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Type 2 Diabetes (T2DM)

NICE guideline [NG28] Type 2 diabetes in adults: management. Last updated: Jun 2022.

NICE CKS Diabetes – type 2. Last revised: Jul 2025.

Background Information

Definition

T2DM is defined as a chronic metabolic disorder characterised by hyperglycemia resulting from a combination of peripheral ​​​​​​insulin resistance and relative insulin deficiency.

Pathophysiology

2 main mechanisms that contribute to T2DM: [Ref]

  • Peripheral insulin resistance (initially)
  • Pancreatic β-cell dysfunction (usually in later stages)
    • Initially, β-cell compensates by increasing insulin secretion
    • However, amylin is co-secreted with insulin → with time amylin can misfold and aggregate into amyloid fibrils
    • Deposition of amyloid fibrils contributes to β-cell dysfunction and death

The above pathophysiological processes are driven by a combination of genetic predisposition and environmental factors (see risk factors).

Risk Factors

Genetic factors: [Ref]

  • Family history of diabetes (1st-degree relatives) is a strong risk factor
  • Ethnicity (Asian, Black African, African Caribbean)
  • Polygenic contribution

Environmental factors: [Ref]

  • Obesity (esp. central obesity / visceral fat) – most important modifiable risk factor
  • Physical inactivity
  • Unhealthy diet (high intake of processed meats, sugar-sweetened beverages, low intake of whole grains and fibres)
  • Socioeconomic deprivation, low education, and psychosocial stress

Medications (that cause hyperglycaemia): [Ref]

  • Systemic glucocorticoids
  • Beta blockers
  • Thiazide diuretics
  • 2nd generation antipsychotics (esp. olanzapine)
  • Protease inhibitors (for HIV)
  • Tacrolimus

Medical conditions: [Ref]

  • Key medical conditions predisposing to T2DM
    • History of gestational diabetes or pre-diabetes
    • Cardiovascular disease, hypertension, dyslipidaemia
    • PCOS
  • Endocrine disorders
    • Cushing’s syndrome
    • Hyperthyroidism
    • Acromegaly
    • Hyperthyroidism and phaeochromocytoma (but usually mild)
  • Pancreatitis disease
    • Haemochromatosis
    • Chronic pancreatitis and pancreatic cancer
    • Cystic fibrosis

Clinical Features

Classic symptoms (NOT specific to T2DM): [Ref]

  • “3 Ps” – classic symptoms of hyperglycaemia
    • Polyuria
    • Polydipsia
    • Polyphagia
  • Unexplained weight loss
  • Fatigue
  • Blurred vision
  • Recurrent infections (esp. candidiasis) / poor wound healing

Cutaneous signs of peripheral insulin resistance: [Ref]

  • Acanthosis nigricans
  • Acrochordons (skin tags)
  • Central obesity

Be aware that the classic symptoms stated above are NOT specific to any type of diabetes. They are simply consequences of hyperglycaemia affecting various body systems.

Features / factors that suggest T2DM:

  • Associated with weight gain and obesity (unlike weight loss in T1DM)
  • Onset >50 y/o
  • Gradual onset
  • Can first present with complications

Complications

Acute Complications

HHS

  • Far more common than DKA in T2DM [Ref]
  • See this article for more details

DKA

  • Rare in T2DM compared to T1DM, but can occur especially in older adults with long-standing T2DM or extreme insulin deficiency [Ref]
  • See this article for more details

Chronic Complications

Microvascular complications: [Ref]

  • Diabetic retinopathy
  • Diabetic nephropathy
  • Diabetic neuropathy +/- charcot arthropathy
  • Diabetic autonomic neuropathy
    • Gastroparesis
    • Sexual dysfunction
    • Orthostatic hypotension
    • Abnormal sweating

Macrovascular disease (from atherosclerosis): [Ref]

  • Coronary artery disease
  • Cerebral vascular disease
  • Peripheral arterial disease

Diabetic foot problems – arise from a combination of peripheral arterial disease and diabetic neuropathy

Diagnosis

Diagnostic Rules

If hyperglycaemia is confirmed by abnormal biochemical tests (below) +/- classic symptoms, and T2DM is suspected clinically, no further tests are needed to diagnose T2DM.

Be aware of features that are suggestive of T1DM (see this article for details on T1DM):

  • Ketosis
  • Rapid weight loss
  • Onset <50 y/o
  • BMI <25 kg/m2
  • Personal and/or family history of autoimmune disease

Diabetes mellitus diagnostic rules:

  • Typical symptoms + 1 abnormal test, or
  • Asymptomatic + 2 abnormal tests (same test on different day or 2 different tests on the same day)

The biochemical cut-offs for diagnosing diabetes mellitus are the same regardless of type:

Test Diabetes Cut-off Pre-Diabetes
Fasting plasma glucose ≥7.0 mmol/L 6.1-6.9 mmol/L (impaired fasting glucose)
Random plasma glucose ≥11.1 mmol/L n/a
2-hour post-oral glucose tolerance test 7.8-11.0 mmol/L (impaired glucose tolerance)
HbA1c ≥48 mmol/mol (6.5%) 42-47 mmol/mol (6.0-6.4%)

A ‘finger prick’ capillary blood glucose level CANNOT be used to diagnose diabetes mellitus.

HbA1c Interpretation

HbA1c should not be used to diagnose diabetes mellitus in the following patient populations: [Ref]

  • All children and young people.
  • Pregnancy – current or recent (< 2 months).
  • Suspected type 1 diabetes, regardless of age
  • Short duration of diabetes symptoms (< 2 months)
  • Patients at high risk of diabetes who are acutely ill
  • Patients recently taking (for < 2 months) medication that may cause rapid glucose rise (e.g., corticosteroids, antipsychotic drugs)
  • Acute pancreatic damage or pancreatic surgery
  • Renal failure
  • Human immunodeficiency virus (HIV) infection

Causes of false HbA1c levels:

Falsely low HbA1c Falsely high HbA1c

(↓ RBC lifespan → less time for glycation)

(↑ RBC lifespan → more time for glycation)

  • Acute blood loss
  • Haemolytic anaemia
  • Haemoglobinopathies
  • Pregnancy
  • Haemodialysis
  • Iron deficiency
  • Vitamin B12 / folate deficiency

Alternative recommended tests if HbA1c monitoring is invalid (due to disturbed erythrocyte turnover, haemoglobinopathies or abnormal haemoglobin type):

  • Quality-controlled plasma glucose profiles 
  • Total glycated haemoglobin estimation (especially useful if abnormal haemoglobin/haemoglobinopathies)
  • Blood fructosamine 

Management

Rescue Therapy

In acute symptomatic hyperglycaemia, consider sulfonylurea or insulin to quickly lower blood sugar.

Long-Term Management

General / Conservative Management

Dietary advice:

  • Eat high-fibre, low-glycaemic-index sources of carbohydrate (e.g. fruit, vegetables, wholegrains and pulses)
  • Choose low-fat dairy products
  • Eat oily fish
  • Control intake of saturated and trans-fatty acids

Lifestyle advice:

  • Lose weight (if overweight)
  • Advice on physical activity
  • Smoking cessation
  • Limit alcohol intake

IMPORTANT, advice on sick-day rules to avoid acute complications like DKA. This is applicable for BOTH type I and II diabetes patients: [Ref]

ALL diabetic patients
  • Increase frequency of monitoring blood glucose and ketones (blood – preferred / urine) to every 2-4 hours
  • Maintain hydration (at least 3L a day to prevent dehydration)
    • If normal / high blood glucose → drink water / carbohydrate-free fluids
    • If low blood glucose → carbohydrate-containing drinks + fast-acting carbohydrate
  • Maintain the person’s normal meal pattern, if possible
    • Replace normal meals with carbohydrate-containing drinks (e.g. milk, fruit juice, sugary drinks) if necessary (e.g. due to reduced appetite)
Patients who take insulin NEVER stop insulin
  • Even if the patient is not eating or vomiting
  • Insulin dose would be maintained or require adjustment based on blood glucose and ketones
Patients who take oral medications Most oral drugs are typically temporarily stopped during acute illness and restarted once the person is  feeling better + eating and drinking for 24-28 hours
  • Metformin (due to risk of lactic acidosis)
  • SGLT-2 inhibitor and GLP-1 agonist (due to risk of euglycaemic DKA)
  • Sulfonylureas (due to risk of hypoglycaemia)

Not directly relevant, other medications like ACE inhibitors, ARBs, diuretics, NSAIDs should also be stopped to reduce the risk of AKI (if there is a risk of dehydration)

Patient should seek medical advice for potential hospital admission if:

  • ↑ Ketone levels (urine ketone >2+ or blood ketones > 3 mmol/L)
  • Persistent vomiting (>2 hours)
  • Unable to keep oral fluids down
  • Signs of severe dehydration
  • Hypoglycaemia (unable to maintain blood glucose >3.9 mmol/L)

Monitoring and Targets

Blood Glucose Monitoring

T2DM should be monitored via HbA1c levels

  • Every 3-6 months initially, and
  • Every 6 months, once HbA1c level is stable

 

HbA1c targets:

  • If the patient is on lifestyle only or 1 drug that does not cause hypoglycaemia: HbA1c 48 mmol/mol (6.5%)
  • If the patient is on sulfonylurea: HbA1c 53 mmol/mol (7.0%)
  • If the patient is on 2 or more drugs: HbA1c 53 mmol/mol (7.0%)

Do not routinely offer self-monitoring blood glucose in T2DM (unlike in T1DM).

 

Only offer self-monitoring if any of the following:

  • Patient is on insulin
  • Evidence of hypoglycaemic episodes
  • Patient is planning pregnancy / is pregnant
  • Patient is on oral medication that may increase risk of hypoglycaemia while driving or operating machinery

 

Only offer intermittently scanned continuous glucose monitoring to:

  • Patients on multiple daily insulin injections, and
  • At least 1 of the following
    • Recurrent / severe hypoglycaemia
    • Impaired hypoglycaemia awareness
    • Inability to self-monitor blood glucose by finger prick

Blood Pressure Monitoring

Blood pressure control and monitoring are important, as patients with T2DM are prone to developing diabetic nephropathy.

 

Blood pressure targets for T2DM are the same as those for diabetic patients

  • Unless there is concurrent CKD with a urine ACR 70 (however, this is a separate indication)
  • Refer to the hypertension article for more details

Pharmacological Management

Note that a lot of students overthink and overcomplicate this section, focusing too much on when exactly to step up and when exactly to add which drug.

In exams, questions tend to provide clean-cut HbA1c (i.e. within range or above range). Students are largely expected to know:

  • Intensify drug treatment if target not met (if within target, usually not necessary)
  • Choice of step 1 drug treatment
  • Choice of further steps of drug treatment relies mainly on the SGLT-2 inhibitor criteria and the side effect / safety profile of other drugs

An important rule to bear in mind is: at any stage, if the patient meets the criteria for SGLT-2 inhibitor (i.e. develops chronic heart failure / atherosclerotic CVD / QRISK >10%) → consider adding or replacing an existing drug with an SGLT-2 inhibitor.

For instance, consider a patient who has developed heart failure, has an HbA1c of 46 mmol/mol (target 48 mmol/mol), and is stable on metformin monotherapy. In strict glycaemic terms, there is no indication to add another drug, as the HbA1c is at target. However, under the “SGLT‑2 rule”, an SGLT‑2 inhibitor should still be considered as an add‑on to metformin because of the new heart failure indication.

Step 1

If the patient has chronic heart failure / atherosclerotic CVD / QRISK ≥10%

  • Offer metforminSGLT-2 inhibitor
  • Don’t start both at the same time: first start metformin, and once tolerability is confirmed, start SGLT-2 inhibitor

All other patients: metformin monotherapy

Always start with standard-release metformin. If the patient cannot tolerate, then attempt modified-release metformin.

Only if the patient cannot tolerate modified-release metformin, consider an alternative drug

  • If the patient meets the criteria for SGLT-2 inhibitor → offer SGLT-2 inhibitor monotherapy
  • Otherwise → offer DPP-4 inhibitor / pioglitazone / sulfonylurea

Step 2

If HbA1c remains >58 mmol/mol (7.5%) despite monotherapy → intensify treatment

Offer dual therapy (add one of the following to the current monotherapy):

  • DPP-4 inhibitor
  • Pioglitazone
  • Sulfonylurea
  • SGLT-2 inhibitor (only if there is chronic heart failure / atherosclerotic CVD / QRISK >10%)

The only clear-cut indication to add a 2nd drug is if HbA1c ≥58 mmol/mol.

If the patient has an HbA1c that is above the agreed target (usually 48 mmol/mol) but is below 58 mmol/L → NICE guideline does NOT give a clean-cut recommendation

  • NICE says that intensification is guided by the individually agreed threshold and shared decision‑making
  • In practice, most local pathways treat this as a “grey zone” and recommend 1) optimise lifestyle, 2) up-titrate metformin to maximum dose (2g per day), 3) check adherence etc.

Step 3

If dual therapy is not controlling HbA1c under the agreed target → consider either of the following:

  • Triple therapy by adding DPP-4 inhibitor / pioglitazone / sulfonylurea / SGLT-2 inhibitor (only if there is chronic heart failure / atherosclerotic CVD / QRISK >10%)

 

  • Insulin (+ metformin) (other oral agents usually stopped to minimise hypoglycaemia risk)
    • 1st line: human isophane insulin (NPH insulin) (once or twice daily basal insulin)
    • 2nd line (1st line option not achieving control): basal bolus insulin regimen or use biphasic insulin twice daily
    • If patient needs assistance to inject insulin: use long-acting insulin (detemir / glargine)

When initiating insulin therapy, metformin and SGLT-2 inhibitors should generally be continued (unless contraindicated). Other glucose-lowering agents, particularly sulfonylureas, are usually stopped to reduce the risk of hypoglycaemia.

Step 4

If triple therapy (including metformin) is not effective → consider switching 1 drug for a GLP-1 mimetic (e.g. liraglutide, semaglutide) if

  • BMI ≥35 kg/m2 + obesity associated medical or psychological problems, or
  • Insulin is not appropriate, or
  • Weight loss would benefit other significant obesity-related comorbidities

T2DM and CKD

Investigation and Diagnosis

ALL T2DM patients should be tested for CKD with:

  • eGFR (creatinine), and
  • Urine ACR (≥3 mg/mmol is defined as clinically important proteinuria)

Management

Offer ACE inhibitor / ARB if ACR >3 mg/mmol (those with T2DM and CKD)

Add SGLT-2 inhibitor (in addition to ACE inhibitor / ARB) if ACR >3 mg/mmol

  • Exact recommendation: offer if >30 mg/mmol and consider if >3 mg/mmol

See this article for more information on CKD management.

DVLA and Diabetes Mellitus

The DVLA guidance on diabetes driving applies to both type 1 and 2 diabetes.

The guidance and restrictions mainly centre around insulin treatment and the occurrence of hypoglycemic episodes, therefore, it is more often applicable to those with T1DM.

When to Notify the DVLA

Inform the DVLA if:

  • Diabetes treated with insulin (type 1 / 2) – a must for all patients
  • Consider if taking medications that can cause hypoglycaemia (e.g. sulfonylurea)

When to Stop Driving

Situations to stop driving IMMEDIATELY and notify the DVLA if:

  • >1 episode of severe hypoglycaemia while awake in the past 12 months
  • Any episode of severe hypoglycaemia while driving
  • Patient developed impaired awareness of hypoglycaemia
  • Visual / peripheral sensation impairment that impairs driving

Starting insulin for less than 3 months may temporarily bar driving, pending medical advice and DVLA notification.

Blood Glucose Monitoring Requirement

For group 1 drivers (car or motorcycle):

  • Check blood glucose at least twice daily on days the person drives
  • Check blood glucose just before driving and at intervals no longer than two hours when driving longer journeys

For group 2 drivers (bus, lorry etc.):

  • Check blood glucose at least twice daily on both driving and non-driving days
  • Must provide 6 weeks of uninterrupted blood glucose records for annual license review

References


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