Anticoag drugs 0504

Question 1

heparin moa

Answer 1

cofactor for activation of ANTITHROMBIN.
antithrombin inactivates thrombin and Xa, which converts prothrombin to thrombin

(decrease thrombin and Xa)

Question 2

heparin use

Answer 2

short half life.
duration of action is only hours.
IMMEDIATE anticoag for PE, stroke, acute coronary syndrome, MI, DVT

Question 3

can heparin be used in pregos?

Answer 3

yes - does not cross placenta

Question 4

how should heparin tx be monitored?

Answer 4

follow PTT - intrinsic pathway
(three letters long, like “Hep”)

also causes increased thrombin time

Question 5

heparin tox

Answer 5

bleeding
thrombocytopenia (HIT)
osteoporosis
drug-drug interaction

Question 6

heparin antidote

Answer 6

protamine sulfate - positively charged molecule that binds negatively charged Hep

Question 7

heparin-induced thrombocytopenia (HIT)

Answer 7

Hep binds factor IV, causing Ab production that binds to and activates plts - lead to plt clearance.

thrombocytopenic, hypercoagulable state.

Question 8

LMWH (enoxaparin) moa

Answer 8

binds antithrombin III ONLY.

acts more to inhibit Xa.

Question 9

enoxaparin pharmacodynamics

Answer 9

better bioavailability.
2-4 times longer half life.
admin SQ.
no lab monitoring.
not easily reversible.

Question 10

fondaparinux

Answer 10

smallest heparin form.
synthetic pentasaccharide inhibitor of Xa.
no activity with antithrombin.

causes increased PT and aPTT.
no effect on thrombin time.

Question 11

hirudin derivatives

Answer 11

lepirudin
bivalirudin
argatroban
dabigatran

Question 12

hirudin derivatives moa

Answer 12

DIRECT thrombin inhibition. prevent new clot formation.
does not require ATIII.
prolongs thrombin time.

Question 13

hirudin derivatives use

Answer 13

alternative to Hep in pts with HIT.

Question 14

warfarin (Coumadin) moa

Answer 14

interferes with normal synthesis and gamma-carboxylation of vit K-dependent factors II, VII, IX, X, prot C and S.

Question 15

warfarin metabolism

Answer 15

cyto P450

Question 16

warfarin lab results

Answer 16

increase PT (affects extrinsic pathway)

Question 17

warfarin use

Answer 17

long half life.
duration of action for days.
CHRONIC anticoag - post STEMI, prophylaxis for venous thromboembolism.

Question 18

how is warfarin use monitored?

Answer 18

follow PT/INR values

Question 19

can warfarin be used in pregos?

Answer 19

NO! can cross placenta

Question 20

what other drug must be administered when warfarin is initiated?

Answer 20

Hep/enoxaparin - anticoag prot C and S are quickly depleted (shortest half lives); can result in paradoxical PROcoagulant state if Hep not given

Question 21

warfarin tox

Answer 21

bleeding
teratogenic
skin/tissue necrosis**
drug-drug interactions

Question 22

warfarin antidote

Answer 22

reverse OD: IV vit K

rapidly reverse SEVERE OD: fresh frozen plasma

Question 23

why is the onset of therapeutic action for warfarin delayed for a few days?

Answer 23

vit K-dependent factors have long half lives

Question 24

route of admin for Hep

Answer 24

parenteral (IV, SC)

Question 25

site of action for Hep

Answer 25

blood

Question 26

Hep structure

Answer 26

large, anionic acidic polymer

Question 27

warfarin structure

Answer 27

small lipid soluble molecule

Question 28

route of admin for warfarin

Answer 28

oral

Question 29

site of action for warfarin

Answer 29

liver

Question 30

can Hep or warfarin inhibit coag in vitro?

Answer 30

Hep does, warfarin does not

Question 31

thrombolytics

Answer 31

streptokinase urokinase tPA (alteplase) APSAC (anistreplase)

Question 32

thrombolytics moa

Answer 32

directly or indirectly aid conversion of PLASMINOGEN to PLASMIN, which cleaves thrombin and fibrin clots

Question 33

thrombolytics lab changes

Answer 33

increase PT increase PTT no change in plt count

Question 34

thrombolytics use

Answer 34

early MI | early ischemic stroke

Question 35

thrombolytics tox

Answer 35

bleeding

Question 36

thrombolytics contraindications

Answer 36

``` pts with: active bleeding history of intracranial bleeding recent surg known bleeding diatheses severe HTN ```

Question 37

thrombolytics antidote

Answer 37

aminocaproic acid - inhibits fibrinolysis

Question 38

aspirin moa

Answer 38

acetylates and IRREVERSIBLY inhibits cyclooxygenase (COX1 and COX2) to prevent conversion of arachidonic acid to thromboxane A2

Question 39

aspirin lab changes

Answer 39

increase bleeding time | no effect on PT, PTT

Question 40

aspirin uses

Answer 40

antipyretic analgesic anti-inflamm anti-platelet

Question 41

aspirin tox

Answer 41

``` gastric ulceration bleeding hyperventilation Reye's syndrome tinnitus (CN VIII) ```

Question 42

clopidogrel, ticlodipine moa

Answer 42

inhibit plt aggregation by irreversibly blocking ADP receptors - block GpIIbIIIa expression, which is needed to bind fibrinogen

Question 43

clopidogrel, ticlodipine use

Answer 43

acute coronary syndrome. coronary steal syndrome. decrease incidence or recurrence of thrombotic stroke.

Question 44

ticlodipine tox

Answer 44

neutropenia

Question 45

cilastazol, dipyridamole moa

Answer 45

phosphodiesterase III inhibitor - increase cAMP in plts to inhibit plt aggregation. also vasodilator.

Question 46

cilastazol, dipyridamole use

Answer 46

intermittent claudication. coronary vasodilation. prevention of stroke or TIAs (combined with aspirin). angina prophylaxis.

Question 47

cilastazol, dipyridamole tox

Answer 47

``` nausea headache facial flushing hypOtension abd pain ```

Question 48

abciximab moa

Answer 48

monoclonal Ab that binds to GpIIbIIIa on activated plts, preventing aggregation

Question 49

abciximab use

Answer 49

acute coronary syndrome. | percutaneous transluminal coronary angioplasty

Question 50

abciximab tox

Answer 50

bleeding | thrombocytopenia