Cardiovascular Pathology Flashcards

1
Q

what are some lifestyle choices that can cause atherosclerosis?

A
  • smoking
  • obesity
  • lack of exercise
  • diet
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2
Q

what are some non-modifiable factors that may contribute to atherosclerosis?

A
  • age
  • gender
  • genes
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3
Q

what is high blood cholesterol known as?

A

hyperlipidaemia

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4
Q

what is atherosclerosis?

A

a chronic inflammatory response followed by the healing response

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5
Q

how is an atheroma formed?

A
  • presence of cholesterol in the vessel walls initiates a chronic inflammatory response
  • the healing response is triggered
  • this causes formation of fibrous tissue
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6
Q

what is vascular pathology?

A

either stenosis/obstruction or weakening of the vessel walls leading to dilation/rupture

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7
Q

what genetic condition may make a patient more likely to develop atherosclerosis?

A

familial hypercholesterolaemia (mutation of LDL receptor gene)

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8
Q

what is the normal state of an endothelial cell known as?

A

basal state

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9
Q

what is the pathological state of an endothelial cell known as?

A

activated state

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10
Q

explain the structure of basal state endothelial cells:

A
  • surface is smooth & non-adhesive (inflammatory cells cannot attach and aggregate on the surface)
  • non-thrombocytic (cannot induce activation of the coagulation system)
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11
Q

explain the structure of an activated endothelial cell:

A
  • surface of endothelial cell becomes changed because of cytokines, bacterial toxins, lipid products… inflammatory cells adhere to the surface of cells
  • permeability changes and inflammatory cells can move in
  • vasoactive substances are released causing vasoconstriction/vasodilation
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12
Q

what are the two phases of a forming atheroma?

A

inflammation phase and healing phase

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13
Q

what occurs during the chronic inflammation phase of atheroma formation?

A
  • endothelial cells change surface cell receptors & become more permeable to lipids
  • altered cell adhesion molecules so monocytes (macrophages and T cells) attach to endothelium & move into blood vessel wall
  • macrophages are phagocytes and engulf the lipid present in the tunica intima
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14
Q

what occurs when macrophages engulf lipids?

A
  • enlarged size
  • pale colour
  • known as FOAM CELLS
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15
Q

what occurs during the healing phase of a forming atheroma?

A
  • proliferation of smooth muscle cells and fibrous tissue in the tunica intima
  • macrophages produce IL-1 which activates T cells
  • more cytokines & chemokines activate inflammatory cells
  • fibrous tissue formation over the lipid & a fatty atheroma (plaque) is formed
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16
Q

what are the resulting effects of atheroma formation?

A
  • ischemia
  • infarction
  • thrombosis
  • embolism
17
Q

what is ischemia?

A

decreased blood supply to tissue/organ

18
Q

what is infarction?

A

complete occlusion of a blood vessel leads to tissue necrosis

19
Q

what is thrombosis?

A

damage of endothelial cells or plaque rupture which causes triggering of the clotting cascade to form a thrombus on the plaque

20
Q

what is meant by embolism?

A

thrombus breaks off and travels in the blood stream

21
Q

how can chronic periodontitis lead to atheroma formation?

A
  • inflammation and the biofilm will result in the presence of growth factors & cytokines in the circulation
  • invitation of an acute phase response in the production of c-reactive protein by the liver
22
Q

what is peripheral vascular disease?

A

ischemia in the muscles of the lower legs

23
Q

what may occur due to peripheral vascular disease?

A
  • claudication = pain and cramps
  • gangrene = complete obstruction of the arteries leading to necrosis of muscles
  • coagulation necrosis and infection due to anaerobic bacteria
24
Q

what is an aneurysm?

A

an abnormal dilation in the wall of a blood vessel

25
Q

what are the main causes of an aneurysm?

A
  • developmental = inherited condition
  • degenerative = infection with mycotic infections or syphilis
  • traumatic = atherosclerosis
26
Q

what occurs in the vessel wall that leads to an aneurysm?

A
  • macrophages (present due to inflammation) produce matrix metalloproteinases
  • MMPs degraded the fibrous tissue leading to weakening of the blood vessel wall
  • this leads to abnormal dilation and an increase in size
27
Q

what occurs during a myocardial infarction?

A
  • myocytes switch to anaerobic respiration to supply energy to the muscles (ineffective)
  • coagulation necrosis of myocardial muscle then occurs
28
Q

how does the cardiac tissue heal after a myocardial infarction?

A

by formation of granulation tissue

- impaired heart function

29
Q

what are tumours of the blood vessels?

A
  • hamartomas

- kaposi sarcoma

30
Q

what are hamartomas?

A
  • collection of cells that are normal but increased in size
  • non-malignant
  • no connective tissue capsule surrounding these structures (normally found in benign tumours)
31
Q

who is most likely to suffer from Kaposi Sarcomas?

A

patients with advanced HIV infection

32
Q

what is the aetiology of kaposi sarcomas?

A

Herpes virus 8

33
Q

what is a haemangioma?

A

hamartoma of the endothelial cells (commonly seen in head & neck)

34
Q

what are examples of benign cardiac tumours?

A
  • myxoma

- lipoma

35
Q

what is an example of a malignant cardiac tumour?

A

angiosarcoma

36
Q

what can pathology of heart valves lead to?

A
  • stenosis (failure of valve to open completely)
  • insufficiency (failure of valve to close properly)
  • vegetations (nodules on the endocardium & valve that may be thrombocytic or infective)
37
Q

what is the most common valve condition?

A

calcification aortic stenosis

38
Q

what occurs to a patient suffering from calcific aortic stenosis?

A
  • dystrophic calcium deposits (result of chronic endothelial injury)
  • narrowing of the valvular orifice which affects valve function
39
Q

what type of reactions are involved in rheumatic heart disease?

A
  • type 2 (cytotoxic type of fibrous sensitivity reaction)

- type 4 (cell-mediated T cell reaction)