Diabetes Types / History / Examination

Classification and Clinical Features of Diabetes Mellitus

Type 1 Diabetes Mellitus (T1DM)

Traditionally regarded as a childhood or adolescent disease.
However, up to 42% of T1DM cases present between ages 30–60.
Often presents acutely with:
- Polyuria, polydipsia, weight loss
- BMI typically <25 kg/m²
- Rapid onset of symptoms
- Presence of ketonuria (though may be absent)
- Absence of features of metabolic syndrome
- Family or personal history of autoimmune disease
Autoimmune markers:
- Positive GAD (glutamic acid decarboxylase) antibodies and/or IA-2 antibodies in ~90% of patients
C-peptide testing:
- Marker of endogenous insulin secretion
- Secreted in equimolar amounts with insulin from β-cells
- Slower clearance than insulin (half-life ~30 min vs 3–5 min), unaffected by hepatic first-pass metabolism
- Reference ranges:
  - Fasting: 0.3–0.6 nmol/L
  - Postprandial: 1–3 nmol/L
- T1DM diagnostic indicator: C-peptide <0.2 nmol/L (non-fasting)
Clinical use:
- Differentiates endogenous vs exogenous insulin production
- May predict long-term need for insulin and risk of complications

Type 2 Diabetes Mellitus (T2DM)

Usually presents in adults, but increasingly seen in overweight children and adolescents
Features:
- Often asymptomatic
- Frequently associated with metabolic syndrome
- Strong family history
Insulin resistance is the hallmark, though insulin deficiency may develop over time

Latent Autoimmune Diabetes in Adults (LADA)

Also termed Type 1.5 diabetes
Autoimmune diabetes with slower β-cell destruction than classic T1DM
Presents in adults aged 30–50 years, often initially misdiagnosed as T2DM
Clinical clues:
- Lean body habitus, rapid deterioration on oral hypoglycaemics
- Early need for insulin (typically within 1–2 years)
- GAD antibody positivity
- Family or personal history of autoimmune disease
Management:
- Early insulin therapy improves glycaemic control and preserves β-cell function
- GAD antibody testing can guide diagnosis and counselling regarding other autoimmune risks

Monogenic Diabetes

Caused by single gene mutations, accounts for 1–2% of diabetes cases
Inherited in an autosomal dominant fashion (unless de novo)
Common subtypes:
- Neonatal Diabetes Mellitus: Presents before 6 months of age (rare)
- Maturity Onset Diabetes of the Young (MODY):
  - Develops <25 years of age
  - Not insulin-dependent
  - May be misdiagnosed as T1DM or T2DM
  - Common gene mutations: HNF1A, GCK, HNF4A
Management:
- Refer to endocrinologist for genetic testing
- Tailored therapy depending on genetic subtype

Gestational Diabetes Mellitus (GDM)

Defined as glucose intolerance first diagnosed during pregnancy
Typically asymptomatic
Risk factors:
- Previous GDM
- Age ≥40 years
- Ethnicity (South Asian, Aboriginal, Middle Eastern, Pacific Islander, non-Caucasian African)
- Obesity (BMI >35 kg/m²)
- PCOS
- Family history of DM
- Previous macrosomic infant (>4500g or >90th percentile)
- Corticosteroid or antipsychotic use
Screening:
- 26–28 weeks gestation: Non-fasting 50g glucose challenge
- If ≥7.8 mmol/L, proceed to fasting 75g OGTT
Diagnosis (per 75g OGTT):
- Fasting glucose >5.5 mmol/L or
- 2-hour glucose ≥8.0 mmol/L
Long-term risks:
- Postpartum T2DM in:
  - 3.7% by 9 months
  - 13.1% by 5 years
  - 18.9% by 9 years

Medication-Induced Diabetes

Most commonly linked to glucocorticoids (e.g., prednisolone) and atypical antipsychotics (e.g., olanzapine)
May require temporary or permanent hypoglycaemic therapy
If offending agent is withdrawn, glycaemic control may improve, but patients remain at elevated cardiovascular risk and should continue long-term monitoring

Other Causes of Diabetes Mellitus

1. Diseases of the Exocrine Pancreas

Any condition that diffusely damages the pancreas can impair β-cell function and lead to diabetes. Significant pancreatic damage is typically required, with pancreatic cancer being a notable exception (often causing diabetes with less extensive destruction).

Examples include:

Chronic or recurrent pancreatitis
Pancreatic trauma or pancreatectomy
Pancreatic neoplasia
Cystic fibrosis – progressive destruction of pancreatic tissue impairs endocrine function
Hemochromatosis – iron deposition damages islet cells
Fibrocalculous pancreatopathy

2. Endocrinopathies

Certain hormone excess states increase insulin resistance and can precipitate diabetes, particularly in those with underlying β-cell dysfunction. Hyperglycemia may resolve if the hormonal imbalance is treated.

Conditions include:

Acromegaly (↑ growth hormone)
Cushing’s syndrome (↑ cortisol)
Glucagonoma (↑ glucagon)
Pheochromocytoma (↑ catecholamines)
Hyperthyroidism
Somatostatinoma
Aldosteronoma (though less common)

3. Drug- or Chemical-Induced Diabetes

Many agents impair insulin secretion or increase insulin resistance. They may not cause diabetes in isolation but can unmask it in predisposed individuals.

Common agents:

Nicotinic acid (niacin)
Glucocorticoids
Thyroid hormone
β-adrenergic agonists
Thiazide diuretics
Phenytoin (Dilantin)
Interferon therapy

4. Infections

Certain viral infections can damage pancreatic β-cells or trigger autoimmune responses, increasing diabetes risk.

Examples:

Congenital rubella
Cytomegalovirus (CMV)

5. Genetic Syndromes Associated with Diabetes

Some chromosomal or genetic disorders are associated with impaired glucose regulation.

Examples:

Down syndrome
Klinefelter syndrome
Turner syndrome

Early-Onset vs. Older-Onset Type 2 Diabetes: Complication Profile

Individuals diagnosed with type 2 diabetes at a younger age face significantly higher lifetime risks:

Increased lifetime risk of complications
Reduced life expectancy
Twice the prevalence of non-alcoholic fatty liver disease (NAFLD)
Earlier and more severe onset of:
- Microalbuminuria and end-stage renal disease (ESRD)
- Diabetic retinopathy
- Peripheral neuropathy
Higher apolipoprotein B levels, even on statins
Myocardial infarction risk is up to 14× higher vs. age-matched peers (compared to 2–4× in older-onset T2DM)
Early diastolic myocardial dysfunction
Reduced fertility and increased pregnancy complications
Higher risk of early cognitive decline
Greater burden of psychological distress and depression
Decreased work capacity, with associated socioeconomic impact
Overall reduction in quality of life

History:

Symptoms and Presenting Features

General Symptoms of Diabetes

Lethargy
Polyuria, polydipsia, polyphagia
Nocturia
Weight loss
Blurred vision
Frequent fungal or bacterial infections
Poor wound healing
Loss of sensation (touch, vibration, temperature)

Symptoms by Glycaemic State

Hypoglycaemic Symptoms
- Sweating, tremor
- Palpitations
- Confusion, dizziness
- Irritability or altered consciousness
Hyperglycaemic Symptoms
- Polyuria, polydipsia
- Polyphagia
- Weight loss
- Nocturia

Sequelae of Chronic Hyperglycaemia

Fatigue/malaise
Visual disturbances
Neuropathy: numbness, pain (feet/toes), loss of proprioception
Autonomic neuropathy:
- Gastroparesis, nausea
- Bladder dysfunction
- Erectile dysfunction
Recurrent infections (skin, urinary tract)
Delayed wound healing
Poor dental hygiene, gingivitis

Risk Factors and Predisposing Conditions

Medical History

Previous gestational diabetes
Pancreatic diseases (e.g., pancreatitis, neoplasia)
Endocrinopathies:
- Cushing’s syndrome
- Hypo-/hyperthyroidism
Obstructive sleep apnoea
Haemochromatosis
Autoimmune diseases
Family history of diabetes or gestational diabetes

Comorbidities

Obesity/overweight
Hypertension
Dyslipidaemia
Cardiovascular disease (CVD)
Multimorbidity

Clinical Considerations

Complications of Diabetes

Eye: Retinopathy, cataracts, macular oedema
Kidney: Microalbuminuria, diabetic nephropathy, end-stage renal disease
Feet: Neuropathy, foot ulcers, Charcot joint; discuss appropriate footwear
Other: Sexual dysfunction, gastroparesis, depression, periodontal disease

Assessment and History-Taking

Specialist Care and Surgical History

Endocrinology, nephrology, ophthalmology, podiatry
Bariatric/metabolic surgery
Any pancreatic surgery or trauma

Lifestyle and Psychosocial History

Physical activity level
Smoking history
Dietary patterns
Emotional wellbeing and mental health
Health literacy and diabetes understanding
Social supports and living arrangements

Medication History

Current and past medications (esp. corticosteroids, antipsychotics)
Complementary/alternative therapies
Diabetes therapies and devices (e.g., insulin, GLP-1, pumps, CGM)

Monitoring and Preventive Care

Self-Monitoring and Technology

Routine and non-routine SMBG (self-monitoring blood glucose)
Continuous glucose monitoring (CGM) or flash monitoring
Insulin pump use
NDSS enrolment and access to support services

Immunisations

Annual influenza vaccine
Pneumococcal vaccine
Tetanus as per general adult guidelines

Reproductive and Occupational Considerations

Pregnancy and Contraception

Pregnancy planning
Safe contraceptive options in diabetes

Driving and Occupation

Assess driving fitness per Austroads “Assessing Fitness to Drive”
Special considerations for high-risk occupations (e.g., diving, machinery)

Examination

Clinical Signs of Insulin Resistance

Acanthosis nigricans
- Hyperpigmented, velvety thickening of the skin
- Commonly located in intertriginous areas: neck, axillae, and groin
Skin tags (acrochordons)
- Benign, pedunculated skin growths
- Often skin-coloured or slightly darker
- Common sites: neck, axillae, eyelids, and trunk
Central (abdominal) obesity
- Defined by:
  - Elevated waist circumference
  - High waist-to-hip and waist-to-thigh ratios
Hirsutism
- Excess terminal hair growth in a male pattern distribution
- Often observed on the face, chest, abdomen, or back in women
- Associated with insulin resistance and hyperandrogenism

General Clinical Examination

Anthropometric Measures
- Body Mass Index (BMI)
- Waist circumference (cm)
Vital Signs
- Blood pressure (evaluate for hypertension)
Vascular Assessment
- Central and peripheral pulses
- Signs of peripheral vascular disease
- Absolute cardiovascular disease (CVD) risk assessment, incorporating relevant history and investigations

Assessment of Diabetes-Related Complications

Foot Examination

Neurological:
- Sensation testing:
  - 10 g monofilament (touch)
  - 128 Hz tuning fork (vibration)
- Tendon reflexes
- Signs of peripheral neuropathy
Vascular:
- Pulses (dorsalis pedis, posterior tibial)
- Capillary refill, temperature
- Signs of peripheral arterial disease
Dermatological and Structural:
- Skin integrity, pressure points, callus formation
- Interdigital maceration or fungal infections
- Deformities: Charcot foot, claw toes, bunions

Cardiovascular System

ECG (if indicated):
- Assess for dysrhythmia, ischaemia, or structural heart disease
- Especially relevant in symptomatic patients or those with longstanding diabetes

Genitourinary Assessment

Sexual dysfunction (both male and female):
- Erectile dysfunction, vaginal dryness, anorgasmia
- May reflect autonomic neuropathy

Ophthalmic Examination

Visual acuity (Snellen chart)
Fundus examination (or retinal photography):
- Assess for diabetic retinopathy, macular oedema

Dermatological Inspection

Insulin injection sites:
- Lipohypertrophy or lipoatrophy
Acanthosis nigricans
Fungal infections (e.g., onychomycosis, intertrigo)

Psychological Assessment

Screen for:
- Depressive symptoms
- Diabetes distress using:
  - Problem Areas in Diabetes (PAID) scale
  - Diabetes Distress Scale (DDS)