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Flashcards in GIT - drugs Deck (48):
1

H2 blockers

"___TIDINE"
[adine = H1G2]

Cemetidine, Ranitidine, famotidine, nizatidine

2

H2 blocker mechanism

[Cemetidine, Ranitidine, famotidine, nizatidine]

REVERSIBLY block H2 receptors of ECL cells

3

H2 blocker use

[Cemetidine, Ranitidine, famotidine, nizatidine]

peptic ulcers, gastritis, mild esophageal reflux

4

H2 blocker toxicity

[Cemetidine, Ranitidine, famotidine, nizatidine]

Cemetidine:
- inhibits p450
- anti-androgen (prolactin, gynecomastia, impotence, libido)
- cross BBB (HA, dizzy, confusion)
- cross placenta
- decrease renal creatinine excretion

Ranitidine:
- decrease renal creatinine excretion

5

Cemetidine

H2 reversible blocker

6

Ranitidine

H2 reversible blocker

7

Famotidine

H2 reversible blocker

8

Nizatidine

H2 reversible blocker

9

PPIs

"___prazole"
[Omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole]

10

PPI mechanism

[Omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole]

IRREVERSIBLY inhibit H/K ATPase in stomach parietal cells
*better than H2 blockers because blocks the final step*

11

PPI use

[Omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole]

PUD, gastritis, esophageal reflux, ZE

12

PPI toxicity

[Omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole]

c. DIFF!, pneumonia, low Mg++ with extended use

13

Omeprazole

PPI

14

Lansoprazole

PPI

15

Esomeprazole

PPI

16

Pantoprazole

PPI

17

Dexlansoprazole

PPI

18

Bismuth mechanism

Binds ulcer base providing physical protection while bicarb is secreted to fix pH in mucus layer

19

Bismuth use

increase ulcer healing
travellers diarrhea

20

Sucralfate mechanism

Binds ulcer base providing physical protection while bicarb is secreted to fix pH in mucus layer
*needs acidic pH .: can't use with PPIs or H2 blockers*

21

Sucralfate use

increase ulcer healing
travellers diarrhea

22

Drugs that promote ulcer healing and treat travellers diarrhea

Bismuth and sucralfate

23

Misoprostol MOA

PGE1 analog, binds Gi
GIT: increases production and secretions gastric mucosal barrier and decreases acid production

Repro: given with Mifepristone (RU-486) to sensitize the receptors to it

24

Misoprostol use

Prevent NSAID-induced ulcers (NSAIDs block PGE1 production, so this replaces it).
MAINTAIN PDA.
Induces labour/ripens cervix + abortions [off-label]

25

Misoprostol AE

Diarrhea
Contraindicated in child-baring age women (abortifacient)

26

Octerotide MOA

Somatostatin analog; mimics splanchnic vasoconstriction hormones

27

Octerotide use

Acute variceal bleeds (VC)
Acromegaly
VIPoma
Carcinoid
Insulinoma

28

Octerotide AE

Steatorrhea
Cramps
Nausea

29

Antacids GENERAL AE:

- Altered absorption, bioavailability, or urinary extortion of other drugs via altered gastric and urinary pH or gastric emptying
- Hypokalemia
- Specific overuse problems

30

Antacids:

Aluminum hydroxide
Calcium carbonate
Magnesium hydroxide

31

Aluminum hydroxide specific overuse AE:

Constipation
Hypophosphatemia
Proximal muscle weakness
Renal Osteodystrophy
Seizures

32

Calcium carbonate specific overuse AE:

Hypercalcemia
Rebound increase in acid
Chealates and decreases effectiveness of other drugs i.e. tetracyclin

33

Magnesium hydroxide specific overuse AE:

Diarrhea
Hyporeflexia
Hypotension
Cardiac arrest

34

Osmotic laxatives

MgOH, MgCitrate, polyethylene glycol (PEG), lactulose

35

Osmotic laxative use

[MgOH, MgCitrate, polyethylene glycol (PEG), lactulose]

Constipation
*Lactulose for hepatic encephalopathy: gut flora degrade it to lactic acid and acetic acid, donates H+ to NH3 which increases NH4+ excretion

36

Osmotic laxative toxicity

[MgOH, MgCitrate, polyethylene glycol (PEG), lactulose]

Diarrhea
Dehydration
Abused by bulimics

37

Sulfasalazine MOA

= sulfapyridine (antibacterial) + 5-ASA (anti-inflammatory)
Activated by colonic bacteria

38

Sulfasalazine use

Ulcerative colitis
Chrons

39

Sulfasalazine toxicity

malaise
nausea
sulfonamide toxicity (G6PD; lupus-like)
reversible oligospermia

40

Ondansetron mechanism

5-HT3 antagonist; decreases vagal stimulation

41

Ondansetron use:

powerful central anti-emetic - post-op and chemo

42

Ondansetron AE

HA
Constipation
QT prolongation

43

Metochlopromide mechanism

D2 antagonist
increases resting tone, contractility, LES tone, and motility = PROKINETIC
[does NOT influence colon transport time]

44

Metochlopromide use

Diabetic and post-surgical gastroparesis
Antiemetic

45

Metochlopromide AE

Increased parkinsonian effects (D2 antagonism)
Interacts with digoxin and diabetic drugs
Contraindicated with small bowel obstructions and parkinsons

46

Orlistat mechanism

inhibits gastric and pancreatic lipases to decrease fat breakdown and thus absorption

47

Orlistat use

weight loss

48

Orlistat AE:

Steatorhea
Decreased absorption of fat-soluble vitamins