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GERICLINICS

GeriQBank · Paper III · Q9

Thrombocytopenia

Moderate YieldAsked ×17-mark note
Topic
Haematology, Oncology & Screening
Chapter
Haematology
Years asked
Not recorded in the source
Frequency
Set 1× in Paper III (2009–2025)

As set in the university paper

  • What are the mechanisms of drug-induced thrombocytopenia?

    Paper III · Haematology & Oncology · asked ×1 · 7-mark note · see in paper list

    Linked automatically by wording similarity — check that this answer matches the question as set.

Detailed answer

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Attempt it firstOutline your answer as a 7-mark note before revealing it — definition, causes, evaluation, management and the geriatric angle.Reveal answer

Well covered: Pathy's Ch. 24 ("Disorders of Platelet Number"), supplemented by Ch. 23 (DIC).

High-Yield Points

1.

Definition: platelet count <1,50,000/µL. Platelet count does NOT change with normal ageing — a low count always signifies disease.

2.

Haemostasis normal above 80,000/µL. Spontaneous haemorrhage (incl. ICH) doesn't occur until <20,000/ µL.

3.

Three mechanisms: decreased production, increased destruction (consumption/immune), splenic pooling. Always consider drugs as a cause.

Immune Thrombocytopenia (ITP)

4.

Adult ITP: insidious onset, chronic course (unlike childhood ITP which is acute, post-viral, self-limiting).

5.

Autoantibody against GPIb/GPIIb-IIIa; platelet survival falls from 7–10 days to hours.

6.

Always repeat count + check film first to exclude pseudothrombocytopenia (EDTA-clumping/clotted sample).

7.

Treatment ladder: prednisolone 1mg/kg or IVIg 1g/kg×2 days (first line) → TPO-RAs/romiplostim/eltrombopag (second line) → splenectomy (third line, needs pre-op vaccination) → azathioprine/cyclophosphamide (last resort).

Drug-Induced & Other Causes

8.

Two mechanisms: direct marrow suppression, or immune-mediated. Common culprits: aspirin, paracetamol, antibiotics, anticonvulsants, diuretics, quinine, quinidine.

9.

HIT is the exception — causes THROMBOSIS not bleeding. Mortality ~30% if untreated. Treatment: stop heparin, start argatroban (acute) then fondaparinux. Warfarin worsens acute HIT.

DIC vs TTP

Test DIC TTP

Coagulation screen Grossly abnormal Normal/mild

Fibrinogen Low (<100 mg/dL) Normal

D-dimer >1000 ng/mL Normal/mild ↑

Key feature Multi-organ failure from microthrombosis Pentad: fever, thrombocytopenia, neuro, renal, MAHA Treatment Treat cause + product support Plasma exchange + steroids/rituximab Two Geriatric Pearls

10.

In MDS, platelet dysfunction coexists with thrombocytopenia — bleeding/infection are commonest causes of death.

11.

In myeloproliferative disorders, bleeding is paradoxically MORE common at very high platelet counts (>10,00,000/µL).

Latest Updates (2023–Present)

Rilzabrutinib (oral BTK inhibitor) — FDA-approved Aug 2025 for persistent/chronic ITP; dual mechanism (blocks autoantibody production AND FcγR-mediated platelet phagocytosis) — LUNA3 trial. Splenectomy moved far down the ladder — ASH now recommends TPO-RAs/rituximab first; delay splenectomy ≥12 months. ITP renamed "immune thrombocytopenia", threshold now <1,00,000/µL. TTP: ISTH 2025 update — recombinant ADAMTS13 (apadamtase alfa) now preferred over FFP in congenital TTP; caplacizumab confirmed standard in immune TTP alongside plasma exchange. HIT now part of a family of "anti-PF4 disorders" (autoimmune HIT, spontaneous HIT, VITT); DOACs now accepted alternatives to argatroban/fondaparinux in stable HIT.

Current Practice Update

Domain Pathy's (2022) Current evidence

ITP later Splenectomy, then Splenectomy deferred ≥12 months; rilzabrutinib (2025) major new MD Geriatrics – Haematology Compendium Page 19 of 34 lines azathioprine/cyclophosphamide option HIT Classic heparin-triggered; Part of anti-PF4 spectrum including VITT; DOACs accepted argatroban→fondaparinux TTP Plasma exchange + steroids/rituximab Adds caplacizumab; recombinant ADAMTS13 first choice in congenital TTP MD Geriatrics – Haematology Compendium Page 20 of 34

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