🩸 Diabetes mellitus is persistently raised blood glucose caused by too little insulin, insulin that does not work properly, or both. It affects over 5 million people in the UK, about 90% of them with type 2. It is a leading cause of blindness, kidney failure, amputation, heart attack and stroke - and most of this harm is preventable.
Your four questions for every patient: Which type of diabetes is it? Is there an emergency (hypoglycaemia, DKA, HHS)? Are glucose, blood pressure and lipids controlled? Are complications being screened for and treated?

What Is Diabetes?

Diabetes is a disorder of fuel metabolism. Without effective insulin, glucose cannot enter muscle and fat cells, the liver keeps releasing glucose, and blood glucose rises. When the level exceeds the kidney's threshold (about 10 mmol/L), glucose spills into the urine and drags water with it.

Symptoms of hyperglycaemia:

Polyuria and nocturia.
Thirst (polydipsia).
Tiredness.
Blurred vision.
Recurrent infections (thrush, skin infections).
Weight loss - especially in type 1, when the body breaks down fat and muscle for fuel.

Long-term damage: Years of raised glucose damage blood vessels:

Small vessels (microvascular): Eyes, kidneys and nerves.
Large vessels (macrovascular): Heart, brain and legs.

The modern approach treats the whole person: glucose control, blood pressure, lipids, smoking, weight, and organ protection with drugs that reduce heart and kidney disease independently of their effect on glucose.

💡 Clinical Pearl: In type 2 diabetes, more people die of cardiovascular disease than of anything else. Treating blood pressure, lipids and smoking saves as many lives as controlling glucose.

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Insulin and Glucose Physiology

Insulin is made by the beta cells of the pancreatic islets. It is the body's only glucose-lowering hormone and the main "fed state" signal:

Moves glucose into muscle and fat cells.
Stops the liver from making and releasing glucose.
Promotes storage as glycogen, fat and protein.
Suppresses fat breakdown and ketone production. This is why even a small amount of insulin prevents DKA, and why DKA occurs mainly when insulin is absent.

Counter-regulatory hormones raise glucose: Glucagon, adrenaline, cortisol and growth hormone. They rise during illness, stress and surgery, which is why glucose rises when people with diabetes are unwell.

Insulin secretion:

There is a steady basal secretion (to control the liver between meals and overnight).
There are bolus surges with meals.
Modern insulin regimens copy this pattern.

Incretins (GLP-1 and GIP) are gut hormones released after eating. They boost insulin release, suppress glucagon, slow stomach emptying and reduce appetite. GLP-1 agonists and DPP-4 inhibitors work through this system.

C-peptide: A fragment released with insulin in equal amounts. It shows how much insulin the patient is making themselves:

Low in type 1 diabetes.
Normal or high in type 2.
Absent when the insulin is injected rather than made by the body.

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Types of Diabetes

Type	Mechanism and key features
Type 1 (about 8–10%)	Autoimmune destruction of beta cells → absolute insulin deficiency. Needs insulin from diagnosis; risk of DKA
Type 2 (about 90%)	Insulin resistance (obesity, inactivity, genetics) plus progressive beta-cell failure
Gestational	Hyperglycaemia first arising in pregnancy; high future risk of type 2
Monogenic (MODY, neonatal)	Single-gene defects in insulin secretion; often misdiagnosed as type 1 or 2
LADA	Slow-onset autoimmune diabetes in adults; looks like type 2 at first
Pancreatic (type 3c)	Pancreatitis, pancreatic cancer, cystic fibrosis, haemochromatosis, pancreatectomy
Endocrine and drug-induced	Cushing's, acromegaly, phaeochromocytoma; steroids, antipsychotics, immunosuppressants, checkpoint inhibitors

💡 Clinical Pearl: The type can be misdiagnosed - about 1 in 5 people over 30 with new type 1 diabetes are initially labelled type 2. If someone is slim, losing weight, has ketones, or fails tablets quickly, reconsider the diagnosis.

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Diagnosing Diabetes

Diagnostic criteria (WHO, used in the UK):

HbA1c 48 mmol/mol (6.5%) or more.
Fasting plasma glucose 7.0 mmol/L or more.
Random plasma glucose 11.1 mmol/L or more with symptoms.
Oral glucose tolerance test (75 g): 2-hour glucose 11.1 mmol/L or more.

Confirming the diagnosis:

With symptoms: One abnormal result is enough.
Without symptoms: A second confirmatory test is needed.

When HbA1c is unreliable - use glucose instead:

Suspected type 1 diabetes, children, and anyone with rapid onset of symptoms. HbA1c reflects the past 2–3 months and lags behind a sudden rise.
Pregnancy (and up to 2 months postpartum).
Haemoglobinopathies (e.g. sickle cell trait, HbC), anaemia, recent blood transfusion or bleeding.
Advanced CKD; some HIV drugs; splenectomy.
Recent acute illness, steroids, or acute pancreatic damage.

⚠️ Safety Pearl: A child or young adult with thirst, polyuria and weight loss needs a same-day capillary glucose and ketone test and same-day specialist referral if raised. Do not wait for an HbA1c or a fasting test - DKA can develop within hours.

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Prediabetes

Definition (NICE calls it "non-diabetic hyperglycaemia"):

HbA1c 42–47 mmol/mol (6.0–6.4%), or
Impaired fasting glucose (6.1–6.9 mmol/L), or
Impaired glucose tolerance (2-hour OGTT glucose 7.8–11.0 mmol/L).

Significance: A high risk of developing type 2 diabetes (about 5–10% a year) and increased cardiovascular risk.

Management:

Refer to the NHS Diabetes Prevention Programme - a structured lifestyle programme.
Weight loss of about 5–10%, regular activity, and dietary change.
Treat cardiovascular risk factors.
Check HbA1c annually.
Metformin is occasionally considered by specialists for high-risk people.

Lifestyle intervention reduces progression to diabetes by about 50–60% in trials.

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Type 1 or Type 2?

Feature	Type 1	Type 2
Age	Any age; peaks in childhood, but half present as adults	Usually over 40; increasingly younger, especially in South Asian and Black people
Onset	Rapid - weeks	Gradual; often found on routine tests
Weight	Often slim; weight loss	Usually overweight or obese
Ketones / DKA	Common	Rare (HHS more typical)
Autoantibodies	Positive (GAD, IA-2, ZnT8)	Negative
C-peptide	Low, falling	Normal or high
Family history	Other autoimmune disease	Strong family history of type 2
Treatment	Insulin from diagnosis	Lifestyle, tablets and injectables; insulin later in some

💡 Clinical Pearl: If in doubt, treat as type 1 and start insulin. Check antibodies at diagnosis, and C-peptide (from about 3 years after diagnosis) to clarify the type later.

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Type 1 Diabetes

Mechanism: T cells destroy the beta cells in genetically susceptible people (HLA-DR3 and DR4), possibly triggered by viral infection. By diagnosis, most insulin-producing capacity is lost. Without insulin, glucose rises, fat is broken down uncontrollably and the liver makes ketones, leading to DKA.

Clinical pattern:

A few weeks of thirst, polyuria, weight loss and tiredness.
About a quarter of children present in DKA.
After starting insulin, many have a temporary "honeymoon" period, needing very little insulin while remaining beta cells recover. Insulin needs rise again later.

Associated autoimmune diseases:

Autoimmune thyroid disease - check TFTs annually.
Coeliac disease.
Addison's disease.
Pernicious anaemia.
Vitiligo.

Management (NICE NG17):

Insulin for life, usually basal–bolus or a pump.
Structured education in carbohydrate counting and dose adjustment (e.g. the DAFNE course) within 6–12 months of diagnosis.
Glucose monitoring: Continuous glucose monitoring (CGM) is offered to all.
HbA1c target: 48 mmol/mol (6.5%) or lower if achievable without problematic hypoglycaemia.
Psychological support.
Screening for complications and associated autoimmune disease.

For the most difficult cases: Islet transplantation or pancreas transplantation (often with a kidney transplant) for severe hypoglycaemia or kidney failure.

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Insulin Types

Type	Examples and action
Rapid-acting analogues	Insulin aspart (NovoRapid, Fiasp), lispro (Humalog), glulisine (Apidra). Onset 10–15 min, peak 1–2 h, lasts 3–5 h. Injected just before meals (bolus); used in pumps
Short-acting (soluble)	Actrapid, Humulin S. Onset 30 min, lasts 6–8 h. Used in IV insulin infusions
Intermediate-acting (isophane, NPH)	Humulin I, Insulatard. Lasts 12–16 h, with a peak. Used once or twice daily; often first-line basal insulin in type 2 and for steroid-induced hyperglycaemia
Long-acting analogues	Glargine (Lantus, Toujeo, Abasaglar), detemir (Levemir), degludec (Tresiba). Flat profile over about 24 h (degludec over 40 h). Basal insulin
Premixed	NovoMix 30, Humalog Mix 25/50, Humulin M3. Fixed mixtures of rapid/short and intermediate insulin, given twice daily before meals

Insulin safety:

Always write "units" in full - never "u" or "iu", which have caused 10-fold overdoses.
Prescribe by brand name and device.
Never draw insulin from a pen or cartridge with a syringe.
Check the strength (U100, U200, U300, U500).
Patients should carry an insulin passport.

Injection technique: Rotate sites. Lipohypertrophy (lumpy fatty swelling from repeated injection in one spot) causes erratic absorption and unexplained hypoglycaemia or high glucose - examine injection sites at every review.

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Insulin Regimens and Targets

Basal–bolus regimen (multiple daily injections) - standard for type 1 (NICE NG17):

Basal insulin: Twice-daily detemir (NICE's first choice), or once-daily glargine or degludec. Covers the liver's background glucose output; should hold glucose steady overnight and between meals.
Bolus insulin: A rapid-acting analogue before each meal, dosed by carbohydrate ratio (e.g. 1 unit per 10 g of carbohydrate) plus a correction dose for high readings.
Typical total daily dose: About 0.5–1 unit/kg/day, roughly half basal and half bolus. Higher in puberty, pregnancy, illness and obesity.

Targets (NICE NG17):

HbA1c: 48 mmol/mol (6.5%) or lower, individualised to avoid disabling hypoglycaemia.
Capillary glucose:
- On waking: 5–7 mmol/L.
- Before meals: 4–7 mmol/L.
- About 90 minutes after meals: 5–9 mmol/L.
- Before driving: at least 5 mmol/L.
CGM metrics: Time in range (3.9–10 mmol/L) over 70%, with time below range (under 3.9 mmol/L) under 4%.

Common patterns:

Dawn phenomenon: Early-morning rise caused by overnight growth hormone and cortisol. Adjust basal insulin or the pump basal rate.
Nocturnal hypoglycaemia: Often from too much basal insulin, evening alcohol or exercise. Check overnight CGM data.
Unexplained variability: Check injection sites (lipohypertrophy), timing, carbohydrate counting, coeliac disease, gastroparesis and adrenal insufficiency.

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CGM, Pumps and Closed Loop

Continuous glucose monitoring (CGM):
- A small sensor under the skin measures interstitial glucose every few minutes.
- Real-time CGM sends alarms; intermittently scanned CGM ("flash") is scanned with a phone.
- NICE (2022): Offer CGM to all adults and children with type 1 diabetes, and to some with type 2 on insulin.
- Interstitial glucose lags blood glucose by about 5–10 minutes - confirm hypoglycaemia symptoms with a finger-prick if they don't match the sensor.
Insulin pump (CSII): Delivers rapid-acting insulin continuously through a cannula, with programmable basal rates and mealtime boluses. Allows fine-tuning for problematic hypoglycaemia, the dawn phenomenon and variable lifestyles.
Hybrid closed loop ("artificial pancreas"):
- How it works: A CGM sensor talks to the pump, and an algorithm automatically adjusts insulin every few minutes. The user still announces meals.
- NICE TA943 (2023): Recommended for people with type 1 diabetes whose HbA1c is 58 mmol/mol or more, or who have disabling hypoglycaemia, and for all children and pregnant women with type 1. It is being rolled out across the NHS.
- Benefit: Improves time in range and reduces hypoglycaemia substantially.
Device problems: A blocked or dislodged pump cannula stops insulin delivery. Because there is no long-acting insulin on board, DKA can develop within hours. Pump users must check ketones if glucose is unexpectedly high and switch to injections if in doubt.

⚠️ Safety Pearl: A pump user admitted to hospital who cannot manage their own pump must be switched to subcutaneous basal–bolus insulin or an IV infusion. Never simply remove the pump without replacing the insulin.

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Living with Type 1

Carbohydrate counting: The basis of flexible insulin dosing. Structured education (DAFNE for adults) improves HbA1c and reduces hypoglycaemia.
Exercise: Increases insulin sensitivity for up to 24 hours, so hypoglycaemia can occur during, after and overnight. Reduce bolus and/or basal insulin, take extra carbohydrate, and check glucose. Intense anaerobic exercise can temporarily raise glucose. Avoid vigorous exercise if ketones are raised.
Alcohol: Blocks the liver's release of glucose, causing delayed hypoglycaemia (often overnight or the next morning). Eat carbohydrate, check glucose before bed, and tell friends about hypoglycaemia.
Hypoglycaemia awareness: Assess with the Gold score. Recurrent hypoglycaemia blunts warning symptoms (impaired awareness); strict avoidance of hypoglycaemia for 2–3 weeks can restore them.
Psychological health:
- Diabetes distress, depression and anxiety are common.
- Disordered eating - including deliberately omitting insulin to lose weight - is a serious and under-recognised cause of recurrent DKA in young women.
Contraception and pregnancy planning: Every woman of child-bearing age should be advised to plan pregnancy, aiming for an HbA1c below 48 mmol/mol, and to take folic acid 5 mg beforehand.

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Children and Young People

Type 1 is the commonest type in children. Type 2 is increasing in adolescents with obesity, especially in South Asian and Black communities.
Presentation: The "4 Ts" - Toilet (polyuria, bedwetting), Thirsty, Tired, Thinner. Diagnosis is often delayed, and about a quarter present in DKA.
Management (NICE NG18):
- Multidisciplinary paediatric diabetes team.
- Multiple daily injections or a pump from diagnosis.
- CGM and hybrid closed loop.
- HbA1c target 48 mmol/mol or lower.
- Education for family and school.
Paediatric DKA is managed with specific BSPED guidance. The fluid regimen is more cautious because of the higher risk of cerebral oedema (headache, falling consciousness, bradycardia, rising BP).
Adolescence: Puberty raises insulin requirements, and adherence often falls. Transition to adult services is a high-risk time for DKA and loss to follow-up.

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Type 2 Diabetes

Mechanism: Two problems combine:

Insulin resistance: Muscle, liver and fat respond poorly to insulin. It is driven by excess fat - particularly fat in the liver and pancreas - inactivity and genetics.
Progressive beta-cell failure: At first the pancreas compensates by making more insulin. Over years it cannot keep up, and glucose rises.

Because some insulin is still produced, ketosis is rare, and the typical emergency is HHS rather than DKA.

Risk factors:

Obesity, especially central obesity.
Inactivity.
Family history.
South Asian, Black African and African-Caribbean ethnicity - diabetes develops at younger ages and lower BMIs.
Previous gestational diabetes.
Polycystic ovary syndrome.
Age.
Antipsychotics and steroids.
Deprivation.

Clinical pattern:

Often asymptomatic, found on routine tests or NHS Health Checks.
Otherwise thirst, polyuria, tiredness and recurrent infections.
About a quarter already have complications at diagnosis, because hyperglycaemia has been present for years.

Early-onset type 2 diabetes (diagnosed under 40) is more aggressive, with faster complications. NICE now recommends more intensive early treatment for this group.

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Lifestyle, Weight Loss and Remission

Structured education: Offer at diagnosis (e.g. DESMOND, X-PERT).
Diet: Reduce refined carbohydrate, sugary drinks, saturated fat and portion size. Several dietary patterns work (Mediterranean, lower-carbohydrate, calorie restriction) - the best diet is one the person can sustain. Very-low-carbohydrate or ketogenic diets need care if the patient takes SGLT2 inhibitors, insulin or sulfonylureas.
Physical activity: At least 150 minutes a week of moderate activity plus strength training. It improves insulin sensitivity independently of weight loss.
Weight loss and remission:
- Losing about 10–15 kg can put type 2 diabetes into remission, especially within the first few years of diagnosis.
- In the UK DiRECT trial, almost half of participants were in remission at 1 year using a low-calorie diet.
- Remission is defined as HbA1c below 48 mmol/mol for at least 3 months off all glucose-lowering drugs.
- People in remission still need annual review - eye screening, foot checks and cardiovascular care.
NHS Type 2 Diabetes Path to Remission: A total diet replacement programme (soups and shakes, about 800–900 kcal/day for 12 weeks, then food reintroduction) for eligible adults with recent-onset type 2 diabetes and overweight.
Weight-loss medicines: GLP-1 agonists and tirzepatide (see below).
Metabolic (bariatric) surgery: Consider expedited assessment for people with recent-onset type 2 diabetes and a BMI of 35 or more (lower thresholds for some ethnic groups). It produces high remission rates.
Smoking cessation and alcohol reduction.

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Drug Treatment: The NICE Pathway

NICE NG28 was substantially updated in February 2026. The approach now focuses on early organ protection as well as glucose lowering. Key recommendations:

First-line for most people: Metformin modified-release plus an SGLT2 inhibitor as dual therapy, even without other comorbidities, unless contraindicated.
- Titrate metformin first for tolerability, then add the SGLT2 inhibitor.
- Use SGLT2 inhibitors cautiously in frailty.
- If metformin is not tolerated, use an SGLT2 inhibitor alone.
Established atherosclerotic cardiovascular disease: Triple therapy - metformin MR, an SGLT2 inhibitor and subcutaneous semaglutide - added in sequence, titrating semaglutide to 1 mg weekly.
Early-onset type 2 diabetes (under 40): Consider triple therapy with metformin MR, an SGLT2 inhibitor and a GLP-1 agonist or tirzepatide.
Heart failure: Continue SGLT2 inhibitors for heart and kidney benefit. Avoid pioglitazone.
Chronic kidney disease: Continue SGLT2 inhibitors for kidney and heart protection even when eGFR is below 45 and their glucose-lowering effect is reduced. A DPP-4 inhibitor may be added for glucose.
Obesity: GLP-1 agonists or tirzepatide are not first-line, but can be the first additional drug when more glucose lowering is needed.
Further glucose lowering: Options are a GLP-1 agonist or tirzepatide (preferred where recommended), a DPP-4 inhibitor, pioglitazone (not in heart failure), a sulfonylurea (if eGFR is above 30), or insulin. Do not combine a GLP-1 agonist or tirzepatide with a DPP-4 inhibitor (same pathway).
Fairness: NICE highlights lower SGLT2 inhibitor uptake in women, older people, some ethnic minority groups and deprived groups. Actively offer them.

💡 Key concept: SGLT2 inhibitors and GLP-1 agonists protect the heart and kidneys beyond their effect on glucose. They are now chosen by the patient's cardiovascular and renal risk, not just by HbA1c.

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Metformin

How it works: Mainly reduces glucose production by the liver and improves insulin sensitivity. It does not cause hypoglycaemia on its own and is weight-neutral.
Dose: Modified-release is now preferred (NICE 2026). Start 500 mg once daily with the evening meal and increase gradually over several weeks to a maximum of 2 g daily. Standard-release can continue if well tolerated, and is used if tablets need crushing.
Side effects:
- GI upset - nausea, diarrhoea, bloating - reduced by slow titration and the MR form.
- Vitamin B12 deficiency with long-term use - check B12 if neuropathy or anaemia develops.
- Rarely, lactic acidosis, mainly in acute illness with poor kidney or liver function or hypoxia.
Kidney function:
- Reduce to a maximum of 1 g daily if eGFR is below 45.
- Do not start if eGFR is below 30, and stop if it falls below 30.
Temporarily stop: During dehydrating illness (sick day rules), and around iodinated contrast in patients with impaired kidney function.

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SGLT2 Inhibitors

Examples: Dapagliflozin 10 mg, empagliflozin 10 mg (25 mg for extra glucose lowering), canagliflozin 100–300 mg, ertugliflozin - once daily.
How they work: Block glucose reabsorption in the proximal tubule, so glucose (and calories and sodium) are lost in the urine.
Benefits beyond glucose:
- Reduce heart failure hospitalisation.
- Slow kidney disease progression.
- Reduce cardiovascular death.
- Modest weight and BP reduction.
- Low risk of hypoglycaemia on their own.
Kidney function: The glucose-lowering effect falls as eGFR declines, but the heart and kidney benefits persist. Continue them in CKD per specialist and licensing advice.
Side effects:
- Genital fungal infections - advise good hygiene.
- Urinary infections.
- Volume depletion and postural hypotension, especially with diuretics and in older people.
- Euglycaemic DKA - rare but serious.
- Fournier's gangrene - rare.
Before starting: Check for previous DKA, dehydration, a very-low-carbohydrate or ketogenic diet, and current acute illness. Do not start during illness.
Sick day rules: Stop during acute illness, vomiting or dehydration. Stop before major surgery (usually the day before and the day of surgery, per local peri-operative guidance) and during prolonged fasting. Restart when eating and drinking normally.

⚠️ Safety Pearl: An unwell patient on an SGLT2 inhibitor with nausea, vomiting, abdominal pain or breathlessness may have DKA with only mildly raised glucose. Always check ketones and a blood gas.

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GLP-1 Agonists and Tirzepatide

Examples and doses:
- Semaglutide SC weekly: 0.25 mg, then 0.5 mg, up to 1 mg for type 2 diabetes.
- Oral semaglutide: Daily; dose depends on the formulation.
- Dulaglutide weekly: 0.75–1.5 mg and higher.
- Liraglutide daily: 0.6 mg, then 1.2–1.8 mg.
- Tirzepatide weekly: A dual GIP/GLP-1 agonist, starting at 2.5 mg and increased in 2.5 mg steps every 4 weeks, to 5–15 mg.
How they work:
- Increase glucose-dependent insulin release (low hypoglycaemia risk on their own).
- Suppress glucagon.
- Slow stomach emptying.
- Reduce appetite strongly, leading to significant weight loss.
Benefits:
- Powerful HbA1c and weight reduction.
- Semaglutide, liraglutide and dulaglutide reduce cardiovascular events in people with cardiovascular disease.
- Semaglutide also slows kidney disease.
Side effects:
- Nausea, vomiting, diarrhoea and constipation - reduced by slow titration.
- Gallstones.
- Pancreatitis - stop if suspected.
- Early worsening of diabetic retinopathy with rapid HbA1c falls - consider informing the eye screening service before starting.
- Rarely NAION (sudden painless visual loss) with semaglutide - warn patients.
- Risk of aspiration under anaesthesia (delayed gastric emptying).
Contraception and pregnancy: Avoid in pregnancy and breastfeeding. Tirzepatide can reduce the effectiveness of oral contraceptives during dose increases - advise barrier or non-oral contraception (MHRA).
When to stop (NICE 2026): If BMI falls below 18.5, or if there is no benefit on glucose or weight and the drug is not being used for cardiovascular protection.
Do not combine with a DPP-4 inhibitor.

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DPP-4 Inhibitors

Examples:
- Sitagliptin 100 mg daily (reduce in renal impairment).
- Linagliptin 5 mg daily (no renal dose adjustment - useful in CKD).
- Alogliptin and saxagliptin.
How they work: Block the enzyme that breaks down the body's own GLP-1 and GIP, giving a modest incretin boost.
Pros: Well tolerated, weight-neutral, low hypoglycaemia risk. Useful in older people and CKD.
Cons:
- Modest glucose lowering only (HbA1c falls by about 5–8 mmol/mol).
- No proven cardiovascular or kidney benefit.
- Rarely pancreatitis and bullous pemphigoid.
- Saxagliptin and alogliptin carry a heart failure caution.

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Sulfonylureas

Example: Gliclazide - 40–80 mg daily initially, up to 160 mg twice daily (or a modified-release preparation).
How they work: Make the beta cells release insulin regardless of the glucose level.
Pros: Cheap and fast-acting; useful for symptomatic hyperglycaemia and in HNF1A-MODY (very sensitive).
Cons:
- Hypoglycaemia - can be prolonged and severe, especially in older people, CKD and with missed meals.
- Weight gain.
- Effect wanes as beta cells fail.
Practical points:
- Patients need glucose monitoring and hypoglycaemia education.
- DVLA rules apply.
- Avoid if eGFR is below 30.
- Reduce or stop if there is hypoglycaemia or weight loss.

💡 Clinical Pearl: Sulfonylurea-induced hypoglycaemia can recur for 24–72 hours. Patients usually need admission and glucose monitoring, even after an initial recovery.

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Pioglitazone

Dose: 15–30 mg daily (maximum 45 mg).
How it works: A thiazolidinedione that activates PPAR-gamma, improving insulin sensitivity in fat, muscle and liver. Low hypoglycaemia risk on its own.
Benefits: Durable glucose lowering; improves fatty liver disease (MASLD).
Side effects:
- Fluid retention - contraindicated in heart failure.
- Weight gain.
- Fractures, especially in women.
- Possible small bladder cancer risk - avoid with active or previous bladder cancer or unexplained haematuria.
- Macular oedema.

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Insulin in Type 2

When needed:

Glucose remains above target despite other treatments (the beta cells continue to fail).
Symptomatic or severe hyperglycaemia.
Pregnancy.
Acute illness.
Uncertainty about whether the diabetes is really type 1 or LADA.

Starting insulin (NICE):

Offer once- or twice-daily basal insulin first:
- Isophane (NPH) insulin, or a long-acting analogue if NPH causes hypoglycaemia or the patient needs once-daily dosing (e.g. given by a district nurse).
- Choose the least expensive suitable insulin; biosimilars are acceptable.
A typical start: About 10 units (or 0.1–0.2 units/kg) at bedtime.
Titration: Increase by about 2 units every 3 days until fasting glucose is 5–7 mmol/L. Reduce if there is hypoglycaemia.
Continue metformin (and the SGLT2 inhibitor for organ protection). Usually reduce or stop sulfonylureas to limit hypoglycaemia.
Intensifying: If HbA1c remains high (e.g. 75 mmol/mol or more), consider adding rapid-acting insulin with meals, or switching to a premixed twice-daily regimen.
Support: A diabetes specialist nurse should support the patient, covering injection technique, monitoring, hypoglycaemia and DVLA requirements.

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Glucose, BP and Lipid Targets

HbA1c - type 2:
- NICE now emphasises individualised targets agreed with the patient.
- Traditionally: about 48 mmol/mol (6.5%) on lifestyle or drugs that do not cause hypoglycaemia, and about 53 mmol/mol (7.0%) on drugs that can cause hypoglycaemia.
- Relax targets in frailty, limited life expectancy, recurrent hypoglycaemia, or for people who drive for a living on insulin.
HbA1c - type 1: 48 mmol/mol or lower if achievable safely.
Blood pressure:
- Type 2 (NICE NG136): Below 140/90 (below 150/90 if aged 80 or over).
- Type 1 (NG17): Below 135/85, or below 130/80 with albuminuria.
- CKD with ACR of 70 mg/mmol or more: Below 130/80.
- First-line: An ACE inhibitor or ARB, especially with albuminuria.
Lipids (NICE NG238):
- Type 2: Atorvastatin 20 mg if QRISK3 is 10% or more.
- Type 1: Offer atorvastatin 20 mg if aged over 40, diabetes for more than 10 years, nephropathy, or other cardiovascular risk factors.
- Established cardiovascular disease: Atorvastatin 80 mg.
Aspirin: Not for primary prevention in diabetes; used for established cardiovascular disease.

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MODY

Mechanism: Maturity-onset diabetes of the young is caused by a single-gene defect in insulin secretion and is autosomal dominant. It accounts for about 1–2% of diabetes, but most cases are misdiagnosed as type 1 or 2.

Clues:

Diagnosis under about 25–30.
A parent with diabetes (and diabetes in several generations).
Antibody-negative, with preserved C-peptide.
No ketosis.
Not overweight.

The MODY probability calculator (Exeter) helps decide who to test.

Main types:

GCK-MODY (glucokinase): The glucose "set point" is slightly high, causing a mild, stable fasting hyperglycaemia (about 5.5–8 mmol/L) from birth. Complications are rare and no treatment is needed outside pregnancy.
HNF1A-MODY (the commonest symptomatic type): Progressive diabetes, often with glycosuria at low glucose levels. Very sensitive to low-dose sulfonylureas - patients can often stop insulin.
HNF4A-MODY: Similar, with sulfonylurea sensitivity. Babies are often large at birth with neonatal hypoglycaemia.
HNF1B-MODY: Diabetes with renal cysts, genital tract abnormalities and pancreatic underdevelopment.

Why it matters: The right diagnosis changes treatment and allows family testing.

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LADA

Mechanism: Latent autoimmune diabetes in adults is a slowly progressive form of autoimmune (type 1) diabetes in adults. It is often initially diagnosed and treated as type 2.

Clues:

Diagnosis over 30.
Slim build.
Personal or family history of autoimmune disease.
Failure of tablets within months to a few years.
Weight loss.
Positive GAD antibodies and falling C-peptide.

Management: Insulin is usually needed early. Avoid sulfonylureas, which may hasten beta-cell exhaustion. Use SGLT2 inhibitors cautiously because of the risk of euglycaemic DKA.

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Pancreatic Diabetes

Mechanism: Damage to the pancreas destroys islets along with the exocrine tissue. Glucagon is often lost too, which makes hypoglycaemia more frequent and severe. Also called type 3c diabetes.

Causes:

Chronic pancreatitis (often alcohol-related).
Pancreatic cancer.
Cystic fibrosis-related diabetes.
Haemochromatosis ("bronze diabetes").
Pancreatectomy; trauma.

Clues: Steatorrhoea and weight loss (exocrine failure), and a history of pancreatitis.

⚠️ Safety Pearl: New-onset diabetes in an older adult with weight loss - especially without obesity - needs pancreatic cancer considered, particularly with abdominal or back pain or jaundice.

Management:

Often needs insulin, in cautious doses.
Pancreatic enzyme replacement (e.g. Creon) for steatorrhoea.
Vitamin D and bone health.
Alcohol cessation.

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Endocrine and Drug-induced Diabetes

Endocrine causes (excess counter-regulatory hormones):
- Cushing's syndrome.
- Acromegaly.
- Phaeochromocytoma.
- Glucagonoma (with necrolytic migratory erythema).
- Hyperthyroidism (worsens control).
Treating the underlying disorder often improves or cures the diabetes.
Drugs:
- Glucocorticoids - the commonest.
- Antipsychotics (olanzapine, clozapine).
- Thiazide diuretics (mild).
- Beta blockers (mild).
- Statins (small increase in risk, outweighed by benefit).
- Tacrolimus and ciclosporin - post-transplant diabetes.
- Protease inhibitors.

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Steroid-induced Hyperglycaemia

Mechanism: Glucocorticoids cause insulin resistance and increase glucose production by the liver. With once-daily morning prednisolone, glucose characteristically rises from late morning, peaks in the afternoon and evening, and falls back overnight. Fasting glucose may look normal and miss the problem.

Monitoring: In patients on significant steroid doses (with or without known diabetes), check capillary glucose before lunch or dinner, ideally once or twice daily.

Management (JBDS guidance):

Morning gliclazide (e.g. 40 mg, titrated), or morning isophane (NPH) insulin (e.g. 10% dose increments), timed to match the steroid peak.
In known insulin-treated diabetes, increase the insulin doses, especially the morning intermediate or daytime doses.
Reduce treatment as the steroid is weaned to avoid hypoglycaemia.

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Rare Forms

Immune checkpoint inhibitor diabetes: Abrupt-onset insulin-deficient diabetes, often presenting in DKA with a very low C-peptide, during or after anti-PD-1/PD-L1 therapy. Lifelong insulin.
Neonatal diabetes (under 6 months): Usually monogenic, e.g. KCNJ11 potassium channel mutations. Many respond to high-dose sulfonylureas instead of insulin.
Mitochondrial diabetes (MIDD): Maternally inherited diabetes with sensorineural deafness.
Wolfram syndrome (DIDMOAD): Diabetes insipidus, diabetes mellitus, optic atrophy and deafness.
Lipodystrophy: Loss of fat tissue with severe insulin resistance, very high triglycerides and fatty liver. It can also be acquired, including with HIV treatment.
Severe insulin resistance: Acanthosis nigricans and very high insulin requirements, e.g. from antibodies to the insulin receptor.

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Hypoglycaemia

Definition: Blood glucose below 4.0 mmol/L in a person with diabetes ("4 is the floor").

Severity:

Level 1: Below 3.9 mmol/L.
Level 2: Below 3.0 mmol/L - clinically significant.
Level 3 (severe): Needs another person's help.

Causes:

Insulin or sulfonylureas, especially with missed meals, exercise or alcohol.
Kidney impairment (reduced clearance of insulin and sulfonylureas).
Weight loss; injection into lipohypertrophy.
Adrenal or pituitary failure; coeliac disease.
Gastroparesis.

Symptoms:

Adrenergic (warning) symptoms: sweating, tremor, palpitations, hunger, anxiety.
Neuroglycopenic symptoms: confusion, slurred speech, odd behaviour, drowsiness, focal neurology (can mimic stroke), seizures, coma.

Management (JBDS guidance):

Conscious and able to swallow:
- 15–20 g of quick-acting carbohydrate - e.g. 150–200 mL of pure fruit juice, or 4–5 glucose tablets.
- Recheck after 10–15 minutes; repeat up to three times.
- Once glucose is above 4 mmol/L, give a longer-acting carbohydrate (e.g. toast, biscuits) or the next meal.
Conscious but unable to swallow safely, or uncooperative:
- Glucose gel on the gums (if able to swallow), or
- IV glucose (10% glucose 150–200 mL over 15 minutes), or
- Glucagon 1 mg IM.
Unconscious or fitting:
- ABC.
- IV 10% glucose 150–200 mL over 15 minutes (or 20% glucose 75–100 mL), repeated as needed.
- If there is no IV access, glucagon 1 mg IM.
When glucagon works less well: In malnutrition, alcohol excess and liver disease (glycogen stores are depleted), and after prolonged hypoglycaemia. It can only be given once.
Afterwards:
- Do not omit the next insulin dose in type 1 (risk of DKA) - review and adjust it instead.
- Find the cause.
- Admit sulfonylurea-induced and long-acting insulin overdose hypoglycaemia for monitoring.

💡 MRCP Pearl: Hypoglycaemia with a high insulin and low C-peptide means injected insulin (factitious or accidental). High insulin and high C-peptide means an insulinoma or sulfonylurea use - send a sulfonylurea screen.

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DKA: Recognition

Mechanism: Absolute or severe insulin deficiency, plus high counter-regulatory hormones, causes three things:

Hyperglycaemia → osmotic diuresis, dehydration and loss of sodium and potassium.
Uncontrolled fat breakdown → the liver makes ketones (beta-hydroxybutyrate, acetoacetate) → metabolic acidosis with a raised anion gap.
Potassium shifts: Insulin deficiency and acidosis move potassium out of cells. Serum potassium may be normal or high, despite a large total-body potassium deficit. Insulin treatment moves potassium back into cells, so the serum level falls sharply.

Precipitants:

New type 1 diabetes.
Infection.
Missed insulin (including deliberate omission and pump failure).
MI, pancreatitis.
SGLT2 inhibitors.
Pregnancy.
Steroids.
Checkpoint inhibitors.

Clinical pattern:

Polyuria, thirst and weight loss.
Nausea, vomiting and abdominal pain (can mimic a surgical abdomen).
Dehydration and tachycardia.
Kussmaul breathing - deep sighing respiration to blow off CO₂.
Ketotic (pear-drop) breath.
Drowsiness.

Diagnosis (JBDS) - all three:

D - Diabetes: blood glucose above 11 mmol/L, or known diabetes (glucose may be lower in euglycaemic DKA).
K - Ketonaemia: blood ketones 3.0 mmol/L or more (or urine ketones 2+ or more).
A - Acidosis: venous pH below 7.3 and/or bicarbonate below 15 mmol/L.

Markers of severe DKA - consider HDU or ICU:

Ketones over 6 mmol/L.
Bicarbonate below 5 mmol/L.
pH below 7.0.
Potassium below 3.5 mmol/L on admission.
GCS below 12.
Oxygen saturations below 92% on air.
Systolic BP below 90 mmHg.
Heart rate over 100 or below 60.
Anion gap over 16.

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DKA: Management

Follow the JBDS DKA guideline and your local care pathway.

1. Fluids (adults; 0.9% sodium chloride):

Shocked (systolic BP below 90): 500 mL over 10–15 minutes, repeated, with senior help.
Typical regimen once not shocked:
- 1 litre over 1 hour.
- Then 1 litre over 2 hours.
- 1 litre over 2 hours.
- 1 litre over 4 hours.
- 1 litre over 4 hours.
- 1 litre over 6 hours.
Slower rates for young adults (18–25, risk of cerebral oedema), older people, and those with heart failure or CKD.

2. Fixed-rate IV insulin infusion:

Soluble insulin at 0.1 units/kg/hour (estimated weight if needed).
Reduce to 0.05 units/kg/hour once glucose falls below 14 mmol/L.
Continue the patient's usual long-acting insulin throughout. This prevents rebound DKA when the infusion stops. Stopping basal insulin is a classic error.

3. Glucose: When glucose falls below 14 mmol/L, add 10% glucose at 125 mL/hour alongside the saline, so the insulin can keep clearing ketones without causing hypoglycaemia.

4. Potassium (added to each litre of 0.9% saline):

Above 5.5 mmol/L: No potassium.
3.5–5.5 mmol/L: 40 mmol per litre.
Below 3.5 mmol/L: Senior review - extra potassium is needed (via a central line or HDU if a high concentration is required).
Check potassium at 1 hour, 2 hours and then 2-hourly.

5. Monitoring - hourly glucose and ketones; venous gas at 1, 2, 4 and 6 hours, then as needed. Targets:

Ketones fall by at least 0.5 mmol/L per hour.
Bicarbonate rises by at least 3 mmol/L per hour.
Glucose falls by about 3 mmol/L per hour.

If the targets are not met, check the infusion line and pump, then consider increasing the insulin rate.

6. Look for the cause: Infection screen, ECG and troponin, amylase, pregnancy test. Give thromboprophylaxis (LMWH); catheterise if needed.

7. Resolution: pH above 7.3 and ketones below 0.6 mmol/L. Then:

Switch to subcutaneous insulin when the patient is eating and drinking.
Give rapid-acting insulin with a meal, and stop the IV insulin 30–60 minutes later.
Refer to the diabetes team before discharge - education, sick day rules, and the cause of the episode.

⚠️ Safety Pearl: The commonest causes of harm in DKA management are hypokalaemia, hypoglycaemia and stopping basal insulin. Monitor potassium closely, start 10% glucose once glucose is below 14, and continue long-acting insulin.

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Euglycaemic DKA

Mechanism: DKA with blood glucose below about 14 mmol/L, so it is easily missed.

Causes:

SGLT2 inhibitors - the commonest. They lower glucose by urinary loss while insulin levels fall and ketone production rises.
Pregnancy.
Starvation or a very-low-carbohydrate diet.
Alcohol.
Insulin given with reduced food intake.
Pancreatitis.

Clinical pattern: A patient on an SGLT2 inhibitor who is nauseated, vomiting, has abdominal pain, is breathless or generally unwell - often after surgery, acute illness or reduced eating - with near-normal glucose but high ketones and acidosis.

Management:

Stop the SGLT2 inhibitor.
Treat as DKA, but start 10% glucose at the outset alongside the fixed-rate insulin, because glucose is already low.
Monitor ketones until they fall below 0.6 mmol/L.
Report to the MHRA (Yellow Card).

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Hyperosmolar Hyperglycaemic State

Mechanism: HHS develops over days to weeks, typically in older people with type 2 diabetes. There is enough insulin to prevent significant ketosis, but not enough to control glucose. Extreme hyperglycaemia causes massive osmotic diuresis - patients lose about 100–220 mL/kg of fluid - and very high plasma osmolality. Mortality (about 10–20%) is higher than in DKA.

Precipitants:

Infection.
Stroke, MI.
Steroids, thiazides.
Sugary drinks.
Reduced access to fluids (dementia, immobility).
Undiagnosed diabetes.

Diagnosis (JBDS) - all of:

Hypovolaemia.
Marked hyperglycaemia (30 mmol/L or more).
Osmolality 320 mOsm/kg or more. Calculated as 2 × Na + glucose + urea.
No significant ketonaemia (below 3.0 mmol/L) or acidosis (pH above 7.3, bicarbonate above 15).

Some patients have a mixed picture with features of both DKA and HHS.

Clinical pattern:

Profound dehydration.
Confusion or reduced consciousness.
Focal neurology or seizures (can mimic stroke).
High risk of thrombosis and foot ulceration.

Management (JBDS): The key principle is gradual correction.

Fluids first: IV 0.9% sodium chloride, e.g. 1 litre over the first hour, then continuing, aiming for a positive balance of about 3–6 litres in the first 12 hours.
Correction targets:
- Osmolality should fall by about 3–8 mOsm/kg per hour.
- Glucose by about 4–6 mmol/L per hour (no more than 10).
Sodium may rise at first as glucose falls. This is acceptable if osmolality is falling.
Insulin:
- Do not start immediately unless there is significant ketonaemia (above 1 mmol/L) - fluids alone lower glucose.
- Start a fixed-rate infusion at a low dose (0.05 units/kg/hour) once glucose stops falling with fluids.
- Rapid falls in glucose and osmolality risk cerebral oedema and osmotic demyelination.
Potassium replacement: As in DKA.
Prophylactic LMWH (very high thrombosis risk).
Foot protection - heel protectors and daily foot checks.
Treat the precipitant.
Recovery: Many patients can later manage on tablets or no treatment, but some need insulin.

💡 Clinical Pearl: DKA: treat with insulin from the start; fast, hours. HHS: treat with fluids first, insulin later at a low dose; slow, days. The danger in HHS is correcting too fast.

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Complications and Annual Review

Raised glucose damages blood vessels over years, and the risk rises steadily with HbA1c, blood pressure, smoking, lipids and duration. Landmark trials (DCCT in type 1, UKPDS in type 2) showed that early good control reduces complications for decades afterwards - the "legacy effect".

Microvascular: Retinopathy, nephropathy, neuropathy.
Macrovascular: Coronary disease, stroke, peripheral arterial disease.
Other: Foot ulcers and amputation, erectile dysfunction, gastroparesis, infections, fatty liver disease, cognitive decline, depression.

Annual review - the "care processes" every person with diabetes should receive:

HbA1c (3–6-monthly until stable).
Blood pressure.
Cholesterol.
Kidney function: eGFR and urine albumin:creatinine ratio (ACR).
Foot examination and risk classification.
Retinal screening through the NHS Diabetic Eye Screening Programme. Usually annual, extended to every 2 years for people at low risk with no retinopathy on two consecutive screens.
Weight and BMI.
Smoking status.
Lifestyle and psychological wellbeing.
Review: Structured education, medicines, hypoglycaemia and injection sites, contraception and pregnancy plans, and driving.

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Retinopathy

Mechanism: High glucose damages retinal capillaries. They leak (causing haemorrhages, exudates and macular oedema) and become blocked (causing ischaemia). The ischaemic retina releases VEGF, which drives fragile new vessel growth. Diabetic retinopathy is a leading cause of sight loss in working-age adults.

Stages:

Background (non-proliferative): Microaneurysms, dot-and-blot haemorrhages, hard exudates. No symptoms.
Pre-proliferative: Cotton wool spots (retinal infarcts), venous beading, multiple haemorrhages, intraretinal microvascular abnormalities. High risk of progression.
Proliferative: New vessels on the disc or elsewhere. Risk of vitreous haemorrhage (sudden visual loss), tractional retinal detachment and neovascular glaucoma.
Maculopathy: Exudates or oedema near the fovea - the commonest cause of visual loss, especially in type 2. Reduced central vision.

Management:

Improve control: Glucose, blood pressure, lipids and smoking.
Proliferative retinopathy: Panretinal laser photocoagulation and/or anti-VEGF injections.
Macular oedema: Intravitreal anti-VEGF (e.g. aflibercept, ranibizumab, faricimab), steroid implants or laser.
Vitreous haemorrhage or detachment: Vitrectomy.

💡 Clinical Pearl: Rapid improvement in HbA1c - after starting insulin or a GLP-1 agonist, after bariatric surgery, or in pregnancy - can temporarily worsen retinopathy. Arrange eye review in people with significant retinopathy.

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Diabetic Kidney Disease

Mechanism: Hyperglycaemia causes high pressure and hyperfiltration in the glomeruli, thickening of the basement membrane and glomerulosclerosis (Kimmelstiel–Wilson nodules). Protein leaks into the urine and kidney function falls. Diabetes is the commonest cause of end-stage kidney disease in the UK. It also greatly increases cardiovascular risk.

Screening: Annual eGFR and urine ACR (early-morning sample).

ACR 3 mg/mmol or more (confirmed on repeat) = albuminuria.
ACR above 30 = significantly increased albuminuria.

Management:

ACE inhibitor or ARB, titrated to the maximum tolerated dose, for diabetes with ACR above 3 (NICE NG203). Check potassium and creatinine - a rise of up to about 30% is acceptable.
SGLT2 inhibitor - slows kidney decline and reduces cardiovascular events. Continue even when eGFR is low (within licence).
Finerenone (a non-steroidal MRA) - add-on for type 2 diabetes with CKD and albuminuria (NICE TA877). Monitor potassium.
Blood pressure target: Below 130/80 if ACR is 70 or more; statin; stop smoking.
Adjust drug doses for kidney function: metformin, sulfonylureas, DPP-4 inhibitors and insulin (risk of hypoglycaemia).
Refer to nephrology for rapidly falling eGFR, ACR of 70 or more, haematuria, or features suggesting another cause.

💡 Clinical Pearl: Kidney disease in diabetes without retinopathy, with active urine sediment (blood, casts) or rapid decline should prompt a search for another cause.

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Peripheral Neuropathy

Mechanism: Damage to the longest nerve fibres first, through metabolic injury and damage to the small vessels supplying the nerves. It causes a symmetrical, length-dependent sensory loss in a "glove and stocking" pattern, starting in the toes.

Clinical pattern:

Numbness, tingling or burning feet.
Loss of protective sensation: a reduced 10 g monofilament response, reduced vibration (128 Hz tuning fork), absent ankle reflexes.
Painful neuropathy - burning, shooting pains, worse at night.
Unsteadiness and falls.
Foot deformity (clawed toes, high arches).

Why it matters: Loss of protective sensation is the main cause of foot ulceration - the patient does not feel a stone in the shoe.

Management:

Good glucose control.
Foot care education and podiatry.
Check B12 (especially on metformin), TFTs and alcohol history.
Painful neuropathy (NICE neuropathic pain guidance):
- Offer amitriptyline, duloxetine, gabapentin or pregabalin; switch to another if one is ineffective or not tolerated.
- Capsaicin cream for localised pain.
- Avoid long-term opioids.

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Autonomic Neuropathy

Cardiovascular:
- Resting tachycardia, loss of heart rate variability.
- Postural hypotension - treat with fluids, stockings, review of antihypertensives, and fludrocortisone or midodrine.
- "Silent" myocardial ischaemia - MI without chest pain.
Gastrointestinal:
- Gastroparesis - early fullness, vomiting, bloating and erratic glucose (food absorbed unpredictably, causing post-meal hypoglycaemia). Manage with small, low-fat, low-fibre meals; prokinetics (metoclopramide or domperidone short-term, erythromycin); adjust insulin timing; gastric electrical stimulation in severe cases.
- Nocturnal diarrhoea; constipation.
Genitourinary:
- Erectile dysfunction - PDE5 inhibitors (e.g. sildenafil); never with nitrates.
- Bladder dysfunction with incomplete emptying and UTIs.
Sudomotor: Dry feet and cracked skin; gustatory sweating (sweating when eating).
Hypoglycaemia unawareness: Loss of the adrenergic warning symptoms.
Pupils: Small, poorly reactive.

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Mononeuropathy and Amyotrophy

Cranial nerve palsies (nerve infarction):
- Third nerve palsy with pupil sparing - the pupil fibres run on the outside of the nerve and keep their blood supply. A dilated pupil instead suggests compression (e.g. a posterior communicating artery aneurysm) and needs urgent imaging.
- Sixth nerve palsy.
- Usually recovers over 3–6 months.
Compression neuropathies (more common in diabetes): Carpal tunnel syndrome, ulnar neuropathy, common peroneal nerve palsy (foot drop).
Diabetic amyotrophy (lumbosacral radiculoplexus neuropathy):
- Typically an older man with type 2 diabetes.
- Severe thigh pain, followed by wasting and weakness of the quadriceps, with weight loss.
- Slow partial recovery over months to years.
- Exclude other causes (spinal stenosis, malignancy).
Truncal radiculopathy: Band-like pain over the chest or abdomen.

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The Diabetic Foot

Mechanism: Neuropathy (no pain warning), ischaemia (poor healing) and infection combine. Foot ulcers precede most diabetic amputations, and about half of ulcers are preventable.

Annual foot risk assessment (NICE NG19): Check sensation (10 g monofilament), pulses, deformity, skin, callus and previous ulcers. Classify risk and review accordingly:

Low risk: No risk factors except callus. Review annually.
Moderate risk: Deformity, or neuropathy, or peripheral arterial disease. Foot protection service review every 3–6 months.
High risk: Previous ulcer or amputation, on dialysis, or neuropathy plus peripheral arterial disease, or either of these with callus or deformity. Review every 1–2 months.
Active diabetic foot problem (ulcer, spreading infection, critical ischaemia, gangrene, suspected Charcot): Refer to the multidisciplinary foot care service within 1 working day.

Assessment of a foot ulcer:

Size and depth; probe to bone (suggests osteomyelitis).
Signs of infection.
Pulses and Doppler or toe pressures (ankle–brachial index can be falsely normal because calcified arteries do not compress).
X-ray, or MRI for osteomyelitis.
Blood glucose, CRP.

Management:

Offloading (casts, special footwear).
Debridement and wound care.
Antibiotics for infection, per local guidance - urgent IV antibiotics for severe infection.
Vascular assessment and revascularisation.
Optimise glucose.
Amputation as a last resort.

⚠️ Safety Pearl: A diabetic foot with spreading cellulitis, crepitus, systemic sepsis or gangrene is a limb- and life-threatening emergency. Same-day surgical and foot team review.

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Charcot Foot

Mechanism: In a neuropathic foot, an often unnoticed injury triggers intense inflammation. Without protective pain, the patient keeps walking on it, and the bones and joints fracture and collapse. Without treatment this leads to severe deformity (e.g. a "rocker-bottom" foot), ulceration and amputation.

Clinical pattern: A hot, red, swollen, often painless or only mildly painful foot in a patient with neuropathy. The affected foot is often more than 2 °C warmer than the other. It is frequently misdiagnosed as cellulitis, gout or DVT.

Investigations: X-ray may be normal early. MRI shows bone marrow oedema and early fractures.

Management:

Urgent referral to the foot team (within 1 working day).
Immediate offloading and immobilisation in a non-removable total contact cast or boot, often for months until the temperature difference settles.
Bespoke footwear afterwards.
Surgery for unstable deformity.

💡 Clinical Pearl: A warm, swollen foot in a diabetic patient with neuropathy is Charcot until proven otherwise. Do not wait for X-ray changes - offload now.

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Cardiovascular Disease

Risk: Diabetes roughly doubles cardiovascular risk. Cardiovascular disease is the leading cause of death in diabetes. Women with diabetes lose much of their usual relative protection.
Presentation: Often atypical or silent because of autonomic neuropathy - breathlessness, fatigue or heart failure rather than chest pain.
Prevention:
- Statins.
- Blood pressure control.
- Stopping smoking.
- Weight loss and exercise.
- Drugs with proven cardiovascular benefit: SGLT2 inhibitors (especially heart failure) and GLP-1 agonists (especially atherosclerotic disease).
Heart failure: Common in diabetes. Use SGLT2 inhibitors; avoid pioglitazone, and saxagliptin/alogliptin with caution.
Peripheral arterial disease: Often distal and calcified - the ankle–brachial index can mislead, so use toe pressures. Major contributor to amputation.
Antiplatelets: For established cardiovascular disease, not for primary prevention.

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Skin and Infections

Skin:

Necrobiosis lipoidica: Shiny, yellow-brown, atrophic plaques with telangiectasia on the shins.
Diabetic dermopathy ("shin spots"): Small brown scars on the shins.
Acanthosis nigricans: Velvety dark skin in the neck folds and axillae - a sign of insulin resistance.
Eruptive xanthomas: Yellow papules from very high triglycerides.
Skin tags, vitiligo (type 1), lipohypertrophy.

Musculoskeletal:

Cheiroarthropathy (limited joint mobility - "prayer sign").
Dupuytren's contracture.
Frozen shoulder.
Trigger finger.
Carpal tunnel syndrome.

Infections - more common and more severe:

Candida (thrush, intertrigo).
Urinary tract infections.
Cellulitis and foot infections.
TB.
Periodontitis.

Rare but classic MRCP infections:

Malignant otitis externa: Pseudomonas, in older diabetic patients. Severe ear pain and discharge; facial nerve palsy; skull base osteomyelitis.
Rhino-orbital mucormycosis: Especially in DKA. Black nasal eschar, facial swelling, ophthalmoplegia - a surgical emergency.
Emphysematous pyelonephritis and cholecystitis: Gas-forming infections.
Necrotising fasciitis, including Fournier's gangrene.

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Pre-existing Diabetes in Pregnancy

Risks: Poorly controlled diabetes around conception and in early pregnancy increases:

Miscarriage.
Congenital anomalies (especially heart and neural tube).
Stillbirth.
Pre-eclampsia.
Large babies (macrosomia) and shoulder dystocia.
Neonatal hypoglycaemia.

Before conception (NICE NG3):

Plan the pregnancy - use effective contraception until HbA1c is optimised.
Aim for HbA1c below 48 mmol/mol (6.5%) if safely achievable. Strongly advise against pregnancy if HbA1c is above 86 mmol/mol (10%).
Folic acid 5 mg daily from before conception until 12 weeks.
Review medication:
- Continue metformin and insulin.
- Stop other glucose-lowering drugs.
- Stop statins and ACE inhibitors/ARBs (switch BP treatment).
Retinal and kidney assessment.

During pregnancy:

Glucose targets: Fasting below 5.3 mmol/L; 1 hour after meals below 7.8 mmol/L (or 2 hours below 6.4 mmol/L). Avoid hypoglycaemia - awareness falls in early pregnancy.
Type 1: Offer CGM and hybrid closed loop. Insulin needs fall slightly in the first trimester, then rise steeply in the second and third.
Aspirin (75–150 mg daily) from 12 weeks to reduce pre-eclampsia risk.
Retinal assessment during pregnancy.
Growth scans.
Plan delivery - usually between 37+0 and 38+6 weeks.

At delivery and after:

A variable-rate insulin infusion during labour if needed.
Reduce insulin immediately after delivery back to pre-pregnancy doses, or lower if breastfeeding.
Monitor the baby's glucose and feed early.

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Gestational Diabetes

Mechanism: Placental hormones cause insulin resistance in the second half of pregnancy. Women whose beta cells cannot compensate develop hyperglycaemia. It affects about 1 in 20 pregnancies in the UK.

Risk factors (NICE):

BMI above 30.
Previous baby weighing 4.5 kg or more.
Previous gestational diabetes.
First-degree relative with diabetes.
High-risk ethnic background (e.g. South Asian, Black Caribbean, Middle Eastern).

Screening: A 75 g OGTT at 24–28 weeks for women with risk factors. Women with previous gestational diabetes are tested early (soon after booking) and again at 24–28 weeks if normal, or offered glucose self-monitoring.

Diagnosis (NICE): Fasting glucose 5.6 mmol/L or more, or 2-hour glucose 7.8 mmol/L or more.

Management:

Diet and exercise advice, with glucose self-monitoring.
Fasting below 7.0 at diagnosis: Diet and exercise for 1–2 weeks; add metformin if targets are not met; then insulin.
Fasting 7.0 or more at diagnosis: Start insulin immediately (with or without metformin).
Fasting 6.0–6.9 with complications (e.g. macrosomia, polyhydramnios): Consider immediate insulin.
Delivery: Usually by 40+6 weeks.

After delivery:

Stop glucose-lowering treatment.
Check fasting glucose at 6–13 weeks, or HbA1c after 13 weeks.
Then HbA1c annually - up to half of women develop type 2 diabetes within 10 years.
Lifestyle advice.
Early testing in future pregnancies.

💡 MRCP Pearl: Gestational diabetes is diagnosed with fasting glucose of 5.6 or more, or 2-hour glucose of 7.8 or more - remember "5-6-7-8".

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Hospital and Surgery

Inpatient glucose target: Generally 6–12 mmol/L (6–10 ideal).
Prevent hospital harm:
- Hypoglycaemia from missed meals and unadjusted insulin.
- DKA from omitted insulin in type 1.
- Insulin prescribing errors.
- Foot pressure ulcers (check feet on admission; heel protection).
Variable-rate IV insulin infusion (VRIII) - the "sliding scale":
- Use for: Patients who cannot eat for more than one missed meal, or are acutely unwell with hyperglycaemia. Not for DKA, which uses a fixed-rate infusion.
- With it: Run a glucose-containing substrate fluid, check glucose hourly, and continue long-acting insulin (often at about 80% of the usual dose).
- Stopping: Overlap with subcutaneous insulin when stopping.
Peri-operative care (Centre for Perioperative Care and JBDS guidance):
- Optimise HbA1c before elective surgery (ideally below 69 mmol/mol).
- Place on the morning list.
- For a short fast (one missed meal), adjust medicines rather than starting a VRIII.
- Reduce basal insulin by about 20% the evening before or the morning of surgery.
- Omit short-acting insulin and sulfonylureas while fasting.
- Omit SGLT2 inhibitors the day before and the day of surgery.
- Check ketones post-operatively in patients on SGLT2 inhibitors.
Self-management: Allow capable patients to manage their own insulin and pumps in hospital where safe.
Refer to the inpatient diabetes team for DKA and HHS, recurrent hypoglycaemia, new insulin starts, pumps and foot problems.

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Sick Day Rules

Type 1 diabetes (and insulin-treated type 2):

Never stop insulin - illness usually increases requirements, even when not eating.
Monitor: Glucose every 2–4 hours and ketones if glucose is above about 13 mmol/L or the patient feels unwell.
Correction doses: Extra rapid-acting insulin according to the glucose and ketone levels, per the patient's sick-day plan.
Fluids: At least 3 litres a day. Use sugary drinks if not eating and glucose is falling.
Seek urgent help if:
- Persistent vomiting, or unable to keep fluids down.
- Ketones above 1.5 mmol/L and rising, or 3 mmol/L or more.
- Abdominal pain or rapid breathing.
- Drowsiness.

Medicines to pause during dehydrating illness (vomiting, diarrhoea, fever, sweats) - "SADMANS":

Sulfonylureas (hypoglycaemia).
ACE inhibitors.
Diuretics.
Metformin.
ARBs.
NSAIDs.
SGLT2 inhibitors (DKA risk).

Restart 24–48 hours after eating and drinking normally. GLP-1 agonists may also be paused if vomiting.

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Driving

This summarises the DVLA rules for Group 1 (car and motorcycle) licences for people on insulin. Patients must check the current DVLA guidance.

Notify the DVLA: If treated with insulin (except temporary use, e.g. gestational diabetes, for 3 months or less).
Check glucose no more than 2 hours before driving and every 2 hours during long journeys. CGM is allowed for Group 1, but a finger-prick check is needed if symptoms or readings suggest hypoglycaemia.
"Five to drive": Glucose should be above 5 mmol/L to drive. Between 4 and 5, eat carbohydrate first. Do not drive if below 4.
If hypoglycaemic while driving:
- Stop safely, remove the keys and move from the driver's seat.
- Treat the hypoglycaemia.
- Wait 45 minutes after glucose has returned to normal before driving.
Must stop driving and inform the DVLA if:
- More than one episode of severe hypoglycaemia (needing another person's help) while awake in 12 months.
- Impaired hypoglycaemia awareness.
Group 2 (lorry and bus) licences have stricter requirements.
Sulfonylureas: Patients need to understand the hypoglycaemia risk and test when appropriate.
Other drugs: Patients on diet, metformin, SGLT2 inhibitors, DPP-4 inhibitors or GLP-1 agonists alone usually do not need to inform the DVLA, unless they have complications such as visual loss.

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Older Adults and End of Life

Priorities change: In frail older people, the main dangers are hypoglycaemia, falls, dehydration and treatment burden - not long-term complications.
Relax targets: Typically HbA1c around 53–64 mmol/mol, and up to about 70 in severe frailty, individualised.
De-intensify when HbA1c is low on hypoglycaemia-causing drugs. Reduce or stop sulfonylureas and simplify insulin regimens (e.g. once-daily long-acting insulin given by a district nurse).
Drug choice: DPP-4 inhibitors are well tolerated. Use SGLT2 inhibitors cautiously (dehydration, falls, genital infection). GLP-1 agonists may cause unwanted weight loss.
Hypoglycaemia may present atypically - confusion, falls, stroke-like symptoms, "funny turns" - and can be mistaken for dementia or TIA.
Care homes: Need clear plans for monitoring, hypoglycaemia, sick days and foot checks.
End of life (Diabetes UK guidance):
- Focus on comfort and avoiding symptomatic hyper- or hypoglycaemia.
- Stop most tablets.
- In type 1 diabetes, continue a low dose of once-daily long-acting insulin to prevent DKA, unless in the last days of life.
- Aim for glucose roughly 6–15 mmol/L.
- Minimise testing.

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Drug Reference Table

Typical adult doses - check the BNF, NICE NG28/NG17 and local protocols. Children are dosed from BNFc.

Drug / use	Dose and key points
Metformin MR Type 2 first-line	500 mg daily with the evening meal, titrated to max 2 g daily. Max 1 g/day if eGFR below 45; stop if below 30. GI upset; B12 deficiency.
Dapagliflozin / empagliflozin Type 2 first-line with metformin; HF; CKD	10 mg once daily (empagliflozin 25 mg for extra glucose lowering). Genital infection, volume depletion, euglycaemic DKA. Sick day rules; omit around surgery.
Semaglutide (SC) Type 2; ASCVD	0.25 mg weekly for 4 weeks, then 0.5 mg, up to 1 mg weekly. GI effects, pancreatitis, gallstones, retinopathy worsening.
Liraglutide / dulaglutide Type 2	Liraglutide 0.6 mg daily, then 1.2–1.8 mg. Dulaglutide 0.75–1.5 mg weekly (higher doses available).
Tirzepatide Type 2; obesity	2.5 mg weekly for 4 weeks, increasing by 2.5 mg every 4 weeks to 5–15 mg. Reduces oral contraceptive effectiveness during titration.
Sitagliptin / linagliptin Type 2	Sitagliptin 100 mg daily (reduce in CKD). Linagliptin 5 mg daily (no renal adjustment). Not with GLP-1 agonists.
Gliclazide Type 2	40–80 mg daily, up to 160 mg twice daily (or MR preparation). Hypoglycaemia; weight gain; avoid if eGFR below 30.
Pioglitazone Type 2	15–30 mg daily (max 45 mg). Contraindicated in heart failure; fluid retention, fractures, bladder cancer caution.
Isophane (NPH) insulin Starting insulin in type 2; steroid hyperglycaemia	E.g. 10 units (0.1–0.2 units/kg) at bedtime, titrated by 2 units every 3 days to fasting 5–7 mmol/L. Morning dose for steroid-induced hyperglycaemia.
Basal–bolus insulin Type 1	Total about 0.5–1 unit/kg/day, roughly half basal (detemir twice daily, or glargine/degludec once daily) and half rapid-acting with meals, by carbohydrate ratio.
Fixed-rate IV insulin DKA	Soluble insulin 0.1 units/kg/hour, reduced to 0.05 units/kg/hour when glucose is below 14 mmol/L. Continue basal insulin. Add 10% glucose at 125 mL/hour when glucose is below 14.
Fixed-rate IV insulin HHS	0.05 units/kg/hour, started only once glucose stops falling with fluids (earlier if ketones above 1).
Potassium chloride DKA / HHS fluids	40 mmol per litre if K⁺ 3.5–5.5; none if above 5.5; senior review if below 3.5.
Glucose 10% IV Severe hypoglycaemia	150–200 mL over 15 minutes, repeated as needed (or 20% glucose 75–100 mL).
Glucagon Severe hypoglycaemia	1 mg IM or SC (once). Less effective in liver disease, alcohol excess and starvation.
Folic acid Pre-conception	5 mg daily from before conception to 12 weeks.
Aspirin Pregnancy (pre-eclampsia prevention)	75–150 mg daily from 12 weeks.
Finerenone Type 2 diabetes with CKD	10–20 mg daily (by eGFR), add-on to ACE inhibitor/ARB. Monitor potassium.
Amitriptyline / duloxetine / pregabalin / gabapentin Painful neuropathy	E.g. amitriptyline 10 mg at night, titrated; duloxetine 60 mg daily; pregabalin 75 mg twice daily, titrated. Adjust for renal function and frailty.

⚠️ Prescribing Safety: Write "units" in full. Never omit basal insulin in type 1. Pause SADMANS drugs in dehydrating illness. Never combine a GLP-1 agonist with a DPP-4 inhibitor. No pioglitazone in heart failure.

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Spot the Diagnosis

Clue	Think of
Teenager with thirst, weight loss, vomiting, Kussmaul breathing	New type 1 diabetes in DKA
Older person, confused, glucose 48, osmolality 360, no ketones	HHS
On dapagliflozin, vomiting, glucose 9, ketones 5, pH 7.15	Euglycaemic DKA
Slim 45-year-old "type 2", tablets failing within a year, GAD+	LADA
Diabetes at 22, parent and grandparent affected, antibody-negative	MODY (HNF1A - try gliclazide)
Lifelong mild fasting glucose of 6.5, no complications	GCK-MODY (no treatment)
New diabetes, weight loss, back pain in a 70-year-old	Pancreatic cancer
Diabetes with deafness, maternal inheritance	Mitochondrial diabetes (MIDD)
Glucose normal in morning, high in afternoon on prednisolone	Steroid-induced hyperglycaemia
Hypoglycaemia, high insulin, low C-peptide	Exogenous (injected) insulin
Erratic glucose, post-meal hypos, early fullness and vomiting	Gastroparesis
Hot, swollen, painless foot in neuropathic patient, normal X-ray	Charcot foot
Third nerve palsy with normal pupil	Diabetic mononeuropathy
Painful thigh, quadriceps wasting, weight loss in a type 2 man	Diabetic amyotrophy
Cotton wool spots and venous beading	Pre-proliferative retinopathy
Shiny yellow-brown plaques on the shins	Necrobiosis lipoidica
Severe ear pain and facial palsy in an older diabetic	Malignant otitis externa (Pseudomonas)
Black nasal eschar in DKA	Mucormycosis
Pregnant, OGTT fasting 5.8	Gestational diabetes
DKA on pembrolizumab with undetectable C-peptide	Checkpoint inhibitor diabetes

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Exam-style Scenarios

Decide your answer before reading on.

1. A 19-year-old has vomiting, abdominal pain and deep breathing. Glucose 28, ketones 5.8, pH 7.12, bicarbonate 9, K⁺ 5.1. Answer: DKA (new type 1 likely). 0.9% saline per JBDS; fixed-rate insulin 0.1 units/kg/h; potassium 40 mmol/L once K⁺ is 5.5 or below; 10% glucose when glucose falls below 14; hourly monitoring; find the precipitant; diabetes team.
2. An 82-year-old care-home resident is drowsy. Glucose 52, Na 152, urea 28, osmolality 380, ketones 0.8, pH 7.34. Answer: HHS. Gradual IV 0.9% saline; no insulin initially; aim osmolality to fall by 3–8 per hour; LMWH, foot protection; treat infection.
3. A 55-year-old with new type 2 diabetes, HbA1c 64, BMI 32, no cardiovascular disease, eGFR 80. Answer: Structured education and lifestyle (consider remission programmes); metformin MR titrated, then add an SGLT2 inhibitor (NICE 2026 dual first-line); statin by QRISK; annual review.
4. Same patient but with a previous MI. Answer: Triple therapy - metformin MR, an SGLT2 inhibitor and subcutaneous semaglutide titrated to 1 mg weekly; atorvastatin 80 mg; antiplatelet; BP control.
5. A 78-year-old on gliclazide 160 mg twice daily with eGFR 32 is found confused with glucose 2.1. Answer: Sulfonylurea-induced hypoglycaemia. IV 10% glucose, then admission for prolonged monitoring; stop or reduce gliclazide; relax targets.
6. A woman on dapagliflozin is 1 day after cholecystectomy, nauseated and tachypnoeic. Glucose 8.4, ketones 4.2, pH 7.21. Answer: Euglycaemic DKA. Stop the SGLT2 inhibitor; treat as DKA with 10% glucose from the start alongside fixed-rate insulin.
7. A man with type 2 diabetes and neuropathy has a warm, swollen, mildly painful foot; X-ray is normal. Answer: Suspected Charcot foot. Urgent foot team referral (within 1 working day), immediate offloading in a total contact cast, MRI.
8. A woman with type 1 diabetes (HbA1c 72) wants to become pregnant. Answer: Effective contraception until HbA1c is below 48; folic acid 5 mg; offer hybrid closed loop and CGM; retinal and renal review; stop statin and ACE inhibitor before conception.

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Key Points

1. Diagnose with HbA1c 48 or more, fasting 7.0 or more, or random 11.1 or more with symptoms; confirm if asymptomatic. Use glucose, not HbA1c, for suspected type 1, children and pregnancy.
2. A thirsty, weight-losing child or young adult needs same-day glucose and ketones.
3. Type 1 needs insulin for life - never stop basal insulin.
4. NICE 2026: metformin MR plus an SGLT2 inhibitor first-line for most people with type 2; add semaglutide in established cardiovascular disease.
5. SGLT2 inhibitors and GLP-1 agonists protect heart and kidneys beyond glucose lowering.
6. Hypoglycaemia (below 4): 15–20 g fast carbohydrate, recheck in 10–15 minutes; unconscious - IV 10% glucose or IM glucagon.
7. DKA: fluids, fixed-rate insulin 0.1 units/kg/h, continue basal insulin, potassium replacement, 10% glucose when below 14; resolution = pH above 7.3 and ketones below 0.6.
8. Euglycaemic DKA on SGLT2 inhibitors - check ketones even with normal glucose.
9. HHS: fluids first, insulin later at 0.05 units/kg/h; correct slowly; thromboprophylaxis.
10. Annual review: HbA1c, BP, lipids, eGFR and ACR, foot check, retinal screening.
11. ACE inhibitor or ARB plus SGLT2 inhibitor for diabetic kidney disease with albuminuria.
12. Active foot problems → foot team within 1 working day; hot swollen neuropathic foot = Charcot.
13. Pregnancy: plan, HbA1c below 48, folic acid 5 mg, aspirin from 12 weeks; gestational diabetes = fasting 5.6+ or 2-hour 7.8+.
14. Sick day rules: never stop insulin; pause SADMANS drugs.
15. In frailty, avoid hypoglycaemia and relax targets.

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Guidelines and Further Reading

NICE NG28: Type 2 Diabetes in Adults - updated February 2026.
NICE NG17: Type 1 Diabetes in Adults.
NICE NG18: Diabetes in Children and Young People.
NICE NG3: Diabetes in Pregnancy.
NICE NG19: Diabetic Foot Problems.
NICE NG203: Chronic Kidney Disease.
NICE TA943: Hybrid Closed Loop Systems.
Joint British Diabetes Societies (JBDS) for Inpatient Care - DKA, HHS, hypoglycaemia, peri-operative, steroid, VRIII and end-of-life guidance.
Centre for Perioperative Care (CPOC) - diabetes management around surgery.
DVLA: Diabetes and Driving.
Diabetes UK - patient information and professional resources.
BNF and BNFc.

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The content on this website is provided for educational and informational purposes only to support exam preparation (e.g., MLA, MRCP, USMLE) and learning. This is NOT medical advice, diagnosis, treatment, or professional guidance. It does not replace consultation with a qualified healthcare professional, official guidelines (e.g., NICE, GMC, BNF), or supervised clinical practice. Always verify information with current, authoritative sources. Makindo and its contributors accept no liability for any reliance on this content, including errors, omissions, or any resulting harm, loss, or consequences. By using this site, you agree to these terms.

Endocrinology: Diabetes (Complete)

What Is Diabetes?

Insulin and Glucose Physiology

Types of Diabetes

Diagnosing Diabetes

Prediabetes

Type 1 or Type 2?

Type 1 Diabetes

Insulin Types

Insulin Regimens and Targets

CGM, Pumps and Closed Loop

Living with Type 1

Children and Young People

Type 2 Diabetes

Lifestyle, Weight Loss and Remission

Drug Treatment: The NICE Pathway

Metformin

SGLT2 Inhibitors

GLP-1 Agonists and Tirzepatide

DPP-4 Inhibitors

Sulfonylureas

Pioglitazone

Insulin in Type 2

Glucose, BP and Lipid Targets

MODY

LADA

Pancreatic Diabetes

Endocrine and Drug-induced Diabetes

Steroid-induced Hyperglycaemia

Rare Forms

Hypoglycaemia

DKA: Recognition

DKA: Management

Euglycaemic DKA

Hyperosmolar Hyperglycaemic State

Complications and Annual Review

Retinopathy

Diabetic Kidney Disease

Peripheral Neuropathy

Autonomic Neuropathy

Mononeuropathy and Amyotrophy

The Diabetic Foot

Charcot Foot

Cardiovascular Disease

Skin and Infections

Pre-existing Diabetes in Pregnancy

Gestational Diabetes

Hospital and Surgery

Sick Day Rules

Driving

Older Adults and End of Life

Drug Reference Table

Spot the Diagnosis

Exam-style Scenarios

Key Points

Guidelines and Further Reading

Categories