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YR5 Histopathology > 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 + fibrosis of the inner layer of the arteries.

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3
Q

What is atherosclerosis characterised by?

A

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 proliferation of endothelium

Soft lipid core

White fibrous cap

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6
Q

What are the 7 main risk factors for atherosclerosis?

A

Age

Sex

Genetics

Hyperlipidaemia

HTN

Smoking

Diabetes Mellitus

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7
Q

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

A

2 RFs increase risk 4-fold

3 RFs increase risk 7-fold

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8
Q

What is the pathogenesis of atherosclerosis according to the response to injury hypothesis?

A
  1. Endothelial injury, disrupted flow, increased permeability
  2. LDL accumulation
  3. Monocyte adhesion to endothelium
  4. Monocyte migration into intima -> macrophages + foam cells
  5. Platelet adhesion
  6. Factor release from activated platelets
  7. Induces smooth muscle cell recruitment, proliferation, ECM production + T cell recruitment
  8. Lipid accumulation: extra + intracellular, macrophages + smooth muscle cells
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9
Q

What is this?

A

Atherosclerosis - smooth muscle proliferation

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10
Q

What is a fatty streak?

A

Earliest lesion

Lipid filled foamy macrophages

No flow disturbance

In ~all children >10yrs

Relationship to plaques uncertain

Same sites as plaques

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11
Q

What characterises an atherosclerotic plaque?

A

Patchy: cause local flow disturbances

Only involve a portion of wall

Rarely circumferential

Appear eccentric

Composed of cells, lipid, matrix

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12
Q

What is this?

A

Atherosclerotic plaque

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13
Q

What are 2 consequences of atheromas?

A

Stenosis

Acute plaque changes

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14
Q

What is stenosis?

A

Critical stenosis: demand > supply

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

Causes “stable” angina

Can lead to Chronic IHD

Acute plaque rupture can occur

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15
Q

What is this?

A

Plaque disruption Type 11 eccentric ragged stenosis

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16
Q

What is this?

A

Normal coronary artery

No atherosclerosis

Widely patent lumen that carries as much blood as the myocardium requires.

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17
Q

What are the acute plaque changes that can occur?

A

Rupture: Exposes prothrombogenic plaque contents

Erosion: Exposes prothrombogenic subendothelial basement membrane

Haemorrhage into plaque: Increase size

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18
Q

What characterises vulnerable plaques?

A

Large lipid core

Thin fibrous cap

Large inflammatory infiltrate

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19
Q

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

A

Adrenaline increases BP + 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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20
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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21
Q

What can vasoconstriction be due to?

A

Adrenergic agonists

Platelet contents

Reduced endothelial relaxing factors

Mediators from perivascular cells

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22
Q

What is this?

A

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

Opposite core = arc of normal vessel wall

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23
Q

What is ischaemic heart disease?

A

Group of conditions resulting from myocardial ischaemia.

Imbalance of supply to demand for oxygenated blood.

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 Sx

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24
Q

What is this?

A

IHD

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25
Q

What is this?

A

IHD

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26
Q

List 4 presentations of IHD

A

Angina pectoris

Myocardial infarction

Chronic IHD with heart failure

Sudden cardiac death

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27
Q

What is the epidemiology of IHD?

A

500,000 deaths yearly USA

50% fall in death rate since 1963 (peak)

Fall due to prevention + tx

But aging population

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28
Q

What is the predominant pathogenesis of IHD? What is this due to?

A

Insufficient coronary perfusion relative to myocardial demand

Due to chronic progressive atherosclerotic narrowing of epicardial coronary arteries + variable superimposed plaque change, thrombosis + vasospasm.

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29
Q

Where do plaques usually occur in IHD?

A

1st few cm of LAD or LCX

Entire length RCA

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30
Q

What is the pathogenesis of acute coronary syndrome?

A

Stable plaque becomes unstable.

Due to rupture, erosion, haemorrhage

Generally leads to superimposed thrombus which increases occlusion.

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31
Q

What is angina pectoris?

A

Transient ischaemia not producing myocyte necrosis.

32
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

33
Q

What is unstable angina pectoris?

A

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

Disruption of plaque.

Superimposed thrombus.

Possible embolisation or vasospasm.

Warning of impending infarction.

34
Q

What is a myocardial infarction? What is the incidence?

A

Death of cardiac muscle due to prolonged ischaemia.

5/1000 yearly UK (STEMI).

IHD most common cause death postmenopausal women.

35
Q

What is the pathogenesis of artery occlusion in MI?

A

Sudden change to plaque

Platelet aggregation

Vasospasm

Coagulation

Thrombus evolves

36
Q

What is the myocardial response to an MI?

A

Myocardial blood supply compromised leading to ischaemia

Loss of contractility within 60s

Therefore HF can precede myocyte death

Potentially reversible

Irreversible after 20-30m

37
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

38
Q

What is the evolution of changes after an MI?

A

< 6h: Normal histology + CK-MB

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

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

5-10d: Removal of debris.

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

Weeks-months: Strengthening, decellularising scar.

39
Q

What is this?

A

MI, 3–7 days

40
Q

What is this? What can be seen?

A

MI 1-3 days.

Coagulation necrosis

Loss nuclei + striations

Neutrophils +++

41
Q

What is this? What can be seen?

A

MI 10-14 days

Granulation tissue

Macrophages.

42
Q

What is this? At what time point?

A

MI
>2 months old

Lots of fibrosis + scar formation

43
Q

What are clinical features of an MI?

A

Common in elderly + diabetes mellitus

10 – 15% asymptomatic

Cardiac enzymes (High CK, Troponin)

Subendocardial infarct may not cause usual ST changes.

44
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.

45
Q

What are 7 short term complications of MI?

A

Contractile dysfunction → Cardiogenic shock

Arrhythmia: conduction disturbance- bradycardia, SVT

Myocardial rupture: LV free wall most common at ~4-5d

Pericarditis (Dressler syndrome): 2-3d after MI

RV infarction

Infarct extension: new necrosis adjacent to old

Infarct expansion: necrotic muscle stretches → mural thrombus

46
Q

What is this?

A

Dressler syndrome

47
Q

What is the mortality associated with an MI?

A

Total mortality = 30% in 1 year.

3-4% mortality per year after

48
Q

What is chronic ischaemic heart disease?

A

Progressive heart failure due to ischaemic myocardial damage.

May not be have had prior infarction.

Can arise with severe obstructive coronary artery disease.

Enlarged heavy heart, hypertrophied, dilated LV.

Atherosclerosis

Maybe mural thrombi

Fibrosis

49
Q

What is sudden cardiac death?

A

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

Usually due to lethal arrhythmia

Usually on background of IHD (90%)

50
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 HTN.

51
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
52
Q

What is this?

A

Pulmonary oedema due to left sided heart failure.

53
Q

What are causes of heart failure?

A

Ischaemic heart disease

Valve disease

HTN

Myocarditis

Cardiomyopathy

Left sided heart failure (Right)

54
Q

What are complications associated with heart failure?

A

Sudden Death

Arrhythmias

Systemic emboli

Pulmonary oedema with superimposed infection

55
Q

What is the histopathology of heart failure?

A

Dilated heart, Scarring + thinning of the walls.

Microscopy: Fibrosis + replacement of ventricular myocardium.

56
Q

What are the types of cardiomyopathy?

A

Dilated

Hypertrophic

Restrictive

(Too thin, too thick, too stiff)

57
Q

What is dilated cardiomyopathy?

A

Progressive loss of myocytes.

Dilated heart.

58
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)

59
Q

What is hypertrophic cardiomyopathy?

A

LV hypertrophy

Familial in 50% (AD, variable penetrance)

Beta-myosin heavy chain

Thickening of septum narrows left ventricular outflow tract.

60
Q

What is restrictive cardiomyopathy?

A

Impaired ventricular compliance

Idiopathic or secondary to myocardial disease eg amyloid, sarcoidosis

Normal size heart, big atria

61
Q

What is chronic rheumatic valvular disease?

A

Sequelae of 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 + fusion of chordae tendineae.

62
Q

What is calcific aortic stenosis?

A

Commonest cause aortic stenosis

Occurs in 70-80s.

Calcium deposits outflow side cusp impairs opening.

Orifice compromised.

Outflow tract obstruction.

63
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.

64
Q

What are 4 conditions associated with aortic regurgitation?

A

Marfan’s Syndrome

Dissecting aneurysm

Syphilitic aortitis

Ankylosing spondylitis

65
Q

What are the two main categories of aneurysms?

A

True: All layers wall

False: Extravascular haematoma

66
Q

What are 4 causes of aneurysms?

A

Weak wall

Congenital e.g. Marfans

Atherosclerosis

Hypertension

67
Q

Which lipids are good and which are bad?

A

LDL = BAD

HDL = GOOD

68
Q

What 7 less obvious risk factors contribute to atherosclerosis?

A

Inflammation: pro inflammatory state

Metabolic syndrome: HTN, hyperlipidaemia

Lipoprotein a: RF for Cerebrovascular + cardiovascular disease

Haemostasis: procoagulation

Lack of exercise

Stress

Obesity: HTN, DM, low HDL

69
Q

What is the response to injury hypothesis?

A

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

70
Q

Why are there many asymptomatic potential victims in atherosclerosis?

A

Majority of plaques show only mild-moderate luminal stenosis prior to acute change

71
Q

How does vasoconstriction contribute to risk of disruption of a vulnerable plaque?

A

Reduced luminal size increases local mechanical forces

71
Q

How does vasoconstriction contribute to risk of disruption of a vulnerable plaque?

A

Reduced luminal size increases local mechanical forces

72
Q

Describe the impact of IHD worldwide

A

Leading cause of death worldwide for M+F (7million/year).

73
Q

In general, what amount of stenosis is required to cause symptoms?

A

75% = Sx precipitated by exercise

Vasodilation cannot compensate above this

90% = pain at rest

74
Q

List 3 long term complications of MI

A

Ventricular aneurysm → thrombus, HF, arrhythmia

Papillary muscle rupture

Chronic IHD: progressive late HF

75
Q

What is this? How common is it?

A

Ventricular aneurysm

Very rare

76
Q

What is this?

A

Papillary muscle rupture

YR5 Histopathology (27 decks)

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