Respiratory Flashcards

1
Q

Define extrinsic allergic alveolitis

A

• Interstitial inflammatory disease of the distal gas-exchanging parts of the lung caused by inhalation of organic dusts. Also known as hypersensitivity pneumonitis

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2
Q

Aetiology extrinsic allergic alveolitis

A

• In sensitised individuals, repetitive inhalation of allergens provokes a hypersensitivity reaction, which varies in intensity and clinical course depending on antigen
• In acute phase, alveoli are infiltrated with acute inflammatory cells
• Early diagnosis and prompt allergen removal can halt and reverse disease progression, so prognosis can be good.
o With chronic exposure, granuloma formation and obliterative bronchiolitis
• Antigenic dusts include microbes and animal proteins
o Bacteria
♣ Actinomycetes
• Farmer’s Lung
• Bagassosis
• Mushroom picker’s lung
o Animal proteins (ie Avian proteins)
♣ Pigeon breeder’s lung
♣ Bird Fancier’s lung

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3
Q
•	Acute 
o	Present 4-12 hrs after exposure 
o	Reversible episodes of:
♣	Dry cough
♣	Dyspnoea
♣	Malaise
♣	Fever
♣	Myalgia 
o	Wheeze and productive cough may develop if repeat high-level exposure
•	Chronic 
o	Slowly increasing breathlessness 
o	↓ exercise tolerance 
o	Weight loss 
o	Exposure is usually chronic, low level and maybe no Hx of previous acute episodes 
•	Acute 
o	Rapid shallow breathing 
o	Pyrexia 
o	Inspiratory crackles 
•	Chronic 
o	Fine inspiratory crackles 
o	Clubbing (rare)
A

extrinsic allergic alveolitis

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4
Q

Investigations extrinsic allergic alveolitis

A

• Immunological response to causative antigen
o Blood checked to determine whether there is antibody to the putative antigen
o Often not diagnostic because may find these in normal individual

•	Bloods
o	FBC
♣	Leukocytosis 
♣	Normocytic, normochromic anaemia 
o	↑ ESR
o	↓ Albumin 
•	CXR
o	Often can be normal in acute episodes 
o	ACUTE
♣	Patchy, nodular infiltrates 
o	CHRONIC: fibrosis 

• CT Chest
o Detects early changes
o Chronic: May show patchy ‘ground glass’ shadowing and nodules, extensive fibrosis

• Pulmonary function tests
o Reversible restrictive defect (low FEV1, low FVC)
o Preserved or increased FEV1/FVC ratio
o Reduced total lung capacity
o Reduced gas transfer during acute attacks

• Bronchoalveolar Lavage
o Increased lymphocytes and mast cells

• Lung biopsy can also be performed

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5
Q

Define ARDS

A
  • Non-cardiogenic pulmonary oedema and diffuse lung inflammation syndrome
  • Syndrome of acute and persistent lung inflammation with ↑ vascular permeability – maybe caused by direct lung injury or occur secondary to severe systemic illness
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6
Q

Aetiology ARDS

A

• Pathophysiology
o Direct lung injury or secondary to systemic illness lung damage release of inflammatory mediators ↑ capillary permeability due to endothelial dysfunction fluid leakage into alveoli as well as ↓ surfactant production impaired gas exchange and ↓ lung compliance

•	Common causes
o	Pulmonary 
♣	Pneumonia
♣	Gastric aspiration 
♣	Smoke inhalation 
♣	Injury 
♣	Vasculitis 
♣	Contusion 
o	Other 
♣	Shock 
♣	Septicaemia 
♣	Haemorrhage 
♣	Multiple transfusions 
♣	DIC
♣	Pancreatitis 
♣	Acute liver failure 
♣	Trauma
♣	Head injury 
♣	Malaria 
♣	Fat embolism 
♣	Burns 
♣	Obstetric events: eclampsia, amniotic fluid embolus 
♣	Drugs/toxins: aspirin, heroin
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7
Q
  • SOB
  • Respiratory distress
  • Cough
  • Acute onset

• Cyanosis
• Tachypnoea
• Tachycardia
• Bilateral widespread fine inspiratory crackles
• Hypoxia refractory to oxygen treatment
Peripheral vasodilation

A

ARDS

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8
Q

Investigations for ARDS

A

• Diagnosis is based on 3 criteria:
o Acute onset (within 1 week)
o Bilateral opacities on CXR
o PaO2/FiO2 (arterial to inspired oxygen) ratio of <300

  • CXR Bilateral infiltrates
  • ABG PaO2/FiO2 (arterial to inspired oxygen) ratio of <300

• Cultures tests for underlying infection
o Sputum
o Blood
o Urine
• Bloods
o Amylase/lipase to check for pancreatitis

  • Echocardiography: severe aortic or mitral valve dysfunction
  • Pulmonary artery catheterisation: PWCP less than or equal to 18mmHg
  • Bronchoscopy: if cause cannot be determined from history, and to exclude differentials
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9
Q

Define asbestosis

A

• Long term inflammation and scarring of the lungs caused by inhalation of asbestos fibres

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10
Q

Aetiology of asbestosis

A

• 3 different types of asbestos:
o Chrysotile (white asbestos) is the least fibrogenic.
o Crocidolite (blue asbestos) is the most fibrogenic.
Amosite (brown asbestos) has intermediate fibrogenicity.
• Asbestos commonly used in building trade always ask about OCCUPATION in resp history degree of exposure = degress of pulmonary fibrosis
• Inflammation gradually causes mesothelial plaques in pleura
• Causes ↑ risk of bronchial adenocarcinoma and mesothelioma
• SMOKING ↑ risk

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11
Q
  • Dyspnoea on exertion
  • Dry non-productive cough
  • Fine end–inspiratory crackles heard at bases and moving up as disease gets worse
  • Clubbing
A

Asbestosis

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12
Q

Investigations asbestosis

A

• CXR
o Lower zone linear interstitial fibrosis
o Pleural thickening

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13
Q

Define mesothelioma

A

• Aggressive tumour of mesothelial cells that usually occurs in pleura (90%), but sometimes in peritoneum, pericardium or testes.
o Mesothelium is thin epithelium that lines several body cavities including pleura, peritoneum, mediastinum and pericardium

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14
Q

Aetiology mesothelioma

A
  • Associated with occupations exposure to asbestos by relationship is complex
  • 90% report prev exposure to asbestos, but only 20% of pts have pulmonary asbestosis
  • Latent period between exposure and development of tumour can be up to 45 years
  • Malignant pleural mesothelioma rarely spreads to distant sites but most patients present with locally advanced disease
  • SMOKING ↑ risk
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15
Q
  • SOB
  • Chest pain (dull, diffuse, developing)
  • Constitutional symptoms: Fever, fatigue, sweats, weight loss
  • Dry and non-productive cough
  • Abdominal pain
  • Occasional palpable chest wall mass
  • Diminished breath sounds due to pleural effusion, trapped lung or bronchial obstruction
  • Dullness to percussion pleural effusion on affected side
  • Abdominal pain/obstruction
A

Mesothelioma

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16
Q

Investigations for mesothelioma

A

• Chest X-ray/CT
o Unilateral pleural effusion
o Irregular pleural thickening
o ↓ lung volumes

  • MRI and PET
  • Pleural fluid: can be sent for cytological analysis and may be blood stained

• Pleural biopsy
o Diagnosis is made on histology, usually following a thoracoscopy (pleural biopsy) – often done post-mortem
o Biopsy of the tumour can be immunostained with a stain that reacts with CALRETININ

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17
Q

Define aspergillus lung disease

A

• Lung disease associated with Aspergillus fungal infection

• There are five different ways this group of fungi can affect the lungs
o Asthma: type I hypersensitivity (atopic) reaction to fungal spores
o Allergic bronchopulmonary aspergillosis (ABPA): type I and type III hypersensitivity reactions to Aspergillus fumigatus
o Aspergilloma (mycetoma): a fungus ball within a pre-existing cavity (often caused by TB or sarcoidosis)
o Invasive aspergillosis
o Extrinsic allergic alveolitis (EAA): due to sensitivity to Aspergillus clavatus (‘malt worker’s lungs’)

18
Q

Aetiology aspergillus lung disease

A

• Aspergilloma
o Growth of an A. fumigates mycetoma ball in pre-existing lung cavity (e.g. post-TB/sarcoidosis, old infarct or abscess)

• Allergic Bronchopulmonary Aspergillosis (ABPA)
o Colonisation of the airways by Aspergillus fumigatus leads to IgE and IgG-mediated immune responses
o Usually occurs in asthmatics and CF patients
o The release of proteolytic enzymes, mycotoxins and antibodies leads to airway damage – this initially causes bronchoconstriction but as inflammation persists, permanent damage occurs causing bronchiectasis

• Invasive Aspergillosis
o Invasion of Aspergillus into lung tissue and fungal dissemination
o This occurs in immunosuppressed patients (e.g. neutropenia, steroids, AIDS) or after broad-spectrum antibiotic therapy

19
Q
•	Aspergilloma
o	Asymptomatic 
o	May cause cough, haemoptysis (potentially massive), lethargy, weight loss 
•	ABPA
o	Difficult to control asthma 
o	Recurrent episodes of pneumonia with wheeze, cough, sputum, dyspnoea, fever and malaise
•	Invasive Aspergillosis 
o	Cough  Non-productive 
o	Dyspnoea
o	Rapid deterioration 
o	Septic picture 
o	Headache 
o	Pleuritic chest pain  peripheral lung lesions 
  • Dullness in affected lung
  • ↓ breath sounds
  • Wheeze (in ABPA)
  • Pleural rub (in IA)
A

Aspergillus lung disease

20
Q

Investigations Aspergillus lung disease

A

Aspergilloma
o CXR
♣ May show a round mass with a crescent of air around it
♣ Usually found in the upper lobes
o CT or MRI - may be used if CXR is unclear
o NOTE: sputum cultures may be negative if there is no communication between the cavity colonised by Aspergillus and the bronchial tree
o Strongly positive serum precipitins
o Aspergillus skin test - +ve in 30%

ABPA
o	Immediate skin test reactivity to Aspergillus antigens 
o	Aspergillus-specific IgE radioallergosorbent test – RAST
o	Eosinophilia 
o	Raised total serum IgE 
o	Raised specific serum IgE and IgG to A. fumigatus – serum precipitins
o	Aspergillus in sputum
o	CXR
•	Transient patchy shadows 
•	Segmental collapse or consolidation
•	Distended mucous-filled bronchi 
•	Signs of complications:
♣	Fibrosis in upper lobes 
♣	Bronchiectasis 
o	CT
•	Lung infiltrates 
•	Central bronchiectasis 
o	Lung Function Tests
•	Reversible airflow limitation 
•	Reduced lung volumes/gas transfer 

Invasive Aspergillosis
o Aspergillus is detected in cultures or by histological examination
o Bronchoalveolar lavage fluid or sputum may be used diagnostically
o Chest CT
• Nodules surrounded by a ground-glass appearance (halo sign)
This is caused by haemorrhage into the tissue surrounding the fungal invasion

21
Q

Define idiopathic pulmonary fibrosis

A

• Chronic inflammatory condition of the lungs resulting in fibrosis of alveoli and interstitium
o Fibrosis excess collagen in connective and interstitial tissue causing thickening

22
Q

Aetiology idiopathic pulmonary fibrosis

A

• Cause is unknown
• Recurrent injury to alveolar epithelial cells = secretion of cytokines and GFs by pneumocytes, ie TGFb1
o Interstitial tissue between alveoli and capillaries contain fibroblasts and macrophages
♣ Cytokines released cause fibroblast activation, recruitment, proliferation, differentiations into myofibroblasts and ↑ collagen sysnthesis and deposition
o Over time = thickened interstitial layer causing problems with ventilation and oxygenation Alveoli are also stiffer
• This is restrictive disease as there is restricted lung expansion due to fibrosis of interstitium
• Loss of alveoli leading to fluid filled cysts surrounded by thick wall – known as honeycombing
• Certain drugs can produce similar illness (e.g. methotrexate, amiodarone)
• Histological Patterns
o Interstitial pneumonia

•	Risk Factors
o	Age
o	Male 
o	Smoking
o	Occupational exposure to metal or wood
o	Chronic microaspiration
o	Animal and vegetable dusts
23
Q
  • Gradual-onset, progressive dyspnoea on exertion
  • Dry irritating cough
  • No wheeze
  • Weight loss, fatigue, and malaise can be common
  • Take full occupational and drug history
  • Clubbing (50%)
  • Bibasal fine end expiratory crackles
A

Idiopathic pulmonary fibrosis

24
Q

Investigations idiopathic pulmonary fibrosis

A

• CXR
o Early disease may show ground glass shadowing
o Later stages bilateral lower zone reiculonodular shadowing
o Signs of cor pulmonale
o Honeycombing

• High resolution CT
o More sensitive in early disease than CXR

• Pulmonary function tests
o Restrictive changes (↓ FEV1 and FVC, with preserved or ↑ FEV1/FVC)
o ↓ lung vol, lung compliance, total lung capacity

• Bloods
o ANA and Rheumatoid factor elevated in 1/3 of patients

  • Bronchoalveolar Lavage - exclude infections and malignancy
  • Lung Biopsy - gold standard for diagnosisbut not always needed, histological changes are referred to as usual interstitial pneumonia (UIP)
25
Q

Define lung Ca

A

• Primary malignant neoplasm of the lung
o WHO classification of bronchocarcinoma:
♣ Small Cell Lung Cancer - 20%
♣ Non-Small Cell Lung Cancer - 80%
• Note: small cell has much worse prognosis with 3 month medial survival
• Small cell – made up of small cells that divide and spread rapidly
• Non-small cell: divide and spread slowly

26
Q

Aetiology Lung Ca

A
  • Smoking
  • Asbestos exposure
  • Other occupational exposure: polycyclic hydrocarbons, nickel, radon gas, chromium, arsenic, iron oxides
  • Atmospheric pollution
27
Q
•	Symptoms due to primary
o	Cough
o	Haemoptysis
o	Chest pain
o	Dyspnoea 
o	Recurrent pneumonia

• Symptoms due to local invasion
o Brachial plexus invasion –> shoulder/arm pain
o Left recurrent laryngeal nerve invasion –> hoarse voice and bovine cough
o Dysphagia
o Arrhythmias
o Horner’s syndrome

•	Symptoms due to metastatic disease or paraneoplastic phenomenon
o	Weight loss 
o	Fatigue
o	Fractures 
o	Bone pain
  • Fixed monophonic wheeze (suggesting that there is a single obstruction)
  • Signs of lobar collapse or pleural effusion
  • Signs of metastases (e.g. supraclavicular lymphadenopathy or hepatomegaly, bone tenderness, confusion, fits, cerebellar syndrome, proximal myopathy, peripheral neuropathy)
  • Cachexia
  • Anaemia
  • Clubbing
  • Hypertrophic pulmonary osteoarthropathy causing wrist pain
  • Lymphadenopathy – supraclavicular or axillary nodes
A

Lung Ca

28
Q

Investigations Lung Ca

A

• Diagnosis
o CXR – peripheral nodule, hilar enlargement, consolidation, lung collapse, pleural effusion, bony secondaries
o Sputum and pleural fluid cytology
o Bronchoscopy with brushings or biopsy – to give histology
o CT/US-guided percutaneous biopsy
o Lymph node biopsy

• Staging - requires CT/MRI of head, chest and abdomen. PET scans may also be useful
Staging = TNM

  • Radionuclide bone scan if suspected mets
  • Lung function tests to assess suitability for lobectomy
•	Bloods
o	FBC 
o	U&amp;Es 
o	Calcium (hypercalcaemia is a common feature)
o	ALP (raised with bone metastases) 
o	LFTs

• Pre-Op - ABG and pulmonary function tests

29
Q

Define OSA

A

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

30
Q

Aetiology OSA

A
  • Occurs due to narrowing of upper airways because of collapse of soft tissues of pharynx
  • Due to ↓ tone of pharyngeal dilators during sleep
•	Risk factors:
o	Weight gain– soft tissue in neck area
o	Surgical swelling
o	Smoking
o	Alcohol
o	Sedative use
o	Enlarged tonsils and adenoids in children
o	Macroglossia
o	Marfan's syndrome
o	Craniofacial abnormalities
31
Q
  • Excessive daytime sleepiness
  • Restless sleep
  • Morning headaches associated with snoring and OSA
  • Dry mouth caused by mouth breathing
  • Loud snoring
  • Episodes of apnoea
  • Episodic gaping
  • Irritability and mood changes, ↓ libido and cognitive performance
•	Macroglossia 
•	Enlarged tonsils 
•	Long or thick uvula
•	Retrognathia (pulled back jaws)
•	Neck circumference 
o	> 42 cm in males, > 40cm in females 
•	Obestiy 
•	HTN
A

OSA

32
Q

Investigations OSA

A

• Sleep Study(polysomnography)
o Monitor overnight with polysomnogram
o Monitor airflow, respiratory effort, pulse oximetry and heart rateand snoring and movement
o Occurrence of 15 or more episodes of apnoea or hypopnoea during 1 hour of sleep indicates significant sleep apnoea

33
Q

Define pneumoconiosis

A

• Fibrosing interstitial lung disease caused by inhalation of mineral dusts
• Types:
o Simple: Coalworker’s pneumoconiosis or silicosis (symptom-free) – due to inhalation of coal dust particles over 15-20 yrs.
♣ Ingested by macrophages which die, releasing their enzymes causing fibrosis
o Complicated: pneumoconiosis results in loss of lung function
o Asbestosis: pneumoconiosis in which diffuse parenchymal lung fibrosis occurs due to prolonged exposure to asbestos

34
Q

Aetiology pneumoconiosis

A

• Caused by inhalation of particles of:
o Coal dust
o Silica
o Asbestos

• Often can co-exists with chronic bronchitis

• Factors
o Occupational exposure (coal mining, quarrying, iron and steel foundries, stone cutting, sandblasting, insulation industry, plumbers, ship builders)
o Risk is dependent on extent of exposure and size/shape of particles
o CO-factors such as smoking and TB contribute

35
Q

o Insidious onset SOB
o Dry non-productive cough
o Black sputum (melanoptysis) - produced occasionally in coalworker’s pneumoconiosis
o Pleuritic chest pain (due to acute asbestos pleurisy) - in patients exposed to asbestos

• Coalworker’s pneumoconiosis and silicosis:
o Decreased breath sounds
• Asbestosis:
o End-inspiratory crackles
o Clubbing
• Signs of pleural effusion or right heart failure (cor pulmonale)

A

Pneumoconiosis

36
Q

Define Pneumothorax

A

• Air in the pleural space – potential space between visceral and parietal pleural

• Variants:
o Haemothorax – blood
o Chylothorax - lymph

37
Q

Aetiology Pneumothorax

A
• Primary/Spontaneous 
o	Occurs in people with typically 
normal lungs 
o	Typically in tall, thin males 
o	Probably caused by rupture 
of subpleural bleb (bulla) 

• Secondary
o Complication of underlying
pulmonary disease (e.g COPD, asthma, TB, pneumonia,
lung abscess, sarcoidosis)

• Traumatic
o Penetrating or blunt injury to chest
• Tension pneumothorax
o Either spontaneous or secondary but a one-way valve is formed. Air from outside can get into pleural space, but it can’t leave.
o Pleural space gets bigger and bigger, thus compressing heart and other structures

• Risk factors:
o Collagen disorders (eg. Marfan’s syndrome, Ehlers-Danlos syndrome)

38
Q
  • Sudden-onset breathlessness
  • Pleuritic chest pain
  • Reduced expansion on affected side
  • Hyper-resonance with percussion on affected side
  • Reduced breath sounds on affected side
A

Pneumothorax

39
Q

o Severe respiratory distress
o Tachycardia
o Hypotension
o Cyanosis
o Distended neck veins
o Tracheal deviation away from side of pneumothorax
o ↑ percussion note, ↓ air entry/breath sounds on affected side

A

Tension pneumothorax

40
Q

Investigations pneumothorax

A

• CXR
o Dark area of film with no vascular markings
o Pleural line identified
o Fluid level seen if there is bleeding
o CXR shouldn’t be performed for tension pneumothorax suspicion as it can delay immediate necessary treatment

41
Q

Management pneumothorax

A

• Tension Pneumothorax (medical emergency)
o Immediate needle decompression
♣ Large bore needle into 2nd intercostal space MCL on affected side, just above 3rd rib to avoid neurovascular bundle
♣ Up to 2.5L of air can be aspirated
♣ Stop if pt coughs or resistance is felt
♣ Then chest drain
♣ Follow up CXR 2hrs and 2 weeks later
o Oxygen therapy – high dose

• Chest drain with underwater Seal
o Performed if:
♣ Aspiration fails
♣ Fluid in the pleural cavity
♣ After decompression of tension pneumothorax
o Inserted in 4-6th interostal space Midax line (safe triangle) ↓ avoids long thoracic nerve and artery
• Advice
o Avoid air travel until follow-up CXR confirms pneumothorax has resolved
o Avoid diving

LOOK AT NOTES FOR PROPER TREATMENT

42
Q

Complications pneumothorax

A
  • Recurrent pneumothoraces

* Bronchopleural fistula