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81 Cards in this Set

  • Front
  • Back
main causes of peptic ulcer disease?
1) increase in attack factors = H. pylori, acid, pepsin
2) decrease in defense factors = < mucous barrier
two besic approaches to therapy?
1) to decrease the acidity and/or peptic activity
2) to enhance the resistance of the mucosa or to protect the base of the ulcer
how to decrease the acidity and/or peptic activity?
1) by blocking secretion of acid and/or pepsin
2) neutralization of HCL or inactivation of pepsin
3) eradicating H.pylori
drugs to decrease attack
1) proton pump inhibitors
2) H2-antihistamines
3) antacids
4) antimuscarinics
5) prostaglandins
6) antibiotics
7) antidepressants
proton pump inhibitors (PPI)
1) Omeprazole (Prilosec) = prototype
2) Lansoprazole (Prevacid)
3) Rabeprazole (Aciphex)
4) Esomeprazole (Nexium)
5) Pantoprazole (Protonix)
2) H2-antihistamines
1) Cimetidine (Tagamet)
2) Ranitidine (Zantac)
3) Famotidine (Pepcid)
4) Nizatidine (Axid)
3) antacids
1) Mg (OH)2
2) Al (OH)3
3) CaCO3
4) NaHCO3
4) antimuscarinics
1) Glycopyrrolate (RObinul)
2) Dicyclomine (Bentyl)
3) Methscopolamine (Pamine)
4) Propantheline (Pro-Banthine)
5) Prostaglandin
1) Misoprostol (Cytotec)
6) Antibiotics
1) Metronidazole (Flagyl)
2) Tetracycline
3) Clarithromycin (Biaxin)
4) Amoxicillin (Amoxil)
7) antidepressant
1) Tricyclics
proton pump involves?
ATPase appears to be?
unique, and is not known to be in other cells = devoid of SE
Omeprazole (Prilosec)
1) prototype inhibitor
2) irreversibly inhibits the ATPase
irreversible inhibition of ATPase cause?
1) profound inhibition of gastric acid secretion (95-100%) for several days
2) GI bacterial overgrowth
3) diarrhea
4) subsequent colonization of the resp. tract
reversible inhibitor of the pump?
Lansoprazole (Prevacid) = gastric acid suppression is not prolonged
drugs which will be decreased in their absorption?
1) ketoconazole
2) ampicillin
3) digoxin
4) iron salts
PPI inhibit metabolism of these drugs
1) phenytoin
2) warfarin
3) diazepam
1) headache
2) diarrhea
3) abd. pain
well tolerated
a major fraction of gastric acid is secreted in response to the activation of?
1) H2-histamine receptors on parietal cell memb. and
2) the subsequent activation of adenylate cyclase
H2-antihistamines have pronounced effects on both?
acid and pepsin secretion
acid and pepsin secretion is elecited by?
1) histamine
2) gastrin
3) caffeine
4) food
5) insulin
6) vagus stimulation
H2-antihistamines do not directly affect?
1) gastrin secretion
2) GI motility
3) LES pressure
H2-antihistamines are most effective when taken at?
H2-antihistamine OTC for?
1) acid indigestion
2) sour stomach
3) heartburn
drugs to increase defense
1) ulcer coating
2) steroid congeners
3) prostaglandins
4) antacids
1) ulcer coating
1) Sucralfate (Carafate)
2) Bismuth compounds (Pepto-Bismol)
3) Graviscon
2) steroid congeners
1) Carbenoxolone
3) Prostaglandins
1) Misoprostol (Cytotec)
4) Antacids
1) Al(OH)3
Sucralfate (Carafate)
1) a complex of sulfated sucrose and aluminum hydroxide
2) for duodenal ulcers
3) bind to free protein in the base of ulcer craters
4) forms a complex which protects from acid, pepsin, and bile salts
5) stimulate local production of PG-E
SE of Sucralfate
1) metalic taste
2) mausea
3) constipation
4) < absorption of some drugs
Bismuth subsalicylate (Pepto-Bismol)
1) selectively bind to ulcers
2) providing a coating and protection from acid and pepsin
3) stimu. mucus production
4) increase PG synthesis
5) to eradicate H.pylori
tripotassium dicitrato-bismuthate
1) available in Europe
2) a stable colloidal complex
SE of bismuth compounds
1) black stools
2) black tongue
3) OD of salicylates
1) antacid
2) contains alginate
3) protects the mucosa and impaired gastric reflux
4) for GERD
1) synth. derevative of glycyrrhizic acid
2) > production , secretion, and viscosity of mucus
3) widely used in Europe
4) for gastric and duodenal ulcers
SE of Carbenoxolone
1) mineralocorticoid activity
2) Na and water retention
3) HTN
4) hypokalemia
Misoprostol (Cytotec)
1) PG-E1 analog
2) > mucus and HCO3 production
3) < acid production
4) only for ulcer pt who cannot discontinue NSAID use
1) neutralize H ion
2) mucosal protection
3) bind injurious substances
4) weak bases, form salt and water
5) > pH to 3.5-4.5
6) consists of metal salts
acid neutralizing capacity (ANC)
the # of mEq of HCL that can be brought to pH 3.5 in 15 min
antacids are used for?
1) dyspepsia
2) adjuncts to other tx for PUD
magnesium hydroxide
1) high neutralizing capacity
2) SE = diarrhea and hyperMg
Aluminum hydroxide
1) high neut. capacity
2) SE = constipation and hypoPhos
3) SE = decrease bone mass
Calcium carbonate
1) moderate neut. capacity
2) liberation of CO2 = abd. distention, nausea, flatulence, belching
large doses of Ca carbonate cause?
1) transient hyperCa
2) rebound acid secretion
3) milk-alkali syndrome
4) nephrolithiasis
sodium bicarbonate
1) high neut.capacity
2) SE = syst. alkalosis, fluid retention, acid rebound, CO2 liberation
3) not for chronic use
added to some antacids, help to relieve gas
for eradication of H. pylori
1) ranitidine bismuth citrate (tritec) + clarithromycin (Biaxin)
tetracycline or amoxicillin + metronidazole + pepto-bismol
eradication of H.pylori
omeprazole + clarithromycin
1) a functional decrease in the tome of LES
2) HCL and bile acids into the esophagus = ulcer, erosive esophagitis
3) heartburn = regurge and dyspepsia
1) decrease LES tone
2) never be used for reflux esophagitis
medications that decrease LES tone?
1) theophylline
2) progesterone
3) nitrates
4) Ca channel blocker
prokinetic agents
1) favor motion and can improve GI proplusion
2) increase gastric emptying
neural regulation of gastric motility
1) acetylcholine
2) dopamine
3) serotonin
gastric motility can be stimulated by?
1) D2 antagonists
2) 5-HT3 antagonists
3) 5-HT4 agonists
motilin receptors
1) in small intestine
2) potential target for prolinetic agents
3) erythromycin also stimulate motilin receptors
Metoclopramide (Reglan)
1) prokinetic
2) 5-HT3 antagonists
3) may act as a D2 antagonists
4) cholinomimetic effect
5) crosses the BBB
SE of reglan
1) extrapyramidal symptoms
2) depression
3) hyperprolactemia
4) hervousness
5) dystonia
6) abd. cramping
7) anticholinergic SE
Domperidone (Motilium)
1) non-US
2) prokinetic
3) D2 antagonist
4) Tx for gastric hypomotility in diabetics
benefit of Domperidone?
does not cross BBB (no extrapyramidal SE) and is not anticholinergic, and better tolerated
antagonists of
1) serotonin
2) dopamine
3) acetylcholine
4) histamine
5-HT3 antagonists
1) receptor in GI tract
N/V believed to be triggered by release of serotonin from ?
the enterochromaffin cells of the small intestine which then activates 5-HT3 receptors on vagal afferents, triggering the vomiting reflex
Ondansetron (Zofran)SE
1) well tolerated
2) HA
3) constipation
4) dizziness
benefit of ondansetron
not an antagonist of dopamine receptors = no extrapyramidal SE
Granisetron HCL (Kytril)
1) for chemo-induced emesis
2) 5-HT3 antagonist
which medication is given with Granisetron HCl to improve acute antiemetic effecacy?
Alosetron (Lotronex)
1) 5-HT3 antagonist
2) severe potential GI SE
Alosetron is only approved for last chance in women with?
irritable bowel syndrome
other 5-HT3 antagonists
1) Dolasetron (Anzemet)
2) Palonosetron (Aloxi)
D2 antagonists
1) Benzamides
2) Metoclopromide (Reglan)
3) Trimethobenzamide (Tigan)
4) Domperidone
5) Phenothiazine
6) Butyrophenones
7) Chlorpromazine (Thorazine)
8) Prochlorperazine (Compazine)
SE of phenothiazine
1) hypotension
2) sedation
3) extrapyramidal movement disorders
Prochlorperazine (Compazine) IM cause
1) D2 antagonists
2) Haloperidol (Haldol)
3) Droperidol (Inapsine)
4) for CA chemo.
5) less sedation and hypotension
1) antiemetic
2) Dexamethasone and other glucocorticoids
3) for moderately emetogenic chemo.
4) reduce SE, diarrhea
1) anti-emetic
2) Delta-9-tetrahydrocannabinol
3) for chemo.
SE of cannabinoids
1) hallucinations
2) disorientation
3) vertigo
tx of motion sickness
histamine H1-receptor antagonists with anticholinergic + antimuscarinic
1) antiemetic
2) Lorazepam (Ativan)
3) Alprazolam (Xanax)