UW table

Question 1

Gastrin. Source?

Answer 1

G cells (antrum of stomach, duodenum)

Question 2

Gastrin. Action? 3

Answer 2

incr. gastric H+ secretion
incr. growth of gastric mucosa
incr. gastric motility

Question 3

Gastrin. Regulation?

Answer 3

incr. by stomach distention/ alkalinization, amino acids, peptides, vagal stimulation via gastrin-releasing peptide (GRP)
decr. by pH < 1.5

Question 4

Gastrin. Increased in what 3 conditions?

Answer 4

incr. by chronic PPI use
incr. in chronic atrophic gastritis
(eg, H pylori)
incr. (2 arrows) in Zollinger-Ellison syndrome (gastrinoma)

Question 5

Somatostatin. Source?

Answer 5

D cells (pancreatic islets, GI mucosa)

Question 6

Somatostatin. Action? 4

Answer 6

decr. gastric acid and pepsinogen secretion

decr. pancreatic and small intestine fluid secretion

decr. gallbladder contraction

decr. insulin and glucagon release

Question 7

Somatostatin. Regulation? 2

Answer 7

incr. by acid 

decr. by vagal stimulation

Question 8

Somatostatin inhibits what?

Answer 8

Inhibits secretion of various hormones (encourages somato-stasis)
Octreotide is an analog used to treat acromegaly, carcinoid syndrome, VIPoma, and variceal bleeding

Question 9

CCK. Source?

Answer 9

I cells (duodenum, jejunum)

Question 10

CCK. Action? 4

Answer 10

Incr. pancreatic secretion
incr. gallbladder contraction
decr. gastric emptying  
incr. sphincter of Oddi
relaxation

Question 11

CCK. regulation?

Answer 11

incr. by fatty acids, amino acids

Question 12

CCK. where acts to cause pancreatic secretion?

Answer 12

Acts on neural muscarinic pathways to cause pancreatic secretion

Question 13

Secretin. Source?

Answer 13

S cells (duodenum)

Question 14

Secretin. Action?

Answer 14

incr. pancreatic HCO3– secretion

decr. gastric acid secretion  incr. bile secretion

Question 15

Secretin. Regulation?

Answer 15

incr. by acid, fatty acids in lumen of duodenum

Question 16

Secretin. What does HCO3?

Answer 16

incr. HCO3– neutralizes gastric acid in duodenum, allowing pancreatic enzymes to function

Question 17

Glucose- dependent insulinotropic peptide. Source?

Answer 17

K cells (duodenum, jejunum)

Question 18

Glucose- dependent insulinotropic peptide. Action?

Answer 18

Exocrine:
decr .gastric H+ secretion
Endocrine:
incr. insulin release

Question 19

Glucose- dependent insulinotropic peptide. Regulation?

Answer 19

incr. by fatty acids, amino acids, oral glucose

Question 20

Glucose- dependent insulinotropic peptide. oral glucose vs iv glucose?

Answer 20

Also called gastric inhibitory peptide (GIP)

Oral glucose load incr. insulin compared to IV equivalent due to GIP secretion

Question 21

Motilin. Source?

Answer 21

Small intestine

Question 22

Motilin. Action?

Answer 22

Produces migrating motor complexes (MMCs)

Question 23

Motilin. Regulation?

Answer 23

incr. in fasting state

Question 24

Motilin. motilin receptor agonists are used for?

Answer 24

Motilin receptor agonists (eg, erythromycin) are used to stimulate intestinal peristalsis.

Question 25

Vasoactive intestinal polypeptide (VIP). Source?

Answer 25

Parasympathetic ganglia in sphincters, gallbladder, small intestine.

Question 26

Vasoactive intestinal polypeptide (VIP). Action?

Answer 26

incr. intestinal water and electrolyte secretion | incr. relaxation of intestinal smooth muscle and sphincters

Question 27

Vasoactive intestinal polypeptide (VIP). Regulation?

Answer 27

incr. by distention and vagal stimulation decr. by adrenergic input

Question 28

Vasoactive intestinal polypeptide (VIP). What pathological finding produce it?

Answer 28

VIPoma—non-α, non-β islet cell pancreatic tumor that secretes VIP; associated with Watery Diarrhea, Hypokalemia, Achlorhydria (WDHA syndrome)

Question 29

Nitric oxide. Source - not specified.

Answer 29

.

Question 30

Nitric oxide. Action?

Answer 30

incr. smooth muscle relaxation, including lower esophageal sphincter (LES)

Question 31

Nitric oxide. regulation - not specified.

Answer 31

.

Question 32

Nitric oxide. NO effect in achalasia?

Answer 32

Loss of NO secretion is implicated in incr. LES tone of achalasia.

Question 33

Ghrelin. Source?

Answer 33

Stomach

Question 34

Ghrelin. Action?

Answer 34

incr. appetite (“ghrowlin’ stomach”)

Question 35

Ghrelin. Regulation?

Answer 35

incr. in fasting state  | decr. by food

Question 36

Ghrelin. in what state increased and in what decr?

Answer 36

incr. in Prader-Willi syndrome decr. after gastric bypass surgery

Question 37

Intrinsic factor. Source?

Answer 37

Parietal cells (stomach)

Question 38

Intrinsic factor. Action?

Answer 38

Vitamin B12–binding protein (required for B12 uptake in terminal ileum).

Question 39

Intrinsic factor. regulation - not specified.

Answer 39

.

Question 40

Intrinsic factor. relation to autoimmune disease?

Answer 40

Autoimmune destruction of parietal cells --> chronic gastritis and pernicious anemia

Question 41

Gastric acid. Source?

Answer 41

Parietal cells (stomach)

Question 42

Gastric acid. Action?

Answer 42

decr. stomach pH

Question 43

Gastric acid. Regulation? 2

Answer 43

``` incr. by histamine, vagal stimulation (ACh), gastrin decr. by somatostatin, GIP, prostaglandin, secretin ```

Question 44

Pepsin. Source?

Answer 44

Chief cells (stomach)

Question 45

Pepsin. Action?

Answer 45

Protein digestion

Question 46

Pepsin. Regulation?

Answer 46

incr. by vagal stimulation (ACh), local acid

Question 47

Pepsin. Made from what source?

Answer 47

Pepsinogen (inactive) is converted to pepsin (active) in the presence of H+

Question 48

Bicarbonate. Source?

Answer 48

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

Question 49

Bicarbonate. Action?

Answer 49

Neutralizes acid

Question 50

Bicarbonate. Regulation?

Answer 50

incr. by pancreatic and biliary secretion with secretin

Question 51

Bicarbonate. where is trapped?

Answer 51

Trapped in mucus that covers the gastric epithelium