Respiratory Flashcards
What is COPD?
Non-reversible, long-term deterioration in air flow through the lungs caused by damage to lung tissue.
Explain the pathophysiology of COPD.
Damage to lung tissue causes air flow obstruction, making it difficult to ventilate the airways and making them more prone to developing infections.
What are the types of COPD?
Chronic bronchitis and emphysema.-Also A1AT deficiency.
Explain the dyspnoea scale.
1 - Breathless of strenuous exercise.
2 - Breathless walking up hill.
3 - Breathless on flat land.
4 - Stop to catch breath after walking 100m on flat land.
5 - Unable to leave house due to breathlessness.
What are two risk factors for COPD?
Smoking and air pollution.
Describe the pathophysiology of chronic bronchitis.
Hypertrophy and hyperplasia of mucous glands, chronic inflammation cells infiltrate bronchi.
Describe the pathophysiology of emphysema.
Destruction of elastin layers in ducts, alveoli and respiratory bronchioles.
-Air is trapped distal to blockage, causing bullae.
Describe the pathophysiology of A1AT deficiency.
What is the inheritance pattern and history?
Autosomal dominant inheritance - no smoking history.-A1AT usually degrades NE which protects elastin, no A1AT means no NE is active and elastin is damaged.
How does COPD present?
Older patient with chronic productive cough (sputum) and SOB.
-Wheezing and recurrent respiratory infections.
Which investigations are used for COPD? What are the results?
Spirometry - Obstructive (FEV1/FVC < 0.7).
Test for reversibility with b2 agonists:
-Large response - Asthma.
-Small/no response - COPD.
CXR and TLCO.
What is the long term management of COPD? (3 lines).
Smoking cessation and flu/pneumonia vaccines.
1st line - SAB2A (salbutamol).
2nd line - SAB2A, LAB2A and LAM3A.
3rd line - SAB2A, LAB2A, LAM3A, ICS.
How is severe COPD managed?
Long term oxygen therapy.
What usually causes exacerbation of COPD?
Viral or bacterial infections.
How is COPD exacerbation managed at home?
Prednisolone, inhalers/nebulisers and antibiotics if evidence of infection.
How is COPD exacerbation managed in hospital?
Nebulised bronchodilators, steroids, antibiotics and ventilation.
What is asthma?
Chronic inflammatory condition of the airways that causes episodic exacerbations of bronchoconstriction.
Explain the pathophysiology of asthma.
Reversible airway obstruction that typically responds to bronchodilators (salbutamol).
-Bronchoconstriction causes an obstruction of airflow in the lungs.
What is the atopic triad?
Atopic rhinitis, asthma and eczema.
What are four risk factors for asthma?
History of atopy, low birth weight, not breastfed and exposure to allergens.
What are the types of asthma?
Allergic and non-allergic.
-Allergic - IgE mediated T1 hypersensitivity due to environmental trigger.
-Non-allergic - Non IgE mediated, usually due to smoking.
What are eight triggers for asthma?
Infections, early night/late night, exercise, animals, cold, dust, strong emotions and drugs (beta-blockers).
How does asthma typically present?
Episodic symptoms of dry cough, wheeze (bilateral widespread polyphonic) and SOB that is usually worse at night.
-Young patient with history and family history of atopy.
What are the investigations for asthma?
FeNO - Increased conc, in breath means inflammation.Spirometry with bronchodilator reversibility.Reduced FEV1, normal FVC. FEV1/FVC < 0.7.
What is the acute management of asthma?
O SHIT ME:
Oxygen, salbutamol (SABA), hydrocortisone, ipratropium bromide, theophylline, IV MgSO4, escalate.
Describe the long term management of asthma. (5 lines).
1st line - SAB2A.
2nd line - SAB2A and ICS
.3rd line - SAB2A, ICS and LTRA.
4th line - SAB2A, ICS, LTRA and LAB2A.
5th line - Increase ICS dose.
Explain the drugs used in asthma.
-SAB2A - Short acting beta-2 agonists (salbutamol): Used as a reliever - cause bronchodilation.
-ICS - Inhaled corticosteroids (beclomethasone): Reduce inflammation in airways - preventer.
-LTRA - Leukotriene receptor antagonists (montelukast): Block leukotrienes which cause inflammation and bronchoconstriction.
-LAB2A - Long acting beta-2 agonists (salmeterol): Same as SAB2As but longer action.
-LAMA -long acting antimuscarinics (tiotropium): Block Ach receptors - bronchodilation.
What is pneumonia?
Infection of the lung tissue which causes inflammation and sputum which fill the airways and alveoli.
How does pneumonia appear on XRAY?
Consolidation.
How is pneumonia classified?
Community (CAP) - Outside of hospital.
Hospital (HAP) - 48h after hospital admission.
Aspiration - As a result of aspirating foreign material like food.
What are five risk factors for developing pneumonia?
Immunocompromised, IVDU, pre-existing respiratory disease, very young/old.
What is the cause of pneumonia?
Typically can bacterial but can also be viral and fungal.
-Flu virus.
-PCP - P, jirovecci (aids defining illness).
What are the organisms that cause CAP? What is the most common? Which are atypical?
S. pnuemoniae (mc), H. influenzae.
-Mycoplasma pnuemoniae and legionella - atypical pneumonia.
What are the organisms that cause HAP?
Pseudomonas, E.coli, klebsiella and MRSA.
What is atypical pnuemonia?
Pneumonia caused by an organism that cannot be cultured in the normal way or detected using a gram stain.
-Don’t respond to penicillin so treated with macrolides (e.g. clarithromycin), fluoroquinolones (e.g. levofloxacin) or tetracyclines (e.g. doxycycline).
-Cause dry cough.
How does pneumonia present?
Productive cough (sputum) with SOB and fever.
-Pleuritic chest pain and haemoptysis.
-Sepsis.
How does atypical pneumonia present?
Dry cough and low grade fever.
What are six signs of pneumonia?
Tachypnoea, tachycardia, hypoxia, hypotension, fever, confusion.
What is the first line investigation of pneumonia?
CXR with consolidation.
What are other investigations for pneumonia?
Bloods - FBC which shows raised WCC. Raised CRP.
What are investigations for severe pneumonia?
Sputum sample and blood culutres.
How is pneumonia severity assessed?
CURB65:
-Confusion.
-Urea > 7.
-RR > 30.
-BP <90/60 mmHg.
-65+ years old.
Why is pneumonia severity assesssed?
Predictor of mortality and guides treatment - home, hospital or ICU.
What is the management for pneumonia?
Analgesia for pain.
Broad spectrum antibiotics - dependent on bacteria and severity.
How is CAP treated?
CURB 0-2 - Amoxicillin.
CURB 3-5 - Co-amoxiclav and clarythromycin.
How is HAP treated?
IV co-amoxiclav and gentamicin.
What are five complications of pneumonia?
Sepsis, pleural effusion, empyema, lung abscesses and death.
What is tuberculosis?
Infectious granulomatous creating disease caused by the mycobacterium tuberculosis bacteria.
How is TB spread?
Airborne.
Is TB common in the UK?
No, more prevalent in non-UK born patients who are immunocompromised.
Where is TB common in the world?
South Asia and Sub-Saharan Africa.
What are four risk factors for TB?
Country/travel, immunocompromised, homeless/crowded housing, IVDU.
What is the difference between active and latent TB?
Active - Active infection in various areas of the body.
Latent - Infection is confined to granulomas but is still alive.
What is secondary TB?
When latent TB reactivates into active infection.
How is TB stained?
Stained via Zeihl-Neelsen stain to bright red due to acid-fastness (resistant to acids in staining procedure).
What is the presentation of latent TB?
Asymptomatic.
What is miliary TB?
When the immune system is unable to control the disease.
What is extrapulmonary TB?
When the TB spreads to other areas.
How does TB usually present?
Fever and night sweats, lethargy, weight loss, cough, haemoptysis.
What are the investigations for TB?
3 sputum cultures with positive Zeihl-Neelsen stains.
-Mantoux test = looks for previous immune response to TB.
CXR.
Describe the Mantoux test.
Tests for previous immune response to TB.
-Tuberculin injected into skin, the bleb is measured and if it is bigger than 5mm it is positive.
-Then test for active disease.
What is the management of latent TB?
Isoniazid and rifampicin for 3 months.
OR:
Isoniazid for 6 months.
What is the management of active TB?
RIPE:
-Rifampicin for 6 months.
-Isoniazid for 6 months.
-Pyrazinamide for 2 months.
-Ethambutol for 2 months.
What are the side effects of active TB treatment?
Rifampicin - Red/orange urine and tears.
Isoniazid - Peripheral neuropathy.
Pyrazinamide - Hepatitis and gout (hyperuricaemia).
Ethambutol - Colour blindness and reduce visual acuity.
-All cause hepatotoxicity.
What is cystic fibrosis?
An autosomal recessive condition affecting the mucous glands.
Describe the genetics of cystic fibrosis.
Mutation on chromosome 7 in the CFTR gene.
-Autosomal recessive inheritance.
Describe the epidemiology of cystic fibrosis.
1 in 25 are carriers, 1 in 2500 children have it.
What is the prognosis for cystic fibrosis?
Median life expectancy is 47y.
-90% develop pancreatic insufficiency.
-50% develop diabetes.
-30% develop liver disease.
What are two risk factors for cystic fibrosis?
Family history and white.
Explain the pathophysiology of CF.
The CFTR gene normally secretes chloride and sodium ions into ductal secretions to make them thin and watery.
-This gene is defective so secretions become thicker with increased chloride and sodium ion retention.
How does CF first present in neonates?
Meconium ileus - earliest stool that is too thick and sticky to pass through the bowel - causing a bowel obstruction and N+V.
What are four symptoms of CF?
Thick sputum with chronic cough, recurrent upper respiratory tract infections, steatorrhoea, salty sweat/saliva.
What is a sign of CF in males?
Bilateral absence/atrophy of vas deferens and epididymis resulting in infertility.
How is CF diagnosed in newborns?
Newborn heel prick test.
What is the gold standard investigation for CF?
Sweat test - chloride concentration is measured. Above 60mmol/L is positive.
How is CF investigated during pregnancy?
Amniocentesis or chorionic villous sampling - genetic testing for CFTR gene.
Why is there recurrent respiratory infections in people with CF?
As patients struggle to clear secretions, there is a perfect environment for microbial colonisers.
What are five common colonisers in people with CF?
S. aureus, pseudomonas, H. influenzae, E. coli, klebsiella.
What is a leading cause of mortality in people with CF and why?
Pseudomonas infection - resistant to antibiotics.
What are four conservative management options of CF?
Chest physiotherapy, exercise, high calorie diet and no smoking.
Explain four medications used in CF.
-Replacing pancreatic enzymes.
-Prophylactic flucloxacillin to reduce risk of infection.
-Bronchodilators (salbutamol).
-Nebulised DNase - making secretions less thick and easier to clear.
Explain the monitoring in CF.
Check ups every 6 months to check for bacteria such as pseudomonas.
-Screening for diabetes, osteoporosis, vitD deficiency and liver failure.
What is bronchiectasis?
Permanent dilation of bronchi/bronchioles with excessive mucous in them.
What are three risk factors for bronchiectasis?
Post infection (pneumonia, TB), CF, HIV.
Explain the pathophysiology of bronchiectasis.
Irreversible dilation, loss of cilia and mucous secretions - increased risk of infection as decreased mucociliary clearance.
How does bronchiectasis present?
SOB with a productive cough and haemoptysis.
-Recurrent chest infections.
What are the investigations for bronchiectasis?
HRCT (GS) and XRAY - shows dilated, thickened bronchi.
What is pleural effusion?
Excess fluid accumulation between visceral and parietal pleural layers.
What are the types of fluid in pleural effusion?
Exudative or trasudative.
Describe exudative fluid in pleural effusion. What causes it?
High protein count due to inflammation causing increased vascular permeability (cloudy fluid).
-Due to lung cancer, TB, pneumonia, RA.
Describe transudative fluid in pleural effusion. What causes it?
Low protein count due to increased hydrostatic or decreased oncotic pressure (clear fluid).
-Due to CHF, hypoalbuminaemia, hypothyroidism.
What is empyema?
Infected pleural effusion.
How does pleural effusion present?
SOB with pleuritic chest pain, cough and decreased breathing sounds.
-Dull percussion.
What is the GS and 1st line investigation for pleural effusion? What does it show?
CXR - shows blunting of costophrenic angles, excess fluid and tracheal deviation.
What is another investigation for pleural effusion?
Thoracocentesis - sample of pleuritic fluid.
-Testing for protein count, WCC, pH, glucose, LDH and microbiology.
What is the management of pleural effusion?
If small - conservative, treat underlying cause.
Larger - aspiration or chest drain.
What is pneumothorax?
Punctured lung - occurs when air gets into pleural space, separating the lungs from the chest wall.
What is the typical patient in pneumothorax?
Young, tall, thin young man with sudden breathlessness and pleuritic chest pain.
What is the difference between simple and tension pneumothorax?
Simple - Air can flow in and out, doesn’t worsen with each breath.
Tension - Medical emergency, one way valve with air only into pleural space and not out. Worsens with each breath.
What are the primary causes of penumothorax?
Sponteanous.
What are three secondary causes of pneumothorax?
Trauma, iatrogenic, lung pathology.
How does pneumothorax present?
SOB with one sided sharp pleuritic chest pain with decreased breathing sounds.
What is the GS and 1st line investigation of pneumothorax?
CXR - shows area between lung and chest wall with no lung markings.
What is the management of simple pneumothorax?
If small (and no SOB) it will self heal.
-Larger = Aspiration. If this fails twice - chest drain.
Why is tension pneumothorax dangerous?
Creates large pressure in thorax which pushes the mediastinum across and can cause cardiorespiratory arrest.
What are four signs of tension pneumothorax?
Tachycardia, hypotension, reduced air entry to affected side, tracheal deviation away from side of pneumothorax.
What is the management of tension pneumothorax?
Insert a large bore cannula into the second intercostal space in the midclavicular line.
Where is the triangle of safety? What is the significance?
This is where chest drains are inserted.
-Triangle is formed by:
5th intercostal space.
Mid axillary line.
Anterior axillary line.
Where are needles inserted in relation to the rib?
Just above the rib to avoid the neurovascular bundle.
What is a pulmonary embolism (PE)?
An embolus typically from a DVT that blocks pulmonary artery circulation.
What are the risk factors for PE?
Virchow’s triad:
-Venous stasis - Immobility, post-surgery, varicose veins, AF.
-Hypercoagulability - Pregnancy, obesity, malignancy, inherited diseases.
-Endothelial injury - Smoking, hypertension, trauma, catheters.
How does a PE present?
SOB with or without blood (haemoptysis) and pleuritic chest pain.
-Tachycardia, raised RR.
-Signs of DVT (unilateral swollen red calf).
-History of immobility.
What are the first investigations for PE?
Perform a Well’s score:
-If >4 and likely a PE, send for a CTPA.
-If unlikely, perform D-dimer and if positive do a CTPA.
What other investigations are there for PE?
DUSS of leg - DVT.
ECG - S1Q3T3:
-S waves in lead I, Q waves in lead III, T waves inverted in lead III.
What is the prophylaxis for VTE?
If increased risk - LMWH and compression stocking (CI - PVD).
What is the supportive management for PE?
Analgesia, oxygen and monitoring.
How is PE treated if patient is haemodynamically stable?
Anticoagulation - DOAC, LMWH, warfarin.
How is PE treated if patient is haemodynamically unstable?
Thrombolysis with alteplase.
What are the options for long term anticoagulation for PE?
Warfarin or DOACs.
-LMWH if pregnant or cancer.
What does low pO2 indicate?
Hypoxia and respiratory failure.
What is the difference between type 1 and type 2 respiratory failure?
Type 1 - Low pO2 and normal pCO2.
Type 2 - Low pO2 and high pCO2.
What is the difference between hypoxia and hypoxemia?
Hypoxia - Low oxygen levels in tissues.
Hypoxemia - Low oxygen levels in blood.
What are interstitial lung diseases?
Umbrella term to describe conditions that affect the lung parenchyma causing inflammation and fibrosis.
How are interstitial lung diseases diagnosed?
HRCT showing ground glass and lung biopsy for histology.
What is pulmonary fibrosis?
Scarring of lung tissue - most common interstitial lung disease commonly seen in smoking older men.
What are the risk factors for pulmonary fibrosis?
Smoking, occupational (dust, coal), drugs (methotrexate) and viruses (EBV, CMV).
How does pulmonary fibrosis present?
Exertional dyspnoea and dry unproductive cough.
What are the investigations for pulmonary fibrosis?
Spirometry shows restriction (FEV1:FVC > 0.7 but FVC < 0.8.
HRCT (GS) - Ground glass.
Inspiratory crackles and finger clubbing.
What is the management of pulmonary fibrosis?
Smoking cessation and vaccines.
-Pirfenidone (antifibrotic and anti-inflammatory).
-Nintendanib (monoclonal antibody against TK).
LR - Lung transplant.
What is sarcoidosis?
Idiopathic granulomatous disease.
What is hypersensitivity pneumonitis?
T3 hypersensitivity - immune antigen-antibody complex deposition at lung tissues.
What causes hypersensitivity pnuemonitis?
Mostly occupation:
-Farmer’s lung (mouldy hay) pigeon fancier’s lung (shite).
How is hypersensitivity pneumonitis treated?
Remove allergen.
What is asbestosis?
Inhalation of asbestos which is fibrogenic and oncogenic.
-Results in lung fibrosis and mesothelioma.
What is Goodpasture’s syndrome?
T2 autoimmune hypersensitivity response where anti-GBM autoantibodies attack lungs and kidneys - pulmonary fibrosis and glomerulonephritis.
Which four drugs cause interstitial lung disase?
Amiodarone, cyclophosphamide, methotrexate and nitrofurantoin.
What is the third most common cancer in the UK?
Lung cancer.
What is the biggest cause of lung cancer?
Smoking.
Are primary or secondary lung tumours more common?
Secondary lung tumours much more common.
Why is secondary lung cancer more common than primary?
As all blood travels to the lungs so it spreads easily there.
What is cancer of the pleura?
Mesothelioma.
What leads to mesothelioma?
Linked to asbestos with very large latent period (up to 45y).
What are the main two types of lung parenchyma cancer? How common are they?
Non-small cell (85%), small cell (15%).
Describe the types of non-small cell lung cancer.
Adenocarcinoma (40%), squamous (20%), large cell carcinoma (10%), other (10%).
What are five risk factors for lung cancer?
Smoking, asbestos, coal, ionising radiation, underlying lung disease.
How does lung cancer present?
SOB with chest pain, cough and haemoptysis and recurrent pneumonia.
-Cancer symptoms - weight loss, TATT, night fever/sweats, pain.
What are the first line and diagnostic investigations for lung cancer?
1st line - CXR and CT.
Diagnostic - Bronchoscopy and biopsy. Confirms type.
What is another investigation to investigate lung cancer?
MRI/PET scan for TNM staging.
Describe small cell lung cancer.
15% of lung cancer - Contain neurosecretory granules that can release neuroendocrine hormones - paraneoplastic syndromes.
What is the management of small cell lung cancer? What is the prognosis?
Chemotherapy and radiotherapy - prognosis is generally worse than NSCLC.
What is the management of non-small cell lung cancer?
Surgery - lobectomy.
Radiotherapy can be curative.
Chemotherapy can improve quality of life and survival.
Which three paraneoplastic syndromes can small cell lung cancer cause?
SIADH due to ectopic ADH.
Cushing’s disease due to ectopic ACTH.
Lambert Eaton syndrome.
What can squamous cell carcinoma in the lung cause?
Hypercalcaemia caused by ectopic PTH.
What are four extrapulmonary manifestations of lung cancer?
-Recurrent laryngeal nerve palsy causing hoarse voice.
-Phrenic nerve palsy - diaphragm weakness and SOB.
-SVC obstruction - facial swelling, SOB and distended veins.
-Horner’s syndrome - Triad of partial ptosis, anhidrosis and miosis. Tumour on pulmonary apex pressing on sympathetic ganglion (Pancoast’s tumour).
What is pulmonary hypertension?
Increased resistance and pressure of the blood in the pulmonary arteries.
Describe the pathophysiology of pulmonary hypertension.
This increases strain on the right side of the heart causing a back pressure of blood into the systemic venous system resulting in cor pulmonale.
What are the five types of pulmonary hypertension?
Group 1 - Primary pulmonary htn.
Group 2 - Left heart side failure due to MI or systemic hypertension.
Group 3 - Chronic lung disease (COPD).
Group 4 - Pulmonary vascular disease (PE).
Group 5 - Miscellaneous disorders.
How does pulmonary hypertension present?
SOB and fatigue.
-Syncope, tachycardia, raised JVP, hepatomegaly, peripheral oedema.
What is the gold standard investigation for pulmonary hypertension?
Right heart catheter to measure pressure.
Describe the ECG and CXR changes in pulmonary hypertension.
CXR - Dilated pulmonary arteries and RVH.
ECG - RBBB, right axis deviation, RVH.
What is the prognosis of pulmonary hypertension?
Poor - 35% 5 year survival, 65% 5 year survival with treatment.
What is pharyngitis?
Inflammation of pharynx with or without exudate.
What are the causes of pharyngitis?
Viral (EBV, adenoviruses), bacterial (group A strep).
How does pharyngitis present?
Sore throat and fever.
-Viral = Cough and congestion.
-Bacterial = Exudate.
What is sinusitis?
Inflamed mucosa of nasal cavity and sinuses.
What are the causes of sinusitis, how does it present and how is it treated?
Mostly viral, bacterial is S. pneumoniae and H. influenzae.
-Nasal discharge, fever, sore throat.
-Self-limiting.
What is otitis media? How is it diagnosed?
Inflamed middle ear typically in children.
Otoscopy shows inflamed erythematous tympanic membrane.
What is epiglossitis?
Inflammation of epiglottis which obstructs the airway.
How does epiglossitis present?
Young child with sore throat, SOB and tripoding (leaning forward and mouth open, tongue out).
How is epiglossitis diagnosed?
GS - Laryngoscopy.
What is whooping cough? Who does it affect?
Chronic cough caused by Bordetella pertussis.
-Pertussis toxin inhibits alveolar macrophages.
Affects mostly children - characteristic whoop in cough.
What is croup?
Occasional complication of URTI particularly parainfluenza and measles.
How does croup present and how is it treated?
Hoarse voice with barking cough and stridor.
-Single dose dexamethasone.
