1. Adrenal Disease Alex Edwards ae11g11@soton.ac.uk

2. DAPSICAMP  Definition  Aetiology  Pathophysiology  Signs and Symptoms  Investigations  Complications  Alternative Diagnosis  Management  Prognosis

3. Anatomy – Arterial Blood Supply

4. Anatomy – Venous Drainage

5. Blood Supply - Summary  Arterial Supply (same on both sides)  Superior Suprarenal Artery  Middle Suprarenal Artery  Inferior Suprarenal Artery  Venous Drainage  LEFT Suprarenal Vein – into  RIGHT Suprarenal Vein – into

6. Adrenal Structure  Cortex –  Medulla –

7. The Medulla  Contains Chromaffin cells  Secrete  Secretion in response to stimulation by ( ) nerve fibres from thoracic segments  ( ) fibres release ACh that binds to Nicotinic type 1 receptors on adrenal medulla  NA/A secreted into circulation

8. The Medulla - effects of cathecholamines  Sympathetic Fight or Flight response  Cause of excess catecholamines:  Tachycardia,( ), tremor, sweating  ( )  NA/A cause an increase in lipolysis, gluconeogenesis and glycogenolysis

9. The Cortex – GFR!  Zona G  ( )  Zona F  ( )  Zona R  ( )

10. The Key Step ( ) Progesterone Mineralocorticoids (ALDOSTERONE) Zona Glomerulosa ( ) Glucocorticoids (CORTISOL) Zona Fasciculata

11. Aldosterone - released by ZG in response to ( ) Angiotensinogen Angiotensin I Angiotensin II Vasoconstriction ALDOSTERONE

12. Aldosterone - effects  Increases renal ( ) in the late DCT  Increases renal ( ) in the early collecting ducts  Increases blood volume and blood pressure

13. Hyperaldosteronism - aetiology

14. Hyperaldosteronism - pathophysiology  Aldosterone acts on principle cells in the late DCT/early collecting ducts causing:  Expression of Na + and K + channels in luminal membrane  Activity of Na + /K + pump on basolateral membrane  Therefore signs and symptoms include: INTERSTITIUM ALDOSTERONE

15. Hyperaldosteronism - investigations  Blood tests  ECG – arrhythmias from electrolyte imbalance  CT/MRI  Special tests  Lying and standing aldosterone/renin levels  Salt loading and aldosterone/renin levels

16. Cortisol - released by ZF in response to ( ) Hypothalamus Anterior Pituitary Gland -Corticotrophs Adrenal Cortex (Zona Fasciculata) CORTISOL HPA axis:

17. Cortisol - effects  Cortisol is a ( ) stress hormone  Anti-insulin – increases plasma glucose  Increases muscle protein degradation  Increases lipolysis and fat deposition  Anti-inflammatory  Immunosuppressant

18. Hypercorticism (Cushing’s Syndrome) - aetiology  ACTH dependent (80-85%)  Secondary SS CC MM  ACTH independent  Primary  Iatrogenic CC

19. Hypercorticism (Cushing’s Syndrome) - Signs and Symptoms  Anti-insulin and increased plasma glucose - ( )  Muscle protein degradation – ( )  Lipolysis and fat deposition – ( ) and ( )  Anti-inflammatory and Immunosuppressant effects – ( )

20. Hypercorticism (Cushing’s Syndrome) - investigations  U&Es  24 hour urinary free cortisol (3 collections)  Dexamethasone suppression test  Dexamethasone supressed corticotropin releasing hormone (CRH) test

21. Adrenal Insufficiency  ADDISON’S DISEASE  Adrenal cortex destruction  Rare  90% autoimmune  Aldosterone deficiency  ( )  ( ) and ( )  Cortisol deficiency  ( )  Caused by increased ACTH from negative feedback  ACTH precursor causes pigmentation

22. Adrenal insufficiency - investigations  U&Es  Blood cortisol levels  ACTH stimulation (Synacthen) test  Fails to produce cortisol in adrenal failure  Managed by synthetic hormonal replacement

23. Summary

24. Any Questions?  ae11g11@soton.ac.uk