Secondary Hypertension.ppt

Secondary Hypertension Jimmy Klemis, MD June 20, 2002 Overview HTN affects 43 million adults in US 95% have “essential HTN” without identifiable and treatable cause “ Secondary” HTN accounts for ~5-10% of other cases and represents potentially curable disease Often overlooked and underscreened Controversy over screening and treatment in some cases Screening Testing can be expensive and requires clinical suspicion and knowledge of limitations of different tests General principles: New onset HTN if 30 or 50 years of age HTN refractory to medical Rx (3-4 meds) Specific clinical/lab features typical for dz i.e., hypokalemia, epigastric bruits, differential BP in arms, episodic HTN/flushing/palp, etc Systemic HTN - Pathophysiology Causes of Secondary HTN Common Intrinsic Renal Disease Renovascular Dz Mineralocorticoid excess/ aldosteronism ? Sleep Breathing d/o Uncommon Pheochromocytoma Glucocorticoid excess/ Cushing’s dz Coarctation of Aorta Hyper/hypothyroidism Renal Parenchymal Disease Common cause of secondary HTN (2-5%) HTN is both cause and consequence of renal disease Multifactorial cause for HTN including disturbances in Na/water balance, depletion or antagonism of vasodepressors/ prostaglandins, pressor effects on TPR Renal disease from multiple etiol, treat underlying disease, dialysis/ transplant if necessary Renovascular HTN Incidence 1-30% Etiology Atherosclerosis 75-90% Fibromuscular dysplasia 10-25% Other Aortic/renal dissection Takayasu’s arteritis Thrombotic/cholesterol emboli CVD Post transplantation stenosis Post radiation Renovascular HTN Renovascular HTN - Pathophysiology Decrease in renal perfusion pressure activates RAAS, renin release converts angiotensinogen? Ang I; ACE converts Ang I? Ang II Ang II causes vasoconstriction (among other effects) which causes HTN and enhances adrenal release of aldosterone; leads to sodium and fluid retention Contralateral kidney (if unilateral RAS) responds with diuresis/ Na, H2O excretion which can return p