Discussion questions are a core component of all short case examinations. In the respiratory station, these discussions commonly cover relevant investigations, differential diagnoses, and knowledge of common conditions.
Here are common questions asked as part of the respiratory short case examination, grouped by underlying pathology.
**Bronchiectasis**
>[!question]- What are the causes of bronchiectasis?
>
>The causes of bronchiectasis can be categorised based on their primary mechanism:
>
>- **Significant, or recurrent, lung infection/injury:**
> - Childhood respiratory infection (e.g. tuberculosis, pertussis)
> - Recurrent respiratory infection (e.g. immunocompromise, chronic aspiration)
> - Autoimmune disease (e.g. Rheumatoid arthritis, Sjogren's, IBD)
>- **Impaired muco-ciliary clearance:**
> - Bronchial obstruction (e.g. malignancy, foreign body)
> - Congenital muco-ciliary defects:
> - Cystic fibrosis: Autosomal recessive disorder affecting CFTR chloride channel. Respiratory, GI, and other manifestations (male infertility).
> - Primary ciliary dyskinesia (PCD): Autosomal recessive disorder, resulting in functional ciliary defect resulting in poor mucous clearance
> - Kartagener's syndrome: Variant of PCD **plus** dextrocardia and situs invertus
> - Young syndrome: Disorder of excessively thick mucous with normal cilia
>- **Comorbid respiratory disease:**
> - Allergic bronchopulmonary aspergillosis (ABPA)
> - Interstitial lung disease with fibrotic change
>[!question]- What is the pathophysiology of bronchiectasis?
>
>- The host response to an infective insult results in transmural inflammation, bronchial wall destruction and dilatation.
>- The destruction and abnormal dilatation of the bronchi impairs muco-ciliary clearance, predisposing to increased bacterial colonisation and respiratory infection
>- This predisposition to respiratory infection results in further bronchial damage/dilatation, impaired mucous clearance, and respiratory infection, which ultimately results in a **vicious cycle** of progressive bronchial destruction and dilatation
>[!question]- What abnormalities can be seen on respiratory function tests in patients with bronchiectasis?
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>Respiratory function testing can be normal in patients with bronchiectasis.
>
>However, patterns that can be seen in bronchiectasis include:
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>- An **obstructive** ventilatory defect (FER <0.7)
>- This may be **associated with a reduction in FVC**.
> - In a patient with bronchiectasis, this can be due to either:
> - Gas trapping (from airway collapsibility/obstruction by secretions)
> - True restriction (e.g. scarring or atelectasis from bronchiectasis, comorbid lung fibrosis)
> - Lung volumes could be performed to evaluate whether this is due to gas trapping, true restriction, or a combination of both
>[!question]- What are the general principles of management in bronchiectasis?
>The main treatment goals in bronchiectasis are to maintain lung health, manage acute/chronic infection, and treat any underlying causes or comorbidities.
>
>- **Preventative/maintenance therapy:**
> - Smoking cessation and avoidance of other airway irritants
> - Chest physiotherapy, routine chest clearance, and pulmonary rehabilitation
> - Use of mucolytic agents and/or airway hydration (nebulised saline)
> - Routine immunisations
>- **Management of acute/chronic infection:**
> - Sputum sampling at periodic intervals and during acute exacerbations, to guide antibiotic therapy and identify *Pseudomonas aeruginosa*
> - Consideration of prophylactic antibiotics (e.g. macrolides, inhaled Tobramycin in some cases)
> - Ensuring adequate duration (10-14 days) and spectrum of antibiotic therapy for exacerbations, based on up-to-date sputum sampling
>- **Management of the underlying cause and comorbidities:**
> - Targeted management of aetiologies such as cystic fibrosis, chronic infection (e.g. NTM, TB), inflammatory disease e.g. RA, Sjogren's), primary immunodeficiency, or recurrent aspiration
> - Assessment for, and treatment of, concurrent airways disease
>[!question]- What is traction bronchiectasis?
>Traction bronchiectasis refers to distortion of the airways that occurs due to mechanical traction on the bronchi, secondary to fibrosis of surrounding lung parenchyma. This leads to airway dilatation and bronchiectasis. This is seen in the setting of fibrotic lung disease.
**Chronic obstructive pulmonary disease (COPD)**
> [!question]- What are the causes of COPD?
> The most common causes of COPD are:
> - Cigarette smoking
> - Other fume/dust exposure (e.g. occupational, household biomass, passive smoke)
>
> Less common causes of COPD include:
> - Alpha-1 antitrypsin deficiency
> - Poorly-controlled asthma with progression to fixed airflow limitation
> - Pulmonary/systemic infections: Tuberculosis, childhood pneumonia, HIV
>[!question]- What are the differential diagnoses for an obstructive ventilatory defect?
>Differentials for an obstructive ventilatory defect include:
>- Chronic obstructive pulmonary disease (COPD)
>- Chronic asthma, with fixed airway obstruction
>- Bronchiectasis
>- Other, less common causes include central airway obstruction or bronchiolitis
>[!question]- What are the general principles of COPD management?
>
> The principles of COPD management are:
>
> - **Smoking cessation** and avoidance of other airway irritants
> - **Pharmacological management:**
> - Inhaled pharmacotherapy: Long-acting bronchodilation (LAMA, or LAMA/LABA), with consideration of ICS if experiencing frequent exacerbations
> - If exacerbations persist, consider addition of other therapies (e.g. prophylactic antibiotics, Dupilumab if Eos >0.3)
> - **Other non-pharmacologic management:**
> - Routine immnunisations (COVID-19, Influenza +/- Pneumococcal)
> - Pulmonary rehabilitation referral
> - **Referral to a Respiratory service** for monitoring/management. In the long-term, consider the role of home oxygen therapy and on-referral to other services as appropriate (e.g. interventional bronchoscopy, transplantation, palliative care).
>[!question]- What are the requirements for long-term oxygen therapy in patients with COPD?
>Patients must have **stopped smoking**, which can be corroborated with a normal carboxyhaemoglobin level. In these patients, arterial blood gas analysis is performed on room air to evaluate for resting, chronic hypoxaemia.
>
>The criteria for long-term oxygen therapy are ***either***:
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>- Arterial PaO2 <55mmHg (equivalent to SpO2 88%)
>- Arterial PaO2 <60mmHg (equivalent to SpO2 90%) **AND** the patient has one of the following: pulmonary hypertension, RV dysfunction, or secondary polycythaemia.
>
**Interstitial lung disease**
>[!question]- What are the causes of chronic interstitial lung disease?
>
>The causes of interstitial lung disease include:
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>- **Idiopathic**: Idiopathic pulmonary fibrosis (IPF)
>- **Connective tissue diseases:** Rheumatoid arthritis, SLE, scleroderma, ANCA, myositis
>- **Inhalational exposure:** Asbestosis, silicosis, hypersensitivity pneumonitis
>- **Medication exposure:** Amiodarone, Methotrexate, Bleomycin, Nitrofurantoin
>
> > [!tip]
> > - In answering this question, suggest focusing on the general categories and citing 1-2 examples each, rather than rattling off an unstructured list of differentials.
> > - Demonstrating a structured, logical approach to your thinking is more valuable than how many differentials you can name. As long as you can remember the general categories, it is typically straightforward to provide 1-2 examples for each.
> > - It is also important to **link** this discussion to your patient. For example, are there signs on clinical examination (e.g. stigmata of CTD, pacemaker/valve disease) that suggest one of these aetiologies?
>[!question]- What are the respiratory causes of nail clubbing?
>
>The respiratory causes of nail clubbing include:
>- Lung malignancy
>- Interstitial lung disease
>- Bronchiectasis
>- Chronic suppurative infection (e.g. lung abscess, empyema, cavitating infection)
>[!question]- How would you investigate a patient with interstitial lung disease?
>> [!tip]
> > *The response to this question is somewhat dependent on what has already been discussed (e.g. if you have already discussed RFTs/HRCT, there is no need to re-cite these and it may be that you start discussion from 'blood tests' onwards). It is also important to cite what you are looking for on these investigations in a concise way.*
> - **Imaging:**
> - **CXR:** Evaluate for reticular or nodular infiltrates suggestive of interstitial lung disease, and features suggestive of the underlying aetiology, such as lymphadenopathy (sarcoidosis) or pleural plaques (asbestosis).
> - **HRCT Chest:** To evaluate pattern, distribution, and extent of any interstitial changes, such as reticular changes, ground-glass opacity, honeycombing, or traction bronchiectasis
>- **Respiratory function tests:**
> - **Spirometry and gas transfer:** May see restrictive pattern and reduced DLCO.
> - **Static lung volumes**: Confirm true restriction (if suggested on spirometry). Expect to see reduced TLC and RV.
>- **Blood tests:**
> - **FBE/CRP:** Evidence of an acute inflammatory process and/or polycythaemia
> - **Autoimmune screen** (e.g. RF, anti-CCP, ANA, dsDNA, ANCA, myositis panel etc.): Evaluate for an underlying CTD
> - **Other tests** to evaluate for an underlying aetiology (e.g. ACE, avian precipitins)
> - **Arterial blood gas**, to evaluate for chronic type 1 respiratory failure
>- **Other tests:**
> - **TTE:** Evaluate for pulmonary hypertension and/or cor pulmonale
>
>[!question]- What are the complications of interstitial lung disease?
>The complications of interstitial lung disease include those related to:
>
>- **Chronic hypoxaemia:** Hypoxaemic respiratory failure, which can lead to pulmonary hypertension and right heart failure (cor pulmonale)
>- **Chronic inflammatory state:** Increased risk of lung malignancy
>- **Complications of therapy**: Increased risk of infection with immunosuppression
**Pleural effusion**
>[!question]- What are the causes of a pleural effusion?
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>There causes of pleural effusion can be classified into transudative and exudative causes.
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>- **Transudative:** Cardiac failure, renal failure (peritoneal dialysis, nephrotic syndrome), hepatic failure (cirrhosis, hepatic hydrothorax), hypoalbuminaemia
>- **Exudative:** Infection (parapneumonic, empyema), inflammation (serositis, pancreatitis, drug reaction), malignancy, trauma (haemothorax)
>[!question]- What are Light's criteria for an exudative pleural effusion?
>
>Light's criteria for an exudative pleural effusion are:
>- (Pleural fluid protein : Serum protein) ratio of >0.5
>- (Pleural fluid LDH : Serum LDH) ratio >0.6
>- Pleural fluid LDH >2/3 the ULN of serum LDH
>
>A pleural effusion is considered exudative if **at least one** criteria is met. Hence, an effusion is transudative if **none** of these criteria are met.
>[!question]- What is the differential diagnosis of dullness to percussion at a lung base?
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>Differentials for this finding can arise from the pleura or nearby structures:
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>- **Pleural:** Pleural effusion, pleural mass/thickening
>- **Lung:** Lung consolidation, lung collapse/obstruction, previous lobectomy
>- **Abdomen**: Raised hemidiaphragm (e.g. phrenic nerve injury/palsy, abdominal mass)
>[!question]- How would you investigate a patient with a pleural effusion?
> > [!tip]
> > *The response to this question depends what has already been discussed (e.g. if you have already discussed pleural fluid results or CT Chest, there is no need to mention these again.*
> >
> - **Pleural fluid sampling**:
> - Biochemistry: Protein, LDH, Glucose, pH
> - Microbiology: Fluid MCS, AFB culture
> - Cytology: Fluid cytology
> - **Chest imaging:**
> - Pleural ultrasound: To characterise size, extent, complexity of effusion
> - CT Chest: To help characterise size, extent, complexity of effusion, and assess for an underlying lung malignancy or other parenchymal findings
> - **Other:**
> - Largely to evaluate for specific aetiologies if these are suggested on examination and/or investigations (e.g. TTE/BNP if heart failure is suspected, CT Abdomen/Pelvis or Mammography if abdominal/breast malignancy suspected)