Coagulation tests Flashcards

1
Q

What pathway is affected if only APTT prolonged

A

Intrinsic or common

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2
Q

What pathway is affected if only PT prolonged

A

Extrinsic

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3
Q

What pathway is affected if both APTT and PT prolonged

A

Common pathway

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4
Q

What factors are part of intrinsic pathway

A

12,11,9,8
Count down from 12 missing 10

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5
Q

What factor represents extrinsic pathway

A

VII/7

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6
Q

Common pathway factors

A

I,II,V,X

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7
Q

What factor joins extrinsic and intrinsic pathways

A

X

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8
Q

Clotting cascade end

A

X+V - Ca2+ + lipids -> thrombin –prothrombin –> fibrinogen -> fibrin clot

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9
Q

Causes of isolated prolonged PT

A

Isolated vit K deficiency (early stages)
Liver disease (early stages)
Warfarin in therapeuti range - INR
Congenital and acquired FVII deficiency

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10
Q

Prolonged APTT

A

Lupus anticoagulant - misnomer
Unfractionated heparin
Congenital intrinsic factor deficiency
Acquired intrinsic factor inhibitors/acquired haemophilia

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11
Q

What is lupus anticoagulant

A

Misnomer - prolongs APTT
Not ass w increased bleeding risk - increased VTE risk
Ass transient transfusion, SLE, antiphospolipid syndrome

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12
Q

What factor deficiency causes haemophilia A

A

FVIII

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13
Q

What facotr deficiency causes haemophilia B

A

FIX

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14
Q

How to test for factor deficiencies singular vs multiple

A

50:50 mix blood test
1:1 patient blood and normal blood

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15
Q

What does non correction in the 50:50 bmix blood test show?

A

Specific or non specific inhibitor OR
multiple factor deficiencies

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16
Q
A
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17
Q

What does a correction of 50:50 mix tes suggest

A

Single factor deficiency as normal blood can provide the missing factor

18
Q

Causes of combined prolonged APTT and PT

A

Severe vit K deficiency
Advance liver disease
DOACs
Supratherapeutic warfarin therapy
Factor consumption eg DIC
Congenital common pathway factor deficiency, acquired inhibitors to common pathway factors

19
Q

What screening test can differentiate DIC, vit K deficiency/warafrin use and liver disease

A

Factor V, VII and VIII

20
Q

Why do mild vit K def and early stage liver disease only prolong PT

A

Factor VII has shorter half life than other factors - first one to be affected

21
Q

Why is DOAC monitoring unreliable

A

Prolonging of APTT and PT depends when checked, cant tell if tehrapuetic or not from levels

22
Q

How is APTT measured

A

Incubate citrated plasma with contact activator first

ADD phospholopid and calcium - time for clot formation in seconds

23
Q

What test for if low factor VIII

A

VWD screen

24
Q

What does a normal VWD screen suggest

A

Haemophilia A

25
Q

What does abnormal VWD screen suggest

A

Von willebrand disease

26
Q

What test do if corect 50/50 mi and normal factor levels

A

Long incubation APTT for early contact factor deficiency

27
Q

What time is not correcting for 50/50 mix

A

> 41 seconds

28
Q

If non correction 50/50 mix and then non specific inhibitor what test for

A

Antiphospholipid antibody testing

29
Q

What test do if consistent with inhibitor after non correction of 50/50 mix

A

Inhibitor assay for factor that is decreased

30
Q

50/50 mix how works

A

APTT reported within 5 minutes of the mix (“immediate”)
after 60 minutes incubation at 37°C -detect progressive inhibitor (this usually indicates a factor VIII inhibitor)

31
Q

What would find if factor VIII inhibitor on 50/50 mix

A

Progressive inhibitor after 60 mins incubation

32
Q

What causes signiicantly prolonged APTT (>100s) but no bleeding

A

Contact factor deficiency (prekallikeren, HMW kininogen)+factor XII

33
Q

What is INR

A

Standardised PT

34
Q

What is ISI

A

International Sensitivity Index (indicates sensitivity of reagent to deficiencies in Vitamin K dependent factors compared to the WHO reference standard)

35
Q

Prolonged PT tests to order after

A

Liver enzymes, albumin, bilirubin
50/50 mix for correction

36
Q

What suspect if correction of 50/50 in prolonged PT

A

Deficiencies

37
Q

What suspect if non-correction of 50/50 in prolonged PT

A

Specific or non sepcific inhibitors to Factor VII

38
Q

Differentials for prolonged APTT AND PT

A
  • Thrombin inhibitors (heparin, direct thrombin inhibitors or direct Xa inhibitors)
  • Vitamin K deficiency (including use of Vitamin K antagonists)
  • DIC
  • Liver disease
  • Paraproteinemia
  • Congenital factor II, V, X or fibrinogen deficiencies
  • Fibrinogen depletion (hemodilution, massive hemorrhage, fibrinolysis)
  • Dysfibrinogenemia (acquired vs congenital)
  • Acquired factor X deficiency from amyloidosis
  • Acquired factor V inhibitors topical bovine thrombin, postoperatively, post-cardiac bypass
  • Any common pathway factor inhibitors
39
Q

Differentiating between factor V, factor VII and factor VIII

A

V - NOT vit K dependent, only made in liver, common
VII - Vit K dependent, only made by liver, exrinsic
VIII -NOT vit K dependent, Lliver and endothelial cells make, intrinsic

40
Q

Why can FVIII be elevated in disorders such as liver disease

A

Acute phase reactant