Acquired bleeding disorders Flashcards Preview

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Flashcards in Acquired bleeding disorders Deck (27)
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1
Q

Clotting requires:

A

platelets; vessel wall; clotting factors

2
Q

Prothrombin time (PT)

A

Measures factors II,V, VII, X, fibrinogen - extrinsic pathway

  • Only test that measures FVII
  • Time in seconds from exposure to clot formation
3
Q

Causes of prolonged PT

A

Vitamin K deficiency

  • Liver disease
  • Massive blood transfusion due to dilution of clotting factors
4
Q

Isolated prolonged PT along with normal APTT =

A

Early liver disease
- (factor 7 drops the quickest as shortest half-life)
-

5
Q

Activated Partial Thromboplastin Time (APTT)

A

Measures other factors, not 7
- Kallikrein and HMWK and Factor XII are contact factors which can mess up APTT and make it look prolonged but deficiencies will not cause bleeding problems

6
Q

Causes of prolonged APTT

A
  • Deficiency or inhibition of factors + fibrinogen

- Liver disease, Warfarin, Haemophilia

7
Q

Thrombin time

A
  • Looking at function and amount of function

- Measures fibrinogen

8
Q

Causes of prolonged TT

A

Dysfibrinogenaemia – no fibrinogen, Hypofibrinogenaemia – low fibrinogen, Hepatocellular disease, DIC, Heparin

9
Q

Lupus anticoagulant (LAC)

A
  • IgG/ IgM autoantibody – antiphospholipid antibody
  • Interferes with APTT test in vitro and prolongs APTT
  • Can do LAC screen
  • In vivo more likely to have thrombosis than bleeding
10
Q

Heparin

A
  • Wraps around antithrombin
  • Inhibits Factor X
  • UFH = inhibits Factor Xa and Thrombin and switch off coagulation cascade
11
Q

Unfractioned heparin monitoring (UFH)

A
  • Badly monitored
  • Half life - 45-90 mins
  • Monitor with APTT
  • Can be hard to anticoagulate some infants
12
Q

Low molecular weight heparin

A
  • More reliable that UFH, renally excreted so may not reach therapeutic range
  • Monitor anti-Xa levels
13
Q

HIT = heparin induced thrombocytopenia

A

Immune complex forms causing drop in platelet count

- Skin/allergic reactions and bleeding

14
Q

Treatment of bleeding

A
  • Patients on UFH - Stop IV heparin, administer protamine sulphate - potential allergy
  • Patients on LMWH - Stop LMWH, Protamine reverses 60% of the effects
15
Q

Warfarin

A
  • prevents activation of vitamin K - Factors 2,7,9,10 are all vitamin K dependant
  • Monitor treatment by INR
16
Q

Treatment of bleeding or excessive anticoagulation on warfarin

A
  • Stop warfarin
  • Give prothrombin complex concentration
  • Vit K IV
  • Measure INR 15 mins and 12 hours after PCC
17
Q

Fondaparinux

A
  • Alternative to heparin – similar action
  • Indirect anti-Xa activity
  • Half-life of 17-20 hours
  • No specific antidote
  • Bleeding – stop treatment and general haemoastatic measures
  • If critical bleeding – consider FVIIa
18
Q

Aspirin

A
  • Anti-platelet agent
  • Inactivates platelet cyclooxygenase
  • Give 2-3 doses of platelets in critical bleeding
19
Q

Bleeding in vitamin K deficiency

A
  • Deficiencies of factors II, VII, IX and X
  • Treatment with IV/oral vitamin K
  • Causes = obstructive jaundice, nutrition deficiency
20
Q

Bleeding in liver disease

A
  • Aka cirrhotic coagulopathy
  • Reduced plasma concentration of coag factors except FVIII
  • Treated with platelet transfusions, FFP or prothrombin complex concentrate
21
Q

Bleeding in renal disease

A

Causes:

  • Anaemia - RBC’s are needed for platelet function (release ADP)
  • Uraemia - Disrupts platelet-platelet and platelet-vessel wall interactions
22
Q

Prevention of bleeding

A
  • Correct anaemia - EPO and transfusions
    DDAVP - Desmopressin - stimulates release of vWF
  • Tranexamic acid
23
Q

Haemostatic abnormalities in massive transfusion

A
  • dilutional depletion of platelets and coagulation factors
  • Acidosis
  • Hypothermia
  • Haemorrhages can cause DIC
24
Q

DIC = disseminated intravascular coagulation

A
  • Characterised by systemic activation of pathways leading to and regulating coagulation, which can result in generation of fibrin clots that may cause organ failure with concomitant consumption of platelets and coagulation factors that may result in clinical bleeding
25
Q

DIC pathogenesis

A
oExcess thrombin generation
Microvascular thrombosis – tissue ischaemia and organ damage
oReduced natural anticoagulant activity
oDecreased fibrinolysis
Aetiology
26
Q

Causes of DIC

A
  • Sepsis
  • Trauma
  • Acute intravascular haemolysis
  • Liver disease
  • Chronic causes = malignancy
27
Q

Diagnosis and management of DIC

A
  • Diagnosed via presence of underlying disorder, Global coagulation tests - Low platelet count, elevated D-dimer, prolonged PT, low fibrinogen
  • Treat underlying cause - antibiotics, Vit K supplementation

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