Haemostasis and Bleeding Disorders for NEET PG Pathology: ITP, Haemophilia, von Willebrand Disease, Vitamin K Deficiency, DIC, TTP

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🎯 Exam priority: Very high. Expect: a boy with a swollen knee and prolonged PTT, a child with petechiae after a viral illness, heavy periods with a family history, a newborn bleeding on day 3, a septic or obstetric patient oozing from lines, and a young woman with thrombosis and recurrent miscarriage.

CBME mapping: PA 20.1–20.2 (and 5.4).

How Bleeding Stops

• Adhesion: von Willebrand factor anchors platelets to exposed collagen via platelet GP Ib/IX.

• Aggregation: fibrinogen bridges GP IIb/IIIa on neighbouring platelets.

• Coagulation: tissue factor with factor VIIa activates factor X (extrinsic pathway). Fibrinolysis: plasmin dissolves fibrin.

• Pattern: skin and mucosal bleeding (petechiae, purpura) = platelet or vessel defect; deep bleeding (joints, muscles) = clotting-factor defect.

The Disorders

Bleeding disorders: bleeding pattern and test results. Drawn by TrackNation.

• ITP: antiplatelet autoantibody, platelets destroyed mainly in the spleen; isolated low platelets with an otherwise normal CBC and smear; most children recover on their own.

• Haemophilia: X-linked recessive; A = factor VIII (about 80%), B = factor IX; joint and muscle bleeds; PTT prolonged, PT and platelets normal; factor assays tell them apart.

• von Willebrand disease: type 1 (commonest) is autosomal dominant; bruising, mucosal bleeding, heavy periods, bleeding after tooth extraction; test VWF antigen and ristocetin cofactor activity; desmopressin or factor VIII concentrate.

• Platelet function: Glanzmann (AR) lacks GP IIb/IIIa — platelets cannot aggregate; Bernard-Soulier is an adhesion defect.

• Vitamin K deficiency: factors II, VII, IX, X not made; PT/INR prolonged, PTT and platelets normal; haemorrhagic disease of the newborn (days 1–7), commoner in breastfed babies; broad-spectrum antibiotics contribute. Severe liver disease also impairs factor synthesis.

• DIC: low platelets, prolonged PT and PTT, high D-dimer, falling fibrinogen; schistocytes; causes include sepsis and obstetric complications (placental abruption). Replace platelets, plasma and fibrinogen (cryoprecipitate).

• TTP: Coombs-negative haemolysis with low ADAMTS13; treated by plasma exchange. HUS: usually children after Shiga-toxin E. coli O157:H7; kidney injury prominent.

• Antiphospholipid syndrome: thrombosis or recurrent pregnancy loss; lupus anticoagulant prolongs the PTT in the lab despite causing clots.

Traps the Examiner Sets

• Prolonged PTT with normal PT: haemophilia (or lupus anticoagulant). Prolonged PT alone: vitamin K deficiency.

• Everything abnormal (platelets, PT, PTT, fibrinogen, D-dimer): DIC.

• Mucosal bleeding with a normal platelet count: think von Willebrand disease.

• APS: a lab test says "bleeding risk" but the patient clots.

Memory Hooks & Shortcuts

Shortcuts to lock in this article's numbers and lists. Each one only re-packages facts proven above.

• 🧠 Ib for Initial (adhesion), IIb/IIIa for Integration (aggregation) — platelet receptors

• 🧠 Haemophilia: boys, joints, PTT — X-linked, haemarthroses, prolonged PTT

• 🧠 Vitamin K: 2, 7, 9, 10 (1972) — vitamin K-dependent factors

• 🧠 DIC: Down platelets, Increased D-dimer, Consumed fibrinogen — DIC labs

• 🧠 TTP: ADAMTS13 Tiny → Thrombi — low ADAMTS13

• 🧠 APS: Prolonged test, Paradoxical clots, Pregnancy loss — lupus anticoagulant

Rapid-Revision Cards

• Platelet adhesion

  VWF + GP Ib/IX.

• Platelet aggregation

  Fibrinogen + GP IIb/IIIa.

• Extrinsic pathway

  Tissue factor + VIIa → X.

• Fibrinolysis

  Plasmin.

• Superficial bleeding

  Platelet or vessel.

• Deep bleeding

  Coagulation factors.

• ITP

  Antiplatelet antibody; isolated thrombocytopenia; children recover.

• Haemophilia

  X-linked; A = VIII (80%), B = IX; PTT ↑, PT normal.

• vWD

  Type 1 AD; mucosal bleeding; ristocetin cofactor; desmopressin.

• Glanzmann

  AR; GP IIb/IIIa; no aggregation.

• Bernard-Soulier

  Adhesion defect.

• Vitamin K

  II, VII, IX, X; PT ↑, PTT normal.

• HDN

  Days 1–7; breastfed infants.

• DIC

  Platelets ↓, PT/PTT ↑, D-dimer ↑, fibrinogen ↓.

• TTP

  Low ADAMTS13; Coombs-neg haemolysis; plasma exchange.

• HUS

  Children; E. coli O157:H7; kidney injury.

• APS

  Clots + pregnancy loss; lupus anticoagulant prolongs PTT.

Sources

Facts in this article were checked against these documents.

• MSD Manual Professional: Overview of Hemostasis; Excessive Bleeding; Immune Thrombocytopenia; Hemophilia; von Willebrand Disease; Inherited Platelet Function Disorders; Overview of Coagulation Disorders; DIC; TTP; HUS; Antiphospholipid Syndrome; Vitamin K Deficiency — Merck & Co. (MSD Manuals), reviewed 2025–2026 (link)

• Competency Based Undergraduate Curriculum, Pathology (PA 20) — National Medical Commission, 2024

Test Yourself: Practice Questions

Twenty-five questions in NEET PG style, most of them clinical vignettes.

Practice Questions (NEET PG pattern)

Original questions written in the style of the exam: +4 for a correct answer, −1 for a wrong one. Every answer was checked against the sources listed above. NEET PG papers are not published by NBEMS, so these are not past-paper questions.

Q1. A 6-year-old boy has a swollen, painful knee after a minor fall; his maternal uncle had similar bleeds. PTT is prolonged; PT and platelets are normal. The diagnosis is

• (a) vitamin K deficiency

• (b) von Willebrand disease

• (c) ITP

• (d) haemophilia

Q2. Haemophilia A is due to deficiency of

• (a) factor IX

• (b) factor VIII (about 80% of haemophilia)

• (c) factor VII

• (d) von Willebrand factor

Q3. Haemophilia A and B are distinguished by

• (a) platelet count

• (b) PT

• (c) bleeding pattern

• (d) specific factor VIII and IX assays

Q4. Bleeding into joints and muscles suggests

• (a) a vessel wall defect

• (b) a platelet defect

• (c) normal haemostasis

• (d) a clotting-factor defect (coagulopathy)

Q5. Petechiae and gum bleeding suggest

• (a) a platelet or vessel problem

• (b) haemophilia

• (c) factor XIII deficiency

• (d) vitamin K deficiency only

Q6. Two weeks after a viral illness, a child has petechiae; platelets are 15,000/µL with an otherwise normal blood count and smear. The diagnosis and outlook are

• (a) immune thrombocytopenia; most children recover spontaneously

• (b) aplastic anaemia; poor

• (c) haemophilia; lifelong

• (d) ALL; poor

Q7. In ITP, platelets are destroyed mainly in the

• (a) spleen

• (b) kidney

• (c) lungs

• (d) liver

Q8. A woman has lifelong heavy periods, nosebleeds and bleeding after a tooth extraction; her mother is similar. Platelets are normal. The likely diagnosis is

• (a) von Willebrand disease (type 1, autosomal dominant)

• (b) Glanzmann

• (c) ITP

• (d) haemophilia A

Q9. A test of von Willebrand factor function is

• (a) PT

• (b) D-dimer

• (c) osmotic fragility

• (d) ristocetin cofactor activity

Q10. Initial platelet adhesion to damaged vessel wall requires von Willebrand factor and the platelet receptor

• (a) thromboxane receptor

• (b) glycoprotein Ib/IX

• (c) glycoprotein IIb/IIIa

• (d) P2Y12

Q11. A child with severe nosebleeds has platelets that do not aggregate; the defect is in GP IIb/IIIa. The diagnosis is

• (a) ITP

• (b) Glanzmann thrombasthenia (autosomal recessive)

• (c) haemophilia

• (d) Bernard-Soulier syndrome

Q12. Bernard-Soulier syndrome is a disorder of platelet

• (a) adhesion

• (b) production

• (c) aggregation only

• (d) survival

Q13. A breastfed baby not given vitamin K at birth starts bleeding on day 3. PT/INR is prolonged; PTT and platelets are normal. The diagnosis is

• (a) DIC

• (b) haemophilia

• (c) haemorrhagic disease of the newborn (vitamin K deficiency)

• (d) ITP

Q14. Vitamin K is needed to make clotting factors

• (a) XI and XII

• (b) V and VIII

• (c) II, VII, IX and X

• (d) I and XIII

Q15. In vitamin K deficiency, the coagulation tests show

• (a) prolonged PTT only

• (b) high D-dimer

• (c) low platelets

• (d) prolonged PT/INR with normal PTT, platelets and fibrinogen

Q16. A woman with placental abruption oozes from IV sites; platelets are low, PT and PTT are prolonged, D-dimer is high and fibrinogen is falling. The diagnosis is

• (a) DIC

• (b) vitamin K deficiency

• (c) haemophilia

• (d) ITP

Q17. In DIC with a very low fibrinogen, fibrinogen is replaced with

• (a) packed red cells

• (b) vitamin K alone

• (c) cryoprecipitate

• (d) albumin

Q18. A woman has confusion, low platelets and Coombs-negative haemolytic anaemia with schistocytes; ADAMTS13 is very low. The diagnosis and treatment are

• (a) DIC — heparin

• (b) TTP — plasma exchange

• (c) HUS — antibiotics

• (d) ITP — steroids alone

Q19. A 4-year-old develops kidney injury, low platelets and haemolysis a week after bloody diarrhoea. The usual cause is

• (a) Giardia

• (b) Salmonella typhi

• (c) rotavirus

• (d) Shiga toxin-producing E. coli O157:H7 (HUS)

Q20. A young woman with recurrent miscarriages and a DVT has a prolonged PTT. The likely diagnosis is

• (a) vitamin K deficiency

• (b) von Willebrand disease

• (c) haemophilia carrier

• (d) antiphospholipid syndrome (lupus anticoagulant)

Q21. Fibrinogen links activated platelets together by binding to

• (a) collagen

• (b) tissue factor

• (c) glycoprotein Ib/IX

• (d) glycoprotein IIb/IIIa

Q22. The extrinsic pathway starts when factor VIIa combines with

• (a) factor XII

• (b) kallikrein

• (c) factor VIII

• (d) tissue factor, activating factor X

Q23. Fibrin is broken down by

• (a) thrombin

• (b) factor XIII

• (c) plasmin

• (d) antithrombin

Q24. A man with cirrhosis bleeds easily with prolonged clotting times. The main reason is

• (a) ITP

• (b) excess vitamin K

• (c) haemophilia

• (d) impaired clotting-factor synthesis by the liver

Q25. A child with severe mucosal bleeding has unusually large platelets that do not aggregate with ristocetin but aggregate normally with ADP, collagen and epinephrine. The defect is in

• (a) ADAMTS13

• (b) glycoprotein Ib/IX (Bernard-Soulier syndrome)

• (c) glycoprotein IIb/IIIa (Glanzmann)

• (d) factor VIII

Active Recall

From memory: describe platelet adhesion and aggregation and the start of coagulation, the bleeding pattern that points to platelets vs factors, and the defect and test pattern in ITP, haemophilia, von Willebrand disease, Glanzmann, vitamin K deficiency, DIC, TTP, HUS and APS.