Upgrade to remove ads
Only $35.99/year

Thrombolytics

Terms in this set (27)

how do thrombolytic agents cause dissolution of fibrin clots
convert plasminogen to plasmin, which then degrades the fibrin clot
why is heparin or aspirin coadministered with thrombolytic agents
prophylactically prevents re-thrombosis (lysed clot-->increased local thrombin conc-->enhanced platelet aggregation and thrombosis)
why better results are achieved when early thrombolytic therapy initiated?
clots become more resistant to lysis as they age
lysis of fibrin clot produces
FDP (fibrin degradation products)
during the mechanism of systemic lytic, fibrinogen is -- and factors I, II, V, and VIII are --
depleted, degraded
the "lytic" states inhibit further -- but also markedly impairs --
clotting, hemostasis
plasminogen activators not only act upon -- bound plasminogen, but also on --- plasminogen, producing a plasmin-generated lytic states
fibrin, circulating
in what (3) ways does plasmin-generated systemic fibrinolysis (thrombolytics) inhibit further clotting and impair hemostasis
-circulating plasmin destroys fibrinogen, V, VII
-FDP inhibits platelet aggregation
-Plasmin-induced proteolysis of GP1b and vWF impairs platelet adhesion
principal ADR and risks of thrombolytic agents
ADR: hemorrhage
risks: allergic reactions (SK only)
who are candidates for thrombolytic therapy post-mi
-ST elevation in >2 leads or new LBBB
-w/in 12 hrs of CP onset
-12-24 after onset with ongoing signs of ischemia

no contraindication to thrombolytic therapy
when are pts no longer candidates for thrombolytic therapy post mi
after 24 hours
absolute contraindications to thrombolytic therapy?
stroke
dissection
pericarditis
intracranial neoplasm
internal bleeding
is advanced age >75 an absolute or relative C/I for thrombolytic therapy
no (just a high risk factor)
what is the MOA of altephase
-recombinant form of tPA that directly converts plasminogen to plasmin
-contains a fibrin binding site which allows tPA to bind to the formed thrombus and generate plasmin preferentially at the thrombus site
explain the relationship of alteplase to endogenous TPA
associated with an increase in intracranial bleeding
what are the 3 principal uses of alteplase
STEMI
PE
acute stroke
why is a 150 mg dose of alteplase C/I
can lead to intracranial bleeding
according to "front-loading" regimen, how do you give 100 mg of alteplase: >67 kg
in 3 IV bolus stages: 1) 15 mg over 1-2 min 2) 50 mg over 30 min
3) 35 mg over 60 min
according to "front-loading" regimen, how do you give 100 mg of alteplase: <67 kg
1) 15 mg IV bolus
2) 0.75 mg/kg (not to exceed 50mg) over 30 minutes
3) 0.50 mg/kg over 60 minutes (not to exceed 35 mg)
reteplase vs alteplase: fibrin clot specificity
reteplase: moderate affinity
reteplase vs alteplase: tendency to systemic fibrinolysis
high
reteplase vs alteplase: half life
longer allows dosing by 2 IV boluses 30 min apart
reteplase vs alteplase: time for drug delivery
10 U IV bolus, second given 30 min later
tenecteplase vs alteplase: fibrin clot specificity
highest specificity for pathologic fibrin clots
tenecteplase vs alteplase: tendency for systemic fibrinolysis
high
tenecteplase vs alteplase: half life
prolonged half life allows for single bolus dosing over 5 seconds
tenecteplase vs alteplase: time for drug delivery
single bolus for 5-10 seconds
Sets found in the same folder