By MRCSA in MRCS Part A — 04 Jul 2026

65 COAGULATION & ANTICOAGULANTS

# 66 COAGULATION & ANTICOAGULANTS

Detailed notes

Haemostasis is the body's response to vessel injury. It must be fast enough to stop blood loss, but tightly regulated to avoid pathological thrombosis. The MRCS Part A consistently tests three things here: the cascade, the drugs that target it, and the disorders that disturb it.

Primary haemostasis — the platelet plug

Within seconds of endothelial injury:

➡ Vasoconstriction — reflex smooth muscle contraction reduces flow.

➡ Platelet adhesion — exposed subendothelial collagen binds platelets via von Willebrand factor (vWF) as a bridge to platelet GpIb.

➡ Platelet activation — releases ADP, thromboxane A2 (TXA2) and serotonin → recruits more platelets.

➡ Aggregation — fibrinogen cross-links activated platelets via the GpIIb/IIIa receptor, forming the soft platelet plug.

This unstable plug must be stabilised by fibrin — the job of secondary haemostasis.

Secondary haemostasis — the coagulation cascade

Two pathways converge on a common final pathway, ending in fibrin.

Pathway	Factors	Test	Trigger
Intrinsic	XII, XI, IX, VIII	APTT	Contact with negatively charged surface (in vivo: collagen)
Extrinsic	VII + tissue factor (III)	PT / INR	Tissue factor released from damaged tissue
Common	X → V → II (prothrombin) → I (fibrinogen) → fibrin	PT and APTT	Activation of factor X

Factor XIII then cross-links fibrin into a stable mesh.

👩‍⚕️ Memory aid — "12 weeks": the intrinsic pathway is the long one (more factors) and is measured by APTT (Activated Partial Thromboplastin Time). "Play tennis indoors → APTT/intrinsic." The extrinsic pathway is short, fast, and uses PT ("Play Tennis outside → PT/extrinsic").

👩‍⚕️ Memory aid — "1972": the vitamin K-dependent factors are II, VII, IX, X (plus protein C and S). Warfarin inhibits all of these by blocking vitamin K epoxide reductase.

──────────────────────────────

Fibrinolysis — taking the clot down

Once the vessel heals, the clot must be cleared.

➡ tPA (tissue plasminogen activator) is released from endothelium.

➡ tPA converts plasminogen → plasmin.

➡ Plasmin degrades fibrin into fibrin degradation products (FDPs), including D-dimer.

A raised D-dimer means fibrin has been broken down somewhere — sensitive but not specific (raised in DVT/PE, but also in sepsis, pregnancy, malignancy, post-op).

Natural anticoagulants

Inhibitor	Target
Antithrombin III	Inactivates IIa and Xa (and to a lesser extent IXa, XIa, XIIa)
Protein C + Protein S	Inactivate Va and VIIIa
Tissue factor pathway inhibitor (TFPI)	Inhibits VIIa/TF complex

👩‍⚕️ Antithrombin III does not inhibit factor VIIIa — that's protein C/S's job. A favourite trap.

Anticoagulant drugs

Drug	Mechanism	Monitoring	Reversal
Unfractionated heparin	Binds antithrombin III → inactivates IIa and Xa equally	APTT	Protamine sulfate (full reversal)
LMWH (enoxaparin, dalteparin)	Antithrombin → mainly Xa (less IIa)	Anti-Xa level (rarely needed)	Protamine (~60% reversal)
Warfarin	Vitamin K epoxide reductase inhibitor → ↓ II, VII, IX, X, protein C/S	PT / INR	PCC (rapid) ± IV vitamin K
Apixaban, Rivaroxaban	Direct Xa inhibitor	None routinely	Andexanet alfa
Dabigatran	Direct thrombin (IIa) inhibitor	None routinely	Idarucizumab
Fondaparinux	Selective Xa via antithrombin	None	No specific antidote

👩‍⚕️ Heparin-induced thrombocytopenia (HIT) — type II is the dangerous one. IgG antibodies against heparin–PF4 complexes form 5–10 days after exposure. Paradoxically causes thrombosis, not bleeding, despite the low platelets. Stop heparin immediately; switch to a non-heparin anticoagulant (e.g. argatroban, fondaparinux).

👩‍⚕️ Warfarin-induced skin necrosis — protein C has a short half-life (~8 h) and falls before procoagulant factors do, creating a transient hypercoagulable window. Worse in patients with congenital protein C/S deficiency. Bridge with LMWH for ≥ 5 days when starting warfarin until INR is therapeutic.

Antiplatelets

Drug	Mechanism
Aspirin	Irreversible COX-1 inhibitor → ↓ thromboxane A2 → ↓ platelet aggregation
Clopidogrel, ticagrelor	Block platelet P2Y12 ADP receptor
Abciximab, tirofiban	Block GpIIb/IIIa — the final common step of aggregation
Dipyridamole	Phosphodiesterase inhibitor → ↑ cAMP in platelets

Aspirin's effect lasts the lifespan of the platelet (~7–10 days) because platelets cannot synthesise new COX-1.

Bleeding disorders

Disorder	Defect	Inheritance	PT	APTT	Bleeding time	Platelets
Haemophilia A	Factor VIII	X-linked recessive	Normal	↑	Normal	Normal
Haemophilia B	Factor IX ("Christmas disease")	X-linked recessive	Normal	↑	Normal	Normal
von Willebrand disease	vWF (and ↓ FVIII carriage)	Autosomal dominant	Normal	↑ (mild)	↑	Normal
DIC	Consumption of everything	Acquired	↑	↑	↑	↓
Vitamin K deficiency	↓ II, VII, IX, X	Acquired	↑	(↑)	Normal	Normal
Liver failure	↓ all factors except VIII	Acquired	↑	↑	Normal	↓ (if portal HTN)
ITP	Antiplatelet antibodies	Acquired	Normal	Normal	↑	↓↓

👩‍⚕️ vWD is the most common inherited bleeding disorder (~1% prevalence). vWF carries factor VIII in plasma — so vWD also gives a mild ↑APTT. Treat with desmopressin (DDAVP), which releases endogenous vWF from endothelium.

Thrombotic disorders (thrombophilias)

Condition	Notes
Factor V Leiden	Most common inherited thrombophilia (~5% Caucasians). FV resistant to protein C cleavage
Prothrombin G20210A	Second most common; ↑ prothrombin levels
Protein C / S deficiency	Loss of natural anticoagulant; risk of warfarin skin necrosis
Antithrombin III deficiency	Severe; heparin resistance (heparin needs ATIII to work). Lifelong warfarin
Antiphospholipid syndrome	Acquired; recurrent thrombosis + miscarriage; paradoxical ↑APTT in vitro

Disseminated intravascular coagulation (DIC)

Pathological activation of coagulation and fibrinolysis simultaneously — clotting factors and platelets are consumed faster than they can be produced.

Triggers: sepsis, major trauma, malignancy, obstetric emergencies (placental abruption, amniotic fluid embolus), massive transfusion.

Picture: ↑PT, ↑APTT, ↓ fibrinogen, ↓ platelets, ↑↑ D-dimer / FDPs, microangiopathic haemolysis on film.

Management: treat the underlying cause; supportive — FFP (replaces factors), cryoprecipitate (fibrinogen), platelets, packed red cells.

👩‍⚕️ Distinguish from dilutional coagulopathy after massive transfusion: ↓ platelets, ↑ INR, but fibrinogen remains relatively normal because plasma factors are diluted rather than consumed.

Thrombocytopenia — the three classic syndromes

	ITP	TTP	HUS
Mechanism	Anti-platelet IgG	ADAMTS13 deficiency → vWF multimers	Shiga toxin (E. coli O157) endothelial injury
Features	Isolated low platelets	Pentad: fever, MAHA, thrombocytopenia, renal failure, neuro signs	Triad: MAHA, thrombocytopenia, AKI (often in children post-diarrhoea)
Treatment	Steroids, IVIG, splenectomy	Plasma exchange (urgent)	Supportive; avoid antibiotics

Perioperative anticoagulation

Drug	Stop pre-op	Bridging
Warfarin	5 days	LMWH if high VTE risk (mechanical valve, recent VTE)
DOACs	24 h (low risk) / 48–72 h (high risk / renal impairment)	Usually none needed
Unfractionated heparin IV	4–6 h	N/A
Therapeutic LMWH	24 h	N/A
Prophylactic LMWH	12 h	N/A
Aspirin / clopidogrel	Often continued for vascular/cardiac patients; stop 7 days pre-op if bleeding risk high	—

Urgent reversal of warfarin (e.g. strangulated hernia, INR 5):

➡ Prothrombin complex concentrate (PCC) IV — contains II, VII, IX, X — works within minutes.

➡ Add IV vitamin K for sustained effect (onset 6–8 h).

➡ FFP only if PCC unavailable.

👩‍⚕️ IVC filter indications: recurrent PE despite therapeutic anticoagulation, or VTE in a patient who cannot have anticoagulation (active bleeding, imminent surgery).

Tranexamic acid

Synthetic lysine analogue that blocks plasminogen's lysine-binding sites → plasminogen cannot bind fibrin → no plasmin activation on the clot. Used in trauma (CRASH-2: give within 3 h), GI bleeding, menorrhagia, and major surgery.

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Test yourself

A 34-year-old pregnant woman develops a hot swollen leg. An iliofemoral DVT is confirmed. Which clotting factor belongs to the intrinsic pathway?

((IXa::☑️ Intrinsic factors are XII, XI, IX, VIII — measured by APTT.))
((VIIa::Extrinsic pathway with tissue factor — measured by PT/INR.))
((VIa::Factor V activates in the common pathway, not VI; no FVI exists clinically.))
((IIa::Thrombin sits in the common pathway, downstream of both arms.))

👩‍⚕️ "Play Tennis Indoors" — APTT goes with the intrinsic pathway.

The extrinsic pathway includes which factor?

((XI::Intrinsic — measured by APTT.))
((X::Common pathway — activated by both arms.))
((IX::Intrinsic — deficient in haemophilia B.))
((VII::☑️ Factor VII binds tissue factor to initiate the extrinsic pathway; measured by PT/INR.))

Which factor is the end result of intrinsic pathway activation?

((IX::Activates earlier in the intrinsic cascade.))
((XI::Activated by XIIa, upstream of IX.))
((Xa::☑️ Both intrinsic and extrinsic pathways converge on activation of factor X — the start of the common pathway.))
((XIII::Cross-links fibrin at the very end — after thrombin acts.))

Which factor is NOT inactivated by antithrombin III?

((VIIIa::☑️ Factor VIIIa is inactivated by activated protein C with protein S — not by antithrombin III.))
((IXa::Inhibited by antithrombin III (to a lesser extent than IIa and Xa).))
((Xa::Major target of antithrombin III — accelerated by heparin.))
((XIa::Inhibited by antithrombin III.))

👩‍⚕️ Classic trap: ATIII hits the cascade factors (II, X, IX, XI, XII). Protein C/S handles the cofactors (V, VIII).

A 51-year-old has surgery while continuing aspirin and clopidogrel until the day before. The wound now oozes. Most likely cause?

((Deranged platelet aggregation from aspirin and clopidogrel::☑️ Aspirin blocks COX-1/TXA2 and clopidogrel blocks P2Y12 — both impair the platelet plug.))
((Decreased extrinsic pathway::Antiplatelets don't affect the cascade factors or PT.))
((Decreased intrinsic pathway::APTT and intrinsic factors are unaffected by antiplatelets.))
((Increased capillary fragility::Seen in scurvy or steroid use, not antiplatelets.))

A man oozes for 2 days after fem-pop bypass. He took aspirin and clopidogrel until 48 h pre-op. Cause?

((Congenital platelet dysfunction::Would have manifested long before this operation.))
((Hypersplenism::Causes thrombocytopenia, not platelet dysfunction; no splenomegaly described.))
((Aspirin-induced platelet dysfunction::☑️ Aspirin irreversibly acetylates COX-1; effect lasts 7–10 days (lifespan of the platelet).))
((Aspirin-induced thrombocytosis::Aspirin doesn't raise the platelet count.))

👩‍⚕️ 48 h is not enough — wait 7 days for full platelet recovery before bleeding-risk surgery.

How does aspirin cause bleeding?

((Inhibits COX-1 → ↓ thromboxane A2::☑️ Reduces platelet aggregation and vasoconstriction; effect lasts the platelet's lifespan.))
((Inhibits COX-2::Affects pain and inflammation, not platelets.))
((Antagonises vitamin K::That's warfarin.))
((Blocks P2Y12::That's clopidogrel.))

A 75-year-old with IHD and PVD has a mid-thigh amputation. Best VTE prophylaxis?

((Aspirin alone::Inadequate for surgical VTE prophylaxis.))
((LMWH::☑️ Mainstay of post-operative VTE prophylaxis; ideally combined with mechanical methods where feasible.))
((TED stockings alone::Mechanical methods alone are insufficient for a high-risk amputation patient.))
((Warfarin::Slow onset, narrow window — not used as prophylaxis post-op.))

A man develops confusion 24 h after femur fracture. Pre-op: aspirin, codeine, flurothiazide; post-op NSAID. Bloods: ↓Na, ↑K, ↑urea, ↑creatinine, ↓GFR. Which enzyme is affected?

((Catechol-O-methyltransferase::Metabolises catecholamines, not relevant here.))
((Carbonic anhydrase::Inhibited by acetazolamide — not by NSAIDs.))
((Cyclooxygenase::☑️ NSAIDs inhibit COX-1 and COX-2; loss of renal prostaglandins → afferent arteriole constriction → AKI in volume-depleted patients.))
((Monoamine oxidase::Relevant to antidepressants, not NSAID nephrotoxicity.))

A heavy smoker is having elective colorectal resection. Best VTE prophylaxis?

((LMWH alone::Effective, but mechanical adjunct is standard in NICE guidance for major abdominal surgery.))
((LMWH plus stockings::☑️ Combined pharmacological and mechanical prophylaxis; extend LMWH to 28 days if cancer surgery.))
((TED stockings alone::Insufficient for major abdominal/pelvic surgery.))
((Warfarin::Not used for acute peri-operative prophylaxis.))

A patient develops recurrent venous emboli despite therapeutic heparin. Management?

((Switch to warfarin::Slow onset; won't address acute embolic risk in a heparin-failure patient.))
((IVC filter::☑️ Indicated when anticoagulation fails to prevent recurrent PE.))
((Increase heparin dose::Already therapeutic — risks bleeding without solving the problem.))
((Thrombolysis::Reserved for massive PE with haemodynamic compromise.))

A 55-year-old on IV heparin for recurrent PE is scheduled for hysterectomy. Best VTE strategy?

((Continue heparin intra-op::Unacceptable bleeding risk during major pelvic surgery.))
((IVC filter::☑️ For high VTE risk where anticoagulation must be paused peri-operatively.))
((Stop heparin only::Leaves the patient unprotected during the highest-risk period.))
((Switch to DOAC::Doesn't address the need to pause anticoagulation peri-op.))

A patient is newly diagnosed with DVT. First-line management?

((LMWH or DOAC::☑️ First-line immediate anticoagulation; transition to long-term oral anticoagulation.))
((Unfractionated heparin::Reserved for renal failure, very high bleeding risk, or when rapid reversal may be needed.))
((Thrombolysis::Only for massive limb-threatening DVT or PE with haemodynamic instability.))
((Embolectomy::Surgical emergency option after failed thrombolysis in massive PE.))

Best long-term measure to prevent post-thrombotic syndrome?

((Lifelong warfarin::Prevents recurrent VTE but not the post-thrombotic venous damage itself.))
((Graduated compression stockings::☑️ Reduce venous hypertension, oedema and pain after a proximal DVT.))
((Aspirin::No role in preventing post-thrombotic syndrome.))
((IVC filter::Prevents PE, not chronic venous insufficiency.))

A patient is diagnosed with antithrombin III deficiency. Best long-term treatment?

((LMWH::Heparin works via antithrombin III — may be ineffective ("heparin resistance").))
((Aspirin::Antiplatelet, inadequate for an inherited thrombophilia.))
((Lifelong warfarin::☑️ Standard for inherited ATIII deficiency; bypasses the defective natural anticoagulant.))
((Observation::Inappropriate — high lifetime VTE risk.))

👩‍⚕️ Heparin resistance is the classic clue to antithrombin III deficiency.

Which physiological mechanism limits thrombus propagation?

((Thrombin::Procoagulant — drives clot formation.))
((Fibrinogen::Substrate for fibrin formation, not its breakdown.))
((Plasmin::☑️ Main fibrinolytic enzyme — degrades fibrin into FDPs/D-dimer.))
((Factor XIII::Cross-links fibrin, stabilising clot rather than degrading it.))

In major trauma, which factor drives hyperfibrinolysis?

((Thrombin::Drives clot formation, not breakdown.))
((Tissue plasminogen activator (tPA)::☑️ Released from injured endothelium; converts plasminogen to plasmin → excessive fibrinolysis.))
((Antithrombin III::Anticoagulant, not fibrinolytic.))
((Factor V::Procoagulant cofactor.))

👩‍⚕️ This is why tranexamic acid (CRASH-2) saves lives in trauma — given within 3 hours.

A woman with AF on warfarin has INR 6.1. Warfarin inhibits synthesis of which factor?

((Antithrombin III::Natural anticoagulant; not vitamin K-dependent.))
((Plasminogen::Fibrinolytic precursor; not vitamin K-dependent.))
((Prothrombin (II)::☑️ Warfarin blocks vitamin K-dependent synthesis of factors II, VII, IX, X and proteins C and S ("1972").))
((von Willebrand factor::Made by endothelium and megakaryocytes; not vitamin K-dependent.))

Which describes the mechanism of warfarin?

((Inhibits antithrombin III::That's heparin's mechanism.))
((Directly inhibits factor X::That's apixaban/rivaroxaban.))
((Inhibits synthesis of factors X, IX, VII and thrombin::☑️ Via vitamin K epoxide reductase inhibition.))
((Kills bacterial flora::No — though gut flora make vitamin K, warfarin doesn't kill them.))

What is used to monitor warfarin?

((APTT::Monitors heparin and the intrinsic pathway.))
((Bleeding time::Tests platelet function.))
((Prothrombin time, standardised as INR::☑️ PT reflects the extrinsic and common pathways — where warfarin's depleted factors (VII, X, II) act.))
((Anti-Xa::Used (rarely) for LMWH or DOAC levels.))

A 65-year-old with strangulated femoral hernia and INR 5 on warfarin. Best IV agent for urgent reversal?

((Fresh frozen plasma::Slower, larger volume; use only if PCC unavailable.))
((Vitamin K alone::Onset 6–8 h — too slow for theatre.))
((Prothrombin complex concentrate::☑️ Contains factors II, VII, IX, X — replaces "1972" within minutes. Give with IV vitamin K for sustained effect.))
((Platelets::No platelet defect — warfarin acts on clotting factors.))

Mechanism of heparin?

((Direct factor Xa inhibition::That's apixaban/rivaroxaban.))
((Activates antithrombin III::☑️ Accelerates ATIII inactivation of thrombin (IIa) and Xa (and to a lesser extent IXa, XIa, XIIa).))
((Inhibits vitamin K epoxide reductase::That's warfarin.))
((Blocks GpIIb/IIIa::That's abciximab.))

👩‍⚕️ Reversal of unfractionated heparin: protamine sulfate (full); LMWH only ~60% reversed.

What is the mechanism of rivaroxaban?

((Antithrombin III activator::That's heparin.))
((Direct thrombin inhibitor::That's dabigatran (reversed by idarucizumab).))
((Direct factor Xa inhibitor::☑️ Blocks Xa → ↓ prothrombin to thrombin conversion → ↓ fibrin formation. Reversed by andexanet alfa.))
((Vitamin K antagonist::That's warfarin.))

Mechanism of tranexamic acid?

((Inhibits thrombin::No — it acts on fibrinolysis, not coagulation.))
((Activates antithrombin III::That's heparin.))
((Inhibits plasmin / plasminogen activation::☑️ Lysine analogue that blocks plasminogen's lysine-binding sites on fibrin → prevents fibrinolysis.))
((Inhibits factor Xa::That's the Xa inhibitor class.))

How long before high-bleeding-risk surgery should apixaban be stopped?

((24 h::Sufficient only for low-bleeding-risk procedures with normal renal function.))
((48–72 h::☑️ Standard for high-bleeding-risk surgery; longer if renal impairment.))
((7 days::Excessive — increases VTE risk in the interim.))
((No need to stop::Unacceptable bleeding risk for major surgery.))

👩‍⚕️ Prophylactic LMWH: stop 12 h pre-op. Therapeutic LMWH: 24 h. IV heparin: 4–6 h.

After 5 units of transfusion: ↓ platelets, normal APTT, ↑ INR, ↑ FDPs, normal fibrinogen. Diagnosis?

((DIC::DIC gives ↓ fibrinogen and ↑ APTT — not seen here.))
((Dilutional coagulopathy::☑️ Massive transfusion dilutes platelets and factors; fibrinogen often preserved.))
((Vitamin K deficiency::Would give isolated ↑ PT; fibrinogen and platelets unaffected.))
((Liver failure::↑ PT, ↑ APTT and ↓ fibrinogen expected.))
((ITP::Isolated thrombocytopenia with a normal coagulation profile.))

After splenectomy following an RTA the patient develops a petechial rash, ↓ platelets, ↓ Hb, ↓ fibrinogen, ↑ PT and ↑ APTT. Diagnosis?

((DIC::☑️ Classic post-trauma picture — consumption of platelets and factors, ↓ fibrinogen, ↑ D-dimer, microangiopathic haemolysis.))
((ITP::Isolated low platelets; clotting profile would be normal.))
((TTP::Pentad of fever, MAHA, thrombocytopenia, renal failure, neuro signs — coagulation usually normal.))
((Vitamin K deficiency::Doesn't drop fibrinogen or platelets.))

👩‍⚕️ DIC labs: everything bad — ↑ PT, ↑ APTT, ↓ fibrinogen, ↓ platelets, ↑↑ D-dimer.

A boy bleeds excessively; his two sisters are unaffected; the condition came from his father's side. Most likely deficient factor?

((XI::Autosomal — would affect both sexes equally.))
((XIII::Rare autosomal recessive; doesn't fit the X-linked pattern.))
((VIII::☑️ Haemophilia A — X-linked recessive (factor VIII). Mother is a carrier; sons affected, daughters carriers.))
((vWF::vWD is autosomal dominant — would affect both sexes.))

👩‍⚕️ Haemophilia A vs B: both ↑ APTT, normal PT. Haemophilia A is FVIII (more common); B is FIX. vWD is autosomal dominant, ↑ APTT and ↑ bleeding time.

Classic feature of vitamin C deficiency (scurvy)?

((Night blindness::Vitamin A deficiency.))
((Neurological deficits::Vitamin B12 deficiency.))
((Bleeding gums and delayed wound healing::☑️ Vitamin C is required for hydroxylation of proline/lysine in collagen synthesis.))
((Dermatitis::Niacin (B3) deficiency — pellagra (dermatitis, diarrhoea, dementia).))

A patient on heparin develops bleeding and a falling platelet count 7 days in. Most likely cause?

((Dilutional coagulopathy::Requires massive transfusion, not described.))
((DIC::No sepsis or trauma trigger; fibrinogen would be low.))
((Heparin-induced thrombocytopenia (type II)::☑️ IgG against heparin–PF4 complexes; develops 5–10 days after exposure. Stop heparin and switch to a non-heparin anticoagulant.))
((ITP::Unrelated to heparin exposure.))

👩‍⚕️ HIT paradoxically causes thrombosis, not bleeding — never restart heparin.

Revision summary

➡ Intrinsic (XII, XI, IX, VIII) → APTT | Extrinsic (VII + TF) → PT/INR | Common (X, V, II, fibrinogen).

➡ Vitamin K-dependent: II, VII, IX, X + protein C/S ("1972"). Warfarin inhibits all.

➡ Heparin: ATIII → IIa + Xa. Monitor with APTT. Reverse with protamine. Beware HIT type II (5–10 d, thrombosis).

➡ LMWH: mainly Xa; no routine monitoring; partial protamine reversal.

➡ Warfarin: monitor INR; reverse with PCC + IV vitamin K for major bleeding; bridge with LMWH at initiation to prevent protein C-mediated skin necrosis.

➡ DOACs: apixaban/rivaroxaban (Xa, andexanet); dabigatran (IIa, idarucizumab). Stop 24 h (low risk) or 48–72 h (high risk) pre-op.

➡ Aspirin = COX-1/TXA2 (irreversible, 7–10 d). Clopidogrel = P2Y12. Abciximab = GpIIb/IIIa.

➡ Haemophilia A (VIII) / B (IX): X-linked recessive; ↑ APTT, normal PT. vWD: autosomal dominant, commonest inherited bleeding disorder, ↑ APTT + ↑ bleeding time.

➡ DIC: ↑ PT, ↑ APTT, ↓ fibrinogen, ↓ platelets, ↑↑ D-dimer. Treat cause + FFP + cryo + platelets.

➡ Factor V Leiden: most common inherited thrombophilia. ATIII deficiency = heparin resistance → lifelong warfarin.

➡ Tranexamic acid: lysine analogue, blocks plasmin binding to fibrin. Give within 3 h in trauma (CRASH-2).

➡ IVC filter: recurrent VTE on anticoagulation, or VTE when anticoagulation must be stopped.