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2nd U2 Path > Other Disorders of Hemostasis > Flashcards

Other Disorders of Hemostasis Flashcards

1
Q

A disorder of platelet destruction that is secondary to heparin therapy…

A

Heparin-induced thrombocytopenia

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2
Q

With heparin-induced thrombocytopenia, how can the development of thrombosis occur?

A

Fragments of destroyed platelets may activate the remaining platelets causing a thrombosis

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3
Q

What does heparin form a complex with in heparin-induced thrombocytopenia and what does this cause the formation of?

A

Forms a complex with PF4 causing the formation of IgG antibodies against the platelets

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4
Q

A pathological activation of the coagulation cascade with widespread microthrombi that results in ischemia and infarction…

A

Disseminated intravascular coagulation (DIC)

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5
Q

What is the mechanism of excessive bleeding from IV sites and mucosal surfaces observed in disseminated intravascular coagulation?

A

With DIC there is a rapid consumption of platelets and coagulation factors which lead to the excessive bleeding

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6
Q

Disseminated intravascular coagulation is almost always secondary to another disease. What are the 5 most common diseases that can cause DIC?

A

1) Obstetric complications
2) Sepsis
3) Adenocarcinoma
4) Acute promyelocytic leukemia
5) Rattlesnake bite

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7
Q

What is the mechanism of disseminated intravascular coagulation formation an obstetrical patient?

A

Tissue thromboplastin within the amniotic fluid activates the coagulation cascade

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8
Q

Sepsis can cause disseminated intravascular coagulation. What is the mechanism of action?

A

Endotoxins from bacterial wall (E. coli or N meningitides) and cytokines induce endothelial cells to make tissue factor.

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9
Q

What activates the coagulation cascade when disseminated intravascular coagulation occurs secondary to adenocarcinoma?

A

Mucin

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10
Q

Patients with acute promyeloctic leukemia can develop disseminated intravascular coagulation. What causes the activation of the coagulation cascade?

A

Primary granules

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11
Q

A bite can cause disseminated intravascular coagulation. What animal can cause this and what is produced by the animal to cause DIC?

A

Rattlesnake bite—venom causes activation of coagulation cascade→ DIC

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12
Q

What are the laboratory findings with disseminated intravascular coagulation with respect to PT, PTT, Platelet count, and Fibrinogen?

A

PT: elevated
PTT: elevated
Platelet count: decreased
Fibrinogen: decreased

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13
Q

What type of anemia is seen with disseminated intravascular coagulation?

A

Microangiopathic hemolytic anemia

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14
Q

What is the best screening test for disseminated intravascular coagulation?

A

Elevated D-dimer

Derived from splitting of cross-linking fibrin

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15
Q

What is the treatment for disseminated intravascular coagulation?

A

Treatment of underlying cause and blood transfusion and cryoprecipitate.

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16
Q

What is the purpose of fibrinolysis?

A

Removal of thrombus after damaged vessel has healed.

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17
Q

What are the 3 steps of fibrinolysis?

A

1) tPA conversion of plasminogen to plasmin
2) Plasmin cleaves fibrin and serum fibrinogen—destroying the coagulation factors and blocks platelet aggregation
3) A2-antiplasmin inactivates plasmin

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18
Q

What is responsible for the conversion of plasminogen to plasmin during fibrinolysis?

A

tPA-(tissue plasminogen activator)

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19
Q

After fibrinolysis has occured, what inactivates the plasmin to stop its function?

A

A2-antiplasmin

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20
Q

Disorders of fibrinolysis usually involve over activity of what substance?

A

Plasmin

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21
Q

Over activity of plasmin seen in disorders of fibrinolysis causes what to occur?

A

Excessive cleavage of serum fibrinogen

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22
Q

What are the 2 most common causes of disorders to fibrinolysis?

A

Radical prostatectomy

Cirrhosis of the liver

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23
Q

What is release during a radical prostatectomy that causes a disorder of fibrinolysis?

A

Urokinase

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24
Q

When urokinase is released during a radical prostatectomy, what occurs to allow for the disorder of fibrinolysis?

A

Urokinase activates plasmin

25
Q

Why does cirrhosis of the liver cause disorders in fibrinolysis?

A

There is a reduction in the production of a2-antiplasmin, which allows plasmin to remain activated.

26
Q

What are the typical laboratory findings seen with disorders of fibrinolysis with respect to PT/PTT, bleeding time, Platelet count, and fibrinogen levels?

A

PT/PTT: elevated
Bleeding time: elevated
Platelet count: normal
Fibrinogen: decreased (without D-dimers)

27
Q

How can a disorder of fibrinolysis be differentiated from disseminated intravascular coagulation?

A

DIC will have D-dimers with the splitting of fibrinogen and DIC will also have a decreased platelet count. Disorder of fibrinolysis will have normal platelet count

A disorder of fibrinolysis will have ABSENCE of D-dimer because fibrin thrombi are absent

28
Q

What is the treatment for a disorder of fibrinolysis?

A

Aminocaproic acid—this blocks the activation of plasminogen

29
Q

Where is the most common location for thrombosis formation?

A

Deep veins (DVT) of the leg below the knee

30
Q

What are the two characteristics of a thrombosis and why are these important findings on autopsy?

A

Lines of Zahn and attachment to vessel wall

If found on autopsy—indicates that thrombosis occur prior to death

31
Q

What are the 3 major risk factors contributing to thrombosis formation also known as Virchow triad?

A

1) Disruption in blood flow
2) Endothelial cell damage
3) Hypercoagulable state

32
Q

What are the 3 common disruptions in normal blood flow that can lead to the formation of thrombosis?

A

1) immobilization—increased risk of DVT
2) Cardiac wall dysfunction—(a-fib, MI)
3) Aneurysm

33
Q

What are the 5 ways in which endothelial cells prevent the formation of thrombosis?

A

1) Blockage of exposure to subendothelial collagen and underlying tissue factor
2) Production of PGI2 and NO—vasodilatation and inhibition of platelet aggregation
3) Secretion of heparin-like molecules—ATIII augmentation causing inactivation of thrombin and coagulation factors
4) Secretion of tPA
5) Scretion of thrombomodulin

34
Q

The production of PGI2 and NO to prevent thrombosis formation works through what mechanism(s)?

A

Cause vasodilation and inhibition of platelet aggregation

35
Q

How does the secretion of heparin-like molecules prevent the formation of thrombosis?

A

Causes augmentation of antithrombin III (ATIII), which in turn inactivates throbin and coagulation factors

36
Q

The secretion of tPA stops the formation of thrombosis through what mechanism?

A

Converts plasminogen to plasmin—this does 3 things

1) cleaves fibrin and serum fibrinogen
2) destroys coagulation factors
3) blocks platelet aggregation

37
Q

The secretion of thrombomodulin prevents the formation of thrombosis through activation of what?

A

Causes redirection of the thrombin to activate protein C—this in turn inactivates factor V and VIII

38
Q

What are the 3 most common causes of endothelial cell damage?

A

Atherosclerosis
Vasculitis
High levels of homocysteine

39
Q

What 2 deficiencies cause a mild elevation of homocysteine levels, which increase the risk of thrombosis formation?

A

Vitamin B12 deficiency

Folate deficiency

40
Q

What is the mechanism for increased homocysteine levels with a vitamin B12 or folate deficiency?

A

Lack of Vitamin B12 or folate leads to the decreased conversion of homocysteine to methionine due to the inability to transfer a methyl group. This leads to a build up of homocysteine

41
Q

A deficiency in cystathionine beta synthase (CBS) causes a high level of what substance?

A

Homocysteine

42
Q

What is the enzymatic function of cystathionine beta synthase (CBS)?

A

Conversion of homocysteine to cystathionine

43
Q

What are the 4 characteristic findings seen in patients who present with a cystathionine beta synthase (CBS) deficiency?

A

1) Vessel Thrombosis
2) Mental retardation
3) Lens dislocation
4) Long slender fingers

44
Q

What is the classic presentation of a patient who presents with a hypercoagulable state?

A

Reccurent DVTs or DVT at a young age

45
Q

What are the most common sites for DVTs to occur?

A

Deep veins of the leg

Hepatic and cerebral veins

46
Q

What deficiency is typically found with patients who have a hypercoagulable state?

A

Protein C and S deficiency

47
Q

What does a protein C and S deficiency cause within the coagulation cascade?

A

Deficiency decreases the negative feedback on the coagulation cascade

48
Q

What is the normal function of protein C and S within the coagulation cascade?

A

Inactivate factors V and VIII

49
Q

Patients who present with a protein C and S deficiency are at an increased risk of developing what type of necrosis?

A

Warfarin skin necrosis

50
Q

A disease involving a mutated form of factor V that results in the factor V without a cleavage site for deactivation by protein C and S…

A

Factor V Leiden

51
Q

What is the most common inherited cause of a hypercoagulable state?

A

Factor V Leiden

52
Q

A disease involving an inherited point mutation in prothrombin resulting in an increased gene expression of prothrombin…

A

Prothrombin 20210A

53
Q

How does prothrombin 20210A promote the production of thrombus?

A

Increased prothrombin→ increased thrombin→ thrombus formation

54
Q

This deficiency decreases the protective effect of heparin-like molecules produced by the endothelium, which increases the risk of thrombus formation…

A

ATIII deficiency

55
Q

What do heparin-like molecules normally activate and what role does this play in the coagulation pathway?

A

Activates ATIII, which inactivates thrombin and coagulation factors

56
Q

What laboratory measurement is used to monitor heparin therapy?

A

PTT

57
Q

A patient presents with ATIII deficiency and is given heparin. What laboratory value will be different when comparing it to a patient WITHOUT ATIII deficiency who was given heparin?

A

The PTT level does not rise with standard heparin dosing in the patient with the ATIII deficiency

58
Q

What is given to overcome an ATIII deficiency and maintain an anticoagulated state?

A

A high dose of heparin is given to activate the limited number of ATIII and then Coumadin is given to maintain an anticoagulated state

59
Q

What is the mechanism by which oral contraceptives increase the risk of developing a hypercoagulable state?

A

Estrogen within the oral contraceptive will increase the production of the coagulation factors—this increases the risk of thrombosis

2nd U2 Path (31 decks)

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