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ACTH-secreting tumours, though rare in general practice, are an important topic in the RCGP curriculum due to their high clinical impact.
Produced by: Anterior pituitary
Regulated by: Hypothalamic–pituitary–adrenal (HPA) axis
Corticotropin-releasing hormone (CRH) → stimulates ACTH release
Target: Adrenal cortex (esp. zona fasciculata, reticularis)
Main effects:
↑ Cortisol
↑ Androgens (DHEA)
Mechanism: Via G protein-coupled receptors → ↑ cAMP in adrenal cells
Cause ↑ ACTH → leads to Cushing’s syndrome.
Two main sources:
Pituitary adenomas (Cushing’s disease) – most common.
Ectopic ACTH-producing tumours – e.g. small cell lung carcinoma, carcinoid tumours.
Often presents with non-specific features (e.g. weight gain, HTN, mood changes) before diagnosis.
Domain | Details |
---|---|
Presentation | Central obesity, moon face, buffalo hump Easy bruising, purple striae HTN, T2DM, mood changes Rapid onset with ↓ K⁺ → consider ectopic source |
Red Flags | Rapid symptom progression Refractory HTN/hyperglycaemia Severe hypokalaemia |
Biochemistry | ↑ Serum cortisol (loss of diurnal rhythm) ↑ Plasma ACTH Low-dose dexamethasone suppression test: No suppression = Cushing’s present High-dose dexamethasone suppression test: • Pituitary: partial suppression → Cushing’s disease • Ectopic: no suppression |
Differentiation... |
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