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Year 3: Sofia COPY COPY > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is aspergillus lung disease?

A

Lung disease associated with Aspergillus fungal infection

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2
Q

What is the aetiology of aspergillus lung disease?

A

Inhalation of the ubquitous Aspergillus spores can produce three different clinical pictures:

1) Aspergiolloma: Growth of an A. fumigatus mycetoma ball in a preexisting lung cavity (e.g. post-TB old infarct or abscess)
2) Allergic bronchopulmonary aspergillosis (ABPA): Aspergillus colonisation of the airways (usually in asthmatics) leads to IgE- and IgG- mediated immune responses. Proteolytic enzymes and mycotoxins released by fungi, CD4/Th2 cells producing IL-4 and IL_5 and mediating eosinophilic inflammation, and IL-8 mediated neutrophilic inflammation result in airway damage and central bronchiectasis

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3
Q

What is invasive aspergillosis?

A

Invasion of Aspergillus into lung tissue and fungal dissemination.
Secondary to immunosuppression (e.g. neutropaenia, steroids, haematopoietic stem cell/ solid organ transplantation, AIDS)

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4
Q

What is the epidemiology of aspergillosis?

A
  • Uncommon

- Most common in elderly and immunocompromised

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5
Q

What are presenting symptoms of aspergillus lung disease?

A
  • Aspergilloma: Asymptomatic, haemoptysis, which may be massive
  • ABPA: Difficult to control asthma, recurrent episodes of pneumonia with wheeze, cough, fever and malaise
  • Invasive aspergillosis: Dyspnoea, rapid deterioration, septic picture
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6
Q

What are the signs of aspergillus lung disease on examination??

A
  • Tracheal deviation in large aspergillomas
  • Dullness in affected lung, reduced breath sounds, wheeze in ABPA
  • Cyanosis may develop in invasive aspergillosis
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7
Q

What are the investigations for aspergilloma?

A
  • Aspergilloma: CXR: Round opacity may be seen with a crescent of air around it (usually in the upper lobes)
  • CT or MR imaging if CXR does not clearly delineate a cavity
  • Cultures of the sputum may be negative if there is no communication between the cavity and the bronchial tree. Also Aspergillus is a common common coloniser of an abnormal respiratory tract
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8
Q

What are the investigations for Allergic bronchopulmonary aspergillosis (ABPA)?

A
  • Immediate skin test reactivity to Aspergillus antigens
  • Eosinophilia
  • Increased serum total IgE
  • Increased serum specific IgE and IgG to A. fumigatus or precipitating antibodies to A. fumigates
  • CXR: Transient patchy shadows, collapse, distended mucus-filled bronchi producing tubular shadows
  • CT: Lung infilitrates
  • LFT: reversible airflow limitation
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9
Q

What are the investigations for invasive aspergillosis?

A
  • Detection of Aspergillus in cultures or by histological examinations
  • Chest CT scan may show nodules surrounded by a ground-glass appearance (halo sign)
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10
Q

What is asthma?

A

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

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11
Q

What is the aetiology of asthma?

A
  • Genetic factors: Positive family history, twin studies. Almost all asthmatic patients show some atopy.
  • Environmental factors: House dust mite, pollen, pets (e.g. urinary proteins, furs), cigarette smoke, viral respiratory tract infection, Aspergillus fumigatus spores, occupational allergens
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12
Q

What is the pathogenesis of asthma with regards to the early phase??

A

Early phase (up to 1 hour): Exposure in inhaled allergens in a presensitised individual results in cross-linking of IgE antibodies on the mast cell surface and release of histamine, prostaglandin D2, leukotrienes and TNF-a. These induce bronchoconstriction, mucous hypersecretion, oedema and airway obstruction

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13
Q

What is the pathogenesis of asthma with regards to the late phase?

A
  • After 6-12 hours
  • Recruitment of eosinophils, basophils, neutrophil and Th2 lymphocytes and their products results in perpetuation of the inflammation and bronchial hyper-responsiveness
  • Structural cells may also release cytokines, profibrogenic and proliferative growth factors and contibute to the inflammation and altered function and proliferation of smooth muscle cells and fibroblasts (‘airway remodelling’)
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14
Q

What is the epidemiology of asthma?

A
  • Affects 10% of children and 5% of adults
  • Prevalence is increasing
  • Male=Female
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15
Q

What are the presenting symptoms of asthma?

A
  • Episodes of wheeze, breathlessness, cough, worse in the morning and at night
  • Ask about interference with exercise, sleeping, days off school and work
  • In an acute attack it is important to ask whether the patient has been admitted to hospital because of his/her asthma, or to ITU, as a gauge of potential severity
  • Precipitating factors: Cold, viral infection, drugs (B-blockers, NSAIDs), exercise, emotions
  • May have a history of allergic rhinits, uticaria, eczema, nasal polyps, acid reflux and family history
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16
Q

What are the signs of asthma on examination?

A
  • Tachypnoea, use of accessory muscles, prolonged expiratory phase, polyphonic wheeze, hyperinflated chest
  • Severe attack: PEFR less than 50% predicted, pulse more than 110/min, respiratory rate more than 25/min, inability to complete sentences
  • Life threatening attack: PEFR less than 33%, silent chest, cyanosis, bradycardia,, hypotension, confusion, coma
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17
Q

What are the investigations for acute asthma?

A
  • Peak flow
  • Pulse oximetry
  • ABG
  • CXR (to exclude other diagnoses e.g. pneumothorax, pneumonia), FBC (increased WCC if infective exacerbation), CRP, U&E, blood and sputum cultures
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18
Q

What are the investigations for chronic asthma?

A
  • PEFR monitoring: often diurnal variation with morning ‘dip’
  • Pulmonary function test: Obstructive defect, with improvement after a trial of B2-agonist.
  • Blood: Eosinophilia, IgE level, Aspergillus antibody titres ( see allergic Aspergillus lung disease)
  • Skin prick tests: May help in identification of allergens
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19
Q

How is acute asthma managed?

A
  • Resuscitate, monitor 02 sats, ABG and PEFR
  • High flow oxygen
  • Nebulized B2-agonist bronchodilator salbutamol, ipatropium
  • Steroid therapy
  • If no improvement: IV Mg sulphate. Consider IV salbutamol
  • Summon anaesthetic help if pt is getting exhausted (PC02 increasing). Treat any underlying cause (infection, pneumothorax). Give antibiotics if there is evidence of chest infection (purulent sputum, abnormal CXR, increased WCC, fever). Monitor electrolytes closely
  • May need ventilation in severe attacks. If not improving or patient tiring, involve ITU early
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20
Q

How is asthma managed on discharge?

A
  • When PEF more than 75% predicted or pts best, diurnal variation less than 25%, inhaler technique checked, stable on discharge medication for 25h, pt own a PEF meter and has steroid and bronchodilator therapy. Arrange follow-up
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21
Q

What is chronic ‘stepwise’ therapy for asthma?

A

Start on step appropriate to initial severity and step up or down to control symptoms. Treatment should be reviewed every 3-6 months

1) Inhaled short acting B2-agonist as needed. If used more than 1/day move to step 2
2) As step 1 plus regular inhaled low dose steroids
3) As step 2 plus long acting B2 agonist (LABA) . If inadequate control with LABA, increase steroid dose. If no response to LABA, stop and increase steroid dose
4) Increase inhaled steroid dose, add a 4th drug e.g. leukotriene receptor antagonist, SR theophylline or B2 agonist tablet
5) Addition of regular oral steroids. Maintain high-dose inhaled steroid. consider other treatments to minimise the use of oral steroids. Refer for specialist care

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22
Q

What advice should be given to pts with asthma?

A

Educate on proper inhaler technique and routine monitoring of peak flow
Develop an individualised management plan, with emphasis on avoidance of provoking factors

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23
Q

What are the possible complications of asthma?

A
  • Growth retardation
  • Chest wall deformity (e.g. pigeon chest)
  • Recurrent infections
  • Pneumothorax
  • Respiratory failure
  • Death
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24
Q

What is the prognosis of asthma?

A
  • Many children improve as they grow older

- Adult-onset asthma is usually chronic

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25
Q

What is bronchiectasis?

A

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

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26
Q

What is the aetiology of bronchiectasis?

A

Severe inflammation in the lung causes fibrosis and dilation of the bronchi.This is followed by pooling of mucous, predisposing to further cycles of infection, damage, and fibrosis to bronchial walls
- Can be idiopathic and post-infectious (after severe pneumonia, whooping cough, tuberculosis)
Host defence defects e.g. Kartagener’s syndrome, cystic fibrosis, immunoglobulin deficiency, yellow nail syndrome
- Obstruction of bronchi: foreign body, enlarged lymph nodes
- Gastric reflux disease
- Inflammatory disorders e.g. rheumatoid arthritis

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27
Q

What is the epidemiology of bronchiectasis?

A
  • Most often arises initially in childhood

- Incidence has reduced with use of antibiotics

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28
Q

What are the presenting symptoms of bronchoiectasis?

A
  • Productive cough with purulent sputum or haemoptysis
  • Breathlessness, chest pain, malaise, fever, weight loss
  • Symptoms usually begin after an acute respiratory illness
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29
Q

What are the signs of bronchiectasis on examination?

A
  • Finger clubbing
  • Coarse crepitations (usually at the bases) which shift with coughing
  • Wheeze
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30
Q

What are the investigations for bronchiectasis?

A
  • Sputum: Culture and sensitivity, common organisms in acute exacerbations. P. auruginosa, H. influenzae, S. aureus, S. pneumoniae, Klebsiella, M. catarrhalis, Mycobacteria
  • CXR: Dilated bronchi may be seen as parallel line radiating from hilum to diaphragm (tramline shadows). May show fibrosis, atelactasis, pneumonic consolidations or may be normal
  • High res CT: Dilated bronchi with thickened walls. Best diagnostic method
  • Bronchography: Determine extent of disease before surgery - Other: sweat electrolytes, serum immunoglobulins, sinus X-ray, mucociliary clearance study
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31
Q

How is bronchiectasis managed?

A
  • Treat acute exacerbations with 2 IV antibiotics with efficcy for Pseudomonas. Prophylactic courses of antibiotics for those with frequent exacerbations
  • Inhaled corticosteroids (e.g. fluticasone) have been shown to reduce inflammation and volume of sputum, although it does not affect the frequency of exacerbations or lung function
  • Bronchodilators
  • Maintain hydration
  • Consider flu vaccination
  • Physiotherapy
  • Bronchial artery embolisation
  • Surgical
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32
Q

What are the possible complication of bronchiectasis?

A
  • Life-threatening haemoptysis
  • Persistent infections
  • Empyema
  • Respiratory failure
  • Cor pulmonale
  • Multi-organ abscesses
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33
Q

What is the prognosis of bronchiectasis?

A

Most patients continue to have the symptoms after 10 yrs

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34
Q

What is chronic obstructive pulmonary disease (COPD)?

A

Chronic, progressive lung disorder characterised by airflow obstruction with the following
- Chronic bronchitis
and/or
- Emphysema

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35
Q

What is chronic bronchitis?

A

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

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36
Q

What is emphysema?

A

Pathological diagnosis of permanent destructive enlargement of the airways, distal to the terminal bronchus

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37
Q

What is the aetiology of COPD?

A

Bronchial and alveolar damage as a result of environmental toxins (e.g. cigarette smoke). A1-antitrypsin deficiency is rare cause

  • Chronic bronchitis: Narrowing of airways resulting from bronchiole inflammation and bronchi with mucosal oedema, mucous hypersecretion and squamous metaplasia
  • Emphysema: Destruction and enlargement of the alveoli. Results in loss of elastic traction that keeps small airways open on expiration. Progressively larger spaces develop- bullae
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38
Q

What is the epidemiology of COPD?

A
  • Very common (prevalence up to 8%)
  • Presence in middle age or later
  • More common in males, but likely to change with increasing female smokers
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39
Q

What are the presenting symptoms of COPD?

A
  • Chronic cough and sputum production

- Breathlessness, wheeze, reduced exercised tolerance

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40
Q

What are the signs of COPD on examination?

A
  • Inspection: may have 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 sometimes present
  • Signs of C02 retention: Bounding pulse, warm peripheries, flapping tremor of the hands (asterixis). In late stages, signs of right heart failure (e.g. right ventricular heave, raised JVP, ankle oedema)
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41
Q

What are the investigations for COPD?

A
  • Spirometry and pulmonary function tests
  • CXR: may appear normal or show hyperinflation, reduced lung markings, elongated cardiac silhouette
  • Blood: FBC
  • ABG: may show hypoxia
  • ECG and echo: Cor pulmonale
  • Sputum and blood cultures
  • Consider a1-antitrypsin levels: in young pts or minimal smoking history
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42
Q

How is COPD managed?

A
  • Stop smoking
  • Bronchodilators: delivered by inhalers or nebulizers
  • Steroids
  • Pulmonary rehabilitation
  • Oxygen therapy
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43
Q

What are the possible complications of COPD?

A
  • Acute respiratory failure
  • Infections (particularly S. pneumoniae, H. influenzae
  • Pulmonary hypertension and right heart failure,
  • Pneumothorax (resulting from bullae rupture)
  • Secondary polycythaemia
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44
Q

What is the prognosis for COPD?

A

High level of morbidity

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45
Q

What is 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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46
Q

What is the aetiology of extrinsic allergic alveolitis?

A

Inhalation of antigenic organic dusts containing microbes or animal proteins induce a hypersensitivity response in susceptible individuals

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47
Q

What are examples of extrinsic allergic alveolitis?

A
  • Farmer’s lung: Moudly hay containing thermophilic actinomycets
  • Pigeon/budgerigar facier’s lung: Bloom on bird feathers
  • Mushroom worker’s lung: Compost containing thermophilic actinomycetes
  • Humidifier’s lung: Water containing bacteria and Naegleria
  • Maltworker’s lung: barley or maltings containing Aspergillus clavatus
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48
Q

What is the epidemiology of extrinsic allergic alveolitis?

A
  • Uncommon

- Marked geographical variation reflecting dependence on occupational causes

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49
Q

What are the presenting symptoms of acute extrinsic allergic alveolitis?

A
  • Presents 4-12 hr post-exposure
  • Reversible episodes of dry cough, dyspnoea, malaise, fever, myalgia
  • Wheeze and productive cough may develop on repeat high level exposures
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50
Q

What are the presenting symptoms of chronic extrinsic allergic alveolitis?

A
  • Poorly reversible manifestation i some
  • Slowly increasing breathlessness and decreasing exercise tolerance, weight loss
  • Exposure is usually chronic, low level and may be no history of previous acute episodes
  • Full occupational history and enquiry into hobbies and pets important
51
Q

What are the signs of extrinsic allergic alveolitis on examination?

A

Acute: Rapid shallow breathing, pyrexia, inspiratory crepitations
Chronic: Fine inspiratory crepitations. Finger clubbing is rare

52
Q

What are the investigations for extrinsic allergic alveolitis?

A
  • Blood: FBC (neutrophilia, lymhonopenia), ABG
  • Serology: Precipitating IgG to fungal or avian antigens in serum, however, these are not diagnostic as are often found in asymptomatic individuals
  • CXR: Often normal in acute episodes, may show ‘ground glass’ appearance with alveolar shadowing or nodular opacities in middle and lower zones. In chronic: fibrosis prominent in upper zones
  • High resolution CT thorax: Detects early change before CXR. Patchy ‘ground glass’ shadowing and nodules
  • Pulmonary function tests: Restrictive ventilatory defect (Reduced FEV1, FVC with preserved or increased ratio)
  • Bronchoalveolar lavage: Increased cellularity with increased CD8+ suppressor T cells. Lung biopsu.
53
Q

What is idiopathic pulmonary fibrosis?

A

Rare, chronic, idiopathic life-threatening disease that manifests over several years and is characterised by scar tissue within the lungs and progressive dyspnoea

54
Q

What is the aetiology of idiopathic pulmonary fibrosis?

A
  • Unknown

- Possible theory= unidentified injury causes damage to alveolar epithelium, endothelium and basement membrane

55
Q

What is the epidemiology of idiopathic pulmonary fibrosis?

A
  • Increasing prevalence with age

- Mean age of dx between 60-70

56
Q

What are the presenting symptoms of idiopathic pulmonary fibrosis?

A
  • Presence of risk factors (advanced age, male sex, FHx, cigarette smoking)
  • Dyspnoea
  • Cough
  • Weight loss, fatigue, and malaise
57
Q

What are the signs of idiopathic pulmonary fibrosis on examination?

A
  • Crackles

- Clubbing (uncommon)

58
Q

What are the investigations for idiopathic pulmonary fibrosis?

A
  • CXR: Basilar, peripheral, bilateral, asymmetrical, reticular opacities
  • High resolution CT: Basilar and subpleural- dominant areas of increased reticulation, honeycombing and possibly traction bronchiectasis
59
Q

What is obstructive sleep apnoea?

A

Characterised by recurrent collapse of the pharangeal airway and apnoea (cessastion of airflow for more than 10s) during sleep, followed by arousal from sleep.
Also known as Pickwickian syndrome

60
Q

What is the aetiology of obstructive sleep apnoea?

A

Obstructive apnoeas occur when the upper airway narrows because of collapse of the soft tissues of the pharynx when tone in pharangeal dilators decreases during sleep. Associated with:

  • Excessive weight gain, smoking alcohol of sedative use
  • Enlarged tonsils or adrenoids in children
  • Macroglossia, Marfan’s syndrome, craniofacial abnormalities
61
Q

What is the epidemiology of obstructive sleep apnoea?

A
  • Common
  • Affects 5-20% men
  • Affects 2-5% of women
  • Over 35 yrs
  • Prevalence increases with age
62
Q

What are the presenting symptoms of obstructive sleep apnoea?

A
  • Excessive daytime sleepiness (at work, driving)
  • Unrefreshing or restless sleep
  • Morning headaches or dry mouth, difficulty concentrating, irritability or mood changes
  • Partner reporting snoring, nocturnal apnoeic episodes or nocturnal choking
63
Q

What are the signs of obstructive sleep apnoea on examination?

A
  • Large tongue, enlarged tonsils, long or thick uvula, retrognathia (pulled back jaws)
  • Neck circumference (more than 42cm in males but 40cm in females) is correlated with presence of disease
  • Obesity and hypertension common
64
Q

What are the investigations for obstructive sleep apnoea?

A

Video recording episodes

  • Sleep study: managed by sleep study centre for polysomnopgraphy or diagnostic sleep studies with monitoring of airflow, respiratory effort, pulse oximetry and heart rate
  • Blood: Thyroid function test, ABG
65
Q

What is 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 lung function
  • Asbestosis: A pneumoconiosis in which diffuse parenchymal lung fibrosis occurs as a result of prolonged exposure to asbestos
66
Q

What is the aetiology of pneumoconiosis?

A

Caused by inhalation of particles of coal dust, silica or asbestos (two main types of fibre: white asbestos and blue asbestos or crocidolite, the latter is more toxic)

67
Q

What are the risk factors for pneumoconiosis

A
  • Occupational exposure: in coal mining, quarrying iron and steel foundries, stone cutting, sandblasting, insulation industry, plumbers, ship builders.
  • Risk depends on extent of exposure, size and shape of particles and individual susceptibility, as well as co-factors such as smoking and TB
68
Q

What is the epidemiology of pneumoconiosis?

A
  • Incidence increasing in developing countries, disability and mortality from asbestosis will increase for the next 20-30 yrs
69
Q

What are the presenting symptoms of pneumoconiosis?

A

Occupational history is important, there may be a long latency between exposure and expression

  • Asymptomatic: Picked up on routine CXR (simple coal or silica pneumoconiosis)
  • Symptomatic: There is usually insidious onset of shortness of breath and a dry cough. Occasionally, black sputum (melanoptysis) is produced in coalworker’s. Workers exposed to asbestos may develop pleuritic chest pain many years after first exposure as a result of acute asbestos pleurisy
70
Q

What are the signs of pneumoconiosis on examination?

A
  • Examination may be normal
  • Decreased breath sound in coalworker’s pneumoconiosis or silicosis
  • End-inspiratory crepitations and clubbing in asbestosis
  • Signs of a pleural effusion or right heart failure (cor pulmonale)
71
Q

What are the investigations for pneumoconiosis?

A
  • CXR: Simple (micronodular mottling is present). Complicated (Nodular opacities in the upper lobes, micronodular shadowing, eggshell calcification of hilar lumph nodes is characteristic of silicosis
  • CT scan: Fibrotic changes can be visualised early
  • Bronchoscopy: Visualises changes. Allows for bronchoalveolar lavage
  • Lung function test: Restrictive ventilatory defect, impaired diffusion
72
Q

What is pneumonia?

A

Infection of distal lung parenchyma. Several ways of categorisation:

  • Community-acquired, hospital acquired or nosocomial
  • Aspiration pneumonia, pneumonia in the immunocompromised
  • Typical and atypical
73
Q

What is the aetiology of community-acquired pneumonia?

A 
- S. pneumoniae, H. influenzae and Moraxella catarrhalis (COPD), Chlamydia pneumonia and Chlamydia pstiiaci (contact with birds/parrots).
Mucoplasma pneumonia (periodic epidemics), Legionella (anywhere with air conditioning), S. aureus ( recent influenza infection, IV drug users)
74
Q

What is the aetiology of hospital-acquired pneumonia?

A
  • Gram-negative enterobacteria (Pseudomonas, Klebsiella)

- Anaerobes (aspiration pneumonia)

75
Q

What are the risk factors for pneumonia?

A
  • Age
  • Smoking
  • Alcohol
  • Pre-existing lung disease
  • Immunodeficiency
  • Contact with pneumonia
76
Q

What is the epidemiology of pneumonia?

A

Community-acquired causes, more than 60,000 deaths in the UK per year

77
Q

What are the presenting symptoms of pneumonia?

A
  • Fever, rigors, malaise, cough, sputum (yellow, green or rusty if S. pneumoniae), breathlessness and pleuritic chest pain, confusion (severe cases, elderly, Legionella)
  • Atypical pneumonia: Headache, myalgia, diarrhoea/abdominal pain
78
Q

What are the signs of pneumonia on 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 expiration phase), coarse crepitation on affect side
  • Chronic suppurative lung disease (empyma, abscess) Clubbing
79
Q

What are the investigations for pneumonia?

A
  • Blood: FBC (abnormal WCC) U&E (reduced Na+, especially with Legionella, LFT, blood cultures (sensitivity 10-20%, ABG (assess pulmonary function), blood film
  • CXR: Lobar or patchy shadowing, may lag behind clinical signs, pleural effusion, Klebsiella often affects upper lobes, repeat 6-8 weeks. May detect complications: Abscess
  • Sputum/pleural fluid: Microscopy, culture & sensitivity, acid fast bacilli
  • Urine: Pneumococcus and Legionella antigens
  • Atypical viral serology
  • Bronchoscopy
80
Q

How is pneumonia managed?

A

Assess severity ( if more than 1 feature present, manage is hosp)
Start empirical antibodies
- Oral amoxicillin (0 markers)
- Oral or IV amoxicillin and erythromycin (1 marker)
- Add metronidazole, if aspiration, lung abscess or empyma suspected
- Switches to appropriate antibiotic as per sensitivity

81
Q

What is the supportive treatment of pneumonia?

A
  • Oxygen (maintain p02 more than 9kPa
  • Parenteral fluids for dehydration or shock, analgesia, chest physiotherapy
  • CPAP, BiPAP or ITU care for respiratory failure
  • Surgical drainage may be needed for empyma/ abscesses
82
Q

How is discharge planned for pneumonia?

A
  • Presence of 2 or more features of clinical instability (raised temperature, heart rate, respiratory rate and reduced BP, oxygen saturation, mental status and oral intake) predict a significant change of re-admission or mortality. Thus this assessment should be considered when planning for discharge
  • Non-resolving pneumonia: Consider other causes
  • Prevention: Pneumococcal, H influenzae, type B vaccination in vulnerable groups
83
Q

What are the possible complications of pneumonia?

A
  • Pleural effusion
  • Empyema (pus in the pleural cavity
  • Localised suppuration-> lung abscess (especially staphylococcal, 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, Guillain-Barre syndrme
84
Q

What is the prognosis of pneumonia?

A

Most resolve with treatment (1-3 weeks). High mortality of severe pneumonia
Markers of Severe pneumonia (CURB-65 score)
- Confusion
- Urea more than 7mmol/L
- Respiratory rate more than 30 mins
- BP: Systolic less than 90mmg or diastolic less than 60 mmHg
- Age: More than 65 tears

85
Q

What is a 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. blood: haemothorax: lymph: chylothorax)
- Tension pneumothorax: Emergency when a functional valve lets air enter the pleural space during inspiration but not leave during expiration

86
Q

What is the aetiology of a pneumothorax?

A
  • Spontaneous: In individuals with previously normal lungs, typically tall thin males. Probably caused by rupture of a subpleural bleb
  • Secondary: Pre-existing lung disease (COPD, asthma, TB, pneumonia, lung carcinoma, cystic fibrosis, diffuse lung disease)
  • Traumatic: Penetrating injury to 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 and Ehlers-Danlos synrome)
87
Q

What is the epidemiology of a pneumothorax?

A
  • Mainly affects 20-40 year olds

- 4x more common in males

88
Q

What are are the presenting symptoms of a pneumothorax?

A
  • May be asymptomatic if pneumothorax is small
  • Sudden onset breathlessness or chest pain, especially on inspiration
  • Distress with rapid shallow breathing with tension pneumothorax
89
Q

What are the signs of a pneumothorax on examination?

A
  • Signs may be absent if small
  • Signs of respiratory distress with reduced expansion, hyper-resonance on percussion, decreased breath sounds
  • Tension: Severe respiratory distress, tachycardia, hypotension, cyanosis, distended neck veins, tracheal deviation away from side of pneumothorax
90
Q

What are the the investigations for a pneumothorax?

A
  • CXR: A pneumothorax is seen as a dark area of film where lung markings do not extend to. Fluid may be seen be seen if there is blood present. In small pneumothoraces, expiratory films may make it more prominent
  • ABG: May be necessary to determine if there is any hypoxaemia, particularly in secondary disease
91
Q

How is a tension pneumothorax managed?

A
  • Emergency
  • Maximum 02, insert large-bore needle into second intercostal space, midclavicular line, on side of pneumothorax to relieve pressure, insert chest drain soon after
92
Q

How is a small pneumothorax (less than 2cm lung-pleural margin) managed?

A
  • If no underlying fluid or clinical compromise, reassure, analgesia if required and moderate pneumothorax (more than 2cm lung-pleural margin)
  • Aspiration using large-bore cannula or catheter with three way tap: Inserted into the second intercostal space in the midclavicular line. Up to 2.5L can be aspirated. Follow up CXR after 2h and 2 weeks later. Advised to avoid diving
  • Chest drain with water seal: If aspiration fails or if fluid in pleural cavity or after decompression of tension pneumothorax. Inserted into 4th to 6th intercostal space in midaxillary line
93
Q

How are recurrent pneumothoraces managed?

A 
Chemical pleurodeces (visceral and parietal pleura fusion with tetracycline or talc) 
- Surgical pleurectomy
94
Q

What advice should be given to patients with a pneumothorax?

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

What are the possible complications of a pneumothorax?

A
  • Recurrent pneumothoraces

- Bronchopleural fistula

96
Q

What is the prognosis of a pneumothorax?

A
  • After 1 spontaneous pneumothorax, at least 20% will have another
  • Frequency increasing with repeated pneumothoraces
97
Q

What is a pulmonary embolism?

A

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

98
Q

What is the aetiology of a pulmonary embolism?

A
  • Thrombus (more than 95% originating from DVT of lower limbs and rarely from right atrium in pts with AF
  • Other agents that can embolise to pulmonary vessels include amniotic fluid embolus, fat emboli, tumour emboli and mycotic emboli from right-sided endocarditis
  • Groups at risk include surgical pts, immobility, obesity, OCP, heart failure, malignancy
99
Q

What is the epidemiology of pulmonary embolisms?

A
  • Relatively common, especially in hospitalised pts
100
Q

What are the presenting symptoms of a pulmonary embolism?

A

Depends on size and site of the pulmonary embolus?

  • Small: May be asymptomatic
  • Moderate: Sudden onset dyspnoea, cough, haemoptysis and pleuritic chest pain
  • Large: All of above plus severe central pleuritic chest pain, shock, collapse, acute right heart failure or sudden death
  • Multiple small recurrent: Symptoms of pulmonary hypertension
101
Q

What are the signs of a pulmonary embolism on examination?

A
  • Clinical probability assessment
  • Small: Often no clinical signs. Earliest sign is tachycardia or tachypnoea
  • Moderate: Tachypnoea, tachycardia, pleural rub, low saturation 02 (despite oxygen supplementation)
  • Massive PE: Shock, cyanosis, signs of right heart strain (raised JVP, left parasternal heave, accentuated S2 heart sounds)
  • Multiple recurrent PE: Signs of pulmonary hypertension and right heart failure
102
Q

What are the investigations for a pulmonary embolism?

A
  • Low probability: D-Dimer blood test
  • High probability: Requires imaging
  • Additional initial investigations: ABG, ECG (tachy, right avis dev. RBBB), CXR
  • Spiral CT pulmonary angiogram
  • Ventilation-perfusion (VQ) scan
  • Pulmonary angiography
  • Doppler USS of lower limb
  • Echocardiogram
103
Q

How is a pulmonary embolism managed?

A
  • Primary prevention: Graduated pressure stockings (TEDs) and heparin prophylaxis in those at risk (e.g. post surgery). Early mobilisation and adequate hydration post surgery
  • If haemodynamically stable: 02 anticoagulation with heparin of LMW heparin, changing to oral warfarin therapy for min 2 months. Analgesics for pain
  • If haemodynamically unstable: Resuscitate, give oxygen, IV fluic resuscitation, thrombolysis with tPa can be considered on clinical grounds alone if cardiac arrest is imminent
  • Surgical or radiological: Embolectomy. IVC filters for recurrent pulmonary emboli
104
Q

What are the possible complications of a pulmonary embolism?

A
  • Death
  • Pulmonary infarction
  • Pulmonary hypertension
  • Right heart failure
105
Q

What is the prognosis of a pulmonary embolism?

A
  • 30% untreated mortality
  • 8% with treatment
  • Pts have an increased risk of future thromboembolic disease
106
Q

What is tuberculosis?

A

Granulomatous disease caused by Mycobacterium tuberculosis.
Primary: Initial infection may be pulmonary (acquired by inhalation from the cough of an infected patient) or, occasionally, gastrointestinal
- Miliary TB: Results when there is haematogenous dissemination
- Post-primary: Caused by infection or reactivation

107
Q

What is the aetiology of tuberculosis?

A

M. tuberculosis is an intracellular organism which survives after being phagocytosed by macrophages

108
Q

What is the epidemiology of tuberculosis?

A
  • Annual mortality 3 million

- Incidence in Asian immigrants more than 30x UK white population?

109
Q

What are the signs and symptoms of primary tuberculosis?

A
  • Mostly asymptomatic
  • May have fever
  • Malaise
  • Cough
  • Wheeze
  • Erythema nodosum
  • Phlyctenular conjunctivits (allergic manifestiations
110
Q

What are the signs and symptoms of miliary tuberculosis?

A
  • Fever
  • Weight loss
  • Meningitis
  • Yellow caseous tubercles spread to other organs (e.g. in bone and kidney may remain dormant dormant for years
111
Q

What are the signs and symptoms of post-primary tuberculosis?

A
  • Fever/night sweats
  • Malaise
  • Weight loss
  • Breathlessness
  • Cough
  • Sputum
  • Haemoptysis
  • Pleuritic pain
  • Signs of pleural effusion
  • Collapse
  • Consolidation
  • Fibrosis
112
Q

What are the signs and symptoms of non-pulmonary tuberculosis?

A

Particularly in immunocompromised

113
Q

What are the signs and symptoms of TB in the lymph nodes

A
  • Suppuration of cervical lymph nodes leading to abscesses or sinuses which discharge pus and spread to skin (scrofuloderma)
114
Q

What are the signs and symptoms of TB in the CNS?

A
  • Meningitis

- Tuberculoma

115
Q

What are the signs and symptoms of TB in the heart?

A
  • Pericardial effusion

- Constrictive pericarditis

116
Q

What are the signs and symptoms of TB in the skin?

A
  • Lupus vulgaris (jelly like reddish-brown glistening plaques)
117
Q

What are the signs and symptoms of TB in the gastrointestinal system?

A
  • Subacute obstruction
  • Change in bowel habit
  • Weight loss
  • Peritonitis
  • Ascites
118
Q

What are the signs and symptoms of TB in the genitourinary system?

A
  • UTI symptoms
  • Renal failure
  • Epididymitis
  • Endometrial or tubal involvement
  • Infertility
119
Q

What are the signs and symptoms of TB in the adrenal system?

A

Insufficiency

120
Q

What are the signs and symptoms of TB in the bones/joints?

A
  • Osteomyelitis
  • Arthritis
  • Paravertebral abscesses and vertebral collapse (Pott’s disease)
  • Spinal cord compression from abscesses
121
Q

What are the investigations for TB?

A
  • Sputum/pleural/bronchial washings: Microscopy (Ziehl-Neelson stain), culture
  • Tuberculin tests: Positive in previous exposure to M.tuberculosis or BCG
  • Mantoux test
  • Heaf test
  • Interfreron-gamma tests
  • CXR
  • HIV testing
  • CT, lymph nodes, pleural biopsy, sampling of other affected systems
122
Q

What would be seen on a CXR in Primary TB?

A
  • Peripheral consolidation

- Hilar lymphadenopathy

123
Q

What would be seen on a CXR in miliary TB?

A

Fine shadowing

124
Q

What would be seen on a CXR in post-primary TB?

A
  • Upper love shadowing
  • Streaky fibrosis and cavitation
  • Calcification
  • Pleural effusion
  • Hilar lymphadenopathy

Year 3: Sofia COPY COPY (16 decks)

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