Chest Medicine (week 6) Flashcards
Name 3 chest pathologies that affect the airways?
COPD
Asthma
Bronchiectasis
Name 3 chest pathologies that affect the Interstitium/parenchyma?
Pulmonary fibrosis
Hypersensitive pneumonitis
(emphysema)
Name 3 chest pathologies that affect the pleura?
Pleural effusion
Pleural maliganancy
Pleural thickening
Name 3 chest pathologies that affect the vasculature?
PE
Pulmonary HTN
Name 4 chest pathologies that affect the lungs ventilation?
Sleep disordered breathing
Obesity hypoventilation
Neuromuscular disease
Thoracic cage abnormalities
What parameters are tested in spirometry?
FEV1 (forced expiratory volume in 1 SEC)
VC (vital capacity)
FVC (forced vital capacity - how much total air)
What is the significance of FEV1/VC ratio?
FEV1/VC ratio <70% = obstructive
FEV1/VC ratio normal = restrictive
What is the FEV1/VC ratio of obstructive disease? Give 3 examples of obstructive pathologies.
FEV1/VC ratio <70% = obstructive
COPD, Asthma, Bronchiectasis
What is the FEV1/VC ratio of restrictive disease? Give 4 examples of restrictive pathologies.
FEV1/VC ratio normal = restrictive Pulmonary Fibrosis Hypersensitivity pneumonitis Neuromuscular disorders Thoracic cage abnormalities
What are the 3 pulmonary function tests?
Spirometry, Lung Volumes (flow volume loop), Transfer Factor
What is the characteristic flow volume loop shape of large airway obstruction?
Hamburger shape
What is the characteristic flow volume loop shape of small airway obstruction?
(COPD) Church and steeple
What are the 2 main measurements of lung volumes?
TLC (total lung capacity)
RV (residual volume)
What patterns of lung volumes are seen in an obstructive pathology?
TLC increases with hyperventialtion
RV increases with gas trapping
What patterns of lung volumes are seen in an Restrictive pathology?
TLC falls (definition of restriction) RV falls but proportionally the same
What are the 2 parameters of transfer factor that we measure?
TLCO (transfer factor of CO)
KCO (coefficient of CO) - per unit volume
What is transfer factor a measurement of?
Functionality of the alveolar-capillary membrane
What factors affect the TLCO? Which conditions are these seen in?
- Ventilation Perfusion Mismatch - common in many lung diseases
- Reduction in the area of alveolar-capillary membrane - e.g. emphysema
- Increased thickness of alveolar-capillary membrane - e.g. pulmonary fibrosis
- Pulmonary Blood flow - e.g. pulmonary hypertension
- Haemoglobin concentration - e.g. anaemia leads to a decrease in TLCO
How do we use TLCO and KCO in unison?
KCO is a useful measurement to give information on functionality ‘per unit volume’ of lung
- I.e. 2 full functioning lungs TLCO = 100%, KCO = 100%.
But in someone with a pneumonectomy (1 lung)
- TLCO = 50% but KCO would be 100%.
What is the TLCO & KCO pattern for the obstructive pathologies (asthma and COPD)?
Asthma - TLCO = normal, KCO = normal
COPD - TLCO = decreased, KCO = decreased
What is the TLCO & KCO pattern for restrictive pathologies, both intrapulmonary (IPF) and extrapulmonary (obesity)?
Intrapulmonary (IPF) - TLCO = decreased, KCO = decreased
Extra-pulmonary (obesity) - TLCO = decreased, KCO = Increased (to keep up with demand)
What are the differentials of a diffusely abnormal CXR?
Cardiac failure/ pulmonary oedema Pneumonia/ ARDS Idiopathic pulmonary fibrosis (IIPs) Sarcoidosis Pneumoconiosis Hypersensitivity pneumonitis
What is the difference between HRCT and spiral/helical CT? When is it appropriate to use each?
HRCT
- Finely detailed pictures of parts of the lung e.g. 1mm slice every 10mm
- Good if suspect diffuse condition [fibrosis; HP; bronchiectasis]
Spiral or Helical
- Less detailed imaging but done in continuum therefore do not miss small nodules etc
What is pneumoconiosis?
Lung disease caused by mineral dust
What is the prevalence of occupational lung disease in terms of % of COPD, asthma, cancer and hypersensitivity pneumonitis?
Asthma - 15% of cases
COPD - 15% of cases
Cancer - 2% of cases
Hypersensitivity pneumonitis - 80% of cases
Name 3 types fibrogenic lung diseases?
Silicosis, Coal worker’s pneumoconiosis, Asbestosis
How does silicosis present? (CXR, biopsy and lung function)
Early CXR: Diffuse nodules (differentiate from TB, sarcoidosis & diffuse malignancy)
Late CXR: Solid mass in upper zone
Restrictive lung function
Biopsy: Dense fibrosis with birefringent particles
What is the characteristic biopsy findings of silicosis?
Biopsy: Dense fibrosis with birefringent particles
sparkly nodules - diagnostic
How does coal workers pneumoconiosis present? (CXR, biopsy and lung function)
Early CXR: Diffuse nodules (differentiate from TB, sarcoidosis & diffuse malignancy)
Late CXR: Solid mass in upper zone
Restrictive lung function
Biopsy: Dust accumulation around terminal bronchioles with fibrosis.
What are the different diseases you can get with asbestos exposure?
Heavy exposure: Lung Ca & asbestosis
Light exposure: pleural plaques, pleural fibrosis & mesothelioma.
(Heavy = lungs, Light = pleura)
What is the prognosis of pleural plaques, characteristic CXR appearance, and the associated clinical pattern?
Not associated with other asbestos conditions (good prognosis)
>10 yr latency, usually asymptomatic
CXR: holly leaf appearance
What is the prognosis of benign diffuse pleural thickening, characteristic CXR appearance, and associated clinical pattern??
Forms a small pleural effusion and leaves patient slightly breathless due to restriction.
Rarely progresses.
CXR: blunt costophrenic angles from effusion
What is asbestosis?
Basal diffuse interstitial fibrosis caused primarily by heavy asbestos exposure
How does asbestosis present clinically and on investigation?
Slow onset SOB with exercise Fine end-inspiratory crackles Restrictive abnormality on PFTs Patients may have clubbed fingers (like IPF) CXR = Basal reticular shadowing
What is the treatment and progression of asbestosis?
No treatment (symptom relief) Progresses slower than IPF
What is the latency and progression of malignant mesothelioma?
~ 25 year latency
Progression to death ~18 months
How will a patient with malignant mesothelioma present?
Breathless, chest pain, sweats, anorexia and w. loss.
CXRL bulky pleural masses, thickening, unilateral pleural effusion
CT: thick grey pleura (reduces size of chest wall (pain) & lung fields (breathless))
What is asthma?
Whats the clinical picture?
Chronic airway inflammation
(Reversible) airflow obstruction caused by airway hyper-responsiveness
Wheeze, cough, shortness of breath, tightness
Nocturnal, early mornings (diurnal variation)
Whats the difference between occupational asthma and work-aggravated asthma?
Occupational Asthma
- Asthma which is caused directly by exposures to some agents at work (or is substantially worsened) – always get worse with increased exposure
“Work-Aggrevated” Asthma
- Previous asthma and symptoms are increased because of exposures at work (eg exercise, dust, cold)
What are the 2 types of Occupational Asthma (OA)?
What is the difference between them?
- Sensitiser-induced OA
- ~90% of cases of OA (like an allergy - IgE)
- Latency period between 1st exposure to a “sensitiser” and immunologically-driven symptoms - Irritant-induced OA
- ~ Reactive airways dysfunction syndrome (RADS)
- Few hours after high concentration exposure to irritant gas, fume, vapours at work. Sometimes 1 exposure is enough.
What is the allergen work exposure limit?
4mg/m3
What are the key investigations in Occupational Asthma?
Total IgE level Skin prick tests Peak flow readings at work and home Airway responsiveness measurements Inhalational challenge test
What is the key feature in history pointing towards occupational asthma?
Symptoms better at weekend or on holiday
Others include:
Onset often within one year of new work
Latent interval of asymptomatic exposure
Worsening during the week
Worse with heavier exposures
Associated nasal/ eye symptoms (IgA sensitisation)
Other workers often affected
Associated with rhinoconjunctivitis and dermatitis
What is the most effective treatment for occupational asthma?
Redeployment to avoid asthmagen exposure
What is the most common agent causing occupational asthma in the UK?
Isocyanates from paint spraying or Wheat Flour (bakers asthma)
What are the key investigations in Occ Asthma?
- Serial PEF measurements (home and work)
- Allergy tests : skin prick/ serum IgE levels
- Challenge tests
• Methacholine challenge (strong bronchoconstrictor)
• Workplace visit/challenge test (take PEFR every hr for 3 days)
• Direct inhalational challenge test
%FeNO is sometimes used in the diagnosis of OA
• Fractional exhaled nitric oxide (NO)
• NO released by inflamed bronchial epithelial cells in asthma and is a surrogate marker for eosinophilic inflammation in the airways. - Sputum eosinophils in OA
• Eosinophilic airway inflammation is a hallmark of asthma.
• Suppressed in cigarette smokers (won’t work as a marker)
What is the Scoring system for occupational asthma? What score indicates Oc Asthma?
OASYS score (range 0-4) ≥2.4 - highly suggestive of Occ Asthma
What is the methacholine challenge test? What score are you looking for in Oc Asthma?
Methacholine (very strong bronchoconstrictor, non-selective muscarinic antagonist)
Take basic FEV1, then breath in increasing doses of methacholine (1.5µg – 3.2mg), repeating the lung function.
You look for a PD20 (the amount of methacholine that causes a 20% drop in FEV1)
Compare this score at work and on holiday
What are the 2 broad categories of Oc asthma causative agents?
High molecular weight allergens
• Flour – bakers, Animals – labs, shops, Enzymes - detergents
Low molecular weight agents
• Isocyanates (most common) – paints, Acrylates - superglue & 100s of others
How do high molecular weight allergens drive Oc Asthma?
Usually proteins with Specific IgE antibodies
- Similar to asthma driven by Cf mites, animals, pollen
How do low molecular weight allergens drive Oc Asthma?
Reactive chemicals with often no specific IgE
- Very small so body barely recognises them, however they are very reactive and react with proteins within your lungs alveoli to make NEOANTIGENS (new proteins). Because there is a change in the protein structure, the body thinks they are foreign and will develop an immune response to them.
What are the risk factors for OA?
Atopy (allergy) increases risk of OA in HMW agents
Smoking increases risk of sensitisation to:
• Platinum salts, Seafood, Flour, Coffee and castor bean
What is the treatment and prognosis of Oc Asthma?
Standard asthma treatment – BTS Asthma guidelines
Anti IgE therapy – Omalizumab (Used for severe asthma.)
1/3 recover completely.
What is the definition of chronic bronchitis?
Chronic (>3 months in a row for 2 consecutive years) or recurrent excessive mucus secretion in the bronchial tree. (improves with smoking cessation)
What is the definition of Emphysema?
An increase (beyond the normal) in the size of the air spaces distal to the terminal bronchiole accompanied by destruction of their walls and without obvious fibrosis. (causes small airway obstruction)
What is the most significant aspect of a Hx in diagnosing COPD?
SH - smoking Hx. (20 pack year Hx)
What is the benefit of pulmonary rehabilitation in COPD patients?
Improves exercise tolerance
Reduces dyspnoea
Improves QOL
Reduced hospitalisations
What is Cor Pulmonale?
RH failure caused by lung disease
Whats the main driver of cor pulmonale in COPD patients?
Directly relates to the V/Q mismatching in the lung.
What is V/Q matching and how does it work?
Matching ventilated areas of the lung with adequate perfusion.
This helps optimise lung function (will put the most perfusion to areas with highest ventialtion).
E.G
If you have an area with pneumonia, ventilation is poor in that area, blood vessels constrict and send blood to areas with better ventilation.
Why does V/Q matching cause issues in COPD?
In EMPHYSEMA HYPOXIA IS EVERYWHERE.
- Your body detects large areas of hypoxia (therefore poor ventilation) and constricts blood vessels to reduce blood supply to the area.
- Vessels constrict, pulmonary vascular resistance increases massively as pulmonary blood supply is effectively pushing against a closed door
- Heart eventually fails = Cor Pulmonale
What is usually the first sign of Cor Pulmonale?
Hypoxia is the driver, but ANKLE OEDEMA usually the first sign
What is the treatment of Cor Pulmonale?
LTOT - Oxygen therapy for 16 hours a day
Diuretics
What is the best treatment for COPD?
Steroid Inhaler
SABA - B2 Agonist (Salbutamol) / LABA (salmeterol)
LAMA - Long acting muscarinic antagonist (tiotropium)
+
Pulmonary rehab & smoking cessation
What is the hallmark of HYPOventilation?
Persistently raised CO2 (hypercapnia)
What are the PO2 parameters for hypoxia and respiratory failure?
Hypoxaemia – PaO2 < 10 kPa on air
Resp failure = < 8 kPa on air
What are the different types of respiratory failure?
Type 1 - PaO2 < 8 kPa on air
Type 2 - PaO2 < 8 kPa on air & PaCo2 > 6 kPa
What happens in Acute on chronic respiratory failure?
Alveolar hypoventilation
In an ABG they will be hypoxic , but the key marker is HYPERCAPNIA.
This is because we aren’t expelling the CO2 from our lungs.
What’s the pathophysiology of Hypoxaemia and Hypercapnia?
Hypoxaemia - Usually caused by V/Q mismatch (ventilation/perfusion) & shunt Hypercapnia - Hypoventilation - Increase in deadspace ventilation - V/Q mismatch can also contribute.
Whats the relationship between alveolar ventilation and hypercapnia?
PaCO2 is inversely proportional to alveolar ventilation (how often and deeply we breathe)
What symptoms suggest respiratory insufficiency?
Breathless on exertion (dyspnoea)
Breathless when lying down (orthopnoea)
Extreme fatigue
Decreased appetite, anxiety & poor concentration
What are the symptoms of nocturnal hypoventilation?
Common as when we sleep our muscles are weaker, therefore respiratory muscles are also weaker.
o Disturbed sleep, frequent awakenings, morning headaches
Name 4 conditions that commonly cause hypoventilation?
COPD
Muscle Disease or diaphragm paralysis
Chest wall deformity and spinal injury
Central and Obstructive Sleep Apnoea
Why does high flow O2 therapy worsen hypercapnia in COPD patients?
Increased O2 will cause V/Q matching to open up all the vessels that have been shut due to V/Q mismatch.
These would take the oxygen but deposit CO2.
This wouldn’t be ventilated and would build up a level of CO2.
What is obstructive sleep apnoea and what causes it?
Recurrent nocturnal upper airway obstruction
Usually causes repeated desaturations, this is due to the soft upper airway closing when it doesn’t have the support of the neck muscles to keep it open.
What are the risk factors for obstructive sleep apnoea?
Obesity - BMI 30+ (40% will have OSA)
Diabetes
Hypertension
Stroke
How can obstructive sleep apnoea present?
Nocturnal problems
• Often partner/spouse complains
• Heavy snoring, Choking/gasping, Apnoeas (stops breathing)
• Awakenings – Brainstem measures O2 in brain. If it gets too low we wake up.
• Nocturnia
• Insomnia
• Morning headaches – High CO2, goes away when you ventilate CO2 away.
Daytime problems
• Excessive daytime sleepiness
• Work-related accidents, Driving accidents,
• Concentration/ability impairment, Cognitive problems
What is the score that quantifies severity of obstructive sleep apnoea?
Epworth sleepiness score
also apnea hypoxic index
What is the treatment of obstructive sleep apnoea?
Depends on symptoms
- CPAP - needs to be severe symptoms for patients to use it. Use for 2-4hr per night
- Tonsillectomy
- Jaw advancement device
Describe the genetic inheritance pattern Duchenne Muscular Dystrophy (DMD)?
X linked recessive disorder
What is the most common cause of death in patients with Duchenne Muscular Dystrophy (DMD)?
73% deaths hypercapnic respiratory failure, due to weak respiratory muscles and diaphragm
What is the best treatment of: a) hypoventilation b) inability to cough c) collapsed lung in patients with Duchenne Muscular Dystrophy (DMD)?
a) NIV - Non Invasive ventilation
b) Cough assist (removes secretion and prevents infection)
c) Lung recruitment (opens up lung)
What is the definition of Interstitial lung disease?
An imprecise term for a range of diseases which affect the lung parenchyma with cellular infiltration (inflammation) of the alveoli, interstitium and distal airways, and which may progress to fibrosis:
- Idiopathic pulmonary fibrosis
- Hypersensitivity pneumonitis
- Sarcoidosis
What is the interstitium?
A lace-like network between alveoli, other alveoli and the capillaries, that contains tiny capillaries that allow gas exchange.
Considering the pathophysiology, what type of abnormality do PFTs show in ILD?
Inflammation causes progressive, patchy digress thickening of the alveolar walls.
This can lead to fibrosis and therefore cause a small stiff lung with impaired gas exchange = RESTRICTIVE PICTURE
What will a CXR show in ILD patients?
Small white lungs (air is black).
Diffuse interstitial shadowing due to fibrosis (reticular (lines) nodular (nodules) shadowing)
NB - normally the interstitium is so thin that it can’t be seen on X-ray.
Name 3 types of ILD - whats the most common?
Most common - Idiopathic Pulmonary Fibrosis (IPF)
Common - Sarcoidosis, Hypersensitivity Pneumonitis (EAA)
Less common - Pneumoconiosis, Connective tissue disease, Drug related interstitial disease
Asbestosis will cause very similar symptoms to IPF
What is the pathophysiology of IPF?
Growth factor etc
What’s the treatment for IPF?
If mild and they are stable - no treatment
Best Supportive Care ie:oxygen/rehab
(LTOT improves quality of life the most)
Pirfenidone / Nintedanib – are the only 2 licensed & are very expensive (antifibrotics, slow progression)
Prednisolone, azathioprine
Transplant (rare)
o Average presentation with IPF is 72, upper age limit of viability for lung transplant is 65
What is the prognosis for IPF?
Average survival from time of diagnosis for IPF patients is 3 years.
What signs are typical of IPF pts?
- Cyanosis – most likely peripheral, but occasionally central (underneath the tongue) (Blue lips is peripheral cyanosis)
- Clubbing – loss of nail angle is most important, curvature of nail, fluctuation of nail.
- Reduced expansion
- Fine Crackles (Velcro-like) – starts at lung bases. (Earliest sign of IPF, will appear before CT evidence.)
NB - IPF is a diagnosis of exclusion - you must ask an extensive history first
What is the difference between fine and coarse crackles?
Fine = Fibrosis
• Dry cough & Restrictive physiology
Coarse = Bronchiectasis
• Wet, productive cough & Obstructive physiology
What is Sarcoidosis? What is the pathophysiology?
Multisystem granulomatous disease of unknown cause, primarily affecting the lung. It is caused by autoimmune processes following exposure to environmental, occupational or infectious agent.
T cells and multinucleated giant cells that cause granulomas all over the body
What are the CXR signs of sarcoidosis patients?
Bilateral Hilar/Mediastinal lymphadenopathy – big dark areas on radiograph.
What investigation do you use to differentiate between IPF and sarcoidosis? What will it show?
High Resolution CT
In sarcoidosis, presence of lymph nodes (near the centre) but also lots of nodules within the lung fields, that tend to bead around the fissures
NB - this is not diagnostic
What is the GOLD STANDARD investigation in IPF, and what does it show?
HRCT (high resolution CT) is the Gold standard of interstitial lung disease diagnosis - look for zone location, type, distribution, cysts, honeycomb, lymphadenopathy, ground glass opacity
Which investigation is used to confirm diagnosis of sarcoidosis? What will it show?
EBUS (EndoBronchial Ultrasound guided FNA). ‘bronchiolar lavage’
• Biopsy will show a non-caseating, non-necrotising granuloma with multinucleated cells (if sarcoidosis)
What is the treatment of Sarcoidosis?
Ideally none as it will be self limiting
Steroids if treatment required as its an immune inflammatory disease
Bilateral hilar lymphadenopathy can be a sign of many things, however 4 big ones to learn are:
- Sarcoid
- TB
- Lymphoma
- Carcinoma
What is Hypersensitivity Pneumonitis (HP) - (AKA Extrinsic Allergic Alveolitis – old name)?
Immune mediated, allergic reaction to something you inhale.
Repeated exposure causes formation of granulomatous inflammatory foci, which can eventually lead to lung fibrosis.
Name 2 causes of Hypersensitivity Pneumonitis?
- Bird fancier’s lung – Most common – Ask about pigeons, many dont see them as pets.
- Farmer’s lung – moldy hay spores
Saw mill worker's lung Mushroom worker´s lung Malt worker´s lung Humidifier lung Cheese washer's lung Suberosis Hot tub lung
What is the characterstic sign of Hypersensitivity Pneumonitis?
Wheeze - terminal bronchiole involvement
What findings of Hypersensitivity Pneumonitis are seen on CT and CXR?
CXR – diffuse shadowing like IPF
HRCT – Mosaicism – Get patient to breath out (expiratory scan)
(Areas of black and grey next to each other. As its an expiratory scan and black means air, the black areas are pathological because the air is trapped due to bronchiole involvement.)
NB - fibrosis will be apical as inhaled agents go to the top of the lung
(in sarcoidosis etc, fibrosis will be basal)
What is the treatment of Hypersensitivity Pneumonitis?
Antigen avoidance and steroids (prednisolone)
LTOT in severe disease
What are the PFT results that would suggest bronchiolitis?
FEV1/FVC <70% - obstructive picture
No response to bronchodilators
TLCO - normal, KCO - normal or increased (obstructive picture)
Flow volume loop = Church and steeple appearance.
Give some examples of isolated bronchiolitis?
Viral infection in children
Transplant rejection
Idiopathic diffuse panbronchiolitis
Rheumatoid disease
What are the 3 different forms of Hypersensitivity Pneumonitis caused by birds?
Acute form (pigeon fancier)
- Flu-like illness 6 hrs after exposure, lasting 3-4 days - SOB, tightness, malaise, crackles
- Poorly formed infiltrate on chest radiograph
Subacute
- Symptoms less severe and last longer
Chronic form (budgeriegar keeper)
- Cyanosis, clubbing, bibasal crackles
- Progressive breathlessness due to low level of exposure
- Upper zone fibrosis and honeycombing on radiograph
- Restrictive ventilatory abnormality
What are the milder and more severe states of coal workers pneumoconiosis?
Mild - anthracosis
Severe - chronic bronchitis
What does biopsy of coal workers pneumoconiosis show?
Dust accumulation around the terminal bronchioles, with fibrosis
How can hypoventilation and OSA be investigated? Which is the gold standard?
- ABG analysis (GOLD STANDARD)
- Pulmonary function tests
- Overnight oximetry transcutaneously
- Venous bicarb
- Sleep studies
Why is venous bicarb measured as well as ABG analysis, in hypoventilation?
Gives a 24 hour average of the total CO2
What 5 variables does polysomnography measure? How does it aid diagnosis of OSA?
- Brain waves
- Oxygen
- HR
- RR
- Chest/leg/arm movements (more pronounced)
For OSA this would show a diagnostic cycle pattern of obstruction then breathing
What are the SIGNS of OSA?
- Crowded pharyngeal airspace
- Increased mallopthi score (ease of intubation)
- Retrognathia
- High epworth score
What organisation needs to be informed if a patient has OSA?
DVLA - 8x risk of RTA
What are the contraindications to NIV?
- Respiratory arrest
- Inability to protect airway
- Facial trauma
- Poor respiratory drive
- Reduced consciousness
- Air leak syndrome
What is the significance of ground glass opacity on X-ray?
Indicates partial filling of alveoli by transudate/exudate
In which disease would you see mosaicism on HRCT?
Hypersensitivity Pneumonitis - due to air trapping
In which disease would you see hilar lymphadenopathy and nodular beading around the fissures on HRCT?
Sarcoidosis
In which connective tissue diseases do you see interstitial lung disease?
Scleroderma Rheumatoid arthritis Sjorgens SLE Dermatomyositis
What are the features of sarcoidosis?
- Erythema nodosum - painful rash with arthralgia, tend to settle after 2 weeks
- Lupus pernio rash across cheeks and nose (might need to take skin biopsy)
- Lung disease - bilateral hilar lymphadenopathy
- Night sweats
- Anterior uveitis - inflammation of iris, choroid, ciliary body, ‘fluid level’
- Neurosarcoidosis
- Hypercalcemia
What would investigations show in sarcoidosis?
Serum ACE - raised ESR/CRP - raised CXR - bilateral hilar lymphadenopathy HRCT Biopsy - non-caseating granulomas
How is acute sarcoidosis managed?
NSAIDS
What is erythema nodosum associated with?
IBD
Sarcoidosis
What is the most appropriate diagnosis to confirm PE?
V/Q mismatch - this is need to confirm diagnosis!!
What is the DEFINITIVE diagnostic test for interstitial lung disease?
Lung biopsy - high T cells, granulomas, fibrosis
What are some differentials for sarcoidosis?
TB
Lymphoma
What side effects does amiodarone cause?
Lung fibrosis
Thyroid issues
What is the treatment for infective exacerbation of COPD?
Oxygen + PO prednisolone + IV/oral abx + NEB salbutamol and ipratropium
