This document discusses anticoagulants and coagulation disorders. It defines anticoagulants as substances that prevent or delay blood clotting. It describes commonly used laboratory and clinical anticoagulants such as heparin, vitamin K antagonists, and aspirin. It also discusses coagulation disorders including defective clotting factors as seen in hemophilia, von Willebrand disease, and disseminated intravascular coagulation (DIC). The document provides details on the causes, symptoms, inheritance patterns, and treatments of various coagulation disorders.

1. Anticoagulants&
Coagulation disorders
Dr Anu Priya J

2. Anticoagulants
Definition
• Substances which prevent or delay clotting of
blood.
Types
• Laboratory anticoagulants
• Clinically used anticoagulants
• Biological / Natural anticoagulants

3. Laboratory anticoagulants
• EDTA
(Ethylene diamine tetraacetic acid)
• Double oxalate - PCV
(Ammonium oxalate+Potassium oxalate)
• Sodium citrate - ESR

4. Criteria
• It should not alter the size of the cell
• It should not produce hemolysis
• It should not disrupt leukocytes
Laboratory anticoagulants

5. Mechanism of action
• Chelating agents – act by removing Ca2+
• Calcium – a part of prothrombin activator
• Removal of Ca2+ : prothrombin not activated
– prevents coagulation
Laboratory anticoagulants

6. Clinically used anticoagulants
• Heparin
• Vitamin K antagonists
• Aspirin

7. Clinically used anticoagulants
Heparin
• Intravenous & Subcutaneous routes
• Potentiates the action of antithrombin III &
prevents coagulation by inhibiting factors IX,
X, XI, XII
• First isolated from liver. Hence the name.
• Present in liver, granules of basophils, and
mast cells.

8. Clinically used anticoagulants
Heparin
• Normally destroyed by heparinase, an enzyme
present in liver.
• Treatment of DVT, MI
• Prophylaxis during heart surgeries,
hemodialysis.
• S/E Heparin induced thrombocytopenia –
Rx Protamine

9. Clinically used anticoagulants
Vitamin K antagonists
• Oral anticoagulants
• Coumarin derivatives – Warfarin sodium,
Dicoumarol
• Competitively inhibits vitamin K by occupying
vitamin K receptors in the liver

10. Vitamin K antagonists
• Vitamin K required for the ϒ carboxylation of
glutamic acid residues of vit K dependent
clotting factors II, VII, IX, X,& Protein C, Protein
S
• Treatment of Atrial fibrillation, Pulmonary
embolism, etc.,
Clinically used anticoagulants

11. Clinically used anticoagulants
Aspirin
• Oral route
• Prophylaxis of thromboembolism

12. Biological/Natural anticoagulants
• Hirudin - leech
• Snake venom
• Heparin
• Anti-thrombin
• Protein C
Naturally occurring anticoagulants in the human body

13. Warfarin cannot be used as a lab
anticoagulant. Why?
• Clotting of blood collected in lab i.e.,invitro -
occurs via intrinsic pathway
• Warfarin inhibits the clotting factors that are
involved in the extrinsic pathway of
coagulation which occurs inside the body i.e.,
in vivo.
• Therefore, warfarin cannot be used as a lab
anticoagulant.

14. Coagulation disorders/
Disorders of hemostasis
I. Defective clotting
II. Vascular defects
III. Platelet defects
IV. Combined defects

15. Defective clotting
 Clotting factor deficiency
 Increased clotting time
Types
Congenital
– Hemophilia
– Von willebrand’s disease
Acquired
– DIC (Disseminated Intravascular Coagulation)
– Liver failure
– Vitamin K deficiency
– Anticoagulant overdose etc.,

16. Vascular defects
Abnormality in the integrity of the vascular
endothelium
Causes
– Infections
– Drugs (Aspirin, Sulpha drugs)
– Vitamin C deficiency
– Allergy
– Vasculitis due to connective tissue disorders,etc.,
Treatment
– ACTH or Corticosteroids – to decrease the fragility of
capillaries

17. Platelet defects
 Quantitative / Thrombocytopenia
 Qualitative / Thrombasthenia

18. Quantitative defect/
Thrombocytopenia
a) Primary / ITP
Idiopathic thrombocytopenic purpura
– Due to autoimmunity (antibodies produced against
platelets)
– (or) Hereditary
– (or) Congenital
b) Secondary
– Drugs
– Infections
– Bone marrow depression
– Hypersplenism (platelets are destroyed in spleen)

19. Qualitative defect/
Thrombasthenia
• Normal platelet count
• Functional defect

20. Terms
Purpura
– Hemorrhage into the skin & mucus membrane from
capillaries due to abnormality in blood vessels or
platelets
– Purpuric spots
– Bleeding time increased; clotting time prolonged
Thrombus
– An abnormal clot that develops in a blood vessel
Embolus
– Thrombus gets detached & is carried to other blood
vessels

22. Hemophilia
• Royal disease
• Defective gene on X chromosome
Hemophilia
Clotting factor
deficiency
Inheritance
Hemophilia A Factor VIII X linked recessive
Hemophilia B/
Christmas disease
Factor IX X linked recessive
Hemophilia C Factor XI X linked dominant

23. Hemophilia
Defect
• In all types of hemophilia – lack of formation
of prothrombinase complex (consists of factor
Xa & factor Va)
• Prothrombinase needed for the conversion of
prothrombin to thrombin in the presence of
calcium

24. Hemophilia
Clinical features
– Spontaneous severe bleeding/ bleeding after
minor trauma
– Subcutaneous & intramuscular hemorrhage
– Hemoptyis
– Hematuria
– Hemorrhage into the joint space – severe joint
pain

26. Hemophilia
Investigations
• Bleeding time – normal
• Clotting time – prolonged to 1 to 12 hours (normal:5-10
min) – formation of a very soft clot
• Prothrombin time (PT) – normal
• Activated partial thromboplastin time (aPTT) – prolonged
• Factor VIII assay - to assess the severity of the disease

27. Hemophilia
Treatment
• Fresh blood/ Fresh plasma transfusion as
factor VIII is destroyed rapidly on storage
• Cryoprecipitate of factor VIII given
intravenously
• Factor IX – not lost during storage – so stored
blood can be given for Hemophilia B.

28. Inheritance

29. Inheritance

30. Inheritance

31. Von Willebrand disease
• Inherited deficiency of von Willebrand factor
(vWf)
• vWf – secreted by platelets & vascular
endothelium – needed for platelet adhesion
to collagen fibers of damaged vessels
• Severe bleeding from small injuries

32. • Also known as pseudohemophilia
• Factor VIII is transported in combination with
vWf – Factor VIII gets activated when it is
separated from vWf
• Deficiency of vWf – secondary deficiency of
factor VIII
Von Willebrand disease

33. DIC
• Disseminated Intravascular Coagulation
• Seen in Septicemia, Abruptio placenta,
mismatched blood transfusion, viper and
scorpion bite.

34. DIC
• Increased traumatized tissues in the body – release
tissue thromboplastin – initiate coagulation
• Formation of numerous small clots that block
peripheral small blood vessels
• Many of the clotting factors – used up for clotting –
so patient begins to bleed after some time – So, DIC
presents with severe bleeding
• Fibrin degradation product formed due to lysis of
intravascular clots – further aggravates bleeding

35. Thank you