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56 Cards in this Set

  • Front
  • Back
most potent stimulus for meal-stimulated HCl acid secretion
gastrin
what receptor does gastrin bind and at what two locations
CCK-B receptor on:
ECL cells - increase histamine synthesis and secretion
Parietal cells - stimulate acid secretion
what produces histamine
enterochromaffin-like (ECL) cells
most important regulator of HCl acid secretion
vagus nerve
how does gastrin releasing peptide (GRP) directly and indirectly stimulate parietal cells
directly - binds to GRP receptor on parietal cells to stimulate HCl secretion
indirectly - binds GRP receptor on G cell to increase gastrin secretion which binds CCK-B receptor on parietal cell
which phase does a vagotomy completely abolish
cephalic phase - acid secretion initiated by sight, smell, taste, and thought of food
3 Actions of somatostatin
1. directly inhibits gastrin release by G cells
2. indirectly inhibits histamine by decreasing gastrin secretion
3. directly inhibits acid secretion by decreasing intracellular cAMP in parietal cells
what produces somatostatin
antral/body D cells
how can somatostatin act as an endocrine and paracrine hormone
endocrine - when Free ions directly stimulate secretion by antral D cells
paracrine - when corpus (body) D cells are stimulated by neurohumoral stimuli
Actions of secretin
inhibits HCl secretion by decreasing G cell gastrin release
increases somatostatin release
what produces secretin
what activates secretin production
release from duodenal S cell in response to decreased intestinal pH
where is gastric HCl and HCO3 derived from
CO2, combines with H20 and forms H and HCO3 via carbonic anhydrase.
what happens to the blood pH following a meal
alkalizes due to HCO3 getting returned to the blood for every H secreted in the parietal cell
4 receptors and second messanger system for gastric acid secretion by parietal cell
1. CCK-B receptor binds gastrin and increases IP3 and DAG leading to increased intracellular Ca
2. H2 receptor binds histamine which increases adenyl cyclase and cAMP
3. M3 muscarinic receptor binds ACh which increases IP3 and DAG
4. GRP receptor binds GRP causing increased IP3 and DAG
pre-epithelial protective mechanism
mucus layer that allows little diffusion and contains HCO3 to counteract the pepsin
epithelial protective mechanism
tight junctions and cellular restitution to replace damaged cells
sub-epithelial protective mechanism
regulated by PGE2 and NO:
increased blood flow, increased mucus secretion, stimulates HCO3 secretion, inhibits HCl secretion by parietal cells (PGE2)
how does CagA+ H. pylori disrupt the gastric mucosal protective mechanism
protease - alters the viscosity and permeability of the mucus barrier
cytotoxin - disrupts the tight junctions between adjacent epithelial cells and allow back diffusion of H ion
how does chronic NSAID therapy disrupt gastric mucosal protective mechanism
decreases COX activity to decrease PGE2 synthesis. Leads to thinning of mucus layer, decreased HCO3 secretion, and decreased blood flow
3 phenotypes of H. pylori infection and types of disease produced
1. mild pangastritis - usually asymptomatic with no disruption of acid secretion
2. antral-predominant - increased gastrin and acid secretory predisposing them to ulcers
3. corpus-predominant - gastric atrophy with decreased gastric acid production, predisposes them to gastric ulcers and adenocarcinoma
patient presents with dyspepsia, awakens at night, and pain is relieved within minutes of food ingestion
peptic duodenal ulcer
patient presents with dyspepsia that worsens upon eating, they have nausea, vomiting, and weight loss
peptic gastric ulcer
how does antral infection with H. pylori lead to peptic duodenal ulcer
H. pylori destroys somatostatin producing D cells, increases gastrin production by G cells, and increases histamine production by ECL cells. Hypergastrinemia increases number of parietal cells leading to gastric metaplasia of duodenum where H. pylori can thrive
How doe H. pylori activate inflammation
tirggers epithelial cells to secrete IL-8 which recruits and activates neutrophils
how does corpus infection with H. pylori lead to peptic gastric ulcer
organism penetrates the mucus layer and alters the mucus secretion and epithelial layer leading to self-digestion of epithelial cells. hypersecretion of acid is not necessary for this process to occur
which H. pylori associated ulcer is hypersecretion of acid necessary
antral-predominant - hypersecretion of acid causes gastric metaplasia of duodenum
corpus-predominant - causes ulcer via normal acid secretion in an area with compromised mucus layer
what are the virulence factors of H. pylori
urease - buffers HCl
catalase - neutralizes H2O2
3 complications associated with peptic ulcer disease and location of each
bleeding - posterior duodenum
perforation - anterior duodenum
ulcer penetration - posterior duodenum
rate of acid secretion seen in:
duodenal peptic ulcer
gastric peptic ulcer
gastric carcinoma
duodenal ulcer - high acid secretion due to hypergastrinemia
gastric ulcer - low acid secretion due to gastric atrophy
gastric carcinoma - associated with achlorhydria (very low acid secretion)
3 conditions associated with elevated gastrin levels
gastrinoma
peptic ulcers
gastric carcinoma
signs that point to gastrinoma present
plasma gastrin concentration > 200 pg/mL
basal acid secretory rate > 15 mmol/hr
ulcers with diarrhea
multiple ulcers develop simultaneously
what electrolyte abnormalities develop from nasogastric suctioning or persistent vomiting
leads to loss of HCl and K causing hypokalemic metabolic alkalosis. the intravascular depletion further worsen this by activating RAAS
what two things are responsible for preventing reflux of gastric contents into the lower esophagus
LES
diaphragmatic crux
what pathophysiologic mechanisms lead to mild and severe forms of GE reflux disease
transient lower esophageal ralaxation, decreased LES pressure leads to mild form
anatomic disruption of GE jxn such as hiatal hernia leads to severe form
patient presents with chest pain, nocturnal coughing, wheezing, laryngitis
GERD
how you differentiate chest pain from GERD vs. angina
acid suppression therapy with proton pump inhibitor resolves the symptoms of GERD
three major causes for peptic ulcers
H. pylori
chronic NSAID use
gastrinoma
what is predominantly responsible for the cephalic phase of acid secretion
vagal activity
what are the three phases of acid secretion
cephalic - initiated by sight, smell, taste, and thought of food. Mediated by ACh and GRP from vagal activity (30%)
gastric - chemical products of digestion stimulate gastrin release (60% of acid secretory response to feeding)
intestinal - amino acids and peptides stimulate gastrin release from G cells in the duodenum (10%)
what converts pepsinogen into pepsin
acid catalyzes this conversion
what secretes pepsinogen
chief cells
what can disrupt the epithelial tight junctions and cause back leak of H ions into gastric epithelial lining
bile agents
alcohol
aspirin
CagA+ H. pylori
mal effects of NSAIDs on the mucosal layer of the stomach
decrease mucosal blood supply
damaged the tight junctions
augments histamine-stimulated acid secretion in parietal cells
increase production of oxygen-derived free radicals
risk factors for developing peptic duodenal ulcers
genetic - increased number of parietal cells or concentration of pepsinogen
smoking - nicotine inhibits pancreatic bicarbonate secretion
emotional stress
urease breath test
ingestion of radiolabeled urea which H. pylori hydrolyzes it into NH3 and radiolabled HCO3. The radiolabeled HCO3 is absorbed into the blood and excreted as radiolabeled CO2 into the breath
where do gastric ulcers tend to be malignant
body/fundus
benign in the antrum
what contributes to mucosal tissue damage in corpus-predominant gastritis
mucosal antibody response caused by H. pylori
what is seen in corpus-predominant gastritis
decreased number of parietal cells
autoimmune antibody tissue damage
increased gastrin secretion
reflux of duodenal contents (bile, lysolecithin, pancreatic enzymes)
differentiate how COX-1 and COX-2 inhibitors lead to increased prevalance of gastric peptic ulcers
COX-1 inhibitor - decreased mucus secretion, bicarbonate secretion, and blood flow
COX - 2 inhibitor - blocks the normal inhibition of leukocyte adherence and the normal epithelial proliferation when damage occurs
what correlates more with ulcerogenic potention, COX-1 or COX-2
COX-1
associated with MEN type I
gastrinoma (zollinger-ellison syndrome)
what normally increases LES tone
ACh and gastrin
what normally decreases LES tone
VIP
NO
PGE2
what aberrantly decreases LES tone
caffeine
nicotine
alcohol
fatty meal
most common cause of severe GERD and erosive esophagitis
combination of hypotensive LES plus and abnormal diaphragmatic sphincter
what can trigger reactive airway disease and pulmonary fibrosis in a patient with GERD
aspiration of refluxed material into the tracheobronchial tree