Diabetes Mellitus Viva

Long Case Viva Defence

Candidate's opening statement (model answer)

"Mr Khan is a 62-year-old retired taxi driver who presents for review of his type 2 diabetes, diagnosed 12 years ago. He has multiple diabetes-related complications and comorbidities. [1]

His past history includes:

• Type 2 diabetes, 12 years duration — currently on metformin 1g BD and gliclazide 80mg
• Ischaemic heart disease — NSTEMI 3 years ago, DES to LAD and RCA
• Hypertension, on perindopril 5mg and amlodipine 10mg
• Diabetic nephropathy — eGFR 38, urine ACR 22 mg/mmol
• Diabetic peripheral neuropathy — bilateral glove-and-stocking sensory loss
• Background diabetic retinopathy — last eye screen showed microaneurysms and hard exudates [1]

His current HbA1c is 74 mmol/mol. Blood pressure today is 144/82. BMI is 31. He has a 1 cm plantar ulcer under the left first metatarsal head with surrounding callus and intact skin around it, palpable dorsalis pedis and posterior tibial pulses, and loss of protective sensation on 10g monofilament testing at both great toes. [1]

His main problems are:

1. Suboptimal glycaemic control on oral agents (HbA1c 74 mmol/mol) — needs escalation
2. Diabetic nephropathy with albuminuria — CKD stage 3B, not on optimised renoprotective therapy
3. Established atherosclerotic cardiovascular disease (post-NSTEMI) — needs organ-protective agents
4. Diabetic foot ulcer — neuropathic, needs offloading and multidisciplinary care
5. Hypertension above target for a proteinuric diabetic patient
6. Obesity (BMI 31) contributing to insulin resistance
7. Polypharmacy and medication adherence" [1]

Examiner probing questions and model answers

Q1: "What is your pharmacological priority for his diabetes?" [1]

"My priority is to add an SGLT2 inhibitor and a GLP-1 receptor agonist, and to stop the gliclifazide. This patient has three indications for organ-protective therapy — established ASCVD (prior NSTEMI), diabetic nephropathy with albuminuria, and obesity. The modern hierarchy for type 2 diabetes is metformin, then an SGLT2i or GLP-1 RA chosen by comorbidity — before sulphonylureas or insulin. The EMPA-REG OUTCOME trial showed empagliflozin reduced cardiovascular death by 38% in diabetics with established CVD. The DAPA-CKD trial showed dapagliflozin reduced the renal composite by 39% in CKD patients with and without diabetes. So I would add dapagliflozin 10mg daily for its combined cardio-renal benefit and a GLP-1 receptor agonist such as liraglutide or semaglutide for ASCVD reduction and weight loss. I would stop the gliclazide — it is now third-line, causes weight gain and hypoglycaemia, and has no organ-protection evidence." [1]

Q2: "His eGFR is 38. Is metformin still safe?" [1]

"Yes, with dose reduction. The current recommendation is to continue metformin down to an eGFR of 30, and to halve the dose when eGFR is between 30 and 45. So I would reduce his metformin from 1g BD to 500mg BD. Metformin should be stopped if eGFR falls below 30. The feared complication is lactic acidosis, but this is rare — approximately 3 per 100,000 patient-years — and occurs in acidaemic or hypoxic patients. I would also check his vitamin B12 level — he has been on metformin for over 4 years and has neuropathy, and metformin causes B12 deficiency which can contribute to neuropathy." [1]

Q3: "His creatinine rises from 140 to 175 after starting the ACE inhibitor and SGLT2i. What do you do?" [1]

"A creatinine rise from 140 to 175 is a 25% increase, which is within the acceptable threshold of 30% when starting RAAS blockade or SGLT2i. This is the expected haemodynamic effect — reduced intraglomerular pressure. I would continue both agents and recheck creatinine and electrolytes in 1 to 2 weeks. If the rise exceeded 30%, I would look for other contributing causes — volume depletion, NSAID use, contrast exposure, or bilateral renal artery stenosis. I would also monitor potassium — if it exceeds 5.5, I would reduce the dose and address contributing factors. The long-term renoprotective benefit of SGLT2i and ACEi far outweighs a modest creatinine rise." [1]

Q4: "Why would you choose a GLP-1 RA over insulin for glycaemic control?" [1]

"Several reasons. First, he is overweight (BMI 31) — GLP-1 RAs cause weight loss (2 to 6 kg for liraglutide, more for semaglutide and tirzepatide), while insulin and sulphonylureas cause weight gain. Second, he has established ASCVD — the LEADER trial showed liraglutide reduced cardiovascular death by 22%, while insulin has neutral cardiovascular outcomes. Third, GLP-1 RAs have a lower hypoglycaemia risk than insulin — they are glucose-dependent insulin secretagogues. Fourth, he is a former taxi driver and may still drive — hypoglycaemia is a major safety concern. The downside is that GLP-1 RAs are injectable (though oral semaglutide exists) and cause gastrointestinal side effects, and they are expensive. Insulin would be indicated if he had catabolic features, marked hyperglycaemia (HbA1c above 86 mmol/mol), or failed to respond to oral and injectable non-insulin agents." [1]

Q5: "How would you manage his foot ulcer?" [1]

"This is a neuropathic plantar ulcer — he has loss of protective sensation, palpable pulses, and surrounding callus without active infection. The management has four pillars: offloading, debridement, wound care, and infection surveillance. The gold standard offloading is a total contact cast, which redistributes pressure away from the ulcer site. He needs sharp debridement of the callus by a podiatrist or foot clinic, appropriate wound dressings, and weekly review. I would perform a probe-to-bone test — if bone is reached, osteomyelitis is likely and I would confirm with MRI. I would assess his vascular status with an ankle-brachial index, but note this may be falsely elevated due to medial arterial calcinosis in diabetes — toe pressures are more reliable. I would not start antibiotics unless there is clinical infection (erythema, purulence, systemic signs). He needs referral to a multidisciplinary diabetic foot clinic and education on daily foot inspection and appropriate footwear." [1]

Q6: "What is the significance of his retinopathy, and how does it affect your management plan?" [1]

"He has background diabetic retinopathy — microaneurysms and hard exudates, which is non-proliferative. The significance is twofold. First, retinopathy and nephropathy are linked — the patient with proteinuric nephropathy nearly always has retinopathy, and vice versa. This confirms that his renal disease is diabetic in origin. Second, rapid improvement in glycaemic control can cause early worsening of retinopathy — this was seen in the DCCT and in the SUSTAIN-6 trial with semaglutide. So I would not escalate his glycaemic control too aggressively, and I would ensure he has a formal ophthalmology review with retinal photography before and during therapy intensification. If he had proliferative retinopathy, I would involve ophthalmology before starting a GLP-1 RA, given the SUSTAIN-6 retinopathy signal." [1]

Q7: "What glycaemic target would you set for him?" [1]

"I would target an HbA1c of 53 to 58 mmol/mol — 7.0 to 7.5%. He is relatively young (62) and active, so he benefits from glycaemic control for microvascular prevention. But he has established ASCVD and CKD, and the ACCORD trial showed that aggressive targets (HbA1c below 42 mmol/mol) increased mortality by 22% in patients with established cardiovascular disease. So I would avoid an overly aggressive target. The most important thing is the organ-protective therapy — the SGLT2i and GLP-1 RA — which reduce cardiovascular and renal events independent of the HbA1c. The glucose number matters, but the drug choice matters more for this patient." [1]

Short Case Discussion

Scenario: "Examine this patient's feet"

Candidate presentation (model): [1]

"I examined Mr Jones's feet. On inspection, there is a 1.5 cm full-thickness ulcer on the plantar surface of the right foot, under the first metatarsal head, with a surrounding rim of callus. The ulcer base is clean and granulating with no slough or exudate. There is no surrounding erythema, warmth, or tracking cellulitis. The skin on both feet is dry with fissuring at the heel — consistent with autonomic neuropathy. The toes are clawed bilaterally and there is prominent callus under both first metatarsal heads. [1]

On palpation, the feet are warm and well-perfused. The dorsalis pedis and posterior tibial pulses are palpable and of normal volume bilaterally. Capillary refill is less than 2 seconds. [1]

Testing for neuropathy: the 10-gram monofilament is not felt at 6 of 10 sites on the right foot and 4 of 10 sites on the left foot, indicating loss of protective sensation. Vibration sense using a 128 Hz tuning fork is reduced at both great toes compared to the medial malleolus. Pinprick sensation is reduced in a stocking distribution to mid-shin bilaterally. Ankle jercles are absent bilaterally. [1]

In summary, these findings are consistent with a neuropathic diabetic foot ulcer — a plantar ulcer under a pressure point, with loss of protective sensation and intact peripheral pulses. The dry fissured skin indicates autonomic involvement. There is no clinical evidence of ischaemia or active infection." [1]

Examiner: "What is the significance of the absent ankle reflexes?" [1]

"Absent ankle reflexes are a common finding in diabetic peripheral neuropathy. The neuropathy is length-dependent, affecting the longest nerves first — so ankle reflexes are lost before knee reflexes, and sensation is lost in the toes before the fingers. The loss of ankle reflexes, combined with the stocking-distribution sensory loss and reduced vibration sense, confirms a distal symmetric polyneuropathy from diabetes. This is the neuropathy that causes the loss of protective sensation that predisposes to foot ulceration." [1]

Examiner: "Why is the skin dry and fissured?" [1]

"The dry, fissured skin is a sign of autonomic neuropathy. Diabetes damages the autonomic fibres innervating the sweat glands of the feet, causing anhidrosis. Without sweating, the skin loses its natural moisture, becomes dry and brittle, and develops fissures. These fissures are entry points for bacteria and are a common precursor to foot infection in the diabetic patient. Management includes daily application of emollient moisturiser (but not between the toes, where maceration is a risk) and prevention of fissuring." [1]

Examiner: "How would you classify this ulcer using the University of Texas system?" [1]

"The University of Texas system grades wounds by depth (0 to III) and stages by the presence of infection and ischaemia (A to D). This ulcer is full-thickness but not to tendon or bone — so it is grade I. There is no clinical infection (stage A) and no ischaemia (palpable pulses). So it is a University of Texas grade 1A neuropathic ulcer. If the probe-to-bone test were positive, it would be grade III (to bone). If there were surrounding cellulitis, it would be stage B. If pulses were absent, stage D." [1]

Examiner: "What is the most important non-pharmacological intervention for this ulcer?" [1]

"Offloading. The total contact cast is the gold standard for plantar neuropathic ulcers. It works by distributing plantar pressure evenly across the entire foot, reducing pressure at the ulcer site by up to 80%. Without offloading, even the best wound care will fail — the patient continues to walk on the ulcer with each step. A removable cast walker is an alternative if a total contact cast is contraindicated (active infection, severe ischaemia). Felted foam and specialised footwear are less effective. The patient must not bear weight on the ulcer until it heals." [1]