BL Hereditary and Acquired Thrombotic disorders Flashcards Preview

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Flashcards in BL Hereditary and Acquired Thrombotic disorders Deck (23):
1

Virchows triad

3 factors that promote thrombosis
1. abnormal blood flow
2. endothelial injury
3. hypercoagulability

- only 1 needs to be present for thrombosis to occur

2

factor V Leiden affects clotting how?

makes clotting harder to turn off --> hypercoagulability

3

disseminated cancer affects clotting how?

makes you more likely to cloth

4

Arterial thrombi:
- Are blood clotting factors or platelets more imp?
- Occurs under high shear stress or slow blood flow?
- Can cause ischemia or not?
- Affected by oral contraceptives?

Arterial:
○ Platelets more imp.
○ Occur in high shear stress
○ If large enough, cause downstream ischemia
○ No - venous thrombi affected by oral contra

5

Venous thrombi:
- Are blood clotting factors or platelets more imp?
- Occurs under high shear stress or slow blood flow?
- More common in young or old?
- Affected by oral contraceptives?

○ Blood clotting factors - Large amounts of fibrin with lots of RBCs (red thrombi)
○ Slow blood flow (stasis)
○ More common with increased age
○ Yes to oral ;)

6

three major clinical symptoms that occur when a patient suffers from an acute iliofemoral thrombosis of the leg

Edema with pain
Dilated superficial veins
Redness and warmth in the area

7

How does Edema with pain occur after an acute iliofemoral thrombosis of the leg?


a. Impaired venous return - "backed up" blood
b. Pain comes from increased hydrostatic pressure

8

How do Dilated superficial veins occur after an acute iliofemoral thrombosis of the leg?

the blood finds another route

9

How does Redness and warmth in the area occur after an acute iliofemoral thrombosis of the leg?

Formation of thrombus triggers an inflammatory response

10

Is Factor V Leiden a deficiency disorder?

No! - it is an Autosomal dominant structural change in factor V

Normally thrombin cleavage leads to Factor V activation (Va), and then APC inactivates Va.

In Factor V Leiden, Factor V is mutated and cannot be inactivated --> hypercoagulability (make more clotting factors!)

11

How do you diagnose Factor V leiden?

DNA analysis

12

Prothrombin Gene Mutation
- leads to increased or decreased prothrombin?
- Assoc. with venous or arterial thrombosis?
-Randomly triggered?

• Polymorphism leads to ↑ prothrombin in circulation
○ Remember that prothrombin leads to more thrombin, which leads to clots. BOOM.
• Associated with venous thrombosis

Most people with the mutation don't clot - need something else to trigger your clot. Not just out of the blue

13

Type I vs Type II antithrombin

○ Type I: ↓ level of protein
○ Type II: ↓ activity (can't bind heparin)

14

Is warfarin used to prevent additional clots?

Yes, but NOT break down already formed cloths

15

If your patient is Protein C deficient, what drug would you give them?

Warfarin bc pt is hypercoagulable, but bridge the therapy with heparin to prevent warfarin induced necrosis

□ Note: warfarin not effective until turnover of the factors because warfarin inhibits activity of vit K, not the factors themselves.→ that's why we give heparin (inactivates activated clotting factors) for ~5 days

16

What factor has the shortest half life? Why is this useful?

VII - 5 hours

good to view a consumptive process

17

Natural anticoagulants

AT III
Protein C
Protein S

18

How do you acquire Protein S deficiency?

○ Pregnancy
○ Active thrombosis
○ DIC
○ Nephrotic syndrome
○ Warfarin use
○ Oral contraceptives

19

Is antiphospholipid antibody syndrome an acquired hypercoagulable state or hemorrhagic state?

Severe hypercoagulable state

20

antiphospholipid antibody syndrome

○ This is a syndrome where thrombotic or obstetric complications are caused by antibodies
○ Can see both venous and arterial thrombosis
○ Can see in any vascular bed, at any age, in any gender

○ Related to drug exposure, infection, and illness

21

Clinical criteria for antiphospholipid antibody syndrome

• Vascular thrombosis:
1+ clinical episodes of thrombosis

• Complications of pregnancy:
1+ unexplained death of fetus > 0 wks
1+ premature births of neonates <10 wks

22

Treating venous thrombi
- Acute vs long term

Use anticoagulant agents

○ Acute:
§ Unfractioned or low molecular weight heparin

○ Long term:
§ Low molecular weight heparin
§ Oral anticoagulation such as warfarin

23

clinical clues suggesting an inherited hypercoagulable disorder.

1. first thrombosis before 50
2. get recurrent thrombosis
3. family hx
4. Neonatal thrombosis
5. idiopathic thrombosis
6. thrombosis at rare sites