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SBL Test 1 > Robbins 14: Bleeding and Clotting > Flashcards

Robbins 14: Bleeding and Clotting Flashcards

1
Q

Disorders due to ABNL platelets vs coagulation facts cause WHAT findings

A
  • 1. ABNL platelets = Mucosal/skin bleeding => peteechiae
  • 2. ABNL coagulation factors = JOINT bleeding, deep tissue bleeding
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2
Q

High platelet counts may indicate _____________

A

Myeloproliferative disease (essential thrombocythemia)

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3
Q

What are causes of thrombocytopenia?

A
  1. Decreased production
  2. Decreased platelet survival
  3. Sequestration in the red pulp of enlarged spleens
  4. Dilution due to massive transfusions
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4
Q

What are causes of decreased platelet production ==> thrombocytopenia?

A
  1. Aplastic anemia
  2. Leukemia
  3. HIV (one of the MC hematologic manifestations of HIV)
  4. Myelodysplastic syndromes
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5
Q

What are causes of decreased platelet survival?

A
  1. ↑ consumption (seen in DIC, TTP, HUS)
  2. Immune-mediated platelet destruction (seen in antiplatelet Ab or immune complex deposition on platelets)
    1. Seen in AI thrombocytopenia: allo-antibodies against platelets are produced when platlets are transfused or cross placenta from fetus => mom.
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6
Q

How may alloantibodies against platelets be generated?

A

When platelets are transfused or IgG cross placenta from fetus —> mother

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7
Q

What are the 2 most important non-immunologic causes of decreased platelet survival leading to thrombocytopenia?

A
  1. DIC
  2. Thrombotic microangiopathies (TTP and HUS)
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8
Q

Primary AI causes of destruction of platelets => ↓ platelet survival

A
  1. Crhronic Immune Thrombocytopenia Purpura (ITP)
  2. Acute immune Thrombocytopenia Purpura (ITP)
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9
Q

Chronic immune thrombocytopenic purpura (ITP) is most commonly seen in whom?

A

Young women < 40YO

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10
Q

Chronic immune thrombocytopenic purpura (ITP)

  1. Definition
  2. Pathogenesis
A
  1. IgG autoantibody destruction of platlets that can be primary or secondary (due to SLE, HIV and B-cell neoplasms/CLL).
  2. Pathogensis:
    1. IgG antiplatelet Ab are directed against membrane glycoproteins
      • IIb/IIIa – Glanzmann Thrombocytopenia
      • Ib/IX – Bernard-Soulier Syndrome
    2. Anti-platelet Abs are recognized by IgG Fc receptors on phagocytes
    3. ↑ platelet destruction by the spleen, however NO splenomegaly occurs.
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11
Q

In Chronic Immune Thrombocytopenic Purpura (ITP), IgG anti-platlet AB are directed against what?

A
  • IIb/IIIa
  • Ib/IX
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12
Q

What is seen in the bone marrow and peripheral blood with chronic immune thrombocytopenic purpura (ITP)?

A
    • Marrow: moderately ↑ number of megakaryocytes
    • Peripheral blood: abnormally large platelets (megathrombocytes)
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13
Q

What are the clinical signs/sx’s of chronic immune thrombocytopenic purpura (ITP); often there is a history of what?

A
  1. Insidious onset characterized by bleeding into the skin and mucosal surfaces
    1. Initially, as pinpoint hemorrhages (petechiae) => ecchymoses
  2. Often there is hx of epistaxis, easy bruising, gum bleding and hemorrhages into soft tissues w/ minor trauma
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14
Q

_________ moderately improves thrombocytopenia seen in chronic immune thrombocytopenic purpura (ITP).

A

Splenectomy

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15
Q

Labs in Chronic Immune Thrombocytopenic Purpura (ITP)

A
  1. Low platlet count (those seen on peripheral blood smear are large)
  2. NL PT and PTT
  3. NL or ↑ megakaryocytes
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16
Q

How is the diagnosis of chronic immune thrombocytopenic purpura (ITP) made?

A

Diagnosis of exclusion after all other causes of thrombocytopenia ruled out

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17
Q

Chronic ITP may sometimes first manifest with what signs/sx’s?

A
  1. Melana
  2. Hematuria
  3. Excessive menstrual flow
18
Q

How does acute ITP differ from chronic ITP in terms of population affected and pathogenesis?

A
  1. Children (M=F)
  2. Sx’s appear abruptly, 1-2 weeks after self-limited viral infection
  3. Self-limited (spontaneously resolves within 6 months)
19
Q

What are 2 serious and sometimes fatal complications of chronic ITP?

A
  1. Subarachnoid hemorrhage
  2. Intracerebral hemorrhage
20
Q

Which 3 drugs are most commonly indicated in causing drug-induced thrombocytopenia?

A
  1. Quinine
  2. Quinidine (Malaria drugs)
  3. Vancomycin
21
Q

MOA of

Drug-Induced Thrombocytopenia

A
  • Drugs act as haptens to glycoproteins on platets => creating AB that can bind to it or form immune complexes that deposit on platelet surfaces
22
Q

What are the complications which may arise with heparin-induced thrombocytopenia, type II?

A

Life threatening venous and arterial thrombosis.

*This is thrombosis occurring in the setting of thrombocytopenia, which is paradoxical to what should be happening.

    • Clots within large arteries may lead to vascular insufficiency and limb loss
    • Emboli from DVT’s can cause fatal PE
23
Q

HIV-Associated Thrombocytopenia: Explain how HIV can cause both ↓ production and survival of platelets?

A
  1. HIV binds CD4 and CXCR4 on megakarytocytes; causing these cells to become prone to apoptosis and ↓ platelet production
  2. HIV causes B-cell hyperplasia => form autoantibodies, which may opsonize platelets => destroy
24
Q

2 Thrombotic Microangiopathies (cause ↓ platelet survival)

A
  1. TTP (thrombotic thrombocytopenic purpura)
  2. HUS (hemolytic uremic syndrome)
25
Q

What are thrombotic microangiopathies?

A

Disorder that causes thrombosis formation in small vessels, which consumes platelets and leads to thrombocytopenia

  • Disorders charactersitzed by:
    1. Thrombocytopenia
    2. Microangiopathic hemolytic anemia
    3. Fever
    4. Transient neurological deficits (in TTP) or renal failure (in HUS)
26
Q

What important process in DIC is NOT a feature of TTP and HUS?

A
  • Activation of the coagulation cascade is NOT of a primary feature; so the PT and PTT = NL in TTP and HUS
    • DIC: PT/PTT is ABNL
27
Q

What is TTP?

A

Disorder that causes thrombosis formation in small vessels, which consumes platelets and leads to thrombocytopenia due to ↓ ADAMTS13 (aka “vWF metalloprotease”/ eznyme that cleaves vWF) bc thery develop an aquired autoAB to it (either acquired or inherited)

  • Normally, ADAMTS13 breaks down vWF multimers
  • With disease = large vWF multimers => abnormal platelet adhesion and microthrombi
  • Worse with endothelial injury
28
Q
  1. Thrombotic thrombocytopenic purpura (TTP) is due to a deficiency in what?
  2. Pentad of symptoms?
A
  1. ADAMTS13 (aka “vWF metalloprotease) because of autoAB to it
    • Fever
  • Thrombocytopenia

- Microangiopathic hemolytic anemia (MAHA)

- Transient neuro deficits

  • Renal failure
    3. Pur
29
Q

How is Hemolytic Uremic Syndrome (HUS) different from TTP?

A
  1. Occurs in children
  2. No neuro symptoms
    • Acute renal failure
  4. Due to GI infection form E.coli O157:H7, which produces Shiga-like toxin => microthrombi.
30
Q

How do typical vs. atypical HUS differ from eachother?

A
    • Typical = commonly caused by shiga-like toxin from E. coli O157:H7 infection, most commonly affecting children/older adults
    • Atypical= commonly caused by complement gene mutation (factor H, membrane cofactor protein (CD46) or factor I) or AI response—> which normally prevent activation of alternative complement pathway
31
Q

TTP typically occurs in _____

HUS typically occurs in _____.

A
  1. TTP = Females
  2. HUS = children
32
Q

3 categories of inherited defective Platelet Dysfunction

A
  1. Defects of adhesion
  2. Defects of aggregation
  3. Disorders of platelet secretion (release reaction)
33
Q

What is a cause of defective platelet adhesion?

A

Bernard-Soulier Syndrome

34
Q

What is

Bernard-Soulier Syndrome?

A

-AR deficiency in GPIb/IX platelet receptor, which allows them to bind to vWF so that platlet can adhere to damaged endothelium

35
Q

What findings do we see in Bernard-Soulier Syndrome?

A
  1. Prolonged bleeding time
  2. Large platelets****
  3. Will aggregate to ADP, collagen, EPI, or thrombin
  4. DO NOT aggregate to ristocetin
36
Q

What is Glanzmann Thrombasthenia?

A

AR deficiency in GPIIB/IIIA, which is the platelet receptor that allows platelets to aggregate and form platelet plug.

37
Q

What findings do we see with Glanzemann Thrombasthenia?

A
  1. NL platelets
  2. Isolated platelets on blood smear (because no clumping)
  3. WILL NOT aggregate to ADP, collagen, EPI, or thrombin
  4. WILL aggregate to ristocetin;
38
Q

What are the 2 most clinically significant acquired defects of platelet function?

A
  1. Aspirin/ other NSAIDs; potent irreversible inhibitor of COX-I, which is needed to make thromboxane A2 and prostaglandins
    • Uremia which involves defects in platelet adhesion, granule secretion, and aggregation
39
Q

How does bleeding due to clotting factor abnormalities differ from those seen with platelet deficiencies?

A
  1. Spontaneous petechiae/purpura = uncommon
  2. Bleeding manifests as large excxymoses or hematomas after injury or prolonged bleeding after laceration/surgery.
  3. Often occurs into the GI/GU tracts and into weight-bearing joints (hemarthrosis)
40
Q

hemarthrosis after minor stress on a knee joint is suggestive of what?

A

hemophilia (A or B), not vWF

SBL Test 1 (15 decks)

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