Hematology

Thrombolytics - tPA & Streptokinase song

Listen to the preview here. The full song is free on YouTube.

Thrombolytics - tPA & Streptokinase

Full song on YouTube ↗

Key points in this song10

tPA (alteplase, tenecteplase) is a recombinant tissue plasminogen activator that converts plasminogen to plasmin, which degrades fibrin clots; it is fibrin-selective, meaning it preferentially activates plasminogen bound to fibrin at the clot site.
Streptokinase is a non-fibrin-selective thrombolytic derived from streptococci that forms a complex with plasminogen to generate systemic plasmin, causing a systemic lytic state and risk of hemorrhage at remote sites.
Absolute contraindications to thrombolytics include any prior intracranial hemorrhage, ischemic stroke within 3 months, known intracranial neoplasm, active internal bleeding, and suspected aortic dissection.
In acute ischemic stroke, IV tPA (alteplase) must be administered within 4.5 hours of symptom onset, with a door-to-needle target of under 60 minutes; blood pressure must be controlled below 185/110 mmHg before administration.
In STEMI, thrombolytics are indicated when primary PCI cannot be performed within 120 minutes of first medical contact; tPA is preferred over streptokinase due to greater fibrin selectivity and superior 90-minute patency rates.
Streptokinase is antigenic and can cause allergic reactions including anaphylaxis; repeat administration within 6–12 months is contraindicated due to neutralizing antibodies from prior streptococcal infection or prior drug exposure.
The major complication of all thrombolytics is hemorrhage, most critically intracranial hemorrhage (ICH), occurring in approximately 0.5–1% of ischemic stroke patients treated with tPA.
Thrombolytics are indicated in massive pulmonary embolism with hemodynamic instability (hypotension, shock); catheter-directed tPA is used in submassive PE with evidence of right heart strain when systemic thrombolysis risk is too high.
Aminocaproic acid (epsilon-aminocaproic acid) inhibits plasminogen activation and is used as the antidote to reverse thrombolytic-induced bleeding by blocking fibrinolysis.
Unlike anticoagulants, thrombolytics actively dissolve already-formed clots by generating plasmin; they do not prevent new clot formation and must be followed by anticoagulation to prevent rethrombosis.