Respiratory Flashcards

1
Q

What is asbestosis?

A

Diffuse interstitial fibrosis of the lung as a consequence of exposure to asbestos fibres

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2
Q

What are the risk factors of asbestosis?

A
Cumulative dose of asbestos 
Cigarette smoking (weak)
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3
Q

What is the aetiology of asbestosis?

A

When asbestos fibres are inhaled, they deposit at alveolar duct bifurcations and cause an alveolar macrophage alveolitis.
These activated macrophages release cytokines, such as tumour necrosis factor and interleukin-1beta and oxidant species, which initiate a process of fibrosis.
Initial interstitial fibrosis typically occurs in the lower lobes and may progress to extensive fibrosis and honeycombing.
Peri-bronchial fibrosis with a cellular infiltrate may narrow the airway and cause reduced air flow

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4
Q

What is the epidemiology of asbestosis?

A

There is a latency period of around 20 years from time of first exposure to asbestos to development of radiographical changes, so the diagnosis is typically seen in individuals who began working with asbestos prior to the 1980s and are now usually more than 50 years of age
More likely to be male, workers in the shipyard, construction, and building maintenance industries

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5
Q

What are the presenting symptoms of asbestosis?

A

Dyspnoea on exertion
Dry, non-productive cough (frequency increases with progression- can be absent in patients with early asbestosis)
Chest tightness from SOB

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6
Q

What are the signs of asbestosis?

A

Clubbing- only found in advanced asbestosis
Crackles, initially heard at bases and increases with progression of disease.
Ask about occupational exposure, smoking Hx

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7
Q

What are the appropriate investigations for asbestosis?

A
1st line:
CXR (PA and lateral): 
-lower zone linear interstitial fibrosis
-progressively involves the entire lung
-pleural thickening
Pulmonary function tests:
-restrictive changes
-may have may have obstructive picture (especially if history of asbestos exposure and smoking)
Others:
High resolution CT chest
Lung biopsy - interstitial fibrosis
Bronchial lavage- presence of asbestos bodies in lavage fluid
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8
Q

What is mesothelioma?

A

An aggressive epithelial neoplasm arising from the lining of the lung, abdomen, pericardium, or tunica vaginalis (pouch of serous membrane that covers the testes)
Asbestos is the chief causative agent

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9
Q

What are the risk factors for mesothelioma?

A
Asbestos exposure
Age 60-85
Weaker risk factors:
-male
-radiation exposure
-genetic predisposition
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10
Q

What is the epidemiology of mesothelioma?

A

More common in men and white people, and typically occurs in older adults

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11
Q

What are the presenting symptoms of mesothelioma?

A

Chest pain
Cough
Shortness of breath
Non-specific symptoms: fatigue, fever, sweats and weight loss

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12
Q

What are the signs of mesothelioma?

A

Diminished breath sounds

Dullness to percussion

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13
Q

What are the appropriate investigations for mesothelioma?

A

1st line:

  • Chest x-ray: unilateral pleural effusion, irregular pleural thickening, reduced lung volumes, and/or parenchymal changes related to asbestos exposure
  • CT scan of chest and abdomen with intravenous contrast: pleural thickening, pleural plaques, pleural effusion, enlarged lymph nodes
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14
Q

What is Aspergillus lung disease?

A

Lung disease associated with Aspergillus fungal infection

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15
Q

What is the aetiology of Aspergillus lung disease?

A

Inhalation of the ubiquitous Aspergillus (usually Aspergillus fumigates) spores can produce three different clinical pictures

  1. Aspergilloma:Growth of an A.fumigatus mycetoma ball in a pre-existing lung cavity (e.g. post TB, abscess)
  2. Allergic bronchopulmonary aspergillosis (ABPA): Aspergillus colonization of the airways (usually in asthmatics) causes mediated immune responses
  3. Invasive aspergillosis: Invasion of Aspergillus into lung tissue and fungal dissemination (secondary to immunosuppression)
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16
Q

What is the epidemiology of Aspergillus lung disease?

A

Uncommon

Most common in elderly and immunocompromised

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17
Q

What are the presenting symptoms of Aspergilloma?

A

Asymptomatic

Haemoptysis, which may be massive

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18
Q

What are the presenting symptoms of Allergic bronchopulmonary aspergillosis (ABPA)?

A

Difficult to control asthma
Recurrent episodes of pneumonia with wheeze, cough,
fever and malaise

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19
Q

What are the presenting symptoms of Invasive aspergillosis?

A

Dyspnoea
Rapid deterioration
Septic picture (high temp, PR, RR, low BP)

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20
Q

What are the signs of Aspergilloma on physical examination?

A

Tracheal deviation in large aspergillomas

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21
Q

What are the signs of Allergic bronchopulmonary aspergillosis (ABPA) on physical examination?

A

Dullness in affected lung
Reduced breath sounds
Wheeze

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22
Q

What are the signs of Invasive aspergillosis on physical examination?

A
Cyanosis may develop
Septic picture (high temp, PR, RR, low BP)
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23
Q

What are the appropriate investigations for Invasive aspergillosis?

A

CXR: nodules, consolidation, non-specific infiltrates, pleural-based lesions and cavities
Sputum culture: Aspergillus
CT scan: nodules surrounded by a ground-glass appearance (halo sign) in invasive pulmonary aspergillosis (haemorrhage into the tissue surrounding the area of fungal invasion)

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24
Q

What are the appropriate investigations for ABPA?

A

Immediate skin test reactivity to Aspergillus antigens
Bloods:
-Eosinophilia
-Raised serum IgE antibodies
CXR: Transient patchy shadows, collapse, distended mucus-filled bronchi producing tubular
shadows (‘gloved fingers’ appearance)
Signs of complications: Fibrosis in upper lobes
(similar to tuberculosis), parallel-line shadows and rings (bronchiectasis)
CT: Lung infiltrates, central bronchiectasis.
Lung function tests: Reversible airflow limitation, reduced lung volumes/gas transfer in progressive cases

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25
Q

What are the appropriate investigations for Aspergilloma?

A

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

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26
Q

What is acute respiratory distress syndrome?

A

A syndrome of acute and persistent lung inflammation with increased vascular permeability

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27
Q

What are the causes of acute respiratory distress syndrome?

A
(TOAST)
Transfusion 
Overdose of drugs 
Aspiration 
Sepsis 
Transplantation 
(PIP) 
Pneumonia 
Injury/burns 
Pancreatitis
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28
Q

What is ARDS characterised by?

A

A - Absence of raised capillary wedge pressure
R - Reduced blood oxygen (hypoxaemia)
D - Double-sided infiltrates (bilateral infiltrates)
S - sudden onset (acute- within 1 week)

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29
Q

What is the aetiology of acute respiratory distress syndrome?

A

Severe insult to lungs
Inflammatory mediators released
Capillary permeability increases
Results in pulmonary oedema, reduced gas exchange and reduced lung compliance
(Injury, inflammation, increased permeability)

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30
Q

What is the epidemiology of acute respiratory distress syndrome?

A

Annual UK incidence 􏰀1 in 6000

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31
Q

What are the pathological stages of ARDS?

A

Exudative
Proliferative
Fibrotic

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32
Q

What are the presenting symptoms of ARDS?

A

Rapid deterioration of respiratory function
Dyspnoea
Cough
Symptoms of cause

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33
Q

What are the signs of ARDS on physical examination?

A
Think SMURF: fast, blue, noisy:
Cyanosis 
Tachypnoea 
Tachycardia 
Widespread crepitations 
Hypoxia refractory to oxygen treatment 
(Usually bilateral but may be asymmetrical in early stages)
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34
Q

What are the appropriate investigations for ARDS? Interpret the results

A

1st line:
CXR- bilateral infiltrates
ABG- low partial oxygen pressure
Sputum/ blood/ urine cultures- positive if underlying infection
Amylase- elevated in cases of acute pancreatitis
Others:
BNP- <100 nanograms/L make HF less likely, so ARDS more likely
Pulmonary artery catheterisation- Pulmonary artery occlusion pressure (PAOP) ≤18 mmHg suggests ARDS

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35
Q

What is asthma?

A

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

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36
Q

What are the risk factors of asthma?

A

Genetic factors:
Family Hx
Atopy (tendency of T lymphocyte (Th2) cells to drive production of IgE on exposure to allergens)- eczema, atopic dermatitis, allergic rhinitis is strongly associated

Environmental factors: 
House dust mite 
Pollen, 
Pets (e.g. urinary proteins, furs) 
Cigarette smoke 
Viral respiratory tract infection 
Aspergillus fumigatus spores
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37
Q

What is the pathogenesis of asthma?

A
Early phase (up to 1 h): 
Exposure to inhaled allergens results in cross-linking of IgE antibodies on the mast cell surface and release of histamine, prostaglandin D2, leukotrienes and TNF-a. These mediators induce smooth muscle contraction (bronchoconstriction), mucous hypersecretion, oedema and airway obstruction. 
Late phase (after 6–12h): 
Recruitment of eosinophils, basophils, neutrophil and Th2 lymphocytes and their products results in perpetuation of the inflammation and bronchial hyper-responsiveness. 

Airway remodelling: the inflammation and altered function and proliferation of smooth muscle cells and fibroblasts from cytokines and proliferative growth factors

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38
Q

What is the epidemiology of asthma?

A

Affects 10% of children and 5% of adults

Acute asthma is a very common medical emergency and still responsible for 1000–2000 deaths/year in the UK

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39
Q

What are the presenting symptoms of asthma?

A
Episodes of wheeze
Breathlessness 
Cough 
Worse in the morning and at night 
Interfering with exercise, sleeping, school/ work
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40
Q

What are the exacerbating factors of asthma?

A
Cold
Viral infections 
Drugs (b-blockers, NSAIDs) 
Exercise 
Emotions
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41
Q

What are the signs of asthma on physical examination?

A
Tachypnoea
Use of accessory muscles 
Prolonged expiratory phase 
Polyphonic wheeze* on expiration 
Hyper inflated chest
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42
Q

What are the signs of a severe asthma attack?

A

PEFR < 50% predicted
HR > 110/min (tachycardia)
RR > 25/min
Inability to complete sentences

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43
Q

What are the signs of a life threatening asthma attack?

A
PEFR<33%
Silent chest 
Bradycardia 
Hypotension 
Confusion 
Coma 
Cyanosis
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44
Q

What are the appropriate investigations for asthma? Interpret the results

A

1st line:

  • FEV1/FVC: <70% of predicted
  • Peak flow
  • CXR: hyper inflated lungs
  • FBC: Eosinophilia
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45
Q

What is the acute management of asthma?

A

O SHIT ME

Oxygen (high flow)

Salbutamol- 2.5-5mg NEB
Hydrocortisone- 100mg IV (or prednisolone 40mg PO)
Ipratropium- 500mcg NEB
Theophylline*: aminophylline infusion- 1g in 1L saline 0.5ml/kg/h

Magnesium sulphate- 2g IV over 20mins 
Escalate care (intubation and ventilation) 

*smooth muscle relaxation (bronchodilation) and suppression of the response of the airways to stimuli

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46
Q

What is the chronic management for asthma? (Stepwise)

A

Step 1: Inhaled short acting B2 agonist as needed (if used >1 / day move to 2)
Step 2: Step 1 + regular inhaled lose dose steroids (400mcg/day)
Step 3: Step 2 + long acting B2 agonist (if inadequate control increase steroid dose to 800mcg/day)
Step 4: Step 3 + increase inhaled steroid dose to 2000mcg/day and add 4th drug (leukotriene receptor antagonist or B2 agonist tablet)
Step 5: Step 4 + addition of regular oral steroids (maintain high dose inhaled steroids) and refer to specialist
review every 3-6 months

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47
Q

What are the complications of asthma?

A

Growth retardation
Pectus carinatum (pigeon chest)
Recurrent infections
Pneumothorax

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48
Q

What is the prognosis for patients with asthma?

A

Children: many improve as they grow
Adults: adult onset is usually chronic

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49
Q

What is Bronchiectasis?

A

The permanent (chronic) dilation of bronchi due to the destruction of the elastic and muscular components of the bronchial wall with impaired mucuociliary clearance and frequent bacterial infections

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50
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 mucus, predisposing to further cycles of infection, damage and fibrosis to bronchial walls
Causes:
-Idiopathic is around 50%
-Post infections e.g. TB
-Obstruction of bronchi: Foreign body, enlarged lymph nodes
-Gastric reflux disease.
-Inflammatory disorders: e.g. rheumatoid arthritis

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51
Q

What are the risk factors for Bronchiectasis?

A

Cystic fibrosis
Host immunodeficiency (increased risk of infection)
Previous infections
Congenital disorders of bronchial airways
Alpha-1 anti-trypsin deficiency

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52
Q

What is the epidemiology of Bronchiectasis?

A

Most often arises initially in childhood

Incidence has decreased with use of antibiotics, approximately 1 in 1000 per year

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53
Q

What are the presenting symptoms of Bronchiectasis?

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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54
Q

What are the signs of Bronchiectasis on physical examination?

A

Finger clubbing
Coarse creptitations (usually at the bases) which shift with coughing
Wheeze.

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55
Q

What are the appropriate investigations for Bronchiectasis?

A

Sputum: Culture and sensitivity
*High-resolution CT: Dilated bronchi with thickened walls. Best diagnostic method.
CXR: Dilated bronchi may be seen as parallel lines radiating from hilum to the diaphragm (‘tramline shadows’)- may also show fibrosis, atelectasis, pneumonic consolidations, or it may be normal
PFTs: Reduced FEV₁, elevated residual volume (RV)/total lung capacity (TLC)
Bloods: raised WCC
Test for cause: rheumatoid factor, Alpha-1 anti-trypsin phenotype

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56
Q

What is the management for Bronchiectasis?

A

Maintenance therapy and treatment of acute 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 may be considered in patients with responsive disease
  • Maintain hydration with adequate oral fluid intake
  • Diet and exercise
  • Pulmonary rehabilitation

*prophylactic courses of antibiotics (oral or aerosolized) for those with frequent (􏰃3/year) exacerbations

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57
Q

What are the common pathogens in Bronchiectasis?

A
Pseudomonas aeruginosa
Haemophilus influenzae
Staphylococcus aureus
Streptococcus pneumoniae
Klebsiella, Moraxella catarrhalis, Mycobacteria
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58
Q

What are the complications of Bronchiectasis?

A

Life-threatening haemoptysis
Persistent infections
Empyema (collection of pus in the pleural cavity)
Respiratory failure
Cor pulmonale (abnormal enlargement of the right side of the heart)
Multi-organ abscesses

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59
Q

What is the prognosis of Bronchiectasis?

A

Most patients continue to have the symptoms after 10 years

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60
Q

What is Chronic obstructive pulmonary disease (COPD)?

A

A preventable and treatable disease state characterised by airflow limitation that is not fully reversible.
It encompasses both emphysema and chronic bronchitis

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61
Q

What is the aetiology of COPD?

A

Bronchial and alveolar damage as a result of environmental toxins (e.g. cigarette smoke). Overlaps and may co-exist with asthma

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62
Q

What is Chronic bronchitis?

A

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

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63
Q

What is emphysema?

A

Pathological diagnosis of permanent destructive enlargement of air spaces distal to the terminal bronchioles

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64
Q

What is the aetiology of Chronic bronchitis?

A

Narrowing of the airways resulting from bronchiole inflammation (bronchiolitis) and bronchi with mucosal oedema, mucous hypersecretion and squamous metaplasia

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65
Q

What is the aetiology of emphysema?

A

Destruction and enlargement of the alveoli
This results in loss of the elastic traction that keeps small airways open in expiration
Progressively larger spaces develop, termed bullae (diameter is >1 cm)

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66
Q

What is the epidemiology of COPD?

A
Very common (prevalence up to 8%)
Presents in middle age or later (65 years and older)
More common in males, but likely to change with increased no. female smokers
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67
Q

What are the presenting symptoms of COPD?

A
Chronic cough and sputum production
Breathlessness
Wheeze
Reduced exercise tolerance
(may present with recurrent lung infections)
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68
Q

What are the signs of COPD on physical examination?

A
Inspection: 
-May have respiratory distress
-use of accessory muscles
-barrel-shaped overinflated chest
-decreased cricosternal distance
-peripheral/central cyanosis
Percussion: 
-Hyper-resonant chest
-loss of liver and cardiac dullness.
Auscultation: 
-Quiet breath sounds
-prolonged expiration
-wheeze
-rhonchi (continuous low pitched, rattling lung sounds- sounds like snoring)
-crepitations
sometimes present.
Signs of CO2 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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69
Q

What are the appropriate investigations for COPD?

A

*Spirometry and pulmonary function tests:
Obstructive picture as reflected by reduced PEFR, reduced FEV1: FVC ratio
Pulse oximetry: low oxygen saturation
CXR: May appear normal or show hyperinflation (>6 ribs visible anteriorly, flat hemi- diaphragms), reduced peripheral lung markings, elongated cardiac silhouette
Bloods: FBC ( increasedHb and PCV as a result of secondary polycythemia)
ABG: May show hypoxia (low PaO2), normal or high PaCO2
ECG and echocardiogram: For cor pulmonale
Sputum and blood cultures: In acute exacerbations for treatment

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70
Q

What could be another cause of COPD?

A

Alpha 1-antitrypsin deficiency (<1%) but should be considered in young patients or in those who have never smoked

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71
Q

What can the FEV1: FVC ratio tell us about the stage of COPD?

A

Mild 60–80%
Moderate 40–60%
Severe <40%

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72
Q

What is the management for COPD?

A

Stop smoking.
Bronchodilators: Short-acting b2-agonists (e.g. salbutamol) and anticholinergics (e.g. ipratropium), delivered by inhalers or nebulisers. Long-acting bronchodilators should be used if >2 exacerbations per year
Steroids: Inhaled beclometasone should be considered for all with FEV1 <50% predicted or
those with >2 exacerbations per year.
Regular oral steroids should be avoided but may be necessary for maintenance.
-Chest physiotherapy: for airway clearance
-Pulmonary rehabilitation
-Diet and exercise, patient education (flu vaccination)
-Long-term home oxygen therapy for non-smokers (improves mortality)

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73
Q

What are the complications of COPD?

A

Acute respiratory failure
Infections (particularly Streptococcus pneumoniae, Haemophilus influenzae)
Pulmonary hypertension and right heart failure
Pneumothorax (resulting from bullae rupture)
Secondary polycythaemia

74
Q

What is the prognosis for COPD?

A

Variable prognosis- depends on several factors including genetic predisposition, environmental exposures, co-morbidities and acute exacerbations
High level of morbidity:Three-year survival rate of:
- 90% if age <60 years and FEV1 >50% predicted
-75% if >60 years and FEV1 40–49% predicted

75
Q

What is Extrinsic allergic alveolitis?

A

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

76
Q

What is the aetiology of extrinsic allergic alveolitis?

A

Inhalation of antigenic organic dusts containing microbes (bacteria, fungi or amoebae) or animal proteins induce a hypersensitivity response (a combination of type III antigen–antibody complex hypersensitivity reaction and a type IV granulomatous lym-phocytic inflammation) in susceptible individuals

77
Q

What are the two main causative organisms in extrinsic allergic alveolitis?

A
Bacteria
Animal proteins (Farmer’s lung: mouldy hay containing thermophilic actinomycetes, Pigeon/budgerigar fancier’s lung:  bloom on bird feathers and excreta)
78
Q

What is the epidemiology of extrinsic allergic alveolitis?

A

Uncommon, 2% of occupational lung diseases- 50% of reported cases affect farm workers

79
Q

What are the presenting symptoms of extrinsic allergic alveolitis?

A

Acute:
-Presents 4–12 h post-exposure
-Reversible episodes of dry cough, dyspnoea, malaise, fever, myalgia
-Wheeze and productive cough may develop on repeat high-level exposures
Chronic:
-Poorly reversible manifestation in some
-Slowly increased breathlessness and decreased exercise tolerance, weight loss
-Exposure is usually chronic, low level and there may be no history of previous acute episodes

80
Q

What are the signs of extrinsic allergic alveolitis on physical examination?

A
Acute: 
-Rapid shallow breathing
-Pyrexia
-Inspiratory crepitations
-Rales (abnormal rattling)
Chronic: 
-Fine inspiratory crepitations 
-Finger clubbing (rare)
81
Q

What are the appropriate investigations for extrinsic allergic alveolitis?

A

Bloods:
-Antibodies to causative antigen
-FBC: leukocytosis- neutrophilia, lymphopenia, elevated ESR
-ABG: (reduced PO2, reduced PCO2)
CXR:
Often normal in acute episodes, may show ‘ground glass’ appearance with alveolar shadowing or nodular opacities in the middle and lower zones. In chronic cases, fibrosis is prominent in the upper zones
High-resolution CT-thorax:
Detects early changes before CXR. 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 increased CD8 and suppressor T cells
Lung biopsy:
Bronchocentric infiltrate consisting of lymphocytes, plasma cells, neutrophils, foamy macrophages, and non-caseating granulomas; in later stages interstitial fibrosis predominates

82
Q

What is idiopathic pulmonary fibrosis?

A

A rare, chronic, life-threatening disease that manifests over several years and is characterised by the formation of scar tissue within the lungs and progressive dyspnoea

83
Q

What is the aetiology of idiopathic pulmonary fibrosis?

A

The cause of IPF is not known- a possible theory is that an unidentified insult causes damage to the alveolar epithelium, endothelium, and basement membrane

84
Q

What are the risk factors for idiopathic pulmonary fibrosis?

A
Over 60 years
Male sex
Family History
Cigarette smoking 
Inhalation of small organic or inorganic particles (weak)
PMH of gastro-oesophageal reflux (weak)
Infection
Diabetes
85
Q

What is the epidemiology of idiopathic pulmonary fibrosis?

A

The prevalence increases with advancing age
Mean age: 60 and 70 years
More common in men

86
Q

What are the presenting symptoms and signs of idiopathic pulmonary fibrosis on physical examination?

A
General: malaise, weight loss, fatigue 
Dyspnoea
Cough
Crackles (End-expiratory, basilar)
Clubbing (25-50% of patients)
87
Q

What are the appropriate investigations for idiopathic pulmonary fibrosis?

A

CXR: basilar, peripheral, bilateral, asymmetrical, reticular opacities
High resolution CT: basilar and subpleural-predominant areas of increased reticulation, honeycombing, bronchiectasis
Anti-nuclear antibodies: normal/mildly elevated
PFTs: Restrictive changes- reduced forced vital capacity, reduced total lung capacity
Surgical lung biopsy: fibrosis of varying ages; areas of normal lung next to areas of honeycombing
Bloods: CRP/ESR mildly elevated, RF and Anti- CCP (exclude underlying rheumatoid cause)

88
Q

What is small cell lung cancer?

A

A malignant epithelial tumour arising from cells lining the lower respiratory tract

89
Q

What are the risk factors for small cell lung cancer?

A

Cigarette smoking
Environmental tobacco exposure
Radon gas exposure
Asbestos exposure (weak)

90
Q

What is the aetiology of small cell lung cancer?

A

Tobacco exposure continues to be the most important cause of lung cancer and approximately 90% of lung cancer is directly attributable to smoking

91
Q

What is the epidemiology of small cell lung cancer?

A

SCLC comprises approximately 15-20% of lung cancers
Incidence is decreasing (most likely due to number of smokers decreasing)
Median age 65-70 years (over 50 years)
Currently more common in men

92
Q

What are the presenting symptoms of small cell lung cancer?

A

May be asymptomatic with radiographical abnormality found
Due to primary tumour: Cough, haemoptysis, dyspnoea, chest pain
Due to metastatic disease: Weight loss, fatigue, bone pain
Due to paraneoplastic syndromes: Weakness, lethargy, seizures, muscle fatiguability

93
Q

What does FLAWS stand for?

A
F-fever
L-lethargy
A-appetite changes
W-weight loss
S-night sweats
*used in history taking for malignancy
94
Q

What are the signs of small cell lung cancer on physical examination?

A

May be no signs on auscultation of the chest
Auscultation of the lungs may demonstrate:
-Wheeze
-Rales
-Decreased breath sounds
-Dullness to percussion
-Signs of lobar collapse or pleural effusion
Signs of metastases, e.g. supraclavicular lymphadenopathy or hepatomegaly
Signs of paraneoplastic syndrome e.g. loss of muscle tone or weakness

95
Q

What are the appropriate investigations for small cell lung cancer?

A

Diagnosis:

  • Sputum cytology
  • Bronchoscopy with brushings and biopsy or percutaneous biopsy (malignant cells- may be within the pleural fluid)
  • Thoracoscopy
  • CXR:central mass, hilar lymphadenopathy, pleural effusion

Staging:

  • CT of chest (massive lymphadenopathy and direct mediastinal invasion are common features of SCLC), abdomen, head
  • Isotope bone scan
  • MRI/CT of brain: brain metastases

Other:

  • Lung function tests
  • Bloods: may show anaemia, mildly elevated LFTs, ADH secreting tumour? - may show hyponatraemia
96
Q

What is lung cancer?

A

A group of malignant epithelial tumours arising from cells lining the lower respiratory tract.
Lung cancer is divided into 2 categories:
-Non-small cell lung cancer (NSCLC) (80%)
-Small cell lung cancer (15%)

97
Q

What can non-small cell lung cancer be classified into?

A
  1. adenocarcinoma
  2. squamous cell carcinoma
  3. large cell carcinoma
98
Q

What are the risk factors for non-small cell lung cancer?

A
Cigarette smoking 
Environmental tobacco exposure
Chronic obstructive pulmonary disease
Family Hx
Radon gas exposure
99
Q

What is the aetiology of non-small cell lung cancer?

A
  • Tobacco exposure continues to be the most important cause of lung cancer
  • 45% of NSCLC are adenocarcinomas, which tend to be located more peripherally in the lung
  • 25% to 30% of lung cancers are squamous cell carcinomas, which tend to involve the central airways
  • Large cell carcinomas, accounting for about 10% of lung cancers, are undifferentiated tumours without histological features typical of a squamous cell or adenocarcinoma and tend to arise centrally
100
Q

What is the epidemiology of non-small cell lung cancer?

A

The most common cause of cancer mortality worldwide
NSCLC accounts for 80% of all lung cancer cases
More common in men
Median age of patients is 70 years (Less than 10% of cases are diagnosed below 50 years)

101
Q

What are the presenting symptoms of non-small cell lung cancer?

A

May be asymptomatic with radiographic abnormality found (5%).
Due to primary: Cough, haemoptysis, chest pain, recurrent pneumonia
Due to local invasion: e.g. brachial plexus (Pancoast tumour, in the apex of the lung) causing
pain in the shoulder or arm, left recurrent laryngeal nerve (hoarseness and bovine cough),
oesophagus (dysphagia), heart (palpitations/arrhythmias).
Due to metastatic disease or paraneoplastic phenomena: Weight loss, fatigue, fits, bone pain or fractures, neuromyopathies

102
Q

What are the signs of non-small cell lung cancer on physical examination?

A

There may be no signs.
Wheeze, rales, decreased breath sounds, and dullness to percussion
Signs of collapse, consolidation or pleural effusion.
Due to local invasion:
-Superior vena cava compression (facial congestion, distension of neck veins, upper limb oedema)
-Brachial plexus (wasting of the small muscles of the hand)
-Sympathetic chain (Horner’s syndrome: pupillary miosis, ptosis and facial anhydrosis) PANCOAST TUMOUR
Due to paraneoplastic phenomena: Hypertrophic osteoarthropathy: clubbing, painful swollen wrists/ankles (periosteal new bone formation)
Due to metastases: Supraclavicular lymphadenopathy, hepatomegaly.

103
Q

What are the appropriate investigations for non-small cell lung cancer?

A

CXR: variable; may detect single or multiple pulmonary nodule(s), mass, pleural effusion, lung collapse, or mediastinal or hilar fullness
Contrast enhanced CT of lower neck, thorax and upper abdomen: shows size, location and extent of primary tumour; evaluates for hilar and/or mediastinal lymphadenopathy and distant metastases
Others:
-Bronchoscopy: endobronchial lesions
-Biopsy: malignant cells
-Sampling of the mediastinal lymph nodes: spread
-Thoracentesis: malignant cells within the pleural fluid
-MRI/CT of brain: brain metastases
-Bone scan: skeletal metastases
-Bloods: may show anaemia, mildly elevated LFTs, hypercalcaemia (squamous cell carcinomas), Alk phosphate (bone mets)
-Contrast enhanced CT of liver and adrenals: metastatic lesions
-ECG: cardiac disease/involvement (pre-operatively)

104
Q

What is obstructive sleep apnoea?

A

characterised by recurrent collapse of the pharangeal airway and apnoea (defined as cessation of airflow for >10 s) during sleep, followed by arousal from sleep
(episodes of complete or partial upper airway obstruction during sleep)

105
Q

What is the aetiology of obstructive sleep apnoea?

A

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

106
Q

What is obstructive sleep apnoea associated with?

A
Obesity
Smoking
Alcohol  
Post menopause
PCOS
Hypothyroidism
In children: enlarged tonsils or adenoids, Down's syndrome
Macroglossia
Marfan’s syndrome
Craniofacial/ maxillomandibular abnormalities
Family Hx
107
Q

What is the epidemiology of obstructive sleep apnoea?

A

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

108
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 chronic snoring, nocturnal apnoeic episodes or nocturnal choking (episodic gasping), nocturnal sweating -particularly in children

109
Q

What are the signs of obstructive sleep apnoea on physical examination?

A
Large tongue
Enlarged tonsils
Long or thick uvula
Retrognathia (pulled back jaws)
Neck circumference (>42 cm males, >40 cm females) is strongly correlated with presence of disease
Obesity and hypertension is common
110
Q

What are the appropriate investigations for obstructive sleep apnoea?

A

*Definitive test: polysomnography (sleep study) monitoring of airflow, respiratory effort, pulse oximetry and heart rate
Bloods: TFTs, ABG
Portable multichannel sleep tests

111
Q

What is Pneumoconiosis?

A

A group of interstitial lung diseases, mostly of occupational origin, caused by the chronic inhalation of mineral or metal dusts

112
Q

What are the different groups of Pneumoconiosis?

A
  1. Simple: Coalworker’s pneumoconiosis or silicosis (symptom-free)
  2. Complicated: Pneumoconiosis (progressive massive fibrosis) results in loss of lung function.
  3. Asbestosis: A pneumoconiosis in which diffuse parenchymal lung fibrosis occurs as a result of prolonged exposure to asbestos
113
Q

What is the aetiology of Pneumoconiosis?

A

Caused by inhalation of particles of coal dust, silica or asbestos (and beryllium)
Risk depends on extent of exposure, size and shape of particles and individual susceptibility, as well as co-factors such as smoking and TB

114
Q

What is the epidemiology of Pneumoconiosis?

A

Incidence is increasing in developing countries, disability and mortality from asbestosis will increase due to previous exposure
Improved recognition of these diseases

115
Q

What are the presenting symptoms of Pneumoconiosis?

A

Occupational history is important (long latency between disease 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 coal worker’s pneumoconiosis
Workers exposed to asbestos may develop pleuritic chest pain many years after first exposure as a result of acute asbestos pleurisy

116
Q

What are the signs of Pneumoconiosis on physical examination?

A

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

117
Q

What are the appropriate investigations for Pneumoconiosis?

A

CXR:
-Simple: Micronodular mottling is present
-Complicated: Nodular opacities in the upper lobes, micronodular shadowing, eggshell calcification of hilar lymph nodes is characteristic of silicosis
-Chronic beryllium disease: progressive upper zone linear interstitial fibrosis
-In asbestosis, there is often bilateral lower zone reticulonodular shadowing and pleural plaques, visible as white lines when calcified, often most obvious on the diaphragmatic pleura or as ‘holly leaf’ patterns
CT scan: Fibrotic changes can be visualized early
Bronchoscopy: Visualizes changes. Allows for bronchoalveolar lavage (fluid introduced and collected)
Lung function tests (spirometry): Restrictive ventilatory defect, impaired gas diffusion
Oxygen sats and ABG: low Oxygen

118
Q

What is pneumonia?

A

Infection of distal lung parenchyma

119
Q

How can be pneumonia be classified?

A
  1. Community-acquired, hospital-acquired or nosocomial (originating in hospital)
  2. Aspiration pneumonia, pneumonia in the immunocompromised
  3. Typical and atypical (Mycoplasma, Chlamydia, Legionella)
  4. Location: lobar
120
Q

What is the aetiology of pneumonia?

A

Community-acquired:
-Streptococcus pneumoniae (70%)
-Haemophilus influenzae and Moraxella catarrhalis (COPD)
-Chlamydia pneumonia and Chlamydia psittaci (contact with birds/parrots)
-Mycoplasma pneumonia (periodic epidemics)
-Legionella (anywhere with air conditioning)
-Staphylococcus aureus (recent influenza infection, IV drug users)
Hospital-acquired:
-Gram-negative enterobacteria (Pseudomonas, Klebsiella), anaerobes (aspiration pneumonia)

121
Q

What are the risk factors for pneumonia?

A
Age (over 65 years)
Smoking (or exposure)
Alcohol
Poor oral hygiene
Pre-existing lung disease e.g. COPD
Immunodeficiency (chronic renal/liver disease, diabetes mellitus)
Contact with pneumonia
122
Q

What is the most common causative organism of Pneumonia?

A

Streptococcus pneumoniae

123
Q

What is the epidemiology of pneumonia?

A

Incidence 􏰄5–11 in 1000 (25–44 in 1000 in elderly)

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

124
Q

What are the presenting symptoms of pneumonia?

A

Fever
Cough with increasing sputum production(yellow, green or rusty in S. pneumoniae)
Rigors, sweating (night sweats)
Malaise
Breathlessness and pleuritic chest pain
Confusion (severe cases, elderly, Legionella).

125
Q

What are the signs of pneumonia on physical examination?

A
Inspection:
-Pyrexia
-Respiratory distress
-Tachypnoea
-Tachycardia
-Hypotension
-Cyanosis
Resp examination:
-Reduced chest expansion
-Dullness to percussion
-Increased tactile vocal fremitus
-Bronchial breathing (inspiration phase lasts as long as expiration phase)
-Coarse crepitations on affected side
*Chronic suppurative lung disease (empyema, abscess): Clubbing
126
Q

What are the presenting symptoms of atypical pneumonia?

A

Headache, myalgia, diarrhoea/abdominal pain

127
Q

What system is used to decide whether to treat a patient with pneumonia in the community or in the hospital?

A
CURB-65 mortality risk score
C- Confusion
U- Urea > 7mmol/L*
R- Respiratory rate > 30
B- BP = SBP < 90 mmHg OR DBP < 60 mmHg
65- age >65 years
*Urea may not be easily measured in community
128
Q

What are the appropriate investigations for pneumonia?

A

CXR: new consolidation (repeat 6–8 weeks)
Pulse oximetry: low arterial oxygen saturation < 94%
ABG: low arterial oxygen saturation
Sputum/pleural fluid: Microscopy, culture and sensitivity, acid-fast bacilli
Urine: Pneumococcus and Legionella antigens
Bloods:
-FBC: leukocytosis (abnormal WCC)
-CRP: elevated
-U&Es: Low sodium
-Blood culture: CMS
-LFTs: usually normal
*When pneumonia fails to resolve or when there is clinical progression: Bronchoscopy (and bronchoalveolar lavage)

129
Q

What is the acid-fast bacilli test for?

A

A type of bacteria that causes tuberculosis

130
Q

What is the management for pneumonia?

A
  1. Assess severity
  2. Start antibiotics:
    -Oral amoxicillin
    -Oral or IV amoxicillin and erythromycin
    -IV cefuroxime/cefotaxime/co-amoxiclav and erythromycin
    *switch to appropriate antibiotic as per sensitivity
  3. Supportive therapy:
    -Oxygen (maintain PO2 > 8 kPa, 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/abscesses
  4. Discharge planning:
    Presence of two or more features of clinical instability (pyrexia, heart rate, respiratory rate and low BP, oxygen saturation, mental status and oral intake) predict a significant chance of re-admission or mortality
131
Q

What are the complications of pneumonia?

A
Pleural effusion
Empyema (pus in the pleural cavity)
Lung abscess (especially staphylococcal, Klebsiella pneumonia- rare)
Septic shock
ARDS
Acute renal failure
Septic schock
Heart failure
132
Q

What is the prognosis of pneumonia?

A

For patients admitted to hospital, mortality rate ranges from 5% to 15%, but increases to 20% to 50% in patients requiring admission to the intensive care unit (ICU)
Patients treated in the community generally have a good prognosis

133
Q

What is a pneumothorax?

A

Air in the pleural space (the potential space between visceral and parietal pleura)

134
Q

What is a tension pneumothorax?

A

Emergency when a functional valve lets air enter the pleural space during inspiration, but not leave during expiration

135
Q

What are the classifications of pneumothoraces?

A
  1. Spontaneous
  2. Secondary
  3. Traumatic
136
Q

What is the aetiology of a spontaneous pneumothorax?

A

In individuals with previously normal lungs, typically tall thin males
Probably caused by rupture of a subpleural bleb (thin walled air containing spaces)

137
Q

What is the aetiology of a secondary pneumothorax?

A

Pre-existing lung disease

COPD, asthma, TB, pneumonia, lung carcinoma, cystic fibrosis, diffuse lung disease

138
Q

What is the aetiology of a traumatic pneumothorax?

A

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

139
Q

What are the risk factors for a pneumothorax?

A
Primary spontaneous:
-Family Hx 
-Tall and slender body 
-Age < 40 years 
Secondary: 
-Acute severe asthma
-COPD
-Active TB
-CF
Traumatic:
-Chest trauma
-Recent invasive medical procedure
*Collagen disorders (e.g. Marfan’s disease and Ehlers–Danlos syndrome)
140
Q

What is the epidemiology of pneumothorax?

A
Spontaneous: 
-Annual incidence is 9 in 100 000
-Mainly affects 20–40 year olds
-Four times more common in males
Traumatic: 
-Seen in as many as 40% to 50% of chest trauma victims
141
Q

What are the presenting symptoms of a tension pneumothorax?

A

Distress with rapid shallow breathing

142
Q

What are the presenting symptoms of a pneumothorax?

A

May be asymptomatic if pneumothorax is small

Sudden onset breathlessness or chest pain, especially on inspiration

143
Q

What are the signs of a pneumothorax on physical examination?

A

Signs may be absent if small
Signs of respiratory distress with reduced expansion, hyper-resonance to percussion, reduced breath
sounds

144
Q

What are the signs of a tension pneumothorax on physical examination?

A
Severe respiratory distress
Tachycardia
Hypotension
Cyanosis
Distended neck veins
Tracheal deviation away from side of pneumothorax
145
Q

What are the appropriate investigations for a pneumothorax?

A

CXR:
-A pneumothorax is seen as a dark area of film where lung markings do not extend to
-Fluid level may be seen if there is blood present
-In small pneumothoraces, expiratory films may make it more prominent (most commonly in the upper zones)
ABG:
May be necessary to determine if there is any hypoxaemia, particularly in secondary disease
Bronchoscopy: visualise endobronchial obstruction

146
Q

What is the management of a tension pneumothorax?

A

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

147
Q

What are the borders of the safety triangle?

A

(Posterior edge) Lateral border of pec major
(Anterior edge) Lateral border of Latissimus dorsi
Upper: axilla
Lower: 4th/5th ICS

148
Q

What is the management of a small pneumothorax (<2cm)?

A

Primary: Discharge, repeat CXR (analgesia if needed)
Secondary: Aspiration

149
Q

What is the management of a moderate pneumothorax (>2cm)?

A

Primary: Aspiration. If unsuccessful: chest drain
Secondary: Chest drain

150
Q

What does aspiration involve?

A

Large-bore cannula or catheter with three-way tap inserted into the 2nd ICS, MCL
Up to 2.5 L of air can be aspirated (stop if patient repeatedly coughs or resistance is felt)
Follow-up CXR should be performed just after, 2 h and 2 weeks later
Patient advised to avoid diving

151
Q

What does a chest drain involve?

A

With water seal: If aspiration fails or if there is fluid in the pleural cavity or after decompression of a tension pneumothorax
It is inserted into the fourth to sixth intercostal space in midaxillary line (safety triangle)

152
Q

What are the complications of pneumothorax?

A

Recurrent pneumothoraces

Bronchopleural fistula

153
Q

What is the management of recurrent pneumothoraces?

A
Chemical pleurodesis (visceral and parietal pleura fusion with tetracycline or talc)
Surgical pleurectomy
154
Q

What is the prognosis for a pneumothorax?

A

After one spontaneous pneumothorax, at least 20% will have another, with the frequency increasing with repeated pneumothoraces
Patients with secondary spontaneous pneumothoraces are at greater risk of recurrences

155
Q

What is a pulmonary embolism?

A

Occlusion of pulmonary vessels, most commonly by a consequence of thrombus formation within a deep vein of the body, most frequently in the lower extremities

156
Q

What is the aetiology of a pulmonary embolism?

A

Thrombus (>95% originating from DVT of the lower limbs and rarely from right atrium in patients with AF)
Other agents that can embolize to pulmonary vessels include amniotic fluid embolus, air embolus, fat emboli, tumour emboli and mycotic emboli from right-sided endocarditis

157
Q

What are the risk factors for developing a pulmonary embolism?

A
Surgery
Immobility
Obesity
PMH of DVT
OCP
Pregnancy
Heart failure
Malignancy
158
Q

What is the epidemiology of pulmonary embolism?

A

Relatively common, especially in hospitalized patients, they occur in 10–20% of those with a confirmed proximal DVT
The incidence and direct mortality from PE increases with age

159
Q

What are the presenting symptoms of a pulmonary embolism?

A

Depends on the size and site of the pulmonary embolus:

  • Small: May be asymptomatic.
  • Moderate: Sudden onset dyspnoea, cough, haemoptysis and pleuritic chest pain.
  • Large (or proximal): All of the above plus severe central pleuritic chest pain, shock, collapse, acute right heart failure or sudden death.
160
Q

What are the presenting symptoms of a pulmonary embolism?

A

Depends on the size and site of the pulmonary embolus:

  • Small: May be asymptomatic
  • Moderate: Sudden onset dyspnoea, cough, haemoptysis and pleuritic chest pain
  • Large (or proximal): All of the above plus severe central pleuritic chest pain, shock, collapse, acute right heart failure or sudden death
  • maybe fever
161
Q

What are the appropriate investigations for pulmonary embolism?

A

Low probability: Use D-dimer blood test (cross-linked fibrin degradation products, highly sensitive but poor specificity)
High probability: Requires imaging
Additional initial investigations:
-Bloods: ABG, consider thrombophilia screen.
-ECG: May be normal or more commonly show a tachycardia, right axis deviation or RBBB.
-CXR: Often normal but to exclude other differential diagnoses

  1. Spiral CT pulmonary angiogram: Poor sensitivity for small emboli, but very sensitive for medium to large emboli
  2. Ventilation-perfusion (VQ) scan: identifies any areas of ventilation and perfusion mismatch (infarction)
  3. Pulmonary angiography: Gold standard, but invasive
  4. Doppler USS of the lower limb: To examine for venous thrombosis
  5. Echocardiogram: May show right heart strain
162
Q

What scoring system is used to predict probability to guide further investigation and management?

A
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 1.0 
Malignancy 1.0
163
Q

What is the management for pulmonary embolism?

A

Primary prevention:

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

If haemodynamically stable:
-O2, anticoagulation with heparin or LMW heparin, changingto oral warfarin therapy (INR 2–3) for a minimum of 3 months. Analgesics for pain

If haemodynamically unstable (massive PE):
-Resuscitate, give oxygen, IV fluid resuscitation, thrombolysis with tPA can be considered on clinical grounds alone if cardiac arrest is imminent (50 mg bolus of tPA)- Tissue plasminogen activator to break down clots

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
164
Q

What are the complications of pulmonary embolism?

A

Death
Pulmonary infarction
Pulmonary hypertension
Right heart failure

165
Q

What is the prognosis for pulmonary embolism?

A

30% untreated mortality, 8% with treatment (due to recurrent emboli or underlying disease)
Patients have increased risk of future thromboembolic disease

166
Q

What is sarcoidosis?

A

A chronic multisystem granulomatous inflammatory disorder

167
Q

What organs are mainly affected in sarcoidosis?

A

Lungs
Skin
Eyes

168
Q

What are the risk factors for sarcoidosis?

A
Family History of sarcoidosis
Transmissible agents (e.g. viruses, atypical mycobacterium)
169
Q

What is the epidemiology of sarcoidosis?

A

Uncommon.

More common in 20–40 year olds, Africans and females

170
Q

What are the presenting symptoms of sarcoidosis?

A

General: Fever, malaise, weight loss
Lungs: dyspnoea, cough (usually unproductive), chest discomfort
Musculoskeletal: Bone cysts, polyarthralgia, myopathy
Eyes:
-dry eyes (keratoconjunctivitis sicca)
-painful red eye, blurred vision, photophobia (uveitis)
Skin:
-Lupus pernio (red–blue infiltrations)
-Erythema nodosum

171
Q

What are the signs of sarcoidosis on physical examination?

A

Lymphadenopathy: enlarged and non-tender
Lungs: Minimal clinical signs (e.g. fine inspiratory crepitations)

172
Q

What are the signs of sarcoidosis on physical examination?

A

Lymphadenopathy: enlarged and non-tender
Lungs: Minimal clinical signs (e.g. fine inspiratory crepitations)
Cardiac and neurological signs

173
Q

What are the five stages of sarcoidosis on a CXR?

A

0: normal
1: bilateral hilar lymphadenopathy
2: bilateral hilar lymphadenopathy plus pulmonary infiltrates
3: pulmonary infiltrates without hilar lymphadenopathy
4: extensive fibrosis with distortion

174
Q

What would a transbronchial lung biopsy show in sarcoidosis?

A
Non-caseating (non-necrotising) granulomas composed of:
epithelioid cells (activated macrophages) 
multinucleate Langhans cells 
mononuclear cells (lymphocytes)
175
Q

What is Tuberculosis?

A

An infectious granulomatous disease caused by Mycobacterium tuberculosis
*notifiable disease

176
Q

What is the aetiology of TB?

A

M. tuberculosis is an intracellular organism (also known as acid-fast bacilli, AFB) which survives after being phagocytosed by macrophages
*predominantly in the upper lobes

177
Q

What is the epidemiology of TB?

A

According to WHO, TB is the 9th leading cause of death worldwide, and is the leading cause of death from a single infectious agent
Both the very young (age <5 years) and older people are at increased risk for progression to disease
*Incidence in Asian immigrants >30 times native UK white population

178
Q

What are the risk factors for TB?

A
Exposure to infection
Birth in a high rid country e.g. Asia, Latin America, and Africa
HIV
Immunosuppressive medication
IV drug use
Malnutrition
179
Q

What are the pulmonary presenting symptoms for TB?

A
*TB is a multi-system disease- but can be LATENT
Primary TB: 
-Mostly asymptomatic*
-May have fever
-Malaise
-Cough
-Wheeze
Miliary TB: 
-Fever
-Weight loss
-Meningitis
-Yellow caseous tubercles spread to other organs
(e.g. in bone and kidney may remain dormant for years)
Post-primary TB: 
-Fever/night sweats
-Malaise
-Weight loss
-Breathlessness
-Cough, sputum, haemoptysis
-Pleuritic pain
180
Q

What are the signs of TB on physical examination?

A

Signs of pleural effusion, collapse, consolidation, fibrosis (abnormal chest auscultation and percussion)
Wheeze
Erythema nodosum and phlyctenular conjunctivitis (allergic manifestations)

181
Q

What are the other features of TB?

A

Lymph nodes: Suppuration (acute onset of tender) 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: Pericardial effusion, constrictive pericarditis
Gastrointestinal: Subacute obstruction, change in bowel habit, weight loss, peritonitis, ascites
Genitourinary: UTI symptoms, renal failure, epididymitis, endometrial or tubal involvement, infertility
Adrenal: Insufficiency
Bone/joints: Osteomyelitis, arthritis, paravertebral abscesses and vertebral collapse (Pott’s disease), spinal cord compression from abscesses.

182
Q

What are the appropriate investigations for TB?

A

*CXR: fibronodular opacities in upper lobes with or without cavitation (hilar lymphadenopathy)
Sputum smear: positive for acid-fast bacilli (AFB)
Sputum culture: positive for Mycobacterium tuberculosis
DNA or RNA amplification tests for rapid diagnosis: +ve
Bloods:
-Latent: exposure of host T cells to TB antigens causes release of interferon
-Active: Raised WCC, low Hb
Bronchoscopy and bronchoalveolar lavage: positive for AFB

*Gastric aspirate if unable to produce sputum