Respiratory Flashcards
Typical causative organisms of CAP
Streptococcus pneumoniae (commonest), Haemophilus influenzae (common in COPD), Moraxella catarrhalis Atypical: Mycoplasma pnuemoniae (dry cough), Staphylococcus aureus
Causative organisms of HAP
Gram neg enterobacteria
Staph aureus
Pseudomonas
Klebsiella
Investigations for pneumonia
Oxygen saturation ABG is sats are low BP Bloods - FBC, U+E, LFT, CRP CXR Sputum for microscopy and cultures
CAP severity scoring system
CURB-65 Confusion (AMT =<8) Urea >7 Resp rate >=30 BP <90 systolic (and/or diastolic 60) Age >= 65
Management (acute and follow up) of CAP depending on severity
CURB65: 0-1 oral abx at home, 2 requires hospital therapy for IV abx, >=3 consider ITU
Abx, oxygen, IV fluids, VTE prophylaxis, analgesia
Follow up at 6 weeks (+/- CXR)
Abx guidelines: amoxicillin (doxycycline or erythromycin if pen allergic), co-amoxiclav if severe
Antibiotics for HAP
Co-amoxiclav
Tazocin if severe
Complications of pneumonia
Pleural effusion, empyema, lung abscess, resp failure, sepsis, brain abscess, pericarditis
Pneumonia in immunocomp patients
Pneumocystis jirovecii
Dry cough, exertional dyspnoea, reduced sats, fever, bilateral creps
Ix: induced sputum MCS, bronchoalveolar lavage
Mx: high dose co-trimoxazole, +/- steroids
What is bronchiectasis
Chronic inflamm of bronchi and bronchioles leading to permanent dilatation and thinning of the airways
Main organisms causing bronchiectasis
Haemophilus influenzae, Strep pneumonia, Staph aureus, Pseudomonas aeruginosa
Causes of bronchiectasis
Congenital: cystic fibrosis, primary ciliary dyskinesia, Kartageners
Post-infection: measles, pertussis, bronchiolitis, pneumonia, TB, HIV
Other: bronchial obstruction, allergic bronchopulmonary aspergillosis, RA, UC, idiopathic
Clinical features of bronchiectasis
Symptoms: persistent cough, copious purulent sputum, intermittent haemoptysis
Signs: clubbing, coarse inspiratory creps, wheeze (asthma, COPD, ABPA)
Complications of bronchiectasis
Pneumonia, pleural effusion, pneumothorax, haemoptysis, cerebral abscess, amyloidosis
Investigations for bronchiectasis
Sputum culture
CXR (cystic shadows, thickened bronchial walls (tramline and ring shadows)
HRCT chest (signet ring)
Spirometry (obstructive)
Bronchoscopy
Other tests - serum immunoglobulins, CF sweat test
Management of bronchiectasis
Chest physiotherapy
Flutter valve devices may air sputum removal
Mucolytics
Antibiotics in acute settings (ciprofloxacin if pseudomonas)
Salbutamol nebs (if asthma, COPD, CF, ABPA)
Prednisolone
Surgery if localised disease
Clinical features of cystic fibrosis (neonates –> children and young adults)
Failure to thrive, meconium ileus, rectal prolapse
Resp - bronchiectasis, recurrent chest infections, pneumothorax, haemoptysis, resp failure, cor pulmonale (finger clubbing, cyanosis, bilateral coarse crackles)
GI - DM, steatorrhoea, gallstones
Other - male infertility, osteoporosis, arthritis, vasculitis, nasal polyps
Management of cystic fibrosis
Antibiotics, postural drainage/ chest physiotherapy, pancreatic supplements (creon), high fat diet, bronchodilators, heart/lung transplant
Ivacaftor and lumacaftor target the CFTR protein
Subtypes of non-small cell lung cancer and their typical features
NSCLC is more common than SCLC
Squamous cell lung cancer - central, PTHrP (hypercalcaemia), finger clubbing, HPOA
Adenocarcinoma - peripheral, most common for non-smokers (although majority of cases are smokers), gynaecomastia, HPOA.
Large cell lung carcinoma - peripheral, poor prognosis, poor differentiation, may secrete beta-HCG
Features of small cell lung cancer
Central, arise from APUD cells, associated with ADH (hyponatraemia) and ACTH secretion (Cushings), Lambert-Eaton syndrome
The ACTH can cause bilateral adrenal hyperplasia and hypokalaemic alkalosis due to cortisol
Features of lung cancer
Persistent cough, haemoptysis, dyspnoea, chest pain, weight loss, anorexia
Complications of lung cancer
Superior vena cava obstruction, hoarseness (recurrent laryngeal nerve palsy), Horners (pancoast tumour), rib erosion, pericarditis, AF, mets to brain, bone, liver, adrenals
Lambert eaton, hypercalcaemia (PTHrP), Cushings (ACTH secretion), hyponatraemia (ADH secretion)
Investigations for lung cancer
CXR (usually the first investigation) CT (investigation of choice) Bronchoscopy (allows for biopsy) PET scan (usually for NSCLC) Bloods (raised platelets)
referral criteria for lung cancer
2-week-wait referral if: CXR suggests lung cancer, or aged 40+ with unexplained haemoptysis
offer 2-week-wait if: 40+ with 2+ unexplained symptoms (or 1+ and a smoker): cough, fatigue, dyspnoea, chest pain, weight loss, anorexia
Consider 2-week-wait if: 40+ with persistent or recurrent chest infections, or finger clubbing, or lymphadenopathy, or chest signs suggestive of lung cancer, or thrombocytosis
Management for NSCLC
Only 20% eligible for surgery
Curative or palliative radiotherapy
Contraindications for surgery in lung cancer
Assess general health, stage 3b/4 (mets), FEV1 <1.5L, malignant pleural effusion, tumour near hilum, vocal cord paralysis, SVCO
Malignant mesothelioma cause, mx, prognosis
Cause - asbestos
Mx - palliative chemo
Prognosis is poor (<2y)
Allergic bronchopulmonary aspergillosis (ABPA)
- what is it
- who does it affect
type 1 and 3 hypersensitivity reaction to Aspergillus fumigatus
Asthmatics and CF patients at risk
Allergic bronchopulmonary aspergillosis (ABPA) symptoms
Bronchoconstriction then permanent damage, causing bronchiectasis -> wheeze, cough, purulent sputum, dyspnoea
Allergic bronchopulmonary aspergillosis (ABPA) investigations
CXR (transient segmental collapse, consolidation, bronchiectasis)
Aspergillus in sputum
Eosinophilia
Serum IgE (raised)
Allergic bronchopulmonary aspergillosis (ABPA) management
Prednisolone
Itraconazole
Bronchodilators
Important questions to ask in asthma history
Symptoms
Precipitants - cold, exercise, emotion, allergens, pollution, NSAIDs, beta blockers
Diurnal variation
Exercise tolerance (quantify)
Disturbed sleep (quantify as nights/week)
Acid reflux?
Other atopic disease - eczema, hayfever, allergy, family history
Home - pets, carpet, feather pillow/duvet, floor cushions?
Job
Days/week off school/work
Investigations for asthma
Spirometry (measures vol and speed of air) - obstructive
FEV1 significantly reduced, FVC normal, FEV1% <70%
reversible obstruction following bronchodilators
Fractional exhaled nitric oxide (FeNO) - rises in inflam cells, so levels will be high in asthma
Consider CXR if old and hx of smoking
Chronic asthma management in children >5
SABA (salbutamol)
- > Low dose ICS (budesonide)
- > Oral LTRA (montelukast)
- > Stop LTRA and start LABA (salmeterol)
- > MART (ICS+LABA)
Side effects of asthma drugs
SABA and LABA - tremor
ICS - oral candidiasis, stunted growth
LTRA - GI discomfort, sleep/movement disorders
Asthma management in adults
SABA
+ICS
+LTRA
+LABA (dont stop LTRA)
SABA + LTRA + MART (ICS + LABA)
Acute asthma management in children
Mild-mod: salbutamol via spacer give 1 puff every 30-60 sec up to 10 puffs, if symptoms not controlled then refer to hospital
Prednisolone should be given to all children with an asthma exacerbation (3-5 days)
Acute asthma severities
Moderate - PEFR 50-75% of best/predicted, normal speech, RR <25, Pulse <110, sats >92
Severe - PEFR 33-50%, cant complete sentences, RR>25, pulse>110, sats <92
Life-threatening - PEFR<33%, silent chest, cyanosis, feeble resp effort (normal pCO2), bradycardia, dysrhythmia, hypotension, exhaustion, confusion, coma
Treatment of acute asthma (severe or life threatening)
O2 (maintain 94-98%) 5mg salbutamol nebs 40-50mg oral prednisolone 500 micrograms ipratropium bromide nebs Consider 2g magnesium sulfate IV
Follow up for acute severe asthma
GP should be notified within 24hours of discharge and should review the patient within 48 hours
Check inhaler technique
Review treatment
Resp specialist should follow up all patients admitted with a severe asthma attack for at least one year
COPD includes which two lung conditions
Chronic bronchitis (chronic cough and sputum production) Emphysema (enlarged alveoli with destruction of alveolar walls)
Pink puffers vs. blue bloaters
Pink puffer - increased alveolar ventilation, near normal pO2 and normal/low pCO2, breathless but not cyanosed. May develop type 1 resp failure
Blue bloater - reduced alveolar ventilation, low pO2 and high pCO2, cyanosed but not breathless and may go on to develop cor pulmonale. Rely on hypoxic drive to maintain resp effort (88-92%) type 2 resp failure.
Investigations for COPD
Spirometry (obstructive, irreversible)
ABG (low pO2 +/- hypercapnia)
CXR (hyperinflation, flat hemidiaphragm, large central pulmonary arteries, reduced peripheral vascular markings)
CT (bronchial wall thickening, air space enlargement)
ECG (right atrial and ventricular hypertrophy if cor pulmonale)
Management of chronic COPD
Stop smoking, exercise, diet advice
If asthmatic features of features of steroid responsiveness:
- SABA or SAMA
- LABA + ICS (if already on SAMA discontinue and switch to SABA)
- LABA + ICS + LAMA
If no asthmatic features or no features of steroid responsiveness:
- SABA or SAMA
- LABA + LAMA (if already taking SAMA, discontinue and switch to SABA)
Flu and pneumococcal vaccinations
Long term oxygen therapy (+ NIV if hypercapnic)
Consider surgery
what is type 1 resp failure and what are some examples
pO2<8kPa with normal/low paCO2
Ventilation/perfusion mismatch, hypoventilation, abnormal diffusion, or right to left cardiac shunts
V/Q mismatch: pneumonia, pulm oedema, PE, asthma, emphysema, pulm fibrosis, ARDS
what is type 2 resp failure and what are some examples
pO2 <8kPa with paCO2 >6kPa
Alveolar hyperventilation +/- V/Q mismatch
Examples: asthma, COPD, pneumonia, end-stage pulm fibrosis, OSA, sedation, cervical cord lesion, MG, GBS, kyphoscoliosis
Management of type 1 resp failure
Treat underlying cause
Oxygen (24-60%) via face mask
Assisted ventilation if pO2 <8kPa despite 60% O2
Management of type 2 resp failure
Treat underlying cause
Controlled O2: start at 24% via venturi
Recheck ABG after 20 min - if pCO2 is steady or lower then increase O2 conc to 28%, if pCO2 has increased by >1.5kPa consider assisted ventilation (non-invasive positive pressure ventilation), if this fails consider intubation and ventilation
Symptoms of PE
Acute breathlessness, pleuritic chest pain, haemoptysis, dizziness, syncope
Signs of PE
Pyrexia, cyanosis, tachypnoea, tachycardia, hypotension, raised JVP, pleural rub, pleural effusion, check for DVT
Investigations for PE
D-Dimer +/- CTPA or V/Q scan
FBC, U+E, baseline clotting
ABG
CXR
ECG (normal, or tachycardia, RBBB, inverted T in V1-V4, S1Q3T3)
Criteria for suspecting PE
Well's Score- Clinical signs and symptoms of DVT (=3) Tachycardia (=1.5) Recently bed ridden or major surgery (=1.5) Previous DVT or PE (=1.5) Haemoptysis (=1) Cancer (=1) Alternative diagnosis less likely than PE (=1)
Score <4 = unlikely
Score >4 = likely
How to investigate PE based on Well’s score
<4 (unlikely) -> D-Dimer
If D-dimer +ve then do CTPA or empirical LMWH
If D-dimer -ve then consider other diagnoses
> 4 (likely) -> immediate CTPA or treat empirically with LMWH fi there will be a delay in CTPA
PE treatment
If haemodynamically unstable -> thrombolyse for massive PE (alteplase)
If haemo stable - LMWH (unfractionated if renal impairment) for 5 days then start DOAC or warfarin (with warfarin stop LMWH when INR 2-3)
Pneumothorax causes
Spontaneous in young thin men
asthma, COPD, TB, pneumonia, lung abscess, cancer, CF, lung fibrosis, sarcoidosis, connective tissue disorders, trauma, iatrogenic
Symptoms of pneumothorax
May be asymptomatic
Sudden onset dyspnoea, pleuritic chest pain
Signs of pneumothorax
Unilateral: Reduced expansion, hyper-resonance to percussion, diminished breath sounds
Tension pneumothorax - trachea deviated away from affected side
Investigations for pneumothorax
CXR (dont bother if tension pneumothorax - delays treatment)
ABG
Types of pneumothorax
Primary - spontaneous, no other lung conditions (young thin male)
Secondary - lung comorbidities
Tension - air drawn into pleural space with each inspiration and no route for escape during expiration (one way valve). EMERGENCY.
Management for non-tension pneumothorax
Primary: SOB or >2cm on CXR -> aspiration (chest drain if unsuccessful)
Primary: <2cm and no SOB -> O/P review in 2-4 weeks
Secondary: SOB or >2cm on CXR -> chest drain
Secondary: <2cm and no SOB -> aspiration if >1cm (chest drain if unsuccessful), if <1cm then admit and observe for 24h with O2
Management of tension pneumothorax
Needle decompression and chest tube insertion.
Insert a large bore (14-16G) needle with a syringe, partially filled with 0.9% saline, into the 2nd intercostal space midclavicular line on the affected side. Withdraw plunger to allow air to to bubble through saline in syringe.
Then insert a chest tube. (5th intercostal mid axillary line)
Pleural effusion transudate vs exudate causes
Transudate (<25g/L protein) - cardiac failure, constrictive pericarditis, fluid overload, cirrhosis, nephrotic
Exudate (>35g/L protein) - infection (pneumonia, TB), inflammation (RA, SLE), malignancy
Pleural effusion signs
Decreased expansion, stony dull percussion, diminished breath sounds on affected side
Reduced vocal resonance
There may be tracheal deviation in large effusions
Pleural effusion investigations
CXR Ultrasound Contrast CT Diagnostic aspiration Pleural biopsy
Management of pleural effusion
Recurrent aspiration
Pleurodesis
Indwelling pleural catheter
Drugs to alleviate symptoms
What is obstructive sleep apnoea syndrome?
Intermittent closure/collapse of the pharyngeal airway causing apnoeic episode during sleep. terminated by partial arousal from sleep
Clinical features of obstructive sleep apnoea
Obese, middle aged man Snoring Tiredness Poor sleep quality Morning headache Decreased libido Nocturia Reduced cognitive performance
Investigations for obstructive sleep apnoea
Epworth sleepiness scale
Diagnostic sleep studies
Management for obstructive sleep apnoea
Weight loss
CPAP
Intra-oral devices (mandibular advancement) if CPAP is not tolerated
Inform DVLA if excessive daytime sleepiness
What is cor pulmonale and what are some causes
Right heart failure due to chronic pulmonary artery hypertension
Causes - chronic lung disease, pulmonary vascular disorders, neuromuscular and skeletal diseases
Clinical features of cor pulmonale
Dyspnoea, fatigue, syncope
Signs: cyanosis, tachycardia, raised JVP, RV heave, loud P2, pansystolic murmur (tricuspid regurg), hepatomegaly, oedema
Sarcoidosis population group
More common in african-caribbean women aged 20-40
Acute sarcoidosis clinical features
Fever, erythema nodosum, polyarthralgia, bilateral hilar lymphadenopathy
Pulmonary features of sarcoidosis
Bilateral hilar lymphadenopathy, fibrosis
Dry cough, progressive dyspnoea, reduced exercise tolerance, chest pain
Non-pulmonary features of sarcoidosis
lymphadenopathy, hepatomegaly, splenomegaly, uveitis, conjunctivitis, dry eyes, glaucoma, bells palsy, erythema nodosum, arrhythmias, hypercalcaemia, renal stones
Investigations for sarcoidosis
Tissue biopsy is diagnostic and shows non-caseating granulomata
Bloods - raised ESR, lymphopenia, deranged LFTs, raised serum ACE, hypercalcaemia, raised immunoglobulins
24hr urine - high calcium
CXR
ECG - arrhythmias, BBB
Lung function tests - restrictive
bronchoalveolar lavage
ultrasound
bone x-rays - punched out lesions in terminal phalanges
CT/MRI
CXR sarcoidosis staging
0- normal 1- BHL 2- BHL + peripheral pulm infiltrates 3- diffuse pulm infiltrates alone 4- progressive pulmonary fibrosis, honey comb, pleural involvement
Management of sarcoidosis
BHL alone requires no treatment, most recovers spontaenously.
Acute sarcoidosis - bed rest, NSAIDs
Consider corticosteroids or immunosuppression.
Clinical features of interstitial lung disease
Dyspnoea on exertion, non-productive paroxysmal cough, abnormal breath sounds, abnormal CXR or HRCT, restrictive pulmonary spirometry
Examples of interstitial lung disease associated with a known cause
Occupational (asbestosis, siliocosis, cotton workers lung, coal workers pneumonconiosis) Drugs (bleomycin, nitrofurantoin, etc) Hypersensitivity pneumonitis (aka. EAA) Infection (TB, fungi, viral) GORD
Examples of interstitial lung disease associated with systemic disorders
Sarcoidosis, RA, SLE, Sjögrens, UC, autoimmune thyroid
Idiopathic examples of interstitial lung disease
Idiopathic pulmonary fibrosis
Cryptogenic organising pneumonia
Non-specific interstitial pneumonitis
What is extrinsic allergic alveolitis (EAA)?
In sensitised inderviduals, repetitive inhalation of allergens provokes a hypersensitivity reaction (acute or chronic phases)
Causes of extrinsic allergic alveolitis
Bird-fanciers and pigeon-fanciers lung
Farmers and mushroom-workers lung
Malt workers lung
Clinical features of EAA (acute and chronic)
Acute (4-6h post exposure): fever, rigors, myalgia, dry cough, dyspnoea, fine bibasal crackles
Chronic: finger clubbing, increasing dyspnoea, weight loss, exertional dyspnoea, type 1 resp failure, cor pulmonale
Acute phase investigations for EAA
FBC (netrophilia), high ESR, ABG, serum antibodies
CXR (upper zone consolidation)
Lung function tests (reversible restriction)
Chronic phase investigations for EAA
Bloods, serum antibodies CXR (upper zone fibrosis, honeycomb) CT chest (nodules, ground glass) Lung function tests (restrictive) Bronchoalveolar lavage (increased lymphocytes and mast cells)
Management of EAA
Acute: remove allergen, give O2, oral prednisolone
Chronic: avoid allergen, wear face mask or positive pressure helmet, long term steroids, compensation
Idiopathic pulmonary fibrosis population group
typically seen in patients aged 50-70 years, twice as common in men
Commonest type of interstitial lung disease
Features of idiopathic pulmonary fibrosis
Progressive exertional dyspnoea
Bibasal fine end-inspiratory crepitations, dry cough, clubbing
Diagnosing idiopathic pulmonary fibrosis
High resolution CT chest diagnostic investigation of choice (honeycombing, traction bronchiectasis, ground glass)
Spirometry - restrictive, FEV1 normal/decreased, FVC decreased, FEV1% increased
Impaired gas exchange - reduced transfer factor (TLCO)
CXR - bilateral interstitial shadowing (ground glass, honeycombing)
ANA positive in 30%, RhF positive in 10%
Management and prognosis of idiopathic pulmonary fibrosis
Pulmonary rehabilitation
Supplementary oxygen
Lung transplant
Poor prognosis (3-4 year life expectancy)
TB primary disease
non-immune host exposed to mycobacterium tuberculosis -> small lung lesion (Ghon focus develops), composed of tubercle-laden macrophages.
In immunocompetent people then initial lesion usually heals by fibrosis. Those who are immunocompromised may develop disseminated disease (miliary TB)
TB secondary disease
Host becomes immunocompromised and the initial infection becomes reactivated, generally at lung apex
Clinical features of TB
Low grade fever, anorexia, weight loss, malaise, night sweats, clubbing, erythema nodosum Cough, haemoptysis Enlarged lymph nodes Bone tenderness TB meningitis UTI symptoms Pericarditis, pericardial effusion
Diagnostic tests for latent TB
Tuberculin skin test - intradermal injection of purified protein derivative tuberculin. Size of skin induration is used to determine positivity depending on vaccination history and immune status
Interferon gamma release assays - measure amount of interferon-gamma released from T cells reacting to TB antigen. More sensitive than TST
Diagnosing active pulmonary TB
CXR - fibronodular/linear opacities in upper zone usually
Sputum smear (three specimens) stained for acid-fast
Sputum culture (takes 1-3 weeks)
Nucleic acid amplification test
Management of TB
ACTIVE: Rifampicin and isoniazid for 6 months. Pyrazinamide and ethambutol for the first 2 months
LATENT: 3 months of isoniazid (with pyridoxine) and rifampicin
Side effects of TB meds
Rifampicin - enzyme inducer, altered liver function, orange-red urine
Isoniazid - peripheral neuropathy (give pyridoxine to prevent), hepatitis
Pyrazinamide - hepatotoxicity
Ethambutol - colour blindness, reduced visual acuity, optic neuritis
Inhaler technique for metered dose inhalers
Remove cap and shake Breath out gently Put mouthpiece in mouth and as you begin to breath in (slowly and deep), press cannister down and continue to inhale steadily and deeply Hold breath for 10 seconds Wait 30sec before next dose
Causes of clubbing
Cardiac - cyanotic congenital heart disease, bacterial endocarditis, atria myxoma
Resp - lung cancer, CF, bronchiectasis, abscess, empyema, TB, asbestosis, mesothelioma, fibrosing alveolitis
Others - Crohns, cirrhosis, PBC, Graves, Whipples, coeliacs
