A 25-year-old woman with type 1 diabetes for 12 years attends for her annual screening appointment. She is asymptomatic with an HbA1c of 62 mmol/mol (7.8%). Digital retinal photography shows microaneurysms and scattered dot haemorrhages in both eyes, but no cotton wool spots, venous beading, or new vessels. Her albumin:creatinine ratio is 2.8 mg/mmol (normal <3), blood pressure is 124/78 mmHg, and monofilament testing of her feet is normal. What is the appropriate follow-up interval for diabetic retinopathy screening in this patient?
Q112
A 58-year-old woman is found to have a TSH of 8.2 mU/L (normal 0.5-5.0) and free T4 of 11 pmol/L (normal 9-25) on routine blood tests. She has no symptoms and no goitre on examination. Anti-thyroid peroxidase (anti-TPO) antibodies are strongly positive. Her lipid profile shows total cholesterol 6.8 mmol/L and LDL cholesterol 4.2 mmol/L. She has no other significant medical history and takes no regular medications. What is the most appropriate management?
Q113
A 19-year-old man with type 1 diabetes for 8 years is reviewed in the diabetes clinic. Over the past 6 months, his HbA1c has risen from 58 mmol/mol to 76 mmol/mol (9.1%). He reports multiple episodes of hypoglycaemia, particularly in the evenings, followed by high glucose readings the next morning. He is currently on a basal-bolus insulin regimen with insulin glargine 28 units at bedtime and insulin aspart before meals. His continuous glucose monitoring shows significant glycaemic variability. What is the most likely explanation for his morning hyperglycaemia?
Q114
A 34-year-old woman who is 8 weeks pregnant presents with fatigue and palpitations. She has no significant past medical history. Examination reveals a fine tremor, warm peripheries, and a resting pulse of 98 bpm. Her thyroid is mildly enlarged but non-tender. Blood tests show: TSH <0.01 mU/L, free T4 28 pmol/L (normal 9-25), free T3 9.2 pmol/L (normal 3.5-7.8), and beta-hCG 85,000 IU/L. TSH receptor antibodies are negative. Which of the following is the most likely diagnosis?
Q115
A 72-year-old woman with type 2 diabetes is brought to the emergency department with reduced consciousness. Her family reports she has been increasingly confused over the past 3 days with reduced oral intake. Her medications include metformin and gliclazide. On examination, she is deeply unresponsive (GCS 6), blood pressure 95/62 mmHg, pulse 118 bpm, temperature 37.8°C, and appears clinically dehydrated. Investigations show: capillary glucose 52.3 mmol/L, sodium 157 mmol/L, potassium 4.8 mmol/L, urea 28.2 mmol/L, creatinine 185 μmol/L, serum osmolality 382 mOsm/kg. Urinalysis shows no ketones. What is the calculated fluid deficit likely to be in this patient?
Q116
A 45-year-old woman presents with palpitations, weight loss, and heat intolerance over the past 3 months. On examination, she has a diffuse, non-tender goitre, a resting pulse of 110 bpm, and lid lag. Blood tests reveal: TSH <0.01 mU/L, free T4 32 pmol/L (normal 9-25), free T3 12.8 pmol/L (normal 3.5-7.8). TSH receptor antibodies are positive. She is commenced on carbimazole 40mg daily. After 6 weeks, her thyroid function tests show: TSH <0.01 mU/L, free T4 14 pmol/L. What is the most appropriate next step in her management?
Q117
A 62-year-old man with type 2 diabetes for 15 years attends his annual diabetes review. He is currently taking metformin 1g twice daily and gliclazide 160mg twice daily. His HbA1c is 68 mmol/mol (8.4%). His BMI is 32 kg/m², blood pressure is 142/88 mmHg, and his eGFR is 48 mL/min/1.73m². He has no history of cardiovascular disease but has background diabetic retinopathy. Which of the following would be the most appropriate addition to his treatment regimen?
Q118
A 28-year-old woman with type 1 diabetes presents to the emergency department with vomiting and abdominal pain. She has been unwell for 2 days with a urinary tract infection. On examination, she is drowsy with a respiratory rate of 28/min and has a fruity odour on her breath. Her capillary blood glucose is 26.4 mmol/L. Venous blood gas shows: pH 7.18, bicarbonate 12 mmol/L, and ketones 5.2 mmol/L. Which of the following is the most appropriate initial fluid management?
Endocrinology & Diabetes UK Medical PG Practice Questions and MCQs
Question 111: A 25-year-old woman with type 1 diabetes for 12 years attends for her annual screening appointment. She is asymptomatic with an HbA1c of 62 mmol/mol (7.8%). Digital retinal photography shows microaneurysms and scattered dot haemorrhages in both eyes, but no cotton wool spots, venous beading, or new vessels. Her albumin:creatinine ratio is 2.8 mg/mmol (normal <3), blood pressure is 124/78 mmHg, and monofilament testing of her feet is normal. What is the appropriate follow-up interval for diabetic retinopathy screening in this patient?
A. Repeat screening in 3 months
B. Urgent referral to ophthalmology within 2 weeks
C. Routine referral to ophthalmology within 13 weeks
D. Repeat screening in 6 months (Correct Answer)
E. Repeat screening in 12 months
Explanation: ***Repeat screening in 6 months***
- The patient exhibits features of **background (mild non-proliferative) diabetic retinopathy**, specifically microaneurysms and **dot hemorrhages** without more advanced lesions.
- According to diabetic eye screening guidelines, the presence of these findings without **maculopathy** or pre-proliferative changes necessitates a shortened surveillance interval of **6 months** to monitor for progression.
*Repeat screening in 3 months*
- A **3-month interval** is not a standard surveillance frequency within national diabetic eye screening protocols for mild non-proliferative changes.
- This interval is generally too frequent for stable **background retinopathy** and does not align with clinical pathway recommendations.
*Urgent referral to ophthalmology within 2 weeks*
- Urgent 2-week referrals are reserved for **proliferative diabetic retinopathy** (new vessels) or sudden, severe vision loss.
- This patient lacks high-risk features such as **neovascularization** or vitreous hemorrhage that would trigger an emergency specialist assessment.
*Routine referral to ophthalmology within 13 weeks*
- Routine ophthalmology referral is indicated for **maculopathy** or **moderate-to-severe non-proliferative retinopathy** (e.g., cotton wool spots, venous beading).
- Since the patient has only microaneurysms and lacks **exudates** or significant hemorrhages near the macula, primary screening surveillance is sufficient over referral.
*Repeat screening in 12 months*
- **Annual (12-month) screening** is only appropriate for patients who show **no evidence of retinopathy** in digital photography.
- Because microaneurysms and hemorrhages are already present, the risk of progression is higher, making the standard **yearly interval** unsafe.
Question 112: A 58-year-old woman is found to have a TSH of 8.2 mU/L (normal 0.5-5.0) and free T4 of 11 pmol/L (normal 9-25) on routine blood tests. She has no symptoms and no goitre on examination. Anti-thyroid peroxidase (anti-TPO) antibodies are strongly positive. Her lipid profile shows total cholesterol 6.8 mmol/L and LDL cholesterol 4.2 mmol/L. She has no other significant medical history and takes no regular medications. What is the most appropriate management?
A. Reassure and repeat thyroid function tests in 3 months (Correct Answer)
B. Commence levothyroxine 50 micrograms daily
C. Commence levothyroxine 25 micrograms daily
D. Commence atorvastatin and repeat thyroid function tests in 3 months
E. Arrange thyroid ultrasound before deciding on treatment
Explanation: ***Reassure and repeat thyroid function tests in 3 months***
- The patient has **subclinical hypothyroidism**, defined by an **elevated TSH** (8.2 mU/L) and a **normal free T4** (11 pmol/L) in an **asymptomatic** individual with no goitre.
- For **asymptomatic** patients with TSH < 10 mU/L, guidelines recommend **observation** and **retesting** thyroid function in 3-6 months to confirm persistent elevation before initiating therapy, even with positive anti-TPO antibodies.
*Commence levothyroxine 50 micrograms daily*
- **Levothyroxine** treatment is typically reserved for **overt hypothyroidism** or **subclinical hypothyroidism** with TSH > 10 mU/L, or if the patient is symptomatic, pregnant, or has a goitre.
- Initiating treatment prematurely in an **asymptomatic** patient with TSH < 10 mU/L risks **unnecessary medication** and potentially **iatrogenic hyperthyroidism**.
*Commence levothyroxine 25 micrograms daily*
- Although 25 mcg is a common starting dose, it is not yet indicated as the diagnosis of persistent subclinical hypothyroidism needs to be confirmed with **repeat testing** in this **asymptomatic** patient.
- Many cases of subclinical hypothyroidism, especially with TSH < 10 mU/L, can **normalize spontaneously** or remain stable without progression, making early intervention unnecessary.
*Commence atorvastatin and repeat thyroid function tests in 3 months*
- **Subclinical hypothyroidism** can cause **dyslipidemia**, but the initial approach is to **manage the thyroid dysfunction** first, if treatment becomes indicated.
- Correcting thyroid function often leads to an **improvement in lipid profiles**, potentially reducing or eliminating the need for **statin therapy**.
*Arrange thyroid ultrasound before deciding on treatment*
- A **thyroid ultrasound** is primarily indicated for evaluating **thyroid nodules** or a palpable goitre, neither of which is present or the main concern here.
- The diagnosis of **subclinical hypothyroidism** is biochemical, and the presence of **anti-TPO antibodies** indicates an autoimmune cause; imaging does not alter the management threshold for **asymptomatic subclinical hypothyroidism**.
Question 113: A 19-year-old man with type 1 diabetes for 8 years is reviewed in the diabetes clinic. Over the past 6 months, his HbA1c has risen from 58 mmol/mol to 76 mmol/mol (9.1%). He reports multiple episodes of hypoglycaemia, particularly in the evenings, followed by high glucose readings the next morning. He is currently on a basal-bolus insulin regimen with insulin glargine 28 units at bedtime and insulin aspart before meals. His continuous glucose monitoring shows significant glycaemic variability. What is the most likely explanation for his morning hyperglycaemia?
A. Dawn phenomenon
B. Somogyi effect (Correct Answer)
C. Waning insulin effect
D. Inadequate basal insulin dosing
E. Insulin antibody formation
Explanation: ***Somogyi effect***
- The **Somogyi effect** occurs when **nocturnal hypoglycaemia** triggers a surge in counter-regulatory hormones (glucagon, adrenaline, and cortisol), leading to **rebound hyperglycaemia** by morning.
- This patient's history of **evening hypoglycaemia** followed by high morning readings is the classic presentation of this phenomenon.
*Dawn phenomenon*
- This refers to early morning hyperglycaemia caused by the physiological release of **growth hormone** and **cortisol** between 4 AM and 8 AM.
- Unlike the Somogyi effect, it is **not preceded by hypoglycaemia** and is a steady climb rather than a rebound from a low.
*Waning insulin effect*
- Occurs when the duration of the **basal insulin** (like glargine) does not last a full 24 hours, leading to a rise in glucose levels before the next dose.
- This would cause a gradual rise in blood sugar throughout the night without the **nocturnal hypoglycaemic episodes** reported by this patient.
*Inadequate basal insulin dosing*
- If the basal insulin dose was simply too low, the patient would experience **persistent hyperglycaemia** throughout the day and night.
- It does not explain the **significant glycaemic variability** or the specific pattern of evening lows followed by morning highs.
*Insulin antibody formation*
- **Insulin antibodies** can neutralize insulin or prolong its action, leading to erratic blood glucose patterns and increased insulin requirements.
- This is **extremely rare** with modern recombinant insulin analogues and does not typically follow a predictable diurnal pattern like the Somogyi effect.
Question 114: A 34-year-old woman who is 8 weeks pregnant presents with fatigue and palpitations. She has no significant past medical history. Examination reveals a fine tremor, warm peripheries, and a resting pulse of 98 bpm. Her thyroid is mildly enlarged but non-tender. Blood tests show: TSH <0.01 mU/L, free T4 28 pmol/L (normal 9-25), free T3 9.2 pmol/L (normal 3.5-7.8), and beta-hCG 85,000 IU/L. TSH receptor antibodies are negative. Which of the following is the most likely diagnosis?
A. Toxic multinodular goitre
B. De Quervain's thyroiditis
C. Hyperemesis gravidarum with secondary thyrotoxicosis
D. Graves' disease
E. Gestational transient thyrotoxicosis (Correct Answer)
Explanation: ***Gestational transient thyrotoxicosis***
- This condition is caused by high levels of **beta-hCG** in early pregnancy, which has structural similarity to **TSH** and cross-reacts with its receptor to stimulate the thyroid.
- The diagnosis is confirmed by biochemical thyrotoxicosis in the **first trimester**, high hCG levels, and the absence of **TSH receptor antibodies** (TRAb).
*Toxic multinodular goitre*
- This typically presents in **older individuals** and is characterized by a nodular, irregular thyroid gland rather than mild, diffuse enlargement.
- It results in autonomous thyroid hormone production that does not correlate with **pregnancy cycles** or hCG levels.
*De Quervain's thyroiditis*
- This is a subacute inflammatory condition that presents with a characteristically **painful, tender thyroid gland**, which is absent in this patient (non-tender).
- It is usually preceded by a **viral upper respiratory tract infection** and is associated with an elevated ESR.
*Hyperemesis gravidarum with secondary thyrotoxicosis*
- While it involves hCG-induced thyrotoxicosis, this diagnosis requires the presence of **severe nausea and vomiting** causing dehydration and weight loss.
- This patient presents with fatigue and palpitations but lacks the **severe gastrointestinal symptoms** characteristic of hyperemesis.
*Graves' disease*
- Graves' disease is the most common cause of hyperthyroidism in pregnancy but would typically feature **positive TSH receptor antibodies** (TRAb).
- It is often associated with clinical signs like **ophthalmopathy** (exophthalmos) or pretibial myxedema, which are not present here.
Question 115: A 72-year-old woman with type 2 diabetes is brought to the emergency department with reduced consciousness. Her family reports she has been increasingly confused over the past 3 days with reduced oral intake. Her medications include metformin and gliclazide. On examination, she is deeply unresponsive (GCS 6), blood pressure 95/62 mmHg, pulse 118 bpm, temperature 37.8°C, and appears clinically dehydrated. Investigations show: capillary glucose 52.3 mmol/L, sodium 157 mmol/L, potassium 4.8 mmol/L, urea 28.2 mmol/L, creatinine 185 μmol/L, serum osmolality 382 mOsm/kg. Urinalysis shows no ketones. What is the calculated fluid deficit likely to be in this patient?
A. Approximately 5-7 litres
B. Approximately 8-10 litres (Correct Answer)
C. Approximately 11-13 litres
D. Approximately 14-16 litres
E. Approximately 3-5 litres
Explanation: ***Approximately 8-10 litres***- This patient presents with **Hyperosmolar Hyperglycaemic State (HHS)**, characterized by severe **hyperglycemia** (52.3 mmol/L), profound **hyperosmolality** (382 mOsm/kg), and clinical signs of severe dehydration, without significant ketosis.- The typical fluid deficit in HHS is significantly higher than in DKA, often ranging from **100-220 mL/kg**, which commonly translates to a total deficit of **8-10 litres** in an average adult patient. *Approximately 5-7 litres*- This fluid volume is more typical of the deficit seen in **Diabetic Ketoacidosis (DKA)**, which usually ranges from 3-6 litres.- Given the patient's extremely high **serum osmolality** (382 mOsm/kg), severe **hypernatremia** (157 mmol/L), and signs of significant organ hypoperfusion, the actual dehydration is much more profound than this range suggests. *Approximately 11-13 litres*- While some patients with very prolonged or severe HHS may accumulate such extensive fluid losses, this represents the **upper end** of the spectrum rather than the average expected deficit.- Overly aggressive initial fluid resuscitation based on this higher estimate carries risks like **cerebral oedema** or fluid overload, especially in an elderly patient. *Approximately 14-16 litres*- This volume indicates **extreme dehydration** and generally exceeds the typical calculated fluid deficit for patients presenting with the described laboratory parameters of HHS.- Rapid replacement of such a large volume can lead to serious complications, including **osmotic demyelination syndrome**, **cerebral oedema**, or acute cardiac decompensation due to fluid overload. *Approximately 3-5 litres*- This range is highly **inadequate** for a patient presenting with marked **hyperglycemia** (52.3 mmol/L), severe **hyperosmolality**, and clear evidence of **pre-renal azotemia** (urea 28.2 mmol/L, creatinine 185 μmol/L).- Such a low estimate fails to account for the massive and sustained **osmotic diuresis** that occurs over several days, leading to profound fluid depletion in HHS.
Question 116: A 45-year-old woman presents with palpitations, weight loss, and heat intolerance over the past 3 months. On examination, she has a diffuse, non-tender goitre, a resting pulse of 110 bpm, and lid lag. Blood tests reveal: TSH <0.01 mU/L, free T4 32 pmol/L (normal 9-25), free T3 12.8 pmol/L (normal 3.5-7.8). TSH receptor antibodies are positive. She is commenced on carbimazole 40mg daily. After 6 weeks, her thyroid function tests show: TSH <0.01 mU/L, free T4 14 pmol/L. What is the most appropriate next step in her management?
A. Continue current dose of carbimazole
B. Reduce carbimazole to 20mg daily (Correct Answer)
C. Stop carbimazole and commence propylthiouracil
D. Add levothyroxine 100 micrograms daily and continue carbimazole
E. Stop carbimazole and arrange radioiodine therapy
Explanation: ***Reduce carbimazole to 20mg daily***
- The patient's initial **free T4** was high (32 pmol/L) and has now normalized to 14 pmol/L, which is within the normal range (9-25 pmol/L) after 6 weeks on 40mg carbimazole. This indicates effective control of hyperthyroidism.
- Reducing the dose is the appropriate next step in a **titration regimen** to prevent **iatrogenic hypothyroidism** while maintaining a euthyroid state. The **TSH** will remain suppressed for longer and should not primarily guide early dose adjustments.
*Continue current dose of carbimazole*
- Continuing 40mg daily would likely lead to **iatrogenic hypothyroidism** because the patient's **free T4** is already within the normal range.
- The goal is to achieve euthyroidism, and maintaining a high dose risks **over-treatment** once thyroid hormone levels have normalized.
*Stop carbimazole and commence propylthiouracil*
- There is no indication to switch to **propylthiouracil (PTU)**, as the patient is responding well to carbimazole and PTU is generally reserved for specific situations like the **first trimester of pregnancy** or **carbimazole intolerance**.
- Switching medications without a clear clinical reason unnecessarily complicates treatment and exposes the patient to potential new side effects.
*Add levothyroxine 100 micrograms daily and continue carbimazole*
- This approach describes a **block-and-replace regimen**, where a high dose of antithyroid drug completely blocks thyroid hormone production, and exogenous levothyroxine replaces it.
- While a valid strategy, it is typically initiated from the outset if chosen, not introduced when a **titration regimen** is successfully bringing thyroid hormones to normal levels.
*Stop carbimazole and arrange radioiodine therapy*
- **Radioiodine therapy** is a definitive treatment for **Graves' disease** but is usually considered after a failed course of antithyroid drugs, relapse, or patient preference for definitive therapy.
- The patient is responding well to **carbimazole**, so stopping it to proceed with radioiodine at this stage would be premature as medical management is still effective.
Question 117: A 62-year-old man with type 2 diabetes for 15 years attends his annual diabetes review. He is currently taking metformin 1g twice daily and gliclazide 160mg twice daily. His HbA1c is 68 mmol/mol (8.4%). His BMI is 32 kg/m², blood pressure is 142/88 mmHg, and his eGFR is 48 mL/min/1.73m². He has no history of cardiovascular disease but has background diabetic retinopathy. Which of the following would be the most appropriate addition to his treatment regimen?
A. Sitagliptin 100mg once daily (Correct Answer)
B. Empagliflozin 10mg once daily
C. Pioglitazone 30mg once daily
D. Insulin glargine 10 units at bedtime
E. Exenatide 10 micrograms twice daily
Explanation: ***Sitagliptin 100mg once daily***
- **Sitagliptin**, a DPP-4 inhibitor, is considered a suitable addition to metformin and sulphonylurea (triple therapy) because it is **weight-neutral** and generally well-tolerated.
- While the dose typically needs adjustment to **50mg** for an eGFR between 30-44 mL/min/1.73m², it remains a safer choice in **chronic kidney disease** (CKD Stage 3a) compared to many other agents.
*Empagliflozin 10mg once daily*
- **SGLT2 inhibitors** have reduced glycemic efficacy as the **eGFR** declines, and while they have cardiorenal benefits, initiation guidelines often require higher renal function for glucose lowering specifically.
- Although some guidelines now allow use down to lower eGFRs, it is not the classic first-line choice for triple therapy in this clinical scenario compared to **DPP-4 inhibitors**.
*Pioglitazone 30mg once daily*
- **Pioglitazone** is associated with **weight gain**, which is undesirable in this patient with a **BMI of 32 kg/m²**.
- It also carries a risk of **fluid retention** and peripheral edema, which can be problematic in patients with declining **renal function**.
*Insulin glargine 10 units at bedtime*
- While effective for glycemic control, **insulin** is usually reserved for when triple oral therapy fails or if the **HbA1c** is significantly higher.
- It carries a high risk of **hypoglycemia** and significant **weight gain**, making it less favorable than adding a third oral agent first.
*Exenatide 10 micrograms twice daily*
- **GLP-1 receptor agonists** like exenatide are usually recommended only if triple therapy with oral agents is ineffective or if the patient's **BMI is >35 kg/m²**.
- Many **GLP-1 analogues** require cautious use or are contraindicated in significant **renal impairment** (eGFR <30-50 mL/min/1.73m² depending on the specific preparation).
Question 118: A 28-year-old woman with type 1 diabetes presents to the emergency department with vomiting and abdominal pain. She has been unwell for 2 days with a urinary tract infection. On examination, she is drowsy with a respiratory rate of 28/min and has a fruity odour on her breath. Her capillary blood glucose is 26.4 mmol/L. Venous blood gas shows: pH 7.18, bicarbonate 12 mmol/L, and ketones 5.2 mmol/L. Which of the following is the most appropriate initial fluid management?
A. 0.9% sodium chloride 1000 mL over 1 hour (Correct Answer)
B. 0.45% sodium chloride 1000 mL over 1 hour
C. Hartmann's solution 1000 mL over 1 hour
D. 5% dextrose 1000 mL over 1 hour
E. 0.9% sodium chloride with potassium chloride 40 mmol/L over 1 hour
Explanation: ***0.9% sodium chloride 1000 mL over 1 hour***- The patient presents with **Diabetic Ketoacidosis (DKA)**, and the priority is volume replacement using an **isotonic crystalloid** to restore circulatory volume.- **0.9% sodium chloride** is the fluid of choice for initial resuscitation to correct dehydration and improve renal perfusion in DKA management.*0.45% sodium chloride 1000 mL over 1 hour*- This is a **hypotonic solution** which can lead to a rapid drop in serum osmolality and increase the risk of **cerebral edema**.- It is generally reserved only for cases of severe hypernatremia and is not indicated for initial **DKA fluid resuscitation**.*Hartmann's solution 1000 mL over 1 hour*- While it is a balanced crystalloid, **Hartmann's solution** contains lactate which might interfere with the monitoring of **ketone clearance** and acid-base status during DKA treatment.- National guidelines traditionally favor **0.9% saline** as the standard initial fluid for volume expansion in diabetic emergencies.*5% dextrose 1000 mL over 1 hour*- Administering **5% dextrose** initially is contraindicated as the patient is already severely **hyperglycemic** (26.4 mmol/L).- Dextrose-containing fluids are only introduced later in the protocol once blood glucose levels fall below **14 mmol/L** to prevent hypoglycemia while insulin continues.*0.9% sodium chloride with potassium chloride 40 mmol/L over 1 hour*- **Potassium** should not be added to the first bag of resuscitation fluid until the patient's **serum potassium** level is confirmed by laboratory testing.- Patients often present with **hyperkalemia** initially due to the shift of ions out of cells in acidosis, and premature administration can lead to dangerous cardiac arrhythmias.
