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Year 3 Knowledge - Conditions and Procedures > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Define acute respiratory distress syndrome.

A

Syndrome of acute and persistent lung inflammation with increased vascular permeability.

  • Acute onset
  • Bilateral infiltrates consistent with pulmonary oedema
  • Hypoxaemia - PaO2 /FiO2 < 200mmHg regardless of the level of positive end-expiratory pressure (PEEP)
  • No clinical evidence for increased left atrial pressure (pulmonary capillary wedge pressure PCWP <18mmHg)
  • ARDS is the severe end of the spectrum of acute lung injury (ALI)
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2
Q

Explain the aetiology /risk factors of acute respiratory distress syndrome.

A

Severe insult to the lungs or other organs induces the release of inflammatory mediators, increased capillary permeability, pulmonary oedema, impaired gas exchange and reduced lung compliance.

Causes:

  • Sepsis
  • Aspiration
  • Pneumonia
  • Pancreatitis
  • Trauma / Burns
  • Transfusion - massive, transfusion-related lung injury
  • Transplantation (bone marrow, lung)
  • Drug overdose / reaction
  • Alcohol misuse
  • Smoke inhalation
  • Drowning
  • E-cigarette and vaping product use
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3
Q

Summarise the epidemiology of acute respiratory distress syndrome.

A

1 in 6000 per year in UK

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4
Q

Recognize the presenting symptoms of acute respiratory distress syndrome.

A
  • Rapid deterioration of respiratory function
  • Dyspnoea
  • Respiratory distress
  • Cough
  • Symptoms of aetiology
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5
Q

Recognize the signs of acute respiratory distress syndrome on physical examination.

A
  • Cyanosis
  • Tachypnoea
  • Tachycardia
  • Widespread inspiratory crepitations
  • Hypoxia refractory to oxygen treatment
  • Bilateral signs
  • May be asymptomatic in early stages
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6
Q

Identify appropriate investigations for acute respiratory distress syndrome and interpret the results.

A
  1. CXR
  2. Bloods
  3. Echocardiography
  4. Pulmonary artery catheterisation
  5. Bronchoscopy

CXR
- Bilateral alveolar and interstitial shadowing

Bloods

  • FBC
  • U&E
  • LFT
  • ESR / CRP
  • Amylase
  • Clotting
  • ABG
  • Blood culture
  • Sputum culture
  • Plasma BNP < 100pg/mL may distinguish between ARDS and heart failure (cannot exclude if critically ill)

Echocardiography
- Severe aortic or mitral valve dysfunction or low left ventricular ejection fraction favours haemodynamic oedema over ARDS

Pulmonary Artery Catheterisation

  • PCWP <18mmHg
  • High PCWP does not exclude ARDS as patients may have concomitant left ventricular dysfunction

Bronchoscopy

  • If cannot determine from history
  • Exclude differentials - e.g. diffuse alveolar haemorrhage
  • To lavage fluid for microbiology - mycobacteria, Legionella pneumophila
  • For cytology - eosinophils, viral inclusion bodies, cancer cells

Diffuse Alveolar Haemorrhage

  • Frothy blood in airways
  • Haemosiderin-laden macrophage from lavage fluid
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7
Q

Define arterial blood gas.

A

A collective term applied to three separate measurements = pH, PCO2 and PO2.
They are generally made together to evaluate acid-base status, ventilation and arterial oxygenation.

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8
Q

Summarise the indications for an arterial blood gas.

A
  • Respiratory failure - both acute and chronic states
  • Any illness that may lead to a metabolic acidosis - e.g. cardiac failure, liver failure, renal failure, hyperglycaemic states (DM), multiorgan failure, sepsis, burns, poisons/ toxins
  • Ventilated patients
  • Sleep studies
  • Severely unwell patients from any cause - affects prognosis.
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9
Q

Identify the possible complications of an arterial blood gas.

A
  • Local haematoma
  • Arterial vasospasm
  • Arterial occlusion
  • Air or thrombus embolism
  • Local anaesthetic anaphylactic reaction
  • Infection at the puncture site
  • Needle-stick injury to healthcare personnel
  • Vessel laceration
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10
Q

Define asbestos-related lung disease (including asbestosis and mesothelioma).

A

Asbestosis - diffuse interstitial fibrosis of the lung as a consequence of exposure to asbestos fibres

Mesothelioma - a tumour of the mesothelial cells that usually occurs in the pleura, and rarely in the peritoneum or other organs, associated with asbestos exposure but relationship is complex

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11
Q

Explain the aetiology / risk factors of asbestos-related lung disease (including asbestosis and mesothelioma).

A

Asbestosis

  • Caused by inhalation of asbestos fibers
  • Commonly sued in building trade for fireproofing, pipe lagging, electrical wire insulation and roofing felt
  • Degree of asbestos exposure is related to degree of pulmonary fibrosis.
  • Onset occurs after 10+ years following initial exposure
  • Increases risk of bronchial adenocarcinoma & mesothelioma

Risk factors:

  • Occupational exposure
  • Longer duration of exposure
  • Smoking history
  • Indirect exposure

Mesothelioma

  • Long latency period (20-40 year latency)
  • Few long-term survivors, high lethal malignancy

Risk factors:

  • Asbestos exposure during home maintenance and renovation
  • 60-85 years
  • Male sex
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12
Q

Summarise the epidemiology of asbestos-related lung disease (including asbestosis and mesothelioma).

A

Asbestosis & Mesothelioma

  • 90% report previous exposure to asbestos
  • 20% of patients have pulmonary asbestosis
  • Latent period between exposure and development of tumour is up to 45 years
  • Incidence in the US is 3200 per year (for malignancy)
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13
Q

Recognize the presenting symptoms of asbestos-related lung disease (including asbestosis and mesothelioma).

A

Asbestosis

  • Asymptomatic
  • Shortness of breath (dyspnoea), especially on exertion
  • Cough
  • Presence of risk factors

Mesothelioma

  • Chest pain
  • Dyspnoea
  • Presence of risk factors
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14
Q

Recognize the signs of asbestos-related lung disease (including asbestosis and mesothelioma) on physical examination.

A

Asbestosis

  • Clubbing
  • Fine end-inspiratory crackles
  • Pleural plaques

Mesothelioma

  • Weight loss
  • Finger clubbing
  • Recurrent pleural effusions

Signs of Metastasis

  • Lymphadenopathy
  • Hepatomegaly
  • Bone pain / tenderness
  • Abdominal pain /obstruction - peritoneal malignant mesothelioma
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15
Q

Identify appropriate investigations for asbestos-related lung disease (including asbestosis and mesothelioma) and interpret the results.

A

Asbestosis

  • CXR (PA and lateral)
  • Pulmonary function tests
  • High-resolution CT chest
  • Lung biopsy
  • Bronchial lavage

Results:

  • Pleural abnormalities
  • Pleural plaques with/without calcification
  • Diffuse pleural thickening
  • Benign pleural effusion
  • Rounded atelectasis
  • In concordance with or in absence of parenchymal fibrosis

Mesothelioma

  • CXR (PA and lateral)
  • CT chest (with contrast)
  • Histology following thoracoscopy
  • Thoracentesis
  • Pleural biopsy
  • Video-associated thoracoscopic surgery
  • Immunohistochemistry

Results:

  • Pleural thickening / effusion
  • Bloody pleural fluid
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16
Q

Define Aspergillus lung disease.

A

Lung disease associated with Aspergillus fungal infection.

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17
Q

Explain the aetiology/risk factors of Aspergillus lung disease.

A

Inhalation of the ubiquitous Aspergillus (usually Aspergillus fumigates) spores produce 3 different clinical pictures:

  • Aspergilloma - growth of an A.fumigatus mycetoma ball in a pre-existing lung cavity (e.g. post-TB, old infarct or abscess)
  • Allergic BronchoPulmonary Aspergillosis (ABPA)
  • Invasive Aspergillosis - invasion into lung tissue and fungal dissemination (secondary to immunosuppression - e.g. neutropenia, steroids, haematopoietic stem cell/ solid organ transplantation, AIDS)

ABPA

  • Aspergillus colonization of airways
  • IgE and IgG mediated immune repsonses
  • Proteolytic enzymes and mycotoxins released by fungi
  • CD4/Th2 cells produce IL-4 and IL-5
  • Eosinophilic inflammation
  • IL-8 mediated neutrophilic inflammation
  • Airway damage and central bronchiectasis
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18
Q

Summarise the epidemiology of Aspergillus lung disease.

A

Uncommon
Elderly
Immunocompromised

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19
Q

Recognize the presenting symptoms of Aspergillus lung disease.

A

Aspergilloma

  • Asymptomatic
  • Haemoptysis (may be massive)

ABPA

  • Difficult to control asthma
  • Recurrent episodes of pneumonia
  • Wheeze
  • Cough
  • Fever
  • Malaise

Invasive Aspergillosis

  • Dyspnoea
  • Rapid deterioration
  • Septic picture
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20
Q

Recognize the signs of Aspergillus lung disease on physical examination.

A
  • Tracheal deviation in large aspergillomas
  • Dullness in affected lung
  • Reduced breath sounds
  • Wheeze (ABPA)
  • Cyanosis (invasive aspergillosis)
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21
Q

Identify appropriate investigations for Aspergillus lung disease and interpret the results.

A

Aspergilloma

  • CXR - round opacity with a crescent of air around it (in upper lobes)
  • CT or MRI imaging (if CXR does not clearly delineate a cavity)
  • Cultures of sputum - if no communication between cavity and bronchial tree

NB: Aspergillus is a common colonizer of an abnormal respiratory tract.

ABPA

  • Immediate skin test reactivity to Aspergillus antigens
  • Eosinophilia
  • High serum total IgE
  • High serum specific IgE and IgG to Aspergillus fumigatus or precipitating serum antibodies to Aspergillus fumigatus
  • CXR
  • CT - lung infiltrates, central bronchiectasis
  • Lung function tests - reversible airflow limitation, reduced lung volumes/ gas transfer in progressive cases

CXR

  • Transient patchy shadows
  • Collapse
  • Distended mucus-filled bronchi producing tubular shadows = gloved fingers
  • Signs of complications
  • Fibrosis in upper lobes (TB)
  • Parallel-line shadows and rings (bronchiectasis)

Invasive Aspergillosis

  • Detection in cultures or histologic examination (septated hyphae with acute angle branching)
  • Risk factors
  • Suggestive clinical findings
  • Microscopic evidence of septate hyphae of examination of bronchoalveolar lavage fluid/sputum / positive serum galactomannan / beta-D-glucan assay
  • Chest CT - nodules surrounded by ground-glass appearance (halo) = haemorrhage into tissue surrounding area of fungal invasion
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22
Q

Define asthma.

A

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

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23
Q

Explain the aetiology/risk factors of asthma.

A

Genetic Factors:

  • Family history (twin studies)
  • Atopy - tendency of TH2 cells to drive production of IgE on exposure to allergens
  • Multiple chromosomal locations (genetic heterogeneity)

Environmental Factors:

  • House dust mite
  • Pollen
  • Pets - e.g. urinary proteins, furs
  • Cigarette smoke
  • Viral respiratory tract infection
  • Aspergillus fumigatus spores
  • Occupation allergens (isocyanates, epoxy resins)

Early Phase (Up to 1h)

  • Exposure to inhaled allergens in a pre-sensitized individual
  • Cross-linking of IgE antibodies on mast-cell surface
  • Release of histamine, PgD2, leukotrienes, TNF-alpha
  • Smooth muscle contraction = bronchoconstriction
  • Mucous hypersecretion
  • Oedema
  • Airway obstruction

Late Phase (After 6-12h)

  • Recruitment of eosinophils, basophils, neutrophil and TH2 lymphocytes and products
  • Perpetuation of inflammation and bronchial hyper-responsiveness
  • Structural cells (e.g. bronchial epithelial cells, fibroblasts, smooth muscle, and vascular endothelial cells) release cytokines, profibrogenic and proliferative GFs
  • Contribute to inflammation and altered function
  • Contribute to the proliferation of smooth muscle cells and fibroblasts = airway remodelling
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24
Q

Summarise the epidemiology of asthma.

A 
10% of children 
5% of adults 
Increasing prevalence
W > M 
1000-2000 deaths from acute asthma per year
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25
Q

Recognize the presenting symptoms of asthma.

A
  • Wheeze
  • Breathlessness
  • Cough
  • Worse in the morning and at night
  • Ask about interference with exercise, sleeping, days off school and work
  • Acute attack - ask about whether admitted before or to ITU as a gauge of severity potential

Precipitating Factors:

  • Cold
  • Viral infection
  • Drugs - e.g. B-blockers, NSAIDs
  • Exercise
  • Emotions
  • History of allergic rhinitis, urticaria, eczema, nasal polyps, acid reflux, family history
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26
Q

Recognize the signs of asthma on physical examination.

A
  • Tachypnoea
  • Accessory muscle usage
  • Prolonged expiratory phase
  • Polyphonic wheeze
  • Hyperinflated chest

Severe Attack:

  • PEFR < 50% predicted
  • Pulse >110/min
  • RR >25/min
  • Inability to complete sentences

Life-Threatening Attack:

  • PEFR < 33%
  • Chest silent
  • Cyanosis
  • Bradycardia
  • Hypotension
  • Confusion
  • Coma
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27
Q

Identify appropriate investigations for asthma and interpret the results.

A

Acute

  • Peak flow
  • Pulse oximetry
  • ABG
  • CXR - to exclude pneumothorax, pneumonia etc
  • FBC - high WCC if infective exacerbation
  • CRP
  • U&E
  • Blood & sputum cultures

Chronic

  • PEPR monitoring - diurnal variation (morning dip)
  • Pulmonary function test - obstructive defect with improvement after trial of B2 agonist
  • Blood - eosinophilia, IgE level, Aspergillus antibody titres
  • Skin prick tests - identification of allergens
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28
Q

Generate a management plan for asthma.

A

Acute

  • Resuscitate, monitor O2 sats, ABG, PEFR
  • High-flow oxygen
  • Nebulized B2-agonist bronchodilator salbutamol (5mg initially continuously, then 2-4 hourly), ipratropium (0.5mg QDS)
  • Steroid therapy (100-200mg IV hydrocortisone followed by 40mg oral prednisolone for 5-7 days)
  • If no improvement - IV magnesium sulphate
  • Consider IV aminophylline infusion or IV salbutamol
  • Summon anaesthetic if patient is getting exhausted - PCO2 increasing
  • Treat any underlying cause (e.g. infection, pneumothorax)
  • Give antibiotics if there is a chest infection - e.g. purulent sputum, abnormal CXR, high WCC fever
  • Monitor electrolytes closely - as bronchodilators and aminophylline reduce K+
  • May need ventilation in severe attacks
  • If not improving or patient tiring then involve ITU early

Discharge

  • PEF > 75% predicted or patient’s best diurnal variation <25%
  • Inhaler technique checked
  • Stable on discharge medication for 24h
  • Own a PEF meter
  • Steroid & bronchodilator therapy
  • Arrange to follow up

Chronic Stepwise Therapy
- Review treatment every 3-6 months
STEP 1: Inhaled short-acting B2-agonist as needed, if used >1/day, move to STEP 2.
STEP 2: STEP 1 plus regular inhaled low-dose steroids (400mcg/day)
STEP 3: STEP 2 plus inhaled long-acting B2-agonist (LABA)

If inadequate control with LABA, then increase steroid dose to 800mcg/day. If no response to LABA then stop and increase steroid to 800mcg/day.

STEP 4: Increase inhaled steroid dose to 2000mcg/day, add 4th drugs (e.g. leukotriene receptor antagonist, SR theophylline or B2 agonist tablet)
STEP 5: Addition of regular oral steroids, maintain high-dose inhaled steroid, consider other treatments to minimize the use of oral steroids and refer for specialist care.

Advice

  • Educate on proper inhaler technique
  • Routine monitoring of peak flow
  • Develop an individualized management plan with emphasis on avoidance of provoking factors
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29
Q

Identify the possible complications of asthma and its management.

A
  • Growth retardation
  • Chest wall deformity - e.g. pigeon chest
  • Recurrent infections
  • Pneumothorax
  • Respiratory failure
  • Death
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30
Q

Summarise the prognosis for patients with asthma.

A

Children usually improve when they grow older

Adult-onset asthma usually chronic

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31
Q

Define bronchiectasis.

A

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

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32
Q

Explain the aetiology / risk factors of bronchiectasis.

A

Severe inflammation in the lung causes fibrosis and dilation of the bronchi. Results in pooling of mucus, predisposing to further cycles of infection, damage and fibrosis to bronchial walls.

Causes

  • Idiopathic (50%)
  • Post-infectious - severe pneumonia, whooping cough, TB
  • Host defence defects - e.g. Kartagener’s Syndrome, cystic fibrosis, immunoglobulin deficiency, yellow-nail syndrome
  • Obstruction of bronchi - e.g. foreign body, enlarged lymph nodes
  • Gastric reflux disease
  • Inflammatory disorders - e.g. rheumatoid arthritis
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33
Q

Summarise the epidemiology of bronchiectasis.

A

Most often arises initially in childhood.
Incidence has decreased with the use of antibiotics
1 in 1000 per year

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34
Q

Recognise the presenting symptoms of bronchiectasis.

A
  • Productive cough
  • Purulent sputum
  • Haemoptysis
  • Breathlessness
  • Chest pain
  • Malaise
  • Fever
  • Weight loss
  • Symptoms begin after acute respiratory illness
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35
Q

Recognise the signs of bronchiectasis on physical examination.

A
  • Finger clubbing
  • Coarse crepitations - usually at the bases
  • Shift with coughing
  • Wheeze
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36
Q

Identify appropriate investigations for bronchiectasis and interpret the results.

A
  1. Sputum
  2. CXR
  3. High-Resolution CT
  4. Bronchography
  5. Other

Sputum

  • Culture and sensitivity
  • Common organisms = Pseudomonas aeruginosa, Haemophilis influenzae, Staphylococcus aureus, Streptococcus pneumoiae, Klebsiella, Moraxella catarrhalis, Mycobacteria

CXR

  • Dilated bronchi seen as parallel lines radiating from hilum to diaphragm = tramline shadows
  • Fibrosis
  • Atelectasis
  • Pneumonic consolidations
  • Normal even

CT

  • Dilated bronchi
  • Thickened bronchial walls

Bronchiography

  • Determine extent of disease before surgery
  • Radioopaque contrast injected through the cricoid ligament or via a bronchoscope

Others

  • Sweat electrolytes
  • Serum immunoglobulins - 10% of adults have some immune deficiency
  • Sinus X-ray - 30% have concomitant rhinosinusitis
  • Mucociliary clearance study
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37
Q

Generate a management plan for bronchiectasis.

A

Acute Exacerbations

  • 2 IV antibiotics - efficacy for pseudomonas
  • Prophylactic antibiotics (oral or aerosolized) for those with >3 exacerbations per year

=>Inhaled corticosteroids

  • e.g. Fluticasone
  • Reduce inflammation and volume of sputum
  • Does not affect the number of exacerbations or lung function

=>Bronchodilators
- If patients have responsive disease

=>Hydration
- Maintain with adequate oral fluid intake

=>Flu Vaccination

=>Physiotherapy

  • Sputum and mucus clearance technique - e.g. postural drainage
  • Position themselves so the lobe to be drained is uppermost, approx 20 min twice daily
  • Reduces frequency of acute exacerbations and aids recovery

=> Bronchial Artery Embolization
- For life-threatening hemoptysis

=> Surgical

  • Localized resection
  • Lung or heart-lung transplantation
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38
Q

Identify the possible complications of bronchiectasis and its management.

A
  • Life-threatening haemoptysis
  • Persistent infections
  • Empyema
  • Respiratory failure
  • Cor pulmonale
  • Multi-organ abscess
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39
Q

Summarise the prognosis for patients with bronchiectasis.

A

Most patients continue to have symptoms after 10 years.

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40
Q

Define COPD.

A

Chronic, progressive lung disorder characterized by airflow obstruction, chronic bronchitis and emphysema.

Chronic Bronchitis - chronic cough and sputum production on most days for at least 3 months per year over 2 consecutive years

Emphysema - pathological diagnosis of permanent destructive enlargement of air spaces distal to the terminal bronchioles.

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41
Q

Explain the aetiology / risk factors of COPD.

A

Bronchial and alveolar damage as a result of environmental toxins - e.g. cigarette smoke.

Rare cause = alpha-1-antitrypsin deficiency (<1%)

  • Young patients
  • Non-smokers
  • Co-presents with asthma

Chronic Bronchitis

  • Narrowing of airways due to bronchiole inflammation = bronchiolitis
  • Bronchi with mucosal oedema
  • Mucous hypersecretion
  • Squamous metaplasia

Emphysema

  • Destruction and enlargement of alveoli
  • Loss of elastic traction that keeps small airways open in expiration
  • Larger spaces develop = bullae (>1cm)
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42
Q

Summarise the epidemiology of COPD.

A

Prevalence 8%
Middle age or later
Males
Change due to increase in female smokers

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43
Q

Recognise the presenting symptoms of COPD.

A
  • Chronic cough
  • Sputum production
  • Breathlessness
  • Wheeze
  • Reduced exercise tolerance
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44
Q

Recognise the signs of COPD on physical examination.

A

Inspection

  • Respiratory distress
  • Use of accessory muscles
  • Barrel-shaped overinflated chest
  • Reduced cricosternal distance
  • Cyanosis

Percussion

  • Hyper-resonant chest
  • Loss of liver and cardiac dullness

Auscultation

  • Quiet breath sounds
  • Prolonged expiration
  • Wheeze
  • Rhonchi and crepitations

Signs of CO2 Retention

  • Bounding pulse
  • Warm peripheries
  • Flapping tremor of hands (asterixis)
  • Late stages = signs of right heart failure (e.g. right ventricular heave, raised JVP, ankle oedema)
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45
Q

Identify appropriate investigations for COPD and interpret the results.

A
  1. Spirometry and Pulmonary Function Tests
  2. CXR
  3. Bloods
  4. ABG
  5. ECG and Echocardiogram - for cor pulmonale
  6. Sputum and Blood Cultures - acute exacerbations for treatment
  7. Consider alpha-1-antitrypsin Levels - in non-smokers, young patients

Spirometry & Pulmonary Function Tests

  • Obstructive picture
  • Reduced PEFR
  • Reduced FEV1:FVC ratio - mild, 60-80%, moderate 40-60%, severe <40%)
  • Increased lung volumes
  • CO gas transfer coefficient reduced when significant alveolar destruction

CXR

  • Normal
  • Hyperinflation - >6 ribs visible anteriorly, flat hemi-diaphragms
  • Reduced peripheral lung markings
  • Elongated cardiac silhouette

Blood
- FBC - high Hb and PCV due to secondary polycythemia

ABG
- Hypoxia (reduced PaO2), normal or high PaCO2

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46
Q

Generate a management plan for COPD.

A

1) Stop Smoking
2) Bronchodilators
3) Steroids
4) Pulmonary Rehabilitation
5) Oxygen Therapy

Bronchodilators

  • Short-acting B2 agonists - e.g. salbutamol
  • Anticholinergics - e.g. ipratropium
  • Delivered by inhalers or nebulizers
  • Long-acting B2 agonists if >2 exacerbations per year

Steroids

  • Inhaled beclomethasone if FEV1 <50% predicted or those with >2 exacerbations per year
  • Regular oral steroids avoided but may be necessary

Oxygen Therapy - only if stopped smoking = long-term home oxygen therapy has been shown to improve mortality
- More economical if used for >8h /day

Indications:

  • PaO2 <7.3kPa on air during a period of clinical stability
  • PaO2 7.3-8.0kPa and signs of secondary polycythaemia, nocturnal hypoxaemia, peripheral oedema or pulmonary hypertension

Treatment of Acute Infective Exacerbations:

  • Provide 24% O2 via non-variable flow Venturi mask
  • Increase slowly if no hypercapnia and still hypoxic (ABG)
  • Corticosteroids (oral or inhaled)
  • Start empirical antibiotic therapy if evidence of infection - follow trust policy
  • Respiratory physiotherapy essential to clear sputum
  • Consider non-invasive ventilation in severe cases
  • Prevention = pneumococcal and influenza vaccination
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47
Q

Identify the possible complications of COPD and its management.

A
  • Acute respiratory failure
  • Infections - e.g. Streptococcus pneumonia, Haemophilus influenzae
  • Pulmonary hypertension
  • Right heart failure
  • Pneumothorax - resulting from bullae rupture
  • Secondary polycythaemia
48
Q

Summarise the prognosis for patients with COPD.

A
  • High level of morbidity

- 3 year survival rate of 90% if age < 60 years and FEV1 > 50% predicted, 75% if >60 years and FEV1 40-49% predicted

49
Q

Define extrinsic allergic alveolitis.

A

Interstitial inflammatory disease of the distal gas-exchanging parts of the lung caused by inhalation of organic dusts.

AKA hypersensitivity pneumonitis.

50
Q

Explain the aetiology / risk factors of extrinsic allergic alveolitis.

A

Inhalation of antigenic organic dusts containing microbes (bacteria, fungi or amoebae) or animal proteins.

Induce a hypersensitivity response = Type III antigen-antibody complex hypersensitivity reaction + Type IV granulomatous lymphocytic inflammation

Farmer’s Lung
- Mouldy hay containing thermophilic actinomycetes

Pigeon / Budgerigar Fancier’s Lung
- Bloom on bird feathers and excreta

Mushroom Worker’s Lung
- Compost containing thermophilic actinomycetes

Humidifier Lung
- Water-containing bacteria and Naegleria (amoeba)

Maltworker’s Lung
- Barley or maltings containing Aspergillus clavatus

51
Q

Recognise the presenting symptoms of extrinsic allergic alveolitis.

A

Acute

  • 4-12h after exposure
  • Reversible episodes
  • Dry cough
  • Dyspnoea
  • Malaise
  • Fever
  • Myalgia
  • Wheeze
  • Productive cough

(last 2 on repeated high-level exposures)

Chronic

  • Poorly reversible manifestation
  • Slowly increased breathlessness
  • Reduced exercise tolerance
  • Weight loss
  • Exposure is usually chronic, low level and no history of previous acute episodes

Full occupational history and enquiry into hobbies and pets important.

52
Q

Recognise the signs of extrinsic allergic alveolitis on physical examination.

A

Acute

  • Rapid shallow breathing
  • Pyrexia
  • Inspiratory crepitations

Chronic

  • Fine inspiratory crepitations
  • Finger clubbing rare
53
Q

Identify appropriate investigations for extrinsic allergic alveolitis and interpret the results.

A
  1. Bloods
  2. Serology
  3. CXR
  4. High-resolution CT-Thorax
  5. Pulmonary Function Tests
  6. Bronchoalveolar Lavage

Bloods

  • FBC - neutrophilia, lymphopenia
  • ABG - low PO2, low PCO2

Serology

  • Precipitating IgG to fungal or avian antigens in serum
  • Not diagnostic as often found in asymptomatic individuals

CXR

  • Acute episodes
  • Ground glass appearance
  • Alveolar shadowing
  • Nodular opacities
  • Located in middle and lower zones
  • Fibrosis prominent in upper zones in chronic cases

CT

  • Early changes
  • Patchy ground-glass shadowing and nodules

Pulmonary Function Tests

  • Restrictive ventilatory defect = reduced FEV1, reduced FVC with preserved or increased ratio
  • Reduced TLCO

Bronchoalveolar Lavage

  • Increased cellularity with high CD8 + suppressor T-cells
  • Lung biopsy - transbronchial or thorascopic
54
Q

Summarise the epidemiology of extrinsic allergic alveolitis.

A

Uncommon
2% of occupational lung diseases
50% of reported cases affect farm workers (4-10 per 100,000 / year )
Marked geographical variation reflecting dependence on occupational causes

55
Q

Define idiopathic pulmonary fibrosis / idiopathic fibrosing alveolitis / cryptogenic fibrosing alveolitis.

A

Inflammatory condition of the lung resulting in fibrosis of alveoli and interstitium.

56
Q

Explain the aetiology / risk factors of idiopathic pulmonary fibrosis / idiopathic fibrosing alveolitis / cryptogenic fibrosing alveolitis.

A
  • Genetically predisposed host - e.g. with telomerase / surfactant protein mutations
  • Recurrent injury to alveolar epithelial cells
  • Secretion of cytokines and growth factors - e.g. TNF-alpha, IL-1, MCP-1
  • Fibroblast activation, recruitment, proliferation
  • Differentiation of fibroblasts into myofibroblasts
  • Increased collagen synthesis and deposition
  • Profibrogenic molecules (e.g. PDGF, TGF-B) secreted by inflammatory, epithelial and endothelial cells

Drugs cause a similar illness

  • Bleomycin
  • Methotrexate
  • Amiodarone

Histological Patterns

  • Usual interstitial pneumonia - e.g. patchy interstitial fibrosis, honeycomb lung
  • Desquamative interstitial pneumonia - diffuse intra-alveolar accumulation of macrophages, mild thickening of alveolar septa, lymphoid aggregates
  • Non-specific interstitial pneumonia

Risk Factors

  • Smoking (75%)
  • Occupational exposure to metal - e.g. steel, brass, lead
  • Occupational exposure to wood (pine)
  • Chronic microaspiration
  • Animal and vegetable dusts
57
Q

Summarise the epidemiology of idiopathic pulmonary fibrosis / idiopathic fibrosing alveolitis / cryptogenic fibrosing alveolitis.

A

Rare
Prevalence 6 in 100,000 in UK
M:F 2:1
67y = mean age

58
Q

Recognise the presenting symptoms of idiopathic pulmonary fibrosis / idiopathic fibrosing alveolitis / cryptogenic fibrosing alveolitis.

A
  • Gradual onset of progressive dyspnoea on exertion
  • Dry irritating cough
  • No wheeze
  • Symptoms preceded by a viral-type illness
  • Fatigue and weight loss common
  • Full occupational and drug history important
59
Q

Recognise the signs of idiopathic pulmonary fibrosis / idiopathic fibrosing alveolitis / cryptogenic fibrosing alveolitis on physical examination.

A
  • Finger clubbing (50%)
  • Bibasal fine late inspiratory crepitations
  • Signs of right heart failure in advanced stages - e.g. right ventricular heave, raised JVP, peripheral oedema
60
Q

Identify appropriate investigations for idiopathic pulmonary fibrosis / idiopathic fibrosing alveolitis / cryptogenic fibrosing alveolitis and interpret the results.

A
  1. Blood
  2. CXR
  3. High-Resolution Ct
  4. Pulmonary Function Tests
  5. Bronchoalveolar Lavage - to exclude infections and malignancy
  6. Lung Biopsy - gold standard for diagnosis
  7. Echocardiography - to look for pulmonary hypertension

Blood

  • ABG - normal in early disease, reduced PO2 on exercise
  • ABG - normal PCo2 which rises in late disease
  • 1/3 have rheumatoid factor or anti-nuclear antibodies

CXR

  • Usually normal
  • Early = small lung fields, ground glass shadowing
  • Late = reticulonodular showing (at bases), signs of cor pulmonale, honeycombing

CT

  • Most sensitive in early disease
  • Affect mainly lower zones and subpleural areas
  • Reticular densities
  • Honeycombing
  • Traction bronchiectasis

Pulmonary Function Tests

  • Restrictive ventilatory defect (reduced FEV1, reduced FVC with preserved or increased ratio)
  • Reduced lung volumes
  • Reduced lung compliance
  • Reduced TLCO
61
Q

Define lung cancer.

A

Non-Small Cell

  • Primary malignant neoplasm of the lung (80%)
  • Squamous cell carcinoma, adenocarcinoma, large cell carcinoma, adenosquamous carcinoma

Small Cell

  • Malignant neoplasm of neuroendocrine Kulchitsky cells of the lung with early dissemination
  • AKA oat cell carcinoma
62
Q

Explain the aetiology / risk factors of lung cancer.

A

Non-Small Cell

  • Genetic alterations that result in neoplastic transformation
  • Mainly in main or lobar bronchi
  • Adenocarcinoma = more peripherally

Risk Factors

  • Smoking (active or passive)
  • Occupational exposure - e.g. polycyclic hydrocarbons, asbestos, nickel, chromium, cadmium, radon
  • Atmospheric pollution

Small Cell

  • Smoking
  • Occupational and environmental exposures
63
Q

Summarise the epidemiology of lung cancer.

A

Non-Small Cell

  • Most common fatal malignancy in the West - 18% of cancer mortality
  • 35,000 deaths per year UK
  • 3x more common in men, but increasing in women

Small Cell
- 20% of all lung cancers

64
Q

Recognize the presenting symptoms of lung cancer.

A

Non-Small Cell

  • Asymptomatic with radiographic abnormality found (5%)
  • Primary = cough, haemoptysis, chest pain, recurrent pneumonia
  • Local invasion = e.g. brachial plexus (Pancoast tumour in apex of lung) causing pain in shoulder or arm, left recurrent laryngeal nerve (hoarseness and bovine cough), oesophagus (dysphagia), heart (palpitations / arrhythmias)
  • Metastatic or paraneoplastic phenomena = weight loss, fits, bone pain, fractures, neuromyopathies

Small Cell

  • Asymptomatic with radiographical abnormality found
  • Primary tumour = cough, haemoptysis, dyspnoea, chest pain
  • Metastatic disease = weight loss, fatigue, bone pain
  • Parneoplastic Syndrome = weakness, lethargy, seizures, muscle fatiguability
65
Q

Recognize the signs of lung cancer on physical examination.

A

Non-Small Cell

  • No signs
  • Fixed monophonic wheeze
  • Signs of collapse, consolidation, pleural effusion
  • Local Invasion = SVC compression (facial congestion, distension of neck veins, upper limb oedema), Brachial plexus (wasting of small muscles of hand), Sympathetic Chain (Horner’s - miosis, ptosis, anhydrosis)
  • Metastases = supraclavicular lymphadenopathy, hepatomegaly
  • Paraneoplastic Phenomena = hypertrophic osteoarthropathy - e.g. clubbing, painful/swollen wrists/ankles due to periosteal new bone formation, dermatological signs

Small Cell

  • No signs or a fixed wheeze on auscultation of the chest
  • Signs of lobular collapse or pleural effusion
  • Signs of metastases - e.g. supraclavicular lymphadenopathy, hepatomegaly
  • Signs of paraneoplastic syndromes
66
Q

Identify appropriate investigations for lung cancer and interpret the results.

A

Non-Small Cell

  1. Diagnosis
  2. TNM Staging
  3. Bloods
  4. Pre-Operative

Diagnosis

  • CXR - coin lesions, lobar collapse, pleural effusion, features of lymphangitis carcinomatosis
  • Sputum cytology
  • Bronchoscopy with brushings or biopsy
  • CT or US-guided percutaneous biopsy
  • Lymph node biopsy

TNM Staging

  • Based on tumour size, nodal involvement and metastatic spread
  • Use CT chest, CT or MRI head and abdomen or ultrasound, bone scan, PET scan
  • Invasive methods - e.g. mediastinoscopy, video-assisted thoracoscopy used

Bloods

  • FBC
  • U&E
  • Ca2+ - hypercalcaemia common
  • AlkPhos - high bone metastases
  • LFT

Pre-Op

  • ABG
  • Pulmonary function tests - FEV1 > 80% predicted to tolerate a pneumonectomy
  • Lung resection is contraindicated if FEV <30% predicted
  • V/Q scan
  • ECG
  • Echocardiogram
  • General anaesthetic assessment

Small Cell

  1. Diagnosis - sputum cytology, bronchoscopy with brushings and biopsy, percutaneous biopsy, thoracoscopy
  2. Staging - CT of chest, abdomen, head, isotope boen scan
  3. Other - lung function tests, FBC, U&E, Ca2+, AlkPhos, LFT
67
Q

Define obstructive sleep apnoea.

A

Characterized by recurrent collapse of the pharyngeal airway and apnoea (defined as the cessation of airflow for >10s) during sleep, followed by arousal from sleep.

AKA Pickwickian Syndrome.

68
Q

Explain the aetiology/risk factors of obstructive sleep apnoea.

A

Occurs when the upper airway narrows because of the collapse of the soft tissues of the pharynx when tone in pharyngeal dilators decreases during sleep.

Associated with:

  • Excessive weight gain
  • Smoking
  • Alcohol
  • Sedative use
  • Enlarged tonsils
  • Enlarged adenoids
  • Macroglossia
  • Marfan’s Syndrome
  • Craniofacial abnormalities
69
Q

Summarise the epidemiology of obstructive sleep apnoea.

A

Common
5-20% of men , 2-5% of women >35 years
Prevalence increases with age.

70
Q

Recognise the presenting symptoms of obstructive sleep apnoea.

A
  • Excessive daytime sleepiness
  • Unrefreshing or restless sleep
  • Morning headaches or dry mouth
  • Difficulty concentrating
  • Irritability or mood changes
  • Partner reporting snoring, nocturnal apnoeic episodes or nocturnal choking
71
Q

Recognize the signs of obstructive sleep apnoea on physical examination.

A
  • Large tongue
  • Enlarged tonsils
  • Long or thick uvula
  • Retrognathia - pulled back jaws
  • Neck circumference - >42cm in M, >40cm females
  • Obesity
  • Hypertension
72
Q

Identify appropriate investigations for obstructive sleep apnoea and interpret the results.

A
  • Sleep study - managed by sleep study centre for polysomnography or diagnostic sleep studies with monitoring of airflow, respiratory effort, pulse oximetry and heart rate
  • Blood - thyroid function tests, ABG
73
Q

Define pneumoconiosis.

A

Fibrosing interstitial lung disease caused by chronic inhalation of mineral dusts.

Simple - Coalworker’s pneumoconiosis or silicosis (symptom free)

Complicated - Pneumoconiosis (progressive massive fibrosis) results in loss of lung function

Asbestosis - Pneumoconiosis in which diffuse parenchymal lung fibrosis occurs as a result of prolonged exposure to asbestos

74
Q

Explain the aetiology/risk factors of pneumoconiosis.

A

Caused by inhalation of particles of coal dust, silica or asbestos.

2 types:

  • White asbestos
  • Blue asbestos or crocidolite = more toxic

Risk Factors:

  • Occupational exposure - e.g. coal mining, quarrying, iron and steel foundries, stone cutting, sandblasting, insulation industry, plumbers, shipbuilders
  • Depends on extent of exposure, size and shape of particles and individual susceptibility
  • Co-factors = smoking, TB

Pathology
- Complicated disease - large nodules in the lung, consisting of dust particles surrounded by layers of collagen and dying macrophages

Methods of Damage:

  • Direct cytotoxicity by particles
  • Particle ingestion by macrophages results in activation and excessive free radical production causing lipid peroxidation and cell injury
  • Proinflammatory cytokines and growth factors from macrophages and epithelial cells stimulate fibroblast proliferation and eventual scarring

Asbestosis:

  • Asbestos bodies consisting of fibres coated with an iron-containing protein seen in fibrotic areas
  • Seen especially in lung bases
75
Q

Summarise the epidemiology of pneumoconiosis.

A

Incidence increasing in developing countries

Disability and mortality from asbestosis will increase for the next 20-30 years

76
Q

Recognize the presenting symptoms of pneumoconiosis.

A
  • Occupational history is very important as there may be a long latency between disease, exposure and epxression

Asymptomatic
- Picked up on routine CXR - simple coal or silica pneumoconiosis

Symptomatic

  • Insidious onset
  • Shortness of breath
  • Dry cough
  • Black sputum - melanoptysis = Coalworker’s Pneumoconiosis
  • Workers exposed to asbestos may develop pleuritic chest pain may years after first exposure due to acute asbestos pleurisy
77
Q

Recognize the signs of pneumoconiosis on physical examination.

A
  • May be normal
  • Decreased breath sounds in Coalworker’s Pneumoconiosis or Silicosis
  • End-inspiratory crepitations
  • Clubbing in asbestosis
  • Signs of a pleural effusion or right heart failure (cor pulmonale)
78
Q

Identify appropriate investigations for pneumoconiosis and interpret the results.

A
  1. CXR
  2. CT Scan - fibrotic changes visualized early
  3. Bronchoscopy - visualizes changes, and allows for bronchoalveolar lavage
  4. Lung-function Tests - restrictive ventilatory defect, impaired gas diffusion

CXR

  • Simple - micronodular mottling
  • Complicated (SILICOSIS) - nodular opacities (upper lobes), micronodular shadowing, eggshell calcification (hilar lymph nodes)
  • Complicated (ASBESTOSIS) - bilateral reticulonodular shadowing (lower zone) and pleural plaques, white lines when calcified (diaphragmatic pleura, holly leaf patterns)
79
Q

Define pneumonia.

A

Infection of the distal lung parenchyma.

Categories:

  • Community-acquired, hospital-acquired or nosocomial
  • Aspiration pneumonia, pneumonia in the immunocompromised
  • Typical and atypical - e.g. Mycoplasma, Chlamydia, Legionella
80
Q

Explain the aetiology / risk factors of pneumonia.

A

Community-Acquired:

  • Streptococcus pneumonia (70%)
  • COPD = Haemophilus influenzae & Morazella catarrhalis
  • Contract with Birds/Parrots = Chlamydia pneumonia & Chlamydia psittaci
  • Periodic epidemics = Mycoplasms pneumonia
  • Anywhere with air con = Legionella
  • Recent influenza infection, IV drug users = Staphylococcus aureus
  • Q Fever, rare = Coxiella burnett
  • TB = may present as pneumonia

Hospital-Acquired:

  • Gram-negative enterobacteria = Pseudomonas, Klebsiella
  • Anaerobes = aspiration pneumonia

Risk Factors:

  • Age
  • Smoking
  • Alcohol
  • Pre-existing lung disease
  • Immunodeficiency
  • Contact with pneumonia
81
Q

Summarise the epidemiology of pneumonia.

A

Incidence 5-11 in 1000 (25-44 in 1000 in elderly)

Community-acquired causes >60,000 deaths/year in UK

82
Q

Recognize the presenting symptoms of pneumonia.

A
  • Fever
  • Rigors
  • Sweating
  • Malaise
  • Cough
  • Sputum (yellow, green or rusty in S pneumoniae)
  • Breathlessness
  • Pleuritic chest pain
  • Confusion - severe cases,elderly, Legionella

Atypical Pneumonia:

  • Headache
  • Myalgia
  • Diarrhoea
  • Abdominal Pain
83
Q

Recognize the signs of pneumonia on physical examination.

A
  • Pyrexia
  • Respiratory distress
  • Tachypnoea
  • Tachycardia
  • Hypotension
  • Cyanosis
  • Reduced chest expansion
  • Dullness to percussion
  • Increased tactile vocal fremitus
  • Bronchial breathing - inspiration phase lasts as long as the expiration phase
  • Coarse crepitations on the affected side
  • Chronic suppurative lung disease (e.g. empyema, abscess): Clubbing
84
Q

Identify appropriate investigations for pneumonia and interpret the results.

A
  1. Bloods
  2. CXR
  3. Sputum
  4. Urine
  5. Atypical Viral Serology
  6. Bronchoscopy & Bronchoalveolar Lavage

Bloods

  • FBC - abnormal WCC
  • U&E - low Na+, especially with Legionella
  • LFT
  • Blood cultures - sensitivity 10-20%
  • ABG - to assess pulmonary function
  • Blood film - RBC agglutination by Mycoplasma caused by cold agglutinins

CXR

  • Lobar or patchy shadowing
  • Pleural effusion
  • Klebsiella - often seen in upper lobes
  • Repeat 6-8 weeks - if abnormal suspect underlying pathology

Sputum/Pleural Fluid

  • Microscopy
  • Culture & sensitivity
  • Acid-fast bacilli

Urine

  • Pneumococcus antigens
  • Legionella antigens

Atypical Viral Serology
- Increased antibody titres between acute and convalescent samples - greater than 2 weeks post onset

Bronchoscopy

  • If Pneumocystis carinii pneumonia is suspected
  • When pneumonia fails to resolve
  • When there is clinical progression
85
Q

Generate a management plan for pneumonia.

A
  1. Assess Severity - see prognosis, if >1 feature presents the manage in hospital
  2. Start Empirical Antibiotics
    - Oral amoxicillin (0 markers)
    - Oral or IV amoxicillin and erythromycin (1 marker)
    - IV cefuroxime / cefotaxime / co-amoxiclav and erythromycin (>1 marker)
    - Add metronidazole, if aspiration, lung abscess or empyema suspected
    - Switch to the appropriate antibiotic as per sensitivity

NB: Levofloxacin and moxifloxacin can provide useful alternatives in selected hospitalized patients with community-acquired pneumonia.

  1. Supportive Treatment
    - Oxygen - maintain PO2 > 8kPa, start with 28% O2 in COPD to avoid hypercapnia
    - Parenteral fluids for dehydration or shock
    - Analgesia
    - Chest physiotherapy
    - CPAP, BiPAP or ITU care for respiratory failure
    - Surgical drainage may be needed for empyema / abscess
  2. Discharge Planning
    - Presence of two or more features of clinical instability predict a significant chance of re-admission or mortality
    - Raised temperature, heart rate, respiratory rate
    - Low BP, oxygen saturation, mental status and oral intake
  3. Non-Resolving Pneumonia
    - Consider other causes

Causes of Non-Resolving Pneumonia

  • Unusual pathogens - e.g. Chlamydia psittaci, C.burnetti, Mycobacterium tuberculosis, Nocardia, Actinomyces israeli, fungi (Aspergillus, histoplasmosis, coccidioidomycosis, blastomycosis)
  • PE
  • Malignancy - e.g. bronchogenic carcinoma, bronchoalveolar cell carcinoma, lymphoma
  • Inflammatory - e.g. vasculitis, Wegener’s granulomatosis, sarcoidosis, systemic lupus erythematosus
  • Congestive heart failure
  • Drug toxicity
  • Diffuse alveolar hemorrhage
  • Bronchiolitis obliterans-organizing pneumonia
  • Eosinophilic pneumonia
  • Acute interstital pneumonia
  • Pulmonary alveolar proteinosis
  1. Prevention
    - Pneumococcal & H.influenzae type B vaccination in vulnerable groups
    - E.g. elderly, splenectomized
86
Q

Identify the possible complications of pneumonia and its management.

A
  • Pleural effusion
  • Empyema (pus in the pleural cavity)
  • Localized superation leading to lung abscess - seen by Staphyloccoal, Klebsiella pneumonia, presenting with swinging fever, persistent pneumonia, copious / foul-smelling sputum
  • Septic shock
  • ARDS
  • Acute renal failure

M.Pneumonia

  • Erythema multiforme
  • Myocarditis
  • Haemolytic anaemia
  • Meningoencephalitis
  • Transverse myelitis
  • Guillian-Barre Syndrome
87
Q

Summarise the prognosis for patients with pnuemonia.

A

Most resolve with treatment (1-3 weeks).

High mortality of severe pneumonia

  • Community-acquired - 5-10%
  • Hospital-acquired - 30%
  • 50% of those in ITU

Markers of Severe Pneumonia (CURB-65 Score)
C = Confusion
U = Urea >7mmol/L
R = RR >30/min
B = BP - Systolic <90mmHg, Diastolic <60mmHg
Age >65 years.

Other markers are:

  • Hypoxia <8kPa
  • ECC <4 or >20 x 10^9 /mm^3
  • Age >50 years
88
Q

Define pneumothorax.

A

Air in the pleural space - the potential space between visceral and parietal pleura

Other variants depend on the substance in the pleural space - e.g. haemothorax, chylothorax (lymph)

Tension Pneumothorax - emergency when a functional valve lets air enter the pleural space during inspiration, but does not leave during expiration.

89
Q

Explain the etiology / risk factors of pneumothorax.

A

Spontaneous

  • In individuals with previously normal lungs, typically tall thin males
  • Rupture of a subpleural bleb

Secondary
- Pre-existing lung disease - e.g. COPD, asthma, TB, pneumonia, lung carcinoma, cystic fibrosis, diffuse lung disease

Traumatic

  • Penetrating injury to the chest
  • Often iatrogenic causes - e.g. during subclavian or jugular venous cannulation, thoracocentesis, pleural or lung biopsy or positive pressure-assisted ventilation

Risk Factors:
- Collagen disorders - e.g. Marfan’s disease, Ehlers-Danlos Syndrome

90
Q

Summarise the epidemiology of pneumothorax.

A

The annual incidence of spontaneous pneumothorax is 9 in 100,000.
20-40 year olds
4x more common in males

91
Q

Recognize the presenting symptoms of pneumothorax.

A
  • Asymptomatic if pneumothorax is small
  • Sudden onset breathlessness or chest pain, especially on inspiration
  • Distress with rapid shallow breathing if tension pneumothorax
92
Q

Recognize the signs of pneumothorax on physical examination.

A
  • Signs may be absent if small
  • Signs of respiratory distress with reduced expansion
  • Hyper-resonance to percussion
  • Breath sounds reduced

Tension Pneumothorax:

  • Severe respiratory distress
  • Tachycardia
  • Hypotension
  • Cyanosis
  • Distended neck veins
  • Tracheal deviation away from the side of the pneumothorax
93
Q

Identify appropriate investigations for pneumothorax and interpret the results.

A

CXR

  • Dark area of film where lung markings do not extend to
  • Fluid level may be seen if blood present
  • Small pneumothoraces, expiratory films may make it more prominent

ABG
- Determine if hypoxaemic, particular in secondary disease

94
Q

Generate a management plan for pneumothorax.

A

Tension Pneumothorax

  • Max O2
  • Insert large bore needle into 2nd ICS, MCL on side of pneumothorax to relieve pressure
  • Insert chest drain soon after

Small Pneumothorax (<2cm lung-pleural margin)

  • Check for underlying lung disease, pleural fluid, clincical compromise
  • If none, reassure, analgesia

Moderate Pneumothorax (>2cm lung-pleural margin)

  • Aspiration using large bore cannula or catheter with three-way tap
  • Inserted into the 2nd ICS MCL
  • 2.5L of air can be aspirated - stop if patient repeatedly coughs or resistance is felt
  • Follow up CXR should be performed just after, 2h and 2 weeks later
  • Advised to avoid diving
  • Chest drain with water seal if the aspiration fails, or if there is fluid in the pleural cavity or after decompression of a tension pneumothorax
  • Inserted into 4-6th ICS in MAL

Recurrent Pneumothoraces

  • Chemical pleurodesis - visceral and parietal pleura fusion with tetracycline or talc
  • Surgical pleurectomy

Advice

  • Avoiding air travel until follow-up CXR confirms resolution of pneumothorax
  • Avoid diving unless bilateral surgical pleurectomy
95
Q

Identify the possible complications of pneumothorax and its management.

A
  • Recurrent pneumothoraces

- Bronchopleural fistula

96
Q

Summarise the prognosis for patients with pneumothorax.

A

After one spontaneous pneumothorax, at least 20% will have another, with the frequency increasing with repeated pneumothoraces.

97
Q

Define pulmonary embolism.

A

Occlusion of pulmonary vessels, most commonly caused by a thrombus that has travelled to the vascular system from another site.

98
Q

Explain the aetiology / risk factors of pulmonary embolism.

A
  • Thrombus
  • 95% originate from DVT of lower limbs
  • Rarely from right atrium in patients with AF
  • Amniotic fluid embolus
  • Air embolus
  • Fat emboli
  • Tumour emboli
  • Mycotic emboli from right-sided endocarditis

Risk factors:

  • Surgical patients
  • Immobility
  • Obesity
  • OCP
  • Heart failure
  • Malignancy
99
Q

Summarise the epidemiology of pulmonary embolism.

A

Fairly common, especially in hospitalized patients

Occur in 10-20% of those with a confirmed proximal DVT.

100
Q

Recognise the presenting symptoms of pulmonary embolism.

A

Depends on site and size.

Small - may be asymptomatic

Moderate

  • Sudden onset dyspnoea
  • Cough
  • Haemoptysis
  • Pleuritic chest pain

Large

  • Sudden onset dyspnoea
  • Cough
  • Haemoptysis
  • Severe pleuritic chest pain
  • Shock
  • Collapse
  • Acute right heart failure
  • Sudden death

Multiple Small Recurrent
- Symptoms of pulmonary hypertension

101
Q

Recognize the signs of pulmonary embolism on physical examination.

A

Clinical Probability Assessment
- Well’s Score - >4 high probability, <3 probability

Clinically suspected DVT = 3.0 
PE is most likely diagnosis = 3.0
Recent surgery (4 weeks) = 1.5
Immobilization = 1.5
Tachycardia = 1.5
History of DVT or PE = 1.5
Haemoptysis = 1
Malignancy = 1
  • Raised Geneva Score - >11 high probability, 4-10 intermediate probability, <3 low probability
>65 = 1
Recent surgery or fracture (28 days) = 2
Previous DVT / PE = 3
Active maliganancy = 2
Unilateral leg pain = 3
Haemoptysis = 2
Heart Rate > 75-94/min = 3
Heart Rate >85/min = 5
Unilateral leg oedema and tenderness = 4

Small

  • No clinical signs
  • Tachycardia
  • Tachypnoea

Moderate

  • Tachycardia
  • Tachypnoea
  • Pleural rub
  • Low O2 sats - despite O2 supplementation

Large

  • Shock
  • Cyanosis
  • Signs of right heart strain - e.g. raised JVP, left parasternal heave, accentuated S2 heart sound

Multiple Recurrent PE
- Signs of pulmonary hypertension and right heart failure

102
Q

Identify appropriate investigations for pulmonary embolism and interpret the results.

A

Low Probability

  • D-dimer blood test - cross-linked fibrin degradation products
  • Highly sensitive
  • Poor specificity

High Probability
- Requires imaging

Additional:

  • Bloods - ABG, thrombophilia screen
  • ECG - normal, tachycardia, right axis deviation, RBBB
  • CXR - exclude other differentials

NB: Classic Si, QIII, TIII pattern uncommon.

  • Spiral CT Pulmonary Angiogram - 1st line, poor sensitivity for small emboli
  • Ventilation-Perfusion (VQ) Scan - administration of IV 99mTc macro-aggregated albumin and inhalation of 81 krypton gas to identify areas of ventilation and perfusion mismatch

(If abnormal CXR or co-existing lung disease, do not use due to difficulty in interpretation)

  • Pulmonary angiography - gold standard, invasive though
  • Doppler USS of lower limb - to examine for VT
  • Echocardiogram - right heart strain shown
103
Q

Generate a management plan for pulmonary embolism.

A

Primary Prevention:

  • Graduated pressure stockings (TEDs)
  • Heparin prophylaxis in those at risk (e.g. undergoing surgery)
  • Early mobilization and adequate hydration post-surgery

If hemodynamically stable:

  • O2
  • Anticoagulation with heparin or LMW heparin
  • Chaing to oral warfarin therapy (INR 2-3) for a minimum of 3 months
  • Analgesics for pain

If haemodynamically unstable:

  • Resuscitate
  • Give O2
  • IV fluid resuscitation
  • Thrombolysis with tPA can be considered on clinical grounds alone if cardiac arrest is imminent - 50mg bolus of tPA

Surgical or Radiological:

  • Embolectomy - when thrombolysis is contraindicated
  • IVC filters - Greenfield filter - may be inserted for recurrent pulmonary emboli despite adequate anticoagulation or when anticoagulation is contraindicated
104
Q

Identify the possible complications of pulmonary embolism and its management, and summarise the prognosis for patients with pulmonary embolism.

A
  • Death
  • Pulmonary Infarction
  • Pulmonary hypertension
  • Right Heart Failure

Prognosis:

  • 30% untreated motrality
  • 8% with treatment - due to recurrent emboli or underlying disease
  • Increased risk of future TE disease
105
Q

Define tuberculosis.

A

Granulomatous disease caused by Mycobacterium tuberculosis.

Primary
- Initial infection may be pulmonary (acquired by inhalation from cough of the infected patient) or occasionally, gastrointestinal

Miliary TB
- Results when there is hematogenous dissemination

Post-Primary
- Caused by re-infection or reactivation

106
Q

Explain the aetiology / risk factors of tuberculosis.

A

M.tuberculosis is an intracellular organism - AKA acid-fast bacilli

Survives after being phagocytosed by macrophages.

107
Q

Summarise the epidemiology of tuberculosis.

A

Annual mortality of 3 million.

95% in developing countries
UK incidence annually 6000

Asian immigrants >30 times native UK white population incidence

108
Q

Recognize the presenting symptoms of tuberculosis.

A

Primary TB

  • Asymptomatic
  • Fever
  • Malaise
  • Cough
  • Wheeze
  • Erythema nodosum
  • Phlyctenular conjunctivitis (allergic manifestations)

Miliary TB

  • Fever
  • Weight loss
  • Meningitis
  • Yellow caseous tubercles spread to other organs - e.g. bone and kidney may remain dormant for years

Post-Primary TB

  • Fever
  • Night sweats
  • Malaise
  • Weight loss
  • Breathlessness
  • Cough
  • Sputum
  • Haemoptysis
  • Pleuritic pain
  • Signs of pleural effusion
  • Collapse
  • Consolidation
  • Fibrosis

Non-Pulmonary TB
- Particularly in immunocompromised

Lymph Nodes
- Suppuration of cervical lymph nodes leading to abscesses or sinuses, which discharge pus and spread to skin = scrofuloderma

CNS

  • Meningitis
  • Tuberculoma

Skin
- Lupus vulgaris - jellylike reddish-brown glistening plaques

Heart

  • Percardial effusion
  • Constrictive pericarditis

Gastrointestinal

  • Subacute obstruction
  • Change in bowel habit
  • Weight loss
  • Peritonitis
  • Ascites

Adrenal
- Insufficiency

Bone/Joints

  • Osteomyelitis
  • Arthritis
  • Paravertebral Abscesses
  • Vertebral collapse - Pott’s disease
  • Spinal cord compression from abscesses
109
Q

Recognize the signs of tuberculosis on physical examination.

A

Primary TB

  • Asymptomatic
  • Fever
  • Malaise
  • Cough
  • Wheeze
  • Erythema nodosum
  • Phlyctenular conjunctivitis (allergic manifestations)

Miliary TB

  • Fever
  • Weight loss
  • Meningitis
  • Yellow caseous tubercles spread to other organs - e.g. bone and kidney may remain dormant for years

Post-Primary TB

  • Fever
  • Night sweats
  • Malaise
  • Weight loss
  • Breathlessness
  • Cough
  • Sputum
  • Haemoptysis
  • Pleuritic pain
  • Signs of pleural effusion
  • Collapse
  • Consolidation
  • Fibrosis

Non-Pulmonary TB
- Particularly in immunocompromised

Lymph Nodes
- Suppuration of cervical lymph nodes leading to abscesses or sinuses, which discharge pus and spread to skin = scrofuloderma

CNS

  • Meningitis
  • Tuberculoma

Skin
- Lupus vulgaris - jellylike reddish-brown glistening plaques

Heart

  • Percardial effusion
  • Constrictive pericarditis

Gastrointestinal

  • Subacute obstruction
  • Change in bowel habit
  • Weight loss
  • Peritonitis
  • Ascites

Adrenal
- Insufficiency

Bone/Joints

  • Osteomyelitis
  • Arthritis
  • Paravertebral Abscesses
  • Vertebral collapse - Pott’s disease
  • Spinal cord compression from abscesses
110
Q

Identify appropriate investigations for tuberculosis and interpret the results.

A
  1. Sputum / Pleural Fluid /Bronchial Washings - microscopy, culture (6 weeks), low sensitivity
  2. Tuberculin Tests - positive in previous exposure, strongly positive = infection (and not BCG)
  3. Mantoux Test - intradermal injection of PPD, induration and erythema after 72h
  4. Heaf Test - place drop of PPD on forearm, fire spring-loaded needled gun, read after 3-7 days, graded according to papule size and vesiculation
  5. Interferon-Gamma Tests - latent TB, esposure of host T-cells to TB antigens causes release of interferon (negative with BCG vaccination)
  6. CXR
    - Primary infection - peripheral consolidation, hilar lymphadenopathy
    - Miliary - fine shadowing
    - Post-primary - upper lobe shadowing, streaky fibrosis, cavitation, calcification, pleural effusion, hilar lymphadenopathy
  7. HIV Testing - to co-incident disease (2% may be HIV positive)
  8. CT, Lymph Nodes, Pleural Biopsy, Sampling of Other Affected Systems
111
Q

Define sarcoidosis.

A

Multisystem granulomatous inflammatory disorder.

112
Q

Explain the aetiology / risk factors of sarcoidosis.

A

Unknown.

Transmissibel agents - e.g. viruses, atypical mycobacterium, Propionibacterium acnes

Environmental triggers
Genetic factors

Unknown antigen presented on MHC Class II complex of macrophages to CD4 Th1 lymphocytes, which accumulate and release cytokines (IL-1, IL-2).

Formation of NON-CASEATING granulomas in a variety of organs.

113
Q

Summarise the epidemiology of sarcoidosis.

A

Uncommon.
20-40 year olds.
Africans.
Females.

Variable prevalence
UK 16 in 100,000
Highest in Irish women.

114
Q

Recognise the presenting symptoms of sarcoidosis.

A

General

  • Fever
  • Malaise
  • Weight loss
  • Bilateral parotid swelling
  • Lymphadenopathy
  • Hepatosplenomegaly

Lungs

  • Breathlessness
  • Cough - usually unproductive
  • Chest discomfort
  • Minimal clinical signs - e.g. fine inspiratory crackles

Musculosksletal

  • Bone cysts - e.g. dactylitis in phalanges
  • Polyarthralgia
  • Myopathy

Eyes

  • Keratoconjunctivitis sicca - dry eyes
  • Uveitis
  • Papilloedema

Skin

  • Lupus pernio - red-blue infiltrations of the nose, cheeky, ears, terminal phalanges
  • Erythema nodosum
  • Maculopapular eruptions

Neurological

  • Lymphocytic meningitis
  • Space occupying lesions
  • Pituitary infiltration
  • Cerebellar ataxia
  • Cranial nerve palsies - e.g. bilateral facial nerve palsy
  • Peripheral neuropathy

Heart

  • Arrhythmia
  • Bundle branch block
  • Pericarditis
  • Cardiomyopathy
  • Congestive cardiac failure
115
Q

Recognise the signs of sarcoidosis on physical examination.

A

General

  • Fever
  • Malaise
  • Weight loss
  • Bilateral parotid swelling
  • Lymphadenopathy
  • Hepatosplenomegaly

Lungs

  • Breathlessness
  • Cough - usually unproductive
  • Chest discomfort
  • Minimal clinical signs - e.g. fine inspiratory crackles

Musculosksletal

  • Bone cysts - e.g. dactylitis in phalanges
  • Polyarthralgia
  • Myopathy

Eyes

  • Keratoconjunctivitis sicca - dry eyes
  • Uveitis
  • Papilloedema

Skin

  • Lupus pernio - red-blue infiltrations of the nose, cheeky, ears, terminal phalanges
  • Erythema nodosum
  • Maculopapular eruptions

Neurological

  • Lymphocytic meningitis
  • Space occupying lesions
  • Pituitary infiltration
  • Cerebellar ataxia
  • Cranial nerve palsies - e.g. bilateral facial nerve palsy
  • Peripheral neuropathy

Heart

  • Arrhythmia
  • Bundle branch block
  • Pericarditis
  • Cardiomyopathy
  • Congestive cardiac failure
116
Q

Identify appropriate investigations for sarcoidosis and interpret the results.

A

Bloods

  • High serum ACE
  • Hight Ca2+
  • High ESR
  • WCC low due to lymphocyte sequestration in lungs
  • Immunoglobulins - polyclonal hyperglobulinaemia
  • LFTs - high AlkPhos & GGT

24h Urine Collection
- Hypercalciuria

CXR

  • Stage 0 - may be clear
  • Stage 1 - bilateral hilar lymphadenopathy
  • Stage 2 - bilateral hilar lymphadenopathy with pulmonary infiltration and paratracheal node enlargement
  • Stage 3 - Pulmonary infiltration and fibrosis

High-Resolution CT Scan
- For diffuse lung involvement

67-Gallium Scan
- Shows areas of inflammation (classically parotids and around eye)

Pulmonary Function Tests

  • Reduced FEV1, FVC and gas transfer
  • Restrictive pattern

Bronchoscopy and Bronchoalveolar Lavage

  • Raised lymphocytes
  • Raised CD4:CD8 ratio

Transbronchial Lung Biopsy (or Lymph Node Biopsy)

  • Non-caseating granulomas composed of epithelioid cells (activated macrophages)
  • Multinucleate Langhans cells
  • Mononuclear cells (lymphocytes)

Year 3 Knowledge - Conditions and Procedures (19 decks)

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