Platelet Disorders Flashcards

1
Q

Qualitative and quantitative PLT disorders may cause what kind of bleeding symptoms: (7)

A
  • Gingival (gum) bleeding
  • Epistaxis (nose bleed)
  • Ecchymosis (excessive bruising)
  • Petechiae (small hemorrhage spots)
  • Purpura (hemorrhage into skin, mucous menbranes (on slide))
  • Prolonged bleeding
  • Menorrhadia (excessive bleeding after tooth surgery)
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2
Q

What is the normal PLT range?

A

150 - 450 x 109/L

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3
Q

A decreased PLT count causes bleeding / results in what symptoms? (4)

A
  • ginigival bleeding
  • Epistaxis
  • Ecchymosis
  • Petichiae
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4
Q

<60 x 109/L PLT count may lead to

A

bleeding in surgery

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5
Q

<30 x 109/L PLT count may lead to

A

Petechial Bleeding

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6
Q

<5 x 109/L PLT count may lead to

A

risk bleeding into CNS

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7
Q

What pre-analytical variables may cause a decreased PLT count? (5)

A
  • Incorrect sample handling
  • Blood reacting with EDTA
  • Bone marrow funtion (Aplasia - lack of megakaryocytes)
    • Cancer (blas cells crown out normal PLT producing cells)
    • Chemotherapy; may destroy PLT producing cells.
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8
Q

What are 5 consumption of PLT disorders?

A
  • Idiopathic (immune) thrombocytopenia purpura (ITP)
  • Thrombotic thrombocytopenic purpura (TTP)
  • Hemolytic Uremic Syndrome (HUS)
  • Altered distribution of PLTs (spleen traps PLTs)
  • Destruction by RES (spleen removes antidrug antibody coated PLTs)
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9
Q

Coagulation samples are drawn in what tube?

A

Blue top (sodium citrate)

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10
Q

What is the blood:anticoag ratio?

A

9:1 (tube must be 90% full)

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11
Q

What is PLT satellitetism?

Leads to?

Corrective action?

A

PLTs form a righ around seg neutrophils, monocytes, and bands.

Leads to falsely low PLT count

sample redrawn in blue tube

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12
Q

What is Neonatal Alloimmune Thrombocytopenia?

A
  • Occurs as a result of materal antibody made against PLT antigens from earlier pregnancy.
  • Antibody is against HPA-1a PLT
  • IgG can cross placenta
  • Infants born have normal PLTs, but soon develop petechia and skin hemorrhages
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13
Q

When is Neonatal Alloimmune Thrombocytopenia treated?

A

only when there is a risk of CNS hemorrhage

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14
Q

What is Idiopathic Thrombocytopenic Purpura?

The autoantibody IgG is against?

A

Decreased PLT count becuse of immune destruction

  • Gp IIb/IIIa or GpIb-IX
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15
Q

What is Thrombotic Thrombocytopenic Purpura (TTP)?

A
  • Deficiency of protein ADAMTS-13, which normally cleaves vWF into smaller proteins. This may lead to excessive PLT clots.
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16
Q

What is the PLT level in Thrombotic Thrombocytopenic Purpura (TTP)?

A
  • PLT .20 x 109/L
17
Q

What is the key factor differentiating Thrombotic Thrombocytopenic Purpura (TTP) from Idiopathic Thrombocytopenia Purpura? (5)

A
  • Microangiopathic Anemia (MHA)
    • Schistocytes and severe anemia
    • Increased LDH
    • Decreased Haptoglobin
    • Hemoglobinuria
18
Q

What are the clinical symptoms of Thrombotic Thrombocytopenic Purpura (TTP)?

A
  • Neurologic symptoms
  • Fever
  • Renal failure
  • Thrombocytopenia
19
Q

T/F: PT and aPTT is in normal reference range in Thrombotic Thrombocytopenic Purpura (TTP)?

A
  • True
20
Q

Renal damage resulting from a toxin produced by E.coli O157:H7, the Shiga toxin leads to cell death in Kidneys.

A

Hemolytic Uremic Syndrome (HUS)

21
Q

Hemolytic Uremic Syndrome (HUS) mimics what disorder?

A

TTP

Clinical symptoms the same except no neurological symptoms

22
Q

Inherited Adhesion Disorder: Von Willebrand Disease genetics?

Symptoms?

What is VWF?

A
  • Auto Dominant
  • Ecchymosis, Epistaxis, menorrhagia, and excessive bleeding after tooth extraction.
  • Intermediary for PLT adhesion and a receptor for GpIIb/IIIa
23
Q

What is the sinlgle best predictive assay for vWF antigen?

A

Ristocetin co-factor activity.

24
Q

Inherited Adhesion Disorder: What is Bernard Soulier syndrome and its genetics? (3)

A
  • Adhesion defect of PLTs involving Gp Ib/IX complex
  • Abscence of ristiocetin induced PLT aggregation
  • Autosomal recessive (rare)
25
Q

Inherited Aggregation Disorder: Glanzmann’s thombasthenia

Genetics?

What is abnormal?

Clinical symptoms?

How is aggregation affected?

Bleeding patterns?

A
  • Rare Auto. recessive
  • Abnormality of Gp IIb/IIIa
  • prolonged bleeding time
  • Abnormal with all aggregating agents EXCEPT ristocetin
  • Variable
26
Q

Acquired defects of PLT function: Drug related abnormalities?

What is the most common drug?

What does it cause? (2)

A
  • Aspirin
    • Inhibits PLT aggregator Thromboxane A2
    • Proloned Bleeding Time
27
Q

Acquired defects of PLT function: Extrinsic PLT abnormalities bare caused by? (2)

A
  • Uremia due to renal disease
  • Hyperviscosity and paraproteinemia
    • multiple myeloma
28
Q

Acquired defects of PLT function: Waldenstrom’s mscroglobulinemia?

What causes this?

What does this prevent?

A
  • IgM interferes with PLTs
  • PLTs circulating in abnormal amounts of protein cannot fully participate in the activation of coagulation factors and fibrin formation.
29
Q

What are the Lab tests for PLT function for the below?

  • PLT function analyzers
  • Von Willebrand’s disease
  • PLT aggregation
A
  • PLT function analyzers - collagen/epinephrine or collagen /ADP membranes
  • vWD antigen measured by immuno assay - Rictocetin
  • Lumi-aggregometer - based in impedence
30
Q

What are PLT aggregation tests used for?

A

Asses PLT function

31
Q

What does the ristocetin cofactor assay assess?

A

vWF Function by measuring ristocetin-meadiated binding of vWF to PLT GpIb

32
Q

What happens to PLT aggregation in Glanzmann’s thrombasthenia?

A

aggregation is decreased with all agonists (ADP, collagen, epinephriine, arachidonate) EXCEPT ristocetin.