Resp Conditions Flashcards

1
Q

Aspergillus Lung Disease

  1. Definition
  2. Aetiology/Risk factors
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
A
  1. Lung disease associated with Aspergillus infection (Asp. fumigatus)
  2. Inhalation of spores produces:
    1. Aspergilloma (growth of A. fumigates mycetoma ball in pre-existing lung cavity), OR
    2. Allergic bronchopulmonary aspergillosis (ABPA)
      1. colonisation of airways by asp leads to IgE and G mediated IR,
      2. usually in asthmatics
      3. release of proteolytic enzymes, mycotoxins and Ab leads to airway damage and central bronchiectasis)
    3. Invasive aspergillosis: invasion of asp into lung tissue and fungal dissemination; occuring in immunosuppressed pts
  3. Uncommon, mainly in elderly and immunocompromised
  4. Aspergilloma = asyx and potentially massive haemoptysis; ABPA = difficult to control asthma, recurrent pneumonia with wheeza, cough, fever and malaise; invasive aspergillosis = dyspnoea, rapid deterioration and septic picture
  5. Tracheal deviation with large aspergilloma; dullness in affected lung; reduced breath sounds; wheeze in ABPA; cyanosis possible in invasive aspergillosis
  6. x
    1. Aspergilloma: CXR = round mass with crescent of air around it; CT/MRI if CXR unclear; sputum culture could be negative
    2. ABPA: immediate skin test reactivity to asp Ag, eosinophilia, raised total sIgE and specific sIgE and IgG to A. fumigatus; CXR = transient patchy shadows, collapse, distended mucous filled bronchi, complications = fibrosis in upper lobes and bronchiectasis; CT = lung infiltrates and central bronchiectasis; lung function tests = reversible airflow limitation and reduced lung volumes/gas transfer
    3. Invasive aspergillosis: cultures/histological exam; broncheoalveolar lavage fluid/sputum may be used diagnostically; Chest CT = nodules with halo sign,
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2
Q

Asthma

  1. Definition
  2. Aetiology/Risk factors
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
  7. Management plan
  8. Complications
  9. Prognosis
A
  1. Chronic inflammatory airway disease characterised by variable reversible airway obstruction, airway hyper-responsiveness and bronchial inflammation
  2. Genetic:FHX, atopy; environment: house dust mites, pollen, pets, cigarette smoke, viral RTI, asp fumigatus spores, occupational allergens
  3. 10% of children, 5% of adults with prevalence increasing
  4. Episodic Hx, wheeze, SOB, cough (worse am and night), previous hospitalisations; precipitating factors: cold, viral infection, drugs, exercise, emotions; check for PMH of atopic disease
  5. Tachypnoea, use of accessory muscles, prolonged exp phase, polyphonic wheeze, hyperinflated chest
    1. SEVERE attack: PEFR < 50% predicted, pulse>110/min, RR >25/min, inability to complete sentences
    2. LIFE THREATENING attack: PEFR <33% predicted, silent chest, cyanosis, bradycardia, hypotension, confusion, coma
  6. Acute: peak flow, pulse oximetry, ABG, CXR, FBC (WCC raised if infective exacerbation), CRP, U&Es, blood and sputum cultures
    1. Chronic: peak flow monitoring (diurnal variation with dip in the morning), pulm function test, bloods: eosinophilia, IgE level, asp Ab titres, skin prick tests (ID allergens)
  7. Management:
    1. Acute: ABCDE, resuscitate, monitor O2 stats, ABG, PEFR, high flow O2, salbutamol nebulizer (5mg, initially continuously then 2-4hrly), ipatropium bromide (0.5mg QDS), steroid therapy (100-200mg IV hydrocortisone; followed by 40mg oral prednisolone for 5-7d and if not improved IV MgSO4), consider IV aminophylline infusion/salbultamol; treat underlying cause (Abx), monitor electrolytes (drop in K), invasive ventilation in severe attacks
    2. Discharge when: PEF >75% predicted, diurnal variaton <25%, inhaler technique checked, stable on discharge meds for 24h, pt owns PEF meter and has steroid and bronchodilator therapy -> arrange follow up
    3. Chronic => Step match severity to pick start =
      1. inhaled SABA, if needed >1/d then onto step 2
      2. inhaled SABA and reg inhaled low dose steroids (400mcg/d)
      3. 2+inhaled LABA; if inadequate control with LABA then increase steroid to 800mcg/day (no control with LABA = stop LABA and up steroid)
      4. increased inhaled steroid (2000 mcg/d), 4th drug (leukotriene antagonist, slow release theophylline or b2 agonist)
      5. Regular oral steroids, maintain high-dose oral steroids, refer to specialist
    4. Advice = teach proper inhaler technique, explain importance of PEFR monitoring and avoid provoking factors
  8. Growth retardation, chest wall deformity (pigeon chest), recurrent infections, pneumothorax, resp failure and death
  9. Many children improve with age; adult onset is usually chronic
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3
Q

Bronchiectasis

  1. Definition
  2. Aetiology/Risk factors
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
  7. Management plan
  8. Complications
  9. Prognosis
A
  1. Lung airway disease characterised by chronic bronchial dilation, impaired mucociliary clearance and frequent bacterial infections
  2. Chronic lung inflammation leads to fibrosis and permanent dilation of bronchi -> mucus pooling and further infections, damage and fibrosis of bronchial walls -> causes:
    1. idiopathic
    2. post-infection (pneumonia, tb)
    3. host-defence defects (cystic fibrosis)
    4. obstruction of bronchi
    5. GORD
    6. inflammatory disorders (rheumatoid arthritis)
  3. often initially in childhood; incidence decreased with Abx
  4. Productive cough with purulent sputum/haemoptysis; SOB; chest pain; malaise; fever; weight loss; syx begin after acute resp illness
  5. clubbing, coarse crepitaions (lung bases, shift with cough), wheeze
  6. Sputum for culture and sensitivity = P. aeruginosa, H influenzae, S aureus, strep pneumo, klebsiella, mycobacteria; CXR = dilated bronchi, fibrosis, atelectasis, pneumonic consolidations; High res CT shows bronchi dilated with thick walls; bronchography; sweat electrolytes for CF, serum Ig, mucociliary clearance study
  7. Acute exacerbations with 2 Abx IV, covering P. aeruginosa; prophhylactic Abx if frequent exacerbations; inhaled corticosteroids; bronchodilators; maintain hydration; flu vaccine; physio for mucus and sputum clearance; bronchial artery embolisation; surgical
  8. Life threatening haemoptysis, prsistent infections, empyema, resp failure, cor pulmonale, multi-organ abcesses
  9. Continue to have syx after 10yrs
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4
Q

COPD

  1. Definition
  2. Aetiology/Risk factors
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
  7. Management plan
  8. Complications
  9. Prognosis
A
  1. Chronic progressive lung disorder characterised by airflow obstruction with the following -> chronic bronchitis (chronic cough and sputum production most days for at least 3m per year or over 2 consecutive years) and emphysema (pathological dx of permanent destructive enlargement of air spaces distal to terminal bronchioles)
  2. Broncheolar and alveolar damage caused by environmental toxins; rarely = alpha 1 antitrypsin deficiency; chronic bronchitis = narrowing of airways, bronchiolitis, bronchial mucosal oedema, mucous hypersecretion and squamous metaplasia; emphysema = destruction and enlargement of alveoli, leads to loss of elasticity, with larger spaces forming = bullae
  3. Very common (8%), middle age or later, more common in males (changing due to increase in female smokers)
  4. Chronic cough, sputum production, SOB, wheeze, reduced exercise tolerance
  5. Inspection = resp distress, accessory msucles, barrel chest, decreased cricosternal distance, cyanosis; Percussion = hyperresonant, loss of liver and cardiac dullness; auscultation = quiet breath sounds, prolonged exp, wheeze, rhonchi, crepitations; sx of CO2 retention = bounding pulse, warm peripheries, asterixis, late stage RHF (RV heave, raised JVP, anlkle oedema
  6. Spirometry and pulm function tests (reduced PEFR/FEV1/FVC, increased lung volumes and decreased CO gas transfer coefficient); CXR = normal, hyperinflation, reduced peripheral lung markings, elongated cardiac silhouette; bloods = FBC = increased Hb and Hct due to 2ry polycythaemia; ABG; ECG and echo; sputum and blood cultures (in acute infective exacerbations); alpha 1 antitrypsin levels
  7. Stop smoking; bronchodilators = SABA, LABA, anticholinergics; steroids = inhaled beclamethasone (FEV1 <50% or > 2 exacerbations per yr; pulm rehab; O2 therapy (stopped smoking and pO2 <7.3kpa); tx of acute exacerbations = 24% O2 with venturi mask, corticosteroids, abx therapy, resp physio for sputum
  8. Acute resp failure, infections, pulm hypertension; RHF; pneumothorax;2ry polycythaemia
  9. high morbidity, 3-years survival = 90% in FEV1 if under 60yrs old; FEV1 >50% predicted,
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5
Q

Extrinsic allergic alveolitis

  1. Definition
  2. Aetiology/Risk factors
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
A
  1. interstitial inflammatory disease of distal gas-exchaning parts of lung caused by inhalation of organic dusts -> hypersensitivity pneumonitis
  2. Inhalation of antigenic dusts causes hypersensitivity response = farmer’s lung, pigeon fancier’s lung, maltworker’s lung
  3. Uncommon, 2% of occupational lung disease, 50% reported cases affect farm workers
  4. Acute = 4-12h after exposure, reversible episodes of = dry cough, dyspnoea, malaise, fever, myalgia (wheeze and productive cough may develop if repeat high level exposure); chronic = slowly increasing SOB, decreased exercise tolerance, weight loss, exposure usually chronic, low-level and may be no Hx of previous acute episodes
  5. Acute = rapid shallow breathing, pyrexia, inspiratory crepitations; chronic = fine inspiratory crep and clubbing (rare)
  6. Bloods = FBC (neutrophilia, lymphopoenia), ABG reduced PO2/CO2; serology = IgG to fungal/avian Ag; CXR = normal in acute episodes, fibrosis seen in chronic cases; high res CT-thorax; pulm function tests = restrictive defect (low FEV1, low FVC, preserved/increased FEV1/FVC, reduced total lung capacity); bronchoalveolar lavage = increased cellularity, lung biopsy can be performed
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6
Q

Idiopathic pulmonary fibrosis

  1. Definition
  2. Aetiology/Risk factors
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
A
  1. Inflammatory condition of the lung resulting in fibrosis of the alveoli and interstitium, known as cryptogenic fibrosing alveolitis
  2. Genetically predisposed individuals, recurrent iinjury to alveolar epithelium = cytokine and growth factor secretion; leads to fibroblast activation, recruitment, proliferation, differentiatiions into myofibroblasts and increased collagen synthesis and deposition; interstitial pneumonia and RF = smoking, occupational exposure to metal/wood, chronic microaspiration, animal and veg dusts
  3. Rare, more common in males, 6/100000
  4. Gradual onset, progressive dyspnoea on exertion, dry irritating cough, no wheeze, may be preceded by viral type illness, fatigue and weight loss common
  5. clubbing (50%), bibasal fine late inspiratory crackles; signs of RHF in advanced stages of disease
  6. Bloods = ABG PCO2 rises in late stages of disease, ANA and RhF (1/3 positive); CXR = normal, ground glass shadowing, later stage reticulonodular shadowing, signs of cor pulmonale and honeycombing; high res CT; pulm function tests = restrictive features, decreased lung vols/compliance/lung capacity; bronchoalveolar lavage; lung biopsy - gold standard for dx; echo
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7
Q

Obstructive sleep apnoea

  1. Definition
  2. Aetiology/Risk factors
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
A
  1. Disease characterised by recurrent prolapse of pharyngeal airway and apnoea (cessation of airflow for >10s) during sleep, followed by arousal for sleep
  2. Narrowing of upper airways because of the collapse of soft tissues of the pharynx, due to decreased tone of the pharyngeal dilators during sleep -> associated with = weight gain, smoking, alcohol, sedative use, enlarged tonsils/adenoids in children, macroglossia, marfan’s syndrome and craniofacial abnormalities
  3. Common, 5-20% men >35, 2-5% women >35 and prevalence increases with age
  4. Excessive daytime sleepiness, unrefreshing/restless sleep, morning headaches, dry mouth, difficulty concentrating, irritability and mood changes, partner reported choking/apnoeic episodes at night
  5. Large tongue, enlarged tonsils, long/thick uvula, retrognathia, neck circumference >42M, >40F; obesity, HTN
  6. Sleep study = monitor airflow, resp effort, pulse oximetry and HR; bloods = TFTs, ABG
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8
Q

Pneumoconiosis

  1. Definition
  2. Aetiology/Risk factors
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
A
  1. Fibrosing interstitial lung disease caused by chronic inhalation of mineral dusts = types:
    1. Simple = coalworker’s pneumoconiosis (syx-free)
    2. Complicated = resulting in loss of lung function
    3. Asbestosis = pneumoconiosis which diffuse parenchymal lung fibrosis occurs as a result of long exposure to asbestos
  2. Caused by inhalation of particles of coal dust, silica and asbestos; RF = occupational exposure, risk is dependent on extent of exposure and size/shapes of particles, individual susceptibility is also important, co-factors such as smoking and TB also contribute
  3. increasing in developing countries; disability/mortality from asbestosis will increase for next 20-30yrs
  4. OCCUPATION, asyx picked up on routine CXR; Syx = insidious onset of shortness of breath, dry cough, black sputum (melanoptysis in coalworkers occasionally), pleuritic chest pain (asbestosis)
  5. Exam may be normal; coalworker’s pneumoconiosis and silicosis = decreased breath sounds; asbestosis = end inspiratory crepitations, clubbing; signs of pleural effusions or RHF
  6. CXR: simple = micronodular mottling, complicated = nodular opacities in upper lobes / micronodular shadowing / eggshell calcification of hilar lymph nodes / bilat lower zone retculonodular shadowing and pleural plaques; CT scan = fibrotic changes can be visualised early; bronchoscopy = visualisation and bronchoalveolar lavage; LFT = restrictive
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9
Q

Pneumonia

  1. Definition
  2. Aetiology/Risk factors
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
  7. Management
  8. Complications
  9. Prognosis
A
  1. Infection of distal lung parenchyma, classified = Community-acquired, nosocomial, aspiration pneumo, pneumo in immunocompromised, typical and atypical (mycoplasma, chlamydia, legionella)
  2. CAP: Strep pneumo 70%, haemophilus influenzae, moraxella catarrhalis (COPD), chlamydia psittaci (psittacosis), legionella (air con), staph aureus, mycoplasma pneumonia, TB, coxiella burnetii (q fever); HAP: GNB (pseudomonas, klebsiella) and anaerobes; RF = age, smoking, alcohol, pre-existing lung disease, immunodeficiency, contact with patients with pneumonia
  3. CAP for >60,000 deaths per year in uk
  4. Fever, rigors, sweating, malaise, cough, sputum, SOB, pleuritic chest pain, confusion; atypical = headache, myalgia, darrhoea/abdo pain, DRY cough
  5. Pyrexia, resp distress, tachypnoea/cardia, hypotension, cyanosis, decreased chest expansion, chronic suppurative lung disease (clubbing), affected areas = dull to percuss , increased vocal fremitus, bronchial breathing and coarse crepitations
  6. Bloods = FBC (^WCC), U&Es, LFT, blood cultures, ABG, blood film (mycoplasma = agglutination of RBC); CXR = lobar/patchy shadowing, pleural effusion; sputum/pleural fluids; urine (pneumococcus and legionella Ag); atypical viral serology; bronchoscopy, bronchoalveolar lavage
  7. Assess severity with british thoracic society guidelines (markers).
    1. Start empirical Abx = oral amoxicillin (0), oral/IV amoxicillin and rythromycin (1), IV cefuroxime/cefotaxime/co-amoxiclav + erythromycin (>1), add metronidazole if aspiration, lung abcess or empyema, and switch based on sensitivity.
    2. Supportive treatment = O2, IV fluids, CPAP/BiPAP/ITU care for resp failure, surgical drainage for lung abcessess and empyema
    3. Discharge planning = 2 or more = high temp, tachycardia/pnoea, hypotension, low O2 sats, means high risk of readmission
    4. Prevention = pneumococcal vaccine, H. influenzae B vaccine
  8. Pleural effusion, empyema, localised suppuration (abcesses = swinging fever, persistent pneumonia, copious, foul smelling sputum), septic shock, ARDS, acute renal failure. Mycoplasma p = erythema multiforme, myocarditis, haemolytic anaemia, meningoencephalitis, transverse myelitis, guillan-barre syndrome
  9. Most resolve within 1-3wks, severe has high mortality. CURB-65 for severity = confusion <8AMTS, Urea >7mmol.L, RR >30/min, BP sys<90 or dias <60, age>65
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10
Q

Pneumothorax

  1. Definition
  2. Aetiology/Risk factors
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
  7. Management
  8. Complications
  9. Prognosis
A
  1. Air in pleural space (haemo = blood, chylo = lymph)
  2. Spontaneous = normal lungs, tall/thin males, rupture of subdural bleb; 2ry = pts with pre-existing lung disease; traumatic = penetrating injury to the chest, iatrogenic (JV cannulation, thoracocentesis); RF = collagen disorders (marfan’s, ehlers-danlos)
  3. annual 9/100,000, mainly 20-40yr olds, 4x more common in M
  4. Asyx if small; sudden onset SOB, pleuritic chest pain, distress with rapid shallow breathing in tension pneumoT
  5. None if small, signs of resp distress, reduced expansion, hyper-resonance to percussion, reduced breath sounds; tension pneumoT = severe resp distress, tachycardia, hypotension, cyanosis, distended neck veins, tracheal deviation (AWAY)
  6. CXR -> dark film area with no vascular markings, fluid level may be seen if bleeding; ABG to check for hypoxaemia
  7. x
    1. Tension = EMERGENCY so max O2, insert large bore needle into 2nd ICS at MCL, aspirate up to 2.5L of air, stop if cough/resistance is felt; follow up CXR 2hr and 2wks later;
    2. Chest drain with underwater seal = performed if aspiration fails, fluid in pleural cavity or after decompression of tension, inserted in 4-6th ICS at mid axillary line;
    3. Recurrent = clhemical pleurodesis (fusing visceral+parietal pleura with tetracycline), surgical pleurectomy.
    4. Advice = avoid air travel until follow up CXR confirms it resolved, avoid diving
  8. Recurrent pneumothoraces, bronchopleura fistula
  9. after having 1, 20% or more have another, with freq increasing with recurrent
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11
Q

Tuberculosis

  1. Definition
  2. Aetiology/Risk factors
  3. Epidemiology
  4. Presenting Syx and Presenting Sx
  5. Investigations
A
  1. Granulomatous disease caused by mycobacterium tuberculosis; 1ry = initial infection may be pulmonary or GI (rare), Miliary = haematogenous dissemination of TB, post-1ry TB caused by reinfection/reactivation
  2. M. TB is an intracellular organism, survives after being phogcytosed; RF = close contact with infected, immunocompromised = HIV, Substance abuse, Silicosis, DM, Severe kidney disease, Low body weight, Head and neck cancer, corticosteroids or organ transplant
  3. Annual mortality = 3 million, in UK 6000 incidence
  4. x
    1. 1ry = asyx, fever, malaise, cough, wheeze, erythema nodosum, phlyctenular conjunctivitis;
    2. miliary = fever, weight loss, meningitis, yellow caseous tubercles;
    3. post-1ry = fever/night sweats, malaise, weight loss, SOB, cough, sputum, haemoptysis, pleuritic chest pain, signs of pleural effusion, collapse, consolidation, fibrosis;
    4. LN has suppuration leading to abcesses,
    5. CNS = meningitis, tuberculoma; skin = lupus vulgaris;
    6. heart = pericardial effusion, constrictive pericarditis;
    7. GI = subacute obstruction, change in bowel habit, weight loss, peritonitis, ascites;
    8. genitourinary = UTI syx, renal failure, epididymitis, endometrial/tubal involvement, infertility;
    9. adrenal insufficiency;
    10. osteomyelitis, arthritis, vertebral collapse, spinal cord compression
  5. Sputum/pleural fluid/bronchial washing, tuberculin tests, mantoux test, heaf test; INF-g test, HIV testing, CT, LN, pleural biopsy, sampling of other affected systems, CXR=
    1. 1ry = peripheral consolidation, hilar lymphadenopathy
    2. Miliary = fine shadowing
    3. Post-1ry = upper lobe shadowing, streaky fibrosis and cavitation, callcification, pleural effusion, hilar lymphadenopathy
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12
Q

Pulmonary embolism

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
  7. Management
  8. Complications
  9. Prognosis
A
  1. Occlusion of pulmonary vessels, commonly by thrombus that travelled to pulm vascular system from another site
  2. Thombus = 95% from DVT in lower limbs, rarely arising in right atrium in AF pts; other embolus causes = Amniotic fluid, air, fat, tumour, mycotic. RF =
    1. Surgical pts
    2. Immobility
    3. Obesity
    4. OCP
    5. HF
    6. Malignancy
  3. Relatively common, esp in hospitalised pts; occurs in 10-20% of pts with confirmed proximal DVT
  4. Small may be asyx; moderate = sudden onset SOB, cough, haemoptysis, pleuritic chest pain; large (or proximal) = as mod and severe central pleuritic chest pain, shock, collapse, acute RHF, sudden death; multiple and recurrent ones = syx of pulm hypertension
  5. Small often has no clinical signs or some tachycardia/pnoea; moderate = tachypneoa/cardia, pleural rub, low O2 sats; massive = shock, cyanosis, signs of RH strain: raised JVP, left parasternal heave, accentuated S2; multiple recurrent = sx of pulm hypertension and RHF
  6. Well’s score used to determine the best investigations = low probability with Wells <4 = d-dimer; high probability with Wells >4 = imaging (CTPA). Others:
    1. bloods = ABG, thrombophilia screen
    2. ECG = normal/tachy, right acis deviation or RBBB/ S1Q3T3 pattern
    3. CXR = normal but helps exclude other dx.
    4. Spiral CT pulm angiogram = 1st line investigation; poor sensitivity for small emboli, very for med-large emboli
    5. VQ scan = indicates area of infarcted lung
    6. Pulm angiography = invasive, rarely necessary
    7. Doppler US of lowe limb
    8. Echo
  7. x
    1. 1ry prevention: compression stocking, heparin prophylaxis and good mobilisation and adequate hydration
    2. If haemodynamically stable = O2, anticoag with heparin/LMWH, switch to oral warfarin for at least 3months (INR at 2-3), analgesia
    3. If haemodynamically unstable = Resuscitate, O2, IV fluids, thrombolysis with tPA if cardiac arrest imminent
    4. Surgical/Radiological = embolectomy, IVC filters (sometimes for recurrent PEs despite adequate anticoag/anticoag contraindicated
  8. Death, pulm infarction, pulm HTN, RHF
  9. 30% mortality if untreated, 8% mortality with treatment; increased risk of future thromboembolic disease
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13
Q

Define

Aspergillus lung disease

A
  1. Lung disease associated with Aspergillus infection (Asp. fumigatus)
  2. Aspergilloma (growth of A. fumigates mycetoma ball in pre-existing lung cavity), OR
  3. Allergic bronchopulmonary aspergillosis (ABPA)
    1. colonisation of airways by asp leads to IgE and G mediated IR,
    2. usually in asthmatics
    3. release of proteolytic enzymes, mycotoxins and Ab leads to airway damage and central bronchiectasis)
  4. Invasive aspergillosis: invasion of asp into lung tissue and fungal dissemination; occuring in immunosuppressed pts
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14
Q

S+S

Aspergillus lung disease

A
  1. Aspergilloma = asyx and potentially massive haemoptysis;
  2. ABPA = difficult to control asthma, recurrent pneumonia with wheeza, cough, fever and malaise;
  3. invasive aspergillosis = dyspnoea, rapid deterioration and septic picture
  4. Tracheal deviation with large aspergilloma;
  5. dullness in affected lung;
  6. reduced breath sounds;
  7. wheeze in ABPA;
  8. cyanosis possible in invasive aspergillosis
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15
Q

Investigations

Aspergillus lung disease

A
  1. Aspergilloma:
    1. CXR = round mass with crescent of air around it;
    2. CT/MRI if CXR unclear; sputum culture could be negative
  2. ABPA:
    1. immediate skin test reactivity to asp Ag, eosinophilia, raised total sIgE and specific sIgE and IgG to A. fumigatus;
    2. CXR = transient patchy shadows, collapse, distended mucous filled bronchi,
    3. complications = fibrosis in upper lobes and bronchiectasis;
    4. CT = lung infiltrates and central bronchiectasis;
    5. lung function tests = reversible airflow limitation and reduced lung volumes/gas transfer
  3. Invasive aspergillosis:
    1. cultures/histological exam;
    2. broncheoalveolar lavage fluid/sputum may be used diagnostically;
    3. Chest CT = nodules with halo sign,
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16
Q

Define

Asthma

A

Chronic inflammatory airway disease characterised by variable reversible airway obstruction, airway hyper-responsiveness and bronchial inflammation

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17
Q

S+S

Asthma

A
  1. Episodic Hx, wheeze, SOB, cough (worse am and night), previous hospitalisations;
  2. precipitating factors: cold, viral infection, drugs, exercise, emotions;
  3. check for PMH of atopic disease
  4. Tachypnoea, use of accessory muscles, prolonged exp phase, polyphonic wheeze, hyperinflated chest
  5. SEVERE attack: PEFR < 50% predicted, pulse>110/min, RR >25/min, inability to complete sentences
  6. LIFE THREATENING attack: PEFR <33% predicted, silent chest, cyanosis, bradycardia, hypotension, confusion, coma
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18
Q

Investigations

Asthma

A
  1. Acute: peak flow, pulse oximetry, ABG, CXR, FBC (WCC raised if infective exacerbation), CRP, U&Es, blood and sputum cultures
  2. Chronic: peak flow monitoring (diurnal variation with dip in the morning), pulm function test, bloods: eosinophilia, IgE level, asp Ab titres, skin prick tests (ID allergens)
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19
Q

Management

asthma

A
  1. Acute:
    1. ABCDE, resuscitate, monitor O2 stats, ABG, PEFR,
    2. high flow O2, salbutamol nebulizer (5mg, initially continuously then 2-4hrly), ipatropium bromide (0.5mg QDS), steroid therapy (100-200mg IV hydrocortisone;
    3. followed by 40mg oral prednisolone for 5-7d and if not improved IV MgSO4),
    4. consider IV aminophylline infusion/salbultamol;
    5. treat underlying cause (Abx),
    6. monitor electrolytes (drop in K),
    7. invasive ventilation in severe attacks
  2. Discharge when: PEF >75% predicted, diurnal variaton <25%, inhaler technique checked, stable on discharge meds for 24h, pt owns PEF meter and has steroid and bronchodilator therapy -> arrange follow up
  3. Chronic =>
    1. Step match severity to pick start =
    2. inhaled SABA, if needed >1/d then onto step 2
    3. inhaled SABA and reg inhaled low dose steroids (400mcg/d)
    4. 2+inhaled LABA; if inadequate control with LABA then increase steroid to 800mcg/day (no control with LABA = stop LABA and up steroid)
    5. increased inhaled steroid (2000 mcg/d), 4th drug (leukotriene antagonist, slow release theophylline or b2 agonist)
    6. Regular oral steroids, maintain high-dose oral steroids, refer to specialist
  4. Advice = teach proper inhaler technique, explain importance of PEFR monitoring and avoid provoking factors
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20
Q

define

Bronchiectasis

A

Lung airway disease characterised by chronic bronchial dilation, impaired mucociliary clearance and frequent bacterial infections

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21
Q

S+S

Bronchiectasis

A
  1. Productive cough with purulent sputum/haemoptysis;
  2. SOB;
  3. chest pain;
  4. malaise;
  5. fever;
  6. weight loss;
  7. syx begin after acute resp illness
  8. clubbing,
  9. coarse crepitaions (lung bases, shift with cough),
  10. wheeze
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22
Q

Investigations

Bronchiectasis

A
  1. Sputum for culture and sensitivity = P. aeruginosa, H influenzae, S aureus, strep pneumo, klebsiella, mycobacteria;
  2. CXR = dilated bronchi, fibrosis, atelectasis, pneumonic consolidations;
  3. High res CT shows bronchi dilated with thick walls;
  4. bronchography;
  5. sweat electrolytes for CF, serum Ig, mucociliary clearance study
23
Q

Management

Bronchiectasis

A
  1. Acute exacerbations with 2 Abx IV, covering P. aeruginosa;
  2. prophhylactic Abx if frequent exacerbations;
  3. inhaled corticosteroids; bronchodilators;
  4. maintain hydration;
  5. flu vaccine;
  6. physio for mucus and sputum clearance;
  7. bronchial artery embolisation;
  8. surgical
24
Q

Define

COPD

A

Chronic progressive lung disorder characterised by airflow obstruction with the following -> chronic bronchitis (chronic cough and sputum production most days for at least 3m per year or over 2 consecutive years) and emphysema (pathological dx of permanent destructive enlargement of air spaces distal to terminal bronchioles)

25
Q

S+S

COPD

A
  1. Chronic cough,
  2. sputum production,
  3. SOB,
  4. wheeze,
  5. reduced exercise tolerance
  6. Inspection = resp distress, accessory msucles, barrel chest, decreased cricosternal distance, cyanosis;
  7. Percussion = hyperresonant, loss of liver and cardiac dullness;
  8. auscultation = quiet breath sounds, prolonged exp, wheeze, rhonchi, crepitations;
  9. sx of CO2 retention = bounding pulse, warm peripheries, asterixis, late stage RHF (RV heave, raised JVP, ankle oedema
26
Q

Investigations

COPD

A
  1. Spirometry and pulm function tests (reduced PEFR/FEV1/FVC, increased lung volumes and decreased CO gas transfer coefficient);
  2. CXR = normal, hyperinflation, reduced peripheral lung markings, elongated cardiac silhouette;
  3. bloods = FBC = increased Hb and Hct due to 2ry polycythaemia;
  4. ABG;
  5. ECG and echo;
  6. sputum and blood cultures (in acute infective exacerbations);
  7. alpha 1 antitrypsin levels
27
Q

Management

COPD

A
  1. Stop smoking;
  2. bronchodilators = SABA, LABA, anticholinergics;
  3. steroids = inhaled beclamethasone (FEV1 <50% or > 2 exacerbations per yr;
  4. pulm rehab;
  5. O2 therapy (stopped smoking and pO2 <7.3kpa);
  6. tx of acute exacerbations = 24% O2 with venturi mask, corticosteroids, abx therapy, resp physio for sputum
28
Q

Define

Extrinsic allergic alveolitis

A

interstitial inflammatory disease of distal gas-exchaning parts of lung caused by inhalation of organic dusts -> hypersensitivity pneumonitis

29
Q

S+S

Extrinsic allergic alveolitis

A
  1. Acute = 4-12h after exposure,
    1. reversible episodes of = dry cough, dyspnoea, malaise, fever, myalgia (wheeze and productive cough may develop if repeat high level exposure), rapid shallow breathing, pyrexia, inspiratory crepitation;
  2. chronic =
    1. slowly increasing SOB,
    2. decreased exercise tolerance,
    3. weight loss,
    4. exposure usually chronic,
    5. low-level and may be no Hx of previous acute episodes,
    6. fine inspiratory crep and clubbing (rare)
30
Q

Investigations

extrinsic allergic alveolitis

A
  1. Bloods = FBC (neutrophilia, lymphopoenia), ABG reduced PO2/CO2;
  2. serology = IgG to fungal/avian Ag;
  3. CXR = normal in acute episodes, fibrosis seen in chronic cases;
  4. high res CT-thorax;
  5. pulm function tests = restrictive defect (low FEV1, low FVC, preserved/increased FEV1/FVC, reduced total lung capacity);
  6. bronchoalveolar lavage = increased cellularity, lung biopsy can be performed
31
Q

Definition

Idiopathic pulmonary fibrosis

A

Inflammatory condition of the lung resulting in fibrosis of the alveoli and interstitium, known as cryptogenic fibrosing alveolitis

32
Q

S+S

Idiopathic pulmonary fibrosis

A
  1. Gradual onset,
  2. progressive dyspnoea on exertion,
  3. dry irritating cough,
  4. no wheeze,
  5. may be preceded by viral type illness,
  6. fatigue
  7. weight loss common
  8. clubbing (50%),
  9. bibasal fine late inspiratory crackles;
  10. signs of RHF in advanced stages of disease
33
Q

Investigations

Idiopathic pulmonary fibrosis

A
  1. Bloods = ABG PCO2 rises in late stages of disease, ANA and RhF (1/3 positive);
  2. CXR = normal, ground glass shadowing, later stage reticulonodular shadowing, signs of cor pulmonale and honeycombing; high res CT;
  3. pulm function tests = restrictive features, decreased lung vols/compliance/lung capacity;
  4. bronchoalveolar lavage;
  5. lung biopsy - gold standard for dx;
  6. echo
34
Q

define

Obstructive sleep apnoea

A

Disease characterised by recurrent prolapse of pharyngeal airway and apnoea (cessation of airflow for >10s) during sleep, followed by arousal for sleep

35
Q

S+S

Obstructive sleep apnoea

A
  1. Excessive daytime sleepiness,
  2. unrefreshing/restless sleep,
  3. morning headaches,
  4. dry mouth,
  5. difficulty concentrating,
  6. Irritability and mood changes,
  7. partner reported choking/apnoeic episodes at night
  8. Large tongue,
  9. enlarged tonsils,
  10. long/thick uvula,
  11. retrognathia,
  12. neck circumference >42M, >40F;
  13. obesity,
  14. HTN
36
Q

Investigations

Obstructive sleep apnoea

A
  1. Sleep study = monitor airflow, resp effort, pulse oximetry and HR;
  2. bloods = TFTs, ABG
37
Q

Definition

Pneumoconiosis

A
  1. Fibrosing interstitial lung disease caused by chronic inhalation of mineral dusts = types:
  2. Simple = coalworker’s pneumoconiosis (syx-free)
  3. Complicated = resulting in loss of lung function
  4. Asbestosis = pneumoconiosis which diffuse parenchymal lung fibrosis occurs as a result of long exposure to asbestos
38
Q

S+S

Pneumoconiosis

A
  1. OCCUPATION, asyx picked up on routine CXR;
  2. Syx = insidious onset of shortness of breath, dry cough, black sputum (melanoptysis in coalworkers occasionally), pleuritic chest pain (asbestosis)
  3. Exam may be normal;
  4. coalworker’s pneumoconiosis and silicosis = decreased breath sounds;
  5. asbestosis = end inspiratory crepitations, clubbing;
  6. signs of pleural effusions or RHF
39
Q

Investigations

Pneumoconiosis

A
  1. CXR:
    1. simple = micronodular mottling,
    2. complicated = nodular opacities in upper lobes / micronodular shadowing / eggshell calcification of hilar lymph nodes / bilat lower zone retculonodular shadowing and pleural plaques;
  2. CT scan = fibrotic changes can be visualised early;
  3. bronchoscopy = visualisation and bronchoalveolar lavage;
  4. LFT = restrictive
40
Q

Definition

Pneumonia

A

Infection of distal lung parenchyma, classified = Community-acquired, nosocomial, aspiration pneumo, pneumo in immunocompromised, typical and atypical (mycoplasma, chlamydia, legionella)

41
Q

S+S

Pneumonia

A
  1. Fever, rigors, sweating, malaise, cough, sputum, SOB, pleuritic chest pain, confusion;
  2. atypical = headache, myalgia, darrhoea/abdo pain, DRY cough
  3. Pyrexia, resp distress, tachypnoea/cardia, hypotension, cyanosis, decreased chest expansion, chronic suppurative lung disease (clubbing), affected areas = dull to percuss , increased vocal fremitus, bronchial breathing and coarse crepitations
42
Q

Investigations

Pneumonia

A
  1. Bloods = FBC (^WCC), U&Es, LFT, blood cultures, ABG, blood film (mycoplasma = agglutination of RBC);
  2. CXR = lobar/patchy shadowing, pleural effusion;
  3. sputum/pleural fluids;
  4. urine (pneumococcus and legionella Ag);
  5. atypical viral serology;
  6. bronchoscopy, bronchoalveolar lavage
43
Q

Management

Pneumonia

A
  1. Assess severity with british thoracic society guidelines (markers).
  2. Start empirical Abx = oral amoxicillin (0), oral/IV amoxicillin and rythromycin (1), IV cefuroxime/cefotaxime/co-amoxiclav + erythromycin (>1), add metronidazole if aspiration, lung abcess or empyema, and switch based on sensitivity.
  3. Supportive treatment = O2, IV fluids, CPAP/BiPAP/ITU care for resp failure, surgical drainage for lung abcessess and empyema
  4. Discharge planning = 2 or more = high temp, tachycardia/pnoea, hypotension, low O2 sats, means high risk of readmission
  5. Prevention = pneumococcal vaccine, H. influenzae B vaccine
44
Q

Definition

Pneumothorax

A
  1. Air in pleural space (haemo = blood, chylo = lymph)
  2. Spontaneous = normal lungs, tall/thin males, rupture of subdural bleb;
  3. 2ry = pts with pre-existing lung disease;
  4. traumatic = penetrating injury to the chest, iatrogenic (JV cannulation, thoracocentesis);
  5. RF = collagen disorders (marfan’s, ehlers-danlos)
45
Q

S+S

Pneumothorax

A
  1. Asyx if small; sudden onset SOB, pleuritic chest pain, distress with rapid shallow breathing in tension pneumoT
  2. None if small, signs of resp distress, reduced expansion, hyper-resonance to percussion, reduced breath sounds;
  3. tension pneumoT = severe resp distress, tachycardia, hypotension, cyanosis, distended neck veins, tracheal deviation (AWAY)
46
Q

Investigations

Pneumothorax

A
  1. CXR -> dark film area with no vascular markings, fluid level may be seen if bleeding;
  2. ABG to check for hypoxaemia
47
Q

Management

Pneumothorax

A
  1. Tension = EMERGENCY so max O2, insert large bore needle into 2nd ICS at MCL, aspirate up to 2.5L of air, stop if cough/resistance is felt; follow up CXR 2hr and 2wks later;
  2. Chest drain with underwater seal = performed if aspiration fails, fluid in pleural cavity or after decompression of tension, inserted in 4-6th ICS at mid axillary line;
  3. Recurrent = clhemical pleurodesis (fusing visceral+parietal pleura with tetracycline), surgical pleurectomy.
  4. Advice = avoid air travel until follow up CXR confirms it resolved, avoid diving
48
Q

Definition

TB

A
  1. Granulomatous disease caused by mycobacterium tuberculosis;
  2. 1ry = initial infection may be pulmonary or GI (rare), Miliary = haematogenous dissemination of TB, post-1ry TB caused by reinfection/reactivation
49
Q

S+S

TB

A
  1. 1ry = asyx, fever, malaise, cough, wheeze, erythema nodosum, phlyctenular conjunctivitis;
  2. miliary = fever, weight loss, meningitis, yellow caseous tubercles;
  3. post-1ry = fever/night sweats, malaise, weight loss, SOB, cough, sputum, haemoptysis, pleuritic chest pain, signs of pleural effusion, collapse, consolidation, fibrosis;
  4. LN has suppuration leading to abcesses,
  5. CNS = meningitis, tuberculoma; skin = lupus vulgaris;
  6. heart = pericardial effusion, constrictive pericarditis;
  7. GI = subacute obstruction, change in bowel habit, weight loss, peritonitis, ascites;
  8. genitourinary = UTI syx, renal failure, epididymitis, endometrial/tubal involvement, infertility;
  9. adrenal insufficiency;
  10. osteomyelitis, arthritis, vertebral collapse, spinal cord compression
50
Q

Investigations

TB

A
  1. Sputum/pleural fluid/bronchial washing, tuberculin tests, mantoux test, heaf test;
  2. INF-g test, HIV testing, CT, LN, pleural biopsy, sampling of other affected systems,
  3. CXR=
    1. 1ry = peripheral consolidation, hilar lymphadenopathy
    2. Miliary = fine shadowing
    3. Post-1ry = upper lobe shadowing, streaky fibrosis and cavitation, callcification, pleural effusion, hilar lymphadenopathy
51
Q

Definition

Pulm embolism

A

Occlusion of pulmonary vessels, commonly by thrombus that travelled to pulm vascular system from another site

52
Q

S+S

Pulm Embolism

A
  1. Small may be asyx;
  2. moderate = sudden onset SOB, cough, haemoptysis, pleuritic chest pain;
  3. large (or proximal) = as mod and severe central pleuritic chest pain, shock, collapse, acute RHF, sudden death;
  4. multiple and recurrent ones = syx of pulm hypertension
  5. Small often has no clinical signs or some tachycardia/pnoea;
  6. moderate = tachypneoa/cardia, pleural rub, low O2 sats;
  7. massive = shock, cyanosis, signs of RH strain:
  8. raised JVP, left parasternal heave, accentuated S2;
  9. multiple recurrent = sx of pulm hypertension and RHF
53
Q

Investigations

Pulm embolism

A
  1. Well’s score used to determine the best investigations = low probability with Wells <4 = d-dimer; high probability with Wells >4 = imaging (CTPA). Others:
  2. bloods = ABG, thrombophilia screen
  3. ECG = normal/tachy, right acis deviation or RBBB/ S1Q3T3 pattern
  4. CXR = normal but helps exclude other dx.
  5. Spiral CT pulm angiogram = 1st line investigation; poor sensitivity for small emboli, very for med-large emboli
  6. VQ scan = indicates area of infarcted lung
  7. Pulm angiography = invasive, rarely necessary
  8. Doppler US of lowe limb
  9. Echo
54
Q

Management

Pulm Embolism

A
  1. 1ry prevention: compression stocking, heparin prophylaxis and good mobilisation and adequate hydration
  2. If haemodynamically stable = O2, anticoag with heparin/LMWH, switch to oral warfarin for at least 3months (INR at 2-3), analgesia
  3. If haemodynamically unstable = Resuscitate, O2, IV fluids, thrombolysis with tPA if cardiac arrest imminent
  4. Surgical/Radiological = embolectomy, IVC filters (sometimes for recurrent PEs despite adequate anticoag/anticoag contraindicated