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(J2) RBCs and Bleeding Disorders > Primary (Platelet) Hemostatic Disorders > Flashcards

Primary (Platelet) Hemostatic Disorders Flashcards

1
Q

What are the types of primary hemostatic diseases?

A

Quantitative

  • decreased platelet count (thrombocytopenia)
  • normal platelet function

Qualitative

  • decreased platelet function
  • normal platelet count
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2
Q

What are common symptoms of primary hemostatic (platelet) disorders?

A

Mucosal bleeding:

  • epistaxis (most common)
  • menorrhagia
  • hemoptysis
  • hematuria
  • menorrhagia

Skin bleeding:

  • petechiae (1-2mm)
  • purpora (>3mm)
  • ecchymosis (>1cm)
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3
Q

What is the most common cause of thrombocytopenia?

A

immune thrombocytopenic purpora (ITP)

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4
Q

What is immune thrombocytopenic purpora (ITP)?

A

Autoimmune disorder; platelet specific IgG

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5
Q

What is the mechanism of immune thrombocytopenic purpora?

A
  • IgG produced in the spleen opsonizes platelets
  • splenic macrophages eat the platelets -> thrombocytopenia
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6
Q

What lab findings would be expected with immune thrombocytopenic purpora?

A
  • decreased platelet count (thrombocytopenia)
  • normal PT/PTT (not involved, primary hemostatis)
  • increased megakaryocytes in bone marrow (increased platelet demand)
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7
Q

What are the different types of immune thrombocytopenic purpora?

A
  • acute
  • chronic
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8
Q

What is acute immune thrombocytopenic purpora?

What is its typical presentation?

A

-children

-weeks after a viral infection/immunization

**self-limiting, resolves within weeks**

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9
Q

What is chronic immune thrombocytopenic purpora?

What is its typical presentation?

A
  • women of childbearing age
  • idopathic (primary) or associated with other autoimmune disease (secondary)
  • commonly associated with SLE
  • also associated with HIV and B cell neoplasms (CLL)
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10
Q

What special consideration should be taken in women with chronic immune thrombocytopenic purpora?

A

IgG can cross the placenta, women with chronic ITP can have children that will display self-limited thrombocytopenia following birth

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11
Q

What is the treatment for immune thrombocytopenic purpora?

A
  • corticosteroids (very effective in children; effective in adults but will likely relapse)
  • splenectomy (eliminates both source of IgG and location of destruction)
  • IVIG
  • rituximab
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12
Q

What is drug-induced thrombocytopenia?

A

platelet destruction either by the direct action of a drug (primary) or immune mediated destruction caused by the drug (secondary)

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13
Q

What are common drugs associated with drug-induced thrombocytopenia?

A
  • heparin
  • quinine
  • quinidine
  • vancomycin
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14
Q

What is HIT?

A

Heparin-induced thrombocytopenia

destruction of platelets following heparin treatment (~5% of the population)

Type 1:

-immediate effect, little clinical significance

Type 2:

  • delayed respone (1-2 weeks)
  • causes platelets to aggregate resulting in paradoxical thromosis with thrombocytopenia

-can lead to loss of limbs or fatal PE

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15
Q

What is the mechanism of HIT?

A
  • heparin binds platelet factor 4 (PF4) on platelets
  • heparin-PF4 complex is recognized by certain antibodies
  • some Ab coated platelets are removed by spleen -> thrombocytopenia
  • some Ab coated platelets fragment and activate other platelets -> thrombosis
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16
Q

What is HIV-associated thrombocytopenia?

What are the mechanisms?

A

One of the most common symptoms of HIV infection

  • platelet destruction and decreased production caused by HIV infection
  • platelets/megakaryocytes have CD4 (target receptor of HIV) and can become infected -> decreased produciton and increased destruction
  • HIV can also cause B-cell dysplasia with increased risk of autoimmune antibodies
17
Q

How does microangiopathic hemolytic anemia relate to hemostasis?

A

the mircrothrombi formed use up platelets -> thrombocytopenia

18
Q

What lab findings would be expected with microangiopathic hemolytic anemia?

A
  • decreased platelets (thrombocytopenia)
  • increased bleeding time
  • normal PT/PTT (not involved, primary hemostasis)
  • anemia w/ schistocytes
  • increased megakaryocytes in bone marrow (increased demand for platelets)
19
Q

What are the main types of microagniopathic hemolytic anemia?

A
  • thrombotic thrombocytopenic purpora (TTP)
  • hemolytic uremic syndrome (HUS)
20
Q

What is TTP?

A

Thrombotic thrombocytopenic purpora

(a microangiopathic hemolytic anemia)

decrease in ADAMTS13 resulting in formation of thrombi resulting in thrombocytopenia

21
Q

What is the mechanism of TTP?

A

caused by decreased ADAMTS13, most commonly autoimmune; can be genetic

ADAMTS13 cleaves multimeric vWF into monomers

decreased ADAMTS13 -> increased multimers -> abnormal aggregation -> microthrombi

22
Q

What is the classic presentation of TTP?

A
  • adult
  • female
  • petechiae/purpora
  • microangiopathic hemolytic anemia
  • fever
  • CNS abnormalities (thrombi in brain)
23
Q

What is the treatment for TTP?

A
  • plasmaphoresis to remove offening Ab
  • corticosteriods
24
Q

What is HUS?

A

Hemolytic uremic syndrome

(a microangiopathic hemolytic anemia)

infection (most commonly dysentery from E coli O157:H7) induced endothelial damage resulting in platelet activation

typically results in renal damage (hence uremic)

25
Q

What is the classic presentation of HUS?

A

children who ate undercooked beef

  • petechiae/purpora
  • microangiopathic hemolytic anemia

-fever

-renal insufficiency (thrombi in kidneys)

26
Q

What is the treatment for HUS?

A

mostly supportive

-late dialysis/renal transplant (renal failure)

27
Q

What is Bernard-Soulier syndrome?

A

Qualitative platelet disorder

-deficiency in GPIb -> impaired platelet adhesion

28
Q

What lab findings would be expected with Bernard-Soulier syndrome?

A
  • normal to mildly decreased platelets
  • giant platelets (BS - big suckers)
  • increased bleeding time
  • normal PT/PTT
29
Q

What is the presentation of Bernard-Soulier syndrome?

A
  • children
  • typically severe bleeding risk
30
Q

What is Glanzmann thrombasthenia?

A

Qualitative platelet disorder

-deficiency in GPIIb/IIIa -> impaired platelet aggregation

31
Q

What lab findings would be expected with Glanzmann thrombasthenia?

A
  • normal platelet number/size
  • increased bleeding time
  • normal PT/PTT
32
Q

What is the presentation of Glanzmann thrombasthenia?

A

-severe bleeding risk

33
Q

How does aspirin affect bleeding risk?

A
  • irreveribly inhibits cycloocygenase
  • no thromboxane A2 or prostaglandin release from platelets -> no aggregation
34
Q

What lab findings would be expected with aspirin overdose?

A
  • normal platelets
  • increased bleeding time
  • normal PT/PTT
35
Q

How does uremia affect bleeding risk?

A

disrupts platelet adhesion and aggregation

36
Q

What lab findings would be expected with bleeding disorders due to uremia?

A
  • normal platelets
  • increased bleeding time
  • normal PT/PTT

(J2) RBCs and Bleeding Disorders (10 decks)

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