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iho week 6 > Thrombotic Disorders > Flashcards

Thrombotic Disorders Flashcards

1
Q

What is a thrombus?

A

A clot that stays in one place

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2
Q

What is an Embolus?

A

A clot that breaks off, moves to a new place and gets stuck

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3
Q

What is visually different in postmortem and premortem clots?

A

Postmortem - current jelly

Premortem - clots have different colored layers

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4
Q

What does an aortic aneurysm with a thrombus look like?

A

Bulge = aortic aneurysm
Very thin wall, all of this is clot in the mass - there was probably turbulent flow here - clot formation is common in aneurysms

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5
Q

What does a thrombosed artery look like on a slide?

A

Looks like a blood clot with many platelets, red cells, and morphs into something more organized over time.

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6
Q

What are the different outcomes that can result from a thrombosis?

A

(1) Thrombus can propagate itself –> moves in direction of blood flow and can move further into vena cava, even into heart
(2) Sometimes body will clear the clot on its own (natural tPA)
(3) Part of clot breaks off, and it gets stuck somewhere in another vessel - these usually happen in the lungs = pulmonary embolism
(4) Clot can recannalize and blood can flow through hole in clot again so it can serve that area of the body
(5) Clot can take care of itself and get small enough to get blood through

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7
Q

What is DVT?

A

Deep Vein Thrombosis

  • Most thrombi happen in the deep veins of the leg
  • Leg becomes edematous, red hot, etc.
  • Often its just the lower leg that gets super red and painful
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8
Q

What did Rudolf Virchow do?

A

He described the things that can predispose you to getting thrombi!
He coined the term embolism and described its process

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9
Q

What are the three main thrombosis risk factors (triad)? what one is most important??

A
  1. Endothelial damage (MOST IMPORTANT)
  2. Stasis
  3. Hypercoagulability
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10
Q

What leads to endothelial damage?

A

Atherosclerosis

  • Hypertension
  • Hyperlipidemia
  • Obesity
  • Smoking
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11
Q

What leads to Stasis?

A
  • Immobilization
  • Varicose veins
  • Cardiac dysfunction
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12
Q

What leads to hyper coagulability?

A
  • Trauma/surgery
  • Carcinoma
  • Estrogen/Postpartum
  • Thrombotic disorders
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13
Q

So your patient has a thrombus, now what?

A
  1. Get a good history! (risk factors, family history)
  2. Order routine lab tests (INR, PTT, TT)
  3. Start to worry if:
    - No obvious cause
    - Family history
    - Weird location
    - Recurrent
    - Patient is young
    - Miscarriages
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14
Q

What are the different Thrombotic Disorders?

A

Most of these are extremely rare

  1. Hereditary
    - Factor V Leiden
    - ATIII deficiency
    - Protein C deficiency
    - Protein S deficiency
    - Factor II gene mutation
    - Homocysteinemia
  2. Acquired
    - Antiphospholipid Ab
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15
Q

If you could only remember two thrombotic disorders?

A
  1. Hereditary - Factor V Leiden

2. Acquired - Antiphospholipid Ab

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16
Q

What MUST you know about Factor V Leiden?

A

Very common hereditary thrombotic disorder

  • Most common cause of unexplained thromboses
  • Point mutation in factor V gene
  • Factor V can’t be turned off
  • Need genetic testing for diagnosis
  • More common in caucasians
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17
Q

What is Factor V Leiden?

A
  1. A mutated factor V gene
    - Single point mutation
    - Discovered in Leiden, Netherlands
  2. Produces abnormal Factor V
    - Participates in the cascade
    - Can’t be cleaves by protein C
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18
Q

Factor V - Yeah, so?

A

You can turn it on. . .but you can’t turn it off!!

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19
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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20
Q

What is the 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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21
Q

How do you diagnose Factor V Leiden?

A
  • PTT and INR are not helpful! (you make fibrin just as fast so they’ll be normal - the main problem is that you can’t turn it off, not that you can’t coagulate!!)
  • Need GENETIC TESTING!! (usually just one mutation related to this)
22
Q

How do you treat 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
23
Q

What MUST you know about Antithrombin III Deficiency?

A
  • ATIII is natural anticoagulant
  • Potentiated by heparin
  • Lots of gene mutations exist
  • Very rare
24
Q

What is Antithrombin III?

A
  • Natural anticoagulant
  • Inhibits IIa, VIIa, IXa, Xa, XIa (don’t need to remember all for Krafts)
  • Potentiated by heparin
25
Q

What’s wrong with the ATIII gene?

A
  • Mutated gene produces LESS ATIII
  • Rara avis ( very RARE
  • Lots of different mutations described –> can’t do single PCR test, so you have to do functional testing
  • Can’t do genetic testing!
26
Q

What’s the risk of getting a clot with ATIII Deficiency?

A
  • Homozygotes: can’t survive
  • Heterozygotes: half get clots
  • Heparin won’t work (obviously).
  • Antithrombin concentrates required
27
Q

What MUST you know about Protein C and S Deficiencies?

A
  • Proteins C and S are natural anticoagulants
  • C is also fibrolytic and anti-inflammatory
  • Warfarin-induced skin necrosis
  • C deficiency is rare; S deficiency is super-rare
28
Q

What is Protein C again?

A
  • Anticoagulant: inactivates Va and VIIIa
  • Fibrinolytic: promotes t-PA action
  • Anti-inflammatory: keeps cytokines low
29
Q

What’s wrong with the mutated protein C gene?

A
  • Mutated gene produces less protein C (or defective protein C)
  • Rara avis (
30
Q

What is the risk of getting a clot with a mutated Protein C gene?

A
  • Heterozygotes: 7 times normal
  • Unique risks:
  • -Warfarin-induced skin necrosis (give patients warfarin and their skin dies - rarely happens)
  • -Purpura fulminans
31
Q

What is this an example of?

  • Young woman with pulmonary embolus
  • Admitted, started on coumadin (warfarin)
  • Day 5; severe pain, right breast
  • Warfarin stopped, heparin started
  • Necrotic tissue eventually excised
A

Diagnosis: Warfarin-induced skin necrosis

32
Q

When a patient has a clot, what do you usually give them??

A

You usually put a patient on both Coumadin and Warfarin at the same time so as to avoid necrosis of the skin

33
Q

What does coumadin inhibit?

A

Factor II, VII, IX and X . . .AND proteins C and S!!

34
Q

What is 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
35
Q

What should you know about Protein S Deficiency?

A
  • Uber rara avis

- Otherwise: same as protein C deficiency

36
Q

What things MUST you know about Factor II Gene Mutation?

A
  • Factor II = prothrombin
  • Mutated gene makes too much prothrombin
  • Prothrombin itself is normal
  • Rare in non-Caucasians
37
Q

What’s wrong with the 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
38
Q

What things MUST you know about Hyperhomocysteinemia?

A
  • Homocystein converts folate
  • Homocysteinuria = rare metabolic disorder
  • Too much homocysteine = thromboses
  • Homocysteinemia has many causes
39
Q

What is Homocysteine?

A
  • Amino acid
  • Made from methionine
  • Maintains myelin
  • Converts dietary folate
40
Q

What is Homocysteinuria?

A

-Rare metabolic disorder (missing enzyme at the bottom)
-Deficienct trans-sulphuration enzyme
[Abnormality in CBS enzyme at end of pathway]
-Inc. in homocysteine in the blood, urine
-Inc. thrombosis, premature atherosclerosis

41
Q

What is the function of B12/folate in homocysteine pathway?

A

B12/folate converts methionine to homocysteine and back!

42
Q

What is Homocysteinemia (MUST KNOW FOR EXAM!!)?

A

NOT METABOLIC DISORDER

  • Not so rare
  • MTHFR gene mutation (MUST KNOW FOR EXAM!!)
  • B12/Folate deficiency
43
Q

What’s so bad about Homocysteine?

A

Toxic to endothelium:
-Forms reactive oxygen species
Interferes with nitric oxide
-NO is a vasodilator and an antithromotic

44
Q

Heterozygous Homocysteinemia?

A
  • Inc. thrombosis, premature atherosclerosis
  • Risk of venous thrombosis: 2.5 x normal
  • Risk of arterial thrombosis: 10 x normal
45
Q

Homocysteinemia in B12/Folate deficiency?

A
  • Less worrisome

- . . .but watch out for other risk factors

46
Q

What MUST you know about Antiphospholipid antibodies?

A
  • Autoantibodies against phospholipids
  • Falsely prolong INR
  • May cause thromboses
  • Antiphospholipid syndrome is serious
47
Q

What are antiphospholipid antibodies?

A
  • IgG antibodies against phospholipids
  • Three variants:
    1. Anticardiolipin antibodies
    2. Lupus anticoagulants
    3. Antibodies against other molecules
48
Q

What do Antiphospholipid Antibodies do?

A
  1. Bind to phospholipids (in vivo and in vitro)
  2. Screw up coagulation tests:
    - Bind up PTT/PT reagnet
    - Specimen can’t clot
    - Test result appears prolonged
  3. Screw up other test:
    - Direct anti globulin test
    - Syphilis test
49
Q

What’s the bottom line about Antiphospholipid Antibodies?

A

These antibodies are called inhibitors.
-Promote coagulation in vivo.
-Promote coagulation in vitro.
So tests results appear contradictory!!

50
Q

Who develops these Anti-phospholipid Antibodies?

A
  1. Children
    - Infection
    - Mild risk
  2. Adults
    - Autoimmune diseases
    - Moderate risk
  3. Elderly
    - Drugs
    - No risk
51
Q

What happens/symptoms of Antiphospholipid Antibody syndrome?

A
  • Recurrent thrombosis
  • Recurrent spontanteous abortions
  • Increased risk of stroke
  • Pulmonary hypertension
  • Renal failure
52
Q

How do you detect the antibodies in Anti-phospholipid Antibody Syndrome?

A
  1. Order a PTT
  2. If prolonged, order a PTT mixing study
    - -If the PTT corrects. . .? That means some factor was missing in blood
    - -If the PTT doesn’t correct. . .? There is something in patients blood that is inhibitory enough to mess up all the normal blood –> this usually happens when you have antibodies present!
  3. If normal, antibody may still be present! Order fancy tests.

iho week 6 (16 decks)

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