MCQs on Thrombocytopenia

Written by Dr. Daniel Fraser (MBBS, FRACP) – Physician

Question 1

Emily, a 28-year-old previously healthy woman, presents to your clinic with a 1-week history of spontaneous bruising on her arms and petechiae on her legs. She reports menorrhagia over the last two cycles but denies any fever, joint pain, recent illness, or medication changes aside from regular use of a combined oral contraceptive pill. There is no family history of bleeding disorders. On examination, there is no hepatosplenomegaly or lymphadenopathy. Initial blood tests reveal:

Hemoglobin: 130 g/L
WBC count: 6.5 × 10⁹/L
Platelets: 18 × 10⁹/L
PT/aPTT: normal
LFTs: normal

What is the most likely diagnosis?

A) Acute leukemia
B) Immune thrombocytopenic purpura (ITP)
C) Thrombotic thrombocytopenic purpura (TTP)
D) Aplastic anemia
E) Systemic lupus erythematosus (SLE)

Correct Answer: B) Immune thrombocytopenic purpura (ITP)

Explanation:
ITP is the most likely diagnosis in this patient with isolated thrombocytopenia and no systemic signs. ITP is an acquired autoimmune condition characterized by the formation of antiplatelet autoantibodies—most often against glycoprotein IIb/IIIa—leading to splenic destruction of platelets. It typically presents with mucocutaneous bleeding (e.g., petechiae, purpura, menorrhagia), especially when platelet count falls below 30 × 10⁹/L.

This patient’s normal hemoglobin and WBC count rule out pancytopenic conditions such as aplastic anemia and leukemia. In leukemia, one would expect blasts or abnormal cells on blood film, plus systemic symptoms like fatigue or weight loss. TTP typically presents with a pentad (fever, microangiopathic hemolytic anemia, thrombocytopenia, renal dysfunction, and neurologic signs), none of which are present here. SLE can present with thrombocytopenia but usually includes other systemic features and positive ANA/autoantibody profile.

The diagnosis of ITP is clinical and by exclusion. Management depends on severity; in asymptomatic or mildly symptomatic patients with platelet count >30 × 10⁹/L, observation may suffice. In more severe cases, corticosteroids are first-line therapy.

Question 2

James, a 70-year-old man, is hospitalized with a proximal deep vein thrombosis (DVT) and started on therapeutic-dose unfractionated heparin. On day 6 of heparin therapy, his platelet count decreases from 210 × 10⁹/L to 85 × 10⁹/L. He has no active bleeding. However, Doppler ultrasound now reveals a new thrombus in the left popliteal vein. He is afebrile and hemodynamically stable. There is no history of autoimmune disease or prior thrombocytopenia.

What is the most appropriate next step in management?

A) Continue heparin and monitor platelet count
B) Transfuse platelets
C) Stop heparin and start warfarin immediately
D) Stop heparin and initiate a direct thrombin inhibitor
E) Administer corticosteroids

Correct Answer: D) Stop heparin and initiate a direct thrombin inhibitor

Explanation:
This is a classic case of Type 2 heparin-induced thrombocytopenia (HIT), a potentially life-threatening, immune-mediated complication of heparin therapy. It typically occurs 5–10 days after starting heparin. The pathophysiology involves antibodies (IgG) against platelet factor 4 (PF4) complexed with heparin, which activate platelets and promote a prothrombotic state—paradoxically increasing the risk of new or progressive thrombosis despite falling platelet counts.

A hallmark of HIT is a ≥50% drop in platelet count (even if still above 50 × 10⁹/L) along with new thrombotic events. HIT is more common with unfractionated heparin than with low-molecular-weight heparin and is not associated with bleeding unless severe.

Immediate cessation of all forms of heparin is critical. Platelet transfusion is contraindicated unless there is active bleeding or the patient is undergoing an invasive procedure, as it can worsen thrombosis. Warfarin should never be started during acute HIT, as it can precipitate venous limb gangrene. Instead, a non-heparin anticoagulant, such as a direct thrombin inhibitor (e.g., argatroban or bivalirudin), or a factor Xa inhibitor (e.g., fondaparinux), should be started promptly.

Question 3

Fatima, a 35-year-old woman, presents to the Emergency Department with confusion and fatigue. Her family reports she had fever and malaise for 2 days. On examination, she is disoriented with petechial rashes on her lower limbs. Blood pressure is 130/80 mmHg, pulse is 98 bpm, and temperature is 38.1°C. Laboratory investigations show:

Hemoglobin: 85 g/L
Platelets: 22 × 10⁹/L
LDH: markedly elevated
Peripheral blood film: schistocytes present
Creatinine: 95 µmol/L
Coagulation profile: normal PT and aPTT

What is the most appropriate immediate management?

A) Platelet transfusion
B) High-dose corticosteroids
C) Plasma exchange therapy
D) Intravenous immunoglobulin (IVIG)
E) Immediate splenectomy

Correct Answer: C) Plasma exchange therapy

Explanation:
This is a classic presentation of thrombotic thrombocytopenic purpura (TTP), a medical emergency characterized by a pentad: microangiopathic hemolytic anemia (MAHA), thrombocytopenia, renal impairment, neurologic symptoms, and fever. Although all five features are not always present, Fatima’s clinical picture and lab findings (low platelets, schistocytes, high LDH) point strongly to TTP.

The pathophysiology involves severe ADAMTS13 deficiency, leading to accumulation of large von Willebrand factor (vWF) multimers, causing platelet aggregation and microvascular thrombosis. The mainstay of treatment is urgent plasma exchange (plasmapheresis), which removes the autoantibodies and replenishes ADAMTS13. Delay in initiating plasma exchange can be fatal.

Platelet transfusions are contraindicated unless there’s life-threatening bleeding, as they can exacerbate thrombosis. Corticosteroids may be used as adjuncts but are not first-line. IVIG is used in ITP, not TTP. Splenectomy is reserved for refractory cases of ITP, not acute TTP.

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6. Hematology Module

6.1 Anemia

6.2 Thrombocytopenia

6.3 Thromboembolism

6.4 Anti-Coagulation

6.5 Lymphomas

6.6 Other Hematological Disorders

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