Patient-directed drug therapy for GERD
INTERMITTENT, MILD HEARTBURN:
lifestyle mod + patient directed therapy w/ antacids and/or OTC H2RA or PPI no more than 2 weeks
ANTACID
1. Mg hydroxide/aluminum hydroxide w/
simethicone (Maalox)
2. antacid/alginic acid (Gaviscon)
3. calcium carb (tums)
OTC H2RA (no more than 2 weeks, up to BID)
1. Cimetidine 200mg
2. famotidine/Pepcid 10mg-20mg
3. nizatidine/Axid AR 75mg
OTC PPI
1. esomeprazole/Nexium 20mg
2. lansoprazole/Prevacid 15mg
3. omeprazole/Prilosec 20mg
4. omeprazole/sodium bicarb (Zegerid)
20mg/1100mg
What are the underlying causes of GERD (physiologically) & what are some things that can worsen GERD symptoms?
DECREASE LES PRESSURE:
1. hiatal hernia (increase pressure, lower LES tone)
2. food: fatty, garlic, onion, coffee/tea, soda, chocolate, ETOH, chili peppers
3. Meds: nicotine, nitrates, progesterone, tetracycline, dopamine, estrogen, barbiturates, anticholinergics
IRRITATE ESOPHAGEAL MUCOSA
1. spicy food
2. tomato or orange juice
3. coffee
4. tobacco
5. ASA or NSAIDs
6. irone
7. KCL
etc.
Patho of GERD
Most common process causing GERD sx
slowed esophageal clearance of gastric contents increasing contact time of refluxate w/ esophageal mucosa NOT increased acid
GERD risk factors
Main typical, atypical, alarm sx GERD
Typical: aggravated by activities/food, heartburn waxing/waning, hypersalvation, regurgitation, bleching
atypical (causality only if typical sx also present): chronic cough, hoarseness, wheezing, asthma, non-cardiac chest pain
alarm (GERD complications Barrett esophagus, esophageal strictures, adenocarcinoma): Odynophagia, dysphagia, weight loss, bleeding
How often sx occur for dx GERD & how dx
2+ times/week
endoscopy, biopsy to test for Barrett esophagus
ambulatory esophageal reflux monitoring
esophageal manometry
what’s dyspepsia
occurs often w/ PUD
epigastric pain and sometimes other upper GI sx like heartburn
consider dx if pain > 1 month
Options of the most appropriate RX drug therapy for gastroesophageal reflux disease
***Moderate-severe PPI should be initial therapy, maintenance if recur
H2RA
1. cimetidine/Tagamet 400mg QID or 800mg
BID
2. famotidine/Pepid 20mg BID
3. Nizatidine/Axid 150mg BID
PPI
1. dexlansoprazole/Dexilant 20mg QD x4 weeks
2. esomeprazole/Nexium 20-40ng QD
3. lansoprazole/Prevacid 15mg QD
4. omeprazole/Prilosec 20mg QD
5. pantoprazole/Protonix 40mg QD
6. rabeprazole/Aciphex 20mg QD
**Doses slightly higher or BID or tx erosive esophagitis **
H2RA side effects
mild: HA and nausea
drug interactions
cimetidine specifically: gynecomastia & vit B12 deficiency
renally eliminated so dose adjustment in renal dysfunction
how do H2RAs work
decrease acid secretion by blocking histamine 2 receptors in gastric parietal cells
how do PPIs work
block gastric acid secretion SIGNIFICANTLY by inhibiting gastric H/K ATP in parietal cells= long-lasting antisecretory effect pH > 4 even during postprandial surges
what PPI can be taken w/o regard to food
dexlansoprazole or omeprazole-sodium bicarb
PPI side effects
Most common= HA, diarrhea, nausea
long-term: AKI/CKD, bone fx, dementia, electrolyte deficiency (ca, mg, B12), bacterial infections (c.diff, PNA)
First line rx tx for GERD
PPI x8 weeks
Can do maintenance or on-demand therapy
Can d/c once sx resolve then reinitiate x2-4 weeks if sx 2+ times in week since d/c
rebound hypersecretion
can occur w/ continual PPI use of at least 2 months
should be tapered (individualized) slowly using H2RAs for breakthrough sx.
Rebound hypersecretion can last > 3 months
3 most common causes of PUD
Plan of care for NSAID induced ulcer
Prevention:
PPI or misoprostol (prostaglandin E1 analog- GI SE); H2RAs less effective
PPI more tolerated
Treatment:
*PPI x4 weeks, Sucralfate if NSAID stopped, H2RA effective w/ DU only
First line tx H. pylori
? amox allergy, ? h/o macrolide abx, ? alcohol (contraindicated metronidazole)
Meds that end in “-pitant”
Ex: aprepitant, rolapitant, netupitant
neurokinin-1 (NK 1) receptor antagonist
act centrally at NK-1 receptors in vomiting centers within the central nervous system to block their activation by substance P released as an unwanted consequence of chemotherapy.
tx acute/delayed CINV when given WITH 5-HT3 antagonist & corticosteroid
prevent PONV
Numerous drug interactions. NOT renally eliminated
Meds that end in “-setron”
Ex: ondansetron, granisetron, dolasetron, palonoestron
5-HT3 antagonists (against serotonin) since 5-HT3 stimulates visceral vagal nerve fibers
tx CINV (chemo releases 5-HT3) & PONV
SE: HA, somnolence, diarrhea, constipation, QT interval changes so ECG if at risk
prevention & tx options CINV
dexamethasone OR 5-HT3 antagonist (“setron”) OR combo
Moderate= steroid with “setron”
high risk= NK1 receptor antagonist AND 5HT3 antagonist AND dexamethasone AND olanzapine
olanzapine for CINV
antipsychotic effects D2, 5HT3, 5HT2C receptors
give in combo therapy for high emetogenic risk chemo
biggest SE= sedation day 2 of chemo
risk factors CINV
poor emetic control prior, female, LOW chronic alcohol use, younger age, motion sickness, NVP