Respiratory Flashcards

(198 cards)

1
Q

What is the pathophysiology of idiopathic pulmonary fibrosis?

A

Progressive fibrosis of interstitium of lungs

This condition leads to scarring and stiffening of lung tissue.

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2
Q

What are the clinical presentations of pulmonary fibrosis?

A
  • Progressive exertional dyspnoea
  • Bibasal fine end-inspiratory creps
  • Dry cough
  • Clubbing

These symptoms indicate the progressive nature of the disease.

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3
Q

What is the spirometry result pattern in pulmonary fibrosis?

A

Restrictive pattern

This indicates a reduced lung volume.

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4
Q

What are the blood test results typically seen in pulmonary fibrosis?

A
  • Reduced TLCO
  • ANA positive in 30%
  • RF positive in 10%

These results help in diagnosing and understanding the disease.

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5
Q

What are the CXR findings in pulmonary fibrosis?

A

B/L interstitial shadowing (small, irregular ground-glass opacities) → later progressing to honeycombing

These findings are characteristic of advanced pulmonary fibrosis.

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6
Q

What is the life expectancy for patients with pulmonary fibrosis?

A

3-4 years

This highlights the severity of the disease.

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7
Q

What are the management options for idiopathic pulmonary fibrosis?

A
  • Pulmonary rehab
  • Pirfenidone (antifibrotic agent) or nintedanib (if FVC 50-80% predicted)
  • Lung transplant

These treatments aim to slow disease progression and improve quality of life.

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8
Q

What are the clinical features of Caplan’s syndrome?

A

Massive fibrotic nodules with occupational coal dust exposure in patients with rheumatoid arthritis

This condition is associated with specific occupational hazards.

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9
Q

What are the causes of transudative pleural effusion?

A
  • HF (most common)
  • Low albumin (liver disease, nephrotic syndrome)
  • Malabsorption
  • Hypothyroid
  • Meig’s syndrome (ovarian tumour + ascites + pleural effusion)

Understanding these causes is crucial for diagnosis.

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10
Q

What are the causes of exudative pleural effusion?

A
  • Infection
  • Connective tissue disease
  • Neoplasia
  • PE
  • Yellow nail syndrome
  • Drugs e.g. nitrofurantoin, methotrexate and amiodarone

These conditions often require different management strategies.

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11
Q

What is the classification of transudate and exudate effusion based on protein levels?

A
  • Transudate = protein <30g/L
  • Exudative = protein >30g/L

This classification helps in determining the underlying cause of the effusion.

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12
Q

What is the clinical presentation of pleural effusion?

A
  • Dyspnoea
  • Non-productive cough
  • Chest pain

These symptoms can vary based on the size and cause of the effusion.

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13
Q

What are the clinical signs in pleural effusion?

A
  • Dullness to percussion
  • Reduced breath sounds
  • Reduced chest expansion

These signs help in physical examination and diagnosis.

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14
Q

What conditions are associated with low glucose in pleural fluid?

A
  • Rheumatoid arthritis
  • TB

Low glucose levels can indicate inflammatory processes.

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15
Q

What conditions are associated with raised amylase in pleural fluid?

A
  • Pancreatitis
  • Oesophageal perforation

Elevated amylase levels can suggest specific underlying conditions.

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16
Q

What condition is associated with low C3/C4 in pleural fluid?

A

SLE

This finding can indicate autoimmune processes.

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17
Q

What conditions are associated with heavy blood staining of pleural fluid?

A
  • Mesothelioma
  • PE
  • TB

Blood-stained pleural fluid can indicate serious underlying conditions.

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18
Q

What are the indications for placing a chest drain in infection?

A
  • If pleural tap fluid is purulent/turbid/cloudy
  • If pleural tap fluid is clear BUT pH <7.2

These criteria help in managing empyema and other infections.

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19
Q

What is the indication for insertion of a surgical chest drain rather than a seldinger chest drain?

A

Pleural tap is blood (not just blood-stained fluid)

This indicates a more urgent need for intervention.

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20
Q

What is a trigger for flash pulmonary oedema in undiagnosed renal artery stenosis?

A

Initiation of ACE inhibitor

This can lead to acute pulmonary complications.

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21
Q

What test is used to determine if turbid/milky pleural fluid is due to an empyema?

A

Centrifugation of pleural aspirate → if supernatant is clear, the fluid is due to cell debris and therefore empyema is likely

This test helps differentiate between types of pleural effusions.

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22
Q

What are the CT findings in silicosis?

A
  • Eggshell calcification
  • Upper zone fibrosing lung disease

These findings are characteristic of silicosis.

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23
Q

What are the occupations at risk of silicosis?

A
  • Miners
  • Slate workers
  • Foundries
  • Potteries

These jobs expose workers to silica dust.

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24
Q

What are the CXR findings in silicosis?

A

Upper zone reticular shadowing

This finding is indicative of silicosis.

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25
What does **CXR left linguinal consolidation** indicate?
Loss of left heart border ## Footnote This can suggest underlying pathology in the lung.
26
What are the causes of **hemithorax whiteout** with trachea pulled towards the white out?
* Pneumonectomy * Complete lung collapse * Pulmonary hypoplasia ## Footnote These conditions can lead to significant radiological findings.
27
What are the causes of **hemithorax whiteout** with trachea central?
* Consolidation * Pulmonary oedema * Mesothelioma ## Footnote These conditions can obscure lung fields on imaging.
28
What are the causes of **hemithorax whiteout** with trachea pushed away from white-out?
* Pleural effusion * Diaphragmatic hernia * Large thoracic mass ## Footnote These findings can indicate significant pathology.
29
What are the **CXR findings** in **pulmonary oedema**?
CXR shows characteristic patterns ## Footnote This imaging is crucial for diagnosis.
30
What are the **clinical features** of **granulomatosis with polyangiitis**?
* ENT + respiratory + kidneys * Epistaxis, saddle-shape nose deformity * Haemoptysis * Rapidly progressive glomerulonephritis * Vasculitic rash ## Footnote These features are indicative of this systemic vasculitis.
31
What is the **antibody** associated with **granulomatosis with polyangiitis** (Wegener’s granulomatosis)?
cANCA PR3 ## Footnote This antibody is a key diagnostic marker.
32
What is the **antibody** associated with **eosinophilic granulomatosis with polyangiitis** (Churg-Strauss syndrome)?
pANCA MPO (myeloperoxidase) ## Footnote This helps differentiate it from other vasculitides.
33
What is the **antibody** associated with **microscopic polyangiitis**?
pANCA MPO ## Footnote This is important for diagnosis.
34
What are the **renal biopsy findings** in **granulomatosis with polyangiitis**?
* Epithelial crescents in Bowman’s capsule * Pauci-immune necrotising crescentic glomerulonephritis ## Footnote These findings are critical for diagnosis.
35
What is the **induction therapy** for **granulomatosis with polyangiitis**?
* High-dose steroids + cyclophosphamide (if severe) WITH mesna * Rituximab is an alternative to cyclophosphamide * PLEX ## Footnote This treatment regimen is aimed at controlling severe disease.
36
What is the **indication for giving mesna** with cyclophosphamide?
Cyclophosphamide can cause haemorrhagic cystitis → mesna binds and detoxifies acrolein (metabolite of cyclophosphamide) which protects bladder lining and prevents haemorrhagic cystitis ## Footnote This is a critical protective measure during treatment.
37
What is the **maintenance therapy** for **granulomatosis with polyangiitis**?
Azathioprine or methotrexate after remission ## Footnote This helps maintain remission and prevent relapse.
38
What is the **prognosis** in **granulomatosis with polyangiitis**?
* Untreated disease is fatal * 5-year survival >80% with treatment * Median survival ~8-9 years ## Footnote Early diagnosis and treatment significantly improve outcomes.
39
What is the **onset of pleural plaques** following exposure?
20-40 years ## Footnote This long latency period is important for monitoring at-risk individuals.
40
What follow-up is required for **pleural plaques** and why?
No follow-up required as they are benign and do not undergo malignant change ## Footnote This reduces unnecessary healthcare burden.
41
What are the **CXR findings** in **pleural plaques**?
CXR shows characteristic patterns ## Footnote This imaging is crucial for diagnosis.
42
What is the **onset of asbestosis** following exposure?
15-30 years where severity is related to length of exposure ## Footnote This highlights the importance of occupational history.
43
What are the **CXR findings** in **asbestosis**?
Lower lobe fibrosis ## Footnote This finding is characteristic of asbestosis.
44
What is the **clinical presentation** of **asbestosis**?
* Dyspnoea * Reduced exercise tolerance * Clubbing * Bilateral end-inspiratory crackles ## Footnote These symptoms indicate lung damage due to asbestos exposure.
45
What are the **spirometry results** in **asbestosis**?
Restrictive pattern with reduced gas transfer ## Footnote This indicates impaired lung function.
46
What is the **management** of **asbestosis**?
Treated conservatively - no interventions offer a significant benefit ## Footnote Supportive care is the mainstay of treatment.
47
What is the **pathophysiology** of **mesothelioma**?
Malignant disease of the pleura ## Footnote This cancer is strongly associated with asbestos exposure.
48
What type of asbestos is most strongly associated with **mesothelioma**?
Crocidolite (blue) asbestos ## Footnote This type poses the highest risk for developing mesothelioma.
49
What is the **onset of mesothelioma** following exposure?
* Progressive SOB * Chest pain * Pleural effusion ## Footnote Symptoms often appear many years after exposure.
50
What is the **management** of **mesothelioma**?
Palliative chemo ## Footnote Treatment focuses on symptom relief.
51
What are the **CXR findings** in **mesothelioma**?
XR shows large peripheral mass left upper zone ## Footnote This finding is indicative of mesothelioma.
52
What is the **most common form of cancer** associated with **asbestos exposure**?
Lung cancer (not mesothelioma) ## Footnote This highlights the broader risks of asbestos exposure.
53
What are the **causes of upper zone pulmonary fibrosis**?
* Coal workers pneumoconiosis * Hypersensitivity pneumonitis (extrinsic allergic alveolitis), histiocytosis * Ankylosing spondylitis * Radiation * Tuberculosis * Silicosis, sarcoidosis ## Footnote These conditions can lead to upper zone fibrosis.
54
What are the **causes of lower zone pulmonary fibrosis**?
* Most connective tissue diseases (e.g. rheumatoid arthritis) * Asbestosis * Idiopathic pulmonary fibrosis * Drugs (e.g. methotrexate) ## Footnote Understanding these causes is essential for diagnosis.
55
What are the **indications for chest drain insertion**?
* Pleural effusion * Pneumothorax not suitable for conservative management or aspiration * Empyema * Haemothorax * Haemopneumothorax * Chylothorax * In some cases of penetrating chest wall injury in ventilated patients ## Footnote These indications guide clinical decision-making.
56
What are the **relative contra-indications** for chest drain insertion?
* INR > 1.3 * Platelet count < 75 * Pulmonary bullae * Pleural adhesions ## Footnote These factors increase the risk of complications.
57
How do you confirm the **correct position** of chest drain insertion?
* Aspiration of fluid from drainage tube (if inserted for effusion) * Swinging of fluid within drain tubing on inspiration and on CXR ## Footnote These methods ensure proper placement.
58
What are the **complications associated with chest drain insertion**?
* Failure of insertion * Bleeding * Infection * Penetration of the lung * Re-expansion pulmonary oedema ## Footnote Awareness of these complications is crucial for safe practice.
59
How can you **reduce the risk of re-expansion pulmonary oedema**?
Regular clamping of drain tubing to avoid rapid fluid output (drain output should not exceed 1L of fluid/6 hours) ## Footnote This practice helps prevent complications during drainage.
60
What are the **indications for chest drain removal**?
* For fluid drainage → drain should be removed when no output >24 hours and imaging shows resolution of fluid collection * For pneumothorax → drain should be removed when no longer bubbling spontaneously or when patient coughs and ideally when imaging shows resolution of pneumothorax * If for penetrating chest injury, to be reviewed by specialist to confirm appropriate time for removal ## Footnote These criteria help ensure safe removal.
61
What is a complication associated with a **bubbling chest drain** (more significant on coughing) that was inserted for an empyema?
Bronchopleural fistula (i.e. an air leak) ## Footnote This complication can lead to persistent issues.
62
What is a complication associated with a **bubbling chest drain** (no change on coughing) that was inserted for an empyema?
Displacement of chest drain ## Footnote This can lead to ineffective drainage.
63
How do you differentiate between a true **haemothorax** and a **traumatic pleural tap**?
If haematocrit of pleural fluid is more than half of patient’s peripheral blood haematocrit → patient has a haemothorax ## Footnote This distinction is critical for management.
64
What is the **management of pneumothorax**?
* Asymptomatic/minimal symptoms → conservative care (regardless of pneumothorax size) * If symptomatic with no high-risk characteristics → conservative or ambulatory device or needle aspiration * If symptomatic with high-risk characteristics → chest drain ## Footnote Management varies based on symptoms and risk factors.
65
What are the **high-risk characteristics** when assessing a patient with a pneumothorax?
* Haemodynamic compromise (suggesting a tension pneumothorax) * Significant hypoxia * Bilateral pneumothorax * Underlying lung disease * ≥ 50 years of age with significant smoking history * Haemothorax ## Footnote These factors necessitate more aggressive management.
66
What encompasses **conservative care** for a pneumothorax?
* Patient to be reviewed every 2-4 days as an OP * If pneumothorax is secondary, conservative care should be as an IP * If pneumothorax stable, follow up in OP in 2-4 weeks time ## Footnote This approach helps monitor recovery.
67
What is the **management of a patient with pneumothorax** who has a persistent air leak or insufficient lung re-expansion despite chest drain insertion OR recurrent pneumothoraces?
VATS (video-assisted thoracoscopic surgery) to allow for mechanical/chemical pleurodesis +/- bullectomy ## Footnote This surgical intervention can prevent recurrence.
68
What is the **fitness to fly** following pneumothorax?
2 weeks after successful drainage if no residual air OR 1 week post-check XR ## Footnote This guideline helps ensure patient safety.
69
What test distinguishes between a **chylothorax** and a **pseudochylothorax**?
* Chylothorax = high triglycerides + high chylomicrons * Pseudochylothorax = high cholesterol ## Footnote This differentiation is crucial for appropriate management.
70
What are the **causes of chylothorax**?
* Damage to thoracic duct during surgery * Malignant melanoma ## Footnote These conditions can lead to chylothorax.
71
What is the cause of **pseudochylothorax**?
Longstanding fibrotic pleura ## Footnote This condition can mimic chylothorax.
72
What are the **clinical features** of **ABPA**?
* Bronchiectasis * Eosinophilia ## Footnote These features are indicative of allergic bronchopulmonary aspergillosis.
73
What are the **CXR findings** in **ABPA**?
Bilateral pulmonary infiltrates ## Footnote This finding is characteristic of ABPA.
74
What are the **CT findings** in **invasive aspergillosis**?
Cavitating lesion with halo sign ## Footnote This imaging finding is critical for diagnosis.
75
What is the **management of ABPA**?
* 1st line - oral prednisolone * 2nd line - itraconazole ## Footnote These treatments aim to control the allergic response.
76
What is the **clinical presentation of cystic fibrosis in adulthood**?
* Recurrent sinusitis * Pancreatitis * Clubbing * Bronchiectasis ## Footnote These symptoms reflect the systemic nature of cystic fibrosis.
77
What is the **Pseudomonas aeruginosa eradication** regimen?
IV ceftazidime and nebulised tobramycin for 14 days ## Footnote This treatment is crucial for managing infections in cystic fibrosis.
78
What is the **management of cystic fibrosis**?
* Regular chest physio and postural drainage * High calories, high fat * Vitamins * Pancreatic enzyme supplements * Lumacaftor/Ivacaftor (Orkambi) ## Footnote This comprehensive approach addresses multiple aspects of the disease.
79
What is a **contraindication to lung transplant** in cystic fibrosis?
Chronic infection with Burkholderia cepacia ## Footnote This infection poses significant risks during transplantation.
80
What organisms are people with **CF** at risk of passing to each other?
* Burkholderia cepacia complex * Pseudomonas aeruginosa ## Footnote These organisms can lead to severe complications.
81
What is the **mechanism of action of Lumacaftor/Ivacaftor** (Orkambi)?
* Lumacaftor increases the number of CFTR proteins that are transported to the cell surface * Ivacaftor is a potentiator of CFTR that is already at the cell surface, increasing the probability that the defective channel will be open and allow chloride ions to pass through the channel pore ## Footnote This dual action improves chloride transport in cystic fibrosis.
82
What is the **normal function of the cystic fibrosis transmembrane regulator**?
Chloride channel ## Footnote This function is critical for maintaining fluid balance in epithelial tissues.
83
On which **chromosome** is the cystic fibrosis transmembrane conductance regulator gene located?
Chromosome 7 ## Footnote This genetic location is important for understanding inheritance patterns.
84
What are the **contraindications for NIV**?
* Recent facial or upper airway surgery or facial injuries * Recent upper gastrointestinal surgery * Confusion/agitation * Bowel obstruction * Upper airway obstruction * Excessive upper airway secretions * Patient actively vomiting ## Footnote These contraindications help prevent complications during NIV.
85
What are the **indications for NIV**?
* COPD with respiratory acidosis pH 7.25-7.35 * The BTS guidelines state that NIV can be used in patients who are more acidotic (i.e. pH < 7.25) but that a greater degree of monitoring is required (e.g. HDU) and a lower threshold for intubation and ventilation should be ## Footnote These guidelines help in the management of acute respiratory failure.
86
What are the **indications for NIV** in COPD?
* COPD with respiratory acidosis pH 7.25-7.35 * Type II respiratory failure secondary to chest wall deformity, neuromuscular disease or obstructive sleep apnoea * Cardiogenic pulmonary oedema unresponsive to CPAP * Weaning from tracheal intubation ## Footnote BTS guidelines state that NIV can be used in patients who are more acidotic (i.e. pH < 7.25) but require greater monitoring.
87
What are the **recommended initial settings for NIV** in COPD?
* Expiratory Positive Airway Pressure (EPAP): 4-5 cm H2O * Inspiratory Positive Airway Pressure (IPAP): 10 cm H2O (RCP) or 12-15 cm H2O (BTS) * Back up rate: 15 breaths/min * Back up inspiration:expiration ratio: 1:3 ## Footnote These settings help manage respiratory distress in COPD patients effectively.
88
What is the **1st line management** for COPD?
SABA or SAMA PRN ## Footnote This is the initial treatment approach for managing COPD symptoms.
89
What are the **2nd line treatments** for COPD if asthmatic features are present?
Add regular LABA + ICS ## Footnote This approach is taken when asthmatic features are identified in COPD patients.
90
What are the **3rd line treatments** for COPD?
PRN SABA plus regular LABA + LAMA + ICS ## Footnote This combination is used for more severe cases of COPD.
91
What are the **clinical features of cor pulmonale**?
* Peripheral oedema * Raised JVP * Systolic parasternally heave * Loud P2 ## Footnote These features indicate right heart failure due to lung disease.
92
What is the **management of cor pulmonale**?
Loop diuretics for oedema ## Footnote This treatment helps alleviate fluid retention associated with cor pulmonale.
93
What are the **factors that may improve survival** in stable COPD patients?
* Smoking cessation * Long term O2 therapy * Lung volume reduction surgery ## Footnote These interventions can significantly enhance the quality of life and longevity in COPD patients.
94
What are the **criteria for lung volume reduction surgery** in COPD?
* Upper lobe emphysema + low exercise capacity * Upper lobe emphysema + high exercise capacity * Non-upper lobe emphysema + low exercise capacity ## Footnote These criteria help determine candidates for surgical intervention.
95
What are the **indications for assessing a patient for LTOT** in COPD?
* Very severe airflow obstruction (FEV1 < 30% predicted) * Cyanosis * Polycythaemia * Peripheral oedema * Raised jugular venous pressure * Oxygen saturations ≤ 92% on room air ## Footnote These signs indicate the need for long-term oxygen therapy.
96
What are the **criteria for LTOT**?
* pO2 <7.3 on 2x occasions at least 3 weeks apart * pO2 7.3 - 8 PLUS either: * Secondary polycythaemia * Peripheral oedema * Pulmonary HTN ## Footnote These criteria help determine eligibility for long-term oxygen therapy.
97
What are the **causes of decreased DLCO** in restrictive lung disease?
* Idiopathic pulmonary fibrosis * Occupational lung disease * Hypersensitivity pneumonitis * Miliary tuberculosis * Pneumonectomy ## Footnote These conditions can lead to reduced diffusing capacity in the lungs.
98
What are the **clinical features of sarcoidosis**?
* Swinging fever * Polyarthralgia * Erythema nodosum * Lupus pernio (violet plaques on nose/face) ## Footnote These symptoms are characteristic of sarcoidosis and can vary in presentation.
99
What is the **prognosis of Lofgren’s syndrome**?
Excellent prognosis ## Footnote Lofgren's syndrome is a form of sarcoidosis with a favorable outcome.
100
What are the **indications for steroids in sarcoidosis**?
* Patients with chest x-ray stage 2 or 3 disease who are symptomatic * Hypercalcaemia * Eye, heart or neuro involvement ## Footnote Steroids are used to manage severe symptoms and complications in sarcoidosis.
101
What are the **contraindications to surgery** in non-small cell lung cancer?
* Stage IIIb or IV (metastases present) * FEV1 < 1.5 litres * Malignant pleural effusion * Tumour near hilum * Vocal cord paralysis * SVC obstruction ## Footnote These factors indicate that surgery may not be safe or effective.
102
Management of **non-small cell lung cancer** for Stage I-II?
* Lobectomy with hilar/mediastinal lymph node resection + adjuvant chemo (complete resection) * Adjuvant radiotherapy (incomplete resection) ## Footnote This approach is aimed at curative intent.
103
Management of **non-small cell lung cancer** for Stage III and not suitable for surgery?
Chemoradiotherapy ## Footnote This is also aimed at curative intent.
104
Management of **non-small cell lung cancer** for Stage III-IV?
Chemotherapy ## Footnote This is intended to improve survival and quality of life.
105
What is the **clinical presentation** of **hypertrophic pulmonary osteoarthropathy**?
Symmetrical, layered thickening along shafts of radius and ulna ## Footnote This condition is often associated with lung cancers.
106
What cancers are associated with **hypertrophic pulmonary osteoarthropathy**?
* Lung adenocarcinoma * Lung squamous cell cancer ## Footnote These types of lung cancer are commonly linked to this condition.
107
Hormone secretion associated with **small cell lung cancer**?
* ADH * ACTH ## Footnote These hormones can lead to paraneoplastic syndromes.
108
Hormone secretion associated with **squamous cell lung cancer**?
* PTH-rp * TSH ## Footnote These hormones can also cause paraneoplastic effects.
109
What syndrome is associated with **small-cell lung cancer**?
Lambert-Eaton syndrome ## Footnote This syndrome affects neuromuscular transmission.
110
What is the **most common lung cancer** in adolescents?
Carcinoid tumour ## Footnote This type of cancer is more prevalent in younger populations.
111
Management of **small cell lung cancer** T1-2a, N0, M0?
Surgery ## Footnote This is the preferred treatment for early-stage disease.
112
Management of **small cell lung cancer** T1-4, N0-3, M0?
4-6 cycles cisplatin +/- radiotherapy ## Footnote This regimen is used for more advanced stages.
113
Management of **small cell lung cancer** T1-4, N0-3, M1a/b?
6 cycles platinum-based combo chemo + thoracic radiotherapy if good response ## Footnote This approach is for metastatic disease.
114
Where is **small cell lung cancer** most commonly located in the chest?
Central ## Footnote This refers to the location of the tumor within the lungs.
115
From which type of cell does **small cell lung cancer** arise?
APUD cells ## Footnote These are neuroendocrine cells involved in hormone secretion.
116
What investigation provides both **diagnosis and staging** of lung cancer?
EBUS (endobronchial ultrasound guided) mediastinal lymph node sampling ## Footnote This technique is minimally invasive and effective.
117
What lung lesions do not require further investigation or monitoring?
Solitary, solid and non-calcified lung nodules of <5mm in size ## Footnote These nodules are generally considered benign.
118
Follow-up required for **5-6mm lung nodules**?
CT at 1 year ## Footnote This is to monitor for any changes.
119
Follow-up required for **6-8mm lung nodules**?
CT at 3 months ## Footnote This is to assess for potential malignancy.
120
Follow-up required for **>8mm lung nodules**?
Malignancy risk calculation using the Brock model then CT or PET if risk > 10% ## Footnote This helps determine the need for further intervention.
121
Type of lung metastases associated with **renal cell cancer**?
Cannonball mets ## Footnote This term describes the appearance of the metastases on imaging.
122
Flow loop volume in **fixed upper airway obstruction**?
Flattened inspiratory and expiratory limbs of the loop ## Footnote This indicates a fixed obstruction pattern.
123
Flow loop volume in **variable extrathoracic obstruction**?
Inspiratory limb flattened and expiratory limb normal ## Footnote This suggests a dynamic obstruction.
124
Flow loop volume in **variable intrathoracic obstruction**?
Expiratory limb flattened and inspiratory limb normal ## Footnote This indicates a different type of dynamic obstruction.
125
Examples of **fixed upper airway obstruction**?
* Tracheal stenosis * Large goitre * Tracheal tumour * Fixed external compression ## Footnote These conditions lead to a consistent obstruction.
126
Examples of **variable extrathoracic obstruction**?
* Vocal cord dysfunction * Laryngeal tumour * Goitre pressing on trachea at neck level ## Footnote These conditions can change with breathing.
127
Examples of **variable intrathoracic obstruction**?
* Tracheomalacia * Intrathoracic goitre * Proximal tracheal tumour inside chest ## Footnote These conditions also vary with respiratory effort.
128
Clinical presentation of **subglottic stenosis**?
* SOB * Inspiratory wheeze * Not responsive to inhaled steroids ## Footnote These symptoms indicate airway obstruction.
129
Investigation results in **subglottic stenosis**?
* CXR normal * Peak flow reduced * Normal eosinophil count * Obstructive spirometry ## Footnote These findings help confirm the diagnosis.
130
Acquired causes of **subglottic stenosis**?
Intubation ## Footnote This is a common cause of airway narrowing.
131
Most common causative organism of **VAP** in patients ventilated >5 days?
Pseudomonas aeruginosa ## Footnote This organism is often resistant to multiple antibiotics.
132
Pathophysiology of **ARDS**?
Increased permeability of alveolar capillaries → fluid accumulation in alveoli (non-cardiogenic pulmonary oedema) ## Footnote This leads to impaired gas exchange.
133
Causes of **ARDS**?
* Infection incl. COVID * Massive blood transfusion * Trauma * Smoke inhalation * Pancreatitis * Cardio-pulmonary bypass ## Footnote These factors can trigger ARDS.
134
Clinical presentation of **ARDS**?
* Dyspnoea * Tachypnoea * B/L lung crackles * Low O2 sats ## Footnote These symptoms indicate severe respiratory distress.
135
Criteria for **ARDS**?
* Acute onset (within 1 week of known risk factor) * Pulmonary oedema (non-cardiogenic) * pO2 <40kPa ## Footnote These criteria help in diagnosing ARDS.
136
Mortality associated with **ARDS**?
40% mortality ## Footnote This highlights the severity of the condition.
137
Management of **ARDS**?
* Oxygenation/ventilation * Organ support e.g. vasopressors * Treat underlying cause e.g. sepsis * Proning ## Footnote These strategies are essential for patient survival.
138
Causes of **pulmonary eosinophilia**?
* Churg-Strauss syndrome * Allergic bronchopulmonary aspergillosis (ABPA) * Loffler's syndrome * Eosinophilic pneumonia * Hypereosinophilic syndrome * Tropical pulmonary eosinophilia * Drugs: nitrofurantoin, sulphonamides * Less common: Wegener's granulomatosis ## Footnote These conditions can lead to increased eosinophils in the lungs.
139
Clinical features of **Loffler’s syndrome**?
* Transient CXR shadowing * Blood eosinophilia ## Footnote These findings are characteristic of the syndrome.
140
Causative organism of **Loffler’s syndrome**?
Ascaris lumbricoides ## Footnote This parasitic infection is a common cause.
141
Causative organism of **tropical pulmonary eosinophilia**?
Wuchereria bancrofti ## Footnote This organism is transmitted by mosquitoes.
142
Management of **acute eosinophilic pneumonia**?
Steroids (highly responsive) ## Footnote This treatment is effective in reducing inflammation.
143
Management of **tropical pulmonary eosinophilia**?
Diethylcarbamazine ## Footnote This medication is used to treat the infection.
144
Clinical features of **obesity hypoventilation syndrome**?
* Chronic hypoventilation * Obesity * Sleep-disordered breathing (particularly OSA) ## Footnote These features are indicative of the syndrome.
145
Clinical presentation of **obesity hypoventilation syndrome**?
* Obesity * Daytime hypoventilation * Sleep-disordered breathing (loud snoring, nocturnal choking/gasping, excessive daytime sleepiness) * Morning headache * Cognitive dysfunction * RHF (peripheral oedema, JVP raised, hepatomegaly) due to chronic hypoxaemia + pulm HTN ## Footnote These symptoms reflect the impact of obesity on respiratory function.
146
Criteria for **obesity hypoventilation syndrome**?
* Obese * Hypoventilation (daytime ABG - raised CO2 and low O2 in absence of other causes) * Sleep disordered breathing (e.g. OSA) ## Footnote These criteria help in diagnosing the syndrome.
147
Management of **obesity hypoventilation syndrome**?
* Weight loss * CPAP or BiPAP * O2 ## Footnote These interventions improve respiratory function.
148
Assessments for **sleepiness**?
* Epworth Sleepiness Scale - questionnaire completed by patient +/- partner * Multiple Sleep Latency Test (MSLT) - measures the time to fall asleep in a dark room (using EEG criteria) ## Footnote These assessments evaluate daytime sleepiness.
149
Diagnostic test for **OSA**?
Sleep studies (polysomnography) ## Footnote This test monitors various physiological parameters during sleep.
150
Management of **OSA**?
* Weight loss * Continuous positive airway pressure (CPAP) is first line for moderate or severe OSAHS * Intra-oral devices (e.g. mandibular advancement) may be used if CPAP is not tolerated or for patients with mild OSAHS where there is no daytime sleepiness ## Footnote These strategies help alleviate symptoms.
151
ABG findings in **untreated OSA**?
Compensated respiratory acidosis ## Footnote This reflects the chronic retention of CO2.
152
1st line investigation for **asthma**?
Eosinophils or FeNO (fractional nitric oxide) ## Footnote These tests help assess airway inflammation.
153
Which condition can **montelukast** unmask?
Churg-Strauss syndrome (eosinophilic granulomatosis with polyangiitis) ## Footnote This highlights the importance of monitoring eosinophil levels.
154
Most common cause of **occupational asthma**?
Isocyanates ## Footnote These chemicals are prevalent in certain industries.
155
Features of **moderate acute asthma**?
* PEFR 50-75% best or predicted * Speech normal * RR < 25 / min * Pulse < 110 bpm ## Footnote These criteria help classify the severity of an asthma attack.
156
Features of **severe acute asthma**?
* PEFR 33 - 50% best or predicted * Can't complete sentences * RR > 25/min * Pulse > 110 bpm ## Footnote These features indicate a more serious condition.
157
Features of **life-threatening acute asthma**?
* PEFR < 33% best or predicted * Oxygen sats < 92% * 'Normal' pCO2 (4.6-6.0 kPa) * Silent chest, cyanosis or feeble respiratory effort * Bradycardia, dysrhythmia or hypotension * Exhaustion, confusion or coma ## Footnote These signs indicate a critical emergency.
158
Features of **near-fatal acute asthma**?
Raised pCO2 and/or requiring I+V with raised inflation pressures ## Footnote This condition requires immediate medical intervention.
159
Management of **acute asthma**?
* 1st line = oxygen, salbutamol nebs, oral prednisolone (40-50mg OD for 5/7) * 2nd line = ipratropium nebs * 3rd line = IV magnesium sulfate (1.2-2g magnesium sulfate in 50mls NaCl 0.9% over 20 minutes) * 4th line = IV aminophylline * 5th line = I+V, ECMO ## Footnote These steps are taken in a stepwise approach to manage acute exacerbations.
160
Criteria for **discharge following acute asthma**?
* Been stable on their discharge medication (i.e. no nebulisers or oxygen) for 12-24 hours * Inhaler technique checked and recorded * PEF >75% of best or predicted ## Footnote These criteria ensure the patient is safe for discharge.
161
Management of **chronic asthma resistant to treatment** with high eosinophils?
Mepolizumab (anti-IL5 monoclonal ab) ## Footnote This treatment targets eosinophilic inflammation.
162
Blood test results in **theophylline poisoning**?
* Hypokalaemia * Hyperglycaemia ## Footnote These findings are indicative of toxicity.
163
Management of **theophylline poisoning**?
* Consider gastric lavage if <1 hour prior to ingestion * Activated charcoal * Whole-bowel irrigation can be performed if theophylline is sustained release form * Charcoal haemoperfusion is preferable to haemodialysis ## Footnote These interventions help reduce theophylline levels.
164
Most common organism associated with **bronchiectasis**?
Haemophilus influenza ## Footnote This organism is frequently isolated in patients with bronchiectasis.
165
Which **HLA** is associated with **bronchiectasis**?
HLA -DR1 ## Footnote This genetic marker is linked to the condition.
166
Pathophysiology of **bronchiectasis**?
Permanent dilatation of airways secondary to chronic infection or inflammation ## Footnote This leads to impaired airway clearance.
167
Causes of **bronchiectasis**?
* Post-infective: tuberculosis, measles, pertussis, pneumonia * Cystic fibrosis * Bronchial obstruction e.g. lung cancer/foreign body * Immune deficiency: selective IgA, hypogammaglobulinaemia * Allergic bronchopulmonary aspergillosis (ABPA) * Ciliary dyskinetic syndromes: Kartagener's syndrome, Young's syndrome * Yellow nail syndrome ## Footnote These factors contribute to the development of bronchiectasis.
168
CXR findings in **bronchiectasis**?
Tramlines (seen most prominent in left lower zone) ## Footnote This radiological sign indicates airway dilation.
169
CT findings in **bronchiectasis**?
Tram-track and signet ring signs ## Footnote These findings are characteristic of bronchiectasis.
170
Clinical features of **klebsiella pneumonia**?
* Red currant jelly sputum * Often affects upper lobes ## Footnote These features are indicative of Klebsiella infection.
171
Klebsiella type of organism?
Gram negative rod ## Footnote This classification helps in identifying the organism.
172
Populations that **klebsiella** is common amongst?
* Alcoholics * Diabetics ## Footnote These groups are at higher risk for infection.
173
Complication associated with **klebsiella**?
Lung abscess formation and empyema ## Footnote These complications can arise from severe infections.
174
Management of **histoplasmosis**?
* Amphotericin B * Intraconazole ## Footnote These antifungal agents are effective against the infection.
175
Histoplasmosis causative organism?
Histoplasma capsulatum ## Footnote This fungus is commonly found in certain environments.
176
Clinical presentation of **histoplasmosis**?
* URTI symptoms * Retrosternal pain ## Footnote These symptoms can mimic other respiratory infections.
177
MERS (Middle East Respiratory Syndrome) causative organism?
Betacoronavirus MERS-CoV ## Footnote This virus is associated with severe respiratory illness.
178
Risk factor for **MERS**?
Contact with camels including drinking camel milk ## Footnote This exposure increases the risk of infection.
179
Pathophysiology of **cryptogenic organising pneumonia**?
Idiopathic interstitial lung disease with granulation tissue plugs (Masson bodies) in alveoli/alveolar ducts/distal bronchioles ## Footnote Underlying lung architecture is preserved, distinguishing it from fibrotic ILD.
180
Clinical presentation of **cryptogenic organising pneumonia**?
* Weeks-months onset * Dry cough * Progressive dyspnoea * Fever * Poor response to abx for suspected pneumonia ## Footnote These symptoms can be misleading.
181
Bronchoscopy/transbronchial biopsy findings in **cryptogenic organising pneumonia**?
Granulation tissue plugs in distal airways with preserved underlying architecture ## Footnote This finding is characteristic of the condition.
182
CT findings in **cryptogenic organising pneumonia**?
B/L patchy consolidation +/- ground-glass opacities ## Footnote These imaging findings are indicative of the disease.
183
Spirometry in **cryptogenic organising pneumonia**?
Restrictive Reduced DLCO ## Footnote These results reflect impaired lung function.
184
Management of **cryptogenic organising pneumonia**?
* Mild disease = observation * Symptomatic disease = oral steroids ## Footnote This approach is based on disease severity.
185
Most common causative organism of **pneumonia**?
Streptococcus pneumoniae ## Footnote This bacterium is the leading cause of community-acquired pneumonia.
186
Clinical features of **psittacosis**?
* LRTI * Splenomegaly * Epistaxis * Can also get diarrhoea and low WCC ## Footnote These symptoms are characteristic of the infection.
187
Psittacosis causative organism?
Chlamydia psittaci ## Footnote This bacterium is transmitted from birds.
188
Common transmission vector for **psittacosis**?
Birds including parrots ## Footnote This highlights the zoonotic nature of the disease.
189
Pharmacological prophylaxis of **acute mountain sickness**?
Acetazolamide ## Footnote This medication helps prevent symptoms at high altitudes.
190
Treatment for **acute mountain sickness**?
Descent ## Footnote This is the most effective treatment.
191
Management of **HACE (high altitude cerebral oedema)**?
* Descent * Dexamethasone ## Footnote These interventions are critical for patient safety.
192
Management of **HAPE (high altitude pulmonary oedema)**?
* Descent * Nifedipine * Dexamethasone * Acetazolamide * Phosphodiesterase type V inhibitors * Oxygen ## Footnote These treatments help alleviate symptoms and improve oxygenation.
193
Definition of **pulmonary hypertension**?
Sustained elevation of mean pulmonary arterial pressure of >20mmHg at rest ## Footnote This condition can lead to significant morbidity.
194
Causes of **group 1 pulmonary hypertension**?
* Pulmonary arterial hypertension - idiopathic, familial, collagen disorders, congenital heart disease, HIV * Persistent pulmonary hypertension of the newborn ## Footnote These causes are primarily related to the pulmonary vasculature.
195
Causes of **group 2 pulmonary hypertension**?
Pulmonary hypertension secondary to left heart disease - left sided atrial/ventricular/valvular disease (MS/MR) ## Footnote This group is related to heart function.
196
Causes of **group 3 pulmonary hypertension**?
Pulmonary hypertension secondary to lung disease/hypoxia - COPD, interstitial lung disease, sleep apnoea, high altitude ## Footnote These conditions affect lung function and oxygenation.
197
Causes of **group 4 pulmonary hypertension**?
Pulmonary hypertension due to thromboembolic disease ## Footnote This group includes conditions like pulmonary embolism.
198
Causes of **group 5 pulmonary hypertension**?
Miscellaneous conditions - lymphangiomatosis e.g. secondary to carcinomatosis or sarcoidosis ## Footnote This group includes various rare conditions.