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Respiratory Flashcards

1
Q

What clinical signs are associated with Pulmonary Fibrosis?

A
  • Clubbing
  • Central cyanosis
  • Tachypnoea
  • Fine end-inspiratory crackles (like Velcro which do not change with coughing
  • Signs associated with autoimmune diseases e.g. rheumatoid arthritis (hands), SLE and systemic sclerosis (face and hands)
  • Signs of treatment e.g. Cushingoid from steroids
  • Discoloured skin (grey) - amiodarone
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2
Q

What investigations would you request in someone who is suspected of having pulmonary fibrosis?

A
  • Bloods: ESR, Rheumatoid factor and ANA
  • CXR: reticulonodular changes, loss of definition of heart border, small lungs
  • ABG: type 1 resp failure
  • Pulmonary Function Tests: FEV1/FVC ratio >0.8 (restrictive) and low TLC (small lungs). Reduced TLco and Kco
  • Bronchoalveolar Lavage: main indication is to exclude infection prior to immunosuppressants plus if lymphocytes>neutrophils indicate a better response to steroids and a better prognosis (sarcoidosis)
  • High-res CT - distribution helps with diagnosis; bibasal subpleural honeycombing typical of UIP; widespread groundglass shadowing more likely to be non-specific interstitial pneumonia often associated with autoimmune disease; if apical in distribution then think of sarcoid ABPA, old TB, hypersensitivity pneumonitia, Langerhan’s cell histiocytosis.
  • Lung Biopsy
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3
Q

How is Pulmonary Fibrosis treated?

A
  • Immunosuppression if likely to be inflammatory
  • Pirfenidone (an anti-fibrotic agent) - for UIP when FEV1 50-80% predicted
  • N-acetyl cysteine - free radical scavenger
  • Single lung transplant - lung transplant patients can present with unilateral fine crackles and contralateral thoracotomy scar with normal breath sounds.
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4
Q

What is the prognosis of Pulmonary Fibrosis?

A
  • Very variable - depends on aetiology
  • Highly cellular with ground glass infiltrate - responds to immunosuppression: 80% 5 year survival
  • Honeycombing CT - no response to immunosuppression - 80% 5-year mortality
  • There is an increased risk of bronchogenic carcinoma
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5
Q

Name some causes of Basal Fibrosis.

A
  • Usual interstitial pneumonia (UIP)
  • Asbestosis
  • Connective Tissue Diseases (except Ank Spond)
  • Asbestosis
  • Aspiration
  • Drug induced: Amiodarone, Bleomycin, Methotrexate
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6
Q

Name some ccauses of upper zone fibrosis.

A
  • Hypersensitivity Pneumonitis (also known as extrinsic allergic alveolitis)
  • Coal worker’s pneumoconiosis
  • Silicosis
  • Sarcoidosis
  • Ank Spond
  • Histiocytosis
  • Tuberculosis
  • Radiation-induced Pulmonary Fibrosis - may develop following radiotherapy for breast or lung cancer. Typically seen between 6-12 months post-radiotherapy course
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7
Q

Name some clinical signs of Bronchiectasis

A
  • Cachexia
  • Tachypnoea
  • Finger Clubbing
  • Mixed character crackles that alter with coughing. Occasional squeaks and wheeze. Sputum +++
  • Cor Pulmonale - ankle swelling, raised JVP, RV heave, loud P2
  • Yellow nail syndrome- yellow nails and lymphoedema
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8
Q

What investigations would you want in someone with suspected Bronchiectasis?

A
  • Sputum culture and cytology
  • CXR - tramlines and ringshadows
  • High-res CT - ‘signet ring’ sign (thickened, dilated bronchi larger than the adjacent vascular bundle)
  • Immunoglobulins: hypogammaglobulinaemia (esp IgG2 and IgA)
  • Aspergillus RAST or skin prick testing: ABPA (upper lobe)
  • Rheumatoid serology
  • Saccharine ciliary motility test: Kartageners
  • Genetic screening: cystic fibrosis
  • History of IBD
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9
Q

Name some causes of Bronchiectasis.

A
  • Congenital: Kartagener’s and Cystic Fibrosis
  • Childhood infections: Measles and TB
  • Immune OVER activity: allergic bronchopulmonary aspergillosis (ABPA), inflammatory bowel disease associated
  • Immune UNDER activity - hypogammaglobulinaemia, Common variable immunodeficiency
  • Aspiration: chronic alcoholics and GORD; localised to RLL.
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10
Q

How do we treat Bronchiectasis?

A
  • Physiotherapy - active cycle breathing
  • Prompt antibiotic therapy for exacerbations
  • Long-term treatment with low dose azithromycin three times per week
  • Bronchodilators/inhaled corticosteroids if there is any airflow obstruction
  • Surgery is occasionally used for localised disease
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11
Q

What complications can arise as a result of bronchiectasis?

A
  • Cor Pulmonale
  • (Secondary) amyloidosis (dip urine for protein)
  • Massive haemoptysis (mycotic aneurysm)
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12
Q

What are the clinical signs of Old TB?

A
  • Chest deformity and absent ribs, thoracoplasty scar
  • Tracheal deviation towards the side of the fibrosis (traction)
  • Reduced expansion
  • Dull percussion but present tactile vocal fremitus
  • Crackles and bronchial breathing
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13
Q

Name the side effects of drugs used to treat TB

A
  • Rifampicin - hepatitis and increased contraceptive pill metabolism
  • Isoniazid - peripheral neuropathy (Pyridoxine to try and reduce risk) and hepatitis
  • Pyrazinamide - hepatitis
  • Ethambutol - retro-bulbar neuritis and hepatitis

Prior to under-going treatment patients must have baseline LFTs and visual acuity checked.

Patients must be told:
- Look at the whites of your eyes every morning - if yellow phone TB nurse
- Notice colours - if red becomes less bright than you expect - ring TB nurse
- If you develop tingling in your toes - keep taking tablets and tell doctor at next clinic app
- Your secretions will turn orange/red. This is because of a dye in the tablet. If you wear contacts they will become permanently stained and should not be worn
- If you are on the OCP, it may fail. Use barrier protection.

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14
Q

Name some clinical signs of a lobectomy.

A
  • Reduced expansion and chest wall deformity
  • Thoracotomy scar: same for either upper or lower lobe
  • Trachea is central
  • Lower lobectomy: dull percussion note over lower zone with absent breath sounds
  • Upper lobectomy: may have normal examination or may have a hyper-resonant percussion note over the upper zone with a dull percussion note at the base where the hemidiaphragm is elevated slightly
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15
Q

What investigations would you order for a patient with a suspected lobectomy?

A
  • CXR - maybe no overt abnormality apparent other than slight raised hemidiaphragm. In health, the R hemidiaphragm should be higher than the L.
  • CT Chest - loss of a lobe with associated truncation of bronchus or pulmonary vessels
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16
Q

What clinical signs can be seen in a patient following a pneumonectomy?

A
  • Thoracotomy scar (indistinguishable from thoracotomy scar performed for a lobectomy)
  • Reduced expansion on side of pneumonectomy
  • Trachea deviated towards the side of the pneumonectomy
  • Dull percussion note throughout hemithorax
  • Absent tactile vocal fremitus beneath the thoracotomy scar
  • Bronchial breathing in the upper zone with reduced breath sounds throughout the remainder of the hemithorax (bronchial breathing is due to transmitted sound from the major airways)
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17
Q

What investigations would you order for a patient with a suspected pneumonectomy?

A
  • CXR - complete white out on side of pneumonectomy. Pneumonectomy space fills with gelatinous material within a few weeks of the operation
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18
Q

What clinical signs would you see in a patient with a suspected Lung Transplant?

A
  • Thoracotomy scar
  • Normal exam on side of scar; may have clinical signs on opposite hemithorax
  • Double lung transplant: clamshell incision - from the one axilla along the line of the lower ribs up to the xiphisternum to the other axilla.
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19
Q

Name some indications for lung transplant.

A
  • Dry conditions: COPD, Pulmonary Fibrosis
  • Wet Conditions: CF, Bronchiectasis or Pulmonary Hypertension
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20
Q

Name some clinical signs associated with COPD

A
  • Inspection: nebulisers/inhalers/sputum pot/dyspnoea/central cyanosis/pursed lips
  • CO2 retention flap, bounding pulse and tar-stained fingers
  • Hyper-expanded
  • Percussion note resonant with loss of cardiac dullness
  • Expiratory polyphonic wheeze (crackles if consolidation too) and reduced breath sounds at apices
  • Cor Pulmonale - raised JVP, ankle oedema, RV heave, loud P2 with pansystolic murmur of tricuspid regurgitation
  • COPD does not cause clubbing therefore, if present consider bronchial carcinoma or bronchiectasis
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21
Q

What are the causes of COPD?

A
  • Environmental: smoking and industrial dust exposure (apical disease)
  • Genetic: alpha1-antitrypsin deficiency (basal disease)
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22
Q

What investigations would you order for a patient with suspected COPD?

A
  • CXR: hyper-expanded lungs and/or pneumothorax
  • ABG: type II resp failure
  • Bloods: high WCC (infection), low alpha1-anti-trypsin (younger patients/FHx), low albumin (severity)
  • Spirometry: low FEV1, FEV1/FVC ratio <0.7
  • Gas transfer - low TLCO
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23
Q

What medical treatments can be considered in COPD?

A

Depends on severity

  • Smoking cessation is the single most beneficial management strategy
  • Cessation clinics and nicotine replacement therapy
  • LTOT
  • Pulmonary rehab
  • Mild (FEV1>80) - beta-agonists
  • Moderate (FEV1 <60%) - tiotropium and beta-agonists
  • Severe (FEV1<40%) or frequent exacerbations - above plus inhaled corticosteroids although avoid if patient has ever had an episode of pneumonia
  • Exercise
  • Nutrition (often malnourished)
  • Vaccinations - pneumococcal and influenza
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24
Q

What surigcal treatments can be considered in COPD?

A
  • Bullectomy (if bullae >1L and compresses surrounding lung)
  • Endobronchial valve replacement
  • Lung reduction surgery - only suitable for a few patients with heterogeneous distribution of emphysema
  • Single lung transplant
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25
Q

What are the criteria for LTOT?

A
  • Non-smoker
  • PaO2 <7.3kPa on air
  • PaCO2 that does not rise excessively on O2
  • If evidence of cor pulmonale, PaO2 <8kPa
  • 2-4L/min via nasal prongs for at least 15 hours a day
  • Improves average survival by 9 months
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26
Q

How would you treat an acute exacerbation of COPD?

A
  • Controlled O2 via Venturi mask monitored closely
  • Bronchodilators
  • Antibiotics
  • Steroids for 5 days
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27
Q

What are the DDx for a wheezy chest?

A
  • Granulomatous polyarteritis (previously Wegener’s): saddle nose, obliterative bronchiolitis
  • Rheumatoid arthritis: wheeze secondary to obliterative bronchiolitis
  • Post-lung transplant: obliterative bronchiolitis as part of chronic rejection spectrum
  • IECOPD
  • Asthma
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28
Q

What are the clinical signs of a pleural effusion?

A
  • Asymmetrically reduced expansion
  • Trachea or mediastinum displaced away from side of effusion
  • Stony dull percussion note
  • Absent tactile vocal fremitus
  • Reduced breath sounds
  • Bronchial breathing above (aegophony)
  • Cancer: clubbing, lymphadenopathy, mastectomy
  • Congestive cardiac failure: raised JVP, peripheral oedema
  • Chronic liver disease: leuconychia, spider naevi, gynaecomastia
  • Chronic renal failure: arteriovenous fistula
  • Connective Tissue Disease: Rheumatoid hands, butterfly rash of SLE
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29
Q

Name some common causes of a dull lung base.

A
  • Consolidation: bronchial breathing and crackles
  • Collapse: tracheal deviation towards the side of the collapse and reduced breath sounds
  • Previous lobectomy - reduced lung volume
  • Pleural thickening - signs are similar to a pleural effusion but with normal tactile vocal fremitus, may have 3 scars suggested of previous VATS pleurodesis
  • Raised hemidiaphragm +/- hepatomegaly
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30
Q

What causes a pleural transudate and exudate?

A

Transudate (<30g/L):
- Congestive cardiac failure
- Chronic renal failure
- Chronic liver failure

Exudate (>30g/L):
- Primary or secondary neoplasm
- Infection
- Infarction
- Inflammation

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31
Q

What would pleural fluid analysis show if the patient had an empyema?

A

Exudate with a low glucose and pH <7.2

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32
Q

What is an empyema?

A

A collection of pus within the pleural space. Most frequent organisms involved includes anaerobes, staphylococci and gram-negative organisms. It is associated with bronchial obstruction, e.g. carcinoma, with recurrent aspiration; poor dentition; alcohol dependence.

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33
Q

How do you treat an empyema?

A
  • Pleural drainage and IV antibiotics
  • Surgical decortication
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34
Q

Name some clinical signs of Lung Cancer.

A
  • Cachectic
  • Clubbing and tar-stained fingers
  • Lymphadenopathy: cervical and axillary
  • Tracheal deviation: towards (collapse) or away (effusion) from the lesion
  • Reduced expansion
  • Percussion note dull (collapse/consolidation) or stony dull (effusion)
  • Absent tactile vocal fremitus (effusion); increased vocal resonance (collapse/consolidation)
  • Auscultation: crackles and bronchial breathing (consolidation/collapse) or reduced breath sounds, absent tactile fremitus (effusion)
  • Hepatomegaly or bony tenderness suggesting mets
  • Treatment: lobectomy scar, sqaure burn and tattoo if radiotherapy
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35
Q

What complications that arise from Lung Cancer can be seen as clinical signs?

A
  • Superior vena caval obstruction: suffused and oedematous face and upper limbs, dilated superficial chest veins and stridor
  • Recurrent laryngeal nerve palsy: hoarse with a ‘bovine’ cough
  • Horner’s sign and wasted small muscles of the hand (T1): Pancoast’s tumour
  • Endocrine: gynaecomastia (ectopic beta hCG)
  • Neurological: Lambert-Eaton myasthenic syndrome, peripheral neuropathy, proximal myopathy and paraneoplastic cerebellar degeneration
  • Dermatological: dermatomyositis (heliotrope rash on eyelids and purple papules on knuckles (Gottron’s papules associated with a raised CK) and acanthosis nigricans
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36
Q

What different types of Lung Cancer are there?

A
  • Squamous cell carcinoma
  • Small cell carcinoma
  • Adenocarcinoma
  • Large cell carcinoma
  • Alveolar carcinoma
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37
Q

How are patient’s with Lung Cancer managed?

A
  1. Diagnosis of a mass
    - CXR: collapse, mass and hilar lymphadenopathy
    - Volume acquisition CT Thorax (so small tumours are not lost between slices) with contrast
  2. Determine cell type
    - Induced sputum cytology
    - Biopsy by bronchoscopy (central lesion and collapse) or percutaneous needle CT guided (peripheral lesion; FEV1>1L)
  3. Stage (CT/Bronchoscopy/EBUS/Mediastinoscopy/thoracoscopy/PET)
    - NSCLC: TNM staging to assess operability
    - Small cell carcinoma (SCLC): limited or extensive disease
  4. Lung function tests for operability assessment:
    - Pneumonectomy contraindicated if FEV1 <1.2L
  5. Complications of the tumour:
    - Mets: deranged LFTs, raised calcium, anaemia
    - NSCLC: raised PTHrP and elevated calcium
    - SCLC: raised ACTH, SIADH and hyponatraemia
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38
Q

What treatment options are available in Lung cancer?

A

NSCLC:
- Surgery: Lobectomy or pneumonectomy
- Radiotherapy: single fractionation (weekly) versus hyper-fractionation (daily for 10 days)
- Chemotherapy: benefit unknown, EGFR positve - erlotinib

SCLC:
- Chemotherapy: benefit with 6 courses

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39
Q

Name some clinical signs of cystic fibrosis

A
  • Inspection: small stature, clubbed fingers, tachypnoeic, sputum pot (purulent+++)
  • Hyperinflated with reduced chest expansion
  • Coarse crackles and wheeze (bronchiectatic)
  • Portex reservoir (Portacath) under the skin or Hickmann line/scars for long-term antibiotics plus PEG for malabsorption
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40
Q

What genetic changes occur in cystic fibrosis?

A
  • Autosomal recessive chromosome 7q
  • Gene encodes for CFTR (Cl- channel)
  • Commonest and most severe mutation is F508 deletion (70%)
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41
Q

Describe the pathophysiology of CF

A

Secretions are thickened and block the lumens of various structures

  • Bronchioles - > bronchiectasis
  • Pancreatic ducts -> loss of exocrine and endocrine function
  • Gut -> distal intestinal obstruction syndrome (DIOS) in adults
  • Seminal vesicles -> male infertilty
  • Fallopian tubes -> reduced female fertility
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42
Q

How would you investigate someone with suspected CF

A
  • Screened at birth: low immunoreactive trypsin (heel prick)
  • Sweat test: Na+ >60mmol/L (can get a false positive in hypothyroidism and Addison’s)
  • Genetic screening
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43
Q

How do you manage patients with CF?

A
  • Physiotherapy - postural drainage and active cycle breathing techniques
  • Prompt antibiotics for intercurrent infections
  • Pancrease and fat-soluble vitamin supplements
  • Mucolytics (DNAse)
  • Immunisations
  • Double lung transplant (50% survival at 5 years)
  • Gene therapy is under development

Poor prognosis if becomes infected with Burkholderia cepacia

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44
Q

Name some clinical signs of pneumonia

A
  • Tachypnoea, O2 mask, sputum pot (rusty sputum associated with pneumococcus)
  • Reduced expansion
  • Dull percussion note
  • Focal coarse crackles, increased vocal resonance and bronchial breathing
  • Ask for the temperature chart
  • If dull percussion note with absent tactile vocal fremitus, think parapneumonic effusion/empyema
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45
Q

What investigations would you arrange if you suspected a patient had pneumonia?

A
  • CXR - consolidation (air bronchogram), abscess, effusion
  • Bloods - WCC, CRP, urea, atypical serology (on admission and at day 10) and immunoglobulins
  • Blood cultures
  • Sputum cultures
  • Urine: legionella antigen (in severe cases), pneumococcal antigen and haemoglobinuria (mycoplasma causes cold agglutinins resulting in haemolysis)
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46
Q

What common organisms cause a CAP?

A
  • Streptococcus pneumoniae (50%)
  • Mycoplasma pneumoniae (6%)
  • Haemophilus influenzae (esp if COPD)
  • Chlamydia pneumoniae
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47
Q

What special considerations should you ave in those who are immunosuppressed with a CAP?

A
  • Fungal - tx with amphotericin
  • Multi-resistant mycobacteria
  • Pneumocystis carinii - tx with co-trimoxazole/pentamidine
  • CMV - tx with ganciclovir
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48
Q

What special considerations should you ave in those who have aspirated with a CAP?

A

Anaerobes - add in Metronidazole

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49
Q

What special considerations should you ave in those who are post-influenza with a CAP?

A

Staph aureus - add in flucloxacillin

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50
Q

Outline the severity score for CAP

A

Confusion
Urea >7
RR >/=30
BP - systolic <90mmHg or diastolic <60mmHg
Age >65 years

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51
Q

What complications can arise from pneumonia?

A
  • Lung Abscess (Staph aureus, Klebsiella, anaerobes)
  • Para-pneumonic effusion/empyema
  • Haemoptysis
  • Septic shock and multi-organ failure
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52
Q

How would you define a moderate asthma exacerbation?

A
  • PEFR 50-75% best or predicted
  • Speech normal
  • RR <25/min
  • Pulse <110bpm
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53
Q

How would you define a severe asthma exacerbation?

A
  • PEFR 33-50% best or predicted
  • Can’t complete sentences
  • RR >25/min
  • Pulse >110bpm
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54
Q

How would you define a life-threatening asthma exacerbation?

A
  • PEFR <33% best or predicted
  • O2 sats <92%
  • Silent chest, cyanosis or feeble respiratory effort
  • Bradycardia, dysarrhythmia or hypotension
  • Exhaustion (normal pCO2), confusion or coma
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55
Q

What treatment should be given in exacerbation of asthma?

A
  • O2
  • Bronchodilators (SABA)
  • Steroids
  • Ipratropium bromide (SAMA)
  • IV Magnesium Sulphate
  • IV aminophylline
  • Intubation/Ventilation
  • Extracorporeal membrane oxygenation (ECMO)
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56
Q

What treatment should be given in exacerbation of COPD?

A
  • O2 - aiming sats 88-92%
  • Nebulised SABA/SAMA
  • Steroids
  • IV theophylline
  • NIV - BiPAP - EPAP 4-5cm H2O and IPAP 10cm H2O
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57
Q

Name some causes of ARDS

A
  • Infection: sepsis, pneumonia
  • Massive blood transfusion
  • Trauma
  • Smoke inhalation
  • Acute pancreatitis
  • COVID 19
  • Cardio-pulmonary bypass
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58
Q

What is the criteria to diagnosis ARDS?

A

American-European Consensus Conference
- Acute onset (within 1 week of a known risk factor)
- Pulmonary oedema: bilateral infiltrates on CXR (not fully explained by effusions, lobar/lung collapse or nodules)
- Non-cardiogenic (pulmonary artery wedge pressure needed if doubt - elevated in ARDS)
- pO2/FiO2 <40kPa (300mmHg)

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59
Q

How do you manage a patient with ARDS?

A
  • Normally in ITU
  • Oxygenation snf ventilation to tx hypoxaemia
  • General organ support e.g. vasopressors as needed
  • Tx of the underlying cause e.g. antibiotics for sepsis
  • Certain strategies such as prone positioning and muscle relaxation have been shown to improve outcomes
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60
Q

What is ABPA and name some clinical features associated with it.

A

Results from an allergy to aspergillus spores. May have a history of bronchiectasis and have a eosinophilia.

Features:
- Bronchoconstriction: wheeze, cough, dyspnoea (may have a previous label of asthma)
- Bronchiectasis (proximal)

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61
Q

What investigations would you arrange in someone with suspected ABPA?

A
  • Bloods - eosinophilia
  • Flitting CXR changes
  • Positive RAST (radioallergosorbent) test to aspergillus
  • Positive IgG precipitans (not as positive as in aspergilloma)
  • Raised IgE
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62
Q

How would you treat a patient with ABPA?

A
  • Steroids
  • Itraconazole is sometimes used as a second-line agent
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63
Q

What is alpha-1 anti-trypsin deficiency?

A

A common inherited condition caused by a lack of protease inhibitor (Pi) normally produced by the liver. The role of A1AT is to protect cells from enzymes such as neutrophil elastase. It classically causes emphysema in patients who are young and non-smokers.

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64
Q

Outline the genetic basis of alpha-1 anti-trypsin deficiency

A
  • Located on chromosome 14
  • Inherited in an autosomal recessive / co-dominant fashion
  • Alleles classified by their electrophoretic mobility - M for normal, S for slow, and Z for very slow.
  • Normal: PiMM
  • Heterozygous: PiMZ - non-smoker at low risk of developing emphysema but may pass on A1AT gene to children
  • Homozygous PiSS - 50% normal A1AT levels
  • Homozygous PiZZ - 10 % normal A1AT levels
65
Q

Name some features of patients with A1AT deficiency

A
  • Lungs: Panacinar emphysema most marked in lower lobes
  • Liver: Cirrhosis and hepatocellular carcinoma in adults, cholestasis in children
66
Q

How would you investigate A1AT deficiency?

A
  • A1AT concentrations
  • Spirometry: obstructive picture
67
Q

How would you manage a patient with A1AT deficiency?

A
  • No smoking
  • Supportive: bronchodilators, physiotherapy
  • IV A1AT protein concentrates
  • Surgery: Lung volume reduction surgery, Lung transplantation
68
Q

Name some features of asbestosis?

A
  • Dyspnoea and reduced exercise tolerance
  • Finger clubbing
  • Bilateral end-inspiratory crackles
  • Lung function tests show a restrictive pattern with reduced gas transfer
69
Q

How would you manage newly diagnosed asthma?

A
  • Step 1: Low dose ICS/LABA
  • Step 2: Low-dose MART (ICS/LABA for maintenance and relief)
  • Step 3: Moderate-dose MART
  • Step 4: Check Fractional exhaled Nitric Oxide (FeNO) if available and blood eosinophil count. If either of these are raised then refer to a specialist. If neither is raised, consider trial of a LTRA or a LAMA in addition to moderate dose MART. If control doesn’t improve, stop and trial alternative.
  • Step 5: Refer
70
Q

What chemicals cause occupational asthma?

A
  • Isocyanates - most common cause. Example occupations include spray painting and foam moulding using adhesives
  • Platinum salts
  • Soldering flux resin
  • Flour
  • Expoxy resins
  • Proteolytic enzymes
71
Q

What is atelectasis and what are the features?

A
  • Basal alveolar collapse that can lead to Resp difficulty. It is caused when airways become obstructed by bronchial secretions
  • It should be suspected in presentation of dyspnoea and hypoxia around 72 hours post-op
72
Q

What are the features of Berylliosis and what are the occupational risk factors?

A
  • Features: Lung fibrosis and bilateral hilar lymphadenopathy
  • Aerospace industry
  • Manufacture of fluorescent light bulbs/golf club heads
73
Q

What are the causes of Bronchiectasis?

A
  • Post-infective: TB, 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
74
Q

What is Bronchiectasis?

A

A permanent dilatation of the airways secondary to chronic infection or inflammation

75
Q

What are the features and signs of bronchiectasis?

A
  • Persistent productive cough. Large volumes of sputum may be expectorated
  • Dyspnoea
  • Haemoptysis
  • Coarse crackles and wheeze on auscultation
  • Finger clubbing
76
Q

How would you manage a patient with bronchiectasis?

A
  • Physical training (e.g. inspiratory muscle training)
  • Postural drainage
  • Antibiotics for exacerbations and long-term rotating antibiotics in severe cases
  • Bronchodilators in selected cases
  • Immunisations
  • Surgery in selected cases (e.g. localised disease)
77
Q

What are the most common organisms isolated from patients with bronchiectasis?

A
  • Haemophilus Influenzae (most common)
  • Pseudomonas aeruginosa
  • Klebsiella spp
  • Streptococcus pneumoniae
78
Q

What is bronchiolitis?

A
  • A common condition characterised by acute bronchiolar inflammation
  • RSV is the pathogen in 75-80% of cases. Other causes include mycoplasma and adenoviruses
  • Most common cause of serious lower respiratory tract infection in those udner 1 year. Maternal IgG provides protection to newborns against RSV.
  • Can be more serious if bronchopulmonary dysplasia (e.g. premature), congenital heart disease or cystic fibrosis
79
Q

What are the features of bronchiolitis?

A
  • Coryzal symptoms (including mild fever) precede:
  • Dry cough
  • Increasing breathlessness
  • Wheezing, fine inspiratory crackles (not always present)
  • Feeding difficulties associated with increased dyspnoea are often the reason for hospital admission
80
Q

Under what circumstances do NICE recommend immediate referral?

A
  • Apnoea (observed or reported)
  • Child looks seriously unwell to a healthcare professional
  • Severe respiratory distress, e.g. grunting, marked chest recession or a RR of over 70
  • Central cyanosis
  • Persistent oxygen saturation of less than 92% when breathing air.
81
Q

How would you manage a patient with bronchiolitis?

A
  • Supportive - oxygen
  • NG feeding may be needed if they cannot take enough fluid/feed by mouth
  • Suction sometimes used for excessive upper airway secretions
82
Q

Name some indications for a chest drain.

A
  • Pleural effusion
  • Pneumothorax not suitable for conservative management or aspiration
  • Empyema
  • Haemothorax
  • Haemopneumothorax
  • Chylothorax
  • Penetrating chest wall injuries in ventilated patients
83
Q

Name some relative contraindications for chest drain

A
  • INR >1.3
  • Platelet count <75
  • Pulmonary bullae
  • Pleural adhesions
84
Q

Name some complications of a chest drain?

A
  • Failure of insertion
  • Bleeding - around the site of the drain or into the pleural space
  • Infection
  • Penetration of lung
  • Re-expansion pulmonary oedema
85
Q

What are the indications for chest drain removal?

A
  • In cases of fluid drainage from the pleural cavity, the drain should be removed when there has been no output for >24 hours and imaging shows resolution of the fluid collection
  • In cases of pneumothorax, the drain should be removed when it is no longer bubbling spontaneously or when the patient coughs and ideally when imaging shows resolution
  • Drains inserted in cases of penetrating chest injury should be reviewed by the specialist to confirms an appropriate time for removal
86
Q

Name some differentials of a cavitating lung lesion

A
  • Abscess (Staph aureus, Klebsiella and Pseudomonas)
  • Squamous cell lung cancer
  • TB
  • Wegener’s Granulomatosis
  • Pulmonary Embolism
  • Rheumatoid arthritis
  • Aspergillosis
  • Histoplasmosis
  • Coccidiodomycosis
87
Q

Name some differentials of a coin lesion

A
  • Malignant tumour: lung cancer or metastases
  • Benign tumour: hamartoma
  • Infection: pneumonia, abscess, TB, hydatid cyst
  • AV malformation
88
Q

Name some differential causes of a lobar collapse

A
  • Lung cancer (most common cause in older adults)
  • Asthma (due to mucus plugging)
  • Foreign body
89
Q

What are the CXR signs of lobar collapse?

A
  • Tracheal deviation towards the side of the collapse
  • Mediastinal shift towards the side of the collapse
  • Elevation of the hemidiaphragm
90
Q

What cancers commonly metastasise to the lung?

A
  • Breast Cancer
  • Colorectal Cancer
  • Renal Cell Cancer
  • Bladder Cancer
  • Prostate Cancer
91
Q

What are the features of pulmonary oedema on CXR?

A
  • Interstitial oedema
  • Bat’s wing appearance
  • Upper lobe diversion (increased blood flow to the superior parts of the lung)
  • Kerley B lines
  • Plueral effusion
  • Cardiomegaly may be seen if there is cardiogenic cause
92
Q

Name some differentials of a white lung lesion

A
  • Consolidation
  • Pleural effusion
  • Collapse
  • Pneumonectomy
  • Specific lesions e.g. tumours
  • Fluid e.g. pulmonary oedema
93
Q

What causes the trachea to be pulled towards a white-out?

A
  • Pneumonectomy
  • Complete lung collapse e.g. endobronchial intubation
  • Pulmonary hypoplasia
94
Q

What causes the trachea to remain central with a lung white out?

A
  • Consolidation
  • Pulmonary oedema (usually bilateral)
  • Mesothelioma
95
Q

What causes the trachea to be pushed away from a white-out?

A
  • Pleural effusion
  • Diaphragmatic hernia
  • Large thoracic mass
96
Q

What are the causes of COPD?

A
  • Smoking
  • A1AT deficiency
  • Cadmium (used in smelting)
  • Coal
  • Cotton
  • Cement
  • Grain
97
Q

What are the features of cystic fibrosis?

A
  • Neonatal period: meconium ileus, less commonly prolonged jaundice
  • Recurrent chest infections
  • Malabsorption: steatorrhoea, failure to thrive
  • Liver disease
  • Short stature
  • Diabetes
  • Delayed puberty
  • Rectal prolapse (due to bulky stools)
  • Nasal polyps
  • Male infertility, female subfertilty
98
Q

How are patients with CF managed?

A
  • Regular chest physio and postural drainage
  • High calorie diet, including high fat intake
  • Minimise contact with other CF patients to prevent cross infection with Burkholderia and Pseudomonas
  • Vitamin supplementations
  • Pancreatic enzyme supplements
  • Lung transplantation
  • Lumacaftor/Ivacaftor (Orkambi) - used to treat patients who are homozygous for delta F508 mutation. Lumacaftor increases the number of CFTR proteins that are transported to the cell surface and 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
99
Q

How do methylxanthines work (e.g. theophylline)?

A
  • Non-specific inhibitor of phosphodiesterase resulting in increase in cAMP
100
Q

Name some features of Eosinophilic granulomatosis with polyangitis (Churg Strauss syndrome).

A
  • Asthma
  • Blood eosinophilia (>10%)
  • Paranasal sinusitis
  • Mononeuritis multiplex
  • Renal involvement occurs in around 20%
  • pANCA positive in 60%
  • LT receptor antagonists may precipitate the disease
101
Q

What are some examples of extrinsic allergic alveolitis?

A
  • Bird Fanciers’ Lung: avian proteins from bird droppings
  • Farmers lung: Spores of Saccharopolyspora rectivirgula from wet hay (formerly Micropolyspora faeni)
  • Malt workers’ lung: Aspergillus clavatus
  • Mushroom workers’ lung: thermophilic actinomycetes
102
Q

How does Extrinsic Allergic Alveolitis present?

A
  • Acute (4-8 hours after exposure): dyspnoea, dry cough, fever
  • Chronic (occurs weeks-months after exposure): lethargy, dyspnoea, productive cough, anorexia and weight loss
103
Q

How would you investigate a patient with suspected EAA?

A
  • Imaging: upper/mid-zone fibrosis
  • Broncho-alveolar lavage: lymphocytosis
  • Serologic assays for specific IgG antibodies
  • Blood: NO eosinophilia
104
Q

What are the features of Granulomatosis with polyangitis?

A
  • Upper respiratory tract: epistaxis, sinusitis, nasal crusting
  • Lower respiratory tract: dyspnoea, haemoptysis
  • Rapidly progressive glomerulonephritis (‘pauci-immune’, 80% of patients)
  • Saddle shaped nose deformity
  • Vasculitis rash
  • Eye involvement (e.g. proptosis)
  • Cranial nerve lesions
  • cANCA positive in >90%
105
Q

How are patients with Granulomatosis with polyangitis managed?

A
  • Steroids
  • Cyclophosphamide
  • Plasma exchange
  • Median survival is 8-9 years
106
Q

What is Histoplasmosis and what features are present? How is it treated?

A
  • Due to fungus Histoplasma capsulatum
  • Most commonly encountered in Mississippi and Ohio River valleys
  • Features: URTI symptoms and retrosternal pain
  • Management is with amphotericin or Itraconazole
107
Q

What is Kartagener’s syndrome and what features would be present in a patient with this condition?

A
  • Primary ciliary dyskinesis
  • Can be associated with dextrocardia
  • Due to dynein arm defect resulting in immotile cilia
  • Dextrocardia or complete situs inversus
  • Bronchiectasis
  • Recurrent sinusitis
  • Subfertility (secondary to diminished sperm motility and defective ciliary action in the fallopian tubes)
108
Q

Name some features of Klebsiella pneumoniae.

A
  • More common in alcoholics and diabetics
  • May occur following aspiration
  • ‘Red-currant jelly’ sputum
  • Often affects upper lobes
  • Commonly causes lung abscess and empyema
109
Q

What is Lofgren’s syndrome?

A
  • Acute form of sarcoidosis characterised by bilateral hilar lymphadenopathy, erythema nodosum, fever and polyarthralgia
  • Typically occurs in young females and carries excellent prognosis
110
Q

Name some causes of Lung Abscess

A
  • Aspiration pneumonia
  • Haematogenous spread e.g. secondary to infective endocarditis
  • Direct extension e.g. from an empyema
  • Bronchial obstruction e.g. secondary from a lung tumour
  • Normally polymicrobial but monomicrobial causes include: staph aureus, klebsiella and pseudomonas aeruginosa
111
Q

What features are seen in patients with a lung abscess?

A
  • Similar features to pneumonia but a more subacute presentation (symptoms develop over weeks).
  • May see systemic features like night sweats and weight loss
  • Fever
  • Productive cough - often foul-smelling sputum. Haemoptysis in a minority of patients
  • Chest pain
  • Dyspnoea
  • Signs - dull percussion and bronchial breathing
  • Clubbing may be seen
112
Q

Causes of fibrosis affecting the upper zones

A
  • EAA
  • Coal worker’s pneumoconiosis
  • Silicosis
  • Sarcoidosis
  • Ank Spond (rare)
  • Histiocytosis
  • TB
  • Radiation-induced fibrosis - may develop following radiotherapy for breast or lung cancer
  • Typically seen between 6-12 months following radiotherapy

Mnemonic - CHARTS (coal worker’s pneumoconiosis, Histiocytosis/Hypersensitivity pneumonitis, Ank Spon, Radition, TB, Silicosis/Sarcoidosis)

113
Q

Name some causes of Fibrosis of the lower lungs

A
  • Idiopathic pulmonary fibrosis
  • Most connective tissue disorders (except ank spond) e.g. SLE
  • Drug induced: amiodarone, bleomycin, methotrexate
  • Asbestosis
114
Q

Name some features of microscopic polyangitis

A
  • Renal impairment: raised creatinine, haematuria, proteinuria
  • Fever
  • Lethargy, Myalgia, Weight loss
  • Rash: palpable purpura
  • Cough, dyspnoea, haemoptysis
  • Mononeuritis multiplex
115
Q

Name some indications for NIV

A
  • COPD with respiratory acidosis
  • T2RF secondary to chest wall deformity, neuromuscular disease or OSA
  • Cardiogenic pulmonary oedema unresponsive to CPAP
  • Weaning from tracheal intubation
116
Q

What are the signs and symptoms of obesity hypoventilation syndrome?

A
  • Obesity: BMI >30 often with central adiposity
  • Daytime hypoventilation: dyspnoea, exercise intolerance, fatigue
  • Sleep-disordered breathing - loud snoring, witnessed apnoeas, nocturnal choking or gasping and excess daytime sleepiness
  • Morning headaches and cognitive dysfunction due to chronic hypercapnia and hyoxaemia
  • Signs of R heart failure: peripheral oedema, jugular venous distention, hepatomegaly due to chronic hypoxaemia and pulmonary hypertension
117
Q

Name some causes of obstructive lung disease

A
  • COPD
  • A1AT deficiency
  • Asthma
  • Bronchiectasis
118
Q

Name some causes of restrictive lung disease

A
  • Idiopathic pulmonary fibrosis
  • EAA
  • Coal worker’s pneumoconiosis
  • Silicosis
  • Sarcoidosis
  • Histiocytosis
  • Drug-induced fibrosis: amiodarone, bleomycin, methotrexate
  • Asbestosis
  • Extra-pulmonary causes: neuromuscular disease: polio, myasthenia gravis, obesity, scoliosis
119
Q

Name some causes of pleural effusion

A
  • Transudate (<30g/protein): HF, hypoalbuminaemia (liver disease, nephrotic syndrome, malabsorption), hypothyroidism, Meig’s syndrome
  • Exudate (>30g/protein): Infection (pneumonia, TB, subphrenic abscess), CTD (RA, SLE), neoplasia (lung, mesothelioma, metastases), pancreatitis, PE, Dressler’s syndrome, Yellow nail syndrome
120
Q

How are pneumothoraxes classified?

A
  • Primary spontaneous pneumothorax - occurs without lung disease often in tall, thin, young individuals. Associated with rupture of blebs or bullae
  • Secondary spontaneous pneumothorax - occurs in those with pre-existing lung disease such as COPD, asthma, CF, lung cancer, pneumocystis)
  • Traumatic pneumothorax - results from penetrating or blunt chest trauma, leading to lung injury and pleural air accumulation
  • Iatrogenic pneumothorax - occurs as a complication of medical procedures such as thoracentesis, CVC placement, ventilation, including NIV or lung biopsy
  • Catamenial Pneumothorax - spontaneous pneumothoraces occurring in menstruating women thought to be caused by endometriosis in the thorax
121
Q

Name some causes of Pulmonary eosinophilia

A
  • Churg Strauss syndrome
  • ABPA
  • Loffler’s syndrome
  • Eosinophilic pneumonia
  • Hypereosinophilic syndrome
  • Tropical pulmonary eosinophilia
  • Drugs: Nitrofurantoin, Sulphonamides
  • Less common: Wegener’s granulomatosis
122
Q

What is Loffler’s Syndrome?

A

Transient CXR shadowing and blood eosinophilia thought to be due to parasites such as Ascaris lumbricoides causing an alveolar reaction. Presents with fever, cough and night sweats which often last for less than 2 weeks.

123
Q

What are the different categories of Pulmonary HTN?

A
  • Group 1: PAH - idiopathic, familial. Associated with collagen vascular disease, congenital heart disease with systemic to pulmonary shunts, HIV, drugs and toxins, sickle cell disease.
  • Group 2: Pulm HTN with L heart disease
  • Group 3: Pulm HTN secondary to lung disease e.g. COPD, ILD, Sleep apnoea and high altitude
  • Group 4: Pulm HTN due to thromboembolic disease
  • Group 5: Miscellaneous conditions e.g. lymphangiomatosis e.g. secondary to carcinomatosis or sarcoidosis
124
Q

Name some causes of respiratory acidosis

A
  • COPD
  • Decompensation in other resp conditions e.g. life-threatening asthma/pulmonary oedema
  • Neuromuscular disease
  • Obesity hypoventilation syndrome
  • Sedative drugs: Benzodiazepines, Opiate overdose
124
Q

Name some causes of respiratory alkalosis

A
  • Anxiety leading to hyperventilation
  • PE
  • Salicylate poisoning
  • CNS disorders: Stroke, SAH, encephalitis
  • Altitude
  • Pregnancy
124
Q

What are the potential respiratory manifestations of rheumatoid arthritis?

A
  • Pulmonary fibrosis
  • Pleural effusion
  • Pulmonary nodules
  • Bronchiolitis obliterans - progressive dyspnoea, obstructive pattern on spirometry, centrilobular nodules, bronchial wall thickening
  • Complications of drug therapy e.g. methotrexate pneumonitis
  • Pleurisy
  • Caplan’s syndrome: massive fibrotic nodules with occupational coal dust exposure
  • Infection (possibly atypical) secondary to immunosuppression
125
Q

Name some features of sarcoidosis

A
  • Acute: erythema nodosum, bialteral hilar lymphadenopathy, swinging fever, polyarthralgia
  • Insidious: dyspnoea, non-productive cough, malaise, weight loss
  • Ocular: uveitis
  • Skin: lupus pernio
  • Hypercalcaemia: macrophages inside the granulomas cause an increased conversion of vitamin D to its active form
126
Q

What is Lofgren’s syndrome?

A

An acute form of sarcoid characterised by bilateral hilar lymphadenopathy, erythema nodosum, fever and polyarthralgia. Usually carries excellent prognosis

127
Q

What is Mikulicz syndrome?

A

There is enlargement of the parotid and lacrimal glands due to sarcoidosis, TB or lymphoma

128
Q

What is Heerfordt’s syndrome?

A

There is parotid enlargement, fever and uveitis secondary to sarcoidosis

129
Q

What CXR changes can be seen in sarcoidosis?

A

Stage 0 = normal
Stage 1 = Bilateral Hilar Lymphadenopathy
Stage 2 = Bilateral Hilar Lymphadenopathy and interstitial infiltrates
Stage 3 = Diffuse interstitial infiltrates only
Stage 4 = Diffuse fibrosis

130
Q

What Ix should be requested if you are suspecting a diagnosis of sarcoidosis?

A
  • CXR
  • ACE
  • Calcium and ESR
  • Spirometry - may show restrictive pattern
  • Tissue biopsy - may show non-caseating granulomas
131
Q

What are the indications for steroids in sarcoidosis?

A
  • Patients with CXR with stage 2 or 3 disease who are symptomatic. Patients with asymptomatic and stable stage 2 or 3 disease who only have mildly abnormal lung function do not require treatment
  • Hypercalcaemia
  • Eye, Heart or Neuro involvement
132
Q

Which occupations are at risk of silicosis?

A
  • Mining
  • Slate works
  • Foundries
  • Potteries
133
Q

What features are seen in silicosis?

A
  • Upper zone fibrosing lung disease
  • ‘Egg-shell’ calcification of the hilar lymphnodes
134
Q

What are the adverse effects of nicotine replacement therapy?

A
  • Nausea and vomiting
  • Headaches
  • Flu-like symptoms
135
Q

What is the mechanism of action of varenicline and what are the adverse effects?

A
  • Nicotinic receptor partial agonst
  • Nausea (most common), headache, insomnia, abnormal dreams
  • Needs to be used in caution in patients with history of depression or self-harm.
  • Contraindicated in pregnancy and breastfeeding
136
Q

What is the mechanism of action of bupropion and what are the adverse effects?

A
  • Norephinephrine-dopamine reuptake inhibitor and nicotinic antagonist
  • Contraindicated in epilepsy, pregnancy and breast feeding. Having an eating disorder is a relative contraindication
  • Small risk of seizures
137
Q

What are the guidelines around a solitary lung nodule?

A
  • <5mm, or clear benign features or unsuitable for treatment - can be discharged
  • > /= 8mm and high risk then CT PET and if CTPET shows high uptake then biopsy
  • Nodule 5-6mm, or >/= 8mm and low risk then CT surveillance
  • CT surveillance - if 5-6mm at 1 year, if >/= 6 then in 3 months
138
Q

What are the features of theophylline poisoning and how is it managed?

A
  • Acidosis, hypokalaemia
  • Vomiting
  • Tachycardia, arrhythmias
  • Seizures

Management:
- 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

139
Q

What is transfer factor?

A

Describes the rate at which gas will diffuse from alveoli into the blood. Carbon monoxide is used to test the rate of diffusion. Results may be given as the total gas transfer (TLCO) or that corrected for lung volume (transfer coefficient, KCO)

140
Q

What are the causes of a raised TLCO?

A
  • Asthma
  • Pulmonary Haemorrhage (granulomatosis with polyangitis, Goodpasture’s)
  • L to R cardiac shunts
  • Polycythaemia
  • Hyperkinetic states
  • Male Gender
  • Exercise
141
Q

What causes a low TLCO?

A
  • Pulmonary fibrosis
  • Pneumonia
  • Pulmonary Emboli
  • Pulmonary oedema
  • Emphysema
  • Anaemia
  • Low Cardiac Output
142
Q

Which conditions cause an increased KCO with a normal or reduced TLCO?

A
  • Pneumonectomy/lobectomy
  • Scoliosis/kyphosis
  • Neuromuscular weakness
  • Ankylosis of costovertebral joints e.g. ank spond
143
Q

Name some DDx for CF?

A
  • Primary immunodeficiency
  • Primary ciliary dyskinesia (PCD)
  • Asthma
  • Chronic aspiration
  • Coeliac disease
144
Q

What medications are used in Lung Transplantation

A

Normally a combination of Tacrolimus, Mycophenolate and Steroid therapy.

145
Q

What is the main cause of death post lung transplant?

A

Bronchiolitis Obliterans

146
Q

What are the contraindications to transplantation?

A
  • Malignancy in the last 5 years or in the last 2 years if malignancy has a low risk of recurrence (eg BCC)
  • If the patient has untreatable significant heart, liver, kidney or brain dysfunction - unless combined organ transplantation can be performed
  • If the patient has atherosclerotic disease with significant end organ ischaemia or dysfunction and/or CAD not amenable to revascularisation
  • Conditions such as sepsis, MI and hepatic failure
  • Chronic infection with highly virulent organisms
  • Significant chest wall or spinal deformities
  • Obese patients (BMI >35)
  • Significant psychiatric or psychological conditions with an inability to cooperate with the healthcare team
  • Inability to adhere to daily medications
  • Substance use/dependence
  • Poor functional status
147
Q

What are the DDx of yellow nail syndrome?

A
  • Psoriasis
  • Lichen Planus
  • Fungal nail infection
  • Drug discolouration (i.e. penicillamine)
  • Local causes of discolouration (i.e. dyes, pollen staining, pesticides, chromium salts)
148
Q

How does yellow nail syndrome present

A
  • Nails appear yellow and excessively curved
  • All nails are affected (hands and feet)
  • Swelling of peri-ungal tissue may occur
  • Onycholysis (lifting of nail plate from nail bed) may also occur
  • Nails become slow growing and thickened
  • The lunula (usually opaque) disappears
  • Condition is usually accompanied by lymphoedema (affects up to 80% with condition). Usually appears after nail changes
  • May also complain of a history of respiratory problems, such as recurrent pleural effusions, sinusitis, bronchitis, pneumonia or bronchiectasis
149
Q
A
149
Q

How are patients with yellow nail syndrome managed?

A
  • Identifying and treating co-existing underlying conditions and lymphoedema
  • Mainstay of direct treatment of the nails is topical vitamin E solution
  • Oral itraconazole is also used although the condition isn’t fungal, it appears to speed up the growth of the nail
  • Some studies suggest oral vitamin E supplementation may help to control or prevent progression of condition.
150
Q

What pattern is seen with consolidation

A
  • No tracheal deviation
  • Normal or reduced chest expansion
  • Normal or duller percussion note
  • Bronchial breathing
  • Coarse crackles
  • Pleural rub
  • Increased whispering pectoriloquoy
151
Q

What pattern is seen with Lobar collapse?

A
  • Yes towards side of collapse
  • Reduced chest expansion
  • Duller percussion note
  • Reduced breath sounds
  • Reduced vocal resonance
152
Q

What pattern is seen with pleural effusion?

A
  • No tracheal deviation or deviation away from side of effusion
  • Reduced chest expansion
  • Stony dull percussion
  • Reduced breath sounds
  • Occasionally pleural rub
  • Reduced vocal resonance
153
Q

What pattern can be seen with pneumothorax?

A
  • No tracheal deviation if no tension
  • Normal or reduced chest expansion
  • Hyperresonant percussion note
  • Reduced breath sounds
  • Occasional click
  • Reduced vocal resonance
154
Q

What are the signs of hyperinflation?

A
  • Increased anteroposterior chest diameter (‘barrel chest’)
  • Indrawing of the intercostal muscles and supraclavicular fossae
  • Flattening of the subcostal angle
  • A shortened cricoid-notch distance (normally greater than 3 finger breadths)
  • Decreased chest expansion
  • Attenuation of heart and liver dullness (with diminished heart sounds)
  • Hyperresonance
155
Q
A

PACES (4 decks)

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