Salivation and Gastric Function Flashcards
how are GI hormones delivered?
they are secreted into capillaries, go through the liver and return in the systemic blood
what is paracrine signaling and what are the three main factors?
chemicals that act in the same tissue that secretes them
serotonin (excites ENS), somatostatin (inhibits pancreatic and gastric secretion and motility) and histamine (stimulates HCl secretion with H2 receptors)
what are neurocrine signals?
signaling molecules synthesized in ENS neurons and released with action potential (neurotransmitters)
where is gastrin secreted and what does it do?
secreted by antral mucosa (G cells)- distension and vagus
increases parietal cell action and mucosal growth
what is CCK secreted by and what does it do?
in duodenum and jejunal I cells- fats and protein
gall bladder contraction, increases pancreatic enzyme and bicarbonate secretion and inhibits gastric emptying
where is secretin secreted and what does it do?
duodenum (S cells)- acidic chyme
increases bicarb and fluid secretion, decreases gastric acid secretion (decreases gastrin), inhibits gastric empty
where is motilin secreted and what does it do?
small intestine mucosa (M cells) during fasting
promotes clearance of indigestible materials
where is glucose dependent insulinopic peptide (GIP) secreted and what does it do?
small intestine mucosa (K cells)- fat and carbohydrates
stimulates insulin secretion and inhibits HCl secretion
digestion of what materials is initiated in the mouth?
carbohydrates and lippids
what type of digestion occurs in the stomach?
protein and lipid (salivary amylase denatured by acid)
where are enzymes in the small intestine located?
secreted into the lumen or anchored to the brush border
what is the function of saliva?
to lubricate (mucus) protect (clear bacteria off teeth and substances that reduce bacterial growth) digest (salivary amylase and lingual lipase)
what is secreted by acinar cells?
alpha amylase and watery substance
what is sjogren syndrome?
autoimmune disease that destroys salivary and lacrimal glands
what is xerostomia?
dry mouth
describe the secretions from salivary glands
basal flow rates: high in K and low in Na and Cl (reabsorbed)
high flow rates: saliva more like plasma with higher bicarb
what is the only agent that affects salivation?
aldosterone- stimulates Na reabsorption and K secretion
where is lingual lipase added to the saliva?
in the mouth
what controls salivary secretion
ANS (unaffected by GI hormones)
PNS increases and sustains secretion
SNS more transient stimulation
what types of mouthfeel stimulate salivation
smooth tactile stimuli- not rough
responses to what GI upset causes salivation?
stomach and small intestine with irritation or nausea
what does the activation of salivary glands cause?
release of kallikrein- results in bradykinin production
vasodilation of capillary increases filtration
where are oxyntic glands located and what cell types do they contain?
in body and fundus
mucous neck cells (mucous), chief cells (pepsinogen and gastric lipase) and parietal cells (IF and HCl)
what occurs when parietal cells are destroled?
achlorhydria and perinicious anemia
what do pyloric glands do? where are they located?
secrete mucus for protenction, gastrin and somatostatin
;pcated om tje amtri,
what do cardiac glands secrete and where are they?
mucus- near LES
what stimulates oxyntic glands?
vagus and ENs
what type of enzyme is pepsin and how is it made
endopeptidase
activated from pepsinogen by HCl (pH 3-5) by removing N terminal
what does mucus do in the stomach?
prevents H+ and pepsin access to mucosa
traps bicarb to be a buffer to H+ and inactivate pepsin
what occurs if H+ reaches the gastric mucosa
degranulation of mast cells increasing blood flow and mucous and bicarb production
what is erosive gastritis and what is it caused by
decreases secretion of mucus and bicarbonate
chronic NSAID use that inhibits prostaglandin synthesis in stomach
what is the main driving force for HCl secretion by parietal cell?
H+ K+ ATP ase in the luminal membrane
Cl follows by diffusion through channels
(targeted by proton pump inhibitors)
where do the H+ ions come from in parietal cells?
CO2 enters the cell and becomes an acid- dissociates into H+ and bicarb
H+ transported into lumen and HCO3- transported into blood with Cl exchanger
where is the vomiting center? what does it cause?
in the medulla
causes salivation, reverse peristalsis, relaxation of UES and expulsion of contents through the mouth
name 4 stimuli that initiate vomiting
irritants in stomach or SI
systemic irritant sensed by 4th ventricle chemoreceptor
head injury
abnormal stimulation of vestibular organs
what does prolonged vomiting cause?
dehydration, lakalosis, hypokalemia
what are 6 stimulators of acid secretion?
vagus (direct and indirect), gastrin (acts on cell and triggers histamine), histamine, insulin, caffeine (increases proton pump) and stress
what are inhibitors of acid secretion?
somatostatin (acts on G cells and parietal cells), GIP (acts on parietal cells) and secretin (acts on G cells)
describe the action of ACh and gastrin on parietal cells.
activate G coupled receptors (separate)> activate phospholipase C> activates protein kinase C> increases intracellular Ca
describe the action of histamine on parietal cells
binds to H2 receptor (g coupled) >activation of adenlyly cyclase> cAMP increase> PKA activation
describe the action of somatostatin and prostaglandins on parietal cells
separate g linked receptors that oppose the action of histamine (decrease cAMP
what do H2 receptor antagonists do?
OTC antacid agents, decrease HCl production
what do proton pump inhibitors do?
block final common pathway of all secretagogues (more effective than histamine antagonists)
describe the cephalic phase
smelling and tasting
vagus directly stimulates parietal cells
indirect stimulation by gastrin productions (gastrin releasing peptide)
describe the gastric phase
distension of the stomach and presence of amino acids
direct and indirect vagal parietal stimulation
distension of antrum and AA> gastrin releasing reflex
describe the intestinal phase
mediated by amino acids
only 10% of gastric acid secretion
when is HCl secretion inhibited? what is the major mediator of this?
when it is no longer needed to activate pepsinogen
somatostatin through direct and indirect effects
what does vagal stimulation of D cells do?
inhibits the release of somatostatin
what are the negative and positive feedback mechanisms of HCl release?
luminal H+ causes release of somatostatin
protein digestion products stimulate gastrin secretion
