GERD/PUD tx

Question 1

dexlansoprazole

Answer 1

PPI

Question 2

Esomeprazole

Answer 2

PPI

Question 3

Lansoprazole

Answer 3

PPI

Question 4

Omeprazole

Answer 4

PPI

** may inhibit metabolism of warfarin, diazepam, phnytoin

Question 5

Pantoprazole

Answer 5

PPI

** use this one if using clopidogrel

Question 6

Rabeprazole

Answer 6

PPI

** use this one if using clopidogrel

Question 7

Cimedtidine

Answer 7

H2RA
** has most DDI’s

see gynecomastia or impotence in men, galactorrhea in women

Question 8

Famotidine

Answer 8

H2RA

** has least amount of DDI’s

Question 9

Nizatidine

Answer 9

H2RA

Question 10

Ranitidine

Answer 10

H2RA

- has moderate amount of DDIs

Question 11

Sodium bicarbonate

Answer 11

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)

Question 12

Calcium carbonate

Answer 12

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

Question 13

Magnesium hydroxide/aluminum hydroxide

Answer 13

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

Question 14

Bismuth Subcitrate

Answer 14

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

Question 15

Bismuth Subsalicylate

Answer 15

“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

Question 16

Misoprostel

Answer 16

agent w/ mucosal protection

MOA: prostaglandin analog

** useful in prevention of NSAID induced ulcers

** not wel tolerated - see diarrhea and cramping/ ab pain

Question 17

Sucralfate

Answer 17

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

Question 18

AB tx for H. pylori?

Answer 18

PPI or H2RA w/ two or more Abs:

• amoxicillin
• clarithromycin
• metronidazole
• tetracycline

Question 19

physio of acid secretion?

Answer 19

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

Question 20

role of prostaglandins?

Answer 20

inhibit the proton pump by reducing cAMP –> result in stimulation of protective factors (mucus and bicarb)

Question 21

NSAIDS

Answer 21

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.

Question 22

tx of mild GERD

Answer 22

antacid or H2RA as needed

Question 23

NERD

Answer 23

antacid or H2RA

Question 24

Erosive esophagitis GERD tx?

Answer 24

PPI for 8 weeks

Question 25

Duodenal ulcer tx?

Answer 25

H2RA or PPI for 4 weeks

Question 26

Gastric ulcer tx?

Answer 26

PPI for 8 weeks

Question 27

PPI's

Answer 27

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

Question 28

AEs of PPIs?

Answer 28

handled well for the most part diarrhea, h/a, ab pain ** increased risk of C. diff ** decreased vit B12 absorption --> increased risk of pneumonia

Question 29

DDI's of PPIs?

Answer 29

must dose adjust for hepatic fn.

Question 30

what to watch out for w/ warfarin?

Answer 30

omeprazole

Question 31

what to watch out for clopidogrel

Answer 31

PPI's: omeprazole, lansoprazole, dexlansoprazole *** use Pantoprazole or Rabeprazole

Question 32

H2RA's

Answer 32

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 >>>>>>>famotidine/nizatidine competes with creatinie and other drugs for renal secretion

Question 33

AE's of H2RA's

Answer 33

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!!!

Question 34

antacids

Answer 34

react with HCl to form a salt and water used for dyspepsia and intermittent heart burn

Question 35

NSAID ulcers tx?

Answer 35

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

Question 36

tx for stress ulcers?

Answer 36

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

Question 37

fastest onset?

Answer 37

antacids > H2RA's > PPis

Question 38

efficacy of acid prevention?

Answer 38

PPIs > H2RA's H2RA's inhibit fasting (basal) acid secretion ; PPI's block both fasting and food stimulated secretion

Question 39

tolerance?

Answer 39

repeated admin. of H2RA's --> reduced effectiveness tolerance with PPI's doesn't occur

Question 40

14 day triple therapy for H. pylori?

Answer 40

1. PPI 2. Clarithromycin 3. Amoxicillin or Metronidazole (for penicillin-allergic individs)

Question 41

14 day quadruple therapy for H. pylori?

Answer 41

1. PPI or H2RA 2. Metronidazole 3. Tetracycline/doxycycline 4. Bismuth subsalicylate

Question 42

AE's of antibiotics?

Answer 42

Clarithromycin: GI upset, diarrhea, altered taste Amoxicillin: GI upset, headache, diarrhea Metronidazole: metallic taste, intolerance to alcohol Tetracycline: GI upset, photosensitivity