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IHO Week 6 > Clotting disorders > Flashcards

Clotting disorders Flashcards

1
Q

thrombosis =

A

an abnormal clot

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2
Q

thrombosis risk factors

A

Endothelial damage
Stasis
Hypercoagulability

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3
Q

Endothelial damage is a result of

A

often atherosclerosis (hypertension, hyperlipidemia, smoking, obesity)

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4
Q

Stasis

A

Immobilization
varicose veins
cardiac dysfunction

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5
Q

Hypercoagulability

A

Trauma/surgery
Carcinoma
Estrogen/postpartum
Thrombotic disorder

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6
Q

When should you worry and your patient has a throbmus?

A 
No obvious cause
Family history
weird location
recurrent
young patient 
miscarriages
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7
Q

Hereditary thrombotic disorders

A 
Factor V Leiden
ATIII deficiency
Protein C deficiency
Protein S deficiency
Factor II gene mutation
Homocysteinemia
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8
Q

Acquired thrombotic disorder

A

Antiphospholipid Ab

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9
Q

About Factor V Leiden

A

Most common cause of unexplained thromboses
Point mutation in factor V gene
Factor V cannot be turned off
Need GENETIC testing for diagnosis

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10
Q

What happens when point mutation occurs in Factor V?

A

Participation in clotting cascade is not stopped because V cannot be cleaved by protein C

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11
Q

How common is factor V leiden?

A

Half of patients with unexplained thrombosis

5% of caucasians

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12
Q

Risk of getting a clot with Factor V Leiden?

A

Heterozygotes 7x normal

Homozygotes 80x normal

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13
Q

How do you diagnose Factor V Leiden?

A

PTT and INR are not helpful (will be normal, cascade will be fine, test stops when fibrin forming)
GENETIC TESTING

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14
Q

How do you treat Factor V Leiden?

A

Don’t.. unless thrombosis
Then: anticoag for awhile
If multiple episodes (or other risk factors) long term anticoag

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15
Q

AT III deficiency - about

A

At III is a natural coag
Potentiated by heparin
Lots of gene mutations exist
Very rare

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16
Q

Antithrombin III

A

Natural anti coag
Inhibits IIa, VIIa, IXa, Xa, XIa (no PCR assay)
Potentiated by heparin

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17
Q

What is wrong with the AT III gene?

A

Mutated gene produces less ATIII
Rare
No genetic testing

18
Q

Risk of clots in AT III deficiency

A

Homozygotes - fatal
Heterozygotes - half get clots
Heparin won’t work
Antithrombin concentrates required

19
Q

Protein C and S deficiencies

A

Natural coagulants
C is also fibrinolytic and anti inflammatory
warfarin induced skin necrosis
C deficiency is rare, S super rare

20
Q

Protein C

A

anticoagulant - Inactivates Va and VIIIa
Fibrinolytic - promotes t-PA action
anti-inflammatory - keeps cytokine levels low

21
Q

What is wrong with gene in protein C deficiency

A

Mutated gene produces less protein C (or defective)

Diagnosis via functional testing

22
Q

Risk of clots in protein C deficiency

A 
7x normal (heterozygotes)
Unique risks: warfarin skin necrosis, purpura fulminans
23
Q

Coumadin and Protein C

A

Coumadin wipes out protein C quickly because short half life

24
Q

Coumadin and protein C deficiency

A

Be careful - coumadin wipes out protein C and become hypercoagulable

25
Q

Purpura Fulminans

A

Thrombotic state + vascular injury
Net result : skin necrosis
Associated with : protein C and S def. and sepsis
Treatment: protein C (last resort)

26
Q

Protein S deficiency

A

So rare, same as C

27
Q

Factor II

A

prothrombin

28
Q

Factor II gene mutation

A

makes too much prothrombin

29
Q

Hyperhomocysteinemia

A

too much cysteine - thromboses
MTHFR mutation
B12/folate deficiency
not so rare

30
Q

Homocysteinuria

A

Rare metabolic disorder

31
Q

What is so bad about cysteine (in context of hyperhomocysteinemia)

A

Toxic to endothelium by forming ROS and Interferes with NO (visodilator and antithrombotic)

32
Q

Heterozygous homocysteinemia

A

Increase thrombosis, premature atherosclerosis (venus 2x risk, arterial 10x normal risk)

33
Q

homocysteinemia in B12 deficiency

A

less worrisome but still need to watch for other risk factors

34
Q

Antiphospholipid Antibodies

A

Autoantibodies against phospholipids
Falsely prolonged INR
May cause thromboses
Antiphospholipid syndrome is serious

35
Q

What are antiphospholipid ab?

A 
IgG ab against phospholipids
3 variants (anticadiolipin, lupus anticoag, antibodies against other molecules)
36
Q

What do antiphospholipid ab do?

A

Bind to phospholipids
Screw up coag tests (bind up PTT, PT reagents so spec. cannot clot, test results appear prolonged)
Screw up DAT and syphilis tests

37
Q

Antiphospholipids ______ coagulation in vivo

A

promote

38
Q

Antiphospholipids ______ coagulation in viro

A

Inhibit

39
Q

Who develops antiphospholipid ab?

A

Children (infection - mild risk)
Adults (autoimmune disorders - moderate risk)
Elderly (drugs - no risk)

40
Q

Antiphospholipid Antibody Syndrome

A 
Recurrent thrombosis
Recurrent Spontaneous Abortions
Increased Risk of Stroke
Pulmonary HT
Renal failure

IHO Week 6 (7 decks)

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