Pathology:                    Cortisol excess from exogenousor endogenous source


Aetiology:                     Exogenous

Steroids: Usually iatrogenic

Pseudo-Cushing’s: ETOH excess, depression



ACTH Dependant (áACTH)

Pituitary adenoma secreting ACTH (Cushing’s disease)

Ectopic ACTH secretion: e.g. small-cell lung cancer,carcinoid.

Presents with hyperpigmentation, hypokalaemicalkalosis, weight loss

ACTH independent (âACTH)

Adrenal adenoma or carcinoma


Symptoms:                 Fluidretention, weight gain, tiredness, depression, headaches


Signs:                              Central obesity,easy bruising, proximal myopathy, thin shiny skin, painful purple striae,oedema, virilisation-excess hair, deep voice, coarse skin osteoporosis


Investigations:         Bloods: FBC,U&E, LFTs, glucose, High or Low dexamethasone suppression test,

Urine: 24 hoururinary free cortisol

Imaging: Inferiorpetrosal sinus sampling (central: peripheral ACTH 4:1),

Pituitary MRI, CT Chest, Abdomen andPelvis


Treatment:                 Medical: Gradualweaning of exogenous steroids, treat hypertension or raised

glucose, bone protection

Surgical: Removalof pituitary tumour, excision of ectopic source, bilateral

adrenalectomy (ACTH dependant whensource not identified).


Complications:          Relapse, osteoporosis, recurrentinfections, metabolic complications, panhypopituitarism, Nelson’s syndrome(aggressive corticotroph tumour post bilateral adrenalectomy in pituitaryCushing’s), diabetes


Prognosis:                    Good prognosis if cured butif poorly controlled complications of vascular disease and diabetes. Adrenalcarcinoma has a poor prognosis


Dexamethasone Dose

Underlying Pathology



Cortisol ↓

Cortisol ↓

No abnormalities.

Dexamethasone suppresses normal Cortisol  production

No change

Cortisol ↓

Cushing’s Disease

No change

No change

Cushing’s Syndrome



Figure 5.5 Dexamethasone Test Results; A low dose is given first andthen a high test performed to distinguish between Cushing’s Disease andCushing’s Syndrome


Conn’s syndrome


Pathology:                    Excessaldosterone production from the adrenal cortex (primary)


Aetiology:                     Adrenocorticaladenoma (60%): F>>M. 3-5th Decade

Idiopathic/hyperplasia (40%): M=F, 5-7thdecade

Adrenal Ca: older group, F>M


Symptoms:                   Usuallyrelated to hypertension. Rarely myopathy, weakness, polyuria/polydipsia due tokidneys being unable to concentrate urine


Signs:                              Moderatesigns of hypertension


Investigations:          Bloods: FBC, U&E, Aldosterone(elevated), plasma renin, (>30-50ng/ml/h).

Imaging:CT/MRI to identify adenomas if biochemical tests suspicious


Treatment:                  Medical: Aldosterone antagonists e.g.Spironolactone or Eplerenone  

Surgical: Resection


Complications:          Allassociated with poorly treated hypertension


Prognosis:                    Adrenalectomycan cure ~ 75% of cases

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