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Histopathology > Cardiovascular Disease > Flashcards

Cardiovascular Disease Flashcards

1
Q

How many deaths in the UK does coronary heart disease cause in men and women?

A
  • 25% in men
  • 16% in women
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2
Q
A

Atheroma in a coronary artery

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3
Q

Define atherosclerosis.

A

An arteriosclerosis characterising by atheromatous deposits in and fibrosis of the inner layer of the arterioles

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4
Q

What its atherosclerosis characterised by?

A
  • There are intimal lesions (atheromatous plaques) that protrude into the vessel lumen
    • (1) Smooth endothelium is damaged, platelets stick to tissue, endothelium proliferates and a fibrous cap form

(2) There is deposition of cholesterol and the plaque enlarges blocking the artery

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5
Q
A

Top aorta has lots of atherosclerosis

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6
Q

What do atheromatous plaques look like?

A
  1. Raised lesion
  2. Soft lipid core
  3. White fibrous cap
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7
Q

What are the RFs of Artherosclerosis?

A
  • Risk factors:
    • Non-modifiable:
      • Age - Atherosclerosis progressive between 40->60 years incidence myocardial infarction (MI) X 5
      • Gender (premenopausal women protected → post-menopausal women = >risk than men)
      • Genetics (FHx, familial hypercholesterolaemia, polymorphisms)
      • Modifiable:
        • Hyperlipidaemia (LDL bad / HDL good, diet, statins inhibit HMG-CoA reductase)
        • Hypertension (increased IHD risk by 60%)
        • Smoking Definite risk in men, probable in women

Prolonged smoking doubles death rate from IHD

Stopping reduces risk considerably

  • Diabetes mellitus (induces hypercholesterolaemia and atherosclerosis)
  • Other risk factors: inflammation, hyperhomocyteinaemia, metabolic syndrome, lipoprotein a, haemostasis (pro-coagulation), lack of exercise, stress, obesity
  • Risk factors have a multiplicative effect – 2 risk factors increase the risk 4x (3 RFs = 7x increase risk)
  • 20% of CVD events occur in absence of RFs and 75% events in healthy women occur in LDL below the risk level
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8
Q

Describe the pathogenesis.

A
  • Pathogenesis – response to injury hypothesis:
  • Chronic inflammatory and healing response of arterial wall to endothelial injury
    • (1) endothelial injury → LDL accumulation
    • (2) monocyte adhesion to endothelium
    • (3) monocyte migration into intima → macrophages & foam cells
    • (4) platelet adhesion → factor release →smooth muscle cell recruitment
    • (5) lipid accumulation → extracellular and intracellular macrophages and smooth muscle cells
    • The early atheroma arises in intact endothelium however, endothelial dysfunction (see below for causes of endothelial dysfunction) is important which increases the permeability, alters gene expression and adhesion
    • Haemodynamic disturbance, hypercholesterolaemia and inflammation → dysfunction and vicious cycle
    • Factor release causes smooth muscle recruitment and lipid accumulation
      • Intimal smooth muscle proliferation
      • Some from circulating precursors (have synthetic & proliferative phenotype)
      • ECM matrix deposition
      • Fatty streak: mature atheroma and growth
      • PDGF, FGF, TGF-alpha implicated
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9
Q

What is role of infection?

A
  • Infection – no conclusive evidence
    • Herpes
    • CMV
    • Chlamydia pneumonia
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10
Q
A

Cracks - cholesterol

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11
Q
A

Fatty streak

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12
Q

What are fatty streaks?

A
  • (1) Fatty streak (these are tiny little streaks in the vessel wall)
    • Earliest lesion
    • Lipid filled foamy macrophages, no flow disturbance
    • In virtually all children <10y/o
    • Relationship to plaques is uncertain but in same sites as plaques
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13
Q
A

Atheroma

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14
Q

What are atherosclerotic plaque, what do they do?

A
  • Patchy: local flow disturbance
  • Only involve portion of the wall: rarely circumferential
  • Appear eccentric and composed of cells, lipid and matrix
  • Can rupture or obstruct
  • Occur in points of disturbed flow: carotids and coronary arteries
    • Bifurcations
    • Curvatures
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15
Q

What are the consequences of stenosis?

A
  • Critical stenosis is when demand > supply
  • Occurs at ~70% occlusion (or diameter <1mm)
  • Causes “stable” angina and can lead to chronic IHD
  • Acute plaque rupture can occur
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16
Q
A

Left to right : build up of atheroma form healthy to stable angina

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17
Q

Describe acute plaque changes.

A
  • Rupture: exposes prothrombogenic plaque contents
  • Erosion: exposes prothrombogenic subendothelial basement membrane
  • Haemorrhage into plaque (increases size)
  • Majority of plaques which show acute change only show mild to moderate luminal stenosis prior to acute change: therefore, there are numerous asymptomatic potential victims
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18
Q

What are the characteristic of vulnerable plaques?

A
  • Lots of foam cells and extracellular lipid
  • Thin fibrous cap
  • Few smooth-muscle cells
  • Clusters of inflammatory cells
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19
Q

What is the mechanism behind rupture of vulnerable plaques?

A
  • Mechanism
    • Adrenaline increases BP and causes vasoconstriction
    • Increases physical stress on plaque
    • Hence emotional stress increases risk of sudden death
    • Circadian periodicity to sudden death (6am-noon)
      • Not all rupture → occlusion – plaque disruption with platelet aggregation/thrombosis common
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20
Q

What is role off vasoconstriction in CVD?

A
  • Vasoconstriction adds to the problem
    • Reduces luminal size
    • Increases local mechanical forces
    • Occurs due to adrenergic agonists, platelet contents, reduced endothelial relaxing factors and mediators from perivascular cells
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21
Q
A

Human coronary atherosclerotic plaque with a yellow core of lipid separated from the lumen by a fibrous cap. Opposite the plaque is an arc of normal vessel wall

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22
Q
A

Cross section of LV - white area is myocardial infarction

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23
Q

What is the epidemiology go IHD? What is it?

A
  • Imbalance of supply to demand for oxygenated blood: less nutrients and less waste removal [2 main features]
    • Therefore, less well tolerated than pure hypoxia
    • 90% of myocardial ischaemia due to reduced blood flow due to atherosclerosis
    • 75%+ stenosis needed to cause symptoms precipitated by exercise (stable angina) → 90% = pain at rest
    • Long silent progression prior to symptoms
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24
Q
A

Cross section - fatty plaques

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25
Q
A

Complete block → death from MI

26
Q

Presentation of IHD?

A
27
Q

IHD epidemiology.

A
28
Q

IHD pathogenesis

A
29
Q

What is acute coronary syndrome?

A
  • Acute coronary syndromes = stable becomes unstable (i.e. rupture, erosion, haemorrhage) → superimposed thrombus
30
Q

What is angina pectoris?

A
  • Transient ischaemia not producing myocyte necrosis
    • Plaques form in first parts of LAD or LCx; or entire length of RCA
    • Stable, Prinzmetal or unstable
    • Stable comes on with exertion, relieved by rest, no plaque disruption
    • Prinzmetal is uncommon but due to artery spasm
31
Q

What is unstable angina?

A
  • Unstable is when is becomes more frequent, longer, onset with less exertion or at rest
    • Disruption of plaque
    • Superimposed thrombus
    • Possible embolisation or vasospasm
    • Warning of impending infarction
32
Q

What is a myocardial infarction? What is the epidemiology?

A
  • Death of cardiac muscle due to prolonged ischaemia
  • Incidence 5/1000 per year UK (ST elevation)
  • 10% less than 40yrs; 45% less than 65yrs; blacks and whites equal; men greater risk than women throughout life

IHD most common cause death postmenopausal women

33
Q

What is the pathogenesis of MI?

A
  • Pathogenesis
    • (1) Artery occlusion:
      • Sudden change of plaque Platelet aggregation Vasospasm
      • Coagulation Thrombus evolves
      • (2) Myocardial response
        • Myocardial blood supply compromised leading to ischaemia
        • Loss of contractility within 60 seconds
        • Therefore, heart failure can precede myocyte death
        • Potentially reversible but irreversible after 20-30 minutes
        • LAD: 50%, anterior wall left ventricle, anterior septum, apex
        • RCA: 40%, posterior wall left ventricle, posterior septum, posterior right ventricle
        • LCx: 20%, lateral left ventricle, not apex
34
Q

Describe the evolution of MI

A
  • <6 hours: normal by histology (CK-MB also normal)
  • 6–24 hours: coagulative necrosis, loss of nuclei and striations
  • 1-4 days: infiltration of neutrophilsmacrophages (clear up debris)
  • 5-10 days: removal of debris (macrophages)
  • 10-14 days: granulation, angiogenesis, collagen synthesis (myofibroblasts, macrophages, angioblasts)
  • Weeks to months: strengthening, decellularising scar
35
Q
A

MI 1-3 days
Coagulation necrosis, loss nuclei & striations,
neutrophils +++

36
Q
A

MI 10-14 days
granulation tissue, macrophages

37
Q
A

MI > 2 month sold

38
Q

What are the clinical features of MIs?

A
  • 10-15% asymptomatic: elderly and DM
  • Cardiac enzymes (CK, troponin)
  • Subendocardial infarct may not cause usual ST changes
39
Q

MI consequences

A
  • General Points:
    • In hospital death rate is 7%
    • Half of deaths occur within 1 hour of onset (most of these do not reach hospital)
    • Age, female, DM and previous MI = worse prognosis
40
Q

What is reperfusion injury?

A
  • Reperfusion injury: due to oxidative stress, Ca2+ overload, inflammation
    • Arrhythmias common
    • Biochemical abnormalities last days to weeks
    • Thought to cause “stunned myocardium”: reversible cardiac failure lasting several days
41
Q

What is hibernating myocardium?

A

chronic sublethal ischaemia causes lowered metabolism in myocytes is reversed with revascularisation

42
Q

What are the complication of MI?

A
  • D Death V Valvular disease
  • A Arrhythmia A Aneurysm of ventricle
  • R Rupture (papillary muscle) D Dressler’s syndrome (pericarditis; 2nd or 3rd day)
  • T Tamponade E Embolism (i.e. bowel ischaemia)
  • H Heart Failure R Recurrence
    • Total mortality is 30% in one year but 3-4% after this due to complications
43
Q
A

Dressler Syndrome

44
Q
A

Normal LV and aneurysm

45
Q
A

Papiillary muscle rupture

46
Q

What is Chronic IHD?

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
  • Atherosclerosis; maybe mural thrombi
  • Fibrosis (microscopic)
47
Q

What is sudden cardiac death? What is the epidemiology?

A
  • “Unexpected death from cardiac causes in individuals without symptomatic heart disease or early (1 hour) after onset of symptoms”; usually due to lethal arrhythmia (from ischaemia-induced electrical instability)
    • Usually on background of IHD (90%) although drugs such a cocaine may be the cause
    • Acute myocardial ischaemia is usual trigger
    • Usually causes electrical instability at sites distant from conduction system (near scars from old MIs)
    • Other conditions also associated (aortic stenosis, mitral valve prolapse, pulmonary hypertension)
48
Q

What is cardiac failure? What are the types?

A
  • The end point of many conditions
  • Types:
    • Left: SOB, pulmonary oedema (CXR = ABCDE)
    • Right: peripheral oedema (nutmeg liver)
    • Left and right = congestive heart failure
49
Q

What are the causes of cardiac failure?

A

•Causes

–Ischaemic heart disease

–Valve disease

–Hypertension

–Myocarditis

–Cardiomyopathy

– Left sided heart failure (Right)

50
Q

What are the complications of cardiac failure?

A
  • Complications: sudden death, arrhythmias, systemic emboli, pulmonary oedema with superimposed infection
51
Q

What is the pathology of cardiac failure?

A
  • Pathology:
    • Dilated heart, scarring and thinning of the walls
    • Microscopy: fibrosis and replacement of the ventricular myocardium
52
Q

What is cardiomyopathy?

A

too thin, too thick, too stiff

53
Q

What are the causes of dilated cardiomyopathy?

A
  • Progressive loss of myocytes
  • Dilated heart
  • Causes:
    • Idiopathic
    • Infective: viral myocarditis
    • Toxic: alcohol, chemotherapy (adriamycin, daunorubicin)
    • Cobalt, iron
    • Hormonal: hyper/hypothyroid, diabetes, peri-partum
    • Genetic: haemochromatosis, Fabry’s, McArdle’s
    • Immunological: myocarditis; inc. viral
54
Q

What are the causes of 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
55
Q

What is restrictive cardiomyopathy?

A
  • Impaired ventricular compliance
  • Idiopathic or secondary to myocardial disease (amyloid, sarcoidosis)
  • Normal heart size but big atria
56
Q

What is chronic rheumatic valvular disease?

A
  • Sequelae of earlier rheumatic fever
  • Predominantly left-sided valves (almost always mitral stenosis)
    • Mitral > Aortic > Tricuspid > Pulmonic
    • Mitral alone 48%; mitral and aortic 42%
    • Thickening of valve leaflet, especially along lines of closure
    • Fusion of commissures
    • Thickening, shortening and fusion of chordae tendineae
57
Q

What his calcific aortic stenosis?

A
  • Commonest cause of aortic stenosis (esp. in elderly; 70s or 80s)
  • Calcium deposits in outflow side cusp which impair opening or orifice is compromised
  • Outflow tract obstruction
58
Q

What causes aortic regurgitation?

A
  • Rigidity: RHD
  • Destruction: IE
    • Left-sided normally (as it is often the more ‘damaged valve’)
    • Right-sided in IVDU (as it is the first valve the bacterium come across)
    • Disease of aortic valve ring: dilatation means that valve is insufficient to cover increased area
      • Marfan’s Syndrome Dissecting aneurysm
      • Syphilitic aortitis Ankylosing spondylitis
59
Q
A

Endocarditis

60
Q

What are the types of aneurysms? What causes them?

A
  • True: all layers of the wall
  • False: extravascular haematoma → aortic dissections
  • Causes: weak wall of large arteries
    • Marfan’s
    • Atherosclerosis
    • Hypertension
60
Q

What are the types of aneurysms? What causes them?

A
  • True: all layers of the wall
  • False: extravascular haematoma → aortic dissections
  • Causes: weak wall of large arteries
    • Marfan’s
    • Atherosclerosis
    • Hypertension

Histopathology (14 decks)

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