Cards Based On Char's 1St Study Questions

Front 1

What is the mechanism of heparin-induced thrombocytopenia?

Back 1

1. Antibodies form against platelet factor 4 + heparin
2. Antibodies bind to platelet's FC receptor
3. Platelets are destroyed by the spleen

Front 2

Besides thrombocytopenia, what is another possible outcome of antibodies formed against platelet factor 4 + heparin?

Back 2

Platelet activation --> Thrombosis

Front 3

Compared to unfractionated heparin, do low molecular weight heparins:

Bind more or less avidly to plasma proteins, platelets, and cells?

Have better or worse bioavailability after SC injection?

Require more or less frequent dosing?

Back 3

Bind less avidly to proteins, platelets, and other cells

Better bioavailability after SC injection (heparin does not cross membranes)

Require less frequent dosing (longer half-life)

Front 4

LMWH and Fondaparinux are both primarily excreted by what organ?

Back 4

Kidney

Front 5

All of the heparin-like molecules must be given either ____ or ____ (modes of drug delivery).

Back 5

Intravenously or subcutaneously

Front 6

Which form of warfarin is more active, R- or S-?

Back 6

S is 3 - 5 times more active

Front 7

S-warfarin is metabolized by what CYP?

Back 7

CYP 2C9

Front 8

What is the mechanism of warfarin-induced skin necrosis?

Back 8

Protein C and S knockout-->unopposed clotting-->platelet microthrombi-->clog up the vasculature-->decreased blood flow-->necrosis

Front 9

What class of hematologic drugs is linked to causing thrombotic thrombocytopenia purpura?

Back 9

The thienopyridines (clopidogrel, ticlopidine)

Front 10

What is the mechanism by which the thienopyridines (clopidogrel, ticlopidine) cause thrombotic thrombocytopenia purpura in some patients?

Back 10

The thienopyridines can induce the formation of antibodies to ADAMTS 13. ADAMTS 13 is a surface protein on endothelial cells that cleaves vWF into smaller pieces. Patients with anti-ADAMTS 13 antibodies have giant vWF molecules --> microthrombi--> mechanical destruction of RBCs + platelet consumption

Front 11

Which strain of influenza (A, B, or C) is amantadine active against? What is its effect on viral vesicles?

Back 11

Active ONLY against influenza A.

Affects pH of vesicles (vesicles need to be acidified for virus release).

Front 12

Zanamivir and Oseltamivir are active against which influenza strains (A, B, or C)?

Back 12

Influenza A and B

Front 13

What drug class combinations are most commonly seen in HAART?

Back 13

At least THREE drugs from TWO different classes. Most common:

TWO NRTIs and ONE NNRTI or TWO NRTIs and ONE PI

Front 14

What HIV anti-viral is associated with skin rashes, inc. Stevens-Johnson, AND hepatotoxicity?
What dosing approach can lower the risk of these S.E.'s?

Back 14

Nivirapine
Start with 14-day lead-in of a reduced dose.

Front 15

Which protease inhibitors can cause kidney stones?

Back 15

Indinavir
Atazanavir

Front 16

What co-receptor is maraviroc limited to?

Back 16

CCR5