IM11.1-24 | Diabetes Mellitus — Glossary

A standardised filament that buckles at 10 g of force; used to test protective sensation in the diabetic foot at 10 plantar sites; inability to feel the filament at ≥4 sites indicates loss of protective sensation and high ulcer risk.

The practice of keeping the pen needle in the injection site for 10 seconds after fully pressing the injection button; prevents leakage of insulin back through the needle track; one of the most commonly neglected injection technique steps.

The standard protocol for treating mild-moderate hypoglycaemia in a conscious patient: consume 15 g of fast-acting carbohydrate (150 mL juice, 3–4 glucose tablets), recheck glucose after 15 minutes, and repeat if still <70 mg/dL.

Standard protocol for treating mild-moderate hypoglycaemia in conscious patients: 15 g fast-acting carbohydrate followed by recheck in 15 minutes; repeat if glucose still <70 mg/dL.

The shortest commonly available pen needle; recommended for most adults (including overweight patients) because average subcutaneous tissue depth is 2.4 mm; injected perpendicular at 90° without a skinfold; reduces intramuscular injection risk.

A velvety, hyperpigmented, thickened skin change in the neck creases, axillae, and groin; a cutaneous marker of insulin resistance; present in T2DM, PCOS, and occasionally malignancy.

Blocks angiotensin-converting enzyme, reducing angiotensin II and aldosterone; dilates efferent arteriole (reducing intraglomerular pressure), lowers BP, reduces proteinuria; first-line for diabetic nephropathy; adverse effects: dry cough (15–20% of Indians), hyperkalaemia, teratogenicity.

Products of non-enzymatic glycation of proteins by glucose; cross-link collagen (increasing basement membrane thickness), activate RAGE receptors (inducing inflammation), and quench nitric oxide; key mediators of diabetic vascular complications.

Spot urine test expressing albumin excretion as a ratio to creatinine concentration; microalbuminuria = 3–30 mg/mmol; macroalbuminuria = >30 mg/mmol; the earliest clinical marker of diabetic nephropathy.

An energy-sensing enzyme activated by metformin (via mitochondrial complex I inhibition); activation suppresses hepatic gluconeogenesis and glycogenolysis; metformin's primary mechanism of glucose lowering.

Blocks angiotensin II at the AT1 receptor; equivalent nephroprotective and antihypertensive effects to ACEi without bradykinin-mediated cough; first choice in ACEi-intolerant patients; same hyperkalaemia and teratogenicity cautions as ACEi.

The calculated difference between the major measured cations and anions: Na+ − (Cl− + HCO₃−); normal 8–12 mEq/L; elevated in HAGMA; in DKA it is typically >20 mEq/L.

The ratio of ankle systolic BP to brachial systolic BP measured by Doppler; normal >0.9; <0.9 indicates peripheral arterial disease; >1.3 indicates non-compressible calcified vessels (common in diabetes).

Intra-vitreal agents (ranibizumab, bevacizumab, aflibercept) that block VEGF, the primary driver of neovascularisation and macular oedema in diabetic retinopathy; now first-line for centre-involving diabetic macular oedema.

Damage to the autonomic nerves in diabetes, causing cardiovascular autonomic dysfunction (orthostatic hypotension, resting tachycardia, loss of heart rate variability), gastroparesis, neurogenic bladder, erectile dysfunction, and anhidrosis.

Long-acting insulin designed to suppress hepatic glucose output overnight and between meals; examples include glargine, detemir (duration 18–24h) and degludec (36–42h, lowest hypoglycaemia risk); the standard approach to insulin initiation in T2DM.

An insulin regimen combining once-daily long-acting basal insulin (suppresses hepatic glucose between meals and overnight) with rapid-acting insulin given before each meal (covers postprandial glucose); the most physiological insulin regimen; typically used in T1DM and some T2DM.

Progressive loss of pancreatic beta-cell mass and secretory function in T2DM, accelerated by glucotoxicity, lipotoxicity, and IAPP amyloid deposition; accounts for rising HbA1c and need for intensifying pharmacotherapy over time.

The predominant ketone body in DKA (BHB:acetoacetate ratio up to 10:1 in severe DKA); NOT detected by the standard nitroprusside urine dipstick; blood BHB measurement is superior for DKA diagnosis and monitoring.

Near-patient glucose measurement from a fingertip capillary blood sample using a glucometer; not diagnostic (±15–20% error); used for monitoring and emergency assessment; technique-sensitive.

Waist circumference ≥90 cm in Indian men or ≥80 cm in Indian women; the single best anthropometric predictor of insulin resistance and metabolic risk in the Indian population.

Progressive destruction of foot bones and joints driven by severe peripheral neuropathy; characterised by a warm, swollen, painless, deformed foot with preserved pulses; results from unperceived repeated microfractures.

Adjustment of measured serum sodium for the dilutional effect of extreme hyperglycaemia; formula: corrected Na = measured Na + 1.6 mEq/L per 100 mg/dL rise in glucose above 100 mg/dL; important for interpreting apparent hyponatraemia in DKA and HHS.

Adjustment for the dilutional effect of hyperglycaemia on measured sodium: corrected Na = measured Na + 1.6 mEq/L per 100 mg/dL rise in glucose above 100 mg/dL; essential for interpreting apparent hyponatraemia in DKA and hypernatraemia in HHS.

Hormones released in response to hypoglycaemia to restore normoglycaemia: glucagon (primary, immediate), adrenaline (secondary), cortisol, and growth hormone (tertiary, hours); impaired counter-regulation in longstanding T1DM leads to hypoglycaemia unawareness.

A group of metabolic disorders characterised by chronic hyperglycaemia resulting from defects in insulin secretion, insulin action, or both; classified as T1DM, T2DM, GDM, MODY, and secondary types.

The characteristic lipid pattern in T2DM: elevated triglycerides, reduced HDL-C, and increased small dense LDL particles; LDL-C may be normal or elevated; confers significantly increased cardiovascular risk.

Acute hyperglycaemic emergency characterised by the triad of hyperglycaemia (usually >250 mg/dL), ketonaemia/ketonuria, and metabolic acidosis (pH <7.3, bicarbonate <18 mEq/L); predominantly in T1DM; precipitated by infection, missed insulin, or new diagnosis.

Length-dependent distal symmetric polyneuropathy affecting the longest nerves first; presents as stocking-and-glove pattern sensory loss (pain, temperature, vibration); creates substrate for painless foot ulcers.

Length-dependent, distal symmetric sensorimotor neuropathy affecting the longest fibres first; presents as stocking-and-glove pattern sensory loss beginning in the feet; the substrate for painless ulceration and Charcot neuroarthropathy.

Microvascular complication of diabetes affecting the retina; classified as non-proliferative (NPDR: microaneurysms, haemorrhages, exudates) and proliferative (PDR: neovascularisation); leading cause of blindness in working-age adults.

All three must be met before transitioning to subcutaneous insulin: blood glucose <200 mg/dL, serum bicarbonate ≥15 mEq/L (or pH ≥7.3), and blood BHB <0.6 mmol/L; glucose normalisation alone is insufficient.

An oral incretin enhancer that inhibits DPP-4 enzyme, preventing degradation of GLP-1 and GIP; weight-neutral, low hypoglycaemia risk; linagliptin requires no dose adjustment in CKD; saxagliptin associated with heart failure hospitalisation.

A serotonin-norepinephrine reuptake inhibitor (SNRI); first-line for painful diabetic peripheral neuropathy; dose 60–120 mg daily; fewer anticholinergic effects than tricyclic antidepressants; also licensed for generalised anxiety disorder.

Calculated estimate of kidney filtration capacity using serum creatinine, age, sex, and ethnicity (CKD-EPI equation); used for KDIGO CKD staging: G1 ≥90, G2 60–89, G3a 45–59, G3b 30–44, G4 15–29, G5 <15 mL/min/1.73m².

A rare form of DKA with blood glucose <250 mg/dL, associated with SGLT2 inhibitor use, prolonged fasting, or alcohol; the normal glucose threshold does not apply and ketone measurement is essential.

Venous plasma glucose measured after ≥8 hours of fasting; diagnostic threshold for diabetes ≥126 mg/dL; prediabetes (IFG) range 100–125 mg/dL.

The standard method of insulin delivery in DKA: 0.1 units/kg/hour of regular/short-acting insulin in 0.9% NaCl infusion; no bolus dose; continued until DKA resolution criteria are met.

A fabric wallet activated by water that maintains temperature at 18–26°C through evaporation; used for insulin storage during travel, in hot climates, and during power outages when refrigeration is unavailable.

A measure of glycated serum proteins reflecting average blood glucose over the preceding 2–3 weeks; used as an alternative to HbA1c when HbA1c is unreliable (haemolytic anaemia, haemoglobinopathies).

An injectable incretin mimetic (except oral semaglutide) that stimulates glucose-dependent insulin secretion, suppresses glucagon, delays gastric emptying, and promotes satiety/weight loss; proven cardiovascular benefit in ASCVD; contraindicated in history of medullary thyroid carcinoma or pancreatitis.

1 mg intramuscular or subcutaneous injection used to treat severe hypoglycaemia when IV access is unavailable; stimulates hepatic glycogenolysis — does NOT work if glycogen stores are depleted (alcoholic hypoglycaemia, prolonged fasting, hepatic failure).

The most widely detectable autoantibody in T1DM; present in 70–80% of cases at diagnosis; useful in distinguishing T1DM from T2DM in ambiguous presentations (LADA).

Haemoglobin A1c reflects the average blood glucose over the preceding 8–12 weeks; a diagnostic threshold of ≥6.5% defines diabetes; unreliable in haemolytic anaemia and haemoglobinopathies.

A metabolic acidosis where the measured serum anion gap (Na+ − [Cl− + HCO₃−]) is elevated above 12 mEq/L; in DKA, caused by ketone bodies (acetoacetate, beta-hydroxybutyrate) accumulating as unmeasured anions.

Statin doses expected to lower LDL-C by ≥50%: atorvastatin 40–80 mg or rosuvastatin 20–40 mg; recommended in T2DM patients with established ASCVD (prior MI, stroke, PAD, angina).

High-risk HLA haplotypes conferring the greatest genetic susceptibility to T1DM; individuals heterozygous for both haplotypes have approximately a 1 in 20 lifetime risk of developing T1DM.

Acute hyperglycaemic emergency with extreme hyperglycaemia (>600 mg/dL), hyperosmolality (>320 mOsm/kg), severe dehydration, and neurological features, but minimal ketosis; predominantly in elderly T2DM; high mortality (up to 20%).

Loss of the adrenergic warning symptoms (sweating, tremor, palpitations) that normally precede neuroglycopenia; develops after repeated hypoglycaemic episodes or with autonomic neuropathy; greatly increases risk of severe hypoglycaemia.

A pre-diabetic state defined by fasting plasma glucose 100–125 mg/dL (WHO) or 100–125 mg/dL (ADA); carries risk of progression to T2DM.

A pre-diabetic state defined by 2-hour OGTT plasma glucose 140–199 mg/dL; indicates significant insulin resistance and beta-cell stress.

A state in which normal concentrations of insulin produce a subnormal biological response; occurs primarily in skeletal muscle, liver, and adipose tissue; driven by visceral adiposity, free fatty acids, and inflammatory cytokines.

A rare insulin-secreting pancreatic beta-cell tumour causing autonomous (non-suppressible) insulin secretion and fasting hypoglycaemia; diagnosed by the 72-hour supervised fast demonstrating low glucose with non-suppressed C-peptide and insulin.

Pathognomonic nodular glomerulosclerosis seen on renal biopsy in advanced diabetic nephropathy; composed of mesangial matrix nodules with peripheral capillary loops.

Deep, slow, laboured breathing pattern compensating for metabolic acidosis in DKA; results from respiratory compensation for low bicarbonate — the depth increases to blow off CO₂ and raise pH.

Firm, painless subcutaneous fatty nodules at insulin injection sites caused by the local anabolic effect of insulin stimulating adipogenesis; results from failure to rotate injection sites; causes erratic insulin absorption due to reduced tissue vascularity.

The first-line biguanide antidiabetic; activates AMPK to reduce hepatic glucose output; does not cause hypoglycaemia; contraindicated if eGFR <30 mL/min due to lactic acidosis risk; causes vitamin B12 deficiency with long-term use.

Urinary albumin excretion 30–300 mg/day or ACR 3–30 mg/mmol; the earliest clinical sign of diabetic nephropathy, indicating early glomerular injury and endothelial dysfunction.

Urinary albumin-creatinine ratio 3–30 mg/mmol (or albumin excretion 30–300 mg/day); the earliest clinical marker of diabetic nephropathy; detected by annual urine ACR testing in all diabetic patients.

A group of monogenic, autosomal dominant forms of diabetes caused by single gene mutations (most commonly GCK-MODY and HNF1A-MODY); typically presents in lean young patients with strong family history; managed differently from T1DM and T2DM.

A rare cutaneous complication of diabetes presenting as pretibial plaques with yellow-atrophic centre, telangiectatic vessels, and erythematous border; indicates long-standing diabetes.

New fragile blood vessels growing on or within one disc diameter of the optic disc; a defining feature of proliferative diabetic retinopathy; indicates ischaemia-driven VEGF release from the retina.

The chemical reaction used in standard urine dipstick ketone pads; detects acetoacetate and acetone but not beta-hydroxybutyrate; responsible for the limitation of dipstick ketone testing in DKA.

Hypoglycaemia occurring during sleep, most commonly between 2 and 4 am; often asymptomatic due to reduced sympathoadrenal response during sleep; detected by 3 am SMBG; associated with NPH peak effect and insufficient bedtime snack; a cause of the Somogyi effect.

The background stage of diabetic retinopathy comprising microaneurysms, dot-blot haemorrhages, hard exudates, and cotton-wool spots; no neovascularisation; subdivided into mild, moderate, and severe.

An intermediate-acting insulin suspension (protamine + zinc); onset 1–2h, peak 4–8h, duration 12–18h; its pronounced peak at 4–8 hours causes nocturnal hypoglycaemia risk when given at bedtime; largely replaced by basal analogues in T1DM.

A standardised test in which 75 g of anhydrous glucose is administered orally after 8–14 hours of fasting; glucose is measured at 0 and 2 hours; 2-hour ≥200 mg/dL = diabetes; 140–199 = IGT.

A fall in systolic BP ≥20 mmHg or diastolic ≥10 mmHg on standing from supine; in diabetes, caused by cardiovascular autonomic neuropathy impairing vasoconstrictor reflexes.

Laser treatment applied to the peripheral retina in proliferative diabetic retinopathy; destroys ischaemic retinal tissue, reducing VEGF production and causing regression of neovascularisation; standard treatment for high-risk PDR.

A nuclear receptor activated by pioglitazone; regulates adipocyte differentiation and lipid storage; activation redistributes fat from visceral to subcutaneous depots, improving insulin sensitivity in muscle and liver.

Anticonvulsants that bind the α₂δ subunit of voltage-gated calcium channels in dorsal horn neurons, reducing neuropathic pain transmission; used for painful diabetic neuropathy; adverse effects: sedation, dizziness, weight gain, peripheral oedema.

A ready-mixed insulin containing 30% short-acting (regular) insulin and 70% intermediate-acting (NPH) insulin; given twice daily before breakfast and dinner; a simplified regimen for patients who cannot manage or prefer not to use separate injections.

Ejection of 2 units of insulin from the pen needle before dosing; removes air bubbles from the cartridge and confirms the needle is patent and delivering correctly; should be performed before every injection.

The advanced stage of diabetic retinopathy characterised by neovascularisation at the disc (NVD) or elsewhere (NVE); new vessels are fragile and prone to haemorrhage and traction retinal detachment, causing severe visual loss.

Artefactually low serum sodium in the context of extreme hyperglycaemia, because glucose draws water from cells into the extracellular space, diluting sodium; corrected sodium formula must be applied.

The practice of patients measuring their own blood glucose using a glucometer and fingerstick at specified times; guides insulin dose titration, detects hypoglycaemia, and allows assessment of dietary and activity impact on glucose.

Estimated from: 2 × [Na+ mEq/L] + [glucose mg/dL]/18 + [BUN mg/dL]/2.8; normal ~285–295 mOsm/kg; >320 mOsm/kg is diagnostic of HHS; >330 mOsm/kg is associated with progressive neurological impairment.

An oral antidiabetic that blocks SGLT2 in the proximal tubule, causing glycosuria; benefits include weight loss, BP reduction, proven renal protection (CKD), and cardiovascular benefit (heart failure hospitalisation, MACE); risk of genital mycotic infections, euglycaemic DKA, and Fournier's gangrene.

The systematic practice of varying insulin injection sites within and between anatomical regions using a grid or zone approach; prevents lipohypertrophy; recommended strategy is to complete a grid within one region before moving to the next.

Rebound fasting hyperglycaemia caused by nocturnal hypoglycaemia triggering a counter-regulatory hormone surge (glucagon, cortisol, adrenaline); associated with NPH insulin; identified by checking 3 am glucose (low = Somogyi); treated by reducing, not increasing, the insulin dose.

The target route for insulin delivery; deposits insulin into the fatty tissue between the skin and muscle layer; provides predictable, gradual absorption; contrasts with intramuscular (faster, unpredictable) and intradermal (too shallow) routes.

A class of oral antidiabetics that stimulate insulin secretion by binding SUR1 on pancreatic beta-cell ATP-sensitive K+ channels; includes gliclazide, glimepiride, glibenclamide; primary risks are hypoglycaemia and weight gain.

An insulin sensitiser acting via PPARγ activation; improves peripheral insulin sensitivity; adverse effects include fluid retention, heart failure exacerbation, weight gain, fracture risk, and possible bladder cancer with long-term use.

The observation by Yajnik that Indians have higher body fat percentage and greater visceral adiposity relative to their weight and BMI than European counterparts, conferring disproportionate metabolic risk at lower BMI; justifies India-specific BMI thresholds (overweight ≥23 kg/m²).

Despite normal or elevated serum K+ at DKA presentation (due to extracellular shift from insulin deficiency and acidosis), total body K+ is depleted by 200–400 mEq (3–5 mEq/kg); insulin administration drives K+ back into cells, risking fatal hypokalaemia unless monitored and replaced.

An autoimmune disorder characterised by progressive immune-mediated destruction of pancreatic beta cells, leading to absolute insulin deficiency; accounts for 5–10% of all diabetes; ketosis-prone.

The dominant form of diabetes (90–95%), characterised by peripheral insulin resistance plus progressive beta-cell secretory failure; strongly associated with obesity, inactivity, and genetic susceptibility.

Low molecular weight heparin (LMWH, e.g., enoxaparin 40 mg SC daily) should be started at HHS admission due to extremely high DVT/PE risk from hyperviscosity, dehydration, and reduced mobility; VTE is a major cause of HHS mortality.

A grading system for diabetic foot ulcers: Grade 0 (no ulcer, high risk), Grade 1 (superficial), Grade 2 (deep to tendon/capsule), Grade 3 (deep with osteomyelitis/abscess), Grade 4 (partial gangrene), Grade 5 (full gangrene).

The three criteria required to diagnose hypoglycaemia in a non-diabetic patient: (1) symptoms consistent with hypoglycaemia, (2) documented low blood glucose at the time of symptoms, and (3) relief of symptoms with glucose administration.