Respiratory Flashcards
Describe FEV1 and FVC in terms of restriction and obstruction
FEV1 / forced expiratory volume - maximum inspiration exhaled as fast as possible. Healthy should be 80% of vital capacity, assessment of lung health
FVC / forced vital capacity - total amount of air expired. Compared to predicted values should be at least 80%
Low forced vital capacity = airway restriction (FEV1 / FVC normal) (entire lungs less)
Parenchyma / chest walls - interstitial lung disease (fibrosing alveolitis, sarcoid)
FEV1 / FVC < 0.7 = airway obstruction (can’t breath out fast), FVC normal
Airways - asthma, COPD obstructive
Describe type 1 and 2 respiratory failure
Type 1 respiratory failure: partial CO2 is low or normal, gas exchange is impaired at level of alveolar-capillary membrane
Pulmonary oedema, pneumonia, asthma, acute respiratory distress syndrome
Type 2 respiratory failure: partial CO2 is high, is due to respiratory pump failure
COPD, Guillain-Barre, opioid overdose
(Type 1 has 1 change (low pO2) type 2 has 2)
Pathophysiology of COPD and common associations
Cigarette smoking major cause (m gland hypertrophy), also chronic exposure to pollutants (working in building, chemicals, cooking), alpha1 antitrypsin causes early onset (proteolytic lung damage)
Increased number of mucus secreting goblet cells especially in larger bronchi, in advanced cases bronchi become inflamed with pus in the lumen
V/Q mismatch leads to fall in PaO2, CO2 excretion less effected, long term insensitivity to CO2 and start relying on hypoxaemia to breathe. Due to risk of hypercapnia have to be careful giving oxygen (target of 88-92%, 94-98 if pCO2 normal)
Associated with chronic bronchitis: hypertrophy and hyperplasia of mucus glands, wall inflammation (infiltration) and mucosal oedema. Inflammation causes scarring and thickening of walls
Also emphysema: dilation and destruction of lung tissue distal to terminal bronchioles, causes loss of elastic recoil, expiratory limitation and airway trapping (premature closing of airways)
Presentation of COPD
Productive cough with white or clear sputum, wheeze, breathlessness, frequent cold and infections, symptoms worsened by cold weather
Usually following many years of smokers cough
Signs: tachypnoea, accessory muscles, hyperinflation, reduced chest expansion, resonant percussion, quiet breath sounds, wheeze, cyanosis, cor pulmonale
Systemic: hypertension, osteoporosis, depression, weight loss, general weakness
Investigations for COPD
Lung function: airway obstruction - FEV1/FVC < 0.7, FEV less than 80% of predicted
FEV1 shows GOLD stages: 1 80%, 2 - 50-79%, 3 - 30-49%, 4 - <30%
Will have little response to salbutamol
Chest x ray (hyperinflation, flat hemidiaphragms, large pulmonary arteries, bullae), CT - emphysema, ABG, alpha1 antitrypsin test, FBC (chronic hypoxia - polycythaemia)
Cor pulmonale - pathophysiology, causes, signs and symptoms
Right sided heart failure caused by respiratory disease, increased pressure + resistance in pulmonary arteries limits RV → back pressure into RA, vena cava and venous system
Causes: COPD, PE, interstitial lung disease, CF, primary pulmonary hypertension
Sx: SOB, peripheral oedema, breathless on exertion, syncope, chest pain
Signs: hypoxia, cyanosis, raised JVP, peripheral oedema, parasternal heave, loud S2 heart sound, murmur (pan systolic tricuspid regurgitation), hepatomegaly
What is the pathogenesis of asthma
Narrowing airways (obstruction) due to smooth muscle contraction (bronchoconstriction), thickening of airway walls (inflammation, cellular infiltration), increased mucus secretions in lumen
Atopic: hypersensitive IgE response to environmental triggers, mast cells become sensitised when IgE bind and respond when allergens present. Histamine released (bronchoconstriction), cytokines - more mast cells and attract eosinophils
Chronic asthma - airway smooth muscle hypertrophy and hyperplasia, further thickening due to deposition of collagens and matrix proteins, epithelium is damaged - loss of ciliated columnar cells
Presentation of asthma
Episodic wheeze + dyspnoea, cough (especially nocturnal), provoking factors, classically diurnal (often worse at 3-4am). 50% have reflux - treating can improve lung function
Signs: tachypnoea, (widespread, polyphonic, expiratory) wheeze, hyperinflation, hyperresonant percussion, reduce air entry, prolonged expiration
During attacks: progressive dyspnoea, use of accessory muscles, tachypnoea, symmetrical expiratory wheeze, reduced air entry. Severe unable to speak, tachycardia, confused
Investigations for asthma
Lung function test: > 12% improvement in PEFR or FEV1 with bronchodilator, reduced FEV1, FEV:FVC <0.7. Fractional exhaled nitric oxide > 40 ppb (airway inflammation)
Peak flow diary: twice daily over 4w, more than 20% is positive
Direct bronchial challenge testing (opposite of reversibility): inhaled histamine / methacholine, reduction in FEV1 by 20%
Severity: RCP3 - recent nocturnal waking? Usual daily asthma symptoms? Interferences with activities of daily living
How is severity of an asthma attack worked out
Moderate PEFR 50-75%, RR < 25, pulse < 100
Severe attack: PEFR 33-50%, inability to complete sentence, pulse > 110, RR > 25
Life threatening attack ACHEST: altered conscious, PaCO2 normal (cyanosis), hypoxia (<92%), exhaustion, silent chest, threatening PEFR < 33%
Management of asthma and asthma attacks
Maintenance: SABA reliever, low dose ICS preventer (beclomethasone); + LTRA (montelukast) (if not enough consider stopping); + LABA fixed dose with ICS (beclometasone/formoterol) or MART (also includes salbutamol) regime; moderate dose ICS; specialist therapies (high dose ICS< LAMA, theophylline, biologicals)
Children 5+ treated the same, stop LTRA if not helping
<5: SABA, + trial of moderate ICS, SABA + low ICS + LTRA, stop LTRA and refer
Intermittent reliever SABA - salbutamol, regular maintenance ICS - beclomethasone (cleanil), initial add on LTRA - montelukast, LABA - salmeterol instead of montelukast
Life threatening: oxygen 15L non breathe, nebulised salbutamol, oral prednisolone (5d following), no response - nebulised ipratropium bromide, IV magnesium sulphate / salbutamol / aminophylline
Pathogenesis of lung cancers
Cigarette smoking accounts for 80%, also occupational (asbestos, coal, chemicals)
Asbestos causes mesothelioma: pleura, latent period, very aggressive
Small cell carcinoma (20%): from endocrine (Kulchitsky) cells, secretes polypeptide hormones - paraneoplastic syndrome (PTH, ADH, ACTH), high grade and aggressive.
Lambert eaton myasthenic syndrome caused by antibodies against small cell
Non-small cell: adenocarcinoma (mucus gland, 40%) usually single lesion, metastases common; squamous (keratin producing epithelium, 20%), frequently caviate with central necrosis; large cell carcinoma
Lungs are a common site for metastases (more common than primary)
Presentation of lung cancer
Local disease: cough (3 weeks merits CXR), SOB, breathlessness, haemoptysis, chest pain, recurrent infections, weight loss
Signs: finger clubbing, lymphadenopathy (subclavicular), cachexia, consolidation, pleural effusion
Metastatic disease: weight loss, bone pain, headache, seizures, neurological deficit, hepatic pain, abdominal pain
Extrapulmonary: recurrent laryngeal / phrenic nerve palsy, superior VC obstruction, paraneoplastic
Investigations + referral and management of lung cancer
X ray (hilar enlargement, peripheral opacity - round / fluffy, lung collapse, pleural effusion), contrast CT (or PET) to stage, bronchoscopy (assessment and biopsy), cytology, bloods - polycythaemia
Molecular testing used to find appropriate adjuvant chemotherapy
Referral criteria - 2w Xray: 40+ clubbing, lymphadenopathy, recurrent chest infections, thrombocytosis, chest signs
Recommend Xray if 2+ unexplained symptoms and never smoked, 1+ unexplained if smoke / asbestos exposure
Small cell: limited disease - combined chemo and radio, extensive - chemo (may respond but often relapses), palliative - endobronchial, pleural drainage, SVC stent if required
Non small cell: if no metastatic spread and peripheral - surgical excision, curative radio if respiratory reserve is poor, chemo +/- radio if advanced disease also monoclonal antibodies (cetuximab)
Pathophysiology of pulmonary embolism
Majority from lower DVT, also pelvic and abdominal veins; run to inferior vena cava, enter the right atrium and pulmonary circulation before lodging
Other causes: RV thrombus (post MI), septic emboli, fat (bone fracture), air, neoplastic, parasites, foreign material from IV drugs
Lung tissue is ventilated not perfused - intrapulmonary dead space, stops producing surfactant and alveoli collapse - hypoxaemia. Reduction in pulmonary area, increased resistance (and pulmonary pressure) so a reduction in cardiac output
Presentation of PE
Depends on number and size, small will often be asymptomatic. Sudden onset dyspnoea is often the only symptom
Dyspnoea, cough, haemoptysis, pleuritic chest pain, dizziness + syncope
Signs: hypoxia + cyanosis, tachycardia, raised respiratory rate, low grade fever, hypotension + haemodynamic instability, raised JVP, pleural rub, DVT
Investigations and scoring of PE
CT pulmonary angiogram + D-dimer (95% sensitive not specific), ventilation perfusion scan
X ray and ECG more to rule out others. Echocardiogram (RVHF) if CTPA not available
Blood gases - may be normal, significant will have arterial hypoxaemia/ type 1 respiratory failure - low PaO2 and CO2, respiratory alkalosis due to hyperventilation
Pulmonary embolism rule out criteria, Well’s score
Management of PE
Haemodynamically stable: apixaban / rivaroxaban FL, enoxaparin / dalteparin SL; continue for 3m
Haemodynamically unstable (hypotension): IV fluids, high flow oxygen, continuous infusion unfractionated heparin (start before thrombolysis), thrombolysis with IV alteplase, morphine
Surgical embolectomy, catheter thrombectomy, vena cava filter, ted stockings
Following: DOAC in most (apixaban), warfarin (INR 2-3) in antiphospholipid / severe CKD, LMWH in pregnancy
Prophylaxis: high risk give enoxaparin / dalteparin (LMWH), compression stockings
Pathogenesis of upper respitatory infections
Overcomes defence: commensal flora (sinuses should be sterile), swallowing, mucus and ciliated epithelium in lungs, cough + sneeze, immune cells + humoral
Viral most common, usually transient: rhinovirus, influenza A, coronavirus, adenovirus
Emergency: SARS, MERS, avian influenza
Most bacterial infections from commensals. Common: group A strep (throat), strep pneumoniae (sinusitis)
Whooping cough is caused by bordetella pertussis, multiple virulence factors (several toxins), lymphoid hyperplasia causes chronic inflammation
Catarrhal phase (1-2w): malaise, anorexia, rhinorrhoea, highly infectious. Paroxysmal (1-6w): coughing spasms terminating in vomiting, inspiratory whoop (only in younger)
Presentation and management of upper respiratory infections
Sore / inflamed: sinuses, pharynx, tonsils, larynx, middle ear
Common symptoms: cough, sore throat, runny nose, nasal congestion, headache, facial pressure
Strep throat: sudden onset, pain with swallowing, fever. No runny nose, cough, voice change
Viruses do not require treatment
Broad spectrum antibiotic given to high risk, or systemically unwell co-amoxiclav; strep throat: phenoxymethylpenicillin (pen V)
Whooping cough - clarithromycin
Management of URTI
Viruses do not require treatment
Broad spectrum antibiotic: co-amoxiclav; strep throat: phenoxymethylpenicillin (pen V)
Whooping cough - clarithromycin
Pathogenesis and presentation of pneumonia
Inflammation and pus in alveoli, acute bronchitis is infection of bronchi and bronchioles
Severe disease will result in excessive inflammation, lung injury, failure to resolve
Complications: respiratory failure, hypotension (dehydration and vasodilation due to sepsis), parapneumonic effusion + empyema, pleural effusion
Cough, purulent sputum production, dyspnoea, fever, generally unwell, haemoptysis, pleuritic chest pain, delirium, malaise, rigours
Signs: increased HR + RR, low BP, fever, hypotension; consolidation (lungs dull to percussion, decreased air entry, bronchial breath sounds), focal crackle / wheeze, increased vocal resonance, pleural rub. Hypoxia and respiratory failure if chronic
Investigations and indications of severity of pneumonia
Investigations: FBC (raised white cells), U+E (severity and other complications), urea, C-reactive protein, pulse oximetry + BP, sputum culture (+blood in severe), CXR
CXR: lobar / multilobar infiltrates, cavitation, pleural effusion
Indicators of severity / sepsis: proinflammatory cytokines (lead to reduced perfusion and tissue hypoxia), delirium, renal impairment, high respiratory rate, low blood pressure.
CURB65 (CRB 65 community) score uses to predict mortality and indicates severity / treatment
Confusion, urea > 7, resp rate > 30, BP < 90/60, age > 65. Urea = systemic / dehydration
Management of pneumonia
Treatment: mild - amoxicillin, moderate - amoxicillin plus clarithromycin, severe - IV co-amoxiclav and clarithromycin (or ceftriaxone). Penicillin allergen - clarithromycin or doxycycline. 5 days enough if moderate
Also depending on bacteria: H influenzae - amoxicillin, s aureus - flucloxacillin, kleb pneumoniae - co-amoxiclav
Hospital acquired: co-amoxiclav, piperacillin tazobactam for gram negative, ceftriaxone
Causes of atypical pneumonia
Atypical pneumonia (can’t use gram stain): mycoplasma pneumoniae, legionella pneumophila, chlamydia pneumoniae, chlamydia psittaci, coxiella burnetii
My legion chlamydia peeS - cox burnt
Pathogenesis of TB
Primary TB: first infection - droplet spread, macrophages take up and present antigen, T cells mediate response. Response is hypersensitive - tissue necrosis (cavities form) and granuloma formation. Initial granuloma and caveated areas become calcified and keep latent bacteria
Also primary lesions in GI tract, bacilli can be taken to lymph nodes - secondary lesions
Reactivation TB (majority of clinical cases): depression of host immune system (often elderly), in HIV this will occur in primary infection. Often spreads to GI, bone, CNS, pericardium, skin
Presentation of TB
Systemic presentation: weight loss (most predictive), low grade fever, anorexia, night sweats, malaise
Pulmonary TB: productive cough (more than 3 weeks), occasional haemoptysis, chest pain, breathlessness. Associated with consolidation, pleural effusion, pulmonary collapse
Extrapulmonary TB: lymph node swelling / discharge, bone (pain, swelling, potts disease), abdominal (ascites, abdominal lymph, ileal malabsorption), GI (epididymis, frequency, dysuria, haematuria), CNS (meningitis, raised ICP)
Diagnosis and management of TB
Diagnosis of active: non specific: anaemia, thrombocytosis, raised ESR + CRP, hypoalbuminaemia, hypercalcaemia, sterile pyuria; suggestive: histopathology - caseating granulomata; definitive: (microbiology) sputum, urine, CSF, pleural fluid
Diagnosing latent: can’t find dormant bacteria, test immune response with Mantoux tuberculin skin test. New interferon gamma release assays
Start with 4 drugs for 2 months (RIPE): rifampicin, isoniazid, pyrazinamide, ethambutol. Rifampicin and isoniazid carried on for further 4 months (6 total).
CNS TB requires 6 months of treatment
TB can be resistant to one or both (1%) rifampicin and isoniazid (7%), have to use older drugs: less effective (22 months) and worse side effects
Prevention: neonatal BCG vaccine - no longer routine but high risk groups. Detection in community
What are the causes of interstitial lung disease
Number of heterogeneous conditions that cause diffuse parenchymal lung disease, chronic inflammation, progressive interstitial fibrosis. TB, sarcoidosis, idiopathic pulmonary fibrosis, hypersensitivity pneumonitis, asbestosis, cryptogenic organising pneumonia
Presentation, investigations and management of idiopathic pulmonary fibrosis
Majority show usual interstitial pneumonitis: dry cough, exertional dyspnoea, no identifiable cause, fatigue
Bibasal fine end inspiratory crackles, finger clubbing (common in OSCEs)
Confirm presence of fibrosis: spirometry (FVC less than 80% but FEV1/FVC above 70%), high resolution CT shows typical ground glass appearance
Rule out other causes: bloods, ABG (severe has low CO2 and O2), CXR, lung biopsy
Oxygen, pirfenidone - slows rate of FVC decline, nintedanib (tyrosine kinase inhibitor) - interferes with proliferation / migration / differentiation
Monitor with lung function testing, lung transplant and pulmonary rehabilitation, palliative care
Presentation, investigations and managment of sarcoidosis
20-40% found incidentally (asymptomatic). Acute sarcoidosis: erythema nodosum (red lumps on shins / thighs / forearms) and polyarthralgia, fever, bilateral hilar lymphadenopathy, resolves
Respiratory: dry cough, progressive dyspnoea and exercise intolerance, chest pain. 90% have bilateral hilar lymphadenopathy, more severe has pulmonary infiltrates
Extra pulmonary: fever, fatigue, weight loss; hepatomegaly, cirrhosis, cholestasis; uveitis, conjunctivitis, optic neuritis; heart block, cardiomyopathy; neuropathy, nerve palsies, pituitary, encephalitis / meningitis; hypercalcaemia, renal stones, nephritis
Bloods - raised ACE and hypercalcaemia, 24h urine calcium, CXR (hilar lymphadenopathy), CT / PET / MRI, biopsy
Also for other organs: U+Es, albumin : creatinine, LFTs, ophthalmology, ECG + echo, US of organs
Non severe will resolve, treat with oral prednisolone (topical if affecting skin), high doses required long term (6-24m) + bisphosphonate; steroid sparing: azathioprine / methotrexate
High dose of steroid originally then lower maintenance. Life threatening give high dose IV
NSAIDs for arthralgia
May need transplant
Pathogenesis and presentation of bronchiectasis
Infection most common but also CF, tumour, foreign body, alpha1, RS, yellow nail syndrome
Bronchial walls become thickened and irreversibly damaged, mucociliary transport mechanism impaired so frequent infections.
Following pneumonia / TB / measles, congenital causes (CF), mechanical obstruction (foreign body)
Most common bacteria; haemophilus influenzae, pseudomonas aeruginosa
PRESENTATION
Productive cough, large amounts of discoloured sputum, weight loss, dyspnoea, recurrent infections
Signs: finger clubbing, cor pulmonale (JVP, peripheral oedema), scattered crackles + wheeze
Investigations and management of bronchiectasis
High resolution CT, sputum culture (also exclude TB), obstruction on spirometry
CXR: tram-track opacities, ring shadows
Airway clearance therapy, lifestyle, pneumococcal + influenza vaccines, oxygen if required
If required: salbutamol, nebulised hypertonic saline (mucoactive)
Acute exacerbation: antibiotics for 14d to clear
Pseudomonas aeruginosa: oral ciprofloxacin. If first case can eradicate with extended regime
Other: amoxicillin (clarithromycin), co-amoxiclav if severe
Frequent exacerbations (>3 per year): long term azithromycin
Pathogenesis and presentation of cystic fibrosis
CF gene mutation, faulty chloride channel transport protein on epithelial cells, defective Cl secretion and increased Na absorption - increased H2O absorption and thickened secretions
In lungs the surface is dehydrated, there is mucus stasis (recurrent infections) and inflammation
Originates in small airways, progressive airway obstruction and bronchiectasis
Multi system disease (80% GI and lung, 15% just lungs) with large range of issues
GI: reduced pancreatic enzymes → diabetes, distal intestinal obstruction, reduced bicarbonate, cholesterol gallstones (P enzymes), peptic ulcers
Other: infertility (females only as progresses), clubbing, osteoporosis
Neonates: failure to thrive, bowel obstruction (meconium ileus), rectal prolapse
Respiratory: cough, wheeze, thick mucus, recurrent infections, sinusitis, nasal polyps
Late stage - haemoptysis and breathlessness
Investigations and management of cystic fibrosis
Sweat test (high sodium and chloride concentrations) GS, all babies have blood spot
Genetic screening in pregnancy (amniocentesis / chorionic villous sampling), blood test after birth
MDT, lung function and BMI monitored, education (nutrition and treatment of exacerbations), chest physio, screening for osteoporosis
Prophylaxis antibiotics, vaccines
Enzymes replacement, beta2 agonists, inhaled corticosteroids, mucolytics (dornase alfa), amiloride inhibits sodium transport
Bilateral lung transplant: have to be on maximal therapy and fully compliant, FEV1 at 30%
Describe microbial colonisation in CF
Microbial colonisers: staph aureus + pseudomonas aeruginosa main, h. Influenzae, klebsiella, e. Coli, burkholderia cepacia
Pseudomonas: very difficult to get rid of due to resistance, significant morbidity + mortality
Nebulised Abx - tobramycin or oral ciprofloxacin
How is pleural effusion classified
Classified by protein content in fluid; transudates (fluid protein < 50% serum protein or < 30g/L) hydrostatic forces in chest favour the accumulation of fluid; exudates < 50% serum or < 30g/L - increased permeability and endothelial cells further apart
Transudates: high venous pressure (heart failure, constrictive pericarditis, fluid overload), hypoproteinaemia (cirrhosis, hypoalbuminaemia, nephrotic syndrome), hypothyroidism
Exudates: pneumonia, malignancy, TB, pulmonary infarction, lymphoma, mesothelioma, asbestos, myocardial infarction
Similarly can use LDH (light’s criteria): exudative pleural LDH / serum LDH >0.6
(Prove, please, please please: pleural protein : serum > 0/5 (5 letters); pleural LDH : serum > 0.6 (6 letters); pleural LDH > 0.66 (6, 6 letters) upper limit of normal)
Presentation, investigations, management of pleural effusion
Can be asymptomatic, symptoms of underlying cause
Shortness of breath, pleuritic chest pain, cough, chest expansion reduced on side of effusion, tracheal deviation
Pleuritic CP = sudden, sharp / stabbing, associated with inhalation and exhalation
X ray - need 300mls to blunt costophrenic angle, fluid in fissures, tracheal deviation, smaller lungs
Ultrasound, CT, aspiration (pH, cytology, microbiology), LDH
Depends on size, symptoms and cause. Small are treated conservatively
Exudates drained if symptomatic, malignant will recur so permanent indwelling pleural catheter
Surgery if persistent collections and increasing pleural thickness, pleurodesis - injection causing visceral and parietal to fuse
What is the pathophysiology of pneumothorax
Air in plueral space leading to partial or complete lung collapse (intrapleural pressure negative), hole from lungs or from chest wall injury. Spontaneous, trauma, iatrogenic
Primary spontaneous: no underlying cause, rupture of apical bleb (small subpleural air filled space)
Increased risk in smoking, tall (stretched), male. Can occur due to even a cough
Secondary spontaneous: COPD, asthma, ILD, CF, cancer, PCP / TB, any cystic disease
Tension pneumothorax: has lead to significant impairment of respiration / blood circulation
Trauma causing one way valve (air in not out), each breath makes worse
Also trauma, iatrogenic (biopsy, mechanical ventilation), lung pathologies
Presentation and investigations of pneumothorax
May be asymptomatic
Sudden onset dyspnoea, unilateral pleuritic chest pain. As enlarges become more breathless, pallor, tachycardia
Reduced expansion, hyper resonance to percussion, diminished breath sounds
Tension: tracheal deviation, reduced air entry in one side, tachycardia, hypotension
Erect CXR,area between lung and chest wall with no lung markings
Size measures horizontally from lung edge to chest wall in line with hilum
CT if too small for CXR, can measure more accurately
If tension is suspected, no investigations just a chest drain
Management of pneumothorax
If trauma / haemothorax / mechanical ventilation requires a chest drain. Also in patients with bilateral, haemodynamic instability, underlying disease
Tension: large bore cannula into 2nd (or 4th) intercostal space, midclavicular line
If small no intervention but consider high flow oxygen, patient choice can have pleural vent ambulatory device or needle aspiration
Pleural vent: catheter in pleural space
Pathogenesis and presentation of pulmonary hypertension
Increased resistance and pressure in pulmonary arteries, strain on the right side of heart, back pressure into the systemic venous system
Damages pulmonary endothelium, release of vasoconstrictors, worsens and RV has to work harder, leads to RV dilatation and eventually failure
Causes: group 1: idiopathic or connective tissue (SLE); 2: left heart failure; 3: chronic lung disease (COPD, fibrosis); 4: pulmonary vascular disease (VTE); 4: misc (sarcoidosis, haematological)
Exertional dyspnoea, lethargy, fatigue, syncope
RHF: ankle swelling, raised JVP (prominent A wave), hepatomegaly + abdominal pain, tachycardia
Investigations and management of pulmonary hypertension
Echo gives estimate of PAP, right heart catheterization GS
ECG: peaked P waves, RVH (tall R v1/2, deep S v5/6), right axis deviation, right BBB
CXR (dilated vessels, RVH), raised NT-proBNP
Treat cause, supportive with oxygen and diuretics (furosemide + K)
Idiopathic: calcium channel blockers, sildenafil (P5 inhibitor), IV epoprostenol (prostanoid), bosentan (endothelin antagonist)
Pathogenesis and types of hypersensitivity pneumonitis
Prior sensitisation to an antigen, IgG form antigen-antibody complexes that are deposited and not properly cleared. Also direct inflammation from the complement pathway. Type III and IV
Alveolar and interstitial macrophages are attracted and activated - progressive pulmonary fibrosis
Acute - infiltration of inflammatory cells, chronic - granuloma formation and obliterative bronchiolitis
Types: bird / pigeon fancier’s lung, farmer / mushroom worker’s lung, malt worker’s lung, sugar worker’s lung
Presentation, investigations, management of hypersensitivity pneumonitis
Acute: dyspnoea, dry cough, fever, rigours, fine bibasal crackles (no wheeze), chest tightness
Symptoms related to level of exposure, will resolve 24-48h after removal of antigen
Chronic: may have no acute history, cyanosis, clubbing, weight loss, increasing dyspnoea, T1 failure
Removing antigen only provides partial improvement
Chest x ray (consolidation / fibrotic shadow in upper zone, diffuse small nodules), restrictive lung function (reduced gas transfer in attacks), FBC (neutrophilia), ESR + CRP, serum antibodies
Acute: removal of antigen, oxygen, oral prednisolone
Chronic: avoid exposure, long term steroids / azathioprine, facemask
Describe obstructive sleep apnoea
Intermittent collapse of the pharyngeal airway, causing apnoeic episodes during sleep, terminated by partial arousal, recurrent episodes lead to chronic intermittent hypoxia + sleep fragmentation
Episodes of apnoea during sleep, snoring, morning headache, waking up unrefreshed, daytime sleepiness, concentration issues
If daytime sleepiness important to ask about their occupation (lorry driver etc)
Sleep study, simple sleep study (at home), respiratory polygraph, polysomnography
Polygraphy: resp rate, flow rate, sats, HR. PSG: EEG, EMG, ECG
Epworth sleepiness scale, likeliness of falling asleep whilst: reading, watching TV, sitting inactive in public, as a passenger for 30 mins, sitting whilst talking, sitting after lunch, in car in traffic
Ranked 0 to 3 (high chance), >9 is abnormal
Mx: weight reduction + exercise + alcohol / smoking reduction, change sleep position, CPAP, surgery to relieve pharyngeal / nasal obstruction
Describe granulomatosis with polyangiitis
Unknown aetiology, ANCA associated vasculitis, antibodies activate neutrophils before they have entered tissues (in vessels)
Recruitment of neutrophils, production of reactive oxygen species, degranulation
Devastating inflammation of many organs including lungs and kidneys
Initially severe rhinorrhoea - nasal mucosal ulceration + saddle nose deformity
Cough, pleuritic pain, haemoptysis, renal disease, peripheral neuropathy, arthritis/ arthralgia
Blood is c-ANCA positive, CXR + CT alveolar haemorrhage, urinalysis - proteinuria and haematuria then confirm with renal biopsy
Corticosteroids to treat induce remission, azathioprine and methotrexate for maintenance
Describe mesothelioma
Very strongly associated with asbestos exposure, but only 20% have pulmonary asbestosis
High grade malignancy of pleura, begins as nodules and extends to surround lungs and extend into fissures, chest wall invaded and infiltrates intercostal nerves
Poor prognosis, average of 8 months after diagnosis
Chest pain, dyspnoea, weight loss, finger clubbing, pleural effusions
Signs of metastases: lymphadenopathy, hepatomegaly, bone pain, abdominal pain + obstruction
CXR + CT - unilateral pleural effusion and pleural thickening, pleural biopsy and fluid aspiration
If localised - surgery, generally resistant to surgery so chemo and radiotherapy
