Respiratory conditions Flashcards
What are examples of obstructive airway disease?
Asthma, chronic bronchitis and emphysema, (COPD).
What is ACOS?
ACOS is asthma/COPD overlap syndrome, patients with features of both COPD and asthma, e.g. COPD with reversibility and eosinophilia who are steroid responsive.
What is asthma?
Asthma is a chronic inflammatory disease of the airways.
What is the asthma triad?
The asthma triad is reversible airflow obstruction, airway hyper-responsiveness and airway inflammation.
What are the hallmarks of remodeling in asthma?
Thickening of the basement membrane, collagen deposition in the submucosa, and hypertrophy of smooth muscle.
Describe the inflammatory cascade in asthma.
A genetic predisposition to asthma and the presence of triggers causes eosinophilic inflammation. Eosinophils release inflammatory mediators in the form of TH2 cytokines. TH2 cytokines cause hyper-reactivity of airway smooth muscle.
How can a genetic predisposition to triggers of asthma be treated?
Avoidance of those triggers, e.g. allergens.
How can eosinophilic inflammation of asthma be treated?
Anti-inflammatory drugs, e.g. corticosteroids or cromones.
How can inflammatory mediators and TH2 cytokines in asthma be treated?
Anti-leukotrienes/histamine, anti-IgE and anti-IL5.
How can hyper-reactivity of asthma be treated?
By bronchodilators, e.g. beta-2-agonists or muscarinic antagonists.
What may inflammation in asthma show on photomicrographs?
Desquamation of airway epithelium, numerous eosinophils, thickening of basement membrane.
What signs and symptoms may point to a diagnosis of asthma?
Episodic symptoms, diurnal variability (worse at night and early morning), non-productive cough, or wheeze due to turbulent airflow. Patient may also experience symptoms in response to triggers, have associated atopy or a FHx of asthma.
What is the forced expiratory ratio in asthma?
Asthmatics have a reduced forced expiratory ratio of <75%, but experience >15% reversibility in response to salbutamol.
How may a diagnosis of asthma be made?
Provocation testing leading to bronchospasm, by exercise or exposure to histamine/methacholine/mannitol.
What are the main components of COPD?
COPD is a multicomponent disease process consisting of: mucociliary dysfunction, inflammation and tissue damage/
What are the characteristics and symptoms of COPD?
A patient experiences frequent exacerbations, reduced lung function. They become increasingly breathless and have a worsening quality of life due to obstruction and disease progression.
What are the triggers and pathophysiology of COPD?
Exposure to inhaled noxious particles or gases causes lung inflammation which may lead to COPD if normal protective/repair mechanisms are defective.
Irritants activate macrophages and airway epithelial cells to release neutrophil cytokines, IL-8 and LTB4. Neutrophils and macrophages release proteases to break down connective tissues in lung parenchyma (alveolar wall destruction–> emphysema) and stimulate mucus hypersecretion (chronic bronchitis).
How may mucociliary function be compromised?
Mucociliary function may be compromised by damage to the cilia due to enzymes, e.g. neutrophil elastase, attracted to airways by toxins.
COPD patients have recurrent resp. tract infection, how may this damage the respiratory mucosa?
Commonly H. influenza, which may break down epithelial cell walls, leading to loss of ciliated cells and damaging airway tissue.
Why does emphysema occur?
Alveolar destruction, causes increased air spaces. Due to proteases, e.g. neutrophil elastase, and may relate to an imbalance of proteases and anti-proteases.
Give 4 features of chronic bronchitis.
- Chronic neutrophilic inflammation.
- Mucus hypersecretion.
- Mucociliary dysfunction.
- Altered lung microbiome.
- Smooth muscle spasm and hypertrophy.
- Partially reversible.
Give the features of emphysema.
- Alveolar destruction.
- Impaired gas exchange.
- Loss of bronchial support.
- Irreversible.
What are indicators of high risk COPD?
2 or more exacerbations within the past year, or an FEV1 <50% of predicted.
What are the signs and symptoms of COPD?
Chronic symptoms, smoker, non-atopic, a daily productive cough, progressive breathlessness, frequent infective exacerbations.
Chronic bronchitis: wheezing.
Emphysema: reduced breath sounds.
Describe the chronic cascade of COPD.
Progressive fixed airflow obstruction leads to impaired alveolar gas exchange, leading to resp. failure (decreased PaO2 and increased PaCO2). This leads to pulmonary hypertension, RV hypertrophy/failure and eventually death.
Non-pharmacological treatment methods of COPD?
smoking cessation, immunization, physical activity, domiciliary oxygen and venesection.
Pharmacological treatment methods of COPD?
LAMA (tiotropium).
LABA (salmeterol or formeterol).
LAMA-LABA combo
LABA-ICS combo: beclometasone+formeterol.
LAMA-LABA/ICS combo: glycopyronnium-formeterol-beclometasone.
What is the FVC and TLCO of asthmatics?
Normal.
What is the FVC and TLCO of COPD?
Reduced.
What is DPLD?
Diffuse parenchymal lung disease. It is an interstitial lung disease caused by disease of alveolar structures. This results in impaired alveolar gas exchange, decreased PaO2 and decreased SaO2. However, CO2 exchange is unimpaired.
Give causes of consolidation of alveolar air spaces.
Infective pneumonia, infarction, rheumatoid disease, drugs.
What is extrinsic allergic alveolitis?
Aka hypersensitivity pneumonitis type 3. It is called farmers lung as it is related to avian keeping, e.g. pigeons, budgies.
What is sarcoidosis?
Sarcoidosis is a multi-system disease, involving lymphadenopathy, erythema nodosum, uveitis, myocarditis and neuropathy,
CXR may show bilateral hilar lymphadenopathy and lung infiltrates.
Non-caseating granuloma may also be found within the lung.
Give examples of drugs which may cause drug-induced alveolitis.
Amiodarone, methotrexate, Gold, bleomycin.
Which gas may cause alveolitis?
Chlorine.
What autoimmune conditions may cause alveolitis?
systemic lupus erythematosus, polyarteritis, Wegeners, Chrug-Strauss, Bechet’s.
What is pneumoconiosis and what are its fibrogenic causes?
Pneumoconiosis is an occupational, restrictive lung disease caused by the inhalation of dust. Fibrogenic causes include asbestosis and silicosis.
What are non-fibrogenic causes of pneumoconiosis?
Iron (siderosis), tin (stenosis), barium (baritosis).
What are the clinical signs and symptoms of DPLD?
Breathless on exertion, cough without wheeze, finger clubbing, inspiratory lung crackles, central cyanosis and pulmonary fibrosis (end-stage due to chronic inflammation).
How may DPLD be diagnosed?
- History: occupation, drugs, pets, arthritis.
- FEV1/FVC ratio <75%. Normal peak flow.
- Reduced gas diffusion, reduced PaO2 and reduced SaO2.
- antibodies.
- Bilateral diffuse alveolar infiltrates on CXR.
- ground glass on high res. CT
Treatment of DPLD.
Remove triggers, treat inflammation with immunosuppressors.
1st line: corticosteroids e.g. oral prednisolone.
2nd line: oral azathioprine.
Anti-fibrotic agents.
Anti-oxidant agents.
Oxygen, if hypoxic.
Lung transplant.
Give an example of effort dependent pulmonary function tests.
Spirometry: forced expiratory flow rate.
Give examples of effort independent pulmonary function tests.
Spirometry: relaxed vital capacity. Helium/N2 washout static lung volumes. Whole body plethysmography. Impulse oscillometry. Exhaled breath nitric oxide.
Give examples of pulmonary function gas diffusion tests.
CO transfer factor.
Arterial blood gases at rest.
SaO2 during exercise.
Describe the spirometry of Asthma.
Asthma has normal FVC and reduced FEV1.
Describe the spirometry of COPD.
COPD has both reduced FVC and FEV1.
Describe the shape of an expiratory flow-volume curve of volume dependent expiratory airway closure diseases, and the diseases that produce this curve.
Asthma and chronic bronchitis. Curve follows shape of normal, but is reduced.
Describe the shape of an expiratory flow-volume curve of pressure dependent expiratory airway closure diseases, and the diseases that produce this curve.
Emphysema. Curve is more rounded, and significantly reduced in comparison to normal curve.
Describe the PEFR, FEV1, FVC, FEV1/FVC ratio and FEV1 response to beta-2-agonist of asthma.
In asthma, PEFR is reduced, FEV1 is reduced, FVC is normal. The FEV1/FVC ratio is <75%, but shows >15% improvement in response to beta-2-agonist.
Describe the PEFR, FEV1, FVC, FEV1/FVC ratio and FEV1 response to beta-2-agonist of COPD.
PEFR is reduced, FEV1 is reduced, FVC is reduced. FEV1/FVC ratio is <75% and shows <15% improvement in response to beta-2-agonist.
Describe the PEFR, FEV1, FVC, FEV1/FVC ratio and FEV1 response to beta-2-agonist of restrictive lung disease.
PEFR is normal, FEV1 is reduced, FVC is reduced. FEV1/FVC ratio is normal and shows no improvement in response to beta-2-agonists.
Describe the static lung volume of COPD.
In COPD there is hyper-inflation of static lung volume.
Describe the static lung volume of restrictive lung disease.
In restrictive lung disease, TLC is reduced.
In which conditions might TLCO be reduced?
TLCO is reduced in anaemia, emphysema, interstitial lung disease, pulmonary oedema, bronchiectasis, pulmonary emboli.
Two methods of measuring airway resistance?
Whole body plethysmography or more commonly - impulse oscillometry.
High levels of exhaled NO reflect what?
Uncontrolled asthmatic inflammation.
Outline the pathology of COPD.
smoking or air pollution causes stimulation of alveolar macrophages, which produce cytokines. Cytokines activate neutrophils, CD8-T-cells. These cause release of matrix metalloproteinases and free radicals.
Describe chronic bronchitis.
Chronic bronchitis is the inflammation of bronchi and bronchioles. Chronic cough productive of sputum. Infective exacerbations produce purulent sputum. Patients present with increasing breathlessness.
Describe emphysema.
Distension and damage to alveoli results in destruction of acinial pouching in alveolal sacs.
When should you image to detect a pulmonary thromboembolism?
If a CXR is normal, perform a V/Q scan.
If radiation is to be avoided/leg is swollen, consider ultrasound (of leg for DVT).
If CXR is abnormal/massive PE is suspected, do a CT pulmonary angiogram.
Symptoms of lung cancer?
25% may be asymptomatic. Symptoms include cough, wheeze, haemoptysis, breathlessness, recurrent pneumonia, hypercalcaemia, weight loss, hoarseness, finger clubbing, persistent enlarged supra-clavicular nodes.
Describe peripheral lung tumours.
Tumours arising beyond the hilum.
Describe central tumours.
Tumours arising at, or close to the hilum.
What are the “cardinal signs” of central lung tumours?
hilar enlargement and distal collapse/consolidation.
What do T, N and M stand for in the international staging system?
T = tumour size. N = lymph node staging. M = metastases.
What is a CT good for with regards to tumours?
Diagnosis. It enables assessment of tumour size, and shows intracranial metastases. It also guides biopsy of peripheral lesions. Can be useful for staging, but a PET scan is better.
What is a PET CT good for with regards to tumours?
Staging. It enables the detection of nodal and distant metastases. It’s also good at outlining tumours within areas of collapse. Often upstages people.
What is an MR good for with regards to lung tumours?
It doesn’t require IV contract, views in 3 planes and good soft tissue differentiation. However its costly and time consuming, and better spatial resolution is achieved with CT.
What is the main treatment method of small cell lung cancer?
Chemotherapy.
What is ultrasound useful for, with regards to the respiratory system?
Pleural effusion, subphrenic collection, seeing diaphragm movement and guiding drainage.
What is stridor?
Worrying. Difficulty breathing in, causing coarse audible wheeze. May be symptom of cancer.
Why might a lung tumour cause a hoarse voice?
It may invade the recurrent laryngeal nerve, causing palsy.
What might invasion of the pericardium by a lung tumour cause?
Breathlessness, atrial fibrillation, pericardial effusion.
What might invasion of the oesophagus by a lung tumour cause?
Dysphagia for solids.
Where are pancoast tumours found?
In the apex of the lung, they may invade the brachial plexus and cause weakness of hands/arms.
what can often happen when a primary lung tumour invades the pleural space?
It may cause large volumes of pleural fluid to accumulate, causing breathlessness.
What may happen when a primary lung tumour invades the SVC?
It obstructs blood drainage from the arms and head. A patient may complain of puffy eyelids and a headache. Distension of veins may also be seen.
What might chest wall invasion by lung cancer cause?
Destruction of ribs, causing localized chest pain made worse by movement. If bone is eroded, patients often have worse pain at night.
What may happen if a tumour encases and erodes into an artery?
It may cause sudden death due to massive haemoptysis.
Where are common sites of metastases for lung cancer?
Liver, brain, bone, adrenal glands, skin, lung.
What symptoms might a patient with cerebral metastases experience?
Slow onset of weakness, visual disturbance, headaches (worse in morning with no photophobia), fits.
What symptoms might a patient with bone metastases experience?
Localised pain which is worse at night, or fractures due to trivial mechanical stress. May be detected by isotope bone scans.
Symptoms of hypercalcaemia?
Headaches, confusion, thirst and constipation.
Why is thrombophlebitis a common manifestation of cancer?
Cancer patients have increased coagulability of the blood.
What are red flag symptoms you must ask about when concerned about lung cancer?
Cough (sputum or not?), haemoptysis, smoker, breathless, weight loss, fatigue, recurrent infection, chest pain.
What should you look for when examining a patient and concerned about lung cancer?
Finger clubbing, breathless, cough, weight loss, bloated face, hoarse voice, lymphadenopathy, dull percussion, tracheal deviation, stridor, enlarged liver.
What is the function of a PET scan?
Analyses tissue uptake of radiolabelled glucose causing tissues with high metabolic activity “light up”. It assessed function, rather than structure.
When might bronchoscopy be used in investigation of lung cancer?
If suspected tumour in central area of bronchial tree.
When might CT guided biopsy be used in investigation of lung cancer?
If there is a suspected peripheral tumour.
When might an endobrachial ultrasound be used in investigation of lung cancer?
To enable visuation of hilar and mediastinal structures, and to target and sample lymph nodes.
When might a thoracoscopy be used in investigation of lung cancer?
Deflation of lungs to visualize and biopsy pleural surfaces.
What are the treatment options for non-small cell lung cancer?
Surgery or radical radiotherapy. Tend to be less responsive to chemotherapy.
Side effects of chemotherapy?
Nausea, vomiting, tiredness, bone marrow suppression (opportunistic infection, anaemia), hair loss and pulmonary fibrosis.
How do radical and palliative radiotherapy differ?
Radical has the intent to cure, and palliative is a delaying tactic useful for metastases.
Radiotherapy disadvantages?
Damage to spinal cord, oesophagus, adjacent lung tissue. Limited to area of beam
Define pleural effusion.
The abnormal collection of fluid in the pleural space. Large unilateral effusions should raise concern. They may be aspirated, to determine if transudate or exudate.
What investigations might you undertake with regards to pleural effusion?
PA CXR. Pleural aspirate. Biochemistry - transudate or exudate? Cytology. Culture. Contrast enhanced CT Pleural tap Bleural biopsy.
what might straw-coloured pleural fluid suggest?
Cardiac failure, hypoalbuminaemia.
What might bloody pleural fluid suggest?
Trauma, malignancy, infection, infarction.
what might milky/turbid pleural fluid suggest?
Empyema, chylothorax
What might foul smelling pleural fluid suggest?
Anaerobic empyema.
What might food particles in the pleural fluid suggest>
Oesophageal rupture.
What might cause bilateral pleural effusions.
LVF, PTE, drugs, systemic pathology.
What is transudative pleural fluid? What are its causes?
Protein <30g/l. It may be caused by heart failure, liver cirrhosis, hypoalbuminaemia, atelectasis, peritoneal dialysis.
What is exudative pleural fluid? What are its causes?
Protein>30g/l. Caused by malignancy, infection inc. TB, pulmonary infarct, asbestos.
What does lymphocytes in pleural fluid cytology suggest?
TB, malignancy. Though, any long standing effusion will eventually become lymphocytic.
What do neutrophils in pleural fluid suggest?
An acute process.
Define mesothelioma,
Mesothelioma is an uncommon, malignant tumour of the lung lining, or rarely of the lining of the abd. cavity. Usually due to asbestos exposure.
What are contributory causes and symptoms of mesothelioma.
Asbestos exposure. Often takes 30-40 years to develop. Symptoms include: breathlessness, chest pain, weight loss, fever, sweating and cough.
What investigations should be carried out when mesothelioma is suspected?
Imaging, pleural fluid aspirate and biopsy (thoracoscopy or CT/US guided).
How is mesothelioma treated?
Pleurodese effusions, radiotherapy, surgery, chemotherapy, palliative care.
How to treat pleural effusion due to LVF?
Diuretics.
How to treat pleural effusion due to infection?
Drain, antibiotics and may require surgery.
How to treat pleural effusion due to malignancy>
Drain, pleurodesis and long term pleural catheter.
What factors make pneumothorax more likely?
Tall thin males, smokers, cannabis use, underlying lung disease.
How do pneumothorax present?
SOB, hypoxia, acute onset pleuritic chest pain. Tachycardia, hyper-resonant, reduced chest expansion, quiet breath sounds on auscultation and a click on auscultation (Hamman’s sign).
How do primary and secondary spontaneous pneumothorax differ in symptoms?
Primary are often asymptomatic, even if moderately sized. Secondary are usually symptomatic, even if small.
Management of pneumothorax?
- Oxygen.
No treatment if pneumothorax is small and asymptomatic.
1st line in PSP: aspiration.
Chest drain, suction, surgical intervention.
Symptoms and signs of tension pneumothorax.
Emergency- may lead to cardiac arrest. Increased pressure in pleural space, pushes other chest organs to opposite side. ARDS. Tracheal deviation to opposite side, hypotension, raised JVP, reduced air entry on affected side.
Treatment of tension pneumothorax.
Needle decompression (typically large bore venflon) in the second intercostal space, anteriorly, mid-clavicular line.
Which conditions affect the upper respiratory tract?
Common cold - coryza. Sore throat- pharyngitis. Sinusitis and epiglottitis.
Which conditions affect the lower respiratory tract?
Acute bronchitis, acute exacerbation of chronic bronchitis, pneumonia and influenza.
Outline the common cold (coryza).
Acute viral infection of nasal passages, often accompanied by sore throat and mild fever. Causative agents include: adenovirus, rhinovirus, and respiratory syncytial virus.
Describe acute sinusitis.
Often preceded by a common cold and purulent nasal discharge. Its usually self-limiting, resolving in roughly 10 days.
Diphtheria.
Life threatening condition, caused by toxin production. Characteristic pseudo-membrane. Not seen in UK due to vaccination.
Acute epiglottitis.
Life threatening airway obstruction in children. Caused by inflammation of the epiglottis, often resulting from haemophilus influenza type B (HiB). Acute onset, sore throat and drooling, severe croup/stridor, high temp.
acute bronchitis.
Preceded by common cold, goes to the chest. Productive cough, possible fever, normal chest exam and CXR, but may have a transient wheeze. Typically self limiting, but significantly increases morbidity in patients with chronic lung disease.
Acute exacerbation of COPD.
Usually preceded by URTI, increased sputum production (chronic), increase sputum purulence, more wheezy and increasingly breathless.
On examination: respiratory distress, wheeze, coarse crackles, cyanosis and ankle oedema (advanced disease).
Treatment of acute exacerbations of COPD?
Antibiotic (e.g. doxycycline or amoxicillin).
Bronchodilator.
Short course of steroids.
May require hospital referral: ABGs, CXR, O2.
Symptoms of pneumonia?
Malaise, anorexia, sweats, rigors, myalgia, arthralgia, headache, confusion, cough, pleurisy, haemoptysis, dyspnea, preceding URTI, abdo. pain, diarrhea.
Signs of pneumonia.
Fever, rigors, herpes labialis, tachypnea, crackles, rub, cyanosis, hypotension. CXR with infiltrates (neutrophil, macrophage, fibrin-rich exudate fluid). Fluid filled spaces lead to consolidation (typically lower lungs).
Pneumonia investigations.
Blood culture, serology, ABGs, FBC, urea, LFTS and CXR.
How is community acquired pneumonia assessed?
CURB65. Confusion (new onset), urea>7, resp rate>30/min, BP<90 or diastolic <61, >65 years. 1 point for each.
Most common causative agent of pneumonia?
Strep. pneumonia.
How often does mycoplasma pneumonia peak?
Peaks every 4 years.
what might cause pneumonia in someone who keeps birds?
Chlamydia psittaci.
Management of community acquired pneumonia.
Antibiotics: amoxicillin, doxycycline. Oxygen 94-98% or 88-92%. Fluids. Bed rest. No smoking.
What are complications of pneumonia?
Respiratory failure, pleural effusion, empyema and death.
Organisation (fibrous scarring), abscess, bronchiectasis.
Clinical presentation of influenza
high, abrupt onset of fever. Malaise, myalgia, headache, cough, fatigue.
Complications of flu?
primary influenzal pneumonia, secondary bacterial pneumonia, bronchitis, otitis media. During pregnancy: perinatal mortality, prematurity, smaller neonatal size and lower birth weight.
Presentation of bronchiolitis.
Presents aged 1/2. Fever, coryza, cough, wheeze, tachypnoea, poor feeding. In severe cases the child may grunt, have reduced PaO2 and show intercostal/sternal indrawing.
Treatment is supportive.
Complications of bronchiolitis.
Resp. and cardiac failure.
Aetiology and confirmation of bronchiolitis.
80% due to respiratory syncytial virus, and confirmed by PCR of swabs.
Metapneumovirus.
First isolated in 2001 in children with RTI. Second most common cause of bronchiolitis in children. Confirmed by PCR.
Presentation of measles.
High fever, runny nose, red eyes, malaise, dry cough. Koplik’s spots, maculopapular rash beginning behind the ears and descending.
Complications of measles.
Bacterial pneumonia, bacterial otitis media, encephalitis. More common in immunocompromised and malnourished.
Croup.
Acute laryngotracheobronchitis. Precipitated by various viruses, harsh cough, stridor. May be treated with humidification if mild, but if admitted- steroids.
Common cold.
Coryza. Caused by many viruses: rhinovirus, coronarvirus etc.
Treatment of epiglottitis?
Ceftriaxone.
cystic fibrosis.
Inherited, abnormally viscous mucous blocking airways. Symptoms are repeated chest infections and chronic colonization (staph. aureus, haemophilus influenza, strep. pneumonia, pseudomonas aeruginosa etc.).
Whooping cough (pertussis).
Acute tracheobronchitis. Experiences cold like symptoms, paroxysmal coughing, violent exhalations with inspiratory “whoop”. Vomiting is common. Caused by bordetella pertussis, a gram -ve coccobacillus.
Bordetella pertussis diagnosis confirmation.
Bacterial culture, PCR, serology.
Treatment of bordetella pertussis.
Clarythromycin, or azithromycin. If pregnant then erythromycin.
What defences does alveolar lining fluid possess?
Surfactant, Ig, complement, alveolar macrophages, neutrophils, FFA, AMP.
Legionella pneumonia aka Legionnaires’ disease.
Atypical, gram -ve. Flu-like symptoms, confusion, cough, SOB, GI upset. May progress to severe pneumonia, and acute renal failure. CXR: consolidation.
Treatment of legionella pneumophilia.
Clarythromycin, erythromycin or quinolones, e.g. levofloxacin.
Treatment of mild/moderate community acquired pneumonia.
Amoxicillin or doxycycline or clarithromycin.
Treatment of severe community acquired pneumonia.
Co-amoxiclav + clarithromycin if penicillin allergic: IV levofloxacin.
Treatment of severe community acquired pneumonia, but in ICU/HDU.
Co-amoxiclav and clarithromycin.
Treatment of severe hospital acquired or aspiration pneumonia.
IV amoxicillin + metronidazole + gentamicin.
If penicillin allergic: IV-co-trimoxazole + metronidazole +/- gentamicin.
Treatment of non-severe hospital acquired pneumonia or aspiration pneumonia.
PO amoxicillin + metronidazole.
Most common pneumonia in the immunosuppressed/AIDS?
Pneumocystis jirovecii pneumonia (PCP).
Symptoms of pneumocystis pneumonia.
Fever, dry cough, SOB, fatigue.
HIV: sub-acute, low grade fever, but more severe pneumonia.
Diagnosis and treatment of pneumocystis pneumonia.
BAL (bronchoalveolar lavage)>Sputum>gargle.
Immunofluorescence.
PCR.
Treatment: co-trimoxazole.
Aspergillus.
Fungal chest infection due to inhalation of fungal spores.
Immunocompromised/suppressed: severe pneumonia and invasive disease.
Immunocompetent patients: localized pulmonary infecton and aspergilloma (fungus ball) in pre-existing chest cavities.
Diagnosis and treatment of aspergillus.
BAL, fungal culture, PCR, histopathology.
Treatment: amphotericin B, voriconazole, or surgery.
tuberculosis.
Caused by mycobacterium tuberculosis, an acid-alcohol-fast-bacilli, with a thick waxy coat. Typically develops into latent TB, and only 10% experience immediate active TB.
Delayed type IV hypersensitivity (caseating granulomas with necrosis).
Symptoms of tuberculosis.
Cough, chest pain, sputum, haemoptysis, weakness or fatigue, weight loss, fever and chills, night sweats.
Upper zone crackles on auscultation.
Diagnosis of TB.
Microscopy of sputum/tissue (ZN stain, mycobacterium stain red/pink).
Culture on selective media.
PCR.
Immune reaction.
Multinucleate giant cell granulomas, caseating necrosis, possible visible mycobacteria.
Tuberculosis CXR.
Dense consolidation of upper lobe(s), cavity formation. Tissue destruction, scarring and shrinkage, heals with calcification.
tuberculous meningitis.
Headaches, drowsy, fits. GI: pain, bowel obstruction, perforation, peritonitis. Spinal: pain, deformity, paraplegia. Lymphadenopathy and cold abscess (pus without pain or inflammation).
Complications of tuberculosis.
Pericardial tamponade, renal failure, septic arthritis and hypoadrenalism.
(never inject steroid into a solitary arthritic joint- could be TB).
Military TB.
Massive seeding of mycobacteria through bloodstream. Untreated, it may be rapidly fatal.
Treatment of TB.
RIPE for 2 months: 1. Rifampicin. 2. Isoniazid. 3. Pyrazinamide. 4. Ethambutol Followed by 4 months of: rifampicin and isoniazid. NB. both rifampicin and isoniazid may disturb liver function.
How might you test for previous TB exposure?
Interferon gamma release assay, or mantoux (tuberculin) skin test - unable to differentiate between BCG and TB.
Which disease is closely associated with HIV?
TB, all TB cases should be offered a HIV test and all HIV cases should be offered a CXR.
What might cause reactivation of latent tuberculosis?
Steroids and other immunosuppressant drugs,
Risk factors for pleural infection?
Diabetes mellitus, immunosuppression inc. corticosteroids, GORD, alcohol misuse, IV drug abuse.
What are the different type of pleural infection?
Simple parapneumonic effusion, complicated parapneumonic effusion and empyema.
Define complicated parapneumonic effusion.
+ve gram stain, pH<7.2, low glucose, septations and loculations.
Define simple parapneumonic effusion.
No characteristics of complicated effusion and may be treated with antibiotics alone, but may later require drainage if change occurs.
Management of pleural infection.
Antibiotics, drainage as required. If persistent sepsis- discuss surgery. Nutrition, VTE prophylaxis. Fibrinolytics/DNAse?
Describe lobar pneumonia.
Lobar pneumonia is often consolidation of a complete lung lobe. Most often due to strep. pneumoniae, but also seen with klebsiella or legionella etc.
Describe bronchopneumonia.
Infection starts in airways and spreads to adjacent alveolar lung. Most often seen in pre-existing disease e.g. COPD, elderly and cardiac failure, influenza, aspiration of gastric contents.
Various causative agents: strep. pneumoniae, H. influenza, staph, anaerobes, coliforms.
Describe bronchiectasis.
Bronchiectasis is the fixed, abnormal dilatation of the bronchi. It is usually de to fibrous scarring resulting from infection, but can also be seen with chronic obstruction (tumour).
The dilated airways accumulate purulent secretions.
Describe immunity and hypersensitivity with regards to TB.
immunity: T-cell responds, enhances macrophage ability to kill mycobacteria.
Hypersensitivity: T-cell responds, causing granulomatous inflammation, tissue necrosis and scarring.
Both processes commonly occur together,
Risk factors for developing chronic pulmonary infection.
Abnormal host response: immunodeficiency or immunosuppression.
Abnormal innate host defence (damaged bronchial mucosa, abnormal cilia, or abnormal secretions).
Repeated insult.
IgA deficiency may have what effect on respiratory health?
Common, increases risk of acute infection.
Hypogammaglobulinaemia may have what effect on respiratory health?
Rare. Increases risk of both acute and chronic infections.
CVID (common variable immunodeficiency) may have what effect on respiratory health?
Commonest cause of immunodeficiency, leading to recurrent respiratory infections.
Immune paresis may have what impact on health?
Myeloma, lymphoma, metastatic malignancy.
Give examples of immunosuppressants.
Steroids, azathioprine, methotrexate, monoclonal antibodies (infliximab), chemotherapy.
What conditions might cause abnormal cilia?
Kartenager’s Syndrome, Young’s syndrome.
What conditions might cause abnormal secretions?
Cystic fibrosis and channelopathies.
What might damage the bronchial mucosa?
Smoking, pneumonia, viral infection, malignancy.
Give examples of chronic respiratory infections.
Intrapulmonary abscess, empyema, chronic bronchial sepsis, bronchiectasis and Cystic fibrosis.
Intrapulmonary abscess.
Weight loss, lethargy, fatigue, weakness, cough, sputum production. Usually follows illness, e.g. pneumonia, virus, foreign body.
High mortality if left untreated.
Describe septic emboli.
Right-sided endocarditis, infected DVT, septicaemia.
Common in IV drug users who inject into the groin -> DVT -> infection -> PE + abscess.
Empyema.
Pus in the pleural space. High mortality rate. D sign on CXR. Treat with amoxicillin + metronidazole. Then direct towards cultured bacteria (2weeks).
Treatment of bronchiectasis.
Stop smoking, vaccines, antibiotics - anti-inflammatory: clarithromycin or azithromycin (pseudomonas).
Complications of cystic fibrosis.
Bronchiectasis, sputum, biliary obstruction, obstructive hepatitis, pancreatic dysfunction (steatorrhoea), male infertility.
Epidemiology of cystic fibrosis.
1 in 25 people carry the gene.
Congenital bilateral absence of vas deferens, fibrotic pancreas and a failure to thrive.
Cystic fibrosis.
What might result from exocrine failure of the pancreas due to cystic fibrosis.
Sludged up ducts, failure to secrete lipase or amylase, resulting in digestive failure.
What might result from endocrine failure of the pancreas due to cystic fibrosis.
Destruction of pancreatic islet cells, fatty replacement of pancreatic tissue. May fail to produce insulin and require insulin injections.
What may happen to the bowels of a CF patient?
Distal intestinal obstruction syndrome, where thick mucus blocks up the large and small intestines. Symptoms are similar to constipation.
what may happen to the liver of a CF patient?
Sludging up of hepatic ducts (intra- and extra-hepatic), portal hypertension and TIPSS.
How are exacerbations of CF managed?
antibiotics: always 2.
physiotherapy
hydration
increased dietary input
Define interstitial lung disease.
Any disease process affecting the interstitium of the lung, e.g. alveoli, terminal bronchi. It interferes with gas transfer and causes restrictive lung patterns. Symptoms vary, but generally include breathlessness and a dry cough.
Give examples of interstitial lung disease.
Sarcoidosis, extrinsic allergic alveolitis, fibrosing alveolitis, idiopathic pulmonary fibrosis, pneumonia, pneumoconiosis and connective tissue disease.
Features of acute sarcoidosis.
Erythema nodosum, bilateral hilar lymphadenopathy, arthritis, uveitis, parotitis and fever.
Features of chronic sarcoidosis.
Lung infiltrates (alveolitis), skin infiltrations, periphera lymphadenopathy, hypercalcaemia and impact on other organs (kidneys, heart, brain, liver and spleen).
Treatment of sarcoidosis.
Acute is usually self-limiting.
Chronic usually requires steroids, and immunosuppression e.g. azathioprine, methotrexate and anti-TNF therapy.
Should monitor CXR and pulmonary function for several years.
Extrinsic allergic alveolitis.
Type III hypersensitivity reaction, causing lymphocytic alveolitis. Often seen in farmers, bird-owners and as a result of medication e.g. sulphasalazine, but may be idiopathic.
Symptoms of acute extrinsic allergic alveolitis type III.
cough, breathlessness, fever, myalgia, flu-like. May have fever and crackles, but no wheeze, and may be hypoxic.
A CXR will show widespread pulmonary infiltrates.
Treatment of acute extrinsic allergic alveolitis.
Oxygen, steroids and antigen avoidance.
Symptoms of chronic extrinsic allergic alveolitis.
Progressive breathlessness and cough. Crackles may be present in the lungs, but finger clubbing is unusual.
CXR: pulmonary fibrosis - commonly in upper lobes.
Restrictive PFTs: low FEV1 and FVC, but a high or normal ratio. TLCO will be low.
Diagnosis of chronic extrinsic allergic alveolitis.
History of exposure to antigen, precipitins (IgG antibodies of antigen) and a lung biopsy if doubt remains.
CXR: pulmonary fibrosis- typically in upper lobes.
Treatment of chronic extrinsic allergic alveolitis.
Antigen avoidance, oral steroids if breathless or if low TLCO.
Idiopathic pulmonary fibrosis (formerly cryptogenic fibrosing alveolitis).
Most common ILD. Unknown aetiology. Not inflammatory disease.
Secondary causes of pulmonary fibrosis.
Rheumatoid, SLE, systemic sclerosis, asbestos, amiodarone, methotrexate.
Symptoms of idiopathic pulmonary fibrosis.
Progressive breathlessness, dry cough, finger clubbing, bilateral fine inspiratory crackles.
Diagnosis of idiopathic pulmonary fibrosis.
Restrictive pattern on PFTs.
CXR: bilateral infiltrates.
CT scan: reticulonodular shadowing, worse at peripheries and lung bases. Honey-combing. Traction bronchiectasis.
A lung biopsy is unnecessary if CT is diagnostic.
Treatment of idiopathic pulmonary fibrosis.
Oxygen if hypoxic.
anti-fibrotic drugs may slow disease (pirfenidone and nintedanib) but will not cure.
Lung transplant may be possible for younger patients.
Terminal disease, median survival of 4 years following diagnosis.
Coal workers pneumoconiosis.
Chronic bronchitis due to coal dust + smoking.
Simple: CXR abnormality but no impairment of lung function.
Complicated: progressive, massive fibrosis, restrictive PFTs and breathlessness.
Silicosis.
15-20 years quartz exposure, e.g. miners, glass workers.
Simple pneumoconiosis: CXR egg-shell calcification of hilar nodes.
Chronic silicosis: restrictive pattern, and pulmonary fibrosis.
Which occupations are at risk of developing asbestos related lung disorders?
Miners, construction, shipbuilders, car workers.
Asbestos related lung disorders.
- Benign pleural plaques - asymptomatic.
- Acute asbestos pleuritis.
- Pleural effusion and diffuse pleural thickening.
- Malignant mesothelioma.
- Pulmonary fibrosis.
- Bronchial carcinoma.
Symptoms of acute asbestos pleuritis.
Fever, pain, bloody pleural effusion.
Symptoms of pleural effusion and diffuse pleural thickening.
Restrictive lung function.
Symptoms of malignant mesothelioma,
incurable pleural cancer, fatal within 2 years. Presents as chest pain and pleural effusion.
Symptoms of asbestosis pulmonary fibrosis.
Prolonged exposure to asbestos. Diffuse pulmonary fibrosis and a restrictive defect. Asbestos bodies seen in sputum and asbestos fibres found in lung biopsy.
Which asbestos fibres are most dangerous?
Straight (amphibole) asbestos is highly dangerous, the serpentine/curved fibres are less so.
Respiratory distress syndrome.
Due to a relative surfactant deficiency. More common in premature babies.
What are the components of surfactant and what might a shortage of it result in>
Phospholipids and apoproteins. Lack of surfactant results in atelectasis and impairment of gas exchange. Its production is stimulated by steroids.
Complications of infant respiratory distress syndrome?
Sudden deterioration and absent breath sounds.
What is a pneumothorax?
A Pneumothorax is air in the pleural space.
Clinical features of asthma
Wheeze, cough, chest tightness, difficulty breathing, atopy, wide spread wheeze on auscultation.
Treating childhood asthma.
- Beta-agonists as required.
- ICS
3a. regular ICS + LABA
3b. ICS + LABA + leukotriene antagonists.
Treatment of acute childhood asthma.
Oxygen. Salbutamol (nebulised). Oral prednisolone. IV salbutamol IV aminophylline IV magnesium ventilator support.
10 year old girl presents with cough, high fever and sputum production. Previously well. On examination: dullness on percussion, increased vocal fremitus and resonance, and bronchial breathing.
Pneumonia.
Most common causative agents of pneumonia in neonates>
GBS (group B strep.), E.coli, Klebsiella, and staph. aureus.
A 2 year old child presents with a barking cough and sudden onset difficulty in breathing. CXR shows steeple sign with narrowing of the tracheal air column at the larynx and distension of the hypopharynx.
Croup. Often caused by viral laryngotracheobronchitis.
Treat with oral steroids to reduce inflammation.
9 month old infant from a developing country presents with irritability, neck rigidity and is afebrile. Upper lobe consolidation.
Mycobacterium tuberculosis. (notifiable disease)!!
Treat with Isoniazid, rifampicin and pyrazinamide for 4 months, followed by 2 months of isoniazid and rifampicin.
New born full-term infant presents with severe breathing difficulties following birth. CXR shows dextrocardia.
diaphragmatic hernia????
What is a pulmonary embolism?
Blockage of a pulmonary artery by a blood clot, fat, tumour or air.
What is a pulmonary infarction?
Compromisation of blood flow and oxygen to lung tissue, resulting in tissue death.
Clinical presentation of DVT?
swollen, hot, red, tender leg or calf.
Investigation of DVT.
Ultrasound Doppler scan of leg.
OR 2nd. CT scan of ileo-femoral veins, IVC and pelvis.
What may large pulmonary emboli cause?
Cardiovascular shock, low BP, central cyanosis, sudden death.
What may medium pulmonary emboli cause?
Pleuritic pain, haemoptysis and breathlessness.
What may small recurrent pulmonary emboli cause?
Progressive dyspnoea, pulmonary hypertension and right heart failure.
Risk factors for DVT?
Thrombophilia, contraceptive pill, smoking, HRT, pregnancy, pelvic obstruction and trauma (RTA).
Surgery, immobility (flights), malignancy, pulmonary hypertension/vasculitis and obesity.
How does pulmonary embolism typically present?
shortness of breath, chest pain, haemoptysis, leg pain/swelling and collapse/sudden death.
Signs of pulmonary embolism.
Tachycardia, tachypnoea, cyanosis, fever, low BP, crackles, pleural rub, pleural effusion.
ABGs: low PaO2, low SaO2 (type 1 resp. failure).
CXR: basal atelectasis, consolidation, pleural effusion.
Investigation and diagnosis of PE.
ECG: acute right heart strain, T wave inversion in V1-3. Raised D-dimers. Ventilation/perfusion scan. CT pulmonary angiogram. Consider ultrasound of leg and pelvis. Echocardiogram.
Prevention of DVT.
Early mobilisation post-op.
Compression stockings.
Calf muscle exercises.
Subcutaneous low dose low mol. wt heparin post op.
Anticoagulant: dabigatran, rivaroxaban/apixaban.
Pulmonary hypertension.
Mean pulmonary arterial pressure>25mmHg.
Causes of pulmonary venous hypertension.
Pulmonary venous hypertension (left heart disease):
- LVSD - ischaemic
- Mitral regurgitation/stenosis.
- cardiomyopathy
Causes of pulmonary arterial hypertension.
Hypoxia- COPD, pulmonary fibrosis, obstructive sleep apnoea.
Multiple PE.
Vasculitis.
Drugs.
HIV
Cardiac left-to-right-shunt (ASD and VSD).
Primary pulmonary hypertension.
Define cor pulmonale.
Right heart disease secondary to lung disease. Causes fluid retention due to hypoxia (+/- right heart failure).
May, e.g. be secondary to COPD.
Clinical signs of pulmonary hypertension and right heart failure.
Central cyanosis if hypoxic, oedema, raised JVP with v waves, RV heave at left parasternal edge, tricuspid regurgitation and loud P2.
Liver may be enlarged or pulsatile.
Investigation of pulmonary hypertension.
ECG, CXR, SaO2 and ABGs. Pulmonary function inc. DLCO. Echocardiogram, Cardiac catheterisation. D dimers and VQ scan if suspected PE. CT pulmonary angiogram. Cardiac MRI
Treatment of pulmonary hypertension.
Anticoagulation, O2 if hypoxic, pulmonary vasodilators (Ca2+ channel blockers), lung transplant.
Define pulmonary oedema.
Pulmonary oedema is the accumulation of fluid in the lung (interstitium and alveolar spaces). It causes a restrictive pattern.
What might cause pulmonary oedema?
Increased hydrostatic pressure, injury to alveolar cells e.g. pneumonia, ARDS.
What is ARDS?
Adult respiratory distress syndrome, aka shock lung. Can be caused by sepsis, diffuse infection (virus, mycoplasma), severe trauma, oxygen.
Outcome of ARDS.
Death, resolution and fibrosis (chronic restrictive lung disease).
Neonatal RDS.
Occurs in premature infants, due to a deficiency in surfactant (type 2 alveolar lining cells). They require increased effort to expand lungs, causing physical damage to cells.
Cor pulmonale
Pulmonary hypertension, complicating lung disease. Signs: RV hypertrophy, RV dilation, RH failure (swollen legs, congested liver etc).
What conditions may cause transudate pleural effusion?
Low protein = transudate.
Cardiac failure or hypoproteinaemia.
What conditions may cause exudate pleural effusion?
Exudate = high protein.
Pneumonia, TB, connective tissue disease, malignancy.
Define respiratory failure.
Gas exchange in the lungs is unable to meet metabolic demand. Type 1 and Type 2.
Examples of type 1 respiratory failure.
Hypoxic conditions: Pneumonia, asthma, pneumothorax, PE, pulmonary fibrosis.
Examples of type 2 respiratory failure.
Hypercapnic conditions: COPD, respiratory muscle weakness, pulmonary oedema.
CO2 retention headache.
Characteristically on wakening, doesn’t change with posture, feels like a “thick head”, similar to hangover.
May feel drowsy/dizzy, SOB, increased HR and BP, sweaty.
Sleep apnoea.
Episodic, awakens from sleep- poor quality, daytime somnolence (drowsiness), and early morning headache.
Obesity hypoventilation.
Snores, dramatic drop in VT, PO2 falls and pCO2 rises steadily causing high CO2 in mornings -> headache.
CXR of acute pulmonary oedema.
Possible: cardiomegaly, upper lobe venous distension, pleural effusion, Kerley B lines, Bat wing opacity (perihilar patchy opacification).
73 y/o male, acute presentation with breathlessness and coughing up frothy pink sputum. Several day history of orthopnoae, PND, and ankle oedema.
Upon examination you find fine bilateral inspiratory crackles at the bases and midzones. Raised JVP and HR of 10.
What is the diagnosis and what might an ECG show?
Acute pulmonary oedema.
Left bundle branch block.
Define stridor.
Stridor is predominantly an inspiratory wheeze due to obstruction of the large airways (larynx/trachea/major bronchi).
Causes of stridor in children.
Infection, foreign body inhalation, anaphylaxis/angioneurotic oedema, burns etc.
Causes of stridor in adults.
Neoplasms, anaphylaxis, goiter, trauma, bilateral vocal cord palsy etc.
Investigation of stridor
Laryngoscopy - NOT in acute epiglottitis. Bronchoscopy. Flow volume loop CXR CT, thyroid scan etc.
Treatment of laryngeal obstruction?
Removal of foreign body/treatment of underlying cause, e.g. anaphylaxis.
Mask bag ventilation with high flow O2.
Cricothyroidotomy.
Tracheostomy.
Treatment of anaphylaxis.
IM adrenaline/epinephrine. IV antihistamine IV corticosteroid High flow O2 NEbulised bronchodilators. Endotracheal intubation
What causes snoring?
Relaxation of pharyngeal dilator muscles during sleep, causes upper airway narrowing, turbulent airflow and vibration of the soft palate and tongue base.
What is obstructive sleep apnoea?
Intermittent upper airway collapse when sleeping, may cause hypoxia, recurrent arousals/sleep fragmentation.
Risk factors for sleep apnoea.
Obesity, enlarged tonsils, hypothyroidism, alcohol, opiates, benzodiazepines.
Consequences of sleep apnoea.
Raised CRP, impaired endothelial function, impaired glucose tolerance, increased risk of cardiovascular events.
Diagnosis of sleep apnoea.
Snoring and raised Epworth score.
Overnight sleep study (oximetry, domicillary recording, full polysomnography).
Treatment of sleep apnoea.
Remove underlying causes.
CPAP: continuous positive airway pressure.
