Hematology Flashcards

1
Q

Which factor is the convergence point and common to both the intrinsic and extrinsic pathways?

A

Factor X

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2
Q

What is the function of fibrin?

Which factor cross links fibrin?

A

It combines with platelets to form a platelet plug, resulting in hemostasis.

Factor XIII helps cross link fibrin

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3
Q

What are the three functions of thrombin?

A
  1. Platelet activation
  2. Activation of factor V and VIII
  3. Converts fibrinogen to fibrin
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4
Q

What are the three functions of antithrombin III?

A
  1. Inhibits factors IX, X, and XI
  2. Bonds to and inhibits thrombin
  3. Binds to heparin
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5
Q

How do proteins C and S work?

A

Protein C: degrades fibrinogen, and factors V and VIII
Protein S: cofactor of protein C

both are vitamin k dependent

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6
Q

What does tissue plasminogen activator do?

A

Converts plasminogen into plasmin

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7
Q

What is the function of plasmin?

A

It degrades factors V and VIII, fibrinogen, and fibrin

- alpha 2 anti plasmin naturally inhibits plasmin

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8
Q

Which factor is the only one not synthesized by the liver?

Where is it synthesized?

A

Factor VIII

It is synthesized in the endothelium

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9
Q

What are the vitamin k- dependent factors?

A

Factors II, VII, IX, X, proteins C and S

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10
Q

What’s the normal half life of RBCs? Of platelets? Of PMNs?

A

RBCs: 120 days
Platelets: 7 days
PMNs: 1-2 days

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11
Q

What’s the function of thromboxane? Where is it released from?
What’s the mechanism of action?

A

Thromboxane causes vasoconstriction and increases platelet activation.

  • it is released by platelets
  • MoA: triggers calcium release, resulting in exposure of GpIIb/IIIa receptor, which allows for platelet-platelet and platelet-collagen binding
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12
Q

What is prostacyclin’s (PGI2) role?

A

Decreases platelet aggregation and promotes vasodilation

- it is releases by endothelium

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13
Q

What is the composition of cryoprecipitate?

When is it used?

A
  1. Cryoprecipitate is composed of: vWF, factor VIII, fibrinogen, and factor XIII
  2. It is used in Von Willebrand’s disease and hemophilia A
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14
Q

What is FFP composed of?

A

All factors, protein C, protein S, and antithrombin III

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15
Q

How does DDAVP work in terms of coagulation?

What other medication works the same way?

A
  1. DDAVP causes release of vWF and factor VIII from endothelium
  2. Conjugated estrogens work in the same way
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16
Q

What does prothrombin complex consist of?

A

Factor X, V, platelet factor 3, and prothrombin

- catalyze formation of thrombin

17
Q

What factors does PT measure?

A

Factors II, V, VIII, and X

- it is the best measure for liver synthetic fxn

18
Q

What factors does PTT measure?

A

All but factors VII and XIII

- doesn’t pick up factor VIII deficiency

19
Q

What’s the therapeutic range of PTT for anticoagulation

A

PTT: 60-90 sec

20
Q

What’s the function of von Willebrand factor?

A

Links GpIb receptor on platelets to collagen

21
Q

What bleeding test is/are abnormal for Von Willebrand’s disease

A

Bleeding time (ristocetin test)

22
Q

How many types of von Willebrand’s disease are there? What’s the treatment for each?

A

Three types

  • types I and III: due to reduced quantity circulating vWF
    • treatment: recombinant VIII, DDAVP, cryoprecipitate,conjugated estrogen
  • type II: defect in vWF
    • treatment: recombinant VIII, cryoprecipitate
23
Q

What’s the difference between hemophilia A and B? Which blood tests are abnormal? What are the treatment differences?

A

Hemophilia A: deficiency in factor VIII
- treatment: cryoprecipitate, recombinant VIII

Hemophilia B: deficiency in factor IX
- treatment: factor IX concentrate, FFP

PTT Prolonged and PT normal in each

24
Q

What bleeding studies are abnormal in factor VIII deficiency? What’s the treatment?

A

Prolonged PT, normal PTT

- treatment: FFP, recombinant factor VII

25
Q

What’s Glanzmann’s thrombocytopenia? What’s the treatment?

A

Deficiency in GpIIb/IIIa receptor on platelets resulting in inability of platelets to bind to each other
- treatment: platelets

26
Q

What’s Bernard Soulier disease? What’s the treatment?

A

Deficiency of GpIb receptor on platelets resulting in inability of platelets to bind to collagen
- treatment: platelets

27
Q

What lab abnormalities are seen with DIC?

A

Decreased platelets, prolonged PT, prolonged PTT, low fibrinogen, high d-dimer, high fibrin split products

28
Q

IgG PF4 is associated with which pathological process? What is the treatment?

A

Heparin induced thrombocytopenia

Stop heparin, anticoagulation with argatroban

29
Q

What is the pathophysiology of Factor V Leiden deficiency? What’s the treatment?

A

Defect of factor V and resistance to activated protein c, leading to hypercoagulability.

Treatment: heparin, warfarin

30
Q

Hyperhomocysteinemia causes 10% of spontaneous venous thromboses. What is the treatment?

A

Treatment: vitamin b12 and folate

31
Q

Other diseases causing hypercoagulability that are deficiencies in what, and deficit in which gene?

A

Protein C or S deficiency and defect in the prothrombin gene

32
Q

Treatment of antithrombin III is

A

Treatment: recombinant antithrombin III, followed by heparin, and then warfarin
- can develop after exposure to heparin

33
Q

Treatment of polycythemia vera:

A

Give aspirin

- also, goal is to keep hct

34
Q

What is the treatment for DVT?

A

1st: Coumadin for 6mo
2nd; Coumadin for 1yr
3rd or significant PE: lifetime Coumadin

35
Q

Indications for IVC filter placement:

A
  1. Contraindication to anticoagulation
  2. Documented PE while on anticoagulation
  3. Free-floating iliofemoral, IVC, or femoral DVT
  4. Those who have undergone pulmonary embolectomy
36
Q

How do you treat a PE?

A

If coded and in shock (despite inotropes): OR

Otherwise, heparin or suction-catheter based intervention