Freeman: Coag

Question 1

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

Answer 1

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)

Question 2

What are these?

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

Answer 2

modifiable risks for hypercoagulation

Question 3

What are these?

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

Answer 3

unmodifiable risks for hypercoagulation

Question 4

How long must patients be kept on heparin?

Answer 4

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

Question 5

What are the Vit K dependent coagulation factors?

Answer 5

2, 7, 9, 10

protein C and protein S

Question 6

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

Answer 6

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

Question 7

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

Answer 7

7-10

Question 8

Is lupus anticoagulant an anticoagulant?

Answer 8

no! it’s actually a procoagulant in vivo

Question 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.

Answer 9

Heparin induced thrombocytopenia Type I

Question 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!

Answer 10

HIT Type II

Question 11

What is the major problem with heparin induced thrombocytopenia?

Answer 11

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

**seen most commonly in major surgery

Question 12

What is the paradox with HIT?

Answer 12

can cause thrombocytopenia and thrombosis

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

Question 13

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

Answer 13

HIT

Question 14

When is HIT most likely to occur?

Answer 14

in surgical patients, as opposed to medical patients

Question 15

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

Answer 15

DIC

Question 16

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

Answer 16

DIC

Question 17

Things that can trigger DIC

Answer 17

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

Question 18

3 things that can activate the coagulation cascade

Answer 18

endotoxin
IL-I
TNF

**these lead to the release of tissue factor

Question 19

What happens to the following in DIC?

PT/PTT
platelets
fibrinogen
D-dimer

Answer 19

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

Question 20

How do you treat DIC?

Answer 20

treat the underlying condition

ex: if secondary to bacterial infection, give antibiotics

Question 21

5 things that can cause major bleeding

Answer 21

trauma
infections
drugs
disorders of coagulation systems
disorders of organ systems

Question 22

3 cases in which you might get a prolonged PT

Answer 22

malnutrition
liver disease (decreased synth of Vit K)
coumadin

Question 23

3 cases in which you might get a prolonged PTT?

Answer 23

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

Question 24

Type 1 von Willebrand Disease is a (blank) deficiency

Answer 24

quantitative

Question 25

Type 2 von Willebrand Disease is a (blank) deficiency

Answer 25

qualitative

Question 26

Type 3 von Willebrand Disease is a (blank) deficiency

Answer 26

total

Question 27

Factor 8 can be thought of as two distinct molecules

Answer 27

Factor 8 vWD

Factor 8 hemophilia

Question 28

What are the 2 major roles of factor 8 vWD?

Answer 28

1. carrier protein for factor 8

2. platelet adhesion to sites of vascular injury

Question 29

What is the major role of factor 8 hemophilia?

Answer 29

procoagulation

Question 30

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

Answer 30

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

Question 31

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

Answer 31

hemophilia

Question 32

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

Answer 32

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

Question 33

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

Answer 33

TTP

Question 34

What are symptoms of TPP?

Answer 34

thrombocytopenia
microangiopathic hemolytic anemia
renal insufficiency
fever

Question 35

2 important lab abnormalities in TPP?

Answer 35

thrombocytopenia

schistocytes (due to microangiopathic hemolytic anemia)

Question 36

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

Answer 36

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

Question 37

Why does heparin cause thrombosis?

Answer 37

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.