HAEMATOLOGY DRUGS
Name Class Clinical Indications Receptor Action Mechanism of Action Adverse Effects and Interactions Administration + PK
Pulmonary embolism Binds to ATIII, inducing a conformational change resulting in increased affinity of ATIII to
Bleeding and haemorrhage,
Arterial thrombus Increases ATIII affinity to thrombin and clotting factors. This amplifies the effects of ATIII, blocking the IV
thrombocytopenia and hypersensitivity
Heparin Anticoagulant Venous thrombus clotting factors and conversion of fibrinogen to fibrin. ATIII also inhibits clotting factors: IX, X, XI and XII, (not absorbed by GI
reactions
Prophylaxis for AF, stasis thrombin blocking the coagulation cascade and preventing further clot formation. tract)
Monitoring is needed
and PE
Arterial thrombus Binds to ATIII, resulting in increased affinity of ATIII to clotting factors. ATIII inhibits
Bleeding and haemorrhage,
Atrial fibrillation clotting factors: IX, X, XI and XII, blocking the coagulation cascade and preventing further
Low molecular Increases ATIII affinity to thrombocytopenia and hypersensitivity
Enoxaparin Cardiomyopathy clot formation. Due to the shorter pentasaccharide sequence compared to unfractionated Subcutaneous injection
weight heparin clotting factors reactions
Venous thromboembolism heparin, it does not induce the conformational change meaning that inhibition of thrombin
Monitoring is not needed
is not affected.
Prophylaxis of: Oral
Anticoagulants Bleeding and haemorrhage, rarely
DVT and PE Antagonises vitamin K reductase which prevents the activation of clotting factors: II, VII, Low Vd due to high
Vitamin K reductase calciphylaxis
Warfarin Anticoagulant Arterial emboli from Afib or IX and X. This blocks the coagulation cascade preventing further clot formation PPB
antagonist Monitoring is needed
valve disease Metabolised by
Contraindications: pregnancy
CYP450
Prophylaxis for:
Oral as prodrug,
Direct thrombin AF Inhibits factor IIA Competitively antagonises free and fibrin bound thrombin (factor IIA). Stopping the Bleeding and haemorrhage
Dabigatran hydrolysed to active
inhibitor Venous thromboembolism (thrombin) coagulation cascade from producing fibrin from fibrinogen. This prevents clot formation. Monitoring is not needed
drug by carboxylases
after knee or hip surgery
Prophylaxis of venous Competitively antagonises clotting factor Xa. This blocks the coagulation cascade, Bleeding and haemorrhage
Rivaroxaban Factor Xa Oral, hepatic
thromboembolism after knee Inhibits factor Xa preventing the conversion of prothrombin into thrombin therefore inhibiting clotting Monitoring is not needed
Apixaban inhibitor metabolism
or hip surgery Contraindications: hepatic impairment
Prophylaxis of arterial Irreversibly inhibits COX-1 in platelets therefore preventing the synthesis of TXA2 Bleeding and haemorrhage and
thrombosis further down in the arachidonic acid pathway. Lower TXA2 resulting is less platelet dyspepsia
Aspirin COX inhibitor Inhibits COX-1 activation and aggregation. Platelets cannot produce more COX-1 therefore inhibition Contraindications: Hypersensitivity to Oral
lasts 7-10 days. other NSAIDs
Antiplatelets
Prophylaxis of thrombosis Irreversibly antagonises P2Y12 receptors on platelets preventing the binding of ADP Bleeding and haemorrhage, diarrhoea,
after coronary stents, TIA, which would usually result in further platelet activation and aggregation. Ultimately prevents GI discomfort Oral as prodrug,
Clopidogrel P2Y12 receptor
Antiplatelet post MI and clot formation due to lack of platelet activation and aggregation. metabolised by
Ticagrelor antagonist
unstable angina CYP450 enzymes
Given with aspirin
Treat clots from MI or stroke Catalyses the conversion of plasminogen to plasmin. Plasmin breaks down fibrin, Bleeding and haemorrhage
Tissue plasminogen
Fibrinolytics Alteplase Fibrinolytic Massive PE hence the fibrinolytic properties. Fibrin is the ‘cement’ of the clot, so when it is broken down, Angioedema (especially if administered IV for immediate effect
activator
the clot dissolves. alongside ACEI)
Interacts with ferriprotoporphyrin IX (heme) and ferrous ions in the plasmodium food
vacuole resulting in the generation of reactive oxygen species that disrupt the Ca2+ Oral
Arthemether Heme and ferrous ions transporters on the parasite. This is effective against the erythrocytic phase but not the Gi disturbance Rapidly metabolised to
hypnozoites in the liver. Headaches active form
Always given alongside Lumefantrine for increased effect Dizziness
Sleep disturbance
Fatigue
Interacts with hemin, inhibiting the formation of beta-hematin (hemozoin) which is used Irreversible hearing loss Oral
by the parasite to detoxify free heme. Without the hemozoin, the parasite is destroyed by Absorbed increased
Lumefantrine Hemin the free heme. Also inhibits nucleic acid and protein synthesis. 6-10x with a fatty
Always given alongside Arthemether for increased effect meal
Slow metabolism
Gi disturbance
Interferes with DNA synthesis in the plasmodium species by inhibiting pyrimidine Rash
Pyrimidine synthesis
Atovaquone synthesis. Headache Oral
inhibitor
Always given alongside Proguanil, a dihydrofolate reductase inhibitor Insomnia
Neutropenia
Antimalarial Gi disturbance
Antimalarials Hypotension and heart block with IV
See table below
Name Class Clinical Indications Receptor Action Mechanism of Action Adverse Effects and Interactions Administration + PK
Pulmonary embolism Binds to ATIII, inducing a conformational change resulting in increased affinity of ATIII to
Bleeding and haemorrhage,
Arterial thrombus Increases ATIII affinity to thrombin and clotting factors. This amplifies the effects of ATIII, blocking the IV
thrombocytopenia and hypersensitivity
Heparin Anticoagulant Venous thrombus clotting factors and conversion of fibrinogen to fibrin. ATIII also inhibits clotting factors: IX, X, XI and XII, (not absorbed by GI
reactions
Prophylaxis for AF, stasis thrombin blocking the coagulation cascade and preventing further clot formation. tract)
Monitoring is needed
and PE
Arterial thrombus Binds to ATIII, resulting in increased affinity of ATIII to clotting factors. ATIII inhibits
Bleeding and haemorrhage,
Atrial fibrillation clotting factors: IX, X, XI and XII, blocking the coagulation cascade and preventing further
Low molecular Increases ATIII affinity to thrombocytopenia and hypersensitivity
Enoxaparin Cardiomyopathy clot formation. Due to the shorter pentasaccharide sequence compared to unfractionated Subcutaneous injection
weight heparin clotting factors reactions
Venous thromboembolism heparin, it does not induce the conformational change meaning that inhibition of thrombin
Monitoring is not needed
is not affected.
Prophylaxis of: Oral
Anticoagulants Bleeding and haemorrhage, rarely
DVT and PE Antagonises vitamin K reductase which prevents the activation of clotting factors: II, VII, Low Vd due to high
Vitamin K reductase calciphylaxis
Warfarin Anticoagulant Arterial emboli from Afib or IX and X. This blocks the coagulation cascade preventing further clot formation PPB
antagonist Monitoring is needed
valve disease Metabolised by
Contraindications: pregnancy
CYP450
Prophylaxis for:
Oral as prodrug,
Direct thrombin AF Inhibits factor IIA Competitively antagonises free and fibrin bound thrombin (factor IIA). Stopping the Bleeding and haemorrhage
Dabigatran hydrolysed to active
inhibitor Venous thromboembolism (thrombin) coagulation cascade from producing fibrin from fibrinogen. This prevents clot formation. Monitoring is not needed
drug by carboxylases
after knee or hip surgery
Prophylaxis of venous Competitively antagonises clotting factor Xa. This blocks the coagulation cascade, Bleeding and haemorrhage
Rivaroxaban Factor Xa Oral, hepatic
thromboembolism after knee Inhibits factor Xa preventing the conversion of prothrombin into thrombin therefore inhibiting clotting Monitoring is not needed
Apixaban inhibitor metabolism
or hip surgery Contraindications: hepatic impairment
Prophylaxis of arterial Irreversibly inhibits COX-1 in platelets therefore preventing the synthesis of TXA2 Bleeding and haemorrhage and
thrombosis further down in the arachidonic acid pathway. Lower TXA2 resulting is less platelet dyspepsia
Aspirin COX inhibitor Inhibits COX-1 activation and aggregation. Platelets cannot produce more COX-1 therefore inhibition Contraindications: Hypersensitivity to Oral
lasts 7-10 days. other NSAIDs
Antiplatelets
Prophylaxis of thrombosis Irreversibly antagonises P2Y12 receptors on platelets preventing the binding of ADP Bleeding and haemorrhage, diarrhoea,
after coronary stents, TIA, which would usually result in further platelet activation and aggregation. Ultimately prevents GI discomfort Oral as prodrug,
Clopidogrel P2Y12 receptor
Antiplatelet post MI and clot formation due to lack of platelet activation and aggregation. metabolised by
Ticagrelor antagonist
unstable angina CYP450 enzymes
Given with aspirin
Treat clots from MI or stroke Catalyses the conversion of plasminogen to plasmin. Plasmin breaks down fibrin, Bleeding and haemorrhage
Tissue plasminogen
Fibrinolytics Alteplase Fibrinolytic Massive PE hence the fibrinolytic properties. Fibrin is the ‘cement’ of the clot, so when it is broken down, Angioedema (especially if administered IV for immediate effect
activator
the clot dissolves. alongside ACEI)
Interacts with ferriprotoporphyrin IX (heme) and ferrous ions in the plasmodium food
vacuole resulting in the generation of reactive oxygen species that disrupt the Ca2+ Oral
Arthemether Heme and ferrous ions transporters on the parasite. This is effective against the erythrocytic phase but not the Gi disturbance Rapidly metabolised to
hypnozoites in the liver. Headaches active form
Always given alongside Lumefantrine for increased effect Dizziness
Sleep disturbance
Fatigue
Interacts with hemin, inhibiting the formation of beta-hematin (hemozoin) which is used Irreversible hearing loss Oral
by the parasite to detoxify free heme. Without the hemozoin, the parasite is destroyed by Absorbed increased
Lumefantrine Hemin the free heme. Also inhibits nucleic acid and protein synthesis. 6-10x with a fatty
Always given alongside Arthemether for increased effect meal
Slow metabolism
Gi disturbance
Interferes with DNA synthesis in the plasmodium species by inhibiting pyrimidine Rash
Pyrimidine synthesis
Atovaquone synthesis. Headache Oral
inhibitor
Always given alongside Proguanil, a dihydrofolate reductase inhibitor Insomnia
Neutropenia
Antimalarial Gi disturbance
Antimalarials Hypotension and heart block with IV
See table below
