Respiratory Flashcards
What scale do you use to grade breathlessness?
MRC dyspnoea scale
1: Not troubled by breathlessness except on strenous exercise
2: SOB when hurrying or walking up a slight hill
3: Walks slower than contempories on level ground because of breathlessness
4: Stops for breath after walking about 100m or a few mins
5: Too breathless to leave the house, at rest
What investigations might you perform in somebody with possible COPD?
Bloods- anaemia, polycythaemia, low albumin
ABG
Sputum culture
alpha 1 antitrypsin level
Lung function tests FEV1/FVC <70%, FEV1 <80%, minimal reversibility
CXR: flattened hemidiapraghm, bullae, cardiomegaly in cor pulmonale
CT
HRCT used to grade and classify emphysema
ECG
What treatments are available to help patients stop smoking?
Behavioural treatment: 5 As Ask about tobacco use Advise to quit Assess willingness to quit Assist in quit attempt Arrange follow up
Nicotine replacment: gum, patch, inhalers
Buproprion: norepinephrine and dopamine reuptake inhibitor and nicotinic antagonist, start 1-2 weeks before stop day. C/I in epilepsy, pregnancy, breast feeding
Varenicline: nicotic partial receptor agonist, start 1 week before stop date. Nausea, headache insomnia, usual dreams. Caution risk of suicide
What are the treatment options in COPD?
Non-pharmacological
- pulmonary rehabilitation: MDT approach, if MRC grade 3+
- optimise nutrition
- vaccination- influenza, pneumococcal
Pharmacological
New GOLD guidelines
Group A (MRC 0-1, 0-1 exacerbations, no admissions)
- Bronchodilator
Group B (MRC >2, 0-1 exacerbations, no admissions)
- LABA or LAMA
- LABA + LAMA
Group C (MRC 0-1, >2 exacerbations or hospital admiss)
- LAMA
- LAMA+ LABA or LABA +ICS
Group D (MRC >2, >2 exacerbations or hospital admiss)
- LAMA
- LAMA + LABA
- LAMA + LABA + ICS
- consider macrolide in former smokers
- consider roflumilast
What are the NICE guidelines for treatment of COPD?
FEV1 > 50%
- LABA or LAMA
- then LABA + ICS
- then LAMA+ LABA + ICS
FEV1 <50%
- LABA + ICS or LAMA
then LAMA + LABA + ICS
When do you qualify for LTOT?
PaO2 <7.3 kPA or
PaO2 <8.0 kPA + secondary polycythaemia, noctural hypoxaemia, cor pulmonale or pul.htn
Describe the role of surgery in COPD
Lung volume reduction surgery
- Symptomatic despite max medical therapy + pul.rehab
- FEV1 <20% predicted, PCO2 <7.3kPA, TLCO >20% prediced
- must have predominantly upper lobe emphysema
- can improve exercise capacity
Bullectomy
- if bullae >1/3 of hemithorax
- can improve lung function, elastic recoil
Lung transplant
- can improve functional capacity
- strick guidelines for referral: FEV1 <25%, resting hypoxaemia + hypercapnia, pul.htn, accelerated decline FEV1
What causes an acute exacerbation of COPD?
Infection 60%
- virus- rhinovirus, influenza, parainfluexna, cornavirus
- Bacteria: Haemophilus influenzae, Moraxella catarrhalis, Strep pneumoniae
- Pollution
- Unknown
How are infective exacerbations treated?
- controlled oxygen therapy
- Short acting beta agonists +/- short acting anti-cholinergics
- PO corticosteroids for 5-7 days
- Antibiotics
- NIV
( should not use aminophylline)
What is NIV and when would you use it in COPD?
Bilevel positive airway pressure provides pressure support with a higher inspiratory positive pressure than expiratory.
Indications
- pH <7.35 despite optimal medical therapy and controlled oxygen
- consent to treatment
Contraindications
- life threatening hypoxaemia
- confusion
- vomiting
- facial injury
- inability to protect own airway
- upper GI surgery
- undrained pneumothorax
How does CPAP differ from BiPAP?
CPAP maintains same pressure support throughout breathing cycle, splinting open the upper airways and recruiting collapsed alveoli, reducing ventilaiton/perfusion mismatch
Used in treatmetn of acute pul.oedema, OSA, T1RF
What is the CURB score?
Confusion Urea >7 RR >30 BP <90 systolic, <60 diastolic Age >65
Score 2= 3% 30 day mortality
3-5 17-57% 30 day mortality
Name the common community acquired pathogens in CAP?
Strep pneumoniae
Haemophilis influenzae: most common in COPD
Mycoplasma pneumoniae: Cold IgM agglutins- haemolytic anaemia, erythema multiforme, GBS, pericarditis, Hepatitis, GN
Chlymydophilia pneumonia: Q fever
Legionella: flu like symptoms, fever, dry cough, bradycardia, confusion, lymphopenia, hyponatraemia, deranged LFTs
Staph aureus: assoc influenza
Moraxella catarrhalis: assoc COPD
Viruses: influenza A+ B
Describe the treatment of CAP
Antibiotics: CURB score low amox, moderate pen+ macrolide
Physio
IVF if fluid depletion
Oxygen
Repeat CXR 6 weeks
Prevention: vaccination for high risk groups
Define hospital acquired pneumonia and what are the likely pathogens?
Occurs >72hrs after admission
Gram negative bacilli, pseudomonas, anaerobes
What is bronchiectasis?
Abnormal permanent dilatation and destruction of bronchi caused by a combination of infection, impaired drainage, airway obstruction +/- defective host response
What are the respiratory causes of clubbing?
ABCDEF Abcess or Asbestosis Bronchiectasis Cystic Fibrosis Dirty tumours (bronchogenic ca) Empyema Fibrosing alveolitis (IPF)
What are the causes of clubbing and crackles?
FAB
Fibrosing alveolitis (IPF)
Asbestosis
Bronchiectasis, bronchogenic carcinoma
What investigations might you do in somebody who you suspect bronchiectasis?
Sputum MCS, AFB, cytology FBC Serum immunoglobulins Alpha-1 antitrypsin Aspergillus precipitans and serum IgA CXR HRCT: high sensitivity and specificity Lung function tests: obstructive Flexible bronchoscopy- rarely needed Specific test- CF sweat test, Kartageners syndrome ( nasal brushings and EM, TB - IGRA
Describe the findings on CXR and CT of a patient with bronchiectasis?
CXR
- tramlines and ring shadows due to dilated thickened airways
- Bronchoceles- mucus plugging
- Hyperinflation
- Honeycomb pattern in severe cases
HRCT
- Bronchial thickening and diltation seen as tram tracking parallel or ring shadowns side on
- Signet ring sign- dilated bronchi >1.5x larger than adjacet pul.artery
- pus/fluid levels
- lack of normal tapering of bronchi seen within 1cm pleura
What are the causes of bronchiectasis?
Congenital
- CF
- Youngs syndrome
- Kartegeners syndrome
- Yellow nail syndrome- lyphoedema, pleural effusion
Mechanical
- Bronchial obstruction- foreign body, carcinoma, granuloma (sarcoid/TB), enlarged LN (TB
Childhood infection- whooping cough, measles, TB
Overactive immune response- ABPA
Underactive immune response: hypogammaglobulinaemia, HIV, leukaemia
Chemical injury: recurrent aspiration
Other resp diseases: fibrosis- traction bronchiectasis, COPD
What is the management of bronchiectasis?
General measures
- Education of patient and family
- optimise nutrition- CF needs pancreatic supplementation and fat soluble vitamins
- smoking cessation
- vaccinations
- respiratory physio- postural drainage, chest percussion, controlled breathing
- devices- acapella device- oscillating PEP
Medical treatments
- antibiotics
- prophylactic antibiotics- less evidence, azithromycin +/- tobramycin neb (pseudomonas)
- bronchodilators
- steroids
- mucolyitics
Transplantation in CF
Immunoglobulins in hypogammaglobulinaemia
What is the pathogenesis of CF
AR
Defect in CFTR gene (CF transmembrane conductance regulator protein) located on chromosome 7.
Over 1250 mutations, most common delta F508
1/2000-3000 live births
CTFR protein in all exocrine tissues
Prevents chloride moving out of cells -> Na hyperabsorption occuring to keep intracellular electrochemical balance -> osmotic pull of water into cells -> dehydration extracellular surfaces -> thick viscous secretions easiily ameanable to colonisation and infection
What systems are affected in CF?
GI
- pancreatic enzyme insuffiency- malabsorption of fat and protein
- diabetes
- meconium ileus in newborns
- focal biliary cirrhosis leading to portal hypertension
- cholelthiasis
Reproductive
- male subfertility due to defective sperm transport
MSK_ osteoporosis
ENT- sinus disease and nasal polyps
What organisms commonly colonise the resp tract of CF patients?
Haemophilus influenzae
Staph aureus
Pseudomonas
Burkholderia cepacia- less common but assoc with accelerated decline
What is the prognosis in CF
Median survival 32 yrs but improving
What are the main complications of bronchiectasis
Pulmonary
- recurrent infections
- haemoptysis
- empyema/abcess
- cor pulmonale
Extrapulmonary
- anaemia
- mets infection eg cerebral abcess
- secondary amyloidosis
What other conditions are known to be assoc with bronchiectasis?
- connective tissue diseasees eg RA
- chronic sinusitis
- iIBD
- Marfans
What are the major pathogens assoc with bronchiectasis?
Pseudomonas aeriuginosa
Haemophilis influenzae
Less common strep
What are the complications of previous TB?
- apical fibrosis
- Bronchiectasis due to LN obstruction causing distal bronchial dilatation, bronchial stenosis and secondary lung fibrosis (traction)
- Aspergilloma in old TB cavity
- Pleural effusion or thickening
What surgeries used to be performed to treat TB?
Based on theory that inducing lobar collapse would starve organism of oxygen (untrue)
Thoracoplasty: ribs resected to reduce intrathoracic volume
Phrenic nerve crush: nerve was crushed to paralyse the diarphragm on that side
Plombage: an inert substance eg wax, gauze was inserted into lung compressing it
What investigations would you perform on somebody with possible TB?
Sputum for ziehl-neelson straining- 3 early morning AFB
Mantoux test (tuberculin skin test) if immunosuppressed can be falsely negative
Interferon gamma release assay (Quantiferon)- measures interferon gamma released by antigen-specific T cells in response to peptides derived from mycobacterium TB
- HIV
-CXR: hilar or paratracheal adenopathy, pul.infiltrates, pul.nodules, consolidation, cavitation
- CT scan- consolidation, caviation, nodules, ground glass opacities, miliary nodules
- Bronchoscopy
- Biopsy LNs
What are the risk factors for active pulmonary TB infection?
- place of birth
- Age
- HIV/Aids
- Homelessness
- Previous prison stays
- sex workers
- co-morbidities- diabetes, renal disease, malignancy
- immunosuppresants- steroids, chemotherapy
How do you treat pulmonary TB?
Contact tracing and notifiable disease
Commence treatment with RIPE while await sensitivities
If fully sensitive can stop PE after to month and continue RI for further 4 months
Prior to tx should have LFTs, visual acuity and colour vision documented
DOT ( direct observed treatment) can be considered
What are the side effects of treatment?
Isoniazid: hepatitis, peripheral neuropathy
Rifampicin: red secretions, GI disturbance
Pyrazinamide: GI disturbance, hepatic toxicity, peripheral neuropathy, gout
Ethambutol: optic neuritis
What are the extra-pulmonary manifestations of TB?
CNS: TB meningitis, tuberculoma Pericardial TB Spinal TB: potts disease, most commonly thoracic GU: prostatitis, epididymitis Miliary TB: haematogenous spread
What are the clinical signs of pulmonary fibrosis?
Tachypnoea- may be on oxygen
Clubbing
Central cyanosis
Tracheal deviation towards fibrosis
Flattened chest
Scars from biopsy
Increased tactile vocal fremitus and resonance
Fine end expiratory crackles- remember creps dissapear on leaning forward
Pul.htn
Steroid purpura
Assoc cause: hands- RA, scleroderma, nicotine
Face- butterfly rash, heliotrope rash, telangiectasia
What causes upper zone fibrosis?
Coal workers pneumoconioses Histoplasmosis Hypersensitivity pneumonitis AS ABPA Radiation TB Sarcoidosis/silicosis
What causes lower zone fibrosis?
RA Asbestosis Connective tissue disease (scleroderma, PM, DM, Sjorgrens, SLE, MCTD Idiopathic pulmonary fibrosis Other- bronchiectasis, chemical or drug
What are the pneumoconioses?
Group of chronic lung disease caused by inhalation of a metal or mineral particle.
Eg silicosis, berylliosis, asbestosis, coal workers
What is hypersensitivity pneumonitis or extrinsic allergic alveolitis?
Inflammation of alveoli of lung secondary to hypersensitivity to inhaled particles.
Acute pul/systemic symptoms occuring 6hrs post exposure to allergen -> cough, pyrexia, malaise and then if chronic dyspnoea, non-causeating granulomas
Farmers lung: mouldy hay
Bird fanciers lung: pigeons
Byssinosis: cotton dust
Mushroom workers lung: mushroom spore
What are the drugs which cause fibrosis?
Bleomycin Busulphan Cyclophosphamide Methotrexate Amiodarone Nitrofurantion Suphasalazine Gold
What are the types idiopathic interstitial fibrosis are there?
UIP: usual interstitial pneumonia: defines IPF, survival 2.5-5.5yrs.
DIP: desquamative interstitial pneumonia: assoc smoking steroid responsive 62%,
Acute interstitial pneumonia: Hamman-Rich syndrome which is rare and fulminant, very high mortality
What are the complications of direct tumour invasion in lung cancer?
Hoarse voice secondary to left recurrent larygeal nerve palsy
Stridor
Horners syndrome: suggests pancoasts tumour. Ipsilateral partial ptosis, miosis, enopthylamous, anhydrosis. Weakness and atrophy of intrinsic muscles of hand
SVC obstruction
What are the complications of metstatic lkung disease
Bone deformity and tenderness
Hepatomegaly and jaundice
FOcal neurology from MSCC or brain mets
Name some musculoskeletal paraneoplastic syndromes?
Hypertrophic pulmonary osteoarthropathy- clubbing pluse pain and swelling at wrists and ankles due to subperiosteal new bone formation, more common with squamous and adenocarcinoma
Polymyositis (anti-Jo)
Name some neurological paraneoplastic syndromes?
Lambert- Eaton syndrome: antibodies against voltage gated calcium channels. Slowly progressive proximal muscle weakness, autonomic dysfunction, can improve after exercise. Present in SCLC
Proximal myopathy
Peripheral neuropathy and cerebellar syndromes (anti-Hu)- small cell lung cancer
Cerebellar syndrome (anti-Yo, mainly ovarian, breast)
Name some endocrine paraneoplastic syndromes
Hypercalcaemia- tumour secrete PTH related peptide, calcitriol. Commonly squamous cell
SIADH: SCLC, fluid restrict demeclocycline
Ectopic ACTH secretion: Cushings syndrome. Commonly SCLC
HCG secreting tumours cause gynaecomastic
What are the dermatological paraneoplastic syndromes?
Thrombophlebitis migrans (Trousseau syndrome): pancreatic cancer
Acanthosis nigrans: adenocarcinoma of GI tract
Erythema gyratym repens: breast cancer
Dermatomyositis
What are the most common paraneoplastic features of small cell lung cancer?
ADH
ACTH - not typical, hypertension, hyperglycaemia, hypokalaemia, alkalosis and muscle weakness are more common than buffalo hump etc
Lambert-Eaton syndrome
WHat are the most common paraneoplastic features of squamous cell lung cancer?
parathyroid hormone-related protein (PTH-rp) secretion causing hypercalcaemia
clubbing
hypertrophic pulmonary osteoarthropathy (HPOA)
hyperthyroidism due to ectopic TSH
What investigations might you do for somebody with possible lung cancer?
Bloods: FBC (anaemia), LFTS (liver mets), U+E (SIADH), bone profile (high ca)
Sputum cytology
Pleural aspiration and cytology
CXR: spiculated, non-calcified lesions, collapse and consolidation
CT chest /abdo with contrast: size, stage, LNs, mets
PET CT: useful for looking for LN involvement
Bone scan
Lung function tests: suitability for resection
Histological sampling
- percutaneous CT guided biopsy- peripherally located
- US guided biopsy/asp of LN
- FLexible bronchoscopy- assess poisiotn, BAL for cytology, endobronchial biopsy, transbronchial needle aspiration
- Mediastinoscopy
- VATs + pleural biopsy
What are the risk factors for lung cancer?
Smoking- 90% of all lung cancers cause by smoking (adenocarcinoma is the only which is not)
Radiation therapy
Environmental exposure to passive smoke, asbestsos
Pulmonary fibrosis
COPD
Alpha 1 antitripsin
genetic factors
Describe the histological classification of lung cancer?
Non-small cell lung cancer: 75-80% of lung cancer
- Squamous > adenocarcinoma> alveolar cell > large cell
Small cell lung cancer: 20-25%, rapidly proliferating, early dissemination
What are the common sites of lung mets?
Liver
Adrenal glands
Bone
Brain
How is small cell lung cancer classified?
Limited disease: confined to ipsilateral hemithorax
Extensive disease: mets outside the ipsilateral hemithorax
How is non-small cell lung cancer classified?
According to TNM staging then can be grouped into Stage 1-4
What prognostic factors help guide treatment of lung cancer?
Performance status - 0-5 (dead)
0 Fully active
1 Restricted in stenous activity, can carry out work
2 Ambulatory >50% of time, capable of self care, unable to work
3 Ambulatory <50% of time
4 Bedbound
5 Dead
Describe the management of patients with NSCLC?
Discussion at lung MDT, CNS involvement
Surgery- lobectomy/pneumonectomy for stage I- IIIa disease
- Pneumonectomy FEV1 >2l
- Lobectomy FEV1 >1.5l
- other contraindications - malignancy pleural effusions, tumour near hilum, vocal cord paralysis, SVC obstruction
Radical radiotherapy- consider in inoperable patients
Chemotherapy- usually platinum based + 3rd generation drug (docetaxel, gemcitabine, paclitaxel, vinorelbine)
Palliative
Describe the management of small cell lung cancer?
If very early can operate but most present with mets
Radiotherapy + platinum based chemotherapy
Prophylactic cranial irradiation
What are the signs of SVC obstruction?
Facial and upper body oedema Facial plethora Cyanotic appearance Superficial vein distention of face and upper body SUffusion of eyes Hoarse voice Inspiratory stridor Elevated fixed JVP Dilated venous angiomata under tongue Pembertons sign: worsening of listed features upon raising both arms above head
What investigations would you perform on somebody with ? SVC?
CXR: mediastinal widening
CT with contrast: defines level and extenet
Conventional venography as a prelude to stenting
What are the common causes of SVC obstruction?
Lung cancer: 10% SCLC, 1.7% NSCLC Lymphoma esp NHL Thymoma Primary mediastinal germ cell tumours Sold tumours with LN mets Post radiation fibrosis Thoracic aortic aneurysm Thrombosis
Describe the management of SVCO?
Steroids in malignancy
Endovascular stenting
Chemo/radiotherapy
What are the causes of a posterolateral thoractomy scar?
Pneumonectomy- empty unilateral cavity which fills with fluid, dull to percussion, decreased or absent breath sounds
Lobectomy:- compensatory hyperinflation of ipsilateral lobes can mask the signs
Open lung biopsy: scar may be shorter only 3-4 cm
List some reasons for performing a pneumonectomy or lobectomy
Lung malignancy, rarely pulmonary mets Localised bronchiectasis Old TB (Prior to anti TB therapy) Fungal infections eg aspergilloma Traumatic lung injury Large bullae Congenital lung disease eg CF Bronchial obstruction with destroyed lung
What are the chest radiographic features of a pneumonectomy/lobectomy?
Pneumonectomy: white out
Lobectomy: volume loss, increase transradiancy of ipsilateral lung, surgical clips, rib resection
Trachea deviated towards pneumo/lobectomy
Compensatory hyperinflation
What is the importance of preoperative evaluation in pneumonectomy?
You lose significant lung function following surgery and it essential to assess functional reserve
What are the subtypes of pneumonectomy?q
Simple: removal of affected lung
Extrapleural: removal of affected lung plus part of diaphragm, parietal pleura and pericardium on ipsilateral side, linings are replaced by surgical Gore-tex. Used in mesothelioma
Comment of the operative mortality of lobectomy and pneumonectomy? Difference between sides?
Mortality for lobectomy is 2-4%
Mortality for pneumonectomy is 6%, right side has higher mortality of 10-12% compared to left 1-3.5%.
What is post pneumonectomy syndrome?
Results from extrinsive compression of distal trachea and main stem bronchus due to mediastinal shifting and compensatory hyperinflation that occurs in remaining lung.
Occurs almost exclusively in right sided pneumonectomy approx 6m after surgery
Progressive dyspnoea, cough, stridor, pneumonia.
Treatment includes repositioning the mediastinum surgically
What is cor-pumonale
Failure of right ventricle and fluid retention due to pulmonary hypertension due to disease affecting the lung and its vasculature
What is the pathophysiology of cor pulmonale?
Fluid retention:
- hypoxia and secondary polycythaemia cause increased sympathetic activity and renal vasoconstriction leading to retention of salt and water.
- Hypercapnia results in increased bicarbonate reabsorption of salt and water
Pulmonary hypertension
- Hypoxia induced pulmonary vasoconstriciton and chronic smooth muscle proliferation that result in increased pul. vascular resistance and pul. htn
- fibrosis of pul. vascular bed
- secondary polycythaemia contributes to resistance in blood flow
RV dysfunction due to increased work load
What are the signs of cor pulmonale?
Bounding pulse, flapping tremor
central cyanosis
Raised JVP: prominant A wave (right atrial hypertrophy) and V wave due to TR
Left parasternal heave due to RV hypertrophy
Palpable 2nd heart sound- pul.htn
Wide splitting of 2nd heart sound, loud P2
PSM due to TR
Early diastolic murmur in pul. area due to functional pulmonary incompetence
4th heart sound
Hepatomegaly
Leg oedema
What investigations would you do in somebody you suspected cor pulmonale?
Pulse oximetry
ABG
CXR: cardiomegaly, enlarge pul.arteries
ECG: RAD, p pulmonale, RBBB
ECHO: dilated, hypertrophied RV, raised pul.artery pressure
Right heart catheterisation- remains gold standard for diagnosing pul.htn
What is the definition of pulmonary htn?
Mean pulmonary artery pressure >25mmHg with pulmonary capillary or left atrial pressure <15mmHg
Name the common causes of cor pulmonale?
COPD
Interstitial lung disease
OSA
Hypoventilation disorders: obesity related hypoventilation, neuromuscular, kyphoscoliosis
How is pul.htn classified by WHO?
- Pulmonary arterial hypertension- includes idiopathic pul.htn, familial pul.htn, HIV, drugs
- Pulmonary venous hypertension- due to left sided heart disease
- Pulmonary hypertension assoc with hypoxaemia- resp disease
- Pul hypertension due to chronic thrombosis/emboli: PE, Sickle cell disease
- Pul hypertension assoc with miscellaneous disorders- sarcoidosis, Langerhans cell histiocytosis
Describe the management of patient with cor pulmonale
- optimise underlying condition
- consider LTOT
- Consider NIV for hypoventilation syndromes
- diurectics (judicious use as can reduce pressure and reduce RV output)
What is Allergic bronchopulmonary aspergillosis and who is more likely to get it?
a hypersensitivity reaction to the colonisation of the airways/sinuses/lungs with Aspergillus spp. This predominantly affects patients with asthma, cystic fibrosis (CF) and bronchiectasis.
Affects 1% of people with asthma and 5-10% of those with CF
How would you diagnose ABPA?
Diagnosis is made on the basis of a deterioration in the patient's clinical condition (the underlying asthma or CF symptoms worsen), being a susceptible patient and the presence of the following: Eosinophilia. Positive skin test to Aspergillus spp. Elevated serum immunoglobulin E (IgE). Positive serology for Aspergillus spp. New infiltrates on CXR or CT scan.
Sputum microscopy and culture may also reveal the presence of Aspergillus spp.
How would you treat ABPA?
Steroids and itraconazole
How would you manage an aspergilloma
Usually treatment started when symptomatic (haemoptysis)
Surgical resection if adequate pul. reserve
Itraconazole long term
Embolisation if massive haemoptysis
