43691 - Dr. Amani A. Noory Khartoum, Sudan The Heart...

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Dr. Amani A. Noory Khartoum, Sudan
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The Heart
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Introduction Hypertension Systolic Blood Pressure (SBP ± Diastolic Blood Pressure (DBP ± < 140 mmHg < 90 mmHg ****************************************************
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Types of Hypertension Essential Secondary A disorder of unknown origin affecting the Blood Pressure regulating mechanisms Secondary to other disease processes Environmental Factors Stress Na+ Intake Obesity Smoking ****************************************************
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Treatment – Why? Symptomatic treatment is Mandatory: Damage to the vascular epithelium, paving the path for atherosclerosis (IHD, CVA) or nephropathy due to high intra-glomerular pressure Increased load on heart due to high BP can cause CHF Hypertension, even asymptomatic needs treatment
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Normal Blood Pressure Regulation Hydraulic equation: Blood Pressure = Cardiac output (CO) X Resistance to passage of blood through precapillary arterioles (PVR) Physiologically CO and PVR is maintained minute to minute by – arterioles (1) postcapillary venules (2) and Heart (3) Kidney is the fourth site – volume of intravascular fluid Baroreflex, humoral mechanism and renin-angiotensin- aldosterone system regulates the above 4 sites Local agents like Nitric oxide In hypertensives – Baroreflex and renal blood-volume control system – set at higher level All antihypertensives act via interfering with normal mechanisms
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Baroreceptor reflex arc Postural baroreflex:
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The Renal response Long-term blood pressure control – by controlling blood volume Reduction in renal pressure - intrarenal redistribution of pressure and increased absorption of salt and water Decreased pressure in renal arterioles and sympathetic activity – renin production – angiotensin II production Angiotensin II: Causes direct constriction of renal arterioles Stimulation of aldosterone synthesis – sodium absorption and increase in intravascular blood volume
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Antihypertensive Drugs Diuretics: Thiazides: Hydrochlorothiazide, chlorthalidone High ceiling: Furosemide K+ sparing: Spironolactone, triamterene and amiloride MOA: Acts on Kidneys to increase excretion of Na and H 2 O – decrease in blood volume – decreased BP Angiotensin-converting Enzyme (ACE) inhibitors: Captopril, lisinopril., enalapril, ramipril and fosinopril MOA: Inhibit synthesis of Angiotensin II – decrease in peripheral resistance and blood volume Angiotensin (AT1) blockers: Losartan, candesartan, valsartan and telmisartan MOA: Blocks binding of Angiotensin II to its receptors
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Centrally acting: Clonidine, methyldopa MOA: Act on central α 2A receptors to decrease sympathetic outflow – fall in BP ß-adrenergic blockers: Non selective: Propranolol (others: nadolol, timolol, pindolol, labetolol) Cardioselective: Metoprolol (others: atenolol, esmolol, betaxolol)
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This note was uploaded on 02/26/2012 for the course PHARM 210 taught by Professor Staff during the Fall '10 term at Rutgers.

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43691 - Dr. Amani A. Noory Khartoum, Sudan The Heart...

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