Adrenal stuff Flashcards
How to diagnose Cushings?
(1) demonstrate cortisol excess
- overnight dexamethasone suppression test
- diurnal cortisol levels
- 24hr urinary free cortisol
How to determine cause in Cushings?
- ACTH suppressed in adrenal Cushings
- ACTH normal/high in ACTH dependent Cushings
(1) high dose dexamethasone to determine cause (pituitary or ectopic ACTH)
–> pituitary - decreased in cortisol
Ectopic - no change to cortisol
(2) CRH test
- bushings - brisk response - Increased ACTH
- Ectopic ACTH - fairly flat
Cushings disease treatment (pituitary)
- trans-sphenoidal hypophysectomy
- adrenelectomy & pituitary radiotherapy
- adrenal synthesis inhibitors (metyrapone, ketoconazole)
- somatostatin analogues - pasireotide
Treatment for Cushings adrenal
laparoscopic adrenelectomy
Treatment for Cushings - ectopic ACTH
- resection of tumour (typically bronchial carcinoid)
- medical therapy
What are the causes of adrenal insufficiency?
Primary (Addison’s disease)
- lack of glucocorticoids and mineralocorticoids
Secondary (hypopituitarism)
- lack of ACTH and glucocorticoids
- normal mineralocorticoids
What are some causes of Addisons?
- Autoimmune (80%)
- infections (HIV/TB)
- congenital
- surgery
- metastases
- amyloid
- hemorrhage
How to tell the difference in primary vs secondary adrenal insufficiency based on symptoms?
Both: weakness, tiredness, fatigue, anorexia, nausea, vomiting, weight loss
Primary: Hyperpigmentation, postural hypotension +++, vitiligo and other autoimmune conditions
Secondary: hypopigmentation, postural hypotension, other hypopituitarism symptoms and signs
How to diagnose adrenal insufficiency?
- Measure ACTH
- Short synACTHen test (synthetic ACTH IM)
Primary - measure U&Es, renin and aldosterone (renin would be high, aldosterone low), adrenal antibodies)
Secondary - investigate as for pituitary disease (anterior pituitary function test and MRI pituitary)
What is the treatment for adrenal insufficiency - emergency and maintenance?
Emergency: IV access +2-3L saline with monitoring of volume status. Hydrocortisone 100mg IV 6 hourly. Maintenance: - hydrocortisone 10-15mg on waking - hydrocortisone - 5-10mg evening - Fludrocortisone - 0.05-0.1mg/day
Three causes of endocrine hypertension?
(1) excess aldosterone from zona glomerulosa
(2) cortisol or precursors from zona fasciculata
(3) catecholamines from medulla
What is the renin-angiotensin system?
Juxtaglomerular cells release renin.
Renin cleaves angiotensinogen to angiotensin 1.
ACE converts this to angiotensin 2 (causes vasoconstriction).
Angiotensin 2 acts on cortex (ZG) to release aldosterone.
Aldosterone acts on MR to increase BP, Na retention, K wasting. –> metabolic alkalosis
What activated renin secretion?
- JG cell baroreceptors detect reduced ECF and renal perfusion pressure
- Macula densa: low plasma Na (low osmolality)
- Carotid arch baroreceptors: low arterial pressure (reduced ECF, cardiac output and vascular tone)
- -> all activate sympathetic innervation of JG apparatus
What is Conn’s syndrome?
- phenotype, treatment
- unilateral adrenal tumour / aldosterone producing adenoma
Phenotype - high plasma aldosterone, high Na - low plasma renin, low K - ECF expansion, hypertension SAME AS BILATERAL ADRENAL HYPERPLASIA
Treatment = surgical
- venous sampling and/or CT scan
- unilateral adrenalectomy
What is bilateral adrenal hyperplasia?
- idiopathic bilateral hyperplasia. 60-70% of PA
Phenotype - high plasma aldosterone, high Na - low plasma renin, low K - ECF expansion, hypertension SAME AS CONN'S SYNDROME
Treatment - pharmacological
- anti-hypertensives e.g. MR blockers
spironolactone, eplerenone