# Hypoglycaemia > Hypoglycaemia in MBBS Physiology: Whipple triad, counter-regulatory hormones, neuroglycopenic thresholds, insulinoma workup and treatment rules. - Canonical URL: https://prepelephant.com/topics/mbbs/physiology/hypoglycaemia-physiology - Exam / course: MBBS · Subject: Physiology - Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team - First published: 2026-10-02 - Last updated: 2026-10-02 - How to cite: "Hypoglycaemia", PrepElephant, https://prepelephant.com/topics/mbbs/physiology/hypoglycaemia-physiology ## Direct answer Whipple's triad — symptoms consistent with hypoglycaemia, a documented low plasma glucose (usually below 50-55 mg/dL) and relief with glucose — is the entry point to the physiology. The brain stores no glucose and makes none, consuming about 100-120 g daily, so it lives hand-to-mouth on arterial supply. Counter-regulation is layered by glucose level: insulin secretion switches off first at about 80-85 mg/dL, glucagon and adrenaline surge at about 65-70, and cortisol with growth hormone reinforce over hours. Adrenergic symptoms — tremor, palpitations, sweating — surface near 50-60 mg/dL, while neuroglycopenia (confusion, drowsiness, seizures, coma) declares below roughly 50. Treatment follows simple arithmetic: conscious patient, 15 g fast carbohydrate rechecked at 15 minutes; unconscious patient, 25 g intravenous 50% dextrose or 1 mg glucagon intramuscularly, and never anything by mouth. ## What you must remember - **Hormonal hierarchy:** insulin off at about 80-85 mg/dL, glucagon and adrenaline on at 65-70, cortisol and growth hormone as slow reinforcement — glucagon is the first responder lost early in type 1 diabetes. - **Symptom thresholds:** adrenergic symptoms at 50-60 mg/dL, neuroglycopenia below about 50 mg/dL; long-standing type 1 diabetes develops hypoglycaemia unawareness from blunted adrenaline responses. - **C-peptide logic:** insulin and C-peptide are co-secreted equimolarly; during true hypoglycaemia, high insulin with high C-peptide means insulinoma, high insulin with low C-peptide means injected insulin or factitious use. - **Drug risk ranking:** sulfonylureas (glibenclamide worst) cause prolonged hypoglycaemia in the elderly and renally impaired — a staple of Indian prescriptions warranting overnight admission; insulin has a plasma half-life near 5 minutes. - **Somogyi versus dawn phenomenon:** a 3 a.m. glucose measurement separates rebound nocturnal hypoglycaemia (Somogyi — low then morning high) from dawn phenomenon (normal 3 a.m. glucose, morning rise from growth hormone and catecholamine-driven insulin resistance). - **Neonatal numbers:** treatment thresholds around 40-45 mg/dL; infants of diabetic mothers are hyperinsulinaemic and crash after clamping the cord. - **Community rule:** 15 g of fast carbohydrate every 15 minutes — in Indian practice, three to four teaspoons of sugar in water remains the taught first response for a conscious diabetic. ## Working up a spontaneous spell A non-diabetic adult presents with recurrent early-morning confusion that relatives abort with tea and biscuits. During a spontaneous episode, draw the four-sample set: glucose, insulin, C-peptide, and ketones (with a sulfonylurea screen if assays allow). Glucose 38 mg/dL with inappropriately normal-or-high insulin and raised C-peptide, ketones suppressed, sulfonylurea screen negative — that is endogenous hyperinsulinism, and imaging follows for insulinoma. The same low glucose with low insulin and high ketones argues fasting adaptation or counter-regulatory failure (adrenal insufficiency, alcohol); low glucose with high insulin but flat C-peptide unmasks injected insulin — factitious or iatrogenic. The discipline is everything drawn during the spell, not after recovery, because insulin's short half-life erases the evidence within the hour. ## Where students slip The Somogyi-dawn pair is answered backwards under pressure: the discriminator is the 3 a.m. glucose, low in Somogyi and normal in dawn phenomenon — one value, question closed. Second, the reason sulfonylurea hypoglycaemia outlasts insulin overdose is pharmacokinetic, not pharmacodynamic: the drug keeps stimulating endogenous insulin release, so observation must be prolonged with glucose ready. Third, glucagon is quoted without its limit — it works by mobilising hepatic glycogen, so it fails in exhausted stores (alcohol fasting, severe malnutrition) and in the glycogen-depleted toddler. And the unconscious patient given oral glucose syrup is the classic unsafe answer in orals; airway protection precedes sweetness, always. ## Frequently asked questions ### What constitutes Whipple's triad? Symptoms compatible with hypoglycaemia, a measurably low plasma glucose at the time of symptoms, and prompt relief after glucose administration. ### In what order do counter-regulatory hormones respond to falling glucose? Insulin secretion is suppressed first (about 80-85 mg/dL), then glucagon and adrenaline rise (65-70 mg/dL), followed by slower cortisol and growth hormone support. ### How does C-peptide distinguish insulinoma from injected insulin overdose? Both show high insulin during hypoglycaemia, but C-peptide is high with insulinoma (co-secreted) and low with exogenous insulin, which suppresses the beta cell. ### Why is sulfonylurea-induced hypoglycaemia prolonged? The drug drives continuing endogenous insulin release, especially in the elderly and renally impaired, so hypoglycaemia recurs and needs extended monitoring with repeated glucose. ### How are the Somogyi phenomenon and dawn phenomenon differentiated? By a 3 a.m. blood glucose: low in Somogyi phenomenon (rebound after nocturnal hypoglycaemia) and normal in dawn phenomenon (morning insulin resistance from counter-regulatory hormones).