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Cardiovascular 2 > Atherosclerosis > Flashcards

Atherosclerosis Flashcards

1
Q

Acute vs chronic obstruction of coronary arteries

A

Chronic causes alternative supplies

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2
Q

Atherosclerosis

A

A chronic inflammatory disorder where lipid plaques form on the inside of the walls of arteries.

Narrowing of the arteries.

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3
Q

Arteriosclerosis

A

Harderning of the arteries

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4
Q

In descending order what arteries are most commonly affected by atherosclerosis?

A

Abdominal aorta
Coronary
Popliteal
Carotid

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5
Q

Modifiable risk factors of arteriosclerosis.

A

Smoking
Hypertension
Diabetes melitus
Dyslipidemia (increase in LDL levels / decrease in HDL levels).

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6
Q

Non-modifiable risk factors of arteriosclerosis.

A

Age
Family history
African-american descent

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7
Q

Inflammatory response to endothelial injury can lead to atherosclerosis, where can this commonly occur?

A

At arterial bifurcations e.g at the carotid bifurcation.

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8
Q

What can cause endothelial injury in arteries?

A

Stress
Smoking
Homocysteinemia (high levels of homocystein in the blood).

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9
Q

How does endothelial injury lead to atherosclerosis?

A

When the endothelium is injured, LDL particles are able to leak into the intimal layer where they get oxidised.

When LDL is oxidised it becomes a pro-inflammatory antigen that induces an immune response in which inflammatory cells such as marcophages come to fight this antigen. The marcophages enter the arterial walls and eat the oxidised LDL’s creating foam cells.

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10
Q

What is the first marker of atherosclerosis?

A

Accumulation of foam cells underneath the arterial endothelium which leads to fatty streaks.

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11
Q

What are the symptoms of fatty streaks?

A

Fatty streaks don’t produce symptoms as they don’t obstruct the lumen and thus don’t cause symptoms like angina.

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12
Q

Endothelial damage causes platelets and endothelial cells to release what factors?

A

PDGF (platelet dependant growth factor)
FGF
TGF-beta

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13
Q

What effect do PDGF, FGF, and TGF-beta have in athersclerosis?

A

These factors stimulate smooth muscle proliferation, and migration of muscle cells from the tunica media to the tunica intima.

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14
Q

Proliferation of smooth muscle in atherosclerosis stimulates production of what?

A

ECM

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15
Q

What does secretion of ECM due to smooth muscle proliferation in atherosclerosis lead to?

A

Formation of a fibrous cap overlying a lipid core in the centre - a PLAQUE.

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16
Q

What is the lipid core of a plaque made up of?

A

Cholesterol crystals.

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17
Q

What effect can necrosis of foam cells have on the fibrous cap?

A

Necrosis of foam cells causes release of matrix metalloproteinases (MMP’s).
These enzymes degrade the fibrous cap thinning it until it ruptures.

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18
Q

What occurs when the fibrous cap of a plaque ruptures?

A

Platelets react forming a fibrin clot at the site of rupture.
- can occlude the lumen even more or detach which can lead to obstruction of other blood vessels such as those in the brain.

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19
Q

What are the complications of atherosclerosis?

A

Ischemia of the supplied organs.

  • angina
  • chronic mesenteric ischemia
  • claudication

Plaque rupturing can lead to clot formation which can cause acute infarction of the supplied organ.

  • MI
  • Stroke
  • Acute mesenteric ischemia
  • Acute limb ischemia

Cholesterol emboli

Aneurysm

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20
Q

Why does atherosclerosis cause angina?

A

Obstruction of the coronary arteries.

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21
Q

Claudication

A

A condition in which cramping pain in the leg is induced by exercise, typically caused by obstruction of the arteries. Type of peripheral vascular disease.

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22
Q

How can atheroma cause aneurysm?

A

Atheroma can weaken the vessel wall leading to aneurysm - especially in areas where the arterial wall is weaker.

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23
Q

What are common sites of aneurysm where the vessel wall is weaker?

A

Abdominal aorta below the level of L2.

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24
Q

Why is the abdominal aorta below L2 more succeptible to aneurysm?

A

This is because it lacks the vaso vasorum, which are small blood vessels in the tunica adventitia supplying the aortic wall. This means the tunica media doesn’t get enough nutrients, causing it to weaken - this increases the risk of aneurysm and haemorrhaging.

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25
Q

How do cholesterol emboli form?

A

The atherosclerotic plaque becomes dislodged leading to a clot free in circulation.

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26
Q

What is a MAJOR risk factor for cholesterol emboli?

A

Cardiac procedure such as percutaneous coronary intervention - caused by a plaque being dislodged during the procedure.

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27
Q

What are the symptoms of cholesterol emboli?

A

Symptoms are dependant on where the embolus ends up, but can include a LIVEDO RETICULARIS, AKI, gangrene of the extremities, hollenhorst plaques.

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28
Q

Livedo reticularis

A

Livedo reticularis is a common skin finding consisting of a mottled reticulated vascular pattern that appears as a lace-like purplish discoloration of the skin. The discoloration is caused by swelling of the venules owing to obstruction of capillaries by small blood clots.

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29
Q

Hollenhorst plaques.

A

Retinal emboli

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30
Q

What are the clinical findings that suggest cholesterol emboli?

A

Eosinophillia

Eosinophiluria

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31
Q

What are the two types of arteriolosclerosis?

A

Hyaline and Hyperplastic

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32
Q

What does arteriolosclerosis effect?

A

Smaller arterioles.

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33
Q

What causes hyaline arteriolosclerosis?

A

Deposition of protein within the vessel wall.

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34
Q

What effect does hyaline arteriolosclerosis have on arterioles.

A

Deposition of protein thickens the arteriole wall and makes it more rigid which can occlude the arteriole lumen.

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35
Q

What are the risk factors of hyaline arteriolosclerosis?

A

Chronic hypertension and diabetes.

36
Q

How does hypertension cause hyaline arteriolosclerosis?

A

The increased arterial wall stress literally pushes plasma proteins into the arterial wall.

37
Q

How does diabetes cause hyaline arteriolosclerosis?

A

Excess glucose combines with the proteins of the arteriolar basement membrane in non-enzymatic glycation.
- Too much sugar in the basement membrane can disrupt the structure allowing plasma proteins to leak in.

38
Q

What are the clinical manifestations of hyaline arteriosclerosis?

A

Hypertension and diabetic nephropathy, small lacunar infarcts in the brain.

39
Q

Why does hyperplastic arteriolosclerosis occur?

A

Hyperplastic occurs due to severe acute elevations in blood pressure.

40
Q

What does hyperplastic atherolosclerosis do?

A

Causes excessive growth of the basement membrane and proliferation of the arteriolar smooth muscle which occludes the lumen.

41
Q

Where does hyperplastic arteriolosclerosis most commonly affect?

A

Renal, retinal and intestinal arterioles.

42
Q

What are the steps of atherosclerosis?

A
  1. Endothelial injury.
  2. LDL particles enter and are oxidised.
  3. Macrophages phagocytose LDL particles, forming foam cells which form the fatty streaks.
  4. Platelets secrete factors such as PDGF stimulating proliferation of smooth muscle cells and their move to the intimal layer, where they lay down ECM.
  5. Over time a atherosclerotic plaque made of a fibrin cap and a lipid core is formed. Calcium is deposited forming a hard calcified core.
  6. Plaque may occlude the lumen, causing ischaemia to distant organs. This can manifest as angina / claudication.
  7. Atheromas can weaken the arterial wall leading to aneurysms.
  8. Atheroma can detach becoming an embolus which can lead to acute infarction, MI or stroke.
43
Q

Summarise hyaline arteriosclerosis.

A

Hyaline arteriosclerosis is associated with chronic hypertension and diabetes, and is associated with plasma protein deposition in the vessel wall.

44
Q

Summarise hyperplastic arteriosclerosis.

A

Hyperplastic arteriosclerosis is associated with severe acute hypertension and is characterised by expansion of the basement membrane.

45
Q

Claudication

A

Lower limb pain on exertion.

46
Q

What is the difference between Arteriosclerosis, Atherosclerosis, and Arteriolosclerosis?

A

Arteriosclerosis is a general umbrella term describing diseases where the wall of the artery becomes thicker, harder, and less elastic than normal.

Arteriolosclerosis is any sort of hardening of small arteries in arterioles.

Atherosclerosis is the hardening of any artery (even though it’s usually medium- to large-sized arteries) which is caused by the buildup of plaque.

47
Q

Plaque =

A

Plaque = Fibrous cap + Lipid core

48
Q

What arteries would be occluded to cause sroke / cerebral atrophy?

A

Internal carotid

Middle cerebral

49
Q

Occlusion of what artery can lead to peripheral ischaemia which can cause gangrene / claudication?

A

Popliteal artery

50
Q

Summarise Monckeberg medial calcific sclerosis.

A

Monckeberg sclerosis is caused by the formation of calcium crystals in the muscular layer of the blood vessel wall, leading to hardening of the blood vessel, but it this does not affect the diameter of the lumen.
- does not produce symptoms.

51
Q

Primary vs Secondary prevention of atherosclerosis:

A

Primary prevention refers to the steps taken by an individual to prevent the onset of the disease, delaying atheroma formation.
Secondary prevention is intended to prevent recurrence of events such as MI and stroke in symptomatic patients.

52
Q

What causes angina?

A

Reduced bloodflow causing ischemia to the heart muscle.

53
Q

Stable angina is most commonly caused by what?

A

When the patient has more than 70% stenosis or the coronary arteries.

54
Q

Why is angina worse during exercise?

A

During exercise and stress the heart works harder and so requires more blood - increased ischemia and pain.

55
Q

Define stable angina.

A

A clinical syndrome characterised by:
Discomfort in the chest, jaw, shoulder back or arms, typically elicited by exertion or emotional stress and relieved by rest or nitroglycerin.

56
Q

What is the normal underlying cause of stable angina?

A

Atherosclerosis of one or more coronary arteries.

57
Q

What are other rarer causes of stable angina?

A

Hypertrophic cardiomyopathy which causes a thickened muscle wall which needs more oxygen.
Aortic stenosis which means the heart has to pump against higher pressures.
Hypertension.

58
Q

Aortic stenosis

A

Narrowing of the aortic valve.

59
Q

Ischaemia in angina most commonly affects which layer of the heart?

A

Subendocardium

60
Q

How does subendocardial ischemia result in anginal pain?

A

Subendocardial ischemia results in release of bradykinin and adenosine which stimulate nerve fibres in the myocardium, resulting in the sensation of pain.

61
Q

Bradykinin

A

Bradykinin is an inflammatory mediator. It is a peptide that causes blood vessels to dilate.

62
Q

What is the classic description of anginal pain?

A

Pressure / squeezing feeling in the chest, pain in the left arm, shoulder, jaw or back.
- symptoms usually last less than twenty minutes and subside after the stress / exertion is taken away.

63
Q

What is unstable angina?

A

When patients experience pain during exercise / stress, yet also at rest.
- pain never really goes away.

64
Q

What is unstable angina usually caused by?

A

Rupture of an atherosclerotic plaque with thrombosis - results in greater occlusion to the vessel.
- causes the heart to feel starved of oxygen even while pumping at a normal rate.

65
Q

How is unstable angina regarded?

A

Unstable angina is regarded as a medical emergency as it has a high chance of progressing to a myocardial infarction.

66
Q

Vasospastic angina aka

A

Prinzmetal angina

67
Q

What causes vasospastic angina?

A

Ischemia due to coronary artery vasospasms.

  • smooth muscle around the coronary arteries constrict extremely tightly, reducing bloodflow enough to cause ischemia.
  • may or may not involve atherosclerosis.
68
Q

Why is prinzmetal angina referred to as transmural?

A

Prinzmetal angina involves ischemia which affects all layers of the heart, hence transmural.

69
Q

How is angina treated?

A

Nitroglycerin

70
Q

What are the three types of angina?

A
  1. Stable angina
  2. Unstable angina
  3. Prinzmetal angina
71
Q

Which substance released by ischaemic myocardium is the main mediator of chest pain in angina?

A

Adenosine

72
Q

How does adenosine cause chest pain?

A

Stimulation of A1 receptors located on cardiac nerve endings.

73
Q

What is stunning regarding angina?

A

Reversible contractile dysfunction that follows ischemia.

74
Q

What is hibernation regarding angina?

A

A chronic but reversible form of contractile dysfunction.

75
Q

What causes myocardial ischaemia?

A

An imbalance between myocardial oxygen supply, consumption and coronary flow.

76
Q

Silent angina

A

Silent ischemia is exactly like angina, except that you don’t feel it, can instead present with shortness of breath and palpitations.

77
Q

How do beta blockers work?

- why are they used in angina?

A

By blocking beta1 receptors in the heart decreases cardiac contractility (decrease force and rate) there by reduce oxygen demand. Thus reduce the ischemia in angina.

78
Q

What is used to treat prinzmetal angina?

A

Nitroglycerin (GTN)

Calcium channel blockers.

79
Q

Explain the general treatment of stable angina.

A

Medical treatment aims to relieve angina and prevent cardiovascular events.

Beta blockers and calcium channel antagonists are first-line options for treatment.

Short-acting nitrates can be used for symptom relief.

Low-dose aspirin and statins are prescribed to prevent cardiovascular events.

80
Q

Shear stress

A

Shear stress is a frictional stress applied parallel to the endothelial wall.

81
Q

Does atherosclerosis develop at points of high shear stress or points of low shear stress?

A

Low shear stress

82
Q

Glycocalyx

A

Fine hair on the arterial endothelium, has a protective function. Bodies first line of defence against atherosclerosis.

83
Q

Atypical symptoms of an acute MI:

A

Stridor
Tooth pain
Headache/Neck pain

84
Q

Matrix metallo proteases

A

Matrix metalloproteinases (MMPs) play an important role in atherosclerosis by degrading the extracellular matrix, which results in cardiovascular remodelling.

85
Q

Arterial thrombosis most commonly occurs due to atherosclerosis what is the most common cause of venous thrombosis?

A

Stasis

Cardiovascular 2 (20 decks)

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