Heme Flashcards

1
Q

How are the mechanisms of unfractionated heparin and LWMH the same? Different?

A

Both bind ATIII

heparin-ATIII inhibits thrombin and Xa equally

LMWH-ATIII preferntially inhibits Xa

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2
Q

What are the two types of HIT?

A

type I: mild, caused by platelet aggregation

type II: severe, caused by activated platelets that adhere, aggregate, and forms clots

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3
Q

What are the vitamin K-dependent clotting factors affected by Coumadin?

A

II, VII, IX, and X

protein C and S

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4
Q

How does DDAVP improve hemostasis?

A

increaes plasma levels of vWF and factor VIII

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5
Q

What does cryoprecipitate contain?

A

vWF, factor VIII, factor XIII, and fibrinogen

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6
Q

How should subsequent transfusion be managed when a patient has received emergency release whole blood?

A

After two units, the patient should continue to get type O blood because they will accumulate anti-A and anti-B antibodies.

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7
Q

How does recombinant factor VII facilitate hemostasis?

A

It directly activates factor X on activated platelets (independent of factors VIII and IX) and causes a “thrombin burst” and a stable fibrin clot

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8
Q

What are the three pedominant roles of vWF in hemostasis?

A

binding platelets to the subendothelium (via GPIb)

binding activated platelets to each other (via GPIIb/IIIa)

stabilizing carrier for inactive factor VIII

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9
Q

What are the three types of von Willebrand’s disease?

A

type 1: mild deficiency of normal vWF

type 2: mutant vWF (mostly affecting multimerization)

type 3: severe deficiency of normal vWF

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10
Q

What type of von Willebrand’s disease is responsive to ddAVP?

A

type 1

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11
Q

What is the primary activator of factor X on the platelet surface?

A

complex of factors VIII and IX

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12
Q

How does platelet aggregation occur?

A

GPIIb/IIIa receptors are exposed on activated platelets and crosslinked by vWF and fibrinogen

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13
Q

What is the role of factor XIII in coagulation?

A

cross-polymerization of fibrin to form a firmer clot

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14
Q

What is the role of factor V in coagulation?

A

co-factor for factor Xa to achieve thrombin activation

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15
Q

What factors limit clot extension?

A

tissue factor pathway inhibitor blocks tissue factor actiation of factor X

protein C (and co-factor protein S) inactivate factor Va and factor VIIIa

tPA initiates fibrinolysis

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16
Q

Why might patients with hemophilia A fail to respond to factor VIII infusion? How can they be managed?

A

30% will develop a neutralizing antibody

can treat with recombinant factor VII, IVIG, plasma exchange

17
Q

What are the indications for FFP?

A

factor deficiency

reversal of coumadin

ATIII deficiency

hereditary angioedema (if C1-esterase inhibitor unavailable)

massive transfusion

18
Q

Can TXA be used in patients with hemophilia A?

A

Yes, but only documented to be effective with minor bleeding

19
Q

What kinds of bleeding are best treated by recombinant factor VII?

A

bleeding confined to a few localized sites, not diffuse bleeding

20
Q

How long are factor VIII levels supplemented after surgery in patients with hemophilia A?

A

2-4 weeks

21
Q

What part of the hemoglobin molecule is affected by sickle cell anemia?

A

beta globin chain

22
Q

What are the four kinds of sickle cell crises?

A

vaso-occlusive

splenic sequestration

aplastic (usually parvovirus B19)

hemolytic (usually with G6PD deficiency)

23
Q

What is acute chest syndrome? How is it treated?

A

New infiltrate and pulmonary symptoms similar to PNA often following a vaso-occlusive crisis

Treat with antibiotics, bronchodilators, and exchange transfusion

24
Q

What are the pre-operative transfusion goals for sickle cell anemia?

A

Hgb > 8

Hgb A fraction > 40%

25
Q

What are the anesthetic considerations particular to sickle cell anemia?

A

maintain O2 content

maintain normothermia

avoid acidosis

avoid touriquet use

avoid venous stasis

avoid hypovolemia