Gastroinstestinal Physiology

Front 1

Effect of sympathetic stimulation in the GI tract

Back 1

↓ motility, ↓ secretions, ↑ contraction of sphincters

Front 2

Effect of parasympathetic stimulation in GI tract

Back 2

↑ motility, ↑ secretions, ↑ relaxation of sphincters (except LES which contracts), ↑ gastrin release

Front 3

Hormones of the GI system

Back 3

Gastrin, CCK, secretin, GIP

Front 4

Stimulus for gastrin secretion

Back 4

Stomach distension. Stomach acid in the duodenum inhibits gastrin release

Front 5

Sources of gastrin

Back 5

G cells of the stomach anthrum, duodenum

Front 6

Actions of gastrin

Back 6

Stimulates acid secretion by parietal cells, increases motility and secretions.

Front 7

Source of secretin

Back 7

S cells of the duodenum

Front 8

Stimulus for secretin release

Back 8

Acid entering the duodenum

Front 9

Actions of secretin

Back 9

Stimulates HCO3 secretion by pancreas to neutralize acid entering duodenum

Front 10

Source of CCK

Back 10

Cells lining the duodenum

Front 11

Stimulus for CCK secretion

Back 11

Fat and amino acids entering duodenum

Front 12

Actions of CCK

Back 12

Inhibits gastric emptying, stimulates pancreatic enzyme secretion, stimulates contraction of the gallbladder and relaxation of sphincter of Oddi.

Front 13

Source of GIP

Back 13

Duodenum

Front 14

Stimulus for GIP secretion

Back 14

Fat, carbs and amino acids

Front 15

Actions of GIP

Back 15

Inhibits stomach motility and secretion

Front 16

Properties of GI smooth muscle

Back 16

Stretch stimulates contraction, electrical syncytium with gap junctions, pacemaker activity

Front 17

Factors that inhibit gastric motility

Back 17

Acid in the duodenum (secretin), fat in the duodenum (CCK), hypoerosmolarity in duodenum, distension of duodenum

Front 18

Factors that stimulate gastric motility

Back 18

Distension of the stomach and ACh

Front 19

What are the different contractions of the intestines?

Back 19

Segmentation contractions (mixing), peristaltic movements (propulsive).

Front 20

What factors control the ileocecal sphincter?

Back 20

Distension of the ileum relaxes, distension of the colon contracts

Front 21

What are the different contractions of the colon

Back 21

Segmentation contractions (haustrations), peristalsis and mass movements

Front 22

Composition of salivary secretions

Back 22

Low in NaCl because of reabsorption; High in K and HCO3 because of secretion; alpha-amylase begins digestion of carbs; fluid is hypotonic due to NaCl reabsorption and impermeability of ducts to water

Front 23

Parietal cells

Back 23

Located in the middle part of the gastric glands. Secrete HCl and intrinsic factor.

Front 24

Chief cells

Back 24

Located in the deep part of the gastric glands. Secrete pepsinogen which is converted to pepsin by acid medium. Pepsin begins digestion of proteins to peptides

Front 25

Mucous cells of the stomach

Back 25

Located in the superficial part if the gastric glands (gastric pits). Secrete mucus and HCO3. Secretion is stimulated by PGE2

Front 26

Ionic composition of gastric secretions

Back 26

High in H+, K+ and Cl-, low in Na+. Vomiting produces metabolic alkalosis and hypokalemia.

Front 27

Control of acid secretion

Back 27

Acetylcholine, histamine and gastrin stimulate parietal cells to secrete acid.

Front 28

Secretion of acid by parietal cells

Back 28

CO2 is extracted from the blood and combined into H2CO3 by carbonic anhydrase. H+ ions are exchanged by the proton pump for K+ ions (active antitransport)

Front 29

Pancreatic amylase

Back 29

Hydrolyzes α-1,4-glucoside bonds forming α-limit dextrins, maltotriose and maltose

Front 30

Pancreatic lipase

Back 30

Needs colipase which displaces bile from surface of micelles. Lipase digests triglycerides to two free fatty acids and one 2-monoglyceride

Front 31

Cholesterol esterase

Back 31

Hydrolizes cholesterol esters to yield cholesterol and free fatty acids

Front 32

Pancreatic proteases

Back 32

Trypsinogen is converted to trypsin by enterokinase --> chymotrypsinogen is converted to chymotrypsin by trypsin --> procarboxypeptidase is converted to carboxypeptidase by trypsin

Front 33

Ionic composition of pancreatic secretions

Back 33

Isotonic due to permeability of ducts to water and high in HCO3. Stimulated by CCK and secretin.

Front 34

What are the primary bile acids?

Back 34

Cholic acid and chenodeoxycolic acid. Synthesized in the liver from cholesterol.

Front 35

How are bile salts formed?

Back 35

Bile acids (cholic and deoxycholic) are conjugated with glycine and taurine which mix with cations to form salts.

Front 36

What are the secondary bile acids?

Back 36

Formed by deconjugation of bile salts by enteric bacteria - deoxycholic acid (from cholic acid) and lithocolic acid (from chenodeoxycholic acid). Lithocholic acid is hepatotoxic and is excreted.

Front 37

Enterohepatic circulation

Back 37

Bile acids are reabsorbed only in the distal ileum. Resection or malabsoption syndromes lead to steatorrhea and cholesterol gallstones.

Front 38

What are the components of bile?

Back 38

Conjugated bile acids (cholic and chenodeoxycholic), billirubin, lecithin and cholesterol.

Front 39

How are carbohydrates absorbed?

Back 39

Glucose and galactose via active secondary Na cotransporter. Fructose is absorbed independently

Front 40

How are amino acids absorbed?

Back 40

Secondary active transport linked to Na and receptor-mediated endocytosis.

Front 41

How are lipids absorbed?

Back 41

Micelles diffuse to the brush border then digested lipids (2-monoglycerides, fatty acids, cholesterol and ADEK vitamins) diffuse into enterocytes. Triglycerides are resynthesized and packaged as chylomicrons with apoB48. Leave the intestine via lymphatics to thoracic duct.