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Endocrine: MRCEM Primary questions with answers

Endocrine is the physiology topic on hormones and the glands that make them. Physiology carries 60 of the 180 questions in MRCEM Primary. You cover the adrenal, pituitary, thyroid and parathyroid glands and the pancreas, with ADH, aldosterone, cortisol, insulin, glucagon, vitamin D and calcium homeostasis. Conditions include Cushing syndrome, adrenal insufficiency, phaeochromocytoma, diabetes insipidus, SIADH and thyroid disease. Emergency physicians meet adrenal crisis, diabetic emergencies and calcium disorders.

5 free questions below, each with the answer and the full explanation · 166 in the full bank · Last updated after the 27 October 2026 MRCEM Primary sitting.

  1. Question 1 · Insulin and Glucagon

    A male aged 45 was found unconscious at home and was brought into the ED by paramedics. On initial assessment at triage, his BM was 1.5mmol/l. According to hypoglycemia management guidelines, which initial treatment should be given in an unconscious patient:

    1. A5% dextrose orally
    2. BIM Pabrinex
    3. C1mg IM glucagon
    4. DWait for iv-line access and give iv 10 % dextrose
    5. E70 to 80 ml of 50% glucose
    Show answer and explanation

    Answer: C. In an unconscious patient, IM glucagon is given initially without waiting for IV access.

    • A: Unsafe orally in an unconscious patient; aspiration risk.
    • B: Pabrinex gives thiamine; not first-line for hypoglycaemia.
    • D: Waiting for IV access delays treatment.
    • E: Hypertonic 50% glucose damages veins; 10% is preferred.

    Full explanation

    IM glucagon should be given initially in an unconscious patient while those patients who are alert and able to swallow oral dextrose should be given

     

  2. Question 2 · Hyperaldosteronism and Renal Insufficiency

    An elderly man attends the ED with acute confusion. Laboratory results show Hyponatremia and hyperkalemia. Deficiency of which one of the following hormones is most likely?

    1. AADH
    2. BThyroxine
    3. CCortisol
    4. DGrowth hormone
    5. EAldosterone
    Show answer and explanation

    Answer: E. Aldosterone deficiency causes sodium loss with potassium retention.

    • A: ADH deficiency causes hypernatraemia.
    • B: Hypothyroidism may cause hyponatraemia, not hyperkalaemia.
    • C: Cortisol deficiency alone does not cause hyperkalaemia.
    • D: Not associated with this electrolyte pattern.

    Full explanation: Hyperaldosteronism and Renal Insufficiency

    Hyperaldosteronism 

    • It is a small group of disorders characterized by excessive secretion of aldosterone (mineralocorticoid). 
    • It is classified into primary and secondary hyperaldosteronism.  

    Primary Hyperaldosteronism

    • It refers to hyperaldosteronism associated with HIGH aldosterone and LOW renin.

    Causes

    •    Aldosterone-secreting adenoma (Conn Syndrome) 
    •    Adrenocortical carcinoma 
    •    Familial hyperaldosteronism. 

    Diagnosis: 

    • Hypertension  
    • Headache, muscle weakness 
    • Polyuria, polydipsia; no peripheral edema 

      Lab Findings:  

    • Hypernatremia (elevated serum sodium) 
    • Hypokalemia 
    • Metabolic alkalosis
    • Elevated aldosterone and decreased plasma renin.
    • Plasma aldosterone: renin ratio > 20. 
    • Sodium suppression test = fails to suppress aldosterone after sodium load. 

    Treatment

    • Spironolactone:  It is an aldosterone antagonist used to normalize whole-body electrolyte balance
    • Followed by surgical removal (adrenalectomy) which is definitive treatment.  

      

    Secondary Hyperaldosteronism

    • It refers to hyperaldosteronism associated with HIGH aldosterone and HIGH renin. 


    • Causes:
    •    Renal artery stenosis 
    •    Congestive heart failure 
    •    Cirrhosis  
    •    Nephritic syndrome  
    •    Pregnancy (estrogen increases renin substrate)  
    •    Renin-secreting renal   tumor                                                                                                                                                                                         

     Lab Findings: 

    •  Elevated aldosterone  
    •  Elevated plasma renin 

     Treatment: 

    • Spironolactone

  3. Question 3 · Parathyroid Hormone

    A male aged 45 years presented to the ED post thyroid surgery with periorbital numbness, paresthesia of hand and feet and abnormal movement. What is the cause of his condition?

    1. AHypothyroidism
    2. BHypokalemia
    3. CThyroid Crisis
    4. DHypocalcemia
    5. EHypomagnesemia
    Show answer and explanation

    Answer: D. Parathyroid damage or removal after thyroid surgery causes hypocalcaemia with perioral and peripheral paraesthesia.

    • A: Causes fatigue and weight gain, not tingling and tetany.
    • B: Causes weakness and cramps, not perioral paraesthesia.
    • C: Causes fever and tachycardia, not tingling.
    • E: Can cause tetany but is less likely than hypocalcaemia post-thyroidectomy.

    Full explanation: Parathyroid Hormone

    Parathyroid hormone (PTH) 

    • Parathyroid hormone is secreted from chief cells of parathyroid gland which is located immediately behind the thyroid gland.  
    • It is a major hormone for regulation of serum calcium.  

    Regulation pf PTH 

    PTH secretion is stimulated by: 

    • Decrease in serum Ca2+
    • Hyperphosphatemia
    • Low calcitriol levels
    • PTH secretion is inhibited by:
    • Increase in serum Ca2+
    • Decrease in serum phosphate.
    • hypomagnesemia

                

    Action of PTH  

    • Are coordinated to produce an increase serum (Ca+) and decrease in serum phosphate. 
    • the second messenger for PTH actions on its target tissue is cAMP.
    • Bone: PTH increases bone resorption, which brings both Ca²+ and phosphate from bone mineral into the ECF (Stimulate the osteoclast cells) 

    kidney 

    • Increases Ca2+ reabsorption in the distal tubule.
    • Decreases phosphate reabsorption in the proximal convoluted tubules.
    • Increases active vitamin D (calcitriol) production via stimulation of 1-alpha-hydroxylase synthesis in the kidneys.

    GIT 

    • PTH increases intestinal Ca+ and phosphate absorption, indirectly by stimulating the production of 1,25-dihydroxycholecalciferol in the kidney.
  4. Question 4 · Aldosterone

    A man aged 25 presents with diabetic ketoacidosis. You start to treat him with short-acting insulin and intravenous fluids as per your local protocol.

    Which electrolyte disturbance is he most at risk of developing as a result of your treatment?

    1. AHypermagnesemia
    2. BHypokalemia
    3. CHypophosphatasemia
    4. DHyperchloremia
    5. EHyponatremia
    Show answer and explanation

    Answer: B. Insulin drives potassium into cells, so hypokalaemia is the main risk during DKA treatment.

    • A: Not a recognised main complication of treatment.
    • C: Can occur, but hypokalaemia is more immediately dangerous.
    • D: Occurs with large saline volumes, but is less dangerous.
    • E: Not the main insulin-driven risk.

    Full explanation

    Insulin excess lowers the serum potassium concentration by driving the K+ into the cells primarily by enhancing the activity of NA-K-ATPase pump.

    ECG changes in hypokalemia and hyperkalemia

  5. Question 5 · Cushing Syndrome

    A lady aged 6o years was brought into the ED with a fracture of the right hip. Which of the following is the primary cause of postmenopausal fractures?

    1. AIncreased bone strength
    2. BIncreased bone density
    3. CIncreased estrogen production
    4. DDecreased estrogen production
    5. EExcessive physical activity
    Show answer and explanation

    Answer: D. Falling oestrogen after menopause accelerates bone loss, leading to osteoporotic fractures.

    • A: Bone strength decreases.
    • B: Bone density decreases.
    • C: Oestrogen production falls after menopause.
    • E: Physical inactivity, not excess activity, contributes.

    Full explanation

    Postmenopausal fractures are often caused by osteoporosis, which is a condition characterized by decreased bone density and increased bone fragility. During menopause, there is a decrease in estrogen production, which can lead to accelerated bone loss and increased risk of fractures. Other factors that can contribute to postmenopausal fractures include age, genetics, nutrition, physical inactivity, smoking, and certain medical conditions or medications that can affect bone health. 

    Note: Choose hormonal imbalance option if question stem is different from this and no other character of osteoporosis is matched in options. 

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