Anteriosclerosis and Hypertension (CVI) Flashcards by Jacob Amato

what disease is responsible for more morbifiy and mortality than any other category of disease

Vacular disaese

How well did you know this?

Not at all

Perfectly

what are the principle mechanisms of vascular disase

Narrowing/obstruction of vascular lumina

weakening of vascular walls leading to dilation/rupture

How well did you know this?

Not at all

Perfectly

what is arteriosclerosis

Hardening of the artery

How well did you know this?

Not at all

Perfectly

what size of arteries does Atherosclerosis

Large and medium arties and arterioles

How well did you know this?

Not at all

Perfectly

what is monckeberg’s medial calcific sclerosis

Medial calcification without luminal narrowing or intimal disruption

How well did you know this?

Not at all

Perfectly

what are the types of arteriolosclerosis

Hyaline

Hyperplastic (proliferative)

How well did you know this?

Not at all

Perfectly

what is hyaline ateriolosclerosis

thickening of basement membrane

How well did you know this?

Not at all

Perfectly

what causes hyaline arteriolosclerosis

Hypertension and diabetes mellitus

How well did you know this?

Not at all

Perfectly

what is hyperplastic (proliferative) arteriosclerosis

Firbocellular intimal thickening

How well did you know this?

Not at all

Perfectly

what causes hyperplastic (proliferative) arteriosclerosis

Malignant hypertension

How well did you know this?

Not at all

Perfectly

clinical signification of medial calcific sclerosis (monckeberg’s) Arteriosclerosis

no encroachment so clinically insignificant

- normal with aging

How well did you know this?

Not at all

Perfectly

what does hyaline arteriolosclerosis look like

lots of transudate PR so it apperas that there is a large basement membrane

How well did you know this?

Not at all

Perfectly

what does hyperplastic arteriolosclerosis look like

s. muscle with collagen intermixed

How well did you know this?

Not at all

Perfectly

what is atherosclerosis associated with

With the formation of intimal lesions called atheromas

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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)

How well did you know this?

Not at all

Perfectly

where is atherosclerosis common

US, western europe

and not common in africa and the far east

How well did you know this?

Not at all

Perfectly

what is the peak death rate of myocardio infarcation

54% in the 60’s

How well did you know this?

Not at all

Perfectly

what is the current death rate for all atherosclerosis related complications

50% (25% for myocardial infarcation

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

what is the most important factors for atherosclerosis

Genetics

How well did you know this?

Not at all

Perfectly

what are the potentially modifiable risk factors for atherosclerosis

Cigarette smoking
diabetes mellitus
Hypertension (no specific level mentioned though)
hypercholesterolemia- specifically more LDL

How well did you know this?

Not at all

Perfectly

how much does cig smoking increase risk for artherosclerosis

200% if a pack a day

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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 ```

Anteriosclerosis and Hypertension (CVI) Flashcards

(71 cards)