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2A revision > Respiratory > Flashcards

Respiratory Flashcards

1
Q

what is chronic obstructive pulmonary disease

A
  • chronic lung condition characterised by breathlessness due to poorly reversible and progressive airflow obstruction.
  • chronic bronchitis and emphysema
  • 1-4 % of population
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2
Q

pathology of chronic bronchitis

A
  • inflammation and scarring of small bronchioles

- Mucous gland hyperplasia and irritant effects of smoke causes productive cough

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3
Q

pathology of emphysema

A
  • inflammation and scarring of the small bronchioles
  • Imbalance of proteases and antiproteases causes destruction of the lung parenchyma with dilation of terminal airspaces (emphysema) and air trapping
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4
Q

pathophysiology of COPD

A
  • hyperinflation, thick mucus, dilated terminal airways
  • +/- bullae
  • finely pigmented macrophages in the respiratory bronchioles
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5
Q

clinical manifestations of COPD

A
  • exertional breathlessness, history of prolonged cough and sputum
  • dyspnoea
  • wheeze
  • FEV1<80 FEV1/FVC<70
  • cyanosis
  • cor pulmonale (R heart enlargement)
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6
Q

pink puffers

A
  • emphysema
  • raised alveolar ventilation, a near normal PaO2 and a normal or low PaCO2.
  • breathless but are not cyanosed
  • may progress to type I respiratory failure
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7
Q

blue bloaters

A
  • chronic bronchitis
  • lowered alveolar ventilation, with a low PaO2 and a high PaCO2.
  • cyanosed, may go on to develop cor pulmonale.
  • Their respiratory centres are relatively insensitive to CO2 and they rely on hypoxic drive
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8
Q

investigations for COPD

A
  • FBC = raised packed cell volume (PCV)
  • CXR: hyperinflation, flat hemidiaphragms
  • CT: bronchial wall thickening, scarring, air space enlargement
  • ECG: right hypertrophy (cor pulmonale)
  • ABG: low PaO2 with hypercapnia
  • Spirometry: obstructive + air trapping
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9
Q

management for COPD

A
  • exercise, weight loss, stop smoking
  • mucolytics (dornase alfa)
  • diuretics for oedema
  • SABA or SAMA (muscarinic antagonist)
  • may need long acting or ICS
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10
Q

acute exacerbations of COPD

A
  • mostly in winter and triggered by infections
  • increased cough, wheeze, breathlessness
  • ABG, ECG, FBC, CXR
  • ensure oxygenation then treat cause
  • salbutamol, IV hydrocortisone, Abx
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11
Q

what is asthma

A
  • A chronic inflammatory disorder of large airways characterised by recurrent episodes of reversible airway narrowing
  • most associated with atopy (asthma, hay fever, eczema) = genetic tendency of immune system to produce IgE in response to common allergens
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12
Q

pathology of asthma

A
  • produce large amount of allergen specific IgE = binds onto surface of mast cells
  • re-exposure = IgE crosslink = degranulation of mast cells
  • airway inflammation and bronchospasm
  • ongoing inflammation = hypersensitive airways = react to exercise, cold air, cigarette smoke
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13
Q

features of asthma

A
  • Inflammation of the mucosa
  • Increased mucous production
  • Bronchodilation
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14
Q

clinical manifestations of asthma

A
  • Intermittent episodes of breathlessness, wheeze, and chest tightness
  • Cough, particularly at night
  • NSAIDs and B blockers can precipitate attack
  • acid reflux
  • poor sleep
  • hyperinflated chest
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15
Q

investigations for asthma

A
  • spirometry, reversibility test (spirometry will increase after dose of salbutamol)
  • PEF
  • CXR = hyperinflation (chronic asthma)
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16
Q

management of asthma

A
  • step 1 = occasional SABA
  • step 2 = + ICS (beclomethasone 200mcg/day)
  • step 3 = Leukotriene receptor antagonist (LRTA, e.g. montelukast)
  • 4 = LABA (e.g. salmeterol)
  • 5 = Increase ICS dose
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17
Q

management of acute severe asthma attack (OSHIT)

A
  • OXYGEN to maintain 94-98%
  • SALBUTAMOL 5mg nebulised
  • add IPRATROPIUM to nebuliser if life-threatening
  • iv HYDROCORTISONE/ prednisolone
  • THEOPHYLLINE IV (bronchodilator)
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18
Q

what is resp failure (type 1 and 2)

A
  • Defined as arterial PO2 <8kPa.
  • Type 1 = normal or low pCO2
  • Type 2 = raised pCO2
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19
Q

causes of type 1 resp failure

A
  • Severe pneumonia
  • Pulmonary embolism
  • Acute asthma
  • Pulmonary fibrosis
  • Acute LVF
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20
Q

causes of type 2 resp failure

A
  • COPD
  • Neuromuscular disorders impairing ventilation e.g. myasthenia gravis
  • Reduced respiratory drive e.g. sedative drugs
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21
Q

pathology of resp failure (1 and 2)

A

1) increased ventilation removes CO2 but can’t compensate for low pO2 (ventilation/perfusion mismatch)
2) generalised alveolar hypoventilation

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22
Q

clinical features of resp failure

A
  • hypoxia = dyspnoea, restlessness, agitation, confusion, central cyanosis (long standing hypoxia = pulmonary hypertension and cor pulmonale)
  • hypercapnia = Headache, peripheral vasodilation, tachycardia, bounding pulse, tremor/flap, papilledema, confusion, drowsiness, coma
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23
Q

investigations for resp failure

A
  • Blood tests: FBC, U&E, CRP, ABG
  • Radiology: CXR
  • Microbiology: sputum and blood cultures
  • Spirometry
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24
Q

management of type 1 resp failure

A
  • Treat underlying cause
  • Give oxygen facemask
  • Assisted ventilation if PaO2 <8kPa despite 60% O2
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25
Q

management of type 2 resp failure

A
  • respiration driven by hypoxia
  • treat cause
  • controlled O2 therapy (start at 24% O2)
  • recheck ABG after 20 min, if PaCO2 lower then increase O2 to 28%
  • may need intubation and ventilation
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26
Q

what is hypersensitivity pneumonitis/ extrinsic allergic alveolitis

A

interstitial lung disease caused by an immunologic reaction to inhaled antigens

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27
Q

causes of hypersensitivity pneumonitis

A
  • Thermophilic bacteria (mouldy hay, compost, air conditioner ducts)
  • Fungi (mouldy maple bark, barley or wood dust)
  • Avian proteins (bird droppings and feathers)
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28
Q

pathology of hypersensitivity pneumonitis

A
  • Inhaled antigens lead to an abnormal immune reaction in the lungs
  • antibody (type 2), immune complex (type 3) and cell-mediated (type 4) hypersensitivity reactions
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29
Q

clinical manifestations of hypersensitivity pneumonitis

A
  • acute disease = severe breathlessness, cough and fever 4-6h after large exposure, resolves in 12-18h
  • chronic disease = prolonged exposure to small amount of antigen, gradual onset of breathlessness, dry cough, fatigue, clubbing, weight loss, type1 RF
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30
Q

investigations for hypersensitivity pneumonitis

A
  • High resolution CT shows middle to upper lobe-predominant linear interstitial opacities and small nodules
  • chronic = honey comb lung on CXR, ground glass appearance on CT
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31
Q

management of hypersensitivity pneumonitis

A
  • identify cause and avoid
  • persistent exposure = fibrosis and honeycomb
  • acute =O2, PO prednisolone, reducing course
  • chronic = avoid allergen or wear facemask, long term steroids
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32
Q

Coal worker pneumoconiosis

A
  • inhalation of coal dust particles over 15-20yrs
    = ingested by macrophages which die, releasing enzymes and causing fibrosis
    -CXR = round opacities in upper zone
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33
Q

progressive massive fibrosis

A
  • due to progression of CWL
  • dyspnoea, fibrosis, cor pulmonale
  • CXR = fibrotic masses in peripheries of upper-mid zone
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34
Q

Caplan’s syndrome

A

The association between rheumatoid arthritis, pneumoconiosis, and pulmonary rheumatoid nodules

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35
Q

silicosis

A
  • inhalation of silica particles, very fibrogenic
  • metal mining, stone quarrying, pottery
  • CXR = nodular pattern, egg-shell calcification of hilar nodes
  • increases risk of TB
  • spirometry = restrictive
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36
Q

asbestosis

A
  • causes pulmonary fibrosis
  • dyspnoea, clubbing, fine-end crackles
  • increased risk of bronchial adenocarcinoma and mesothelioma
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37
Q

byssinosis

A
  • cotton mill worker
  • symptoms start on first day back then improve through week
  • endotoxins in bacteria in raw cotton
  • no CXR changes
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38
Q

what is bronchiectasis

A
  • abnormal permanent dilation of bronchi accompanied by inflammation in their walls and in adjacent lung parenchyma
  • causes in developed countries = obstruction due to tumour/foreign body or CF related
  • post infection (measles, pertussis, bronchiolitis, pneumonia, TB, HIV)
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39
Q

pathology of bronchiectasis

A
  • weakening in bronchial walls caused by recurrent inflammation
  • Scarring in the adjacent lung parenchyma places traction on the weakened bronchi, causing them to permanently dilate.
  • Permanent thinning of these airways.
  • Main organisms: H. influenzae, Strep. Pneumoniae, Staph. Aureus, Pseudomonas aeruginosa
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40
Q

signs and symptoms of bronchiectasis

A
  • Persistent cough, Copious purulent sputum, Intermittent haemoptysis
  • Finger clubbing, Coarse inspiratory crepitations, Wheeze
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41
Q

complications of bronchiectasis

A
  • Pulmonary hypertension and RVF
  • Pneumothorax
  • Deposition of serum amyloid A protein in β-pleated sheets in multiple organs (AA amyloidosis)
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42
Q

investigations for bronchiectasis

A
  • Sputum culture
  • CXR: cystic shadows, thickened bronchial walls
  • spirometry = obstructive
  • bronchoscopy
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43
Q

management of bronchiectasis

A
  • Airway clearance techniques (chest physio) and mucolytics
  • Abx
  • bronchodilators
  • surgery if severe haemoptysis
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44
Q

what is cystic fibrosis

A
  • An inherited disorder caused by a mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene
  • AR
  • CFTR is on chromosome 7q and codes for a chloride ion channel
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45
Q

pathology of CF

A
  • deletion of phenylalanine 508 (F508 mutation) causes abnormal folding of the CFTR protein
  • Lack of normal CFTR = defective electrolyte transfer across epithelial cell membranes = thick mucus secretions
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46
Q

clinical manifestations of CF

A
  • Neonate: failure to thrive, meconium ileus (cause bowel obstruction), rectal prolapse
  • Children and young adults: cough, wheeze, recurrent infections, pancreatic insufficiency (DM), gallstones, cirrhosis, male infertility, osteoporosis, arthritis, vasculitis, nasal polyps
  • liver failure develops late
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47
Q

investigations for CF

A
  • neonatal screening = raised serum immunoreactive trypsin
  • sweat test = sodium and chloride >60mmol/L
  • CXR = hyperinflation, bronchiectasis
  • abdo US = fatty liver, cirrhosis, chronic pancreatitis
  • spirometry = obstructive
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48
Q

management of CF

A
  • multidisciplinary
  • chest physio (postural drainage), bronchodilators
  • Abx for infective exacerbations
  • treat other symptoms (eg DM), fat-soluble vitamins
  • may need ventilation or lung transplant later on
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49
Q

what is a pleural effusion

A
  • accumulation of excess fluid within the pleural space
  • Blood = haemothorax
  • Pus = empyema
  • Chyle (lymph with fat) = chylothorax
  • Both blood and air = hemopneumothorax
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50
Q

what can cause pleural effusion

A
  • VF, Pneumonia, Pulmonary embolism, Malignancy
  • Multisystem autoimmune disease e.g. lupus, RA
  • Transudates =raised venous pressure (cardiac failure, constrictive pericarditis, fluid overload) or hypoproteinaemia (cirrhosis, nephrotic syndrome, malabsorption).
  • Exudates = increased leakiness of pleural capillaries secondary to infection, inflammation or malignancy
51
Q

clinical manifestations of pleural effusion

A
  • small = asymptomatic
  • large = breathlessness and pleuritic chest pain
  • Decreased expansion, Stony dull percussion note, Diminished breath sounds
52
Q

investigations for pleural effusion

A
  • CXR
  • aspiration
  • pleural biopsy
53
Q

management of pleural effusion

A
  • drainage
  • pleurodesis = irritant drug to stick lung to chest wall
  • surgery if persistent and thickening of pleura
54
Q

what is pneumothorax

A
  • air in pleural space
55
Q

causes of pneumothorax

A
  • spontaneous = thin, tall young men (rupture of small apical blebs of lung tissue from stretching of lung)
  • underlying lung issue (COPD, asthma, pneumonia)
  • Trauma e.g. penetrating chest wound, rib fractures
  • Iatrogenic e.g. subclavian vein cannulation, lung biopsy
56
Q

what is a tension pneumothorax

A
  • rare
  • tissues near the lung defect and act as a one-way valve, preventing the equalization of pressure = continuous build-up of pressure and volume on each breath
  • causes cardiorespiratory arrest
  • respiratory distress, tachycardia, hypotension, distended neck veins
57
Q

clinical manifestations of pneumothorax

A
  • Sudden onset of unilateral pleuritic chest pain
  • Breathlessness
  • asthma/COPD = sudden deterioration
58
Q

investigations for pneumothorax

A
  • CXR will show air (don’t do if tension pneumothorax suspected unless air removed first)
  • expiratory film
59
Q

management of pneumothorax

A
  • chest drain

- aspiration

60
Q

what is a lung carcinoma

A
  • malignant epithelial tumour arising in the lung
  • small cell carcinoma (SCLC)
  • NSCLC = adenocarcinoma, squamous cell carcinoma,
  • rare subtypes
61
Q

carcinogenesis of lung carcinomas

A
  • likely to arise from a precursor phase of epithelial dysplasia = neoplastic transformation
  • Adenomatous dysplasia/ adenocarcinoma in situ precedes adenocarcinoma
  • Squamous dysplasia/ squamous carcinoma in situ precedes squamous cell carcinoma
62
Q

clinical manifestations of lung carcinoma

A
  • local growth = progressive breathlessness, cough, chest pain, hoarseness or loss of voice, haemoptysis, weight loss, and recurrent pneumonia
  • metastases = Abdo pain, bony pain, and neuro symptoms
  • small cell carcinomas can present with paraneoplastic syndromes (cushings, ADH, PTH, HCG) or the superior vena cava syndrome
63
Q

treatment of NSCLC

A
  • lobectomy

- radical radiotherapy

64
Q

treatment of SCLC

A
  • surgery
  • chemo/radiotherapy
  • SVC stent + radiotherapy + dexamethasone
  • analgesia, steroids, anti-emetics
65
Q

risk factors of carcinoma of the bronchus

A
  • smoking, asbestos, Chromium, arsenic, iron oxides, and radiation
66
Q

signs of carcinoma of the bronchus

A
  • Cachexia (wasting)

- Anaemia

67
Q

complications of carcinoma of the bronchus

A
  • Local: recurrent laryngeal nerve palsy
  • Phrenic nerve palsy
  • SVC obstruction
68
Q

investigations for carcinoma of the bronchus

A
  • CXR: peripheral nodule, hilar enlargement, lung collapse
  • Cytology: sputum and pleural fluid
  • Fine needle aspiration or biopsy
  • Lung function tests
69
Q

bronchial adenoma

A
  • rare, slow-growing. 90% are carcinoid tumours.

- Treatment – surgery

70
Q

hamartoma

A
  • rare, benign.
  • CT: lobulated mass with flecks of calcification
  • Excise
71
Q

what is a mesothelioma

A
  • malignant tumour arising in the pleura from mesothelial cells and showing a diffuse pattern of growth over the pleural surfaces
  • asbestos fibres become coated in iron (asbestos bodies) and are permanently trapped in lungs
72
Q

clinical manifestations of mesothelioma

A
  • Breathlessness (large pleural effusion)
  • Chest pain
  • Weight loss and malaise
  • Signs of metastases; Lymphadenopathy, Hepatomegaly, Bone pain/tenderness, Abdominal pain/ obstruction
73
Q

management of mesothelioma

A
  • pemetrexed + cisplatin chemo

- pleurodesis, indwelling pleural drain

74
Q

what is pulmonary hypertension

A
  • mean pulmonary artery pressure >25mmHg at rest or >30mmHg during exercise.
  • secondary = complication of chronic lung or cardiac disease
  • primary (idiopathic, certain drugs, HIV, collagen vascular disease, congenital systemic-to-pulmonary shunts)
75
Q

pathology of pulmonary hypertension

A

Chronic hypoxia and obliterative pulmonary fibrosis = raised pressure in the pulmonary arterial circulation

76
Q

clinical manifestations of pulmonary hypertension

A
  • exertional dyspnoea and fatigue

- dizziness, syncope

77
Q

investigations for pulmonary hypertension

A
  • CXR: enlarged proximal pulmonary arteries which taper distally
  • ECG: RVH, and P pulmonale (peaked P waves)
  • Echo: right ventricular dilation/ hypertrophy
78
Q

management of pulmonary hypertension

A
  • oxygen
  • warfarin (due to high risk of intrapulmonary fibrosis)
  • diuretics
  • oral CCBs
  • treat cause
79
Q

microbiology of TB

A
  • Myocbacterium tuberculosis, an acid-fast rod-shaped bacillus
  • Active infection occurs when containment by the immune system (T-cells/macrophages) is inadequate from primary infection or re-activation
  • respiratory spread from patient with active pulmonary TB
80
Q

latent TB

A
  • infection without disease
  • persistent immune system containment
  • Risk factors for reactivation include new infection, HIV, organ transplantation, immunosuppression, silicosis, illicit drug use, malnutrition, high-risk settings
81
Q

pathology of TB

A
  • Inhaled bacilli are engulfed by alveolar macrophages but can survive and multiply within them
  • spread to O2 rich sites (lung apices, kidneys, bone, meninges)
  • mycobacteria-specific CD4+ helper T-cells are activated following MHC class II antigen presentation
  • Th1 subset helper T-cells secrete interferon (IFN)-gamma = macrophages into epithelioid macrophages = granulomas = wall off the mycobacteria in an anoxic and acidic environment = scarring
82
Q

clinical manifestations of TB

A
  • chronic pneumonia = persistent cough, fever, night sweats, weight loss and loss of appetite
  • Extrapulmonary TB = Meningitis, Lymphadenopathy, Genitourinary symptoms, Bone or joint pain
  • can affect any organ
83
Q

investigations for TB

A
  • acid fast bacilli (Ziehl-Neelsen stain) in sputum, pleural fluid, or bronchoalveolar lavage (BAL) fluid
  • culture = definitive but takes 12 weeks
  • Tuberculin skin testing (TST) = Mantoux test
    Interferon-gamma release assays (IGRAS)
84
Q

treatment for TB

A
  • Rifampicin – 2 months intensive, 4 months continuation
  • Isoniazid – 2 months intensive, 4 months continuation
  • Pyrazinamide – 2 months intensive
  • Ethambutol – 2 months intensive
85
Q

what is pneumonia and its 4 classifications

A
  • infection of the lung parenchyma caused by bacterial organisms
  • community-acquired, hospital-acquired, aspiration, immunosuppression
86
Q

microbiology of pneumonia

A
  • Community-acquired: streptococcus pneumoniae, mycoplasma pneumoniae, Haemophilus influenzae, Legionella pneumophila.
  • Hospital-acquired: gram-negative bacteria, e.g. Klebsiella, Escherichia coli, Pseudomonas
  • Aspiration: mixed aerobic and anaerobic bacteria
  • Immunosuppression: all
87
Q

clinical manifestations of pneumonia

A
  • Productive cough
  • Breathlessness
  • Chest pain
  • Fever
  • Haemoptysis
  • pyrexia, cyanosis, confusion, tachycardia, tachypnoea
88
Q

investigations for pneumonia

A
  • sats, blood tests, sputum culture
  • CXR = lobar or multilobar infiltrates, cavitation, or pleural effusion
  • check urine for Legionella/ Pneumococcal urinary antigens
89
Q

severity of pneumonia (CURB-65)

A
  • 1 point each
  • Confusion
  • Urea >7mmol/L
  • Respiratory rate >30/min
  • BP <90 systolic and/or 60mmHG diastolic
  • Age 65+
90
Q

management of pneumonia

A
  • severity 0-1 = Abx/ home treatment
  • 2 = hospital therapy
  • 3 = severe pneumonia (mortality 15-40%)
  • give O2, treat hypotension, keep hydrated, find pathogen, Abx, analgesia
91
Q

what antibiotics for pneumonia

A

amoxicillin/ flucloxacillin + clarithromycin

92
Q

common cold (acute coryza)

A
  • usually rhinovirus spread by droplets
  • incubation 12h-5d
  • malaise, slight pyrexia, sore throat, watery nasal discharge
93
Q

sinusitis

A
  • Infection of paranasal sinuses
  • Strep pneumoniae or H. influenzae
  • frontal headache, facial pain, nasal discharge
  • co-amoxiclav, topical corticosteroids ( fluticasone propionate nasal spray), steam inhalations
94
Q

rhinitis

A
  • Sneezing attacks, nasal discharge or blockage occurring for more than 1h for most days;
  • For a limited period of the year (seasonal rhinitis) = hayfever = itching of eyes and soft palate
  • Throughout the whole year (perennial or persistent rhinitis) = allergic or non-allergic +/- nasal polyps
  • skin prick testing
  • avoid allergens, antihistamines (loratadine/ cetirizine), beclomethasone spray twice daily (decongestant)
95
Q

acute pharyngitis

A
  • adenoviruses
  • sore throat and fever
  • More persistent and severe pharyngitis implies bacterial infection – haemolytic Strep, Haemophilus influenzae, staphylococcus aureus = IV penicillin 4x daily for 10d
96
Q

acute laryngotracheobronchitis (croup)

A
  • parainfluenza virus or measles virus
  • severe in <3 y/o
  • Inflammatory oedema involving larynx = hoarse voice, barking cough (croup) and stridor
  • Tracheitis = burning retrosternal pain
  • O2, oral/IM corticosteroids, nebulised adrenaline
97
Q

influenza

A
  • mostly type A and B
  • coated with haemagglutinin (H) and neuraminidase (N) = for attachment to resp epithelium
  • human immunity against surface proteins
  • influenza A = antigenic shift = major changes to H and N antigens = pandemic
  • seasonal influenza in winter
98
Q

presentation of influenza

A

Fever, dry cough, sore throat, coryzal symptoms, headache, malaise, myalgia, conjunctivitis, eye pain, photophobia

99
Q

diagnosis of influenza

A
  • clinical = acute onset + cough +fever
  • public health surveillance
  • viral PCR, rapid antigen testing, viral culture of clinical samples
100
Q

treatment of influenza

A
  • uncomplicated = symptomatic treatment (paracetamol)
  • complicated or high risk = antivirals = hospital admission
  • antiviral inhibitors of influenza neuraminidase: Oseltamivir, Zanamivir
101
Q

pathology of PE

A
  • thrombus in deep vein (DVT) embolises > R side of heart > pulmonary arterial circulation >loges in pulmonary artery
102
Q

clinical manifestations of PE

A
  • blockage of major artery = instant death due to sudden huge rise in pulmonary arterial pressure
  • medium = area of ventilation/perfusion mismatch and breathlessness
  • small = subtle breathlessness, chest pain, dizziness
103
Q

investigations for PE

A
  • FBC, U&E, baseline clotting, D-dimers
  • ABG may show lowered PaO2 and PaCO2
  • Imaging: CXR may be normal, or show oligaemia of affected segment
  • ECG: sinus tachycardia
104
Q

management of PE

A
  • O2 if hypoxic
  • Aspirin
  • morphine IV with anti-emetic
  • IV alteplase to thrombolyse massive PE
  • if haemodynamically stable then start LMWH
105
Q

prevention of PE

A
  • Give heparin to all immobile patients.

- Stop HRT and the combined contraceptive pill pre-op

106
Q

what is interstitial lung disease (ILD)

A
  • describe a number of conditions that primarily affect the lung parenchyma in a diffuse manner.
  • chronic inflammation and/or progressive interstitial fibrosis
107
Q

clinical features of ILD

A
  • Dyspnoea on exertion
  • Non-productive paroxysmal cough
  • Abnormal breath sounds
  • Abnormal CXR
  • Restrictive pulmonary spirometry
108
Q

pathological features of ILD

A
  • Fibrosis and remodelling of the interstitium
  • Chronic inflammation
  • Hyperplasia of type II epithelial cells or type II pneumocytes
109
Q

classification of ILD

A
  • known cause = occupation, drugs, hypersensitivity etc
  • associated with systemic disorders = sarcoidosis, RA, SLE etc
  • idiopathic = idiopathic pulmonary fibrosis, non-specific interstitial pneumonitis
110
Q

idiopathic pulmonary fibrosis

A
  • idiopathic interstitial pneumonia limited to the lung
  • histological appearance of usual interstitial pneumonia (UIP)
  • abnormal repair mechanism to alveolar injury = overexpress profibrotic cytokines = irreversible lung damage
111
Q

clinical manifestations of idiopathic pulmonary fibrosis

A
  • breathlessness, non-productive cough, malaise, weight loss, arthralgia, cyanosis, clubbing, fine end-inspiratory crepitations
112
Q

investigations for idiopathic pulmonary fibrosis

A
  • ABG = low PaO2 (severe = raised PaCO2)
  • CXR = decreased TLV, honeycomb lung
  • spirometry = restrictive
  • lung biopsy
113
Q

management of idiopathic pulmonary fibrosis

A
  • oxygen, pulmonary rehabilitation, opiates, palliative care input
  • consider for lung transplant and clinical trials
114
Q

what is sarcoidosis

A
  • multisystem disease of unknown cause in which tissues are infiltrated by granulomas
  • granulomatous inflammation
115
Q

clinical manifestations of sarcoidosis

A
  • any organ affected, most common is lymph nodes, lungs and skin
  • acute = presents suddenly, erythema nodosum
  • chronic = insidious, lupus pernio, pulmonary fibrosis, posterior uveitis
  • pulmonary = dry cough, dyspnoea, low exercise tolerance
  • lymphadenopathy, hepatomegaly, glaucoma
116
Q

investigations for sarcoidosis

A
  • Blood: raised ESR, lymphopenia
  • 24h urine: raised calcium
  • CXR is abnormal
  • Tissue biopsy: diagnostic and shows non-caseating granulomata
117
Q

management of sarcoidosis

A
  • acute = bed rest, NSAIDs
  • corticosteroids if uveitis, hypercalcaemia, neuro/cardio involvement
  • severe illness = IV methylprednisolone
118
Q

what is Goodpasture’s syndrome ( anti-GBM disease)

A
  • Rare.
  • Auto-antibodies to type IV collagen which is present in glomerular and alveolar basement membranes (anti-GBM Abs).
  • A pulmonary-renal syndrome
119
Q

clinical manifestations of Goodpasture’s syndrome

A
  • Renal disease – oliguria/anuria, haematuria, AKI, renal failure
  • Lung disease – pulmonary haemorrhage, SOB, haemoptysis
  • crescent glomerulonephritis
120
Q

management of Goodpasture’s syndrome

A
  • Plasma exchange
  • Corticosteroids
  • Cyclophosphamide
  • Treat shock
121
Q

what is Wegener’s granulomatosis (granulomatosis with polyangiitis [GPA])

A
  • A systemic ANCA-associated vasculitis characterised by dominant upper respiratory tract, lung and renal involvement and cANCA positivity.
  • necrotising granulomatous inflammation and vasculitis of small and medium vessels
122
Q

clinical manifestations of Wegener’s granulomatosis

A
  • Nasal symptoms – nasal obstruction, ulcers, or destruction of nasal septum
  • Acute renal failure
  • Pulmonary symptoms – cough, haemoptysis or pleuritis
  • Skin purpura or nodules
  • Peripheral neuropathy
  • Mononeuritis multiplex
123
Q

management of Wegener’s granulomatosis

A
  • severe = corticosteroids and cyclophosphamide

- aggressive immunosuppression needed

2A revision (10 decks)

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