Ch4 - 3) Other disorders of Hemostasis Flashcards

1
Q

What is Heparin induced thrombocytopenia?

A

Platelet destruction that arises secondary to heparin therapy

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2
Q

How does Heparin induced thrombocytopenia lead to thrombosis?

A

Fragments of destroyed platelets may activate remaining platelets, leading to thrombosis

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3
Q

What is disseminated intravascular coagulation?

A

Pathologic activation of the coagulation cascade

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4
Q

What does disseminated intravascular coagulation result in?

A
  1. Widespread microthrombi result in ischemia and infarction, 2. Consumption of platelets and factors results in bleeding, especially from IV sites and mucosal surfaces (bleeding from body orifices).
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5
Q

Is disseminated intravascular coagulation usually primary or secondary?

A

Almost always secondary to another disease process

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6
Q

What are some situations that may result in disseminated intravascular coagulation?

A

Obstetric complications, sepsis, adenocarcinoma, Acute promyelocytic leukemia, Rattlesnake bite

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7
Q

Obstetric complications and disseminated intravascular coagulation

A

Tissue thromboplastin in the amniotic fluid activates coagulation

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8
Q

Sepsis and disseminated intravascular coagulation

A

(especially with E. coli or Neisseria meningitidis) ? Endotoxins from the bacterial wall and cytokines (e.g TNF and IL-1) induce endothelial cells to make tissue factor.

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9
Q

Adenocarcinoma and disseminated intravascular coagulation

A

Mucin activates coagulation.

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10
Q

Acute promyelocytic leukemia and disseminated intravascular coagulation

A

Primary granules activate coagulation.

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11
Q

Rattlesnake bite and and disseminated intravascular coagulation

A

Venom activates coagulation

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12
Q

Laboratory findings for disseminated intravascular coagulation include?

A

decreased platelet count, increased PT/PTT, decreased fibrinogen, Microangiopathic hemolytic anemia, Elevated fibrin split products, particularly D-dimer

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13
Q

What is the best screening test for DIC?

A

Elevated D-dimer

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14
Q

D dimer is derived from?

A

splitting of cross-linked fibrin; D-dimer is not produced from splitting of fibrinogen.

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15
Q

Treatment of DIC involves?

A

addressing the underlying cause and transfusing blood products and cryoprecipitate (comains coagulation factors), as necessary.

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16
Q

What does normal fibrinolysis do?

A

Normal fibrinolysis removes thrombus after damaged vessel heals

17
Q

Tissue plasminogen activator (tPA)

A

converts plasminogen to plasmin

18
Q

Plasmin

A

cleaves fibrin and serum fibrinogen, destroys coagulation factors, and blocks platelet aggregation.

19
Q

a2-antiplasmin

A

inactivates plasmin.

20
Q

What are the disorders of fibrinolysis due to? What does this result in?

A

plasmin overactivity resulting in excessive cleavage of serum fibrinogen.

21
Q

What are some examples of disorders of fibrinolysis?

A

radical prostatectomy, cirrohsis of the liver

22
Q

How does radical prostatectomy lead to a disorder of fibrinolysis?

A

Release of urokinase activates plasmin

23
Q

How does cirrhosis of the liver lead to a disorder of fibrinolysis?

A

reduced production of a2-antiplasmin

24
Q

How does disorders of fibrinolysis present?

A

with increased bleeding (resembles DIC)

25
Q

Laboratory findings for disorders of fibrinolysis include

A

Increased PT/PTT, increased bleeding time with normal platelet count, Increased fibrinogen split products without D-dimers

26
Q

Why is there increased fibrinogen split products without D-dimers in disorders of fibrinolysis?

A

Serum fibrinogen is lysed; however, D-dimers are not formed because fibrin thrombi are absent

27
Q

Why is there increased bleeding time with disorders of fibrinolysis?

A

Plasmin blocks platelet aggregation

28
Q

Why is there increased PT/PTT with disorders of fibrinolysis?

A

Plasmin destroys coagulation factors.

29
Q

What is the treatment for disorders of fibrinolysis?

A

it is aminocaproic acid, which blocks activation of plasminogen.