Acid Secretion & PUD Flashcards
anatomy of the stomach
*cardia
*fundus
*body
*antrum
*pylorus
oxyntic glands
*located in the gastric BODY
-mucous neck cells
-parietal cells
-chief cells
-ECL cells
pyloric glands
*located in the gastric ANTRUM
-mucous cells
-G cells
parietal cells - functions
1) hydrochloric acid
-kills microorganisms
-cleaves pepsinogen to pepsin
-activates pepsin at pH < 4
2) intrinsic factor
-binds vitamin B12, which allows absorption in the terminal ileum
production of HCl by parietal cells
- carbonic anhydrase converts water + Co2 into carbonic acid
- carbonic acid dissociates into H+ and bicarb
- H+/K+ ATPase (proton pump) pumps H+ ions into gastric lumen, and chloride follows
- chloride-bicarbonate counter-transporter on the opposite (basolateral) membrane pumps bicarb into the blood
note - 3 inputs on the parietal cell stimulate the production of acid (acetylcholine, HISTAMINE, and gastrin)
what 3 inputs stimulate acid production by the parietal cell?
- HISTAMINE
- acetylcholine
- gastrin
chief cells - function
*SECRETE PEPSINOGEN
-cleaved to active form by HCl
-pepsin is a proteolytic enzyme
ECL cells - function
*SECRETE HISTAMINE (histamine stimulates the parietal cell to secrete HCl)
stimulation/inhibition of histamine release from ECL cells
*stimulated by: (1) gastrin; (2) acetylcholine (vagus)
*inhibited by: somatostatin
G cells - function
*SECRETE GASTRIN:
-gastrin stimulates ECL cells to release histamine and stimulates other oxyntic glands to secrete HCl and pepsinogens
stimulation/inhibition of gastrin release from G cells
*stimulated by: (1) gastric distension; (2) amino acids
*inhibited by: (1) somatostatin; (2) secretin; (3) gastric acid
D cells - function
*SECRETE SOMATOSTATIN
-somatostatin inhibits: (1) histamine release by ECL cells; (2) gastrin release by G cells; (3) inhibits HCl secretion by parietal cells
stimulation/inhibition of somatostatin release by D cells
*stimulated by: (1) acid; (2) CCK; (3) gastrin
*inhibited by: acetylcholine (vagus)
control of HCl secretion - AGONISTS
**HISTAMINE
control of HCl secretion - ANTAGONISTS
**SOMATOSTATIN
cephalic phase of acid secretion
*elicited by sight, smell, and taste of food
*entirely mediated by the VAGUS NERVE (stimulates parietal cells, ECL cells, and G cells; inhibits D cells)
*feedback inhibition: low gastric pH evokes inhibition of parietal cells & G cells
gastric phase of acid secretion
*once the food moves into stomach
*gastric distension (mechanoreceptors in the gastric wall initiate vasovagal reflexes)
*amino acids & peptides stimulate G cells to secrete gastrin
intestinal phase of acid secretion
*STIMULATION: duodenal distension initiates vasovagal reflex & peptides/amino acids stimulate duodenal G cells
*INHIBITION:
1) acid in the duodenum: inhibits the vasovagal reflex & releases secretin (inhibiting acid secretion)
2) ingested fat & protein in the duodenum releases CCK (inhibiting acid secretion)
mucosal protection of the stomach
*mucus secretion
*bicarbonate secretion
*epithelial barrier
*mucosal blood flow
causes of peptic ulcer disease
1) H. pylori (helicobacter pylori)
2) NSAIDs
H. pylori - overview
*small, gram negative rod with flagella
*colonizes the mucous layer (NOT invasive)
*elaborates UREASE (produces ammonia and thereby neutralizes acid)
H. pylori & gastric malignancy
associated with:
*gastric adenocarcinoma
*MALT lymphoma
tests used to diagnose H. pylori infection
**urea breath test!
**stool antigen assay!
other: biopsy urease test (CLO), histology, culture, serology
action of NSAIDs
*inhibition of cyclo-oxygenase enzymes (COX-1 and COX-2)
*COX-1: produces PROSTACYCLIN (important for protection of gastric mucosa)
*COX-2: induced by inflammation and cytokines
