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IHO Week 6 (EH) > Thrombotic Disorders > Flashcards

Thrombotic Disorders Flashcards

1
Q

layers of thrombus if formed in life (vs. after death)

A

Lines of Zahn

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2
Q

Outcomes of thrombi

A

Degraded completely by body
Degraded partially
Could propagate in direction of blood flow (backwards towards heart)
Dislodged, flow in direction of blood flow that it can no longer fit through

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3
Q

Thrombosis risk factors (3)

A

endothelial damage
Stasis
hypercoagulability

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4
Q

what leads to endothelial damage

A

atherosclerosis

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5
Q

what leads to stasiss

A

immobilization
varicose veins
cardiac dysfunction

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6
Q

what leads to hypercoagulability

A

trauma/surgery
carcinoma
estrogen/postpartum
thrombotic disorders

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7
Q

If patient has a thrombus

A 
get a good history
order routine lab tests
start to worry if --> 
No obvious cause
Family history
Weird location (not in deep vein of leg)
Recurrent
Patient is young
Miscarriages
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8
Q

Factor V Leiden TYMK

A

Most common cause of unexplained thromboses
Point mutation in factor V gene
Factor V can’t be turned off
Need genetic testing for diagnosis

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9
Q

Underlying mutations in Factor V Leiden

A

A mutated factor V gene
Single point mutation
Discovered in Leiden, Netherlands

Produces abnormal factor V
Participates in the cascade
Can’t be cleaved by protein C
Can turn it on, but can’t turn it off

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10
Q

How common is factor V leiden

A

Half of patients with unexplained
thromboses!
5% of Caucasians have it
VERY rare in non-Caucasians

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11
Q

Risk of getting a clot with factor V leiden

A

Heterozygotes: 7 times normal
Homozygotes: 80 times normal
Normal risk = 1-2 patients per 1000 (per year)

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12
Q

How do you diagnose factor V leiden

A

PTT and INR are not helpful because you can’t speed up clotting, factor V works just fine, just do more clotting than you should

Genetic testing

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13
Q

tx factor V leiden

A

DON’T…unless there is a thrombosis.
Then: give an anticoagulant for a while.
If there are multiple episodes (or other risk factors), give long-term anticoagulation.

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14
Q

Antithrombin III Deficiency TYMK

A

ATIII is a natural anticoagulant
Potentiated by heparin
Lots of gene mutations exist
Very rare

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15
Q

What is ATIII?

A

Natural anticoagulant
Inhibits IIa, VIIa, IXa, Xa, XIa
Potentiated by heparin

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16
Q

What’s wrong with the ATIII gene?

A 
Mutated gene produces less ATIII
   Rara avis (
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17
Q

ATIII risk of getting a clot

A

Homozygotes: can’t survive.
Heterozygotes: half get clots.
Heparin won’t work (obviously).
Antithrombin concentrates required.

18
Q

Protein C and S deficiencies TYMK

A

Proteins C and S are natural anticoagulants
C is also fibrinolytic and anti-inflammatory
Warfarin-induced skin necrosis
C deficiency rare; S deficiency super-rare

19
Q

what is protein c

A

Anticoagulant: inactivates Va and VIIIa
Fibrinolytic: promotes t-PA action
Anti-inflammatory: keeps cytokines low

20
Q

whats wrong with protein C gene

A 
Mutated gene produces less protein C        
     (or defective protein C)
   Rara avis (
21
Q

dx protein C deficiency

A

Diagnosis: functional testing

22
Q

risks with protein C def

A

Heterozygotes: 7 times normal clot risk
Unique risks:
Warfarin-induced skin necrosis
Purpura fulminans

23
Q

Coumadin inhibits

A

II, VII, IX, and X

AND protein C and S

24
Q

Purpura fulminans

A 
Thrombotic state + vascular injury
   Net result: skin necrosis
   Associated with: 
   protein C and S deficiency
   sepsis
   Treatment may include administering protein C
25
Q

Warfarin induced skin necrosis

A

Coumadin inhibits II, VII, IX, and X AND proteins C and S
Protein C has a very short half life (shorter than 7 - will be the first thing to go down)
If person is already deficient in Protein C and you inhibit this, people are hypercoagulable w/ coumadin d/t inhibition of protein C
After a few days, factors will also be decreased and not at a risk for clotting
Usually do coumadin and heparin for first few days

26
Q

Protein S deficiency

A

VERY RARE

otherwise same as protein C def

27
Q

Factor II gene mutation TYMK

A

Factor II = prothrombin
Mutated gene makes too much prothrombin
Prothrombin itself is normal
Rare in non-Caucasians

28
Q

Gene mutaton in factor II gene

A 
Mutated gene produces 
     too much prothrombin!
   Prothrombin itself is normal
   5% of caucasians (rare in others)
   Clot risk: 2 - 20 times normal
29
Q

Hyperhomocysteinemia TYMK

A

Homocysteine converts folate
Homocysteinuria = rare metabolic disorder
Too much homocysteine = thromboses
Homocysteinemia has many causes

30
Q

Homocysteine

A

Amino acid
Made from methionine
Maintains myelin
Converts dietary folate

31
Q

Homocysteinuria

A

Rare metabolic disorder
Deficient trans-sulphuration enzyme
↑ homocysteine in blood, urine
↑ thrombosis, premature atherosclerosis

32
Q

homocysteine pathogenesis

A

Toxic to endothelium
Forms reactive oxygen species
Interferes with nitric oxide
NO is a vasodilater and an antithrombotic

33
Q

homocysteinemia

A

Not so rare
MTHFR gene mutation
B12/folate deficiency

34
Q

Heterozygous homocysteinemia

A

Inc. thrombosis, premature atherosclerosis
Risk of venous thrombosis: 2.5 x normal
Risk of arterial thrombosis: 10 x normal

35
Q

Homocysteinemia in B12/folate def.

A

Less worrisome

…but watch out for other risk factors

36
Q

antiphospholipid antibodies TYMK

A

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

37
Q

antiphospholipid antibodies

A 
IgG antibodies against phospholipids
   Three variants
  anticardiolipin antibodies
  lupus anticoagulants
  antibodies against other molecules
38
Q

what do antiphospholipid abs do

A 
Bind to phospholipids (in vivo and in vitro) 
   Screw up coagulation tests:
   bind up PTT/PT reagent
   specimen can’t clot
   test result appears prolonged
    Screw up other tests:
   direct antiglobulin test
   syphilis test
39
Q

antiphospholipid abs = inhibitors?

A

Promote coagulation in vivo
Inhibit coagulation in vitro
Test results appear contradictory

40
Q

Who develop anti-phos abs

A 
Children
   Infection
   Mild risk
Adults
   Autoimmune diseases
   Moderate risk
Elderly
   Drugs
   No risk
41
Q

anti-phos ab syndrome

A 
Recurrent thrombosis
   Recurrent spontaneous abortions
   Increased risk of stroke
   Pulmonary hypertension 
   Renal failure
42
Q

How to detect anti-phos abs

A 
Order a PTT.
If prolonged, order a PTT mixing study.
If the PTT corrects…?
If the PTT doesn’t correct…?
If normal, antibody may still be present!  
Order fancy tests.

IHO Week 6 (EH) (9 decks)

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