Cardiovascular & Renal Endocrinology ©  IOS/S Nussey

Mineralocorticoid excess

Box Adrenal steroid biosynthesis

Box 4.33

Clinical Case 4.1 bp 200/100

Conn’s 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 Conn’s 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