Cardiovascular I Flashcards
What are the two principle mechanisms of vascular disease?
Narrowing or obstruction of vascular lumina
Weakening of vascular walls, leading to dilation and/or rupture
Artherosclerosis
Involves the large and medium arteries
Characterized by atheroma - atheromas protrude into the lumen of the vessel
May weaken the underlying media of the arteria
Plaques can rupture, resulting in catastrophic vessel thrombosis
What are the two types of Arteriosclerosis?
Hyaline
Hyperplastic
Hyaline Arteriosclerosis
Thickening of basement membrane
Hypertension and diabetes mellitus
Hyperplastic Arteriosclerosis
Malignant hypertension
Where is Atherosclerosis most and least prevalent?
Most prevalent in western cultures
Least prevalent in eastern cultures and africa
What are the non-modifiable risk factors for artherosclerosis?
Age - peak age is 40-60
Gender - men > premenopausal women
Genetics - familial history is the most important factor
What are the potentially modifiable risk factors for artherosclerosis?
Cigarette smoking - smoking increases death rate by 200%
Diabetes mellitus
Hypertension
Hypercholesterolemia - specifically LDL
Monkeberg’s Medial calcific sclerosis
Medial calcification without luminal narrowing or intimal disruption
What is Arteriosclerosis
Hardening of the arteries
What are some additional risk factors for artherosclerosis?
Inflammation (CRP levels) Hyperhomocysteineia Lipoprotein levels Metabolic syndrome (obesity) Type A personality (stress) Lack of exercise
What is the Response-to-Injury Hypothesis?
Endothelial injury results in endothelial dysfunction
LDLs and cholesterols accumulate in the vessel wall
Monocytes migrate and adhere, and differentiate into macrophages and “foam cells” (macrophages that ingested lipids)
Lipids accumulate in the macrophages, with release of inflammatory cytokines
Smooth muscle cell recruitment due to factors released from activated platelets, macrophages, and vascular wlals
Smooth muscle poliferates and ECM (mostly collagen) produciton proliferates
We get fully developed plaque with collage and central lipid core
Fatty streaks
Appear in most children independent of geography, gender, race, and environment
Occur at sites both prone and not prone to develop atherosclerosis
Some may progress to atheromas (can also regress)
Characterized by lipid-laden cell in the initia
What do plaques contain?
Collagen Lipid Myofibroblasts Macrophafes Neurovaculature
What is the fibrous cap comprised of?
Smooth muscle cells (myofibroblasts) and collagen
Central core of lipid/cellular debris with cholesterol
What are some progressive changes in plaques?
Ulceration Fissure formation Thrombosis Embolization Calcification Hemorrhage Medial weakening
What are some common sites of atheroma formation?
Major arterial branch points Abdominal aorta Coronary arteries Popliteal arteries Carotid arteries Cerebral arteries
What are some complications of atherosclerosis?
Ischemic heart disease (MI) Cerebral vascular accident (stroke) Gangrene Renal artery stenosis Aortic aneurysm
Normal Blood pressure level
Mild hypertension BP level
140/90 - 159/104 mmHg
Moderate-Severe hypertension BP level
> 160/106 mmHg
How common is hypertension in the US?
Approx. 20% of adults have it
What are the symptoms of hypertension?
None at early, low and moderate Headache Fatigue Dizziness Palpitations
Essential Hypertension. Prevalence and contributing factors
90-95% of all cases Contributing factors: -Genetics -Stress -Obesity -Inactivity -Smoking -High salt intake
Secondary Hypertension
There are many diseases which may produce hypertension
The hypertension is controlled when the underlying disease is treated
Malignant Hypertension
Relatively rapid onset of very high BP
Complications can include cerebral edema, retinal hemorrhage, headache, vomiting, convulsions, transient blindness, encephalopathy, renal failure, heart failure
This is a medical emergency requiring prompt but cautious blood pressure lowering
What is the pathogenesis of Essential Hypertension?
Hereditary Factors
Reduced renal Na excretion, increased plasma volume, increase cardiac output
Increased peripheral vascular resistance
Environmental factors
What are complications of Hypertension?
Concentric left ventricular hypertrophy: compensated
LVH and ventricular dilation: decompensated
Atherosclerosis and arteriosclerosis
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 is no longer adequate to provide normal CO due to decreased myocardial contractility.
This results in left ventricle dilation and gradual onset of CHF
Concentric hypertrophy
Thickening of the left ventricular wall at the expense of the left ventricular chamber with little or no increase in the outside cardiac dimensions
