Ch.9 Hypertension 20221.pdf

Chapter 7 Pathophysiology for Pharmacy Students Cardiovascular Disorders – II Vascular Diseases B. Hypertension...

Chapter 7 Pathophysiology for Pharmacy Students Cardiovascular Disorders – II Vascular Diseases B. Hypertension Lectures by Prof. Dr. Mahmoud Abu-Samak., Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings  Hypertension : Definition Hypertension is defined as a consistent elevation of arterial pressure above the normal range expected for a particular age group. Nearly 25% of adults in the United States may have hypertension. Approximately 90% of all hypertension cases are classified as primary hypertension. This form of hypertension is also called essential or idiopathic hypertension since its etiology is uncertain. Approximately 5 to 10% of patients are afflicted with secondary hypertension, in which the cause of the elevated blood pressure is clearly defined. Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings  Hypertension : Risk Factors A number of genetic, environmental and dietary factors are associated with an increased risk for the development of essential hypertension: Familial history of hypertension Increasing age. Race and gender: incidence of hypertension is significantly higher in black men High dietary salt intake : salt sensitivity Hyperinsulinemia Heavy alcohol consumption Obesity Cigarette smoking Low dietary intake of potassium, calcium and magnesium Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings  Hypertension : Pathogenesis Current guidelines for Prevention, Detection, Evaluation, and Treatment of High Blood Pressure define normal BP as systolic pressure of < 120 mm Hg and diastolic pressure of < 80 mm Hg. 120/80 ; Normotensive ; + 10 = pre-hypertensive Hypertension is defined as an arterial pressure greater than 140/90 mm Hg in adults on at least three consecutive visits to the doctor's office. People whose blood pressure is between normal and 140/90 mm Hg are considered to have pre-hypertension and people whose blood pressure falls in this category should appropriately modify their lifestyle to lower their blood pressure to below 120/80 mm Hg. As noted (Figure 11–7), systolic pressure normally rises throughout life, and diastolic pressure rises until age 50–60 years but then falls, so that pulse pressure continues to increase. Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings  Hypertension : Pathogenesis In the past, emphasis has been on treating individuals with elevated diastolic pressure. However, it now appears that, particularly in elderly individuals, treating systolic hypertension is equally important or even more so in reducing the cardiovascular complications of hypertension. The most common cause of hypertension is increased peripheral vascular resistance. However, because blood pressure equals total peripheral resistance times cardiac output (BP= TPR. CO) , prolonged increases in cardiac output can also cause hypertension. These are seen, for example, in hyperthyroidism and beriberi. In addition, increased blood volume causes hypertension, especially in individuals with mineralocorticoid excess or renal failure (see later discussion); and increased blood viscosity, if it is marked, can increase arterial pressure. Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings  Hypertension : Clinical Presentation Hypertension by itself does not cause symptoms. Headaches, fatigue, and dizziness are sometimes ascribed to hypertension, but nonspecific symptoms such as these are no more common in hypertensives than they are in normotensive controls. Instead, the condition is discovered during routine screening or when patients seek medical advice for its complications. These complications are serious and potentially fatal :. They include MI, CHF , thrombotic and hemorrhagic strokes, hypertensive encephalopathy, and renal failure (Figure 11– 17). This is why hypertension is called "the silent killer." Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings  Hypertension : Complications Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings  Hypertension : Rationale for essential hypertension Early detection of hypertension in a patient is essential to prevent organ and tissue damage. Comprehensive and frequent blood pressure screening is key. Once diagnosed, the treatment of essential hypertension is often multifaceted and will depend on the severity and responsiveness of the particular patient to various therapies. Management of the hypertensive patient should always include some modification of lifestyle and diet. In the mildly hypertensive patient, these lifestyle modifications alone might reduce blood pressure sufficiently such that pharmacologic interventions are not necessary. Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings  Hypertension : Rationale for essential hypertension In moderate to severely hypertensive patients, pharmacologic interventions should be instituted (started) promptly (on time), in addition to lifestyle changes, to lower blood pressure and prevent the serious consequences of untreated hypertension. Patients who are diagnosed with hypertension at an early stage and who receive effective therapy for the condition will have a significantly lower morbidity and mortality than patients with uncontrolled hypertension. Regular blood pressure screenings are the key to early diagnosis. Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings  Hypertension : Treatment Rationale for treatment of essential hypertension Treatment: I. Lifestyle modifications Weight loss Exercise Sodium-restricted diet Cessation of smoking Cessation alcohol intake Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings  Hypertension : Treatment II. Pharmacologic a. Diuretics ( thiazides, furosemide) — Lower blood pressure by reducing vascular volume. Thiazide diuretics inhibit sodium reabsorption in the distal convoluted tubules of the kidney, while loop diuretics such as furosemide inhibit sodium reabsorption in the thick ascending portion of the loop of Henle. b. β -Blockers ( selective β 1and nonselective) — Lower blood pressure by decreasing heart rate and cardiac output. c. Diuretics + β -blockers — This combination has been shown to reduce overall mortality in patients with hypertension Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings  Hypertension : Treatment d. ACE (angiotensin-converting enzyme) inhibitors ( captopril, enalapril) Block the formation of angiotensin II, which is a powerful vasoconstrictor. Also reduces the formation of aldosterone , an adrenal hormone that stimulates salt and water retention. e. Calcium channel blockers ( nifedipine, diltiazem) — Reduce blood pressure by relaxing vascular smooth muscle around blood vessels. Some calcium channel blockers may also reduce cardiac output. f. Direct-acting vasodilators (α1antagonists hydralazine, diazoxide) - Directly relax smooth muscle around peripheral blood vessels. g. Central-acting agents ( methyldopa ) — Reduce blood pressure by decreasing sympathetic output from the brain. Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings  Hypertension : Treatment Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings  Hypertension : Associated diseases Normal blood flow through arteries and veins requires an intact system of blood vessels and adequate perfusion pressure to drive the blood through these vessels. A number of disease processes can affect normal function of the arteries and/or veins. Disease-induced changes may impair blood flow through arteries and disrupt delivery of oxygen and nutrients to tissues while disease processes affecting veins will disrupt removal of waste products from tissues and the return of blood to the heart. Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings An aneurysm is a localized, balloon-like swelling in the wall of an artery caused by weakening of the arterial wall. Aneurysm may occur in any artery, but the aorta is most susceptible to aneurysm due to the constantly high pressure on the walls of that vessel. Cerebral aneurysms may also occur. Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings  Varicose veins Varicose veins are veins that have become distended (swollen) over time due to the pooling of blood in the lower extremities. This condition occurs most frequently in individuals who spend long periods of time standing or who have impaired return of blood from the lower extremities. Veins are thin-walled vessels that are easily distended by the chronic pooling of blood in the lower extremities. Chronic distention of veins can reduce effectiveness of one-way venous valves that are present in the lumen to prevent the back flow of blood and lead to a condition termed valvular incompetence (Figure 7.4). These venous valves work in conjunction with skeletal muscle pumps in the legs to move blood back to the heart from the extremities. The most common manifestations of varicose veins are aching and edema. Their appearance through the skin is also unsightly (ugly). Treatment often involves the use of support stockings to prevent venous pooling. Surgical interventions may also be used to improve appearance and reduce discomfort. Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings  Varicose veins Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings  Venothromosis : DVT A thrombus is a blood clot that forms in the lumen of a blood vessel. A thrombus may form in an artery, but it is more common in veins due to the lower pressure and reduced blood flow found in the venous circulation. Factors that may contribute to the formation of a thrombus include the following: 1. Stasis of blood due to poor blood flow, immobility, heart failure, myocardial infarction and hypotension 2. Damage to blood vessels from trauma, surgery, IV drugs, catheters or immune response 3. Hypercoagulability of blood resulting from pregnancy, malignancies, coagulation disorders, dehydration or use of oral contraceptives Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings  Venothromosis : DVT Venous thrombus Thrombi may form in superficial vessels of the skin and extremities or in deep veins of circulation or tissues. Most superficial thrombi are benign and self-limiting, but deep vein thrombus (DVT) can be much more dangerous. Treatment and prevention of venous thrombus : Prevent blood stasis in susceptible patients through ambulation, use of elastic stockings, exercise or elevation of legs Anticoagulation therapy (warfarin, heparin) Thrombolytic therapy to dissolve clots (streptokinase, TPA) Surgical removal of clots Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings  Venothromosis : DVT : Pulmonary Embolism Embolism Unfortunately, for many patients with DVT the first manifestation of the thrombus is a pulmonary embolism. An embolism is a thrombus that breaks loose and travels through circulation. Common sites for lodging of emboli are the small pulmonary blood vessels of the lungs. Emboli that lodge in cerebral or coronary blood vessels may be rapidly fatal. A bolus of fat released by the breakage of long bones or an injection of air or foreign matter into the bloodstream through intravenous or intra-arterial lines can also act as an embolism. Ischemia and possible death of tissues may occur when blood flow is blocked by an embolus. Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings Copyright © 2005 Pearson Education, Inc. publishing as Benjamin Cummings