Flashcards in El Stomacho Deck (22)
Vagus nerve is cholinergic. Cutting it decreases contraction of smooth muscle and decreases relaxation of the sphincters
proton pump inhibitors- They are absorbed in the intestine and travel via the blood to the stomach. When PPIs reach the parietal cell-canaliculi, the acidic environment converts these drugs into sulfonamide/sulfenic acid, which interact with sulfhydryl groups in H+-K+-ATPase and inactivate the proton pump irreversibly.
binds to histamine H2RA receptors on parietal cells and prevents the action of histamine.
Most side effects: complicates warfarin therapy by inhibiting liver enzyme that metabolizes it (cytochrome p450), therefore extrinsic clotting cascade does not have crucial cofactors bc warfarin metabolizes those-> prolonged PT time
side effects: laxative, Hypermagnesemia and renal failure (kidney excretes magnesium)
useful in treating gastroparesis for two reasons. 1) It binds to dopamine D2 receptors on the neurons in the myenteric plexus and thereby prevents the inhibitory effect of dopaminergic neurons. 2) Metoclopramide activates serotonin 5HT4-receptors on vagal neurons and thereby increases parasympathetic action
side effects: tardive dyskinesia, oculogyric crisis, dystonia
enhances mucosal protection. It is a complex salt of sucrose sulfate and aluminum hydroxide. At pH<4, sucralfate becomes a gel-like substance that binds preferably to defective mucosa
side effects: constipation
H. pylori infection
secretes the enzyme urease, an enzyme produced by the bacteria, converts urea into ammonia. The ammonia increases the pH around the bacteria further allowing it to survive in the stomach.
also secretes catalase and oxidase
dx: A commonly used clinical diagnostic test for urease activity involves drinking 13C-urea and measuring 13CO2 in the breath
tx: acid-suppressing agent (e.g. PPI or H2RA) and an antibiotic (commonly clarithromycin)
binds to ulcers, allowing a physical protective barrier. It also suppresses H. pylori infection
anatomical divisions of the stomach
FCAP- Fundus/Cardia, Corpus, Antrum, Pylorus
paralyzed stomach muscle -> food and secretions do not empty normally from the stomach, and there is nausea and vomiting
causes: disease of either the stomach muscle itself or the nerves controlling the muscle. most common cause of gastroparesis is diabetes mellitus
stimulate gastric motility
Acetylcholine, gastrin and motilin increase action potentials and contractions
Erythromycin, an antibiotic that binds to motilin receptors, increases action potentials and gastric contractions
inhibit gastric motility
Epinephrine, norepinephrine, dopamine, secretin, gastric inhibitory peptide decrease action potentials and contractions
increased by: intragastric volume
decreased by: intraduodenal volume, fat and protein -> release GIP, VIP, PYY, hyper-osmolality (trigers osmoreceptors and chemoreceptors), acid -> secretin, acid -> H+ receptors -> myenteric signal to inhibit gastrin
symptoms: bleeding -> melena (black stool), perforate ulcers -> acid contents in peritoneal cavity -> peritonitis, diarrhea, low pH inactivates pancreatic lipase -> steatorrhea (fat in stool)
cause: gastrinoma (gastrin secreting tumor)
dx: high fasting serum gastrin
symptoms: liquids empty stomach faster, solids don't. Vomiting
causes: decrease in the amplitude of the antral contractions or an increase in sphincter resistance. usually due to scarring from chronic peptic ulceration.
prostaglandin analog that is approved for the treatment of NSAID-mediated ulcers.
Histamine H2 receptor blockade
Cimetidine, Ranitidine, Famotidine are examples of H2RAs
Muscarinic M3 receptor blockade
muscarinic M3 receptors and triggers acid secretion
side efects: acid rebound (Ca stimulates parietal cells) and milk alkali syndrome (absorbed calcium elevates serum concentrations -> renal calcinosis)
symptoms: Weakness, dizziness and excessive sweating 1-2 hours after meals in a gastrectomized patient
causes: triggers rapid absorption of glucose from the intestine, hyperglycemia, abrupt rise in insulin secretion, resulting in a secondary hypoglycemia 2 hours after meals
stimulated by: vagus nerve (Ach and GRP), histamine, gastrin
Steps during secretion of hydrogen ions from parietal cells
CO2 (produced by metabolism) and water combine in parietal cells to form carbonic acid in the presence of the enzyme carbonic anhydrase. Carbonic acid (H2CO3) rapidly dissociates into H+ and HCO3-.
Proton pump: H+ ions are pumped into the stomach lumen through the proton pump in the apical membrane of the parietal cell. The proton pump (H+-K+-ATPase) requires ATP and pumps H+ in exchange for K+ (i.e. the exchange is electroneutral).
Anion exchanger: The HCO3- produced in the cell is transported into the blood through the HCO3-/Cl- anion exchanger on the basolateral surface of the parietal cell. The transfer of HCO3- into the blood accounts for the “post-prandial alkaline tide” (high pH of blood) after a meal. The exchange of HCO3- for Cl- is passive.
Steps during secretion of chloride ions from parietal cells.
Na+-K+-ATPase: Sodium-potassium ATPase on the basolateral membrane of the parietal cell pumps 3Na+ into the blood in return for 2K+ entering the parietal cell. There is a net loss of one positive charge. The interior of the parietal cell becomes negative.
Potassium ions diffuse back out into the blood through potassium channels on the basolateral membrane of the parietal cell and into the stomach lumen through potassium channels on the luminal membrane. This diffusion of K+ out of the cell further increases the intracellular negativity of the parietal cells.
Chloride ions: The high intracellular negativity forces Cl- into the stomach lumen through chloride channels located in the apical membrane of the parietal cell.
H+ and Cl- combine to form HCl (hydrochloric acid) in the stomach lumen.