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Medicine Year 3 > Week 8 - Respiratory > Flashcards

Week 8 - Respiratory Flashcards

1
Q

What CXR changes are seen in lung cancer?

A

Mass lesion

Lobar or lung collapse

Mediastinal widening or hilar lymph nodes

Pleural effusion

Slowly resolving consolidation

Normal

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2
Q

How are pleural effusions treated?

A
  • Dependent on cause
  • Take fitness into account
  • Chest drain, pleurodesis etc.
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3
Q

In which conditions would transfer factor be reduced in?

A

Emphysema

Interstitial lung disease

Pulmonary vascular disease

Anaemia (increased in polycythaemia)

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4
Q

Describe the features of adenocarcinomas

A
  • Common tumour in females
  • Also seen in non-smokers (but also associated with smoking)
  • 2/3 arise in periphery sometimes in relation to scarring
  • Appearance
    • Glandular, solid, papillary or lepidic (grows along walls of airway)
    • Mucin production
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5
Q

Which factors which impact passive diffusion of gases in the lungs?

A

Varies inversely with distance (0.3uM)

Varies directly with area (70-100m) - Fick’s law

Solubility = Henry’s law

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6
Q

Describe the side effects of anti-muscarinics

A
  • Blurred vision, dry mouth, urinary retention, nausea, constipation
  • Nebulised ipratropium may precipitate acute angle closure glaucoma - use a mouthpiece not a mask (keep it out of the eyes)
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7
Q

How are patients with high and low exacerbation risk and levels of symptoms treated?

A
  • A (few symptoms and exacerbations) - short acting beta 2 agonist, short acting muscarinic antagonist
  • B (symptomatic with few exacerbations) - long acting beta 2 agonist and/or long acting muscarinic antagonist
  • C (few symptoms, many exacerbations) - long acting muscarinic antagonist, long acting beta 2 agonist + inhaled corticosteroid
  • D (symptomatic, many exacerbations) - long acting beta 2 agonists + long acting muscarinic antagonists + inhaled corticosteroids + theophylline + macrolide
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8
Q

What are the two main categories of pleural effusion?

A

Exudate - fluid protein usually >30g/l - e.g. in pneumonia, malignancy, TB

Transudate - fluid protein <30g/l (usually <20g/l) - heart failure, liver failure, nephrotic syndrome

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9
Q

What are the consequences of untreated OSAS?

A

Hypertension

Right heart strain

Cardiovascular disease

Increased risk of CVA

Increased accident at work/poor concentration

Increased road traffic accidents

4x more likely to have a RTA

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10
Q

What is the effect of ventilation perfusion mismatch?

A
  • Main cause of hypoxaemia in medical patients
  • Mixing of blood from poorly ventilated and well ventilated parts of the lung causes hypoxaemia
  • Does not fully correct with oxygen administration
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11
Q

Describe the mechanism of action of amphotericin B

A
  • Amphotericin B also exploits the ergosterol/cholesterol difference
  • It is not an enzyme inhibitor
  • Exploits the presence of ergosterol
    • Binds directly to ergosterol in fungal membrane
    • Hydrophilic and hydrophobic sides - hydrophilic side faces outwards
    • Water and ions can freely pass amphotericin B - creates transmembrane port (punches a hole in the membrane) –> fungus death
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12
Q

What is the difference between atopic and non-atopic asthma?

A
  • Atopic asthma (Extrinsic asthma) - usually starts in childhood
    • Atopic - raised total serum IgE and presence of specific IgE against common aeroallergens, or positive skin tests to common aeroallergens
  • Non-atopic (intrinsic asthma) - often starts in middle age, possible triggers include respiratory viruses, air pollutants
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13
Q

What are the main causes of lung cancer?

A
  • 79% of lung cancer cases in UK are preventable
  • Smoking main risk factor - 72% attributable
  • Other risk factors:
    • Environmental tobacco smoke
    • Ionising radiation - radon, uranium (5%)
      • Radon is a decay product of uranium which is relatively common in the Earth’s crust
    • Air pollution
    • Asbestos
    • Other e.g. fibrosing conditions of the lung, human papilloma virus, hereditary (polymorphisms in cytochrome p450)
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14
Q

What kind of clinical signs can be seen in sarcoidosis?

A

Pulmonary findings

Dermatological

Ocular

Cardiac

Neurological (rare)

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15
Q

What are the effects of allergy in the airways?

A
  1. Affects airflow
  • Increases resistance
  • Causes wheeze/stridor - turbulence
  • Measured by spirometry
  • Imaging (CXR) not helpful
  • Gas transfer not affected
  1. Affects parenchyma
  • Gas transfer and compliance affected
  • CXR/imaging helpful
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16
Q

What is the consequence of the structural changes which occur in emphysema?

A

Consequent loss of surface area for gas exchange

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17
Q

What is the hygiene hypothesis? How does it contribute to the development of asthma?

A

Growing up in relatively ‘cleaner’ environment predisposes to the development of allergy/Th2 responses

Bacterial components direct the immune system to Th1 responses

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18
Q

What typical pathological features are seen in pulmonary fibrosis?

A
  • Collagen (pink) - scar tissue (fibrosis)
  • Cysts - produce honeycombing on radiology
  • Thickened alveolar wall - more than 1 cell thick
  • Fibroblastic foci
    • Loose area of fibrosis, ongoing fibrosis
  • Temporal heterogeneity
    • Established and ongoing fibrosis
  • Spatial heterogeneity
  • Smooth muscle - develops due to scarring/repair
  • End stage ARDS
    • Microvascular damage - fibrinous exudate into alveolar airspace is terminal event
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19
Q

Who is most commonly affected by idiopathic pulmonary fibrosis?

A
  • Age >50
  • M:F - 2:1
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20
Q

List the features of small cell carcinomas

A
  • Most aggressive form of lung cancer
  • Metastasises early and widely
  • Often initial good response to chemotherapy - but most patients relapse
  • Appearance
    • Cells smaller than 2 lymphocytes
    • Oval to spindle shaped cells
    • Inconspicuous nucleoli
    • Scant cytoplasm
    • Nuclear molding (more prominent in cytology)
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21
Q

How does oximetry work?

A

Non-invasive measurement of saturation of haemoglobin by oxygen

Depends on oxyhaemoglobin and deoxyhaemoglobin absorbing infrared light differently

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22
Q

How is a pleural effusion due to empyema diagnosed? What is the prognosis?

A
  • Presence of pus or bacteria
  • 15% mortality
  • 15-40% require surgery
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23
Q

Describe the pathophysiology of allergic disease in the lung parenchyma

A
  • Trigger - first exposure
    • Antigen-presenting cell + T cells recognise
    • IL-12 and IFN produced
    • Reactive T cells produce IgG
    • Delayed response
  • Trigger - re-exposure
    • Immunological memory in T cells - reactive T cells produce IgG rapidly on second exposure
    • IgG - antigen immume complex
      • Acute illness, fever, wheeze
    • Tissue remodelling
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24
Q

Give causes of transudative pleural effusion vs exudative pleural effusion

A
  • Transudate
    • Heart failure
    • Cirrhosis
    • Renal failure
    • Hypothyroidism
    • Hypoalbuminaemia
  • Exudate
    • Malignancy
    • Infection
    • Empyema
    • TB
    • Haemothorax
    • Autoimmune
    • Pulmonary embolism
    • Post CABG? MI
    • Drug induced
    • Pancreatitis
    • Chylothorax
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25
Q

How can lung volumes be measured?

A
  • Unable to measure residual volume by spirometry
  • 2 methods of measuring:
    • Helium dilution (inspire known quantity of inert gas)
    • Body plethysmography (respiratory manoeuvres in a sealed box lead to changes in air pressure - can derive lung volumes)
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26
Q

Describe normal PTH production/regulation and how this is effected by tumour secretion of parathyroid hormone related peptide

A
  • Parathyroid hormone produced by parathyroid gland in response to low serum calcium
  • Stimulates osteoclast activity in bones
  • Serum calcium raised, negative feedback to parathyroid gland to stop excessive PTH production
  • When PTHrP secreted by tumour there is no negative feedback on tumour so secretion is constant
  • Hypercalcaemia
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27
Q

Describe the natural history of COPD

A

FEV1 <80% - worsening airflow limitation and shortness of breath typically developing on exertion

FEV1 <50% - increased breathlessness and repeated exacerbations impact patient quality of life (increasing number and severity of exacerbation will likely lead to increasing hospitalisation

FEV1 <30% - severe breathlessness and respiratory failure, marked by hypoxaemia. Pulmonary hypertension usually develops following severe hypoxaemia. Systemic, extrapulmonary effects may include systemic inflammation and skeletal muscle dysfunction.

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28
Q

How are the lungs specialised for their function?

A
  • Able to force air through small spaces quickly - average man breathes out 4-5L of air in 6 seconds (woman 4L)
    • Flexible tubes for high speed flow
    • Significant vulnerability - few tubes for large volume of air
  • Large surface area for gas exchange
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29
Q

How does hypercapnia develop in patients with COPD?

A
  • Respiratory failure = low pO2 (paO2 <8kPa on room air - 21% inspired oxygen)
    • Type 1 - low pO2, low/normal CO2 (e.g. PE, pneumonia)
    • Type 2 - low pO2, CO2 high (acidotic) e.g. COPD
      • Respiration driven by levels of CO2 in blood
      • In COPD airways tight so don’t breathe out CO2 as effectively so CO2 levels constantly high
      • Brain relies less on CO2 as drive to breathe - uses low O2 level as indicator to increase respiratory drive
      • Low pO2, in hospital given oxygen
      • When relying on being hypoxic to breathe lose respiratory drive, respiratory rate drops, get much more ill –> comatose
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30
Q

Describe the appearance of a central lung tumour with surrounding obstructive pneumonia

A

Lots of lipid due to retention of secretions including surfactant = yellowish colour

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31
Q

How can the risk of exacerbation in COPD be determined?

A
  • Spectrum of increasing symptoms/breathlessness, number of exacerbations in past year and severity of airflow limitation
  • Severe airflow limitation = more exacerbations
    • A = few symptoms, mild airflow limitation
    • B = very symptomatic, mild airflow limitation
    • C = severe airflow limitation, few symptoms
    • D = severe airflow limitation, very symptomatic
  • High risk of exacerbations - severe airflow limitation
    • C, D
  • Low risk of exacerbations - mild airflow limitation
    • A, B
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32
Q

When is measurement of lung function used?

A
  • Evaluation of the breathless patient
  • Screening for COPD (e.g. in symptomatic smokers) or occupational lung disease
  • Lung cancer - fitness for treatment
  • Pre-operative assessment (anaesthetic risk)
  • Disease progression and treatment response
  • Monitoring of drug treatment toxic to the lungs
  • Pulmonary complications of systemic disease
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33
Q

Give examples of non-metastatic effects of lung cancers

A
  • Inappropriate ACTH secretion by tumour
    • Adrenal hyperplasia, raised blood cortisol –> Cushing’s syndrome
  • Inappropriate ADH secretion by tumour
    • Retention of water by kidneys, dilutional hyponatraemia (SIADH - syndrome of inappropriate antidiuretic hormone secretion)
  • Parathyroid hormone related peptide secretion
    • Osteoclastic activity –> hypercalcaemia
  • Other non-metastatic effects:
    • Encephalopathy
    • Cerebellar degeneration
    • Neuropathy
    • Myopathy
    • Eaton Lambert myasthenia-like syndrome
    • Cancer associated retinopathy - antibodies to photoreceptor cells produced
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34
Q

What is the difference between tolerance and intolerance?

A

Tolerance - not a medical state (expected)

Intolerance

  • Inability to cope with something normally acceptable
  • Not same as poison - everyone reacts the same
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35
Q

Describe the pharmacokinetics/pharmacodynamics of methylxanthines

A
  • Time to steady state 2-3 days - plasma theophylline levels at 5 days/3 days after dose adjustment
  • Narrow therapeutic window: 10-20mg/L
    • Drug monitoring 4-6 hours post-dose
    • Toxicity - severe vomiting, hypokalaemia/hypocalcaemia, seizures, arrhythmias, hypotension
    • Weight based dosing for IV infusions
  • Metabolised in the liver - caution in liver disease and with concomitant use of some antibiotics including rifampicin, clarithromycin, ciprofloxacin
    • Rifampicin reduces levels, clarithromycin/ciprofloxacin increases
  • Smoking increases theophylline clearance - dose may need adjusted following smoking cessation
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36
Q

What investigations should be done in a patient with a suspected pleural effusion?

A
  • Imaging
  • Bloods
  • Sampling
    • As few interventions as possible
    • Never drain an undiagnosed effusion - easier to get samples to aid diagnosis if not drained fully
    • Local anaesthetic thoracoscopy
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37
Q

Describe the prevalence of pleural effusion in pleural infections

A

Up to 50% of pneumonias will have an associated effusion

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38
Q

How useful are reference ranges in spirometry?

A
  • FEV1 of 85% predicted may be considered ‘normal’ in some patients
  • FEV1 of 100% predicted may represent significant decline if values supra-normal at the start
  • Corrected for age, gender, race, height and atmospheric values
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39
Q

What is the differential diagnosis in a pneumothorax?

A

PTE, musculoskeletal pain, pleurisy/pneumonia

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40
Q

What is central apnoea?

A

Brainstem related - brain not giving signal to maintain respiration e.g. due to opioids

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41
Q

What are the differences between upper/extra-thoracic airway disease and bronchial disease?

A
  • Upper/extra-thoracic airways
    • Not susceptible to intra-thoracic pressure - thick walled, tubes held open so linear airflow
    • Narrowing causes stridor - whistling on inspiration
    • E.g. laryngeal oedema - thyroid, scarring, epiglottis
      • Stridor
      • Flow-volume loops
      • CXR not helpful
      • Aspiration to right middle/lower lobe
  • Bronchial disease
    • Susceptible to intra-thoracic pressure
    • Thin-walled airways, susceptible to changes in resistance
    • Easily collapsible e.g. due to allergy
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42
Q

How is thoracoscopy used in diagnosis of a pleural effusion?

A
  • Direct visual examination of the pleura with a thoracoscope
  • Indicated in undiagnosed cytology negative pleural effusion
  • Performed under local anaesthesia and mild sedation
    • Direct visualisation of the pleural surface
    • Biopsy of areas which appear abnormal
    • Definitive effusion management
  • Diagnostic rate approx. 90% for malignant pleural disease
    • E.g. nodular plaques = asbestos exposure, loculations = infection
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43
Q

What is the alveolar oxygen equation?

A

PAO2 = FiO2 – (1.25 x PaCO2)

PAO2 = Alveolar oxygen partial pressure, kPa

FiO2 = Inspired oxygen concentration, kPa

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44
Q

List the causes of pulmonary fibrosis

A
  • Occupational and environmental - silicosis, asbestosis, hypersensitivity pneumonitis (EAA)
  • Drug induced - amiodarone, nitrofurantoin, methotrexate, cocaine
  • Connective tissue diseases - lupus, RA, scleroderma
  • Primary diseases - sarcoidosis, LAM
  • Idiopathic (25%)- IPF, NSIP
  • Genetics

>200 causes

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45
Q

Does small cell or non-small cell lung carcinoma have a better prognosis?

A

Non-small cell carcinoma generally has the better prognosis

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46
Q

List the symptoms associated with lung cancer

A

Cough

Haemoptysis

Shortness of breath

Chest pain

Weight loss/anorexia

General malaise

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47
Q

Describe the appearance of COPD on CXR

A
  • Hyperinflated - air spaces destroyed w big balls of air, lose recoil of lung
    • Count no. of ribs above diaphragm - more than 6 anterior or 10 posterior = hyperinflation
  • Dark lungs due to loss of BVs (white)
  • Heart thin
  • Flattened hemidiaphragms
  • Ribs flattened
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48
Q

Describe normal ADH production/regulation and how this is effected by tumour secretion of ADH

A
  • ADH secreted by posterior pituitary in response to low sensed volume/low BP/low osmolality
  • Acts on kidneys to retain water - negative feedback to stop over secretion of ADH
  • When secreted by tumour there is no negative feedback on the tumour so secretion of ADH is constant
  • Kidneys always stimulated to retain water
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49
Q

Describe the steps involved in management of an acute pulmonary embolism

A

Acute PE

  1. Risk stratify
  • High risk - thrombolysis
  • Intermediate risk - ?thrombolysis
  • Low risk - ?early discharge
  1. LMWH
  • LMWH
  • 3-6/12 warfarin
  • 3-6/12 novel agent
  1. Risk stratify
  • Long term anticoagulation?
  • CTEPH screening
  • Cancer screening?
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50
Q

What are the indications for beta 2 agonists in respiratory disease?

A

Treatment of asthma

Treatment of COPD

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51
Q

Why is amphotericin B toxic? How can this be improved?

A
  • Amphotericin B has to be infused intravenously
  • Quite toxic - high concentration locally when injected, interacts w/ cholesterol at high concentration, destroys cells
  • New formulation
    • Amphotericin B integrated into part of liposomes - infused into bloodstream, diffuses slowly to where fungal infection is
    • Much more safe
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52
Q

Describe the infections caused by dermatophytes

A
  • Fungi that cause common infections of skin, nails and hair
  • Do not colonise ‘live’ tissues, instead keratinised areas such as nails and outer skin
    • Specialised niche, use keratinases, elastase and other proteinases from digestion of skin/hair/nails as virulence factors
    • Slow growing/slow response to treatment - slowly digest tissues to release virulence factors to feed themselves and grow
  • Also known as ‘ringworm’ or ‘tinea’
    • Spreads radially outwards from principal contact point
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53
Q

How may respiratory failure in COPD present?

A
  • Blue Bloater - chronic bronchitis
    • Low respiratory drive
    • Type 2 respiratory failure
    • Low pO2, high pCO2
    • Signs
      • Cyanosis
      • Warm peripheries
      • Bounding pulse
      • Flapping tremor
      • Confusion, drowsiness
      • Right heart failure
      • Oedema, raised JVP
  • Pink Puffer - emphysema
    • High respiratory drive
    • Type 1 respiratory failure
    • Low pO2, low pCO2
    • Signs
      • Desaturates on exercise
      • Pursed lip breathing - automatic response to prevent airways collapsing
      • Use accessory muscles
      • Wheeze
      • Indrawing of intercostals
      • Tachypnoea
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54
Q

What are the indications for anti-muscarinics in respiratory disease?

A

Treatment of asthma

Treatment of COPD

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55
Q

How should a patient with suspected OSA be assessed?

A
  • History - esp. from partner v important
  • Clinical examination
    • Weight
    • BMI
    • BP
    • Neck circumference (>40cm)
    • Craniofacial appearance (Retrognathia, Micrognathia)
    • Tonsils
    • Nasal patency
    • Mallampati score - relates tongue size to pharyngeal size, visualise size of airway
  • Risk criteria/scores for excessive daytime sleepiness
    • The Epworth sleepiness score - how likely would you be to fall asleep in different situations?
    • The STOP-BANG questionnaire - risk criteria for how likely to have OSA
    • The Berlin questionnaire
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56
Q

Describe the mortality associated with IPF/UIP

A
  • Very high mortality and short life expectancy following diagnosis
  • UIP mortality 50% by 2 years
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57
Q

Is a biopsy needed in the diagnosis of sarcoidosis?

A

If CXR shows bilateral hilar lymphadenopathy and all other causes have been excluded 99% are sarcoidosis, don’t really need biopsy

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58
Q

Which patients should be hospitalised following an acute PE?

A

High, intermediate-high and intermediate-low risk patients should be hospitalised

Low risk patients do not need hospitalisation - early discharge and home treatment

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59
Q

Describe the oxygen dissociation curve

A
  • Relates oxygen saturation to partial pressure of oxygen in the blood (pO2) - determined by haemaglobin affinity for oxygen
  • As the partial pressure of oxygen increases the affinity of haemoglobin for oxygen increases and so the oxygen saturation increases
  • Plateaus as saturation reaches close to 100%
  • Normal partial pressure = 12kPa
    • Increase beyond normal makes very little difference to oxygen saturation - oxygen carrying capacity not improved (giving oxygen if normal sats is useless)
    • If saturation is low, increasing pO2 by a small amount increases saturation significantly (can give a small amount of O2 to correct low sats)
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60
Q

What would serial peak flow measurement show in asthma?

A

Thickened smooth muscle of airways is ‘twitchy’ - saw-toothing of peak flow morning to night and reduces as week goes on

Consequence of hyperactivity of smooth muscle in airway

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61
Q

What FBC results would be seen in a patient with COPD and resultant chronic hypoxaemia?

A

Polycythaemia - raised Hb and PCV

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62
Q

What symptoms are associated with EAA?

A
  • Flu-like illness
  • Cough
  • High fever, chills
  • Dyspnoea, chest tightness
  • Malaise, myalgia
  • 4-8 hours after exposure
  • Chronic disease - dyspnoea in strain, sputum production, fatigue, anorexia, weight loss
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63
Q

What are the main causes of hypoxaemia?

A
  • Hypoventilation (e.g. drugs, neuromuscular disease)
  • Ventilation/perfusion mismatch (e.g. COPD, pneumonia - perfusing parts of lung which aren’t ventilated)
  • Shunt e.g. congenital heart disease
  • Low inspired oxygen (altitude, flight)
    • Assessment for fitness to fly can be done
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64
Q

Describe the pathogenesis of chronic bronchitis

A
  • Smoking induces inflammatory infiltrate around airways
    • Infiltration with neutrophils and CD8+ lymphocytes
    • Neutrophils not very responsive to steroids (unlike asthma)
  • Inflammation = squamous metaplasia
  • Increased epithelial mucous cells + mucous gland hyperplasia –> more mucous, clogs airways (further inflammation)
  • Free oxygen radicals - loss of interstitial support
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65
Q

What determines the symptoms of lung cancer?

A
  1. Is the tumour central or peripheral in the lung?
  2. Has the cancer spread locally or distantly?
  3. Non-metastatic effects of the tumour
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66
Q

What are the other causes of malignant pleural effusion? (other than mesothelioma)

A
  • Metastatic spread
    • Lung most common
    • Breast, ovarian
    • Also bowel, renal, lymphoma etc.
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67
Q

What is spirometry? How is it performed?

A
  • Forced expiration manoeuvre from total lung capacity followed by full inspiration
    • Take a big breath in as far as you can and blow out as hard as you can for as long as possible - then take a big breath all the way in
    • Best of 3 acceptable attempts (within 5%)
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68
Q

List the features which encompass the clinical definition of asthma

A
  • Appropriate symptoms with signs
    • Wheeze, cough, yellow/clear sputum
    • Breathlessness, exercise intolerance
  • Episodic, triggered, variable - paroxysmal
    • Exercise
    • Allergy e.g. cats
    • Chemical/physical (salicylate/aspirin) - hyper-reactivity
      • 15% asthmatics can’t tolerate aspirin - side effects exaggerated due to hyper-reactivity
    • Diurnal - nocturnal awakening
  • Respond to asthma therapies
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69
Q

Describe the clinical signs and CXR changes of a pleural effusion

A

Clinical signs

  • Decreased breath sounds, stony dull to percussion, decreased tactile or vocal fremitus

CXR Appearance:

  • Need >300ml of fluid to be present to be seen on CXR
  • Uniformly white appearance
  • Blunting of the costophrenic and cardiophrenic angles
  • A meniscus at the upper edge
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70
Q

How is asthma diagnosed?

A

Appropriate clinical story

Supportive physiological tests:

  • Serial peak flow measurement
  • Bronchial challenge test
  • Reversibility of airflow obstruction
  • Skin prick test
  • Plethysmography
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71
Q

What are the mechanisms which lead to airway obstruction in COPD?

A
  • Loss of elasticity and alveolar attachments due to emphysema - airways collapse on expiration
    • Causes air-trapping and hyperinflation –> increased work of breathing –> breathlessness
  • Goblet cell metaplasia with mucous plugging of lumen
  • Inflammation of the airway wall
  • Thickening of the bronchiolar wall
    • Smooth muscle hypertrophy and peri-bronchial fibrosis
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72
Q

Describe the pathogenesis of lung cancers

A
  • Probably a multi-step process
  • Chronic irritation/stimulation of cells by carcinogens
  • Increased cell turnover
  • Metaplasia - from normal pseudostratified columnar ciliated with goblet cells to squamous
  • Progressive accumulation of genetic abnormalities in molecules involved in cell cycle, signalling and angiogenesis pathways
  • Little known about rate of progression/regression
  • Phenotypic changes potentially reversible (but genotypic alterations persist)
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73
Q

When is maxillary-mandibular surgery used in OSAS?

A

Problematic patients, severe retrognathia/micrognathia

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74
Q

Why are NOACs/DOACs replacing heparin in anti-coagulation therapy?

A

NOACs/DOACs:

  • Fixed dose
  • No monitoring
  • Few drug-drug or drug-food interactions
  • Lots of studies show efficacy in VTE
  • Just as good as warfarin at preventing further clots, with lower bleeding risk (safer)
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75
Q

What investigations can be done in a patient with suspected OSA?

A
  • Limited polysomnography
  • Full polysomnography
  • Transcutaneous oxygen saturations and carbon dioxide assessment (TOSCA)
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76
Q

What are the effects of cigarette smoking?

A
  • Cilia are damaged/destroyed by smoking, cilial motility reduced - don’t clear secretions as effectively leading to increased susceptibility to infection and damage to the lungs
  • Airway inflammation
  • Hypertrophy of goblet cells and mucous cells, higher mucous production - cough more
  • Increased protease activity (released from inflammatory cells), anti-proteases inhibited
  • Digestion of lung, not enough anti-protease activity to inhibit
  • Oxidative stress - free radicals
  • Squamous metaplasia –> higher risk of lung cancer
    • Carcinogens absorbed and circulate - higher risk of other cancers
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77
Q

What is the impact of a PE on the heart?

A
  • Pulmonary hypertension causes pressure overload of RV
  • RV does not cope well with overload, dilatation and reduced stroke volume
  • Increase pressure from normal mean pulmonary artery pressure of 14mmHg –> >25, stroke volume of RV drops massively
  • Small clots can have big impact on function of heart
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78
Q

Describe the side effects associated with corticosteroids

A
  • Multiple - not very specific agents
  • Diabetes, osteoporosis, hypertension, muscle wasting, peptic ulceration, cataracts, Cushing’s syndrome, adrenal suppression, acute pancreatitis, hyperlipidaemia, increased appetite, salt and water retention, immune suppression
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79
Q

What investigations may be done to investigate a patients fitness for surgery in lung cancer?

A
  • Lung function tests - need full PFTs if considering surgery
  • ECG
  • PET-CT for staging, to check if surgically treatable
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80
Q

What is typically seen on an ECG in PE?

A

Can be normal

Common features - sinus tachycardia, S1Q3T3 appearance (pathopneumonic of acute PE but only in 20% cases)

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81
Q

What are the possible side effects of clarithromycin?

A
  • Rapidly absorbed orally, can cause phlebitis intravenously so avoid if possible
  • Undergoes hepatic metabolism therefore caution in liver failure and reduce dose in significant renal impairment
  • Inhibits CYP450 - risk of adverse drug interactions
    • Withhold simvastatin
  • Cardiac cautions: QT prolongation, giving risk of arrhythmia
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82
Q

What is the significance of BMI in COPD?

A

Low BMI (<21) associated with poorer prognosis

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83
Q

How is OSAS treated?

A
  • Treat the symptomatic - OSAS (daytime sleepiness)
  • AIM = improve daytime somnolence and quality of life
  • Explain OSAS
  • Weight loss
  • Avoid triggering factors e.g. alcohol
  • Treat underlying conditions - tonsils, hypothyroidism, nasal obstruction
  • Come off sedating medications overnight
  • Continuous positive airway pressure (CPAP)
  • Mandibular advancement device (MAD)
  • Maxillary-mandibular surgery
  • Sleep position trainers
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84
Q

Define extrinsic allergic alveolitis/hypersensitivity pneumonitis

A

Immunologically mediated inflammatory reaction in the alveoli and in the respiratory bronchioles

It is NOT atopy, it is a T-cell mediated response

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85
Q

What can cause restrictive spirometry?

A

Interstitial lung disease (stiff lungs)

Kyphoscoliosis - chest wall abnormality

Previous pneumonectomy

Neuromuscular disease - Guillain-Barre, MND

Obesity

Poor effort/technique

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86
Q

How does CPAP treat sleep apnoea?

A
  • Mask over nose gently directs air into the throat to keep the airway open
    • Splints airway open
    • Stops snoring
    • Stops sleep fragmentation
    • Improves daytime sleepiness and quality of life
  • Need compliance >4 hours for >70% days
  • Fixed vs autoset CPAP
    • Fixed = same pressure throughout
    • Auto = varying pressure calculated by machine throughout sleep, generally tolerated better
  • Nasal vs full face mask
  • Follow up - annually by physiology once CPAP established
  • 2 way remote monitored CPAP - can remotely monitor compliance and oxygen/CO2 levels etc.
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87
Q

How does chronic bronchitis contribute to the syndrome of COPD?

A
  • Larger airways >4mm in diameter
    • Inflammation leads to scarring and thickening of airways
    • Breathing inefficient - trapped air, can’t breath out efficiently
    • Exercise - respiratory rate increases, not enough time to breathe out properly so become hyperinflated (causes discomfort)
  • Small airways disease:
    • ‘Bronchiolitis’ in airways of 2-3mm
    • May be an early feature of COPD
    • Narrowing of the bronchioles due to mucous plugging, inflammation and fibrosis
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88
Q

What are the indications for methylxanthines in respiratory disease?

A

Adjunct to inhaled therapy in asthma/intravenous infusion in severe exacerbations of asthma

Not very effective in COPD

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89
Q

What imaging modalities can be used in the diagnosis of PE?

A
  • CTPA - most common, time contrast to maximise in main pulmonary artery to see vasculature
  • VQ - ventilation perfusion scanning, inhale radioactive gas and inject radioactive albumin, sits in pulmonary vasculature, look at two and see if they match up (if ventilation but no perfusion suggests PE)
  • VQ spect - used in pregnant women, lower radioactive dose
  • Pulmonary angiography - inject dye
  • CT - look at pulmonary artery and RV function
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90
Q

What is the prognosis of idiopathic pulmonary fibrosis?

A
  • Outcome - Median survival 3 -5 years from time of diagnosis
  • Rate of progression varies - generally have a steady, progressive decline but may also have sudden steps of decline after exacerbations/infections
  • Most patients (around 75%) will die of respiratory illness. Approximately 1in 10 patients will develop lung cancer.
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91
Q

How is a bronchial challenge test done? What would be seen in asthma?

A
  • How well can they tolerate breathing in histamine, methacholine or mannitol (which causes histamine release by making mast cells in the lung burst)
  • Everyone would eventually react but asthmatics show bronchial hypersensitivity
    • FEV1 dips faster than normal in asthmatics
    • Positive = fall by >20% FEV1 by <8mg/ml methacholine/histamine/mannitol
  • Not an allergy to histamine, just hypersensitivity compared to normal
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92
Q

How is an empyema managed?

A
  • Drainage (12-16F)
    • Larger drains more painful and no more effective
  • IV antibiotics
  • Fibrinolytics - enzymes to break down
  • Surgery
  • Ongoing clinical trials
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93
Q

Describe the cell types involved with the pathogenesis of IPF

A
  • Damaged epithelial cells
    • Activated to release growth factors - TGFβ1 one of most important
  • Fibroblasts/myofibroblasts
    • Myofibroblasts secrete excessive amounts of extracellular matrix proteins, mainly collagens
  • Type 1 pneumocytes are reduced
    • Injured cells produce TGFβ1 which promotes the transformation of fibroblasts to myofibroblasts
    • Fail to develop from type 2 pneumocytes add to the deveopment of dysfunctional alveolar epithelium
    • Reduced levels of calveolin 1, an anti-fibrotic molecule produced by these cells
  • Eosinophils, mast cells, macrophages and lymphocytes
    • Release cytokines such as IL-4, IL-1, TNFα and IFNγ
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94
Q

What additional treatments might be considered in a life threatening asthma attack which is not improving?

A

If not improving after 15-30 minutes (or if life-threatening features are present):

  • Discuss with senior clinician and ICU tam
  • Consider giving infusion of IV magnesium sulphate 1.2-2g infusion over 20 minutes and then either IV aminophylline or IV salbutamol (or terbutaline)
  • Consider transfer to ITU for mechanical ventilation if no improvement
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95
Q

What are the investigations which are used to give a clinical diagnosis of asthma?

A
  • Serial peak expiratory flow measurements - look for diurnal variation
  • Spirometry - have airflow obstruction, >400ml improvement in FEV1 following bronchidilator
  • Metacholine or histamine bronchial provocation test- look for a drop of 20% in FEV1 from baseline
  • Exhaled nitric oxide - a marker of airway inflammation (raised level >25 ppb)
  • CXR - usually normal, pneumothorax in acute asthma or infiltrates in ABPA
  • Skin prick tests or specific IgE levels - should be done, common allergens
  • Blood and sputum tests - may have raised blood eosinophils, often have raised sputum eosinophils but not routinely done
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96
Q

What symptoms can be seen in metastases to the brain?

A

Patients can experience headache, blurred vision, epilepsy, can be silent depending on location

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97
Q

Describe the appearance of acute HSP on CXR

A

Numerous poorly defined small (<5mm) opacities throughout both lungs

Sometimes with sparing of the apices and bases

Airspace disease - usually seen as ground glass opacities

Fine reticulation may also occur

Zonal distribution

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98
Q

Define allergy, and describe the steps which lead to an allergic reaction

A
  • Allergy is immune system mediated intolerance
    • Requires exposure to a trigger
    • Memory
    • Characteristic clinical features
      • Dependent on which arm of the immune system
  • Clinical reaction
    • Acute - sudden or slow - progressive
  • Chronic allergy leads to tissue remodelling
    • Acute inflammation - repair
  1. Trigger (which most people are tolerant of)
  2. Immune system recognises as foreign (external, not part of own body)
  • Antigen-presenting cell, T cell
  • IL-4, IL-33 or IL-12, IFN
  1. Memory
  2. Response
  • IL-4, IL-33 –> IgE, mast cell - immediate response (anaphylaxis, asthma etc.)
  • IL-12, IFN –> reactive T cells - delayed response
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99
Q

Degine extrinsic allergic alveolitis (hypersensitivity pneumonitis)

A
  • Acute illness due to type II reaction
    • Serum sickness or immune complex disease
  • Sub-acute days to weeks
    • Type IV T-cell mediated reaction (like chronic dermatitis of lung)
  • Chronic disease - fibrosis and emphysema
    • Final pathway of all chronic inflammatory conditions
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100
Q

Describe the histological classification of lung cancer

A

From a practical point of view division into -

  • Small cell and non-small cell lung cancer is the most important decision for treatment
  • Small cell - usually advanced at diagnosis and responds to chemotherapy
  • Non-small cell - may be localised at diagnosis and can be treated by surgery or radiotherapy
  • With advancement in therapies subdivision of non-small cell cancers is increasingly important
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101
Q

When/how are sleep position trainers used in the treatment of OSAS?

A

Supine OSA

Vibration when on back

Weeks to change sleeping position

Appropriate in few patients with supine OSA

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102
Q

How is the alveolar oxygen equation used?

A

Arterial pO2 (PaO2) can be directly measured- ABG

The difference between the calculated alveolar pO2 and the arterial pO2 is the alveolar arterial (A-a) oxygen gradient

Difference between alveolar and arterial oxygen partial pressures should be <2-4 kPa- more than this suggests V/Q mismatch

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103
Q

What symptoms are associated with SVC obstruction?

A
  • Oedema of face and arms
  • Raised JVP
  • Dilated veins on chest wall
  • Plethoric face
  • Headache worse on stooping
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104
Q

What treatments are available for dermatophyte fungal infections?

A
  • Straightforward
  • Many over the counter products
    • Sprays, creams, tablets, powders, liquids
  • Topical administration usually
  • Oral medication
    • Severe infections, nail infections
    • Topical medication has not worked
    • Adults only
  • Active ingredients
    • Terbinafine (Lamisil)
    • Itraconazole
    • Ketoconazole
    • Miconazole
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105
Q

List imaging which can be useful in pleural effusion

A
  • Chest X-ray
  • CT
  • Ultrasound
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106
Q

Define idiopathic pulmonary fibrosis

A
  • A specific form of chronic fibrosing interstitial pneumonia of unknown aetiology
  • Limited to the lung
  • Histopathological appearance of usual interstitial pneumonia (UIP) on surgical lung biopsy
  • Known causes of ILD such as drugs, environmental exposure and connective tissue disease have been excluded
  • Abnormal lung function tests with evidence of restriction and/or impaired gas exchange
  • Characteristic abnormalities on CXR or HRCT chest (bibasal reticular abnormalities with minimal or no ground glass opacities on HRCT)
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107
Q

What are the most common investigations done in suspected lung cancer?

A
  • Routine bloods - FBC, U&Es, LFTs, serum calcium, CRP
  • CT chest and upper abdomen - look for lymph nodes, evidence of liver or adrenal metastases
  • Bronchoscopy - will detect more central lesions
  • Percutaneous needle biopsy - peripheral lesions
  • CT/CT-PET - combined imaging to look for metastases
  • Endobronchial ultrasound - to visualise and guide needle biopsy of mediastinal lymph nodes
  • Ultra-sound guided aspiration of supraclavicular lymph nodes
  • VATS (video-assisted thoracoscopic surgery) - to diagnose and treat pleural effusion
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108
Q

Describe the prevalence of lung cancer

A
  • 3rd most common cancer in the UK
    • In men second commonest after prostate
    • In women second commonest after breast
  • Accounts for 13% of all new cancer cases
  • >44% in over 75s, highest in 85-89 y/o
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109
Q

Describe the use and mechanism of action of leukotriene receptor antagonists (Montelukast and Zafirlukast)

A
  • For asthma maintenance - not for treatment of acute attacks
  • Taken orally
  • High affinity antagonist of cysteinyl leukotriene receptor (CysLT1) inhibiting the action of LT-D4 in smooth muscle cells of the airway and airway macrophages –> reduces airway oedema and smooth muscle contraction
  • Useful for prophylaxis of exercise-induced asthma, allergic rhinitis
  • Short half-life - often take at night (when symptoms are worse)
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110
Q

How can blood gas analysis be interpreted (from a respiratory perspective)?

A
  • Always look at the pO2 first - normal approx. 13
    • Is the patient in respiratory failure (<8) requiring additional oxygen (<6)?
  • Then look at the PCO2 (type 1 vs type 2 respiratory failure)
    • pCO2 >6 - type 2 respiratory failure
    • pCO2 <6 - type 1 respiratory failure
  • Then consider acid base balance
    • Acute (decompensated) respiratory acidosis- elevated pCO2, normal bicarbonate, acidosis (H+ > 44)
    • Compensated respiratory acidosis- elevated pCO2, elevated bicarbonate (renal compensation), not acidotic (H+ normal)
    • Acute on chronic respiratory acidosis - elevated pCO2, elevated bicarbonate, acidotic
      • = mixed picture - chronic respiratory failure with acute respiratory event which prevents compensation
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111
Q

What are the clinical consequences of extrinsic allergic alveolitis?

A
  • Pathology - thickening of the septae, filling of the alveolus with fluid
    • Impact on passive diffusion of gases
  • Loss of O2 - hypoxaemia
    • Normal CO2 - soluble in water so can still transfer in fluid
  • Air space shadowing on CXR

Chronic Exposure:

  • Fibrosis
    • Interstitial scarring from chronic tissue remodelling/repair pathways
    • More exposure = more fibrosis
  • Emphysema
    • Interstitial destruction from neutrophilic enzyme release

Passive Diffusion Consequences:

  • Emphysema - reduced surface area, reduced amount of BV available to oxygen
    • Increased distance for O2 to travel to be absorbed
  • Pulmonary fibrosis
    • Thicker alveolar walls, reduced solubility of oxygen

= Reduced oxygen transport into the bloodstream, measured by carbon monoxide gas transfer during full PFTs. Airspace shadowing on CXR

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112
Q

What is the advice for OSAS and driving?

A

British Thoracic Society (BTS) Statement on Driving and OSA/OSAS

  • DVLA need to be informed if moderate/severe OSAS with excessive sleepiness or mild OSAS with excessive sleepiness which can’t be controlled after 3 months
  • DVLA do not need to be informed without symptoms of excessive sleepiness
  • OSA without daytime somnolence, do not need to stop driving
  • OSAS (DTS) - likely impairment of driving, inform DVLA on diagnosis
  • OSAS can hold license if compliant with treatment and reduced DTS
  • CAT 2 license require ongoing monitoring by DVLA with regards to treatment compliance
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113
Q

How is transfer factor measurement done?

A

Single breath of a very small concentration of carbon monoxide

CO has very high affinity to Hb (100x O2)

Measure concentration of CO2 in expired gas to derive uptake in the lungs

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114
Q

What is plethysmography? How is it used in asthma diagnosis?

A
  • Patient inside sealed box, breathing monitored
  • Could introduce potential trigger and measure response
  • Not done - could trigger potentially life-threatening asthma attack
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115
Q

Define obstructive sleep apnoea and obstructive sleep apnoea syndrome

A

Obstructive Sleep Apnoea:

Recurrent episodes of partial or complete upper (pharyngeal) airway obstruction during sleep, intermittent hypoxia sleep fragmentation

Obstructive Sleep Apnoea Syndrome:

Manifests as excessive daytime sleepiness

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116
Q

Which stages of non-small cell carcinoma are usually operable?

A

<25% operable, stage 1 operable, some stage II

Gives best chance of cure

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117
Q

How can COPD and asthma be distinguished using spirometry?

A
  • Reversibility Testing:
    • Nebulised or inhaled salbutamol given
    • Spirometry before and 15 minutes after salbutamol
    • 15% and 400ml reversibility in FEV1 suggestive of asthma
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118
Q

Describe a normal tide/volume plot

A
  • Sharply rises as most of forced vital capacity expired in first second, then plateaus
  • Can measure
    • Peak expiratory flow rate - first 0.1 seconds
    • Forced expiry volume in one second - should be most of functional lung capacity
    • Forced vital capacity
    • FEV1:FVC ratio
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119
Q

Describe systemic fungal infections

A

Mostly infected through airways, can spread through meninges to CNS

Only causes infection in immunocompromised

Treatment can be problematic

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120
Q

What type of infection does crytococcus neoformans cause?

A
  • Causes cryptococcosis of lungs, and meningitis
    • Often secondary infection with HIV
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121
Q

What signs can be seen on CXR which aid diagnosis of pleural effusion?

A
  • Unilateral pleural effusion - more likely to be exudative
  • Bilateral pleural effusion - more likely to be transudative
  • D sign - doesnt follow gravity, suggests infection/empyema (more complex)
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122
Q

What is sarcoidosis?

A
  • Common multisystem inflammatory disease of unknown aetiology that predominantly affects the lungs and intrathoracic lymph nodes
  • Cause is unknown - efforts to identify a possible infectious aetiology unsuccessful
  • Characterised by ‘non-necrotising granulomatous inflammation’
    • Inflammation in interstitium of organ (working tissue)
  • Diagnosis of exclusion
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123
Q

List the possible phenotypes in COPD

A

Frequent exacerbations

Persistent breathlessness

Chronic bronchitis

Muscle wasting syndrome (emphysema)

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124
Q

What is the immediate management of a tension pneumothorax?

A
  • Medical emergency
  • Immediate management - insert Venflon 2nd intercostal space mid-clavicular line to relieve pressure
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125
Q

List the causes of EAA/HSP

A
  • Causes
    • Organic dusts (<5um - have to be small enough to escape mucous and cilia of airways)
    • Moulds
    • Foreign proteins (animals)
    • Some chemicals
    • Often heavy, repeated exposure, most often at the work place
  • Farmer’s lung - mouldy hay
  • Saw mill worker’s lung - mouldy wood dust
  • Bird fancier’s lung - proteins in bird dropping
  • Mushroom worker’s lung - spores, moulds
  • Malt worker’s lung - mouldy malt
  • Humidifier lung - contaminated humidifier water
  • Cheese washer’s lung - penicillium casei
  • Suberosis - cork dust mould
  • Disocyanate lung - polyurethane hardeners
  • Hard metal worker’s lung - hard metal dust, cobalt
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126
Q

Describe the genetic abnormalities involved in lung cancer development

A
  • Oncogenes (ras, myc)
  • Growth factors receptors (epidermal growth factor, bombesin-like peptide)
  • Genetic predisposition (Li-Fraumeni syndrome, Hippel-Lindau)
  • Antioncogenes (P53, 3P, rb)
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127
Q

What would the expected symptoms be in a small central lung tumour with bronchial obstruction?

A

Cough, haemoptysis

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128
Q

Give examples of actionable driver genetic mutations in lung cancer

A

KRAS

EGFR

ALK

HER2

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129
Q

Define Horner’s syndrome

A

Due to invasion of cervical sympathetic chain

Ptosis, exophthalmos, miosis, anhidrosis

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130
Q

How are moderate asthma exacerbations, acute severe asthma attacks, life threatening asthma attacks and near fatal asthma attacks categorised?

A
  • Moderate Exacerbation:
    • Increasing symptoms
    • PEF >50-75% best or predicted
    • No features of acute severe asthma
  • Acute Severe:
    • Any one of
      • PEF 33-50% best or predicted
      • Respiratory rate >25/min
      • Heart rate >110/min
      • Inability to complete sentences in one breath
  • Life Threatening:
    • In a patient with severe asthma, any one of
      • PEF <33% best or predicted
      • SpO2 <92%
      • PaO2 <8kPa
      • Normal PaCO2 (4.6-6kPa)
      • Silent chest
      • Cyanosis
      • Poor respiratory effort
      • Arrhythmia
      • Exhaustion, altered conscious level
  • Near Fatal:
    • Raised PaCO2 and/or requiring mechanical ventilation with raised inflation pressures.
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131
Q

How do sleep studies give a diagnosis of obstructive sleep apnoea?

A
  • Calculated by adding the number of apnoea and hypopnoeas and dividing by the total sleep time (in hours)
    • AHI>15 is diagnostic of OSA
    • AHI 5-15 with compatible symptoms
      • AHI <5 normal
      • AHI 5-15 mild
      • AHI 16-30 moderate
      • AHI >30 severe
  • Oxygen Desaturation Index (ODI)
    • The number of times per hour of sleep that the SpO2 falls >4% from baseline
132
Q

Name the cell types and inflammatory mediators involved in airway inflammation in asthma

A

Inflammatory cells seen:

  • Activated T helper (Th2) lymphocytes produce IL-3, 4, 5 and 14 which maintain the allergic phenotype
  • IL-4 stimulates IgE production, IL-5 activates eosinophils, IL-13 stimulates mucous secretion and promotes IgE production
  • Eosinophils - in bronchial walls and secretions of asthmatics, attracted to airways by IL-3 and 5, GMCSF and chemokines (eotaxin, RANTES), release mediators such as LTC4 when activated
  • Mast cells - increased in mucous glands, smooth muscle and epithelium, produce histamine, PGD2, cysteinyl leukotrienes, tryptase
  • Dendritic cells - present allergens to T lymphocytes

Mediators in the (late) acute asthma response

  • Leukotrienes (LT C4, D4, E4) - bronchoconstriction, increase vascular permeability, increase mucous secretion
  • Acetyl choline - released from intrapulmonary nerves, directly stimulates muscarinic receptors on airway smooth muscle
  • Histamine - bronchoconstriction
  • Prostaglandin PGD2 - bronchoconstriction and vasodilation
  • Others - platelet-activating factor, IL-1, TNF, IL-6, chemokines, neuropeptides (eotaxin), nitric oxide
133
Q

How can drugs target ergosterol to treat fungal infections?

A
  • Target steps in ergosterol synthesis
    • Azoles inhibit 14-methylsterol alpha-demethylase
    • Terbinafine inhibits squalone 2,3-epoxidase
  • Amphotericin B binds to ergosterol and creates pores
134
Q

Describe the histological changes seen in the airways of asthmatics

A

Epithelium damaged due to inflammation, undergoing continuous repair (scarring/fibrosis)

BM thickened

Smooth muscle hypertrophy - target of asthma therapies

135
Q

What causes ventilation perfusion mismatch?

A
  • Happens to a degree in normal lungs
    • Due to gravity apices are well ventilated, bases are less well ventilated
  • Areas of lungs that are perfused but not well ventilated e.g. pneumonic consolidation
  • Shunt an ‘extreme’ form of V/Q mismatch where blood bypasses the lungs entirely, does not correct with oxygen administration
136
Q

How long should anticoagulation therapy be for patients post-PE?

A
  • Therapeutic anticoagulation for >3 months is recommended for all patients with PE
  • For patients with first PE/VTE secondary to a major transient/reversible risk factor, discontinuation of therapeutic oral anticoagulation is recommended after 3 months
  • Oral anticoagulant treatment of indefinite duration is recommended for patients presenting with recurrent VTE (at least one previous episode of PE/DVT) not related to a major transient or reversible risk factor
  • Oral anticoagulant treatment with a VKA for an indefinite period is recommened for patients with antiphospholipid antibody syndrome
137
Q

Describe the acute illness associated with extrinsic allergic alveolitis

A

4-6 hours after exposure

Wheeze, cough, fever, chills, headache, myalgia, malaise, fatigue

May last several days

Serum sickness illness

138
Q

What is the criteria for long term oxygen therapy in patients with COPD?

A

Long-term oxygen therapy in COPD patients who have:

  • PaO2 <7.3kPa when stable - his paO2 is too good at present
  • OR PaO2 7.3-8kPa
  • And any of
    • Secondary polycythaemia
    • Nocturnal hypoxaemia
    • Peripheral oedema
    • Pulmonary hypertension
  • And non-smoker for >3 months
139
Q

In which patients should a diagnosis of COPD be considered?

A
  • Consider the diagnosis of COPD for people who are over 35, and smokers or ex-smokers, with any of:
    • Exertional breathlessness
    • Chronic cough
    • Regular sputum production
    • Frequent winter ‘bronchitis’
    • Wheeze
140
Q

Describe the changes which have occurred in the incidence of lung cancers by histology

A
  • Recent rise in adenocarcinoma and small cell carcinoma with fall in squamous carcinoma
  • Due to changes in smoking habits or composition of cigarettes
    • Change in smoking demographics (more women now getting lung cancer)
    • Filter tips, lower tar and nicotine
    • Deeper inhalation exposes more peripheral airways to carcinogens
141
Q

How can sarcoidosis be staged?

A

CXRs in patients with sarcoidosis have been classified into 4 stages:

  • Stage I - bilateral hilar lymphadenopathy without infiltration
  • Stage II - bilateral hilar lymphadenopathy with infiltration
  • Stage III - infiltration alone
  • Stage IV - fibrotic bands, bullae, hilar retraction, bronchiectasis, diaphragmatic tenting

Represent radiographic patterns and do not indicate disease chronicity or correlate with changes in pulmonary function.

142
Q

Define malignant mesothelioma

A
  • Malignant mesothelioma - malignant tumour of the pleural caused by asbestos exposure
    • Encases lung and spreads in interlobar fissure
    • Compresses lung
143
Q

Describe the physiological, pathological and clinical aspects of asthma

A

Wheeze due to:

  • Reversible/variable airflow obstruction - physiological
  • Airways inflammation/allergy - pathological
  • Triggers, cold, exercise, cats, nocturnal/diurnal - clinical

Variable clinical presentation - used to direct management

  1. Physiological
  • Yellow mucous
  • Repair pathways
  • Non-elastic airways
  • Increased responsiveness/sensitivity
  1. Pathological
  • Inflammation
  • Scabby epithelium
  • Thickened BM
  • Thickened smooth muscle
  • Mast cells in smooth muscle
  1. Clinical
  • Cough
  • Wheeze
  • Hyper-reactivity
  • Hyper-sensitivity
144
Q

Describe the effects of local spread of lung cancer

A
  • Pleural - haemorrhagic effusion
  • Hilar lymph nodes (–> cervical)
  • Adjacent lung tissue - may involve large blood vessel leading to haemoptysis
  • Pericardium - pericardial effusion with subsequent involvement of pericardium
  • Mediastinum
    • Superior vena caval obstruction - raised JVC, visible veins on chest, swelling of face, headache
    • Recurrent laryngeal nerve compression as it hooks under arch of aorta and travels up side of larynx - hoarseness
    • Phrenic nerve - hemidiaphragm paralysis
  • Pancoast tumour
    • Involvement of brachial plexus giving sensory and motor symptoms
    • Horner’s syndrome/oculosympathetic palsy (cervical sympathetic chain)
145
Q

What treatment is available for non-small cell lung cancer vs small cell lung cancer?

A

NSCLC - surgery, radiotherapy, chemotherapy, palliative care

SCLC - radiotherapy, chemotherapy, palliative care

146
Q

Describe the features of squamous cell carcinoma

A
  • Tend to arise centrally from major bronchi
  • Often within dysplastic epithelium following squamous metaplasia
  • Slow growing and metastasise late therefore may be good candidate for surgery
  • May undergo cavitation - outgrow blood supply, necrosis in centre
  • May block bronchi leading to retention pneumonia or collapse
  • Appearance
    • A malignant epithelial tumour showing keratinisation and/or intercellular bridges (desmosomes, same as stratum spinosum layer of skin)
    • In situ squamous cell carcinoma may be seen in the adjacent airway mucosa
147
Q

Which diseases increase/decrease lung volumes?

A
  • Lung volumes reduced in restrictive lung disease
  • Increased residual volume and residual volume/total lung capacity in obstructive lung disease
148
Q

How is COPD treated?

A
  • Inhaled bronchodilators
    • Short-acting - salbutamol (beta 2 agonist - SABA)
    • Long-acting - salmeterol (beta 2 agonist) - LABA, tiotropium (muscarinic antagonist - LAMA)
  • Inhaled corticosteroids
    • Budesonide and fluticasone - combination inhalers
    • Oxygen therapy
  • Oral theophylline
    • Mucolytics - carbocysteine (symptomatic relief)
    • Nebulised therapy
149
Q

What is the effect of aspergillus fumigatus?

A

Can give rise to 3 different conditions:

  • Allergic bronchopulmonary aspergillosis
    • Allergic reaction to fungal infection
    • Association with cystic fibrosis, asthma
    • Prednisone (anti-allergic agent)
  • Invasive pulmonary aspergillosis
    • Becomes systemic and spreads throughout the body
    • Common in immunocompromised
    • Treatment - voriconazole, amphotericin B
  • Aspergilloma
    • A fungal ball that develops in an area of past lung disease or lung scarring - encapsulated in lung tissue
      • E.g. tuberculosis or lung abscess
    • No treatment unless bleeding occurs - surgery (excision)
      • Irresponsive to drugs as encapsulated
150
Q

List the types of emphysema which cause airway obstruction

A
  1. Centri-acinar (acinus = area of lung supplied by one respiratory bronchiole)
  • Damage around respiratory bronchioles
  • More in upper lobes
  1. Pan-acinar
  • Uniformly enlarged from the level of terminal bronchiole distally
  • Can get large bullae
  • Associated with alpha 1 anti-trypsin deficiency
  1. Paraseptal
    * Peripheral alveolar damage around the septae of the lungs/pleura
151
Q

Describe the guidelines for management of a pneumothorax

A
  • Spontaneous pneumothorax - if bilateral/haemodynamically unstable proceed to chest drain
  • Age >50 and signifcant smoking history, evidence of underlying lung disease on exam or CXR?
    • No - primary pneumothorax
    • Yes - secondary pneumothorax
  • Primary
    • Size >2cm and/or breathless - aspirate 16-18G cannula, aspirate <2.5L
      • Success (<2cm and breathing improved) - consider discharge review in OPD in 2-4 weeks
      • No success - chest drain, size 8-14 Fr, admit
    • Size <2cm, not breathless - consider discharge review in OPD in 2-4 weeks
  • Secondary
    • >2cm or breathless - chest drain, size 8-14Fr, admit
    • Size 1-2cm - aspirate 16-18G cannula, <2.5L
      • Success (size now <1cm) - admit, high flow oxygen (unless suspected oxygen sensitive), observe for 24 hours
      • No success - chest drain, size 8-14Fr, admit
    • Smaller than 1cm - admit, high flow oxygen (unless suspected oxygen sensitive), observe for 24 hours
152
Q

Describe the side effects associated with beta 2 agonists

A

Due to action on beta 1 receptors

  • Tremor, hypokalaemia, hyperglycaemia, hypomagnesaemia
  • Flushing, tachycardia, arrhythmias, headache, muscle cramps
153
Q

Give examples of the non-small cell lung carcinomas other than adenocarcinomas, squamous cell carcinomas and large cell carcinomas

A
  • Tumours of mesenchymal tissues
    • Inflammatory myofibroblastic tumour
  • Salivary gland-type tumours
    • Adenoid cystic carcinoma
  • Tumours of ectopic origin
    • Germ cell tumours
  • Tumours of neuroendocrine cells
    • Carcinoid
  • Tumours of lymphatic system
    • Lymphoma
154
Q

Describe the features of large cell carcinoma

A
  • A diagnosis of exclusion
  • Usually arises centrally
  • An undifferentiated malignant epithelial tumour that lacks the cytological features of SCLC and glandular or squamous differentiation
155
Q

What are the potential side effects of co-amoxiclav?

A

Predominantly renally excreted therefore reduce dose in severe renal impairment

Can cause cholestatic jaundice, Stevens Johnson syndrome or toxic epidermal necrolysis

156
Q

Describe the pharmacokinetics/pharmacodynamics of anti-muscarinics

A

Short-acting - ipratropium bromide

Long-acting - tiotropium, glycopyrronium, umeclidinium

Renally excreted

157
Q

Describe the MRC dyspnoea scale

A
  • Grade 1 - dyspnoea on strenuous exercise
  • Grade 2 - short of breath when hurrying or walking up a slight hill
  • Grade 3 - walks slower than contemporaries on level ground because of breathlessness, or has to stop for breath when walking at own pase
  • Grade 4 - stops for breath after walking about 100m or after a few minutes on level ground
  • Grade 5 - too breathless to leave the house, or breathless when dressing and undressing
158
Q

How can genetics predispose to COPD?

A
  • Alpha 1 antitrypsin deficiency - genetic
    • Alpha 1 antitrypsin - anti-protease (serine protease inhibitor), prevents protease digestion of lung tissue
    • Present in 1-3% of COPD patients
    • M alleles normal variant
    • SS and ZZ homozygotes have clinical disease
  • Unable to ‘counterbalance’ destructive enzymes in lung
  • Non-smokers get emphysema in 30-40s, smokers get emphysema much earlier
  • Smokers have increased risk of COPD if it is in the family
159
Q

Describe the appearance of phrenic nerve paralysis on CXR

A

Elevated domed hemidiaphragm on affected

160
Q

Describe inflammation in asthma

A
  • Inflammatory response from epithelium due to repeated damage
  • Epithelial lining regrows - GF, cytokines released by mast cells, macrophages, lymphocytes and epithelial cells
  • Cytokines - IL-5, TSLP, IL-13
    • IL-5/13 important targets for treatment
    • Drives eosinophilic inflammation
  • Growth factors - TNF alpha, TGF beta, VEGF
    • Fibrosis, remodelling cytokines, responsible for growth of smooth muscle, angiogenesis, epithelial cell damage, airway remodelling

Inflammation

  • Corticosteroid responsive disease
  • Routinely identified in airways of asthma
  • If stimulated will drive an asthma phenotype
    • Viral infections, late allergic reactions
  • Multiple candidate genes and non-hierarchical genes associated with asthma are inflammatory
161
Q

What is NSIP? How is it treated?

A

Cause of pulmonary fibrosis

NSIP = non-specific interstitial pneumonia, treat with immune modulating drugs

162
Q

Describe the staging of non-small cell carcinomas

A

T – tumour size

N – regional lymph node involvement

M – presence or absence of distant metastases

TNM used together to give stage of disease - helps decide treatment options

TNM Staging

Stage I: localized, no LN involvement

Stage IA - < 2 cm in size

Stage IB – 2 - 3 cm in size

Stage 2: 3 – 7 cm or involves main bronchus/visceral pleura/lobar collapse or hilar LN

Stage 2A – 3 – 5cm in size

Stage 2B – 5 -7 cm in size

Stage 3: > 7 cm in size or invades into adjacent structures or whole lung collapse

Stage 3A- any size and spreads into mediastinal lymph nodes or local spread to chest wall, pleural or mediastinum

Stage 3B – spread to contralateral or supraclavicular nodes, or spread to another major structure such as the oesophagus, heart, trachea or major vessel, or two or more tumours in the same lung, or pleural effusion

Stage 4 – distant spread

163
Q

List the types of non-small cell carcinoma

A

Squamous cell carcinoma

Adenocarcinoma

Large cell carcinoma

Other

164
Q

Describe the Epworth Sleepiness Score

A
  • How likely would you be to fall asleep in different situations?
    • Sitting and reading
    • Watching TV
    • Sitting, inactive in a public place (e.g. a theatre or a meeting)
    • As a passenger in a car for an hour without a break
    • Lying down to rest in the afternoon when circumstances permit
    • Sitting and talking to someone
    • Sitting quietly after lunch without alcohol
    • In a car, while stopped for a few minutes in the traffic
165
Q

What tests are used in asthma investigation?

A
  • PEFR testing
    • Look for diurnal variation and variation over time
    • Response to inhaled corticosteroid
    • Occupational asthma
  • Bronchial provocation
  • Spirometry before and after trial of inhaled/oral corticosteroid
166
Q

Describe the mechanism of OSAS

A
  • Pharyngeal narrowing
  • Negative thoracic pressure
  • Arousal
    • Sleep disruption - sleepiness, reduced quality of life, road traffic accidents
    • Blood pressure surge - heart attacks, strokes
167
Q

Which symptoms and signs should alert you to a possible diagnosis of lung cancer?

A

Symptoms suspicious of lung cancer:

  • Cough - that doesn’t go away or is long-standing and gets worse
  • Recurrent infections
  • Breathlessness - lobar/lung collapse (co-existing COPD)
  • Haemoptysis
  • Unexplained weight loss
  • Chest and/or shoulder pains
  • Hoarse voice

Clinical signs which may be associated with lung cancer:

  • Finger clubbing
  • Signs of lobar collapse or a pleural effusion
  • From metastases - hepatomegaly, cervical lymphadenopathy, bone tenderness
  • Cachexia
  • Horner’s syndrome (Pancoast tumour)
  • Evidence of superior vena cava obstruction (SVCO) or spinal cord compression (SCC)
  • Cushingoid
168
Q

How does sarcoidosis typically present?

A
  • Approximately 5% of cases are asymptomatic and incidentally detected by CXR
  • Presentation depends on the extent and severity of the organ involved
  • Systemic symptoms occur in 45% of cases such as
    • Fever
    • Anorexia
    • Fatigue
    • Night sweats
    • Weight loss
  • Macrophages produce systemic effect
  • Pulmonary - dyspnoea on exertion, cough, chest pain and haemoptysis (rare) occur in 50% of case
169
Q

What are the risk factors for a spontaneous pneumothorax?

A

Smoking, male gender and height are risk factors

Young, tall, slim males most at risk

Underlying lung disease (secondary)

Recurrence rate 40-50% after first episode

170
Q

Which pathogens commonly cause COPD exacerbations?

A

Strep pneumoniae, haemophilus influenzae

171
Q

What is the role of a pulmonary embolism response team?

A

Like a virtual MDT

Multi-professional

Consult on the complex sub-massive/massive PTEs

Rapid risk stratification

172
Q

How can reversibility of airflow obstruction in suspected asthma be tested?

A
  • Measure FEV1 before and after inhaled/nebulised salbutamol (or other bronchodilator)
  • In asthma - >15% improvement in FEV1 after bronchodilator
173
Q

How is crytococcus neoformans infection contracted?

A

Inhaled opportunistic pathogen

Encapsulated yeast - fluffy surrounding capsule, easily airborne

Contracted from environment e.g. pigeon droppings

174
Q

Describe the difference between immediate asthma (early reaction) and late phase reactions

A
  • Immediate asthma (early reaction)
    • Starts within minutes, maximal at 15-20 minutes, subsides by 1 hour
    • Bronchoconstriction triggered by direct stimulation of subepithelial vagal receptors, increased mucous production, vasodilation and increased vascular permeability
  • Late-phase reactions
    • Follows immediate reaction, more sustained attack of airflow limitation that may respond less well to bronchodilators
    • Inflammation with recruitment of eosinophils, neutrophils and lymphocytes
175
Q

How should an exacerbation of COPD be managed in hospital?

A
  • Assess severity: Symptoms, ABG, CXR
  • Controlled oxygen therapy: 24 -28 % oxygen, aim to maintain SpO2 88 – 92 %; repeat ABGs at 1 hour
  • Bronchodilators: nebulised salbutamol 2.5 – 5 mg and ipratropium bromide 0.5 mg qds (and PRN)
    • Consider IV aminophylline if not improving
  • Corticosteroids: prednisolone 30 – 40 mg od
  • Antibiotics: if signs of bacterial infection (purulent sputum, increased sputum volume, ­WCC, ­CRP
  • Non-invasive ventilation (NIV): for acidotic type II respiratory failure
  • Other: consider DVT prophylaxis (LMWH), monitor fluid balance and nutrition, manage co-morbidities
176
Q

How are targetted therapies used in lung cancer treatment?

A
  • Population targeting oncogenic drivers has transformed the care of patients with lung adenocarcinoma
  • Those with actionable genes do better than those without - can target therapy, much better outcomes
  • In NHS GGC
    • 13% have mutation in EGFR receptor and may respond to tyrosine kinase inhibitors
    • 2% of NSCLC patients have EML4-ALK gene fusions present in their tumours - may respond to ALK inhibitors
    • Approximately 1-2% of NSCLC patients have ROS-1 oncogenic fusion which may respond to targeted therapies
    • PD-L1 is overexpressed on some tumours in some patients with NSCLC - may be treated with PD-L1 inhibitors
177
Q

How is extrinsic allergic alveolitis managed?

A
  • Allergy - avoid trigger (occupation)
  • Inflammation - corticosteroids
    • Neutrophils are modestly steroid responsive
    • Cytotoxics
  • Oxygen supplementations
178
Q

How is pulmonary fibrosis diagnosed?

A
  • HRCT
  • Video-assisted thoracoscopic surgery (VATS)
    • Need 3 biopsies for diagnostically competent sample
    • Don’t take biopsy from lingula (damaged by heart) or points of lungs (damaged by infections)
179
Q

What pathological features would be seen in a lymph node biopsy in sarcoidosis?

A

Pink abnormal infiltrate - macrophages

Surrounded by normal purple lymphocytes

180
Q

What should be examined in a patient with a suspected pleural effusion?

A

Systemic examination - clubbing, ascites, lymphadenopathy

Chest

Cardiovascular

181
Q

Is there overlap between COPD and asthma

A

Diseases of airflow limitation - emphysema, chronic bronchitis and asthma, can have overlap between all

Asthma-COPD overlap syndrome

182
Q

What factors affect transfer factor?

A

Alveolar surface area

Pulmonary capillary blood volume

Haemoglobin concentration

Ventilation perfusion mismatch

183
Q

What are the symptoms/signs associated with IPF?

A
  • Bibasilar crackles, clubbing
  • Peripheral interstitial pattern
  • Subpleural honeycombing (holes in lung tissue)

Symptoms:

  • Breathlessness (worse with exercise)
  • Hacking dry cough
  • Fatigue and weakness
  • Appetite and weight loss
184
Q

Define a pancoast tumour

A

Tumour of the pulmonary apex which can involve the brachiocephalic vein, brachial plexus, subclavian vein/artery

Causes severe pain in the shoulder/scapula, pain the in arm and weakness of the hand on the affected side and Horner’s syndrome

185
Q

List the signs and symptoms of a pneumothorax

A

Pleuritic chest pain - worse when breathing in

Breathlessness, can be minimal if primary

Respiratory distress (especially if secondary)

Reduced air entry on affected side

Hyper-resonance to percussion (?)

Reduced vocal resonance

Tracheal deviation if tension (+/- circulatory collapse) - late sign

186
Q

Define COPD

A

COPD characterised by airflow obstruction

Airflow obstruction usually progressive, not fully reversible and does not change markedly over several months

187
Q

Define COPD

A

Irreversible airflow obstruction

(Reversibility - if given a bronchodilator the airways open)

188
Q

Describe the treatment of non-small cell carcinomas

A
  • Surgery - early stages (usually stage I or II)
  • Radiotherapy
    • Curative intent (radical radiotherapy) in some with early stages if not thought to be fit for surgery
      • Side effects - radiation pneumonitis in 10-15% (acute infiltrate <3 months after treatment), radiation fibrosis around one year after
    • For symptom control (palliative radiotherapy) - good for bone and chest wall pain, haemoptysis, occluded bronchi, SVCO
  • Chemotherapy
    • Platinum based chemotherapy (cisplatin/carboplatin) in combination with paclitaxel or gemcitabine
    • Can be used to down-stage tumours for surgery or to palliate symptoms
189
Q

What are the most common types lung cancer by histology?

A
  • Adenocarcinoma - 40%
  • Squamous cell carcinoma - 30%
  • Small cell lung carcinoma - 15%
  • Large cell carcinoma - 10%
  • Other non-small cell lung carcinoma - 3%
190
Q

How does a pneumothorax develop?

A
  • Pleural cavity usually a potential space
  • Negative intrapleural pressure
    • Opposing forces of chest wall (outwards) and lung (inwards - natural elastic recoil)
  • Any breach of the pleural space leads to collapse of the elastic lung
191
Q

What are the recommendations for post-PE long term anti-coagulation therapy?

A
  • Initiation of anticoagulation is recommended without delay in patients with high or intermediate clinical probability of PE, while diagnostic workup is in progress
  • If anticoagulation is initiated parenterally, LMWH or fondaparinux is recommended (over UFH) for most patients
  • When oral anticoagulation is started in a patient with PE who is eligible for a NAOC (apixaban, dabigatran, edoxaban or rivaroxaban), a NOAC is recommended in preference to a VKA
  • When patients are treated with a VKA, over-lapping with parenterally anticoagulation is recommended until an INR or 2.5 is reached
  • NOACs are not recommended in patients with severe renal impairment, during pregnancy and lactation, and in patients with antiphospholipid antibody syndrome
192
Q

What are azoles? Give examples.

A
  • Largest class of antifungal agents
  • Pharmacologically active part of molecule = azole
  • Many applications
  • Examples
    • Miconazole (Micatin or Daktarin)
    • Ketoconazole (Nizoral, Fungoral and Sebizole)
    • Clotrimazole (Lotrimin, Lotrimin AF and Canesten)
    • Econazole
    • Isoconazole
    • Fluconazole
    • Itraconazole
    • Abafungin
193
Q

Which investigations should be done in suspected interstitial lung disease?

A
  • CXR
  • CT chest
  • Routine blood tests
    • FBC
    • U+Es
    • LFTs
    • Calcium
    • ESR
    • CRP
  • Immunology
    • Rheumatoid factor
    • ANA screen
    • ANCA screen
    • Avian precipitans and aspergillus precipitans
    • Serum angiotensin converting enzyme level (sarcoid)
    • Serum immunoglobulins (sarcoid)

As condition progresses or if felt to have evidence of respiratory failure or cor pulmonale at presentation:

  • Arterial blood gases - Type 1 Respiratory Failure
    • Caused by a combination of alveolar capillary block (loss of capillary volume) and V/Q mismatch
    • PaCO2 normal or low owing to hyperventilation
      • High in obstructive disease – not breathing out effectively
  • Six-minute walk test/ambulatory oxygen assessment - to assess if desaturation on exertion.
  • Echocardiogram - to look for the development of pulmonary hypertension
194
Q

List alternative drugs used in COPD

A
  • Roflumilast
    • Selective inhibitor of phosphodiesterase-4
    • Inhibits hydrolysis of cAMP in inflammatory cells –> increased intracellular cAMP –> reduces release of pro-inflammatory mediators and cytokines
    • Orally administered, metabolism by cytochrome P450
    • Reduction in exacerbations of COPD - but many side effects
  • Azithromycin
    • Macrolide antibiotic with immunomodulatory and anti-inflammatory effects - inhibition of pro-inflammatory AP-1, NFkB and mucin release
    • Reduction in exacerbations of COPD
  • Carbocysteine
    • Mucolytic that increases concentrations of sialomucins and reduces concentrations of fucomucins, resulting in reduced sputum viscosity
    • Less viscose sputum means secretions are cleared more easily, reduction in retained secretions = reduction in infections/exacerbations
195
Q

List the possible endotypes in COPD

A

Persistent systemic inflammation

Eosinophilic or Th2 high COPD

Persistent pathogenic bacterial colonisation - long term antibtioics

Alpha-1 antitrypsin deficiency

196
Q

Define an exacerbation of COPD

A

An exacerbation is a sustained worsening of the patient’s symptoms from their usual stable state which is beyond normal day-to-day variations, and is acute in onset. Commonly reported symptoms are worsening breathlessness, cough, increased sputum production and change in sputum colour. The change in these symptoms often necessitates a change in medication.

197
Q

What is the commonest tumour found in the lungs?

A
  • Secondary spread to lungs is very common - the commonest tumour in the lungs is metastatic
    • Multiple tumours in lungs suggests metastatic spread
    • Many primary tumours spread to lung
198
Q

Is IPF genetic?

A

No genetic factors consistently associated with sporadic cases of IPF

MUC5B gene polymorphisms is associated with familial cases of IPF

199
Q

What are the symptoms of obstructive sleep apnoea?

A

Snorer

Witnessed apnoeas

Disruptive sleep - nocturia, choking, dry mouth, sweating

Unrefreshed sleep

Daytime somnolence

Fatigue/low mood/poor concentration

200
Q

Describe the formation of asbestos bodies in mesotheliomas

A
  • Asbestos inhaled - macrophages try to digest, indigestible
  • Creates reactive oxygen species which cause iron deposits to be laid down
201
Q

What could the revelant points in a clinical history for idiopathic pulmonary fibrosis be?

A

Occupation

Past medical history

Travel

Environment

Drugs

Smoking

202
Q

Describe the prevalence of asthma

A
  • 15% adult population have/had
    • If not currently symptomatic but diagnosed in childhood - well controlled or not currently presenting
  • Life long - expensive
  • 80% easy to manage, 20% severe asthma - difficult to manage
  • 2014 - 198 deaths
203
Q

How is a PE treated medically?

A
  1. Parenteral therapy - short, quick acting, given in hospital
  • LMWH
  • Unfractionated heparin
  • Fondaparinux
  • Thrombolytic agents
  1. Oral medication (anticoagulation)
  • Mainstay is vitamin K antagonists - warfarin
  • Used much less frequently now - monitoring is difficult, many interactions
  • Novel agents with less bleeding risk are becoming available
  • Not suitable in all cases for example cancer
  • Difficulties with warfarin include time TTR (time in therapeutic range)
  • Drug/food interactions
  • Pharmacogenomic approach
204
Q

When should sputum samples be taken in COPD?

A

Send for analysis in acute exacerbations

205
Q

Define a tension pneumothorax

A

‘One way valve’ leads to increased intrapleural pressure

Air can move into the intrapleural space but not out

Build up of air in the intrapleural space

206
Q

Describe palliative care in lung cancer

A

Opiates to treat pain and breathlessness (important as lung cancer often diagnosed at an advanced stage in patients with other health problems e.g. COPD, IHD)

207
Q

How is obstructive sleep apnoea typically referred?

A
  • Often initiated by partner or media coverage
  • GP
  • ENT
  • Pre-operative assessment for elective surgery
  • Post-operative presentation
  • Weight management clinics
  • Diabetes clinic
  • Neurology
208
Q

What is the mechanism of action of methylxanthines (aminophylline/theophylline)?

A
  • Non-selective inhibition of phosphodiesterases –> increased intracellular cAMP –> bronchial smooth muscle relaxation
  • Immunomodulatory action - improved mucociliary clearance and anti-inflammatory effect (inhibits synthesis of leukotrienes and TNF alpha)
209
Q

How can lung function be measured and in which settings?

A
  • At home
    • Peak flow
    • Oximetry (patients often buy)
  • At the GP
    • Spirometry (quality varies)
    • Oximetry
  • In a specialist lab
    • Spirometry
    • Transfer factor
    • Lung volumes
    • Blood gases
    • Bronchial provocation testing
    • Respiratory muscle function
    • Exercise testing
210
Q

Describe the infection caused by pneumocystic jiroveci

A
  • Common environmental fungus
  • No pathology in immunocompetent
  • Pneumonia
    • Fever
    • Cough
    • Shortness of breath, rapid breathing
  • Treatment and prophylaxis
    • Trimethoprim-sulfamethoxazole
211
Q

Which radiological features would support a diagnostic of idiopathic pulmonary fibrosis?

A
  • Radiology - changes predominantly at lung bases
  • CXR - ground glass changes→ irregular reticulonodular shadowing → honeycombing
  • High resolution CT Chest
    • Subpleural reticular abnormalities
    • Honeycombing - thick-walled cysts 0.5 - 2 cm in diameter in respiratory and terminal bronchioles
    • Traction bronchiectasis – scar tissue pulling bronchiole wider, thickened

Ground glass changes - hazy areas of increased attenuation in the lung with preserved bronchial and vascular

212
Q

How is a chest drain inserted?

A
  • Aseptic technique
  • Local anaesthetic - can be painful (pleural highly innervated)
  • If pneumothorax should be lying back with hand above head, expose ‘triangle of safety’
  • Use big introducer needle with syringe on end, head air escaping as enter the intrapleural space
  • Feed guide wire in, make incision to make hole bigger
  • Use dilator to make space bigger to insert drain into
  • Chest drain fed over guide wire, remove guide wire
  • Attach 3 way trap + underwater seal
213
Q

Describe the key histological features of UIP

A

Macroscopically

  • Pleural surfaces of the lung are “cobblestoned”
  • Fibrotic areas of lung - firm rubbery and white
  • Disease mainly basal and subpleural, with thickening of the interlobular septae

Histology

  • Patchy interstitial fibrosis, varies in intensity and age (temporal heterogeneity)
  • Fibroblastic foci in early fibrosis - areas of fibroblastic/myofibrobalastic proliferation - become less cellular as disease progresses and collagen deposited
214
Q

Define cor pulmonale

A

Cor pulmonale – pumping against high resistance due to fibrosis, pre-load in R heart increased, R heart hypertrophy then failure

215
Q

What are the causes of a pneumothorax?

A
  • Can be traumatic, iatrogenic or spontaneous
    • Traumatic - stabbing, fractured rib
    • Iatrogenic - CT guided lung biopsy, TBLB (transbronchial lung biopsy), pleural aspiration
    • Spontaneous -
      • Primary - young patient, no underlying lung disease
      • Secondary - underlying lung disease (e.g. COPD, cystic fibrosis)
216
Q

What other causes of masses in the lungs can be mistaken for cancer?

A

TB

  • Granulomatous - creamy, necrotic encapsulated mass
  • Necrosis
  • Multinucleated giant cells
  • Ziehl-Neelson staining
217
Q

List the causes of drug-induced ILD

A
  • Antibiotics - nitrofurantoin
  • Disease-modifying antirheumatic drugs - methotrexate, sulphasalazine, gold, pencillinamine, lefluonamide, etanercept
  • Cardiovascular agents - amiodarone, ACE-inhibitors, statins
  • Chemotherapeutic agents - bleomycin, cyclophosphamide
  • Ilicit drugs - heroin, methadone, talc
  • Miscellaneous - oxygen, radiation, aspirin, interferons
218
Q

What are the pitfalls of oximetry?

A

Depends on adequate perfusion (shock, cardiac failure)

Does NOT measure carbon dioxide, so no measurement of ventilation

False reassurance in patient on oxygen with normal saturations (acute asthma, COPD, hypoventilation)

219
Q

How is sarcoidosis diagnosed?

A
  • Chest X-ray
  • Pathology
220
Q

Describe the side effects associated with methylxanthines

A

GI upset, palpitations, tachycardia/arrhythmias, headache, insomnia, hypokalaemia

221
Q

Describe the pharmacokinetics/pharmacodynamics of beta 2 agonists

A
  • Short acting - salbutamol, terbutaline (elimination half life 3-5 hours)
  • Long acting - salmeterol, formoterol, vilanterol, indacaterol
  • Salbutamol can be given via inhaled, nebulised, oral, intravenous routes
  • Inhalation route preferable/nebulised if severe
222
Q

How are high risk PE patients immediately managed?

A
  • Reperfusion treatment
    • Systemic/catheter directed thrombolysis
  • Haemodynamic support
    • Inotropic support e.g. ECMO
223
Q

Why should ECG/echocardiography be done in COPD patients?

A
  • To assess cardiac status if has clinical features of cor pulmonale
    • Enlargement of the right side of the heart due to disease of the lungs or pulmonary vessels
224
Q

What is the mechanism of action of anti-muscarinics?

A
  • Antagonist of cholinergic M1 and M3 (muscarinic) receptors in the lung, countering the parasympathetic direct broncho-constriction of muscarinic receptor activation, which is coupled to Gq G-proteins and hence to phospholipase P, IP3 production and intracellular Ca
  • On vasculature, M3 activation increases NO production, causing vasodilation
225
Q

What is the difference between a transudative and exudative pleural effusion? How are they distinguished?

A
  • Different causes in transudative vs exudative pleural effusion
    • Transudate = pressure effect, fluid pushed out
    • Exudate = something added which disrupts fluid drainage
  • Light’s criteria
    • Fluid protein : serum protein >0.5
    • Fluid LDH : serum LDH >0.6
    • Fluid LDH >2/3 maximum serum normal
    • Any 1 of 3 = exudate
  • Always send paired samples
226
Q

What immediate treatment should be given in a life threatening asthma attack?

A

Oxygen 40-60% (maintain spO2 94-98%)

Salbutamol 5mg or terbutaline 10mg via an oxygen-driven nebuliser

Ipratropium bromide 0.5mg via an oxygen-driven nebuliser

Prednisolone tablets 40-50mg or IV hydrocortisone 100mg or both if very ill

No sedatives of any kind

Chest radiography only if pneumothorax or consolidation suspected

227
Q

Describe the subtypes of non-small cell carcinoma

A

Squamous cell (40-60%) - closely linked to smoking history, keratinization and/or intercellular bridges on histology, central airways, high frequency of p53 mutations

Adenocarcinoma (10 -20%) - glandular differentiation or mucin production, most common form in women and non-smokers, more peripherally located, TTF-1 positive, if EGFR mutations present may benefit from treatment with EGFR inhibitors

Large cell (5-15%) - undifferentiated epithelial tumour

228
Q

How is asthma treated?

A

Target pathology with specific treatments:

  • Established therapies
    • Anti-IgE biological therapy - type 1 allergies driven by IgE, block pathways
    • Corticosteroids (inhaled - bad to swallow)
    • Anti-leukotriene receptor drugs
    • Bronchodilators - relax smooth muscle
  • New Therapies
    • Immunotherapy
    • Biological therapies - TNF, IL-5, IL-13
      • Anti-TNF tried but doesn’t work - get a bit better then get cancer
      • IL-5/12 very effective - injectable monthly
    • Thermoplasty - heat airway
      • Gets rid of smooth muscle bulk - deinnervates
229
Q

What are the main risk factors for the development of lung cancer?

A

Smoking in 85%

Passive smoking

Occupation asbestos

Silica and nickel exposure

Pulmonary fibrosis

230
Q

Define pneumothorax

A

Air within the pleural cavity

231
Q

Describe the inflammatory process in COPD compared with asthma

A
  • Asthma sensitising agent
    • Asthmatic airway inflammation - CD4+, T lymphocytes, eosinophils
    • Completely reversible
  • COPD noxious agent
    • COPD airway inflammation - CD8+, T lymphocytes, macrophages, neutrophils
    • Irreversible
232
Q

Describe transcutaneous oxygen saturation and carbon dioxide assessment

A

Home or inpatient

Shows periodic dips in oxygen and peaks in CO2 when not breathing properly

233
Q

How does a PE typically present?

A

Most to least common clinical characteristics:

  • Dyspnoea
  • Pleuritic chest pain
  • Cough
  • Substernal chest pain
  • Fever
  • Haemoptysis
  • Syncope
  • Unilateral leg pain
  • Signs of DVT (unilateral extremity swelling)
234
Q

Describe the pathogenesis of IPF

A
  • “Repeated cycles” of epithelial activation/injury by some unidentified agent
    • Abnormal activation of epithelial cells leads to a dysregulated repair process
  • Abnormal epithelial repair at site of injury/inflammation leads to the formation of the fibroblastic foci
  • Inflammatory pathways also promote fibrosis
235
Q

Describe the appearance of a pneumonectomy 6 weeks post-op

A

Fluid fills the empty hemithorax - white

236
Q

Describe clinical risk stratification in PEs

A
  • Used to determine risk of mortality within 30 days post-PE
  • Early mortality risk high
    • Shock or hypotension
    • PESI class II-V or sPESI > 1 (pulmonary embolism severity index)
    • Signs of RV dysfunction on imaging test
    • Cardiac laboratory biomarkers
  • Intermediate-high early mortality risk
    • No shock or hypotension
    • PESI class III-IV or sPESI > 1
    • Signs of RV dysfunction on imaging
    • Cardiac laboratory biomarkers
  • Intermediate-low early mortality risk
    • No shock or hypotension
    • PESI class III-IV or sPESI > 1
    • One (or none) of signs of RV dysfunction on imaging or cardiac laboratory biomarkers positive
  • Low early mortality risk
    • No shock or hypotension
    • Not PESI class III-IV or sPESI >1
    • Assessment of RV function/cardiac laboratory biomarkers optional, if assessed both negative
237
Q

What comprises the clinical syndrome of COPD?

A
  1. Chronic Bronchitis:
  • The production of sputum on most days for at least 3 months in 2 years (when other causes of chronic cough have been excluded)
  • Narrowing of airways due to inflammation, lack of support around airways
  1. Emphysema:
    * Abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles
238
Q

Describe spirometry in restrictive lung disease

A
  • Time/volume plot
    • FEV1 and FVC both reduced in proportion
    • FEV1/FVC ratio >70%
  • Flow volume loop
    • Normal shape but smaller - reduced capacity of lungs
239
Q

What are the clinical consequences of bronchial disease?

A
  • Medium-small airways flaccid walls
    • Not supported by cartilage
    • Expiratory phase narrowing - wheeze
    • Muco-ciliary clearance impairment - sputum
  • Characteristic flow-volume loops
  • CXR - unhelpful (except for hyperinflation)
240
Q

Describe the shape of a flow/volume loop

A
  • Positive = expiration (initially effort dependent and rapid then passive effort independent)
    • Tails off due to airway resistance meaning the pressure of airflow decreases from alveoli –> mouth
  • Negative = inspiration
241
Q

How does distant spread of lung cancer occur?

A
  • Haematogenous
    • Common due to invasion of pulmonary veins
    • Liver, bone, brain, adrenal
  • Lymphatic
    • Hilar lymph nodes –> cervical lymph nodes
242
Q

Describe the pathophysiology of a primary pneumothorax

A
  • Development of subpleural blebs/bullae at lung apex
    • Shape of lungs and chest cavity in tall thin people mean they are more prone to these defects
  • Possible additional diffuse, microscopic emphysema below the surface of the visceral pleura
  • Spontaneous rupture leads to tear in visceral pleura
  • Air flows from airways to pleural space (pressure gradient)
  • Elastic lung then collapses
243
Q

What are the pitfalls of spirometry testing?

A

Need appropriately trained technician

Effort and technique dependent

Patient frailty

Pain, patient too unwell

244
Q

What treatments are available for idiopathic pulmonary fibrosis?

A

Pirfenidone

  • Approved for use in IPF (patients with FVC 50 - 80 % predicted)
  • Antifibrotic and anti-inflammatory effects; slows lung function decline
  • Mechanism of action unclear but likely to suppress fibroblast proliferation, so reducing the production of fibrosis-associated proteins and cytokines
  • Reduces pO2 max capacity in lung

Nintedanib

  • Intracellular inhibitor of multiple tyrosine kinases
  • Slows lung function decline in recent trial.

Steroids and immunosuppressants are not routinely recommended for treatment of IPF

  • Steroids not effective in most cases
  • Azathioprine may worsen prognosis when used with prednisolone

No longer advised to give the “triple therapy” of steroids + azathioprine + N-acetylcysteine

Trial of steroids may be considered if there is felt to be a possibility of an inflammatory component in some cases e.g. younger women with a possible underlying connective tissue disease.

N-acetyl cysteine

  • Does not improve survival or slow lung function decline
  • Is a mucolytic, so might be tried if a patient has cough or sputum, as has little toxicity

For many patients, especially if over 80 years old therapy for IPF is essentially aimed at symptom control

  • Long term oxygen therapy – home oxygen eventually (stop smoking)
  • Diuretics for fluid retention if develop cor-pulmonale
  • Antibiotics to treat infection
  • Lung transplantation in younger patients (age < 65)
245
Q

How is a pneumothorax managed?

A
  • Size is less important than symptoms
    • Small pneumothorax very symptomatic if bad COPD
    • Can tolerate complete lung collapse very well if healthy
  • 2cm rim of air at axilla = 50% lung volume
    • <2cm defined as small, >2cm large
  • Options for management
    • Observation (serial CXR) if small or not very symptomatic - can be as outpatient
    • Aspiration (small bore catheter 2nd intercostal space midclavicular line - aspirate air with syringe/3 wat tap) - up to 2.5L
    • Intercostal drain with underwater seal
  • Good guideline developed by British Thoracic Society
246
Q

Describe the pathogenesis of the acute illness associated with extrinsic allergic alveolitis

A
  • Antibodies from past exposure collect in lungs - complexes of proteins develop when antigen-antibody binding occurs
  • Infarction of capillaries in lungs
  • Inflammatory fluid fills lungs
  • Wall thickened with inflammation

Immune complex disease = acute inflammation –> neutrophils –> consolidation

247
Q

How is crytococcus neoformans treated?

A
  • 2 weeks of IV amphotericin B for meningitis
    • V unpleasant, toxic
  • Fluconazole or flucytosine (non-CNS)
    • Doesn’t penetrate CNS well enough for meningitis treatment on its own but less toxic
    • Can give combination therapy
248
Q

When is a mandibular advancement device used in OSAS treatment?

A

Mild-moderate OSAS unable to tolerate CPAP

Needs good dentition

249
Q

If a chest drain fails to work, what are the further management options for a pneumothorax?

A
  • VATS - video assisted thoracic surgery
    • Considered if not resolved in 5 days
  • Can staple blebs
  • Talc pleurodesis - causes inflammatory reaction and pleural adhesion, highly effective
  • Pleural abrasion/stripping
  • Surgical pleurodesis considered if 2nd pneumothorax on same side, first contralateral event
  • Professional considerations e.g. airline pilots, scuba divers
    • After spontaneous pneumothorax should wait 7 days before flying, should not dive again
250
Q

List causes and triggers of asthma

A
  • Environmental exposure to allergen - house dust mite (dermatophagoides pteronyssinus), gross pollen, domestic pets
  • Occupation sensitisers
    • Non-IgE related - isocyanates, colophony fumes
    • IgE related - latex, animal allergens
  • Viral infections - rhinovirus, parainfluenza virus, RSV
  • Atmospheric pollution - sulphur dioxide, ozone, particulates
  • Drugs - NSAID, beta-blockers
  • Irritant drugs, vapours and fumes - perfume cigarette smoke
  • Exercise
  • Cold air
  • Emotion
  • Genetic factors - IL-4, IL-13 pathways, ADAM 33, others
251
Q

Generally, how can spirometry be interpreted?

A
  • First look at FEV1:FVC ratio
    • If <70% - obstruction
    • If obstructed, look at %predicted FEV1 (severity) and any reversibility (COPD vs asthma)
  • If FEV1/FEV ratio normal, look at % predicted FVC (if low, suggests restrictive abnormality)
  • Can also get mixed picture e.g. obesity and COPD - obstructive and restrictive
252
Q

Describe the appearance of a R tension pneumothorax on X-ray

A

Mediastinum shifted to left, collapse of R lung

253
Q

What pathological features are seen in lung biopsies in sarcoidosis?

A
  • Macrophages try to phagocytose something they can’t digest and present so they become activated and can form giant cells (coalescence of cells with multiple nuclei) in the alveolar tissue (not in air spaces)
  • Giant cells can have some calcification, are multinucleated
  • Asteroid body - cytokeratin, specific structure in giant cells
254
Q

What is the effect of E-cigarette smoking/vaping? How does this compare to smoking cigarettes?

A
  • No evidence to suggest they cause COPD
  • Do have potential to induce inflammation and hypersensitivity pneumonitis, and have effects on blood pressure
  • UK advice - reasonable alternative to cigarette smoking, harm reduction but not harm free
255
Q

Define a pleural effusion

A
  • Abnormal volume of fluid in the pleural space
    • Normal is 15ml per hemithorax, anything more is abnormal
    • >300ml before seen on X-ray
256
Q

Compare the clinical features of COPD with asthma

A
  • COPD
    • Nearly all smoker/ex-smoker
    • Rarely symptoms under age 35
    • Common to have chronic productive cough
    • Breathlessness persistent and progressive
    • Uncommon to have night time waking with breathlessness and/or wheeze
    • Uncommon to have significant diurnal or day-to-day variability of symptoms (progressively worsening)
  • Asthma
    • Possibly smoker/ex-smoker
    • Often symptoms under age 35
    • Chronic productive cough uncommon
    • Variable breathlessness
    • Common night time waking with breathlessness and/or wheeze
    • Common significant diurnal or day-to-day variability of symptoms
  • If have >400ml reversibility on spirometry, asthma more likely
257
Q

Define pulmonary fibrosis

A
  • Scarring of lung tissue
  • Lots of possible causes (including sarcoidosis + EAA)
  • Idiopathic pulmonary fibrosis (IPF) is the clinical manifestation or equivalent of the pathological diagnosis of usual interstitial pneumonia (UIP)
  • It is a difficult diagnosis to make in some cases and the whole picture has to add up - radiology, pathology and clinical picture
258
Q

Which values are directly measurable using spirometry? Which values are not?

A
  • Directly measurable
    • Vital capacity
    • Inspiratory capacity
    • Inspiratory reserve volume (difference between tidal inspiration and full inspiration)
    • Tidal volume (volume in and out of lungs in quiet breathing) - 500ml normally
    • Expiratory reserve volume (difference between tidal expiration and full expiration)
  • Indirectly measureable
    • Residual volume - left over air in lung after full expiration, prevents collapse of lung
    • Total lung capacity
    • Functional residual capacity
259
Q

Describe endobronchial treatments of lung cancers

A

Laser, stents to deal with tumour obstructing large airways

260
Q

How should oxygen therapy be administered in hypoxaemic COPD patients?

A
  • Give controlled oxygen - smaller amounts more controlled
  • Aim for lower pO2 in COPD - 88-92% to stop patients developing hypercapnia
  • When oxygen is given, should expect PaO2 to be roughly 10-15 units below inspired O2 - i.e. for 28% O2 should expect levels of 13-18kPa
261
Q

How does the site of lung cancers vary with histology types?

A

Central tumours arise in and around hilus of the lung and are usually squamous or small cell carcinomas

Peripheral tumours are predominantly adenocarcinomas

262
Q

Which inflammatory cells and mediators are involved in COPD?

A
  • Chemoattractant substances in cigarette smoke attract inflammatory cells to the alveoli
  • Cell types
    • Macrophages, CD8 and CD4 T lymphocytes, neutrophils
  • Inflammatory mediators
    • TNF, IL8 and other chemokines
    • Neutrophil elastase, proteinase 3, cathepsin G (from activated neutrophils)
    • Elastase and MMPs (from macrophages)
    • Reactive oxygen species
  • Airway inflammation persists after smoking ceased
263
Q

Who is affected by dermatophyte fungal infections?

A

Healthy and immunocompromised people

264
Q

What are the consequences of a tension pneumothorax?

A

Venous return impaired, cardiac output and blood pressure fall

PEA (pulseless electrical activity) arrest without intervention

265
Q

What the effect of the recurrent laryngeal nerve paralysis?

A

Controls muscles of larynx, long root

Hoarseness - 80% of patients

Usually L side affected

266
Q

How is a complex parapneumonic effusion diagnosed?

A
  • pH <7.2
  • LDH >1000
  • Glucose <2.2
  • Loculated on ultrasound
267
Q

What is the aim of PE follow up clinics?

A
  • Confirm diagnosis
  • Assess precipitating factor
  • Duration of anticoagulation
  • Selected thrombophilia testing
  • Selected malignancy screening
  • CTEPH screening - 4%
    • Pulmonary hypertension persists
    • Clots don’t resolve, scar tissue
  • Counselling, for example family (e.g. COCP)
268
Q

In which patients should a diagnosis of COPD be considered?

A

Consider diagnosis of COPD in those over 35 y/o, smokers or ex-smokers, with any of:

  • Exertional breathlessness
  • Regular sputum production
  • Wheeze
  • Chronic cough
  • Frequent winter ‘bronchitis’
269
Q

Define mesothelioma

A
  • Primary pleural tumour (also occurs in peritoneum, pericardium and tunica vaginalis testis)
  • Almost always due to asbestos exposure
    • High incidence in GGC due to Clyde shipbuilding industry
  • Very long lag period before disease develops
  • Tumour has either an epithelial or sarcomatoid appearance or a mixture of both (biphasic)
270
Q

What is the most common primary pleural malignancy?

A
  • Mesothelioma
    • Highest incidence worldwide, 200 cases per year in Scotland
    • Poor prognosis (1 year), treatment supportive
271
Q

Describe airway remodelling in chronic asthma

A
  • Leads to irreversible airflow obstruction
    • Overall thickening of the airway wall
    • Epithelium - loss of ciliated columnar cells, increased number and activity of mucous secreting goblet cells
    • Epithelial basement membrane - sub-basement membrane fibrosis due to deposition of collagen and proteoglycans
    • Smooth muscle - hypertrophy and/or hyperplasia of smooth muscle layer
  • In the inflammation of chronic asthma - Th1 cells also activated, TNF alpha production
272
Q

What are the triggers for extrinsic allergic alveolitis?

A
  • Bird dander
    • Pigeon fancier’s lung, budgie lung
  • Mushroom worker’s lung
  • Farmer’s lung (fungal spores)
  • Aspergillus lung
  • Cheese workers
  • Wheat weevil
  • Mollusc shell workers
  • Malt worker’s lung
  • Humidifier lung

Each with an antibody that can be measured in serum e.g. avian precipitatans

273
Q

Describe the stages of COPD and their classification

A

Post-bronchodilator FEV1 % predicted

Stage 1 (mild) = 80 %

Stage 2 (moderate) = 50 - 79 %

Stage 3 (severe) = 30 - 49 %

Stage 4 (very severe)** = < 30

Or FEV1 <50% with respiratory failure

FEV1% doesn’t always correlate to loss function

274
Q

What should the FEV1:FVC ratio be?

A

Normal = >70%

275
Q

Describe spontaneous pneumothorax incidence

A

16.7/100,000 (men), 5.8/100,000 (women)

Mortality rate very low (1/million/year)

Recurrence rate 40-50% after first episode

276
Q

How should a history be taken from a patient with a suspected pleural effusion?

A
  • Associated symptoms
  • Red flag symptoms - weight loss, haemoptysis
  • Onset - fall, change in medications (e.g. Warfarin), travel?
  • Past medical history
    • Previous cancer
    • TB - travel
  • Smoking history
  • Occupation history
277
Q

Describe the pathogenesis of pulmonary fibrosis

A
  • Age, genetic factors, environmental factors, nature of injury –> repetitive alveolar epithelial injury
    • oxidative stress, profibrotic cytokines, chemokines, eicosnoid imbalance, impaired fibrinolysis, TIMPs-MMPs imbalance = altered alveolar microenvironment
  • Dysregulated repair, loss of epithelial cells, accumulation of mesenchymal cells
  • = fibrosis
278
Q

How is malignant pleural effusion managed?

A
  • Management is symptom driven, patient centered
    • Chest drain +/- talc pleurodesis (80% success)
    • Indwelling pleural catheter
    • Patient choice unless talc failed/lung trapped
279
Q

What can be detected by sleep studies?

A
  • Apnoea
    • The cessation, or near cessation of airflow
    • 4% oxygen desaturation, lasting >10 seconds
  • Hypopnoea
    • Hypopnoea is a reduction of airflow to a degree insufficient to meet the criteria for an apnoea
  • Respiratory effort related arousals
    • Arousals associated with a change in airflow that does not meet the criteria for apnoea or hypopnoea
280
Q

What causes COPD?

A
  • The disease is commonly cause by smoking
    • Only 15-20% of smokers get COPD
    • Can also be caused by environmental pollution, burning of biomass fuels, occupational dusts, alpha 1 anti-trypsin deficiency (genetic)
281
Q

How is the risk of PTE recurrence estimated?

A
  • Low (<3% per year)
    • Major transient or reversible factors associated with >10 fold increased risk for the index VTE event (compared to those without risk factor) e.g. surgery with general anaesthesia for >30 mins, confined to bed in hospital for >7 day due to acute illness or acute exacerbation of chronic illness, trauma with fractures
  • Intermediated (3-8% per year)
    • Transient or reversible factors associated with <10-fold increased risk for first VTE e.g. minor surgery (general anaesthesia for <30 mins), admission to hospital for <3 days with an acute illness, oestrogen therapy/contraception, pregnancy or post-partum, leg injury (without fracture) associated with reduced mobility for >3 days, long haul flight
    • Non-malignant persistent risk factors - inflammatory bowel disease, active autoimmune disease, no identifiable risk factor
  • High (>8% per year) - active cancer, one or more previous episodes of VTE in the absence of a major transient or reversible factor, antiphospholipid antibody syndrome
282
Q

Describe the use and mechanism of action of mepolizumab

A
  • Anti-IL5 monoclonal antibody
  • Reduces circulating eosinophils
  • Severe refractory eosinophilic asthma
  • Subcutaneous injection every 4 weeks
  • Headaches commonly reported
283
Q

How are small cell carcinomas staged?

A

Staged as limited or extensive disease

  • Limited - confined to one hemithorax and the ipsilateral supraclavicular fossa (30%)
  • Extensive disease - all other patients (70%)
  • Without treatment - survival 2-3 months in limited disease, 4 weeks in extensive disease
  • With treatment - limited disease survival 15-20 months, 10-13% 5 year survival, extensive disease 8-13 months median survival, 1-2% survive 5 years
284
Q

Describe the use and mechanism of action of omalizumab

A
  • Monoclonal anti-IgE antibody
  • Severe persistent allergic asthma
  • Subcutaneous injection every 4 weeks
  • Dose based on IgE and weight
  • Risk of severe hypersensitivity reaction
285
Q

Describe the epidemiology of OSA/OSAS

A

25,000,000 snorers in UK (40% population)

5% of UK adults thought to have undiagnosed OSA (2.5 million)

250,000 men have OSA in UK

Men 2-3 > premenopausal females

Average age of presentation 40-50 y/o

Incidence increasing with obesity epidemic

286
Q

Define asthma

A
  • Chronic inflammatory condition of the airways, causes recurrent episodes of wheezing, breathlessness, chest tightness and cough - particularly at night and/or early morning
  • Symptoms usually associated with widespread but variable bronchoconstriction and airflow limitation that is at least partly reversible, either spontaneously or with treatment
  • Airflow limitation usually reversible in early disease, but may have an irreversible component in longstanding disease

Key Features:

  • Increased airways hyper-responsiveness to a variety of stimuli resulting in episodic bronchoconstriction
  • Inflammation of the bronchial walls
  • Increased mucous secretion
287
Q

How is malignant pleural effusion diagnosed?

A
  • Aspiration
  • Often need tissue for genetics
288
Q

How has lung cancer incidence been influenced by smoking rates?

A
  • In men lung cancer peaked in 1970s then decreased by around 45% reflecting reduction in smoking since 1940s
  • In women lung cancer rates have increased by 64% reflecting increased smoking rates in women between WW2 and the 1970s
289
Q

List the maintenance drugs used in asthma

A
  • Leukotriene receptor antagonists (Montelukast and Zafirlukast)
  • Omalizumab
  • Mepolizumab
290
Q

How does the incidence of lung cancer in Scotland compare to the UK as a whole? Why is this?

A
  • In the UK incidence rates for lung cancer highest in Scotland
  • Scotland is the only UK nation where lung cancer remains the overall most common cancer
  • Lung cancer incidence is 1/3 higher in GGC compared with Scotland as a whole
  • Reflects the high smoking prevalence
291
Q

What can be seen on ultrasound which can aid diagnosis of pleural effusion?

A

Pleural fluid more grey = exudate (due to high protein content)

292
Q

What is the difference between hyperreactivity and allergy?

A

E.g. Rhinitis

  • Can occur due to hyperreactivity to a stimulus e.g. spicy food, cold air - most people will react if extreme but varying tolerance at low levels
    • Dose dependent - the more you are exposed the more likely you are to react
  • Can occur due to allergy to a stimulus e.g. cats - if not allergic will never react, if allergic will always react
    • Not dose dependent - if allergic to cats will react to one cat or 3 cats
293
Q

What are the contraindications for amoxicillin prescription?

A

Predominantly renally excreted - caution prescribing in renal impairment

294
Q

What subsequent management should be done in a patient following a life threatening asthma attack who is improving?

A

If patient is improving continue

  • 40-60% oxygen
  • Prednisolone 40-50mg daily (should continue for at least 5 days or until recovery)
  • Nebulised B2 agonist and ipratropium 4-6 hourly
295
Q

How can alpha 1 antitrypsin deficiency be managed?

A

Can give replacement - not a wide-spread therapy, quitting smoking more effective

296
Q

Describe the known and unknown causes of interstitial lung disease

A
  • Known
    • Occupational - asbestos, beryllium
    • Environmental - hypersensitivity pneumonitis (birds, mould etc)
    • Medication
    • Connective tissue disease - scleroderma, polymyositis, rheumatoid arthritis
  • Unknown
    • Idiopathic interstitial pneumonia - IPF, NSIP, other
    • Granulomatous - sarcoidosis
    • Other - vasculitis, eosinophilic
297
Q

What is the mechanism of action of corticosteroids?

A
  • Bind to activated glucocorticoid receptors to suppress multiple pro-inflammatory genes that are activated in asthmatic airways by reversing histone acetylation (promotes histone deacetylase 2)
  • Reduces number of inflammatory cells in airways and release of pro-inflammatory cytokines, reduces airway oedema and mucous secretion, allows beta 2 agonist to work better by freeing beta 2 receptors
298
Q

What are the symptomatic differences between central and peripheral lung cancers?

A
  • Central - bronchi and hila
    • Ulceration of bronchus - cough, haemoptysis
    • Bronchial obstruction - pneumonia, lung abscess, bronchiectasis, wheeze, shortness of breath
    • Build up of secretions - retention pneumonia, irritation (chronic cough)
  • Peripheral - out towards chest wall
    • May not have symptoms - have extra lung capacity
    • If involves chest wall may have chest wall pain
    • Pleural involvement - pain, effusion
    • Apical lung cancer
      • Compression of - sympathetic chain (Horner’s syndrome), T1 and T2 roots to brachial plexus (wasting of hand muscle, pain down arm)
299
Q

Describe limited vs full polysomnography

A
  • Limited polysomnography (limited sleep study)
    • 5 channel home study
    • Oxygen saturations
    • Heart rate
    • Flow
    • Thoracic and abdominal effort
    • Position
  • Full polysomnography
    • EEG - sleep staging
    • Video
    • Audio
    • Thoracic and abdominal bands
    • Position
    • Flow
    • Oxygen saturations
    • Limb leads
    • Snore

Advantages of Full PSG:

  • Correct patient
  • Accurate assessment of sleep efficiency
  • Sleep staging via EEG
  • Parasomnic activity - acting out dreams, sleep talking
  • Can diagnose other sleep disorders e.g. narcolepsy
300
Q

Why is PaCO2 normal in a life threatening asthma attack?

A

During an asthma exacerbation there is air trapping and ventilation/perfusion mismatch, resulting in hypoxemia. Initially compensation occurs and hyperventilation causes the PCO2 to decrease. When further air trapping leads to decreased lung compliance and increased work of breathing, the PCO2 will begin to increase. Thus, a “normal” pCO2 in a wheezing patient is a sign of a severe/life-threatening attack.

301
Q

In an acute COPD exacerbations, what do the following ABGs indicate?

H+ 37 nmol/l, PaCO2 5.7kPa, PaO2 18.1 kPa, Bic 29 mmol/l

(H+ 35 – 45, PaCO2 4 – 6 kPa, PaO2 12 – 14, HCO3 21 - 30)

A
  • Not acidotic, pCO2 normal, bicarbonate normal
  • pO2 high - recieving too much oxygen
    • Patients with COPD develop hypercapnia (CO2 retention, hypoventilation) when pO2 too high
302
Q

How is COPD diagnosed?

A

Spirometry:

Obstructive pattern - FEV1:FVC ratio <70% (both reduced)

303
Q

How can inhaled medication be stepped up in poorly controlled asthma?

A
  • Step-wise approach to asthma management in Adults (BTS SIGN Guideline 2019)
  • Drug treatment is directed at relieving smooth muscle spasm and reducing underlying airway inflammation - use of the lowest effective doses of convenient medications to minimise short-term and long-term side effects.

Short acting beta 2 agonist as required +

  1. Regular preventer - low dose inhaled corticosteroid (ICS)
  2. Initial add-on therapy - add inhaled LABA to low dose ICS (fixed fose or MMT)
  3. Additional controlled therapies - consider increasing ICS to medium dose or adding LTRA (if no response to LABA consider stopping LABA)
  4. Specialist therapies - refer patient for specialist case
304
Q

Describe spirometry in obstructive lung disease

A
  • Generally asthma or COPD
  • FEV1:FVC ratio <70%
  • Time/volume plot - much slower rising curve
  • Flow/volume loop
    • Loss of support holding airway open –> airway obstruction
    • Typical ‘church and steeple’ pattern - scooped out appearance of expiratory loop
    • Passive exhalation of air not occurring as efficiently
305
Q

How does a pleural effusion typically present?

A
  • Shortness of breath
  • Weight loss
  • Cough
  • Haemoptysis
  • Chest pain/pressure
  • Lethargy
  • Fever
306
Q

What are the possible side effects of doxycycline?

A
  • Many resistance mechanisms documented - efflux via ABC-transporters, ribosome protection proteins (RPPs) preventing tetracycline binding
  • Well absorbed orally
  • Avoid/caution in patients with hepatic impairment
  • Chelates calcium (avoid in young children and pregnancy)
    • Brown discolouration of teeth, abnormal bone development
307
Q

Describe genetic testing in lung adenocarcinomas

A

Adenocarcinomas now tested for genetic mutations, and if positive, specific treatments may be offered

  • EGFR mutations - erlotinib
  • ALK mutations - crizotinib
  • PD-L1 mutations - immunotherapy e.g. Nivolumab
  • ROS-1 mutations - crizotinib, increased senstivity to premetrexed
308
Q

What is aminophylline?

A

Aminophylline is a mixture of theophylline and ethylenediamine (ratio 2:1). This formulation improves solubility and is preferred for IV administration, also non-selective adenosine receptor antagonist.

309
Q

What complications can occur following PTE?

A

Most common to least common complications following PTE:

  • Reduced functional status
  • Persistent thrombi
  • Measurable limitations in cardiopulmonary function
  • CTEPH
  • Post-PE syndrome
310
Q

Describe the mechanism of action of azoles

A
  • Azoles are inhibitor of 14-methylsterol alpha-demethylase which produces ergosterol
  • Ergosterol is an essential component of the fungal plasma membrane
    • Sterols insert themselves into the lipid bilayer and are essential for its proper functioning and viscosity
  • Does not occur in animal or plant cells
  • Equivalent of cholesterol in yeast, fungi
  • Eradicate fungus without affecting human cells
  • Resistance to azoles emerging
311
Q

List the types of fungal infections

A
  1. Dermatophytes
  2. Systemic fungal infections
312
Q

Explain the physiological reason for the wheeze heard in asthmatics

A

When lungs working well airflow is linear - evenly straight down

Airflow partially interrupted by divisions in airways, which causes turbulence

Turbulence increased by narrowing of airways - air circulates round making high pitched noise –> wheeze

313
Q

Describe the benefit of smoking cessation in patients with COPD

A

For smokers who have already developed moderate obstruction, stopping smoking at the age of 45 can make the difference between a normal lifespan and premature death

If continue to smoke - disability and death occur more quickly

314
Q

What is the mechanism of action of beta 2 agonists?

A
  • Higher specificity for pulmonary beta 2 receptors vs. cardiac beta 1 receptors
  • Stimulate adenyl cyclase to increase intracellular cAMP –> relaxation of bronchial smooth muscle
315
Q

Describe the features of carcinoid tumours

A
  • Tumour of neuroendocrine cells
  • Central or peripheral
  • Classified as typical or atypical
  • Can metastasise but much better prognosis than other conventional lung cancers (5 year survival for typical 85-90%, atypical 5 year survival 50-75%)
  • Appearance
    • Polypoid projections in airways
    • Yellowish brown colour
316
Q

Describe the pathophysiology of a secondary pneumothorax

A
  • Inherent weakness in lung tissue e.g. emphysema
  • Increased airway pressure e.g. asthma, ventilated patient (high positive pressure)
  • Increased lung elasticity e.g. pulmonary fibrosis
  • Patient is generally much more symptomatic
    • Poor underlying lung function
  • Management more complex, prognosis less good
  • More likely to require intervention
317
Q

Explain the physiological basis for ‘pink puffers’ and ‘blue bloaters’ and what would be seen on examination of each

A

Pink Puffer

  • High respiratory drive, low PaO2, PaCO2, desaturates on exercise, type 1 respiratory failure
  • O/E - pursed lip breathing, use accessory muscles, wheeze, indrawing of intercostals, tachypnoea

Blue Bloater - loss of central sensitivity to CO2 and reliance on hypoxic drive to stimulate breathing

  • Low respiratory drive, low PaO2, high PaO2 right heart failure (oedema), type 2 respiratory failure
  • O/E - confusion, drowsiness, cyanosis, wheeze, hypoventilation, warm peripheries and bounding pulse, flapping tremor, peripheral oedema
318
Q

Describe the typical pathology seen in EAA

A

Bronchiolocentric pattern

Foamy macrophages in alveolar spaces - lung produces surfactant, washed out by staining process so looks foamy

Chronic interstitial inflammation

Organising pneumonia

319
Q

What are the indications for corticosteroids in respiratory disease?

A

Asthma - mainstay of asthma therapy

COPD with recurrent exacerbation

Exacerbations of asthma/COPD

320
Q

Give examples of combination inhalers

A

LABA/LAMA - usually once daily

E.g. Anoro Ellipta (umeclinidium/vilanterol)

LABA/ICS

E.g. Relvar Ellipta (fluticasone/vilanterol), seretide accuhaler/evohaler (fluticasone/salmeterol) - increases risk of pneumonia

321
Q

List the signs/symptoms of Cushing’s syndrome

A
  • Emotional disturbance
  • Enlarged sella turcica
  • Moon facies
  • Osteoporosis
  • Cardiac hypertrophy (hypertension)
  • Buffalo hump
  • Obesity
  • Adrenal tumour or hyperplasia
  • Thin, wrinkled skin
  • Abdominal striae
  • Amenorrhoea
  • Muscle weakness
  • Purpura
  • Skin ulcers (poor wound healing)
322
Q

What are the key clinical features of idiopathic pulmonary fibrosis?

A
  • Age of onset >50
  • Male>female
  • Progressive breathlessness, productive cough, cyanosis
  • Respiratory failure, cor pulmonale, pulmonary hypertension
  • Fine bilateral end-inspiratory crackles
  • Finger clubbing (2/3)
  • Usually a history of cigarette smoking
323
Q

Give examples of systemic fungal infections and their causative organisms

A
  • Fungal meningitis
    • Cryptococcus neoformans
  • Aspergillosis of the lungs
    • Aspergillus fumigatus
  • Pneumocystis pneumonia
    • Pneumocystis Jiroveci
324
Q

What systemic effects does alpha 1 antitrypsin deficiency have?

A

Can cause cirrhosis - proteases in liver

To avoid need to minimise alcohol intake/stop smoking

325
Q

Describe the risks of lung cancer associated with smoking

A
  • Smoking is the main avoidable risk for lung cancer - 72% of cases
  • Predisposes to lung cancer of all major histological types but link strongest for squamous and small cell
  • Smoking risks
    • <5% are life long non-smokers
    • 10-20 cig/day - 30x risk
    • 60cig/day - 60x risk
  • Stopping smoking reduces risk but depends on number of years of smoking and takes time

Medicine Year 3 (15 decks)

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