Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI II Exam I > Pharm - treatment of GERD and PUD CIS- Waller > Flashcards

Pharm - treatment of GERD and PUD CIS- Waller Flashcards

1
Q

Proton-Pump Inhibitors (PPIs)

- list

A 
Dexlansoprazole (Dexilant)
Esomeprazole (Nexium)
Lansoprazole (Prevacid)
Omeprazole (Prilosec, Zegerid)
Pantoprazole (Protonix)
Rabeprazole (Aciphex)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

H2-Receptor Antagonists (H2RAs)- list

A

Cimetidine (Tagamet)
Famotidine (Pepcid)
Nizatidine (Axid)
Ranitidine (Zantac)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Antacids

- list

A 
Sodium bicarbonate (Alka Seltzer)
Calcium carbonate (Tums, Os-Cal)
Magnesium hydroxide/aluminum hydroxide (Mylanta, Maalox)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Agents Which Provide Mucosal Protection- list

A

Bismuth subcitrate
Bismuth subsalicylate (Pepto-Bismol)
Misoprostol
Sucralfate (Carafate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Antibiotic Treatment of Helicobacter pylori Infection

- list

A 
PPI or H2RA combined with             two or more antibiotics
Amoxicillin
Clarithromycin
Metronidazole
Tetracycline
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

PPIs- MOA, PK, ADRS

A

Agents: dexlansoprazole, esomeprazole, lansoprazole, omeprazole, pantoprazole, rabeprazole

MOA: covalently bind H+/K+-ATPase, irreversibly inactivating the enzyme.

PK:
Inactive pro-drug, delayed-release, acid resistant, enteric coated – to protect acid labile drug from destruction
Administer on an empty stomach; 30 minutes before meals

ADRs:
Diarrhea, headache, abdominal pain (1-5%)
Clostridium difficile (2-3x risk)
↓ vitamin B12 absorption, ↑ risk of nosocomial pneumonia, modest ↑ risk of hip fracture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

H2-Receptor Antagonists (H2RAs)- MOA, PK, ADRs

A

Agents: cimetidine, famotidine, nizatidine, ranitidine

MOA: competitive inhibition at parietal cell H2-receptors.

PK:
Duration of action dependent on dose used

ADRs:
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

PPIs vs. H2RAs

A

PPI DDIs:
Decreased acidity may alter drug absorption (ketoconazole, itraconazole, digoxin, atazanavir)
Extensive CYP P450 metabolism (2C19 & 3A4)
Clinically significant interactions rare (short t1/2)
Omeprazole may inhibit metabolism of warfarin (↑ INR), diazepam, phenytoin….

H2RAs DDIs:
CYP1A2, 2C9, 2D6, 3A4 (cimetidine&raquo_space;> ranitidine)
Theophylline, warfarin, phenytoin, lidocaine (↑ levels)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

PPIs and Clopidogrel

A

Clopidogrel (pro-drug) requires activation by CYP2C19 for anti-platelet activity
PPIs could ↓ activation = ↓ anti-platelet activity
Especially omeprazole, esomeprazole, lansoprazole, dexlansoprazole
If co-administration required, pantoprazole or rabeprazole preferred

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

amtacid use and side effects

A

Mg has laxative effects

Al causes constipation

Antacids combining Al and Mg are used to lower stomach acid w/o producing undesirable constipation or diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Clinical Pharmacology – GERD

A

PPIs
Greater efficacy for ERD and NERD, esophageal complications, and extra-esophageal manifestations

H2RAs
Used intermittently for infrequent heartburn or dyspepsia

Recommendations:
Mild, intermittent symptoms – antacid or H2RA as needed
NERD – antacid or H2RA (PPI may be required)
Erosive esophagitis – PPI x 8 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Lifestyle Modification in GERD

A

Unlikely to control symptoms in most patients.
Recommend in target populations:

overweight- weight loss
lying down- head of bed elevation
nocturnal- avoid meals 2-3 hours before bedtime
tobacco- smoking cessation
relief after trigger avoidance– quit eating those foods

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Clinical Pharmacology – PUD

A

PPIs
Greater symptom relief & faster ulcer healing

H2RAs
Replaced by PPIs but still used occasionally for duodenal ulcers (nocturnal acid inhibition)

Recommendations:
Duodenal ulcer – H2RA or PPI x 4 weeks
Gastric ulcer – PPI x 8 weeks
Prevention of re-bleeding – PPI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Clinical Pharmacology – NSAID Ulcers

A

Discontinue ASA or NSAID (faster healing)

PPIs
Preferred if ASA or NSAID continued

H2RAs
May be used if ASA or NSAID discontinued

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Treatment of H. pylori

A 
Antibiotics
Amoxicillin
Clarithromycin
Metronidazole
Tetracyclines
Two or three antibiotics + PPI

14-day triple therapy (all BID): PPI, clarithromycin, amoxicillin or metronidazole

14-day quadruple therapy: PPI or H2RA (BID), Tetracycline, Metronidazole, Bismuth subsalicylate (all QID)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Adverse Drug Reactions in H pylori treatment

A

Mild side effects to drug regimens common

Significant side effects reported in 5-20%
Clarithromycin: GI upset, diarrhea, altered taste
Amoxicillin: GI upset, headache, diarrhea
Metronidazole: metallic taste, intolerance to alcohol
Tetracycline: GI upset, photosensitivity

17
Q

Self-treatment of GERD is fine in the absence of what?

A

alarm symptoms- bleeding, trouble swallowing, anemia,

severe or frequent heartburnt, more than 2 days/ week more than 3 months
extraesophageal- asthma, cough, laryngitis
Persistent symtoms despite appropriate therapy

18
Q

Creates physical barrier at base of erosions

A

sucralfate and bismuth

19
Q

Inhibits 30S bacterial ribosome

A

tetracycline

20
Q

Prostaglandin analog

A

misoprostol

21
Q

reacts with HCl forming CO2 and CaCl2

A

Calcium Carbonate

22
Q

H2-receptor antagonist

A

famotidine

23
Q

You recommend an agent (to a GERD patient) which is generally well tolerated but may have a low incidence of headache and diarrhea. What is this drug’s likely mechanism of action?

choices: 
Creates physical barrier at base of erosions
H2-receptor antagonist
Inhibits 30S bacterial ribosome
Prostaglandin analog
Reacts with HCl forming CO2 and CaCl2
A

H2-receptor antagonist

24
Q

heartburn drugs that may impact warfarin’s CYP metabolism?

A

PPIs and H2RAs

most likely: Omeprazole and cimetidine

25
Q

PPIs less likely to inhibit CYP

A

Pantoprazole or rebprazole

26
Q

when do we dose adjust PPIs?

A

with hepatic impairment, but not renal impairment

27
Q

pt with frequent heartburn, difficulty swallowing, moderate esophagitis, an esophageal stricture, and no evidence of Barrett metaplasia

Should we give antacids vs H2RAs vs. PPIs?

A

PPI is appropriate - most effective and goodo for esophageal copmlications and extra-esophageal manifestations

28
Q

why do we use delayed-release PPIs?

A

so they are not destroyed by the acid of the stomach and can reach their site of action

29
Q

drug that inhibits H+/K+ ATPase as continuous IV infusion?

A

PPI

e.g. pantoprazole

30
Q

In PUD, if an NSAID must be continued, is a PPI or H2RA preferred?

A

PPI; an H2RA will not be as effective

31
Q

what drugs are not recommended for aspirin allergy?

A

Busmuth subsalicylate

32
Q

drug that is not compatible with alcohol?

A

metronidazole

GI II Exam I (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions