Review of Week 2 Flashcards
screening test for primary haemostasis?
platelet count
no simple screening test really for other components
screening tests for secondary haemostasis?
prothrombin time (PT) activated partial thromboplastin time (APTT)
what does PT test?
CF 7
tissue factor
(intrinsic pathway??)
what does APTT test?
CF 8 and 9
extrinsic pathway??
acquired causes of thrombocytopaenia?
reduced production (marrow problem) increased destruction (coagulopathy such as DIC, autoimmune such as ITP, hypersplenism)
what is ITP?
immune thrombocytopenic purpura
acquired causes of platelet dysfunction?
drugs (aspirin, NSAIDs)
renal failure
what can cause failure of formation of fibrin clot?
multiple clotting factor deficiency (eg DIC0
single clotting factor deficiency (e.g haemophilia)
which is inherited and which is acquired out of multiple and single clotting factor deficiency?
multiple = acquired single = inherited
what can cause multiple clotting factor deficiency?
liver failure
vit K dependency/warfarin therapy
complex coagulopathy such as DIC
how are PT and APTT affected in multiple clotting factor deficiency?
both prolonged
describe DIC
excessive and inappropriate activation of all parts of the haemostatic system (often after trauma, sepsis etc)
causes formation of multiple microvascular thrombus resulting in end organ failure
body tried to break down clots but more are continually made
results in clotting factors being used up
features of DIC?
bruising
purpura
generalised bleeding
causes of DIC?
sepsis
obstetric emergencies
malignancy
hypovolaemic shock
signs of shock?
pale, clammy hands (warm and flushed in distributive)
tachycardia
hypotension
hypoxia
causes of shock in general?
sepsis blood loss obstruction pump failure etc
treatment pathway in shock?
get help IV access fluid replacement oxygen treat cause
signs of PE?
SOB
pleuritic chest pain
pleuritic rub
hypoxia
virchows triad?
relates to venous thrombosis
stasis, vessel wall injury, hypercoagulability
risk factors for venous thromboembolism?
age obesity pregnancy/puerperium oestrogen previous VTE thrombophilia trauma/surgery malignancy heart failure recent MI immobility infection abdo/pelvic mass
how is VTE diagnosed?
imaging
- doppler US
- can do venography/VQ/angiography if needed
- history and clinical examination
- D-dimers
what are D-dimers?
breakdown products of fibrin clot
produced whenever fibrin is generated therefore produced when coagulation has been activated
presence indicates coagulation
efficiency of D-dimer test?
sensitive but not specific
(lots of things can cause elevated D dimers but D dimers are basically always generated in DVT)
i.e elevated D dimers doesn’t confirm DVT but normal D dimers basically rules it out
when should D dimer test be done?
use D dimers to exclude need for imaging
if patient is deemed low risk of DVT by scoring system then a D dimer can rule out DVT without need for imaging
what gives 1 point in clinical scoring system for DVT (wells score)?
active cancer paralysis, plaster bed bound > 3 days or surgery within 4 weeks tenderness along vein entire leg swollen calf swollen >3cm pitting oedema collateral veins low risk = 0 mod = 1-2 high = 3+
DVT prophylaxis?
TED stockings
physio
early mobilisation
DVT treatment?
heparin
warfarin
how does heparin work?
binds to anti-thrombin and potentiates its effect on thrombin
also inactivates CF 10
vit K dependant clotting factors?
2, 7, 9 and 10
also proteins C and S
vit K needed for carboxylation in final step needed to function
how does Vit K carboxylate clotting factors?
adds second COOH group which stabilises bond between coagulation factor and platelet
what is the INR?
international normalised ratio
correction of PT which allows comparison of results between labs and standardises reporting of PT
step wise reversal of warfarin action in event of raised IRN or bleeding?
INR raised but no big bleeding = omit dose/reduce future doses
persistently high INR but no massive bleeding = oral vit K (takes 6 hrs to work)
massive bleeding = clotting factors (works immediately)
