GI and acid-peptic dz's Flashcards

1
Q

what are 3 acid-peptic dz’s?

A

GERD, peptic ulcer (gastric or duodenal), or stress-related mucosal injury

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

over 90% of peptic ulcers are caused by…

A

infxn w/ H. pylori and use of NSAIDs

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

where is the site of damage in H. pylori and NSAID induced ulcers?

A

H. pylori – duodenum

NSAIDs – stomach

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

2 classes of drugs used in tx for acid-peptic dz’s?

A

agents that reduce intragastric acidity and those that promote mucosal defense

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

what receptors do parietal cells contain?

A

gastrin (CCK-B)
histamine (H2)
acetylcholine (muscarinic, M3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what agents reduce intragastric acidity?

A

Antacids
H2 receptor antagonists (H2 blockers)
Proton Pump inhibitors (PPI)

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

how do antacids neutralize the acidity in the stomach?

A

antacids = weak base

they react w/ gastric HCl to form a salt and water

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

MOA antacids (sodium bicarbonate)

A

Reacts rapidly with hydrochloric acid (HCL) to produce carbon dioxide and sodium chloride

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

ADE’s of antacids (sodium bicarbonate)

A

CO2 gastric distention and bleching, metabolic alkalosis, exacerbate fluid retention

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

ADE’s antacids (calcium carbonate)

A

metabolic alkalosis

w/ dairy products –> hypercalcemia, renal insufficiency

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

ADE’s antacids (Magnesium hydroxide or aluminum hydroxide)

A

(belching does not occur)

metabolic alkalosis, osmotic diarrhea, constipation

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

what can be given w/ Magnesium hydroxide or aluminum hydroxide to control bowel function?

A

Gelusil, Maalox, Mylanta

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

antacids should not be given within 2 hours of doses of…

A

Tetracycline
Fluoroquinolone
Itraconazole
Iron

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

what are some H2 receptor antagonists (h2 blockers)?

A

Cimetidine (Tagament), ranitidine (Zantac), famotidine (Pepcid), nizatidine (Axid)

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

what pts need a dose reduction of H2 receptor antagonists?

A

mod-severe renal insufficiency and elderly

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

MOA of H2 receptor antagonists?

A

competitive inhibition at parietal cell H2 receptors

suppress acid secretion

highly selective

Volume of pepsin reduced

reduce acid secretion stimulated by histamine as well as by gastrin and cholinomimetic agents

histamine released from ECL cells by gastrin or vagal stimulation is blocked from binding to the parietal cell H2 receptor

direct stimulation by gastrin or acetylcholine diminished effect on acid secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

best time to give H2 blockers?

A

at bedtime

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

which H2 receptor blocker is the most potent?

A

famotidine

19
Q

H2 receptor antagonists Rx vs. OTC duration of action?

A

rx = 10 hrs

OTC = 6 hrs

20
Q

uses of H2 blockers?

A

Gastroesophageal Reflux Disease (GERD)
Peptic Ulcer Disease (PUD)
Nonulcer Dyspepsia (NUD)
Prevention of Bleeding from Stress-Related Gastritis

21
Q

ADE’s for H2 receptor antagonists?

A

D, ha, fatigue, myalgias, constipation

mental status changes

22
Q

ADE’s of cimetidine?

A

inhibits binding of dihydrotestosterone to androgen receptors

males – gynecomastia, impotence

females – galactorrhea

crosses placenta

23
Q

Cimetidine drug interactions

A

Interferes (inhibitor) with several important hepatic cytochrome P450 drug metabolism pathways including: CYP1A2, CYP2C9, CYP2D6, and CYP3A4

24
Q

ranitidine drug interactions

A

binds 4–10 times less avidly than cimetidine to cytochrome P450

25
Q

what are some PPI’s

A
Omeprazole (Prilosec)
Esomeprazole (Nexium)
Lansoprazole (Prevacid)
Dexlansoprazole (Dexilant)
Rabeprazole (Aciphex) 
**Pantoprazole (Protonix)
26
Q

when should you administer PPI’s? why?

A

30-60mins before a meal preferably before breakfast

PPIs inactivate acid pumps that are actively secreting, but they have no effect on pumps in quiescent

27
Q

Pharmacokinetics of PPI’s

A

18 hours are required for synthesis of new H+/K+-ATPase pump molecules

rapid first-pass systemic hepatic

acid suppression by irreversible inactivation of PP

28
Q

PPI uses

A

GERD
PUD
Nonulcer dyspepsia
Prevention of Stress-Related Mucosal Bleeding
Gastrinoma and other Hypersecretory Conditions

29
Q

ADE’s of PPI

A

hypersecretion if not tapered off

diarrhea, ha, abd. pain

promotes absorption of food-bound minerals (Fe, Ca, Mg)

pneumonia, incr risk of C. diff

30
Q

PPI drug interactions

A

alter absorption of ketoconazole, digoxin

omeprazole inhibit metabolism of warfarin, diazepam

reduce clopidogrel activation

**pantoprazole no significant drug interactions

31
Q

MOA Mucosal protective agents

A

Mucosal prostaglandins important in stimulating mucus/bicarbonate secretion and mucosal blood flow

restrict back diffusion of acid and pepsin

32
Q

what are some Mucosal protective agents?

A

Sucralfate
Prostaglandin analogs
Bismuth

33
Q

How does Sucralfate work?

A

in water or acidic sol’ns –> forms viscous tenacious paste

Stimulates mucosal prostaglandin and bicarbonate secretion

34
Q

uses for sucralfate?

A

prevention of stress-related bleeding

35
Q

pharmacodynamics of misoprostol (prostaglandin analogs)?

A

Both acid inhibitory and mucosal protective properties

36
Q

ADE’s for misoprostol?

A

diarrhea, cramping, stimulates uterine contractions, dysmenorrhea, hypophosphatemia

37
Q

what are the 2 bismuth compounds available?

A

bismuth subsalicylate

bismuth subcitrate potassium

38
Q

how does bismuth subsalicylate work?

A

undergoes rapid dissociation within the stomach, allowing absorption of salicylate

Reduces stool frequency and liquidity in acute infectious diarrhea

39
Q

why does bismuth work for traveler’s diarrhea?

A

has direct antimicrobial effects and binds enterotoxins

40
Q

ADE’s for bismuth compounds

A

Harmless blackening of the stool and darkening of the tongue

bismuth toxicity (encephalopathy), or salicylate toxicity

avoid in renal insufficiency

41
Q

ADE’s for sucralfate

A

constipation

42
Q

indications for Tx of H. pylori infection

A

Gastric or duodenal ulcer
MALT lymphoma
After endoscopic resection of gastric cancer
Uninvestigated dyspepsia

43
Q

recommended 1st therapies for H. pylori infxn?

A

clarithromycin triple (PPI, clarithromycin, amox or metronidazole)

bismuth quadruple (PPI, bismth subitrate, tetracycline, metronidazole)

clarithromycin-based