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a path 3 > HISTO: Cardiovascular > Flashcards

HISTO: Cardiovascular Flashcards

1
Q

True or false

“In the Western world atheroma causes half of all deaths and more morbidity and mortality that any other disorder”

A

True

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2
Q

What is shown?

A

Atherosclerosis

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3
Q

Define atheroscelrosis.

A

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

Atheroscelrosis is characterized by intimal lesions - atheroma (atheromatous plaques) - that protrude into vessel lumen

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4
Q
A
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5
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A
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6
Q

What are the characteristics of an atheromatous plaque?

A
  • Raised lesion
  • Soft lipid core
  • White fibrous cap
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7
Q

What are the risk factors for atherosclerosis?

A
  • Age
  • Gender
  • Genetics
  • Hyperlipidaemia
  • Hypertension
  • Smoking
  • Diabetes Mellitus
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8
Q

What kind of effect does having multiple RFs have on risk of atherosclerosis?

A

Risk factors have a MULTIPLICATIVE EFFECT e.g.

  • 2 risk factors increase the risk fourfold
  • 3 risk factors increase the risk sevenfold
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9
Q

Hwo does age affect atherosclerosis risk?

A

Atherosclerosis progressive between 40->60 years

incidence myocardial infarction (MI) X 5

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10
Q

How does gender affect atherosclerosis?

A

Premenopausal women protected (HRT no protection)

Postmenopausal risk increases (older ages greater than men)

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11
Q

How do genetics affect risk of atherosclerosis?

A

Family history most significant independent risk factor

Some mendelian disorders (eg Familial Hypercholesterolaemia)

Most multifactorial (genetic polymorphisms -> clustered risk factors HT, DM)

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12
Q

What is a modifiable risk factor for atherosclerosis? How is this risk modified?

A
  1. Hyperlipidaemia (Hypercholesterolaemia)
  • LDL – bad HDL – good
  • Diet rich in cholesterol/saturated fat – bad
  • Statins inhibit HMG-CoA reductase rate limiting enzyme in liver cholesterol synthesis - good
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13
Q

How does HTN affect risk of atherosclerosis?

A

Modifiable RF 2: HTN

  • Systolic & Diastolic important
  • Ht alone increases risk of IHD by 60%
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14
Q

How does smoking affect risk of athrosclerosis?

A
  1. Smoking
  • Definite risk in men, probable in women
  • Prolonged smoking doubles death rate from IHD
  • Stopping reduces risk considerably
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15
Q

Why is DM a RF for atherosclerosis?

A
  1. DM
  • Induces hypercholestrolaemia
  • Increases risk of atherosclerosis
  • 2 x risk IHD in DM if all other factors equal
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16
Q

Which of these is not a major RF for ischaemic heart disease?

  • Age
  • Male sex
  • High alcohol
  • Smoking
  • HTN
A

High alcohol consumption is not a major RF

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17
Q

What are some other RFs for atherosclerosis?

A
  • Inflammation
  • Hyperhomocyteinaemia
  • Metabolic syndrome
  • Lipoprotein (a)
  • Haemostasis (procoagulation)
  • Lack of exercise
  • Stress
  • Obesity (Ht, Dm, low HDL)
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18
Q

What is the pathogenesis of atherosclerosis? (Response to Injury Hypothesis)

A

Response to Injury Hypothesis

  1. Chronic inflammatory and healing response of arterial wall to endothelial injury
  2. Endothelial injury
    • Lipoprotien accumulation (LDL)
    • Monocyte adhesion to endothelium
  3. Monocyte migration into intima -> macrophages & foam cells
  4. Platelet adhesion
  5. Factor release
  6. Smooth muscle cell recruitment
  7. Lipid accumulation -> extra & intracellular, macrophages & smooth muscle cells
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19
Q

How does endothelial damage occur?

A

Early atheroma arises in intact endothelium

Endothelial dysfunction important – increase permeability, gene expression & adhesion

  • Haemodynamic disturbance -> dysfunction
  • Hypercholesterolaemia -> dysfunction
  • Inflammation -> vicious circle
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20
Q

What are the characteristics of smooth muscle proliferation in atherosclerosis pathogenesis?

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 implicated
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21
Q

What are the layers seen here in an artery?

A
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22
Q

What is the earliest lesion in atherosclerosis?

A

Fatty streak

  • 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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23
Q

What is seen here?

A

Fatty streak

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24
Q

What are the characteristics of 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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25
Q

What sites of an arterial tree does atherosclerosis usually occur in?

A

bifurfations and curvatures

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26
Q

What are the complications of an atheromatous plaque?

A

Can obstruct or rupture

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27
Q

At what % occlusion does stenosis usually occur in atheroma? What is the result?

A

>70% occlusion demand>supply OR diameter <1mm

–> Stable angina

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28
Q

What type of plaque disruption is this?

A

Type II - eccentric ragged edges stenosis

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29
Q

What are 3 ways in whch atherosclerotic plaques can change?

A
  • Rupture – exposes prothrombogenic plaque contents
  • Erosion - exposes prothrombogenic subendothelial basement membrane
  • Haemorrhage into plaque – increase size
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30
Q

Which plaques are most at risk of complications?

A
  • Lots foam cells or extracellular lipid
  • Thin fibrous cap
  • Few smooth muscle cells
  • Clusters inflammatory cells
  • Stress -
    • 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)
  • Vasoconstriction - reduces luminal size e.g. sue to adrenergic factors, platelet factors, reduced endothelial relaxing factors, mediators from perivascular cells
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31
Q

What characteristics of atherosclerosis are seen here?

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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32
Q

What is the leading cause of death for men and women worldwide?

A

IHD

7million/year

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33
Q

What does IHD refer to ?

A

Group of conditions resulting from myocardial ischaemia

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34
Q

What % of blood flow obstruction occurs fo MI to occur?

A

90%

long silent progression prior to symptoms

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35
Q

What 4 conditions can IHD present as?

A
  1. Angina pectoris
  2. Myocardial infarction
  3. Chronic IHD with heart failure
  4. Sudden cardiac death.
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36
Q

What is the pathogenesis of IHD?

A

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

37
Q

What % stenosis is require to cause chest pain during exercise vs at rest?

A

75% for pain precipitated by exercise

90% for pain at rest

38
Q

After which level of stenosis can vasodilation no longer compensate for?

A

>75%

39
Q

Where do atherosclerosis usually occur in IHD?

A
  • Plaques mainly in first few cm of LAD or LCX
  • Entire length RCA
40
Q

What is acute coronary syndrome caused by?

A

Stable plaque becomes unstable

Due to rupture, erosion, haemorrhage etc

Generally leads to superimposed thrombus which increases occlusion

41
Q

What is the difference between Prinzmental vs Stable vs Unstable angina?

A

Stable = comes on with exertion, relieved by rest, no plaque disruption

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

Prinzmetal = uncommon, due to artery spasm

42
Q

What is angina pectoris? Is there ischaemia?

A

Yes - transient ischaemia but not producing myocyte necrosis

43
Q

What is MI? How common is it in the UK?

A

Death of cardiac muscle due to prolonged ischaemia

Incidence 5/1000 per year UK (ST elevation)

44
Q

What is the most common cause of death in postmenopausal women?

A

MI

45
Q

What is the myocardial response to 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
46
Q

Which artery is most commonly affected in 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

47
Q

Which part of the myocardium does LAD supply?

A
  • Ant wall LV
  • Ant septum
  • Apex
48
Q

Which part of the myocardium does the RCA supply?

A
  • Post wall LV,
  • Post septum
  • Post RV
49
Q

What part of the myocardium does LCx supply?

A
  • Lat LV
  • NOT apex
50
Q

What is the gross pathology of the myocardium post-MI (1hr to 6 weeks)?

A
  1. Under 6 hours – normal by histology (CK-MB also normal)
  2. 6–24 hrs loss of nuclei, homogenous cytoplasm necrotic cell death
  3. 1-4 days – infiltration of polymorphs then macrophages (clear up debris)
  4. 5-10 days removal of debris
  5. 1-2 weeks granulation tissue, new blood vessels, myofibroblasts, collagen synthesis
  6. Weeks-months strengthening, decellularising scar
51
Q

When does loss of nuclei, homogenous cytoplasm necrotic cell death occur post MI?

A

6–24 hrs

52
Q
A

1

53
Q

Which days post MI is this and what is seen?

A

MI 10-14 days
granulation tissue, macrophages

54
Q

How long after MI would this appearance occur?

A

>2 months

55
Q

What % of MI is asymptomatic?

A

10 – 15% asymptomatic

Common in elderly & diabetes mellitus

56
Q

Which type of MI will not cause usual ST changes?

A

Subendocardial infarct

57
Q

What time frame do most MI deaths occur in?

A

50% of deaths within the first hour (most do not reach hospital)

58
Q

Who has worse prognosis with MI?

A

Age

Female

DM

Previous MI history

59
Q

What is the cause or reperfusion injury post angioplasty? What are the clinical features?

A

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
60
Q

What is a hibernating myocardium? Is it reversible?

A

Chronic sub lethal ischaemia -> lowered metabolism in myocytes “hibernating myocardium”

Reversed with revascularisation

61
Q

What are the complications of MI? When do they usually occur?

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
  • Mural thrombus
  • Ventricular aneurysm, late -> thrombus, heart failure, arrhythmia, do not rupture
  • Papillary muscle rupture
  • Chronic IHD = progressive late heart failure
62
Q

What is Dressler syndrome and when does it occur?

A

Pericarditis post-MI = Dressler syndrome

2nd or 3rd day post MI

63
Q

Complication time frames:

A
64
Q

What is the mortality with a year of MI?

A
  • Total mortality = 30% in one year
  • 3-4% mortality per year after first
65
Q

What is chronic IHD?

A

Progressive heart failure due to ischaemic myocardial damage. There may be no prior infarction.

66
Q

What are the gross histopathological features of chronic IHD?

A
  • Enlarged heavy heart, hypertrophied, dilated LV
  • Atherosclerosis
  • Maybe mural thrombi
  • Fibrosis (microscopic)
67
Q

Define sudden cardiac death. What is the usual cause?

A

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

Usually due to lethal arrhythmia on background of IHD in most (90%). In most cases triggered by myocardial ischaemia.

68
Q

What % of sudden cardiac death is caused by atherosclerosis?

A

90% due to marked atherosclerosis (of >75% stenosis)

10% due to non atherosclerotic cause (long QT etc, some cases heritable)

69
Q

What symptoms are usually caused by left vs right sided heart failure?

A

Left sided -> SOB, pulmonary oedema

Right sided -> peripheral oedema

70
Q

What side of the heart does congestive heart failure affect?

A

Left and right

71
Q

What are the causes of cardiac failure?

A
  • Ischaemic heart disease
  • Valve disease
  • Hypertension
  • Myocarditis
  • Cardiomyopathy
  • Left sided heart failure (Right)
72
Q

What are the complications of cardiac failure?

A
  • Sudden Death
  • Arrhythmias
  • Systemic emboli
  • Pulmonary oedema with superimposed infection
73
Q

What are the histopathological features of cardiac failure including gross and microscopic?

A

Gross: Dilated heart, scarring & thinning of the walls

Microscopy: fibrosis and replacement of ventricular myocardium

74
Q

Name these types of cardiomyopathy.

A

Left to right

  1. Normal
  2. Dilated
  3. Hypertrophic
  4. Restrictive
75
Q

What is the pathophysiology of dilated cardiomyopathy?

A

Progressive loss of myocytes –> dilated heart

76
Q

What are the causes of dilated cardiomyopathy?

A
  1. Idiopathic
  2. Infective – viral myocarditis
  3. Toxic: alcohol, chemotherapy (adriamycin, daunorubicin), cobalt, iron
  4. Endocrine– hyper-, hypo- thyroid, diabetes, peri-partum (?)
  5. Genetic – haemochromatosis, Fabry’s, McArdle’s
  6. Immunological – myocarditis incl. Viral (hypersensitivity component
77
Q

What type of cardiomyopathy is shown?

A

Dilated

78
Q

What is the most common cause of hypertrophic cardiomyopathy?

A

Familial in 50% - autosomal dominant inheritance with variable penetrance

Mutation to the beta-myosin heavy chain

79
Q

What is the gross histopathology of hypertrophic cardiomyopathy (HCM)?

A

Left ventricular hypertrophy

Thickening of septum narrows left ventricular outflow tract

80
Q

What is shown?

A

Hypertroophic cardiomyopathy (left ventricular)

81
Q

What are the gross histopathological features of restrictive cardiomyopathy? What is it caused by ?

A
  • Impaired ventricular compliance
  • Normal size heart – big atria

Idiopathic or secondary to myocardial disease eg amyloid, sarcoidosis

82
Q

What are the features of chronic rheumatic valvular disease? Which valve is most commonly affected?

A

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

83
Q

What is the cause of chronic rheumatic valvular disease?

A

Sequelae of earlier rheumatic fever predominantly affecting left-sided vlaves (mitral)

84
Q

What is the most common cause of aortic stenosis?

A

Calcification of the aortic valve

Affects patients aged 70-80yrs

85
Q

What are the complications of calcified aortic stenosis?

A
  • Impairs opening
  • Orifice is compromised
  • Outflow tract obstruction
86
Q

What are the causes of aortic regurgitation?

A
  • Rigidity - rheumatic, degenerative
  • Destruction - microbial endocarditis
  • Disease of aortic valve ring –> dilatation –>valve insufficient to cover increased area
    • Marfan’s Syndrome
    • Dissecting aneurysm
    • Syphilitic aortitis
    • Ankylosing spondylitis
87
Q

What is a true vs false aneurysm?

A

True - all layers wall

False – extravascular haematoma

88
Q

What are the causes of aneurysms?

A

Causes: Weak wall

  • Congenital eg Marfans
  • Atherosclerosis
  • HTN
89
Q

What is shown?

A

Aneurysm

  • Atherosclerosis may weaken the wall of the aorta such that it bulges out to form an aneurysm.
  • This typically occurs in the abdominal portion below the renal arteries, as shown here.
  • Aortic aneurysms that get bigger than 6 or 7 cm are likely to rupture.

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