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Block 7 Week 4 > Coagulation-Freeman > Flashcards

Flashcards in Coagulation-Freeman Deck (90)
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1

(blank) pathway is the main system that causes clotting

Extrinsic pathway

2

Why do you get hypercoag because of factor V Leiden?

In this disorder, the Leiden variant (form) of factor V cannot be inactivated (switched off) by activated protein C, and so clotting is encouraged

3

What does normal factor 5 do?

APC binds to factor V and cleaves it into 2 inactive fragments

4

(blank) thrombophilia is a genetically inherited disorder of blood clotting. It is a variant (mutated form) of human factor V that causes an increase in blood clotting (hypercoagulability)

Factor V Leiden

5

In the normal person, factor V functions as a cofactor to allow factor (blank) to activate an enzyme called thrombin. Thrombin in turn cleaves fibrinogen to form fibrin, which polymerizes to form the dense meshwork that makes up the majority of a clot. Activated protein C (aPC) is a natural anticoagulant that acts to limit the extent of clotting by cleaving and degrading factor V.

Xa

6

What is the incidence of factor V leiden?

3-8%

7

What is the risk of hypercoagulable in heterozyg of factor V leiden?

8X

8

What is the risk of hypercoagulable of homozy factor V leiden?

20X

9

What do heparins do?

bind to Anti thrombin III to block Xa

10

What is the key to degrading clots or preventing them?

inhibiting fibrin formation

11

(blank) and (blank) can cause vasoconstriction

epi and nicotine

12

What are the two components in flow dynamics?

mechanical and chemical

13

What are the components for flow dynamics?

prior sites of thrombus
compression (obesity)
chemical (nictone, vasoconstricting agents)

14

What are the modifiable factors for coagulation?

-Obesity
-Sedentary life-style
-Travel
-BCPs
-Pregnancy
-Surgery (elective)
-Smoking
-Prior DVT

15

What are the unmodifiable factors for coagulation?

-factor V leiden
-prothrombin gene mutation
-malignancy
-surgery (emergent)
-chronic illness
-lupus anticoagulant

16

The body need how many risk factors to clot?

4 (the body has a near perfect system to prevent clotting)

17

In acute thrombogenesis, what should you give patients?

7-10 days of full heparinization (LMWH) (regardless of coumadin levels)

18

What are the vit-K dependent factors?

2,7,9,10
Protein C/S

19

What is the 1/2 life of factor X?
What is the 1/2 life of protein C?

48H
6H
***notice that protein C has shorter half life so you might get a hypercoag state)

20

When can you initiate coumadin?

at time of heparin-> course of coumadin is based on etiology of thrombogenic event

21

(blank) anticoagulants may be seen at time of acute thrombotic events (acute phase reactants).

Lupus anticoagulants (LA)

22

Repeat serology is recommeneded (blank) months after acute events prior to making long-term therapeutic coumadin decisions.

3

23

Lupus anticoagulant is actually a (Blank)

pro-coagulant (misnomer)

24

If you have LA in vitro, what will you see?

prolonged PTT

25

If you have LA in vivo, what will you see?

procoagulant

26

If your patient has HIT what should you give them?

agatroban

27

What are the 2 types of HIT?

Type I and Type II

28

What is this:
modest, transient decrease in platelets 2/2 heparin-induced platelet agglutination. Self-limited; plt counts can return to normal while heparin is continued.

Type I HIT

29

What is this:
a drug-induced, immune-mediated response 2/2 abs directed against heparin-plt factor 4 complex that results in 50% or greater drop in platelet counts. Severe thrombocytopenia w/ bleeding is rare!

HIT (type II)

30

Severe hit involves heparain and what clotting factor?

factor 4