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Phase 3 > Week 8 - Respiratory > Flashcards

Week 8 - Respiratory Flashcards

1
Q

What is spirometry?

A

Forced expiratory manoeuvre from total lung capacity followed by a full inspiration .

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2
Q

How might you instruct a patient who is doing a spirometry test?

A

“Take a deep breath in as far as you can then blow out as hard as you can for as long as you can and then take a deep breath all the way in.”

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3
Q

What are some of the pitfalls of spirometry?

A

Result depends on patient technique and effort, requires a trained technician, patients may be too ill or in pain to do the test.

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4
Q

What would a normal FEV1/FVC ratio be?

A

> 70%

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5
Q

What type of lung disease is asthma and COPD? What would you expect the FEV1/FVC ratio to be?

A

Obstructive lung disease

<70%

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6
Q

Severity of COPD is stratified by % of predicted FEV1. What % corresponds to mild, moderate, severe and very severe COPD?

A

Mild >80%
Moderate 50-80%

Severe 30-50%

Very severe <30%

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7
Q

How is reversibility testing done? What result would be suggestive of asthma?

A

Nebulised or inhaled salbutamol given, spirometry done before and 15 minutes after salbutamol.
15% and 400ml reversibility in FEV1 suggestive of asthma.

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8
Q

What effect would a restrictive lung disease have on the FVC and the FEV1? What would the expected FVC/FEV1 ratio be?

A

FEV1 and FVC reduced.

FEV1/FVC ratio >70%.

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9
Q

What are some of the causes of a restrictive spirometry?

A

Interstitial lung disease, kyphoscoliosis, previous pneumonectomy, neuromuscular disease, obesity, poor effort/technique.

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10
Q

How is transfer factor measured? What conditions is it reduced in?

A

Single breath of very small concentration of carbon monoxide inhaled, then the concentration in expired gas measured to derive uptake in the lungs. (CO has a very high affinity for haemoglobin).

Emphysema

Anaemia

Interstitial lung disease

Pulmonary vascular disease.

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11
Q

What effect does restrictive and obstructive lung diseases have on lung volumes?

A

Restrictive - lung volume reduced

Obstructive - lung volume can increase.

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12
Q

What equation allows you to measure the alveolar oxygen partial pressure?

A

PAO2 = FiO2 - (1.25 x PaCO2)

FiO2 - inspired oxygen concentration
PaCO2 - arterial CO2 concentration

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13
Q

What is the difference in arterial gas results in type 1 and type 2 respiratory failure?

A

Type 1 - low oxygen without increased CO2

Type 2 - low oxygen and elevated CO2.

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14
Q

Describe COPD, including its aetiology.

A

COPD is a disease characterised by airflow obstruction which is normally progressive and not fully reversible.
Commonly caused by smoking but also pollution, occupational dusts and alpha 1 antitrypsin deficiency.

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15
Q

What are some of the effects of cigarette smoking on the respiratory system?

A
  • cilial motility reduced
  • airway inflammation
  • goblet cell and mucous hypertrophy
  • increased protease activity
  • oxidative stress
  • squamous metaplasia - higher risk of lung cancer.
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16
Q

What is the function of alpha 1 anti-trypsin and how does it contribute to lung disease?

A

There to counterbalance destructive enzymes in the lung, if you are deficient you get destruction of lung tissue and COPD much earlier.

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17
Q

What are the two clinical syndromes of COPD? Describe them.

A

Chronic bronchitis - production of sputum on most days for 3 months for at least 2 years in a row.
Emphysema - abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles due to destruction of lung parenchyma.

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18
Q

Chemoattractant substances in cigarette smoke attract inflammatory cells to the alveoli. What cells types are involved? What inflammatory mediators are involved?

A

Macrophages, T lymphocytes, neutrophils.

TNF, IL-8, MMPs, reactive oxygen species.

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19
Q

What is the difference in pathology and aetiology between centri-acinar and pan-acinar emphysema?

A

Centri-acinar - damage around the respiratory bronchioles, more in the upper lobes. Caused by smoking and inhaling fumes.
Pan-acinar - uniformly damaged from the level of the terminal bronchiole distally, associated with alpha 1 antitrypsin deficiency.

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20
Q

What treatment is available for COPD?

A

Inhaled bronchodilators - i.e. LAMAs, LABAs (salmeterol), SAMAs, SABAs (i.e salbutamol).
Inhaled corticosteroids - budesonide, fluticasone.
Oxygen therapy, mucolytics, nebulised therapy.

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21
Q

What percentage of oxygen would you aim to give acute COPD patients? What oxygen saturation are you aiming for? What is the reason for this?

A

24-28% oxygen
88-92% sats

Too much oxygen and too high sats in COPD patients can reduce respiratory drive and lead to worsening hypercapnia.

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22
Q

Define allergy.

A

Allergy is an immune system mediated intolerance.

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23
Q

How would you define asthma clinically?

A

Appropriate symptoms with signs which is episodic, triggered and variable with some response to asthma therapies.

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24
Q

What is asthma?

A

Inflammation of the airway causing reversible airflow obstruction brought on by a trigger which may be allergic.

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25
Q

Asthma leads to airway remodelling in the long term. What changes may occur in the airway of an asthmatic?

A

Smooth muscle hypertrophy, angiogenesis, epithelial cell damage, fibrosis and scarring.

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26
Q

What cytokines are increased in asthmatics? Which inflammatory cells are activated as a result?

A

IL-5, IL-13, TNF-alpha

Mast cells, lymphocytes, macrophages, eosinophils, basophils.

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27
Q

What is the clinical presentation of extrinsic allergic alveolitis (EAA)? What are some of the triggers?

A

Symptoms of wheeze, cough, fever, chills, headache, myalgia, malaise, fatigue 4-6 hours after exposure to a trigger.
Pigeon dander, aspergillus.

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28
Q

What would be the outcome of chronic EAA? What causes the damage?

A

Fibrosis and emphysema in the lung.

Immune complexes activating complement in the lung which causes tissue damage.

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29
Q

Which type of hypersensitivity is EAA? What mediators are involved?

A

Type 3

IL-12 and interferon gamma.

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30
Q

What is a pneumothorax? What are it’s three potential aetiologies?

A

Air within the pleural cavity.

Traumatic, iatrogenic, spontaneous.

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31
Q

What is the difference between a primary and secondary spontaneous pneumothorax?

A

Primary - no underlying lung disease.

Secondary - underlying lung disease i.e. COPD, CF

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32
Q

What is the treatment of a tension pneumothorax?

A

Immediate insertion venflon into the second intercostal space, midclavicular line to relieve the pressure.
Will always require ICD.

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33
Q

What are the risk factors for a spontaneous pneumothorax?

A

Smoking, male gender, height, underlying lung disease?

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34
Q

How does a primary pneumothorax occur?

A

A subpleural bleb ruptures and leads to a tear in the visceral pleura.

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35
Q

What are the symptoms of pneumothorax? What are the signs?

A

Pleuritic chest pain, breathlessness, respiratory distress.
Reduced air entry on affected side, hyper-resonance to percussion, reduced vocal resonance, tracheal deviation if tension +/- circulatory collapse.

36
Q

What are the management options for pneumothorax?

A

Observation (with serial CXR) if small and not very symptomatic.
Aspiration
Intercostal drain with underwater seal

37
Q

What are the options if a chest drain is unsuccessful in resolving a pneumothorax?

A

VATS (video assisted thoracic surgery).
Staple blebs.
Using medical or surgical pleurodesis. (adheres lung to the chest wall)

38
Q

Define obstructive sleep apnoea (OSA). How does obstructive sleep apnoea SYNDROME manifest?

A

Recurrent episodes of partial or complete upper (pharygeal) airway obstruction during sleep, intermittent hypoxia and sleep fragmentation.
Excessive daytime sleepiness.

39
Q

What are the symptoms of OSA?

A 
Snoring
Noisy/laboured breathing while sleeping
Frequently waking up during the night (may be nocturia, night sweats, dry mouth)
Daytime somnolence 
Fatigue, low mood concentration
40
Q

How would you assess someone for potential obstructive sleep apnoea?

A 
History - especially from partner. 
Weight
BMI
Neck circumference (>40cm)
Tonsils
Nasal patency
Craniofacial appearance (retrognathia, micrognathia)
Blood pressure
The Epworth sleepiness score
41
Q

What different investigations can be done to assess sleep for OSA?

A 
Limited polysomnography (done at home)
Full polysomnography (inpatient)
TOSCA - transcutaneous oxygen saturations and Carbon dioxide assessment. (home or inpatient)
42
Q

Explain the terms:
Apnoea
Hypopnoea
Respiratory effort related arousals

A

Apnoea - cessation or near cessation of airflow - 4% oxygen desaturation lasting ≥ 10 secs.
Hypopnoea - reduction in airflow to a degree insuffiecient to meet the criteria for an apnoea.
Respiratory effort related arousals - arousals associated with a change in airflow that doesn’t meet criteria for apnoea or hypopnoea.

43
Q

What is the Apnoea-Hypopnoea Index (AHI)?

What is the oxygen desaturation index (ODI)?

A

Number of apnoeas and hypopnoeas divided by the total sleep time in hours.
Number of times per hour of sleep that the SpO2 falls ≥ 4% below the baseline.

44
Q

What Apnoea-Hypopnoea Index (AHI) is diagnostic of OSA?

A

≥15 is diagnostic of OSA

5-15 + symptoms

45
Q

How can OSAS be treated? What is the aim of treatment?

A

Continuous positive airway pressure (CPAP)
Mandibular advancement device. (MAD)
Sleep position trainers
Improve daytime somnolence and QOL.

46
Q

What is the risk of untreated OSAS?

A 
Hypertension 
Right heart strain 
Cardiovascular disease
Increased risk of CVA
Increased RTAs
Increased accidents at work/poor concentration
47
Q

What is the rules surrounding OSAS and driving?

A

OSA without daytime somnolence - no need to stop driving.
OSAS with daytime somnolence - must inform DVLA of diagnosis but can keep licence if compliant with treatment and reduced DTS.

48
Q

What is sarcoidosis?

A

Sarcoidosis is a multisystem inflammatory disease of unknown aetiology that predominantly affects the lungs and intrathoracic lymph nodes.

49
Q

What type of inflammation is sarcoidosis characterised by?

A

Non-necrotising granulomatous inflammation.

50
Q

What are some of the symptoms of interstitial pulmonary fibrosis?

A

Breathlessness (worse with exercise), hacking dry cough, fatigue and weakness, appetite and weight loss, clubbing.

51
Q

What are some of the non idiopathic causes of pulmonary fibrosis?

A

Asbestosis, hypersensitivity pneumonitis, cocaine, nitrofurantoin, rheumatoid arthritis, lupus, sarcoidosis.

52
Q

What is EAA/HSP (extrinsic allergic alveolitis/hypersensitivity pneumonitis)?

A

Immunologically mediated inflammatory reaction in the alveoli and in the respiratory bronchioles (not atopy!)

53
Q

Give some examples of aetiologies of EAA/HSP?

A

Bird fancier’s lung - proteins in bird dropping.
Farmer’s lung - mouldy hay
Mushroom worker’s lung - spores/moulds

54
Q

What are the symptoms of EAA/HSP? How long post exposure does it present?

A 
flu-like illness
cough
high fever, chills
dyspnea, chest tightness
malaise, myalgia
4-8 hours after exposure
Chronic - dyspnea in strain, sputum production, fatigue, anorexia, weight loss.
55
Q

What is a pleural effusion? What are the clinical signs of pleural effusion?

A

Fluid in the pleural space.

Deceased breath sounds, stony to dull percussion, decreased tactile or vocal fremitus.

56
Q

What are the three broad causes of pleural effusion? Give examples of each.

A

Traumatic - i.e. stabbing, rib fracture.
Iatrogenic - i.e. CT guided lung biopsy
Spontaneous - primary (young, healthy patient) Secondary (underlying lung disease).

57
Q

What are the symptoms and signs of pneumothorax?

A 
Pleuritic chest pain 
Breathlessness 
Respiratory distress
Reduced air entry on affected side
Hyperresonance to percussion 
Reduced vocal resonance 
Tracheal deviation if tension
58
Q

What is the immediate management of a tension pneumothorax?

A

Insert venflon into 2nd intercostal space midclavicular line to relieve pressure.

59
Q

What are the management options for pneumothorax?

A

Observation as outpatient with CXR if small and not very symptomatic.
Aspiration.
Intercostal drain with underwater seal.

60
Q

What are the management options if a chest drain fails to resolve pneumothorax?

A 
VATS (Video Assisted Thoracic Surgery) 
Bleb stapling 
Talc pleurodesis 
Pleural abrasion/stripping 
Surgical pleuodesis
61
Q

What are some common causes of transudative and exudative pleural effusion?

A

Transudative - cardiac failure, hepatic cirrhosis, nephrotic syndrome

Exudative - bacterial pneumonia, malignancy, TB

62
Q

What is interstitial lung disease?

A

Term used to describe a number of conditions that primarily affect the lung parenchyma in a diffuse way. They are characterised by chronic inflammation and/or progressive interstitial fibrosis.

63
Q

What are the clinical features of idiopathic pulmonary fibrosis?

A

Progressive breathlessness, productive cough, cyanosis, respiratory failure, pulmonary hypertension, cor pulmonale, fine bilateral end inspiratory crackles, finger clubbing, usually history of cigarette smoking.

64
Q

Name some things which can cause pulmonary fibrosis.

A

Drugs i.e. Nitrofurantoin, methotrexate
Environmental - asbestosis, hypersensitvity pneumonitis
Connective tissue disease - lupus, RA, scleroderma.
Sarcoidosis

65
Q

What investigations would you do for suspected IPF?

A 
Lung function tests 
CXR
HRCT chest 
Routine Blood tests and immunology tests 
Lung biopsy
66
Q

What is the macroscopic and histological appearance IFP?

A

Looks like usual interstitial pneumonia (UIP).
Macroscopically - pleural surfaces are cobblestoned, fibrotic areas of lung (firm and rubbery white). Thickening of interlobular septae.
Histologically - patchy interstitial fibrosis, fibroblastic foci and collagen deposition.

67
Q

What is the pathogenesis of IPF?

A

Repeated cycles of epithelial injury by an unknown agent, results in abnormal repair at the site of injury leading to formation of fibroblastic foci. Inflammatory pathways also promote fibrosis.

68
Q

In IPF, damaged epithelial cells release growth factors and myofibroblasts secrete ECM proteins. Name one of each.

A

GF - TGFβ1

ECM protein - collagen

69
Q

What inflammatory cells are involved in IPF?

A

Eosinophils, mast cells, macrophages, lymphocytes.

70
Q

What treatments are available for IPF?

A

Pirfenidone - slows decline
Nintedanib - slows decline
N-acetyl cysteine - mucolytic so may be used in patient has cough or sputum.
Long term oxygen therapy
Diuretics for fluid retention if develop cor pulmonare
Antibiotics for infection
Lung transplant in young patients.

71
Q

Define sarcoidosis.

A

Sarcoidosis is a multisystem inflammatory granulomatous disease of unknown aetiology that predominantly affects the lungs and intrathoracic lymph nodes.

72
Q

Name some of the symptoms occuring in sarcoidosis including systemic symptoms?

A

Pulmonary dyspnea on exertion, cough, chest pain and haemoptysis.
Fever, anorexia, weight loss, fatigue, night sweats.

73
Q

What are the 4 stages of sarcoidosis as seen on CXR?

A

stage 1, bilateral hilar lymphadenopathy without infiltration.
stage 2, bilateral hilar lymphadenopathy with infiltration.
stage 3, infiltration alone.
stage 4, fibrotic bands, bullae, hilar retraction, bronchiectasis, and diaphragmatic tenting.

74
Q

What type of inflammation is seen with sarcoidosis?

A

Non-necrotising granulomatous inflammation.

75
Q

What are the main risk factors for developing lung cancer?

A

Smoking

Passive smoking, occupational asbestos, silica and nickel exposure, pulmonary fibrosis.

76
Q

What investigations would be done for suspected lung cancer?

A

Routine bloods
Chest X-ray
CT chest
CT guided percutaneous needle biopsy/bronchoscopy

77
Q

What are some of the symptoms of lung cancer?

A 
Cough - that doesn’t go away or a long standing cough gets worse
Recurrent infections. 
Breathlessness – lobar/lung collapse.
Haemoptysis.
Unexplained weight loss.
Chest and/or shoulder pains.
Hoarse voice.
78
Q

What are some of the signs of lung cancer?

A

Finger clubbing
Signs of lobar collapse and pleural effusion
Signs of metastases i.e. hepatomegaly, cervical lymphadenopathy, bony tenderness.
Cachexia.
Horner’s syndrome
Evidence of SVC obstruction i.e. oedema in arms/face, or spinal cord compression.
Cushingoid.
Hypercalcaemia.

79
Q

Where are squamous, small cell and adenocarcinomas normally located in the lung?

A

Squamous and small cell - predominantly central tumours

Adenocarcinoma - predominantly peripheral tumours.

80
Q

Describe small cell carcinoma including histology.

A

Most aggressive form of lung cancer.
Metastasizes early and widely. Often good initial response to chemotherapy but most patients relapse.
Oval to spindle shaped cells, nuclear moulding.

81
Q

Describe squamous cell carcinoma and its histology.

A

Tend to arise centrally from major bronchi. Slow growing and metastasize late therefore may be good candidate for surgery. May block bronchi leading to retention pneumonia or collapse. May be cavitating.
Histology - keratinization, intercellular bridges.

82
Q

Describe adenocarcinoma and its appearance.

A

Common in females. Also seen in non-smokers. Mainly found in the peripheries.
Appearance - glandular, solid, papillary or lepidic. Mucin production.

83
Q

Describe large cell carcinoma.

A

A diagnosis of exclusion. Usually arises centrally. Undifferentiated malignant epithelial tumour that lacks cytological features of SCLC and glandular or squamous differentiation.

84
Q

Name 2 molecular targets used in treatment of lung cancer and what drug targets them.

A

EGFR - tyrosine kinase inhibitors
PDL1 - inhibitors
EML4-ALK gene - ALK inhibitors

85
Q

What is the name of the primary pleural tumour caused by asbestos exposure?

A

Mesothelioma.

Phase 3 (14 decks)

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