Pharmacology Flashcards

1
Q

Drugs for H2 blockers

A

Cimetidine
ranitidine
famotidine
nizatidine

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2
Q

Mechanism of action of H2 blockers

A

reversible block of histamine H2-receptors => decrease H+ secretion by parietal cells

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3
Q

Clinical use for H2 blockers

A

peptic ulcer, gastritis, mild esophageal reflux

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4
Q

Which H2 blockers are associated w/ strong toxicities?

A

Cimetidine &raquo_space;> Ranitdine&raquo_space;»»»»>famotidine, nizatidine

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5
Q

Name toxicity of Cimetidine

A
potent inhibitor of cytochrome P-450;
antiandrogenic effects (prolactin release, gynecomastia, impotence, decreased male libido)
cross BBB (confusion, dizziness, headaches) & placenta;

decrease renal excretion of creatinine

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6
Q

Name toxicity of Ranitidine

A

decrease renal excretion

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7
Q

Drugs used as proton pump inhibitors

A
omeprazole
lansoprazole
esomeprazole
pantoprazole
dexlansoprazole
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8
Q

mechanism of action of PPIs

A

irreversibly inhibit H/K ATPase in stomach parietal cells

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9
Q

clinical use of PPIs

A

peptic ulcer, gastritis, esophageal reflux,

Zollinger-Ellison syndrome

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10
Q

Toxicity of PPIs

A

increased risk of C. difficile infection, pneumonia;
hip fractures;
decreased serum Mg+ w/ long term use

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11
Q

Chronic use of PPIs will cause a sustained elevation in what GI hormone?

A

gastrin

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12
Q

What is used to increase ulcer healing?

A

bismuth or sucralfate

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13
Q

What is used to Tx Sx of traveler’s diarrhea?

A

bismuth or sucralfate

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14
Q

Mechanism of action for bismuth and sucralfate

A

bind to ulcer base, providing physical protection and allowing HCO3 secretion to re-establish pH gradient in mucous layer

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15
Q

Mechanism of action for misoprostol

A

PGE-1 analog =>
increases production & secretion of gastric mucous barrier,
decreases acid production

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16
Q

Clinical use of misoprostol

A

prevention of NSAID-induced peptic ulcers;
maintenance of patent ductus arteriosus;
used to induce labor => ripens cervix

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17
Q

Toxicity of misoprostol

A

Diarrhea

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18
Q

Who and why is misoprostol contraindicated for?

A

contraindicated in women of childbearing potential bc it is an abortifacient

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19
Q

mechanism of action for octreotide

A

long acting somatostatin analog

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20
Q

clinical use for octreotide

A

acute variceal bleeds,
acromegaly,
VIPoma,
carcinoid tumors

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21
Q

toxicity of octreotide

A

nausea, cramps, steatorrhea

22
Q

Antacid use can affect what?

A

absorption, bioavailability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying

23
Q

All antacids can cause what?

A

hypokalemia

24
Q

Overusing an antacid containing aluminum hydroxide can cause what problems?

A

constipation and hypophosphatemia;
proximal muscle weakness, osteodystrophy, seizures

aluMINIMUM amount of feces

25
Q

overusing an antacid containing Magnesium hydroxide can cause what problems?

A

diarrhea, hyporeflexia, hypotension, cardiac arrest

Mg = Must Go to the bathroom

26
Q

overusing an antacid containing calcium carbonate can cause what problems?

A

hypercalcemia, rebound acid production

27
Q

Which antacid formula would most cause absorption, bioavailability, or urinary excretion problems? why?

A

Calcium carbonate => can chelate and decrease effectiveness of other drugs => tetracycline

28
Q

What is used as osmotic laxatives?

A

Mg hydroxide;
Mg citrate;
polyethylene glycol;
lactulose

29
Q

mechanism of action for osmotic laxatives?

A

provide osmotic load to draw water out

30
Q

What drug can be used w/ decrease in neurological ability w/ increased liver failure? How does this work?

A

lactulose => hepatic encephalopathy;

gut flora degrade lactulose into metabolites (lactic acid & acetic acid) that promote Nitrogen excretion as NH4+

31
Q

clinical use for osmotic laxatives

A

constipation

32
Q

toxicity of osmotic laxatives

A

diarrhea, dehydration;

abuse by bulimics

33
Q

mechanism of action for infliximab

A

monoclonal Ab to TNF-a

34
Q

clinical use of infliximab

A

Crohn’s disease, ulcerative colitis, rheumatoid arthritis

35
Q

toxicity of infliximab

A

infection => REACTIVATES LATENT TB;
fever;
hypotension

36
Q

mechanism of action for sulfasalazine

A

combination of sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-inflam) => activated by colonic bacteria

37
Q

clinical use of sulfasalazine

A

ulcerative colitis, Crohn’s disease

38
Q

Toxicity of sulfasalazine

A

malaise,
nausea,
sulfonamide toxicity,
reversible oligospermia

39
Q

mechanism of action for ondansetron

A

5-HT3 antagonist=> powerful central acting antiemetic

Keep ON DANCing w/ ONDANSetron

40
Q

clinical use of ondansetron

A

control vomiting post-op and in patients undergoing chemotherapy

41
Q

toxicity of ondansetron

A

headache, constipation

42
Q

mechanism of action of metoclopramide

A

D2 receptor antagonist => increases resting tone, contractility, LES tone, motility => does NOT INFLUENCE colon transport time

43
Q

clinical use of metoclopramide

A

diabetic and post-op gastroparesis,

anti-emetic

44
Q

toxicity of metoclopramide

A

increase parkinsonian effects;

restlessness, drowsiness, fatigue, depression, nausea, diarrhea

45
Q

What are drug drug interactions assoc w/ metoclopramide?

A

digoxin and diabetic agents

46
Q

Who is metoclopramide contraindicated for?

A

small bowel obstruction;

parkinson’s disease

47
Q

Which drugs work on the ulcer bed of the GI?

A

misoprostol;

sucralfate and bismuth

48
Q

What drug classes will block parietal cell function by blocking what receptor?

A

Muscarinic antagonists => block M3-r

H2 blockers => block H2-r

49
Q

What drug or classes block a receptor on ECL cell to block its release?

A

Muscarinic antagonist => block M1-r

Octreotide (somatostatin)=> ST-2r

50
Q

What drug classes work in the stomach lumen and how?

A

PPI’s inhibit H/K ATPase at apical border of stomach

Antacids => bind H+ in lumen

Misoprostol, sucralfate, bismuth work on ulcers in lumen