Coagulation tests Flashcards

(40 cards)

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

24
Q

What does a normal VWD screen suggest

A

Haemophilia A

25
What does abnormal VWD screen suggest
Von willebrand disease
26
What test do if corect 50/50 mi and normal factor levels
Long incubation APTT for early contact factor deficiency
27
What time is not correcting for 50/50 mix
>41 seconds
28
If non correction 50/50 mix and then non specific inhibitor what test for
Antiphospholipid antibody testing
29
What test do if consistent with inhibitor after non correction of 50/50 mix
Inhibitor assay for factor that is decreased
30
50/50 mix how works
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
What would find if factor VIII inhibitor on 50/50 mix
Progressive inhibitor after 60 mins incubation
32
What causes signiicantly prolonged APTT (>100s) but no bleeding
Contact factor deficiency (prekallikeren, HMW kininogen)+factor XII
33
What is INR
Standardised PT
34
What is ISI
International Sensitivity Index (indicates sensitivity of reagent to deficiencies in Vitamin K dependent factors compared to the WHO reference standard)
35
Prolonged PT tests to order after
Liver enzymes, albumin, bilirubin 50/50 mix for correction
36
What suspect if correction of 50/50 in prolonged PT
Deficiencies
37
What suspect if non-correction of 50/50 in prolonged PT
Specific or non sepcific inhibitors to Factor VII
38
Differentials for prolonged APTT AND PT
* 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
Differentiating between factor V, factor VII and factor VIII
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
Why can FVIII be elevated in disorders such as liver disease
Acute phase reactant