Cardiovascular 1 Flashcards
(28 cards)
vascular disease
responsible for more morbidity and mortality than any other cetegory of disease
two principal mechanisms:
narrowing or obstruction of vascular lamina
weakening of vascular walls, leading to dilation and/or rupture
arteriosclerosis
hardening of the arteries
artherosclerosis
affects larger arteries
characterized by atheroma, involves large and medium arteries
associated with formation of intimal lesions called atheromas plaques
atheromas protrude into the lumen of the vessel
atheromas can enlarge and obstruct blood flow
may weaken underlying media of the artery
plaques can rupture- resulting in catastrophic vessel thrombosis
atherosclerosis epidemiology
high prevalence- united states, western europe
low prevalence- africa, far east
peak death rate from myocardial infarction- 54% in late 1960s
current death rate- 50% for all atherosclerosis- related complications (25% due to MI)
monckeberg’s medial calcific sclerosis
medial calcification without luminal narrowing or intimal disruption
arteriolosclerosis
affects arterioles
hyaline- thickening of basement membrane- hypertension and diabetes mellitus
hyperplastic (proliferative)-fibrocellular intimal thickening- malignant hypertension and scleroderma
non modifiable risk factors of atherosclerosis
age- risk of acute myocardial infaction increases 5x in men between 40 and 60 years
gender- men>premenopausal women
genetics- most important factor- family history of MI
potentially modifiable risk factors of atherosclerosis
cigarette smoking- 1 pack per day increases death rate by 200%. after cessation- risk gradually decreases
diabetes mellitus
hypertension- no specific level identifies increased risk
hypercholesterolemia- the higher the level of cholesterol and LDL, the greater the risk (Especially above 160 mg/dl)
HDL is inversely associated with atherosclerosis
additional risk factors of atherosclerosis
inflammation (CRP- inflmmatory marker) hyperhomocysteinemia lipoprotein a levels metabolic syndrome (obesity) type a personality (stress) lack of exercise
common sites of atheroma formation
major arterial branch points abdominal aorta coronary arteries popliteal arteries carotid arteries cerebral arteries
morphologic features of atheroma
plaques contain collagen, lipid, myofibroblasts, macrophages, neovascularization
fibrous cap- composed of smooth muscle cells (myofibroblasts) and collagen, develops over a central core of lipid/cellular debris with cholesterol
progressive changes in plaques include ulceration, fissure formation, thrombosis, embolization (thrombus or debris from the central core), calcification, hemorrhage into plaque from neovascularization , medial weakening
response to injury hypothesis
endothelial injury- endothelial dysfunction
accumulation of lipoproteins- LDL and cholesterol in the vessel wall
monocyte adhesion- migration into intima with differentiation into macrophages and foam cells
lipid accumulation in the macrophages, with release of inflammatory cytokines
smooth muscle cell recruitment due to factors released from activated platelets, macrophages and vascular wall cells
smooth muscle cell proliferation and ECM (mostly collagen) production
fully developed plaque with collagen (fibrous cap) and central lipid core
fatty streak
occurs in infants and children in atherosclerotic and nonatherosclerotic prone geographic areas
they can regress, some may progress to atheromas
characterized by lipid laden cells in the intima
complications of atherosclerosis
ischemic heart disease cerebral vascular accident (stroke) gangrene nephrosclerosis aneurysm formation due to pressure atrophy of the media with altered balance of collagen synthesis/degradation
prevalence of hypertension
25% of adults- increases with increasing age
guidelines of hypertension
normal bp160/106
symptoms of hypertension
none (early) at low and moderate hypertension headache fatigue dizziness palpitations
secondary hypertension
primary renal disease renal artery narrowing or adrenal disorders- diseases that produce hypertension
hypertension is controlled when underlying disease is treated
essential hypertension
accounts for 90% or more of all hypertension
contributing factors include genetics, stress, obesity, increased salt intake, inactivity, cigarette smoking
untreated hypertension tends to get higher and shortens life expectancy
symptoms and complications of essential hypertension
most patients have no symptoms until organ damage has occurred
high bp causes headaches, fatigues, dizziness, palpitations
pathogenesis of hypertension
hereditary factors
reduced renal sodium excretion-salt and water retention increased plasma volume- increased cardiac output
increased peripheral vascular resistance (vasoconstriction)
environmental factor- stress
complications of hypertension
concentric left ventricular hypertrophy: compensated
LVH and ventricular dilation: decompensated (leads to CHF)
atherosclerosis and arteriolosclerosis
retinal injury
nephrosclerosis
dissecting hematoma of the aorta
compensated hypertensive heart disease
left ventricular concentric hypertrophy provides normal cardiac output
decompensated hypertensive heart disease
hypertrophy no longer adequate to provide normal cardiac output due to decreased myocardial contractility resulting in left ventricular dilation and gradual onset of CHF
