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
Most significant lab findings of DIC
- fibrinogen level has decreased markedly and the platelet count is low
26
Syndrome caused by lupus anticoagulant
antiphospholipid antibody syndrome
27
The lupus anticoagulant prolongs the ___. Why?
PTT | IgG antibody binds the phospholipid that is added to test tube to start the reaction
28
Normal plasma mixed with plasma from patient with lupus anticoagulant->
PTT does not correct
29
Lupus coag + phospholipid and repeat PTT
partial correction
30
Other method of detecting lupus anticoagulant
dilute Russell's Viper Venom Test
31
Why should you not give whole blood Group O even though it is the universal donor?
Contains anti-B and A antibodies
32
Antibody to mono reacts to
horse red blood cells
33
antibody to syphilis reacts to
phosphodiester group in bacterium Treponema pallidum | and cardiolipin from beef heart
34
AIDS is diagnosed when CD4 levels fall below
200/microliter
35
Least likely infections in HIV
High grade extracellular pathogens | - maintained ability to make Tfh independent antibody responses
36
Standard antiretroviral therapy uses 2 _ and
NRTIs and a third drug from a different class
37
Postthrombotic syndrome following DVT
- chronic venous insufficiency and chronic venostasis | - extremities become chronically wollen and show dark skin discoloration
38
DVT restricted to calf veins
clinically insignificant
39
DVT of popliteal of more proximal veins
stongly associated with PE
40
Common studies for PE
CT and V/Q scan
41
Arterial thrombi treatment
- heparin (further prevent clot formation) | - fibrinolytic agent (to lyse existing clot)
42
Treatment of venous thrombi
since activation of the coagulation cascade and formation of a fibrin clot is the main pathophysiologic mechanism, agents that inhibit coagulation are indicated
43
With arterial thrombi the | pathophysiology of thrombus formation is primarily related to
platelet activation and aggravation ** therefore treat with antiplatelet in long term setting
44
Dabigatran etexilate
Pradaxa | - direct inhibitor of thrombin
45
Apixaban and rivaroxaban
(Eliquis and Xarelto_ | - directly inhibit factor Xa
46
Antiplatelet drugs are used to treat
acute coronary syndrome
47
3 general classes of anti-platelet drugs
1. platelet products (aspirin) 2. prevent activation/aggregation (ADP receptor antagonists) 3. Block adhesion proteins (glycoprotein IIb/IIIa inhibitors)
48
Thienopyridines (3)
ADP receptor antagonists 1. clopidogrel 2. ticlopine 3. prasugrel
49
Onset of action thienopyridines
slow onset of action
50
Onset of action ticagrelor
more rapid action than thienopyridines
51
3 GPIIb/IIIa
1. abciximab- Monoclonal Ab, given IV 2. Eptifibatide 3. Tirofiban
52
Indications for cryoprecipitate use
low or absent fibrinogen
53
Transfuse PRBCs
4 hours
54
Problem with using cryoprecipitate
IgM isoagglutinins can also be concentrated and cause hemolysis
55
Delayed hemolytic reactions due to
alloantibody production
56
Acute lung injury within 6 hours of infusion->
Transfusion related lung injury
57
Transfusion associated circulatory overload (TACO)
fluid overload related to excessive amounts of products and or/ cardiac dysfunction
58
Drug used in treatment of Philadeplephia chrom neg ALL that uses BiTE
blinatumomab
59
mABs in transplant are directed to ___ and ____
CD3 and IL-2 receptor