Gastrointestinal - Physiology

eliot2014's version from 2016-01-27 20:14

GI Hormones

HormoneWhere its madeactionregulationnotes
GastrinG cells (antrum of stomach, duodenum)increase gastric H+ secretion,
growth of gastric mucosa,
↑ gastric motility
↑: by stomach distention/alkalinization, amino acids, peptides, vagal stimulation via gastrin releasing peptide
↓: stomach pH < 1.5
↑↑ in Zollinger-Ellison syndrome
↑ by chronic PPI use, chronic atrophic gastritis
Potent stimulators: phenylalanine, typtophan
CCKI cells (duodenum and jejunum)↑ pancreatic secretion
↑ gallbladder contraction
Decreases gastric emptying
Increases sphincter of Oddi relaxation
↑ by fatty acids, amino acidsacts on neural muscarinic pathways to cause pancreatic secretion
SecretinS cells (duodenum)↑ pancreatic HCO3 & bile excretion
↓ gastric acid secretion
↑ by acid, fatty acids in duodenal lumen↑ HCO3 neutralizes gastric acids in duodenum, allowing pancreatic enzymes to function
SomatostatinD cells (pancreatic islet cells, GI mucosa)"Desist GI tract!"
↓ gastric acid and pepsinogen secretion
↓ pancreatic and small intestine fluid secretion
↓ gallbladder secretion
↓ insulin and glucagon release
↑ by acid
↓ by vagal stimulation
Inhibitory secretion of GH, insulin, and other hormones (encourages somatostasis)
Octreotide is an analog used to treat acromegly, insulinoma, carcinoid syndrome, and variceal bleeding
GIP (glucose-dependent insulinotropic peptide)K cells (duodenum, jejunum)↓ gastric H+ secretion, ↑ insulin release↑ by fatty acids, amino acids, oral glucose (it is the only GI hormone that is secreted in response to 3 types of nutrients)AKA "gastric inhibitory peptide
Because of GIP, oral glucose causes a larger insulin release compared to IV glucose
VIP (vasoactive intestinal peptide)parasympathetic ganglia in sphincters,
small intestine
↑ intestinal water and electrolyte secretion
↑ relaxation of intestinal smooth muscle and sphincters
Increase HCO3- release
Decrease H+ release
↑ by distention and vagal stimulation
↓ by adrenergic input
VIPoma: non-α, non-β islet cell pancreatic tumor that secretes VIP.
Copius watery diarrhea, hypokalemia, achlorhydria (WDHA syndrome)
Motilinsmall intestinein fasting state, produces migrating motor complexes↑ in fasting stateMotilin receptor agonists (erythromycin) used to stimulate intestinal peristalsis
Intrinsic Factorparietal cells (stomach)vitamin B12 binding protein-autoimmune destruction of parietal cells → chronic gastritis and pernicious anemia
Gastric acidparietal cells (stomach)↓ stomach pH↑ by histamine, ACh, gastrin
↓ by somatostatin, GIP, prostaglandin, secretin
Gastrinomas: high levels of acid secretion and ulcers refractory of medical therapy
pepsinchief cells (stomach)protein digestion↑ by vagal stimulation, local acidInactive pepsinogen → pepsin by H+
HCO3Mucosal cells (stomach, duodenum, salivary glands, pancreas)
Brunner's glands (duodenum)
Neutralizes acid↑ by pancreatic and biliary secretion with secretinHCO3 is trapped in mucus that covers the gastric epithelium
NO-Increases smooth muscle relaxation, including lower esophageal sphincter; --Loss of NO secretion is implicated in increased LES tone of achalasia
GhrelinStomachIncreases appetiteincreased in fasting state and decreased by foodincreased in Prader-Willi syndrome and decreased after gastric bypass surgery


Question Answer Column 3
Vagal stimulation-↑ gastrin, 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 testdistinguishes GI mucosal damage from other causes of malabsorption
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's patches differentiate into IgA-secreting plasma cells → lamina propria
IgAA receives protective secretory component and is then transported across the epithelium to the gut to deal with intraluminal antigen
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
Excretion of conjugated (direct) bilirubinUrobilinogen → 20% to kidney(10%)/liver(90%), 80% to feces as stercobilin