GI Physiology & Anatomy

Question 1

Retroperitoneal structures

Answer 1

“SAD PUCKER”:

• Suprarenal (adrenal glands
• Aorta and IVA
• Duodenum (2nd - 4th parts)
• Pancreas (except tail)
• Ureters
• Colon (descending and ascending)
• Kidneys
• Esophagus (lower 2/3)
• Rectum

Question 2

Gastrin

Answer 2

Hormone; Gastrin-CCK homology

Produced by G cells of stomach antrum in response to small peptides and amino acids (especially phenylalanine and tryptophan), dissension of stomach, vagus (via GRP; not affected by atropine).

Increases gastric H+ secretion directly via CCKb receptor on parietal cells (IP3 mediator) and indirectly via ECL cells (releases histamine); also increases gastric motility and growth of gastric mucosa

Inhibited by decreased gastric pH and somatostatin

Question 3

Cholecystokinin (CCK)

Answer 3

Hormone; Gastrin-CCK homology

Produced by I cells of duodenum/jejunum in response to amino acids and fatty acids.

Stimulates contraction of gallbladder and relaxation of sphincter of Oddi; stimulates pancreatic enzyme and bicarb secretion (via potentiation of secretin and neural muscarinic pathways); stimulates growth of exocrine pancreas, inhibits gastric emptying.

Question 4

Secretin

Answer 4

Hormone; Secretin-glucagon homology

Produced by S cells of duodenum in response to H+ and fatty acids in duodenum.

Increases pancreatic bicarb secretion, increases biliary bicarb and bile secretion, and decreases gastric H+ secretion (allows pancreatic enzymes to function)

Question 5

Glucose-depending insulinotropic peptide (GIP)

Answer 5

Hormone; Secretin-glucagon homology

Produced by K cells of duodenum and jejunum in response to oral glucose, fatty acids, and amino acids.

Increases insulin release and decreases gastric H+ secretion

Oral glucose load is more rapidly used than the equivalent load give via IV due to GIP secretion.

Question 6

Somatostatin

Answer 6

Paracrine (diffuse over short distances to act on target cells)

Produced by D cells of the GI mucosa and pancreatic islets in response to H+ in the lumen

Inhibits the release of all GI hormones (downregulates cAMP in the parietal cell)

Somatostatin is inhibited by vagal stimulation

Question 7

Histamine

Answer 7

Paracrine

Produced by ECL cells in response to gastrin.

Increases H+ secretion via H2 receptor on parietal cells (via cAMP); blocked by H2 blockers

Question 8

Vasoactive intestinal peptide (VIP)

Answer 8

Neurocrine (synthesized in neurons of the GI tract); Secretin-glucagon homology

Produced by parasympathetic ganglia in sphincters, gallbladder, and small intestine in response to distention and vagal stimulation.

Produces relaxation of GI smooth muscle and sphincters; stimulates pancreatic HCO3 secretion and inhibits gastric H+ secretion

VIP presumed to mediate pancreatic cholera (WDHA Syndrome: Watery Diarrhea, Hypokalemia, Achlohydria)

Inhibited by adrenergic input

Question 9

Enkephalins

Answer 9

Neurocrine

Produced by nerves in the mucosa and smooth muscle of the GI tract

Stimulate contraction of GI smooth muscle (sphincters) and inhibit intestinal secretion of fluid and electrolytes

Opiates are useful in the treatment of diarrhea

Question 10

Motilin

Answer 10

Produced by cells in the small intestine in response to fasting

Produces migrating motor complexes (MACs)

Motilin receptor agonists (e.g. erythromycin) are used to stimulate intestinal peristalsis

Question 11

Nitric oxide

Answer 11

Increases smooth muscle relaxation (LES)

Loss of NO secretion is implicated in the increases LES tone of achalasia

Question 12

Stimulators and inhibitors of gastric acid production

Answer 12

Stimulators: Histamine, ACh, Gastrin

Inhibitors: Somatostatin, GIP, Prostaglandin, Secretin, VIP, H2 blockers, PPIs, Atropine