Heme Rx

Question 1

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Heparin

Answer 1

1) immediate anticoag for PE, ACS, MI, DVT (pregnancy safe)
2) Anti-thrombin: antithrombin cofactor –> decr thrombin* + decr factor Xa
3) toxicity: bleeding, HIT, osteoporosis, Rx interactions; protamine sulfate antidote (pos charge molec that binds neg charge heparin)
4) short 1/2 life

Question 2

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Enoxaparin

Answer 2

1) immediate anticoag for PE, ACS, MI, DVT (pregnancy safe)
2) LMWH antithrombin: act more on factor Xa
3) toxicity but less risk than heparin: bleeding, HIT, osteoporosis, Rx interactions; no antidote
4) compared to heparin: better bioavail, 2~4x longer 1/2 life; sub-Q; no need to monitor

Question 3

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Dalteparin

Answer 3

1) immediate anticoag for PE, ACS, MI, DVT (pregnancy safe)
2) LMWH antithrombin: act more on factor Xa
3) toxicity but less risk than heparin: bleeding, HIT, osteoporosis, Rx interactions; no antidote
4) compared to heparin: better bioavail, 2~4x longer 1/2 life; sub-Q; no need to monitor

Question 4

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Lepirudin

Answer 4

1) immediate anticoag for pts w/ HIT
2) antithrombin
3) N/A
4) deriv of hirudin (leeches)

Question 5

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Bivalirudin

Answer 5

1) immediate anticoag for pts w/ HIT
2) antithrombin
3) N/A
4) deriv of hirudin (leeches)

Question 6

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Warfarin (Coumadin)

Answer 6

1) chronic anticoag: post STEMI, VTE prophylaxis, prevent stroke in afib (teratogenic)
2) antiplt: interfere w/ nl syn + carboyxlation of vit-K clotting factors (1972: X, IX, VII, II) + proteins C, S
3) bleeding, teratogenic, skin/tissue necrosis*, Rx interactions; give vit K for OD, give FFP for severe OD
4) cyt P450 met; incr PT (extrinsic path); long 1/2 life; follow PT/INR; PO

Question 7

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Alteplase (tPA)

Answer 7

1) early MI, early ischemic stroke, direct thrombolysis of severe PE
2) thrombolytic: aid plasminogen –> plasmin to cleave thrombin + fibrin clots
3) bleeding (contraindicate in active bleed, intracranial bleed hx, recent sx, known bleed diathese, severe HTN); tx toxicity w/ aminocaproic acid (inhibits fibrinolysis)
4) incr PT, PTT; no change in plt ct

Question 8

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Reteplase (rPA)

Answer 8

1) early MI, early ischemic stroke, direct thrombolysis of severe PE
2) thrombolytic: aid plasminogen –> plasmin to cleave thrombin + fibrin clots
3) bleeding (contraindicate in active bleed, intracranial bleed hx, recent sx, known bleed diathese, severe HTN); tx toxicity w/ aminocaproic acid (inhibits fibrinolysis)
4) incr PT, PTT; no change in plt ct

Question 9

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Tenecteplase (TNK-tPA)

Answer 9

1) early MI, early ischemic stroke, direct thrombolysis of severe PE
2) thrombolytic: aid plasminogen –> plasmin to cleave thrombin + fibrin clots
3) bleeding (contraindicate in active bleed, intracranial bleed hx, recent sx, known bleed diathese, severe HTN); tx toxicity w/ aminocaproic acid (inhibits fibrinolysis)
4) incr PT, PTT; no change in plt ct

Question 10

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Aspirin (ASA)

Answer 10

1) antipyretic, analgesic, anti-infl, anti-plt (decr aggregation)
2) irreversibly inhibits COX-1 (and -2) via covalent acetylation –> decr TxA2 + prostaglandins
3) gastric ulcer, tinnitus (CN VIII); chronic use: acute renal failure, interstitial nephritis, upper GI bleed; Reye’s syn in kids w/ viral infct; OD: respir alkalosis + met acidosis
4) plts can’t syn new COX so effect lasts until new plts made; incr bleeding time; no effect on PT, PTT

Question 11

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Clopidogrel

Answer 11

1) ACS, coronary stenting, decr incidence + recurr of thrombotic stroke
2) ADP R inhibitor: inhibit plt aggregation by irreversibly blocking ADP R; inhibit fibrinogen binding via Gp IIb/IIIa
3) N/A
4) N/A

Question 12

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Ticlopidine

Answer 12

1) ACS, coronary stenting, decr incidence + recurr of thrombotic stroke
2) ADP R inhibitor: inhibit plt aggregation by irreversibly blocking ADP R; inhibit fibrinogen binding via Gp IIb/IIIa
3) neutropenia (unique)
4) N/A

Question 13

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Prasugrel

Answer 13

1) ACS, coronary stenting, decr incidence + recurr of thrombotic stroke
2) ADP R inhibitor: inhibit plt aggregation by irreversibly blocking ADP R; inhibit fibrinogen binding via Gp IIb/IIIa
3) N/A
4) N/A

Question 14

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Ticagrelor

Answer 14

1) ACS, coronary stenting, decr incidence + recurr of thrombotic stroke
2) ADP R inhibitor: inhibit plt aggregation by irreversibly blocking ADP R; inhibit fibrinogen binding via Gp IIb/IIIa
3) N/A
4) N/A

Question 15

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Cilostazol

Answer 15

1) intermittent claudication, coronary vasodilation, prevent stroke/TIAs (w/ ASA), angina prophylaxis
2) PDE III inhibitor –> incr cAMP in plts –> inhibit plt aggregation; vasodilator
3) nausea, HA, facial flush, hypotension, ab pain
4) N/A

Question 16

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Dipyridamole

Answer 16

1) intermittent claudication, coronary vasodilation, prevent stroke/TIAs (w/ ASA), angina prophylaxis
2) PDE III inhibitor –> incr cAMP in plts –> inhibit plt aggregation; vasodilator
3) nausea, HA, facial flush, hypotension, ab pain
4) N/A

Question 17

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Abciximab

Answer 17

1) ACS, PTCA
2) Gp IIb/IIIa inhibitor: bind R on activated plts –> prevent aggregation
3) bleeding, thrombocytopenia
4) made from monoclonal ab Fab fragments (unique)

Question 18

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Eptifibatide

Answer 18

1) ACS, PTCA
2) Gp IIb/IIIa inhibitor: bind R on activated plts –> prevent aggregation
3) bleeding, thrombocytopenia
4) N/A

Question 19

1) uses 2) class/ MOA 3) ADE 4)Fun fact/note

Tirofiban

Answer 19

1) ACS, PTCA
2) Gp IIb/IIIa inhibitor: bind R on activated plts –> prevent aggregation
3) bleeding, thrombocytopenia
4) N/A