Cardiovascular & Renal Endocrinology IOS/S Nussey Mineralocorticoid excess Box Adrenal steroid biosynthesis Box 4.33 Clinical Case 4.1 bp 200/100 Conns syndrome Clinical features - hypertension - hypokalemia - + weakness - + headache Screening test End-organ damage Renal artery stenosis Mineralocorticoid excess - Investigation - Establish aldosterone excess Investigate renin suppression e.g. renin/aldo ratio Attempt to suppress aldosterone e.g. saline infusion or captopril test Differentiate adrenal adenoma from hyperplasia e.g. postural test Imaging/lateralisation Imaging in Conns syndrome Catecholamine excess Box 4.41 Pheochromocytoma - Investigations - Think of the diagnosis Establish serum/urinary catecholamine concentrations Localise the tumor Imaging in Pheochromocytoma Box 4.43 MIBG scan Cardiac failure Box Q8.2 Endocrinology of heart failure Baroreflex activation leads to sympathetic activation and increased myocardial contractility, tachycardia, arterial vasoconstriction (increasing afterload) Increased sympathetic tone and decreased perfusion pressure increases renin secretion by the JGA (and, therefore, RAA activity) Increased sympathetic tone and RAA activity leads to renal Na + (and, hence, water retention) Baroreflex mediated non-osmotic AVP release results in a decrease in free water excretion LV dysfunction (producing BNP release) leads to an increase in LA pressure and ANP release resulting in increased glomerular filtration, decreased Na + reabsorption and reduced RAA activity Sepsis Pathways activated in sepsis Endothelium in sepsis