IM11.1-24 | Diabetes Mellitus — Practice Quiz

Correct. In an asymptomatic patient, a single elevated fasting glucose (even above 126 mg/dL) requires confirmation on a separate day. The diagnostic criteria require either two abnormal values on two separate occasions, or a single unequivocal result in a symptomatic patient with classic features (polyuria, polydipsia, unexplained weight loss) and random glucose 200 mg/dL or above.

Diabetes diagnostic thresholds: fasting plasma glucose 126 mg/dL or above, 2-hour OGTT 200 mg/dL or above, HbA1c 6.5% or above, or random glucose 200 mg/dL or above with symptoms. In asymptomatic patients, a single value must always be confirmed on a separate day.

A single fasting plasma glucose of 126 mg/dL or above meets the diagnostic threshold only in a symptomatic patient or when confirmed by a second test on a separate day. In this asymptomatic man, the diagnosis must be confirmed by repeating the fasting plasma glucose (or performing HbA1c or OGTT) on a different day before treatment is initiated.

Correct. The potassium is 3.2 mEq/L, which is already low. Starting insulin in this state is dangerous: insulin drives potassium into cells, causing a further fall in serum potassium that can precipitate fatal cardiac arrhythmias. The rule is absolute — if serum potassium is below 3.5 mEq/L, potassium must be replaced and the level corrected to 3.5 mEq/L or above before insulin is started. IV fluids (0.9% saline) should also be commenced immediately.

DKA management rule: K+ below 3.5 mEq/L = HOLD insulin and replace potassium first. Begin IV 0.9% saline immediately for fluid resuscitation. IV insulin at 0.1 units/kg/hour is started only after potassium is at or above 3.5 mEq/L. Bicarbonate is not routinely given (reserve for pH below 6.9).

In DKA with serum potassium below 3.5 mEq/L, insulin must NOT be started until potassium has been replaced and the level is 3.5 mEq/L or above. Insulin drives potassium into cells, and starting it with an already-low potassium risks fatal hypokalaemia and cardiac arrest. This is the single most important safety rule in DKA management.

Correct. SGLT2 inhibitors (empagliflozin, dapagliflozin, canagliflozin) have proven cardiovascular outcome benefits and are indicated in T2DM with established cardiovascular disease or high CV risk. They also significantly reduce progression of diabetic kidney disease, including reduction of proteinuria and slowing eGFR decline. At eGFR 42, SGLT2 inhibitors can still be used for cardiorenal benefit (check specific agent thresholds: dapagliflozin can be used for CKD benefit down to eGFR 25).

Modern T2DM treatment is outcome-driven. SGLT2 inhibitors are indicated in T2DM with: established CVD or high CV risk (reduce MACE), heart failure (reduce hospitalisation), or CKD with proteinuria (reduce progression). They work by glucosuria and have haemodynamic and anti-fibrotic renal mechanisms. Check eGFR thresholds for the specific agent.

SGLT2 inhibitors are the preferred add-on class in T2DM with proteinuric CKD and high cardiovascular risk, given their proven renal protective and cardiovascular outcome benefits (EMPA-REG OUTCOME, CREDENCE, DAPA-CKD trials). Sulfonylureas carry hypoglycaemia risk and no organ-protective benefit. TZDs cause fluid retention. DPP-4 inhibitors are weight-neutral and have no proven renal outcome benefit.

Correct. GLP-1 receptor agonists (semaglutide, liraglutide, dulaglutide) are the class of choice in overweight/obese T2DM patients who are concerned about weight gain. They stimulate glucose-dependent insulin secretion (low hypoglycaemia risk), suppress glucagon, slow gastric emptying, and reduce appetite — resulting in significant weight loss (3-5 kg average, up to 15 kg with semaglutide 2.4 mg weekly). They also have cardiovascular outcome benefits in high-risk patients.

Drug effect on weight: GLP-1 RA and SGLT2i cause weight loss; metformin is weight-neutral; DPP-4i is weight-neutral; SU, TZD, and insulin cause weight gain. In an obese T2DM patient, prefer GLP-1 RA or SGLT2i as add-on to metformin. GLP-1 RA is biguanide class misclassification trap — it is a separate incretin-based class.

GLP-1 receptor agonists are the preferred add-on in obese T2DM when weight loss is a treatment priority. Sulfonylureas and insulin both cause weight gain. TZDs cause weight gain and fluid retention. DPP-4 inhibitors are weight-neutral. GLP-1 RAs lower HbA1c substantially and promote weight loss through central appetite suppression and delayed gastric emptying.

Correct. HHS (hyperosmolar hyperglycaemic state) is characterised by extreme hyperglycaemia (typically above 600 mg/dL, often 800-1200 mg/dL), marked hyperosmolality (effective osmolality above 320 mOsm/kg), severe dehydration, and absence of significant ketosis or acidosis. It predominantly occurs in elderly type 2 diabetic patients and is often precipitated by an intercurrent illness with inadequate fluid intake. Mortality is 10-20%, significantly higher than DKA.

HHS vs DKA: HHS = glucose commonly above 600 mg/dL, effective osmolality above 320 mOsm/kg, no significant ketosis (ketones negative or trace), pH normal or near-normal, typically elderly T2DM. DKA = glucose commonly 250-600 mg/dL, ketonaemia, metabolic acidosis (pH below 7.3), predominantly T1DM. Both may overlap.

DKA is characterised by the triad of hyperglycaemia, ketosis, and metabolic acidosis (pH below 7.3, HCO3 below 15 mEq/L) — predominantly in T1DM. This patient has pH 7.36 (normal), no ketones, but extreme hyperglycaemia and hyperosmolality in an elderly T2DM patient — the classic HHS profile. Management differs: slower fluid replacement over 48-72 hours, low-dose insulin (only once glucose falls below 300 mg/dL initially).

Correct. In an unconscious patient with severe hypoglycaemia who cannot swallow, oral glucose is contraindicated (aspiration risk). IV access should be obtained immediately and 50% dextrose (25-50 mL, providing 12.5-25 g glucose) administered as a bolus. This rapidly raises blood glucose. If IV access is not immediately available, IM glucagon 1 mg is the alternative while IV access is established, but IV dextrose is preferred when IV access is available.

Severe hypoglycaemia management: conscious and able to swallow = 15-20 g oral fast-acting carbohydrate; unresponsive or unable to swallow = IV 50% dextrose (25-50 mL) OR IM glucagon 1 mg (if no IV access). After resolution, give a slow-acting carbohydrate snack, monitor glucose, and identify the precipitant.

Oral glucose must never be given to an unconscious or unresponsive patient — the aspiration risk is unacceptably high. The priority is IV access and immediate IV 50% dextrose 25-50 mL. IM glucagon 1 mg is a valid alternative if IV access cannot be established quickly. After recovery, the cause of severe hypoglycaemia must be identified and recurrence prevented.

Correct. The most common form of diabetic neuropathy is the length-dependent distal symmetrical sensorimotor polyneuropathy — affecting the longest nerves first (feet before hands, stocking-and-glove distribution). Key features: bilateral symmetrical symptoms, burning/paraesthesiae worse at night, reduced vibration sense (large fibre), absent ankle jerks, and later motor involvement. It is caused by metabolic and vascular injury to peripheral nerves related to chronic hyperglycaemia.

Diabetic peripheral neuropathy: most common pattern is length-dependent distal symmetrical polyneuropathy (DSPN) — affects longest axons first (feet before hands), burning/aching at night, reduced vibration and proprioception, absent ankle jerks. Screen annually with 10 g monofilament and 128 Hz tuning fork. Poor glycaemic control is the strongest modifiable risk factor.

This presentation — bilateral symmetrical burning pain and paraesthesiae in feet, absent ankle jerks, reduced vibration sense, normal pulses — is classic length-dependent distal symmetrical polyneuropathy, the most common diabetic neuropathy. Mononeuritis multiplex involves multiple individual nerves asymmetrically. Amyotrophy causes proximal weakness and wasting. Autonomic neuropathy causes orthostatic symptoms, gastroparesis, or erectile dysfunction.

Correct. ACE inhibitors (e.g., ramipril) or ARBs (e.g., losartan) are the cornerstone of treatment for diabetic nephropathy. They reduce intraglomerular pressure by dilating the efferent arteriole, thereby reducing proteinuria and slowing GFR decline — an effect independent of blood pressure lowering. In a diabetic patient with albuminuria (uACR 30-300 mg/g = microalbuminuria) and hypertension, an ACE inhibitor or ARB is the preferred antihypertensive class, addressing both blood pressure and renal protection simultaneously.

Diabetic nephropathy treatment: ACE inhibitor or ARB is first-line in all diabetic patients with albuminuria (uACR above 30 mg/g), regardless of blood pressure. Target BP in diabetic kidney disease is below 130/80 mmHg. Monitor potassium and creatinine after starting. Add SGLT2 inhibitor if eGFR allows for additional renoprotection (CREDENCE/DAPA-CKD evidence).

ACE inhibitors and ARBs have renoprotective effects in diabetic nephropathy beyond blood pressure control — they reduce intraglomerular hypertension by dilating the efferent arteriole, decreasing proteinuria and slowing CKD progression. They are the preferred antihypertensive class in T2DM with any degree of albuminuria (uACR above 30 mg/g). Note: never combine ACE inhibitor with ARB (increased hyperkalaemia and AKI risk without added benefit).

Correct. Lipohypertrophy is a firm, painless, rubbery subcutaneous mass that develops at sites of repeated insulin injection. It is painless, which is why patients prefer these sites — creating a vicious cycle. Insulin absorption from lipohypertrophic tissue is erratic and unpredictable (delayed or variable), causing unexplained hypo- and hyperglycaemic episodes. The solution is to rotate injection sites systematically and avoid previously lipohypertrophic areas.

Lipohypertrophy is the most common complication of insulin injection technique. It is painless (so patients keep using the site), firm/rubbery on palpation, and causes erratic insulin absorption. Always inspect injection sites annually. Teach patients to rotate sites systematically (abdomen, thighs, upper arms, buttocks) and to use a different spot within each area each time.

Lipohypertrophy (firm, painless subcutaneous mass at injection sites) is caused by the local anabolic effect of insulin at repeatedly-used injection sites. The absorbed insulin becomes erratic from these abnormal tissue depots — causing unexplained hypoglycaemia and hyperglycaemia. The patient prefers the site because it is painless, perpetuating the problem. Systematic site rotation prevents and resolves lipohypertrophy over time.

Correct. Non-proliferative diabetic retinopathy (NPDR) is characterised by intraretinal changes only: microaneurysms (earliest sign), dot-blot haemorrhages, hard exudates (lipid deposits), soft exudates (cotton-wool spots — ischaemia), and intraretinal microvascular abnormalities (IRMA). In NPDR, there are no new vessels growing outside the retina. Progression to proliferative DR (PDR) is defined by neovascularisation — new vessel formation on the disc (NVD) or elsewhere (NVE).

Diabetic retinopathy staging: NPDR = intraretinal changes only (microaneurysms, haemorrhages, exudates, IRMA); PDR = neovascularisation (NVD or NVE), vitreous haemorrhage, pre-retinal haemorrhage, tractional retinal detachment. Diabetic macular oedema (DME) can occur at any stage and is the most common cause of visual impairment. Annual fundus examination is mandatory from diagnosis in T2DM.

New vessels on the disc (NVD), pre-retinal haemorrhage, and tractional retinal detachment are all features of PROLIFERATIVE diabetic retinopathy (PDR). NPDR is confined to intraretinal changes: microaneurysms (earliest sign), dot-blot haemorrhages, hard exudates, cotton-wool spots, and IRMA. The defining feature of proliferation is neovascularisation — pathological new vessel growth beyond the retinal boundaries.