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LSB658 > Atherosclerosis and MI > Flashcards

Atherosclerosis and MI Flashcards

1
Q

What is cardiogenic shock?

A

Loss of perfusion due to malfunction of the heart

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2
Q

What is ischaemic heart disease?

A

All heart diseases resulting from reduced O2 supply to heart muscle

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3
Q

List three forms of acute coronary syndrome (ACS)

A
  • Angina
  • Acute coronary occlusion
  • Myocardial infarction
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4
Q

Describe how an atheroma is formed

A

There is a tear in an artery wall; fatty material is deposited in the wall and the narrowed artery becomes blocked by a blood clot

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5
Q

What are statins?

A

Drugs that reduce/prevent cholesterol build-up in vessels

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6
Q

What two things may occur when fatty acids are present via diet/liver synthesis?

A

Oxidised for fuel, or converted to triglycerides and stored in adipose tissue

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7
Q

Free fatty acids travel through blood bound to which protein?

A

Albumin

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8
Q

Triglycerides (TAGs) and cholesterol are transported between organs in ____.

A

Lipoproteins

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9
Q

What are lipoproteins?

A

Lipid droplets assembled around protein particles called apo-lipoproteins

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10
Q

Apo-lipoproteins drive the metabolism of particles by…

A

Binding to receptors on cell membranes

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11
Q

What is the relevance of LDL to cardiovascular disease?

A

LDL is small enough to enter the arterial wall and deposit lipids between endothelium and smooth muscle

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12
Q

Macrophages in blood vessels cannot regulate cholesterol uptake and so become what kind of cells?

A

Foam cells

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13
Q

What are foam cells?

A

Lipid-loaded macrophages that secrete pro-inflammatory cytokines

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14
Q

What is the major function of HDL?

A

To remove cholesterol from peripheral tissues and return it to the liver to be degraded to bile acids and excreted; this is why they are associated with CVD prevention

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15
Q

Describe Tangier’s disease

A
  • Rare genetic disease
    • Mutation in a cholesterol transporter required to move cholesterol out of cells
  • Almost complete lack of HDL
  • Hypertriglyceridaemia (high TAG levels)
  • Early onset atherosclerosis
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16
Q

Describe the development of atherosclerosis

A
  1. LDL deposits lipids between endothelium and smooth muscle
  2. Accumulation of LDL in sub-endothelial space triggers endothelial cells to secrete chemokines
  3. Chemokines induce monocyte infiltration
  4. Monocytes differentiate into macrophages
  5. Macrophages phagocytose LDL
  6. Sustained LDL uptake induces foam cell formation
  7. Foam cells cannot leave the lesion, and recruit other inflammatory cells
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17
Q

Give three examples of how atherosclerotic lesions can become unstable

A
  • Necrosis/apoptosis of foam cells
  • Increased inflammation
  • Breakdown of the fibrous cap
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18
Q

What can trigger the core necrosis in an atherosclerotic lesion?

A

Necrosis of the foam cells can occur as a consequence of:

  • Growth factor deprivation
  • Hypoxia
  • Toxic cytokines
  • ER stress due to excess cholesterol accumulation in the ER membrane
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19
Q

Activated mast cells promote which conversion process?

A

Macrophages into foam cells

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20
Q

How do mast cells become activated and what do they release to trigger conversion?

A

Mast cells bind to molecules and become ‘activated’, and release secretory granules which contain enzymes (proteases), heparin and histamine

21
Q

What is the effect of mast cells in relation to macrophage function?

A

Mast cells make LDL more accessible to macrophages, promoting foam cell conversion, while removing HDL from the region

22
Q

How do ACE inhibitors contribute to hypertension rx?

A

Inhibit activation of angiotensin, an enzyme that increases BP

23
Q

How do diuretics contribute to hypertension rx?

A

Reduce blood volume, therefore BP

24
Q

How do calcium channel blockers contribute to hypertension rx?

A

Reduce muscle tone in artery walls

25
Q

How do beta blockers (particularly B1 blockers) contribute to hypertension rx?

A

Counteract sympathetic NS-mediated vasoconstriction

26
Q

In general terms, explain how smoking causes atherosclerosis

A
  • Releases toxins into bloodstream
  • Toxins cause inflammatory effect
  • Inflammation causes cellular damage
  • Cell damage increases incidence of thrombotic events
27
Q

Give two ways smoking effects endothelial cells

A
  • Damages endothelial cells leading to unstable vessel walls
  • Decreases NO availability, causing vasoconstriction
28
Q

What is the effect of smoking on platelets?

A

Increases platelet aggregation

29
Q

What is the effect of smoking on the clotting cascade?

A

Smoking has a pro-coagulant effect through:

  • Decreased tPA
  • Increased fibrinogen
  • Increased tissue factor
30
Q

What is the effect of smoking with regard to inflammation?

A

Reactive oxygen species generation and other effects of these molecules create a strong pro-inflammatory environment (which promotes atherosclerosis)

31
Q

What is the effect of smoking on blood lipids?

A

Decreases HDL, increases LDL

32
Q

Where does an arterial thrombosis occur?

A

Directly at the site of the atheroma

33
Q

What is an embolism?

A

An object that travels in the bloodstream and does not dissolve

34
Q

What is a thromboembolism?

A

A clot that travels

35
Q

True or false: GTN dilates coronary vessels

A
36
Q

What is ischaemic heart disease?

A

Progressive constriction of coronary arteries

37
Q

What triggers stable angina pectoris?

A

Exercise

38
Q

What is acute coronary occlusion?

A

A sudden change in atherosclerotic plaque in which platelets start to adhere to the plaque, creating a small clot

39
Q

Acute coronary occlusion often precedes what event?

A

Myocardial infarction

40
Q

What is myocardial infarction?

A

Death of cardiac muscle cells due to ischaemia

41
Q

What are the two main types of myocardial infarction?

A

Transmural and subendocardial

42
Q

Differentiate between transmural and subendocardial myocardial infarctions

A
  • Transmural MI - transverses entire portion of heart wall
  • Subendocardial MI - impact is partially through the heart wall
43
Q

Describe the electrophysiology and relevant ECG characteristics of a non-transmural myocardial infarction

A
  • Injured area: depolarised
  • Depolarising current travels toward the positive electrode
  • Baseline voltage prior to QRS will be elevated (depolarised)
  • ST segment appears lower in comparison (ST depression)
    • Isoelectric point has shifted up, so when it actually depolarises and reaches the level of the ST segment, the segment looks lower
44
Q

Describe the electrophysiology and relevant ECG characteristics of a transmural myocardial infarction

A
  • Injured area: depolarised
  • Depolarising currents are travelling away from the positive electrode
  • Baseline voltage prior to QRS will be lowered (hyperpolarised; more negative)
  • ST segment appears higher in comparision (STEMI)
45
Q

What is the function of tenecteplase?

A

Converts plasminogen to plasmin which then breaks down the fibrin around the clot

46
Q

What is the function of clopidogrel/aspirin?

A

Inhibits receptors on the surface of platelets to inhibit platelet aggregation

47
Q

What is the function of enoxaparin?

A

Irreversibly inactivates clotting factor Xa, preventing formation of new clots

48
Q

What is tested in hospital to determine MI?

A

Cardiac enzymes, namely troponin levels

LSB658 (11 decks)

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