27258951
Description
Flashcards by Jenna Paterson, updated more than 1 year ago
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Created by Jenna Paterson
about 5 years ago
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| Question | Answer |
| What factors are part of the intrinsic clotting pathway? | Factors XII, XI, IX and VIII |
| What factors are part of the extrinsic clotting pathway? | Factor VII |
| What is the APTT and what is it a reflection of? | Activated partial thromboplastin time - Reflection of the intrinsic pathway - factors VIII, IX, XI, XII. |
| What is the PT and what is it a reflection of? | Prothrombin time - Reflection of extrinsic pathway - VII |
| What is the INR and what is a normal value? | International normalised ratio (INR) is the standardised form of prothrombin time. INR should be close to 1.0. |
| What can cause an isolated prolonged PT? | - Liver disease (although can also cause a mild APTT increase) - Drugs (warfarin, apixaban, rivaroxaban) - Isolated factor VII deficiency |
| What can cause an isolated prolonged APTT, and how can you determine the case? | Mix patient's serum with someone known to have normal coagulation factor levels - 50:50 mix. ○ If APTT normalises - likely factor deficiency ○ If doesn’t, something is inhibiting coagulation - commonly lupus anticoagulant. |
| What can cause a combined prolongation of PT and APTT? | - Liver disease - Malabsorption - Drugs (warfarin - although more likely to cause isolated PT) - DIC - Massive transfusions in major haemorrhage - Common pathway deficiencies - II, V and X or combination factor deficiency of V and VIII (although more rare) |
| What is TCT and what does it depend on? | TCT - thrombin clotting time - Measurement of conversion of fibrinogen to fibrin clot. - Depends on how much fibrinogen is present in the plasma, and how well that fibrinogen works. |
| What causes low fibrinogen? | ○ DIC ○ Liver disease (synthetic function of liver not working) ○ Massive transfusion ○ Hypofibrinogenemia (low fibrinogen) ○ Dysfibrinogenaemia (good quantity but lack of function) ○ Afibrinogenemia (lack of fibrinogen) |
| What causes high fibrinogen? | ○ Pregnancy ○ Oestrogen effect in females, those on OCP ○ Advancing age ○ Disseminated malignancy |
| What is haemophilia A and its mode of inheritance? | - Factor VIII deficiency - X-linked recessive |
| What is haemophilia B and its mode of inheritance? | - Factor IX deficiency - X-linked recessive |
| What is haemophilia C and its mode of inheritance? | - Factor XI deficiency - Autosomal recessive - Rare in this part of the world |
| What is Von Willebrand Disease and its mode of inheritance? | - Lack of VWF (used to bind factor VIII and platelets together to form clots - 3 types ○ type 1 - mild = autosomal dominant ○ type 2 - mixed = tend to be autosomal dominant ○ type 3 - severe = autosomal recessive (rarer) |
| How is haemophilia A managed? | - Mild: tranexamic acid and/or DDAVP (desmopressin) or recombinant factor VIII - Moderate to severe: recombinant factor VIII (Refacto AF, advate) - Often BD regime however, when bleeding is stable, may be OD (especially in mild/moderate) - Once factor given, 20 mins later factor level from opposite arm |
| How is haemophilia B managed? | - Mild: DDAVP - Moderate to severe: recombinant factor IX (Benefix) |
| How is VW Disease managed? | - Type 1: tranexamic acid ± DDAVP - or rarely voncento (VWF rich product) if major surgery. - Type 2: as above - 2B - associated with low platelets which can worsen with DDAVP - Type 3: Voncento BD regime if using voncento usually, again can be reduced to OD depending on levels and clinical indication. |
| What are the main types of platelet disorder? | Glanzmann thrombaesthenia Bernald Soullier |
| How is Glanzmann Thrombaesthenia managed? | Can be treated with rVIIa (novoseven) and HLA matched platelets |
| How is Bernald Soullier managed? | Tranexamic acid and DDAVP for mild bleeding. HLA matched platelets in more significant bleeding. |
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