Haemostasis Screening Tests

Overview

Haemostasis = 5 components: vessel wall, platelets, coagulation factors, fibrinolysis, inhibitors. Each has screening + special/confirmatory tests. Ties together Von Willebrand Disease, Immune Thrombocytopenic Purpura, Vascular and Platelet Function Disorders.

Screening tests

Whole blood coagulation time: 4-9min, insensitive/nonspecific, limited value. APTT: plasma+Ca+phospholipid+kaolin, normal 30-40sec. ↑ by heparin, factor deficiency, liver disease, circulating anticoagulants. PT: tissue thromboplastin+Ca, normal 10-14sec. ↑ by oral anticoagulants, liver disease, vit K deficiency, DIC. Fibrinogen: TT (normal <20sec) + fibrinogen titre (normal up to 1:32). Both ↑ with hypofibrinogenaemia (DIC), ↑FDP, heparin.

Special tests

Coagulation factor assays (substrate plasma minus one factor, compare to standard, % of normal). Quantitative immunological/chemical assays.

Fibrinolytic system tests

Screening: fibrinogen, serum FDP, ethanol gelation test, euglobulin lysis time. Special: functional/ELISA/chromogenic assays.

Coagulation inhibitors

Antithrombin III — binds thrombin, blocks coagulation. Protein C+S — activated protein C inactivates factors V/VIII (cofactor protein S). Deficiency, or factor V Leiden (resistance to protein C), → hypercoagulable state.

Pattern table (memorise)

Clinical relevance

Highest-yield table in the whole bleeding-disorders section — most questions reduce to “given this pattern, name the disorder.” PT↑ alone → extrinsic pathway (early warfarin, vit K deficiency, mild liver disease); APTT↑ alone → intrinsic pathway (heparin, haemophilia A/B, vWD). FDP positive = the one thing that separates DIC from everything else in the table. Vit K deficiency and liver disease give an IDENTICAL screening pattern (both make vit K-dependent factors, made in liver) — distinguished clinically, not by this table alone.

Overview

Haemostatic balance depends on five components: the blood vessel wall, platelets, coagulation factors, the fibrinolytic system, and coagulation inhibitors. Each has its own screening tests (first-line) and special/confirmatory tests (used when screening is abnormal). This topic collects the laboratory tests referenced throughout the bleeding-disorder topics into one reference framework — see Von Willebrand Disease, Immune Thrombocytopenic Purpura, and Vascular and Platelet Function Disorders for how these tests apply to specific diseases.

Screening Tests by Component

Individual Test Detail

• Whole blood coagulation time — normal 4–9 minutes at 37°C; capillary or tube methods; of limited value — insensitive and nonspecific.
• APTT (or PTTK) — plasma is combined with calcium, phospholipid, and a surface activator (kaolin); normal range 30–40 seconds. Prolonged by: heparin, factor deficiency, liver disease, circulating anticoagulants.
• One-stage PT — tissue thromboplastin (e.g. brain extract) and calcium added; normal range 10–14 seconds. Prolonged by: oral anticoagulants, liver disease (especially obstructive), vitamin K deficiency, DIC.
• Fibrinogen measurement — via semiquantitative fibrinogen titre and thrombin time; normal TT under 20 seconds, normal fibrinogen titre up to 1:32 dilution. Both are prolonged/raised by hypofibrinogenaemia (e.g. DIC), raised FDP, or heparin.

Special (Confirmatory) Tests

Used once a screening abnormality is identified:

• Coagulation factor assays — bioassays using substrate plasma containing every factor except the one under study; the unknown sample’s activity is compared against a standard control and expressed as % of normal activity.
• Quantitative assays — immunological and other chemical methods for direct factor quantification.

Investigation of the Fibrinolytic System

Increased circulating plasminogen activator indicates hyperfibrinolysis. Screening tests: fibrinogen estimation, serum FDP, ethanol gelation test, euglobulin (whole blood) lysis time. More specific tests: functional assays, ELISA-based immunological assays, chromogenic assays of plasminogen activators/plasminogen/plasminogen activator inhibitor/FDP.

Investigation of Coagulation Inhibitors

The body’s built-in braking system, keeping coagulation localised:

• Antithrombin III — binds thrombin, forming a thrombin-antithrombin complex that blocks further coagulation.
• Protein C and S — activated protein C cleaves and inactivates activated factors V and VIII (an anticoagulant action), augmented by cofactor protein S. Deficiency of protein C/S, or resistance of activated factor V to protein C due to a mutation at the target site (factor V Leiden), produces a hypercoagulable state.

Pattern Recognition: Major Haemostatic Disorders Contrasted

Clinical Relevance

• This table is the single highest-yield reference for the entire bleeding-disorders section — most exam questions on this topic reduce to “given this pattern of platelet count/BT/PT/APTT, identify the disorder,” and every disease covered elsewhere in this batch has its defining row here.
• The PT/APTT split maps directly onto the extrinsic-vs-intrinsic (plus common) pathway division — an isolated prolonged PT points to factor VII or an extrinsic-pathway problem (early warfarin effect, vitamin K deficiency, mild liver disease), while an isolated prolonged APTT points to the intrinsic pathway (heparin, haemophilia A/B, vWD) — this is the practical logic clinicians use before ordering specific factor assays.
• FDP positivity is the one parameter that cleanly separates DIC from every other disorder in the table — every other condition listed leaves FDP absent, making it the single most specific discriminating test when DIC is suspected against a background of multiple deranged screening parameters.
• Vitamin K deficiency and liver disease produce an identical screening pattern (↑PT, ↑APTT, normal platelets/TT/FDP) because vitamin K-dependent factor synthesis happens in the liver — the two are distinguished clinically (history, other liver function tests) rather than by this table alone.

No Rendered Diagram for This Topic

This topic is a laboratory reference table (which test measures what, and the resulting pattern per disorder), not a disease mechanism — a rendered diagram would only redraw the pattern table already in notes.md.

Hand-Draw Suggestion

Draw the pattern table from notes.md by hand as an active-recall exercise: list the 10 disorders down one side, and try to fill in the platelet count/BT/PT/APTT/TT/FDP columns from memory before checking against the reference — this table is the single highest-yield piece of the entire haemostasis section and is best learned by repeated blind recall, not by a diagram.