Ch4 - 3) Other disorders of Hemostasis

Question 1

What is Heparin induced thrombocytopenia?

Answer 1

Platelet destruction that arises secondary to heparin therapy

Question 2

How does Heparin induced thrombocytopenia lead to thrombosis?

Answer 2

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

Question 3

What is disseminated intravascular coagulation?

Answer 3

Pathologic activation of the coagulation cascade

Question 4

What does disseminated intravascular coagulation result in?

Answer 4

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).

Question 5

Is disseminated intravascular coagulation usually primary or secondary?

Answer 5

Almost always secondary to another disease process

Question 6

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

Answer 6

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

Question 7

Obstetric complications and disseminated intravascular coagulation

Answer 7

Tissue thromboplastin in the amniotic fluid activates coagulation

Question 8

Sepsis and disseminated intravascular coagulation

Answer 8

(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.

Question 9

Adenocarcinoma and disseminated intravascular coagulation

Answer 9

Mucin activates coagulation.

Question 10

Acute promyelocytic leukemia and disseminated intravascular coagulation

Answer 10

Primary granules activate coagulation.

Question 11

Rattlesnake bite and and disseminated intravascular coagulation

Answer 11

Venom activates coagulation

Question 12

Laboratory findings for disseminated intravascular coagulation include?

Answer 12

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

Question 13

What is the best screening test for DIC?

Answer 13

Elevated D-dimer

Question 14

D dimer is derived from?

Answer 14

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

Question 15

Treatment of DIC involves?

Answer 15

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

Question 16

What does normal fibrinolysis do?

Answer 16

Normal fibrinolysis removes thrombus after damaged vessel heals

Question 17

Tissue plasminogen activator (tPA)

Answer 17

converts plasminogen to plasmin

Question 18

Plasmin

Answer 18

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

Question 19

a2-antiplasmin

Answer 19

inactivates plasmin.

Question 20

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

Answer 20

plasmin overactivity resulting in excessive cleavage of serum fibrinogen.

Question 21

What are some examples of disorders of fibrinolysis?

Answer 21

radical prostatectomy, cirrohsis of the liver

Question 22

How does radical prostatectomy lead to a disorder of fibrinolysis?

Answer 22

Release of urokinase activates plasmin

Question 23

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

Answer 23

reduced production of a2-antiplasmin

Question 24

How does disorders of fibrinolysis present?

Answer 24

with increased bleeding (resembles DIC)

Question 25

Laboratory findings for disorders of fibrinolysis include

Answer 25

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

Question 26

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

Answer 26

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

Question 27

Why is there increased bleeding time with disorders of fibrinolysis?

Answer 27

Plasmin blocks platelet aggregation

Question 28

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

Answer 28

Plasmin destroys coagulation factors.

Question 29

What is the treatment for disorders of fibrinolysis?

Answer 29

it is aminocaproic acid, which blocks activation of plasminogen.