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Cell Pathology 2 (Pathology) > Hem I and II/Hemostasis and Thrombosis > Flashcards

Hem I and II/Hemostasis and Thrombosis Flashcards

1
Q

What are the 4 general stages of hemostasis?

A
  1. Transient vasoconstriction
  2. Platelet adhesion to surface of disrupted vessel
  3. Platelet degranulation
  4. Platelet aggregation
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2
Q

When injury damages subendothelial tissue, what factor is released?

A

von Willebrand factor

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3
Q

Via which receptor does vWF contribute to platelet adhesion?

A

Gp1b to result in platelet adhesion

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4
Q

What two sources do vWF come from?

A

Weibel-Palade bodies of endothelial cells (vast majority) and some from alpha-granules of platelets

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5
Q

What is the disease which is a Gp1b deficiency? What is the result?

A

Bernard-Soulier disease; impaired platelet adhesion which leads to bleeding

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6
Q

What two factors are released by activated endothelial cells?

A

They synthesize tissue factor and secrete plasminogen activator inhibitor (PAI) which limits fibrinolysis

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7
Q

What are the following skin bleeding signs called:
1-2 mm
>3 mm
>1 cm

A

1-2 mm = petechiae (usually due to platelet deficiency or vit C deficiency; also sign of thrombocytopenia)
3-5 mm = purpura (also due to vasculitis or trauma)
>1 cm are ecchymoses (bruises)

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8
Q

What causes immune thrombocytopenic purpura (ITP)?

A

Autoimmune production of IgG against platelet antigens (e.g., GPIIb/IIIa)

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9
Q

In what organ does the events that eliminate platelets in immune thrombocytopenic purpura take place?

A

Most of the events take place in the spleen; the spleen will make the plasma cells that create the antibodies and they have macrophages that consume the antibody bound platelets

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10
Q

What are the two types of cytoplasmic granules that platelets have, and what do each contain?

A

Alpha granules: fibrinogen, factor V and VIII, vWF

Delta granules: ADP, ATP, calcium, serotonin, epinephrine

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11
Q

What would the PT/PTT values be for ITP?

A

Normal PT/PTT; it is a disorder of primary hemostasis and the coagulation cascade is unaffected.

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12
Q

What is microangiopathic hemolytic anemia?

A

Is the pathologic formation of platelet microthrombi in small vessels; the thrombi formation consumes platelets and shears RBCs resulting in hemolytic anemia with schistocytes

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13
Q

What two diseases is microangiopathic hemolytic anemia seen?

A

thrombocytopenic purpura and hemolytic uremic syndrome

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14
Q

What is the genetic cause of TTP?

A

Decreased ADAMTS13 which normally cleaves vWF Thus the resulting large multimers of vWF lead to platelet adhesion.

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15
Q

What is the cause of hemolytic uremic syndrome (HUS)?

A

Due to endothelial damage by drugs or via infection (esp. with undercooked beef)

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16
Q

What is the PT/PTT value for microangiopathic hemolytic anemia diseases?

A

Both are normal because this is a disease of primary hemostasis, not of coagulation cascade

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17
Q

What is the genetic defect in Glanzmann thromasthenia?

A

Due to a genetic GPIIb/IIIa deficiency; impairs platelet aggregation

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18
Q

What vasoconstrictor does aspirin block the synthesis of and where does this vasoconstrictor come from?

A

Aspirin blocks the synthesis of TXA2 from activated platelets. TXA2 is a prostaglandin made by COX enzymes which are inhibited by aspirin.

19
Q

What role does ADP released from dense granules of platelets have?

A

It is a potent mediator of platelet aggregation

20
Q

How are GIIb/IIIa receptors activated?

A

These receptors are expressed on activated platelets which bind fibrinogen and promotes platelet aggregation; this forms the platelet plug. Their exposure is promoted by ADP release from delta granules on other platelets

21
Q

What is the overarching goal of secondary hemostasis and generally how is this accomplished?

A

Overall goal is to support the primary platelet plug. Accomplished via conversion of fibrinogen to fibrin which is cross linked.

22
Q

How is fibrinogen converted to fibrin?

A

Via thrombin

23
Q

What organ produces the factors of the coagulation cascade?

A

Liver

24
Q

What activates the extrinsic pathway of the coagulation cascade?

A

Tissue thromboplastin

25
Q

What activates the intrinsic pathway of the coagulation cascade?

A

Subendothelial collagen

26
Q

The liver produces the factors of the coagulation cascade in an inactive form. What is required for their activation (3 things)?

A
  1. Exposure to activating substance (tissue thromboplastin or subendothelial collagen)
  2. Phospholipid surface of platelets
  3. Calcium (derived from platelet dense granules)
27
Q

What factors make up the intrinsic pathway? What activates the intrinsic pathway?

A

Factor XII -> XI -> IX -> VIII -> X

Activated by subendothelial collagen

28
Q

What factors make up the extrinsic pathway? What activates the extrinsic pathway?

A

Factor VII -> X

Activated by thromboplastin

29
Q

What lab measure assesses the extrinsic pathway, and which lab measure assesses the intrinsic pathway?

A

Extrinsic pathway is assessed by prothrombin time (PT) while intrinsic pathway is assessed by partial thromboplastin time (PTT)

30
Q

What factors make up the common pathway of the coagulation cascade?

A

X -> V -> II -> I (II = thrombin and I = fibrin; technically Ia is fibrin and is cleaved due to thrombin)

31
Q

What factors are activated by thrombin?

A

Thrombin converts fibrinogen into fibrin which allows for clotting. Also activates factor XI, VIII and V. Also, XIII which cross links fibrin.

32
Q

How does thrombin lead to platelet activation?

A

Via activation of protease-activated receptors (PARs)

33
Q

How does thrombin mediate proinflammatory effects?

A

PARs are on immune cells in addition to being present on platelets and mediates these proinflammatory effects

34
Q

What genetic defect is present in hemophilia A? What lab result (PT or PTT) would you expect to be abnormal?

A

Factor VIII deficiency. Part of the intrinsic pathway so PTT should be abnormal (is elevated) and PT normal.

35
Q

What genetic defect is hemophilia B a result of?

A

Factor IX deficiency (also resembles hemophilia A because it is also part of the intrinsic pathway)

36
Q

What causes coagulation factor inhibitor disease?

A

Is a result of an acquired antibody against a coagulation factor resulting in impaired factor function. mostly against factor VIII (thus resembles hemophilia A)

37
Q

Which factors require vitamin K?

A

factors II, VII, IX, X and proteins C and S where gamma carboxylation is needed for functioning protein.

38
Q

What is warfarin’s mechanism of action?

A

Inhibits vitamin K synthesis and thus

39
Q

Is tissue plasminogen activator a coagulation promoter or inhibitor?

A

tPA inhibits coagulation via conversion of plasminogen to plasmin on endothelial cells which breaks clots.

40
Q

What prevents the activity of plasmin?

A

alpha2-antiplasmin

41
Q

How does liver failure lead to abnormal secondary hemostasis?

A
  1. Decreased production of the coagulation factors.

2. Decreased activation of vitamin K by epoxide reductase

42
Q

What is the molecule that inactivates thrombin? What organ produces it?

A

Antithrombin III made by the liver and is activated by heparin-like molecules on endothelial cells.

43
Q

What is the mechanism of action of heparin?

A

Is an anticoagulant that potentiates the antithrombin III activity

44
Q

How does protein C inhibit clotting and what is its required cofactor (and what do both of these factors require)?

A

Protein C is made by the liver, requires cofactor of protein S and both protein C and S are vitamin K dependent. Inhibits clotting factors Va and VIIIa

Cell Pathology 2 (Pathology) (9 decks)

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