Respiratory Flashcards
Signs of COPD on Examination
Inspection
Inhalers
Peak flow meter
Nebuliser
Pursed lip breathing
Splinting diaphragm
Cushingoid
Cyanosed
Cachetic
Hands
Tar staining
CO2 retention flap
Face
Plethora - polycythaemia
Central cyanosis
Chest
Barrel-shaped
Decreased cricosternal distance
Decreased expansion bilaterally
Resonant PN
Auscultation: reduced breath sounds, expiratory wheeze, prolonged expiratory wheeze
Hyperexpansion
Decreased cricosternal distance
Loss of cardiac dullness
Palpable liver edge
Extras
Cor pulmonale: Raised JVP, left parasternal heave, loud P2 and S3, mid-diastolic murmur of tricuspid regurg, ascites, peripheral oedema, hepatomegaly (pulsatile)
Significant negatives: CO2 retention, Cor pulmonale, clubbing
Differential for COPD
Chronic asthma
Bronchiectasis
Definition of COPD
Disease state characterised by airflow limitation that is not fully reversible.
It encompasses both emphysema and chronic bronchitis. The airflow limitation is usually progressive and is associated with an abnormal inflammatory response of the lungs to noxious particles or gases.
Management of COPD
Conservative / General management
smoking cessation advice
Pulmonary rehabilitation programme
annual influenza vaccination
one-off pneumococcal vaccination
Bronchodilator therapy
a short-acting beta2-agonist (SABA) or short-acting muscarinic antagonist (SAMA) is first-line treatment
for patients who remain breathless or have exacerbations despite using short-acting bronchodilators the next step is determined by the FEV1
FEV1 > 50%
long-acting beta2-agonist (LABA), for example salmeterol, or:
long-acting muscarinic antagonist (LAMA), for example tiotropium
FEV1 < 50%
LABA + inhaled corticosteroid (ICS) in a combination inhaler, or:
LAMA
For patients with persistent exacerbations or breathlessness
if taking a LABA then switch to a LABA + ICS combination inhaler
otherwise give a LAMA and a LABA + ICS combination inhaler
Oral theophylline
NICE only recommends theophylline after trials of short and long-acting bronchodilators or to people who cannot used inhaled therapy
the dose should be reduced if macrolide or fluoroquinolone antibiotics are co-prescribed
Mucolytics
should be ‘considered’ in patients with a chronic productive cough and continued if symptoms improve
Cor pulmonale
features include peripheral oedema, raised jugular venous pressure, systolic parasternal heave, loud P2
use a loop diuretic for oedema, consider long-term oxygen therapy
ACE-inhibitors, calcium channel blockers and alpha blockers are not recommended by NICE
Factors which may improve survival in patients with stable COPD
smoking cessation - the single most important intervention in patients who are still smoking
long term oxygen therapy in patients who fit criteria
lung volume reduction surgery in selected patients
Home Emergency Pack (rescue)
Antibiotics
Surgical Mx
Recurrent pneumotjoraces or large bullae
Bullectomy or lung reduction surgery
Factors that Improve Patient Survival
Factors which may improve survival in patients with stable COPD
Smoking cessation - the single most important intervention in patients who are still smoking
Long term oxygen therapy in patients who fit criteria (15h / day)
Lung volume reduction surgery in selected patients
Obstructive spirometry
Increased Total Lung Capacity (TLC)
Increased Residual Volume (RV)
FEV1: <80%
FEV1: FVC ratio: 0.7
Decreased transfer factor (not tested on spirometry)
Hyperinflation
>10 posterior ribs
flat diaphragm
DDx: long-standing asthma, COPD, bronchiectasis
Criteria for LTOT in COPD
Offer LTOT to patients with a pO2 of < 7.3 kPa
OR
pO2 of 7.3 - 8 kPa and one of the following:
- secondary polycythaemia
- nocturnal hypoxaemia
- peripheral oedema
- pulmonary hypertension
GOLD Staging
Stage I - IV
All have FEV1 : FVC ratio <0.7
Mild: FEV1% >80%
Moderate: FEV1% 50-79%
Severe: FEV1% 30-49%
Very Severe: FEV1% <30%
CXR signs of COPD
Acute
Consolidation
Pneumothorax
Chronic
Hyperinflation
Pulmonary HTN
Bullae
BODE Index
Body-mass index, airflow Obstruction, Dyspnea, and Exercise
Calculates index of function for COPD patients
Used to long-term outcomes
Four factors to predict risk of death from the disease
Weight loss = bad
Good lung function = good
modified MRC dyspnea scale, less SOB = good
6-min walk test, greater distance = good
Definition of Chronic Bronchitis
Cough productive of sputum on most days for >3 months on 2 or more consecuitive years
Definition of Emphysema
Histological description of alveolar wall destruction with airway collapse and air trapping
Investigations for COPD
Invx
spirometry
pulse oximetry
ABG
CXR
ECG: RV strain/hypertrophy
echo: RVH
sputum culture
PFTs
chest CT scan
alpha-1 antitrypsin level
Signs of Asthma on Chronic Examination
Inspection
Inhalers
Peak flow meter
Nebuliser
General: cushingoid
Specific: oral thrush
Chest
Harrison sulcus
Auscultation: Usually normal, may be decreased air enrty and mild wheeze
Significant negatives: CO2 retention, Cor pulmonale, clubbing
Differential:
Pulmonary oedema: cardiac wheeze
COPD
Definition of Asthma
Chronic inflammatory airway disease characterised by intermittent airway obstruction and hyper-reactivity
Investigations for Asthma
Bedisde: PEFR
exhaled nitric oxide
Bloods:
FBC (eosinophilia)
Increased IgE
Aspergillus serology
CXR: hyperinflation
Spirometry: obstructive
Reduced FEV1:FVC ration <0.75
Reduced FEV1
Increased residual volume
>12% improvement with inglaed SABA
PEFR diary
Atopy
Skin-prick testing
RAST
Spirometry results for Asthma
Spirometry: obstructive
Reduced FEV1:FVC ration <0.75
Reduced FEV1
Increased residual volume
>12% improvement with inglaed SABA
Management of Asthma
General
MDT: GP, specialist nurse, respiratory team
TAME
Technique for inhaler
Avoidance of allergens, smoke, dust
Monitor: peak flow diary
Educate: specialise nurse, develop action plan
Medical
ICS, SABA, LABA, LTRA
Well controlled: no exacerbations, no reliever therapy, no night time waking, <20% diurnal variation, normal lung function
Signs of Pulmonary Fibrosis on Examination
General
Clubbing
cushingoid
No sputum
Tachypnoea
Central cyanosis
Evidence of cause:
Rheumatoid arthritis
Sarcoidosis: erythema nodosum
Systemic sclerosis: sclerodactyl, calcinosis, microstomia, beak nose, telangiectasia
SLE: malar rash
Ankylosing spondylitis: kyphosis
Radiation: skin tattoos on chest
Chest
Thoracotomy scar: single lung trasplant
Tracheal shift towards fibrosis: upper lobe
Fine end-inspiratory crackles: No change with coughing
Extras: cor pulmonae
Apex beat
Peripheral oedema
Differential:
Bronchiectasis
Chronic lung abscess
Significant negatives: signs of causes (e.g. RA hands), cor pulmonale, cyanosis
Causes of Pulmonary Fibrosis
Commonest: idiopathic pulmonary fibrosis
Upper Lobe: PATEN
Pneumoconiosis: coal, silica
Aspergillosis: Allergic bronchopulmonary aspergillosis
TB
Extrinsic allergic alveolitis
Negative, sero-arthopathy
Lower Lobe: STARI
Sarcoidosis
Toxins: BANSME
Asbestosis
Rheumatological: Rheumatoid arthritis, Systemic Lupus Erythematosus, Sjogren’s
Idiopathic Pulmonary Fibrosis
BANSME
Bleomycin, Busulfan
Amiodarone
Nitrofurantoin
Sulfasalazine
MEthotrexate
Investigations for Pulmonary Fibrosis
Bedside:
PEFR
ECG (RVH)
Bloods
FBC: anaemia exacerbates SOB
ABG: decreased PaO2, Increase PaCO2
Idiopathic PF: increased ESR, increased CRP, ANA+ve in 30%, Rheumatoid factor +ve 10%, Increase Ig
Extrinsic allergic alveolitis: +ve serum precipitins
Connective tissue disease: C3/C4, RF, ANA, scl-70, centromere
Sarcoid: serum ACE, Calcium
Spirometry
Normal or increased FEV1: FVC ratio
Reduced FEV1
Reduced TLC, FVC and RV
TLCO: reduced transfer factor
Imaging
CXR: reticulonodular shadowing, reduced lung volume
HRCT: honeycomb, fibrosis
Echo
Pulmonary hypertension
Bronchoalveolar lavage
Lung biopsy: usual interstitial pneumonia
Management of Pulmonary Fibrosis
MDT: GP, respiratory team, Physio, Psych, Pallative care, specialist nurse
Specific to Idiopathic Pulmonary Fibrisos: Pirfenidone (an antifibrotic agent)
Acute flare: give 4 weeks of prednisolone
Treat specific cause:
Extrinsic allergic alveolitis: steroids
Sarcoidosis: steroids
Connective tissue disease: steroids
Supportive care
Smoking cessation: most beneficial
Pulmonary rehabilitation
Long term oxygen therapy
Symptomatic relief: anti-tussive (codiene), Heart failure (b-blockers, ACE-i)
Surgery: lung transplant
Signs of Bronchiectasis on Examination
General
Clubbing
Sputum pot
Small and young = Cystic fibrosis
Cachexia
Tachypnoea
Evidence of specific cause:
Rheumatoid arthritis: rheumatoid hands
Yellow nails
Cystic fibrosis: Young, nasal polyps
Hypogammaglobulinaemia: splenomegaly
Inflammatory bowel disease: abdo scars
Chest
Thoracotomy scars
Portacath or hickman lines + scars: Cystic fibrosis
Coarse, wet crackles - may change with cough,
Localised patchy crackles = focal consolidation
Widespread crackles = secondary to systemic disease
+/- monophonic wheeze
Dextrocardia –> Primary ciliary dyskinesia
Extras: cor pulmonale
Completion: examine nose for nasal polyps, examine abdo for scars and splenomegaly
Significant negatives: cor pulmonale, specific cause e.g. rheumatoid hands
Differential
Pulmonary fibrosis
Chronic lung abscess
Causes of Bronchiectasis
Congenital
Cystic fibrosis
Primary ciliary dyskinesia (Kartagener’s)
Young’s: azoospermia and bronchiectasis
Hypogammaglobulinaemia: X-linked, CVID, specific antibody def
Acquired
Idiopathic
Post-infectious: pertussis, TB, measles
Obstructive: tumour, foreign body
Associated: Rheumatoid arthritis, ulcerative colitis (and corhn’s), ABPA
Investigations for Bronchiectasis
Bedside
PEFR
Urine dip: proteinuria —> amyloidosis
Sputum: MC+S, cytology
Bloods
FBC:
Serum Ig
Aspergillus: RAST, precipitins, IgE, eosinophilia
Precipitins: These tests detect the presence of IgG antibodies to Aspergillus fumigatus
RA: anti-CCP. RF, ANA
Imaging
CXR: tramlines and ring shadows (bunch of grapes)
HRCT:
signet ring sign = thickended dilated bronchi and small adjacent vascular bundle
Pools of mucus in saccular dilatations
Spirometry: obstructive
Other
Bronchoscopy + biopsy
CF sweat test
Aspergillus skin prick testing
Complications of Bronchiectasis
Cachexia
Pulmonary HTN
Massive haemoptysis
Type 2 respiratory failure
Amyloidosis
Management of Bronchiectasis
MDT approach: GP, Respiratory team, Dietician, Immunologist, Genetics
Physio:
Postural drainage
Active cycle breathing
Rehabilitation
Medical
Antibiotics: Ciprofloxacin for 7 days, Azithromycin for prophylaxis
Bronchodilators: nebulised salbutamol
Treat underlying cause:
CF: DNAse, Creon, ADEK vitamins
ABPA: steroids
Immune def: IV Ig
Vaccination: flue, pneumococcus
Cause of Cystic Fibrosis
Autosomal recessive
Mutation in CFTR gene on chromosome 7
Cystic fibrosis transmembrane conductase regulator
Commonly deltaF508
Deletion of three nucleotides = loss of phenylalanine (F)
Decreased luminal CI- secretion and Increased Na resorption leading to viscous secretions
Because chloride is negatively charged, this modifies the electrical potential inside and outside the cell that normally causes cations to cross into the cell. Sodium is the most common cation in the extracellular space. The excess chloride within sweat ducts prevents sodium resorption by epithelial sodium channels and the combination of sodium and chloride creates the salt, which is lost in high amounts in the sweat of individuals with CF. This lost salt forms the basis for the sweat test.
CFTR not only allows chloride ions to be drawn from the cell and into the ASL, but it also regulates another channel called ENac, which allows sodium ions to leave the ASL and enter the respiratory epithelium. CFTR normally inhibits this channel, but if the CFTR is defective, then sodium flows freely from the ASL and into the cell. As water follows sodium, the depth of ASL will be depleted and the cilia will be left in the mucous layer
Bronchioles –> bronchiectasis
Pancreatic duct –> DM, malabsorption
GIT –> Distal intestinal obstruction syndrome
Liver –> gallstone, cirrhosis
Fallopian tubes —> decrease female fertility
Seminal vesicles —> Male infertility
Diagnosing Cystic Fibrosis
Immunoreactive trypsinogen on heel-prick (neonatal screening)
AND
Sweat test >60mM Cl- = diagnostic
(false positive in hypothyroidism and Addison’s)
Faecal elastase - test of pancreatic exocrine function
Investigations in Cystic Fibrosis
Bloods
FBC, LFTs, clotting, ADEK levels, GGT
Sputum: MC+S
CXR
Diffuse tramlines and rings
Abso USS
Fatty liver, cirrhosis, pancreatitis
Spirometry
Obstruction
Aspergillus serology / skin prick test (20% develop allergic bronchopulmonary aspergillosis)
Management of Cystic Fibrosis
MDT: GP, Gastroenterologist, Chest, Physio, Dietician, Specialist nurse
Portacath insertion
Physio
Postural drainage
Active cycle breathing
Chest
Antibiotics: Prophylaxis and Acute
Mucolytics: DNAse
Segregation from other CF patients, reduce risk of pseudomonas and burkholderia transmission
Advanced disease ==> heart lung transplant
GI
Creon
Overnight feeds to increase nutrition
ADEK supplements
Insulin
Other
Fertility and genetic counselling
DEXA and osteoporosis screen
Mx complicatiosn e.g. DM
Mean survival 35 years
Primary Ciliary Dyskinesia
Autosomal recessive defect in ciliary motility
Poor mucociliary clearance –> chronic recurrent inflammation and bronchiectasis
Decreased sperm motility in males –> infertility
Kartagener’s Syndrome: Situs invertus + Primary ciliary dyskinesia
Situs invertus
Chronic sinusitis
Bronchiectasis
Yellow Nail Syndrome
Very rare
Yellow dystrophic nails
Pleural effusions
Lymphoedema: lymphatic hypoplasia
Bronchiectasis
Allergic Bronchopulmonary Aspergillosis
ABPA
Type 1 and Type 3 hypersensitivity reaction to Aspergillus fumigatus
Causes bronchoconstriction —> Bronchiectasis
Presentation
Dyspnoea
Wheeze
Cough
Bronchiectasis
Invx
Increased IgE and eosinophilia
positive IgG precipitins (not as positive as in aspergilloma)
+ve skin prick test or RAST
CXR
Mx
Prednisolone
Itraconazole is sometimes introduced as a second line agent
Bronchodilators
Signs of Pleural Effusion on Examination
Inspection
Chest drain
Evidence of cause:
Cancer: clubbing, cachexia, LNs
Pneumonia: febrile
CCF: increased JVP, S3, ascites, ankle oedema
CLD: clubbing leukonychia, spider naevi, gynaecomastia
CTD: rheumatoid hands, malar rash
Chest
Tracheal shift away from effusion
Decreased expansion on the affacted side
Stony dull percussion
Recuded air entry
Reduced tactile fremitus
Significant negatives: Fever, Clubbing, Peripheral oedema, CTD
Management of Pleural Effusion
Treat underlying cause
May use drain / repeated aspiration
Drain <2L per day!
Pleurodesis if recurrent malignant effusion
Persistent effusions may require surgery
Signs of Lung Cancer on Examination
Inspection
Cachexia
Hoarse voice or stridor
Hands
Clubbing
Hypertrophic pulmonary osteoarthropathy (HPOA)
Tar staining
Claw hand and wasting of interossei
Face
Anaemia
Horner’s
Plethora
Neck
LNs
Dilated veins
Chest
Thoracotomy scar
Radiotherapy square birn + tattoo
Acanthosis nigrans
Collapse
Tracheal deviation towards collapse
Decreased expansion
Dull percussion note
Absent air entry
Increased VR
Effusion
Tracheal deviation away from effusion
Reduced expansion
Stony dull percussion
Reduced air enrty
Reduced VR
Hypertrophic Pulmonary Osteoarthopathy
HPOA
Present in up to 10% lung cancers
More common in non-small cell cancer
Complications of Lung Cancer
Superior vena cava obstruction
Plethroic
Oedematous face
Oedematous upper limbs
Dilated neck and chest veins
Stridor
Recurrent laryngeal nerve palsy
Hoarse voice
Bovine cough
Pancoast tumour
Horner’s
Claw hand with wasting of interossei - compression of ulnar nerve
Dermatomyositis
Signs of Lobectomy / Pneumonectomy on Examination
Inspection
Clubbing
Cachexia
Scars
Lateral throacotomy
Clamshell: double lung transplant
Chest drains
VATS
Chest wall asymmetry or deformity
Pneumonectomy
Tracheal and apex shift to abnormal side
Decreased expansion
Dull percussion
NO breath sounds
Lobectomy
Tracheal shift (mainly upper lobectomy)
Focal signs
Reduced expansion
Dull percussion
Reduced breath sounds
Paraneoplastic Lung Cancer
ADH –> SIADH —> hyponatraemia
Cushing’s syndrome (ACTH)
Carcinoid syndrome (Serotonin)
Hypercalcaemia (PTHrP)
SCC
Paraneoplastic Signs of Lung Cancer
Endocrine
ADH –> SIADH
ACTH –> Cushing’s
Serotonin –> Serotonin syndrome
PTHrP –> primary hyperparathyroidism (Squamous cell)
Rheumatological
Dermatomyositis
Polymyositis
Neuro
Cerebellar degeneration
Peripheral neuropathy
Derm
Acanthosis nigricans
Trousseau syndrome: thrombophlebitis migrans
Signs of Pneumonia on Examination
Inspection
Febrile
Looks unwell
Tachypenoeic
Tachycardia
Cough
Rusty sputum
Chest: Consolidation
Decreased expansion
Dull percussion
BRonchial breathing
Decreased air entry
Focal coarse crackles
Pleural rub
Increased vocal resonance
Para-pneumonic effusion
Erthyema multiforme = mycoplasma pneumonia
DDx
Collapse
Effusion
Signs of Old TB on Examination
Inspection
Asymmetry: absent ribs
Scars: thoracoplasty (removal of several ribs to collpase upper portion of lung)
ScarL supraclavicular fossa - phrenic nerve crush
Chest
Tracheal deviation towards apical fibrosis
Decreased expansion
Dull to percussion
+/- bronchial breathing
Reduced air entry
Crackles
Increased vocal resonance
