Prevalence and Incidence of Cerebral Arteriosclerosis
Cerebral Arteriosclerosis Prevalence: Book Excerpts
Prevalence/Incidence of Cerebral Arteriosclerosis: Online Medical Books
16 MEDICAL BOOKS ONLINE!
Review excerpts from medical books online, free, without registration,
for more information about the prevalence and/or incidence of Cerebral Arteriosclerosis.
Hypertension:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
Hypertension affects 25% of adults in the United States. If untreated, it carries a high mortality. Risk factors for hypertension include family history, race (most common in blacks), stress, obesity, a diet high in saturated fats or sodium, tobacco use, sedentary lifestyle, and aging.
Secondary hypertension may result from renal vascular disease; pheochromocytoma; primary hyperaldosteronism; Cushing’s syndrome; thyroid, pituitary, or parathyroid dysfunction; coarctation of the aorta; pregnancy; neurologic disorders; and use of hormonal contraceptives or other drugs, such as cocaine, epoetin alfa (erythropoietin), and cyclosporine.
Cardiac output and peripheral vascular resistance determine blood pressure. Increased blood volume, cardiac rate, and stroke volume as well as arteriolar vasoconstriction can raise blood pressure. The link to sustained hypertension, however, is unclear. Hypertension may also result from failure of intrinsic regulatory mechanisms:
❑ Renal hypoperfusion causes release of renin, which is converted by angiotensinogen, a liver enzyme, to angiotensin I. Angiotensin I is converted to angiotensin II, a powerful vasoconstrictor. The resulting vasoconstriction increases afterload. Angiotensin II stimulates adrenal secretion of aldosterone, which increases sodium reabsorption. Hypertonic-stimulated release of antidiuretic hormone from the pituitary gland follows, increasing water reabsorption, plasma volume, cardiac output, and blood pressure.
❑ Autoregulation changes an artery’s diameter to maintain perfusion despite fluctuations in systemic blood pressure. The intrinsic mechanisms responsible include stress relaxation (vessels gradually dilate when blood pressure rises to reduce peripheral resistance) and capillary fluid shift (plasma moves between vessels and extravascular spaces to maintain intravascular volume).
❑ When the blood pressure drops, baroreceptors in the aortic arch and carotid sinuses decrease their inhibition of the medulla’s vasomotor center, which increases sympathetic stimulation of the heart by norepinephrine. This, in turn, increases cardiac output by strengthening the contractile force, increasing the heart rate, and augmenting peripheral resistance by vasoconstriction. Stress can also stimulate the sympathetic nervous system to increase cardiac output and peripheral vascular resistance.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Pregnancy-induced hypertension:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
The cause of pregnancy-induced hypertension is unknown, but geographic, ethnic, racial, nutritional, immunologic, and familial factors and pre-existing vascular disease may contribute to its development. Age is also a factor. Primiparas who are older than age 35 are at higher risk for preeclampsia.
Preeclampsia develops in about 7% of pregnancies. Incidence is significantly higher in low socioeconomic groups. About 5% of females with preeclampsia develop eclampsia; of these, about 15% die from PIH itself or its complications. Fetal mortality is high due to the increased incidence of premature delivery and uteroplacental insufficiency.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Pulmonary hypertension:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
Pulmonary hypertension begins as hypertrophy of the small pulmonary arteries. The medial and intimal muscle layers of these vessels thicken, decreasing distensibility and increasing resistance. This disorder then progresses to vascular sclerosis and obliteration of small vessels.
In most cases, pulmonary hypertension occurs secondary to an underlying disease process, including:
❑ alveolar hypoventilation from chronic obstructive pulmonary disease (most common cause in the United States), sarcoidosis, diffuse interstitial disease, pulmonary metastasis, and certain diseases such as scleroderma (In these disorders, pulmonary vascular resistance occurs secondary to hypoxemia and destruction of the alveolocapillary bed. Other disorders that cause alveolar hypoventilation without lung tissue damage include obesity, kyphoscoliosis, and obstructive sleep apnea.)
❑ vascular obstruction from pulmonary embolism, vasculitis, and disorders that cause obstruction of small or large pulmonary veins, such as left atrial myxoma, idiopathic veno-occlusive disease, fibrosing mediastinitis, and mediastinal neoplasm
❑ primary cardiac disease, which may be congenital or acquired. Congenital defects that cause left-to-right shunting of blood — such as patent ductus arteriosus or atrial or ventricular septal defect — increase blood flow into the lungs and, consequently, raise pulmonary vascular pressure. Acquired cardiac diseases, such as rheumatic valvular disease and mitral stenosis, increase pulmonary venous pressure by restricting blood flow returning to the heart.
Primary (or idiopathic) pulmonary hypertension is rare, occurring most commonly — and with no known cause — in women between ages 20 and 40. Secondary pulmonary hypertension results from existing cardiac, pulmonary, thromboembolic, or collagen vascular diseases or from the use of certain drugs.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Renovascular hypertension:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
Stenosis or occlusion of the renal artery stimulates the affected kidney to release the enzyme renin, which converts angiotensinogen — a plasma protein — to angiotensin I. As angiotensin I circulates through the lungs and liver, it converts to angiotensin II, which causes peripheral vasoconstriction, increased arterial pressure and aldosterone secretion and, eventually, hypertension.
Atherosclerosis (especially in older males) and fibromuscular diseases of the renal artery wall layers — such as medial fibroplasia and, less commonly, intimal and subadventitial fibroplasia — are the primary causes in 95% of all patients with renovascular hypertension. Other causes include arteritis, anomalies of the renal arteries, embolism, trauma, tumor, and dissecting aneurysm. Less than 5% of patients with high blood pressure display renovascular hypertension; it’s most common in persons younger than age 30 or older than age 50.
PEDIATRIC TIP Fibromuscular dysplasia is the most common cause of renovascular hypertension in children. The surgical cure rate is very high.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
About prevalence and incidence statistics:
The term 'prevalence' of Cerebral Arteriosclerosis usually refers to the estimated population
of people who are managing Cerebral Arteriosclerosis at any given time.
The term 'incidence' of Cerebral Arteriosclerosis refers to the annual diagnosis rate,
or the number of new cases of Cerebral Arteriosclerosis diagnosed each year.
Hence, these two statistics types can differ:
a short-lived disease like flu can have high annual incidence but low prevalence,
but a life-long disease like diabetes has a low annual incidence but high prevalence.
For more information see about prevalence and incidence statistics.
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