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T yr: IOD > Cardiovascular Pathology > Flashcards

Cardiovascular Pathology Flashcards

1
Q

What is haemostasis?

A
  • Occurs when there is damage to a blood vessel
    – it involves the formation of a solid plug from the constituents of blood – it stops loss of blood from the circulation at the site of injury
    – it is physiological (ie. it’s a good thing)
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2
Q

What factors determine haemostasis?

A

close interactions between the

  • vessel wall
  • platelets
  • coagulation cascade
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3
Q

How does endothelial damage result in haemostasis?

A
  1. injury
  2. adhesion
  3. platelet aggregation
  4. formation of loose platelet plug
  5. Tissue factor expo
  6. intrinsic clotting cascade
  7. insoluble fibrin forms
  8. stable platelet plug (due to fibrin)
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4
Q

What is fibrinolysis?

A

activated by the same injury that initiates haemostasis

plasminogen -> plasmin

plasmin degrades insoluble fibrin into soluble products

ensures that haemostasis is very tightly isolated to the site of injury
(if this didn’t happen, then you would get DIC)

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5
Q

When does thrombosis occur?

A

following inappropriate activation of haemostasis

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6
Q

How does thrombosis occur?

A
  1. platelets and coagulation system interact with vessel wall
  2. thrombus forms
  3. process overwhelms the regulation on coagulation system (e.g. fibrinolysis etc)
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7
Q

What is a thrombus made up of?

A

same components as a haemostat plug

  • platelets
  • fibrin
  • RBCs

However, it is PATHOLOGICAL

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8
Q

How does a clot differ from a thrombus?

A

Thrombus contains PLATELETS but a clot does not

technically, a clot is formed from stationary blood or outside the CVS e.g. post-mortem or in a test tube

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9
Q

What is Virchow’s triad?

A

[3 main predisposing factors to thrombus formation]

  • endothelial injury
  • abnormal flow (turbulent or static flow)
  • hypercoagulability
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10
Q

What is the most important RF in ARTERIAL thrombosis?

A

atherosclerosis

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11
Q

What are the most important RFs in VENOUS thrombosis?

A
  • stasis

- hypercoagulability

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12
Q

What are the 3 main outcomes of thrombi formation?

A
  1. PARTIAL occlusion at site of thrombosis
  2. COMPLETE occlusion at site of thrombosis
  3. EMBOLISM to a distant site and occlusion of that vessel
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13
Q

What is an embolism?

A
  • occlusion of a vessel by undissolved material

- transported via the blood stream

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14
Q

What can partial or complete vessel occlusion by a thrombus cause?

A

ischaemia of the tissue supplied by that vessel

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15
Q

What is ischaemia?

A
  • tissue dysfunction
  • interference with blood flow
  • reversible
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16
Q

What can occur if a vessel occlusion is not reversed?

A

ischaemia can progress to infarction

17
Q

What is infarction?

A
  • tissue death (necrosis)
  • interference with blood flow to a tissue
  • irreversible
18
Q

What are the clinical effects of a vessel occlusion?

A

dependent on

  • which vessel is occluded
  • type of tissue supplied
19
Q

What will thromboemoli originating in the VENOUS system go on to occlude?

A

a pulmonary artery

20
Q

What will thromboemoli originating in the ARTERIAL system or LHS of heart go on to occlude?

A

a systemic artery

e.g. renal arteries

21
Q

What initiates atherosclerosis?

A
  • chronic inflammatory process

- initiated by endothelial injury

22
Q

What are the established RFs for endothelial injury?

A
  • smoking
  • HTN
  • DM
  • dyslipidaemia
23
Q

What are atherosclerotic plaques composed of?

A

core: lipid debris and foam cells and lymphocytes
roof: fibrous cap

24
Q

By what mechanisms does atherosclerosis cause clinical disease?

A
  1. Gradual enlargement of a STABLE plaque -> luminal stenosis
  2. Sudden disruption of a VULNERABLE plaque + thrombosis in lumen
    - > occlusion at that site
    - > embolism at another site
  3. Aneurysm formation
    - > rupture
    - > thromboembolism
25
Q

What are the features of a STABLE atherosclerotic plaque?

A
  • thick fibrous cap
  • resistant to rupture
  • stable lesions grow more slowly over decades
  • gradual stenosis
26
Q

What are the features of an UNSTABLE ‘vulnerable’ atherosclerotic plaque?

A
  • plaques contain more inflammatory cells

- thinner fibrous cap more prone to acute rupture

27
Q

What determines stability of atherosclerotic plaques?

A

A balance between:

  • smooth muscle cells (produce fibrous cap that stabilises the plaque)
  • inflammatory cells (MMPs digest the fibrous cap and kill SMCs -> destabilise the plaque)
28
Q

What does Poiseuille’s law say?

A

flow is proportional to (vessel radius)^4

therefore a subtle reduction in lumen size will have a great effect on (laminar) blood flow

29
Q

What is stable angina?

A
  • imbalance between O2 supply and demand in the myocardium
  • myocardial ischaemia
  • cardiac-type pain

Clinically:

  • PREDICTABLE cardiac-type pain
  • precipitated by exertion
  • relieved by rest
30
Q

What is the cause of stable angina?

A
  • STENOSIS

- due to stable plaque in a coronary artery

31
Q

What are acute coronary syndromes (ACS)?

A
  • spectrum of conditions
  • caused by a SUDDEN severe reduction in myocardial perfusion
  • > ischaemia or infarction
32
Q

What is the pathology of the ACS?

A

acute change in coronary artery atherosclerotic plaque

T yr: IOD (11 decks)

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