GI PHysio Flashcards
Endocrine hormones
released into circulation and reach all tissues
i.e. secretin, gastrin, CCK, GIP and motilin
Paracrine
released from endocrine cells and diffuse through extracellur space to target
i.e. histamine
Neurocrine
GI peptides located in nn. acting as neurotransmitters.
i.e. ACh
Secretin
“natures antacid”
stimulus: released from duodenal mucosa by HCl when pH falls below 4.5
site: released from duodenal mucosa
actions: stimulates pancreatic and liver bicarb. secretion, inhibits gastric emptying
inhibits gastrin release
Gastrin
Stimulus: distension due to food
Site of release: G cells in gastric mucosa, duodenum, and pancreas
Action: stimulates release of HCl by pareital cells of stomach via release of histamine from ECL cells
- aids in gastric motility
- acid feeds back to inhibit gastrin release, also inhibited by secretin and glucagon release
CCK (cholecystokinin)
Stimulus: proteins and fat in duodenum
Site of release: mucosal cells of small intestine and duodenum
Actions: stimulates gallbladder contractions to release bile for fat digestion and pancreatic bicarb. release
Gastric inhibatory peptide (GIP)
stimulus: glucose, fat, protein
site of release: intestinal mucosa
action: inhibits gastric secretions and stimulates insulin release
Motilin
stimulus: cyclical release every 90 minutes under neural control during periods of fasting or presence of acid/fat in duodenum
site of release: upper small intestine
action: stimulates gastric motility and upper GI motility via the interdigestive migrating myoelectric complex (MMC)
gastrin CCK interaction
- they can both activate each others receptors b/c they have similar chemical structures
Enteroglucagon
similar to secretin
- release stimulated by fat
- releases insulin, inhibits gastric secretion and delays gastric emptyig
- pancreatic alpha cells
Pancreatic polypeptide
- polypeptide isolated from insulin
- release stimulated by protein, fat, glucose
- inhibits pancreatic bicarb. and enzyme secretion
Peptide YY
release stimulated by fat
inhibits gastric secretion and emptying as well as intestinal motility
Nuerocrine peptides
substance P, neurotensin, VIP, bombesin, enkephalins
substance P
stimulates intestinal motility and gallbladder contraction
neurotensin
increases blood glucose by stimulation of glycogenolysis. inhibits release of insulin
VIP
mediates relaxation of intestinal smooth muscle and vasodilates SM via NO
Bombesin
like GRP - released by vagal stimulation with resulting release of gastrin
Enkephalins
opiates slow intestinal motility and is used to treat diarrhea
Paracrine peptides
somatostatin, histamine,
somatostatin
found in gastric duodenal mucosa and pancreas
inhibits gastrin release and gastric acid secretion
histamine
produced by ECL cells
- released by gastrin, stimulate acid secretion from parietal cells
- potentiates action of gastrin and ACh on acid secretion
- binds with H2 receptors
Gastrinoma/Zollinger-Ellison Syndrome
tumor of pancreas/duodenum
continually release gastrin into blood
results in peptic ulcers, diarrhea, steatorrhea, hypokalemia
Pancreatic Cholera
- watery diarrhea syndrome
- overproduction of VIP due to pancreatic islet cell tumor
- results in signifiant intestinal secretion of fluid and electrolytes with production of copious diarrhea
- frequently lethal due to large volume of fluid lost
what do parietal cells secrete?
HCl: activates pepsinogen to pepsin (this is stimulated after a meal by gastrin and histamine)
IF –> absorbs vit B12
Chief/zymogenic cells
Peptic cells: secretes pepsinogen/zymogens
Oxyntic glands of stomach
located in fudus/body
Parietal, peptid, mucous cells
Pyloric glands
G cell and mucous cells
G cells
secrete gastrin: stimulates HCl and pepsinogen release (too much gastrin, drops pH and increases pepsin resulting in ulcers)
Alkaline tide
H+ is pumped out into gastric lumen via H+/K+ ATPase
Cl- is pumped into parietal cells and gastric lumen via HCO3-/Cl- co transporter, thus directly after eating the blood becomes alkaline
M3 Receptors;
respond to ACh secreted from Vagus n.
results in neuronal stimulation of parietal cells –> increased HCl secretion
H2 receptors
histamine secreted from ECL cells stimulates parietal cells, thus increasing HCl secretion. Paracrine stimulation
CCK receptor
Gastrin is secreted from G cells, works on CCK receptors. stimulates parietal cells and thus increases HCl. this is hormonal
Somatostatin
inhibits G cell release of gastrin, inhibits parietal cell release of HCl
Gastric inhibitory peptide
inhibits parietal cells in duodenum and jejunum
secretin
inhibits gastrin
“natures anacid”
HCO3- release in duodenum
phases of secretion
- cephalic: reflex sends impulses to medulla oblongata stimulating vagus n.
- gastric phase: food distends gastric mucosa: stimulates vagus and ENS
- Intestinal phase: peptides in duodenum stimulate gastrin secretion
- secretin released when pH is too low in duodenum, results in HCO3- release
CCK: released when fatty food in duodenum, results in bile release
Vagotomy
cutting of vagus n. to inhibit gastric acid secretion
used to treat peptic ulcers
Pepsinogen
secretion activated by vagus n. via Ach.
secreted by Chief cells
Is converted to enzyme Pepsin via HCl.
Pernicious anemia
results from absence of IF, no B12 absorption, resulting in defective erythrocyte production
Components of mucous?
HCO3- in mucous. results in acid being neutralized
- If H+ penetrates cells, destroys mast cells, histamine is released, more H+ released resulting in further damage.
- damage can be caused by alcohol, H. pylori, bile acids
Peptic ucler disease
often asscoated with H. pylori
- acid and pepsin break through mucosal barrier, stimulates mast cells to release histamine, results in parietal cells releasing more HCl
- can include gastric ulcer disease or duodenal ulcer disease
gastric ulcer disease
- assoc. with H. pylori
- gastrinoma: too much release of gastrin
- prob. with pepsin staying active too long
Duodenal ulcer disease
increased acid secretion in gastric region
increased pepsin activation
pancreatitis: decreased HCO3- secretion
Pentagastrin
has similar effect to gastrin, used to challenge people with peptic ulcer problems.
gastrinoma/duodenal ulcer –> gastric is already elevated, won’t go up much further
Gastrinoma/Zollinger-Ellison Syndrom
increased gastrin secretion, at rest and after meals
- results in gastric ulcers
Atrophic gastritis
H. pylori infection, results in increased gastric acid
Pernicious anemia
Abs produced against parietal cells, results in decreased H+, no gastrin produced, no B12 absorption
Omeprazole/Priolosec
proton pump inhibitor
decreases H+ release
used to treat peptic ulcers
can results in pneumonia, C. diff growth, osteoporosis.
Xerostomia
dry mouth only
absence of saliva production
resulting from drugs, radiation, AI disease
Sjoren’s syndrome
dry mouth and no tears
AI targets salivary and lacrimal glands
difficulty chewing, swallowing, speech and dental problems
ductal cells?
reabsorb Na+, Cl- ; secrete K+ HCO3- in saliva
results in hypotonic saliva
via NA/K+ ATPase and Cl-/HCO3- exchanger
how is saliva controlled?
only through ANS
PS: Ach –>M3 receptors –> fluid secretion
stimulated by smell, taste, sound site, chewing
inhibited by : sleep, fear, antidepreesant meds
