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Path U2 > Ch4 - 1) Primary Hemostasis and Bleeding Related Disorders > Flashcards

Ch4 - 1) Primary Hemostasis and Bleeding Related Disorders Flashcards

1
Q

What is hemostatsis?

A

Damage to the wall is repaired by hemostasis,

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2
Q

Hemostasis involves the formation of?

A

a thrombus (clot) at the site of vessel injury

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3
Q

Hemostasis stages?

A

primary and secondary.

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4
Q

Primary hemostasis?

A

forms a weak platelet plug

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5
Q

Primary hemostasis is mediated by?

A

interaction between platelets and the vessel wall

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6
Q

Secondary hemostasis?

A

stabilizes the platelet plug

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7
Q

Secondary hemostasis is mediated by?

A

the coagulation cascade.

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8
Q

What is Step 1 in secondary hemostasis?

A

Transient vasoconstriction of damaged vessel

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9
Q

How is Step 1 in secondary hemostasis mediated?

A

by reflex neural stimulation and endothelin release from endothelial cells

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10
Q

What is Step 2 in secondary hemostasis?

A

Platelet adhesion to the surface of disrupted vessel

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11
Q

In step 2 of secondary hemostasis, how does platelet adhesion occur?

A

Von Willebrand factor (vWF) binds exposed subendothelial collagen,

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12
Q

How do platelets bind to vWF?

A

via the GPIb receptor

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13
Q

vWF is derived from?

A

the Weibel-Palade bodies of endothelial cells and a-granules of platelets.

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14
Q

What is Step 3 in secondary hemostasis?

A

Platelet degranulation

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15
Q

In step 3 of secondary hemostasis what does Adhesion induce?

A

shape change in platelets and degranulation with release of multiple mediators

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16
Q

What are the mediators released in step 3 of secondary hemostasis?

A

ADP and TXA

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17
Q

What is the role of ADP in step 3 of secondary hemostasis?

A

it is released from platelet dense granules; promotes exposure of GPIIb/IIIa receptor on platelets.

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18
Q

What is the role of TXA in step 3 of secondary hemostasis?

A

it is synthesized by platelet cyclooxygenase (COX) and released; promotes platelet aggregation

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19
Q

What is step 4 in secondary hemostasis?

A

Step 4?Platelet aggregation

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20
Q

Where and how do Platelets aggregate in step 4 of secondary hemostasis?

A

at the site of injury via GPIIb/IIIa using fibrinogen (from plasma) as a linking molecule;

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21
Q

What does platelet aggregation result in?

A

formation of platelet plug

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22
Q

Platelet plug?

A

It is weak; coagulation cascade (secondary hemostasis) stabilizes it.

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23
Q

What are disorders of primary hemostasis usually due to?

A

Usually due to abnormalities in platelets;

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24
Q

Disorders of primary hemostasis are divided into?

A

quantitative or qualitative disorders

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25
Q

What are some Clinical features for disorders of primary hemostasis?

A

mucosal and skin bleeding.

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26
Q

What is the most common overall symptom in mucosal bleeding?

A

epistaxis

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27
Q

What are symptoms of mucosal bleeding?

A

epistaxis, hemoptysis, GI bleeding, hematuria, and menorrhagia. Intracranial bleeding occurs with severe thrombocytopenia.

28
Q

What are the symptoms of skin bleeding?

A

include petechiae (1-2 mm), ecchymoses (> 3 mm), purpura (> 1 cm), and easy bruising;

29
Q

Petechiae are a sign of what?

A

thrombocytopenia and are not usually seen with qualitative disorders.

30
Q

What are some useful laboratory studies for disorders of primary hemostasis?

A

platelet count, bleeding time, blood smear, bone marrow biopsy

31
Q

Platelet count

A

normal 150-400 K/pL; < 50 K/pL leads to symptoms,

32
Q

Bleeding time

A

normal 2-7 minutes; prolonged with quantitative and qualitative platelet disorders

33
Q

Blood smear

A

used to assess number and size of platelets

34
Q

Bone marrow biopsy

A

used to assess megakaryocytes, which produce platelets

35
Q

What is immune thrombocytopenic purpura?

A

(ITP) is an autoimmune production of IgG against platelet antigens (GPIIb/IIIa)

36
Q

What is the most common cause of thrombocytopenia in children and adults?

A

immune thrombocytopenic purpura

37
Q

In ITP what results in thrombocytopenia?

A

Antibody-bound platelets are consumed by splenic macrophages

38
Q

ITP is divided into?

A

acute and chronic forms

39
Q

Acute form of ITP?

A

arises in children weeks after a viral infection or immunization;selflimited, usually resolving within weeks of presentation

40
Q

Chronic form of ITP?

A

arises in adults, usually women of chilbearing age. May be primary or secondary (e.g SLE).

41
Q

What is the risk involved in chronic ITP?

A

May cause short-lived thrombocytopenia in offspring since antiplatelet IgG can cross the placenta.

42
Q

laboratory findings for ITP include

A

decreased platelet count, often < 50 K/pL, Normal PT/FTT, Coagulation factors are not affected. increased megakaryocytes on bone marrow biopsy

43
Q

What is the Initial treatment for ITP?

A

corticosteroids.

44
Q

How will children and adults respond to the initial treatment for ITP?

A

Children respond well; adults may show early response, but often relapse.

45
Q

In addition to corticosteroids what else is used in the treatment of ITP?

A

IVIG is used to raise the platelet count in symptomatic bleeding, but its effect is short-lived,

46
Q

What is a permenant solution for patients with ITP?

A

Splenectomy eliminates the primary source of antibody and the site of platelet destruction (performed in refractory cases).

47
Q

What is microangiopathic hemolytic anemia?

A

Pathologic formation of plateletmicrothrombin small vessels

48
Q

How are plateletmicrothrombin formed and what is the result?

A

Platelets are consumed in the formation of microthrombi sheering the RBCs as they cross microthrombi, resulting in hemolytic anemiawith schistocytes

49
Q

What is microangiopathic hemolytic anemia seen in?

A

thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS)

50
Q

What is TTP due to?

A

decreased ADAMTS13 which is an enzyme that normally cleaves vWF multimers into smaller monomers for eventual degradation.

51
Q

How does TTP lead to microangiopathic hemolytic anemia?

A
  1. Large, uncleaved multimers lead to abnormal platelet adhesion, resulting in microthrombi.
52
Q

Decreased ADAMTS13 is usually due what?

A

an acquired autoantibody;

53
Q

TTP is most commonly seen in?

A

adult females

54
Q

HUS is due to?

A

Hemolytic uremic syndrome is due to endothelial damage by drugs or infection.

55
Q

HUS is classically seen in?

A

children with E coli G157;H7 dysentery, which results from exposure to undercooked beef

56
Q

How is E Coli related to microangiopathic hemolytic anemia?

A

E coli verotoxin damages endothelial cells resulting in platelet microthrombi

57
Q

The clinical findings for HUS and TTP include

A

Skin and mucosal bleeding, Microangiopathic hemolytic anemia, Fever, Renal insufficiency, CNS abnormalities

58
Q

Renal insufficiency is more common in HUS or TTP?

A

HUS ? thrombi involve vessels of the kidney

59
Q

CNS abnormalities are more common in HUS or TTP?

A

TTP ? Thrombi involve vessels of the CNS

60
Q

Laboratory findings for microangiopathic hemolytic anemia include?

A

Thrombocytopenia with increased bleeding time Normal PT/PTT (coagulation cascade is not activated), anemia with schistocytes, increased megakaryocytes on bone marrow biopsy

61
Q

Treatment for microangiopathic hemolytic anemia?

A

involves plasmapheresis and corticosteroids, particularly in TTP.

62
Q

What are the qualitative platelet disorders?

A

bernard-soulier, Glanzmann thrombasthenia, asprin, uremia

63
Q

Bernard-Soulier syndrome

A

is due to a genetic GPIb deficiency; platelet adhesion is impaired.

64
Q

In Bernard-Soulier what lab test are you interested in?

A

Blood smear which shows mild thrombocytopenia with enlarged platelets.

65
Q

Glanzmann thrombasthenia is due to?

A

a genetic GPIIb/IIIa deficiency; platelet aggregation is impaired.

66
Q

Aspirin and microangiopathic hemolytic anemia?

A

it irreversibly inactivates cyclooxygenase; lack of TXA, impairs aggregation.

67
Q

Uremia and microangiopathic hemolytic anemia

A

disrupts platelet function; both adhesion and aggregation are impaired.

Path U2 (25 decks)

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