2.11 GI Pharm: GERD, Ulcers, Gastroparesis Flashcards

1
Q

What is the general MOA of antacids or ionic salts?

A

Weak bases that react to gastric acid H+ to neutralize them

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2
Q

Who should avoid using antacids?

A

People with renal insufficiency or drugs that need acidic environments like tetracyclines or FQ

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3
Q

What kind of monitoring do you need to do with patients taking antacids?

A

Electrolyte imbalance and renal function

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4
Q

What are antacids used to treat?

A

Mild GERD and occasional heartburn
NOT ulcers

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5
Q

What antacids salt ADSE include diarrhea or hyper magnesia that can lead to renal insuffiency?

A

Magnesium salts

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6
Q

What antacid slat can lead to hypercalcemia, alkalosis, or milk-alkali syndrome?

A

Calcium salt

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7
Q

What antacid salt ADSE includes constipation, neurotoxicity, hypophosphatemia, and anemia in renal failure?

A

Aluminum salts

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8
Q

What is the MOA of cimetidine, famotidine, ranitidine (“-idine”)?

A

H2 receptor antagonist (on parietal cells) reducing gastric acid secretion

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9
Q

What are cimetidine specific ADSE?

A

Gynecomastia, galactorrhea, CYP450 interactions

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10
Q

Although rare, what are the side effects of a competitive H2 receptor antagonist?

A

Headache, diarrhea, fatigue

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11
Q

What are the contraindications for cimetidine, famotidine, ranitidine?

A

Pregnancy (cross placenta)

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12
Q

What monitoring should you do for patients on H2 receptor antagonist?

A

Mental status (if IV) or drug interactions (cimetidine)

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13
Q

What are the “-tidine” H2 receptor antagonists used to treat?

A

GERD, peptic ulcer, mild acid reflux

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14
Q

What are the PPI drugs?

A

Omeprazole, lansoprazole, esomeprazole
“-prazoles”

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15
Q

What is the MOA of “-prazoles”?

A

Irreversible inactivate H+/K+ ATPase parietal cells

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16
Q

What is the specific ADME for PPIs?

A

Enteric coated activated in acidic environments
Take 1 hr before meal

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17
Q

What ADSE should you consider for PPIs?

A

Diarrhea, headache, decreased B12 absorption, hypomagnesia, acid rebound, infection risk

18
Q

What should you avoid in patients taking omeprazole, lansoprazole, and esomeprazole?

A

Caution long term use (osteoporosis, hypomagnesia)
Avoid with CYP2C19 drugs (clopidogrel)

19
Q

What do you monitor with patients taking the “-prazoles”?

A

Magnesium levels and infection signs

20
Q

What do you use to treat GERD, peptic ulcers, H. Pylori infections, and NSAID-induced ulcers?

A

PPIs “-Prazole” drugs
Omeprazole, lansoprazole, esomeprazole

21
Q

What are some mucosal protective agents you can use?

A

Sucralfate, Bismuth, Misoprostol

22
Q

Sucralfate MOA?

A

Has aluminum that reduces pepsin access creating protective barrier on ulcers promoting healing

23
Q

What is used to treat GERD in pregnancy?

A

Sucralfate

24
Q

What is a Sucralfate ADSE?

A

Constipation (aluminum)

25
Q

Can cause black stool, darken the tongue?

A

Bismuth

26
Q

What are the contraindications for Bismuth?

A

Pregnancy and renal insufficiency

27
Q

What is the MOA or bismuth?

A

Enhances prostaglandin production, binds to ulcer craters, and antimicrobial effects to H. Pylori (salicylates)

28
Q

What is used to prevent NSAID ulcer damage?

A

Misoprostol

29
Q

Prostaglandin E1 analog that reduced acid secretion by decreasing cAMP?

A

Misoprostol

30
Q

Misoprostol ADSE and CONTRA?

A

Diarrhea + cramping
NO to pregnancy

31
Q

What is the triple therapy for H. Pylori eradication?

A

Clarithromycin, amoxicillin, PPI

32
Q

What is the quadruple therapy for H. Pylori eradication?

A

Metronidazole, tetracycline, PPI, Bismuth

33
Q

Clarithromycin MOA?

A

Macrolide inhibiting bacterial 50S ribosome

34
Q

Amoxicillin MOA?

A

Penicillin derivative disrupting cell wall synthesis

35
Q

Metronidazole MOA?

A

DNA damage with free radicals (anaerobic bacteria)

36
Q

Tetracycline MOA?

A

Protein synthesis inhibitor bacterial 30S ribosome

37
Q

What is metroclopramide used for?

A

GERD, gastroparesis, antiemetic

38
Q

What are the ADSE for a prokinectic agent like metoclopramide?

A

CNS: restless, drowsy, extrapyramidal (tardive dyskinesia** with long term use)

39
Q

What is the MOA for metoclopramide?

A

D2 receptor antagonist with some 5-HT4 agonist activity

(Increase GI motility and accelerate gastric emptying)

40
Q

Where does metoclopramide act?

A

Brain (CNS) - dopamine receptors
It blocks the 5HT released from mucosal enterochromaffin cells