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Flashcards in Freeman: Coag Deck (37):
1

What does it mean if you have factor V leiden? What happens to patients with Factor V Leiden?

you have a mutation in factor 5, so you can't bind protein C and cannot degrade factors 5a and 8a, so you get a state of hypercoagulation; usually nothing happens to these patients; however, if they have other predisposing symptoms, then they will be at increased risk of hypercoagulation (clotting)

2

What are these?

Obesity
Sedentary life-style
Travel
BCP’s
Pregnancy
Surgery
*elective, particularly
ortho
Smoking
Prior DVT

modifiable risks for hypercoagulation

3

What are these?

Factor V Leiden
Prothrombin Gene Mutation
Malignancy
Surgery
*emergent
Chronic Illness
Lupus Anticoagulant

unmodifiable risks for hypercoagulation

4

How long must patients be kept on heparin?

7-10 days, even if you start the heparin with coumadin

5

What are the Vit K dependent coagulation factors?

2, 7, 9, 10
protein C and protein S

6

Why must a patient who is on both heparin and coumadin be kept on heparin for 7-10 days?

because coumadin takes a while to take effect, because it works on the Vit K dependent coag factors (2, 7, 9, 10, protein C and S) - these factors have long half-lives, so if you give coumadin, some coag factors will still be floating around for awhile

7

Patients require (blank) days of full heparinization regardless of
when adequate coumadinization
occurs.

7-10

8

Is lupus anticoagulant an anticoagulant?

no! it's actually a procoagulant in vivo

9

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.

Heparin induced thrombocytopenia Type I

10

What is this?

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

HIT Type II

11

What is the major problem with heparin induced thrombocytopenia?

the creation of a prothrombotic state, which can occur even after heparin has been discontinued

**seen most commonly in major surgery

12

What is the paradox with HIT?

can cause thrombocytopenia and thrombosis

**thrombosis w/ declining platelets seen in 50% of pts w/ recent hospitalization

13

This should be considered in all recently hospitalized patients returning w/ acute thrombosis w/i 1-2 weeks of their hospital stay

HIT

14

When is HIT most likely to occur?

in surgical patients, as opposed to medical patients

15

Widespread activation of the clotting cascade causing a consumption of clotting factors and platelets w/resultant bleeding

DIC

16

Thrombin formation causes microvascular compromise and results in tissue ischemia with resultant organ damage

DIC

17

Things that can trigger DIC

gram - septicemia (gram + too)
damaged cerebral tissue
damaged cerebral tissue
placental tissue from obstetric catastrophies
snake venoms
acute hemolytic transfusion rxns
massive tissue injury

18

3 things that can activate the coagulation cascade

endotoxin
IL-I
TNF

**these lead to the release of tissue factor

19

What happens to the following in DIC?

PT/PTT
platelets
fibrinogen
D-dimer

increased PT/PTT
decreased platelets
decreased fibrinogen
increased D-dimer

20

How do you treat DIC?

treat the underlying condition

ex: if secondary to bacterial infection, give antibiotics

21

5 things that can cause major bleeding

trauma
infections
drugs
disorders of coagulation systems
disorders of organ systems

22

3 cases in which you might get a prolonged PT

malnutrition
liver disease (decreased synth of Vit K)
coumadin

23

3 cases in which you might get a prolonged PTT?

lupus anticoagulant/acquired factor inhibitors
factor 8/9 deficiency or inhibitor
heparin

24

Type 1 von Willebrand Disease is a (blank) deficiency

quantitative

25

Type 2 von Willebrand Disease is a (blank) deficiency

qualitative

26

Type 3 von Willebrand Disease is a (blank) deficiency

total

27

Factor 8 can be thought of as two distinct molecules

Factor 8 vWD
Factor 8 hemophilia

28

What are the 2 major roles of factor 8 vWD?

1. carrier protein for factor 8
2. platelet adhesion to sites of vascular injury

29

What is the major role of factor 8 hemophilia?

procoagulation

30

In which disease would you see mucosal "oozing" after surgery or trauma?

von Willebrand disease, because there is no platelet adhesion to sites of vascular injury

31

In which disease would you see spontaneous hemarthroses, or bleeding into muscles and joints?

hemophilia

32

How do you treat mild cases of vWD? What else can you use?

DDAVP (increases endogenous release of vWF by stimulating endothelial cells); factor 8 replacement

33

this disorder is due to an autoantibody directed against ADAMTS13, a metalloproteinase involved in the normal processing of von Willebrand factor

TTP

34

What are symptoms of TPP?

thrombocytopenia
microangiopathic hemolytic anemia
renal insufficiency
fever

35

2 important lab abnormalities in TPP?

thrombocytopenia
schistocytes (due to microangiopathic hemolytic anemia)

36

What are some causes of TPP? Why do you get this auto-antibody to ADAMTS13?

E. Coli 0:157
idiopathic
other autoimmune disease
drug-associated (ex: quinine)
pregnancy/postpartum

37

Why does heparin cause thrombosis?

So, heparin can cause HIT. HIT is caused by IgG antibodies binding to the heparin-PF4 complex. Heparin-PF4 antibodies activate platelets, causing the release of prothrombotic platelet-derived microparticles, platelet consumption, and thrombocytopenia. The microparticles in turn promote excessive thrombin generation, frequently resulting in thrombosis.