IM11.1-24 | Diabetes Mellitus — Graded Quiz

Correct. Positive islet cell autoantibodies (ICA, GADA, IA-2A, ZnT8A) are the defining immunological hallmark of type 1 diabetes, confirming autoimmune destruction of pancreatic beta cells. Undetectable C-peptide confirms absolute insulin deficiency. Young age and lean BMI are suggestive but not diagnostic — LADA (latent autoimmune diabetes in adults) can present at any age. Autoantibody positivity is the most specific criterion.

T1DM classification: autoantibody positive (ICA/GADA/IA-2/ZnT8) + low/undetectable C-peptide. T2DM: autoantibody negative, detectable C-peptide (residual beta-cell function). LADA: autoantibody positive but initially insulin-independent. MODY: single gene mutation, autoantibody negative, strong family history (autosomal dominant).

Age of onset and BMI overlap between T1DM and T2DM — obese T1DM exists, and T2DM can present acutely. Autoantibody positivity (ICA, GADA, IA-2A) is the specific marker of type 1 diabetes, confirming autoimmune beta-cell destruction. Undetectable C-peptide confirms absolute insulin deficiency. These two findings together definitively classify this as T1DM.

Correct. On the WHO 2013 / IADPSG criteria for GDM using a 75 g OGTT, GDM is diagnosed if ANY ONE of the following thresholds is met: fasting glucose 92 mg/dL or above, 1-hour glucose 180 mg/dL or above, or 2-hour glucose 153 mg/dL or above. This patient's 1-hour value of 192 mg/dL exceeds 180 mg/dL, fulfilling the diagnosis of GDM. Only one abnormal value is sufficient for diagnosis under IADPSG/WHO criteria.

GDM diagnostic thresholds (IADPSG/WHO 2013, 75 g OGTT): fasting 92 mg/dL or above, 1-hour 180 mg/dL or above, 2-hour 153 mg/dL or above. ONE abnormal value is sufficient. The DIPSI single-step test (2-hour 75 g non-fasting glucose 140 mg/dL or above) is used in India for universal screening. GDM increases risk of macrosomia, birth injury, neonatal hypoglycaemia, and future T2DM in mother.

IADPSG/WHO 2013 GDM criteria (75 g OGTT): GDM diagnosed if ANY ONE threshold is met — fasting 92 mg/dL or above, 1-hour 180 mg/dL or above, or 2-hour 153 mg/dL or above. This patient's 1-hour glucose of 192 mg/dL meets the diagnosis. The older Carpenter-Coustan criteria required 2 of 4 abnormal values, but current Indian (DIPSI) and WHO guidelines require only one abnormal threshold.

Correct. In T2DM with established atherosclerotic cardiovascular disease (ASCVD — prior MI, stroke, PAD), current ADA/EASD guidelines recommend adding a GLP-1 receptor agonist (liraglutide — LEADER trial, semaglutide — SUSTAIN-6) or SGLT2 inhibitor (empagliflozin — EMPA-REG OUTCOME, canagliflozin — CANVAS) regardless of HbA1c, to reduce cardiovascular mortality and MACE. Among the options given, GLP-1 RA is the most appropriate, as it has class I recommendation for CV mortality reduction in established CVD.

ADA 2024 cardiometabolic priority algorithm: In T2DM with established ASCVD, prescribe GLP-1 RA (liraglutide/semaglutide/dulaglutide) or SGLT2i (empagliflozin/canagliflozin/dapagliflozin) for cardiovascular benefit. In T2DM with HF or CKD, SGLT2i is preferred. These are independent of HbA1c targets. Choose based on: ASCVD→both classes; CKD→SGLT2i preferred; HF→SGLT2i preferred.

In T2DM with established CVD, the ADA/EASD algorithm prioritises drugs with proven CV outcome benefit: SGLT2 inhibitors and GLP-1 RAs. DPP-4 inhibitors (saxagliptin) are CV-neutral and can even increase HF hospitalisation. Sulfonylureas have no CV benefit and increase hypoglycaemia risk. The key principle: when established CVD or high CV risk is present, choice of glucose-lowering agent is outcome-directed, not only HbA1c-directed.

Correct. In DKA management, when blood glucose falls to approximately 250 mg/dL, IV fluid is switched to 5% dextrose (or 10% dextrose with normal saline — 'dextrose-saline') with potassium supplementation, while the insulin infusion is continued at a reduced rate (0.05-0.1 units/kg/hour). This prevents hypoglycaemia while keeping insulin running to suppress ketogenesis and correct the acidosis. DKA is resolved by ketosis clearance (HCO3 above 18, pH above 7.3, anion gap closure), not by glucose normalisation alone — hence insulin must continue.

DKA resolution criteria: pH above 7.3, HCO3 above 18 mEq/L, anion gap below 12 mEq/L (not glucose). When glucose reaches approximately 250 mg/dL: switch to 5% dextrose plus 0.45% NaCl, continue insulin at 0.05-0.1 units/kg/hour. Keep K+ between 3.5-5 mEq/L throughout. Transition to subcutaneous insulin only when patient tolerating oral intake, ketones cleared, and acidosis resolved.

The key principle: DKA resolution is defined by correction of acidosis and closure of the anion gap — NOT glucose normalisation. When glucose approaches 250 mg/dL, add dextrose to the IV fluid (5% or 10%) to prevent hypoglycaemia while continuing insulin to resolve ketosis. Stopping insulin at glucose 246 mg/dL would halt ketone clearance and leave the patient in active DKA. The resolution criteria are: pH above 7.3, HCO3 above 18 mEq/L, anion gap below 12 mEq/L.

Correct. This patient has both peripheral neuropathy (painless ulcer, loss of monofilament sensation) and peripheral arterial disease (absent dorsalis pedis pulse, toe pressure below 40 mmHg — critical ischaemia threshold). This combination defines a neuroischaemic diabetic foot — the most dangerous category because neuropathy masks ischaemic pain (the patient does not feel the ischaemia) while poor perfusion impairs wound healing. Urgent vascular surgery review for revascularisation is required alongside wound management.

Diabetic foot examination: always assess both neuropathy (10 g monofilament, 128 Hz tuning fork, ankle jerk) AND vascularity (foot pulses, ankle-brachial index, toe pressures). Neuroischaemic ulcers account for 50-60% of diabetic foot ulcers. Critical ischaemia: ankle pressure below 50 mmHg or toe pressure below 30-40 mmHg — requires urgent vascular review. Charcot foot: hot, swollen, erythematous foot ± bony destruction on X-ray.

Pure neuropathic foot: palpable pulses, normal ankle-brachial index, sensation loss only. Pure ischaemic foot: sensation intact, absent/reduced pulses. Neuroischaemic: both neuropathy AND PAD — loss of monofilament sensation (neuropathy) plus absent pulses and low toe pressures (PAD). This is the most common and highest-risk pattern in T2DM. Charcot neuroarthropathy causes bony destruction and deformity, not typically plantar pressure ulcers at presentation.

Correct. When adding basal insulin to an oral regimen, the standard approach is: start long-acting basal insulin (glargine or detemir) once daily at bedtime (or morning for some agents), titrated based on fasting glucose targets. Metformin is continued as it complements insulin action. Glibenclamide should be stopped (or replaced with a shorter-acting SU) to reduce hypoglycaemia risk when insulin is started — combining glibenclamide (long-acting SU) with insulin substantially increases hypoglycaemia risk.

Basal insulin initiation in T2DM: start glargine/detemir 10 units at bedtime; continue metformin; STOP glibenclamide (long-acting SU + insulin = high hypoglycaemia risk). Titrate up by 2 units every 3 days targeting fasting glucose 80-130 mg/dL. If HbA1c remains above target after basal optimisation, add rapid-acting (prandial) insulin or a GLP-1 RA before proceeding to full basal-bolus.

Starting basal insulin: add long-acting insulin (glargine/detemir) once daily; continue metformin; STOP sulfonylurea (especially long-acting glibenclamide) to avoid dual insulin-secretagogue hypoglycaemia. The initial dose is 10 units (or 0.2 units/kg) at bedtime, titrating by 2 units every 3 days to achieve a fasting glucose of 80-130 mg/dL. Basal-bolus regimen may be needed later if post-prandial hyperglycaemia persists.

Correct. Gastroparesis (delayed gastric emptying) is a form of diabetic autonomic neuropathy affecting the enteric nervous system and vagal control of gastric motility. It causes early satiety, nausea, vomiting of partially digested food, bloating, and erratic glycaemic control (unpredictable insulin absorption relative to food absorption). It is most common in patients with long-standing poorly controlled diabetes. Diagnosis is confirmed by gastric emptying scintigraphy (4-hour technetium-labelled solid meal).

Diabetic autonomic neuropathy manifestations: gastroparesis (early satiety, nausea, erratic glucose); diabetic diarrhoea (nocturnal, watery); constipation; erectile dysfunction; orthostatic hypotension (dizziness on standing, systolic BP fall above 20 mmHg or diastolic above 10 mmHg); neurogenic bladder; hypoglycaemia unawareness. Gastroparesis management: small frequent meals, prokinetics (metoclopramide, domperidone), optimise glucose control.

Early satiety, nausea, vomiting, and postprandial bloating with normal endoscopy in a patient with long-standing T2DM is classic gastroparesis — diabetic autonomic neuropathy of the stomach. The vagus nerve controlling gastric motility is damaged. This explains erratic glucoses: food stays in the stomach unpredictably, so the timing of insulin action does not match nutrient absorption. Uraemia would cause more systemic symptoms; metformin GI effects are typically diarrhoea and occur early in treatment.

Correct. Metformin is renally cleared and accumulates in renal impairment, increasing the risk of lactic acidosis (metformin-associated lactic acidosis, MALA). Current guidelines state: DO NOT START metformin if eGFR below 30; WITHHOLD if eGFR 30-45 (use clinical judgment); DOSE-REDUCE if eGFR 45-60. At eGFR 28, metformin must be stopped. Sitagliptin (DPP-4 inhibitor) can be continued in CKD but requires dose reduction at eGFR below 45 (to 50 mg/day) and below 30 (to 25 mg/day).

Metformin and renal function: eGFR 45-60 = dose-reduce; eGFR 30-45 = withhold (assess risk vs benefit); eGFR below 30 = contraindicated (STOP). Also withhold before iodinated contrast and reintroduce after 48 hours if eGFR stable. Lactic acidosis from metformin accumulation is rare but potentially fatal. DPP-4 inhibitors (except linagliptin) require dose reduction in renal impairment — linagliptin is excreted in bile and requires no renal dose adjustment.

Metformin must be stopped when eGFR falls below 30 mL/min/1.73 m2 due to accumulation and risk of lactic acidosis. This is an absolute contraindication. In the eGFR 30-45 range, metformin should be used with caution or withheld. Sitagliptin does not need to be stopped but requires dose reduction in CKD: eGFR 30-45 = 50 mg/day; eGFR below 30 = 25 mg/day. For this patient, the appropriate action is: STOP metformin, REDUCE sitagliptin dose.

Correct. Perioperative insulin management: basal insulin (glargine) should be given at 75-80% of the usual dose the night before surgery — stopping it entirely risks ketosis and hyperglycaemia; giving the full dose risks hypoglycaemia in a fasting patient. Prandial (mealtime) insulin is omitted while nil by mouth. Blood glucose should be monitored 1-2 hourly throughout. The target perioperative glucose is 6-10 mmol/L (108-180 mg/dL). IV insulin infusion ('sliding scale') is reserved for major surgery or poor control.

Perioperative insulin management: basal insulin reduced to 75-80% of usual dose the evening before surgery; prandial insulin withheld while fasting; glucose monitored 1-2 hourly; target 6-10 mmol/L (108-180 mg/dL) perioperatively. IV insulin infusion used for major surgery, prolonged fasting, or uncontrolled diabetes. Resume usual regimen when eating normally postoperatively.

Stopping all insulin in a type 2 diabetic on insulin-only risks hyperglycaemia and ketosis. Giving the full glargine dose to a fasting patient risks hypoglycaemia. The standard approach: reduce basal insulin to 75-80% of usual dose before surgery (maintains basal coverage without hypoglycaemia risk in a fasting state); omit all bolus/prandial insulin while nil by mouth; monitor glucose 1-2 hourly and correct with a correction insulin scale as needed.

Correct. The principal maternal complications of poorly controlled pre-existing diabetes in pregnancy are: pre-eclampsia (3-5x increased risk), worsening nephropathy and retinopathy, DKA (which carries 20-30% fetal mortality), and increased risk of caesarean section. The principal fetal/neonatal complications are: macrosomia (from fetal hyperinsulinism in response to maternal hyperglycaemia), congenital malformations (cardiac, neural tube — associated with first-trimester hyperglycaemia), neonatal hypoglycaemia (from fetal hyperinsulinism persisting after cord clamping), and perinatal mortality.

Diabetes in pregnancy: macrosomia = fetal hyperinsulinism (insulin is a growth factor) responding to maternal hyperglycaemia; neonatal hypoglycaemia = fetal hyperinsulinism persists after cord clamping. Congenital malformations highest with HbA1c above 10% in first trimester. Target HbA1c in pregnancy: below 6.5% pre-conception (if achievable without hypoglycaemia), below 7% in second and third trimesters. DKA threshold is lower in pregnancy (euglycaemic DKA can occur).

Poorly controlled T1DM in pregnancy causes: maternal — pre-eclampsia, DKA (more frequent in pregnancy, fetal mortality 20-30%), worsening retinopathy/nephropathy; fetal — macrosomia, congenital anomalies (cardiac, neural tube), neonatal hypoglycaemia (hyperinsulinism persists after delivery), polycythaemia, respiratory distress. IUGR is more typical of vasculopathic disease or very tight control. HbA1c below 6.5% pre-conception reduces congenital malformation risk but does not eliminate all fetal risks.

Correct. The right eye has NVD (new vessels on the disc) and a pre-retinal haemorrhage — both are hallmarks of PROLIFERATIVE diabetic retinopathy (PDR), the advanced stage characterised by pathological neovascularisation beyond the retinal plane. The left eye has only intraretinal changes (microaneurysms, hard exudates) — classic NON-PROLIFERATIVE diabetic retinopathy (NPDR). This patient needs urgent ophthalmology referral for pan-retinal photocoagulation (laser) for the PDR eye, and monitoring plus optimisation of metabolic control for NPDR.

Diabetic retinopathy: NPDR grading = mild (microaneurysms only) → moderate (haemorrhages, exudates, cotton-wool spots) → severe (4-2-1 rule: haemorrhages in all 4 quadrants, venous beading in 2 quadrants, IRMA in 1 quadrant). PDR = any neovascularisation. PDR treatment: pan-retinal photocoagulation (PRP laser) or intravitreal anti-VEGF (bevacizumab/ranibizumab). Screen T2DM: at diagnosis then annually. Screen T1DM: 5 years after diagnosis then annually.

The staging criteria: NPDR = intraretinal only (microaneurysms, haemorrhages, hard exudates, cotton-wool spots, IRMA). PDR = neovascularisation (NVD or NVE), pre-retinal or vitreous haemorrhage, fibrovascular proliferation, or traction retinal detachment. Right eye has NVD + pre-retinal haemorrhage = PDR. Left eye has microaneurysms + hard exudates only = NPDR. Urgent pan-retinal laser photocoagulation is the treatment for PDR to prevent vitreous haemorrhage and blindness.

Correct. Recurrent nocturnal hypoglycaemia at a predictable time (3-4 AM) with normal bedtime glucose points to excessive basal insulin with its peak action coinciding with this window — common with NPH insulin (peak 4-8 hours) or over-dosed long-acting analogues. The first step is to reduce the bedtime basal insulin dose. If using NPH, switching to a peakless long-acting analogue (glargine U300, detemir, or degludec) eliminates the nocturnal peak and substantially reduces nocturnal hypoglycaemia risk. Continuous glucose monitoring (CGM) is valuable for identifying this pattern.

Nocturnal hypoglycaemia pattern: 3-4 AM low = peak of basal insulin (typically NPH at 4-8 hours). Management: reduce basal dose, switch to peakless analogue. Hypoglycaemia unawareness: counterregulatory responses blunted by repeated low glucose; restore by strict avoidance of hypoglycaemia for 2-3 weeks. CGM is transformative for identifying nocturnal hypoglycaemia patterns invisible to standard SMBG.

Somogyi effect = rebound hyperglycaemia after nocturnal hypoglycaemia (controversial, over-diagnosed). Dawn phenomenon = pre-dawn rise in blood glucose from GH/cortisol surge, causing morning hyperglycaemia. Recurrent 3-4 AM hypoglycaemia with normal bedtime glucose = excessive basal insulin peaking at that time. First-line: reduce basal insulin dose; consider switching from NPH (has a peak) to peakless analogues (glargine, detemir, degludec). Hypoglycaemia unawareness develops with recurrent hypoglycaemic episodes — requires strict avoidance of hypoglycaemia for 2-3 weeks to partially restore awareness.