1 hypertension

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1 hypertension

  1. 1. INTERNAL MEDICINE<br />
  2. 2. Hypertension<br />Def:<br />Blood pressure is defined as the pressure that is put on the walls of the arteries as blood is pumped through the circulatory system.<br />
  3. 3. Hypertension<br />Types of HTN:<br />A)Essential HTN or Primary HTN<br />B)Secondary HTN<br />
  4. 4. Hypertension<br />Causes:<br />A)Essential HTN or Primary HTN-<br />Idiopathic <br />Age<br />Genetic and familial factor<br />Socioeconomic condition<br />Obesity <br />
  5. 5. Hypertension<br />Causes:<br />B)Secondary HTN-<br />Adrenal gland tumor <br />Alcohol abuse<br /> Anxiety and stress <br />Arteriosclerosis <br />Birth control pills<br />Coarctation of the aorta <br />Cocaine use <br />Cushing syndrome <br />Diabetes <br />
  6. 6. Hypertension<br />Causes:<br />B)Secondary HTN-<br />Kidney disease, including: <br />Glomerulonephritis<br />Kidney failure <br />Renal artery stenosis<br />Renal vascular obstruction or narrowing<br />
  7. 7. Hypertension<br />Causes:<br />B)Secondary HTN-<br />Corticosteroids<br />Pregnancy <br />Primary hyperaldosteronism<br /> Renal artery stenosis<br />
  8. 8. Hypertension classification<br />
  9. 9. Hypertension<br />Pathogenesis of hypertension:<br />The pathogenesis of essential hypertension is multifactorial and highly complex. Multiple factors modulate the blood pressure for adequate tissue perfusion and include humoral mediators, vascular reactivity, circulating blood volume, vascular caliber, blood viscosity, cardiac output, blood vessel elasticity, and neural stimulation. A possible pathogenesis of essential hypertension has been proposed in which multiple factors, including genetic predisposition, excess dietary salt intake, and adrenergic tone, may interact to produce hypertension. Although genetics appears to contribute to essential hypertension, the exact mechanism has not been established.<br />
  10. 10. Hypertension<br />Pathogenesis of hypertension:<br />The natural history of essential hypertension evolves from occasional to established hypertension. After a long invariable asymptomatic period, persistent hypertension develops into complicated hypertension, in which target organ damage to the aorta and small arteries, heart, kidneys, retina, and central nervous system is evident. The progression begins with prehypertension in persons aged 10-30 years (by increased cardiac output) to early hypertension in persons aged 20-40 years (in which increased peripheral resistance is prominent) to established hypertension in persons aged 30-50 years, and, finally, to complicated hypertension in persons aged 40-60 years.<br />
  11. 11. Hypertension<br />Pathogenesis of hypertension:<br />One mechanism of hypertension has been described as high-output hypertension. High-output hypertension results from decreased peripheral vascular resistance and concomitant cardiac stimulation by adrenergic hyperactivity and altered calcium homeostasis. A second mechanism manifests with normal or reduced cardiac output and elevated systemic vascular resistance due to increased vasoreactivity. Another (and overlapping) mechanism is increased salt and water reabsorption (salt sensitivity) by the kidney, which increases circulating blood volume.<br />
  12. 12. Hypertension<br />Pathogenesis of hypertension:<br />The vasoreactivity of the vascular bed, an important phenomenon mediating changes of hypertension, is influenced by the activity of vasoactive factors, reactivity of the smooth muscle cells, and structural changes in the vessel wall and vessel caliber, expressed by a lumen-to-wall ratio. Patients who develop hypertension are known to develop a systemic hypertensive response secondary to vasoconstrictive stimuli. Alterations in structural and physical properties of resistance arteries, as well as changes in endothelial function, are probably responsible for this abnormal behavior of vasculature. Furthermore, vascular remodeling occurs over the years as hypertension evolves, thereby maintaining increased vascular resistance irrespective of the initial hemodynamic pattern.<br />
  13. 13. Hypertension<br />Clinical features:<br />Most of the time, there are no symptoms. Symptoms that may occur include:<br />Chest pain <br />Confusion<br />Ear noise or buzzing<br />Irregular heartbeat<br />Nosebleed<br />Tiredness<br />Vision changes<br />Headache<br />Vertigo<br />Palpitation<br />Dizziness <br />
  14. 14. Hypertension<br />Investigation:<br />Urine analysis<br />CXR P/A view<br />ECG<br />Plasma lipid profile<br />BUN<br />Sr.creatitine<br />Plasma electrolytes<br />IVU<br />USG of KUB<br />Angiography<br />MRI<br />
  15. 15. Hypertension<br />Management:<br />A)general management<br />Diet- avoidance of excess salt consumption and alcohol<br />Weight reduction in obese<br />Stop smoking<br />Exercise and relaxation<br />
  16. 16. Hypertension<br />Management:<br />B)Antihypertensive drug therapy<br />1.Diuretics-<br />Thiazide diuretics 2.5 mg daily<br />Potassium sparing diuretics 50-200 mg daily<br />Loop diuretics 40 mg daily<br />
  17. 17. Hypertension<br />Management:<br />B)Antihypertensive drug therapy<br />βadrenoceptor antagonists-<br />Atenolol 50-100 mg daily<br />Metoprolol 100-200 mg daily<br />Propranolol 40-120 mg thrice daily<br />Labetalol 100-200 mg twice daily(combined α and βadrenoceptor antagonist)<br />
  18. 18. Hypertension<br />Management:<br />ACE inhibitors-<br />Captopril 25 to 75 mg 12 hrly<br />Enalapril 20 mg daily<br />Lisinopril 10 mg daily<br />Ca-antagonists-<br />Diltiazem 60 mg 8 hrly<br />Amlodipine 5-10 mg daily<br />Nifedipine 20 mg twice daily<br />Drug combination- <br />β blockers and thiazide combination<br />

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