Respiratory Flashcards
Upper versus lower lobe fibrosis
Basal crackles are caused by CIAD
- CTDs (other than AS)
- IPF
- Asbestosis
- Drugs
Think: basal predominance more likely to be UIP pattern (IPF, RA)
Predominant upper zone causes (SCHARTS):
- Silicosis
- Coal worker’s pneumoconiosis
- Histiocytosis
- Ankylosing spondylitis
- Allergic bronchopulmonary aspergillosis
- Radiation
- Tuberculosis
- Sarcoidosis
Predominant lower zone causes (DRASID)
- Dermatomyositis/polymyositis
- Rheumatoid arthritis
- Asbestosis
- Scleroderma
- IPF
- Drugs
ILD findings on exam
No trachea displacement
Symmetrical, reduced lung expansion
Resonant percussion note
Vesicular breath sounds
Added fine late inspiratory crackles (or pan if more severe)
Exam findings of COPD
Midline trachea
Symmetrical, reduced chest expansion
Resonant percussion note
Reduced vesicular breath sounds
+/- added wheeze
Euqal vocal resonance
Pleural effusion exam findings
Trachea displaced away if severe
Asymmetrical reduced chest expansion on side of effusion if severe
Stony dull percussion note
Absent / reduced breath sounds over effusion, may be bronchial at border
No added sounds, maybe pleural rub
Exam findings in consolidation?
Midline trachea (or displaced toward pathology if associated collapse)
Chest wall movement (may be asym reduced if severe area of consolidation)
Dull percussion note
Bronchial breath sounds (coarse and pan-inspiratory)
Increased vocal resonance
What are the causes of crackles?
What other signs would be in keeping with each?
ABC-I
- Alveolar oedema
- Medium crackles (fine or coarse)
- Bilateral
- May be a/w signs of pleural effusion
- Increased body mass for increased CV risk
- CV exam for signs of L sided cardiac failure
- Displaced apex beat
- L sided valvulopathies
- Bronchiectasis
- Coarse crackles
- Unilateral or bilateral
- If unilateral may have tracheal deviation to affected side
- Clubbing (may not be present)
- Productive cough
- Co-existant obstructive airways disease - wheeze and reduced chest expansion
- Consolidation eg. secondary to an infective process or maligancy
- Coarse
- Usually unilateral / asymmetrical
- Dullness to percussion note
- Reduced vocal resonance
- Bronchial breath sounds
- Interstital lung disease
- Fine: late in early disease or pan in severe disease)
- Clubbing in IPF
- Reduced chest expansion
Causes of clubbing
Cardiac
- infective endocarditis
- cyanotic heart disease
Respiratory
- malignancy (not SCLC)
- suppurative lung diseases (bronchiectasis, CF, lung abscess, empyema)
- IPF
- Asbestosis
Other
- IBD
- Liver cirrhosis
- Coeliac disease
What are the causes of ILD?
DR COVID
Drugs (MTX, amiodarone)
Radiation
CTDs (RA, systemic sclerosis, poly/dermatomyositis)
Occupational (asbestos, sillicosis)
Vasculitis (PAN, eGPA, MPA)
IPF
Don’t forget drugs
How to investigate causes of ILD?
The diagnostic test for ILD would be HRCT, however more basic investigations (and investigation to explore aetiology) include:
- Medication chart and drug history
- FBE - anaemia of chronic disease or polycythaemic in a chronic hypoxic state
- ABG - evidence of respiratory failure
- CRP, ESR
- RhF, anti-CCP, CK, ANA, ENA
- ANCA
- Serum ACE, Vitamin D
- CXR
- HRCT
- BAL or lung biopsy to support diagnosis or if any uncertainty
How do you diagnose obstruction on PFTs?
- If FEV1/FVC < 70% obstruction is present
- If FVC > 80% - pure obstruction
- If either FEV1 or FVC change is > 12% AND 200mL = reversibility
- RV/TLC is usually 25%
- If > 25% –> gas trapping
- If DLCO low - emphysema (reduced membrane SA)
- If DLCO normal - other forms of obstruction
How would you diagnose restrictive lung disease on PFTs?
- If FEV1/FVC > 70% this is normal
- But if FVC < 80% this is suggestive of restriction
- Check by looking at TLC if this is < LLN (dependent on height/weight) = restriction
- Then check DLCO
- If DLCO > normal = extrinsic restirction
- If DLCO < normal = intrinsic restriction
- if DLCO IS FAR MORE REDUCED THAN TLC, THINK PULMONARY HYPERTENSION
What does a BLSTx scar look like?
Clamshell
(joined in the middle)
What are the causes of clubbing?
What does systemic sclerosis cause?
Causes of clubbing:
- Idiopathic pulmonary fibrosis (IPF) (idiopathic lung disease (ILD))
- Bronchiectasis.
- Suppurative lung diseases eg cystic fibrosis
- Lung cancer
- Also:
- thyroid disease
- CLD
- cyanotic heart disease
- IE
- IBD
- Coeliac
- HIV
- TB
Systemic sclerosis can cause pseudo clubbing due to loss of pulp / finger atroptht
What are the types of quality of breath sounds?
Vesicular = normal
Think: vesicular = alveoli
Normal to hear this over most of the lung
Insp > expiration
Gap between inspiration and expiration (because alveoli are filled)
Soft
Bronchial
Making the sound it would through the bronchi, but if heard through the lungs it means the alveoli are clogged up
Expiration > inspiration, with no gap between (think: going through a tube)
Loud
Often he
What is normal chest expansion?
What causes reduced asymmetrical or symmetrical lung expansion?
Normal expansion
- symmetrical
- 5 - 10 cm
Asymmetrical expansion:
- Unilateral lung disease
- Lung resection
- Pneumonectomy
- Unilateral lung transplantation with normal expansion of the transplanted lung and reduced expansion of the native lung.
Symmetrical but reduced:
- Chronic obstructive lung disease.
- Interstitial lung disease.
Scar of single lung transplant
Anterior thoracotamy scar
(also used for lobectomy, pneumoectomy, LVRS –> or a posterolateral thoracotomy scar)
Scar of double lung transplant
clamshell
or bilateral anterior thoracotomies
Heart borders on a CXR
How to identify pulmonary trunk on CXR?
ABove the left main bronchus but below the aortic knuckle
Features of right atrial enlargement on a chest xray?
Occupies more of the retrosternal space
How to identify the heart borders on a lateral chest xray?
Right heart border anteriorly
Left atrium posteriorly at the top, ventircle down the bottom
(remember they are closest to the oesophagus)
What are the radiological criteria for UIP?
Definite:
- Subpleural (around the edges), basal (down the bottom) i.e. an apicobasal gradient (worse down the bottom of the lung)
- Reticular
- Honeycombing (think: sweet - I have the DDx!, not groundglass - shattered, I can’t make the Dx)
- Absence of atypical features
What are the differences in HRCT in non-specific interstitial pneumonia, compared to UIP?
Why is it important to differentiatie between the two?
In NSIP, there is ground glass change, traction bronciectasis, sub-pleural sparing and little honeycombing.
Much better prognosis in NSIP compared to UIP IPF.
