Which of the following statements best describes the underlying mechanism of heparin-induced thrombocytopenia?

Antibodies are formed against heparin-platelet factor 4 complexes.

Low molecular weight heparin can also cause heparin-induced thrombocytopenia.

Vitamin K is not an antidote for heparin-induced thrombocytopenia.

Heparin-induced thrombocytopenia can occur after several days of heparin therapy.

Disseminated intravascular coagulation (DIC) differs from thrombotic thrombocytopenic purpura. In this reference, DIC is most likely characterized by:

Low levels of coagulation factors

Presence of schistocytes in the blood smear

A previously healthy child has sudden onset of red spots on body. There is a history of a preceding viral infection 1-4 weeks before the onset.

Idiopathic thrombocytopenic purpura

Thrombotic thrombocytopenic purpura

Thrombotic thrombocytopenic purpura is a syndrome characterized by which of the following?

Thrombocytopenia, anemia, neurological abnormalities, progressive renal failure and fever

Thrombocytopenia, anemia, neurological abnormalities, progressive hepatic failure and fever

Thrombocytopenia, normal anemia, neurological abnormalities, progressive renal failure and fever

Thrombocytopenia, anemia, no neurological abnormalities, progressive renal failure and fever

A 45-year-old lady presents with normal PT and increased aPTT. About 2 years ago, she underwent cholecystectomy and did not have any bleeding episode. What is the next investigation for clinical diagnosis?

Dilute Russell viper venom assay

The following is not true of platelet transfusion -

Effects decrease with repeated usage

Platelet Disorders for NEET-PG: High-Yield Internal Medicine Lessons

Platelet Essentials - Hemostasis Heroes

Small, anucleated cells derived from bone marrow megakaryocytes. Lifespan: 7-10 days. Normal count: 1.5 - 4.5 lakhs/µL.
Key players in primary hemostasis: forming the initial platelet plug.
Contain α-granules (vWF, fibrinogen) & dense granules (ADP, Ca²⁺, serotonin).
Key surface receptors: GPIb (binds vWF for adhesion), GPIIb/IIIa (binds fibrinogen for aggregation).

⭐ Glanzmann thrombasthenia results from a deficiency or dysfunction of the GPIIb/IIIa receptor, leading to impaired platelet aggregation.

Thrombocytopenia: Causes & Approach - Count Catastrophe

Platelets < 150,000/μL. Severe: < 50,000/μL. Bleed risk ↑ if < 10,000-20,000/μL.
Always rule out 📌 Pseudothrombocytopenia (EDTA clumping) with citrate tube/smear.
Major Mechanisms & Causes:
- ↓ Production: Marrow disorders (aplasia, leukemia, MDS), B12/folate def., drugs, viral (HIV).
- ↑ Destruction:
  - Immune: ITP, HIT, drugs, SLE.
  - Non-immune: DIC, TTP-HUS, sepsis, HELLP.
- Sequestration: Splenomegaly (e.g., cirrhosis).
- Dilutional: Massive transfusion.
Approach Algorithm:

⭐ ITP is a diagnosis of exclusion: isolated thrombocytopenia, normal marrow (if done), no other cause. Often follows viral illness in children.

Immune Thrombocytopenias - Self Sabotage

Feature	ITP	HIT	Drug-Induced
Mechanism	Anti-GpIIb/IIIa autoAbs	Abs vs PF4-heparin	Drug-dependent Abs
Onset	Insidious/Acute	5-10 days post-heparin	Acute post-drug
Platelets	<30k/µL often	↓ >50%; rarely <20k/µL	Variable, severe
Hallmark	Isolated thrombocytopenia	Thrombosis risk; 📌 4Ts Score	Drug link; resolves on stop
Diagnosis	Exclusion; Anti-platelet Abs	4Ts; HIT Ab assay	Drug Hx
Treatment	Steroids, IVIG, TPO-RAs	Stop heparin; DTI (e.g. Argatroban)	Stop drug; supportive

⭐ HIT: prothrombotic despite thrombocytopenia due to Ab-mediated platelet activation.

MAHAs & Consumptive Coagulopathies - Fragmented Frenzy

RBC fragmentation (schistocytes) & thrombocytopenia define Microangiopathic Hemolytic Anemias (MAHAs). Schistocytes and platelets in MAHA peripheral blood smear

Comparison:

Feature	TTP	HUS	DIC
Cause	↓ADAMTS13 (<10%)	Shiga toxin (E.coli)	Sepsis, trauma, malignancy
Clinical	📌 FAT RN Pentad (Fever, Anemia, Thrombocytopenia, Renal, Neuro)	Triad (Anemia, Thrombocytopenia, AKI - esp. kids)	Bleeding & thrombosis
Coags	Normal	Normal	↑PT/PTT, ↑D-dimer, ↓Fibrinogen
Rx	Plasma Exchange (PEX)	Supportive	Treat cause, FFP, Cryo

⭐ In TTP, initiate plasma exchange emergently upon suspicion, pre-ADAMTS13 results.

Platelet Dysfunction & Thrombocytosis - Sticky & Swarming

Platelet Dysfunction (Qualitative)
- Inherited:
  Feature Glanzmann's (GT) Bernard-Soulier (BSS)
  Defect GpIIb/IIIa (Aggregation) GpIb (Adhesion)
  Inheritance AR AR
  Ristocetin Agg. Normal ↓ / Absent
  Platelet Size Normal Giant (📌 Big Suckers)
- Acquired: Uremia, drugs (Aspirin, Clopidogrel).
Thrombocytosis (Quantitative): Platelet count > 450,000/μL.
Feature Reactive Clonal (ET)
Cause Infection, inflammation, Fe def JAK2 mut. (MPN)
Platelet Func. Normal Often Abnormal
Splenomegaly No (or from cause) Possible
Treatment Treat cause Cytoreduction, Aspirin

Feature	Glanzmann's (GT)	Bernard-Soulier (BSS)
Defect	GpIIb/IIIa (Aggregation)	GpIb (Adhesion)
Inheritance	AR	AR
Ristocetin Agg.	Normal	↓ / Absent
Platelet Size	Normal	Giant (📌 Big Suckers)

Feature	Reactive	Clonal (ET)
Cause	Infection, inflammation, Fe def	JAK2 mut. (MPN)
Platelet Func.	Normal	Often Abnormal
Splenomegaly	No (or from cause)	Possible
Treatment	Treat cause	Cytoreduction, Aspirin

⭐ BSS: Absent Ristocetin aggregation. Giant platelets. Defect in GpIb (vWF receptor).

High‑Yield Points - ⚡ Biggest Takeaways

ITP: Isolated thrombocytopenia from anti-GpIIb/IIIa antibodies. First-line: steroids.

TTP: ADAMTS13 deficiency; Pentad (Fever, MAHA, Thrombocytopenia, Renal, Neuro). Plasma exchange is crucial.

HUS: Often post-E. coli O157:H7; Triad (MAHA, Thrombocytopenia, ARF). Primarily supportive.

Bernard-Soulier Syndrome: GpIb defect (adhesion); Giant platelets, thrombocytopenia.

Glanzmann Thrombasthenia: GpIIb/IIIa defect (aggregation); Normal count, impaired aggregation.

von Willebrand Disease (vWD): Most common inherited bleeding disorder; ↓vWF, ↓FVIII. Desmopressin for Type 1.

DIC: Consumptive coagulopathy; ↓platelets, ↓fibrinogen, ↑PT/APTT, ↑D-dimer. Treat underlying cause.

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