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Path U2 > Ch4 - 2) Secondary Hemostasis and Related Disorders > Flashcards

Ch4 - 2) Secondary Hemostasis and Related Disorders Flashcards

1
Q

What does secondary hemostasis do?

A

Stabilizes the weak platelet plug via the coagulation cascade

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2
Q

In secondary hemostasis the coagulation cascade generates?

A

thrombin, which converts fibrinogen in the platelet plug to fibrin.

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3
Q

In secondary hemostasis what happens to fibrin?

A

It is cross-linked, yielding a stable platelet-fibrin thrombus.

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4
Q

Where are the factors of the coagulation cascade produced?

A

In the liver in an inactive state.

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5
Q

What does activation of the factors of the coagulation cascade require?

A

exposure to an activating substance, Phospholipid surface of platelets, calcium

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6
Q

What are the activating substances involved in the activation of the factors of the coagulation cascade?

A

Tissue thromboplastin activates factor VII (extrinsic pathway). Subendothelial collagen activates factor XII (intrinsic pathway).

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7
Q

Where does the Calcium involved in the activation of the factors of the coagulation cascade come from?

A

derived from platelet dense granules

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8
Q

Disorders of secondary hemostasis are usually due to?

A

factor abnormalities

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9
Q

What are the clinical features of disorders of secondary hemostasis?

A

they include deep tissue bleeding into muscles and joints (hemarthrosis) and rebleeding after surgical procedures (e.g circumcision and wisdom tooth extraction).

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10
Q

Laboratory studies for Disorders of secondary hemostasis include?

A

PT (prothrombin time) and PTT (partial thromboplastin time)

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11
Q

Prothrombin time (PT)

A

measures extrinsic (factor VII) and common (factors II, V, X, and fibrinogen) pathways of the coagulation cascade

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12
Q

Extrinsic pathway of the coagulation cascade

A

factor VII

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13
Q

Common pathway of the coagulation cascade

A

factors II, V, X, and fibrinogen

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14
Q

Partial thromboplastin time (PTT) measures

A

intrinsic (factors XII, XI, IX, VIII) and common (factors II, V, X, and fibrinogen) pathways of the coagulation cascade

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15
Q

What is involved in Hemophilia A?

A

Genetic factor VIII (FVIII) deficiency, X-linked recessive (predominantly affects males)

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16
Q

Does Hemophilia A require a family history of it?

A

Can arise from a new mutation (de novo) without any family history

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17
Q

Hemphilia A presents with?

A

deep tissue, joint, and postsurgical bleeding

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18
Q

Clinical severity of hemophilia A depends on?

A

the degree of deficiency

19
Q

Laboratory findings of hemophilia A include

A
  1. increased PTT; normal PT 2. decreased FVIII 3. Normal platelet count and bleeding time
20
Q

What does treatment of hemophilia A involve?

A

recombinant FVIII.

21
Q

What is christmas disease?

A

Hemophilia B - Genetic factor IX deficiency, Resembles hemophilia A, except FIX levels are decreased instead of FVIII

22
Q

What is coagulation factor inhibitor?

A

Acquired antibody against a coagulation factor resulting in impaired factor function; anti-FVIII is most common,

23
Q

Clinical and lab findings for hemophilia B?

A

its similar to hemophilia A, PTT does not correct upon mixing normal plasma with patient’s plasma (mixing study) due to inhibitor; PTT does correct in hemophilia A.

24
Q

How can you tell the difference between hemophilia A and B?

A

mixing study

25
Q

von Willebrand Disease

A

Genetic vWF deficiency

26
Q

What is the most common inherited coagulation disorder?

A

von Willebrand disease

27
Q

Does von Willebrand Disease result in qualitative or quantitative disorders?

A

Multiple subtypes exist, causing quantitative and qualitative defects;

28
Q

What is the most common type of von Willebrand Disease?

A

is autosomal dominant with decreased vWF levels

29
Q

von Willebrand Disease presents with?

A

mild mucosal and skin bleeding; low vWF impairs platelet adhesion.

30
Q

Laboratory findings for von Willebrand Disease include

A
  1. increased bleeding time 2. increased PTT: normal PT ? Decreased FVIII half-life (vWF normally stabilizes FVIII); 3. Abnormal ristocetin test
31
Q

What is usually not seen with von Willebrand Disease that is unusual

A

deep tissue, joint, and postsurgical bleeding are usually not seen.

32
Q

Why is there an Abnormal ristocetin test in von Willebrand disease

A

Ristocetin induces platelet aggregation by causing vWF to bind platelet GPIb; lack ofvWF ?> impaired aggregation ?> abnormal test.

33
Q

What is the treatment for von willebrand disease?

A

desmopressin (ADH analog), which increases vWF release from Weibel-Palade bodies of endothelial cells

34
Q

How does vitamin K deficiency relate to hemostasis?

A

Disrupts function of multiple coagulation factors

35
Q

What is involved in Vitamin K activation?

A

Vitamin K is activated by epoxide reductase in the liver

36
Q

What does Activated vitamin K do?

A

it gamma carboxvlates factors II, VII, IX, X, and proteins C and S; gamma carboxylation is necessary for factor function.

37
Q

Vitamin K deficiency occurs in?

A
  1. Newborns 2. Long-term antibiotic therapy 3. Malabsorption
38
Q

Why is there vitamin K deficiency in newborns?

A

its due to lack of GI colonization by bacteria that normally synthesize vitamin K; vitamin K injection is given prophylactic ally to all newborns at birth to prevent hemorrhagic disease of the newborn

39
Q

How does Long-term antibiotic therapy elad to Vitamin K deficiency?

A

disrupts vitamin K-producing bacteria in the GI tract

40
Q

How does Malabsorption lead to Vitamin K deficincy?

A

leads to deficiency of fat-soluble vitamins, including vitamin K

41
Q

What are some other causes of secondary hemostasis?

A

liver failure, large volume transfusion,

42
Q

How does liver failure lead to secondary hemostasis?

A

decreased production of coagulation factors and decreased activation of vitamin K by epoxide reductase;

43
Q

How is the effect of liver failure on coagulation followed?

A

followed using PT.

44
Q

How does Large-volume transfusion lead to secondary hemostasis?

A

it dilutes coagulation factors, resulting in a relative deficiency

Path U2 (25 decks)

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