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!Final Year > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is acute bronchitis?

A

A type of chest infection which is usually self-limiting in nature and involves inflammation of the trachea and major bronchi

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2
Q

What is the aetiology of acute bronchitis?

A

A result of inflammation of the trachea and major bronchi and is therefore associated with oedematous large airways and the production of sputum from a number of pathogens (viral infection is the leading cause)

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3
Q

What is the epidemiology of acute bronchitis?

A

Viral infection is the leading cause and around 80% of episodes occur in autumn or winter

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4
Q

What is the prognosis of acute bronchitis?

A

The disease course usually resolves before 3 weeks
25% of patients will still have a cough beyond this time

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5
Q

What are the features of acute bronchitis?

A

An acute onset of:
1. Cough: may or may not be productive
2. Sore throat
3. Rhinorrhoea
4. Wheeze

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6
Q

What are the signs of acute bronchitis on examination?

A

Majority of patients will have a normal chest examination
Some patients may present with:
1. Low-grade fever
2. Wheeze

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7
Q

What is the difference in acute bronchitis and pneumonia on history?

A

Sputum, wheeze, breathlessness may be absent in acute bronchitis whereas at least one tends to be present in pneumonia

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8
Q

What is the difference in acute bronchitis and pneumonia on examination?

A

No other focal chest signs (dullness to percussion, crepitations, bronchial breathing) in acute bronchitis other than wheeze
Systemic features (malaise, myalgia, and fever) may be absent in acute bronchitis, whereas they tend to be present in pneumonia

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9
Q

What are the investigations for acute bronchitis?

A

Typically a clinical diagnosis
If CRP testing is available: may be used to guide whether antibiotic therapy is indicated

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10
Q

What is the management for acute bronchitis?

A
  1. Analgesia
  2. Good fluid intake
  3. Consider antibiotic therapy: first line is doxycycline (not in children or pregnancy), or amoxicillin
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11
Q

When would a patient with acute bronchitis require antibiotic therapy?

A

Usually a viral infection
But if they are:
1. Systemically very unwell
2. Have pre-existing co-morbidities
3. A CRP of 20-100mg/L (offer delayed prescription) or a CRP >100mg/L (offer antibiotics immediately)

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12
Q

What is acute respiratory distress syndrome?

A

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

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13
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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14
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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15
Q

What are the causes of ARDS?

A

Infection: sepsis, pneumonia
Massive blood transfusion
Trauma
Smoke inhalation
Acute pancreatitis
Covid-19
Cardio-pulmonary bypass

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16
Q

What is the aetiology of acute respiratory distress syndrome?

A
  1. Severe insult to lungs
  2. Inflammatory mediators released
  3. Capillary permeability increases
  4. Results in pulmonary oedema, reduced gas exchange and reduced lung compliance
    (Injury, inflammation, increased permeability)
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17
Q

What are the pathological stages of ARDS?

A

Exudative
Proliferative
Fibrotic

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18
Q

What are the presenting symptoms of ARDS?

A

Rapid deterioration of respiratory function
Dyspnoea
Cough
Symptoms of cause

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19
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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20
Q

What are the clinical features of ARDS?

A

Dyspnoea
Elevated respiratory rate
Bilateral lung crackles
Low oxygen saturations

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21
Q

What are the appropriate investigations for ARDS?

A

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

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22
Q

What are the two key investigations for ARDS?

A

Chest x-ray and ABG

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23
Q

What is the criteria for ARDS (American-European Consensus Conference)?

A
  1. Acute onset (within 1 week of a known risk factor)
  2. Pulmonary oedema: bilateral infiltrates on chest x-ray (‘not fully explained by effusions, lobar/lung collapse or nodules)
  3. Non-cardiogenic (pulmonary artery wedge pressure needed if doubt)
  4. pO2/FiO2 < 40kPa (300 mmHg)
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24
Q

What is the management for ARDS?

A

Due to the severity of the condition patients are generally managed in ITU
Oxygenation/ventilation to treat the hypoxaemia
General organ support e.g. vasopressors as needed
Treatment of the underlying cause e.g. antibiotics for sepsis
Certain strategies such as prone positioning and muscle relaxation have been shown to improve outcome in ARDS

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25
Q

What is an arterial blood gas (ABG)?

A

A procedure to measure the acidity (pH) and the levels of oxygen and carbon dioxide in the blood from an artery

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26
Q

What are the indications for an arterial blood gas?

A

Respiratory failure - in acute and chronic states.
Any severe illness which may lead to a metabolic acidosis:
- Cardiac/ Liver/ Renal failure
- Hyperglycaemic states associated with diabetes mellitus
- Multiorgan failure
- Sepsis
- Burns
Poisons/toxins
Ventilated patients

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27
Q

What are the possible complications of an arterial blood gas?

A

Local hematoma
Arterial vasospasm
Arterial occlusion
Air or thrombus embolism
LA anaphylactic reaction
Infection at the puncture site

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28
Q

What is type 1 respiratory failure?

A

Normal pCO2
Low pO2
Hypoxia

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29
Q

What is type 2 respiratory failure?

A

Raised pCO2
Low pO2
Hypercapnic and hypoxic

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30
Q

What can exposure to asbestos cause?

A

A variety of lung conditions from benign pleural plaques to asbestosis and mesothelioma

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31
Q

What are pleural plaques following asbestos exposure?

A

Benign and do not undergo malignant change therefore no follow up needed
Most common form of asbestos-related lung disease
Generally occur after a latent period of 20-40 years

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32
Q

What is asbestosis?

A

Diffuse interstitial fibrosis (of the lower lobes) as a consequence of asbestos exposure

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33
Q

What is the pathophysiology of asbestosis?

A
  1. When asbestos fibres are inhaled, they deposit at alveolar duct bifurcations and cause an alveolar macrophage alveolitis
  2. These activated macrophages release cytokines, such as tumour necrosis factor and interleukin-1beta and oxidant species, which initiate a process of fibrosis
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34
Q

What is the severity of asbestosis related to?

A

Length of exposure

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35
Q

What is the latent period of asbestosis?

A

15-30 years

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36
Q

What are the features of asbestosis?

A
  1. Dyspnoea and reduced exercise tolerance
  2. Clubbing
  3. Bilateral end-inspiratory crackles
  4. Lung function tests show a restrictive pattern with reduced gas transfer
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37
Q

What are the investigations for asbestosis?

A

Imaging: CXR and CT
CXR:
1. lower zone interstitial fibrosis
2. pleural thickening
CT:
1. interstitial fibrosis
Others: bronchial lavage = presence of asbestos bodies, pulmonary function tests = restrictive changes

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38
Q

What is the management for asbestosis?

A

Treated conservatively
No interventions offer a significant benefit

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39
Q

What is mesothelioma?

A

A malignant disease of the pleura
Even a limited exposure of asbestos can cause disease

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40
Q

What are the features of mesothelioma?

A
  1. Progressive shortness of breath
  2. Chest pain
  3. Pleural effusion
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41
Q

What are the investigations for mesothelioma?

A

Imaging
CXR:
1. Unilateral pleural effusion
2. Irregular pleural thickening
CT:
1. Pleural thickening and plaques
2. Pleural effusion
3. Enlarged lymph nodes

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42
Q

What is the management of mesothelioma?

A

Palliative chemotherapy (limited role of surgery and radiotherapy)

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43
Q

What is the prognosis of mesothelioma?

A

Very poor
Median survival from diagnosis is 8-14 months

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44
Q

What is the most common form of cancer associated with asbestos exposure?

A

Lung cancer due to increased risk of smoking (therefore smoking cessation is very important in smokers who have a history of asbestos exposure)

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45
Q

What is Aspergillus lung disease?

A

Lung disease associated with Aspergillus fungal infection

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46
Q

What are the three types of Aspergillus lung disease?

A
  1. Aspergilloma
  2. Allergic bronchopulmonary aspergillosis
  3. Invasive aspergillosis
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47
Q

What is an aspergilloma?

A

A mycetoma (mass-like fungus ball) which often colonises a pre-existing cavity e.g. secondary to TB, CF or lung cancer

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48
Q

What are the features of Aspergilloma?

A

Usually asymptomatic
May have cough and/or haemoptysis (can be severe)

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49
Q

What are the investigations for Aspergilloma?

A
  1. CXR: round opacity, crescent sign may be present
  2. Aspergillus precipitin titres = high
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50
Q

What is the management for Aspergilloma?

A

Surgical
Medical = antifungals including Amphotericin B

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51
Q

What is Allergic bronchopulmonary aspergillosis?

A

Allergic reaction from Aspergillus spores
Most patients have a history of bronchiectasis and eosinophilia

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52
Q

What are the features of Allergic bronchopulmonary aspergillosis?

A

Bronchoconstriction:
1. Wheeze
2. Cough
3. Dyspnoea
Bronchiectasis (proximal)
Some patients may have previously labelled asthma

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53
Q

What are the investigations for Allergic bronchopulmonary aspergillosis?

A
  1. Eosinophilia
  2. Fitting CXR changes
  3. Positive radioallergosorbent (RAST) test to Aspergillus
  4. Positive IgG precipitins (not as positive as in aspergilloma)
  5. Raised IgE
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54
Q

What is the management for Allergic bronchopulmonary aspergillosis?

A

Oral glucocorticoids is first choice
Second-line agent: itraconazole

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55
Q

What is invasive aspergillosis?

A

A systemic Aspergillus infection that is the leading cause of death in immunocompromised patients

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56
Q

What are the risk factors for invasive aspergillosis?

A
  1. HIV
  2. Leukaemia
  3. Following broad-spectrum antibiotics
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57
Q

What are the signs of invasive aspergillosis on examination?

A

Septic picture with pyrexia, tachycardia, high RR and hypotension
May develop cyanosis

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58
Q

What is the management of invasive aspergillosis?

A

Antifungals: voriconazole (Vfend) and Amphotericin B
If it does not improve with medical treatment, it eventually leads to death

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59
Q

Who is at risk of developing invasive aspergillosis?

A

Immunocompromised patients

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60
Q

What is asthma?

A

Chronic inflammatory airway disease characterised by:
1. Variable reversible airway obstruction
2. Airway hyper-responsiveness
3. Bronchial inflammation

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61
Q

What is the epidemiology of asthma?

A

Affects around 8% in the UK
More common in boys until teenage years
More common in women

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62
Q

What is the pathology of asthma?

A

Chronic airway inflammation (often eosinophilic inflammation)
Bronchial hyperreactivity to a variety of stimuli causing reversible airway obstruction

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63
Q

What are some of the stimuli in asthma?

A

Allergens e.g. pets, house dust mites
Emotion
Exercise
Change in air temperature
Pollution (indoors and outdoors)
Viruses
Occupational exposure e.g. flour dust, latex, chemicals (hairdresser)

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64
Q

What are some of the features in the history for asthma?

A

Wheeze
Chest tightness
Cough
Breathlessness
Symptoms can be diurnal e.g. nocturnal cough
Ask about triggers
Ask about smoking history which exacerbates asthma

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65
Q

What are the examination findings for asthma?

A

Mouth: oral candida (inhaled steroids without rinsing mouth out), nasal polyps
Hands: fine tremor (excess bronchodilator use)
HR: high (exacerbation or excess bronchodilator use)
Skin: eczema
Chest: audible expiratory wheeze, cough (poor control or acute exacerbation), high RR (acute), polyphonic expiratory wheeze (poor control or acute exacerbation)

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66
Q

What are the two types of wheeze heard in asthma patients?

A

Audible expiratory wheeze
Polyphonic expiratory wheeze = poor control or acute exacerbation

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67
Q

How is the diagnosis of asthma made in adults?

A
  1. Ask if their symptoms are better on days away from work/ during holidays - could be occupational asthma
  2. Spirometry with a bronchodilator reversibility (BDR) test
  3. All patients should have a FeNO test
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68
Q

What is a FeNO test for suspected asthma?

A

Fractional exhaled nitric oxide
Levels of NO correlate with levels of eosinophils inflammation which is found in asthma
Considered positive is equal to or above 40 parts per billion (35 ppb for children)

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69
Q

What are the spirometry findings for someone with asthma?

A

FEV1/FVC ratio less than 70% is considered obstructive

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70
Q

What is a positive result in bronchodilator reversibility for patients with asthma?

A

Indicated by an improvement in FEV1 of 12% or more and increase in volume of 200ml or more

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71
Q

What are the investigations for asthma?

A

No gold standard test
Evidence of airway obstruction:
1. Peak flow diary showing diurnal variation > 20%
2. Spirometry: FEV1/FVC < 0.7, after bronchodilation FEV1 improved by 12% and 200ml
3. FeNO > 40 ppb for eosinophil inflammation
Blood test: eosinophil count and IgE levels
Skin prick test (alternative to IgE blood tests)
Chest x-ray: should be normal, may show hyperinflation

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72
Q

What are the two main differentials for a nocturnal cough?

A

Asthma
GORD

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73
Q

What is the management of low probability asthma?

A

Investigate for other more likely diagnoses
Test for airway obstruction: spirometry and bronchodilator reversibility
If positive then follow intermediate possibility of asthma

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74
Q

What is the management of intermediate probability of asthma?

A

Test for airway obstruction: spirometry and bronchodilator reversibility
Test for variability: reversibility, PEF charting, bronchial challenge
Test for eosinophilic inflammation or atopy: FeNO, IgE, eosinophil count
Then either watchful waiting if asthmatic or commence treatment

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75
Q

What is the management for high probability of asthma?

A

Initiate treatment and assess response objectively e.g. lung function. validated system score
Adjust maintenance dose
Provide self-management advice
Arrange on-going review

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76
Q

What are the principles of medical management of asthma?

A
  1. Short acting beta-2 agonist (SABA)
  2. SABA + low dose ICS
  3. SABA + low dose ICS + leukotriene receptor antagonist (LTRA)
  4. SABA + low dose ICS + Long acting beta-agonist (LABA) ± LTRA
  5. SABA ± LTRA + MART
  6. SABA ± LTRA + medium dose MART (or moderate dose ICS +LABA separately)
  7. SABA ± LTRA and either:
    a) high dose ICS
    b) trial of an additional drug e.g. LAMA
    c) Seeking advice from specialist
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77
Q

What are examples of the medical management of asthma?

A

SABA = salbutamol
ICS = Flovent® (fluticasone) Pulmicort® (budesonide)
LTRA = montelukast
LABA = Serevent (salmeterol)

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78
Q

What are some other considerations alongside medical management of asthma?

A

Regular asthma review - either GP or specialist
Trigger avoidance e.g. pets
Adherence
Inhaler technique
Asthma management (action) plan
Vaccinations = flu, covid
Smoking cessation
Cormorbid management e.g. obesity, allergic rhinitis

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79
Q

What are some indications for severe asthma?

A

Frequent asthma exacerbations e.g 4 per year
Raised eosinophils/ FeNO/ IgE/ atopy

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80
Q

What is MART in asthma management?

A

Maintenance and reliever therapy
Form of combined ICS and LABA treatment in which a single inhaler contained both
Used for both daily maintenance therapy and relief of symptoms as required

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81
Q

What are the doses of inhaled corticosteroids in asthma management?

A

Low = < 400 mcg budesonide
Moderate = 400-800 mcg budesonide
High = > 800 mcg budesonide

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82
Q

What are the principles of stepping down treatment in asthma?

A

Consider stepping down treatment every 3 months or so (taking into account duration of treatment, side effects and patient preference)
When reducing dose of ICS, do this by 25-50% at a time

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83
Q

What are some differentials for asthma?

A

COPD (can have an overlap with asthma)
Allergic bronchopulmonary aspergillosis (ABPA)
Bronchiectasis
Bronchiolitis

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84
Q

What are the typical features of asthma?

A

Wheeze
Cough (nocturnal)
Breathlessness
Chest tightness
History of triggers and diurnal variation

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85
Q

What are the features of acute asthma?

A

History of asthma
Worsening dyspnoea, wheeze and cough that is NOT responding to salbutamol (SABA)
May be triggered by a respiratory tract infection

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86
Q

How are patients with acute asthma stratified?

A

Moderate
Severe
Life-threatening

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87
Q

What are the features of someone with moderate acute asthma?

A

PEFR 50-75% best or predicted
Speech normal
RR < 25/ min
Pulse < 110 bpm

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88
Q

What are the features of someone with severe acute asthma?

A

PEFR 33-50% at best
Can’t complete sentences
RR > 25/min
Pulse > 110 bpm

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89
Q

What are the features of someone with life-threatening acute asthma?

A

PEFR < 33% at best
Oxygen saturations < 92%
PaO2 < 8kPa, “normal” PaCO2
Silent chest
Cyanosis
Poor respiratory effort
Bradycardia
Arrhythmia
Hypotension
Exhaustion
Altered conscious level (confusion or coma)

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90
Q

What are the features of near-fatal asthma?

A

Raised PaCO2 and/or requiring mechanical ventilation with raised inflation pressures

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91
Q

What is the management for severe or life-threatening asthma?

A

ABCDE assessment
Call for help: ITU/HDU
Oxygen: aim for sats 98%
Bronchodilators: nebuliser salbutamol ± ipratropium bromide, IV magnesium
Steroids: PO prednisolone, if not IV hydrocortisone
Re-assess
Later → ventilatory support

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92
Q

What is the management for improved severe or life threatening asthma after initial management?

A

Continue bronchodilators and steroids (5-7 days)
Wean off oxygen
Serial PEF, discharge if PEF over 75%
TAME asthma:
1. Technique
2. Avoid triggers
3. Monitor PEF
4. Educate

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93
Q

What are the doses of medical management for severe or life threatening acute asthma?

A

Oxygen (15L high flow or with nebulisers)
Nebulised beta agonists: 2.5 mg salbutamol every 15 minutes
Nebulised ipratropium: 0.5mg every max 4 hours
Steroids: Oral 40/50mg OD or 100mg IV hydrocortisone

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94
Q

What is bronchiectasis?

A

A permanent dilatation of the airways secondary to chronic infection or inflammation

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95
Q

What is the pathophysiology of bronchiectasis?

A

Permanent dilation of the bronchi due to the destruction of the elastic and muscular components of the bronchial wall

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96
Q

What are the causes of bronchiectasis?

A
  1. Post infective: TB, measles, pertussis, pnuemonia
  2. Cystic fibrosis
  3. Bronchial obstruction e.g. lung cancer, foreign body
  4. Immune deficiency: selective IgA, hypogammaglobulinaemia
  5. Allergic bronchopulmonary aspergillosis (ABPA)
  6. Ciliary dyskinetic syndromes
  7. Yellow nail syndrome
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97
Q

What are the features of bronchiectasis?

A

Persistent productive cough
Large volumes of sputum
Dyspnoea
Haemoptysis

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98
Q

What are the signs of bronchiectasis on examination?

A

Abnormal chest auscultation: coarse crackles, wheeze
Clubbing may be present

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99
Q

What are the investigations for bronchiectasis?

A

CXR and CT imaging
Can also offer sputum culture, pulmonary function tests and tests to diagnose underlying disease e.g. immune assays, Mantoux test for TB

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100
Q

What are the chest x-ray findings for bronchiectasis?

A

Tramlines:
1. Predominantly in the lower zones
2. Dilated bronchi seen as parallel lines radiating from the hilum to the diaphragm

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101
Q

What are the CT findings for bronchiectasis?

A
  1. Widespread tram-track signs
  2. Signet ring sign = enlarged bronchi
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102
Q

What is the best diagnostic test for bronchiectasis?

A

High resolution CT

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103
Q

What is the management for bronchiectasis?

A

After assessing for treatable causes e.g. immune deficiency
1. Physical training e.g. inspiratory muscle training
2. Postural drainage
3. Antibiotics for exacerbations and long-term rotating antibiotics (severe cases)
4. Bronchodilators in selected cases
5. Immunisations
6. Surgery in selected cases e.g. localised disease

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104
Q

What is the best management option for non-CF bronchiectasis?

A

Physical training e.g inspiratory muscle training

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105
Q

What are the common organisms found in patients with bronchiectasis?

A
  1. Most common: haemophilus influenzae
  2. Pseudomonas aeruginosa
  3. Klebsiella spp
  4. Streptococcus pneumoniae
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106
Q

What are the complications of bronchiectasis?

A
  1. Life- threatening haemoptysis
  2. Persistent infections
  3. Empyema: collection of pus in the pleural cavity
  4. Respiratory failure
  5. Cor pulmonale: abnormal enlargement of the R side of the heart
  6. Multi-organ abscess
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107
Q

What is the prognosis of bronchiectasis?

A

Most patients continue to have symptoms after 10 years

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108
Q

What is a chest drain?

A

A tube inserted into the pleural cavity which creates a one way valve: allows the movement of air or liquid out of the cavity

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109
Q

What are the indications for a chest drain?

A
  1. Pleural effusion
  2. Pneumothorax not suitable for aspiration or conservative management
  3. Empyema
  4. Haemothorax/ haemopneunomothorax
  5. Some cases of penetrating chest wall injuries in ventilated patients
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110
Q

What are the relative contraindications for a chest drain?

A
  1. INR > 1.3
  2. Platelet count < 75
  3. Pulmonary bullae
  4. Pleural adhesions
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111
Q

How is a chest drain inserted?

A
  1. Patient positioned in a supine position or at 45 degrees
  2. Identify the 5th intercostal space in the mid-axillary line
    (can be ultrasound guided especially if fluid in the pleura)
  3. LA (lidocaine max 3mg/kg)
  4. Drainage tube inserted using a Seldinger technique
  5. Drain tubing should then be secured using either a straight stitch or an adhesive dressing
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112
Q

What is a Seldinger technique?

A
  1. The desired vessel is punctured with a sharp hollow needle
  2. The syringe is detached and a guide wire is advanced through the lumen of the needle
  3. The needle is then withdrawn
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113
Q

How can the position of a chest drain be confirmed?

A
  1. Aspiration of fluid from the drainage tube
  2. ‘Swinging’ of the fluid within the drain tubing when the patient inspires
  3. On chest x-ray
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114
Q

What are the complications of a chest drain?

A
  1. Failure of insertion (may go into the wrong place- should be removed and re-sited)
  2. Bleeding: around the site of the drain or into the pleural space
  3. Infection
  4. Penetration of the lung
  5. Re-expansion pulmonary oedema
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115
Q

What is re-expansion pulmonary oedema?

A

Uncommon complication following drainage of a pneumothorax or pleural effusion

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116
Q

What symptoms often precede re-expansion pulmonary oedema?

A

Cough and/or shortness of breath

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117
Q

How can re-expansion pulmonary oedema be prevented and managed?

A

Prevention: the drain tubing should be clamped regularly in the event of rapid fluid output i.e. drain output should not exceed 1L of fluid over a short period of time (less than 6 hours)
Management: the chest drain should be clamped and an urgent chest x-ray should be obtained

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118
Q

When should a chest drain be removed?

A

Dependent on the indication for insertion:
1. If for fluid drainage = the drain should be removed when there has been no output for > 24 hours and imaging shows resolution of the fluid collection
2. For pneumothorax = the drain should be removed when it is no longer bubbling spontaneously or when the patient coughs and ideally when imaging shows resolution of the pneumothorax

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119
Q

What is COPD?

A

An umbrella term encompassing chronic bronchitis and emphysema

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120
Q

What is the most common cause of COPD?

A

Smoking

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121
Q

What is COPD characterised by?

A
  1. Airflow limitation that is not fully reversible
  2. Chronic bronchitis + emphysema
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122
Q

What is the aetiology of COPD?

A
  1. Bronchial and alveolar damage as a result of environmental toxins (e.g. cigarette smoke)
  2. Overlaps and may co-exist with asthma
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123
Q

What is the second common cause of COPD?

A

Alpha -1 antitrypsin deficiency (not as common as smoking)

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124
Q

Aside from smoking and alpha-1 antitrypsin deficiency, what are the other causes of COPD?

A

Not as common
1. Cadmium (used in smelting)
2. Coal
3. Cotton
4. Cement
5. Grain

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125
Q

What are the features of COPD?

A
  1. Cough, often productive
  2. Dyspnoea
  3. Wheeze
  4. In severe cases = right-sided HF may develop leading to peripheral oedema
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126
Q

What are the investigations for suspected COPD?

A
  1. Spirometry with bronchodilator: demonstrate airflow obstruction, FEV1/FVC < 70%
  2. Chest x-ray
  3. Bloods: FBC to exclude secondary polycythaemia
  4. BMI index
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127
Q

What are the signs of COPD on a chest x-ray?

A
  1. Hyperinflation
  2. Bullae: if large can mimic a pneumothorax
  3. Flat hemidiaphragm
  4. Exclude lung cancer
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128
Q

Why is peak expiratory flow (PEF) of limited value in COPD?

A

May underestimate the degree of airflow obstruction

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129
Q

What is the severity of COPD categorised by?

A

FEV1: forced expiratory volume in 1 second

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130
Q

When should COPD diagnosis be considered in patients?

A

If over 35 years who are smokers or non-smokers and have symptoms such as:
1. Exertional breathlessness
2. Chronic cough
3. Regular sputum production

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131
Q

What value of post-bronchodilator spirometry FEV1/FVC is needed to make a diagnosis of COPD?

A

< 0.7 (< 70%)

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132
Q

What are the stages of severity of COPD based on the FEV1?

A

Stage 1 (>80%): Mild, symptoms should be present to diagnose COPD in these patients
Stage 2 (50-79%): Moderate
Stage 3 (30-49%): Severe
Stage 4 (<30%): Very severe

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133
Q

What stage of COPD does a patient have if their post-bronchodilator FEV1/FVC is < 0.7 but their FEV1 is greater than 80%?

A

Stage 1, mild COPD (even though their FEV1 is over 80% it is still COPD, but must have symptoms for diagnosis)

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134
Q

What is the general management of COPD?

A
  1. Smoking cessation advice (includes offering nicotine replacement therapy)
  2. Annual influenza vaccination, one-off pneumococcal vaccination
  3. Pulmonary rehabilitation
  4. Bronchodilator therapy, first-line SABA or SAMA
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135
Q

What is the medical management of COPD?

A
  1. SABA or SAMA
  2. Determine whether they have asthmatic/ steroid responsive features
    a. If yes: SABA or SAMA as required, LABA + ICS (often one inhaler)
    b. If no: SABA as required, LABA + LAMA regularly
  3. If patient remains breathlessness or have exacerbations:
    SABA as required, triple therapy regularly = LABA + LAMA + ICS
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136
Q

What are the NICE criteria to determine whether a COPD patient has asthmatic/ steroid responsive features?

A
  1. Any previous secure diagnosis of asthma/ atopy
  2. Higher blood eosinophil count (as part of the recommended FBC)
  3. Substantial variation in FEV1 over time ( at least 400ml)
  4. Substantial diurnal variation in PEF (at least 20%)
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137
Q

When would oral theophylline be recommended in COPD management?

A
  1. Only after trials of short and long-acting bronchodilators or to people who cannot use inhaled therapy
  2. The dose should be reduced if macrolide or fluoroquinolone antibiotics are co-prescribed
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138
Q

When are oral prophylactic antibiotic therapy recommended in the management of COPD?

A
  1. Azithromycin in select patients
  2. Patients should not smoke, have optimised standard treatments and continue to have exacerbations
  3. Need to have a CT thorax to exclude bronchiectasis
  4. Need to have a sputum culture to exclude atypical infections and TB
  5. ECG prior to starting to exclude QT prolongation (as azithromycin can cause this) and LFTs
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139
Q

When would mucolytic be considered in COPD management?

A

Should be considered in patients with a chronic productive cough and continued if symptoms improve

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140
Q

What are the features of cor pulmonale in the context of COPD?

A
  1. Peripheral oedema (due to right-sided heart failure)
  2. Raised jugular venous pressure
  3. Systolic parasternal heave
  4. Loud P2
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141
Q

What is the management of cor pulmonale in COPD patients?

A
  1. Use a loop diuretic for the oedema
  2. Consider long-term oxygen therapy
    (NOT ACEi, CCB or alpha blockers)
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142
Q

What are the factors which may improve survival in patients with stable COPD?

A
  1. Smoking cessation
  2. Long-term oxygen therapy in patients who fit the criteria
  3. Lung volume reduction surgery in selected patients
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143
Q

What is the single most important intervention in COPD patients who are still smoking?

A

Smoking cessation

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144
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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145
Q

What is emphysema?

A

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

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146
Q

What is the aetiology of chronic bronchitis?

A

Narrowing of the airways resulting from:
1. Bronchiole inflammation (bronchiolitis) and
2. Bronchi with mucosal oedema
3. Mucous hypersecretion

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147
Q

What is the aetiology of emphysema?

A
  1. Destruction and enlargement of the alveoli
  2. Results in loss of the elastic traction that keeps small airways open in expiration
  3. Progressively larger spaces develop, termed bullae (diameter is >1 cm)
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148
Q

Which COPD patients should be assessed for long-term oxygen therapy?

A
  1. Very severe outflow obstruction, FEV1 <30% (considered if FEV1 is 30-49%)
  2. Cyanosis
  3. Polycythaemia
  4. Peripheral oedema
  5. Raised jugular venous pressure
  6. Oxygen saturations < 92% on room air
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149
Q

What is the assessment for long-term oxygen therapy in COPD patients?

A

Measure ABG on 2 occasions at least 3 weeks apart in patients with stable COPD on optimal management

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150
Q

When should COPD patients be offered long-term oxygen therapy?

A
  1. ABG: pO2 of <7.3 kPa
  2. ABG pO2 of 7.3-8 kPa and one of the following:
    a. Secondary polycythaemia
    b. Peripheral oedema
    c. Pulmonary hypertension
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151
Q

What is the advice on long-term oxygen therapy and smoking?

A

Do not offer long-term oxygen therapy to people who continue to smoke despite being offered smoking cessation advice and treatment and referral to specialist

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152
Q

What is important in regards to the risk assessment for long-term oxygen therapy?

A
  1. Risk of falls from tripping over the equipment
  2. Risk of burns and fires (increased risk for people who live in homes where someone smokes)
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153
Q

What is an acute exacerbation of COPD?

A

Where patients with COPD experience more severe symptoms, often due to an infective cause

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154
Q

What are the most common bacterial causes of acute exacerbation of COPD?

A
  1. Haemophilus influenzae (most common)
  2. Streptococcus pneumoniae
  3. Moraxella catarrhalis
155
Q

What is the most common bacterial causative organism for an acute exacerbation of COPD?

A

Haemophilus influenzae

156
Q

What are the viral causes of an acute exacerbation of COPD?

A
  1. Respiratory viruses, account for 30% of exacerbations
  2. Human rhinovirus is most important
157
Q

What are the features of an acute exacerbation of COPD?

A
  1. Increase in dyspnoea, cough and wheeze
  2. May be increase in sputum (suggestive of infective cause)
  3. Patients may be hypoxic and in some cases have acute confusion
158
Q

What is the criteria for admission of an acute exacerbation of COPD?

A
  1. Severe breathlessness
  2. Acute confusion or impaired consciousness
  3. Cyanosis
  4. O2 sats < 90% on pulse oximetry
  5. Social reasons e.g. inability to cope at home/ living alone
  6. Significant comorbidity e.g. cardiac disease, insulin dependent DM
159
Q

What is the management of non-severe acute exacerbation of COPD?

A
  1. Increase the frequency of bronchodilator use (and consider giving via a nebuliser)
  2. Give prednisolone 30mg daily for 5 days
  3. Antibiotics if sputum is purulent or clinical signs of pneumonia: oral amoxicillin, clarithromycin or doxycycline
160
Q

What is the management of severe acute exacerbation of COPD (requiring secondary care admission)?

A
  1. Oxygen therapy
  2. Nebulised bronchodilator
  3. Steroid therapy: prednisolone 30mg daily for 5 days or IV hydrocortisone
  4. Consider IV theophylline
  5. Non-invasive ventilation if T2RF development
161
Q

What is the oxygen therapy in the management of severe exacerbation of COPD?

A
  1. Risk of hypercapnia therefore aim for oxygen target of 88-92%
  2. Initially use 28% Venturi mask at 4L/min, aim for 88-92% whilst waiting for ABG results
  3. Adjust target range to 94-98% if the pCO2 is normal
162
Q

What nebulised bronchodilators are used in the management of severe exacerbation of COPD?

A
  1. Beta adrenergic agonist: salbutamol
  2. Muscarinic antagonist: ipratropium bromide
163
Q

When is IV theophylline therapy considered in severe exacerbations of COPD?

A

For patients not responding to nebulised bronchodilators

164
Q

When is non-invasive ventilation used in the management of severe exacerbations of COPD?

A
  1. If the patient develops type 2 respiratory failure: low O2 and high CO2
  2. Typically used for COPD with respiratory acidosis: pH 7.25-7.35 (can be for <7.25 but require more monitoring and has a lower threshold of intubation and ventilation)
165
Q

What type of non-invasive ventilation is used in severe exacerbations of COPD?

A

Bi-level positive airway pressure (BiPAP), initial settings:
1. Expiratory Positive Airway Pressure (EPAP): 4-5 cm H2O
2. Inspiratory Positive Airway Pressure (IPAP): RCP advocate 10 cm H20 whilst BTS suggest 12-15 cm H2O

166
Q

What is extrinsic allergic alveolitis?

A
  1. Also known as hypersensitivity pneumonitis
  2. Hypersensitivity induced lung damage due to a variety of inhaled organic particles
167
Q

What is the aetiology of extrinsic allergic alevolitis?

A
  1. Mainly by immune-complex mediated tissue damage (type 3 hypersensitivity)
  2. Delayed hypersensitivity ( type 4) plays a role in the chronic phase
168
Q

What are some of the examples of extrinsic allergic alveolitis?

A
  1. Bird fanciers’ lung: avian proteins from bird droppings
  2. Farmers lung: spores of Saccharopolyspora rectivirgula from wet hay
  3. Malt workers’ lung: Aspergillus clavatus
  4. Mushroom workers’ lung: thermophilic actinomycetes
169
Q

What is the acute presentation of extrinsic allergic alveolitis?

A

4-8 hours after exposure:
1. Dyspnoea
2. Dry cough
3. Fever

170
Q

What is the chronic presentation of extrinsic allergic alveolitis?

A

Occurs weeks-months after exposure
1. Lethargy
2. Dyspnoea
3. Productive cough
4. Anorexia and weight loss

171
Q

What are the investigations for extrinsic allergic alveolitis?

A
  1. Imaging: upper/mid zone fibrosis
  2. Bronchoalveolar lavage: lymphocytosis
  3. Serologic assays for specific IgG antibodies
  4. No eosinophilia on bloods
172
Q

What is the management of extrinsic allergic alveolitis?

A
  1. Avoid precipitating factors
  2. Oral glucocorticoids
173
Q

What are the findings of extrinsic allergic alveolitis on CXR and CT?

A

CXR:
1. Often normal in acute episodes
2. May show ‘ground glass’ appearance with alveolar shadowing or nodular opacities in the middle and lower zones
3. In chronic cases, fibrosis is prominent in the upper zones
High-resolution CT-thorax:
1. Detects early changes before CXR
2. Patchy ‘ground glass’ shadowing and nodules

174
Q

What is idiopathic pulmonary fibrosis?

A

A chronic lung condition characterised by progressive fibrosis of the interstitium of the lungs

175
Q

What are some of the causes of pulmonary fibrosis?

A
  1. Medications e.g. nitrofurantoin
  2. Connective tissue disease
  3. Asbestos
    Idiopathic pulmonary fibrosis: reserved for when there is no underlying cause
176
Q

What is the epidemiology of idiopathic pulmonary fibrosis?

A
  1. Patients aged 50-70 years
  2. Twice as common in men
177
Q

What are the features of idiopathic pulmonary fibrosis?

A
  1. Progressive exertional dyspnoea
  2. Bi-basal fine end-inspiratory crepitations on auscultation
  3. Dry cough (non-productive)
  4. Clubbing
178
Q

What can be heard on auscultation on patients with idiopathic pulmonary fibrosis?

A

Bi-basal fine end-inspiratory crepitations

179
Q

What are the investigations for idiopathic pulmonary fibrosis?

A
  1. Spirometry
  2. Imaging
  3. Antibodies- limited role
180
Q

What are the findings of spirometry in patients with idiopathic pulmonary fibrosis?

A

Classically a restrictive picture:
1. FEV1 normal or decreased
2. FVC decreased
3. FEV1/FVC increased

181
Q

What is the investigation of choice for idiopathic pulmonary fibrosis?

A

High-resolution CT

182
Q

What are the findings on imaging in patients with idiopathic pulmonary fibrosis?

A
  1. Bilateral interstitial shadowing
  2. Typically small, irregular, peripheral opacities = ‘ground-glass’ (sub-pleural reticular opacities increase from apex to base)
  3. Later progresses to ‘honeycombing’
183
Q

What antibodies are tested in idiopathic pulmonary fibrosis?

A

Usually ANA are positive in 30% and rheumatoid factor positive in 10% but this does not always mean that the pulmonary fibrosis is secondary to connective tissue disease

184
Q

What is the management of idiopathic pulmonary fibrosis?

A
  1. Pulmonary rehabilitation
  2. Medications: few have shown benefit, some evidence of pirfenidone (an antifibrotic agent) in some patients
  3. Many patients will require supplementary oxygen
  4. Eventually patients will need a lung transplant
185
Q

What is the prognosis of idiopathic pulmonary fibrosis?

A
  1. Poor
  2. Average life expectancy is 3-4 years
186
Q

What are the two broad types of lung cancer?

A

Histologically classified into:
1. Small cell lung cancer (SCLC) = 15%
2. Non-small cell lung cancer (NSCLC) = 85%

187
Q

Which class of lung cancer carries a worse prognosis?

A

Small cell lung cancer

188
Q

What are the different types of non-small cell lung cancer?

A
  1. Adenocarcinoma (most common)
  2. Squamous
  3. Large cell
  4. Alveolar cell carcinoma
  5. Bronchial adenoma
189
Q

What is adenocarcinoma lung cancer?

A
  1. A subtype of non-small cell lung cancer
  2. Most common type of lung cancer
  3. Often seen in non-smokers
190
Q

What are the features of lung cancer?

A
  1. Persistent cough
  2. Haemoptysis
  3. Dyspnoea
  4. Chest pain
  5. Weight loss and anorexia
  6. Hoarseness (Pancoast tumours pressing on the recurrent laryngeal nerve)
  7. Superior vena cava syndrome: oncological emergency due to compression of SVC
191
Q

What are the findings of lung cancer on examination?

A
  1. Fixed, monophonic wheeze may be noted
  2. Supraclavicular lymphadenopathy or persistent cervical lymphadenopathy
  3. Clubbing
192
Q

What is superior vena cava syndrome?

A

An oncological emergency due to compression of the SVC- most commonly seen in lung cancer

193
Q

What are the features of superior vena cava syndrome?

A
  1. Dyspnoea (most common symptom)
  2. Swelling of the face, neck and arms - conjunctival and periorbital oedema may be seen
  3. Headache: often worse in the mornings
  4. Visual disturbance
  5. Pulseless jugular venous distension
194
Q

What are some of the other causes of superior vena cava syndrome?

A
  1. Common malignancies e.g small cell lung cancer, lymphoma
  2. Other malignancies: Kaposi’s sarcoma, breast cancer
  3. Aortic aneurysm
  4. Mediastinal fibrosis
  5. Goitre
  6. SVC thrombosis
195
Q

What is the management of superior vena cava syndrome?

A
  1. Dependent on the individual patient and their malignancy (or cause)
  2. Endovascular stenting is often treatment of choice: provides symptom relief
196
Q

When should an urgent chest x-ray be considered within 2 weeks to assess for lung cancer?

A

Over 40 years of age and any of the following:
1. Persistent or recurrent chest infections
2. Finger clubbing
3. Supraclavicular lymphadenopathy or persistent cervical lymphadenopathy
4. Chest signs consistent with lung cancer
5. Thrombocytosis

197
Q

When should an urgent chest x-ray be offered within 2 weeks to assess for lung cancer?

A

Over 40 years of age if they have 2 or more of the following unexplained symptoms, or if they have ever smoked and have 1 or more of the following unexplained symptoms:
1. Cough
2. Fatigue
3. Shortness of breath
4. Chest pain
5. Weight loss
6. Appetite loss

198
Q

When should someone be referred on the suspected lung cancer pathway (appointment within 2 weeks)?

A
  1. Have chest x-ray findings that suggest lung cancer
  2. Are aged over 40 years with unexplained haemoptysis
199
Q

What is squamous cell cancer of the lung?

A
  1. Type of NSCLC
  2. Typically central
  3. Associated with parathyroid hormone-related protein secretion causing hypercalaemia
  4. Strongly associated with finger clubbing
  5. Cavitating lesions
  6. Hypertrophic pulmonary oestoarthropathy (HPOA)
200
Q

What is adenocarcinoma of the lung?

A
  1. Type of NSCLC
  2. Typically peripheral
  3. Most common type of lung cancer in non-smokers (but majority of patients who develop these are smokers)
201
Q

What is large cell lung carcinoma?

A
  1. Type of NSCLC
  2. Typically peripheral
  3. Anaplastic, poorly differentiated tumours
  4. Poor prognosis
  5. May secrete b-hCG
202
Q

What are the features of small cell lung cancer?

A
  1. Usually central
  2. Associated with ectopic ADH and ACTH secretion
    a. ADH: hyponatraemia
    b. ACTH: Cushing’s syndrome
  3. ACTH secretion can cause bilateral adrenal hyperplasia: hypokalaemic acidosis
203
Q

What is Lambert-Eaton syndrome in small cell lung cancer?

A

Antibodies to voltage gated calcium channels causing myasthenic like syndrome

204
Q

What are the investigations for lung cancer?

A
  1. Chest x-ray (often the first test)
  2. CT = investigation of choice
  3. Bronchoscopy (for biopsy)
  4. PET scanning: typically for NSCLC
  5. Bloods: raised platelets
205
Q

What is the investigation of choice for suspected lung cancer?

A

CT

206
Q

What is the role of bronchoscopy in the diagnosis of lung cancer?

A
  1. Allows a biopsy to be taken to obtain a histological diagnosis
  2. Sometimes aided by an endobronchial ultrasound
207
Q

What is the role of PET scanning in the diagnosis of non-small cell lung cancer?

A
  1. To establish eligibility for curative treatment
  2. Uses 18-fluorodeoxygenase which is preferentially taken up by neoplastic tissue
  3. Has been shown to improve diagnostic sensitivity of both location and distant metastasis spread in NSCLC
208
Q

What is the management for non-small cell lung cancer?

A
  1. Only 20% are suitable for surgery
  2. Can be offered curative or palliative radiotherapy
  3. Has poor response to chemotherapy
209
Q

What needs to be performed prior to surgery for NSCLC?

A
  1. Mediastinoscopy
  2. This is because CT does not always show mediastinal lymph node involvement
210
Q

What are the contraindications for surgery in the management of NSCLC?

A
  1. Assess general health
  2. Staged 3b or 4 = metastases present
  3. FEV1 < 1.5 L for lobectomy
  4. Malignant pleural effusion
  5. Tumour near hilum
  6. Vocal cord paralysis
  7. SVC obstruction
211
Q

What is the management for small cell lung cancer?

A
  1. Usually metastatic disease by the time of diagnosis
  2. Patients with very early stage disease are now considered for surgery (T1-2a, N0, M0)
  3. Most patients with early/ limited disease receive a combination of chemotherapy and radiotherapy
  4. Patients with more extensive disease are offered palliative chemotherapy
212
Q

Which type of lung cancer generally carries a worse prognosis?

A

Small cell lung cancer

213
Q

What are the paraneoplastic features of small cell lung cancer?

A
  1. ADH: hyponatraemia
  2. ACTH: not typical, HTN and hyperglycaemia, hypokalaemia alkalosis and muscle weakness
  3. Lambert- Eaton syndrome
214
Q

What are the paraneoplastic features of squamous cell lung cancer?

A
  1. Parathyroid hormone-related protein secretion: causes hypercalcaemia and clubbing
  2. Hypertrophic pulmonary osteoarthropathy
  3. Hyperthyroidism due to ectopic TSH
215
Q

What are the paraneoplastic features of adenocarcinoma of the lung?

A
  1. Gynaecomastia
  2. Hypertrophic pulmonary oesteoarthropathy
216
Q

What is obstructive sleep apnoea?

A

A condition in which the muscles in the throat relax and narrow, interrupting normal breathing

217
Q

What is apnoea?

A

When there is a blockage of the airway for 10 seconds or more

218
Q

What are the features of obstructive sleep apnoea?

A
  1. Interrupted sleep
  2. The partner often complains of excessive snoring and may report periods of apnoea (airway obstruction)
219
Q

What are the predisposing factors for obstructive sleep anpoea?

A
  1. Obesity
  2. Macroglossia: acromegaly, hypothyroidism, amyloidosis (AL)
  3. Large tonsils
  4. Marfan’s syndrome
220
Q

What are the consequences of obstructive sleep apnoea?

A
  1. Daytime somnolence (drowsiness/ desire to sleep)
  2. Compensated respiratory acidosis
  3. Hypertension
221
Q

How do you assess sleepiness in obstructive sleep apnoea?

A
  1. Epworth sleepiness scale: questionnaire completed by patient/ partner
  2. Multiple Sleep Latency Test: measures the time to fall a sleep in a dark room (using EEG criteria)
222
Q

What are the investigations for obstructive sleep apnoea?

A

Sleep studies (polysomnography):
1. Ranging from monitor of pulse oximetry at night to full polysomnography
2. Polysomnography is where a wide variety of physiological factors are studied, e.g. EEG, respiratory flow, thoraco-abdominal movement, snoring and pulse oximetry

223
Q

What is the management for obstructive sleep apnoea?

A
  1. Weight loss
  2. Continuous positive airway pressure (CPAP): first line for moderate or severe
  3. Intra-oral devices e.g. mandibular advancement for patient who can’t tolerate CPAP or with mild OSA where there is no sleepiness in the daytime
  4. DVLA should be infored if is is causing excessive daytime sleepiness
224
Q

What is the aetiology of obstructive sleep apnoea?

A
  1. Occurs when the upper airway narrows
  2. This is because the soft tissues of the pharynx collapse when tone in pharangeal dilators decreases during sleep
225
Q

What are some of the presenting features of obstructive sleep apnoea?

A
  1. Excessive daytime sleepiness (at work, driving)
  2. Unrefreshing or restless sleep
  3. Morning headaches or dry mouth
  4. Difficulty concentrating, irritability or mood changes
  5. Partner reporting chronic snoring, nocturnal apnoeic episodes or nocturnal choking (episodic gasping), nocturnal sweating -particularly in children
226
Q

What is Pneumoconiosis?

A
  1. A group of interstitial lung diseases
  2. Mostly of occupational origin caused by the chronic inhalation of mineral or metal particles
227
Q

What does pneumoconiosis mean?

A

Accumulation of dust in the lungs and the response of the bodily tissue to its presence- most commonly used in relation to coal worker’s pneumoconiosis

228
Q

What are the different types of penumoconiosis?

A
  1. Simple: Coal worker’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
229
Q

What is the aetiology of penumoconiosis?

A
  1. Occupational lung disease caused by long term exposure to coal dust particles (or asbestos)
  2. Severity is linked to the extent of exposure
  3. Often there is a long lead time between the first exposure and the development of the disease
  4. Risk also depends on smoking and other lung disease e.g. TB
230
Q

What is the epidemiology of pneumoconiosis?

A
  1. Prevalence is higher in populations with higher levels of exposure e.g. areas with large coal mining industries
  2. Coal worker’s pneumoconiosis makes up around 7% of all Pneumoconiosis
  3. Diagnosis is usually 15-20 years after initial exposure to the coal dust
231
Q

What is the pathophysiology of coal worker’s pneumoconiosis?

A
  1. Coat dust is inhaled and enters the lungs
  2. The dust reaches the terminal bronchioles and is engulfed by alveolar and interstitial macrophages
  3. The dust particles are moved by the macrophages and removed from the body as mucus
  4. Over many years, the system is overwhelmed and the macrophages begin to accumulate in the alveoli → immune response, causing damage to the lung tissue
232
Q

What is simple pneumoconiosis?

A
  1. Commonest type
  2. Patients are often asymptomatic
  3. It’s presence increases the risk of lung diseases such as COPD
  4. May lead to Progressive Massive Fibrosis
233
Q

What is the staging of pneumoconiosis?

A

Appearance of the chest X-ray:
Category 1: some opacities but normal lung markings visible
Category 2: large number of opacities but normal lung markings visible
Category 3: large number of opacities with normal lung not visible

234
Q

What is Progressive Massive Fibrosis?

A
  1. Dust exposure causes patients to develop round, fibrotic masses (can be several cm in diameter)
  2. Most common in upper lobes
  3. Often symptomatic: breathlessness on exertion and cough, some may have black sputum (coal worker’s)
  4. LFTs: mixed obstructive/ restrictive picture
235
Q

What are the investigations for pneumoconiosis?

A
  1. Chest x-ray: upper zone fibrosis
  2. Spirometry: restrictive lung function tests, normal or slightly reduced FEV1 and FVC
236
Q

What is the management for pneumoconiosis?

A
  1. Avoid further exposure to coat dust and other respiratory irritants e.g. smoking
  2. Manage symptoms of chronic bronchitis (analgesia, good fluid intake, consider antibiotics)
  3. Patients may be eligible for compensation via Industrial Injuries Act
237
Q

What is Pneumonia?

A
  1. Any inflammatory condition affecting the alveoli of the lungs
  2. Commonly this is secondary to a bacterial infection
238
Q

What are the two broad categories of Pneumonia?

A
  1. Community acquired: majority of patients
  2. Hospital acquired: occurs 48 hours or more after admission
    * Important due to causative organisms
239
Q

How can 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
240
Q

What is the most common causative pathogen for pneumonia?

A

Bacterial pneumonia

241
Q

What is the most common causative organism for pneumonia?

A
  1. Streptococcus pneumoniae (pneumococcus)
  2. Accounts for 80% of cases
  3. Particularly associated with high fever, rapid onset and herpes labialis
242
Q

What is the most common causative organism for pneumonia in patients with COPD?

A

Haemophilus influenzae

243
Q

What are the two common typical organisms for pneumonia?

A
  1. Streptococcus pneumoniae
  2. Haemophilus influenzae
244
Q

What are the atypical causative organisms for pneumonia?

A
  1. Mycoplasma pneumoniae
  2. Legionella pneumophilia
  3. Klebsiella pneumoniae
  4. Staphylococcus aureus
245
Q

Which organism causes pneumonia often following influenza vaccination?

A

Staphylococcus aureus

246
Q

What is Mycoplasma pneumoniae?

A
  1. Atypical causative organism
  2. Often presents as a dry cough and atypical chest signs/x-ray findings
  3. Autoimmune haemolytic anaemia and erythema multiforme may be seen
247
Q

Which organism causes pneumonia classically seen in alcoholics?

A

Klebsiella pneumoniae

248
Q

What is Legionella pneumophilia?

A
  1. One of the atypical pneumonias
  2. Hyponatraemia and lymphopenia common
  3. Classically seen secondary to infected air conditioning units
249
Q

What is Pneumocystis jiroveci?

A
  1. Type of pneumonia typically seen in HIV patients
  2. Presents with a dry cough, exercise-induced desaturations and the absence of chest signs
250
Q

What are the symptoms of Pneumonia?

A
  1. Cough
  2. Sputum
  3. Dyspnoea
  4. Chest pain: may be pleuritic
  5. Fever
251
Q

What are the signs of pneumonia on examination?

A
  1. Signs of systemic inflammatory response: tachycardia, fever
  2. Reduced oxygen saturations
  3. Auscultation: reduced breath sounds, bronchial breathing
252
Q

What are the investigations for pneumonia?

A
  1. Bloods
  2. ?ABG
  3. Chest x-ray
  4. In intermediate or high-risk patients, NICE recommend blood and sputum cultures, pneumococcal and legionella urinary antigen tests
253
Q

When is an ABG indicated in the investigation of pneumonia?

A

If the oxygen saturations are low or if the patient has pre-existing respiratory disease e.g. CODP

254
Q

What are the blood work findings in pneumonia?

A
  1. FBC: neutrophilia in bacterial infections
  2. U&Es: check for dehydration, ‘Urea’ as part of CURB-65, maybe hyponatraemia in atypical pneumonia (Legionella)
  3. CRP: elevated
  4. Blood and sputum cultures: identify pathogen
255
Q

What are the chest x-ray findings of pneumonia?

A
  1. Consolidation
  2. Abnormal opacification
  3. Lobar - fissures divide the infection
256
Q

What is the risk stratification system used in pneumonia?

A

CURB-65:
C. Confusion: abbreviated mental test score < 8/10
U. Urea > 7 mmol/L (not always available in primary care)
R. RR > 30/min
B. BP: SBP < 90 mmHg and/or DBP < 60mmHg
65. Aged > 65 years

257
Q

What are the NICE recommendations of the CURB-65 scoring system for pneumonia?

A
  1. Home-based care for patients with a CURB-65 score of 0, oral amoxicillin
  2. Hopsital assessment for all other patients, particularly those with a CRB65 score of 2 or more
258
Q

What are the risk stratification for mortality from pneumonia using CURB-65?

A

0: low risk (< 1% mortality risk), NICE recommend that treatment at home(alongside clinical judgement)
1 or 2: intermediate risk (1-10% mortality risk)
NICE recommend that hospital assessment should be considered (particularly for people with a score of 2)
3 or 4: high risk (> 10% mortality risk)
NICE recommend urgent admission to hospital

259
Q

What is the point-of-care CRP test in Pneumonia?

A
  1. Not currently widely available
  2. CRP is used to guide antibiotic therapy
  3. If < 20 mg/L = do not routinely offer
  4. CRP 20-100 mg/L = consider delayed antibiotic prescription
  5. CRP > 100 mg/L = offer antibiotic therapy
260
Q

What is the management of low-severity community acquired pneumonia?

A
  1. First line = amoxicillin
  2. If pencillin allergic = macrolide or tetracycline
  3. NICE recommend a 5 day course of antibiotics
261
Q

What is the management of moderate and high-severity community acquired pneumonia?

A
  1. Dual antibiotic therapy = amoxicillin and a macrolide e.g. clarithromycin
  2. 7-10 day course is recommended
  3. NICE recommend considering a beta-lactamase stable penicillin such as co-amoxiclav, ceftriaxone or piperacillin with tazobactam and a macrolide in high-severity community acquired pneumonia
262
Q

What are the criteria for not routinely discharging patients for pneumonia?

A

If in the past 24 hours they had 2 or more of the following:
1. temperature > 37.5°C
2. RR > 24 breaths/min
3. HR > 100 beats/ min
4. SBP 90 mmHg or less
5. Oxygen saturation under 90% on room air
6. Abnormal mental status
inability to eat without assistance

263
Q

What is the prognosis for pneumonia?

A

1 week: fever should have resolved
4 weeks: chest pain and sputum production should have substantially reduced
6 weeks: cough and breathlessness should have reduced
3 months: Most symptoms should have resolved, fatigue may still be present
6 months: most people will feel back to normal

264
Q

What should happen to all patients who had pneumonia 6 weeks after clinical resolution?

A
  1. Repeat chest x-ray
  2. To ensure that consolidation has resolved and there is no underlying secondary abnormalities e.g. lung cancer
265
Q

What is the pathophysiology of pneumonia?

A
  1. Once a pathogen has entered the lower respiratory tract an inflammatory cascade begins
  2. Neutrophils migrate to the infected alveoli and release cytokines which activate an immune response and induce fever
  3. This process leads to an accumulation of fluid and pus within the alveoli that impairs gaseous exchange, leading to a hypoxic state which is characteristic of pneumonia
266
Q

What are the risk factors for pneumonia?

A
  1. Aged under 5 or over 65-years-old
  2. Smoking
  3. Recent viral respiratory tract infection
  4. Chronic respiratory diseases e.g. CF, COPD
  5. Immunosuppression: e.g. cytotoxic drug therapy and HIV
  6. Patients at risk of aspiration e.g. those with neurological diseases such as Parkinson’s disease
  7. IV drug users
    Other non-respiratory co-morbidities e.g. DM, CVD
267
Q

What is aspiration pneumonia?

A
  1. Pneumonia that develops as a result of foreign materials entering the bronchial tree
  2. Usually oral or gastric contents such as food and saliva
  3. Depending on the acidity of the aspirate, a chemical pneumonitis can develop, plus bacterial pathogens
268
Q

What is the aetiology of aspiration pneumonia?

A
  1. Often results from an incompetent swallow mechanism
  2. Causes include neurological disease or injury e.g. stroke, MS, intoxication
  3. Intubation can also increase risk of aspiration
269
Q

What are the risk factors for aspiration pneumonia?

A
  1. Poor dental hygiene
  2. Swallowing difficulties
  3. Prolonged hospitalisation or surgical procedures
  4. Impaired consciousness
  5. Impaired mucociliary clearance
270
Q

What are the most common sites of aspiration pneumonia?

A

Right middle and lower lung lobes:
1. Right bronchus has a more vertical orientation
2. Right bronchus has a larger calibre

271
Q

What are the common bacteria implicated in aspiration pneumonia?

A
  1. Streptococcus pneumoniae
  2. Staphylococcus aureus
  3. Haemophilus influenzae
  4. Pseudomonas aeruginosa
  5. Klebsiella: often seen in aspiration lobar pneumonia in alcoholics
  6. Anaerobic e.g. bacteriodes
272
Q

What are the investigations and management of aspiration pneumonia?

A
  1. Similar to that of pneumonia: bloods, Chest x-ray
  2. Antibiotic therapy: amoxicllin ± macrolide
  3. If high-severity: beta lactamase stable penicillin e.g. co-amoxiclav
273
Q

What is co-amoxiclav a mixture of?

A
  1. Amoxicillin
  2. Clavulanic acid
274
Q

What are the complications of pneumonia?

A
  1. Pleural effusion
  2. Empyema
  3. Lung abscess
  4. Sepsis
275
Q

What is a penumothorax?

A

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

276
Q

What are the classification for pneumothoraces?

A
  1. Spontaneous (primary)
  2. Secondary
  3. Tension pneumothorax
277
Q

What is a primary (spontaneous) pneumothorax?

A
  1. Air in the pleural space in patients with no underlying lung disease
  2. Typically tall, thin males
278
Q

What is a secondary pneumothorax?

A
  1. Air in the pleural space in a patient with underlying lung disease
  2. E.g. COPD, asthma, TB, CF
279
Q

What are the risk factors for a pneumothorax?

A
  1. Pre-existing lung disease: COPD, asthma, CF, lung cancer, Pneumocystis pneumonia
  2. Connective tissue disease: Marfan’s syndrome, rheumatoid arthritis
  3. Ventilation, including non-invasive
  4. Endometriosis (in primary pneumothoraces - catamenial pneumothorax)
280
Q

What are the symptoms of a pneumothorax?

A

Tend to come on suddenly:
1. Dyspnoea
2. Chest pain: often pleuritic, on inspiration
3. Sweating
4. tachypnoea
5. Tachycardia
May be asymptomatic if small

281
Q

What are the signs of a pneumothorax on examination?

A
  1. May be absent if small
  2. Signs of respiratory distress
  3. Reduced expansion, hyper-resonance and reduced breath sounds
282
Q

What are the investigations for a pneumothorax?

A
  1. Chest x-ray: lung markings do not extend all the way to the periphery, fluid level if blood present (small pneumothoraces are usually in upper lobes)
  2. ABG: determine if there is hypoxia, especially secondary to pre-existing lung disease
283
Q

How is the management of a primary pneumothorax divided?

A

Size of pneumothorax:
1. If < 2cm and not SOB = consider discharge or aspiration attempted
2. if >2cm or SOB = aspiration attempted, if this fails, chest drain should be inserted

284
Q

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

A
  1. Primary: Discharge, repeat CXR (analgesia if needed)
  2. Secondary: Aspiration
285
Q

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

A
  1. Primary: Aspiration. If unsuccessful, chest drain
  2. Secondary: Chest drain
286
Q

What does aspiration involve?

A
  1. Large-bore cannula or catheter with three-way tap inserted into the 2nd ICS, MCL
  2. Up to 2.5 L of air can be aspirated (stop if patient repeatedly coughs or resistance is felt)
  3. Follow-up CXR should be performed just after, 2 h and 2 weeks later
  4. Patient advised to avoid diving
287
Q

What does a chest drain involve?

A
  1. It is inserted into the fourth to sixth intercostal space in midaxillary line (safety triangle)
  2. With water seal
  3. Used if aspiration fails or if there is fluid in the pleural cavity or after decompression of a tension pneumothorax
288
Q

What are the borders of the safety triangle?

A
  1. (Posterior edge) Lateral border of pec major
  2. (Anterior edge) Lateral border of Latissimus dorsi
  3. Upper: axilla
  4. Lower: 4th/5th ICS
289
Q

What is the management of a secondary pneumothorax which is less than 1 cm?

A

Give oxygen and admit for 24 hours

290
Q

What is the management of an iatrogenic pneumothorax?

A
  1. Less likelihood of recurrence than a primary/ spontaneous pneumothorax
  2. Majority will resolve with observation
  3. If treatment is required = aspiration
  4. Ventilated patients will need chest drains
291
Q

What is the management of persistent/ recurrent pneumothoraces?

A
  1. If persistent air leak or insufficient lung re-expansion despite chest drain insertion or recurrent pneumothoraces
  2. Video-assisted thoracoscopic surgery (VATS)
  3. Allows for mechanical/ chemical pleurodesis ± bullectomy (fuse visceral and parietal pleura together)
292
Q

What are the three main considerations when discharging patients post-pneumothorax?

A
  1. Stop smoking (reduce the risk of further episodes)
  2. Fitness to fly: absolute contraindication (may travel 2 weeks after if no residual air)
  3. Scuba diving: permanently avoided (unless bilateral surgical pleurectomy, with normal lung function and chest CT postoperatively)
293
Q

What is a tension pneumothorax?

A
  1. May occur following thoracic trauma when a lung parenchymal flap is created
  2. This acts as a one way valve and allows pressure to rise
  3. Trachea shifts away from affected side (due to pressure build up)
  4. Hyper-resonance is apparent on affected side
294
Q

What is the aetiology of a tension pneumothorax?

A
  1. Trauma
  2. When a functional valve lets air enter the pleural space during inspiration, but not leave during expiration
295
Q

What are the presenting symptoms of a tension pneumothorax?

A

Distress with rapid shallow breathing

296
Q

What are the signs of a tension pneumothorax on examination?

A
  1. Severe respiratory distress
  2. Tachycardia
  3. Hypotension
  4. Cyanosis
  5. Distended neck veins
  6. Trachea deviated away from affected side (due to pressure build up)
297
Q

What is the management of a tension pneumothorax?

A
  1. Maximum Oxygen
  2. Needle decompression via a large-bore cannula into 2nd ICS, MCL on side of pneumothorax to relieve the pressure
  3. Insert chest drain soon after
298
Q

What is the prognosis for a pneumothorax?

A
  1. After one spontaneous pneumothorax, at least 20% will have another, with the frequency increasing with repeated pneumothoraces
  2. Patients with secondary pneumothoraces are at greater risk of recurrences
299
Q

What is a pulmonary embolism?

A
  1. Occlusion of pulmonary vessels
  2. Most commonly by a consequence of thrombus formation within a deep vein, most frequently in the lower extremities
300
Q

What is the aetiology of a pulmonary embolism?

A
  1. Thrombus (>95% originating from DVT of the lower limbs, rarely from right atrium in patients with AF)
  2. 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
301
Q

What are the risk factors for a pulmonary embolism?

A
  1. Surgery
  2. Immobility
  3. Obesity
  4. PMH of a DVT
  5. OCP
  6. Pregnancy
  7. Malignancy
302
Q

What are the potential features of a pulmonary embolism?

A
  1. Chest pain: pleuritic
  2. Dyspnoea
  3. Haemoptysis
  4. Tachycardia
  5. Tachypnoea
303
Q

How can the features of a PE vary with size?

A
  1. Small = may be asymptomatic
  2. Moderate = sudden onset of dyspnoea, cough, haemoptysis, pleuritic chest pain
  3. Large (or proximal) = all of the above plus severe central pleuritic chest pain, shock, collapse, RHF or death
304
Q

What is the classic triad associated with a PE?

A
  1. Pleuritic chest pain
  2. Dyspnoea
  3. Haemoptysis
305
Q

What are the findings of a PE on examination?

A
  1. Classically the chest is clear
  2. Commonly have tachypnoea (RR > 16)
  3. Crackles
  4. Tachycardia
  5. Fever
306
Q

What are the investigations for a suspected PE?

A
  1. Thorough history
  2. Respiratory examination
  3. Chest x-ray
  4. PERC rule - rule out PE/ 2-level PE Wells score
307
Q

What is the PERC rule?

A
  1. All the criteria must be absent to have negative PERC result, i.e. rule-out PE
  2. This should be done when you think there is a low pre-test probability of PE, but want more reassurance that it isn’t the diagnosis
  3. A negative PERC reduces the probability of PE to < 2%
308
Q

What are the criteria for the PERC rule?

A
  1. Age ≥ 50 years
  2. HR ≥ 100
  3. Oxygen sats ≤ 94
  4. Previous DVT or PE
  5. Recent surgery or trauma
  6. Haemoptysis
  7. Unilateral leg swelling
  8. Oestrogen use e.g. HRT, contraception
309
Q

When can the PERC rule exclude a PE?

A

When all of the PERC rule criteria are absent (probability would be less than 2%)

310
Q

What should be performed if a PE is suspected and/or the PERC rule is positive?

A

2-level PE Wells score

311
Q

What is the 2-level PE Wells score?

A
  1. Clinical signs and symptoms of DVT = 3
  2. An alternative diagnosis is less likely than PE = 3
  3. HR > 100 beats per minute = 1.5
  4. Immobilisation for more than 3 days or surgery in the previous 4 weeks = 1.5
  5. Previous DVT/PE = 1.5
  6. Haemoptysis = 1
  7. Malignancy (on treatment, treated in the last 6 months, or palliative) = 1
312
Q

How does the Wells score define likelihood of PE?

A
  1. Likely if more than 4 points
  2. Unlikely if 4 or less points
313
Q

What are the next steps if a PE is ‘unlikely’ (4 or less points)?

A

Arrange a D-dimer test:
a. If positive = arrange for an immediate CTPA (if a delay is expected give interim therapeutic anticoagulation in meantime)
b. If negative = then PE is unlikely, stop anticoagulation and consider an alternative diagnosis

314
Q

What are the next steps if a PE is ‘likely’ (more than 4 points)?

A
  1. Arrange an immediate CTPA (if there is a delay give interim anticoagulant until scan is performed)
  2. If positive = PE is diagnosed
  3. If negative = consider a proximal leg vein US if DVT is suspected
315
Q

What is the use of an interim anticoagulant use in the diagnosis of a PE?

A
  1. Used if there is a delay in requesting a CTPA
  2. NICE recommend using an anticoagulant that can be continued if the scan is positive
  3. This is normally a direct oral anticoagulant (DOAC) such as apixaban or rivaroxaban
316
Q

What is the benefit of performing a CTPA or a V/Q scan?

A
  1. Speed
  2. Easier to perform out-of-hours
  3. Reduced need for further imaging
  4. Possibility of providing an alternative diagnosis if PE is excluded
317
Q

When is a V/Q scan the investigation of choice over a CTPA?

A

In patients who have renal impairment and a suspected PE (due to the use of contrast)

318
Q

What are some of the other investigations for a PE?

A
  1. D dimer (if 4 or less points on Well’s) = poor specificity
  2. ECG = S1Q3T3 change only seen in 20% of patients, may also see RBBB, right axis deviation and sinus tachycardia
  3. Chest x-ray = recommended in all patients, typically normal, maybe wedged-shape opacification
319
Q

What is the management of a PE?

A

DOACs: Apixaban or rivaroxaban should be offered first-line following the diagnosis of a PE

320
Q

What is the management of a PE in a patient with renal impairment?

A

If severe (e.g. < 15/min) then LMWH, unfractionated heparin or LMWH followed by a VKA

321
Q

How is the length of management for a PE divided?

A

Provoked vs unprovoked:
1. Provoked: obvious precipitating event e.g. immobilisation following major surgery, event was transient and the patient is no longer at increased risk
2. Unprovoked: absence of an obvious precipitating event, i.e. there is a possibility that there are unknown factors (e.g. mild thrombophilia) making the patient more at risk from further clots

322
Q

How long should a patient be on anticoagulation for a PE?

A

All patients should be on anticoagulation for at least 3 months

323
Q

How long should a patient be on anticoagulation for a provoked PE?

A

Typically stopped after the initial 3 months

324
Q

How long should a patient be on anticoagulation for an unprovoked PE?

A

Typically continued for another three months after the initial 3 months = total 6 months

325
Q

What scoring system can be used to determine risk of bleeding in patients on long-term anticoagulation?

A

ORBIT score

326
Q

How long should a patient with active cancer be on anticoagulation for a PE?

A

DOAC for 3-6 months

327
Q

What extra management option is available for patients with a PE that is haemodynamically unstable?

A

Thombolysis: now recommended as the first-line treatment for massive PE where there is circulatory failure (e.g. hypotension)

328
Q

What might patients who have repeated PEs despite adequate anticoagulation be offered?

A

Inferior vena cava (IVC) filters: work by stopping clots formed in the deep veins of the leg from moving to the pulmonary arteries

329
Q

What is the dose of rivaroxaban for the treatment of PE?

A

Initially 15 mg twice daily for 21 days, then maintenance 20 mg once daily, to be taken with food, for duration of treatment (3 -6 months)

330
Q

What is sarcoidosis?

A

A multi-system disorder characterised by non-caseating granulomas

331
Q

Which organs are most commonly affected in sarcoidosis?

A
  1. Lungs
  2. Eyes
  3. Skin
332
Q

What is the epidemiology of sarcoidosis?

A

More common in young adults and in people of African descent

333
Q

How can the features of sarcoidosis be divided?

A
  1. Acute
  2. Insidious
334
Q

What are the acute features of sarcoidosis?

A
  1. Erythema nodosum
  2. Bilateral hilar lymphadenopathy
  3. Swinging fever
  4. Polyarthralgia
335
Q

What are the insidious features of sarcoidosis?

A
  1. Dyspnoea
  2. Non-productive cough
  3. Malaise
  4. Weight loss
336
Q

What are the eye signs of sarcoidosis?

A
  1. Dry eyes (keratoconjunctivitis sicca)
  2. Painful red eye
  3. Blurred vision
  4. Photophobia (uveitis)
337
Q

What is the main skin sign of sarcoidosis?

A

Lupus pernio: red-blue infiltrations, also get erythema nodosum

338
Q

What is a biochemical feature of sarcoidosis?

A

Hypercalcaemia:
Macrophages inside the granulomas cause an increased conversion of vitamin D to it’s active form = 1,25-dihydroxycholecalciferol

339
Q

What are some syndromes associated with sarcoidosis?

A
  1. Lofgren’s syndrome: acute form of sarcoidosis, good prognosis
  2. Mikulicz/ Sjogren’s syndrome: enlargement of parotid and lacrimal glands secondary
  3. Heerfordt’s syndrome: parotid enlargement, fever and uveitis secondary to sarcoidosis
340
Q

What is the diagnostic test for sarcoidosis?

A

No one diagnostic test:
1. Chest x-ray
2. ACE levels: may have role in monitoring
3. Hypercalcaemia and raised ESR on bloods

341
Q

What are the 5 stages of sarcoidosis on chest x-ray?

A

Stage 0: normal
Stage 1: bilateral hilar lymphadenopathy
Stage 2: bilateral hilar lymphadenopathy + interstitial infiltrates
Stage 3: diffuse interstitial infiltrates only
Stage 4: Diffuse fibrosis

342
Q

What are some other investigations which may be helpful in diagnosing sarcoidosis?

A
  1. Spirometry: restrictive effect
  2. Tissue biopsy: non-caseating granulomas
343
Q

What type of granulomas are seen in sarcoidosis?

A

Non-caseating

344
Q

What is the management of sarcoidosis?

A

Steroids

345
Q

What are the indications of steroids in the management of sarcoidosis?

A
  1. Chest x-ray with stage 2 or 3 disease and are symptomatic (if asymptomatic they do not require treatment)
  2. Hypercalcaemia
  3. Eye, heart or neuro involvement
346
Q

What is the prognosis of sarcoidosis?

A

Remits without treatment in 2/3rds of people

347
Q

What are the factors associated with poor prognosis of sarcoidosis?

A
  1. Insidious onset, symptoms that are present > 6 months
  2. Absence of erythema nodosum
  3. Extra-pulmonary manifestations e.g. lupus pernio, splenomegaly
  4. CXR: stage 3 or 4 features
  5. If the patient is of black ethnicity
348
Q

What is tuberculosis?

A

An infection caused by Mycobacterium tuberculosis (most commonly affects the lungs)

349
Q

What is the aetiology of TB?

A
  1. Mycobacterium tuberculosis is an intracellular organism (also known as acid-fast bacilli, AFB)
  2. It can survive after being phagocytosed by macrophages
    *predominantly in the upper lobes
350
Q

How can TB be classified?

A

Primary and secondary

351
Q

What is primary TB?

A
  1. When a non-immune host is exposed to M. tuberculosis
  2. In immunocompetent people, the initial lesion (Ghon focus + hilar lymph nodes = Ghon complex) heals by fibrosis
  3. In immunocompromised people, they may develop disseminated disease = miliary TB
352
Q

What is secondary (post-primary) TB?

A
  1. If the host becomes immunocompromised the initial infection may become reactivated
  2. Causes of immunocompromised are: immunosuppressive drugs e.g. steroids, HIV, malnutrition
  3. Reactivation generally occurs in the apex of the lungs, can spread to distant sites
353
Q

What is the most common site for secondary TB?

A

The lungs (usually the apex)

354
Q

What are some of the other sites (extra-pulmonary) for secondary TB?

A
  1. Central nervous system: tuberculous meningitis (most serious complication)
  2. Vertebral bodies: Pott’s disease
  3. Cervical lymph nodes (scrofuloderma)
  4. Renal
  5. GI tract
355
Q

What are the risk factors for TB?

A
  1. Having lived in Asia, Latin America, Eastern Europe, or Africa for years
  2. Exposure to an infectious TB case
  3. HIV: are 20 to 30 times more likely to develop active TB
  4. Immunocompromised individuals: DM, patients on immunosuppressive therapy, malnourished, or those with haematological malignancies)
  5. Silicosis
  6. Apical fibrosis
356
Q

What are the risk factors for developing active TB (from latent)?

A
  1. Silicosis
  2. Chronic renal failure
  3. HIV positive
  4. Solid organ transplantation with immunosuppression
  5. IV drug use
  6. Haematological malignancy
  7. Anti-TNF treatment
  8. Previous gastrectomy
357
Q

What is silicosis?

A

A type of pneumoconiosis due to inhalation of a large amount of crystalline silica dust resulting in pulmonary fibrosis

358
Q

What are the features of primary TB?

A
  1. Mostly asymptomatic
  2. May have fever, malaise, cough
359
Q

What are the features of miliary TB?

A
  1. Fever
  2. Weight loss
  3. Meningitis
  4. Yellow caseous tubercules, can spread to other organs e.g. bone and kidney and remain dormant for years
360
Q

What are the features of secondary (post-primary) TB?

A
  1. Fever/ night sweats
  2. Malaise
  3. Weight loss
  4. Breathlessness
  5. Cough ± sputum, haemoptysis
  6. Pleuritic pain
361
Q

What are the signs of TB on examination?

A
  1. Weight loss
  2. Abnormal chest percussion and auscultation: pleural effusion/ collapse/ consolidation/ fibrosis
  3. Extra-pulmonary features e.g. meningitis, pericarditis, GI (subacute obstruction), adrenal insufficiency, GU (renal failure), skin: lupus vulgaris
  4. Lymph nodes: cervical, acutely tender leading to abscesses and spread to skin: scrofuloderma
  5. Bones: Osteomyelitis, arthritis, paravertebral abscesses and vertebral collapse (Pott’s disease), spinal cord compression from abscesses
362
Q

What are the investigations of TB divided into?

A
  1. Screening of latent TB
  2. Diagnosis of active TB
363
Q

What is the main screening technique for latent TB?

A

Mantoux test

364
Q

What is the Mantoux test?

A
  1. Involves injecting a small amount (0.1ml of 1:1,000) of purified protein derivative tuberculin intradermally
  2. The result is read 2-3 days later
  3. Dependent on the diameter of the wheal (circular shape formed in response to tuberculin)
365
Q

What is the interpretation of a diameter of induration of < 6mm in the Mantoux test?

A
  1. Negative: no significant hypersensitivity to tuberculin protein
  2. Previously unvaccinated individuals may be given the BCG
366
Q

What is the interpretation of a diameter of induration of 6-15mm in the Mantoux test?

A
  1. Positive: hypersensitive to tuberculin protein
  2. Should not be given the BCG
  3. Result may be due to previous TB infection or the BCG
367
Q

What is the interpretation of a diameter of induration of > 15mm in the Mantoux test?

A
  1. Strongly positive: strongly hypersensitive to the tuberculin protein
  2. Suggests TB infection
368
Q

What are some of the causes of a false negative Mantoux test?

A
  1. Miliary TB
  2. Sarcoidosis
  3. HIV
  4. Lymphoma
  5. Very young age (e.g. < 6 months)
369
Q

What is the interferon-gamma blood test used for in TB screening?

A
  1. When the Mantoux test is positive or equivocal
  2. In people where a Mantoux test may be falsely negative e.g. HIV, sarcoidosis
370
Q

What are the investigations for active TB?

A
  1. Chest x-ray
  2. Sputum smear
  3. Sputum culture
  4. Nucleic acid amplification test (NAAT)
371
Q

What is the gold standard investigation for active TB?

A

Sputum culture:
1. More sensitive than a sputum smear and NAAT
2. Can also assess drug sensitivities
3. But can take 1-3 weeks for results to come back

372
Q

What are the findings of active TB on chest x-ray?

A
  1. Upper lobe cavitation (classic finding of reactivated TB)
  2. Bilateral hilar lymphadenopathy
373
Q

What is a sputum smear in the investigation of active TB?

A
  1. Rapid and inexpensive test
  2. Three specimens are needed
  3. Stained for the presence of acid-fast bacilli: Ziehl-Neelsen stain
  4. Sensitivity is between 50-80% and decreased in individuals with HIV
  5. All mycobacteria will be stained positive (not specific)
374
Q

What is a NAAT test for active TB?

A
  1. Allows rapid diagnosis: within 24-48 hours
  2. More sensitive than sputum smears but less sensitive than sputum culture
375
Q

What is the standard medical therapy for the management of active TB?

A
  1. Initial phase (2 months = 4 drugs)
    (RIPE)
    a. Rifampicin
    b. Isoniazid
    c. Pyrazinamide
    d. Ethambutol
  2. Continuation phase ( 2 drugs for next 4 months)
    a. Rifampicin
    b. Isoniazid
376
Q

What are the adverse effects of rifampicin?

A
  1. Orange secretions
  2. Potent liver enzyme inducer
  3. Hepatitis
  4. Flu-like symptoms
377
Q

What are the adverse effects of Isoniazid?

A
  1. Peripheral neuropathy: prevent with pyridoxine (Vitamin B6)
  2. Hepatitis
  3. Agranulocytosis
  4. Liver enzyme inhibitor
378
Q

What are the adverse effects of pyrazinamide?

A
  1. Hyperuricaemia causing gout
  2. Arthralgia, myalgia
  3. Hepatitis
379
Q

What are the adverse effects of ethambutol?

A

Optic neuritis: check visual acuity before and during treatment

380
Q

What is the treatment of latent TB?

A
  1. 3 months of isoniazid (with pyridoxine) and rifampicin
    OR
  2. 6 months of isoniazid (with pyridoxine)
381
Q

What is the treatment of meningeal TB?

A

Treated for a prolonged period (at least 12 months) with the addition of steroids

382
Q

What is directly observed therapy in the management of TB?

A

Three times a week dosing regimen may be
indicated in certain groups:
1. Homeless people with active TB
2. Patients who are likely to have poor concordance
3. All prisoners with active or latent TB

383
Q

What is immune reconstitution disease?

A
  1. Complication of TB treatment
  2. Occurs typically 3-6 weeks after starting treatment
  3. Often presents with enlarging lymph nodes

!Final Year (26 decks)

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