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IHO Week 5 > Clotting Disorders > Flashcards

Clotting Disorders Flashcards

1
Q

When a clot breaks free it is called an:

A

embolus

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2
Q

What are the risk factors for atherosclerosis?

A

Hypertension
Hyperlipidemia
Obesity
Smoking

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3
Q

What are the risk factors for stasis?

A

Immobilization
Varicose veins
Cardiac dysfunction

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4
Q

What are the risk factors for hypercoagulability?

A

Trauma/surgery
Carcinoma
Estrogen/postpartum
Thrombotic disorders

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5
Q

What is the most common cause of unexplaned thromboses

A

Factor V leiden

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6
Q

What is the problem with the factor V gene in Factor V Leiden?

A

Protein can’t be turned off

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7
Q

What factor cleaves factor V (and can’t cleave it if the mutation is there?

A

Protein C

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8
Q

Why are PTT and INR not helpful in diagnoses of Factor V Leiden?

A

PTT and INR will be normal because the protein works fine

Genetic testing is needed

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9
Q

How do you treat Factor V leiden?

A

Don’t unless there’s a thrombosis, then give anticoagulant for a while

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10
Q

A deficiency in this protein will result in a significantly decreased effect of heparin.

A

ATIII

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11
Q

What is the result of the mutation in the ATIII gene that causes ATIII deficiency?

A

Makes LESS ATIII

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12
Q

Homozygotes of ATIII deficiency have this prognosis:

Heterzygotes of ATIII deficiency have this prognosis:

A

Homozygotes: Will not survive into infancy
Heterozygotes: Half get clots

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13
Q

Along with being an anticoagulant, protein C has these two effects:

A

Firbinolytic (promotes t-PA), anti-inflammatory (decreased cytokines)

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14
Q

What happens to someone with a Protein C deficiency when given warfarin?

A

Warfarin induced skin necrosis

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15
Q

What is the role of protein S?

A

Endothelial cell receptor for protein C

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16
Q

What is requried for diagnosis of protein C deficiency

A

functional testing

17
Q

If you give this drug to someone with a protein C deficiency, they will very likely get skin necrosis.

A

Coumadin

18
Q

What is purpura fulminans?

A

A thrombotic state associated with vascular injury, resulting in skin necrosis

19
Q

How do you treat purpura fulminans?

A

Give protein C

20
Q

What is the result of the gene deficiency in which factor II (prothrombin) is the culprit?

A

Makes TOO MUCH prothrombin

21
Q

Too much homocysteine results in what vascular effect?

A

thromboses

22
Q

What is the most common gene defect for homocysteinemia?

A

MTHFR: Methylene tetrahydrofolate reductase

23
Q

What are the other two enzyme defects known for hyperhomocysteinemia?

A

Methionine synthase

Cystathionine beta synthase

24
Q

What enzyme is deficient in homocysteinuria?

A

Trans-sulphuration enzyme

25
Q

What is the effect of homocysteinuria?

A

Increased homocysteine in blood and urine

Increased thrombosis, premature artherosclerosis

26
Q

What dietary deficiency can result in homocysteinemia?

A

B12/folate deficiency

27
Q

What are the two distinct toxicities to increased homocysteine levels?

A

Toxic to endothelium, forms ROS

Interferes with NO, which is a vasodilater and antithrombotic

28
Q

When a patient has antibodies against phospholipids, what tests are deceitful?

A

INR is falsely prolonged
PTT/PT reagents bound
DAT test and syphilis tests screwed up

29
Q

What is different about coagulation in vivo/in vitro for Antiphospholipid antibodies?

A

Promote coagulation in vivo

Inhibit coagulation in vitro

30
Q

What are the main results of antiphospholipid antibody syndrome? (5)

A 
Recurrent thrombosis
Recurrent spontaneous abortion
Increased risk of stroke
Pulmonary hypertension
Renal failure
31
Q

What is the more definitive test to find antiphospholipid antibody syndrome

A

PTT mixing study

IHO Week 5 (9 decks)

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