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PathY5 > Cardiovascular Pathophysiology > Flashcards

Cardiovascular Pathophysiology Flashcards

1
Q

What is the biggest cause of death in men under 75 in the UK?

A

Coronary Heart Disease

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2
Q

What is the biggest cause of death in women under 75 in the UK?

A 
Other cancers (20%) 
Coronary Heart Disease (16%)
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3
Q

What is this?

A

Atherosclerosis

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4
Q

What is atherosclerosis?

A

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

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

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5
Q

What is the process of atherosclerosis?

A
  1. Endoethelial damage
  2. Platelets stick to damaged tissue
  3. Endothelium proliferates
  4. Fibrous cap forms on top of endothelium
  5. Deposition of cholesterol
  6. Plaque enlarges, blocking artery
  7. fatty core, foam cells etc.
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6
Q

What is the structure 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 effect do RFs have on atherosclerosis?

A
  • Risk factors have a MULTIPLICATIVE EFFECT
  • 2 risk factors increase the risk fourfold
  • 3 risk factors increase the risk sevenfold
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9
Q

Why is age bad?

A

Atherosclerosis progressive between 40->60 years incidence myocardial infarction (MI) X 5

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10
Q

Why is gender bad?

A

Premenopausal women protected (HRT no protection)

Postmenopausal risk increases (older ages greater than men)

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11
Q

Why are genetics bad?

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 the implication of hyperlipidaemia?

A

•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

Why is HTN bad?

A

Systolic & Diastolic important

Ht alone increases risk of IHD by 60%

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14
Q

Why is smoking bad?

A

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 diabetes bad?

A

Induces hypercholestrolaemia

Increases risk of atherosclerosis

2 x risk IHD in DM if all other factors equal

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16
Q
  • 20% cardiovascular events occur in absence of Ht, Hyperlipidaemia,smoking, Dm
  • 75% events in healthy women occur with LDL below risk level
  • Other risk factors must be involved
A
  • 20% cardiovascular events occur in absence of Ht, Hyperlipidaemia,smoking, Dm
  • 75% events in healthy women occur with LDL below risk level
  • Other risk factors must be involved
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17
Q

What is the pathogenesis of atherosclerosis?

A

Chronic inflammatory and healing response of arterial wall to endothelial injury

  • Endothelial injury
  • Lipoprotien accumulation (LDL)
  • Monocyte adhesion to endothelium
  • Monocyte migration into intima -> macrophages & foam cells
  • Platelet adhesion
  • Factor release
  • Smooth muscle cell recruitment
  • Lipid accumulation -> extra & intracellular, macrophages & smooth muscle cells
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18
Q

What is endothelial injury?

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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19
Q

What is 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 implicated
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20
Q
  • Herpes, CMV, Chlamydia pneumonia
  • No conclusive evidence
A
  • Herpes, CMV, Chlamydia pneumonia
  • No conclusive evidence
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21
Q

What is 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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22
Q

What is 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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23
Q

Why is atherosclerotic plaque bad?

A
  • Obstruct
  • Rupture
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24
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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25
Q

What is acute plaque change?

A

Rupture – exposes prothrombogenic plaque contents

Erosion - exposes prothrombogenic subendothelial basement membrane

Haemorrhage into plaque – increase size

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26
Q

What are the consequences of atheroma?

A
  • Majority of plaques that show acute change show only mild to moderate luminal stenosis prior to acute change
  • Therefore numerous “asymptomatic potential victims”
  • Plaques dynamic
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27
Q

What are vulnerable plaques?

A
  • Lots foam cells or extracellular lipid
  • Thin fibrous cap
  • Few smooth muscle cells
  • Clusters inflammatory cells
  • Adrenalin 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)
  • Not all rupture causes occlusion
  • Plaque disruption with platelet aggregation & thrombosis probably common
  • Important mechanism for plaque growth
28
Q

What is the implication of vasoconstriction?

A
  • Reduces luminal size
  • Increases local mechanical forces -> plaque disruption
  • Occurs due to:
  • Adrenergic agonists
  • Platelet contents
  • Reduced endothelial relaxing factors
  • Mediators from perivascular cells
29
Q

What is IHD?

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
30
Q

What is the presentation of IHD?

A
  • Angina pectoris
  • Myocardial infarction
  • Chronic IHD with heart failure
  • Sudden cardiac death.
31
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
32
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
  • >90% have atherosclerosis of 1 or more epicardial coronary arteries
  • 75% stenosis or more generally needed to cause symptoms precipitated by exercise
  • Vasodilation cannot compensate above this level of stenosis
  • 90% stenosis can lead to pain at rest
  • Plaques mainly in first few cm of LAD or LCX
  • Entire length RCA
33
Q

What is acute coronary syndrome?

A
  • Stable plaque becomes unstable
  • Due to rupture, erosion, haemorrhage etc
  • Generally leads to superimposed thrombus which increases occlusion
34
Q

What is angina pectoris?

A
  • Transient ischaemia not producing myocyte necrosis
  • 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?

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 the epidemiology of a MI?

A
  • Death of cardiac muscle due to prolonged ischaemia
  • Incidence 5/1000 per year UK (ST elevation)
  • 1.5 million MIs per year USA
  • 10% less than 40yrs
  • 45% less than 65yrs
  • Blacks & whites equal
  • Men greater risk than women throughout life
  • IHD most common cause death postmenopausal women
37
Q

How does artery occlusion occur in MI?

A
  • Sudden change to plaque
  • Platelet aggregation
  • Vasospasm
  • Coagulation
  • Thrombus evolves
38
Q

What is the myocardial response in MI pathogenesis?

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

Which arteries get affected?

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 MI pathology?

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 happens on day 1-3 post MI?

A

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

43
Q

What happens 10-14 days after an MI?

A

granulation tissue, macrophages

44
Q

What are the 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
45
Q

What are the consequences of an MI?

A
  • In hospital death rate 7% down from 30% in 1960s
  • ½ deaths occur within 1 hr of onset
  • Most of thee do not reach hospital
  • Age, female, DM, previous MI

-> worse prognosis

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 MI complications?

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)

49
Q

What are later MI complications?

A
  • 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
50
Q

MI complications pt 3

A
  • Ventricular aneurysm, late -> thrombus, heart failure, arrhythmia, do not rupture
  • Papillary muscle rupture
  • Chronic Ischaemic Heart Disease (Chronic IHD) = progressive late heart failure
51
Q

What is the mortality of MI?

A
  • Total mortality = 30% in one year
  • 3-4% mortality per year after first
52
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)
53
Q

What is sudden carduac 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%)
  • 300,000 - 400,000 per annum in USA
  • 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 eg Aortic stenosis, mitral valve prolapse, pulmonary hypertension
  • Marked atherosclerosis (>75% stenosis) in one or more vessels usually >90%
  • 10% non atherosclerotic cause

(long QT etc)

  • ½ have plaque rupture.
  • 25% have MI changes but conflicting data on role of MI
  • Felt to be ischaemia induced electrical instability
  • Some cases heritable
54
Q

What is 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 are the complications of left and right sided HF?

A

Left = pulmonary oedema

Right = Pedal oedema

56
Q

What are the causes of cardiac failure?

A

–Ischaemic heart disease

–Valve disease

–Hypertension

–Myocarditis

–Cardiomyopathy

– Left sided heart failure (Right)

57
Q

What are the complications of HF?

A

Sudden Death
Arrhythmias
Systemic emboli
Pulmonary oedema with
superimposed infection

58
Q

What is the pathology of HF?

A
  • Dilated heart, Scarring & thinning of the walls
  • Microscopy: fibrosis and replacement of ventricular myocardium,
59
Q

What is dialted cardiomyopathy?

A
  • Progressive loss of myocytes
  • Dilated heart
60
Q

What are the causes of dilated caardiomyopathy?

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)

61
Q

What is HCM?

A
  • Left ventricular hypertrophy
  • Familial in 50% (autosomal dominant, variable penetrance)
  • Beta-myosin heavy chain
  • Thickening of septum narrows left ventricular outflow tract
62
Q

What is restrictive cardiomyopathy?

A
  • Impaired ventricular compliance
  • Idiopathic or secondary to myocardial disease eg amyloid, sarcoidosis
  • Normal size heart – big atria
63
Q

What is CHRONIC RHEUMATIC VALVULAR DISEASE?

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

–Mitral > Aortic > Tricuspid > Pulmonic

–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
64
Q

What is calcific aortic stenosis?

A
  • Commonest cause aortic stenosis
  • 70s or 80s
  • Calcium deposits outflow side cusp
  • Impairs opening
  • Orifice compromised
  • Outflow tract obstruction
65
Q

What is aortic regurgitation?

A

–Rigidity - rheumatic, degenerative

–Destruction - microbial endocarditis

–Disease of aortic valve ring

–Þ dilatationÞvalve insufficient to cover increased area

  • Marfan’s Syndrome
  • Dissecting aneurysm
  • Syphilitic aortitis
  • Ankylosing spondylitis
66
Q

What are aneurysms?

A
  • True - all layers wall
  • False – extravascular haematoma
  • Causes: Weak wall

–Congenital eg Marfans

–Atherosclerosis

–Hypertension

PathY5 (98 decks)

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