Unit IV Flashcards

1
Q

Factor XIII is a ___ that forms ___ bonds between ___ and ____ residues

A

transglutaminase
amide
lysine and glutamine

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2
Q

TF is expressed by

A

fibroblasts and smooth muscle cells surrounding blood vessels

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3
Q

Structure of fibrinogen

A

3 pairs of polypeptide chains (2
Aα-chains, 2 Bβ-chains, and 2 γ-chains)
arranged into identical half molecules in an
elongated polypeptide composed of three
globules: a central globule (labelled the E
domain) containing the N-terminal domain
of all of the polypeptides, and globules on
each end of the molecule, designated D
domains

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4
Q

Factor XIII cross links ___ domains

A

D

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5
Q

What happens to the phospholipid membrane during platelet activation?

A

anionic phospholipid phosphatidylserine translocated from inner to outer leaflet

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6
Q

Abnormal test in thrombocytopenia

A

platelet count

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7
Q

abnormal test in platelet dysfunction

A

bleeding time

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8
Q

abnormal test in hemophilia

A

APTT

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9
Q

abnormal test in factor VII def

A

APTT

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10
Q

abnormal test in dysfibrinogenemia

A

Thrombin clotting time (TCT)- fibrinogen defects

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11
Q

abnormal test in hypofibrinogenemia

A

fibrinogen

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12
Q

Only vitamin K dependent factor that is not a serine protease

A

Protein S

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13
Q

Homozygous protein C deficiency

A

fatal in neonates

neonatal purpuea fulminans

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14
Q

Tissue factor pathway inhibitor expressed by

A

constitutively by endothelial cells

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15
Q

Plasmin cleaves

A

both fibrionogen and fibrin

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16
Q

t-PA is a poor activator of plasmin in the absence of ____

A

fibrin

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17
Q

Thrombin-activatable fibrinolysis inhibitor mechanism

A
  • factor XIII covalently attaches it to fibrin
  • cleaved to active form by thrombin-thrombomodulin complex
  • removes C terminal of fibrin polecules and FDPs
  • reduces plasminogen binding sites on fibrin
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18
Q

Plasminogen activator inhibitor-q (PAI-1) is present in

A

alpha granules of platelets

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19
Q

Deficiency in alpha 2 antiplasmin causes

A

bleeding disorder

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20
Q

two things that cause abnormal bleeding times

A
  1. decrease in platelet count

2. VW disease

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21
Q

Post operative hemorrhage in Ashkenazi Jew or middle eastern, possibly after prostectomy

A

Factor XI deficiency

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22
Q

Most common acquired factor inhibitor

A

factor VIII

- antibody to it

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23
Q

In a lab test of Factor VIII, the ___ will be abnormal. When you do a mixing study what will happen?

A

PTT

It will not correct

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24
Q

Prognosis of Factor VII def

A

excellent long term

25
Q

Most significant lab findings of DIC

A
  • fibrinogen level has decreased markedly and the platelet count is low
26
Q

Syndrome caused by lupus anticoagulant

A

antiphospholipid antibody syndrome

27
Q

The lupus anticoagulant prolongs the ___. Why?

A

PTT

IgG antibody binds the phospholipid that is added to test tube to start the reaction

28
Q

Normal plasma mixed with plasma from patient with lupus anticoagulant->

A

PTT does not correct

29
Q

Lupus coag + phospholipid and repeat PTT

A

partial correction

30
Q

Other method of detecting lupus anticoagulant

A

dilute Russell’s Viper Venom Test

31
Q

Why should you not give whole blood Group O even though it is the universal donor?

A

Contains anti-B and A antibodies

32
Q

Antibody to mono reacts to

A

horse red blood cells

33
Q

antibody to syphilis reacts to

A

phosphodiester group in bacterium Treponema pallidum

and cardiolipin from beef heart

34
Q

AIDS is diagnosed when CD4 levels fall below

A

200/microliter

35
Q

Least likely infections in HIV

A

High grade extracellular pathogens

- maintained ability to make Tfh independent antibody responses

36
Q

Standard antiretroviral therapy uses 2 _ and

A

NRTIs and a third drug from a different class

37
Q

Postthrombotic syndrome following DVT

A
  • chronic venous insufficiency and chronic venostasis

- extremities become chronically wollen and show dark skin discoloration

38
Q

DVT restricted to calf veins

A

clinically insignificant

39
Q

DVT of popliteal of more proximal veins

A

stongly associated with PE

40
Q

Common studies for PE

A

CT and V/Q scan

41
Q

Arterial thrombi treatment

A
  • heparin (further prevent clot formation)

- fibrinolytic agent (to lyse existing clot)

42
Q

Treatment of venous thrombi

A

since activation of the coagulation cascade and formation of a fibrin clot is the main
pathophysiologic mechanism, agents that inhibit coagulation are indicated

43
Q

With arterial thrombi the

pathophysiology of thrombus formation is primarily related to

A

platelet activation and aggravation

** therefore treat with antiplatelet in long term setting

44
Q

Dabigatran etexilate

A

Pradaxa

- direct inhibitor of thrombin

45
Q

Apixaban and rivaroxaban

A

(Eliquis and Xarelto_

- directly inhibit factor Xa

46
Q

Antiplatelet drugs are used to treat

A

acute coronary syndrome

47
Q

3 general classes of anti-platelet drugs

A
  1. platelet products (aspirin)
  2. prevent activation/aggregation (ADP receptor antagonists)
  3. Block adhesion proteins (glycoprotein IIb/IIIa inhibitors)
48
Q

Thienopyridines (3)

A

ADP receptor antagonists

  1. clopidogrel
  2. ticlopine
  3. prasugrel
49
Q

Onset of action thienopyridines

A

slow onset of action

50
Q

Onset of action ticagrelor

A

more rapid action than thienopyridines

51
Q

3 GPIIb/IIIa

A
  1. abciximab- Monoclonal Ab, given IV
  2. Eptifibatide
  3. Tirofiban
52
Q

Indications for cryoprecipitate use

A

low or absent fibrinogen

53
Q

Transfuse PRBCs

A

4 hours

54
Q

Problem with using cryoprecipitate

A

IgM isoagglutinins can also be concentrated and cause hemolysis

55
Q

Delayed hemolytic reactions due to

A

alloantibody production

56
Q

Acute lung injury within 6 hours of infusion->

A

Transfusion related lung injury

57
Q

Transfusion associated circulatory overload (TACO)

A

fluid overload related to excessive amounts of products and or/ cardiac dysfunction

58
Q

Drug used in treatment of Philadeplephia chrom neg ALL that uses BiTE

A

blinatumomab

59
Q

mABs in transplant are directed to ___ and ____

A

CD3 and IL-2 receptor