Two video sessions will describe anticoagulants, thrombolytics, and antiplatelet agents.


There often exists a confusion in the three terms – Anticoagulant, Antiplatelet, and Thrombolytic. Let us be sure about them right at the beginning.

Anticoagulants = Prevent coagulation by affecting the various mechanisms of coagulation: (means – Heparin, Warfarin sodium)

Antiplatelet = Prevent aggregation of platelets (means – low-dose aspirin, clopidogrel etc)

Thrombolytic = Dissolve the thrombus/clot (means tenecteplase, reteplase, alteplase, streptokinase etc; which are tissue plasminogen activators which activate plasminogen into plasmin; and the plasmin dissolves the clot)


Classify anticoagulants with examples.

Anticoagulants prevent blood coagulation. Those used to prevent the blood coagulation inside the body for therapeutic purposes are called In vivo anticoagulants; and those used to prevent the clotting of blood when the blood is collected for investigations are the In vitro anticoagulants.

In vivo drugs may be RAPIDLY ACTING (which mainly includes HEPARIN and its related drugs, which produce a rapid action and their effect lasts for comparatively short time); and SLOW ACTING (which mainly includes warfarin sodium, which begins the effect slowly and its effect lasts longer)


In vivo

Rapidly acting:

1. Traditional/Unfractionated: Heparin

2. Low-molecular weight heparins (LMWH)/Fractionated heparins: Enoxaparin, Dalteparin, Reviparin,Tinzaparin, Pamaparin, Nadroparin, Ardeparin

3. Direct thrombin inhibitors (Heparinoids): Hirudin/Lepirudin/Bivalirudin, Argatroban, Danaparoid, Heparan sulfate

4.Factor Xa Inhibitors: Fondaparinux, Idraparinux, Idrabiotaparinux

5.Human antithrombin concentrate

Slow acting:

1.Coumarins: Warfarin sodium, Nicoumalone, dicoumarol

2. Inandiones: Phenindione

3. Directly acting oral anticoagulants-DOACs) (Non-Vitamin K antagonists):

—a. -Direct thrombin inhibitors: Dabigatran

—b. –Factor Xa Inhibitors: Rivaroxaban, Apixoban, Betrixaban, Edoxaban                           

In vitro


-Calcium complexing agents: Na oxalate, Na citrate, Na edetate

Heparin is used by parenteral route of administration. Warfarin is used orally.

Heparin binds and forms a complex with antithrombin III and activates antithrombin. This complex inhibits coaulation factors – IIa, IXa, Xa, XIa, XIIa, XIIIa ; therefore the action of heparin begins instatntaneouly and it starts its anticoagulant effect.

Whereas warfarin opposes vitamin K and inhibits the synthesis of vitamin K dependent coagulation factors – II, VII, IX, X). Synthesis of new coagulation factors is a long process (for example – Factor II- 60 hours, VII – 6 hours, IX – 24 hours, X – 4 hours), and therefore it takes time to inhibit the process of synthesis of new coagulation factors. Naturally the coagulation factors which are already present, they keep acting.  This is the reason why warfarin is slow acting, and has a time lag in its beginning the action.

Heparin is an anticoagulant of choice during pregnancy, because warfarin is fetotoxic/teratogenic.

Because anticoagulants prevent the process of clotting, their overdose will mean excess anticoagulation – which means bleeding – so the common adverse effect of anticoagulants will be bleeding (Just as for antihypertensives – it is hypotension, antithyroid drugs – it is hypothyroidism, and for hypoglycemic drugs – it is hypoglycemia !!!)

And for heparin overdose the antidote is Protamine sulfate; whereas for warfarin overdose, the antidote is Vitamin K.

We are going to compare and contrast between heparin and warfarin sodium, in the form of a table, which will enable us to know individually about both drugs; plus it will help us to quickly overview the differences between them,


Compare and contrast: Heparin and Warfarin sodium

1 Vitro / Vivo In vitro, In vivo both Only in vivo
2 Route Subcutaneous / Intravenous Usually used by oral route
3 Onset of action Rapidly acting Slow acting
4 Time for onset IV: Instant SC: 1-2 hours Time lag 24-48 hours
5 Duration Short acting Long acting
6 Antidote Protamine sulfate Vitamin K
7 Placenta Does not cross placenta Crosses placenta
8 Pregnancy Used in pregnancy Cannot be used in pregnancy: Fetal warfarin syndrome / warfarin embryopathy: Skeletal and neurological defects
9 CT/PT Increases clotting time Increases prothrombin time
10 Adverse effects BLEEDING



Allergic reactions


Increased transaminase levels





Dermatitis, GI toxicity, Cutaneous and oral ulcers


11 Effect measured by Effect is measured by aPTT  (activated partial thromboplastin time) Effect is measured by INR
12 Drug Interactions Comparatively less drug interactions Comparatively more drug interactions
13 Mechanism of action Binds and activates antithrombin III, its complex with antithrombin III inhibits the factors IIa, Xa, Xia, XIIa, XIIIa Inhibits activation of Vitamin K epoxide and regeneration of its active form – hydroxyquinone; and thus inhibits the synthesis of vitamin K dependent coagulation factors – mainly II, VII, IX, X
14 Antiplatelet action Heparin has additional antiplatelet action Warfarin DOES NOT HAVE antiplatelet action




Mention uses of anticoagulants.

Anticoagulants are mostly useful in venous thrombi because they are fibrin thrombi. They have a less role to play in arterial thrombosis. (Arterial thrombosis has platelet aggregation as its main reason)

1.Prevention and treatment of deep vein thrombosis (DVT)

2.Prevention and treatment of venous thrombosis

3.Prevention and treatment of pulmonary embolism 

      In (1), (2), and (3) – the prophylaxis against thrombosis is needed for

       high-risk patients. namely —

        – Bed-ridden patients with prolonged immobilization

         -Old patients

         -Patients undergoing elective surgery

          -Patients on prolonged immobilization

         -Post-operative patients

         -Post-stroke patients

         -Post-partum patients

         -Patients with leg fractures

4. Prevention of thrombosis in patients with –

     Prosthetic heart valves

     Vascular surgeries

     Joint replacement

     Retinal vessel thrombosis

     Extracorporeal circulation


5. Prevention of thrombosis during –

     cardiac bypass surgery, coronary angioplasty, stent placement

6. Prevention and treatment of stroke (Transient ischemic attack) and cerebral embolism    -in patients with rheumatic valvular heart disease (mitral valve disease) and atrial fibrillation

7. Prevention of myocardial infarction in patients with unstable angina


Mention low molecular weight heparins/Fractionated heparins. Mention the differences and advantages over traditional heparin.

Low molecular weight heparins are fractionated heparins of molecular weights between 3000 and 7000.

Examples: Enoxaparin, Dalteparin, Nadroparin, Tinzaparin, Reviparin, Pamparin, Ardeparin

They are different than traditional heparin due to many pharmacodynamic (actions and mechanisms of action) and pharmacokinetic (bioavailability, dose calculation etc) advantages.

Pharmacodynamic Advantages/differences of LMWH (Low molecular weight heparins)  

  1. More selective action on  FactorXa
  2. Less action on Factor IIa (Thrombin)
  3. Produce Conformational change in antithrombin-III
  4. Less effect on aPTT and whole blood CT
  5. Less antiplatelet effect
  6. Less thrombocytopenia
  7. Less hemorrhagic complications
  8. Lower risk of osteoprosis
  9. Safer than traditional heparin for long-term / short-term administration

Pharmacokinetic Advantages/differences of LMWH (Low molecular weight heparins)

  1. More bioavailability
  2. Longer half life
  3. Convenient Once/twice a day S/C dosing is possible for prophylaxis as well as treatment
  4. More predictable response
  5. Easy to monitor (Less stringent requirements for monitoring and less expenditure on repeated laboratory investigations)
  6. Simplified dose calculation on the basis of body weight is possible (Because clearance is dose-independent)


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