Respiratory Flashcards
What are the paraneoplastic syndromes associated with lung cancer?
SIADH
Cushings
Hypercalcemia
Which lung cancer causes Cushings?
ACTH is released from small cell lung cancer
Which lung cancer causes SIADH?
ADH is released from small cell lung cancer
Which lung cancer causes hypercalcemia?
Parathyroid related peptide (PTHrP) from squamous cell carcinoma –> increased Ca absorption from gut, reabsorption from kidneys + bone resorption
Small cell lung cancer
Very aggressive + poor prognosis
Poorly differentiated neuroendocrine tumour
Often present with more disease in lymph nodes than lungs
Surgery usually pointless due to amount of extrapulmonary tissue therefore chemo
Histologically –> small cells with large, dark, irregular nuclei
Squamous cell carcinoma
- Thought to derive from squamous metaplasia of the airways (from smoking)
- Better prognosis than adenocarcinoma but more associated with smoking
- Central forming cancer
Histologically –> must show keratin formation + intercellular bridges
Which carcinoma is described as lepidic?
Adenocarcinoma - spreads along surface of alveolar walls
Adenocarcinoma
- Thought to derive from atypical adenomatous hyperplasia
- Peripherally forming
- Commonest type of lung Ca
- More likely to have no smoking hx than SCC
- Can show lepidic pattern which shows a groundglass appearance on CXR like infection
Histologically –> gland formation or mucin production
Which is the commonest type of lung Ca?
Adenocarcinoma
Metastasis in the lung
Actually the commonest type of tumour in the lung!
Commonest site of metastasis because dense capillary network captures circulating tumour
Usually multiple peripheral nodes on imaging
What staging is used for lung cancer?
TNM
What is a carcinoid tumour?
Low grade neuroendocrine tumour (other end of spectrum to small cell)
Low grade malignancy as behaviour difficult to predict - some do metastasise
Usually very well defined on imaging - diagnosis suspected before tissue diagnosis
What mutations are tested for in order to determine treatment of NSCLC?
EGFR mutation
ALK translocation
ROS1 translocation
PD-L1 expression
Which is the most malignant type of pleural tumour?
Metastases from lung + breast
What is the lag period between asbestos exposure and mesothelioma developing?
20-30 years
Clinical features of mesothelioma
Tumour encases lung + burrows into chest wall
Lymph node + distant metastases unusual
Indistinguishable from lung Ca on history but more chest pain + no lymphadenopathy
Diagnosis of mesothelioma
CT is distinctive - tumour wraps around lung, infiltrating into fissures
Histology of mesothelioma
Atypical mesothelial cells infiltrating surrounding tissue
What is a primary spontaneous pneumothorax?
Occurs in young people without known respiratory illness
Pneumothorax
Accumulation of air in the pleural space
What is a secondary spontaneous pneumothorax?
Occurs in people with pre-existing pulmonary disease
Clinical signs/symptoms of pneumothorax
May be minimal/absent in PSP
- Sudden onset of pain
- SOB (depending on size)
- Tachycardia (>135 suggests tension)
- Pulsus paradoxicus (HR slows with inspiration)
- Hypotension
- Raised JVP
- Hyper-resonance + reduced breath sounds over area
Type 1 respiratory failure
Hypoxic but normal normocapnia
- V/Q mismatch (amount of air in doesn’t match BF to lung)
Give oxygen + treat cause: pneumonia, PE, pneumothorax, acute asthma, ARDS, COPD, pulmonary oedema
Type 2 respiratory failure
Hypoxia + hypercapnia
Alveolar hyperventilation
Acute - respiratory acidosis but normal bicarb
Chronic - high bicarb to maintain acid-base balance
Causes: COPD, exhaustion in asthma, obstructive sleep apnoea, opiates, NM disorders
Oxygen mask concentrations
Air: 21% Nasal cannula: 24-40% Simple mask: 40-60% Non-rebreathe: 90% Venturi: 24, 28, 35, 40, 60%
Treatment for primary spontaneous pneumothorax
If >2cm + SOB - aspirate and if this doesn’t work then use chest drain
If <2cm and no SOB - leave it and review
Treatment for secondary spontaneous pneumothorax
If >2cm or SOB - Aspirate - if successful (<1cm) then admit + observe. If fails then add chest drain
If <2cm and no SOB - if 1-2cm then aspirate, if <1 then admit + observe
Examples of lung fibrosis affecting the lower, mid and upper zones
Lower - idiopathic pulmonary fibrosis
Mid - sarcoidosis
Upper - hypersensitivity pneumonitis
Clinical features of fibrosing lung disease
SOBOE, dry cough, fine end inspiratory crackles, joint or skin disease, clubbing
Histological features of fibrosing lung diseases
Fibrosis + remodelling of IS
Chronic inflammation
Hyperplasia of type II epithelial cells or type II pneumocytes
Most common interstitial lung disease?
Idiopathic pulmonary fibrosis
Idiopathic pulmonary fibrosis
Commonest cause of ILD
M>F 70yrs
Poor prognosis
Often associated with autoimmune disease
Features: SOB, dry cough, malaise, WL, arthralgia, clubbing, cyanosis, bilateral end-inspiratory crackles basally
Which drug slows disease progression in IPF?
Pirfenidone + nintedanib
How does coal workers pneumoconiosis occur?
Inhalation of coal particles - taken up by macrophages - die - release enzymes - cause fibrosis
What is progressive massive fibrosis?
progression of coal workers pneumoconiosis causing SOB, fibrosis and eventually cor pulmonale.
On a CXR - bilateral upper mid zone fibrotic masses developing from periphery towards the hilum
What does silicosis show on a CXR?
Diffuse military or nodular pattern in upper + mid zones and egg shell calcification of hilar nodes
What does asbestosis show on a CXR?
Pleural plaques
What is extrinsic allergic alveolitis?
Hypersensitivity to inhaled particles
Granuloma formation + obliterative bronchiolitis
4-6h post exposure - fever, rigors, malaise, SOB, dry cough, bibasal crackles
Chronic - clubbing, SOB, SOBOE, WL, type 1 respiratory failure
Avoid trigger!! Steroids may help
What is spirometry used for?
Differentiating between obstructive + restrictive disease
Can monitor disease progression
Obstructive pattern in spirometry
FEV1 reduced
FVC reduced but not as much
–> Fev1/FVC ratio reduced
Restrictive pattern in spirometry
Fev1 reduced
FVC reduced
–> Fev1/FVC normal
Bronchiectasis
Permanent dilatation + thickening of the airways characterised by chronic cough, excessive sputum production, bacterial colonisation + recurrent acute infections
Causes of bronchiectasis
50% idiopathic
CF
Post infection e.g. pneumonia, measles, pertussis
ABPA - allergic bronchopulmonary aspergillosis
Signs + symptoms of bronchiectasis
Chronic cough, sputum, SOB, chest pain, WL
Clubbing, coarse inspiratory crackles, wheeze
Cause of fine crackles
Fibrosis
Cause of coarse crackles
COPD
Pneumonia
Bronchiectasis
TB
Which 2 diseases make up COPD?
Chronic bronchitis
Emphysema
Emphysema
Alveoli are destroyed causing a loss of elasticity so air becomes trapped in them
Histological dx of enlarged air spaces distal to terminal bronchioles with destruction of alveolar walls
Chronic bronchitis
inflammation of the lining of bronchial tubes
Cough + sputum on most days for 3m of 2 successive years
Which disease are pink puffers?
Emphysema
Thin, less hypoxic, SOB, hyperinflated, tachypnoeaic, pink, low PCO2
Which disease are blue bloaters?
Hypoxic, cyanosis + swollen feet/ankles/legs (HF or cor pulmonale)
Signs + symptoms of COPD
SOB, cough + sputum, WL, frequent winter bronchitis, barrel chested, wheeze, coarse crackles
Investigations of COPD
Bedside: sputum sample, ECG
Bloods: ABG, FBC (anaemia + polycythaemia), could check AAT level
Imaging: CXR, echo
Special tests: spirometry + reversibility
Management of COPD
Conservative:
- Lifestyle (stop smoking, exercise)
- Chest physio
- Pulm rehab + MDT
- Vaccinate
- Assess impact (MRC scale)
Medical:
- SABA or SAMA. If still breathless then next step determined by asthmatic features e.g. steroid responsiveness so LABA + LAMA +/- ICS
- Then specialist e.g. theophylline, LTOT
- Consider carbocysteine
What is in a COPD rescue pack?
5 days supply of prednisolone, 5 day supply of amoxicillin/doxy (use if purulent sputum)
CXR findings of COPD
- Hyperinflation - >6 anterior ribs
- Prominent pulmonary arteries
- Peripheral oligaemia
- Bullae
Who gets LTOT?
Non-smokers with: PaO2 <7.3, PaO2 7.3 - 8 when stable + 2nd polycythemia, nocturnal hypoxaemia, peripheral oedema, pulmonary HTN
Required for 15h a day for benefit
Severity of COPD
Mild - FEV1 >80% predicted
Mod - FEV1 50-79%
Severe - FEV1 30-49%
V. severe - FEV1 <30% (or <50% with resp failure)
MRC dyspnoea scale
- Not troubled by breathlessness except on vigorous exertion
- SOB when hurrying or walking up inclines
- Walks slower than contemporaries because of breathlessness or has to stop for breath when walking at own pace
- Stops for breath after walking 100m or stops after a few minutes walking on level
- Too breathless to leave the house or breathless on dressing or undressing
What is the most common organise of an infective exacerbation of COPD?
Haemophilus influenza
Things to not forget in an asthma history
C - compliance with medication R - reliever usage O - occupation S - sleep interference S - smoking E - eczema, atopy? D - days missed from work
Management of acute asthma
O - oxygen 15L non rebreathe, sit pt up S - nebulised salbutamol back to back H - hydrocortisone IV I - nebulised ipatropium T - IV theophylline Magnesium sulphate IV if no improvement
Normal/high CO2 is very worrying - ITU
Inhaler technique
Remove cap Shake If not used for wk/new then spray Hold upright Breathe out as much as possible Start to breathe in slow + deep then press Hold breath for as long as possible If need 2nd dose - wait 30secs
% of oxygen for litres
4l = 35% 6l = 50% 8l = 55% 10l = 60%
HAP
Occurs 48h after admission or anytime from an institution
Always typical
CAP
Can be typical or atypical
Signs + symptoms of pneumonia
Fever, rigors, malaise, cough + sputum, haemoptysis, pleuritic chest pain
Increased RR, increased HR, cyanosis, confusion, consolidation - reduced air entry + expansion, dull to percuss, crackles, bronchial breathing, pleural rub
Typical of CAP
Strep pneumonia, haemophilus influenza
Atypical of CAP
chlamydophila, legionella, pneumocystis
HAP organisms
Gram -ve enterobacteria
Staph aureus
CURB 65 score
Confusion
Urea >7
RR >30
BP <90/60
Age 65
0-1 = outpatient
2 = hospital
3 or more = consider itu
What is a pleural effusion
Fluid in the pleural space
Name for blood in the pleural space
Haemothorax
Pus in pleural space
Empyema
Blood + air in pleural space
Haempneumothorax
Chyle (lymph + fat) in pleural space
Chylothorax
Causes of a transudative pleural effusion
Increased venous pressure (HF, constrictive pericarditis, fluid overload)
Hypoproteinaemia (LD, malabsorption)
Hypothyroidism
Causes of an exudative pleural effusion
‘Leaky capillaries’
Infection, malignancy, TB, SLE, mesothelioma
Signs + symptoms of pleural effusion
SOB, pleuritic chest pain
Stony dull percussion, decreased expansion, diminished breath sounds, may have bronchial breathing in rest of the lung above effusion, may be trachea deviation away from effusion if very large
Pleural effusion on a CXR
Blunted costophrenic angles
Level of protein in exudative v transudative
Transudative <25
Exudative >35
If 25-35 then use lights criteria to distinguish - if protein/serum >0.5 then exudative
Primary TB infection
Non-immune host who is exposed may develop primary infection of the lungs - Ghon focus develops in lungs which can turn into Ghon complex (combination of ghon focus with hilar lymph node involvement)
Secondary TB infection
When TB that may have been latent becomes reactivated in a person - usually when they have become immunocompromised. Can spread locally or distally - military TB
What happens when TB is inhaled?
Ingested by macrophages - form giant cells with central necrosis
What increases the probability of TB being transmitted?
Infectiousness of case i.e. number expelled into air
Enviro factors e.g. air flow
Duration, proximity and frequency of exposure
Susceptibility of exposed person
Is extrapulmonary TB infectious?
Not usually
Latent TB contact screening
Mantoux (tuberculin skin test)
IGRA (IFN g release assay) - blood test with blood with TB and see if WBCs produce IFNg - if yes then do they have TB? if no then do they need the BCG?
If signs of active TB DO NOT use these tests
Symptoms of TB
Long hx as slow growing e.g. 3m of fever
Fever, WL, fatigue, night sweats (TNFa), cough, haemoptysis
How to diagnose TB?
- Acid fast bacilli test for initial screen (if +ve then highly infectious) if +ve do ziel nelson stain to confirm
- CXR - infiltration of upper zones + hilar lymphadenopathy
- Broncho-alveolar or gastric lavage
- Grow the organism (takes 4wks!) then another 4 wks to see what abx!!
- Whole genome sequencing effective tool for predicting drug susceptibility + resistance - get results in 5-7d (looks at SNPs)
