Bleeding Disorders Flashcards
What can cause failure of primary haemostasis (i.e. the platelet plug)?
Vascular
- e.g. lack of collagen
Platelets
- Reduced number or function
Von Willebrand Factor
What vascular abnormalities can cause failure of primary haemostasis?
Hereditary (weak collagen)
- Marfan’s
- Hyperflexibility Disorders
Acquired
Vasculitis
eg Henoch-Schonlein Purpura
(not actually problem with platelets, just leaky vessels)
What can cause a reduced NUMBER of platelets?
Decreased production
- Bone marrow problem
Increased Destruction (caused by:)
- Disseminated Intravascular Coagulation (DIC)
- Immune Thrombocytopenic Purpura (ITP)
- Hypersplenism
What can decrease platelet function?
Drugs (eg Aspirin, NSAIDs)
- this is often deliberate (antiplatelets used to prevent arterial thrombosis in at risk patients)
Renal failure
- uraemia can interfere with platelet function
How is vWF deficiency normally inherited?
Autosomal dominant
If platelets are being prematurely destroyed, production of platelets increases in the bone marrow to compensate. What would the blood film look like if this was the case?
Large platelets
(larger on Day 1 than Day 7)
=> more large platelets = increased production
What are the main causes for failure of secondary haemostasis?
Multiple clotting factor deficiencies
- acquired (eg DIC)
Single clotting factor deficiency
- hereditary (eg Haemophilia)
What are the potential causes for multiple clotting factor deficiencies?
- Liver failure (makes clotting factors)
- Vitamin K Deficiency/Warfarin therapy (Vit K antag.)
[Factor II, VII, IX, X all rely on Vit K] - Complex coagulopathy
- DIC
Why may a platelet transfusion not be useful in patients who have increased destruction due to an autoimmune cause?
platelets will be destroyed by autoantibodies soon after they are given
- instead steroids should be used to suppress immune system and Ab
- platelet transfusion may be more useful if marrow failure
If multiple clotting factors are affected, will PT or APTT be abnormal?
Both will be prolonged
Where do we find vitamin K and how is it absorbed?
- Diet (green leafy veg)
BUT can also be produced by bacteria in gut - Absorbed in upper intestine
- Requires bile salts for absorption
What can cause a vitamin K deficiency?
- Poor dietary intake
- Malabsorption
- Obstructive jaundice
- Vitamin K antagonists (warfarin)
- Haemorrhagic disease of the newborn (lack of vit K as none in breast milk, and not enough bacteria in bowel)
WHat is disseminated intravascular coagulation?
- activation of clotting EVERYWHERE
- Primary and secondary haemostasis and fibrinolysis
- Microvascular thrombus formation => end organ failure
- Clotting factors used up
=> Bruising, purpura
Using up all clotting factors has what effect on PT and APTT?
Prolonged (as body takes longer to clot if it cant find clotting factors)
Which of PT and APTT is first to become abnormal in DIC?
PT first as Factor VII has shortest T1/2