Respiratory Flashcards
What are some environmental triggers for asthma?
Allergens (pollen, animal dander, dust mites)
Respiratory infections (e.g., viral infections)
Tobacco smoke
Air pollution
Occupational exposures (chemical irritants, industrial dust).
What are the main risk factors for developing asthma?
Personal/family history of atopy
Maternal smoking (during pregnancy and around child)
Low birth weight
Not being breastfed
Exposure to high concentrations of allergens
Air pollution
Hygiene hypothesis: reduced exposure to infections in childhood, leading to a Th2-dominant immune response.
What other atopic conditions are commonly associated with asthma?
Atopic dermatitis (eczema) and allergic rhinitis (hay fever).
How is asthma defined?
Asthma is a chronic inflammatory disorder of the airways secondary to type 1 hypersensitivity, characterized by reversible bronchospasm causing airway obstruction.
What causes bronchoconstriction in asthma?
Contraction of airway smooth muscle triggered by inflammatory mediators such as histamine and leukotrienes.
What is airway remodeling in asthma?
Chronic inflammation leads to structural changes in the airway wall, such as:
Subepithelial fibrosis
Increased smooth muscle mass
Mucus gland hypertrophy
Angiogenesis
What are the common symptoms of asthma?
–> Wheezing: A high-pitched, whistling sound during expiration due to narrowed airways.
–> Cough: Dry or productive, often worse at night or early morning, triggered by allergens, cold air, exercise, or respiratory infections.
–> Dyspnoea (shortness of breath): Caused by bronchoconstriction, airway inflammation, and mucus production, experienced during physical exertion or at rest.
–> Chest tightness: A sensation caused by airway obstruction and increased work of breathing, often accompanied by coughing and shortness of breath.
What objective tests are used to diagnose asthma in patients ≥ 5 years old according to NICE 2017 guidelines?
FeNO (Fractional Exhaled Nitric Oxide):
Adults: Positive if FeNO ≥ 40 parts per billion (ppb).
Children: Positive if FeNO ≥ 35 parts per billion (ppb).
Spirometry:
Obstruction is indicated by an FEV1/FVC ratio < 70% or below the lower limit of normal.
Bronchodilator Reversibility (BDR) Test:
Adults: Positive if FEV1 improves by ≥ 12% and volume increases by 200 ml or more.
Children: Positive if FEV1 improves by ≥ 12%.
What are the key steps in managing asthma according to NICE 2017?
- Newly diagnosed asthma:
SABA as needed. - Not controlled on Step 1 / symptoms ≥ 3/week:
SABA + low-dose ICS. - Not controlled on Step 2:
SABA + low-dose ICS + LTRA. - Not controlled on Step 3:
SABA + low-dose ICS + LABA.
Continue LTRA based on response.
- Not controlled on Step 4:
Switch to MART (low-dose ICS/LABA). - Not controlled on Step 5:
Medium-dose ICS MART or return to fixed-dose ICS + LABA. - Not controlled on Step 6:
High-dose ICS or add a new drug (e.g., LAMA, theophylline).
Seek specialist advice if needed.
MART:
Combined ICS/LABA inhaler for daily and relief use (only with fast-acting LABA).
Inhaled Corticosteroid Doses (Adults):
Low: ≤ 400 mcg budesonide
Moderate: 400-800 mcg
High: > 800 mcg
How are acute asthma exacerbations classified according to NICE?
Moderate Acute Asthma Exacerbation:
Symptoms: Increasing.
PEFR: >50-75% of best/predicted.
Other: No severe features.
Acute Severe Asthma Exacerbation:
PEFR: 33-50% of best/predicted.
RR: ≥ 25 breaths/min.
HR: ≥ 110 beats/min.
Other: Unable to complete sentences in one breath.
Life-Threatening Asthma Exacerbation:
PEFR: <33% of best/predicted.
SpO₂: <92%.
PaO₂: <8kPa.
Other: Silent chest, cyanosis, new arrhythmia, exhaustion, reduced GCS, hypotension.
Near-Fatal Asthma Exacerbation:
PaCO₂: >6kPa (raised) and/or mechanical ventilation required.
What are the common triggers and symptoms of acute asthma exacerbations?
Triggers:
Viruses (e.g., rhinovirus)
Bacteria
Allergens (e.g., mold, pet dander)
Tobacco smoke
Symptoms:
Progressive breathlessness
Cough
Wheeze
Chest tightness
Signs of Severe Exacerbation:
Tachypnoea
Tachycardia
Inability to speak in full sentences
Silent chest
What investigations are recommended for managing acute asthma exacerbations?
PEFR / FEV1
Assesses severity of exacerbation.
PEFR is preferred in acute settings; expressed as a percentage of the patient’s best/predicted score.
Predicted score is based on age and height if best score is unavailable.
SpO₂ Measurement
Normal saturation: >94%.
<92% indicates life-threatening exacerbation requiring urgent treatment and increased risk of hypercapnia.
Pulse oximetry is unreliable in shock or anaemic patients.
Arterial Blood Gas (ABG)
Indicated if SpO₂ <92% or PEFR ≤30% of best/predicted.
Measures PaO₂ and PaCO₂; lower PaO₂ correlates with obstruction severity.
Hypercapnia (PaCO₂ >6kPa) suggests near-fatal attack, correlating with FEV1 around 20% of predicted.
Most patients exhibit respiratory alkalosis; hypercapnia can lead to acidosis.
Venous blood gas may be used if ABG is not possible, though it’s less useful.
Chest X-ray
Not generally required unless another diagnosis (e.g., pneumonia) is suspected.
What are some differential diagnoses to consider in patients presenting with severe acute asthma exacerbation?
–> Acute Exacerbation of COPD
More likely diagnosed later in life, often with a history of smoking (≥20 pack-years).
Lacks diurnal variation and day-to-day worsening typical in asthma.
–> Pneumothorax
Similar presentation but often causes pleuritic pain.
Chest X-ray is essential if pneumothorax is suspected.
–> Foreign Body Aspiration
May cause wheezing with more acute onset.
Differentiated by chest X-ray to identify radiopaque structures.
–> Vocal Cord Dysfunction
Presents with dyspnoea and stridor; can be difficult to differentiate from asthma.
Evidence may be found on video laryngostroboscopy.
–> Pulmonary Embolism
Usually presents more acutely than asthma exacerbation.
Commonly associated with pleuritic pain and haemoptysis, which are not typical in asthma.
What is the management protocol for patients with near-fatal or life-threatening acute asthma?
–> Admission to Hospital
Immediate admission for near-fatal or life-threatening exacerbations.
Admission for severe cases failing to respond to initial treatment.
–> Oxygen Therapy
Start supplemental oxygen if hypoxaemic.
Administer 15L via non-rebreather mask; titrate to maintain SpO₂ 94-98%.
Consider nasal cannulae or Venturi masks.
Initial Treatment
–> High-dose inhaled SABA (e.g., salbutamol, terbutaline).
Standard pressurised metered-dose inhaler (pMDI) or oxygen-driven nebulizer for non-life-threatening cases.
Nebulised beta₂-agonists for life-threatening cases.
–> Corticosteroids
Administer 40-50mg prednisolone orally daily for at least 5 days.
–> Additional Treatments
Nebulised ipratropium bromide (0.5mg every 4-6 hours) for severe cases.
Consider magnesium sulfate (IV or nebulized) and/or intravenous aminophylline if no response to initial treatments.
–> Mechanical Ventilation
Considered for coma, arrest, severe fatigue, or cardiovascular compromise.
Consult senior physicians and anaesthesia for guidance.
Post-Exacerbation Review
identify possible triggers for the attack.
Review inhaler use and technique.
Optimize treatment and develop a plan for preventing further exacerbations.
What are the key features of Chronic Obstructive Pulmonary Disease (COPD)?
Cough: Often productive
Dyspnoea: Difficulty breathing
Wheeze: Whistling sound during breathing
Right-sided Heart Failure: May develop in severe cases, resulting in peripheral oedema
What investigations are recommended for suspected Chronic Obstructive Pulmonary Disease (COPD)?
–> Post-Bronchodilator Spirometry:
FEV1/FVC ratio < 0.7 indicates airflow obstruction
–> Chest X-ray:
Assess for hyperinflation, bullae (can mimic pneumothorax), and flat hemidiaphragm
Exclude lung cancer
–> Full Blood Count:
Exclude secondary polycythaemia
–> Body Mass Index (BMI) Calculation:
Assess nutritional status
What factors should be considered for diagnosing COPD according to NICE?
Age: Patients over 35 years
Smoking History: Current or ex-smokers
Symptoms:
Exertional breathlessness
Chronic cough
Regular sputum production
How is the severity of COPD categorized based on FEV1?
Stage 1 - Mild: FEV1/FVC < 0.7 with FEV1 > 80% predicted; symptoms should be present to diagnose COPD.
Stage 2 - Moderate: FEV1/FVC < 0.7 with FEV1 50-79% predicted.
Stage 3 - Severe: FEV1/FVC < 0.7 with FEV1 30-49% predicted.
Stage 4 - Very Severe: FEV1/FVC < 0.7 with FEV1 < 30% predicted.
What criteria should be assessed to determine if a COPD patient is eligible for long-term oxygen therapy (LTOT)?
Very severe airflow obstruction (FEV1 < 30% predicted)
Severe airflow obstruction (FEV1 30-49% predicted) may also be considered
Cyanosis
Polycythaemia
Peripheral oedema
Raised jugular venous pressure
Oxygen saturations ≤ 92% on room air
What pO2 levels qualify a COPD patient for long-term oxygen therapy (LTOT)?
pO2 < 7.3 kPa
pO2 between 7.3 - 8 kPa if they also have:
Secondary polycythaemia
Peripheral oedema
Pulmonary hypertension
What are the key components of general management for COPD according to the 2018 NICE guidelines?
Smoking cessation advice, offering nicotine replacement therapy, varenicline, or bupropion
Annual influenza vaccination
One-off pneumococcal vaccination
Pulmonary rehabilitation for those functionally disabled by COPD (usually MRC grade 3 and above)
What is the first-line bronchodilator therapy for COPD patients according to NICE?
A short-acting beta2-agonist (SABA) or short-acting muscarinic antagonist (SAMA) is the first-line treatment.
How does NICE recommend determining if a COPD patient has asthmatic or steroid-responsive features?
Previous, secure diagnosis of asthma or atopy
Higher blood eosinophil count
Substantial variation in FEV1 over time (≥ 400 ml)
Substantial diurnal variation in peak expiratory flow (≥ 20%)
What bronchodilator therapy is recommended for COPD patients without asthmatic or steroid-responsive features?
Add a long-acting beta2-agonist (LABA) + long-acting muscarinic antagonist (LAMA). If already using a SAMA, switch to a SABA.
What therapy is recommended for COPD patients with asthmatic or steroid-responsive features?
LABA + inhaled corticosteroid (ICS)
If symptoms persist, offer triple therapy (LAMA + LABA + ICS)
If already using a SAMA, switch to a SABA
When is oral theophylline recommended in COPD management?
Oral theophylline is recommended after trials of short and long-acting bronchodilators or for patients who cannot use inhaled therapy. The dose should be reduced if macrolide or fluoroquinolone antibiotics are co-prescribed.
Under what circumstances does NICE recommend oral prophylactic azithromycin for COPD patients?
Azithromycin prophylaxis is recommended if patients:
Do not smoke
Have optimised standard treatments
Continue to have exacerbations
Have had a CT thorax to exclude bronchiectasis and sputum culture to exclude atypical infections and tuberculosis
Have normal LFTs and an ECG to exclude QT prolongation
What criteria must be met for the use of phosphodiesterase-4 (PDE-4) inhibitors in COPD?
NICE recommends PDE-4 inhibitors like roflumilast for patients with:
Severe COPD (FEV1 < 50% predicted normal)
Two or more exacerbations in the last 12 months despite triple therapy with LAMA + LABA + ICS
What features indicate cor pulmonale in COPD patients, and how should it be managed?
Features: peripheral oedema, raised jugular venous pressure, systolic parasternal heave, loud P2. Management includes loop diuretics for oedema and considering long-term oxygen therapy. ACE inhibitors, calcium channel blockers, and alpha blockers are not recommended.
What are the key factors that improve survival in COPD patients?
Smoking cessation (most important for smokers)
Long-term oxygen therapy (LTOT) in eligible patients
Lung volume reduction surgery in selected patients
What are the most common bacterial causes of acute COPD exacerbations?
Haemophilus influenzae (most common cause)
Streptococcus pneumoniae
Moraxella catarrhalis
What respiratory viruses are commonly associated with COPD exacerbations?
Respiratory viruses account for around 30% of exacerbations
Human rhinovirus is the most important pathogen
What are the clinical features of an acute COPD exacerbation?
Increase in dyspnoea, cough, and wheeze
Increased sputum production, suggestive of an infective cause
Hypoxia and acute confusion in severe cases
What is the NICE recommendation for treating an acute exacerbation of COPD?
Increase the frequency of bronchodilator use (consider nebulisers)
Give prednisolone 30 mg daily for 5 days
Use antibiotics if sputum is purulent or there are signs of pneumonia (first-line options: amoxicillin, clarithromycin, doxycycline)
When do the NICE guidelines recommend hospital admission for a COPD exacerbation?
Severe breathlessness
Acute confusion or impaired consciousness
Cyanosis
Oxygen saturation < 90%
Social reasons (e.g., inability to cope at home)
Significant comorbidity (e.g., cardiac disease or insulin-dependent diabetes)
What oxygen saturation target should be aimed for in COPD patients with risk of hypercapnia during an exacerbation?
An initial oxygen saturation target of 88-92% should be used.
What is the recommended oxygen therapy for COPD exacerbations before blood gas results are available?
Use a 28% Venturi mask at 4 l/min and aim for oxygen saturation of 88-92% in patients with risk factors for hypercapnia but no prior history of respiratory acidosis.
What are the typical bronchodilator treatments for COPD exacerbations?
Beta adrenergic agonists (e.g., salbutamol)
Muscarinic antagonists (e.g., ipratropium)
What corticosteroid therapies are used during severe exacerbations of COPD?
Prednisolone 30 mg orally for 5 days
Intravenous hydrocortisone may be considered in certain cases
When is intravenous theophylline considered for COPD exacerbations?
It may be considered in patients who do not respond to nebulised bronchodilators.
What type of respiratory failure can COPD patients develop during an exacerbation, and what therapy is often used?
Type 2 respiratory failure may develop, and non-invasive ventilation (NIV) is typically used, especially for respiratory acidosis (pH 7.25-7.35).
What is acute bronchitis?
Acute bronchitis is a self-limiting chest infection caused by inflammation of the trachea and bronchi, leading to sputum production and airway swelling.
What is the typical duration and cause of acute bronchitis?
Acute bronchitis usually resolves within 3 weeks, but 25% of patients may still have a cough after that. Viral infections are the main cause, especially in autumn and winter (80% of cases).
What is the presentation of acute bronchitis?
Patients typically present with an acute onset of:
–> cough: may or may not be productive
–> sore throat
–> rhinorrhoea
–> wheeze
The majority of patients with have a normal chest examination, however, some patients may present with:
–> Low-grade fever
–> Wheeze
What are the investigations for acute bronchitis?
acute bronchitis is typically a clinical diagnosis
however, if CRP testing is available this may be used to guide whether antibiotic therapy is indicated
How can acute bronchitis be differentiated from pneumonia based on history and examination?
In acute bronchitis, sputum, wheeze, and breathlessness may be absent, while in pneumonia, at least one is usually present.
Acute bronchitis typically lacks focal chest
signs (like dullness to percussion, crepitations, or bronchial breathing) seen in pneumonia.
Additionally, systemic features such as malaise, myalgia, and fever are often absent in acute bronchitis but common in pneumonia.
What is the recommended management for acute bronchitis?
Management includes analgesia, good fluid intake, and consideration of antibiotics if the patient is systemically unwell, has pre-existing comorbidities, or a CRP level of 20-100 mg/L (offer delayed antibiotics) or >100 mg/L (offer antibiotics immediately). Doxycycline is first-line (not for children or pregnant women), with alternatives like amoxicillin.
What lung diseases can asbestos exposure cause?
Asbestos exposure can lead to a variety of lung diseases, ranging from benign pleural plaques to malignant mesothelioma. Other conditions include pleural thickening, asbestosis, and lung cancer.
What are pleural plaques, and what is their significance in asbestos exposure?
Pleural plaques are benign and do not undergo malignant change. They are the most common form of asbestos-related lung disease, typically occurring after a latent period of 20-40 years, and do not require follow-up.
What is pleural thickening in relation to asbestos exposure?
Pleural thickening is a condition caused by asbestos exposure that may resemble changes seen after empyema or haemothorax. The exact pathophysiology is not fully understood.
What is asbestosis, and how is its severity related to asbestos exposure?
Asbestosis is a lung disease caused by prolonged asbestos exposure, typically with a latent period of 15-30 years. Its severity is related to the length of exposure, leading to lower lobe fibrosis.
What are the features of asbestosis?
Features include dyspnoea, reduced exercise tolerance, clubbing, bilateral end-inspiratory crackles, and lung function tests showing a restrictive pattern with reduced gas transfer. It is treated conservatively, as no interventions offer significant benefit.
What is mesothelioma, and how does it relate to asbestos?
Mesothelioma is a malignant disease of the pleura caused by asbestos exposure, particularly crocidolite (blue asbestos). It presents with progressive shortness of breath, chest pain, and pleural effusion.
What is the prognosis for patients with mesothelioma?
Patients with mesothelioma are typically offered palliative chemotherapy, with limited roles for surgery and radiotherapy. The prognosis is poor, with a median survival of 8-14 months from diagnosis.
How does asbestos exposure relate to lung cancer?
Lung cancer is the most common cancer associated with asbestos exposure, with a synergistic effect with cigarette smoke. Smoking cessation is crucial, as the risk of lung cancer is significantly higher in smokers with a history of asbestos exposure
What is bronchiectasis, and what are its primary effects?
Bronchiectasis involves permanent dilation of the bronchi, leading to sputum accumulation, chronic cough, continuous sputum production, and recurrent infections due to organisms growing in the wide tubes.
What are potential causes of bronchiectasis?
Idiopathic
post infection (Pneumonia)
Whooping cough (pertussis)
Tuberculosis
Alpha-1-antitrypsin deficiency
Connective tissue disorders (e.g., rheumatoid arthritis)
Cystic fibrosis
Yellow nail syndrome
What is the significance of yellow nail syndrome in relation to bronchiectasis?
Yellow nail syndrome is characterized by yellow fingernails, bronchiectasis, and lymphoedema. Patients are stable with good clinical signs, making it notable in exams, though it is rare.
What are the key presenting symptoms of bronchiectasis?
Shortness of breath
Chronic productive cough
Recurrent chest infections
Weight loss
Haemoptysis
What signs may be observed during the examination of a patient with bronchiectasis?
Sputum pot by the bedside
Oxygen therapy (if needed)
Weight loss (cachexia)
Finger clubbing
Signs of cor pulmonale (e.g., raised JVP and peripheral oedema)
Scattered crackles and wheezes in the chest
What investigations are used to diagnose bronchiectasis?
Sputum culture to identify organisms (most common: Haemophilus influenzae, Pseudomonas aeruginosa)
Chest x-ray for tram-track opacities and ring shadows
High-resolution CT (HRCT) is the test of choice for diagnosis.
What is the general management approach for bronchiectasis?
Vaccines (e.g., pneumococcal, influenza)
Respiratory physiotherapy
Pulmonary rehabilitation
Long-term antibiotics (e.g., azithromycin) for frequent exacerbations
Inhaled colistin for Pseudomonas colonization
Long-acting bronchodilators for breathlessness
Long-term oxygen therapy for low oxygen saturation
Surgical lung resection for specific disease areas
Lung transplant for end-stage disease
What is cystic fibrosis (CF), and what causes it?
Cystic fibrosis is an autosomal recessive genetic condition caused by a mutation in the cystic fibrosis transmembrane conductance regulator gene on chromosome 7, most commonly the delta-F508 mutation. It affects mucus glands and leads to thick secretions.
What are the key consequences of the cystic fibrosis mutation?
–> Thick pancreatic/biliary secretions causing blockage and lack of digestive enzymes - billiary ducts blocked leading to liver diseases
–> Low volume thick airway secretions leading to bacterial colonization and infections which lead to progressive lung damage (bronchiectasis)
–> Congenital bilateral absence of the vas deferens in males, resulting in infertility
What is the typical presentation of cystic fibrosis?
CF is screened at birth with a blood spot test. Meconium ileus, characterized by thick, sticky meconium causing bowel obstruction, is often the first sign. Later signs include recurrent respiratory infections, failure to thrive, and gastrointestinal symptoms.
What are common symptoms of cystic fibrosis?
Chronic cough
Thick sputum production
Recurrent respiratory tract infections
Loose, greasy stools (steatorrhoea)
Abdominal pain and bloating
Salty-tasting skin
Poor weight and height gain (failure to thrive)
What signs may indicate cystic fibrosis?
Low weight or height on growth charts
Nasal polyps
Finger clubbing
Crackles and wheezes on auscultation
Abdominal distention
How is cystic fibrosis diagnosed?
Newborn blood spot testing
Sweat test (gold standard, chloride concentration >60mmol/L)
Genetic testing for CFTR gene
What is the sweat test, and why is it important?
The sweat test measures chloride concentration in sweat. It involves inducing sweating with pilocarpine and testing the sweat for chloride levels. A concentration over 60mmol/L confirms cystic fibrosis.
What are common microbial colonisers in cystic fibrosis patients?
Staphylococcus aureus
Pseudomonas aeruginosa
Haemophilus influenzae
Klebsiella pneumoniae
Escherichia coli
Burkholderia cepacia
How is pseudomonas aeruginosa managed in cystic fibrosis?
Pseudomonas colonization leads to increased morbidity. Management includes long-term nebulized antibiotics like tobramycin and oral ciprofloxacin.
What are the key management strategies for cystic fibrosis?
Chest physiotherapy and exercise
High-calorie diet
CREON tablets for pancreatic insufficiency
Prophylactic flucloxacillin
Treatment of chest infections
Bronchodilators (e.g., salbutamol)
Nebulized DNase and hypertonic saline
Regular vaccinations
What are additional treatment options for cystic fibrosis?
Lung transplantation for end-stage respiratory failure
Liver transplantation for liver failure
Fertility treatments for male infertility
Genetic counseling
What monitoring is required for cystic fibrosis patients?
Patients need regular monitoring for bacterial colonization, diabetes, osteoporosis, vitamin D deficiency, and liver failure, typically in specialist clinics every 6 months.
What are the key screening and diagnostic tests for cystic fibrosis, and how are they monitored
–> Newborn Screening: Measures immunoreactive trypsinogen (IRT) levels; elevated levels prompt further testing.
–> Sweat Chloride Test: Gold standard for diagnosis; chloride levels >60 mmol/L are diagnostic.
–> Genetic Testing: Identifies mutations in the CFTR gene for diagnosis and treatment guidance.
–> Sputum Culture: Regular analysis to identify pathogens and guide antibiotic therapy.
–> Pulmonary Function Tests (PFTs): Assess lung function and monitor disease progression.
–> Chest Radiography and CT: Evaluate lung disease severity and identify complications.
–> Blood Tests: Screen for cystic fibrosis-related diabetes via oral glucose tolerance tests.
–> Bone Density Assessment: DXA scans evaluate bone mineral density and identify osteopenia or osteoporosis.
What is interstitial lung disease (ILD)?
ILD includes conditions causing inflammation and fibrosis of lung parenchyma, leading to the replacement of functional lung tissue with non-functional scar tissue.
Key conditions include:
Idiopathic pulmonary fibrosis (IPF)
Secondary pulmonary fibrosis
Hypersensitivity pneumonitis
Cryptogenic organizing pneumonia
Asbestosis
What are the key presenting features of interstitial lung disease?
Shortness of breath on exertion
Dry cough
Fatigue
In IPF, expect:
Bibasal fine end-inspiratory crackles
Finger clubbing
What are the diagnostic methods for interstitial lung disease?
High-Resolution CT Scan (HRCT): Shows “ground glass” appearance.
Spirometry: May be normal or show a restrictive pattern (FEV1 and FVC reduced, FEV1 >70%).
Other Investigations: If unsure, consider lung biopsy or bronchoalveolar lavage (BAL).
What is the general management strategy for interstitial lung disease?
Management is primarily supportive due to poor prognosis:
Remove or treat underlying causes
Home oxygen therapy for hypoxia
Smoking cessation
Physiotherapy and pulmonary rehabilitation
Vaccinations (e.g., pneumococcal, flu)
Advanced care planning and palliative care
Lung transplant (evaluate risks and benefits)
What is idiopathic pulmonary fibrosis (IPF) and its management?
IPF features progressive pulmonary fibrosis with no known cause, presenting insidiously over 3+ months. It primarily affects adults over 50 years old, with a poor prognosis (2-5 years life expectancy).
Medications:
Pirfenidone: Reduces fibrosis and inflammation.
Nintedanib: Inhibits tyrosine kinase to reduce fibrosis.
What are the causes of secondary pulmonary fibrosis?
Secondary pulmonary fibrosis can be caused by:
Medications: Amiodarone, cyclophosphamide, methotrexate, nitrofurantoin.
Conditions: Alpha-1 antitrypsin deficiency, rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, sarcoidosis.
What is hypersensitivity pneumonitis and its management?
Hypersensitivity pneumonitis (extrinsic allergic alveolitis) is an immune response to inhaled allergens, leading to lung inflammation.
Management:
Remove allergen
Provide oxygen if needed
Administer steroids
Examples of Causes: Bird-fancier’s lung, farmer’s lung, mushroom worker’s lung, malt worker’s lung.
What is cryptogenic organizing pneumonia (COP) and how is it treated?
COP involves focal lung inflammation, which can be idiopathic or triggered by infections, inflammatory disorders, medications, or allergens.
Presentation: Symptoms resemble infectious pneumonia.
Diagnosis: Lung biopsy is definitive; treatment involves systemic corticosteroids.
What is pneumonia?
Pneumonia is an infection of the lung tissue, causing inflammation in the alveolar space, often seen as consolidation on a chest X-ray.
How is pneumonia classified based on acquisition?
Community-acquired pneumonia (CAP): Develops in the community.
Hospital-acquired pneumonia (HAP): Develops after more than 48 hours in a hospital.
Ventilator-acquired pneumonia (VAP): Develops in intubated patients in the intensive care unit.
Aspiration pneumonia: Develops due to aspiration of food or fluids, associated with anaerobic bacteria.
What are the presenting symptoms of pneumonia?
Cough
Sputum production
Shortness of breath
Fever
General malaise
Haemoptysis (coughing up blood)
Pleuritic chest pain (sharp pain worsened by inspiration)
Delirium (acute confusion)
What are the characteristic chest signs of pneumonia?
Bronchial breath sounds (harsh inspiratory and expiratory sounds)
Focal coarse crackles
Dullness to percussion
What observations may indicate sepsis secondary to pneumonia?
Tachypnoea (raised respiratory rate)
Tachycardia (raised heart rate)
Hypoxia (low oxygen levels)
Hypotension (shock)
Fever
Confusion
What is the CRB-65 scoring system?
The CRB-65 score assesses pneumonia severity in out-of-hospital patients:
C: Confusion (new disorientation)
U: Urea > 7 mmol/L
R: Respiratory rate ≥ 30
B: Blood pressure < 90 systolic or ≤ 60 diastolic
65: Age ≥ 65 years
