Flashcards in GI drugs I Deck (49):
what is the cause of ulcers
increased acidity or decreased mucosal resistance. caused or promoted by gastric acid
where is a peptic ulcer located
in the duodenum
what three receptors are present on the parietal cell in the stomach and what do they do?
gastrin, Ach, and histamine. all act to stimulate the K+/H+ ATPase.
what does histamine do the cell
increases the formation of cyclic AMP
what does gastrin and cholinergics do the parietal cell
increases intracellular calcium
where does gastrin come from in the stomach
where does Ach come from in the stomach
from vagal input
where does histamine come from in the stomach
stimulated by both Ach and gastrin
define the mucosal protection from acid
there is a pH gradient from very low, to 7 caused by the secretion of bicarbonate. this protects the mucosa from damage. there is reduced bicarb secretion in DU patients.
what is the approach to treating ulcers
relief of symptoms, promotion of healing, prevention of complications, prevention of recurrence.
what is the treatment plan for ulcers
neutralize acid, decrease acid production, increase resistance
only effective when they can elevate the pH to above 5. stops pepsins damage as well as acidic erosion. best if taken 1 hour after eating when gastrin activity is highest. liquids work better
reacts slowly with HCl to form calcium chloride and carbonic acid. it is constipating so given with magnesium compounds as laxatives
what are the SE of calcium carbonate
milk-alkali syndrome, nephrocalcinosis, rebound acidity, digitalis antagonism d
rarely used because of systemic alkalosis, enhanced effects of amphetamine, quinidine, cinchophen. high sodium content
magnesium hydroxide and carbonate
hydroxide is more potent. may cause magnesium intoxication in renal disease.
magnesium hydroxide and carbonate SE
diarrhea, hypokalemia, hypermagnesemia, iron deficiency
combines to form al-Cl and water. aluminum is excreted in the feces when it combines with phosphate. this is also useful in protecting the mucosa and doesnt perturb the electrolytes in the body. useful in renal patients.
adverse of effects of aluminum chlorides
constipation, phosphate depletion, weakness, anemia, tetany, apnea, delayed gastric emptying, concretions, fecaloma, perforation, peritonitis, encephalopathy. impaired absorption of tetracycline and digoxin.
what is defoaming agent and what does it do
within an antacid preparation, claims to disperse the antacid.
what is an adverse effect of all antacids
increases the luminal pH
antacids cause the decreased absorption of what
antacids cause the increased absorption of what
phenothiazines, INH, nalidixic acid, nitrofurantoin, pen G, sulfonamides, premature release of enteric coated tablets.
anticholinergics for ulcer treatment
vagotomy effect reduction of HCl secretion. spasmolytic effect.
adverse effects of anticholinergics
dry mouth, blurred vision, atony of the bladder, constipation, drowsiness, mental confusion.
when are anticholinergics contraindicated
pyloric obstruction, hiatal hernia, peptic esophagitis,
what are the common anticholinergics
atropine, propantheline, metantheline bromide.
when to administer anticholinergics
30 min before meals and at bedtime.
why give the anticholinergics before bed
to reduce nocturnal secretion by vagal block when antacids are not being consumed.
H2 blockers agents
cimetidine, ranitidine, famotidine, nizatidine
H2 blockers do what
lower acid secretion by blocking the receptor on parietal cells which mediates the release of acid. decreases both basal and food stimulated. can be given prophylactically to reduce stress ulcers.
adverse effects of H2 blockers
uncommon. HA, lethargy, confusion, depression and hallucinations.
what are the drug interactions for the H2 blockers
P450, theophylline, warfarin, dilatin, lidocaine.
H+/K+ ATPase inhibitors agents
omeprazole, lansoprazole, rabeprazole, esomeprazole, pantoprazole, dexlansoprazole.
general H+/K+ ATPase inhibitors
these are noncompetitive inhibitors. acitvated by acidic pH. inhibits 90% of 24 hr secretion. better pain relief and healing than the H2-blockers. will even heal H2 refractory ulcers.
adverse effects of the H+/K+ ATPase inhibitors
headache gynecomastia, inhibition of 450, gastric hyperplasia. not recommended for long-term use due top carcinoid tumors.
what drugs do the H+/K+ ATPase inhibitors interact with
warfarin, diazepam, dilantin
what are the agents that decrease the mucosal defenser
NSAIDs, H. pylori, smoking, genetics, stress.
hat drugs coat the ulcer/crater
bismuth salts (pepto), sucralfate
how do bismuth salts work
in acid they form crystals that precipitate on the ulcer. they have a lower ulcer recurrence rate than H2.
how does sucralfate work
aluminum hydroxide complex of sucrose binds to the ulcerated tissue after activation in the acid environment.
what are the SE of the coating agents
no adverse effects. constipation, aluminum tox, renal failure.
prostaglandin E2 analogs agent
misoprostol does what
decreased acid production, increase mucous and bicarbonate secretion. less effective than H2. t
what is misoprostol mainly used for
to prevent NSAID induced gastric ulcer
adverse effects of misoprostol
transient diarrhea, cannot use in pregnancy
drugs that eradicate H pylori
bismuth salts and antibiotics (metronidazole + tetracycline/amoxicillin
what is triple therapy for h pylori
a PPI/ranitidine bismuth citrate 2X/day and 2 of amoxicillin/clarithromycin/metronidazole.