ATHEROSCLEROSIS AND HYPERTENSION
ATHEROSCLEROSIS AND HYPERTENSION
1. Define the types of arteriosclerosis. Be able to list and briefly discuss the major risk factors for atherosclerosis.
2. Describe the gross and microscopic features of atherosclerosis. List the complications.
3. Be able to describe the pathogenesis of atherosclerosis according to the reaction to injury hypothesis.
4. Know the contributing factors, complications and pathogenesis for essential hypertension.
REFERENCE: Kumar, Cotran, Robbins, Pathologic Basis of Disease, 8th ed., Chapter 10, pages 343-357, 398-399.
I. ARTERIOSCLEROSIS (“HARDENING OF THE ARTERIES”)
1. Atherosclerosis characterized by the atheroma, involves large and medium arteries.
2. Monckeberg’s medial calcific sclerosis medial calcification without luminal narrowing or intimal disruption.
a. hyaline thickening of basement membrane
hypertension and diabetes mellitus
b. hyperplastic (proliferative) fibrocellular intimal thickening
hypertension and scleroderma
4. Fibroelastic hyperplasia (proliferative arteriosclerosis) – concentric smooth muscle proliferation and collagen deposition in small muscular arteries.
II. RISK FACTORS
A. COMMON RISK FACTORS
1. Age – risk of acute MI increases 5x in men between 40 and 60 years
2. Gender men > premenopausal women
3. Genetic factors
1. Cigarette smoking – 1 pack per day increases death rate by 200%. After cessation, risk gradually decreases.
2. Diabetes mellitus
3. Hypertension no specific level separates risk and no risk increase
4. Hypercholesterolemia, the higher the level of cholesterol and LDL, the greater the risk (especially above 160 mg/dl). HDL is inversely associated with atherosclerosis.
5. C-reactive protein – a marker of inflammatory activity
B. “SOFT” 0R UNCERTAIN RISK FACTORS
1. Lack of exercise
3. Type A personality (stress)
4. High carbohydrate intake
5. Lipoprotein (a)
6. Chlamydia pneumonia, infection
III. MORPHOLOGY OF THE ATHEROMA หลินจือ มะเร็ง
A. COMMON SITES OF ATHEROMA FORMATION
1. Major arterial branch points
2. Abdominal aorta
3. Coronary arteries
4. Popliteal arteries
5. Carotid arteries
6. Cerebral arteries
B. MORPHOLOGIC FEATURES
1. Plaques contain collagen, lipid, myofibroblasts, macrophages, neovascularization.
2. A cap, composed of smooth muscle cells (myofibroblasts) and collagen, develops over lipid/cellular debris with cholesterol
3. Progressive changes in plaques include ulceration, fissure formation, thrombosis, embolization (thrombus or debris from the central core, calcification, hemorrhage into the plaque from neovascularization.
IV. FATTY STREAK
1. Occurs in infants and children in atherosclerotic and nonatherosclerotic
prone geographic areas.
2. They can regress, some may progress to atheromas.
3. Characterized by lipid-laden cells in the intima.
V. COMPLICATIONS OF ATHEROSCLEROSIS
1. Thrombosis and embolization
2. Organ ischemia and/or infarction
3. Aneurysm formation due to altered balance of collagen synthesis / degradation in the media below the plaque
VI. PATHOGENESIS – (Refer to Figure 10-6 Page 347 for description of the Response-To-Injury Hypothesis).
1. Hypertension is very common in the U.S. with a prevalence in
adults ranging from 20% to 40%. The prevalence increases with
2. Guidelines for diagnosing hypertension include:
a) BP < 140/90 normal
b) BP > 160/106 moderate or severe
c) BP = 140/90 to 159/104 mild
B. ESSENTIAL HYPERTENSION
1. Accounts for 90% or more of all hypertension.
2. Contributing factors include genetics, stress, obesity, salt intake,
inactivity, cigarette smoking.
3. Untreated hypertension tends to get higher and shortens life expectancy.
4. Symptoms and complications include:
a) Most patients have no symptoms until organ damage has occurred.
b) High BP causes headaches, fatigue, dizziness, palpitations.
– concentric left ventricular hypertrophy (compensated)
– left ventricular hypertrophy plus dilation and congestive heart failure
– atherosclerosis leads to ischemic heart disease, stroke and ischemic injury in other organs
– arteriolosclerosis leads to retinal injury (visual disturbances) and kidney damage or nephrosclerosis (renal failure)
5. Other complications from hypertension
– Nephrosclerosis – scarring of kidney due to atherosclerosis and
– dissecting hematoma of the aorta – longitudinal tear in the media
5. Pathogenesis of hypertension (environmental and hereditary factors)
a) Peripheral vascular resistance (vasoconstriction)
b) Reduced sodium excretion salt and water retention increased plasma volume and cardiac output
C. SECONDARY HYPERTENSION
There are many diseases which may produce hypertension. The hypertension is controlled when the underlying disease is treated.
D. MALIGNANT HYPERTENSION
1. Relatively rapid onset of very high blood pressure
2. Complications include cerebral edema with papilledema, retinal hemorrhage, severe headache, vomiting, convulsions, transient blindness, encephalopathy, renal failure, heart failure, cerebral hemorrhage
3. This is a medical emergency requiring prompt but cautious blood pressure lowering
Key Points สมุนไพรเบาหวาน
1. Atherosclerosis – Arteriolosclerosis – Fibroelastic Hyperplasia
2. Atherosclerosis modifiable risk factors: DM, hypertension, smoking, cholesterol
3. Atherosclerotic plaque: fibrous cap, central lipid core, progressive changes
4. Atherosclerosis complications: heart, brain, kidneys, lower legs/feet, AAA
5. Atherosclerosis: Reaction-to-Injury
6. Hypertension: Symptoms and risk factors
7 Hypertension: Risk Factors
8 Hypertension Complications: Heart (compensated – decompensated), arteries (arteriosclerosis, arteriolosclerosis, dissecting hematoma), kidneys (nephrosclerosis)