Hemeonc 7

Question 1

What 3 factors make up Virchow’s triad? And what is the end result?

Answer 1

1) hypercoaguability
2) Abnormal blood flow
3) Epithelial injury

Results in thrombosis

Question 2

What is the degradation product of fibrin clot? What does it mean if you find positive results of this on a lab test? Negative results?

Answer 2

D-dimer, positive is inconclusive, could mean many things. Negative would rule out a clot

Question 3

What would you expect to see on the CXR of a patient with a PE?

Answer 3

Nothing, most CXR’s are normal for PE. Rarely see infarction of pleural effusion

Question 4

What are the ideal tests for detecting VTE’s?

Answer 4

US, CT, VQ scan (MRI for brain only)

Question 5

What is the most common preventable cause of in-hospital death?

Answer 5

PE

Question 6

underlying predisposition to thrombosis

Answer 6

Thrombophilia

Question 7

For most people with thrombophilia, how would you adjust your treatment of a clot when compared to a patient without thrombophilia?

Answer 7

Treat them the same

Question 8

What are the 5 inherited thrombophilias?

Answer 8

Antithombin III deficiency
Protein C deficiency
Protein S deficiency
Factor V Leiden mutation
Prothrombin G20210A mutation

Question 9

What inhibits multiple clotting factors (natural anticoagulants)?

Answer 9

Antithrombin III (ATIII), it is a SERine Protease INhibitor (SERPIN)

Question 10

__________ disease can cause acquired ATIII deficiency, because that is where ATIII is synthesized.

Answer 10

Liver disease

Question 11

What is the Vit K dependent protein synthesized in the liver that is also a potent anticoagulant through inactivation of FVIIIa and FVa

Answer 11

Protein C (after it is activated and becomes “activated protein C”)

Question 12

Acquired Protein C deficiency is much more common than congenital. What could cause this?

Answer 12

Decreased synthesis (synthesized in liver, so liver dz, vit K deficiency, warfarin)
Increased turnover/consumption (DIC, sepsis, acute thrombosis)

Question 13

What is a co-factor used with protein C as a natural anticoagulator? It is also a Vit K dependent protein synthesized by liver, endothelium, megakaryocytes

Answer 13

Protein S

Question 14

Aquired Protein S deficiency is also much more common than congenital. What causes it?

Answer 14

Decreased synthesis
Increased consumption
PREGNANCY is much bigger risk factor

Question 15

What happens in the Prothrombin 20210 Gene Mutation?

Answer 15

Mutation essentially leads to increased prothrombin levels in the plasma, which consequently means more thrombin and more clots.

Question 16

What clinical signs would you expect from a patient with Prothrombin 20210 Gene Mutation? How would you diagnose it?

Answer 16

Recurrent VTE’s, multiple fetal losses.

Dx by DNA testing (common, 2% of Caucasians)

Question 17

Which inherited thrombophilia is associated with a resistance to the activated protein C? How common is this?

Answer 17

Factor V Leiden, fairly common 5% Caucasians are heterozygous for this mutation

Question 18

If you have a prolonged PTT and normal PT and your 1:1 mixture corrects, what do you suspect?
If it does NOT correct, what do you suspect?

Answer 18

Corrects: there is a clotting deficiency

Does NOT correct: there is NOT a clotting deficiency (Ex: Antiphospholipid Antibodies)

Question 19

What is a disorder in which your immune system mistakenly produces antibodies against certain normal proteins that bind a type of fat that plays a key role in coagulation? It can cause blood clots to form within your arteries or veins as well as pregnancy complications, such as miscarriages and stillbirths. Also associated with a red lacy rash.

Answer 19

Antiphospholipid Antibodies. Considered primary if there are no known autoimmune issues. Secondary in presence of Lupus, HIV, etc

Question 20

Unprovoked, ie idiopathic thrombosis are a red flag for what? What should you do for a patient who develops a clot for no obvious reason?

Answer 20

Malignancy, make sure they are UTD on all screenings

Question 21

Why does pregnancy place you at higher risk for thrombosis?

Answer 21

Virchow’s triad:
stasis (due to edema and being fat and tired)
hypercoaguability (body producing more clotting factors in preparation for birth)
endothelial injury (especially post partum)

Question 22

What is the “multiple hit theory”?

Answer 22

Thrombotic risk over time increases with age and multiple exposures to high risk clotting situations

Question 23

What disorder is characterized by long, uncleaved strands of von Willebrand Factor which attract aggregated platelets? It causes lots of “microclots” throughout the body which results in 1) consumptive thrombocytopenia and 2) microangiopathic hemolytic anemia (lots of schistocytes)

Answer 23

Thrombotic Thrombocytopenic Purpura (TTP)

Question 24

What deficiency is responsible for all the uncleaved von Willebrand factor in TTP?

Answer 24

ADAMPTS13 deficiency

Question 25

What is an alternate type of TTP that occurs in children with the frequent prodrome of diarrhea and renal insufficiency?

Answer 25

HUS--hemolytic uremic syndrome

Question 26

“white clot syndrome” refers to platelet-rich arterial thrombosis (rather than fibrin-rich venous thrombosis) Common in cardiac and orthopedic surgery patient who get exposed to frequent or long-standing heparin. Clots are often "micro clots"

Answer 26

Heparin induced thrombocytopenia (HIT)