Pathogenesis of Essential Hypertension, Factors Influencing BP Regulation, Etiology of Essential Hypertension. The pathophysiology of hypertensive emergencies is not well understood. Failure of normal autoregulation and an abrupt rise in systemic vascular resistance (SVR) are typically initial steps in the disease process. Increases in SVR are thought to occur from the release of humoral vasoconstrictors from the wall of a stressed vessel. The increased pressure within the vessel then starts a cycle of endothelial damage, local intravascular activation of the clotting cascade, fibrinoid necrosis of small blood vessels, and the release of more vasoconstrictors. If the process is not stopped, a cycle of further vascular injury, tissue ischemia, and autoregulatory dysfunction ensues. The pathophysiology of hypertensive renal damage discussed suggests 3 broad targets for. Hypertension: Pathophysiology. PDF Free; PPT Slides of All. Start your free trial and access books. Hypertension- is an intermittent or sustained elevation of diastolic or systolic blood. Activate Your Free Trial! Hypertension, also called high blood pressure. Hypertension is a common comorbid condition in patients with type 1 or type. PATHOPHYSIOLOGY OF DIABETES . Yes it can make them endure more serious illnesses later but they are able to still break free from things. Two- organ involvement is found in 1. This leads to left ventricular failure and pulmonary edema or myocardial ischemia. Chronic hypertension causes increased arterial stiffness, increased systolic blood pressure (BP), and widened pulse pressures. These factors decrease coronary perfusion pressures, increase myocardial oxygen consumption, and lead to left ventricular hypertrophy (LVH). Cardiac myocytes respond by hypertrophy, allowing the heart to pump more strongly against the elevated pressure. However, the contractile function of the left ventricle remains normal until later stages. Eventually, LVH lessens the chamber lumen, limiting diastolic filling and stroke volume. The left ventricular diastolic function is markedly compromised in long- standing hypertension. The mechanisms of diastolic dysfunction apparently include an aberration in the passive relaxation of the left ventricle during diastole. Over time, fibrosis may occur, further contributing to the poor compliance of the ventricle. As the left ventricle does not relax during early diastole, left ventricular end- diastolic pressure increases, further increasing left atrial pressure in late diastole. The exact determinants of left ventricular diastolic dysfunction have not been well studied; possibly, the abnormality is governed by abnormal calcium kinetics. Cardiac involvement in hypertension manifests as LVH, left atrial enlargement, aortic root dilatation, atrial and ventricular arrhythmias, systolic and diastolic heart failure, and ischemic heart disease. LVH is associated with an increased risk of premature death and morbidity. A higher frequency of cardiac atrial and ventricular dysrhythmias and sudden cardiac death may exist. Possibly, increased coronary arteriolar resistance leads to reduced blood flow to the hypertrophied myocardium, resulting in angina despite clean coronary arteries. Hypertension, along with reduced oxygen supply and other risk factors, accelerates the process of atherogenesis, thereby further reducing oxygen delivery to the myocardium. Hypertension and cerebrovascular disease. Cerebral autoregulation is the inherent ability of the cerebral vasculature to maintain a constant cerebral blood flow (CBF) across a wide range of perfusion pressures. Rapid rises in BP can cause hyperperfusion and increased CBF, which can lead to increased intracranial pressure and cerebral edema. However, such patients also have increased cerebrovascular resistance and are more prone to cerebral ischemia when flow decreases, especially if BP is decreased into normotensive ranges. Hypertension and renal disease. Hypertension is commonly observed in patients with kidney disease, with chronic hypertension causing pathologic changes to the small arteries of the kidney. As hypertensive damage occurs, the renal arteries develop endothelial dysfunction and impaired vasodilation, which alter renal autoregulation. When the renal autoregulatory system is disrupted, the intraglomerular pressure starts to vary directly with the systemic arterial pressure, thus offering no protection to the kidney during BP fluctuations. During a hypertensive crisis, this can lead to acute renal ischemia. Volume expansion is the main cause of hypertension in patients with glomerular disease (nephrotic and nephritic syndrome). Hypertension in patients with vascular disease is the result of the activation of the renin- angiotensin system, which is often secondary to ischemia. The combination of volume expansion and the activation of the renin- angiotensin system is believed to be the main factor behind hypertension in patients with chronic renal failure. The renin- angiotensin system. The activities of the renin- angiotensin system influence the progression of renal disease. Angiotensin II acts on the afferent and efferent arterioles, but more so on the efferent arterioles, leading to increased intraglomerular pressure and, in turn, to microalbuminuria. Reducing intraglomerular pressure using an ACE inhibitor has been shown to be beneficial in patients with diabetic nephropathy, even if they are not hypertensive. The beneficial effect of ACE inhibitors on the progression of renal insufficiency in patients who are nondiabetic is less clear. The benefit of ACE inhibitors is greater in patients with more pronounced proteinuria. Renovascular hypertension. The term renovascular hypertension (RVHT) denotes the causal relationship between anatomically evident arterial occlusive disease and elevated BP. RVHT is the clinical consequence of renin- angiotensin- aldosterone activation. As demonstrated by Goldblatt, renal artery occlusion creates ischemia, which triggers the release of renin and a secondary elevation in BP. Hyperreninemia promotes conversion of angiotensin I to angiotensin II, causing severe vasoconstriction and aldosterone release. The ensuing cascade of events varies, depending on the presence of a functioning contralateral kidney. In the setting of 2 kidneys, aldosterone- mediated sodium and water retention is handled properly by the nonstenotic kidney, precluding volume from contributing to the angiotensin II. By contrast, a solitary, ischemic kidney has little or no capacity for sodium and water excretion; hence, volume plays an additive role in the hypertension. Hypertension and end- stage renal disease. Despite widespread treatment of hypertension in the United States, the incidence of end- stage renal disease continues to rise. The explanation for this rise may be concomitant diabetes mellitus, the progressive nature of hypertensive renal disease despite therapy, or a failure to reduce BP to a protective level. A reduction in renal blood flow in conjunction with elevated afferent glomerular arteriolar resistance increases glomerular hydrostatic pressure secondary to efferent glomerular arteriolar constriction. The result is glomerular hyperfiltration, followed by development of glomerulosclerosis and further impairment of renal function. Hypertension and ocular changes. The pathophysiologic effects of hypertensive ocular changes can be divided into acute changes from malignant hypertension and chronic changes from long- term, systemic hypertension. Optic changes that can result from malignant hypertension include the development of the following acute retinal lesions. Focal intraretinal periarteriolar transudates. Inner retinal ischemic spots (cotton- wool spots). Microaneurysms. Shunt vessels. Collaterals. Chronic hypertensive retinal changes include the following. Arteriolosclerosis - Localized or generalized narrowing of vessels. Copper wiring and silver wiring of arterioles as a result of arteriolosclerosis. Arteriovenous (AV) nicking as a result of arteriolosclerosis. Retinal hemorrhages. Nerve fiber layer losses. Increased vascular tortuosity. Remodeling changes due to capillary nonperfusion, such as shunt vessels and microaneurysms. Hypertension and metabolic syndrome. The metabolic syndrome is an assemblage of metabolic risk factors that directly promote the development of atherosclerotic cardiovascular disease. The combination of these risk factors leads to a prothrombotic, proinflammatory state in humans and identifies individuals who are at elevated risk for atherosclerotic cardiovascular disease. Hypertensive patients who are obese have a sympathetic overdrive, higher cardiac output, and a rise in peripheral vascular resistance due to reduced endothelium- dependent vasodilation. Plasma aldosterone and endothelin are increased, the increase in cardiac output manifests secondary to increased preload, and the end- diastolic volume and pressure are elevated, leading to left ventricular dilatation. Left ventricular wall thickening occurs secondary to increased afterload, heightening the risk of congestive heart failure. The concomitant diabetes that is often present in patients who are obese produces a devastating effect on the kidneys and leads to a much higher incidence of renal failure. Obstructive sleep apnea confers additional risk of resistant hypertension.
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