Insulin Therapy in Diabetes

Also written as Insulin, Exogenous insulin.

Insulin replaces deficient endogenous hormone, controls hyperglycaemia and prevents acute complications. Understanding its physiology, indications, and safe use is essential for low‑resource settings.

Overview

Insulin is a peptide hormone secreted by pancreatic β‑cells that promotes glucose uptake, inhibits hepatic glucose production and regulates lipid and protein metabolism.

• Acts via insulin receptors on muscle, fat and liver
• Rapidly lowers plasma glucose by facilitating cellular uptake
• Deficiency or resistance leads to diabetes mellitus

Key concepts

Clinically insulin is used when endogenous secretion is insufficient (type 1 diabetes, advanced type 2, gestational diabetes, steroid‑induced hyperglycaemia) or when oral agents fail.

• Random blood glucose: Is the patient hyperglycaemic? ≥200 mg/dL confirms diabetes in symptomatic patients
• Urine dipstick for glucose/ketones: Detects uncontrolled hyperglycaemia; presence of ketones suggests insulin deficiency
• HbA1c (if available): Shows chronic control; ≥6.5 % supports diabetes diagnosis

• Absolute insulin deficiency → type 1 diabetes, pancreatic disease, severe malnutrition
• Relative deficiency with high insulin resistance → advanced type 2, infection, HIV, TB, malaria
• Pregnancy increases insulin requirements by 30‑50 %

Clinical relevance

In low‑resource hospitals, insulin is often the only option to treat diabetic ketoacidosis (DKA) and severe hyperglycaemia, and to bridge periods of infection or pregnancy.

• Serum potassium: Guides replacement before insulin; low K⁺ (<3.3 mmol/L) contraindicates insulin until corrected
• Blood gas (if available): Detects metabolic acidosis in DKA; pH <7.3 confirms DKA
• Capillary glucose monitoring: Tracks response to insulin; aim 150‑200 mg/dL after initial bolus

• DKA: treat with regular insulin infusion, monitor glucose and electrolytes
• Hyperosmolar hyperglycaemic state: high‑dose regular insulin required
• Pregnant women: basal‑bolus regimen to avoid fetal macrosomia

Exam pearls

Examiners test understanding of insulin’s mechanism, when to start, how to monitor, and pitfalls in low‑resource settings.

• Explain why insulin is mandatory in DKA regardless of oral drug availability
• Describe the ‘rule of 15’ for hypoglycaemia management
• Identify causes of insulin resistance common in East Africa (infection, malnutrition, herbal remedies)

Common mistakes

Errors often arise from dosing misconceptions, ignoring potassium status, and misinterpreting lab results.

• Starting insulin with serum K⁺ <3.3 mmol/L without replacement can precipitate cardiac arrest
• Assuming normal glucose in a patient on insulin means adequate control; missed hypoglycaemia is common
• Using only short‑acting insulin for basal needs leads to glucose variability

Questions an examiner may ask

• A 28‑year‑old woman with type 1 diabetes presents with nausea, abdominal pain and glucose 480 mg/dL – what is your immediate management and why? — Recognise DKA, give IV regular insulin, replace fluids and potassium, monitor pH.
• Explain how infection with TB can alter insulin requirements in a diabetic patient – what physiologic changes occur? — Inflammation increases insulin resistance via cytokines, raises counter‑regulatory hormones, and may precipitate hyperglycaemia.
• A patient on basal‑bolus insulin develops a serum potassium of 3.0 mmol/L – what steps do you take before continuing insulin? — Stop insulin, give potassium replacement until >3.3 mmol/L, then restart insulin cautiously.
• Why is regular (short‑acting) insulin preferred over rapid‑acting analogues for DKA in a low‑resource setting? — Regular insulin is inexpensive, widely available, and its pharmacokinetics are well studied for continuous infusion.
• Distinguish between hyperglycaemic hyperosmolar state and DKA in a patient with glucose 650 mg/dL – what key investigations differentiate them? — Check serum ketones and arterial pH; HHS has minimal ketones and pH >7.3.
• A pregnant woman with gestational diabetes is on oral metformin but glucose rises to 210 mg/dL – what is the next step? — Initiate insulin therapy (basal‑bolus) because oral agents are less reliable in pregnancy and risk fetal overgrowth.
• How can herbal remedies common in East Africa interfere with insulin therapy? — Some herbs contain hypoglycaemic compounds that can cause unexpected lows when combined with insulin, requiring closer glucose monitoring.
• What are the warning signs of insulin‑induced hypoglycaemia that require urgent care? — Altered mental status, seizures, loss of consciousness, or cardiac arrhythmia.

When to seek help

• Unexplained loss of consciousness (possible severe hypoglycaemia)
• Persistent vomiting with high glucose (>300 mg/dL) – risk of DKA
• Signs of cardiac arrhythmia after insulin initiation

Quick questions

Why is potassium checked before starting insulin?

Insulin drives potassium into cells; low serum potassium can cause life‑threatening arrhythmias.

Can oral hypoglycaemic agents be used in DKA?

No, insulin is the only effective therapy to suppress ketogenesis and lower glucose rapidly.