Week 3 - Investigations of haemostasis - Primary/Secondary, PT/APTT, V.W.D, Heparin/Warfarin, D.I.C Flashcards
- What is meant by primary haemostasis? How does it occur?
Primary haemostasis is the formation of the platelet plug When there is damage to the endothelial wall, this exposes the subendothelium and collagen + vWF are exposure which cause platelets to come and bind - this is platelet adhesion, then the platelets release chemicals to bring about platelet aggregation and this is primary haemostasis The platelet release phosholipids and calcium which bind to the surface of the plug and the positively charged calcium allows clotting factors to bind for secondary haemostasis
- What is the extrinsic, intrinsic and final common pathway? Which out of extrinsic and intrinsic is the quicker pathway? What coagulation tests measure which pathway?
- Extrinsic pathway is quicker than the intrinsic
- Extrinsic pathway - factor VII - prothrombin time (PT) measures this
- Intrinisc pathway - factor VIII,IX,XI,XII - activated partial thromboplastin (APTT) time measures this
- Common pathway - factors V,X,II,I
- What tests constitute a basic coagulation screen? How are the basic coagulation screenings carried out?
This would be the PT and APTT tests For both, blood is collected and added a test tube containing an anti-coagulant to prevent the blood clotting straight away - usually citrate To both calcium infused phospholpid substance is added To test PT - TF is added to test the extrinsic pathway To test APTT - Kaolin is added to test the intrinsic pathway (platelet count, is also part of basic coag screen) (bleeding time - the platelet function is rarely measured)
A) 19 year old with menorrhagia and easy bruising Platelets 241 x 109 /l Prothrombin time 12 secs Activated partial thromboplastin time 61 secs Platelet count is normal, PT is normal, only APTT is high What are the differentials here? State which is most likely? Does this look like a problem with primary or secondary haemostasis?
Looks like a problem with primary haemostasis due to the bleeding from mucous membranes Increased APTT time, (PT and platelets normal) * Haemophilia is X-linked recessive so very unlikely as she is female * Anti-phospholipid syndrome increases the APTT * VWD also increases the APTT as it binds to factor VIII to prevent its destruction in circulation
A) 19 year old with menorrhagia and easy bruising Platelets 241 x 109 /l Prothrombin time 12 secs Activated partial thromboplastin time 61 secs Platelet count is normal, PT is normal, only APTT is high This patient did indeed have von willebrands disease Why could we rule out liver disease and DIC?
Can rule these out as they would result in a raised PT and APTT usually also causing a low platelet count Anti-phospholpid would also usually cause a mild thrombocytopenia and have thomboses
Which drug can cause an increased APTT?
This would be heparin - usually unfractionated heparin Heparin potentiates the action of anti-thrombin which inhibits mainly thrombin and factor X Unfractionated mainly affects thrombin and therefore APTT would be raised if the patient was on heparin
b) 59 year old male with past history of thromboembolic disease Platelets 325 x 109 /l Prothrombin time 29 secs Activated partial thromboplastin time 53 secs What are likely causes of this patients tests? What is the most likely cause?
Platelet count normal PT and APTT high Patient could have a vitamin K deficiency Could have DIC or liver failure although usually would have low platelets with these conditions Most likely that the patient is on wafarin due to past thromboembolic disease
What are other causes of vitamin K deficiency? How does warfarin cause an increased PT?
Dietary intake - mostly from leafy vegetables and malabsorption ie coeliacs Also requires bile salts for absorption so gallstones blocking gallbladder can cause the disease Warfarin acts on clotting factors 2,7,9,10 (the ones vitK carboxylates) and prevents vitamin K carboxylating these Factor VII has a very short half life and therefore PT is usually the first to rise
c) 40 year old male with multiple injuries following a road traffic accident Platelets 72 x 109 /l Prothrombin time 78 secs Activated partial thromboplastin time >180 secs Thrombin clotting time >180 secs Describe the results? What is the thrombin clotting time? WHat are the possible causes of the results?
Platelet count is low (thrombocytopenic) Prothrombin time is very high APTT is very high Thrombin time is also massively prolonged (tests how long it takes to convert fibrinogen to thrombin via the addition of thrombin) Could have liver disease although platelets are usually mild thrombocytopenia in this, likely he has DIC due to trauma
What are the causes of DIC? Which may have causes this mans blood results?
* Causes of DIC - anything that causes release of tissue factor can potentially set it off * Malignancy, Obstetric emergencies, Infection, Hypovalaemia * Likely this patient was hypovalaemic due to the road traffic accident causing DIC DIC results in the inappropriate and excessive activation of primary and secondary hemostasis and fibrinolysis
Why may there be thrombocytopenia in liver failure even though platelets are made in the marrow?
Liver failure can cause portal hypertension which then causes splenomegaly due to pressure of blood flow, splenomegaly can lead to hypersplenism increasing platelet destruction
What is the treatment of disseminated intravascular coagulation? What is the normal platelet level for platelet transfusion and what is it in this disease?
Would treat by replacing the clotting factors - give fresh frozen plasma Replace the red cell loss if hypovalaemia is the cause - red cell transfusion Replace fibrinogen - cryoprecipitate Also would give platelets when platelet level goes below 50x10^9 / L - want to maintain a good level Usually platelets are replaced when platelet <10x10^9/L
