Membership of the Royal College of Physicians (MRCP UK) Endocrinology and Metabolic Medicine Syllabus

Endocrinology and Metabolic Medicine syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Endocrinology and Metabolic Medicine in Membership of the Royal College of Physicians (MRCP UK), not a summary of it.

1. 1

   Diabetes Mellitus

   4 topics

   • Type 1 diabetes management
     • Insulin regimens and technology
   • Type 2 diabetes and oral/injectable therapy
     • SGLT2 inhibitors and GLP-1 receptor agonists
   • Diabetic emergencies
     • Diabetic ketoacidosis
     • Hyperosmolar hyperglycaemic state
     • Hypoglycaemia
   • Microvascular and macrovascular complications
2. 2

   Pituitary and Hypothalamic Disorders

   4 topics

   • Pituitary adenomas and hypopituitarism
   • Acromegaly and prolactinoma
   • Cushing's disease and syndrome
     • Diagnostic testing and localisation
   • Diabetes insipidus and SIADH
3. 3

   Thyroid and Parathyroid Disease

   4 topics

   • Hyperthyroidism and thyroid storm
     • Graves' disease management
   • Hypothyroidism and myxoedema coma
   • Thyroid nodules and thyroid cancer
   • Calcium and parathyroid disorders
     • Hyperparathyroidism and hypercalcaemia
     • Hypocalcaemia
4. 4

   Adrenal, Gonadal and Reproductive Disorders

   5 topics

   • Adrenal insufficiency and Addisonian crisis
   • Phaeochromocytoma and primary hyperaldosteronism
   • Congenital adrenal hyperplasia
   • Hypogonadism and disorders of reproduction
   • Polycystic ovary syndrome and hirsutism
5. 5

   Lipid and Metabolic Bone Disorders

   4 topics

   • Dyslipidaemia and familial hypercholesterolaemia
   • Obesity and metabolic syndrome
   • Osteoporosis and fracture risk assessment
   • Osteomalacia, Paget's disease and metabolic bone disease

Endocrinology and Metabolic Medicine flashcards for Membership of the Royal College of Physicians (MRCP UK)

25 of 58 cards from the Endocrinology and Metabolic Medicine deck — real questions with worked answers.

1. In Type 1 diabetes, what is the recommended HbA1c target for most adults, and what fasting plasma glucose target on waking is advised?

   Target HbA1c of $\leq 48\ \mathrm{mmol/mol}$ ($6.5\%$) or lower if achievable without disabling hypoglycaemia. On waking, aim for a fasting plasma glucose of $5\text{–}7\ \mathrm{mmol/L}$; pre-meal at other times $4\text{–}7\ \mathrm{mmol/L}$.

2. What is the first-line insulin regimen recommended for adults with Type 1 diabetes, and which long-acting basal insulin is preferred?

   A multiple daily injection (MDI) basal–bolus regimen is first-line. The preferred basal is twice-daily insulin detemir; alternatives include once-daily glargine or degludec. Rapid-acting analogues (aspart, lispro, glulisine) are used for mealtime bolus rather than soluble human insulin.

3. Define the diagnostic biochemical triad for diabetic ketoacidosis (DKA).

   DKA requires all three: (1) ketonaemia $\geq 3\ \mathrm{mmol/L}$ (or significant ketonuria $\geq 2+$); (2) blood glucose $> 11\ \mathrm{mmol/L}$ (or known diabetes); and (3) bicarbonate $< 15\ \mathrm{mmol/L}$ and/or venous pH $< 7.3$.

4. Outline the initial fluid and insulin management of adult DKA.

   Give $0.9\%$ saline IV (e.g. 1 L over the first hour, then titrated). Start a fixed-rate IV insulin infusion at $0.1\ \mathrm{units/kg/h}$. When glucose falls below $14\ \mathrm{mmol/L}$, add $10\%$ glucose alongside saline. Replace potassium once $K^{+} < 5.5\ \mathrm{mmol/L}$ and patient is passing urine. Continue long-acting basal insulin.

5. How does the hyperosmolar hyperglycaemic state (HHS) differ biochemically from DKA?

   HHS features marked hyperglycaemia (often $> 30\ \mathrm{mmol/L}$), serum osmolality $> 320\ \mathrm{mosmol/kg}$, significant dehydration, but NO significant ketosis ($< 3\ \mathrm{mmol/L}$) and pH $> 7.3$ / bicarbonate $> 15\ \mathrm{mmol/L}$. It evolves over days, typically in older type 2 patients, with higher mortality than DKA.

6. Give the formula for calculated serum osmolality used in HHS.

   $$\text{Osmolality} = 2[\mathrm{Na^{+}}] + [\text{glucose}] + [\text{urea}]$$ (all in $\mathrm{mmol/L}$). Normal range is approximately $275\text{–}295\ \mathrm{mosmol/kg}$.

7. What is the first-line oral pharmacological agent for Type 2 diabetes, its main mechanism, and a key contraindication?

   Metformin (a biguanide) is first-line. It reduces hepatic gluconeogenesis and increases peripheral insulin sensitivity, and does not cause hypoglycaemia or weight gain. Avoid/withhold when eGFR $< 30\ \mathrm{mL/min/1.73m^{2}}$ (lactic acidosis risk); review dose below $45$.

8. Which class of diabetes drug should be added to metformin in a Type 2 patient with established cardiovascular disease or heart failure, and why?

   An SGLT2 inhibitor (e.g. empagliflozin, dapagliflozin). They reduce cardiovascular death and heart-failure hospitalisation and slow CKD progression by promoting glycosuria/natriuresis. Caution: euglycaemic DKA, genital infections, volume depletion.

9. Compare the mechanism and weight effect of sulfonylureas versus GLP-1 receptor agonists.

   Sulfonylureas (e.g. gliclazide) stimulate insulin secretion by closing $\beta$-cell $K_{ATP}$ channels — risk of hypoglycaemia and weight gain. GLP-1 receptor agonists (e.g. semaglutide, liraglutide) are injectable incretin mimetics that enhance glucose-dependent insulin release, suppress glucagon, slow gastric emptying — causing weight loss and low hypoglycaemia risk.

10. What is the mechanism of DPP-4 inhibitors (gliptins) and how do they differ from GLP-1 agonists in effect?

    DPP-4 inhibitors (e.g. sitagliptin) block degradation of endogenous incretins (GLP-1, GIP), raising their levels. They are oral, weight-neutral, and have modest glucose-lowering effect — weaker and weight-neutral compared to the injectable, weight-reducing GLP-1 receptor agonists.

11. In diabetic nephropathy, what is the first sign and the recommended first-line drug class for renoprotection?

    The earliest sign is microalbuminuria (urine albumin:creatinine ratio $\geq 3\ \mathrm{mg/mmol}$). First-line renoprotection is an ACE inhibitor or ARB (titrated to maximum tolerated dose), which reduces intraglomerular pressure; add an SGLT2 inhibitor for further protection.

12. Classify diabetic retinopathy and state which features define proliferative disease.

    Non-proliferative (background): microaneurysms, dot/blot haemorrhages, hard exudates. Pre-proliferative: cotton-wool spots, venous beading, IRMA. Proliferative retinopathy is defined by neovascularisation (new vessels at disc/elsewhere), risking vitreous haemorrhage and traction detachment — treated with pan-retinal photocoagulation.

13. What are the macrovascular complications of diabetes, and what is the target blood pressure in a diabetic patient?

    Macrovascular: coronary artery disease (MI), cerebrovascular disease (stroke), and peripheral arterial disease. Blood pressure target is generally $< 140/90\ \mathrm{mmHg}$, or $< 130/80\ \mathrm{mmHg}$ if there is kidney, eye, or cerebrovascular damage.

14. List the anterior and posterior pituitary hormones.

    Anterior pituitary (adenohypophysis): ACTH, TSH, FSH, LH, GH, and prolactin. Posterior pituitary (neurohypophysis) stores and releases hypothalamic hormones: ADH (vasopressin) and oxytocin.

15. In hypopituitarism, in what order are anterior pituitary hormones typically lost, and which deficiency is most life-threatening?

    Classic sequence of loss: GH first, then gonadotrophins (LH/FSH), then TSH, then ACTH, with prolactin usually last (it may rise with stalk compression). ACTH deficiency causing secondary adrenal insufficiency (cortisol loss) is the most immediately life-threatening.

16. What is pituitary apoplexy and its classic presentation?

    Pituitary apoplexy is sudden haemorrhage or infarction of a (usually adenomatous) pituitary gland. It presents with sudden severe headache, visual disturbance/ophthalmoplegia, and features of acute hypopituitarism (especially adrenal crisis). It is a medical emergency requiring urgent hydrocortisone and possible surgical decompression.

17. Why does a pituitary macroadenoma classically cause bitemporal hemianopia?

    The tumour compresses the optic chiasm from below. The crossing nasal retinal fibres (which carry information from the temporal visual fields) are affected, producing a bitemporal hemianopia — typically starting in the upper temporal quadrants.

18. What is the biochemical screening and confirmatory test for acromegaly?

    Screen with serum IGF-1 (raised for age). Confirm with an oral glucose tolerance test: in acromegaly GH fails to suppress to $< 1\ \mathrm{\mu g/L}$ (often $< 0.4$ with sensitive assays) after a 75 g oral glucose load. Then image the pituitary with MRI.

19. What is the first-line treatment for acromegaly, and which medical therapies are used if it fails?

    First-line is trans-sphenoidal surgical resection of the GH-secreting adenoma. If not cured: somatostatin analogues (octreotide, lanreotide), the GH-receptor antagonist pegvisomant, dopamine agonists (cabergoline), and/or radiotherapy.

20. What is the first-line treatment for a prolactinoma, even when it is a large macroadenoma causing visual field loss?

    Dopamine agonists (cabergoline first-line, or bromocriptine) are first-line for prolactinomas of any size — they both lower prolactin and shrink the tumour, often restoring vision. Surgery is reserved for drug intolerance/resistance or apoplexy.

21. List physiological and drug causes of hyperprolactinaemia that must be excluded before diagnosing a prolactinoma.

    Physiological: pregnancy, breastfeeding, stress, nipple stimulation. Pathological non-tumour: primary hypothyroidism, chronic kidney disease, stalk compression (disconnection). Drugs: dopamine antagonists — antipsychotics (especially risperidone), metoclopramide, domperidone, and some antidepressants.

22. Distinguish Cushing's disease from Cushing's syndrome.

    Cushing's syndrome is the clinical state of chronic glucocorticoid excess from any cause (most commonly exogenous steroids). Cushing's disease specifically refers to an ACTH-secreting pituitary adenoma — the commonest endogenous cause of Cushing's syndrome.

23. Name the first-line screening tests for Cushing's syndrome.

    Any of: (1) overnight 1 mg dexamethasone suppression test (failure to suppress cortisol $< 50\ \mathrm{nmol/L}$); (2) 24-hour urinary free cortisol ($\times 2$); (3) late-night salivary cortisol (loss of diurnal rhythm). Confirm with low-dose dexamethasone suppression.

24. How does the high-dose dexamethasone suppression test and ACTH level distinguish causes of Cushing's syndrome?

    Pituitary (Cushing's disease): ACTH detectable/high, cortisol SUPPRESSES on high-dose dexamethasone (>50%). Ectopic ACTH: ACTH high, NO suppression. Adrenal tumour: ACTH suppressed (low), no suppression of cortisol. Inferior petrosal sinus sampling confirms a pituitary source.

25. Contrast central diabetes insipidus, nephrogenic diabetes insipidus, and how the water deprivation test plus desmopressin distinguishes them.

    Central DI: deficient ADH secretion; urine concentrates after desmopressin. Nephrogenic DI: renal resistance to ADH; urine does NOT concentrate after desmopressin. After water deprivation both fail to concentrate urine; the response to exogenous desmopressin separates them.

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