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
overusing an antacid containing Magnesium hydroxide can cause what problems?
diarrhea, hyporeflexia, hypotension, cardiac arrest Mg = Must Go to the bathroom
26
overusing an antacid containing calcium carbonate can cause what problems?
hypercalcemia, rebound acid production
27
Which antacid formula would most cause absorption, bioavailability, or urinary excretion problems? why?
Calcium carbonate => can chelate and decrease effectiveness of other drugs => tetracycline
28
What is used as osmotic laxatives?
Mg hydroxide; Mg citrate; polyethylene glycol; lactulose
29
mechanism of action for osmotic laxatives?
provide osmotic load to draw water out
30
What drug can be used w/ decrease in neurological ability w/ increased liver failure? How does this work?
lactulose => hepatic encephalopathy; | gut flora degrade lactulose into metabolites (lactic acid & acetic acid) that promote Nitrogen excretion as NH4+
31
clinical use for osmotic laxatives
constipation
32
toxicity of osmotic laxatives
diarrhea, dehydration; abuse by bulimics
33
mechanism of action for infliximab
monoclonal Ab to TNF-a
34
clinical use of infliximab
Crohn's disease, ulcerative colitis, rheumatoid arthritis
35
toxicity of infliximab
infection => REACTIVATES LATENT TB; fever; hypotension
36
mechanism of action for sulfasalazine
combination of sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-inflam) => activated by colonic bacteria
37
clinical use of sulfasalazine
ulcerative colitis, Crohn's disease
38
Toxicity of sulfasalazine
malaise, nausea, sulfonamide toxicity, reversible oligospermia
39
mechanism of action for ondansetron
5-HT3 antagonist=> powerful central acting antiemetic Keep ON DANCing w/ ONDANSetron
40
clinical use of ondansetron
control vomiting post-op and in patients undergoing chemotherapy
41
toxicity of ondansetron
headache, constipation
42
mechanism of action of metoclopramide
D2 receptor antagonist => increases resting tone, contractility, LES tone, motility => does NOT INFLUENCE colon transport time
43
clinical use of metoclopramide
diabetic and post-op gastroparesis, | anti-emetic
44
toxicity of metoclopramide
increase parkinsonian effects; | restlessness, drowsiness, fatigue, depression, nausea, diarrhea
45
What are drug drug interactions assoc w/ metoclopramide?
digoxin and diabetic agents
46
Who is metoclopramide contraindicated for?
small bowel obstruction; | parkinson's disease
47
Which drugs work on the ulcer bed of the GI?
misoprostol; | sucralfate and bismuth
48
What drug classes will block parietal cell function by blocking what receptor?
Muscarinic antagonists => block M3-r H2 blockers => block H2-r
49
What drug or classes block a receptor on ECL cell to block its release?
Muscarinic antagonist => block M1-r Octreotide (somatostatin)=> ST-2r
50
What drug classes work in the stomach lumen and how?
PPI's inhibit H/K ATPase at apical border of stomach Antacids => bind H+ in lumen Misoprostol, sucralfate, bismuth work on ulcers in lumen