bleeding disorderd Flashcards
ISTH-BAT
- Bleeding assessment tool
- Can help structure questions when taking a bleeding history
- Higher scores may increase likelihood of bleeding disorder
what components are measured during a coagulation screen time?
- Prothrombin time
- Activated partial thromboplastin time
- Clauss fibrinogen
TIME BASED TESTS
Coagulation screen
how coag screen works
- Bottle has an anticoagulant in it to prevent clotting before testing
- Sample is spun to remove effect of platelets
- Time for clot to form – analyser measures light passing through
what does a coag screen tell you?
Only tell you about components of coagulation cascade
NOT platelets, NOT natural anticoagulants
Does not tell you whether there is a deficiency or a loss of function
normal PT time
10-14s
what does PT tell you?
EXTRINSIC AND COMMON PATHWAY
- Factor VII (+ common pathway factors: X, V, II, I)
- add excess tissue factor, phsopholipid and Ca so if theres a longer clot time it will be primarily because of deficiency in clotting factors
- identify issues with clotting factors, vitamin K + liver disease
what does activated partial thromboplastin time tell you?
INTRINSIC AND COMMON
- Factors XII, XI, IX, VIII (+ common pathway factors: X, V, II, I)
- Add a contact activator (to bypass need for extrinsic system), phospholipid and calcium in excess
- Deficiency in factors of the intrinsic or common pathway are the rate limiting step
prolongued PT
- remember both PT and APTT also test common pathway so if APTT is fine but PT is prolongued - it must be deficiency in VII
causes for deficiency in VII
- liver disease
- early vitamin K mutation (Bc factor VII has the earliest half life)
Prolonged APTT
FVIII/IX/XI/XII deficiency
ISOLATED prolonged APTT
All other causes also prolong PT
when theres an issue with the factors and tests are prolongued, what can this be?
- deficiency
- not functioning factors
- inherited
- aquired
assessing patients with prolonged PT or APTT
How prolongued is it?
- greater - the more likely theres a problem
has it been prolongued before?
- if no - aquired
is the patient bleeding now?
- if yes - investigated asap
take a thourough bleeding history
- think about anticoagulants, liver disease and nutrition
if emergency / unlear - call haemotology
if not urgent - consider a trial with vitamin K - discuss with haematology is persists
clauss fibrinogen assay
Thrombin is added to the patient’s plasma.
Fibrinogen is converted into fibrin, forming a clot.
The clotting time is measured and compared to a standard curve to determine fibrinogen concentration (g/L or mg/dL).
causes of low class fibrinogen
- liver disease
- disseminated intravscular coagulation
- dilutional coagulopathy
- after thrombolysis
- hypofibrinogenaemia
- dysfibrinogaenemia
what are some bleeding disorders which dont show up on a coag screen?
- VW disease
- mild factor deficiencies
- factor XIII deficicency
- platelet function disorders
- collagen vascular disorders
- thrombocytopenic disorders - inherited or aquired - have abnormal FBC
inheritance - haemophillia
mutation on X chromosome
Classic presentation haemophillia
- Young boy with recurrent bleeds in childhood – often when starts mobilising
- No family history in 1/3
Acquired haemophilia
- Immune mediated condition – often triggered by malignancy, pregnancy
- Antibodies target and destroy FVIII
- Very severe acute soft tissue/joint/muscle bleeds
- Acutely prolonged APTT
- Treated with immunosuppression
