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151 Cards in this Set
- Front
- Back
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describe the extrinsic innervation: 2 components
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autonomic: PSNS and SNS
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describe the components of PSNS innervation
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vagus n.
pelvic n. synapse with cells in enteric NS vagovagal reflex |
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describe vagus innervation of GI
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innervates esophagus, stomach, SI, upper colon
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pelvic n.
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innervates descending colon, sigmoid colon, rectum, and anal canal
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describe the vagovagal reflex of the GI tract
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info from receptors in mucosa and smooth m. relayed to CNS via vagus afferents
response carried back to GI via vagus efferents |
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describe the SNS of GI
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most preganglionic synapse outside GI in prevertebral ganglia
some innervate smooth m, blood vessels and secretory cells directly postganglionic innervate cells in enteric NS |
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where do sympathetic postganglionic fibers synapse?
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innervate enteric NS cells
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what forms the intrinsic NS?
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(enteric NS)
formed by myenteric and submucosal plexuses |
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how does the intrinsic NS relay info to/from the gut?
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via the enteric NS
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how does the intrinsic NS promote communication within the GI tract?
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stimulus in one part of GI can prod a resp in another part w/o the entrinsic NS via the intrinsic
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what stim the rel of gastrin?
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(hormone)
rel in resp to meal, peptides and aa, stomach distention, vagus stim (GRP) |
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what cells rel gastrin?
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G cells of stomach
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what inhibits the rel of gastrin?
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ph < 3 in stomach
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action of gastrin
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stim HCl rel by parietal cells of stomach
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what is zollinger-ellison syndrome?
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pt with a gastrinoma
rel xs gastrin and gastric acid dev duodenal ulcers, diarrhea, steatorrhea |
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what stim rel of CCK?
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small peptides, aa, FFA and monoglycerides
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where is CCK rel?
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rel from I cells of proximal SI
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action of CCK?
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stim gallbladder contraction, pancreatic enzyme secretion
potentiates pancreatic bicarb rel stim by secretin inhibits gastric emptying |
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why do fatty meals take longer to digest?
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fatty meals stim CCK rel which inhibits gastric emptying
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what stim the rel of secretin? from where?
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rel by S cells of prox SI in resp to acid
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actions of secretin
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overall: reduce acid in SI lumen
bicarb and water secretion in pancreas, liver incr bile prod inhibit gastric acid secretion by parietal cells |
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what stim GIP rel? from where?
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rel from prox SI in resp to fat, protein, CHO
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what is special abt GIP?
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only hormone rel in resp to all 3 foodstuffs
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actions of GIP
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stim insulin rel
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why does oral glucose stim insulin rel more than IV glucose?
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b/c GIP is only rel in resp to oral glucose load-> insulin
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what stim motilin rel? from where? what inhibits its rel?
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rel every 90 min from prox SI when fasting
rel inhibited by eating |
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action of motilin?
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stim migrating myoelectric complex in stomach, SI
helps to clear remaining food |
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what are 2 paracrines?
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somatostatin and histamine
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when/from where is somatostatin rel?
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rel by cells throughout GI in resp to acid in lumen
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action of somatostatin
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inhibits rel of gastrin and gastric acid
inhibits rel of all GI hormones |
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from where is histamine rel?
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rel from gastric enterochromaffin-like cells
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action of histamine? where is it found in high concentrations?
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incr gastric acid secretion directly and indirectly- potentiating effects of gastrin and ACh
found in high conc in acid-rel portions of stomach |
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what are the 3 neurcrines?
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vasoactive intestinal peptide (VIP)
gastrin-rel peptide (GRP)/ bombesin enkephalins |
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from where is VIP rel?
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rel from nn in mucosa and smooth m of GI
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action of VIP
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relax GI smooth mm
stim intestinal and pancreatic secretion (can mediate cholera syndromes) |
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from where and when is GRP rel? action?
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rel from nn of gastric mucosa in resp to vagal stimulation
stim gastrin rel |
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from where are enkephalins rel?
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nn in mucosa and smooth m of GI
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actions of enkephalins
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stim contraction of GI smooth m- esp sphincters (lower esophageal, pyloric, ileocecal)
inhibits intestinal secretion of fluid, electrolytes |
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why are opiates used to tx diarrhea?
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opiates act as enkephalins- inhibit secretion of fluid and electrolytes
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what is the basic electrical rhythm?
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periodic changes in resting mbr potential of smooth m cells in GI
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what are the pacemakers of the slow wave?
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interstitial cells of cajal
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what makes up a slow wave?
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NOT ACTION POTENTIALS
consist of upstroke/depolariztion and plateau |
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what has to occur for contraction to occur?
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plateau phase must reach threshold
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are slow waves action potentials?
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NO- but they determine the pattern of APs
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what happens once threshold is reached?
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VG Ca channels open-> APs/spike potentials
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how do the APs contribute to the contraction/?
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incr strength and duration
greater # of APs-> greater F of contraction |
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can contractions occur without APs?
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yes, but only in stomach (not in rest of GI tract)
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how do neural and hormonal inputs affect freq of slow waves and APs?
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have little effect on freq of slow waves;
greatly affect APs-> det strength of contractions |
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what det the max frequency of contractions?
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freq of SLOW WAVES
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3 fxns of salivation
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digestion of starches, fats
facilitates swallowing antibacterial |
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order of contribution of 3 salivary glands
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submaxillary> parotid> sublingual
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structure of gland
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acinus- blind end with cells secreting saliva
intercalated duct- conn acinus and striated duct striated duct- modifies composition of saliva |
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where are myoepithelial cells located in the gland?
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acinus and intercalated duct
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in which part of the gland is saliva modified?
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striated duct
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what controls saliva prod? what doesnt?
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under ANS control (PSNS and SNS)
NOT under hormonal control |
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how does PSNS lead to salivation?
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incr transport in acinus and ductal cells
vasodilation of vessels prov water for saliva prod stim gland metabolism |
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how does SNS contribute to saliva prod?
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transiently incr prod of saliva
contraction of myoepithelial cells constriction of bld vessels |
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what induces salivation?
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food in mouth
smells, reflexes (pavlov) nausea |
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what inhibits salvation?
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sleep, fatigue, dehydration, fear, anticholinergics (block PSNS)
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composition of saliva
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pH 5.5-6
water, electrolytes, organic cmpds bacteriocidal subst |
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what proteins does saliva contain?
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alpha amylase to digest starches
lingual lipase to digest fats mucin for lubrication |
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how does the ionic composition of saliva compare to plasma?
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ALWAYS HYPOTONIC to plasma b/c is an ultrafiltrate
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how do striated ducts modify ionic composition of saliva?
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reabsorb Na, Cl
secrete K and HCO3 relatively impermeable to water |
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how does flow rate affect saliva ion concentrations?
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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 |
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what is xerostomia?
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dry mouth
due to lack of salivary secretion assoc with chronic infections of buccal mucosa and dental cavities |
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what is xerostomia most commonly due to?
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antidepressants (which are anticholinergic and inhibit PSNS)
also, beta blockers and antihistamines sjogrens radiation damage |
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describe the oral phase of swallowing
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voluntary
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pharyngeal phase of swallowing
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involuntary
breathing inhibited nasopharynx closed by soft palate peristalsis begins in pharynx laryngeal mm contract, close glottis upper esophageal sphincter relaxes |
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what triggers the swallowing reflex?
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initiated voluntarily but req something to trigger reflex
swallowing center in medulla |
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lesions in swallowing center leads to...?
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loss of pharyngeal phase of swallowing
aspiration |
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basic structure of esophagus mm
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upper 1/3 striated
lower 1/2 smooth |
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what makes up the UES? fxn?
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cricopharyngeal mm
sep esophagus from oral cavity prevents entry of air |
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LES? fxn?
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sep esophagus from stomach
prevents reflux of gastric acid |
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primary peristaltic contraction in esophagus
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initiated by swallowing
creates zone of incr pressure behind bolus |
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what happens as bolus reaches LES?
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LES relaxes to let bolus pass, then constricts to prevent reflux
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describe smooth m of esophagus when quiescent
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LES tonically contracted
remainder flaccid |
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secondary peristaltic contraction
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initiated by presence of food in esophagus
cont until all material removed from esophagus |
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GERD
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decr tone of LES
-> heartburn, esophagitis tx with lifestyle changes: lose weight, stop smoking |
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what can longterm exposure to acid reflux lead to?
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barrett's esophagus
metaplasia and esophageal cancer |
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what is achalasia?
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n/m disorder of lower 2/3 esophagus
peristalsis absent LES cant relax |
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what are s/s of achalasia?
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food accumulated in esophagus
takes hrs to digest meals dysphagia, regurgitation of food, wt loss |
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what is eructation?
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belching
swallowed air etc forms bubbles in stomach air enters esophagus when LES relaxes |
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what are the 2 functional regions of stomach?
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orad-proximal; receives meal
caudad-distal; contracts to mix food and propels it into duodenum |
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describe the thickness of the smooth m layers in the stomach
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thickness incr distally towards pylorus
stronger contractions in caudad |
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what is receptive relaxation?
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orad relaxes to accept meal (up to 1.5 L) without incr pressure
mediated by vagovagal reflex which is stim by stretch of stomach |
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what abolishes receptive relaxation?
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vagotomy
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what causes the caudad to contract?
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presence of food
produces chyme |
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where do peristalsis contractions begin in the stomach?
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midstomach (near fundal-corpus border)
move caudally; incr force and velocity |
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where is the pacemaker in the stomach and what does it initiate?
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near border of orad/caudad
prod slow waves |
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what is retropulsion?
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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 |
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what is the migrating myoelectric complex? when is it active?
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contractions that occur every 90 min when fasting
clear stomach of residual food abolished with eating |
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what det rate of gastric emptying?
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food ingested (liq vs solid)
(CHO > protein > fat) rate inversely proportional to pressure in orad stomach (eat big meal, takes longer to empty) |
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what is gastric emptying mainly controlled by?
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signals from duodenum
prevents flow of chyme from exceeding ability of SI to handle it |
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what inhibits gastric emptying?
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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 |
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what is gastroparesis? (s/s, causes)
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impaired or delayed emptying
sx include fullness, nausea, vomiting caused by diabetes (neuropathy), anticholinergics, peptic ulcers that obstruct gastroduodenal canal |
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how do duodenal ulcers cause diarrhea?
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stomach acid damages duodenal lining and impairs reabsorption
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what is dumping syndrome? who is it freq seen in?
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lower SI fills too fast with undigested food from stomach
right after meal or 1-3 hrs later stomach surgery/gastric bypass |
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what are the 2 regions of the stomach based on secretory fxn?
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oxyntic gland mucosa- prox 80%; rel acid, pepsinogen, intrinsic factor, mucus
pyloric gland mucosa- distal 20%; rel mainly gastrin; some mucus, pepsinogen |
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where are the stem cells located in the oxyntic gland?
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stem cells in mucous neck cell area give rise to parietal or epithelial surface cells
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what do parietal cells secrete?
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intrinsic factor and acid
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what do chief cells secrete?
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pepsinogen
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what is the order of cells in the oxyntic gland from lumen out?
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chief cells-> parietal cell-> mucous neck cells-> surface epithelial cells-> goblet cells
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what do the surface epithelial cells in the oxyntic gland secrete?
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bicarb and mucous
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what are the 4 components of gastric juice?
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HCl
pepsin mucus intrinsic factor |
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fxn of HCl in gastric juice
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rel by parietal cells
begins protein digestion activates pepsinogen-> pepsin kills bacteria |
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fxn of pepsin in gastric juice
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stored/rel as pepsinogen; converted by HCl and pepsin to pepsin
begins protein digestion rel due to vagal stimulation |
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what are the 2 forms of mucus?
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soluble and insoluble
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when is soluble mucus secreted?
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rel by mucous neck cells after vagal stimulation
lubricates chyme not present in resting stomach |
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when is insoluble mucus secreted?
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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 |
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what happens when the insoluble mucus contacts acid?
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precipitates into clumps and moves into duodenum with chyme
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fxn of intrinsic factor in gastric juice
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rel by parietal cells
binds B12 and allows reabsorption in ileum absence leads to pernicious anemia |
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mxn of HCl secretion
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parietal cells rel HCl into the lumen of stomach and rel HCO3 into the blood when stimulated
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how is H+ formed in the parietal cell and how is it secreted?
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dissoc of H20-> H+ + OH-
H+ secreted into lumen in exchange for K+ via H/K ATPase |
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how is HCO3 rel into blood from parietal cell?
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exchanged for Cl-; Cl- then moves through channel into lumen
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how does HCl form in the lumen of the stomach?
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H+ and Cl- secreted separately from the parietal cell; forms HCl in the lumen
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what is the alkaline tide?
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in venous blood of actively secreting stomach
created by HCO3 being rel into blood |
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how does gastric juice composition change with rate of secretion?
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at basal rates: primarily NaCl from nonparietal secretion
high rates: primarily HCl from parietal secretion |
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how does the conc of K in gastric juice compare to that in plasma?
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more K in gastric juice than plasma
chronic vomiting-> hypokalemia from loss of K |
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what are 3 stimulants of acid secretion in the stomach?
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ACh
histamine gastrin |
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how does ACh incr acid secretion?
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binds muscarinic R on parietal cells
activated PLC---> Ca |
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how does histamine incr acid secretion?
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binds H2 R on parietal cells
activates adenylate cyclase-->cAMP |
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how does gastrin incr acid secretion?
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binds gastrin/CCK-B R on parietal cells
activates PLC--> Ca |
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which stimulants of acid secretion in the stomach work via PLC?
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ACh and gastrin
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when does potentiation occur in the stomach?
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histamine potentiates actions of ACh and gastrin in acid secretion
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what is the best MOA to block acid secretion in the stomach?
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H2-R blocker because also blocks potentiating effects of histamine on ACh and gastrin
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in addn to parietal cells, what other cells have R for gastrin and ACh?
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enterochromaffin-like cells (ECL)
gastrin stim syn and rel of histamine and cell proliferation ACh also slightly stim syn and rel of histamine |
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what are 2 inhibitors of acid secretion in the stomach?
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low pH (< 3.0)in stomach and chyme in duodenum
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how does somatostatin effect acid secretion in stomach?
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inhibits acid secretion by parietal cells and inhibits gastrin secretion by G cells
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how does chyme in the duodenum inhibit acid secretion in stomach?
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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 |
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what are the 4 phases of acid secretion in the stomach?
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basal
cephalic gastric intestinal |
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describe basal secretion of acid in stomach
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occurs w/o gastric stimulation, b/w meals
circadian rhythms-highest in evening (but gastrin stays level) |
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describe cephalic phase of acid secretion
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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 |
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what stim the gastric phase of acid secretion in stomach?
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entry of food into stomach raises pH--> vagal stim initiates gastrin rel via cephalic phase while gastric phase maintains gastrin rel
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what stim gastrin rel in the gastric phase of acid secretion?
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distention of stomach act mechanoR
initiate local and vagovagal reflexes stim gastrin rel via GRP stim acid secretion vi ACh |
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what is the only nutrient that causes direct rel of gastrin from G cells?
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protein (broken into peptides and aa)
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what effect do Ca and caffeine have on acid secretion in stomach?
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incr
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what initiates the intestinal phase of acid secretion?
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protein digestion products in duodenum-->prox duodenum rel gastrin
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which phase of acid secretion contributes most?
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gastric 60%
cephalic 30% intestinal 10% |
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gastric ulcers
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pain with eating
barrier breaks down distal stomach |
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duodenal ulcers
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more common than gastric
less pain with meal incr levels of pepsin, acid, gastrin |
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causes of peptic ulcers
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H. pylori (urease to neutralize)
NSAIDS (asprin) alcohol |
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Tx of peptic ulcers
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H+ pump inhibitor
antibiotic combo pepto bismol |
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where does the mxn for vomiting begin?
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anti-peristalsis begins in distal SI
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what is retching?
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involves involuntary motions of vomiting but without the vomit
(ex: cats) |
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what are some sx before and during vomiting and what causes them?
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incr salivation, sweating, rapid breathing, irregular heartbeat due to incr ANS
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where is the vomiting center and what occurs with direct activation?
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medulla
vomiting w/o nausea/retching |
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what activates the vomiting center?
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afferents triggered by:
tickle throat distended stomach, duodenum motion sickness pain to genitourinary |
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when do we just get retching w/o vomiting?
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activation of separate second medullary area
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what is the chemoR trigger zone? (for vomiting)
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in 4th ventricle of brain
activated by emetics, radiation, motion sickness |
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what is hyperemesis of pregnancy?
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severe nausea and vomiting that causes weight loss
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effects of prolonged vominting
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hypokalemia
hyponatremia metabolic alkalosis |
