GIT - drugs Flashcards

1
Q

H2 blockers

A

“___TIDINE”
[adine = H1G2]

Cemetidine, Ranitidine, famotidine, nizatidine

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2
Q

H2 blocker mechanism

A

[Cemetidine, Ranitidine, famotidine, nizatidine]

REVERSIBLY block H2 receptors of ECL cells

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3
Q

H2 blocker use

A

[Cemetidine, Ranitidine, famotidine, nizatidine]

peptic ulcers, gastritis, mild esophageal reflux

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4
Q

H2 blocker toxicity

A

[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

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5
Q

Cemetidine

A

H2 reversible blocker

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6
Q

Ranitidine

A

H2 reversible blocker

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7
Q

Famotidine

A

H2 reversible blocker

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8
Q

Nizatidine

A

H2 reversible blocker

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9
Q

PPIs

A

“___prazole”

[Omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole]

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10
Q

PPI mechanism

A

[Omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole]

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

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11
Q

PPI use

A

[Omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole]

PUD, gastritis, esophageal reflux, ZE

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12
Q

PPI toxicity

A

[Omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole]

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

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13
Q

Omeprazole

A

PPI

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14
Q

Lansoprazole

A

PPI

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15
Q

Esomeprazole

A

PPI

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16
Q

Pantoprazole

A

PPI

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17
Q

Dexlansoprazole

A

PPI

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18
Q

Bismuth mechanism

A

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

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19
Q

Bismuth use

A

increase ulcer healing

travellers diarrhea

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20
Q

Sucralfate mechanism

A

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
Q

Sucralfate use

A

increase ulcer healing

travellers diarrhea

22
Q

Drugs that promote ulcer healing and treat travellers diarrhea

A

Bismuth and sucralfate

23
Q

Misoprostol MOA

A

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
Q

Misoprostol use

A

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

25
Q

Misoprostol AE

A

Diarrhea

Contraindicated in child-baring age women (abortifacient)

26
Q

Octerotide MOA

A

Somatostatin analog; mimics splanchnic vasoconstriction hormones

27
Q

Octerotide use

A
Acute variceal bleeds (VC)
Acromegaly
VIPoma
Carcinoid
Insulinoma
28
Q

Octerotide AE

A

Steatorrhea
Cramps
Nausea

29
Q

Antacids GENERAL AE:

A
  • Altered absorption, bioavailability, or urinary extortion of other drugs via altered gastric and urinary pH or gastric emptying
  • Hypokalemia
  • Specific overuse problems
30
Q

Antacids:

A

Aluminum hydroxide
Calcium carbonate
Magnesium hydroxide

31
Q

Aluminum hydroxide specific overuse AE:

A
Constipation
Hypophosphatemia
Proximal muscle weakness
Renal Osteodystrophy
Seizures
32
Q

Calcium carbonate specific overuse AE:

A

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

33
Q

Magnesium hydroxide specific overuse AE:

A

Diarrhea
Hyporeflexia
Hypotension
Cardiac arrest

34
Q

Osmotic laxatives

A

MgOH, MgCitrate, polyethylene glycol (PEG), lactulose

35
Q

Osmotic laxative use

A

[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
Q

Osmotic laxative toxicity

A

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

Diarrhea
Dehydration
Abused by bulimics

37
Q

Sulfasalazine MOA

A

= sulfapyridine (antibacterial) + 5-ASA (anti-inflammatory)

Activated by colonic bacteria

38
Q

Sulfasalazine use

A

Ulcerative colitis

Chrons

39
Q

Sulfasalazine toxicity

A

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

40
Q

Ondansetron mechanism

A

5-HT3 antagonist; decreases vagal stimulation

41
Q

Ondansetron use:

A

powerful central anti-emetic - post-op and chemo

42
Q

Ondansetron AE

A

HA
Constipation
QT prolongation

43
Q

Metochlopromide mechanism

A

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

44
Q

Metochlopromide use

A

Diabetic and post-surgical gastroparesis

Antiemetic

45
Q

Metochlopromide AE

A

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

46
Q

Orlistat mechanism

A

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

47
Q

Orlistat use

A

weight loss

48
Q

Orlistat AE:

A

Steatorhea

Decreased absorption of fat-soluble vitamins