GERD/PUD tx Flashcards
dexlansoprazole
PPI
Esomeprazole
PPI
Lansoprazole
PPI
Omeprazole
PPI
** may inhibit metabolism of warfarin, diazepam, phnytoin
Pantoprazole
PPI
** use this one if using clopidogrel
Rabeprazole
PPI
** use this one if using clopidogrel
Cimedtidine
H2RA
** has most DDI’s
see gynecomastia or impotence in men, galactorrhea in women
Famotidine
H2RA
** has least amount of DDI’s
Nizatidine
H2RA
Ranitidine
H2RA
- has moderate amount of DDIs
Sodium bicarbonate
Antacid
“baking soda”
- has high amount of CO2 production –> gas, belching, distension
- can cause metabolic alkalosis and fluid retention, may pose risk for pts. w/ HF, HTN and renal insuffiecncy
Sodium bicarbonate + HCl –> NaCl and CO2
CO2 (distension and belching)
Alkali absorption (metabolic alkalosis)
NaCl absorption (fluid retention)
Calcium carbonate
Antacid = “tums”
Calcium carbonate + HCl –> CaCl2 and CO2
- has high amount of CO2 production –> gas, belching, distension
- can lead to hypercalcemia, renal insufficiency, metabolic alkalosis
Magnesium hydroxide/aluminum hydroxide
Antacid
no gas generated so belching doesn’t occur, metabolic alkalosis is also uncommon
however,
Mg2+ salts – osmotic diarrhea
Al3+ salts – constipation
watch out for renal insufficiency
Bismuth Subcitrate
agent w/ mucosal protection
Bismuth coats ulcers and erosions; stimulates intestinal prostaglandin, mucus, and bicarbonate secretion
ADRs:
Harmless blackening of stool and tongue
Salicylate toxicity (high doses)
Therapeutic use:
Dyspepsia and acute diarrhea
Traveler’s diarrhea
H. pylori
Bismuth Subsalicylate
“pepto-bismol” : agent w/ mucosal protection
Bismuth coats ulcers and erosions; stimulates intestinal prostaglandin, mucus, and bicarbonate secretion
Salicylate (like ASA) inhibits intestinal prostaglandin and chloride secretion
ADRs:
Harmless blackening of stool and tongue
Salicylate toxicity (high doses)
Therapeutic use:
Dyspepsia and acute diarrhea
Traveler’s diarrhea
H. pylori
Misoprostel
agent w/ mucosal protection
MOA: prostaglandin analog
** useful in prevention of NSAID induced ulcers
** not wel tolerated - see diarrhea and cramping/ ab pain
Sucralfate
agent w/ mucosal protection
MOA: unknown - forms viscous paste in water/acid sol’n which binds ulcers for up to six hours
** use: stress-related mucosal injury (slightly less effective than H2RA’s IV) - used preferentially over acid-inhibitory therapies due to concern of increased risk of pneumonia created by alkaline envirnment
AB tx for H. pylori?
PPI or H2RA w/ two or more Abs:
- amoxicillin
- clarithromycin
- metronidazole
- tetracycline
physio of acid secretion?
ACh - attaches to M3 receptors:
- stimulates Gastrin to be released from G cells
- directly stimulates parietal cells –> acid
- stimulates Histamine to be released from ECL cells
Gastrin (from G cells): binds CCKB-R of parietal cells –> stimulates acid secretion
Histamine (from ECL cells): binds H2R on Parietal cells–> acid section
(is stimulated by both ACh and Gastrin)
THus - ACh provides direct parietal stimulation while gastrin effects are primarily mediated through indirect release of histamine from ECL cells
role of prostaglandins?
inhibit the proton pump by reducing cAMP –> result in stimulation of protective factors (mucus and bicarb)
NSAIDS
block PG production –> more acid secretion, less mucus and bicarb production and diminished blood flow –> thus NSAIDs are ulcerogenic and should be avoided in ulcer pts.
tx of mild GERD
antacid or H2RA as needed
NERD
antacid or H2RA
Erosive esophagitis GERD tx?
PPI for 8 weeks
Duodenal ulcer tx?
H2RA or PPI for 4 weeks
Gastric ulcer tx?
PPI for 8 weeks
PPI’s
they are lipophilic prodrugs that readily cross lipid membrane and are protonated and activated in parietal cells –> forms a covalent disulfide bond w/ H+/K+ ATPase –> irreversibly inactivating the enzyme
** they have short half life and longer duration! :)
** they are well tolerated and work to inhibit 90% of all total acid secretion
used for tx of GERD, PUD (better sx control than H2RA), H. pylori infection, NSAID ulcers, ZE syndrome
AEs of PPIs?
handled well for the most part
diarrhea, h/a, ab pain
** increased risk of C. diff
** decreased vit B12 absorption –> increased risk of pneumonia
DDI’s of PPIs?
must dose adjust for hepatic fn.
what to watch out for w/ warfarin?
omeprazole
what to watch out for clopidogrel
PPI’s: omeprazole, lansoprazole, dexlansoprazole
*** use Pantoprazole or Rabeprazole
H2RA’s
Histamine2 receptor antagonists - tidine
MOA: competitively inhibit parietal cell H2 receptors and block histamine released from ECL cells
** suppresses basal more than meal stimulated acid secretion ** thus most useful for nocturnal acid secretion (only modest effect for meal inhibited acid)
** must be dosed multiple times per day - and dose adjust for BOTH hepatic and renal fn
tx: used for GERD, PUD (largely replaced by PPI’s except for DU’s), NSAID ulcers, stress injury
DDI’s: Cimetidine»>rantidine»_space;»»>famotidine/nizatidine
competes with creatinie and other drugs for renal secretion
AE’s of H2RA’s
Diarrhea, headache, fatigue, myalgia (< 3%)
Mental status changes (ICU patients, elderly, renal or hepatic impairment)
Nosocomial pneumonia, rare blood dyscrasias, bradycardia/hypotension (rapid IV infusion)
inhibits gastric acid (except famotidine) first-pass metabolism of alcohol - dont use w/ alcoholics!!!
antacids
react with HCl to form a salt and water
used for dyspepsia and intermittent heart burn
NSAID ulcers tx?
Discontinue ASA or NSAID (faster healing)
PPIs - Preferred if ASA or NSAID must be continued (pantoprazole, rabeprazole)
H2RAs - May be used if ASA or NSAID discontinued
tx for stress ulcers?
use PPIs for stress ulcer prophylaxis : Omeprazole sodium bicarbonate only PPI FDA approved – given per tube
H2RA’s Preferred IV over PPI IV if no nasoenteric tube present or with significant ileus
fastest onset?
antacids > H2RA’s > PPis
efficacy of acid prevention?
PPIs > H2RA’s
H2RA’s inhibit fasting (basal) acid secretion ; PPI’s block both fasting and food stimulated secretion
tolerance?
repeated admin. of H2RA’s –> reduced effectiveness
tolerance with PPI’s doesn’t occur
14 day triple therapy for H. pylori?
- PPI
- Clarithromycin
- Amoxicillin or Metronidazole (for penicillin-allergic individs)
14 day quadruple therapy for H. pylori?
- PPI or H2RA
- Metronidazole
- Tetracycline/doxycycline
- Bismuth subsalicylate
AE’s of antibiotics?
Clarithromycin: GI upset, diarrhea, altered taste
Amoxicillin: GI upset, headache, diarrhea
Metronidazole: metallic taste, intolerance to alcohol
Tetracycline: GI upset, photosensitivity
