh and gastrin
in addn to parietal cells, what other cells have R for gastrin and ACh?
enterochromaffin-like cells (ECL)
gastrin stim syn and rel of histamine and cell proliferation
ACh also slightly stim syn and rel of histamine
what are 2 inhibitors of acid secretion in the stomach?
low pH (< 3.0)in stomach and chyme in duodenum
how does somatostatin effect acid secretion in stomach?
inhibits acid secretion by parietal cells and inhibits gastrin secretion by G cells
how does chyme in the duodenum inhibit acid secretion in stomach?
via neural and humoral mxns
triggered by acidity, osmolarity and fat content in chyme
inhibit rel of gastrin from G cells and secretion by parietal cells
what are the 4 phases of acid secretion in the stomach?
describe basal secretion of acid in stomach
occurs w/o gastric stimulation, b/w meals
circadian rhythms-highest in evening (but gastrin stays level)
describe cephalic phase of acid secretion
stim is thought, sight, taste, smell of food
afferents to vagal nucleus; vagal efferents to stomach
incr acid via: ACh stim parietal cell directly and ACh causes rel of GRP
what stim the gastric phase of acid secretion in stomach?
entry of food into stomach raises pH--> vagal stim initiates gastrin rel via cephalic phase while gastric phase maintains gastrin rel
what stim gastrin rel in the gastric phase of acid secretion?
distention of stomach act mechanoR
initiate local and vagovagal reflexes
stim gastrin rel via GRP
stim acid secretion vi ACh
what is the only nutrient that causes direct rel of gastrin from G cells?
protein (broken into peptides and aa)
what effect do Ca and caffeine have on acid secretion in stomach?
what initiates the intestinal phase of acid secretion?
protein digestion products in duodenum-->prox duodenum rel gastrin
which phase of acid secretion contributes most?
gastric 60%
cephalic 30%
intestinal 10%
gastric ulcers
pain with eating
barrier breaks down
distal stomach
duodenal ulcers
more common than gastric
less pain with meal
incr levels of pepsin, acid, gastrin
causes of peptic ulcers
H. pylori (urease to neutralize)
NSAIDS (asprin)
Tx of peptic ulcers
H+ pump inhibitor
antibiotic combo
pepto bismol
where does the mxn for vomiting begin?
anti-peristalsis begins in distal SI
what is retching?
involves involuntary motions of vomiting but without the vomit
(ex: cats)
what are some sx before and during vomiting and what causes them?
incr salivation, sweating, rapid breathing, irregular heartbeat due to incr ANS
where is the vomiting center and what occurs with direct activation?
vomiting w/o nausea/retching
what activates the vomiting center?
afferents triggered by:
tickle throat
distended stomach, duodenum
motion sickness
pain to genitourinary
when do we just get retching w/o vomiting?
activation of separate second medullary area
what is the chemoR trigger zone? (for vomiting)
in 4th ventricle of brain
activated by emetics, radiation, motion sickness
what is hyperemesis of pregnancy?
severe nausea and vomiting that causes weight loss
effects of prolonged vominting
metabolic alkalosis