Flashcards in CV lecture 1- Arteriosclerosis and Hypertension Deck (44):
____________ is responsible for more morbidity and mortality than any other category of disease
name the 2 principal mechanisms of vascular disease
1) Narrowing or obstruction of vascular lumina
2) Weakening of vascular walls, leading to dilation and/or rupture
atherosclerosis is characterized by _________, which are A fatty deposit in the inner lining (intima) of an artery
ahterosclerosis effects the _________ and _________ arteriolies
medium and large
what condition is classified by: medial calcification without luminal narrowing or intimal disruption
Mönckeberg's medial calcific sclerosis
what are the 2 types of atherosclerosis? (describe both types)
1) hyaline type: thickening of basement membrane
2) hyperplastic (proliferative) type: fibrocellular intimal thickening
malignant hypertension and scleroderma both cause what type of atherosclerotic formation?
hyaline type athrosclorosis is caused by _________ and ________
hypertension and diabetes mellitus
Atheromas protrude into the ______ of the vessel
how can atheromas cause injury to the body?
1) can enlarge and obstruct blood flow
2) May weaken the underlying media of the artery (aneurysm)
3) Plaques can rupture, resulting in catastrophic vessel thrombosis
what regions of the world have a high prevalence for atherosclerosis? which regions have a low prevalence?
High Prevelance – United States, Western Europe
Low Prevelance – Africa, Far East
name the Non-modifiable (“constitutional”) modifiers for risk of atherosclerosis
Genetics (family history) – most important in this group
what are the major modifiable risk factors for atherosclerosis?
Hypercholesterolemia – high LDL, low HDL
what modifiable risk factor will increase your risk for Atherosclerosis by 200%?
smoking one pack of cigarettes a day
what are the steps involved in the "Response-to-injury" hypothesis for atherosclerosis?
1) endothelial cell injury
2) accumulation of lipoproteins
3) monocyte adhesion
what are the common sites for atheroma formations?
1. Major arterial branch points
2. Abdominal aorta
3. Coronary arteries
4. Popliteal arteries
5. Carotid arteries
6. Cerebral arteries
atheroma plaques contain what substances?
plaques contain collagen, lipid, myofibroblasts, macrophages, neovascularization.
during atheroma formation, a fibrous cap, composed of __________ and ________, develops over a central core of lipid/cellular debris with cholesterol
smooth muscle cells (myofibroblasts) and collagen
Progressive changes in atheroma plaques include:
(hint: theres 6 of them)
2) fissure formation
4) embolization (thrombus or debris from the central core)
6) hemorrhage into the plaque from neovascularization
Fatty streaks appear in atherosclerosis involving __________, and is independent of geography, gender, race and environment
T/F: Fatty streaks will form in almost any location, regardless of if that location is prone to atheroma formation
T/F: fatty streaks signal the start of atheromas formation
not all atheroma formations will start as fatty streaks
- its a possible step in formation, but not always present
what complications are associated with atherosclerosis?
Ischemic heart disease (MI)
Cerebral infarct (stroke)
Renal artery stenosis (narrowing)
Aortic aneurysm (dilation/bulge)
what is mild hypertension?
what is mild to severe hypertension?
Mild: BP between 140/90 - 159/104 mmHg
Moderate – severe: BP greater than 160/106 mmHg
Hypertension affects approximately _____% of the US population
the "peak death rate" for Myocardial infarctions (heart attacks) was ______% in the 1960s
what is the current death rate for all atherosclerosis-related complications ?
___________ hypertension Accounts for 90% or more of all hypertension
Contributing factors for hypertension include:
increased salt intake
what are the symptoms of low, and moderate, hypertension?
name the symptoms of severe hypertension:
what is "essential hypertension"
hypertension that has no identifiable cause
what are the FOUR factors involved in the pathogenesis of ESSENTIAL hypertension?
a) Peripheral vascular resistance (vasoconstriction)
b) hereditary factors
c) Reduced sodium excretion → salt and water retention→ increased plasma volume and cardiac output
d) environmental factors
what are the COMPLICATIONS of hypertension?
(theres 6 of them)
1) Concentric left ventricular hypertrophy (LVH)
2) LVH + ventricular dilation
3) Atherosclerosis and arteriolosclerosis
4) Retinal injury
6) Dissecting hematoma of the aorta
which complication of hypertension, if "decompensated", can lead to coronary heart failure (CHF)?
LVH + ventricular dilation
(LVH = left ventricular hypertrophy)
what occurs during decompensated hypertensive heart disease?
- hypertrophy no longer adequate to provide normal cardiac output due to decreased myocardial contractility
- results in left ventricle dilation and gradual onset of CHF
what are the characteristics of "Concentric Hypertrophy"?
- Thickening of the left ventricular wall at the expense of the left ventricular chamber
- little or no increase in the outside cardiac dimensions.
(heart increases muscle mass at the expense of chamber volume)
name the characteristics of Accelerated (Malignant) Hypertension:
- Relatively rapid onset
- Often superimposed on previous hypertension
- Very high systolic and diastolic pressures
the complications of accelerated (malignant) hypertension include:
the thickness of what structure will determine if it is a vulnerable plaque or a stable plaque?
the fibrous cap
- it surrounds the lipid core of the plaque
thick cap = stable
thin cap = vulnerable
what are the PRE-clinical phases of plaque formation?
1) normal artery
2) fatty streak (may not be part of progression)
3) Fibrofatty plaque
4) Advanced/vulnerable plaque
what differentiates a foam cell from a macrophage?
foam cells are macrophages that have become engorged with lipoproteins (cholesterol)
during atherosclerosis progression, what happens once monocytes adhere to the lipoprotein deposits?
- migration into intima
- differentiation into macrophages and “foam cells” (macrophages that have ingested lipid)