Respiratory Flashcards
What is silicosis ?
Occupations at risk?
Features?
Silicosis is a fibrosing lung disease caused by inhalation of fine particles of crystalline silicon / silica.
Occupations at risk - Miners, slate works, potteries, foundry worker ( metal casting)
Features - upper zone fibrosing lung disease
“Egg shell” calcification of hilar lymph nodes
Common causes of IECOPD
NICE guidance on mx
Bacterial - haemophilus influenza, streptococcus pneumoniae and moraxella catarrhalis.
Viral - Rhinovirus most important pathogen.
NICE guidance:
Increased freq of bronchodilator and consider giving via nebuliser.
Prednisilone 30 mg OD for 5 days
Oral abx only if sputum is purulent or there are clinical signs of pneumonia. 1st line abx –> amoxicillin, clarithromycin or doxycyline.
NICE recommendation for admission with IECOPD?
Severe SOB
Acute confusion / reduced concious level
Cyanosis
o2 sats < 90%
Social reasons - living alone or unable to cope at home
Significant comorbidity e.g cardiac or insulin dependent diabetes.
Hospital mx of IECOPD
Controlled oxygen therapy. All patients on high flow o2 via non rebreathe if hypoxic. ABG should be completed to determine if pt is CO2 retainer. ( CO2 retainers have lost hypercapnic drive for respiration and rely on hypoxia to drive RR, if giving too much o2 can suppress resp drive). If non retainer, aim sats 94-98%, CO2 retainer 88-92%.
Nebulised bronchodilators - salbutamol and ipratroprium
Steroid therapy - Oral prednisilone or IV hydrocortisone
IV theophylline if failure to respond to above.
Abx - 1st line Amoxicillin / 2nd line if pen allergy - doxycycline, if received abx recently in past 5 days co trimoxazole (5 day course)
Development of T2RF - NIV. Typically for pts with respiratory acidosis pH 7.25- 7.35. BTS state NIV can be used in patients who are more acidotic but HDU monitoring required. BiPaP typically used with initial settings - EPAP 4-5 cm H20 and IPAP 10-15 cm
Pneumothorax mx
Primary PT
Secondary PT
Iatrogenic PT
Primary PT: No underlying respiratory disease.
If rim of air < 2cm & patient asymptomatic then d/c considered.
If < 2cm but symptomatic then aspiration should be considered.
If aspiration fails or remain SOB then chest drain should be inserted.
Secondary PT:
If > 50 yrs old, rim of air > 2cm and / or pt SOB then chest drain should be inserted.
If rim of air 1-2cm then aspiration. If aspiration fails then chest drain. All patients admitted for at least 24 hours
If PT < 1cm then o2 and observation for 24 hours.
Iatrogenic PT:
Less likelihood of recurrence than Spont PnT
Majority resolve with observation, if treatment required then aspiration used.
Ventilated pts need chest drains / COPD pts.
Recommendation for persistent pneumothorax
If persistent air leak/ insufficient lung re-expansion or recurrent pneumothoraces then video assisted thorascopic surgery ( VATS) should be considered to allow for mechanical/ chemical pleurodesis +/- bullectomy
D/C advice for patients with PT?
Smoking - avoid to reduce further risk of PT
Flying - not before 6 weeks or for 1 week post a check xr
Diving - never unless surgical BL pleurectomy and normal lung function and CT scan post op.
2WW referral for lung cancer when?
CXR suspicious for lung cancer
> 40 yrs and unexplained haemoptysis.
Offer urgent CXR ( 2 weeks) for ? Lung cancer when?
> 40 YRS and they are a non smoker with two of the following unexplained symptoms or smoker with one of the following unexplained symptoms:
Cough
Fatigue
SOB
Chest pain
WL
Appetite loss
Consider an urgent chest x-ray (to be performed within 2 weeks) to assess for lung cancer in people aged 40 and over with any of the following..?
Persistent/ recurrent chest infections
Finger clubbing
Supraclavicular lymphadenopathy or persistent cervical lymphadenopathy
Chest signs consistent with Lung cancer
Thrombocytosis *raised platelets > 450 x 10 9
Lung CA RF’s
Smoking - increases risk by 10 x
Asbestos - increases risk by 5 x
Both smoking & asbestos are synergistic ( if both 50x risk)
Others:
Arsenic / radon/ nickel
Aromatic hydrocarbons
Cryptognic fibrosing alveolitis
NOT related is COAL dust.
Sleep apnoea - Predisposing factors?
Presentation?
RF’s:
Male
Middle aged
Obesity
Macroglossia - acromegaly, hypothyroid, amyloidosis
Large tonsils
Marfans syndrome
Alcohol intake
Ob sleep apnoea - episodes or partial or complete airways obstruction. Episodic obstruction is associated with oxyHG desaturation and arousal from sleep.
Presentation:
-often noticed by partner, excessive snoring & may report periods of apnoea.
Chronic snoring & gasping
Unrefreshing sleep
Morning headache
Daytime somnolence
Reduced concentration
Insomnia and restless sleep
Depression and anxiety
Compensated respiratory acidosis and hypertension.
AX of sleep apnoea?
Epworth scale
Referral to ENT for polysomnography studies - overnight oximetry
Mx of sleep apnoea
Conservative - lifestyle modification including weight loss, reduced alcohol and stop smoking
Medical mx - CPAP 1st line for moderate to severe OSA.
CPAP improves survival, sleepiness and mood. Needs pt education and adherence, proper facial mask fitting.
2nd line if CPAP not tolerated intra oral devices or for mild OSA with no daytime sleepiness.
- DVLA need to be informed if daytime sleepiness *
Indications for BiPAP?
COPD with resp acidosis pH 7.25-7.35.
T2RF secondary to chest wall deformity, Neuromuscular disease or OSA.
Cardiogenic pulmonary oedema unresponsive to CPAP.
Weaning from tracheal intubation.
Bipap - cycle of high and low prssure to corrspond with inspiration and expiration.
Insipiratory PAP - prssure to force air into lungs 10-15 cm
Expiratory PAP - to keep airways open during expiration 4-5 cm
Main indications for placing chest drain in pleural infection?
Frankly purulent / turbid/ cloudy pleural fluid on sampling.
The presence of organisms identified by Gram stain and/or culture from a non-purulent pleural fluid sample indicates that pleural infection is established and should lead to prompt chest tube drainage.
Pleural fluid pH < 7.2 in patients with suspected pleural infection indicates a need for chest tube drainage.
Define pleural effusion
Pathophysiology of pleural effusions
Pleural effusion = abnormal collection of fluid within the pleural space commonly detected on CXR as blunting of costophrenic angles / consolidation with a meniscal line.
Pathophysiology:
Pleura is formed of mesothelial cells and connective tissue. Two layers, the visceral layer ( covering lung tissue) and parietal layer ( covering chest wall) and between them the pleural space. Pleural space normally contains around 10 mls fluid & lubricates the surfaces allowing for easier respiration and generates surface tension ( pulling the parietal and visceral pleura together).
Under normal circumstances there is a constant balance between fluid entry and exit into the pleural space. Related to three things 1) Hydrostatic pressure in vessels 2) oncotic pressure of vessels 3) lymphatic drainage.
Increase in fluid entry:
1) increased vasc permeability - infection or malignancy
2) increased microvascular pressure - e.g. HF or cirrhosis
3) reduced plasma oncotic pressure - Nephrotic syndrome/ cirrhosis
Reduced fluid exit:
Altered lymph drainage after radiotherapy or extrinsic physical compression.
Causes of pleural effusion split into transudate vs exudate
Exudate - protein content > 35g/L or 3.5 g/dL with high protein and cellular content.
Due to increased vascular permeability or reduced lymphatic drainage. Causes:
1) Parapneumonic effusion
2) malignancy
3) Trauma
4) TB
5) PE
6) Pancreatitis
7) Radiation pleuritis
8) Systemic inflammation - RA or SLE
Transudate - low protein content ( < 25g/L or 2.5g / dL). Due to increased hydrostatic pressure or reduced oncotic pressure:
Heart Failure
Cirrhosis
Nephrotic syndrome
Meig’s syndrome - Triad of benign ovarian tumour, pleural effusion and ascites.
Peritoneal dialysis
Presenting sx of pleural effusion
Pleuritic CP
SOB
Cough - productive favours parapneumonic , dry favours transudative cause.
O2 requirement
Reduced Ex Tol
Examination :
Reduced chest expansion
Stony dullness to percussion
Reduced breath sounds
Decreased vocal resonance
Tracheal deviation if large ( > 1L)
Clubbing - lung cancer.
Imaging in pts with suspected pleural effusion?
PA & lateral CXR - Key findings blunting of costophrenic angles, meniscus level, fluid in fissures, tracheal/ mediastinal deviation with large effusions. Complete white out seen in large effusions.
Pleural USS- increases likelihood of successful pleural aspiration and sensitive for detecting pleural septations.
Contrast CT - for underlying cause in exudative effusions.
Outline investigation in Pleural effusion
Bedside - Sputum sample and gram stain
Bloods - FBC/ CRP/ U&ES/ LFTs / NTproBNP/ Blood cultures if ? infective
Imaging. - CXR, pleural USS , CT CAP. ECHO for ? HF.
Special tests:
Pleural aspiration / drainage.
Generally BL pleural effusions are assumed to be transudative and pleural aspirations not done unless unsuccessful trial of treatment / cause unclear.
If unilateral pleural effusion, pleural tap usually done to confirm if transudative vs exudative.
What is sent for from pleural fluid during a pleural paracentesis?
USS guided pleural aspiration done to avoid complications. Fluid is sent for:
1) pH - pleural fluid alkaline pH ( 7.6). pH < 7.3 abnormal - parapneumonic effusion. pH < 7.2 - empyema.
2) Protein - transudate vs exudate. Transudate < 30g/ L , exudate > 30g/L. IF intermediate level of protein ( 25- 35) use Lights criteria.
3) LDH - Part of lights criteria, High in exudate, low in transudate.
4) MCS - gram stain, culture, sensitivity & TB
5) Cytology - ? malignant cells
6) Glucose - Glucose < 3.3 mol/L suggests parapneumonic/ empyema/ malignant/TB/SLE
7) Haematocrit - > 50% = haemothorax
8) WCC - high neutrophils in parapneumonic effusion , high leucocytes in TB/lymphoma/sarcoid
9) Amylase - high in pancreatitis / oesphageal rupture or malignancy
10) Lipids - > 110 / dL - chylothorax
What is Lights criteria and when is it used?
Used to distinguish between exudate and transudate when there is intermediate levels of protein ( 25-35 g/L) .
Exudate if:
Pleural fluid protein / serum protein ratio > 0.5
Pleural fluid LDH / serum LDH > 0.6
Pleural fluid LDH more than 2/3rds upper limit of normal serum LDH
Other characteristic pleural fluid findings:
low glucose: ? differentials
raised amylase: ? differentials
heavy blood staining: ? differentials
low glucose - TB / Empyema/ RA
Raised amylase - pancreatitis, oesphageal perforation
Heavy blood staining - mesothelioma, PE, TB
Characteristic of pleural fluid in:
1) Parapneumonic effusion
2) Empyema
3) TB
4) HF
5) Malignant
Parapneumonic - Turbid/ straw coloured, pH < 7.3, High protein, +ve gram stain, LOW glucose < 3.3
Empyema - Pus on aspiration, pH < 7.2, high protein, low glucose < 3.3 , +Ve gram stain
TB - Turbid/bloody/straw coloured, Very high protein, Very low glucose, low pH & +ve for acid fast bacilli.
HF - straw colourd, low protein count, negative MCS, normal glucose
Malignant - blood stained fluid, high protein , LOW glucose. -ve mcs, Cytology positive for malignant cells
When should a chest drain be placed in suspected pleural infection?
All patients admitted with sepsis or pneumonic illness should have diagnostic pleural fluid sampling.
if pleural fluid is cloudy/ purulent or turbid a chest drain should be placed.
If fluid is clear but pH less than 7.2 chest tube should be placed.
Management of pleural effusions?
Treat the cause. Dependent on size may need aspiration or drainage. Small asymptomatic effusions often do not need intervention.
Large effusion ( > 1L) - therapeutic and diagnostic paracentesis or chest drain.
Recurrent pleural effusions - Pleurodesis after drainage via chest drain using sclerosing agents ( fibroses the pleural space).
OR surgical management - if pleural biopsy is required, video assisted thorascopic surgery ( VATS) for biopsy, washout and pleuredectomy.
Empyema - always requires chest drain and empirical abx. ( coamoxiclav + metronidazole or Tazocin).
Asthma management in adults
1) New diagnosis - SABA
2) Not controlled on previous step OR new diagnosis with symptoms >= 3x / week OR night time waking –> SABA + Low dose ICS
3) SABA + low dose ICS + Leukotriene receptor antagonist ( LRTA).
4) SABA + Low dose ICS + LABA . Can continue LRTA if benefit.
5) SABA +/- LTRA. Switch ICS/LABA for one inhaler, MART ( maitenance and reliever therapy) which includes a low dose ICS & fast acting LABA e.g. formoterol.
6) SABA +/- LTRA + medium dose ICS MART . Or consider changing back to fixed dose Moderate ICS and separate LABA.
7) SABA +/- LTRA and one of the following:
- Increase ICS to high dose ( not as MART as part of fixed dose regime).
-Trial LAMA (tiotroprium) or Theophylline ( methylxanthine / PDE inhibitor)
-Referral to secondary care for specialist advice.
Low vs Med vs High ICS dosing?
Low dose - < = 400 micrograms budesonide
400-800 micrograms moderate dose budesonide
> 800 micrograms - high dose budeosonide
What is intersitial lung disease?
What is the most common type?
Interstitial lung disease - umbrella term for group of conditions that lad to progressive fibrosis and scarring of the lung tissue. Leads to restrictive disease and impaired gas exchange.
Most common type is idiopathic pulmonary fibrosis
Pathophysiology of interstitial lung disease
Inflammation and scarring of the lung interstitium. Some diseases driven mainly by inflammation that may respond to treatment, once scarring has occurred it is irreversible. Repeated injury of lung tissue leadings to fibroblast activation and laying down of new ECm. In ILD genetic mutations in fibroblasts leads to excess ECM depositing and scarring. The lung interstitium is thicker which increases the diffusion distance and compromising gas exchange.
Causes of interstitial lung disease?
Idiopathic - IPF
Autoimmune / connective tissue disease - sarcoidosis, RA, SLE/ Sjogrens/ systemic sclerosis/ Alpha 1 antitrypsin/ UC
Environmental:
Asbestosis
Silicosis
Occupational:
Hypersensitivity pneumonitis
Bird fanciers lung ( droppings)
Farmers lung ( mouldy spores in hay)
Mushroom workers lung
Malt workers lung ( mould on barley)
Infective: - mycoplasma pneumonia / pneumocystis pneumoniae
Drugs : BANSMe
Bleomycin
Amiodarone
Nitrofurantoin
Sulfasalazine
Methrotrexate
Investigations of ILD
Bloods - FBC ( chronic anaemia ) , CRP, ESR ( raised) , U&E ( vasculitis) & autoimmune screen. ( RF/AntiCCP RA, ANA SLE).
Imaging- CXR –> reticular fine opacities.
HRCT - Ground glass appearance, later honeycombing ( destruction of airspaces) , traction bronchiectasis ( dilated airways pulled apart by fibrosis) .Reticular opacities with thickening of lung interstitium.
Special tests - BAL / Transbronchial biopsy or surgical lung biopsy
Common features of ILD
Symptoms:
Progressive exertional SOB
& Reduced exercise tolerance ( progresses over weeks - months)
Chronic dry cough
General fatigue and malaise
Symptoms of CTD e.g. arthralgia, dysphagia, dry eyes etc
Examination features:
Clubbing
Skin - raynauds ( systemic sclerosis) / erythema nodosum ( sarcoidosis)
Bibasal fine end inspiratory crackles
Dullness to percussion and pleural effusion
Painful joints
Causes of upper zone fibrosis - CHARTS
Coal worker pneumoconiosis
Hypersensitivity pneumonitis
Ankylosing spondylitis / ABPA
Radiation
TB
Silicosis / sarcoidosis
Ix of mesothelioma
CXR - features suspicious for mesothelioma / asbestos exposure. Lower zone fibrosis, pleural plaques, pleural thickening or pleural effusion/ pleural mass.
Pleural CT
Pleural aspiration - exudative with malignant cells.
Local anaesthetic thoracoscopy increasingly used to ix cytology negative exudative effusions ( high diagnostic yield) - camera inserted into pleural space to visualise and take biopsy.
If pleural nodularity is seen on CT then image guided pleural biopsy.
Outline the pharmacological management of COPD
Step 1: SAMA ( ipratroprium) or SABA ( salbutamol or terbutaline) as required
Then - any features of asthma?
Includes previous diagnosis of asthma or atopy, raised eosinophil count, FEV variation or PEFR diurnal variation > 20%.
For Asthmatic features:
Step 2 - SABA/ SAMA PRN & Regular LABA + ICS.
Step 3 - Remain symptomatic or freq exacerbations then Above PLUS LAMA. ( SABA / LABA/ LAMA / ICS
For no Asthmatic features:
Step 2 : SABA PRN, LABA + LAMA
Step 3 : if remaining symptomatic Add ICS trial for 3 months, if no improvement revert back.
What is sarcoidosis?
What are the risk factors ?
Sarcoidosis is a chronic granulomatous disorder. Granulomas are inflammatory nodules full of macrophages and cause of granulomas is unknown.
Usually presents as a respiratory disease 90% but has many extra pulmonary manifestations. Commonly skin manifestations are tested - erythema nodosum and lupus pernia
Risk factors:
Female
Aged 20-40 or 60
Black ethnic origin or Scandinavian origin
Fhx
Lofgrens syndrome?
Specific presentation of sarcoidosis with classic triad:
Erythema nodosum
BL Hilar lymphadenopathy
Polyarthralgia
Heerfordt’s syndrome
Heerfordts syndrome - Parotid enlargement, fever and uveitis secondary to sarcoidosis.
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Key facts to inform patients of if found with pleural plaques?
Pleural plaques are benign. They are the most common form of asbestos related lung disease, they do not undergo malignant change and do not increase your risk of lung cancer or mesothelioma. No FU required and patient can be reassured. Ongoing FU of asbestos related disease encouraged.
Pathophysiology of bronchiectasis
Vicious cycle –> initial infection with pathogen, leads to inflammation of airways, activation of neutrophils and release of elastase –> impaired mucociliary clearance –> airway mucus hypersecretion and obstruction –> microbial colonisation / infection —> further inflammation and bronchial dilatation / airways destruction
Outline the severities of COPD and FEV1 predicted values
