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Pathology - Y5 > Cardiovascular Disease > Flashcards

Cardiovascular Disease Flashcards

1
Q

What is this?

A

Atherosclerosis

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2
Q

What is atherosclerosis?

A

An arteriosclerosis characterized by atheromatous deposits in and fibrosis of the inner layer of the arteries.

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3
Q

What is atherosclerosis characterised by?

A

Atheroscelrosis characterized by intimal lesions.

Atheroma (atheromatous plaques) - that protrude into vessel lumen.

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4
Q

What is this?

A

Atherosclerosis

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5
Q

What is an atheromatous plaque?

A

Raised lesion

Soft lipid core

White fibrous cap

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6
Q

What are the main risk factors for atherosclerosis?

A

Age

Gender

Genetics

Hyperlipidaemia

Hypertension

Smoking

Diabetes Mellitus

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7
Q

How do the number of risk factors affect the risk of getting atherosclerosis?

A

2 risk factors increase the risk fourfold

3 risk factors increase the risk sevenfold

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8
Q

What is the pathogenesis of atherosclerosis?

A

Chronic inflammatory and healing response of arterial wall to endothelial injury.

  1. Endothelial injury
  2. Lipoprotien accumulation (LDL)
  3. Monocyte adhesion to endothelium
  4. Monocyte migration into intima -> macrophages & foam cells
  5. Platelet adhesion
  6. Factor release
  7. Smooth muscle cell recruitment
  8. Lipid accumulation -> extra & intracellular, macrophages & smooth muscle cells
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9
Q

What is the pathogensis of smooth muscle proliferation?

A
  • Intimal smooth muscle proliferation
  • Some from circulating precursors – (have synthetic & proliferative phenotype)
  • ECM matrix deposition
  • Fatty streak -> mature atheroma & growth
  • PDGF, FGF, TGF-alpha implicate
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10
Q

Which infections can predispose to atherosclerosis?

A

Herpes

CMV

Chlamydia pneumonia

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11
Q

What is this?

A

Atherosclerosis - smooth muscle proliferation

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12
Q

What is a fatty streak?

A

Earliest lesion

Lipid filled foamy macrophages

No flow disturbance

In virtually all children >10yrs

Relationship to plaques uncertain

Same sites as plaques

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13
Q

What is an atherosclerotic plaque?

A

Patchy – local flow disturbances

Only involve portion of wall

Rarely circumferential

Appear eccentric

Composed of – cells, lipid, matrix

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14
Q

What is this?

A

Atherosclerotic plaque

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15
Q

What are the consequences of atheromas?

A

Stenosis

Acute plaque changes

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16
Q

What is stenosis?

A

Critical stenosis – demand > supply

Occurs at ~70% occlusion (or diameter <1mm)

Causes “stable” angina

Can lead to Chronic Ischaemic Heart Disease

Acute plaque rupture can occur

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17
Q

What is this?

A

Plaque disruption Type 11 eccentric ragged stenosis

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18
Q

What is this?

A

This is a normal coronary artery with no atherosclerosis and a widely patent lumen that can carry as much blood as the myocardium requires.

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19
Q

What are acute plaque changes which can occur?

A

Rupture: Exposes prothrombogenic plaque contents

Erosion: Exposes prothrombogenic subendothelial basement membrane

Haemorrhage into plaque: Increase size

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20
Q

What are vulnerable plaques?

A

Lots foam cells or extracellular lipid

Thin fibrous cap

Few smooth muscle cells

Clusters inflammatory cells

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21
Q

What is the mechanism for a rupture of a vulnerable plaque?

A

Adrenaline increases blood pressure & causes vasoconstriction.

Increases physical stress on plaque.

Hence emotional stress increases risk of sudden death.

Circadian periodicity to sudden death (6am-noon).

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22
Q

How do vulnerable plaques contribute to plaque growth?

A

Not all rupture causes occlusion.

Plaque disruption with platelet aggregation & thrombosis probably common.

Important mechanism for plaque growth.

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23
Q

What can vasoconstriction be due to?

A

Adrenergic agonists

Platelet contents

Reduced endothelial relaxing factors

Mediators from perivascular cells

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24
Q

What is this?

A

Human coronary atherosclerotic plaque with a yellow core of lipid separated from the lumen by a fibrous cap.

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25
Q

What is ischaemic heart disease?

A

Leading cause of death worldwide for men and women (7million/year).

Group of conditions resulting from myocardial ischaemia.

Imbalance of supply to demand for oxygenated blood.

Also less nutrients & less waste removal.

Therefore less well tolerated than pure hypoxia.

90% myocardial ischaemia due to reduced blood flow due to atherosclerosis.

Long silent progression prior to symptoms.

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26
Q

What is this?

A

IHD

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27
Q

What is this?

A

IHD

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28
Q

What is the presentation of IHD?

A

Angina pectoris

Myocardial infarction

Chronic IHD with heart failure

Sudden cardiac death

29
Q

What is the epidemiology of IHD?

A

500,000 deaths per year USA

50% fall in death rate since 1963 (peak)

Fall due to prevention & treatment

But aging population

30
Q

What is the pathogenesis of IHD?

A

Predominant cause is insufficient coronary perfusion relative to myocardial demand due to chronic progressive atherosclerotic narrowing of epicardial coronary arteries and variable degrees of superimposed plaque change, thrombosis and vasospasm.

31
Q

Where do plaques usually occur in IHD?

A

Plaques mainly in first few cm of LAD or LCX

Entire length RCA

32
Q

What is the pathogenesis of acute coronary syndrome?

A

Stable plaque becomes unstable.

Due to rupture, erosion, haemorrhage etc.

Generally leads to superimposed thrombus which increases occlusion.

33
Q

What is angina pectoris?

A

Transient ischaemia not producing myocyte necrosis.

34
Q

What are the different types of angina?

A

Stable, Prinzmetal, Unstable

  • Stable comes on with exertion, relieved by rest, no plaque disruption.
  • Prinzmetal: Uncommon, due to artery spasm
35
Q

What is unstable angina pectoris?

A

Unstable more frequent, longer, onset with less exertion or at rest.

Disruption of plaque.

Superimposed thrombus.

Possible embolisation or vasospasm.

Warning of impending infarction.

36
Q

What is a myocardial infarction?

A

Death of cardiac muscle due to prolonged ischaemia.

Incidence 5/1000 per year UK (ST elevation).

IHD most common cause death postmenopausal women.

37
Q

What is the pathogenesis of artery occlusion in MI?

A

Sudden change to plaque

Platelet aggregation

Vasospasm

Coagulation

Thrombus evolves

38
Q

What is the myocardial response to an MI?

A

Myocardial blood supply compromised leading to ischaemia

Loss of contractility within 60 seconds

Therefore heart failure can precede myocyte death

Potentially reversible

Irreversible after 20-30 minutes

39
Q

What are common sites of occlusion in an MI?

A

LAD: 50%, ant wall LV, ant septum, apex

RCA: 40%, post wall LV, post septum, post RV

LCx: 20%, lat LV not apex

40
Q

What is the evolution of an MI?

A

Under 6 hours: Normal by histology (CK-MB also normal)

6–24 hrs: Loss of nuclei, homogenous cytoplasm necrotic cell death.

1-4 days: Infiltration of polymorphs then macrophages (clear up debris).

5-10 days: Removal of debris.

1-2 weeks: Granulation tissue, new blood vessels, myofibroblasts, collagen synthesis.

Weeks-months: Strengthening, decellularising scar.

41
Q

What is this?

A

MI, 3–7 days

42
Q

What is this?

A

MI 1-3 days.

Coagulation necrosis, loss nuclei & striations, neutrophils +++

43
Q

What is this?

A

MI 10-14 days granulation tissue, macrophages.

44
Q

What is this?

A

MI
>2 months old

45
Q

What are clinical features of an MI?

A

10 – 15% asymptomatic

Common in elderly & diabetes mellitus

Cardiac enzymes (CK, Troponin etc)

Subendocardial infarct may not cause usual ST changes.

46
Q

What is a reperfusion injury?

A

Clinical importance uncertain

Due to oxidative stress, Ca overload, inflammation

Arrhythmias common

Biochemical abnormalities last days -> weeks

Thought to cause “stunned myocardium” – reversible cardiac failure lasting several days.

47
Q

What is hibernating myocardium?

A

Chronic sub lethal ischaemia -> lowered metabolism in myocytes “hibernating myocardium” reversed with revascularisation.

48
Q

What are complications of MI?

A

Contractile dysfunction: 40% infarct-> cardiogenic shock with 70% mortality rate.

Arrhythmia: Due to myocardial irritability & conduction disturbance.

Myocardial rupture: Free wall most common, septum less common, papillary muscle least common. (At mean 4-5days, range 1-10 days).

Pericarditis (Dressler syndrome): 2nd or 3rd day

RV infarction

Infarct extension: New necrosis adjacent to old.

Infarct expansion: Necrotic muscle stretches ->mural thrombus.

49
Q

What is this?

A

Dressler syndrome

50
Q

What is the mortality associated with an MI?

A

Total mortality = 30% in one year.

3-4% mortality per year after first.

51
Q

What is chronic ischaemic heart disease?

A

Progressive heart failure due to ischaemic myocardial damage.

May not be prior infarction.

Can arise with severe obstructive coronary artery disease.

Enlarged heavy heart, hypertrophied, dilated LV.

52
Q

What is sudden cardiac death?

A

Unexpected death from cardiac causes in individuals without symptomatic heart disease or early (1hr) after onset of symptoms.

Usually due to lethal arrhythmia

Usually on background of IHD (90%)

53
Q

Which conditions are associated with sudden cardiac death?

A

Acute myocardial ischaemia is usual trigger.

Usually causes electrical instability at sites distant from conduction system often near scars from old MIs.

Other conditions also associated e.g. Aortic stenosis, mitral valve prolapse, pulmonary hypertension.

54
Q

What is cardiac failure?

What are the two types of cardiac failure?

A

End point of many conditions.

Congestive Heart Failure (L&R).

  • Left sided: SOB, pulmonary oedema
  • Right sided: Peripheral oedema
55
Q

What is this?

A

Pulmonary oedema due to left sided heart failure.

56
Q

What are causes of heart failure?

A

Ischaemic heart disease

Valve disease

Hypertension

Myocarditis

Cardiomyopathy

Left sided heart failure (Right)

57
Q

What are complications associated with heart failure?

A

Sudden Death

Arrhythmias

Systemic emboli

Pulmonary oedema with superimposed infection

58
Q

What is the histopathology of heart failure?

A

Dilated heart, Scarring & thinning of the walls.

Microscopy: Fibrosis and replacement of ventricular myocardium.

59
Q

What are the types of cardiomyopathy?

A

Dilated

Hypertrophic

Restrictive

(Too thin, too thick, too stiff)

60
Q

What is dilated cardiomyopathy?

A

Progressive loss of myocytes.

Dilated heart.

61
Q

What are causes of dilated cardiomyopathy?

A

Idiopathic

Infective: Viral myocarditis

Toxic: Alcohol, chemotherapy (adriamycin, daunorubicin), cobalt, iron

Hormonal: Hyper-, hypo- thyroid, diabetes, peri-partum (?).

Genetic: Haemochromatosis, Fabry’s, McArdle’s.

Immunological: Myocarditis incl. Viral (hypersensitivity component)

62
Q

What is hypertrophic cardiomyopathy?

A

Left ventricular hypertrophy

Familial in 50% (autosomal dominant, variable penetrance)

Beta-myosin heavy chain

Thickening of septum narrows left ventricular outflow tract.

63
Q

What is restrictive cardiomyopathy?

A

Impaired ventricular compliance

Idiopathic or secondary to myocardial disease eg amyloid, sarcoidosis

Normal size heart – big atria

64
Q

What is chronic rheumatic valvular disease?

A

Sequelae of earlier rheumatic fever. Predominantly left-sided valves (almost always mitral).

  • Mitral > Aortic > Tricuspid > Pulmonary
  • Mitral alone 48%, Mitral + aortic 42%

Thickening of valve leaflet, especially along lines of closure.

Fusion of commissures.

Thickening, shortening and fusion of chordae tendineae.

65
Q

What is calcific aortic stenosis?

A

Commonest cause aortic stenosis, occurs in 70s or 80s.

Calcium deposits outflow side cusp impairs opening.

Orifice compromised.

Outflow tract obstruction.

66
Q

What are causes of aortic regurgitation?

A

Rigidity: Rheumatic, degenerative

Destruction: Microbial endocarditis

Disease of aortic valve ring: Results in dilitation. Valve insufficient to cover increased area.

67
Q

What are conditions associated with aortic regurgitation?

A

Marfan’s Syndrome

Dissecting aneurysm

Syphilitic aortitis

Ankylosing spondylitis

68
Q

What are the two main categories of aneurysms?

A

True: All layers wall

False: Extravascular haematoma

69
Q

What are causes of aneurysms?

A

Weak wall

Congenital e.g. Marfans

Atherosclerosis

Hypertension

Pathology - Y5 (59 decks)

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