Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
22 Cards in this Set
- Front
- Back
|
Give 3 activating functions of thrombin. |
FVa - increases FXa activity 300 000 FVIIIa - +FIXa: FX->FXa FXI - FIX -> FIXa |
|
|
What is the function of FXIIIa? |
Activated by thrombin, cross links fibrin clot. |
|
|
What common symptoms do coagulopathies present with? What medical diseases cause these? |
Epistaxis, menorrhagia, gingival haemorrhage, bruising, , post-surgical bleeding, traumatic bleeding, childbirth, ENT haemorrhage. Renal disease, cushings, HHT, CTD, leukaemia, aspirin, NSAIDs, SSRIs, family history. |
|
|
What does haemophilia (X linked) present in lab results? |
Raised aPPT - intrinsic pathway, normal PT/TT/FBC/vWF. Differential diagnosis by specific assay. |
|
|
How do you treat haemophilia A both mild/moderate/severe? |
Mild/moderate -> DDAVP: ADH replacement Severe ->FVIIIa concentrates. |
|
|
What is the function of vWF and what is vWF disease? |
Binds FVIII stops rapid degradation, released by thrombin. Binds to collagen, exposed to endothelial damage. Binds to platelet receptors and assists in platelet aggregation.
vWD - heterogenous - mucosal/platelet type bleeding. Increased aPPT & bleeding time. Normal PT, TT, Pt count. Decreased FVIII, vWF. |
|
|
Name 3 causes of vitamin K dependent factor deficiency. |
Haemorrhagic disease newborn
Biliary obstruction/malabsorption
Vit K antagonists. |
|
|
How does liver + renal disease cause coagulopathy? |
Liver: Failure of production clotting factors. Failure of vit K production/use. Abnormal fibrinogen production - increased TT, excess sialic acid. Hypersplenism and portal hypertension -> Pt low.
Renal: uraemia, low pt. |
|
|
Give the mechanism for DIC induced bleeding. |
Systemic activation coagulation - starts subclinical compensation -> decompensated.
Intravascular deposition of fibrin -> thrombus small & medium vessels. Depletion of pts and coagulation proteins -> bleeding.
Causes: septicaemia, viraemia, metastasis, AML (M3), shock, burns, trauma, cirrhosis, acute rejection, ABO mismatch. |
|
|
What is massive transfusion syndrome? |
Transfusion >5L in 24 hours. Loss FV & FVIII. Defect likely with >80% blood replaced. Everything low/prolonged. Treat with FFP/pt/cryoppt |
|
|
How does platelet release reaction affect vasoconstriction and the coagulation cascade? |
Vasoconstriction - serotonin release
Coagulation cascade - release of platelet phospholipid |
|
|
What is the most common presentation of haematological malignancy? |
Bleeding |
|
|
What are specific symptoms of inherited disorders? |
Haemoptysis Poor wound healing |
|
|
What is the incidence of haemophilia A & B? |
A: 1/5000-10000 male births B: 1/30000 male births
|
|
|
What is FIX? |
FIX: single chain vit K dependant serine protease. With FVIII convert FX-> Xa |
|
|
What are the complications of haemophilia A? |
Progressive joint disease Neurovascular damage from 'tight bleeds' Social concerns |
|
|
Why does haemorrhagic disease of the newborn cause lowered vit K? How does it present? |
Low vit K at birth, not in breast milk, no gut synthesis vit K, liver immaturity, levels may fall in first few days.
Raised aPPT & PT, normal TT, Pts. Prophylactic vit k at birth/IV vit k |
|
|
In what circumstances can GI absorption affect Vit K? |
Vit K; absorption requires bile salts, seen in: obstructive jaundice, biliary obstruction, CF, surgical ileal resection, IBD, malabsorption, antibiotics - gut flora synthesis.
Prolonged PT/aPPT, low II, VII, IX, X. Prophylaxis vit K oral. |
|
|
What is vit k derived from? |
0.1-0.5 ug/kg from green vegetables and bacterial gut synthesis. Requires bile salts. |
|
|
How do haemostatic problems in liver disease present? |
Prolonged PT/aPPT, TT - dysfibrinogenaemia, FDPS - failure to be cleared or increased fibrinolysis, thromocytopoenia.
Treat with vit K/FFP |
|
|
How do haemostatic problems in renal disease present? |
Due to uraemia, low pt.
CNS haemorrhage, GI bleeding, purpura, haemorrhagic pericarditis, epistaxis
Normal aPPT, PT, TT. Normal/slightly low Pt, prolonged bleeding time, abormal pt aggregation studies. |
|
|
How do you treat haemostatic problems in renal disease? |
Reduction uraemic products - dialysis. Platelet transfusion. DDAVP/Cryoppt Blood tranfusion to >0.3Hct. |
