1. Occupational history techniques

A. Start with broad screening questions

• “What kind of work do you do?”
• “Please describe a usual workday.”
• “Have you ever thought your symptoms might be related to work?”
• “Do symptoms improve on days off, weekends, holidays, or vacation?”
• “Do coworkers have similar symptoms?”
• “Do you have unpaid work, hobbies, or home exposures such as renovations, farming, crafts, or vehicle repair?”

B. Take a chronological job history

• Job title, industry, employer, and location
• Dates of employment and duration
• Main duties rather than job title alone
• Training, job changes, unemployment, and military service
• Work relationships, job satisfaction, conflict, responsibility, and current feelings about work

C. Characterize workplace exposures

• Inhalational: dust, silica, asbestos, fumes, smoke, welding gases, vapors, aerosols, molds, animal proteins
• Chemical: solvents, pesticides, metals, dyes, disinfectants, acids/alkalis, pharmaceuticals
• Physical: noise, vibration, heat/cold, radiation, poor lighting
• Ergonomic: repetitive movements, lifting, awkward posture, prolonged sitting/standing
• Biological: blood/body fluids, animals, infectious patients, waste
• Psychosocial: workload, shift work, harassment, job insecurity, violence, low job control

D. Establish a work-symptom time relationship

• When did symptoms begin relative to starting the job or a new task?
• Do they occur during a shift, after work, or at night?
• Do they improve away from work?
• Was there an acute high-level exposure?
• Have similar symptoms occurred in previous jobs?

E. Assess consequences and safety

• Work restrictions or sickness absence
• Ability to perform duties safely
• Risk to coworkers, family members, or the public
• Need for workplace modification, occupational-health referral, reporting, or compensation documentation
• Patient consent before contacting an employer

2. Cultural considerations in patient assessment

Principles

• Ask the person how they identify themselves. Do not assign identity based on appearance, surname, or language.
• Treat culture as broader than ethnicity or religion. It may include language, migration history, gender identity, sexual orientation, age, socioeconomic position, occupation, disability, caste, spirituality, and community.
• Recognize that one person may hold several intersecting identities.
• Avoid stereotyping. Cultural information should guide individualized care, not replace clinical reasoning.

A. Cultural identity and communication

• Preferred language for speaking and reading
• Health literacy and numeracy
• Preferred name, pronouns, and family role
• Country/place of origin, migration or displacement experience
• Religion, spiritual practices, and community supports
• Need for an interpreter

B. Patient’s explanatory model of illness

• “What do you think is causing this problem?”
• “What worries you most about it?”
• “What name do you give this illness?”
• “What treatments do you think would help?”
• “Who should be involved in decisions about your care?”

C. Physical examination considerations

1. Explain each step and obtain permission, especially before touching sensitive areas.
2. Offer privacy and draping appropriate to the examination.
3. Offer a chaperone and, where feasible, a clinician of the preferred gender.
4. Ask about religious or modesty requirements, including head coverings or clothing.
5. Adapt communication for disability and literacy needs.
6. Avoid misinterpreting behavior: limited eye contact, silence, reluctance to disclose, emotional restraint, or family-centered decision-making may have cultural meanings.
7. Do not overlook discrimination and structural barriers such as racism, migration-related insecurity, financial hardship, workplace exploitation, transport barriers, or prior negative healthcare experiences.

D. Negotiating a treatment plan

• Respect safe traditional remedies and practices.
• Ask specifically about herbs, supplements, traditional medicines, fasting, and healers because of possible toxicity or drug interactions.
• Explain where medical recommendations are non-negotiable for safety.
• Negotiate practical options that fit the person’s beliefs, work, finances, literacy, diet, and family circumstances.
• Include family or community supports only with the patient’s permission.

Brief documentation example

Patient prefers Hindi for detailed health discussions; professional interpreter used. Attributes fatigue partly to work stress and sleep disruption, with no concern about spiritual cause. Requests spouse involvement in treatment decisions. Reports rotating night shifts and solvent exposure at a printing job; headaches worsen during shifts and improve on days off. Uses gloves inconsistently because they interfere with tasks.

Respiratory assessment in occupational lung disease

1. Chest X-ray interpretation in pneumoconioses

Stepwise approach

1. Check film quality
   • Correct patient, date, PA view, inspiration, rotation, exposure/penetration.
   • Compare with prior radiographs whenever possible.
2. Assess the general lungs
   • Lung volumes: hyperinflation, volume loss
   • Distribution: upper versus lower zones; central versus peripheral
   • Type of opacity: small rounded, small irregular, or large opacity
   • Extent/profusion of abnormalities
3. Assess pleura
   • Pleural plaques, diffuse pleural thickening, calcification, costophrenic-angle blunting.
4. Assess hila and mediastinum
   • Lymph-node enlargement or calcification, including eggshell calcification.
5. Look for complications
   • Progressive massive fibrosis
   • Tuberculosis or other infection
   • Lung cancer
   • Emphysema or chronic obstructive pulmonary disease
   • Cor pulmonale in advanced disease

ILO classification: what to report

Typical chest X-ray patterns

Progressive massive fibrosis

Key caution

2. Spirometry in occupational lung disease

Purpose

• Baseline assessment before or early in exposure
• Periodic surveillance of exposed workers
• Detecting airway disease due to dust, fumes, sensitizers, or irritants
• Assessing disability and change over time
• Investigating suspected work-related asthma or chronic obstructive pulmonary disease

Core variables

Major spirometric patterns

Application to specific occupational disorders

Silicosis and coal workers' pneumoconiosis

• Simple disease may have normal spirometry.
• Obstruction can occur due to dust-related small-airway disease, chronic bronchitis, emphysema, or smoking.
• Restriction, low DLCO, hypoxemia, and reduced exercise capacity are more likely in advanced fibrosis or progressive massive fibrosis.
• A normal test does not exclude radiographic pneumoconiosis.

Asbestosis

• Typical physiological pattern is restriction:
  • Low FVC
  • Preserved or elevated FEV1/FVC ratio
  • Reduced TLC
  • Often reduced DLCO
• Pleural plaques alone often cause little or no major spirometric abnormality.

Occupational asthma

• Baseline spirometry may be normal between episodes.
• Obstruction may improve after bronchodilator.
• Serial peak expiratory flow or serial FEV1 measurements at work and away from work are often more informative than a single clinic test.

Work-related COPD

• Persistent obstruction may be present.
• Consider additive effects of smoking plus occupational dust, fumes, biomass smoke, or chemical exposure.

Quality and interpretation principles

• Ensure patient effort is acceptable and repeatable.
• Record height, age, sex, and reference equation used.
• Compare with previous tests, not just predicted values.
• A consistent decline in FEV1 over time may signal harmful exposure even if individual values remain within the reference range.
• Interpret changes after considering smoking, weight change, respiratory infection, equipment variation, and test quality.
• Abnormal spirometry should trigger exposure review, clinical evaluation, and consideration of full pulmonary function testing, imaging, and occupational-medicine referral.

Examination correlation

• Tachypnea and reduced exercise tolerance
• Reduced chest expansion
• Fine late inspiratory basal crackles, especially in asbestosis
• Wheeze or prolonged expiration when airflow obstruction is present
• Cyanosis, signs of pulmonary hypertension, peripheral edema, or raised JVP in advanced respiratory failure/cor pulmonale

Nephrotic syndrome

Definition

• Nephrotic-range proteinuria: >3.5 g/day in adults, or a high spot urine protein-to-creatinine ratio
• Hypoalbuminemia
• Edema: periorbital, dependent, genital, ascites, pleural effusions
• Hyperlipidemia and lipiduria

Important complications

• Venous and arterial thrombosis, including renal-vein thrombosis
• Infection, especially cellulitis and spontaneous bacterial peritonitis
• Acute kidney injury
• Dyslipidemia and accelerated cardiovascular risk
• Malnutrition and vitamin D deficiency

Differential diagnosis of nephrotic syndrome

A. Primary glomerular diseases

B. Secondary causes

C. Conditions that can mimic edema of nephrotic syndrome

Evaluation

Initial tests

• Urinalysis and urine microscopy
• Spot urine protein-to-creatinine ratio or albumin-to-creatinine ratio
• Serum creatinine/eGFR, albumin, electrolytes
• Lipid profile, full blood count
• HbA1c or glucose
• Hepatitis B, hepatitis C, HIV testing when indicated
• ANA, anti-dsDNA, complement C3/C4 if autoimmune disease suspected
• Serum protein electrophoresis, urine immunofixation, and serum free-light chains if amyloidosis or monoclonal gammopathy is possible
• Anti-PLA2R antibody in suspected primary membranous nephropathy
• Renal ultrasound

Role of kidney biopsy

General treatment of nephrotic syndrome

Supportive treatment

1. Treat edema
   • Sodium restriction
   • Loop diuretic, adjusted to edema severity, renal function, blood pressure, and electrolytes
   • Severe edema may require specialist-directed combination diuretics or, rarely, albumin plus diuretic in selected patients
2. Reduce proteinuria and control blood pressure
   • ACE inhibitor or ARB when tolerated
   • Monitor creatinine and potassium after initiation or dose changes
   • SGLT2 inhibitors may be appropriate in selected proteinuric CKD, particularly diabetes, depending on eGFR and the underlying diagnosis
3. Manage cardiovascular risk
   • Statin therapy when indicated
   • Smoking cessation, diabetes control, weight management, vaccination
4. Prevent and detect complications
   • Assess thrombosis risk individually, especially with severe hypoalbuminemia, membranous nephropathy, immobility, previous thrombosis, or additional prothrombotic risk factors
   • Do not prescribe routine anticoagulation to every patient without individualized bleeding-risk assessment
   • Evaluate fever, abdominal pain, cellulitis, chest pain, or new dyspnea promptly for infection or thrombosis
5. Avoid nephrotoxins
   • Avoid NSAIDs where possible
   • Review herbal products, contrast exposure, and other nephrotoxic medicines

Disease-specific therapy

• MCD: glucocorticoids are first-line; relapse-prone disease may need steroid-sparing immunosuppression.
• Primary FSGS: glucocorticoids or calcineurin inhibitor in selected primary disease; treat secondary or genetic FSGS mainly with supportive therapy and cause-directed care.
• Membranous nephropathy: risk-stratified therapy. Rituximab, cyclophosphamide plus glucocorticoids, or calcineurin inhibitors may be selected by nephrology.
• Lupus nephritis: immunosuppressive therapy based on biopsy class.
• Diabetic kidney disease: optimized glycemic and blood-pressure management, RAAS blockade where appropriate, and kidney-protective drugs.

Kidney amyloidosis

What it is

Main causes of renal amyloidosis

Clinical features

• Heavy, often nonselective proteinuria
• Nephrotic syndrome
• Gradual decline in eGFR
• Enlarged kidneys may occur early, though size can later decrease in advanced CKD
• Hypertension may be absent early
• Renal-vein thrombosis may occur due to nephrotic syndrome

Diagnosing renal amyloidosis

1. Confirm amyloid in tissue

2. Type the amyloid correctly

• Immunohistochemistry or immunofluorescence in an experienced pathology service
• Laser microdissection with mass-spectrometry-based proteomics, where available
• Genetic testing when hereditary disease is suspected

3. Investigate the cause

• Serum free-light-chain assay
• Serum and urine immunofixation
• Bone marrow examination
• Cardiac staging and evaluation

• Search for active inflammatory, infectious, or autoinflammatory disease
• Measure and follow inflammatory markers, including CRP and, where available, serum amyloid A

Treatment of renal amyloidosis

1. Support kidney function and nephrotic syndrome

• Sodium restriction and careful diuresis for edema
• RAAS blockade where blood pressure and kidney function allow
• Treat hyperlipidemia and reduce cardiovascular risk
• Assess thrombosis risk
• Avoid NSAIDs and other nephrotoxins
• Prepare for kidney replacement therapy if progressive kidney failure develops

2. AL amyloidosis: suppress the plasma-cell clone

3. AA amyloidosis: suppress the underlying inflammation

• Familial Mediterranean fever: colchicine
• Rheumatologic disease: disease-modifying treatment or biologics appropriate to the underlying illness
• Chronic infection: definitive antimicrobial or surgical source treatment
• Autoinflammatory disorders: cytokine-directed therapy, often IL-1 or IL-6 pathway treatment when indicated

4. Hereditary amyloidosis

5. Kidney transplantation

High-yield distinction