Chest medicine Flashcards
Zone = pathology
- Upper zone
- Middle zone
- Lower zone
- Sarcoidosis (most common), silicosis (nodular/widespread), coal workers pneumoconiosis CWP, TB
- Pulmonary oedema (groundglass), hypersensitivty pneumonitis
- Idiopathic pulmonary fibrosis, asbestosis (also both reticular)
Heart failure / pulmonary oedema Xray ABCDE
Alveolar oedema (batwing distribution) kerley B lines Cardiomegaly upper lobe Diversion pleural Effusion
Restrictive PFTs
Obstructive PFTs
Restrictive:
FEV/FVC both reduced + reduced TLC
Impaired gas transfer - TCO, KCO both reduced
Obstructive:
FEV1/FVC reduced <75% + increased TLC (hyperinflated) + residual volume
>15% reversible post bronchodilator = asthma
Increased gas transfer/KCO in…
Goodpastures syndrome (alveolar haemorrhage) + polycythemia
Extrapulmonary restriction such as pleural, chest wall and respiratory neuromuscular disease = raised KCO thus raised KCO = extrapulmonary cause
Low KCO is due to restriction from intrapulmonary causes such as emphysema and interstitial lung disease - thus a another way to dinstinguish asthma and COPD
Breath sounds:
- Stridor
- Bronchial breathing
- Wheeze
- Pleural rub
- Fine inspiratory crackles
- Coarse expiratory crackles
- Obstruction
- Consolidation + fibrosis
- Asthma + COPD
- Pneumonia + PE + pleuritis
- Pulmonary oedema + pulmonary fibrosis
- Bronchiectasis
1. Nodular 2, Reticular (lace) 3. Honeycombing + bronchiectasis 4. Groundglass 5. Eggshell calcification
- Widespread - sarcoidosis, silicosis
- Pulmonary fibrosis, asbestosis (lower zone)
- Pulmonary fibrosis
- Pulmonary fibrosis + oedema
- Silicosis
How to tell difference between TB and sarcoidosis
TB has different risk factors/exposure rates, positive TB test
Sarcoidosis has non-caseating granuloma on biopsy + intrathoracic lymphadenopathy + joint pain
General pneumoconiosis Mechanism Presentation Ix Mx
NOT hypersensitivity just inhalation of large mineral particles > inflammation > fibrosis
PROGRESSIVE SoB, dry cough + fine end inspiratory basal crackles like VELCRO + clubbing
- CXR + PFTs - low DLCO + mixed spiro
- High res CT
- Biopsy
Palliative - Oxygen therapy, pulmonary rehabilitation, and, if obstruction is present, bronchodilator therapy + stop smoking
Silicosis Mechanism Presentation Ix Complications
Inhaled silica/sand causes macrophages to release inflammatory cells which cause fibrosis AROUND silica particles
Dry non productive cough + pulmonary oedema if acute
CXR: Upper zone nodules + eggshell calcification of hilar lymph nodes
HRCT: Upper zone - DIAGNOSTIC
Biopsy: Birefringent silica particles
Increased risk of TB and lung ca
Coal Workers Pneumoconiosis
Mechanism
Presentation
Ix
+ Rheumatoid arthritis?
Underground coal mines dust again causes macrophages to cause inflammatory response - requires 10x more than silica
Black sputum dry cough
CXR: Upper zone nodules - indistinguishable from silicosis on CXR
HRCT: Upper zone - DIAGNOSTIC
Biopsy: Reticulin formation + dust around terminal bronchioles
Caplan’s syndrome
Asbestosis Mechanism Presentation Ix Complications
Inhaled asbestos fibres activate macrophages
Dry non productive cough + SoB if pleural effusion
CXR: LOWER ZONE RETICULAR (lace/linear) PLEURAL PLAQUES/THICKENENING + holly leaf shadowing
HRCT: Lower zone fibrosis with pleural thickening
Biopsy: Asbestos bodies + ferruginous bodies. Required for court cases?
Mesothelioma is a malignant unilateral tumour of the pleura. It is not exclusive to those exposed to asbestos; however, the vast majority are due to this cause. Frequently presents with a malignant pleural effusion - exudate. Diagnosis is usually by CT imaging with/without thorascopically guided biopsy.
Occupational asthma Mechanism Presentation compared to normal asthma Diagnosis Mx options Prognosis
Can either be caused by high molecular weight allergens which stimulate IgE or low molecular weight allergens which are so small that they only affect proteins in airway
Onset within 1 year of new work (not immediate)
Rhinitis and conjuctivitis
Sx improve on wekkends/holiday
Evening/nightime Sx 4-6hours after workplace exposure
History and examination
Immunological investigations: Skin prick tests + RAST: Specific IgE
Serial PEF measurements
Serial airway responsiveness measurements - methacholine
Inhalation/workplace challenge tests
Give him an additional corticosteroid inhaler
Tell him to stop work
Suggest he wears a mask at work
Early identification + avoidance is key to reducing morbidity and finances. Non removal of exposure by 2 years means the asthma may become severe/chronic despite removal of causative agent.
Pulmonary hypertension Definition Types/causes Presentation Ix Mx
RARE but common in those with systemic sclerosis, portal hypertension, heart failure
Hypoxia > Polycythemia
Pulmonary artery pressure >25mmHg - assessed via RH catheterisation
Pulmonary artery hypertension - rare idiopathic or associated with HIV CTD etc = fibrosis of vessels causes RV hypertrophy to push blood
- Pulmonary hypertension due to left heart disease = backpressure
- Hypoxic pulmonary hypertension = low oxygen causes vasoconstriction, seen in COPD
- Chronic thromboembolic pulmonary hypertension = recurrent clots physically block and cause release of vasoconstrictive factors
SoB, fatigue + syncope related to exertion
RV heave, raised JVP, loud 2nd heart sound, ABSENCE of crackles
CXR - exclude other lung pathology
ECG - RV hypertrophy
Echo - assess RV function + estimate PA pressure
GOLD STANDARD: Pulmonary angiogram + R cardiac catheterisation
If unsure whether pulmonary/cardiac cause check LH pressure if normal = pulmonary cause
Inconclusive Mx - vasodilators such as prostacyclin, diuretics to treat oedema + HF, digoxin to pump blood, LONG TERM HOME OXYGEN if PaO2 below 8
COPD Sx Dx Mx Complications
SoB, cough, sputum, wheeze. hyperinflated chest, reduced cricosternal distance
FEV1/FVC <70% (if improves by 15% after bronchodilator = asthma)
- Everyone gets SABA as required
- FEV1 >50% use LABA or LAMA
- FEV1 <50% use LABA + ICS + LAMA
Mucinolytics for cough
Psychological - anxiety
Pulmonary deconditioning - use PULMONARY REHABILITATION
Cor-pulmonale:
COPD > hypoxia > pulmonary vasculature constricts > pulmonary artery htn > right heart failure
Secondary polycythemia
Chronic bronchitis vs Emphysema
Blue bloaters vs pink puffers
Chronic bronchitis:
Daily productive cough for 3 months in 2 consecutive years
Overweight and cyanotic
Wheeze
Emphysema:
Destruction of alveolar wall > collapse
Old and thin but barrel chest due to hyperinflation
Long term oxygen therapy in patients with COPD if O2 is ? when stable
OR
when O2 is ? when stable and which 4 conditions
<7.3
<8
Secondary polycythemia
Nocturnal hypoxaemia
Peripheral oedema
Pulmonary hypertension
Cause and consequence of hypoventilation in COPD, OSA, NMD
COPD:
Overinflated lung compresses capillaries + destruction of pulmonary vasculature (emphysema) = Reduced perfusion to ventilated alveolar = hypoventilation = hypercapnia/type2 resp failure = low co2, low o2 + acidosis treat with NIV 88-92%
Obstructive sleep apnea:
Repeated collapsed of upper airway with subsequent arousal needed to reactive the pharyngeal dilator leads to fragmented sleep.
Failure of upper airway tone + obesity + obstruction of pharynx by soft tissue = OSA
Neuromuscular disorders:
Secondary to decreased muscle weakness
Chest wall deformities
Some of the consequences of hypoventilation, such as cor pulmonale and pulmonary hypertension, may be irreversible.
Obstructive sleep apnoea Presentation Screening Dx Mx Complications
Snoring, unrefreshing sleep, excessive sleepiness, obese, crowded pharyngeal space
Epsworth Sleepiness Screening Score tallies likelihood of falling asleep in various situations >9 = abnormal
- Rule out alternatives TFTs, ABG, drug Hx, PFTs
- Sleep studies: 5+ events (hypopnoea/apnoea/ arousals) PER hour in association with sx of sleep disordered breathing = DIAGNOSIS
- GOLD STANDARD: Polysomnography + overnight oximetry + CO2 + EEG etc
CPAP splints airway open with positive pressure (often don’t need O2)
Weight loss + tonsil surgery + Mandibular assist device
Inform DVLA
Associated with HTN! T2DM + stroke + IHD
Hypersensitivity pneumonitis Mechanism Sx - FLU Ix Mx
Alveoli and distal bronchioles diffuse granulomatous inflammation due to IgG type 3/4 hypersensitivity reaction to inhaled antigens: birds, bacteria, animals
(compared to asthma which is type 1 IgE hypersensitivity)
Productive cough, FEVER + systemic symptoms, weight loss, clubbing, diffuse bibasal RALES
Mixed spirometry, +ve blood test for antibody to alleged IgG antigen, high ESR + autoantibodies
CXR: Patchy opacity but clear between attacks
HRCT: Mosaic attenuations (white = alveolitis, black = bronchiolitis) + groundglass in UPPER ZONE
Biopsy: Granulomatous inflammation
Bronchoalveolar lavage: Lymphocytosis + CD8+
Antigen avoidance + steroids for acute exacerbations
Idiopathic Pulmonary Fibrosis
Mechanism/Cause
Presentation
70year old Male
Unknown insult (smoking, organic dust, GORD, infection, CTD/SLE/RA, scleroderma, amiodarone/ methotrexate/nitrofuratoin) causes influx of macrophages + pro-fibrotic cells = alveolar destruction + fibrosis
SoB on exertion, dry cough + velcro crackles, clubbing »_space;> RH failure
Restrictive spiro + reduced KCO + TLC
CXR:LOWER ZONE reticular peripheral fibrosis
HRCT: LOWER ZONE reticular peripheral fibrosis + honeycombing
Acute: Corticosteroids
Ongoing: Antifibrotic therapy – Pirfenidone or Nintedanib AND PPI (GORD prophylaxis)
Sarcoidosis Pathology Sx Ix Mx
Black Scandanavian 20-40s
Persistent and poorly degradable antigen induces a T cell response > alveolar macrophages release inflammatory cells = non-caseating granulomas with multinucleated giant cells in the centre
Non-productive cough, wheeze, non-tender lymphadenopthy, uveitis
Löfgren syndrome: Erythema nodosum + Hilar lymphadenopathy + Arthralgia
Uveoparotid fever
Abnormal ECG
Bloods: High calcium due to production of calcitriol/Vit D by activated macrophages and granulomas
Elevated ACE + ALT
Spirometry: Restrictive
CXR: UPPER ZONE ilfiltrates > fibrosis + hilar lymphadenopathy
HRCT: Nodules follow division of lobes/fissures or bronchovascular distribution + groundglass
Biopsy: Can easily biopsy skin lesions. Flexible bronchoscopy with transbronchial lung biopsy = Non-caseating granulomas - DIAGNOSTIC
Lavage: Lymphocytosis CD4 > CD8, unlike hypersensitivity pneumonitis which has more CD8 cells
Corticosteroids
Which ILD are LESS common in smokers?
DDx for bilateral hilar/mediastinal lymphadenopathy
Hypersensitivty pneumonitis
Sarcoidosis - lungs less sensitive?
UC + Alzheimers
Sarcoidosis
TB
Lymphoma
Lung cancer
Distinguishing features between IPF, HP and Sarcoidosis
Sx
Ix
Mx
Sx:
Productive cough, FEVER aka FLU and diffuse basal RALES = HP
VELCRO crackles = IPF
Lupus pernio, uveitis, lymphadenopathy, erythema nodosum, arthralgia = Sarcoidosis
Ix:
Specific IgG antibodies + ESR, Mixed spiro, Mosaic attenuations in UPPER ZONE but clear between attacks, CD8 cells = HP
Low KCO, LOWER ZONE reticular peripheral fibrosis + honeycombing = IPF
High calcium + ACE, hilar lymphadenopathy + UPPER ZONE fibrosis along fissures + non-caseating granulomas + CD4 cells = Sarcoidosis
Mx:
All given corticosteroids, IPF trial Antifibrotic therapy – Pirfenidone or Nintedanib AND PPI
Conditions associated with NORMAL breath sounds even if CXR abnormal
Coal workers pneumoconiosis
Silicosis
Sarcoidosis
Asthma/COPD have wheeze but otherwise normal breath sounds
Asbestosis/IPF have fine end-insp basal crackles + finger clubbing
