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Pharmacology 3 > Drugs > Flashcards

Drugs Flashcards

1
Q

Rimantadine is poor at crossing the? and has less what?

A

BBB CNS effects

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2
Q

Warfarin

MOA

how to monitor

AE

A
  • Inhibits vitamin K epoxide reductase
  • Teratogenic-fetal hemorrhage
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3
Q

Dipyridamole

A
  • Inhibits reuptake of adenosine and inhibits phosphodiester that degrades cAMP
  • Contraindicated in CHF
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4
Q

Nonnucleotide RTI are different than side and tide inhibitors in what way?

A

Dont require phosphorylation

Dont compete with dNTPs

Resistance develops rapidly

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5
Q

Activated partial thromboplastin time deals with what meds?

A

Heparin, also helpful in diagnosis of hemophilia

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6
Q

What does amantadine block?

A

Blocks the M2 proton ion channel

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7
Q

Rudins are? Monitored by?

A

Direct thrombin inhibitors Monitored by aPTT same as Heparin

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8
Q

Direct oral Factor Xa inhibitors?

A

xabans A fib - Cant be reversed

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9
Q

Tenofovir inhibits?

A

viral reverse transcriptase DNA chain terminator

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10
Q

Clopidogrel

MOA

DI

A
  • Irreversible inhibition of platelet ADP receptor
  • Bleeding GI
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11
Q

Zidovudine ZDV or AZT

AE

A
  • Bone marrow toxicity causing anemia
  • Lactic acidosis
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12
Q

If someone takes too much warfarin what do you do?

A

Vitamin K

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13
Q

Heparin is reversed by?

A

Proxamine

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14
Q

Rimantadine is a?

A

Uncoating inhibitor

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15
Q

Apixaban is a ______

A

Direct factor Xa inhibitors

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16
Q

Oseltamivir is a?

A

Inhibitor of influenza neuraminidase oral

17
Q

Nucleoside RT inhibitors need to be activated by?

A
  • Need to be activated within the cell by phosphorylation
18
Q

Clopidogrel

A
  • Irreversible inhibition of platelet ADP receptor
  • Bleeding, GI
19
Q

Tenofovir?

A

Nucleotide RTI

20
Q

Plase

A

Drugs that activate tissue plasminogen to create plasmin Given soon after event

21
Q

Rimantadine is ___ compared to amantadine

A

longer lived

22
Q

Plase drugs do what?

A

Activate plasminogen to plasmin

23
Q

Nevirapine, delavirdine and efavirenz are?

MOA

AE

A
  • NNRTI
  • They are not active against HIV-2
  • NNRTIs bind directly noncompetitively to the RT enzyme at a site distinct from NRTI binding site
  • Block DNA polymerase by causing a conformational change and disrupt the catalytic site of the enzyme
24
Q

Tipranavir

A
  • Antiretroviral protease inhibitor
  • non-peptidic protease inhibitor
  • AE
    • Dose-dependent hepatotoxicity, lipodytrophy
25
Q

Nucleotide RTI differ from nucleoside analogs in what way?

A

They are already phosphorylated so they can skip the nucleoside-kinase reaction

26
Q

Zidovundine ZDV or AZT is a?

Nucleoside ot tide?

A

NRTI

27
Q

How do nucleoside reverse transcriptase inhibitors cause termination of viral growth

A
  • The lack of 3’-OH analog prevents the formation of the 5’ to 3’ phosphodiester linkage needed for chain elongation
28
Q

Integrase inhibitors?

A

Raltegravir, prevent virus DNA from integrating into host genome

29
Q

Aspirin MOA Drug interactions and AE

A
  • Irreversible COX1 inhibitor Reduces the production of thromboxane A2
  • Can cause nephrotoxicity
30
Q

Ritonavir?

MOA

DI AE

A
  • Antiretroviral protease inhibitor
  • Competitive inhibitor of HIV protease responsible for cleaving gag-pol precursor molecule
  • Inhibit both HIV-1 and 2

DI

  • Ritonavir is a substrate and potent inhibitor of CYP3A4
  • Can act as a pharmacokinetic enhancer of drug metabolized by CYP450 3A

AE

  • Hyperlipidemia, with large increases in total cholesterol and TG concentrations
31
Q

Abciximab

MOA

AE DI

A
  • Inhibits platelet aggregation by interfering with GPIIb/IIIa binding to fibrinogen and other ligands
  • Bleeding thrombocytopenia with prolonged use
32
Q

Oseltamivir blocks?

A

Neuraminidase

33
Q

Lamivudine 3TC

As well as being used for HIV can also inhibit replication of?

Side or tide?

A

NRTI

HBV

34
Q

Maravoroc?

A

HIV entry inhibitor that stops binding with CCR5 receptor - Can interfere with immune response, not effective at all with CXCR4 because CCR5 isnt used

Pharmacology 3 (20 decks)

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