1. Cardiovascular & Renal Endocrinology ©  IOS/S Nussey

3. Mineralocorticoid excess

5. Box 4.5 - Adrenal steroid biosynthesis

6. Box 4.33

8. Clinical Case 4.1 bp 200/100

9. Conn’s syndrome Clinical features - hypertension - hypokalemia - + weakness - + headache Screening test

10. End-organ damage

11. Renal artery stenosis

13. 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

14. Imaging in Conn’s syndrome

15. Catecholamine excess

19. Box 4.41

20. Pheochromocytoma - Investigations - Think of the diagnosis Establish serum/urinary catecholamine concentrations Localise the tumor

21. Imaging in Pheochromocytoma

22. Box 4.43 MIBG scan

24. Cardiac failure

25. Box Q8.2

26. 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

30. Sepsis

32. Pathways activated in sepsis

36. Endothelium in sepsis