Download Adrenal OVERLOAD (Cushing`s syndrome)

Adrenal problems
Anatomy
Patho-physiology
Adrenal
OVERLOAD
(Cushing’s
syndrome)
Zona glomerulosa: outer; aldosterone
Zona fascitulata: middle; cortisol
Zona reticularis: inner; androgens
CRH from hypothalamus  ACTH from APG  Cortisol from adrenal cortex
Effects of cortisol: decr release of CRH and ACTH
Gluconeogenesis, lipolysis, decr ketogenesis, decr insulin release  incr BSL
Decr effects of cytokines, decr cell mediated immunity, anti-inflammatory
RAA  aldosterone from adrenal cortex
Effects of aldosterone: incr Na (incr reabsorption), incr H20 excretion
decr K (incr excretion) in DCT
alkalosis (incr H excretion)
Cause: Iatrogenic (steroids, ACTH; most
common cause)
Pituitary adenoma (Cushing’s disease)
Adrenal adenoma/Ca/hyperplasia
Ectopic CRH (eg. Pancreas, bronchial carcinoid, thymic Ca)
Ectopic ACTH (20%; eg. Oat cell Ca lung)
OE: moon face, buffalo hump, truncal obesity, acne, striae, hursutism, atrophic skin, OP, HTN, peri oedema, DM,
psych (>70%), bitemporal hemianopia, adrenal Ca
if 2Y to ACTH – no Cushingoid fetaures, but HTN, oedema, prox myopathy, hyperpigmentation, cachexia
Ix: hyper HTN / G
Hypo K
Metabolic alkalosis
Aldosterone
OVERLOAD
incr Hb, incr neuts
Cortisol: at 00:00; >200 = Cushings
24hr urinary cortisol: 85% sens; false –ive if dilute urine
Corticotropin
Dex supp test: 24hr urine for 2/7; cortisol and ACTH blood test at 09:00; dex 1mg given at 11pm; normal
should be decr to <50% baseline level
Cause: 1Y: Conn’s syndrome (F:M 2:1; adenoma in F, hyperplasia in M)
2Y: due to RAA from decr blood flow or perfusion p; underlying oedematous disorder; CCF, CLF, CRF; RAS;
Bartter’s syndrome (normal BP, no oedema, hypoNa)
OE: HTN, weakness, paraesthesia, polyuria
Ix: hyper Na / volaemia / HTN
Hypo K / Ca
Metabolic alkalosis
Adrenal
insufficiency
Renin and aldosterone mid-morning
Cause: can be precipitated by: surgery, MI, GA, hypoG, hypothermia, trauma, psych illness, drugs
1Y: there is an aldosterone deficiency  hypovolaemia, high K
adrenal haem (anticoagulants, neonates, sepsis – Freidrich-Waterhouse syndrome)
Addison’s disease (80%)
Autoimmune diseases (70%; eg. Antiphospholid syndrome)
Surgical removal
Drugs (long term steroids most common cause – recovery post-steroids takes 1-12/12; ketoconazole)
Infection (TB – most common infectious cause worldwide, AIDS – mot common infectious cause in
USA (20%), protozoa, CMV, HSV); 60% patients with sepsis have decr cortisol
Ca (usually 1Y; lung and lymphoma most common cause of 2Y)
Congenital adrenal hyperplasia: vague presentation at 2wks; look for virilisation
Other (sarcoidosis, haemochromatosis, hereditary)
2Y: aldosterone is normal  euvolaemia, low K
pituitary failure, hypothalamic failure, head trauma, meningitis, irradiation / post op, Sheehan
syndrome
Pathophysiology: 90% of gland must be destroyed to cause hypo
Results in: 1Y: Hypo Cl / Na / osm / volaemia (Na rarely <120; total body depletion + intracellular mvmt)
Hyper K (rarely >7; extracellular mvmt + decr excretion)
NAGMA
Always consider if fluid-resistant hypotension
2Y: no vol depletion; low K; high / low Na; little other change in elecrolytes as aldosterone normal
Sx: anorexia, N+V+D+AP, lethargy, weight loss, weakness, postural syncope
OE: pigmentation if 1Y; SBP <100 with postural drop
Ix: as above + incr Cr, mild incr Ca (in 10-20%), mild hypoG; anti-adrenal ab
Cortisol: within 1hr of waking; <200 = insufficiency; 200-500 = needs ACTH stimulation test
ACTH stimulation test: bloods  Synacthen IM  bloods 30mins  bloods 60mins  cortisol >550 =
normal; if normal response = 2Y
ACTH: high = 1Y; low = 2Y
Mng: IVF (may need ++); trt hypoG; trt K if needed; vasopressors may be needed
If uncertain diagnosis: Dexamethasone 10mg IV stat  4mg QID
If certain: hydrocortisone 250mg IV stat  100mg QID; 25mg IV if neonate, 50mg IV toddler to school
child, 100mg to adolescents
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