GIT - drugs

Question 1

H2 blockers

Answer 1

“___TIDINE”
[adine = H1G2]

Cemetidine, Ranitidine, famotidine, nizatidine

Question 2

H2 blocker mechanism

Answer 2

[Cemetidine, Ranitidine, famotidine, nizatidine]

REVERSIBLY block H2 receptors of ECL cells

Question 3

H2 blocker use

Answer 3

[Cemetidine, Ranitidine, famotidine, nizatidine]

peptic ulcers, gastritis, mild esophageal reflux

Question 4

H2 blocker toxicity

Answer 4

[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

Question 5

Cemetidine

Answer 5

H2 reversible blocker

Question 6

Ranitidine

Answer 6

H2 reversible blocker

Question 7

Famotidine

Answer 7

H2 reversible blocker

Question 8

Nizatidine

Answer 8

H2 reversible blocker

Question 9

PPIs

Answer 9

“___prazole”

[Omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole]

Question 10

PPI mechanism

Answer 10

[Omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole]

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

Question 11

PPI use

Answer 11

[Omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole]

PUD, gastritis, esophageal reflux, ZE

Question 12

PPI toxicity

Answer 12

[Omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole]

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

Question 13

Omeprazole

Answer 13

PPI

Question 14

Lansoprazole

Answer 14

PPI

Question 15

Esomeprazole

Answer 15

PPI

Question 16

Pantoprazole

Answer 16

PPI

Question 17

Dexlansoprazole

Answer 17

PPI

Question 18

Bismuth mechanism

Answer 18

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

Question 19

Bismuth use

Answer 19

increase ulcer healing

travellers diarrhea

Question 20

Sucralfate mechanism

Answer 20

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

Question 21

Sucralfate use

Answer 21

increase ulcer healing

travellers diarrhea

Question 22

Drugs that promote ulcer healing and treat travellers diarrhea

Answer 22

Bismuth and sucralfate

Question 23

Misoprostol MOA

Answer 23

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

Question 24

Misoprostol use

Answer 24

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

Question 25

Misoprostol AE

Answer 25

Diarrhea | Contraindicated in child-baring age women (abortifacient)

Question 26

Octerotide MOA

Answer 26

Somatostatin analog; mimics splanchnic vasoconstriction hormones

Question 27

Octerotide use

Answer 27

``` Acute variceal bleeds (VC) Acromegaly VIPoma Carcinoid Insulinoma ```

Question 28

Octerotide AE

Answer 28

Steatorrhea Cramps Nausea

Question 29

Antacids GENERAL AE:

Answer 29

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

Question 30

Antacids:

Answer 30

Aluminum hydroxide Calcium carbonate Magnesium hydroxide

Question 31

Aluminum hydroxide specific overuse AE:

Answer 31

``` Constipation Hypophosphatemia Proximal muscle weakness Renal Osteodystrophy Seizures ```

Question 32

Calcium carbonate specific overuse AE:

Answer 32

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

Question 33

Magnesium hydroxide specific overuse AE:

Answer 33

Diarrhea Hyporeflexia Hypotension Cardiac arrest

Question 34

Osmotic laxatives

Answer 34

MgOH, MgCitrate, polyethylene glycol (PEG), lactulose

Question 35

Osmotic laxative use

Answer 35

[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

Question 36

Osmotic laxative toxicity

Answer 36

[MgOH, MgCitrate, polyethylene glycol (PEG), lactulose] Diarrhea Dehydration Abused by bulimics

Question 37

Sulfasalazine MOA

Answer 37

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

Question 38

Sulfasalazine use

Answer 38

Ulcerative colitis | Chrons

Question 39

Sulfasalazine toxicity

Answer 39

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

Question 40

Ondansetron mechanism

Answer 40

5-HT3 antagonist; decreases vagal stimulation

Question 41

Ondansetron use:

Answer 41

powerful central anti-emetic - post-op and chemo

Question 42

Ondansetron AE

Answer 42

HA Constipation QT prolongation

Question 43

Metochlopromide mechanism

Answer 43

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

Question 44

Metochlopromide use

Answer 44

Diabetic and post-surgical gastroparesis | Antiemetic

Question 45

Metochlopromide AE

Answer 45

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

Question 46

Orlistat mechanism

Answer 46

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

Question 47

Orlistat use

Answer 47

weight loss

Question 48

Orlistat AE:

Answer 48

Steatorhea | Decreased absorption of fat-soluble vitamins