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Thrombolytics and Fibrinolytics

As the name suggests these drugs:

a. break down thrombosis – Arterial / Venous

b. Fibrinolysis –degrade fibrinogen and fibrin

so clot formation decreases.

Naturally when endothelial injury occurs, after some time clot is formed, and endothelial tissue releases tissue plasminogen activator. This acts on plasminogen converting it into plasmin, when acts on fibrin polymers, breaking them down, leading to thrombus breakdown.


Not only break pathological thrombi but also normal haemostatic plugs in body, which are protective in nature.

There is a generalized lytic state. Increased internal bleeding and hemorrhage might occur, thus patients are carefully selected.

 1. Streptokinase

Protein in nature obtained from streptococci. It forms one to one complex with plasminogen, activating it, plasminogen forms and fibrin polymer breakdown takes place.

It is given parentally, having half life of 2 minutes.

2. Urokinase

Enzyme obtained from fetal kidney cells, grown on tissue culture.

Longer half life than streptokinase of about 15 minutes.

3. Anistreplase

Anisoylated plasminogen streptokinase activator complex (APSAC), a complex of human plasminogen and streptokinase obtained from streptococci. The active site of enzyme is covered with acyl group.

On administration, acyl group is hydrolyzed, the complex and plasminogen is activated.

Drug has more clot selectivity.

Thrombolytic duration of action is 70 minutes.

Tissue plasminogen activator (t-PA)

Naturally present in the body. Also prepared by recombinant DNA technology. Different preparations are available:

1. Alteplase –mutant form of tissue plasminogen activator

2. Reteplase – less fibrin specific than alteplase

3. Tenecteplase – more fibrin specific


1. Acute MI

Main use. Proper patient selection must be done in emergency. Thrombolytic therapy has best outcome when administered as early as possible. Best results are obtained within 6 hours of attack, although administered up to 24 hours, the benefits decrease as time from onset of attack is increased. Administered in patients with ST elevation, indicating patient has complete obstruction of coronary vessel by clot, so needs this treatment.

2. Pulmonary embolism

3. Severe DVT – sup. vena caval syndrome
4. Ascending thrombophlebitis – ileofemoral vein
5. Cerebrovascular ischemia with stroke

Adverse effects

1. Bleeding –due to lytic state.

All contraindications of heparin are same here.

2. Micro-emboli –when thrombus breaks
3. Arrhythmias –due to sudden reperfusion after acute MI
4. Allergy –streptokinase is obtained from streptococci, which are antigenic in nature, body may form antibodies, esp. in patients with streptococcal infections.

If suspect infection in the last 2 weeks, then not given.  


Bleeding tendency

 Fibrinolytic Inhibitors

Aminocaproic acid

Similar in structure to Lysine. As the name suggests, its action is opposite to fibrinolytics. It binds plasminogen and inhibits the binding of fibrinogen with plasmin.

Tranexamic acid

Analogue of aminocaproic acid, used orally and parentally.

  1. Bleeding –adverse effect of fibrinolytic therapy
  2. Adjunctive in hemophilia –dental extraction etc. when chances of bleeding
  3. Prophylaxis –intracranial  aneurysms to prevent bleeding
  4. Postsurgical bleeding –esp. GIT / prostate
  5. Bladder hemorrhage –due to cystitis, drugs or radiations
  6. Menorrhagia
 Adverse effects

1. Thrombosis

2. Hypotension

3. Myopathy

4. GIT disturbance

  1. Disseminated intravascular coagulation (DIC)
  2. Upper genito-urinary tract bleeding – involving kidney, ureter.
  3. Clot Colic

Hemeaturia occurs due to urinary tract bleeding, clot forms, leading to clot colic, which is not dissolved as giving therapy

Serine Protease inhibitor

Aprotinin (serpin) acts directly on plasmin, inhibiting its actions. It used during surgeries where extracorporeal circulation (outside body) is required (e.g. liver transplant/cardiac bypass).

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