GERD/PUD Flashcards
List a few Paxton lifestyle interventions for GERD.
- do not lie down for at least 2hr after eating/drinking
- elevate head of bed
- weight loss
- routine avoidance of foods that have been thought to trigger reflux (chocolate, caffeine, alcohol, spicy) is no longer recommended **
Describe the general pharm management of GERD (based on severity)
Mild, infrequent: antacid or H2RA PRN
Inadequate control or severe, frequent sxs: PPI qd x 8wk
Continued sxs: BID PPI or switch to different PPI
Nocturnal sxs despite BID PPI: add H2RA
What are the 3 main salts used as antacids?
- Al (OH)3 - aluminum hydroxide
- CaCO3 - calcium carbonate
- Mg (OH)3 - magnesium hydroxide
What is the MOA of antacids? Clinical use?
MOA:
- neutralize gastric acidity by increasing pH
- inhibit proteolytic activity of pepsin when gastric pH > 4
Clinical indication: dyspepsia, GERD prn
What are two different drug interactions related to antacids?
- DEC TTC/FQ absorption (cations)
2. DEC absorption d/t “alkalization” of stomach - Fe***
also - ketoconazole, digoxin, phenytoin
List the three ADRs associated with Al(OH)3.
- hypophosphatemia
- aluminum intoxication (encephalopathy, seizure, coma in CKD pt)
- constipation**
List the two ADRs associated with CaCO3.
- Constipation**
- Milk-alkali syndrome (HA, Nausea, irritability, weakness, hypercalcemia, metabolic alkalosis, hypophosphatemia)
What are two ADRs associated with Mg(OH)2.
- hyperMg
- laxative effects **
Reiteration - which two antacids cause constipation? Which causes laxative effects?
Constipation: aluminum hydroxide, calcium carbonate
Laxative: magnesium hydroxide
What is the MOA of Sucralfate (Carafate) and clinical indications?
Aluminum hydroxide complex of sucrose
MOA: forms a “protective coating” by binding with positively charged proteins in exudates
Indications:
- GERD/PUD
- Tx NSAID-induced mucosal damage
- prevent stress ulcer
** suspension - topical tx of stomatitis d/t chemo **
What drug interaction should you be aware of with sucralfate? What are two ADRs?
Interaction: DEC absorption of digoxin, phenytoin, warfarin, ketoconazole, theophylline, TTC, FQ
ADRs: constipation, aluminum tox in CKD pt
Name two first gen and two second gen H2RAs.
First gen: cimetidine & ranitidine*
Second gen: famotidine* & nizatidine
Why was ranitidine pulled off the shelves?
Concern for NDMA in the drug
Currently being investigated by the FDA
Describe the MOA of H2RAs.
- inhibit gastric secretion by blocking H2
- reduces basal acid secretion primarily (some food stimulated secretion)
- good for PRN use
- less potent at reducing nocturnal secretion
What are the clinical indications of H2RAs?
- dyspepsia / GERD / PUD
- SUP in critically ill pt [may lead to more pneumonia and CDI**]
- gastric hypersecretory states (ZES, MEN) but PPIs often more effective
What is a class drug effect of H2RAs? What CYP ish should you know?
- DEC absorption Fe*** (ketoconazole, digoxin, phenytoin)… these require acidic environment to be absorbed
CYP
- Cimetidine: inhibits all isoenzymes, don’t use*
- Ranitidine, famotidine*, nizatidine - fairly clean
What are two class ADRs related to H2RAs?
- acid rebound possible
- confusion in cognitive impairment / demented* elderly pt
What are three ADRs related to cimetidine specifically?
- anti-androgen effects w/chronic use
- drug fever
- agranulocytosis
What is the PPI suffix? Which two are IV?
-prazole
IV: Esomeprazole, Pantoprazole
What is the MOA of PPIs?
Inhibit parietal cell H+/K+ ATP pump
- suppress gastric basal and food stimulated acid secretion
** PPIs should be administered 30-60 min before first meal
What are the clinical indications for PPIs?
- GERD
- intermittent vs. on-demand vs. continuous - PUD* +/- bleeding (commonly H. pylori)
- SUP in critically ill pt
- not routine hospitalized pt**
- larger doses for more than 2d increase risk of CDI** - Gastric hypersecretory states (ZES, MEN)
- H. pylori infection
There are 4 main concerns related to PPI use, what are they?
- INC CDI
- CAP / HAP d/t DEC gastric acid allowing bacterial overgrowth
- INC fracture risk in PMP
- recommend Ca citrate* and Vit D - Other deficiencies
- hypoMg d/t DEC absorption
- DEC absorption of iron and Vit B12
Who truly needs a PPI?
Those at high risk for ulcers or GI bleeding d/t severe GERD, erosive esophagitis, NSAIDs, etc.
Use lowest effective dose for shortest possible duration**
Consider Fe, Ca, Vit B12 supplementation
Is there any clinical difference b/t PPIs for symptom relief, esophagitis / ulcer healing? *
No
Pt may respond to one and not another
What should you monitor with your pt taking a PPI?
Mg - baseline and periodically in pt on long-term therapy (> 2wk) or who take diuretics or digoxin
Who should you avoid extended PPI therapy (> 2wk) in?
Pt w/risk of TdP and those w/long QT syndrome
TdP secondary to altered Mg levels
Which CYP interactions are important to know regarding PPIs?
Substrates: 2C19, 3A4
Most agents inhibit 2C19
** Clopidogrel - remember, use PANTOPRAZOLE** instead of omeprazole
2C9 inhibitor - Omeprazole
- careful with Warfarin**
What are three other important drug interactions to be aware of with PPIs?
- all DEC absorption of ketoconazole, Mg, Fe, Ca, Vit B12, digoxin, phenytoin
- DEC MTX clearance
- PPI + diuretic –> DEC Mg –> TdP
Old thinking says PPIs are fairly well tolerated. What must you remember when discontinuing these meds?
Taper!!
Acid rebound may occur with d/c
Consider H2RAs or antacids for breakthrough
What are some newer ADRs to be aware of with PPIs?
- nosocomial infections (HAP/VAP, CDI)
- anemia (Fe def, pernicious)
- fractures (hip, wrist, spine)
- CKD with long-term use?
