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Spring 15 - CM Heme.Onc > Platelets > Flashcards

Platelets Flashcards

1
Q

How are platelets formed?

A
  • liver makes thrombopoietin
  • megakaryocytes get bigger b/c of its dividing DNA and the cytoplasm stretches
  • platelets are shed from disintegrating megakaryocyte
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2
Q

What do phospholipids and glycoprotein receptors on the platelet cell membrane do?

A
  • phospholipids important in coagulation and fibrin clot formation
  • glycoprotein receptors needed for platelet adhesion and aggregation
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3
Q

What do dense granules in platelets do?

A

-contribute to platelet aggregation and anticoagulation activity

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4
Q

What do alpha granules do in platelets?

A

-contain proteins that contribute to adhesion, aggregation and coagulant activity

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5
Q

What does a high platelet volume suggest?

A

-young platelets and a destructive process

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6
Q

What does a low platelet volume suggest?

A

-older platelets and a marrow production issue

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7
Q

Platelet Function Assay

A

-in vitro test of platelet function that has replaced bleeding time test
-esp useful in von Willebrand’s disorder
-if collagen/epinephrine and collagen/ADP are both long, platelet dysfunction
(if epi only, ASA or drug effect)

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8
Q

Myeloproliferative Disorders

A
  • abnormal platelets and too many platelets
  • thrombosis is a big worry
  • treat dz, give ASA or other antiplatelet med
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9
Q

Examples of Myeloproliferative Disorders

A
  • essential thrombocytopenia
  • chronic myelogenous leukemia
  • polycythemia vera
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10
Q

Reactive Platelet Disorders

A
  • normal platelets but too many

- will resolve with time

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11
Q

Causes of Reactive Platelet Disorders

A
  • infection
  • post-splenectomy
  • malignancy
  • iron deficiency
  • inflammation
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12
Q

What are 3 mechanisms that can cause thrombocytopenia (too low platelets)?

A
  • decreased production
  • increased destruction
  • hypersplenism
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13
Q

What might cause decreased platelet production?

A
  • bone marrow failure (aplastic anemia)
  • marrow replacement (lymphoma, leukemia)
  • marrow toxins (drugs, radiation, ethanol)
  • nutritional deficiency (B12, folic acid)
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14
Q

What might cause drug-induced thrombocytopenia?

A
  • myelosuppression: chemo, sulfa drugs, VPA, anti-retrovirals
  • immunologic: drug might induce antibody response
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15
Q

Clinical/Lab Presentation of Drug-Induced Thrombocytopenia

A

-severe, rapid onset of thrombocytopenia

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16
Q

Treatment of Drug-Induced Thrombocytopenia

A
  • stop drugs

- transfuse platelets if necessary

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17
Q

Clinical Features of Heparin-Induced Thrombocytopenia

A
  • thrombocytopenia starts 5-10 days after starting heparin
  • absence of other causes of thrombocytopenia
  • return to normal platelet count when heparin is discontinued
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18
Q

Lab Features of HIT

A
  • low platelets

- variable INR, PTT, fibrinogen

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19
Q

What is concerning about HIT?

How is HIT treated?

A

-can cause life or limb-threatening venous and/or arterial thrombosis

  • stop all forms of heparin ASAP
  • alternative anticoagulants (fondaparinux, argatroban, etc)
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20
Q

What is immune thrombocytopenic purpura?

A

loss of tolerance to self and IgG antibody against platelet glycoproteins

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21
Q

Immune Thrombocytopenia Purpura in Kids

A
  • acute onset often after viral illness

- often resolves spontaneously

22
Q

Immune Thrombocytopenia Purpura in Adults

A
  • insidious onset

- many pts go on to have chronic ITP

23
Q

Clinical Features of ITP

A
  • most kids have no health issues
  • most adults have other issues like autoimmune or malignancy
  • petechiae in dependent regions, ecchymoses
  • menorrhagia, epistaxis, gingival bleeding, blood in stool or urine
  • no lymphadenopathy or splenomegaly
24
Q

Lab Features of ITP

A
  • very low platelets (< 10,000)
  • CBC otherwise normal
  • normal coagulation times (INR, PTT, fibrinogen)
25
Q

How is ITP treated in adults?

A
  • steroids
  • IVIg
  • WinRho
  • Rituxan
  • splenectomy
  • observation
26
Q

How is ITP treated in kids?

A
  • observation (75%)
  • IVIg
  • WinRho
  • steroids
27
Q

What is the downside of steroid and IVIg treatment?

A

-very few have a durable response beyond a few weeks

28
Q

What is a downside of WinRho treatment?

A

only works in Rh+ patients

29
Q

What is disseminated intravascular coagulation (DIC)?

A
  • life threatening coagulation disorder –> excessive activation of coagulation system
  • thrombi can cause tissue ischemia and multiple organ dysfunction
30
Q

Lab Features of DIC

A
  • thrombocytopenia
  • prolonged coagulation times (INR, PTT)
  • low fibrinogen
31
Q

Treatment of DIC

A
  • treat underlying cause
  • transfuse platelets, FFP as needed
  • consider low dose heparin
32
Q

Thrombotic Thrombocytopenic Purpura

A

-poorly understood pathophys involving von Willebrand factor and ADAMTS13

33
Q

Thrombotic Thrombocytopenic Purpura

CLASSIC PENTAD

A
  • thrombocytopenia
  • microangiopathic hemolytic anemia (MAHA)
  • neurologic sxs
  • fever
  • renal dysfunction
34
Q

Lab Features of Thrombotic Thrombocytopenic Purpura

A
  • hemolysis
  • thrombocytopenia
  • coagulation should be normal or slightly prolonged
35
Q

Treatment of Thrombotic Thrombocytopenic Purpura

A

-plasma exchange has been main tx since early 1980s

36
Q

Hemolytic Uremic Syndrome Clinical Features

A
  • seen mostly in kids
  • mostly renal sxs, anemia, thrombocytopenia
  • associated w/ E coli and Shigella infections
37
Q

Hemolytic Uremic Syndrome Treatment

A
  • pts often require dialysis

- supportive therapy

38
Q

Gestational Thrombocytopenia

A

-most common cause of low platelets in pregnancy

39
Q

Hypersplenism

A
  • mild to moderate thrombocytopenia in pts w/ splenomegaly

- normally 30% of platelets in spleen –> up to 90% in an enlarged spleen

40
Q

What are some causes of splenomegaly?

A
  • congestive: CHF or portal HTN
  • infections: bacterial, CMV, HIV, TB
  • malignancy: leukemia, lymphoma
  • infiltrative (metabolic disorders)
  • collagen vascular dz
41
Q

What are some examples of qualitative platelet disorders?

A
  • Bernard Soulier syndrome
  • Glanzmann’s thrombasthenia
  • gray platelet syndrome
  • May-Heglin anomaly
42
Q

Bernard Soulier Syndrome

A

-defective glycoproteins and von Willebrand factor receptors

43
Q

Glanzmann’s Thrombasthenia

A

-defective glycoproteins and fibrinogen receptors

44
Q

Gray Platelet Syndrome

A

-alpha granule deficiency

45
Q

May-Heglin Anomaly

A

-inclusions in WBCs

46
Q

How might qualitative platelet disorders present?

A
  • early age
  • nosebleeds, mouth bleeding, bruising, petechiae
  • low platelet counts and/or abnormal platelet function
47
Q

Therapy for Qualitative Platelet Disorders

A
  • supportive care
  • tx of underlying medical disorders
  • platelet transfusions
48
Q

MC Causes of Bleeding Disorders in Women

A
  • von Willebrand dz
  • platelet disorders
  • connective tissue disorders
  • hemophilia carrier state
49
Q

What is the problem with platelets in:

  • HIT
  • ITP
  • DIC
  • TTP/HUS
A

-all have falling platelets

50
Q

What is the problem with INR/PTT/fibrinogen in:

  • HIT
  • ITP
  • DIC
  • TTP/HUS
A
  • HIT: variable clotting times and fibrinogen
  • ITP/TTP/HUS: normal clotting and fibrinogen
  • DIC: prolonged INR/PTT and low fibrinogen

Spring 15 - CM Heme.Onc (6 decks)

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