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Flashcards in Coag Screening Deck (18):

APTT- tests what factors



Method aptt

Platelet poor plasma [PPP] is incubated at 37°C then phospholipid (cephalin) and a contact activator (e.g. Kaolin, micronized silica or ellagic acid) are added followed by calcium (all pre-warmed to 37°C). Addition of calcium initiates clotting and timing begins. The APTT i


Prolonged aptt

Factor Deficiencies of either XII, XI, IX & VIII. However, the APTT can be normal with mild deficiencies of these clotting factors (<20-40% of normal before the APTT is prolonged)
Contact factor deficiency e.g. pre-kallikrein
Acquired inhibitors
Paraprotein- anti x
Renal- lose factors
Ribaroxaban and Dabigatran


Long pt and aptt

Vitamin K deficiency

Liver disease due to low vit k abs
- Decreased synthesis of clotting factors
- An acquired dysfibrinogenemia due to changes in the sialic acid content of the fibrinogen. This is similar to the effect seen in the newborn infant - the so-called 'fetal fibrinogen.'

Direct thrombin inhibitors including Hirudin, Argatroban and Dabigatran.

DIC - due to the consumption of clotting factors

Massive blood transfusion leading to a dilutional coagulopathy

In patients receiving thrombolytic therapy, the APTT may be prolonged due to a reduction in fibrinogen levels.

In multiple clotting factor deficiencies the APTT becomes prolonged with less severe reductions in factor levels.

Combined deficiency of clotting factors e.g. Factors V and VIII

'Common Pathway' deficiency - FV, F, FII [Prothrombin] and Fibrinogen.


Increased APTT
± Prolonged PT

Hep in high doses
Acquired f v fx
Antiphospholipid ab


Prolonged PT ± Prolonged APTT



Short APTT

An acute phase response leading to high FVIII levels -
anti-Xa assays should be performed to monitor
Dice if ass w hypercoagulable state
Difficulties in the collection of samples leading to activation of coagulation within the collection tube.


General coag assay techniques

Tilt tube is gold standard
Optical density -allow clot waveform analysis and include
Scattered light detection for clotting assays (660 nm)
The turbidity during the formation of a fibrin clot is measured as an increase in scattered light intensity when exposed to light at a wavelength of 660 nm.
Transmitted light detection for chromogenic assays -Colour production leads to a change in light absorbance, which is detected as a change in transmitted light. Over time, the change in absorbance per minute is calculated (OD/min). Transmitted light detection for immunoassays (405 nm, 575 nm, 800 nm) The change in light absorbance caused by the antigen–antibody reaction is detected as the change in transmitted light. Over time, the change in absorbance per minute is calculated (OD/min). Some analysers detect light transmittance at multiple wavelengths between 395 and 710 nm.chromogenic immuno
affected by turbid samples
Mechanical The sample cuvette rotates and a steel ball remains stationary in a magnetic field until the formation of fibrin strands around the ball produces movement. This is detected by a change in the magnetic field and the coagulation


International guide for lupus testing

Dilute Russell’s viper venom time (DRVVT) in conjunction with the platelet neutralization test. 2. An APTT test that has a low concentration of phospholipid and uses silica as an activator, thus making it sensitive to the presence of LAC.


Recommendations for the optimal laboratory detection of lupus anticoagulant (LAC)4

(A) Blood collection -before the start of any anticoagulant drug or a sufficient period after its discontinuation
2. Fresh venous blood in sodium citrate 9:1
3. Double centrifugation
4. Quickly frozen plasma is required if LAC detection is postponed
5. Frozen plasma must be thawed at 37°C
(B) Choice of the test
1. Two tests based on different principles
2. DRVVT should be the first test considered 3. The second test should be a sensitive APTT (low phospholipids and silica as activator)
4. LAC should be considered as positive if one of the two tests gives a positive result
(C) Mixing test
1. Pooled normal plasma (PNP) for mixing studies 2. A 1:1 proportion of patient:PNP should be used, without preincubation within 30 min
3. LAC cannot be conclusively determined if the thrombin time of the test plasma is significantly prolonged
(D) Confirmatory test 1. Confirmatory test(s) must be performed by increasing the concentration of phospholipid content of the screening test(s) 2. Bilayer or hexagonal (II) phase phospholipid (PL) should be used to increase the concentration of PL (E) Expression of results Results should be expressed as ratio patient:PNP for all procedures (screening, mixing and confirm) (F) Transmission of results A report with an explanation of the results should be given


D dimer assay

30 different assays
All based on principle of using antibodies against d dimer- eg latex immunoassay-


Raised dimer

Pgy malignancy burns liver ex snake bites. Cardiac failure
renal failure
Aortic dissection DIC
Vaso-occlusive sickle cell crisis


Prolonged Aptt in massive detail
Pre analytic

1- FVIII, IX, XI,XII, contact factors(pre kalikikrein), common pathway(7,5,10)' hypofibrinogen dysfib
Drug - warfarin, thrombolyse, noacs lmwh
Acquired- amyloid(fx) fxii( nephrotic) dic, liver dysfunction, bl loss fluid replacement
Inh- 8, 9, aq fv, lupus AC, paraproteins
Pre analytic- tube fill, clotted sample, aged blood, wrong ac


Components of initiation phase

Thrombin burst


Important anticoagulant pathway component

Anti thrombin
Protein C & S


Which factor def gives long aptt and normal PT

XI deficiency and factor XII deficiency cause prolongation of the APTT without prolongation of the PT. However factor XII deficiency does not cause haemorrhage.


Attributes of anti xa

Linear against range of concentration calibrated to drug specific standards
Available 24 hrs and fast


Xa assay

Add known concentration thrombin and pt plasma and measure xa activity based on colour change
Inversely proportional to amount of drug