Thrombosis and Embolus Flashcards

(34 cards)

1
Q

What distinguishes a thrombus from a postmortem clot?

A
  • Lines of Zahn

- Attachment to vessel wall

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2
Q

What do layers of Zahn look like on histology?

A

Lines of RBCs and fibrin

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3
Q

What is Virchow’s triad?

A
  • Endothelial injury
  • Stasis
  • Hypercoguable state
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4
Q

WHat does the endothelium produce to reduce risk of thrombosis?

A
  • PGI2 (prostaglandin I2) - blocks platelet aggregation
  • NO - vasodialtion
  • Heparin-like molecules - activate AT3 (inactivates thrombin)
  • tPA
  • Thromobomodulin - redirects function of thrombin to activate protein C
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5
Q

What does endothelial damage cause?

A
  • Atherosclerosis
  • Vaculitis
  • High levels of homocysteine (B12 and folate also increase these levels slightly)
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6
Q

What does can an increased homocysteine level cause?

A
  • Thrombosis
  • Homocystinuria

CBS deficiency (Cystathionine beta synthase)

  • Thrombosis
  • Mental retardation
  • Lens discolouration
  • Long slender fingers
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7
Q

What does CBS (Cystathionine beta synthase) do?

A

Converts homocysteine to cystathionine

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8
Q

What are the characteristic signs of a inherited hypercoagulable disorders?

A
  • Recurrent DVTs
  • DVTs at young age
  • Thrombosis in hepatic or cerebral veins
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9
Q

What type of adverse drug reaction are individuals with a protein C or S deficiency at risk of?

A

Warfarin skin necrosis

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10
Q

What does vitamin K epoxide reductase activate?

A

Vitamin K

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11
Q

What does vitamin K activate?

A
  • Factors II, VII, IX, X

- Protein C and S

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12
Q

How does warfarin cause warfarin skin necrosis?

A
  • Proteins C and S are degraded first, before the clotting factors
  • This causes an increased risk of thrombus as factors 2,7,9,10 are increased relatively
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13
Q

What medication is given with warfarin?

A

Heparin - to reduce the risk of thrombus formation - warfarin skin necrosis

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14
Q

What is factor V Leiden?

A

Mutated factor V that lacks cleavage site for deactivation by proteins C and S

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15
Q

What is prothrombin 20210A?

A
  • Point mutation in prothrombin
  • Results in increased gene expression
  • Promotes thrombus formation
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16
Q

What is ATIII deficiency?

A
  • Decreases protective effect of heparin-like molecules produced by endothelium, increasing the risk of thrombus
17
Q

What happens when patients with AT3 deficiency are given heparin?

A
  • PTT does not rise with standard dosing - high doses are needed to activate limited supply
  • Warfarin is given after to maintain hypercoagulable state
18
Q

What does estrogen increase the production of/

A

Coagulation factors

19
Q

Name the hypercoagulable disorders?

A
  • Protein C or S deficiency
  • AT3 deficiency
  • Factor V Leiden (most common)
  • Prothrombin 20210A
20
Q

What are the different types of embolus?

A
  • Thromboembolus (~95%)

- Atherosclerotic embolus (due to plaque that dislodges)

21
Q

What is a characteristic finding in atherosclerotic emboli?

A

Presence of cholesterol clefts (crystals) in the embolus

22
Q

When would a patient get a fat embolus?

A
  • After bone fractures (long bones) and soft tissue trauma

- Develops while fracture is still present or shortly after repair

23
Q

What is a characteristic finding in a patient with a fat embolus?

A

Dyspnea and petechiae on the skin overlying the chest

- Circular white spaces in lumen on histology

24
Q

Where else will there be pain in patients with a gas emboli?

A

Joint and muscle pain (the bends) as well as resp symptoms

25
What is the chronic form of decompression sickness?
Caisson disease - Mutifocal ischemic necrosis of bone - Chronic nitrogen emboli
26
When else other than from decompression can a patient get a gas embolus?
- Laproscopic surgery
27
What are the characteristic symptoms of an amniotic fluid embolus?
- During labour or delivery - SOB, Neurological symptoms - DIC (due to tissue thromboplastin in amniotic fluid) - Squamous cell and keratin debris in amniotic fluid
28
Why are PEs often clinically silent?
- Lung has dual blood supply | - Embolus is usually small and self-resolves
29
How many PEs cause infarction and what may this be due to?
- ~10% | - Obstruction of large or medium sized artery with pre-existing cardiopulmonary compromise
30
What are the clinical features of PE?
- SOB - Hemoptysis, pleuritic chest pain, pleural effusion - V/Q mismatch - Spiral CT shows a vascular filling defect in the lung - Elevated d dimer - Doppler US in leg
31
What will a PE show on imaging?
- Hemorrhagic | - Wedge shaped infarct
32
How may a PE cause sudden death?
- Large saddle embolus or significant occlusion of a large pulmonary artery - Death due to electromechanical dissociation
33
How can emboli cause pulmonary hypertension?
Chronic emboli may reorganise over time
34
What is the source of most systemic emboli?
Arise in the left heart | - Travel down systmeic circulation to occlude flow to organs, most commonly lower extremities