GI Physiology

Question 1

Make a table of the GI regulatory substances

Answer 1

….

Question 2

CCK lesser known facts

Answer 2

I cells in duodenum, jejunum.
Relaxes sphincter of Oddi, slows gastric emptying, increases pancreatic secretion (not bicarb, that’s secretin) Activated by increased fatty and amino acids.
Acts on neural muscarinic pathways to cause pancreatic secretion.

Question 3

Gastrin lesser known facts

Answer 3

G cells from antrum. Inc. gastric H+ secretion, growth of gastric mucosa, and gastric motility. Activated by stomach distention/alkalinization, amino acids, peptides, vagal stimulation, dec. by pH<1.5.
Phenylalanine and tryptophan are potent stimulators.

Question 4

Glucose-dependent insulinotropic peptide

Answer 4

K cells in duodenum, jejunum.
Dec. gastric H+ secretion. Increases insulin release.
Inc. by fatty acids, amino acids, oral glucose.
AKA Gastric Inhibitory Peptide (GIP)/Incretin
Oral glucose has higher insulin release because of this

Question 5

Motilin

Answer 5

Small intestine
Produces migrating motor complexes (MMCs)
Inc. in fasting state
Erythromycin is a motilin receptor agonist.

Question 6

Secretin

Answer 6

S cells in duodenum. inc. pancreatic bicarb secretion, dec. gastric acid secretion, inc. bile secretion.
Inc. by acid, fatty acids in lumen of duodenum
SORT OF LIKE CCK WITH MORE BICARB release/ACID sensitivity

Question 7

Somatostatin

Answer 7

D cells (pancreatic islets, GI mucosa), decrease acid/pepsinogen, pancreatic and small intestine fluid secretion, gallbladder contraction, dec. insulin and glucagon. DECREASES EVERYTHING. 
Inc. by acid, dec. by vagal stimluation.

Question 8

NO

Answer 8

Inc. smooth muscle relaxation including lower esophageal sphincter (LES). Loss of NO secretion is implicated in inc. tone of achalasia.

Question 9

Vasoactive Intestinal Polypeptide (VIP)

Answer 9

Parasympathetic ganglia in sphincters, gallbladder, small intestine.
Inc. intestinal water and electrolyte secretion and inc. relaxation of intestinal smooth muscle and sphincters.
Increased by distention and vagal stimulation and dec. by adrenergic input.

Question 10

VIPoma

Answer 10

non-alpha, non-Beta islet cell pancreatic tumor that secrete VIP.
WDHA syndrome: Copious watery diarrhea, hypokalemia, and achlorhydria

Question 11

Parietal cells of stomach produce

Answer 11

Intrinsic factor and acid

Question 12

What affects parietal cell acid production

Answer 12

Histamine, ACh, gastrin increase

Dec. by somatostatin, GIP, prostaglandin, secretin

Question 13

What makes pepsin

Answer 13

Chief cells

Question 14

What increases pepsin

Answer 14

vagal stimulation, local acid. It is activated by acid.

Question 15

What makes bicarb

Answer 15

Mucosal cells (stomach, duodenum, salivary glands, pancreas) and Brunner glands (duodenum).

Question 16

Gastric parietal cell receptors and ligands

Answer 16

ACh - M3 receptor
Gastrin - CCKb receptor
Histamine - H2 receptor
Prostaglandins/misoprostol and somatostatin: activate Gi

Question 17

Signal transduction in parietal cell

Answer 17

M3 and CCKb activate Gq - IP3/Ca2+ pathway to activate H/K ATPase.
H2 activates Gs - cAMP to activate H/K ATPase
Gi from prostaglandins/somatostatin blocks cAMP

Question 18

Low flow pancreatic secretion

Answer 18

high Cl-. isotonic

Question 19

High flow pancreatic secretion

Answer 19

high HCO3. isotonic.

Question 20

Pancreatic enzymes

Answer 20

alpha-amylase, lipase, phospholipase A, colipase, proteases, trypsinogen

Question 21

Pancreatic protease activation

Answer 21

Trypsinogen to trypsin through enterokinase/enteropeptidase on brush border of duodenum and jejunum. Activates chymotrypsin, elastase, carboxypeptidases, and more trypsin.

Question 22

Glucose and galactose transporter in gut

Answer 22

SGLT1 (Na+ dependent)

Question 23

Fructose transporter

Answer 23

GLUT-5 facilitated diffusion

Question 24

What carbs can be absorbed

Answer 24

Only monosaccharides: once in the enterocytes, they move into bloodstream via GLUT-2

Question 25

Absorption of Folate, B12, and Iron

Answer 25

[Iron Fist, Bro] Iron absorbed as Fe2+ in duodenum, Folate in jejunum and ileum, B12 in terminal ileum with bile acids (requires intrinsic factor)

Question 26

Peyer patches

Answer 26

Have M cells which are APCs. Unencapsulated lymphoid tissue in lamina propria and submucosa of ileum. IgA-secreting plasma cells is the end result, residing in lamina propria.

Question 27

immunology fact: B cells mature in the bone marrow and while floating around get activated by an antigen. They divide and create a few short lived IgM producing plasma cells. Most move into the germinal centers of lymph nodes to interact with T cells which also have found similar antigens which leads to affinity maturation and proliferation and isotype switching.

Answer 27

.

Question 28

What are bile salts

Answer 28

Bile acids conjugated to glycine or taurine, water soluble, along with phospholipids, cholesterol, bilirubin, water, and ions.

Question 29

Rate-limiting step of bile synthesis

Answer 29

7alpha-hydroxylase

Question 30

How does body get rid of cholesterol

Answer 30

Bile is the only way

Question 31

Pathway of bilirubin metabolism

Answer 31

Heme is broken down to bilirubin which is bound to albumin and taken up by the liver. In the liver it undergoes glucuronidation through UDP-glucuronosyl-transferase into conjugated bilirubin which is excreted into the gut. Then turned by gut bacteria into urobilinogen. 80% of urobilinogen is passed into the stool as stercobilin. 20% is reabsorbed. 90% of that is taken up into the liver, 10% goes to the kidney and is excreted as urobilin.

Question 32

Enzyme that conjugates bilirubin

Answer 32

UDP-glucuronsyl-transferase