Respiratory Flashcards
In which lung is an aspiration more likely to happen?
Right lower lung
The right bronchus is more vertical and wider so a foreign object is likely to fall down this path over the left bronchus
What cells are involved in the mucociliary apparatus?
Goblet cells - secrete mucus to trap pathogens
Ciliated columnar cells - move mucus towards main bronchi and trachea to be expelled by coughing or swallowed
How does the innate immune system act as a defence mechanism for the respiratory tract against inhaled pathogens?
Alveolar Macrophages - recognise microbes via surface receptors - immobilise + destroy bacteria
Type II alveolar cells - secrete surfactant proteins to enhance phagocytosis and agglutination of gram-positive bacteria
Neutrophils - chemoattraction to alveolar space - phagocytose bacteria and kill via respiratory burst
What are neuraminidase and haemaglutinin and is their function?
Glycoproteins on influenza membranes
Haemaglutinin binds to sialic acid receptors on host respiratory epithelial cells for fusion and neuraminidase cleaves sialic acid residues to promote release and spread of viruses
What is the role of spike proteins on coronavirus?
A glycoprotein that facilitates the fusion and penetration of host cell by binding to ACE2 along our airways
S1 - recognise and bind to receptors on the host cell
S2 - fuses envelope of the virus with the host cell membrane
What is Antigenic Drift?
Small changes or mutations in the genes of influenza virus that can lead to changes in the surface proteins of the virus - HA, NA
Loss or reduction in protection from existing antibodies and vaccines - susceptible to the flu again
What is Antigenic Shift?
A major change where 2 or more strains combine to form new subtypes of HA, NA glycoproteins
e.g. When an zoonotic virus gains the ability to infect humans
Normally would result in a pandemic, no previous immunity, occurs infrequently
How can soap kill corona virus?
Tear apart the lipid shell surrounding the virus to make the inside susceptible to our immune system
What is the role of furin in viruses?
A protease released by the golgi apparatus
Cleaves glycoproteins once bound to host cell to allow for fusion and penetration into membrane
Increasing infectious and pathogenic nature of virus
What are common pathogens that cause a sore throat?
Influenza, Rhinovirus, Coronavirus
Adenovirus
EBV
CMV
Strep A
What are infections of the URT?
Common cold
Tonsilitis
Laryngitis
Pharyngitis
Sinusitis
Otitis Media
Mainly viral pathogens as causative agent
What are infections of the LRT?
Pneumonia
Tuberculosis
Lung abscess
Bronchiolitis
Mainly bacteria pathogens as causative agent
How can you distinguish between URT and LRT infections?
URTI - normal chest x-ray and breath sounds on auscultation
Symptoms - runny nose, dry cough, headache, sore throat, sneezing, myalgia
LRTI - changes/consolidation on x-ray and coarse crackles on auscultation
Symptoms - productive cough, SOB, breathlessness, wheezing, tight chest
What is the most common infective cause of COPD exacerbations?
Haemophilus Influenzae
What is the common causative bacteria of Pneumonia in HIV?
Pneumocystis jiroveci - PCP
What is the common causative bacteria of Pneumonia in alcoholics and diabetics?
Klebsiella pneumoniae
What type of bacteria are asplenic patients more susceptible to and why? Give 3 examples.
Insufficient splenic macrophages to opsonise and phagocytose encapsulated bacteria
Streptococcus pneumoniae
Haemophilus influenzae
Neisseria meningitis
What is the common causative bacteria of Pneumonia in someone recently exposed to air con and hot tubs?
Legionella pneumophilia
What is the difference between tuberculosis and sarcoidosis?
TB - caseating granuloma
Sarcoidosis - non-caseating granuloma
What are similarities in tuberculosis and sarcoidosis?
Granulomatous disease
Erythema nodosum
Hilar lymphadenopathy
Arthralgia
Systemic symptoms - fever, malaise, weight loss
Affect upper lobes of lungs
What is the management of active TB?
Isoniazid, rifampicin, ethambutol, and pyrazinamide
for 2 months
Isoniazid and rifampicin for a further 6 months
Longer courses if extra-pulmonary TB, HIV, immunosuppressed
What is the pathophysiology of the primary infection in TB?
M.tuberculosis inhaled as aerosolized droplets
M.T lodge in the alveoli and engulfed by macrophages
M.T continues proliferating intracellulary
AM travels to lymph nodes = hilar lymphadenopathy
Granuloma forms with caseous necrosis (TNF-alpha and IFN-Gamma activate to mature macrophages) = ghon focus
If healthy patient - heals by fibrosis and disease becomes latent
Ranke complex once Ghon focus calcified
What is a Ghon complex?
Primary lesion/ghon focus in the lungs and hilar lymphadenopathy
What is secondary and miliary TB?
Secondary - reactivation of TB - cavitating lesions of upper lobes of lung + systemic symptoms (Weight loss, fever, haemoptysis)
Miliary - haematogenous spread of TB (Potts disease - in spinal cord, meninges, kidneys, hepititis)
Mainly in immunocompromised
How can TB be diagnosed?
Sputum Smear - 3 specimens on 3 different days - Ziehl-Neelsen - stain red
Sputum Culture - Lowenstein-Jensen media
Tuberculin/Mantoux Test - Purified Protein Deviate injected into skin - reaction if immune recognition of TB(positive in those who have had BCG)
IFN-Gamma Release Assay - measure response - can’t tell difference between latent or active TB
Which drug class is contra-indicated in TB and why?
TNF-alpha inhibitors
Disrupt granuloma formation and can reactivate TB
What is the common causative bacteria of Pneumonia?
Streptococcus pneumoniae
What is the criteria for CURB 65?
C - confusion
Urea >7 mol
RR > 30/min
BP < 90/60
What result of CURB 65 would warrant consideration for hospital admission?
2+
What is the time frame for HAP?
Pneumonia occurring 48 hours or more after admission
What is the treatment for low severity CAP?
Amoxicillin - 500mg TDS for 5 days
If Penicillin allergy
- Doxycycline - 200mg loading dose + 100mg OD - 5 days total
- Clarithromycin 500mg BD for 5 days
What is the management after pneumonia has been treated?
Repeat chest x-ray 6 weeks after clinical resolution to ensure consolidation has resolved and no underlying secondary abnormalities
What is the management for moderate-severe CAP?
Dual antibiotic therapy for 7-10 days
Moderate: Amoxicillin + Doxycycline/Clarithromycin
Severe: Co-amoxiclav/Benzylpenicillin/Vancomycin + Clarithromycin
What are features of sputum from different causative bacteria?
Strep pneumonia - rust coloured
Psuedomonas - green
Klebsiella - redcurrant jelly
Anaerobes - bad smell/bad taste
How is an infective exacerbation of COPD treated?
Amoxicillin PO 500mg TDS for 5 days
Doxycycline 200mg stat dose day 1 - 100mg 4 days OD - if penicllin allergy
What are features of Klebsiella?
Common in alcoholics and diabetics
Red-currant jelly sputum
Often affects upper lobes
Commonly causes lung abscess formation and empyema
What are features of PCP - pneumocystis jiroveci?
Typically seen in HIV patients
Dry cough, exercise-induced desaturations, absence of chest signs
Clear chest - may hear end inspiratory crackles
Treated with co-trimoxazole
In which patients are at risk of staphylococcal pneumonia?
Intravenous drug users
Elderly patients
Patients who already have an influenza infection
What are features of mycoplasma pneumonia?
Flu like symptoms - flu, arthralgia, myalgia, dry cough and headache
Auto-immune manifestation - erythema multiforme, hepatitis, cold autoimmune haemolytic anaemia
Primarily affects younger patients.
Associated with erythema multiforme, stevens-johnson syndrome, guillain-barre syndrome
How can Legionella pneumonia present in a patient and on labs?
Hyponataemia + Deranged LFTs, Raised CK
Diarrhoea, vomiting
Typically travel related - hot tubs and air con
How often is the pneumococcal vaccine given in at-risk individuals?
5 years
What bacteria can cause pneumonia in patients exposed to birds, parrots etc?
Chlamydophilia psittaci
Associated fevers, joint pain, nose bleeds
What is Q fever?
Disease caused by Coxiella burnetii
From exposure to sheep and goats
Q fever = fever, myalgia, headache, hepatitis - can present as pneumonia
What are the histological classifications of pneumonia?
Lobar - affects one or more lobes of the lungs
Bronchopneumonia - affects patches throughout both lungs
How is aspiration pneumonia treated?
Amoxicillin/Clarithromycin and Metronidazole
How is HAP treated?
1st line - co-amoxiclav 500/125mg TDS 5 days
2nd line - doxycyline
What test can identify the Legionella antigen?
Urinary antigen testing
How is severe HAP with sepsis/non-responsive treated?
IV tazocin - piperacillin/tazobactam
What is the pathophysiology of Pneumonia?
Infection leads to inflammatory response
Inflammatory response leads to exudate formation and alveoli oedema
Consolidation forms in lung tissue
What are typical features of atypical pneumonia?
Often fever, headache, sweating, myalgia
Moderate sputum production, often no consolidation on CXR, small increase in WCC
Less likely to present with typical ‘resp’ symptoms
What are common causative bacteria of aspiration pneumonia?
Streptococcus pneumoniae
Staphylococcus aureus
Haemophilus influenzae
Enterobacteriaceae
Pseudomonas
Anaerobic bacteria
What is the inheritance pattern of cystic fibrosis and what is the mutation?
Autosomal recessive disorder
Mutation in CFTR gene on chromosome 7 - DF508 mutation
What is the pathophysiology of cystic fibrosis?
CFTR protein - a channel that normally transports chloride ions out from mucus cells into mucus to attract water and make it less viscous
In CF - defective CFTR - chloride ions trapped in cell = mucus will be abnormally thick - builds up and obstructs organs. Chloride ions also stuck in sweat glands - unable to be reabsorbed - high chloride in sweat
What are symptoms of CF in a newborn?
Meconium ileus - rigid abdomen, green vomit, fever, can’t passed first stool
What are symptoms of CF in childhood?
Failure to thrive
Delayed puberty
Pancreatic insufficiency - pale stools, pancreatitis, gallstones
Chronic wet cough
Recurrent infections, pneumonia, bronchiectasis
What are symptoms of CF in adulthood?
Infertility
Amenorrhea
Clubbing
Diabetes
What are investigations for CF?
Heel prick test - screening at birth - detects IRT = pancreatic damage
Sweat test - chloride ion levels > 60
Genetic testing
Spirometry - obstructive disease - bronchiectasis
Faecal elastase
Sputum cultures
FBC
What can be seen on an x-ray in CF?
Bronchiectasis - tram-track lines
Hyperinflation
Soap bubbles
Ring shadows - clusters of cysts in upper lobes
What are common bacteria responsible for infections in CF?
Pseudomonas aeruginosa
Staphylococcus aureus
Haemophilus influenzae
Burkholderia cepacia
Aspergillus
How does Lumacaftor/Ivacaftor work to treat CF?
CFTR Modulators
Lumacaftor - increases the number of CFTR proteins on the cell surface
Ivacaftor - potentiator of CFTR to open channel and allow chloride ion to pass through
Which mucolytics are used in CF and how do they work?
Dornase alfa - Mucolytic peptide that cleaves DNA of mucus
Hypertonic saline - acts as a expectorant to increase airway surface fluid and improve clearance
What is Young Syndrome and what are the main differentials?
Characterised as…
- Male infertility
- Bronchiectasis
- Sinusitis
Differentials - CF, kartagener syndrome
What is Kartagener Syndrome?
Primary ciliary dyskinesia +
Situs inversus(or dextrocardia)
Bronchiectasis
What is the inheritance of primary ciliary dyskinesia?
Autosomal recessive disease producing defective cilia
= recurrent infections, sinusitis, otitis media, subfertily, bronchiectasis
What are symptoms related to the different URTI?
(rhinosinusitis, pharyngitis, tonsillitis, laryngitis, epiglottis, bronchitis, croup)
Rhinosinusitis - pain/pressure on face
Pharyngitis - sore throat
Tonsillitis - pain swallowing
Laryngitis - hoarse voice and dry cough
Epiglottitis - trouble breathing
Bronchitis - productive cough for up to 3 weeks, chest tightness, wheeze
Croup - harsh barking cough, stridor
What guides antibiotic treatment for acute bronchitis and what is the criteria?
CRP
20-100 - offer delayed prescription of doxycycline
>100 - prescribe doxycycline 5 days
How long do URTIs last?
Acute otitis media: 4 days
Acute sore throat/acute pharyngitis/acute tonsillitis: 1 week
Common cold: 1+1/2 weeks
Acute rhinosinusitis: 2+1/2 weeks
Acute cough/acute bronchitis: 3 weeks
What is part of the centor criteria that helps guide the decision of whether to prescribe abx in URTIs?
Presence of tonsillar exudate
Tender anterior cervical lymph nodes/ Lymphadenopathy or lymphadenitis
History of fever
Absence of cough
(3+ indicates to prescribe abx, also high chance strep A is causing sore throat)
When should immediate abx be prescribed in an URTI?
Systemically very unwell
Symptoms suggestive of serious illness
High risk complications due to co-morbidities
Children<2 with bilateral otitis media
Centor criteria 3+
>65 with acute cough + 2 of … hospitalisation in previous year, diabetes, CHF, steroid use
>80 with acute cough + 1 of … hospitalisation in previous year, diabetes, CHF, steroid use
What fibres in epithelial cells are involved in the cough reflex?
C fibres - chemical driven, inflammation
RAR - mechanically driven
SAR - mechanically driven
Send signals down vagus nerve
What is the mechanism behind the cough?
C fibres/RAR/SAR in respiratory epithelial cells stimulated - send signals down vagus nerve - reach tractus solitarus in the brainstem - goes to cough and respiratory pattern generator = synapse with efferent nerve fibres - output of cough
What can activate the tractus solitarus to stimulate a cough?
Vagus nerve - from respiratory epithelium
Ear, Heart, Oesophagus, Stomach
How do ACEi cause a dry cough as a side effect?
ACEi prevent the inactivation of bradykinin and cause it to accumulate in the respiratory tract.
Accumulation of bradykinins, substance P and prostaglandins act as chemical irritants of the c-fibres of the respiratory tract which induces the cough reflex
What are the 3 phases of the cough reflex?
Inspiratory phase
- glottis opens wide, diaphragm and external intercostal muscle contract, big breath in, increase pressure inside the lungs
Compress phase
- glottis closes, increase pressure in the lungs
Expiratory phase
- abdominal and internal intercostal muscles contract, glottis opens - air pushed out due to high pressure in the lungs = cough
Differentials for acute, sub-acute, chronic cough?
Acute < 3 weeks
- URTI
- Allergens
- PE
Sub-acute 3-8 weeks
- Post-infectious - covid, bronchitis
- ACEi
Chronic > 8 weeks
- COPD
- Asthma
- GORD
- Lung cancer
- TB
Causes of bronchiectasis?
Post-Infection: Tuberculosis; HIV; Measles; Pertussis; Pneumonia
Bronchial Pathology: Obstruction by foreign body or tumour
Allergic Bronchopulmonary aspergillosis (ABPA)
Congenital: Cystic fibrosis; Kartagener’s syndrome; Primary ciliary dyskinesia; Young syndrome
Hypogammaglobulinaemia
Idiopathic
Features of bronchiectasis?
Productive cough - large amounts of purulent sputum
Dyspnoea
Haemoptysis
Halitosis
Coarse crackles
Wheeze
Clubbing
Spirometry - obstructive pattern
X-ray - thickened, dilated airways - tramtrack sign, ring shadows
CT scan - thickened, dilated airways, signet ring
What is the most common bacteria found in bronchiectasis?
Haemophilus influenzae
What is bronchiectasis?
Permanent dilation of bronchi due to irreversible destruction of the elastic and muscular components of the bronchial wall, causing them to dilate and thicken
What is the management of bronchiectasis?
Smoking cessation
Treat underlying disease
Chest physiotherapy
Postural drainage
Patient education
Antibiotics - 10-14 days - amoxicillin or ciprofloxacin
Bronchodilators
Immunisations
Surgery for localised disease
Carbocysteine
What is the pathophysiology behind asthma?
1.Dendritic cells pick up allergens from environmental triggers and present them to T helper 2 cells.
- TH2 cells produce IL-4 and IL-5.
- IL-4 + IL-13 leads to the production of IgE antibodies which stimulate the release of granules from mast cells. Histamine, leukotrienes and prostaglandins released in this type 1 hypersensitivity reaction to give the common symptoms known as allergies.
- IL-5 activate eosinophils which release more cytokines and leukotriene
What drugs can trigger asthma?
Beta blockers
NSAIDs
Aspirin
What is Samter’s triad?
Asthma
Nasal polyps
Aspirin sensitivity
What is the spirometry reading in asthma?
FEV1/FVC < 70%
FEV1 < 80%
Bronchodilator reversibility - FEV1 > 12% and 200ml after 20 min use with SABA
What other investigations are done in asthma after spirometry?
Peak flow - 20% variability QDS for 2-4 weeks
FeNO - 40ppm
Eosinophils > 0.15
Methocholine < 8mg/ml
Skin prick allergy test
IgE in blood
What is the step up for asthma treatment?
SABA
SABA + Low dose ICS
SABA + Low dose ICS + LABA
SABA + Medium dose ICS + LABA
SABA + Medium dose ICS + LABA + LTRA
What is the treatment for an acute exacerbation of asthma?
OSHITME
- Oxygen - 94-98%
- Salbutamol - 5mg nebs - driven by oxygen
- Hydrocortisone - give oral steroids if can swallow or IV if not, minimum 5 days
- Ipratropium - 500 micrograms nebs
CALL FOR SENIOR - Theophylline - give aminophylline IV bolus plus IV - specialist give only
- Magnesium - 1.2-2g IV infusion 20 minutes
- Escalate - need ITU if still unwell for non-invasive ventilation/mechanical
What is the discharge criteria following an acute exacerbation of asthma?
Stable on discharge meds for 12 - 24 hours with no nebulisers or oxygen
PEFR > 75% with diurnal variability of < 20%
Inhaler technique checked and recorded
What are features of a moderate asthma attack?
PEFR 50-75% best or predicted
Increasing symptoms
RR > 25 / min
Pulse > 110 bpm
What are features of a severe asthma attack?
PEFR 33 - 50% best or predicted
Can’t complete sentences
RR > 25/min
Pulse > 110 bpm
What are features of a life-threatening asthma attack?
PEFR < 33% best or predicted
Oxygen sats < 92%
Silent chest, cyanosis or feeble respiratory effort
Bradycardia, dysrhythmia or hypotension
Exhaustion, confusion or coma
Normal pCO2 - indicates exhaustion
What are features of a near fatal asthma attack?
Raised pCO2
Requiring mechanical ventilation with raised inflation pressures
Differentials for asthma?
ABPA
GORD
Churg-strauss syndrome
COPD
CF
What is a complication of a mucus plug in asthma?
Lobar collapse
What are the classifications of COPD?
Stage 1 - Mild - FEV > 80%
Stage 2 - Moderate - FEV 50-79%
Stage 3 - Severe - FEV 30-49%
Stage 4 - Very Severe - FEV <30%
What is the pathophysiology of emphysema in COPD?
Imbalance between antiprotease < protease activity
Activate Protease -> Smoking stimulates macrophages and neutrophils which stimulate release of elastase that destroys elastin in alveolar wall
Inactivate anti-protease -> Free radicals from smoking/pollutants inhibit alpha1-antitrypsin
Results in destruction of alveolar wall - unable to recoil so collapses during expiration and traps air
What is the criteria for chronic bronchitis in COPD?
Productive cough for more than 3 months each year for 2+ consecutive years
What is the role of alpha-1 antitrypsin?
An anti-protease synthesised in the liver that inhibits neutrophil elastase to protect cells.
In deficiency - causes liver cirrhosis and allows build up neutrophil elastase in lungs(destroys elastin-leads to emphysema in lower lobes-loss of recoil in alveoli)
Complications of COPD?
Secondary polycythaemia - due to hypoxemia
Pulmonary hypertension
Cor pulmonale
Pneumothorax
What are examination findings in COPD?
Anteroposterior diameter of chest upwards - hyperinflation
Reduction of the cricosternal distance
Percussion - hyperresonance
Auscultation - expiratory wheeze
Reduced chest expansion
Decreased/quiet breath sounds
Cyanosis
Cor pulmonale
What is the spirometry results in COPD?
Obstructive
FEV1/FVC < 70%
FEV1 <80%
No bronchodilator reversibility
What is seen on a chest x-ray in COPD?
Hyperinflated chest (>6 anterior ribs)
Bullae
Decreased peripheral vascular markings
Flattened hemidiaphragms
Patients with what should be assessed for LTOT in COPD?
Very severe airflow obstruction (FEV1 < 30% predicted). Assessment should be ‘considered’ for patients with severe airflow obstruction (FEV1 30-49% predicted)
Cyanosis
Polycythaemia
Peripheral oedema
Raised jugular venous pressure
Oxygen saturations less than or equal to 92% on room air
Who should be offered LTOT in COPD?
pO2 of < 7.3 kPa
pO2 of 7.3 - 8 kPa and one of the following:
secondary polycythaemia
peripheral oedema
pulmonary hypertension
(measurements taken on 2 occasions at 3 weeks apart, NON smokers)
What is the pharmacological management of chronic COPD?
SABA/SAMA
Asthmatic Features: LABA + ICS -> + LAMA
NO Asthmatic Features: LABA + LAMA
Mucolytics
Prophylactic azithromycin
DIuretics if cor pulmonale
What are asthmatic features that can suggest steroid responsiveness in COPD?
Previous diagnosis of asthma or atopy
High blood eosinophil count
Variation in FEV1
Diurnal variation in peak flow >20%
What are factors contributing to ‘difficult to treat’ asthma?
Non adherence
- Unintentional
- Lack of knowledge about necessity
- Concerns of adverse effects
- Regimen burden
- Cost of medicines
Poor inhaler technique
Medications - NSAIDs, beta-blockers, aspirin
Smoking or second-hand smoking
Exposure to asthma triggers - allergy/environment
Female hormones - symptoms can worsen around periods, menopause, pregnancy
Co-morbidities
- Acid reflux/GORD
- Anxiety and depression
- COPD
- Rhinosinusitis
- Rhinitis
- Overweight
- ABPA
What is the management in acute exacerbation of COPD?
Oxygen - 88-92% target
Salbutamol - 5mg nebs driven by oxygen
Hydrocortisone - oral steroids if can swallow, if not give IV
Ipratropium - 500 microgram nebs
- CALL FOR SENIOR
Theophylline - give aminophylline IV
Escalate - need ITU if unwell not ventilation, pH<7.35
What is acute respiratory distress syndrome?
Non-cardiogenic pulmonary oedema and diffuse lung inflammation - secondary to underlying illness
What is the pathophysiology behind acute respiratory distress syndrome?
Inflammation results in diffuse bilateral alveolar injury mediated by TNF-alpha, IL-1, IL-8
Endothelial injury activates neutrophils in the pulmonary capillaries releasing ROS and proteases that damage the alveolar endothelium and type 2 alveolar cells
Increased permeability of alveolar capillaries leading to fluid accumulation in the alveoli = non-cardiogenic pulmonary oedema + hypoxemia
Deficiency in surfactant in alveoli = alveoli collapse
What are causes of ARDS?
Pneumonia
Sepsis
Aspiration
Acute pancreatitis
Transfusion reactions
Trauma and fractures
Fat embolism
COVID-19
Smoke inhalation
What is the presentation of ARDS?
Dyspnoea - severe SOB
Elevated respiratory rate - fast, shallow breathing
Bilateral lung crackles - rails
Low oxygen saturations - fails to improve with oxygen
Cyanosis
Feeling faint, Tiredness, drowsiness, confusion
Fever, cough, pleuritic chest pain
What does ARDS look like on an x-ray?
Bilateral alveolar infiltrates on chest x-ray
NO features of heart failure
What are differentials of ARDS?
COVID-10
Acute heart failure
Bilateral pneumonia
Hypersensitivity pneumonitis
Acute interstitial pneumonia
What are respiratory causes of chronic breathlessness?
Asthma
COPD
Lung cancer
Interstitial lung diseases
TB
Sarcoidosis
Pulmonary hypertension
What are non-respiratory causes of breathlessness?
Anaemia
Obesity
Anxiety
IHD
Cardiac arrhythmias
CHF
Is wheeze normally heard on expiration or inspiration?
Expiration
What are the two types of wheeze sounds?
Polyphonic - widespread airflow obstruction - asthmatics
Monophonic - single airway partially obstructed - tumour, mucus plug
What are key differentials for wheeze?
Asthma
COPD
Pulmonary oedema
Bronchial spasm
CF
Allergies
Resp tract infections
Excessive secretions
What is the difference between a high or low pitched wheeze
High pitched - narrowing of smaller bronchi
Low pitched - narrowing of large bronchi - rhonchi
What is the difference between stridor and wheeze?
Wheeze - typically high-pitched music sound during expiration - indicating smaller lower airway obstruction
Stridor - typically harsh monophonic sound during inspiration - indicating large upper airway obstruction
What is allergic bronchopulmonary aspergillosis?
Hypersensitivity reaction of IgG and IgE to the fungus aspergillus which leads to a lung disease
More common in asthmatics and CF patients
What are features of ABPA?
Frequent productive cough
Lots of mucus - brown mucus plugs, blood
Wheezing
SOB
Chest pain or tightness
Bronchiectasis
Chest x-ray - infiltrates, aspergilloma
High levels of IgE and eosinophils
Skin testing of aspergillus
How is ABPA treated?
Oral steroids
Anti-fungals - itraconazole
Optimizing underlying condition - asthma, CF
What is the most dangerous type of asbestos?
Blue asbestos - Crocidolite
Extremely fine sharp fibers - greatest ability to inhale and reach alveoli
What are common features of asbestosis?
SOB and reduced exercise tolerance
Cough
Clubbing
Typically 15-30 years after asbestos exposure
What is found on investigations in asbestosis and idiopathic pulmonary fibrosis - spirometry, auscultation, x-ray, CT
Spirometry - restrictive pattern with reduce gas transfer
Auscultation - bilateral basal fine end-inspiratory crackles
X-ray - Reticular shadowing - basal predominance
CT - honeycombing, traction bronchiectasis, reticular scarring
How does asbestosis occur?
Inhalation of asbestos fibres
Remain in alveoli indefinitely, can not be degraded - become coated in iron to form asbestos bodies - cause fibrosis and disease
What is the management of asbestosis, coal workers pneumoconiosis?
Removal of triggers
Smoking cessation
Oxygen therapy
Treatment of symptoms
Lung transplant
Industrial compensation
What is the benign change that can happen from asbestos exposure?
Pleural plaques
Benign and do not undergo malignant change - no follow ups necessary
Which lung diseases form granulomas and are they caseating/ non-caseating?
Caseating - Tuberculosis
Non-caseating - Sarcoidosis + Hypersensitivity pneumonitis
What is the pattern seen on spirometry for interstitial lung diseases?
Restrictive pattern with reduced transfer factor
What is the immunology pathophysiology behind hypersensitivity pneumonitis?
Type III hypersensitivity(acute) and Type IV hypersensitivity(chronic), reaction to inhaled organic particles causing lung damage
Inflammation leads to (non-caseating) granuloma formation(acute) and fibrosis(from chronic exposure)
How is hypersensitivity pneumonitis treated?
Removal of trigger
Steroids
What can increase the transfer factor(TLCO)?
Asthma
Pulmonary haemorrhage (Wegener’s, Goodpasture’s)
Left-to-right cardiac shunts
Polycythaemia
Hyperkinetic states
Male gender, exercise
What can lower the transfer factor (TLCO)?
Pulmonary fibrosis
Pneumonia
Pulmonary emboli
Pulmonary oedema
Emphysema
Anaemia
Low cardiac output
What are features of hypersensitivity pneumonitis?
Acute - SOB, dry cough, fever
Chronic - lethargy, productive cough, SOB
Diffuse crackles, wheeze, squeaks
Which lung diseases show predominantly as upper lung fibrosis?
CHARTS
Coal workers pneumoconiosis
Hypersensitivity pneumonitis
Ankylosing spondylitis
Radiotherapy
Tuberculosis
Silicosis and sarcoidosis
What are extra-pulmonary causes of a restrictive lung breathing pattern?
Neuromuscular - muscular dystrophies, guillain-barre, myasthenia gravis
Musculoskeletal - kyphoscoliosis, obesity, anky spon
What does hypersensitivity pneumonitis show on x-ray and CT?
X-ray = reticular shadowings, micronodular changes
CT = ground glass, mosaicism
Apical dominance
What drugs are given in idiopathic pulmonary fibrosis?
Anti-fibrotic drugs - when FVC 50-80%
- Pirfenidone - S/E: nausea, photosensitivity rash
- Nintedanib - S/E: diarrhoea
What is the histological features of asbestosis?
Asbestosis bodies and fibrosis
What is the histological features of hypersensitivity pneumonitis?
Non-caseating granuloma
Honeycomb - alveolar space
What is the histological features of idiopathic pulmonary fibrosis?
Collagen deposition and fibrosis in the alveolar interstitium
What are features of malignant mesothelioma?
Dyspnoea, weight loss, chest wall pain
Clubbing
Pleural effusion - 30% present as painless pleural effusions
Asbestosis - 20%
Is mesothelioma or asbestosis linked to length of exposure of asbestos ?
Asbestosis severity related to length of exposure
Mesothelioma - even limited exposure can cause disease
What are types of coal worker’s pneumoconiosis ?
Simple - typically asymptomatic
Progressive massive fibrosis
- Features: Breathlessness, Cough, Black sputum
- X-ray: fibrotic masses in upper lobes
What is caplan syndrome?
Combination of RA and pneumoconiosis with nodules
What is the pathophysiology of coal workers pneumoconiosis?
Coal dust reaches terminal bronchioles - engulfed by alveolar macrophages - overwhelmed, unable to clear the coal - macrophages accumulate and settle on alveoli lining - aggregates into fibrotic masses - can cavitate and necrose
Which interstitial lung disease increases your risk for TB?
Silicosis
Silica impairs the formation of phagolysosome and so more susceptible to tuberculosis
What does silicosis look like on an x-ray?
Upper zone fibrotic opacities
Egg shell calcification of hilar lymph nodes
What is Lofgren syndrome characterised by?
Acute sarcoidosis
- Fever
- Hilar lymphadenopathy
- Erythema nodosum
- Polyarthralgia
What are the 1-4 stages of sarcoidosis via x-ray?
Stage 1 - Bilateral hilar lymphadenopathy (BHL)
Stage 2 - BHL with interstitial infiltrates
Stage 3 - Diffuse interstitial infiltrates only
Stage 4 - Diffuse fibrosis
What findings would you see in investigations for sarcoidosis?
Hypercalcaemia
Increased ACE levels
High ESR
Non-caseating granuloma - biopsy
What features would you see in sarcoidosis?
Pulmonary - dry cough, SOB
Skin - lupus pernio, erythema nodosum
Eyes - uveitis
Abdominal - hepatosplenomegaly, renal stones
Constitutional - fever, weight loss, arthralgia, fever, lymphadenopathy
Neurological - meningitis, peripheral neuropathy, bell’s palsy, seizures
Heart - arrhythmias
When do you use steroids to treat sarcoidosis?
Hypercalcaemia
Eye, heart or neuro involvement
Evidence of fibrosis on x-ray - stage 2+
What is the 4 criteria for diagnosis of ARDS?
- Acute presentation
- Chest x-ray/CT - white out in both lungs
- PF ratio <300mmHg
- NOT due to cardiac causes
Why are tall, slender men at an increased risk of a pneumothorax?
More negative pressure at the apex of the lung compared to the base
More likely to have pleural blebs (these burst and let air in)
How does a tension pneumothorax occur?
A one-way valve is created in which air can enter the pleural cavity but is unable to leave - progressive accumulation of air in the pleural cavity - mediastinal shift and compromise of cardiovascular system
Tracheal deviation
Low blood pressure
High heart rate
What is the management of a primary pneumothorax?
<2cm + clinically well = send home, review in 2-4 weeks + safety net - resolves without intervention
> 2 cm or unwell = aspirate - safe triangle, measure success - if still not better = needs chest drain
What is the management of a secondary pneumothorax?
<1cm and symptomless - admitted for observation for 24 hours + oxygen PRN
1-2cm - aspiration 16-18 gauge cannula
> 2cm intercostal chest drain
What is the management of a tension pneumothorax and where should it be inserted?
Immediate needle decompression using 16 gauge cannula
Second intercostal space - just above third rib, mid-clavicular line
Lifestyle advice following a pneumothorax?
Smoking cessation
No flying for a week after a clear x-ray
Can never scuba dive
Where should a chest drain be inserted?
5th intercostal space
Safe triangle:
Anterior - lat border of pec major
Inferior - line of 5th ICS - along nipple line
Lateral - anterior edge of lat dorsi
Superior - base of axilla
What is found on examination on a chest with a pneumothorax?
Reduced chest expansion of affected side.
Hyper-resonant percussion note on affected side.
Reduced or absent breath sounds on affected side, with no added sounds.
Vocal resonance reduced on the affected side
What are exudative causes of a pleural effusion?
Inflammation of pulmonary capillaries - increase capillary permeability
Infections - pneumonia, TB
Malignancy - bronchial carcinoma, mesothelioma, or lung metastases.
Inflammatory conditions - RA, SLE, acute pancreatitis.
Pulmonary infarct (for example secondary to a pulmonary embolism) and trauma.
What are transudative causes of pleural effusion?
Increase hydrostatic pressure, decrease oncotic pressure
Heart failure
Liver cirrhosis
CKD
Coeliac disease
Hypothyroidism
Meigs syndrome
What is the difference between exudative and transudative pleural effusions?
Exudative - typically unilateral, high protein content >30g/L - cloudy liquid
Transudative - typically bilateral - low protein content <30g/L - clear liquid
What is Light’s criteria for exudative pleural effusion
Pleural protein/Serum protein > 0.5
Pleural lactate dehydrogenase (LDH)/serum LDH >0.6
Pleural LDH > than two-thirds of upper limit of normal for serum
What is meigs syndrome?
Triad of…
1. Benign ovarian tumour
2. Ascites
3. Pleural effusion - transudate
What is found on examination of the chest in a pleural effusion?
Trachea central or deviated away from affected side
Stony dullness when percuss over effusion
Reduced chest expansion
Vocal resonance reduced over effusion
Reduced or Absent breath sounds
Bronchial breathing at upper border of pleural effusion
What is the criteria for an empyema?
Pleural liquid - pH < 7.2
What other substances can be seen in the pleural fluid findings?
Low glucose - RA, TB
Raised amylase - pancreatitis, oesophageal perforation
Blood staining - mesothelioma, PE, TB
How is a pleural effusion treated?
Ultrasound-guided pleural aspiration
Intercostal drain - if large effusion or empyema
Treating underlying factor
Pleurodesis if recurrent
What is a chylothorax?
When the thoracic duct is obstructed by tumours or surgery and lymphatic fluid accumulates in the pleural space = lymphatic pleural effusion
What is the difference between atelectasis and pleural effusion on an x-ray?
Similar - white out
Different
- Pleural effusion - Mediastinum shifted to opposite side
- Atelectasis - Mediastinum pulled to same side
What are causes of atelectasis?
Obstruction - mucus plugs, tumours, foreign objects
Lack of surfactant - neonatal respiratory distress syndrome, ARDS
Compressive - Pleural effusion, pneumothorax
Contraction - scarring - sarcoidosis, ILD
Anaesthesia
Respiratory depression
What are common contra-indications for surgery in lung cancer?
Tumour near the hilum
Vocal cord paralysis
SVC obstruction
Stage IIIb + (mets present)
FEV <1.5 litres
Malignant pleural effusion
Poor general health
In which cancer can cavitary lesions be seen on an x-ray?
squamous cell carcinoma
What is a specific presentation for bronchoalveolar carcinoma?
Lots of mucus production - golden brown colour
What are paraneoplastic features of small cell lung cancer?
ACTH - increase cortisol - cushings syndrome
SIADH - increases water reabsorption = high BP, hyponatraemia, oedema, concentrated urine
Lambert-Eaton Syndrome - antibodies against voltage gated calcium channels = muscle weakness, double vision, drooping eyelids, difficulty swallowing
Which cancer has the worst prognosis where surgery is not normally an option and why?
Small cell lung cancer
Very aggressive - frequently metastasized to mediastinal lymph nodes and normally disseminated on presentation
Where does small cell lung cancer typically grow and from what cell does it develop from?
Develops centrally near a main bronchus
Arise from endocrine cells - Kulchitsky cells
What cancer is common in non-smokers?
Adenocarcinoma
What are some non-respiratory symptoms associated with bronchial carcinoid tumours and how?
Serotonin secretion = increase peristalsis - diarrhoea, facial flushing, wheeze
What are paraneoplastic syndromes associated with adenocarcinomas?
HPOA - clubbing
Gynaecomastia
What are paraneoplastic syndromes associated with squamous cell carcinomas?
PTHrp - bone resorption - high calcium
HPOA - clubbing
Where does lung cancer typically metastasize to?
BALLS
Brain
Adrenal glands
Liver
Lung
Skeleton
How does horner’s syndrome present and why?
Ptosis, meiosis, anhydrosis
Pancoast tumour in apical region - pressing on sympathetic trunk
What does mesothelioma express?
Calciretinin
What can compression of the recurrent laryngeal nerve present as?
Hoarseness of voice
What can compression of the phrenic nerve present as?
Difficulty breathing
How does SVC obstruction present?
Swollen, flushed face and upper body
Shortness of breath
Swollen veins in chest or neck
When do you refer people for the 2WW suspected lung cancer?
Have chest x-ray findings that suggest lung cancer
Aged 40 and over with unexplained haemoptysis
SVC obstruction
Neck nodes in smokers
Symptoms suggestive lung cancer
Where does squamous cell typically develop and what do they produce?
Develops centrally
Produce keratin
Where do adenocarcinomas typically develop in the chest?
Develop peripherally - of the bronchial or alveoli wall
Where is large cell lung cancer more common in the lungs?
More common in periphery but found throughout
From where does cannonball mets seen in the lung metastasize from?
Renal cell carcinoma
Who should be referred for an urgent x-ray when suspecting cancer?
Persistent unexplained haemoptysis
Chest or shoulder pain
Hoarseness
Cough>3 weeks
SOB
Weight loss
What are the 2 features to look at when deciding whether to do surgery in lung cancer?
- Resectability - ability to completely excise the tumour at surgery - disease features
- Operability - risk of morbidity/mortality - patient features
What is Type I Respiratory Failure and how do you treat?
Low oxygen with normal or low carbon dioxide
Typically due to V/Q Mismatch
Once optimum medical management reached and still symptomatic - NIV - CPAP
What is Type II Respiratory Failure and how do you treat?
Low oxygen with high carbon dioxide
Can be acute or chronic - distinguish on ABG by metabolic compensation
Once optimum medical management reached and still symptomatic - NIV -BiPAP
Symptoms of hypoxia?
Dyspnoea
Restlessness and agitation
Confusion
Cyanosis
Symptoms and signs of hypercapnia?
Headaches
Drowsiness
Confusion
Tachycardia with bounding pulse
CO2 retention hand flap
Peripheral vasodilation
Papilloedema
Risk factors for obstructive sleep apnoea?
- More common with increasing age
- Obesity
- Male
- Maxillomandibular anomalies - micrognathia, retrognathia
- Macroglossia
- Large neck circumference
- Family history of OSA
- Tobacco smoking
- Hypothyroidism
- Down’s syndrome
- Marfans
- Post-menopausal women
- Increased volume of soft tissues
When does REM and non-REM sleep occur whilst we sleep and what is the differences between the two?
Non-REM Sleep - first half of sleep
- N1 - light sleep
- N2 - slightly deeper slee
- N3 - deep sleep - to make ourselves feel refreshed
- Breathing is normal, muscles has tone
REM(rapid eye movement) sleep - 2nd half of sleep
- After 3/4am
- Dreaming
- Muscles are atonic except diaphragm, erratic breathing
What is the pathology for obstructive sleep apnoea?
Recurrent episodes of partial or complete upper airway obstruction during sleep, leading to intermittent hypoxia and arousals from sleep
- On inspiration upper-airway pressure becomes negative, but airway patency is maintained by upper-airway muscle tone. During deep sleep, these muscles relax causing narrowing of the upper airways as the norm. If the airway is already narrowed, the airway collapses and OSA results.
Features of obstructive sleep apnoea?
- Snoring
- Witnessed apnoea
- Excessive day time sleepiness
- Restless sleep
- Insomnia
- Nocturia - increased frequency to pass urine at night > 4 times
- Unrefreshed sleep
- Morning headaches
- Dry throat
- Mood swings
- Loss of libido
- Difficulty concentrating
What is the score of Epsworth Sleepiness Scale that is pathological for OSA and what are the negatives of this scale?
> 11/24 = pathological
Shows excessive sleepiness but not the score
Limitations - not telling the truth, exaggerations
What is the definition of apnoea?
Cessation of breathing for 10 seconds or more for 15+ episodes - usually scored with >4% desaturation SpO2 - diagnostic
What is the definition of hypopnea?
Reduction in the airflow (nasal flow) by 50% or more. May not cause O2 desaturations
What is the difference between OSA Syndrome and OSA?
OSA syndrome = abnormal sleep study and excessive day time sleepiness
OSA = abnormal sleep study and no excessive day time sleepiness
What is the criteria for categorising OSA?
Desaturation Index > 4%
Apnoea Hyponoea Index /hour
- Normal: <5
- Mild OSA: 5-15
- Moderate OSA: 15-30
- Severe OSA: >30
What are driving regulations in OSA?
- Declare to DVLA of diagnosis or receiving treatment
- CPAP compliance > 4 hours a night
- HGV/Bus/Taxi drivers - declare to employer
What is the management of mild-moderate OSA?
Lifestyle modifications
Weight reduction
Sleep hygiene
- Reduction of caffeine
- 8 hours a night
- Avoiding alcohol
Positional training
Mandibular advancement device
- Gum shield device to create more room at the back of the throat to breathe
- Fitted by dental practitioner
What is the management of moderate-severe OSA?
CPAP
- Blows continuous air into lungs to keep them expanded
- Minimum 4 hours a night
Features of Obesity Hypoventilation Syndrome?
- Morbid Obesity: BMI > 35kg/m2
- Mean SpO2 < 90% in sleep study, hyperventilate at night
- Time spent < 90% SpO2 in sleep study
- Daytime CO2 retention and/or elevated HCO3 > 27mmol/L
- TX: Weight loss, Non-invasive ventilation
What is the gold standard investigation for OSA?
Polysomnography
Possible complications from OSA?
Accidents related to excessive daytime sleepiness
Systemic hypertension, MI, CVD, stroke
Psychological consequences - depression, stress
Pulmonary arterial hypertension
Impaired glucose metabolism - diabetes
Associated with increase in all cause mortality
Associated symptoms with chest pain and differentials?
- Autonomic disturbance - sweating, nausea, vomiting - aortic dissection, PE, MI
- Breathlessness, cough, wheeze - respiratory causes
- Prodromal viral illness - myocarditis or pericarditis
- Throat tightness, perioral tingling, emotional distress - anxiety
Different onset types of chest pain with differentials?
- During exertion - angina, musculoskeletal or psychological in origin
- Sudden - aortic dissection, PE, pneumothorax
- Several minutes - MI
- Worse after eating and in supine position, regurgitation, dysphagia - GERD
Characteristics of chest pain with differentials?
- Sharp - catching chest pain aggravated by deep breathing - respiratory pathology
- Sharp catching pain during inspiration, coughing, lying flat - myocarditis, pericarditis
- Dull, constricting, choking, squeezing, crushing, burning, aching - MI
- During exertion and relieved by rest, exacerbated by cold weather, emotion - angina, asthma
What are risk factors for pulmonary hypertension?
- Systemic sclerosis + other connective disease
- Heart failure
- Lung disease - COPD, ILD
- Drugs - amphetamines, leflunomide, fenfluramine, SJW
- History of clots
- Group 1 - Family history - mutation in BMPR2 - member of TGF-Beta superfamily
- Schistosomiasis
- Female for group 1
What are the 5 different classifications of pulmonary hypertension?
- Pulmonary arterial hypertension - drugs, HIV, geneS, CTD
- PH due to left heart disease
- PH due to lung disease
- CTEPH - recurrent clots increasing pressure
- Unclear and multifactoral mechanisms
What is the criteria for pulmonary arterial hypertension diagnosis and what is the gold standard diagnostic investigation?
> 25mmHg at rest or
30mmHg on exercise
Right heart catheterisation (only when high suspicion for diagnosis and all other tests done to rule out differentials)
What is the main complication of pulmonary hypertension?
Cor Pulmonale
- Peripheral oedema
- Ascites
- Elevated JVP
- Cyanosis
- Hepatomegaly
- Parasternal heave - right ventricular enlargement
Arrhythmias - AF or atrial flutter
Haemoptysis
Compression of recurrent laryngeal nerve - hoarseness
What is an heritable gene mutation in Pulmonary Arterial Hypertension
Mutation in BMPR2 gene = excessive proliferation of smooth muscle cells in blood vessels = narrowing vessel = hypertension
What are investigations done in pulmonary hypertension - not diagnostic?
Chest x-ray - enlarged pulmonary arteries
Echo - enlarged right ventricle, increased arterial pressure
Spirometry - underlying causative lung disease
V/Q Perfusion Scan - rule out chronic thrombus
Antibody screen - rule out autoimmune diseases
What are signs of pulmonary hypertension on an ECG?
Right ventricular hypertrophy
- right axis deviation
- T inversion in anterior leads
- persistent s wave
- RBBB
What is the functional classification in pulmonary hypertension?
Class I - comfortable at rest and exertion
Class II - comfortable at rest, slight limitation of activity on exertion
Class III - comfortable at rest, marked limitation of physical activity even on mild exertion
Class IV - symptoms at rest and severe on exertion
What is the pathophysiology behind pulmonary arterial hypertension
Disruption in major signalling pathways = increases pulmonary vascular resistance
1. Nitric oxide and prostacyclin pathway disrupted = impaired vasodilation
2. Disrupted endothelin pathway = increased vasoconstriction
What are supportive therapies in pulmonary hypertension?
- Diuretic therapy
- Anticoagulants - increased risk clots
- Long term oxygen therapy
- Vaccinations
