Anteriosclerosis and Hypertension (CVI) Flashcards
what disease is responsible for more morbifiy and mortality than any other category of disease
Vacular disaese
what are the principle mechanisms of vascular disase
Narrowing/obstruction of vascular lumina
weakening of vascular walls leading to dilation/rupture
what is arteriosclerosis
Hardening of the artery
what size of arteries does Atherosclerosis
Large and medium arties and arterioles
what is monckeberg’s medial calcific sclerosis
Medial calcification without luminal narrowing or intimal disruption
what are the types of arteriolosclerosis
Hyaline
Hyperplastic (proliferative)
what is hyaline ateriolosclerosis
thickening of basement membrane
what causes hyaline arteriolosclerosis
Hypertension and diabetes mellitus
what is hyperplastic (proliferative) arteriosclerosis
Firbocellular intimal thickening
what causes hyperplastic (proliferative) arteriosclerosis
Malignant hypertension
clinical signification of medial calcific sclerosis (monckeberg’s) Arteriosclerosis
no encroachment so clinically insignificant
- normal with aging
what does hyaline arteriolosclerosis look like
lots of transudate PR so it apperas that there is a large basement membrane
what does hyperplastic arteriolosclerosis look like
s. muscle with collagen intermixed
what is atherosclerosis associated with
With the formation of intimal lesions called atheromas
how do atheromas cause problems
Protrude into the lumen of a vessel
- can enlarge and obstruct blood flow
- weaken the underlying media of the artery
- plaque can rupture resulting in catastrophic vessel thrombosis
what is a atheromas ook like
- A fibrous cap (s. muscle, macrophage, foam cels, lymphcytes, collagen, elastin, proteoglycan, neovascularization)
- necrotic center (cell debris, cholesterol crystals (LDL), foam cels, calcium)
where is atherosclerosis common
US, western europe
and not common in africa and the far east
what is the peak death rate of myocardio infarcation
54% in the 60’s
what is the current death rate for all atherosclerosis related complications
50% (25% for myocardial infarcation
non-modifiable risk factors for Atherosclerosis
- Age(risk of acute myocardial infarction increases by 5x in men between 40 and 60)
- Gender: men more than premenopausal women
- genetics: family history of acute myocardial infarction
what is the most important factors for atherosclerosis
Genetics
what are the potentially modifiable risk factors for atherosclerosis
Cigarette smoking
diabetes mellitus
Hypertension (no specific level mentioned though)
hypercholesterolemia- specifically more LDL
how much does cig smoking increase risk for artherosclerosis
200% if a pack a day
what are the added risk factors for artherosclerosis
inflamtion (C-reactive protein, CRP-inflammatory marker) hyperhomocysteinemia Lipoprotein (a) levels Metabolic syndrome (obesity) Type A personality (stress) Lack of exercise
what are the common sites of atheroma formation
Major arterial branch points Abdominal aorta Coronary arteries Popliteal arteries Cerebral arteries
what are the progressive changes in plaques
Ulceration
fissure formation
Thrombosis
embolization (thrombus or debris from the central core)
calcification
hemorrhage into plaque from neovascualrization
what are the first steps in the response-to-injury hypothesis for atherosclerosis
- Endothelial injury/dysfunction
- accumulation of
- lipoproteins in the vessel wall
Monocyte adhesion
how does Monocyte adhesion lead to atherosclerosis
Migration into intima with differentiation into macrophages and foam cells
what are foam cells
MAcrophages that have ingested lipid
how does foam cells cause problems
Tend to release lots of cytokines
how doew release of cytokines from foam cells lead to atherosclerosis
Smooth muscle cell recruitment due to factors from activated platelets, macrophages, and vascular wall cells
what does smooth muscle cell recruitment lead to
Cell proliferation and ECM(collagen) production to eventually create a fibrous cap and central lipid core
when do fatty streaks appear
In most children independent of geograph, gender, race, and environment
where do fatty streaks appear
Both sites prone and not prone to develop aterosclerosis
can fatty straks develop in atheromas
Yes, some may
do fatty streaks elevate themsleves
No, so no clinical remifications
how can an atherosclerotic plaque change
Calcification ulceration fissure formation thrombosis Embolization hemorrhage into plauqe medial weakening
where do lymphocytes tend to gether in an arthroma
Near the shoulder
what can an advanced/vulnerable plaque develop into
Aneurysm and Rupture
Occlusion by Thrombus
Critical stenosis
how can an advance/vulnerable plaque develop into an aneurysm and rupture
Mural thrombosis
embolization
wall weakening
how can an advanced/vulnerable plaque develop into occlusion by thrombus
Plaque ruptures Plaue erosed Plaue hemorrhages Mural thrombosis embolization
how can an advanced/vulnerable plaque develop into critical stenosis
Progressive plaque growth
complications of atherosclerosis
Ischemic heart diseaes Cerebral infarct (stroke) gangrene Renal artery stenosis Aortic aneurysm
how common is hypertension
very common, with 25% of US adults, soon to grow to 50%
what are the guidelines for hypertension
Normal: less than 129/79
stage I: 130-139/80-89
stage II: greater than 140/90
crisis: greater than 180/120
when do people show symptoms of hypertension
at stage II usually
what are the guidlines for treatement for dentists with patients with hypertension
180/120: emergency room
160-> question
how common is essential hypertension
90% of all hypertensios
what is the contributing factors for essential hypertension
Genetics Stress obesity increased salt intake Inactivity cigs
hat does untreated hypertension lead to
gets higher and shortens life
when do symptoms of hypertension appear
once organ damage occurs
what are some symptoms of hypertension that are not so bad
High BP leads to headaches, fatigue, dizziness, palpitations
what is compensated hypertension
Concentric left ventricular hypertrophy
what is decompensated hypertension
Left ventricular hypertrophy plus dilation and congestive heart failure
what can artherosclerosis from essential hypertension lead to
Ischemic heart disease, stroke, and ischemic injury in other organs
what does arterioloscerlosis from essential hypertension do to the eyes and kindey
retinal injury for visual disturbances
kidney damge or nephrosclerosis
how can the kidney lead to essential hypertension
Reduced renal sodium excretion leads to increased plasma and increased cardiac output
how can the vessels lead to essential hypertension
Increased peripheral vascular resistance (increased vascular reactivity
what factors can lead to a change in blood volume
Sodium
mineralocorticoids
Atrial natriuretic peptide
what humoral factors lead to constriction
Angiotensin II Catecholamines Thromboxane Leukotrienes Endothelin
what humoral factors lead to dilation
Postaglandins
Kinins
NO
what neural factors lead to constriction and dilation
Constriction: Alpha adrenergic
Dialtion: beta adrenergic
what local factors lead to peripheral resistance
Autoregulation
pH
hypozia
what is compensated hypertensive heart disease
left ventricular concentric hypertrophy provides normal cardiac output
what is decompensated hypertensive heart disease
hypertrophy no longer adequate to provide normal cardiac outpute deu to decreased myocardiacl contractility
- LV dilation and graduatl onset of congestive Heart failure
what is concentric hypertrophy
Thickening of the left ventricle wall at the expense of the left ventricular chamber, with little to no increase in outside cardiac dimensions (lumen gets small)
what is secondary hypertesion
kidney causes hypertesion due to lack of conrol
what is dissection hypertension
blood blows into the media and pulls away the lining
how long does ti take for accelerated (malignant) hypertension to start
Relatively rapid onset
- superimposed on previous hypertension
what pressures are associated with accelerated malignant hypertesion
high systolic and diastolic pressure(200/120_)
what complications are associated with Accelterated (malignant) hypertension
Cerebral edema Papiledema encephalopathy renal failure cerebtral hemorrhage
