GI Hormones

eesohbel's version from 2015-07-30 21:27


Question Answer
Secreted by G cells (Antrum, Duodenum)Gastrin
Secreted by Parietal cellsIntrinsic Factor (IF) and Gastric acid
Secreted by Chief cellsPepsin
Secreted by Mucosal cellsHCO3-
Secreted by D cells (Pancreas, GI mucosa)Somatostatin
Secreted by I cells (duodenum and jejunum)Cholecystokinin (CCK)
Secreted by S cells (duodenum)Secretin
Secreted by K cells (duodenum)GIP
Secreted in the Small intestineMotilin
Parasympathetic gangliaVIP
Gastrin↑ H+ secretion
↑Gastric motility
IFBinds B12 to help it be reabsorbed in the ileum
PepsinProtein digestion
HCO3-Neutralizes acid in the stomach, duodenum (brunner glands), pancreas
SomatostatinUniversal inhibitor! Used to treat variceal bleeding, carcinoid syndrome, acromegaly and insulinoma
Cholecystokinin↑Pancreatic secretion
↑GB contraction!!
Relaxes sphincter of oddi
Slows gastric emptying
Secretin↑Pancreatic HCO3-
↑Bile secretion
Inhibits gastric acid
GIPExocrine: ↓Gastric H+
Endocrine: ↑Insulin
VIP↑Water and electrolyte secretion
↑Relaxation of intestinal SM
NORElaxes SM and LES
Stimulated by stomach distentionGastrin
Increased by acidSomatostatin
Increase by FACCK, Secretin, GIP
Stimulated by HIstamine, ACh and gastrinParietal cells releasing gastric acid!
Stimulated by vagusPepsin and Gastric acid
chronic PPI use leads to an increase in what hormonegastrin
In achalasia what hormone is lossNO leads to increased LES tone
Gastrin increases acid secretion primarily through its effects onECL cells rather than through direct effect on parietal cells
Function of secretionincrease pancreatic HCO3 secretion; decrease gastric acid secretion; bile secretion
phenyalanine, calcium and tryptophan are potent stimulators of what hormonegastrin
what hormone stimulates the release of bicarb-rich secretions from the exocrine pancreassecretin
most potent stimulus for secretin releaseHCL

Islet cell tumors

Question Answer
somatostainoma symptomsachlorhydria (blockage of gastrin), cholelithiasis (blockage of CCK), steatorhhea (blockage of secretin), diabetes (blockage of GIP release)
Treatment for a somatostainomastreptozotocin
VIPomaneoplasm that produces ectopic VIP
Symptoms of VIPomasecretory diarrhea, aclorhydria. Remember WDHA (Watery Diarrhea, Hypokalemia and Achlorhydria)
Treatment of VIPomaoctreotide
Serology of VIPomahypokalemia, normal anion gap metabolic acidosis
PPI leads to an increase in what hormonegastrin as a reaction to blocked parietal cells
If you block any one three parietal cell receptors (gastrin, acetylcholine or histamine)you will inhibit acid production to a great extent


Question Answer
Vagal stimulationgastrin, gastric acid, VIP, pepsin
↓ Somatostatin
Hormones released from the duodenumI cells - CCK
S cells - Secretin
K cells - GIP
Hormones released from the antrumD cells - Somatostatin
Mucous cells - mucus
G cells - Gastrin (into circulation), GRP is the neurotransmitter, not ACh
Hormones released in the body of the stomachChief cells - pepsinogen
Parietal cells - HCL, IF
How does gastrin cause release of gastric acid?Gastrin released into circulation by G cells in antrum → + ECL cells → produce histamine → + parietal cells → gastric acid
Inhibitors of gastric parietal cells/Gastric acid releaseAtropine blocks the M3 receptor (and inhibits the Gq, Ip3/CA, ATPase pathway
H2 blockers block H2 receptor and block the cAMP activation of the ATPase
Proton pump inhibitors block the ATPase (H+ release) directly
Brunner's gladnsDuodenal submucosa
Secretes alkaline mucus
Peptic ulcer disease → hypertrophy of Brunner's glands

Digestion enzymes & extras

α-amylasestarch digestion
Secreted in active form
Lipase, phospholipase A, colipaseFat digestion
ProteasesProtein digestion
Trypsin, chymotrypsin, elastase, carboxypeptidases
Secreted as proenzymes (zymogens)
TrypsinogenCoverted to trypsin, which activates other proenzymes and releases more trypsinogen
Converted to trypsin by enterokinase/enteropeptidase, secreted by duodenal mucosa
Salivary amylaseStarts digestion in mouth
hydrolyzes α-1,4 linkages to yield disaccharides (maltose and α-limit dextrins)
Pancreatic amylaseHydrolyzes starch to oligosaccharides and disaccharides in duodenum
Oligosaccharide hydrolasesAt bush border of intestine
rate-limiting step in carbohydrate digestion
produces monosaccharides from oligo- and disaccharides
Carbohydrate absorptionOnly monosaccharides
Glucose & galactose - SGLT1 (Na dependent)
Fructose - facilitated diffusion by GLUT-5
All are transported to blood by GLUT-2
D-xylose absorption testdifferentiates small bowel disease from pancreatic disease and bile salt deficiency. An oral form is given which does not need pancreatic enxymes. if levels continue to be low then not absorbed because of small intestine problems
Iron absorptionas Fe2+ in duodenum
Folate absorptionin jejunum
B12 absorptionin terminal ileum along with bile acids
requires intrinsic factor
Peyer's patchesunencapsulated lymphoid tissue found in lamina propria and submucosa of ileum
Contain specialized M cells that take up antigen
The immunology of peyer's patchesB cells stimulated in germinal centers of Peyer patches differentiate into IgA-secreting plasma cells which reside in the lamina propria
Bile compositionBile salts: bile acids conjugated to glycine or taurine, making them water soluble
Rate limiting step of bile synthesisCatalyzed by cholesterol 7α-hydroxylase
Functions of bileDigestion and absorption of lipids and fat-soluble vitamins
Cholesterol excretion
Antimicrobial activity via membrane disruption
Bilirubinproduct of heme metabolism
Removed from blood by liver, conjugated with glucuronate, and excreted in bile
Direct bilirubinconjugated with glucuronic acid in the liver
water soluble
Indirect bilirubinunconjugated
water insoluble
increased indirect bilirubinexcess hemolysis or severe liver damage
increased direct bilirubinindicates blockage of bile ducts
Excretion of conjugated (direct) bilirubinUrobilinogen → 20% to kidney(10%)/liver(90%), 80% to feces as stercobilin
iron absorptiondoudenum

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