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MSN II: CVS DISORDERS
TOPIC - VASCULAR DISORDERS
BY
BELLO, SA’AD MOHD (RNE)
ATHEROSCLEROSIS, ARTERIOSCLEROSIS & ANEURISMS
Atherosclerosis
• Def: is the deposition of Atheromatous plaques in the wall of tunica Intima
of large and medium-sized arteries which reduces the diameter of the artery.
• Mature plaques consist of accumulations of cholesterol and other lipids,
excess smooth muscle and fat-filled monocytes (foam cells).
• The plaque is covered with a rough fibrous cap. As plaques grow and
thicken they spread along the artery wall and protrude into the lumen.
• Eventually the whole thickness of the wall and long sections of the vessel
may be affected.
• Plaques may rupture, exposing subintimal materials to the blood.
• This may cause thrombosis and vasospasm and will compromise blood
flow.
• Arteries most commonly involved are those in the heart, brain, kidneys,
small intestine and lower limbs.
Causes/risk factors
• The origin of atheromatous plaques is uncertain. But its believe that Fatty
streaks present in artery walls of infants are usually absorbed but their
incomplete absorption may be the origin of atheromatous plaques in later
life.
• Atherosclerosis (the presence of plaques) is considered to be a disease of
older people because it is usually in these age groups that clinical signs
appear. Plaques, however, start to form in childhood in developed countries.
Incidence
• The incidence of atheroma is widespread in developed countries. Why
atheromatous plaques develop is not clearly understood, but the
predisposing factors appear to exert their effects over a long period.
• This may mean that the development of atheroma can be delayed or even
arrested by a change in lifestyle.
Risk factors
Non modifiable factors
• Heredity – family history
• Gender – males are more susceptible than females,
• until after the female menopause
• Increasing age
• Diabetes mellitus
• Hypertension
• Hyperlipidaemia, especially high levels of LDL
Modifiable factors
• Obesity
• Diet – high in refined carbohydrates and/or saturated fats and
cholesterol
• Cigarretes smoking
• Excessive emotional stress
• Sedentary lifestyle
• Excessive alcohol consumption
Pathophysiology
• Atherosclerosis begins as fatty streaks, lipids that are deposited in the intima of
the arterial wall.
• Although they are thought to be the precursors of atherosclerosis, fatty streaks
are common, even in childhood.
• The continued development of atherosclerosis involves an inflammatory
response.
• T lymphocytes and monocytes (that become macrophages) infiltrate the area to
ingest the lipids and then die; this causes smooth muscle cells within the vessel to
proliferate and form a fibrous cap over the dead fatty core.
• These deposits, called atheromas or plaques, protrude into the lumen of the
vessel, narrowing it and obstructing blood flow.
• If the fibrous cap of the plaque is thick and the lipid pool remains relatively
stable, it can resist the stress from blood flow and vessel movement.
• If the cap is thin, the lipid core may grow, causing it to rupture and hemorrhage
into the plaque, allowing a thrombus to develop.
• The thrombus may obstruct blood flow, leading to sudden cardiac death or an
acute myocardial infarction (MI).
Clinical manifestations
• 15 % of cases are asymptomatic
• Others clinical signs and symptoms depend on the organ
affected
• Cerebral atherosclerosis – headache, loss of consciousness,
loss of functions etc.
• Coronary atherosclerosis – chest pain/angina pain,
tarchycardia etc
• Renal atherosclerosis – loin pain
• Intestinal atherosclerosis – abdominal pain
Stages in the formation of atherosclerosis
Effects of atherosclerosis
• Atheromatous plaques may cause partial or complete obstruction of an
artery.
• The blockage may be complicated by clot formation. The consequences of
this depend on the site and size of the artery involved and the extent of
collateral circulation.
Narrowing of an artery
• The tissues distal to the narrow point become ischaemic.
• The cells may receive enough blood to meet their minimum needs, but not
enough to cope with an increase in metabolic rate, e.g. when muscle activity
is increased.
• This causes acute cramp-like ischaemic pain, which disappears when
exertion stops. Cardiac muscle and skeletal muscles of the lower limb are
most commonly affected.
• Ischaemic pain in the heart is called angina pectoris and in the lower limbs,
intermittent claudication.
Occlusion of an artery
• When an artery is completely blocked, the tissues it supplies rapidly
degenerate (ischaemia), which leads to infarction.
• If a major artery supplying a large amount of tissue is affected, the
consequences are likely to be more severe than if the obstruction
occurs in a minor vessel.
• If the tissue is well provided with a collateral circulation (such as the
circulus arteriosus provides in the brain), tissue damage is less than if
there are few collateral vessels (which may be the case in the heart).
• When a coronary artery is occluded myocardial infarction occurs.
Occlusion of arteries in the brain causes cerebral ischaemia and this
leads to cerebral infarction.
Treatment
• Treatment consists of risk factor modification, life style changes and
medications through the following processes
• Weight loss.
• Diet change: lower sodium, lower cholesterol and fat, decreased calorie
intake, increased dietary fiber.
• Administer low doses of aspirin.
• Administer beta-adrenergic blockers to reduce workload of heart: e.g
metroprolol, propranolol, nadolol.
• Administer calcium channel blockers to reduce heart rate, blood pressure,
and muscle contractility; helps with coronary vasodilation; slows AV node
conduction.
• Administer nitrate if patient has symptomatic chest pains to reduce
discomfort and enhance blood flow to myocardium.
• Platelet inhibitors:e.g dipyridamole, clopidogrel, ticlopidine
• Revascularization
Complications of the atherosclerosis
•Thrombosis
•Embolism
•Infarction
•Hypertension
•Myocardial infarction
•Heamorrhage
•Aneurysm
•Deep vein thrombosis (DVT)
Arteriosclerosis
• Def: This is a progressive degeneration of arterial walls, associated with
ageing and accompanied by hypertension.
Causes/predisposing factors
• Old age
• Cigarrete smooking
Pathology
• In large and medium-sized arteries, the tunica media is infiltrated with
fibrous tissue and calcium.
• This causes the vessels to become dilated, inelastic and tortuous.
• Loss of elasticity increases systolic blood pressure, and the pulse pressure.
• When small arteries (arterioles) are involved, their lumen is narrowed
because of a deposition of a substance called hyaline material, which
reduces the elasticity of the vessel wall.
• Because arterioles control peripheral resistance this narrowing
increases peripheral resistance and blood pressure.
• Damage to small vessels has a disproportionate effect on blood flow,
leading to ischaemia of tissues supplied by affected arteries.
• In the limbs, the resultant ischaemia predisposes to gangrene, which is
particularly serious in people with diabetes mellitus.
• If arteries supplying the brain are affected, cerebral ischaemia can
result in progressive deterioration of higher order functions.
Complication
• Hypertension
• Ischaemia
• Gangrene
Arteriosclerotic artery
Aneurysms
• Def: Aneurysms are abnormal local dilations of arteries,
which vary considerably in size which may be caused by
atheroma, hypertension and defective formation of collagen
in the arterial wall.
• It commonly occurs in the aorta.
Causes/predisposing factors
• Atheromatous plague
• Old age
• Hypertension
• Defective collagen formation
• Genetic/familial tendency
Types of aneurisms
• Saccular aneurysms: this is the type of aneurism that bulge out on
one side of the artery. When they occur in the relatively thin-walled
arteries of the circulus arteriosus in the brain they are sometimes
called ‘berry’ aneurysms. It is also called cerebral aneurism.
• They may be congenital, or be associated with defective collagen
production or with atheroma.
• Fusiform or spindle-shaped distensions aneurisms: this is the type
od anrurism that occur mainly in the abdominal aorta. They are usually
associated with atheroma. It called abdominal aortic aneurism (AAA)
• Dissecting aneurysms: this is the type of aneurism that occur mainly
in the arch of the aorta. They are caused by infiltration of blood
between the endothelium and tunica media, beginning at a site of
endothelial damage. Also known as thoracic aortic aneurism (TAA)
Types of aneurism
Treatment of aneurisms
The treatment of aneurisms is mainly surgical that involved
• Repair of the aneurisms and or
• Catheter embolization
Complications of aneurisms
• Ruptured aneurisms
• Thrombosis
• Embolism
• Stroke
• Internal haemorrhage
Thank you for
listening.
Any questions?
Group assignment
Write on the following problems of peripheral circulation
• Group A - Shock
• Group B - Oedema
• Group C - Deep vein thrombosis (DVT)
• Group D - Vericose veins

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CVS DISORDERS LECTURE 2.pptx

  • 1. MSN II: CVS DISORDERS TOPIC - VASCULAR DISORDERS BY BELLO, SA’AD MOHD (RNE)
  • 2. ATHEROSCLEROSIS, ARTERIOSCLEROSIS & ANEURISMS Atherosclerosis • Def: is the deposition of Atheromatous plaques in the wall of tunica Intima of large and medium-sized arteries which reduces the diameter of the artery. • Mature plaques consist of accumulations of cholesterol and other lipids, excess smooth muscle and fat-filled monocytes (foam cells). • The plaque is covered with a rough fibrous cap. As plaques grow and thicken they spread along the artery wall and protrude into the lumen. • Eventually the whole thickness of the wall and long sections of the vessel may be affected. • Plaques may rupture, exposing subintimal materials to the blood. • This may cause thrombosis and vasospasm and will compromise blood flow. • Arteries most commonly involved are those in the heart, brain, kidneys, small intestine and lower limbs.
  • 3. Causes/risk factors • The origin of atheromatous plaques is uncertain. But its believe that Fatty streaks present in artery walls of infants are usually absorbed but their incomplete absorption may be the origin of atheromatous plaques in later life. • Atherosclerosis (the presence of plaques) is considered to be a disease of older people because it is usually in these age groups that clinical signs appear. Plaques, however, start to form in childhood in developed countries. Incidence • The incidence of atheroma is widespread in developed countries. Why atheromatous plaques develop is not clearly understood, but the predisposing factors appear to exert their effects over a long period. • This may mean that the development of atheroma can be delayed or even arrested by a change in lifestyle.
  • 4. Risk factors Non modifiable factors • Heredity – family history • Gender – males are more susceptible than females, • until after the female menopause • Increasing age • Diabetes mellitus • Hypertension • Hyperlipidaemia, especially high levels of LDL
  • 5. Modifiable factors • Obesity • Diet – high in refined carbohydrates and/or saturated fats and cholesterol • Cigarretes smoking • Excessive emotional stress • Sedentary lifestyle • Excessive alcohol consumption
  • 6. Pathophysiology • Atherosclerosis begins as fatty streaks, lipids that are deposited in the intima of the arterial wall. • Although they are thought to be the precursors of atherosclerosis, fatty streaks are common, even in childhood. • The continued development of atherosclerosis involves an inflammatory response. • T lymphocytes and monocytes (that become macrophages) infiltrate the area to ingest the lipids and then die; this causes smooth muscle cells within the vessel to proliferate and form a fibrous cap over the dead fatty core. • These deposits, called atheromas or plaques, protrude into the lumen of the vessel, narrowing it and obstructing blood flow. • If the fibrous cap of the plaque is thick and the lipid pool remains relatively stable, it can resist the stress from blood flow and vessel movement. • If the cap is thin, the lipid core may grow, causing it to rupture and hemorrhage into the plaque, allowing a thrombus to develop. • The thrombus may obstruct blood flow, leading to sudden cardiac death or an acute myocardial infarction (MI).
  • 7. Clinical manifestations • 15 % of cases are asymptomatic • Others clinical signs and symptoms depend on the organ affected • Cerebral atherosclerosis – headache, loss of consciousness, loss of functions etc. • Coronary atherosclerosis – chest pain/angina pain, tarchycardia etc • Renal atherosclerosis – loin pain • Intestinal atherosclerosis – abdominal pain
  • 8. Stages in the formation of atherosclerosis
  • 9. Effects of atherosclerosis • Atheromatous plaques may cause partial or complete obstruction of an artery. • The blockage may be complicated by clot formation. The consequences of this depend on the site and size of the artery involved and the extent of collateral circulation. Narrowing of an artery • The tissues distal to the narrow point become ischaemic. • The cells may receive enough blood to meet their minimum needs, but not enough to cope with an increase in metabolic rate, e.g. when muscle activity is increased. • This causes acute cramp-like ischaemic pain, which disappears when exertion stops. Cardiac muscle and skeletal muscles of the lower limb are most commonly affected. • Ischaemic pain in the heart is called angina pectoris and in the lower limbs, intermittent claudication.
  • 10. Occlusion of an artery • When an artery is completely blocked, the tissues it supplies rapidly degenerate (ischaemia), which leads to infarction. • If a major artery supplying a large amount of tissue is affected, the consequences are likely to be more severe than if the obstruction occurs in a minor vessel. • If the tissue is well provided with a collateral circulation (such as the circulus arteriosus provides in the brain), tissue damage is less than if there are few collateral vessels (which may be the case in the heart). • When a coronary artery is occluded myocardial infarction occurs. Occlusion of arteries in the brain causes cerebral ischaemia and this leads to cerebral infarction.
  • 11. Treatment • Treatment consists of risk factor modification, life style changes and medications through the following processes • Weight loss. • Diet change: lower sodium, lower cholesterol and fat, decreased calorie intake, increased dietary fiber. • Administer low doses of aspirin. • Administer beta-adrenergic blockers to reduce workload of heart: e.g metroprolol, propranolol, nadolol. • Administer calcium channel blockers to reduce heart rate, blood pressure, and muscle contractility; helps with coronary vasodilation; slows AV node conduction. • Administer nitrate if patient has symptomatic chest pains to reduce discomfort and enhance blood flow to myocardium. • Platelet inhibitors:e.g dipyridamole, clopidogrel, ticlopidine • Revascularization
  • 12. Complications of the atherosclerosis •Thrombosis •Embolism •Infarction •Hypertension •Myocardial infarction •Heamorrhage •Aneurysm •Deep vein thrombosis (DVT)
  • 13. Arteriosclerosis • Def: This is a progressive degeneration of arterial walls, associated with ageing and accompanied by hypertension. Causes/predisposing factors • Old age • Cigarrete smooking Pathology • In large and medium-sized arteries, the tunica media is infiltrated with fibrous tissue and calcium. • This causes the vessels to become dilated, inelastic and tortuous. • Loss of elasticity increases systolic blood pressure, and the pulse pressure. • When small arteries (arterioles) are involved, their lumen is narrowed because of a deposition of a substance called hyaline material, which reduces the elasticity of the vessel wall.
  • 14. • Because arterioles control peripheral resistance this narrowing increases peripheral resistance and blood pressure. • Damage to small vessels has a disproportionate effect on blood flow, leading to ischaemia of tissues supplied by affected arteries. • In the limbs, the resultant ischaemia predisposes to gangrene, which is particularly serious in people with diabetes mellitus. • If arteries supplying the brain are affected, cerebral ischaemia can result in progressive deterioration of higher order functions. Complication • Hypertension • Ischaemia • Gangrene
  • 16. Aneurysms • Def: Aneurysms are abnormal local dilations of arteries, which vary considerably in size which may be caused by atheroma, hypertension and defective formation of collagen in the arterial wall. • It commonly occurs in the aorta. Causes/predisposing factors • Atheromatous plague • Old age • Hypertension • Defective collagen formation • Genetic/familial tendency
  • 17. Types of aneurisms • Saccular aneurysms: this is the type of aneurism that bulge out on one side of the artery. When they occur in the relatively thin-walled arteries of the circulus arteriosus in the brain they are sometimes called ‘berry’ aneurysms. It is also called cerebral aneurism. • They may be congenital, or be associated with defective collagen production or with atheroma. • Fusiform or spindle-shaped distensions aneurisms: this is the type od anrurism that occur mainly in the abdominal aorta. They are usually associated with atheroma. It called abdominal aortic aneurism (AAA) • Dissecting aneurysms: this is the type of aneurism that occur mainly in the arch of the aorta. They are caused by infiltration of blood between the endothelium and tunica media, beginning at a site of endothelial damage. Also known as thoracic aortic aneurism (TAA)
  • 19. Treatment of aneurisms The treatment of aneurisms is mainly surgical that involved • Repair of the aneurisms and or • Catheter embolization Complications of aneurisms • Ruptured aneurisms • Thrombosis • Embolism • Stroke • Internal haemorrhage
  • 21. Group assignment Write on the following problems of peripheral circulation • Group A - Shock • Group B - Oedema • Group C - Deep vein thrombosis (DVT) • Group D - Vericose veins