Pharm Heme Flashcards
What is the mechanism of heparin? Clinical use? Half life? What must be followed during clinical use? Toxicity? Antidote? Mechanism of antidote?
Activator of antithrombin leading to decr. thrombin and factor X
Short half life
Immediate anticoag for PE, acute coronary syndrome, MI, DVT
Used during pregnancy
Follow PTT
Bleeding, HIT, osteoporosis, drug drug interaction
Protamine sulfate (positively charge molecule bind neg)
What class of drug are enoxaparin and dalteparin? Mechanism? Clinical use? How do they differ from their parent drug?
LMWH
Same mechanisms and use as heparin
Act more on factor Xa Have better bioavailability Longer halflife Can be administered Sub w/o monitoring Not easily reversible
What is the mechanism of fondaparinux? Clinical use? How does it differ from similar drugs?
Factor Xa inhibitor
Very similar to LMWHs
What is HIT? Pathophys? Symptoms?
Development of IgG antibodies against heparin bound platelet factor 4.
The complex activates platelets
Thrombosis and thrombocytopenia
What is the mechanism of argatroban, bivalirudin (1), and dabigatran? Origin of 1? Clinical use?
Inhibit thrombin directly
1=related to hirudin, anticoag used by leaches
Alternatives to heparinn for pts. with HIT
What is the mechanism of warfarin? What must be followed? half life? Clinical use? CI? Toxicity? Reversal? What is heparin bridging?
Interferes with gamma carboxylation of vitamin k clotting factors II, VII, IX, X and proteins C and S (epoxide reductase)
Long half life
Chronic anticoag
Not used in pregnant women
Follow PT/INR
Bleeding, teratogenic, skin/tissue necrosis
Rapid reversal=FFP
reversal=vitamin K
Giving heparin before starting warfarin to avoid a pro coag state.
What class of drug are apixaban and rivaroxaban (1)? Mechanism? Clinical use both? Of just 1? Monitoring? Toxicity? Reversal?
Direct factor Xa inhibitors
Bind to and directly inhibit factor Xa
Treatment and prophylax for DVT
Stroke prophylaxis in pts with a fib
1=treatment and prophylaxis of PE
Oral agents do not require monitoring
Bleeding
No reversal agent
What class of drug are alteplase, reteplase, streptokinase, and tenecteplase? Mechanism? Clinical use? Toxicity? Contraindications? Toxicity treatment?
thrombolytics
Directlly or indirectly aid conversion of plaminogen to plasmin, which cleaves thrombin and fibrin clots, inhibits other factors
Incr. PT
Incr. PTT
No change in platelet count
Early MI
Early ischemic stroke
direct thrombolysis of severe PE
Bleeding
CI=pts w/ active bleeding, history of IC bleeding, recent surgery, known bleeding diathesis, or severe hypertension
Aminocaproic acid, an inhibitor of fibrinolysis
FFP to correct factor deficiencies
What is the mechanism of aspirin? What is its effect on lab findings? Clinical use? Toxicity? Chronic toxicity? Toxicity in children? Overdose?
Irreversibly inhibit COX-1 and COX-2 enzyme by covalent acetylation
Platelets cannot synthesize new enzyme, so more platelets must be formed
Incr. bleeding time, decr. TXA2 and PGs, no effect on PT or PTT
Antipyretic, analgesic, anti-inflammatory, antiplatelet
Gastric ulceration, tinnitus
Acute renal failure, interstitial nephritis, upper GI bleed
Reye syndrome in children w/ viral infection
Hyperventilation and respiratory alk then transitions to mixed metabolic acidosis/resp alk
What class of drug are clopidogrel, prasugrel, ticagrelor (1), and ticlodipine (2)? Mechanism of all? Of just 1? Clinical use? Toxicity of 2? Of others?
ADP receptor Inhibitors
Inhibit platelet aggregation by irreversibly blocking ADP receptors
Prevent expression of IIb/IIIa on platelet surface (no fibrinogen aggregation)
1=reversible
Acute coronary syndrome
coronary stinting
Decr. incidence or recurrence of thrombotic stroke
2=Neutropenia
TTP maybe
What is the mechanism of cilostazol and dipyridamole?Clinical use? Toxicity?
Phosphodiesterase III inhib
Incr. cAMP in platelets=inhibition of platelet aggregation
vasodilators
Intermittent claudication,
coronary vasodilation
Prevention of stroke and TIAs (with aspirin)
Angina prophylaxis
nausea, headache, facial flushing, hypotension, abdominal pain
What class of drug are abciximab , eptifibatide, and tirofiban? Mechanism? Clinical use? Toxicity?
GP IIb/IIIa inhib
Bind to GP IIb/IIIa on activated platelets, preventing aggregation
Unstable angina
Percutaneous transluminal coronary angioplasty
Bleeding, thrombocytopenia
