week 6: cardiovascular disease processes. outline structure and function of blood vessels...
TRANSCRIPT
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Week 6:Cardiovascular Disease
Processes
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Outline
• Structure and function of blood vessels– Differences between arteries and veins
• Pathophysiology of atherosclerosis– Atherosclerosis and acute
cardiovascular syndromes
• Physiology of risk factors for atherosclerosis
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Structure of Vessel Walls
Figure 21-1
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Structure of Blood Vessels
Figure 21-2
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Arteries and Pressure
• Elasticity allows arteries to absorb pressure waves that come with each heartbeat
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Vasoconstriction & Vasodilatation
• The contraction of arterial smooth muscle by the ANS
• The relaxation of arterial smooth muscle• Enlarging the lumen • Affect:
– afterload on heart– peripheral blood pressure– capillary blood flow
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Vascular Endothelium
Regulation of own
Permeability
Localised Vascular Control
Enzymatic Actions on
Plasma
Inflammation & Immune
Response Angiogenesis
Sensed by shear and O2 tension
Releases: NO vasdodilatory, inhibits smooth muscle proliferation, leucocyte binding, platelet aggregation.
Prostacyclin: vasodilator, inhibits plateley aggregation
ACE
Involved in white blood cell actions.
Immunoglobulins: mediate leucocyte adhesion to endothelial cells
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Atherosclerosis and Arteriosclerosis
Disease Progression & Risk Factors
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Atherosclerosis & Arteriosclerosis
• Atherosclerosis• ‘The formation of plaques of cholesterol,
platelets, fibrin, and other substances on the arterial walls.’
• Arteriosclerosis• Imprecise term for various disorders of
arteries, particularly hardening due to fibrosis or calcium deposition, often used as a synonym for atherosclerosis.
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The Processes: Arterial Narrowing & Thrombus
Formation
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LDL Cholesterol accumulates in the arterial wall & undergoes chemical changes.
Signals – endothelial cells to latch on to white blood cells.
Triggers inflammatory response LDS- foam cells
The fat-laden foam cells form a fatty streak.
Plaque grows and a fibrous cap forms to ‘heal’ the plaque.
If it breaks, the it can form a blood clot.
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The fatty streak - earliest identifiable morphological change.
This is pre-dated by endothelial dysfunction
Characterised by accumulation of macrophage foam cells and a local chronic inflammatory infiltrate.
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Chronic local inflammatory response.
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The complex plaque is characterised by:
smooth muscle cell migration, formation of a fibrous cap,
a necrotic lipid core
increasing inflammatory infiltrate.
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Plaque rupture may occur after fibrous cap weakened by the production of: degradative enzymes reactive oxygen species by the inflammatory cellular infiltrate.
Plaque rupture exposes highly prothrombotic material, that may result in the clinically recognised acute coronary syndromes.
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Risk Factors
Physiological Explanations
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Lipids
• Low density lipoproteins (LDLs)• Associated with endothelial injury• Taken up by macrophages• Worse when:
– glycated – oxidised
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Diabetes
• Impaired endothelium-related relaxation– Via advanced glycosylation end-
products
• Increased platelet aggregation– Decreased response to a number of
agonists
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Hypertension
• Reduces endothelial function (via NO)
• Increases permeability to macromolecules
• Increases growth and proliferation vascular smooth muscle cells– Via Angiotensin II
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Hypertension 2
• Increases smooth muscle lipoxygenase activity oxidation of LDL inflammatory processes
• Pro-inflammatory response free radical production NO leukocyte adhesions peripheral resistance
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Smoking
• Promotes endothelial dysfunction• Enhanced platelet activity• Increased whole blood viscosity
– Associated with secondary polycythaemia
• Lowers HDL, increases oxidation of LDL– Via free radical exposure
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Obesity and Physical Inactivity
• Only small direct increase in atheroclerosis
• Effects via links with diabetes, hypertension and dyslipidaemia
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Summary
• The general process of atherosclerotic plaque / thrombus formation
• Several physiologial risk factors for atherosclerosis
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Hypertension
The Silent Killer
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Hypertension• Primary (essential)
• Secondary– Tumor, kidney disorder, adrenaline gland
disorder• ADH, renin, aldosterone, adrenaline, ACE.
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Effect of obesity
• When metabolised abdominal fat releases more triglycerides per g
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Valvular Disorders
Common Examples
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Mitral stenosis
• Narrowing of mitral valve opening due to progressive scarring
• Rheumatic Fever
• Atrial remodelling– >50% AF
• Pulmonary Hypertension
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Mitral StenosisLeads to obligatory increases in pulmonary arterial pressure
Reactive arteriolar constriction and structural changes in pulmonary artery (fibrosis)
Sustained >70 mm/Hg pressuresRV hypertrophy - increased afterload
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Mitral Regurgitation
• Leaky Mitral Valve
• Breathlessness• Heart Murmur• Ultrasound
• Tolerated for years due to compensation
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Causes of Mitral Regurgitation
• Rheumatic fever• Mitral valve prolapse syndrome • Hypertrophic cardiomyopathy• Myocardial infarction
– Damage to ventricle where the chordae are attached.
– Can cause rupture of the chordae
• Some congenital heart problems• Infection of the valve (endocarditis)
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Cardiac Myopathy and (Congestive) Heart Failure
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Cardiac Myopathy
• Disorder of the heart muscle• Usually an enlargement of:
– Chambers (dilated)– Muscle tissue (hypertrophic)
• Systolic myopathies
• But may be simply due to stiffening of myocardium
• Diastolic myopathy
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Causes of Cardiomyopathy
• Mostly idiopathic• Alcohol• Pregnancy• Viral – myocarditis
• MI• Valvular disorders• Secondary to hypertension
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Hypertrophic or Dilated Cardiomyopathy
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(Chronic) Heart Failure
• Cardiomyopathies are commonly compensatory mechanisms
• (C)HF is failure to meet Q-demands• Outcomes:• Sudden Death• Pump Failure• Transplantation
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Congestive Heart Failure
• Left sided failure: increased pulmonary circuit pressure
• Pulmonary hypertension• Fluid in lungs
– (congestion)
• Common to diagnose this way
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Signs to look out for
• Shortness of breath on exertion• Weight gain• Peripheral fluid retention• Chronic ‘bronchitis’
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Getting to Heart Failure
• HF occurs after an accumulation of problems that may include:– Idiopathies, Viruses, drugs
• More commonly in CR secondary to:– Valvular disorders– Hypertension– MI
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