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4 Hemostasis and Related Disorders > 4.4 Thrombosis > Flashcards

4.4 Thrombosis Flashcards

1
Q

CBS (cystathionine beta synthase)

  • how is related to hemostasis disorders?
  • mech
A
  • CBS deficiency: causes homocysteinemia/homocysteinuria
  • increased risk of thrombosis from high homocysteine, which damages endothelium
  • homocysteine is normally converted by CBS to cystathione for degradation.
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2
Q

Vit B12/Folate deficiency

  • effect on hemostasis
  • mech
A
  • increased risk of thrombosis from high homocysteine, which damages endothelium
  • lack of either means homocysteine is not methylated into methionine
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2
Q

Prothrombin 20210A

A
  • leads to hypercoagulable state.
  • mutation in prothrombin leads to increased expression, leading to excessive thrombin, cross linking more fibrinogen.
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3
Q

Thrombosis can be caused by endothelial damage. What conditions cause this damage (3)

A
  1. atherosclerosis
  2. vasculitis
  3. high levels of homocysteine
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3
Q

Pt using oral contraceptives.

-why increased risk for thrombosis?

A

Estrogen increases production of coag factors.

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3
Q

You see a pt who has recurring DVTs, is mentally retarded, has poor vision, and has long slender fingers.

Think what?

A

CBS deficiency homocysteinuria

  1. thrombosis
  2. mental retardation
  3. lens dislocation
  4. long slender fingers
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4
Q

Factor V Leiden

A
  • leads to hypercoagulable state.
  • mutated Factor 5 leads to excessive Factor 5. Mutation makes F.5 lack cleavage site for protein C and S deactivation.
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5
Q

Virchow Triad

A
  • 3 risk factors of thrombosis:
    1. Abnormal blood flow
    2. Endothelial damage
    3. Hypercoagulable state–excessive procoagulants or defective anticoagulants
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6
Q

Antiphospholipid antibodies -examples

A

-example of acquired hypercoag, leads to increased risk of thromboses -Acquired Ab against phospholipid complexes -ex: 1. “lupus anticoagulant”– it is not an anticoagulant, although it paradoxically increases PTT (lab test artifact) and is associated with SLE 2. anti-cardiolipin Ab

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7
Q

Pt with thrombosis that you treat with heparin, but no change in PTT.

  • Suspect what?
  • If so, how to induce anticoagulated state?
A

Possible ATIII deficiency.

-If so, use warfarin, along with temporary high dose heparin to prevent warfarin skin necrosis (there may still be existing ATIII to be activated).

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8
Q

CBS deficiency:

-clinical presentation (4)

A

homocysteinemia/homocystenuria

  1. vessel thrombosis
  2. mental retardation
  3. lens dislocation
  4. long slender fingers

1/4 die before age 30 from thrombosis complications.

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9
Q

Protein C or S deficiency

  • what does this cause
  • what is there increased risk of?
A
  • leads to hypercoagulable state.
  • Protein C and S are anticoagulants, normally inactivate F.5, F.8
  • increased risk of warfarin skin necrosis (acute loss of protein C,S from warfarin can induce thrombosis of skin vessels)
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10
Q

ATIII deficiency

  • mech
  • what lab test is changed?
A
  • leads to hypercoagulable state.
  • ATIII is an anticoagulant activated by heparin that inactivates thrombin and coag factors.
  • PTT does not rise when heparin is given, b/c there is no ATIII to bind to.
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11
Q

Pts with genetic hypercoagulable state

-classic presentation

A
  • DVTs (possibly recurrent) at a young age.
  • usu in leg, but also hepatitic and cerebral veins
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13
Q

How to distinguish thrombus from postmortem clot?

A

Histology of thrombus:

  1. Lines of Zahn (alternating layers of platelets/fibrin and RBCs)
  2. attachment to vessel wall
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15
Q

What do endothelial cell secrete to prevent thrombosis? (4)

A
  • Endothelial cells secrete:
    1. PGI2/NO–both vasodilate and inhibit platelet aggregation
    2. HLM (heparin-like molecules)–activate ATIII, which inactivates thrombin and coag factors
    3. tPA, activating plasmin (remember: it cleaves fibrin and serum fibrinogen, destroys coag factors, and blocks platelet agg)
    4. thrombomodulin (modulates thombin to activate protein C, which inactivates factors 5,8)
17
Q

Thrombosis from Abnormal blood flow

-example disorders

A
  • DVT from lack of movement
  • AFib
  • Aneurysm
18
Q

How do oral contraceptives affect hemostasis?

A

-Estrogen increases production of coag factors, leading to increased risk of thrombosis

19
Q

warfarin skin necrosis

  • what is it
  • what condition has an increased risk of this?
A
  • Skin necrosis can occur from clotting when using warfarin. (paradoxical)
  • Warfarin inactivates Vit K, inactivating 2,7,9,10,C,S. C and S (anticoags) are inactivated first, creating a window of hypercoagulable state, which can lead to thrombosis, esp in the skin. Prevent this by giving heparin with warfarin.
  • increased risk in Protein C or S deficiency
20
Q

homocysteine

  • how is it related to hemostasis disorders
  • mech
  • specific disorders (3)
A
  • high levels cause endothelial damage, increasing risk of thrombosis
  • THF becomes methylated, donating the methyl to Vit B12, which donates to homocysteine, creating methionine. Also, homocysteine is normally converted by CBS to cystathione for degradation.

1,2. Vit B12/Folate deficiency
-lack of either means homocysteine is not methylated into methionine

  1. CBS (cystathionine beta synthase) deficiency
21
Q

thrombomodulin

  • made from where
  • what does it do?
A
  • secreted by endothelium
  • modulates thrombin to activate Protein C, which inactivates Factors 5, 8. Therefore, inhibits clotting.
22
Q

Pt with a DVT.

How to start thinking about your differential?

A

Think Vichow’s triad:

  1. blood stasis
    - immobilization, AFib, aneurysm, etc
  2. endothelial damage
    - atherosclerosis, vasculitis, homocysteinemia
  3. hypercoag state
    - oral contraceptives
    - genetic: Factor 5 leiden, Protein C/S deficiency, ATIII deficiency, prothrombin 20210A
23
Q

Thrombosis can be caused by a hypercoagulable state. What conditions cause this?(5)

-which is most common?

A

-excessive procoagulants or defective anticoagulants

Genetic:

  1. Protein C or S deficiency–lack of anticoags
  2. Factor 5 Leiden–mutated in F.5 cleavage site for deactivation by proteins C and S
  3. Prothrombin 20210A–mutation in prothrombin that increases its expression
  4. ATIII deficiency–lack of anticoag

Non-genetic:
5. Oral contraceptives–estrogen increases production of coag factors

Factor 5 Leiden is most common.

4 Hemostasis and Related Disorders (5 decks)

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