Specialist & Consultant Endocrinology oral assessment prep

Knowledge: This is pituitary apoplexy, a haemorrhage into a previously unrecognised macroadenoma. The most immediate threat is acute adrenal insufficiency from ACTH deficiency, shown here by hypotension, hyponatraemia and hypoglycaemia. The second threat is compression of the optic chiasm and cavernous sinus nerves. Subarachnoid haemorrhage, meningitis and basilar artery thrombosis are the main differentials and are excluded by imaging and clinical review. MRI defines the haemorrhage, its extent and chiasmal compression. Decisions about surgery rest on visual acuity, field loss and conscious level, and many patients with only ocular palsy recover with conservative care.

Management: I would give hydrocortisone 100 mg intravenously at once, without waiting for cortisol results, and then 50 mg every 6 hours or a continuous infusion. I would take blood for cortisol, thyroid function, prolactin, IGF-1, gonadotrophins and testosterone before the dose if it causes no delay. I would correct glucose and give isotonic fluids with careful sodium monitoring. I would arrange urgent MRI, formal visual acuity and fields, and an early joint review with neurosurgery and ophthalmology. Reduced acuity, severe persistent field loss or falling consciousness favour early transsphenoidal decompression. Otherwise, conservative care with daily visual assessment is reasonable. I would monitor fluid balance for diabetes insipidus. Long-term, he needs pituitary function reassessment, imaging and hormone replacement.

Ethics and communication: This cannot wait for the morning, and I would say so clearly to the emergency team. I would explain the diagnosis and options to him and his family in plain language, including uncertainty about vision recovery. He must not drive until his visual fields meet the required standard, and I would document this advice. I would document the time of steroid treatment and each specialist review.

Reference: Society for Endocrinology UK Guidelines for the Management of Pituitary Apoplexy, 2011; Williams Textbook of Endocrinology, 15th edition

Knowledge: She has active Graves' hyperthyroidism in the first trimester. Uncontrolled thyrotoxicosis raises the risk of miscarriage, pre-eclampsia, preterm birth and growth restriction, so stopping treatment is unsafe. Carbimazole and methimazole carry a recognised embryopathy risk in the period of organogenesis, roughly weeks 6 to 10. Propylthiouracil is preferred in the first trimester, but it carries a rare risk of severe liver injury. High TSH receptor antibodies can cross the placenta from mid-pregnancy and cause fetal and neonatal thyrotoxicosis. Radioiodine is contraindicated in pregnancy. Gestational transient thyrotoxicosis is unlikely with positive antibodies and a known history.

Management: I would switch carbimazole to propylthiouracil today, at an equivalent dose of about 100 mg two or three times daily. I would add a beta-blocker, such as propranolol, at the lowest dose for symptoms and stop it once controlled. I would aim to keep free T4 at or just above the upper reference limit, using the lowest effective dose, and check thyroid function every 2 to 4 weeks. After the first trimester, I would consider switching back to carbimazole. I would repeat TSH receptor antibodies at around 18 to 22 weeks and again late in pregnancy. If they remain high, I would arrange fetal growth and heart rate surveillance with maternal-fetal medicine. I would alert the neonatal team to check the baby after birth. She should report sore throat, fever, jaundice or dark urine immediately.

Ethics and communication: She is an adult with capacity, and the decision is hers, informed by the evidence. With her permission, I would include her husband or mother-in-law to explain why stopping treatment risks the baby. I would document the counselling on drug risks and her consent. I would coordinate care with her obstetrician.

Reference: American Thyroid Association Guidelines for the Diagnosis and Management of Thyroid Disease During Pregnancy and the Postpartum, 2017; American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism and Other Causes of Thyrotoxicosis, 2016

Knowledge: This is severe symptomatic PTH-independent hypercalcaemia, most likely humoral hypercalcaemia of malignancy from PTHrP, often seen with squamous cell lung cancer. Bone metastases and myeloma are other causes. Primary hyperparathyroidism is excluded by a suppressed PTH. Volume depletion from vomiting and calcium-induced diuresis drives the kidney injury and worsens the hypercalcaemia. Severe hypercalcaemia can cause arrhythmia, coma and kidney failure. Endocrine Society guidance supports intravenous fluids, then denosumab or an intravenous bisphosphonate. In severe cases it suggests adding calcitonin for its rapid effect. The ECG may show a short QT interval, and digoxin toxicity is more likely if he takes it.

Management: I would start intravenous 0.9% saline, aiming for good urine output, while watching for fluid overload. I would give zoledronic acid 4 mg intravenously, or denosumab if kidney function stays poor, and add subcutaneous calcitonin for the first 48 hours. I would stop thiazides, calcium supplements and vitamin D, and review drugs that worsen kidney function. I would monitor calcium, electrolytes, renal function and ECG. I would request PTHrP, myeloma screen, and a CT of chest, abdomen and pelvis. Dialysis is reserved for refractory hypercalcaemia with kidney failure. I would use furosemide only for fluid overload after rehydration. I would refer to the lung cancer team for tissue diagnosis.

Ethics and communication: I would acknowledge the sons' concern, which is common and loving in the region. Once his confusion improves, I would ask him how much he wants to know and who should be present. A capacitous patient has the right to information about his diagnosis, and I would not lie to him. If he prefers that his sons receive the details, I would respect that choice. I would document his wishes and the conversations.

Reference: Endocrine Society Clinical Practice Guideline: Treatment of Hypercalcemia of Malignancy in Adults, 2023; Williams Textbook of Endocrinology, 15th edition

Knowledge: A lipid-poor adrenal mass over 10 Hounsfield units with paroxysms and a plasma normetanephrine 6 times the upper limit is phaeochromocytoma until proven otherwise. Beta-blockade before alpha-blockade can cause unopposed alpha stimulation and a hypertensive crisis. Surgery without preparation risks severe intraoperative instability. A significant proportion of phaeochromocytomas have a germline mutation, such as SDHB, VHL, RET or NF1. Endocrine Society guidance recommends genetic testing for all patients. Functional imaging helps assess extra-adrenal or metastatic disease, particularly with SDHB variants. Biopsy of a possible phaeochromocytoma is contraindicated because it can provoke a crisis.

Management: I would stop bisoprolol now and advise the surgeon to postpone surgery. I would start alpha-blockade with doxazosin or phenoxybenzamine, titrated over 7 to 14 days. I would advise a high-sodium diet and good fluid intake to restore volume. I would add a beta-blocker only after adequate alpha-blockade if tachycardia persists. I would aim for seated blood pressure below about 130/80 mmHg with mild orthostatic fall. I would request genetic testing and consider functional imaging before surgery. I would liaise with an experienced anaesthetist and surgeon. Postoperatively I would watch for hypotension and hypoglycaemia. I would recheck metanephrines a few weeks after surgery and arrange lifelong follow-up.

Ethics and communication: I would discuss the change of plan with the surgeon directly, without undermining him in front of the patient. I would explain the risks to her and record her consent to the delay. If a germline variant is found, I would explain the implications for relatives and support her to share them. I would not contact relatives without her consent.

Reference: Endocrine Society Clinical Practice Guideline: Pheochromocytoma and Paraganglioma, 2014; ESE Clinical Practice Guideline on the Management of Adrenal Incidentalomas, 2023

Knowledge: Under IDF-DAR risk scoring, type 1 diabetes with poor control, recent severe hypoglycaemia and impaired awareness places him in the highest risk category. People at this risk are advised not to fast. Fasting increases risks of hypoglycaemia, hyperglycaemia, ketoacidosis and dehydration. Many scholars recognise illness as an exemption from fasting, but the decision remains his. Continuous glucose monitoring and structured education reduce risk if he fasts. Insulin pump therapy also helps but takes time to establish. A sudden change in sleep and meal timing also disrupts insulin needs. Without changes, his HbA1c and hypoglycaemia history predict a high chance of a severe event.

Management: I would first review his injection technique, sites and recent glucose data. I would advise him clearly that fasting is not recommended. If he still fasts, I would provide a written plan. I would start continuous glucose monitoring and teach him to act on alerts. I would reduce glargine by about 20 to 30% and adjust it according to fasting glucose. I would give aspart with suhoor and iftar, matched to carbohydrate content. He must break the fast for glucose below 3.9 mmol/L, above 16.7 mmol/L, or symptoms. He should check ketones if glucose stays high. I would arrange contact after one week and after Ramadan, and improve his overall control for the longer term.

Ethics and communication: He is an adult with capacity, and I would respect his decision while advising honestly. I would avoid pressuring him or judging his faith. If he agrees, I would suggest talking to a trusted religious scholar about exemptions. I would document the risk counselling and the plan.

Reference: IDF-DAR Diabetes and Ramadan Practical Guidelines, 2021; ADA Standards of Care in Diabetes

Knowledge: This is severe hypoglycaemia from a tenfold overdose of long-acting insulin. Glargine absorption is prolonged, so hypoglycaemia may recur for 24 hours or more. Her kidney disease further reduces insulin clearance. Neuroglycopenia can cause seizures, arrhythmia and permanent brain injury, and hypokalaemia can follow as glucose and insulin drive potassium into cells. The error type, a misread U for units, is a recognised cause of insulin overdoses. Glucagon may work less well when glycogen stores are low, as in acute illness. Repeated hypoglycaemia in the first hours often means a continuing insulin depot, not a failure of treatment. I would also confirm that no sulfonylurea was given, since that changes the plan.

Management: I would give 150 to 200 mL of 10% glucose intravenously over 15 minutes, or 75 to 100 mL of 20%, and repeat the glucose at 10 minutes. I would then start a continuous 10% glucose infusion and monitor glucose hourly. I would check potassium regularly and replace it as needed. If she becomes alert and can swallow, she should eat. I would monitor her in a high-dependency area for at least 24 hours, as recurrence is expected. I would withhold all insulin until glucose rises without the infusion. I would check whether other patients received orders from the same handwriting or chart that day. I would review her diabetes treatment before discharge.

Ethics and communication: I would explain the error honestly to her and her family as soon as she is able, with an apology. I would report the incident through the hospital system. I would support the nurse while the review looks at systems, such as handwritten insulin orders. I would document the error, treatment and disclosure clearly.

Reference: JBDS-IP: The Hospital Management of Hypoglycaemia in Adults with Diabetes Mellitus; Federal Decree-Law No. 4 of 2016 on Medical Liability