Endocrine and metabolic · Hard
This case is fictional and exists for study. It describes no real patient.
34 years · female
A 34-year-old female presents to the emergency department via ambulance with a 3-day history of worsening profound fatigue, nausea, recurrent vomiting, and severe dizziness upon standing. Her family notes that she has experienced a 6 kg weight loss over the past 3 months and recently developed progressive darkening of her skin. On physical examination, she appears lethargic and moderately dehydrated with distinct hyperpigmentation over her buccal mucosa and palmar creases. Her abdomen displays diffuse tenderness on palpation without guarding or rebound tenderness. Initial laboratory evaluation demonstrates severe hyponatraemia, hyperkalaemia, impaired renal function, and hypoglycaemia.
Vital signs
- HR
- 118 bpm
- BP
- 82/50 mmHg
- RR
- 22/min
- Temp
- 37.8 °C
- SpO₂
- 96%
Examination findings
- Hyperpigmentation over palmar creases and buccal mucosa
- Dry mucous membranes and decreased skin turgor
- Diffuse abdominal tenderness without peritonitis
Investigations
| Sodium | 118 mmol/L | reference: 135-145 |
| Potassium | 6.2 mmol/L | reference: 3.5-5.0 |
| Urea | 14.2 mmol/L | reference: 2.5-7.8 |
| Creatinine | 140 µmol/L | reference: 44-80 |
| Blood Glucose | 3.1 mmol/L | reference: 4.0-7.0 |
| Serum Cortisol (Random) | 80 nmol/L | reference: 180-550 |
Question 1 of 3
What is the most likely diagnosis?
The clinical presentation of severe hyponatraemia, hyperkalaemia, hypoglycaemia, postural hypotension, and mucocutaneous hyperpigmentation is diagnostic of primary adrenal insufficiency (Addisonian crisis). Loss of mineralocorticoid (aldosterone) leads to renal sodium wasting and potassium retention, while cortisol deficiency causes hypoglycaemia and loss of negative feedback on ACTH production (causing hyperpigmentation). SIADH presents with euvolaemic hyponatraemia without hyperkalaemia, hypoglycaemia, or hyperpigmentation. Secondary adrenal insufficiency preserves aldosterone secretion (regulated by the renin-angiotensin system) and does not cause hyperkalaemia or hyperpigmentation. Diabetic ketoacidosis presents with severe hyperglycaemia rather than hypoglycaemia.
Teaching point: Primary adrenal insufficiency features both glucocorticoid and mineralocorticoid deficiency alongside high ACTH (hyperpigmentation), distinguishing it from secondary adrenal insufficiency.
Question 2 of 3
Which of the following is the single most appropriate immediate management step?
Immediate management of an acute Addisonian crisis requires rapid volume expansion with IV 0.9% sodium chloride to treat hypovolaemic shock and IV hydrocortisone (100 mg bolus followed by 200 mg/24 hours). High-dose hydrocortisone provides sufficient mineralocorticoid activity, so oral fludrocortisone is unnecessary in the acute phase. Hypertonic saline is reserved for severe acute hyponatraemia causing seizures or coma. Calcium gluconate and insulin-dextrose treat hyperkalaemia, but volume expansion and glucocorticoid administration correct potassium retention in adrenal crisis without needing immediate hyperkalaemic emergency protocol unless ECG changes are present. Resuscitation must never be delayed for a short Synacthen test.
Teaching point: In suspected acute adrenal crisis, immediate resuscitation with IV isotonic saline and high-dose IV hydrocortisone must be initiated without waiting for diagnostic confirmation.
Question 3 of 3
Which physiological mechanism best accounts for the presence of skin hyperpigmentation in this patient?
In primary adrenal insufficiency, destruction of the adrenal cortex reduces serum cortisol, removing normal negative feedback on the hypothalamus and anterior pituitary. This leads to compensatory hypersecretion of pro-opiomelanocortin (POMC), the common precursor for both ACTH and alpha-MSH. Elevated levels of ACTH and MSH cleavage products act on melanocortin-1 receptors on dermal melanocytes, leading to hyperpigmentation. Mineralocorticoid deficiency, renal impairment, and hyperkalaemia do not directly cause cutaneous hyperpigmentation.
Teaching point: Hyperpigmentation in primary adrenal disease is caused by loss of cortisol negative feedback, driving elevated ACTH and POMC synthesis.
Key learning points
- Primary adrenal insufficiency causes combined cortisol and aldosterone deficiency, producing hyponatraemia, hyperkalaemia, hypoglycaemia, and hypotension.
- Cutaneous hyperpigmentation (buccal mucosa, palmar creases) is specific to primary adrenal insufficiency due to high ACTH/POMC cleavage products.
- Acute Addisonian crisis is a medical emergency treated immediately with aggressive IV 0.9% sodium chloride and IV hydrocortisone.
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