UW table Flashcards
Gastrin. Source?
G cells (antrum of stomach, duodenum)
Gastrin. Action? 3
incr. gastric H+ secretion
incr. growth of gastric mucosa
incr. gastric motility
Gastrin. Regulation?
incr. by stomach distention/ alkalinization, amino acids, peptides, vagal stimulation via gastrin-releasing peptide (GRP)
decr. by pH < 1.5
Gastrin. Increased in what 3 conditions?
incr. by chronic PPI use
incr. in chronic atrophic gastritis
(eg, H pylori)
incr. (2 arrows) in Zollinger-Ellison syndrome (gastrinoma)
Somatostatin. Source?
D cells (pancreatic islets, GI mucosa)
Somatostatin. Action? 4
decr. gastric acid and pepsinogen secretion
decr. pancreatic and small intestine fluid secretion
decr. gallbladder contraction
decr. insulin and glucagon release
Somatostatin. Regulation? 2
incr. by acid
decr. by vagal stimulation
Somatostatin inhibits what?
Inhibits secretion of various hormones (encourages somato-stasis)
Octreotide is an analog used to treat acromegaly, carcinoid syndrome, VIPoma, and variceal bleeding
CCK. Source?
I cells (duodenum, jejunum)
CCK. Action? 4
Incr. pancreatic secretion incr. gallbladder contraction decr. gastric emptying incr. sphincter of Oddi relaxation
CCK. regulation?
incr. by fatty acids, amino acids
CCK. where acts to cause pancreatic secretion?
Acts on neural muscarinic pathways to cause pancreatic secretion
Secretin. Source?
S cells (duodenum)
Secretin. Action?
incr. pancreatic HCO3– secretion
decr. gastric acid secretion incr. bile secretion
Secretin. Regulation?
incr. by acid, fatty acids in lumen of duodenum
Secretin. What does HCO3?
incr. HCO3– neutralizes gastric acid in duodenum, allowing pancreatic enzymes to function
Glucose- dependent insulinotropic peptide. Source?
K cells (duodenum, jejunum)
Glucose- dependent insulinotropic peptide. Action?
Exocrine:
decr .gastric H+ secretion
Endocrine:
incr. insulin release
Glucose- dependent insulinotropic peptide. Regulation?
incr. by fatty acids, amino acids, oral glucose
Glucose- dependent insulinotropic peptide. oral glucose vs iv glucose?
Also called gastric inhibitory peptide (GIP)
Oral glucose load incr. insulin compared to IV equivalent due to GIP secretion
Motilin. Source?
Small intestine
Motilin. Action?
Produces migrating motor complexes (MMCs)
Motilin. Regulation?
incr. in fasting state
Motilin. motilin receptor agonists are used for?
Motilin receptor agonists (eg, erythromycin) are used to stimulate intestinal peristalsis.
Vasoactive intestinal polypeptide (VIP). Source?
Parasympathetic ganglia in sphincters, gallbladder, small intestine.
Vasoactive intestinal polypeptide (VIP). Action?
incr. intestinal water and electrolyte secretion
incr. relaxation of intestinal smooth muscle and sphincters
Vasoactive intestinal polypeptide (VIP). Regulation?
incr. by distention and vagal
stimulation
decr. by adrenergic input
Vasoactive intestinal polypeptide (VIP). What pathological finding produce it?
VIPoma—non-α, non-β islet cell pancreatic tumor that secretes VIP; associated with Watery Diarrhea, Hypokalemia, Achlorhydria (WDHA syndrome)
Nitric oxide. Source - not specified.
.
Nitric oxide. Action?
incr. smooth muscle relaxation, including lower esophageal sphincter (LES)
Nitric oxide. regulation - not specified.
.
Nitric oxide. NO effect in achalasia?
Loss of NO secretion is implicated in incr. LES tone of achalasia.
Ghrelin. Source?
Stomach
Ghrelin. Action?
incr. appetite (“ghrowlin’ stomach”)
Ghrelin. Regulation?
incr. in fasting state
decr. by food
Ghrelin. in what state increased and in what decr?
incr. in Prader-Willi syndrome decr. after gastric bypass surgery
Intrinsic factor. Source?
Parietal cells (stomach)
Intrinsic factor. Action?
Vitamin B12–binding protein (required for B12 uptake in terminal ileum).
Intrinsic factor. regulation - not specified.
.
Intrinsic factor. relation to autoimmune disease?
Autoimmune destruction of parietal cells –> chronic gastritis and pernicious anemia
Gastric acid. Source?
Parietal cells (stomach)
Gastric acid. Action?
decr. stomach pH
Gastric acid. Regulation? 2
incr. by histamine, vagal stimulation (ACh), gastrin decr. by somatostatin, GIP, prostaglandin, secretin
Pepsin. Source?
Chief cells (stomach)
Pepsin. Action?
Protein digestion
Pepsin. Regulation?
incr. by vagal stimulation (ACh), local acid
Pepsin. Made from what source?
Pepsinogen (inactive) is converted to pepsin (active) in the presence of H+
Bicarbonate. Source?
Mucosal cells (stomach, duodenum, salivary glands, pancreas) and Brunner glands (duodenum).
Bicarbonate. Action?
Neutralizes acid
Bicarbonate. Regulation?
incr. by pancreatic and biliary secretion with secretin
Bicarbonate. where is trapped?
Trapped in mucus that covers the gastric epithelium
