Clinical revision guide — diabetes care

Managing Hypo- & Hyperglycaemia, and the Medications Used to Treat Diabetes

A practical rundown for interview preparation: recognising and treating acute glucose emergencies, and knowing the main drug classes a diabetic specialist nurse is expected to understand.

1. Managing Hypoglycaemia

Hypoglycaemia is usually defined as a blood glucose below 4.0 mmol/L, though symptoms and the threshold for treatment vary by individual, especially in those with hypo unawareness or tight targets in pregnancy.

Recognise it Autonomic (adrenergic) symptoms — sweating, tremor, palpitations, hunger, anxiety — usually appear first. Neuroglycopenic symptoms follow if untreated: confusion, slurred speech, poor coordination, drowsiness, irritability, and eventually seizure or loss of consciousness.

Conscious and able to swallow — the "15/15 rule"

  1. Give 15–20g fast-acting carbohydrate. E.g. 150–200ml fruit juice or non-diet fizzy drink, 4–5 glucose tablets/dextrose tablets, or a glucose gel. Avoid chocolate/biscuits as the first-line treatment — fat slows absorption.
  2. Recheck blood glucose after 15 minutes.
  3. Still below 4.0 mmol/L? Repeat the fast-acting carbohydrate. Can repeat up to 3 times before escalating and seeking medical review.
  4. Once above 4.0 mmol/L, give a longer-acting carbohydrate (e.g. slice of toast, 2 biscuits, next meal if due) to prevent rebound hypo.
  5. Review the cause — missed meal, exercise, wrong insulin dose/timing, alcohol, interacting medication — and document/adjust the care plan accordingly.

Conscious but unable to safely swallow / uncooperative

  1. Do not give oral treatment — aspiration risk.
  2. Glucogel/dextrose gel can sometimes be massaged into the buccal mucosa in small amounts if the patient can protect their airway, but this is a judgement call, not a substitute for the steps below if in doubt.
  3. Glucagon 1mg IM (adult) if trained/available and no contraindication (ineffective in glycogen-depleted states — starvation, chronic alcohol excess, adrenal insufficiency).
  4. Escalate for IV access and treatment as below.

Unconscious, seizing, or severe hypoglycaemia

  1. ABCDE approach, protect the airway, call for emergency help per local protocol.
  2. IV glucose — typically 10% glucose infusion (e.g. 150–200ml over 15 min) is preferred in hospital over concentrated 20%/50% boluses, which are more sclerosant and prone to overshoot; follow local trust guideline/PGD.
  3. IM Glucagon 1mg if IV access is delayed or unavailable.
  4. Recheck glucose every 10–15 minutes until stable and conscious level recovers, then give oral longer-acting carbohydrate once safe to swallow.
  5. Monitor for rebound hypo, especially with long-acting insulin or sulfonylureas on board — these patients often need extended observation (sulfonylurea-induced hypos in particular can be prolonged and recurrent).
Key teaching points Always ask why the hypo happened — this drives patient education and any medication review. Repeated or severe hypos should trigger a review of the whole regimen, driving/DVLA implications, and hypo-awareness status (Gold score). Document every episode.

2. Managing Hyperglycaemia

Hyperglycaemia management depends heavily on context: an isolated high reading in someone otherwise well is managed very differently from suspected Diabetic Ketoacidosis (DKA) or Hyperosmolar Hyperglycaemic State (HHS).

Simple/isolated hyperglycaemia (no ketones, well patient)

  1. Check blood glucose and ketones (blood or urine) to rule out evolving DKA, particularly in Type 1 patients.
  2. Encourage hydration with sugar-free fluids.
  3. Correction dose of rapid-acting insulin if on an insulin regimen and a correction factor/sick-day plan is in place.
  4. Identify the trigger — illness/infection, steroids, missed doses, diet, stress, pump/device failure.
  5. Sick day rules: never stop insulin during illness (doses may need increasing), monitor glucose and ketones more frequently, maintain fluid and carbohydrate intake.
Suspect DKA when Glucose usually >11 mmol/L (can be lower, e.g. "euglycaemic DKA" with SGLT2 inhibitors) + ketones ≥3 mmol/L (or ++ urine) + acidosis (venous bicarb <15 mmol/L or pH <7.3). Symptoms: nausea/vomiting, abdominal pain, Kussmaul breathing, fruity/acetone breath, drowsiness, dehydration.
Suspect HHS when Usually Type 2, older adults. Marked hyperglycaemia (often >30 mmol/L), high serum osmolality, significant dehydration, little/no ketosis or acidosis. Onset is typically slower and more insidious than DKA; confusion is common.

DKA — outline of hospital management

  1. ABCDE, IV access, bloods (glucose, ketones, VBG, U&Es, FBC, cultures if infection suspected), continuous cardiac monitoring if severe/K⁺ abnormal.
  2. Fixed-rate IV insulin infusion — typically 0.1 unit/kg/hour soluble insulin, per local protocol. Do not stop long-acting basal insulin.
  3. IV fluid resuscitation — 0.9% sodium chloride, front-loaded, then rate-adjusted; caution and slower rates in young people (cerebral oedema risk) and the elderly/cardiac disease.
  4. Potassium replacement guided by hourly/2-hourly levels — insulin drives K⁺ into cells and hypokalaemia is the major risk to monitor for.
  5. Add 10% glucose infusion once blood glucose falls below ~14 mmol/L, alongside the ongoing fixed-rate insulin, to allow ketone clearance to continue safely.
  6. Monitor hourly: capillary glucose, ketones (aim for ketone fall ≥0.5 mmol/L/hr and bicarbonate rise ≥3 mmol/L/hr), VBG, and clinical status until resolution criteria are met.
  7. Resolution: ketones <0.6 mmol/L, venous pH >7.3/bicarb >18, and patient eating/drinking — then transition back to subcutaneous insulin, overlapping the SC dose with the IV infusion by at least 30–60 minutes to prevent rebound ketosis.
  8. Treat the precipitant (infection, missed insulin, new diagnosis, illicit substance use, pump failure) and arrange diabetes team follow-up/education before discharge.

HHS — outline of hospital management

  1. Fluid resuscitation is the priority — 0.9% sodium chloride, more cautious/slower rate than DKA given typically older patients and very high osmolality; large fluid deficits (often 100–220 ml/kg) need to be corrected gradually, generally over 48+ hours.
  2. Insulin is usually withheld initially or given at a low rate (e.g. 0.05 unit/kg/hr) — glucose often falls substantially with fluids alone, and dropping it too fast risks central pontine myelinolysis and cardiovascular collapse.
  3. VTE prophylaxis — HHS carries a high thrombosis risk due to hyperviscosity.
  4. Monitor osmolality, glucose and electrolytes closely and involve senior/specialist review — these patients are often frail with comorbidities.
Key teaching points Know your local Trust's DKA/HHS pathway numbers and thresholds — questions often probe whether you'd follow protocol vs. know when to escalate. Be ready to explain why potassium and fluid balance matter as much as the insulin itself.

3. Diabetes Medications by Class

Insulins

Insulin types by onset/duration profile
TypeExamplesOnsetDurationTypical use
Rapid-acting analogueNovorapid, Humalog, Fiasp, Apidra10–20 min3–5 hrsMealtime/bolus dosing, correction doses, pumps
Short-acting (soluble)Actrapid, Humulin S30–60 min6–8 hrsMealtime dosing (older regimens), IV infusions in DKA/surgery
Intermediate-actingHumulin I, Insulatard1–2 hrs~14–18 hrsBasal cover, often twice daily
Long-acting analogueLantus, Levemir, Abasaglar1–2 hrs~20–24 hrsOnce/twice daily basal cover
Ultra-long-acting analogueTresiba, Toujeo1–2 hrsup to 36–42 hrsFlatter profile, once daily basal
Biphasic/mixedNovomix 30, Humalog Mix2510–20 minup to 16 hrsCombined bolus+basal, twice-daily regimens

Non-insulin agents (mainly Type 2)

Biguanides

First-line, Type 2
Example
Metformin
Mechanism
Reduces hepatic glucose output, improves peripheral insulin sensitivity
Watch for
GI upset, B12 deficiency long-term, lactic acidosis risk (avoid/caution in significant renal impairment)
Hypo risk
Very low as monotherapy

Sulfonylureas

Insulin secretagogue
Example
Gliclazide, glimepiride
Mechanism
Stimulates pancreatic beta cells to release more insulin
Watch for
Hypoglycaemia (can be prolonged), weight gain
Hypo risk
Significant — key teaching point for patients

DPP-4 inhibitors ("gliptins")

Incretin-based
Example
Sitagliptin, linagliptin, alogliptin
Mechanism
Blocks breakdown of GLP-1/GIP, boosting glucose-dependent insulin release
Watch for
Generally well tolerated; rare pancreatitis reports
Hypo risk
Low

SGLT2 inhibitors ("gliflozins")

Renal-acting
Example
Dapagliflozin, empagliflozin, canagliflozin
Mechanism
Blocks glucose reabsorption in the kidney, so excess glucose is excreted in urine
Watch for
Genital/urinary infections, euglycaemic DKA risk (important — ketones can rise with a "normal" glucose), sick-day rule guidance is essential; also used for heart failure/CKD benefit
Hypo risk
Low alone, higher combined with insulin/sulfonylurea

GLP-1 receptor agonists

Injectable, incretin-based
Example
Liraglutide, semaglutide (Ozempic/Wegovy), dulaglutide, exenatide
Mechanism
Mimics GLP-1 — boosts glucose-dependent insulin release, suppresses glucagon, slows gastric emptying, promotes satiety
Watch for
Nausea/GI side effects (usually settle), significant weight loss, rare pancreatitis; increasingly central to current NICE/Type 2 pathways
Hypo risk
Low alone

Thiazolidinediones ("glitazones")

Insulin sensitiser
Example
Pioglitazone
Mechanism
Improves peripheral insulin sensitivity via PPAR-gamma activation
Watch for
Fluid retention/heart failure risk, weight gain, bone fracture risk, used less commonly now
Hypo risk
Low alone

Alpha-glucosidase inhibitors

Less commonly used
Example
Acarbose
Mechanism
Slows carbohydrate digestion/absorption in the gut
Watch for
Flatulence, GI discomfort — limits tolerability
Hypo risk
Low alone; if a hypo occurs, must treat with glucose (not sucrose) as absorption of complex sugars is blocked
BiguanidesSulfonylureasDPP-4 inhibitors SGLT2 inhibitorsGLP-1 agonistsThiazolidinediones Alpha-glucosidase inhibitorsInsulins

4. What an Interviewer Will Likely Probe

  1. Scenario questions. "A patient calls you with a glucose of X and symptoms Y — talk me through what you'd do." Expect to structure your answer logically (assess → treat → recheck → escalate → educate).
  2. Sick day rules. Being able to explain these clearly to a patient is a core competency — especially insulin never being stopped, and SGLT2 inhibitors being paused temporarily during acute illness.
  3. Holistic/education focus. A diabetes specialist nurse role leans heavily on patient education, self-management support, and MDT working (dietitians, podiatry, ophthalmology screening, psychological support) — not just acute treatment algorithms.
  4. Awareness of national guidance. Familiarity with NICE guidelines (NG17 Type 1, NG28 Type 2, NG18 in children/young people) and local Trust DKA/HHS protocols is often asked about directly.
  5. Safeguarding and holistic risk. Recognising when recurrent hypos or poor control might reflect wider issues — mental health, insulin omission, social/financial barriers to self-care.

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