AMC MCQ Endocrinology: Diabetes, Thyroid & Adrenal Key Topics

Last reviewed: May 2026 | Written by the MplusX Editorial Team

📌 Key Takeaways

Diabetes Dominates: Type 2 diabetes management — HbA1c targets, SGLT2 inhibitor and GLP-1 RA indications, metformin in renal impairment — accounts for the majority of endocrinology questions across AMC MCQ sittings.
DKA Is a Protocol Question, Not a Knowledge Question: The AMC MCQ tests your sequential management steps, fluid choice, potassium replacement rules, and insulin timing — not pathophysiology.
Thyroid Tests the Threshold: Subclinical hypothyroidism treatment thresholds, Graves’ disease drug choice, and thyroid emergency recognition are common exam setups.
Adrenal Disease Is Low Frequency, High Specificity: Addison’s disease crisis management and sick day rules appear infrequently but are almost always correct-answer scenarios when they appear.
Primary CTA: Read the General Medicine High-Yield Guide — internal medicine topics including endocrinology, with eTG-cited clinical decision points.

Endocrinology is the subject that looks like it should be about pathophysiology but is actually about management thresholds.

The AMC MCQ does not ask you to explain the mechanism of insulin resistance in type 2 diabetes. It asks you what you prescribe when the patient’s eGFR is 28 mL/min and they are already on metformin.

It does not ask you to explain the hypothalamic-pituitary-thyroid axis. It asks you whether to treat a TSH of 6.2 mIU/L with a normal free T4 in a 62-year-old woman.

Endocrinology in the AMC MCQ rewards candidates who know the decision rules precisely — and penalises candidates who know the biology without knowing the thresholds.

This guide maps the highest-yield decision points across all five major endocrine topics tested in the AMC MCQ examination.

1. The AMC MCQ Endocrinology Blueprint

Topic Area	Relative Frequency	Most Tested Decision Point
Type 2 diabetes management	Very high	HbA1c targets, second-line agent selection, metformin in renal impairment
DKA management	High	Fluid protocol, potassium replacement, insulin timing
Thyroid disease	High	TSH interpretation, treatment thresholds, Graves’ management
Type 1 diabetes	Moderate	Sick day rules, hypoglycaemia management
Adrenal disorders	Moderate	Addison’s crisis, sick day rules, Cushing’s screening
Hypercalcaemia	Lower	PTH-dependent vs. independent differential

2. Type 2 Diabetes Management

2.1 HbA1c Targets — 2026 Australian Standards

The eTG 2026 and Diabetes Australia 2026 guidelines set HbA1c targets individualised by patient characteristics — not one-size-fits-all.

Patient Population	HbA1c Target
Most adults with T2DM (general target)	< 53 mmol/mol (< 7.0%)
Younger adults, newly diagnosed, no major comorbidities	< 48 mmol/mol (< 6.5%)
Frail elderly patients, limited life expectancy, recurrent hypoglycaemia	< 64 mmol/mol (< 8.0%) — less aggressive
Adults with significant CVD risk	< 53 mmol/mol; prioritise agents with proven cardiovascular benefit

The AMC MCQ frequently presents a frail 82-year-old with type 2 diabetes and offers answer options that include tightening glycaemic control. The correct answer in this context is the less-aggressive HbA1c target and avoiding hypoglycaemia-prone agents.

2.2 First-Line Pharmacotherapy

Metformin remains first-line for most adults with type 2 diabetes in Australia per eTG 2026, provided renal function is adequate.

Renal impairment thresholds for metformin (eTG 2026):

eGFR (mL/min/1.73m²)	Action
≥ 45	Continue at standard dose
30–44	Reduce dose by 50%; monitor renal function every 3 months
< 30	Contraindicated — stop metformin
Acute kidney injury or hospitalisation with contrast	Withhold temporarily

The AMC MCQ examiner frequently sets a vignette with a patient on metformin whose eGFR has declined below 30. The correct answer is to stop metformin — not reduce it.

2.3 Second-Line Agent Selection — The 2026 Paradigm Shift

The choice of second-line agent in type 2 diabetes is no longer primarily about glucose lowering. It is driven by comorbidity profile.

SGLT2 Inhibitors (empagliflozin, dapagliflozin, canagliflozin):

Indicated as add-on (or initial alternative to metformin) in patients with:

Established cardiovascular disease (CVD) — reduces MACE (major adverse cardiac events) Reading about best AMC MCQ resources might also be helpful.
Heart failure with reduced ejection fraction (HFrEF) — reduces hospitalisation and mortality
Chronic kidney disease (CKD, eGFR 25–60) — reduces progression to ESKD

PBS-funded indications for SGLT2 inhibitors in Australia (2026):

Type 2 diabetes + inadequate glycaemic control on ≥ 1 oral agent
Type 2 diabetes + chronic kidney disease (dapagliflozin under extended PBS listing)

Key safety rules for SGLT2 inhibitors:

Withhold before surgery, prolonged fasting, or severe illness (euglycaemic DKA risk)
Do not use with eGFR < 30 (reduced efficacy; dapagliflozin for CKD has a different threshold — check eTG)
Genital mycotic infections are common — counsel patients

GLP-1 Receptor Agonists (semaglutide, dulaglutide, liraglutide):

Indicated in patients with:

Established CVD and need for weight reduction
Obesity (BMI > 30) as part of diabetes management
Inadequate glycaemic control on SGLT2 inhibitor + metformin

GLP-1 RAs reduce HbA1c, promote weight loss, and have cardiovascular benefits. They do not cause hypoglycaemia when used without insulin.

DPP-4 Inhibitors (sitagliptin, saxagliptin, vildagliptin):

Weight-neutral, low hypoglycaemia risk
Second-line option when SGLT2 and GLP-1 are contraindicated or not tolerated
Saxagliptin: avoid in heart failure (increases hospitalisation risk)

Sulfonylureas (glipizide, glibenclamide, gliclazide MR):

Cheap, effective glucose lowering
High risk of hypoglycaemia — especially in elderly, those with irregular meals
Gliclazide MR is preferred over older-generation sulfonylureas (lower hypoglycaemia risk)
AMC MCQ will often present a case where a sulfonylurea is appropriate for cost-effective glycaemic control in a patient without CVD or CKD

2.4 Insulin in Type 2 Diabetes

Insulin initiation is appropriate when:

HbA1c remains above target despite optimised oral combination therapy
Patient has symptomatic hyperglycaemia at diagnosis (HbA1c > 75 mmol/mol or > 9%)
Acute illness driving acute decompensation

Starting insulin (per eTG 2026):

Basal insulin (insulin glargine or detemir): starting dose 10 units subcutaneous at bedtime
Titrate by 2 units every 3 days until fasting glucose 4.0–7.0 mmol/L
Hypoglycaemia counselling mandatory before initiation

graph TD A[T2DM: HbA1c above target on Metformin] –> B{Patient has CVD or CKD?} B –>|Yes — established CVD| C[Add SGLT2 inhibitor or GLP-1 RA — proven MACE benefit] B –>|Yes — HFrEF or CKD eGFR 25–60| D[Add SGLT2 inhibitor dapagliflozin/empagliflozin] B –>|No CVD/CKD, weight concern| E[Add GLP-1 RA semaglutide/dulaglutide — weight loss] B –>|No CVD/CKD, cost concern| F[Add Sulfonylurea gliclazide MR — lowest cost] B –>|No CVD/CKD, neutral weight| G[Add DPP-4 inhibitor sitagliptin — weight neutral] C –> H[Titrate + monitor HbA1c 3-monthly] D –> H E –> H F –> H G –> H

style A fill:#0F2D5C,stroke:#fff,color:#fff style C fill:#166534,stroke:#fff,color:#fff style D fill:#166534,stroke:#fff,color:#fff style E fill:#2A7D7B,stroke:#fff,color:#fff style F fill:#2A7D7B,stroke:#fff,color:#fff style G fill:#2A7D7B,stroke:#fff,color:#fff

3. Diabetic Ketoacidosis (DKA)

3.1 Recognising DKA

DKA is the most commonly tested endocrine emergency across AMC MCQ sittings.

Diagnostic triad: 1. Hyperglycaemia (BGL typically > 14 mmol/L, though BGL can be normal in euglycaemic DKA — SGLT2 inhibitor-associated) 2. High anion-gap metabolic acidosis (pH < 7.3, bicarbonate < 15 mmol/L) 3. Ketonaemia (blood ketones > 3.0 mmol/L) or ketonuria (++ or more on urinalysis)

Precipitants to identify in the vignette:

Missed insulin dose
Intercurrent infection (most common — UTI, pneumonia)
New-onset type 1 diabetes presenting in crisis
SGLT2 inhibitor use (euglycaemic DKA — normal or mildly elevated glucose)

3.2 DKA Management Protocol — eTG 2026

Step 1 — Resuscitation (first hour):

IV access × 2 (large bore)
1,000 mL 0.9% sodium chloride (normal saline) over 1 hour — initial bolus
If shocked or severely dehydrated: more aggressive fluid resuscitation

Step 2 — Ongoing fluid replacement:

Continue 0.9% NaCl at 250–500 mL/hour for the next 2–4 hours, then titrate based on clinical status
Switch to 0.45% NaCl if sodium is correcting too rapidly or hypernatraemia develops Reading about MplusX vs AMEDEX might also be helpful.
Once BGL falls below 14 mmol/L: add 5% dextrose to the fluid regimen (to prevent hypoglycaemia while continuing insulin)

Step 3 — Potassium replacement (critical):

Serum K⁺	Action
< 3.5 mmol/L	Delay insulin; replace potassium urgently before starting insulin (insulin drives K⁺ intracellular)
3.5–5.5 mmol/L	Start insulin; add KCl 40 mmol/L to IV fluids
> 5.5 mmol/L	Start insulin; withhold potassium until K⁺ < 5.5 mmol/L

This potassium rule is the single most tested decision point in DKA management. The AMC MCQ will present a patient with a serum K⁺ of 3.2 mmol/L and ask what you do before starting insulin. The answer is: replace potassium first.

Step 4 — Insulin infusion:

Fixed-rate intravenous insulin infusion (FRIII): 0.1 units/kg/hour (regular insulin)
Continue until blood ketones < 0.3 mmol/L AND pH > 7.3 AND patient can eat/drink
Do not stop insulin infusion just because glucose has normalised — ketone clearance is the endpoint

Step 5 — Monitoring:

Hourly BGL, urine output, vital signs
2-hourly blood ketones (if bedside ketone meter available) or every 2–4 hours via blood gas
4-hourly EUC (electrolytes, urea, creatinine)
Continuous cardiac monitoring (ECG changes with hypo/hyperkalaemia)

Step 6 — Bicarbonate:

Do NOT routinely administer sodium bicarbonate in DKA
Reserve for life-threatening acidosis (pH < 6.9) only, and only after senior review
Routine bicarbonate administration in DKA was abandoned due to evidence of harm

graph TD A[“DKA Diagnosis: BGL >14 + pH <7.3 + Ketones >3.0″] –> B[“Step 1: IV Access x2 + 1000 mL 0.9% NaCl over 1 hour”] B –> C[Step 2: Check Serum Potassium] C –> D{K⁺ level?} D –>|”K⁺ < 3.5 mmol/L"| E["HOLD INSULIN Replace K⁺ urgently first"] D -->|”K⁺ 3.5–5.5 mmol/L”| F[Start insulin + add KCl to fluids] D –>|”K⁺ > 5.5 mmol/L”| G[“Start insulin Withhold K⁺ until <5.5"] E --> H[“Start Insulin: 0.1 units/kg/hr FRIII”] F –> H G –> H H –> I{“BGL < 14 mmol/L?"} I -->|Yes| J[“Add 5% Dextrose to fluids Continue insulin”] I –>|No| H J –> K{“Ketones < 0.3 AND pH > 7.3?”} K –>|Yes| L[“Transition to SC insulin Resume eating”] K –>|No| J

style A fill:#0F2D5C,stroke:#fff,color:#fff style E fill:#991B1B,stroke:#fff,color:#fff style H fill:#D69E2E,stroke:#fff,color:#fff style J fill:#2A7D7B,stroke:#fff,color:#fff style L fill:#166534,stroke:#fff,color:#fff

4. Type 1 Diabetes Management

4.1 Sick Day Rules

The AMC MCQ regularly tests sick day management in type 1 diabetes.

The core principle: never stop insulin in type 1 diabetes during illness, even if the patient is not eating.

Without insulin, type 1 diabetics will develop DKA rapidly regardless of oral intake.

Sick day action plan (per RACGP and Diabetes Australia 2026): 1. Continue all usual insulin doses 2. Check BGL every 2–4 hours 3. Check blood ketones every 4 hours 4. If BGL > 14 mmol/L AND ketones > 0.6 mmol/L: correction dose of rapid-acting insulin required 5. Maintain fluid intake — at least 200 mL/hour if vomiting prevents solids 6. Present to ED if: vomiting preventing oral hydration, ketones > 3.0 mmol/L, pH < 7.3, altered consciousness

4.2 Hypoglycaemia Management in Type 1 Diabetes

Mild-moderate hypoglycaemia (patient conscious, can swallow):

Rule of 15: 15 g of fast-acting carbohydrate (e.g., 150 mL juice, 4 glucose tablets)
Recheck BGL in 15 minutes
If BGL still < 4.0 mmol/L: repeat 15 g carbohydrate
Once BGL normalises: follow with a snack containing complex carbohydrate

Severe hypoglycaemia (impaired consciousness, cannot swallow safely):

IV dextrose (50 mL of 50% dextrose) if IV access available
OR glucagon 1 mg IM if no IV access (e.g., home setting)
Do NOT give oral glucose to an unconscious patient (aspiration risk)

The AMC MCQ will present a hypoglycaemic patient at home, no IV access, with impaired consciousness. The correct answer is intramuscular glucagon — not oral glucose, and not waiting for IV access.

5. Thyroid Disease

5.1 TSH Interpretation

TSH is the first-line screening test for thyroid disease.

TSH Level	Free T4	Diagnosis	Action
High (> 4.0 mIU/L)	Low	Primary hypothyroidism (overt)	Treat with levothyroxine
High (> 4.0 mIU/L)	Normal	Subclinical hypothyroidism	Treatment depends on TSH level and patient factors
Low (< 0.4 mIU/L)	High	Overt hyperthyroidism	Treat (see below)
Low (< 0.4 mIU/L)	Normal	Subclinical hyperthyroidism	Monitor or treat based on degree and risk

5.2 Subclinical Hypothyroidism — Treatment Thresholds

The AMC MCQ tests this threshold repeatedly.

Per eTG 2026:

TSH 4.0–10.0 mIU/L with normal free T4:

– Treat if: symptomatic, pregnant, planning pregnancy, TPO antibodies positive, TSH > 10 mIU/L (regardless of symptoms) – Monitor without treatment if: asymptomatic, no risk factors, TSH < 10 mIU/L, no antibodies — repeat TFT in 3–6 months

TSH > 10.0 mIU/L with normal free T4: Treat with levothyroxine regardless of symptoms (per current eTG guidance)

The AMC MCQ vignette: a 55-year-old woman, no symptoms, TSH 7.8, normal free T4, no antibodies. What do you do? Monitor — not treat yet.

5.3 Graves’ Disease Management

Graves’ disease is the most common cause of hyperthyroidism in younger Australians.

Initial pharmacological management (per eTG 2026):

Carbimazole — first-line antithyroid drug in Australia

– Starting dose: 15–40 mg/day (depending on severity) – Side effects: agranulocytosis (rare but serious — warn patient to seek urgent review if fever, sore throat, mouth ulcers develop) – Do not use carbimazole in the first trimester of pregnancy — use propylthiouracil (PTU) instead (teratogenicity of carbimazole)

Propranolol — for symptomatic relief of tremor, palpitations, anxiety during initial thyroid storm or severe hyperthyroidism

– Not an antithyroid agent; does not affect thyroid hormone production

Definitive treatment options: 1. Radioactive iodine (RAI / ¹³¹I): Preferred definitive treatment in non-pregnant adults. Contraindicated in pregnancy and severe ophthalmopathy. May worsen Graves’ ophthalmopathy. 2. Total thyroidectomy: Indicated if large goitre, suspected malignancy, severe ophthalmopathy, patient prefers surgical option, or RAI failed.

Post-RAI or post-thyroidectomy: Hypothyroidism expected. Start levothyroxine.

5.4 Thyroid Emergencies

Myxoedema Coma:

Severe, life-threatening hypothyroidism
Presentation: altered consciousness, hypothermia, bradycardia, hyponatraemia, respiratory failure
Treatment: IV levothyroxine (T4) ± IV liothyronine (T3), IV hydrocortisone (exclude concurrent adrenal insufficiency first), supportive care in ICU

Thyroid Storm:

Life-threatening hyperthyroidism with systemic decompensation
Presentation: fever > 38.5°C, HR > 140, agitation, confusion, vomiting/diarrhoea, jaundice
Burch-Wartofsky Point Scale (BWPS) used clinically to quantify probability
Treatment (sequential, per eTG 2026):

1. Propylthiouracil (PTU) 200–250 mg every 4 hours — blocks new hormone synthesis AND peripheral conversion of T4 to T3 2. Potassium iodide (Lugol’s iodine) — 1 hour AFTER PTU (not before; iodine given before PTU will worsen storm) 3. Propranolol IV or oral — rate control 4. Hydrocortisone 100 mg IV 8-hourly — suppresses T4→T3 conversion, covers possible relative adrenal insufficiency 5. ICU admission

The timing of iodine administration relative to PTU is a high-yield AMC MCQ trap.

6. Adrenal Disorders

6.1 Addison’s Disease (Primary Adrenal Insufficiency)

Presentation:

Fatigue, weight loss, nausea, postural hypotension
Hyperpigmentation (excess ACTH stimulating melanocytes — characteristic of PRIMARY adrenal insufficiency)
Hyponatraemia, hyperkalaemia, hypoglycaemia (cortisol and aldosterone both deficient)

Diagnosis:

Short synacthen (ACTH stimulation) test: cortisol < 500 nmol/L at 30–60 minutes post-ACTH = adrenal insufficiency

Maintenance therapy:

Hydrocortisone 15–25 mg/day in divided doses (morning-weighted)
Fludrocortisone 50–200 mcg/day (for mineralocorticoid replacement — only in primary, not secondary, adrenal insufficiency)

6.2 Adrenal Crisis

Precipitants: Infection, surgery, trauma, missed steroid doses, acute illness

Presentation: Severe hypotension, vomiting, confusion, shock

Emergency management (eTG 2026): 1. IV hydrocortisone 100 mg immediately (do not wait for investigations) 2. IV 0.9% NaCl — aggressive fluid resuscitation (corrects hypovolaemia and hyponatraemia) 3. IV 5–10% dextrose if hypoglycaemia present 4. Identify and treat precipitant (usually infection) 5. ICU or HDU monitoring

The AMC MCQ principle: In suspected adrenal crisis, administer hydrocortisone immediately — do not delay treatment while waiting for cortisol results.

6.3 Sick Day Rules for Addison’s Disease

AMC MCQ candidates must know the “sick day rule” for patients with Addison’s disease:

Severity of Illness	Steroid Adjustment
Minor illness (fever, mild infection)	Double oral hydrocortisone dose
Moderate illness (vomiting, cannot take oral meds)	IM hydrocortisone 100 mg immediately; seek medical review
Major illness or surgery	IV hydrocortisone 50–100 mg 6-hourly; ICU/HDU care

6.4 Cushing’s Syndrome — Screening

Cushing’s syndrome (cortisol excess) is less common than adrenal insufficiency on the AMC MCQ but appears as a clinical recognition question.

Screening tests (eTG 2026): 1. Overnight dexamethasone suppression test: 1 mg dexamethasone at midnight; 8 am cortisol < 50 nmol/L = normal suppression 2. 24-hour urinary free cortisol (UFC): Elevated in Cushing’s 3. Late-night salivary cortisol: Loss of diurnal variation in Cushing’s

Localising the source:

Low-dose dexamethasone suppression test + ACTH level:

– High ACTH + no suppression → ACTH-dependent (pituitary = Cushing’s disease; ectopic ACTH = small cell lung cancer) – Low/suppressed ACTH → ACTH-independent (adrenal adenoma/carcinoma)

7. Hypercalcaemia

7.1 Causes and Differential

Hypercalcaemia is not rare on the AMC MCQ. It typically appears as an investigation-result question requiring source identification.

PTH-dependent hypercalcaemia (PTH elevated or inappropriately normal):

Primary hyperparathyroidism — most common cause overall (parathyroid adenoma)
Familial hypocalciuric hypercalcaemia (FHH) — benign, low urinary calcium, normal PTH

PTH-independent hypercalcaemia (PTH suppressed):

Malignancy — commonest cause in hospitalised patients (PTHrP from solid tumours; lytic bone metastases)
Sarcoidosis — granulomatous 1,25-dihydroxyvitamin D production Reading about AMC MCQ recalls might also be helpful.
Vitamin D toxicity
Milk-alkali syndrome
Thiazide diuretics (mild)
Immobilisation

7.2 Acute Hypercalcaemia Management

Symptomatic severe hypercalcaemia (> 3.5 mmol/L or symptomatic): 1. IV normal saline — vigorous hydration (corrects dehydration, promotes renal calcium excretion) 2. IV bisphosphonate — zoledronic acid or pamidronate (if malignancy-related) 3. Calcitonin — rapid short-term calcium lowering 4. IV glucocorticoids — if sarcoidosis or vitamin D toxicity (inhibit 1,25-dihydroxyvitamin D production)

Do not give thiazide diuretics in hypercalcaemia — they reduce urinary calcium excretion and will worsen the hypercalcaemia. The AMC MCQ will offer furosemide as a distractor — furosemide (loop diuretic) increases urinary calcium excretion and may be used. Thiazides are wrong.

8. High-Yield Distractor Deconstruction

Scenario 1 — Metformin and Renal Impairment

A 68-year-old man with type 2 diabetes on metformin 1g BD has an eGFR that has declined to 28 mL/min. What is the most appropriate action regarding metformin?

Trap: Reduce metformin dose to 500 mg BD.

Correct answer: Stop metformin. eGFR < 30 mL/min is a contraindication to metformin use in Australia per eTG 2026.

Scenario 2 — DKA Potassium Rule

A patient presenting with DKA has serum potassium of 3.1 mmol/L. What is the next step?

Trap: Start insulin infusion at 0.1 units/kg/hour immediately.

Correct answer: Correct hypokalaemia (IV potassium replacement) before starting insulin. Insulin drives potassium intracellularly, worsening hypokalaemia and risking fatal arrhythmia.

Scenario 3 — Thyroid Storm Iodine Timing

A patient in thyroid storm is to receive propylthiouracil, potassium iodide, and propranolol. In what order should these be given?

Trap: Potassium iodide first to acutely block iodine organification.

Correct answer: PTU first → wait at least 1 hour → potassium iodide. Giving iodine before PTU provides excess substrate for hormone synthesis and can precipitate worsening of the storm.

Scenario 4 — Graves’ in Pregnancy

A 26-year-old woman in her first trimester is diagnosed with Graves’ disease. Which antithyroid drug is preferred?

Trap: Carbimazole — it is first-line for Graves’ in most patients.

Correct answer: Propylthiouracil (PTU). Carbimazole is associated with aplasia cutis and other teratogenic effects in the first trimester. PTU is used in the first trimester; carbimazole may be used from second trimester if PTU is not tolerated.

Scenario 5 — Adrenal Crisis Management

A patient with known Addison’s disease presents in shock, vomiting, and confusion. Cortisol results will take 2 hours from the lab. What do you do?

Trap: Wait for cortisol result before giving steroids to ensure you do not mask adrenal function.

Correct answer: Administer IV hydrocortisone 100 mg immediately. In a suspected adrenal crisis, treatment takes priority over diagnostic confirmation. Waiting for results in an unstable patient can be fatal.

Frequently Asked Questions

What is the most tested endocrinology topic in AMC MCQ?

Type 2 diabetes management — specifically second-line agent selection (SGLT2 inhibitor and GLP-1 RA indications), metformin in renal impairment, and HbA1c targets. DKA management and thyroid disease are close behind.

Do I need to know all DKA fluid rates in exact numbers?

You need to know: normal saline is the initial fluid, potassium must be replaced before insulin if K⁺ < 3.5, the insulin infusion rate is 0.1 units/kg/hour, and you switch to dextrose-containing fluid when BGL falls below 14 mmol/L. Exact mL/hour rates are less likely to be tested than these key decision rules.

Is sodium bicarbonate ever given in DKA in 2026 Australian practice?

Rarely, and only for life-threatening acidosis (pH < 6.9) under senior specialist guidance. Routine bicarbonate administration in DKA is no longer recommended and would be a wrong answer in AMC MCQ unless the stem specifically specifies pH < 6.9 with haemodynamic deterioration.

What is the difference between Addison’s disease and secondary adrenal insufficiency in AMC MCQ?

Addison’s disease (primary) presents with hyperpigmentation, hyperkalemia, and both glucocorticoid AND mineralocorticoid deficiency. Secondary adrenal insufficiency (pituitary cause) does not cause hyperpigmentation (ACTH is low) and does not cause hyperkalaemia (aldosterone is intact). In management, secondary adrenal insufficiency does not require fludrocortisone.

When should I refer a patient with subclinical hypothyroidism?

Refer to endocrinology when: TSH > 10, patient is pregnant or planning pregnancy, clinical uncertainty about treatment threshold, or coexisting conditions complicate management decisions.

Drill Endocrinology With Precision

Endocrinology questions on the AMC MCQ are winnable.

The thresholds are fixed. The protocols are sequential. The distractor traps are predictable.

A candidate who can recite the metformin eGFR thresholds, the DKA potassium rule, the thyroid storm drug sequence, and the adrenal crisis hydrocortisone dose has command of the majority of endocrinology marks on offer.

Read the General Medicine High-Yield Guide — the companion guide covering internal medicine topics with the same precision, including cardiology, respiratory, nephrology, and haematology.

Written by the MplusX Editorial Team — dedicated to providing clinically accurate, structured, and practical resources for international medical graduates pursuing licensing with the Australian Medical Council.

References

John Murtagh‘s General Practice (8th Edition): Chapter 11: Diabetes mellitus, Page 249; Chapter 14: Endocrine and metabolic disorders, Page 348
RACGP Red Book (10th edition): Chapter 8.4: Type 2 diabetes, Page 92
Therapeutic Guidelines (eTG): Part 2 DM (Diabetes Mellitus): Chapter 1: Management of type 2 diabetes, Page 335

Disclaimer: This article is written for AMC MCQ examination preparation and general informational purposes only. It does not constitute medical advice, diagnosis, or treatment recommendations. Clinical decisions should always be based on individual patient assessment, current Australian Therapeutic Guidelines (eTG), and consultation with qualified healthcare professionals. MplusX is an exam preparation platform and is not a substitute for supervised clinical training.