Respiratory Flashcards
Chronic obstructive pulmonary disorder (COPD) definition
A disease state characterised by airflow limitation that is not fully reversible.
Encompasses emphysema and chronic bronchitis.
Airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases. Associated with type 2 respiratory failure (decreased PaO2, increased PaCO2)
Chronic bronchitis
- airways inflammation and narrowing
- increased mucus production
- bronchitis is often temporary but need to be chronic to cause COPD
Emphysema
- destruction and dilation of air spaces
- can’t recoil and expel air
COPD aetiology
Smoking is the cause in over 90% of cases
Other causes: cystic fibrosis, industrial exposure to irritants eg mining, heavy industry etc alpha-1-antitrypsin deficiency (ver rare, about 2% of emphysema)
COPD pathophysiology
Chronic bronchitis: airways become inflamed due to irritants, narrowing them and leading to increased mucus producing. Smoking causes mucus glands to increase in number and the irritants damage the cilia meaning that the mucus can’t effectively be removed from the airway, causing a chronic cough and mucus/phlegm production
Emphysema: alveoli become large and lose their elasticity - they therefore cannot recon and expel all of the air out. Smoking causes this damage as it causes release of inflammatory factors (to fight off irritants) which break down collagen and elastin in the airways. When breathing the alveoli become more full than they should, causing a barrel chest.
Alpha-1-antitrypsin (A1AT) deficiency: A1AT regulates elastase activity. No A1AT leads to uncontrolled elastase activity. Elastase builds up in the liver causing cirrhosis. Elastase destroys alveoli leading to emphysema. In A1AT deficiency, the lower acinar (alveoli) are more affected whereas those at the top are more affected in normal COPD (irritants get less far down the lungs)
COPD clinical manifestations
Signs: dyspnoea, tachypnoea, barrel chest, ankle swelling (caused by resulting heart failure), cyanosis may be present
Symptoms: SOB, chronic cough, recurring chest infections
Chronic bronchitis (blue boater):
- clinical diagnosis
- daily productive cough for three or more, in at least two consecutive years
- chronic respiratory infections
- overweight and cyanotic
- elevated haemoglobin
- peripheral oedema
- hypoxemia and hypercapnia - may lead to cyanosis
- crackles *due to airways opening when large amounts of mucus is present)
- rhonchi (coarse respiratory sounds due to secretions I the bronchial airways) and wheezing
- hypoxic vasoconstriction of the pulmonary arterioles leads to increased pulmonary vascular resistance and therefore pulmonary hypertension - putting strain on the right side of the heart which leads to right heart enlargement - leading to right sided here failure (COR PULMONE)
Emphysema (pink puffer):
- pathological diagnosis
- permanent enlargement and destruction of airspace’s distal to the terminal bronchiole
- older and thin
- severe dyspnea - may exhale slowly through pursed lips to increase pressure I airways and keep them from collapsing (puffer)
- weight loss can result from increased breathing effort
- can lead to hypoxemia
- cough with some sputum (less then chronic bronchitis) may be present
- air trapping and hyperinflation can lead to barrel chest
- quiet chest
- CXR - hyperinflation with flattened diaphragms
- hypoxic vasoconstriction of the pulmonary arterioles leads
A1AT deficiency: always consider in young COPD patients with deranged LFTs or other liver signs eg ascites, jaundice
COPD 1st line investigations
CXR
- emphysema: hyperinflation of the lungs, a flattened diaphragm and a barrel shaped chest
- do to exclude cancer
COPD gold standard investigations
Spirometry: obstructive picture, FEV1/FVC < 70%, does not respond to reversibility testing with SABA
COPD other investigations
FBC: chronic hypoxia may cause polycythemia
BMI: weight loss - lung cancer
Serum A1AT
DLCO: shows how well CO2 is diffusing in and out of the blood, reduced in COPD patients as the exchange pathway is impaired.
COPD management
Acute:
- oxygen
- nebuliser SABA - salbutamol
- inhaled steroids
- treat any current infection
Chronic Fundamentals of COPD care - smoking cessation - offer pneumococcal and influenza vaccines - pulmonary rehabilitation if indicated
Start inhaled therapy if: previous advice given, clinical need for inhaled therapies
Step 1:
- SABA (ie salbutamol or terbutaline) or SAMA (ipratropium bromide)
Step 2:
- if no asthmatic/steroid response: LABA (ie salmeterol) + LAMA (ie tiotropium)
- if asthmatic/steroid response: LABA (ie salmeterol) and ICS (ie budesonide); can be given in combined Symbicort inhaler (Formoterol (LABA) + budesonide (ICS))
Step 3:
- add long term oxygen therapy
Exacerbations:
Steroids (hydrocortisone/prednisolone) + nebuliser bronchodilators (salbutamol/ipretropium bromide) + Abx
If severe: IV aminophylline (bronchodilator), may need ventilation (usually BiPAP as tends to cause type II respiratory failure)
COPD monitoring
MRC Dyspnea Scale
- Grade 1: not troubled by breathlessness except on strenuous exercise
- Grade 2: SOB when hurrying on a level or when walking up a slight hill
- Grade 3: walks slower than most people on the level, stops after a mile or so or stops after 15 mins walking at own pace
COPD complications
Infective exacerbations (IE COPD) Emphysema: increased pneumothorax risk due to bullae
Asthma definition
Reversible chronic obstructive disease. Asthma is sometimes called bronchial hyperrespnsiveness (twitchy airways). Characterised by bronchocontricton and excessive secretion production.
Asthma aetiology
In most cases is an allergic disease (atopic asthma) often associated with atopy and allergy. Allergic inflammation is characterised by the recruitment of eosinophils. Atopy is the tendency to develop IgE mediated reactions to common aeroallergens.
Atopic triad: asthma, eczema, allergic rhinitis (hay fever)
Can divide asthma into eosinophils and non-eosinophilic. Asthma is often linked to COPD especially in smokers. Eosinophilic asthma can be further divided into atopic and non-atopic. Non-eopsinophilic asthma is often smoking or obesity related.
Asthma exacerbates
Infection, menstrual cycle, allergens, pollution, smoking, mould, stress, some medications (ACEi, beta blockers (cause bronchoconstriction), NSAIDs and aspirin), cold weather, obesity, laughter, emotions
Occupational: animals, fumes, dusts
Asthma pathophysiology
Airflow limitation
- caused by bronchial muscle contraction, mucosal inflammation and increased mucus production
Characterised by muscular hypertrophy and inflammation
Asthma clinical manifestatins
Auscultation: episodic wheeze - widespread (localised suggests foreign body), polyphonic, generally no crackles
Diurnal variation (typically worse in morning and night)
Can have mucus (usually clear)
Cough, breathless ness
Characteristically comes and goes and depends on triggers
Classic progression is childhood onset, better in teenage years and recurrence
Brittle asthma: recurrent, severe attacks. Can be type 1 - chronic severe variability of PEFR or type 2 - sudden unpredictable drops in PEFR
COPD is more of a relentless progressive disease and there is less diurnal variation
Associated problems: eczema, hay fever, nasal disease, food and drug allergies, reflux disease (reflex at night can exacerbate asthma)
Asthma classification
Classifying attacks: Uncontrolled/moderate - PEFR > 50% - RR < 25 - pulse < 110 - Normal speech, no severe markers
Severe: ano ONE of:
- PEFR 33-50% predicted
- RR >/= 25
- HR >/= 110
- inability to complete sentences
Life-threatening: any ONE of:
- PEFR < 33%
- SaO2 <92% or PaO2 < 8kPa
- normal PaCO2
- altered consciousness, exhaustion, arrhythmia, hypotension, silent chest, poor effort cyanosis
Near fatal:
- raised PaCP2 and/or requiring ventilation
Asthma 1st line investigations
Spirometry with reversibility testing (patients >5yrs)
- obstructive pattern: FEV1 <80% of predicted normal, FEV1/FVC ratio <0.7
- peak flow (PEFR)
- use bronchodilator to test reversibility
Asthma other investigations
Blood count: eosinophils, raised
Tests for atopy and allergy: SPTs (skin prick tests) and IgE
CXR often useful
O2 stats
Specific tests of airway inflammation
- becoming more common
- exhaled nitric oxide (PeNO), a marker of eosinophilic inflammation - not specific as elevated in smokers, viral infections an rhinitis
Asthma management
Drug classes:
- bronchodilators: beta agonists, leukotrine receptor antagonists, theophylline, LABAs, anticholinergics
- anti–inflammatory drugs: steroids - important as these actually reduce inflammation unlike bronchodilators which only relieve symptoms. Inhaled steroids given due to less side effects
- new biologics: omalizumab, mepolizumab
Treatment pathway:
- SABA (eg sabutamol)
- Inhaled corticosteroid (ICS eg budesonide)
- Leukotriene receptor antagonist (LRTA eg Montelukast)
- LABA (eg salmetrol)
- Increase ICS dose
Emergency management of severe or life-threatening asthma:
- oxygen (40-60%)
- salbutamol nebulizer 5mg (+ipratropium neb 0.5mg if life threatening)
- prednisolone 30-60mg (+/- hydrocortisone 200mg IV)
- consider magnesium or aminophylline IV
- ABGs
- CXR
Very important to monitor PEFR regularly as well as K= and glucose, aim for SATs >92
Asthma complications
Emergency: pneumothorax, arrhythmias, hypokalaemia
Lung cancers classification
Bronchial carcinoma
- non small cell (80-85%)
Squamous - most strongly associated with cigarette smoking
Adenocarcinoma (MOST COMMON TYPE and most common in non-smokers)
- small cell (10-15%) - strongly associated with cigarette smoking
- metastatic: prostate, kidney, breast, bone, thyroid, ovary, colon
Cancer of the Pleura
- mesothelioma
Lung cancers risk factors
Lung cancers: smoking, metal dusts (chromium), asbestos, radon exposure, pulmonary, HIV, genetics
Mesothelioma: asbestos exposure
Lung cancers clinical manifestations
Lung cancers
- symptoms: persistent cough, SOB, chest pain, haemoptysis (coughing)
- signs: anaemia, weight loss, finger clubbing, supreclavicular or axillary node enlargement
Basic form of staging seen here. TNM (tumour, node, metastasis) staging used for pre-surgical staging
Metastatic symptoms
- bone pain
- headaches, seizures, neuro deficit
- abdominal pain
Preneoplastic changes (rare but important)
- raised PTH - hyperparathyroidism
- raised ADH - SiADH
- raised ACTH - Cushing’s disease
Mesothelioma:
- classic cancer symptoms: weight loss, fever, SOB, fatigue
- persistent cough
- clubbing
- pain near affected site
Lung cancers management
Stage I/II: surgical intervention and radiotherapy
Stage III/IV: palliative chemo, radiotherapy and palliative care
Mesothelioma: almost always palliative as usually presents much later and progresses quickly
Lung cancers complications
- Pancoast’s Tumour (tumour in the apex of the lung) causing Horner’s syndrome - tumour in the lung invades sympathetic plexus in the neck causing compression of the plexus causing Horner’s (ptosis, mitosis (constricted pupil)), anhidrosis (decreased sweating))
- recurrent laryngeal nerve palsy - can lead to a hoearse voice
- metastasis (to outside the lung): liver, bone, adrenal glands, brain
- phrenic nerve palsy
- SVC obstruction
- Lambert eat syndrome (SCLC)
- neuroendocrine tumours:
- raised PTH - hyperparathyroidism
- raised ADH - SiADH
- raised ACTH - Cushing’s disease
Pulmonary embolism definition
A consequence of thrombus formation with a deep vein of the body. Thrombus formation occurs due to Virchow’s triad: venous states, trauma and hyper coagulability
Pulmonary embolism risk factors
Recent immobility, previous DVT/PE, pregnancy, thrombophilic syndromes eg antiphospholipid, malignant, hormone therapy eg HRT or COCP, smoking
Pulmonary embolism key presentation
Sudden onset SOB and pleuritic chest pain and Hx of painful calves (DVT) and recent long haul flight/immobilisation = think PE
Pulmonary embolism signs and symptoms
Signs: hyperaemia, pyrexia, cyanosis, tachycardia, tachypnoea, hypertension, raised JVP, red swollen leg, haemoptysis, syncope, hyperaemia, crepitations
Pulmonary embolism investigations
Well’s Score w/pints:
- clinical signs of PE/DVT: 3
- PE most likely diagnosis: 3
- tachycardia >100: 1.5
- immobility (>3/7, surgery in last 4/52): 1.5
- previous PE/DVT: 1.5
- haemoptysis: 1
- malignancy +/- treated in last 6 months: 1
Well’s score = 4 moderate possibility, do a D-dimer
Well’s score >4, PE likely do immediate CTPA, offer interim anticoagulation if CTPA delay
D-dimer - negative excludes PE but positive does not prove it. If positive, do imaging
GOLD STANDARD: CTPA
Pulmonary embolism management
Oxygen
Analgesia
Anticoagulation - apixaban or rivaroxaban or LMWH
- 3 months if provoked PE, >3 months if unprovoked PE
If haemodynamically unstable
- presents with hypotension, raised JVP - patient is acutely unwell
- continuous unfractionated heparin + thrombolysis (alteplase)
Otheroptions: surgical embolectomy, vena cava filter
Infections - TB definition
Pulmonary Tuberculosis is caused by mycobacterium tuberculosis. TB most commonly involves the lungs and is communicable in this form but can affect many organs: lymph nodes, CNS, liver, bones, GU tract and GI tract. Associated with restrictive disease
Infections - TB epidemiology
Majority of cases from Africa and Asia (India and China). About 2 billion people are infected with mycobacterium tuberculosis
Infections - TB aetiology
Mycobacterium tuberculosis
- aerobic, non-motile, non-sporing, slightly curved-bacilli with a thick waxy capsule
- acid-fast bacilli - turns red/pink with Ziehl-neelsen stain
- slow growing
- resistant to phagolysosomal killing and able to remain dormant
Spread is via airborne droplets
Infections - TB risk factors
Recent foreign travel or exposure to a person who has travelled eg India
Risk factors for developing active TB:
- recent tuberculin skin test conversion (test goes from negative to positive within 24hrs)
- homeless, IV drug users
- smokers
- immunocompromised (diabetes, corticosteroid therapy, renal disease, malnutrition, HIV, haematological malignancy
Infections - TB pathophysiology
Development of TB requires infection by Mycobacterium tuberculosis and inadequate containment by the immune system. Latent TB describes Mycobacterium tuberculosis infection without clinical, bacteriological or radiographic evidence of active TB
Active TB may occur from re-activation of previously latent infection or from progression of primary infection
- Alveolar macrophages insect bacteria and rods proliferate inside them. At this point the patient has primary tuberculosis (signs of infection after exposure), most people are asymptomatic or have a mild flu like illness
- About 3 weeks later, cell-mediated immunity kicks in forming a granuloma with a necrotic core (caveating granuloma). This granulomatous area is known as a Gohn focus
- TB can spread to the hilarity lymph nodes (via lymphatic spread or infiltration from John focus), caseating necrosis can also occur here. These hilarious lymph nodes and gohn focus make up a Gohn Complex (usually in lower lobes)
- These can become fibrosed and calcified and are then called a Ranke Complex
- In some cases the TB is killed off but it can remain viable (although dormant), reactivation of the Gohn complex may occur due to immunocomprimisation (AIDS, ageing etc), infection can spread and it usually occurs in the upper lobes (greatest oxygenation, TB is highly aerobic)
- Memory T cells release cytokines causing further caseous necrosis although this time it tends to lead to cavity formation
- This can allow the TB to disseminate (spread) via airways or lymphatics, causing bronchopneumonia, it can also spread through the vascular system and can affect other parts of the body - systemic miliary TB
- Systemic miliary TB can lead to the following complications
Kidneys: sterile pyuria (WBCs in urine)
Meninges: meningitis
Lumbar vertebrae: Pott disease (osteomyelitis and arthritis in the vertebrae)
Adrenal glands: Addison’s disease
Liver: hepatitis
Cervical lymph nodes: lymphadenitis (chronic inflammation), also known as scrofula
This is an example of delayed hypersensitivity reaction. Successful containment of TB is particularly dependent on T-helper cells as they, along with macrophages, form a granuloma with a necrotic caseous centre.
Approximately 10% of people with latent infection will progress to active disease in their lifetime (highest risk is within 2yrs)
Infections - TB clinical manifestations
Systemic symptoms: weight loss, low grade fever, anorexia, drenching night sweats, malaise
Pulmonary symptoms: productive cough, haemoptysis, cough > 3 weeks (dry or productive), breathlessness, sometimes chest pain
Signs: signs of bronchial breathing, dullness to percuss, decreased breathing, fever, crackles
Infections - TB 1st line investigations
1st line:
- CXR - typically shows fibronodular opacities in upper lobes with or without cavitation (abnormal thick-walled gas-filled spaces within the lung), may see Gohn focus - small calcified nodule often in upper lower lobes or lower upper lobes, these occur where bacteria settle
- sputum test (3x) w/ acid-fast bacilli smear - Ziehl-Neelsen stain (used for acid-fast organisms). Follow up with nucleic acid amplification for confirmation
Sputum culture: most sensitive and specific test but can take weeks for results, grow on Lowenstein Jansen agar
Diagnosing latent TB:
Tuberculin skin test ‘Mantoux’: negative does not rule out active TB
- immune reaction occurs if there has been previous exposure
- reaction can take 2-3 days, induration (hardening) >5mm is generally considered positive regardless of BCG vaccination history
- shows that there has been some sort of exposure
Interferon gamma release assay - detects WBCs response to TB antigens
Infections - TB management
Ntoifiable disease - report to public health England immediately
1st Line for ACTIVE TB: RIPE abx regimen
- Rifampicin (6 months - bactericidal - blocks protein synthesis) Side effects: red urine, hepatitis
- Isoniazid (6 months - bactericidal - blocks cell wall synthesis) Side effects: hepatitis, neuropathy
- Pyrazinamide (2 months - bactericidal initially, less effective later) Side effects: gout, arthralgia, rash, hepatitis
- Ethambutamol (2 months - bacteriostatic, blocks cell wall synthesis) Side effects: optic neuritis
Treatment for LATENT TB:
Usually 9 months of isoniazid
Infections - pneumonia (CAP & HAP) definition
Pneumonia is inflammation of the lungs with consolidation (a region of lung is filled with liquid instead of air) or interstitial lung infiltrates, most often categorised according to the causative organism. Causes 30% of ICU deaths
Infections - pneumonia aetiology
Community-acquired pneumonia (CAP) - pneumonia acquired outside hospital or healthcare facilities
- streptococcus pneumoniae is the most common - characterised by rusty sputum
- haemophiliac influenzae
- mycoplasma pneumoniae
- other: staphylococcus aureus (inc MRSA), group A streptococci and Moraxella catarrhalis
Hospital-acquired pneumonia (HAP) - acute lower respiratory tract infection that is acquired after at least 48hrs of admission to hospital and is not incubating at the time of admission. Mostly caused by aerobic gram-negative bacilli:
- Pseudomonas aeruginosa
- Escherichia coli
- Klebsiella pneumoniae
- HAP after 5 days admission is more likely to be Pseudomonas aeruginosa or MRSA. Within 4 days after admission the causative organism is most likely the same as in CAP ie S.pneumoniae/S.aureus
Atypical pneumonia - bacterial pneumonia caused by atypical organisms not detectable on Gram stain and cannot be cultures using standard methods
- mycoplasma pneumoniae
- Chlamydophila pneumoniae
- Legionella pneumophila - consider if travel Hx (eg Spain)
Pneumonia in immunocompromised patients
- eg pneumocystis jiroveci (fungal) - occurs in severely immunocompromised patients eg HIV
Infections - pneumonia risk factors
- infants and elderly
- COPD, other lung disease
- immunocompromised eg HIV
- nursing home residents
- impaired swallowing
- diabetes
- cardiovascular disease and congestive heart failure
- alcoholics and IV drug users
Infections - pneumonia clinical manifestations
Clinical features: fever, productive cough, dyspnoea/tacypnoea, tachycardia, low BP, confusion (esp elderly), rights, malaise, pleuritic chest pain
Signs: dull to percussion, decreased air entry, bronchial breath sounds
Infections - pneumonia investigations
FBC - elevated WBC Determine causative organism - sputum sample and blood cultures - urinary antigen test - Legionellas - Thoracentesis (pleural tap)
Gold standard: CXR showing consolidation
- Multilobar: Streptococcus pneumoniae, Staphylococcus aureus
- Multiple abscesses: S.aureus
Infections - pneumonia assess severity
CURB-65 (each score 1 point) C - confusion U - blood urea nitrogen (BUN) >7mmol/L R - respiratory rate >/= 30 B - blood pressure = 90 systolic OR diastolic = 60 - >/= 65 yrs old Max score is 5
Score 1: treat as an outpatient
Score 2: consider short stay in hospital/monitor closely as outpatient
Score 3+: hospitalisation, consideration for ITU
Can use CRB-65 in a community setting
Infections - pneumonia management
ABCDE approach: IV fluids, CPAP etc
Analgesia for chest pain eg paracetamol
Abx - start empirically then guided after cultures
Thromboprophylaxis - risk of venous thromboembolism
Abx for community acquired pneumonia (CAP) (done by CURB-65 score)
Mild (0-1): oral amoxicillin at home
Moderate (2): oral amoxicillin and macrolide (eg clarithromycin), consider hospitalisation
Severe (3+): IV co-amoxiclav and macrolide (eg clarithromycin), consider ITU
Abx for Legionellas
- ciprofloxacin and clarithromycin
Interstitial Lung Disease definition
Interstitial lung disease (ILD) is an umbrella term used for a group of diseases that cause scarring (fibrosis) of the lungs. Most interstitial lung disease fall into the category of restrictive disease
Interstitial Lung Disease aetiology
Can be divided into acute or chronic
Acute ILDs
- trauma, infection, drugs (therapeutic and recreational), radiation, aspiration, gas inhalation, paraquat (herbicide) poisoning
- leading to ARDS - adult respiratory distress syndrome
Chronic ILDs
- idiopathic
- idiopathic pulmonary fibrosis (IPF)
- scarring of the lungs -> pulmonary fibrosis -> respiratory failure -> cor pulmonale
- shows classic ‘honeycombed’ CXR due to fibrosis with inflammatory infiltrate
- IPF has a median survival of 2-5 yrs from diagnosis
- previously thought to be inflammatory, now known that drugs targeting inflammation do more harm than good
- generally presents >60yrs, more common in men
- autoimmune
- rheumatoid arthritis ILD, Sjorgens, SLE, polymyositis, dermatomyositis, systemic sclerosis
- pneumoconiosis - inhalation of something causing lung damage
- coal worker pneumoconiosis - inhales coal gets taken up by macrophages and congregate in the lungs
- silicosis - inhaled stone.sand from mining
- asbestosis - inhaled asbestos irritates lungs
- extrinsic allergic alveolitis/hypersensitivity pneumonitis (covered in separate table)
- inflammation driven process
- Type III hypersensitivity (IgG) and immune complex from causing inflammation in the lungs -> chronic exposure leads to pulmonary fibrosis
- may also have fever, weight loss etc
- eg Farmer’s lung, pigeon fanciers lung etc
- secondary to other disease: TB, pneumonia, sarcoidosis
- sarcoidosis
- chronic granulomatous disorder of unknown aetiology affecting the lungs, skin and eyes
- lungs and mediastinal lymph nodes are most affected
- bimodal age distribution with 2 peaks in 3rd and 5th decades
- non-caveating granulomas form due to CD-4 interactions - type 4
- check serum ACE levels- secreted from nodules
Some ILDs will go on to become progressive fibrosis ILD “Pulmonary Fibrosis” such as idiopathic pulmonary fibrosis but others will not necessarily
Interstitial Lung Disease pathophysiology
Idiopathic pulmonary fibrosis
- fibroblasts repair damaged tissue
- fibroblasts migrate to the lungs and become myofibroblasts
- myofibroblasts deposit collagen in the extracellular matrix
- IPF these fibroblasts proliferate and form fibroblastic foci
- the thickened tissue leads to lower gas exchange efficiency in the lungs
Histology shows spatial heterogeneity (normal lung tissue next to abnormal tissue)
Interstitial Lung Disease clinical manifestations
Idiopathic pulmonary fibrosis
- dyspnoea, cough, crackles
- weight loss, fatigue, malaise
Sarcoidosis
- cough, dyspnoea, wheezing, rhonchi
- lymphadenopathy
- photophobia, red painful eye, blurred vision
- arthralgia, chronic fatigue
Interstitial Lung Disease investigations
Idiopathic pulmonary fibrosis
CXR - generally lungs look smaller
Spirometry - restrictive
TLCO or DLCO - reduced (reduced gas exchange due to thickening of alveolar layer)
HRCT (best imaging) - honeycombing is characteristic, typically affects periphery and base of the lungs, thickened dilated bronchus are seen, often has a ground glass appearance
Exercise testing
Sarcoidosis
CXR - hisar or mediastinal nodal enlargement is most common at presentation, although may present with parenchymal disease only or end stage disease (pulmonary fibrosis)
Serum ACE: often elevated
Calcium: often raised
Interstitial Lung Disease complications
GORD, pulmonary infections, pulmonary hypertension
