1. RESPIRATORY
Diseases of the Respiratory Tract
Coryza (commoncold)
Acute viral infection of the nasal passages; highly infectious due to rhinoviruses, coronaviruses and
adenoviruses. Spread via droplets, facilitated by overcrowding and poor ventilation.
Symptoms:
 Watery nasal discharge
 Sneezing
 Tiredness
 Mild pyrexia (fever)
 Malaise
 Sore nose and throat
Complications:
 Sinusitis
 Acute bronchitis
 Secondary infections (minority)
 Otitis media (sore ear)
Investigations: none really needed.
Treatment: herbal extracts, bed rest, fluids, isolation.
Sinusitis
Bacterial/fungal infection of paranasal sinuses, usually preceded by Coryza. Can occur with asthma.
Symptoms:
 Frontal headache, facial pain
 Purulent rhinorrhoea
 Fever
 Acute: lasts 1 week-1 month
 Subacute: 1-3 months
 Chronic: >3 months
Investigations: CT of paranasal sinuses, MRI to demonstrate bony landmarks
Treatment:
 Nasal decongestants (xylometazoline)
 Broad-spec antibiotics (co-amoxiclav)
 Topical corticosteroid (fluticasone
propionate nasal spray)
 FESS for ventilation and drainage
Rhinitis
Sneezing attacks, nasal blockage/discharge occurring >1hr on most days.
Seasonal/Intermittent
Limited period of the year; “hayfever” but not restricted to grass pollen.
Symptoms:
 Nasal irritation, rhinorrhoea, sneezing
 Itchy eyes and ears
 Irritated soft palate
 Wheeze
Perennial/Persistent
Throughout the whole year.
Symptoms:
 Nasal blockage, rhinorrhoea  Loss of smell and taste
Allergic: caused by faeces of dust mites; cats; industrial dust and fumes.
Non-allergic: no identifiable stimulus, but eosinophilic granulocytes are present in secretions.
Treatment of rhinitis in general:
 Antihistamines (loratidine, cetirizine)
 Topical corticosteroids (beclometasone,
fluticasone propionate)
 CysLT antagonist (montelukast)
 Anti-inflammatory (sodium cromoglicate)

2. RESPIRATORY
Pharyngitis
Endemic adenovirus infection, causing reddened oropharynx and soft palate and inflamed tonsils.
Symptoms:
 Sore throat
 Tonsillar lymph nodes enlargement
 Localised endemics of fever and
conjunctivitis
Treatment:
 Phenoxymethylpenicillin or cefaclor if severe
Acute Laryngotracheobronchitis
Occasional complication of URTIs, particularly those caused by parainfluenza viruses and measles.
Most severe in children <3yrs. Inflammatory oedema usually present which can spread to vocal cords.
Symptoms:
 Hoarseness
 Barking cough (croup)
 Stridor
 Progressive airway obstruction
Treatment:
 Nebulised adrenaline
 Oral/IM corticosteroids (dexamethasone)
 Oxygen and adequate fluids
 Tracheostomy (rare!)
Acute epiglottitis
Life-threatening airway obstruction in children <5yrs caused by H. influenzae.
Symptoms:
 Severe airflow obstruction  High fever
Complications (mainly of H. influenzae):
 Meningitis
 Diphtheria
 Septic arthritis
 Osteomyelitis
Treatment:
 Urgent endotracheal intubation
 IV antibiotics (ceftazidime,
chloramphenicol)
 Prevention vaccine given to infants
 Do NOT inspect epiglottis until airway is
patent
Influenza
Influenza A (pandemics) and Influenza B (localised outbreaks) incubate within 3 days. Not a cold!
Symptoms:
 Abrupt fever
 Shivering and aching
 Severe headache
 Sore throat + dry cough
Complications:
 Secondary bacterial infection/pneumonia  Encephalomyelitis (rare)
Investigations:
 Increase in complement-fixing antibody (hemagglutinin) between onset and after 1-2 weeks
 Nasal/throat secretion analysis
Treatment:
 Bed rest
 Paracetamol
 Neuraminidase inhibitors (first 48hrs)
 Antibiotics >65yrs (zanamivir, oseltamivir)

3. RESPIRATORY
Acute Bronchitis
“Cold which goes to the chest” – acute infection of bronchi causing them to become inflamed.
Usually arises from Strep. pneumoniae/H. influenzae infections, or in people with COPD.
Symptoms:
 Irritating dry cough; becomes productive
 Wheeze
 Breathlessness
 Mild fever
Treatment: NO antibiotics unless there is underlying chronic lung disease (amoxicillin).
Pneumonia
Acute infection of the lungs causing inflammation. Community, Hospital and Immunocompromised
acquired pneumonia. Mainly caused by Strep. pneumoniae, H. influenzae, Staph. aureus, Influenza A.
Atypical causes: Mycoplasma, Legionella, Chlamydophila pneumoniae/psittaci, coxiella burnetti.
Symptoms:
 Fever and rigors
 Pleuritic chest pain
 Anorexia
 Breathlessness
 Cough – dry or productive
Investigations:
 CXR consolidation, effusions,
collapse
 FBC + U&Es, CRP
 Sputum culture to detect organisms
 CURB65 for CAP
Treatment:
 Antibiotics
o CAP (see Antibiotic Man)
 Mild/Moderate: (7 days) oral amoxycillin + clarythromycin,
If penicillin allergy doxycycline + levofloxacin/moxifloxacin
 Severe: (10 days) IV co-amoxiclav + clarithromycin/doxycycline
If penicillin allergy levofloxacin + clarythromycin
o HAP
 Severe: (7-10days) IV amoxicillin + metronidazole + gentamicin
 Non-severe: (7 days) amoxicillin + metronidazole
o Specific
 Staph. aureus = flucloxacillin/vancomycin if MRSA
 Klebsiella = cefotaxime
 Pseudomonas = ceftazidime, ciprofloxacin + aminoglycide
 Mycoplasma = clarithromycin/ciprofloxacin
 Legionella = levofloxacin/moxifloxacin/consider rifampicin
 Chlamydophila = doxycycline
 Pneumocystis jiroveci = co-trimoxazole

4. RESPIRATORY
COPD (Chronic ObstructivePulmonary Disease)
Encompasses 2 main clinical syndromes: chronic bronchitis and emphysema.
Characterised by airflow obstruction that is irreversible.
Symptoms:
 Productive cough
 Wheeze
 Breathlessness
 Infective exacerbations
Complications:
 Hypertension
 Osteoporosis
 Weight loss
 Cor pulmonale
Investigations:
 Smoking history/chronic history of
symptoms
 Family history (α1-antitrypsin deficiency)
 LFTs (reduced FEV1/FVC, low PEFR)
 CXR classically normal
 ABGs desaturate over time
Treatment:
 Smoking cessation and lifestyle advice
 SABA (salbutamol) mild COPD, LABA
(formoterol, salmeterol) mod-sev COPD
 SAMA (ipratropium) or LAMA
(tiotropium)
 Inhaled corticosteroid (beclometasone),
oral corticosteroid if sev (prednisolone)
 Seretide (salmeterol + beclometasone)
 Xanthine (theophylline)
 Anti-mucolytics (carbocysteine)
Treatment of acute exacerbation of COPD:
 Oral prednisolone
 Oxygen (24%)
 Nebulised salbutamol
 Antibiotics if purulent sputum
(amoxicillin, doxycycline)

5. RESPIRATORY
Asthma
Chronic inflammatory condition where reversible obstruction of the airways occurs.
Airflow limitation -> airway hyper-responsiveness -> bronchial inflammation.
Symptoms:
 Chest tightness
 Wheeze
 Dry cough
 Breathlessness (worse at night)
Investigations:
 Allergen skin prick test
 LFTs (reduced PEFR: mod<80%,
severe<50%, life-threatening<30%)
 Bronchial challenge testing (histamine,
methacholine)
 CO transfer (normal in asthma)
Treatment:
 SABA (salbutamol)
 LABA (salmeterol)
o + inhaled corticosteroid (beclometasone)
+ sodium cromoglicate
+ CysLT antagonist (montelukast)
+ oral corticosteroid (prednisolone)
Treatment of acute severe asthma (O SHIT MAn):
 Oxygen (40-60%)
 Salbutamol (nebulised)
 Hydrocortisone (IV)
 Ipratropium (nebulised)
 Theophylline (oral)
 Magnesium sulphate (IV)
 Anaesthetist!

6. RESPIRATORY
Obstructive Sleep Apnoea
Airway becomes closed during sleep; muscles hypotonic during sleep and thus do not open airway.
Partial occlusion results in snoring; complete occlusion results in apnoea (cessation of breathing).
Symptoms:
 Loud snoring
 Daytime sleepiness
 Unrefreshed/restless sleep
 Headache
Risk factors:
 Obesity
 Narrow pharyngeal opening
 Co-existent COPD
 Respiratory depressants
Investigations:
 Epworth Sleepiness Scale
 Overnight pulse oximetry
 Diagnose if >10-15 apnoeas in any 1hr of
sleep
Treatment:
 Nasal Continuous Positive Airway Pressure (via mask during sleep)
 CNS stimulant (modafinil)
Bronchiectasis
Abnormal permanent dilatation of airways, resulting inflammation and thickening of walls.
Mucociliary transport mechanism is impaired and thus recurrent bacterial infections ensue.
Cystic fibrosis = most common cause.
Symptoms:
 Productive cough (yellow-green sputum,
can become haemoptysis)
 Halitosis (bad breath)
 Recurrent febrile episodes, malaise
 Clubbing
 Coarse crackles, pneumonic episodes
Complications:
 Pneumonia, pneumothorax
 Empyema
 Metastatic cerebral abscesses
 Life-threatening haemoptysis
Investigations:
 CXR dilated + thickened bronchi
 CT thickened bronchi, cysts
 Sputum Staph. aureus, Pseudomonas,
HiB
 IgA deficiency
Treatment:
 Postural drainage!
 Antibiotics (mild-cefaclor, ciprofloxacin,
flucloxacillin if S. aureus;
persistent-ceftazidime)
 Bronchodilators + anti-inflammatory
agents
Lung abscess
Localised suppuration assoc. with cavity formation on CXR/CT.
Aetiology: aspiration, TB, Stap/Klebs pneumonia, septic emboli, foreign body inhalation.
Symptoms: persisting pneumonia, foul sputum, malaise, weight loss, raised inf. markers.
Treatment: guided by culture results, surgical drainage.

7. RESPIRATORY
Cystic Fibrosis
Autosomal recessive disorder in which there is a defect in the CFTR gene, a critical chloride channel.
Failed opening of Cl channel -> ↑cAMP, resulting in ↓Cl and ↑Na -> ↑viscosity of airway secretions.
Symptoms:
 Recurrent infections
 Sinusitis, nasal polyps
 Breathlessness
 Haemoptysis
 Steatorrhoea
 Meconium ileus (SI obstruction)
 Malabsorption
 Abnormal teenage milestones
Investigations:
 Family history  Gene testing
Treatment:
 Lifestyle (smoking, vaccines)
 Antibiotics (as per bronchiectasis)
 SABAs, ICS for symptoms
 Inh recombinant DNAse (dornase)
Tuberculosis
Airborne infection spread by droplets by Mycobacterium species. Affects 1/3 of population.
Caseating granulomatous inflammation (necrotic centre; surrounded by epitheloid cells and Langhan’s
giant cells; formation of Ghon focus/complex). Primary=first infection. Latent=asymptomatic, smear –ve.
Symptoms:
 Persistent productive cough (>3weeks) +
occasional haemoptysis.
 Weight loss, night sweats, fever, fatigue
 Hoarseness, pleuritic pain
Investigations:
 CXR consolidation +/- cavitation, fibrosis, calcification, pleural effusion, widening of mediastinum
 Latent: tuberculin skin test/Mantoux test (possible false –ve if previous BCG). If +ve do ifG test.
 Active: obtain tissue/fluid (induced sputum, bronchoalveolar lavage if unproductive cough,
aspiration of pleural fluid/biopsy, pus, ascites, urine, bone marrow, CSF)
 Culture > PCR > ZN stain (but culture takes weeks, PCR is rapid)
Treatment:
 2 months RIPE, 4 months RI
 Rifampicin SE hepatitis, discolouration of
urine/tears, flu-like illness
 Isoniazide SE neuropathy,
agranulocytosis, allergic reaction
 Pyrazinamide SE hepatic toxicity (rare),
reduced renal excretion of urate, gout
 Ethambutol SE colour blindness
developing into blindness
Sarcoidosis
Multisystem non-caseating granulomatous Type IV hypersensitivity disorder of unknown aetiology.
Symptoms:
 Erythema nodosum
 Fatigue, weight loss
 Uveitis
 Peripheral lymphadenopathy
Investigations:
 CXR multiple abnormalities, BHL
 Restrictive lung pattern
 Hypercalcaemia, raised ACE level
 Transbronchial biopsy
Treatment: corticosteroids (oral prednisolone)

8. RESPIRATORY
Wegener’s Granulomatosis
Granulomatous disease predominantly affecting small arteries. Lesions in URT, lungs, kidney.
Symptoms:
 Severe rhinorrhoea ->nasal mucosa ulcer
 Cough, haemoptysis, pleuritic pain
 Occasionally involves skin and nervous
system.
Investigations:
 CXR nodular masses/pneumonia infiltrates with cavitation
 Renal biopsy reveals necrotising microvascular glomerulonephritis
Treatment: responds well to cyclophosphamide or rituximab
Churg-Strauss syndrome
Eosinophilic infiltration with high blood eosinophil count, vasculitis of small arteries and veins.
Predominately affects 40 year old males.
Symptoms:
 Rhinitis and asthma, breathlessness
 Systemic vasculitis (fever, sweats, fatigue,
weight loss, rash)
 Cough
 Difficulty passing urine
 Cold peripheries
Investigations:
 CXR pneumonic shadows (bilateral)  ANCA +ve
Treatment: responds well to corticosteroids
Systemic Lupus Erythematosis
Chronic disease that causes inflammation in various parts of body.
Symptoms:
 Joint pain, fatigue
 Skin rash
 Pleurisy with or w/o effusion
 Effusions (usually small/bilateral)
 Basal pneumonitis (restricted chest
movement due to pleural pain)
Idiopathic Pulmonary Fibrosis
Patchy scarring of lung with collagen deposition and honeycombing. Late onset. Commoner in males.
Symptoms:
 Progressive breathlessness
 Dry cough
 Cyanosis
 Fine bilateral end-inspiratory crackles
 Clubbing
 Assoc. with autoimmune diseases
Investigations:
 CXR initially ground-glass -> honeycomb
 CT bilateral changes, thick-walled cysts
 Restrictive lung pattern, ↓CO transfer
 Anti-nuclear antibodies
Treatment:
 Corticosteroids (oral prednisolone)  Anti-fibrotic (pirfenidone)
For rarer diffuse disease of the lung parenchyma, visit Kumar & Clark p850 -853.

9. RESPIRATORY
Extrinsic Allergic Alveolitis (Hypersensitivity Pneumonitis)
Widespread diffuse inflammatory reaction in small airways and alveoli due to inhalation of foreign
antigens, usually from animals. Cigarette smokers actually have decreased risk. Type III hypersensitivity.
Symptoms (typically several hours after exposure):
 Fever, malaise
 Cough, breathlessness, wheeze
 Coarse end-inspiratory crackles
 Weight loss and IPF features (chronic)
Investigations:
 CXR fluffy upper zone nodular shadows
 CT ground glass opacity
 Restrictive lung pattern, ↓CO transfer
 Raised leucocytes + T cells
Treatment:
 Prevent exposure  Oral prednisolone in early stages
Coal-worker’s Pneumoconiosis
Dust particles typically 2-5 micrometres in diameter are retained in small airways and alveoli.
Simple Pneumoconiosis
More common form; refers to deposition of coal dust in lung.
Symptoms usually COPD-related. CXR fine micronodular shadowing.
Progressive Massive Fibrosis
Round fibrotic masses several cm in diameter develop in upper lobes -> apical destruction of lung.
Necrotic central cavities.
Symptoms:
 Considerable effort dyspnoea  Cough + black sputum
Investigations:
 Rheumatoid factor and anti-nuclear antibodies
 Mixed restrictive/obstructive lung pattern with loss of lung volume, ↓gas transfer
Asbestosis
Fibrosis causes by asbestos dust exposure.
Symptoms:
 Progressive breathlessness, clubbing  Bilateral basal end-inspiratory crackles
No treatment alters progression, but corticosteroids can help symptoms.
For more on occupational lung diseases, visit Kumar & Clark p854 -856.

10. RESPIRATORY
Pneumothorax
Air in the pleural space. May be spontaneous (tall, thin males) or the result of trauma to the chest.
Symptoms:
 Sudden onset pleuritic pain
 Increasing breathlessness
 Pallor, tachycardia
 Mediastinal shift (tension pneumothorax)
Treatment:
 Needle aspiration (2nd
IC space, mid-
clavicular line)
 Chest drain if recurs using large bore
cannula
Empyema
Pus in the pleural space. Usually complication of pneumonia. Exudate of pH<7.2 suggestive.
Symptoms:
 Ongoing fever  Persistent pneumonic symptoms
Treatment: surgical drainage.
Pleural Effusions
Excessive fluid in the pleural space.
Transudate = protein <30g/l, LDH <200, ratio <0.6. Heart failure, nephrotic syndrome, pericarditis.
Exudate = protein >30g/l, LDH >200. Pneumonia, cancer, TB, autoimmunity, MI, pancreatitis.
Symptoms: breathlessness, sometimes chest pain but rarely.
Investigations:
 Clinically detect when >500ml present
 CXR detects when >300ml present, obliterated costophrenic angle, raised hemidiaphragm
Treatment: treat underlying cause but drain if empyema (purulent fluid).
Cor Pulmonale (Pulmonary Hypertension/Right Heart Failure)
Fluid overload secondary to lung disease. Fluid retention due to failure of excretion of sodium and water
by hypoxic kidney rather than heart failure.
Can occur in advanced COPD: alveolar collapse (emphysema) results in hypoxia which causes
vasoconstriction, increasing pressure in the right side of the heart.
Symptoms:
 Progressive breathlessness
 Ankle oedema
 Parasternal heave
 Pulmonary hypertension
 RV hypertrophy
 Elevated JVP, ascites
For more on disorders of the chest wall and pleura, visit Kumar & Clark p862 -863.

11. RESPIRATORY
Respiratory Failure
Occurs when gas exchange is inadequate, resulting in hypoxia. It is defined as PaO2 <8kPa, subdivided
according to PaCO2 level.
Type I Respiratory Failure = hypoxia (PaO2 < 8kPa) with normal or low PaCO2
Aetiology:
o Pneumonia
o Pulmonary oedema
o PE, fibrosing alveolitis
o Asthma, emphysema, ARDS
Treatment:
 Treat underlying cause
 Oxygen (15L) non-rebreather (hypoxia)
 Assisted ventilation if PaO2 < 8kPa
despite 60% O2
Type II Respiratory Failure = hypoxia (PaO2 < 8kPa) + hypercapnia (PaCO2 > 6.0 kPa)
Aetiology:
o Pulmonary disease (asthma, COPD, pneumonia, fibrosis, obstructive sleep apnoea)
o Reduced respiratory drive (sedation drugs, CNS tumour/trauma)
o Neuromuscular disease (cervical cord lesion, diaphragmatic paralysis, poliomyelitis, MG, Guillain-
Barre Syndrome)
o Thoracic wall disease (flail chest, kyphoscoliosis)
Treatment:
 Oxygen (24%), recheck ABGs after 20min
 If PaCO2 is steady/lower, increase O2 concentration to 28%
 If PaCO2 rises >1.5kPa and patient is still hypoxic, consider a respiratory stimulant (doxapram) or
assisted ventilation (NIPPV)

12. RESPIRATORY
Lung Cancer
Bronchial carcinoma is the most common.
Symptoms:
 Cough (3 week cough merits a CXR)
 Breathlessness (central tumours occlude large airways)
 Haemoptysis (tumour bleeding into airway)
 Chest pain (peripheral tumour invade the chest wall/pleuritic pain
 Wheeze (monophonic when due to partial obstruction of airway by tumour)
 Hoarseness (compression of the recurrent laryngeal nerve)
 Dysphagia (invasion of phrenic nerve/oesophagus)
Small Cell Carcinoma
Arise from neuroendocrine (APUD) cells.
Often centrally located.
Rapid metastasis.
Squamous Cell Carcinoma
Most common type. Arises from epithelial cells.
Occasionally cavitates; central necrosis.
Local, slow metastasis.
Adenocarcinoma
Most common in non-smokers.
Arises from mucus-secreting glandular cells.
Metastasises widely.
Large Cell Carcinoma
Poorly differentiated.
Metastasises early on.
Investigations:
 CXR may be initially normal due to small lesion/confined to central structures.
Common presentations: mass lesions, pleural effusion (large, unilateral), mediastinal widening or
hilar adenopathy, slow resolving consolidation, collapse, reticular shadowing.
 CT indicates extent of disease. Includes liver, adrenal glands. TNM staging can be done.
 PET characterises extent of mediastinal nodal involvement or distant metastases (2nd
line to CT).
PET + CT for best correlation.
 Assess fitness for surgery.
Treatment:
 Surgery: early stage NSCLC surgery can be curative.
If Stage III, treat with chemotherapy to downstage then surgical resection.
 Radical radiotherapy: for patients with early stage NSCLC but adequate lung function, this is ideal
if surgery is not possible due to co-morbidities.
 Chemotherapy: effective against SCLC only.