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Clinical Chemistry

Quantitative Platelet Disorders Thrombocytopenia

Vocabulary:

Thrombosis:

Stagnation of blood flow caused by:

  • Arterial Disease

  • or mechanical impedance disturbs the endothelial cell anticoagulant effect

Thrombosis leads to the formation of thrombus clot & hypercoagulable states 

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Cascade:

Process of involving interlinked steps

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Hemostasis:

The cascade mechanism of stopping the bleeding from a blood vessel by forming a "plug" that closes up the damaged part of the blood vessel to control the bleeding.

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Primary Hemostasis:

Platelet adhesion to exposed collagen with the endothelium of the vessel wall

  • Interaction results in clump of platelets (primary hemostatic plug or soft clot)

  • The primary hemostatic plug temporarily stops bleeding, but it is fragile & easily dislodged from the vessel 

What is Thrombocytopenia? 

Definition: A decrease in the number of circulation platelets

  • Thrombocytopenia: <50 x 10^9 /L

  • Normal Reference Range: 150,000-450,000 platelets

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Clinical Evidence of Thrombocytopenia:

  • Increased amount of petechiae​

  • Hemorrhages

  • Prolonged bleeding time

  • Impaired clot retraction

What are the Causes of Thrombocytopenia?

Causes:

  • Decreased platelet production in the bone marrow

    • Decreased amount of megakaryocyte​

    • Ineffective platelet production

  • Disorders of distribution & dilution of platelets ​in the circulation

  • Destruction of platelets

Thrombocytopenia%20Chart_edited.jpg
Levels of Thrombocytopenia
A Closer Look Into Thrombocytopenia

Let's take a closer look into major disorders/diseases associated to thrombocytopenia.

Fanconi's Anemia

Mechanism: Decreased # of Megakaryocytes

  • Inherited Megakaryocytic Hypoplasia

Description:

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Fanconis Anemia.png

Decreased # of Megakaryocytes

May Hegglin Anomaly (MHA)

Mechanism: Decreased # of Megakaryocytes

  • Acquired Megakaryocytic Hypoplasia

*NOTE: Also associated with Qualitative Platelet Disorders

Description:

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[See Qualitative Platelet Disorders for More Info]

May Hegglin Anomaly.jpg

Bernard-Soulier Syndrome

Mechanism: Decreased # of Megakaryocytes

  • Acquired Megakaryocytic Hypoplasia

*NOTE: Also associated with Qualitative Platelets Disorders

Description: Rare inherited bleeding disorder

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[See Qualitative Platelet Disorders for More Info]

Wiskott-Aldrich Syndrome

Mechanism: Decreased # of Megakaryocytes

  • Acquired Megakaryocytic Hypoplasia

*NOTE: Also associated with Qualitative Platelets Disorders

Description:

​

[See Qualitative Platelet Disorders for More Info]

Wiskott Aldrich Syndrome.jpg

Drug-Induced Thrombocytopenia

Mechanism: Ineffective Platelet Production

Description:

​

Tylenol.jpg

Di Guglielmo's Syndrome

(Erythroleukemia)

Mechanism: Ineffective Platelet Production

Description:

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Di guglielmo Disease.jpg

Paroxysmal Nocturnal Hemoglobinuria (PNH)

Mechanism: Ineffective Platelet Production

Description:

​

Paroxysmal%20Nocturnal%20Hemoglobinuria_

Increased Destruction/Consumption

*The main thrombocytopenic disorders that needed to be studied & distinguished from.

Immune Thrombocytopenic Purpura (ITP)

Also known as Idiopathic Thrombocytopenic Purpura

Mechanism: Increased Platelet Destruction/ Consumption

  • Immune (Autoimmune)

Description:

  • Diagnosis of Exclusion

Immune Mediated platelet destruction following a recent infection

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ITP

Pathogenesis:

  • ↑ bone marrow platelet production

Acute ITP (self limiting: 2-6 weeks)​​

Spontaneous remission in 80%

  • Viral attachment & antigenic alteration of platelet membrane proteins

    • Forms platelet autoantibodies (IgG) coating platelets & are removed by macrophages in the spleen

Chronic ITP​ (Last months or years)

  • Associated with systemic lupus erythematosus (SLE)

Clinical Presentation:

​

Target Presentation:

Acute ITP

  • Occurs in children 2-6 years of age

  • Often following viral infection(s)

    • Rubella​

    • Chickenpox

    • Cytomegalovirus (CMV)

    • Toxoplasmosis

Chronic ITP​

  • Occurs in adults 20-40 years of age

    • Women are 3 times more than in men​

Lab Test Results

↑ Mean Platelet Volume (MPV)

↓ Platelet count 

↑ Marrow megakaryocyte

Normal Bleeding time

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Acute ITP

< 20,000 platelets

Chronic ITP

~55,000 platelets (not as severe)

Blood Smear:  Schistocytes

Heparin Induced Thrombocytopenia (HIT)

Mechanism: 

Increased Platelet Destruction/ Consumption

  • Alloimmune 

    • Clearance of activated platelets & antibody-coated platelets by the reticuloendothelial system (RES)

Description:

​Formation of antibodies that activate the platelets following heparin administration

  • Most important & most frequent form of drug-induced thrombocytopenia 

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HIT

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Thrombotic Thrombocytopenic Purpura (TTP)

Mechanism: Increased Platelet Destruction/ Consumption

  • Non-immune

Description: Microangiopathic hemolytic anemia causing nonimmune hemolysis

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Lab Test Results

↑ Bleeding Time 

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Blood Smear:  Schistocytes

TTP

Pathophysiology:

  • ADAMS-13 deficiency causing ↑ vonWillebrand factor

Clinical Presentation:

  • Thrombocytopenia

  • Anemia

  • Fever

  • Neurologic Symptoms

  • Renal Dysfunction

Hemolytic Uremic Syndrome (HUS)

Mechanism: Increased Platelet Destruction/ Consumption

  • Non-immune

Description:

​

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Lab Results

↑ Bleeding time

Thrombocytopenia

↑Creatinine

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Blood Smear: Schistocytes

HUS

Pathogenesis:

  • Shiga toxin-mediated hemolysis

    • Infection of pathogenic E. coli 0157:H7 or another E.coli strain​​

Clinical Presentation:

  • Kidney Failure following E.coli infection

  • Bloody Diarrhea

Target Population:

  • Occurs often in children who ingested the toxin

Disseminated Intravascular Coagulation (DIC)

Mechanism: Increased Platelet Destruction/ Consumption

  • Non-immune

Description: Inappropriate widespread clotting activation usually secondary to:

  • trauma

  • sepsis

  • obstetric complications

​

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Lab Results:

↓PLT

↑ Bleeding Time

↑ PT

↑ PTT

↑ D-Dimer

↓Fibrinogen

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Blood Smear: Schistocytes

DIC

Pathogenesis:

​Uncontrolled thrombin & plasmin causing excess tiny clots & bleeding, respectively

Clinical Presentation:

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Target Population

Sources:

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