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Year 3 > Block 31 Week 5 > Flashcards

Block 31 Week 5 Flashcards

1
Q

pneumothorax =

A
  • air in the pleural space
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2
Q

spontanous pneumothorax?

A
  • spontaneous pneumothorax: presence of air in pleural space in absence of trauma or intervention
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3
Q

managemtn options of a pneumothorax?

A
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4
Q

primary SP?

A
  • no prev pulm disease
  • some have emphysema on CT
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5
Q

Secondary spont pneumothorax?

A
  • established chronic lung disease
  • 50 yrs or older w smoking history
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6
Q

conservative management of

A
  • if no symptoms, and good lungs - primary spont pneumothorax
  • outpatient review every 2-3 days
  • CXR to monitor resolution
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7
Q

surgical referral criteria for a pneumothorax

A
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8
Q

spontaneous secondary pneumothorax?

A
  • conservative management but as inpatient
  • CXR to monitor
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9
Q

needle aspiration ?

A
  • mostly for PSP, outcomes for SSP not great
  • recommended for people with minimal symptoms
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10
Q

Heimlich valve?

A
  • one way valve
  • plastic tube connected to chest wall, air comes through the tube
  • plastic collapses when breathing in so air can’t come back in
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11
Q

Ambulatory management of a pneumothorax?

A
  • PSP only
  • can go home w this
  • more freq follow up due to risk of valve problems
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12
Q

chest drain requires?

A
  • daily inpatient review
  • remove drain when resolved
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13
Q

chance of reoccurance of a pneumothorax?

A
  • PSP - 30% chance
  • recurrence after surgical intervention is v low
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14
Q

what means that thoracic surgery is required at initial presentation?

A
  • tension pneumothorax
  • high risk occupations
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15
Q

prevention/ pleurodesis of pneumothorax?

A
  • during the first ep if patient sig decompensated i.e. COPD
  • not for young people with normal lungs bc risk of fibrosis
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16
Q

surgical procedures for a pneumothorax?

A
  • VATS for chemical pleurodesis
  • resection of lung parenchyma to stop air leak
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17
Q

advice for a pneumothorax?

A
  • smoking cessation
  • can fly 7 days after full resolution
  • diving discourgaged permanently
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18
Q

Pleural effusion?

A
  • fluid between the pleura
  • cancer, HF, infection
  • TB
  • PE
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19
Q

bilateral vs unlateral pleural effusion?

A
  • bilateral - usually due to systemic diseases
  • unilateral - usually a local cause
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20
Q

pleural effusion history?

A
  • asbestos exposure/ occupational histiry
  • medications - tyrosine kinase inhibitirs
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21
Q

Ix for a pleural effusion?

A
  • XR, US, CT
  • pleural effusion aspiration
  • pleural biopsy
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22
Q

pleural effusion caused by TB?

A
  • pleural fluid high in adenosine deaminase +/- inteferon gamma
  • high prevalence area
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23
Q

Pleural biopsy?

A
  • for thickened pleura
  • mesothelioma
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24
Q

pleural infection - empyema?

A

purulent effusion - requires drainage

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25
Q

intrapleural TPA?

A
  • for failed drainage
  • use alteplase
  • streptokinase should not be used
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26
Q

Mesothelioma?

A

-Mesothelioma is a cancer of the mesothelial layer of the pleural cavity that is strongly associated with asbestos exposure
- can present as a painless pleural effusion
- latent period of 30-40 yrs

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27
Q

normal chest X ray?

A
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28
Q

looking at cxr?

A
  • left hilum is higher than the right
  • right D higher than left
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29
Q

pleural effusion CXR?

A
  • fluid doesn’t build up like a line it builds up like a crescent
  • could be from bleeding after a fall and the patient is on an AC
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30
Q

asthma involves (3)?

A
  • Reversible airflow limitation
  • Airway hyperresponsiveness
  • Inflammation of the bronchi
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31
Q

early phase of asthma?

A
  • inhalation of allergens leads to type 1 hypersensitivity reaction in the airways
  • Sensitisation occurs during theallergen exposure causing the release of IgE antibodies from plasma cells.
  • IgE bind to high affinity receptors on mast cells.
  • Subsequent exposure to antigens cause mast cell degranulation and histamine release.
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32
Q

The mediators relased in the early phase of asthma cause…

A
  • These mediators cause smooth muscle contraction and bronchoconstriction whilst inflammation contributes to airway obstruction.
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33
Q

late phase of asthma?

A
  • recruitment of inflammatory cells e.g. T cells
  • overtime the airways lay down fibrous tissue
  • causing airway remodelling and leads to fixed airway obstruction - irreversible narrowing
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34
Q

Sx of asthma?

A
  • Cough(may be worse at night)
  • Dyspnoea
  • Chest tightness
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35
Q

signs of asthma?

A
  • Expiratory wheeze - polyphonic
  • Prolonged expiratory phase
  • Tachypnoea
  • harrison’s sulcus
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36
Q

harrison’s sulcus?

A

a groove at the inferior border of the rib cage that may be seen in children with chronic severe asthma.

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37
Q

signs of resp failure that can occur in a severe asthma attack:

A
  • Tachypnoea
  • Tachycardia
  • Inability to complete sentences
  • Exhaustion
  • Reduced respiratory effort
  • Silent chest
  • Altered conscious level
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38
Q

Asthma exacerbation - moderate?

A

PEFR > or equal to 50-70%

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39
Q

Severe asthma exacerbation PEFR?

A

33-50%

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40
Q

life threatening asthma exacerbation PEFR

A

<33%

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41
Q

near fatal asthma exacerbation?

A

raised PaCO2 or requires mechanical ventilation with raised inflation pressures

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42
Q

Asthma exacerbations summary table?

A
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43
Q

Spirometry results for an obstructive lung disease?

A
  • FVC:may be normal but often reduced due to air trapping.
  • FEV1:reduced.
  • FEV1/FVC:< 70%.
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44
Q

PEFR values in asthma?

A
  • Asthma demonstrates characteristic variability on PEFR diaries
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45
Q

asthma FeNO level?

A
  • > 40 supports diagnosis of asthma
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46
Q

inhaler types - beta agonists?

A
  • Short-acting beta-agonists(SABA): Salbutamol
  • Long-acting beta-agonists(LABA): Salmeterol
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47
Q

Steroid inhaler for asthma?

A

Beclomethasone

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48
Q

LABA-ICS inhaler in asthma?

A

Seretide (salmeterol/fluticasone)

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49
Q

Stepwise management of asthma?

A
  • 1) ICS - regular preventer
  • 2) add LABA - salmeterol: can be MART (combined inhaler)
  • 3) increase LAB or add leukotriene receptor antagonist
  • 4) referral
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50
Q

Asthma chronic management summary?

A

ICS -> add LABA -> inc LABA or add montelukast

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51
Q

Acute asthma management ?

A
  • oxygen
  • steroids - prednisolone or IV hydrocortisone
  • ipatropium bromide - for patients with severe or life-threatening asthma not responding to nebulised salbutamol.
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52
Q

second line therapies in the management of acute asthma?

A
  • Mg sulfate IV
  • beta 2 agonist infusion
  • aminophylline
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53
Q

BTS asthma pathway

A

1) SABA
2) ICS
3) laba

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54
Q

chronic bronchitis =

A
  • Chronic bronchitis: chronic productive cough for at least 3 months over two consecutive years.
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55
Q

Emphysema =

A
  • emphysema: abnormal airspace enlargement distal to terminal bronchioles with evidence of alveoli destruction and no obvious fibrosis
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56
Q

aetiology of COPD?

A
  • 90% of cases associated with smoking but only 10% of smokers develop it
  • alpha-1 antitrypsin deficiency - AR condition
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57
Q

Pack years =

A

(number of cigarettes smoked per day, divided by 20, multiplied by the number of years smoked)

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58
Q

chronic bronchitis vs asthma?

A
  • characterised by chronic inflammation with neutrophilic infiltration, CD8+ T lymphocytes and macrophages.
  • This differs from asthma, which has a predominant eosinophil infiltration with CD4+ T lymphocytes.
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59
Q

CB leads to (4)?

A
  • Goblet cell hyperplasia
  • Mucus hypersecretion
  • Chronic inflammation and fibrosis
  • Narrowing of small airways
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60
Q

bullae formation in COPD?

A
  • permanent enlargement of airspaces distal to the terminal bronchiole
  • Destruction of the lung parenchyma results in a reduced area for gas exchange and chronic hypoxia.
  • loss of elastin within alveoli leads to collapse and dilatation and bullae formation - alveoli dilate and may eventually join with neighbouring alveoli forming bullae.
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61
Q

Cor pulmonale =

A
  • right ventricular impairment secondary to COPD
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62
Q

what happens in cor pulmonale?

A
  • Chronic hypoxia causes vasocontriction of pulmonary arteries, which leads to elevated pulmonary arterial pressure.
  • The chronic elevation of pulmonary arterial pressure subsequently leads to right heart failure.
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63
Q

how does cor pulmonale present?

A
  • raised jugular venous pressure,
  • cyanosis,
  • ankle oedema,
  • parasternal heave
  • hepatomegaly.
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64
Q

COPD symptoms?

A
  • Chronic cough: usually productive
  • Sputum production
  • Breathlessness: usually on exertion in early stages
  • Frequent episodes of ‘bronchitis’: usually in the winter
  • Wheeze
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65
Q

Sigsn of COPD - respiratory?

A
  • Dyspnoea
  • Pursed lip breathing:(prevents alveolar collapse by increasing the positive end expiratory pressure)
  • Wheeze
  • Coarse crackles
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66
Q

signs of copd - cardiac?

A
  • Loss of cardiac dullness:due to hyperexpansion of lungs from emphysema
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67
Q

GI sign of COPD?

A
  • Downward displacement of liver:due to hyperexpansion of lungs from emphysema
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68
Q
A
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68
Q

Signs of COPD retention?

A
  • Drowsy
  • Asterixis
  • Confusion
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69
Q

signs of CP?

A
  • Peripheral oedema
  • Left parasternal heave: caused by right ventricular hypertrophy
  • Raised JVP
  • Hepatomegaly
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70
Q

Severity of breathlessness =

A
  • MRC dyspnoea scale
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71
Q

Symptoms of an acute exacerbation of copd

A
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72
Q

diagnosis of COPD?

A
  • spirometry - FEV1/ FVC <70%
  • post-bronchodilator ratio of <0.7 consistent with diagnosis of COPD
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73
Q

Distinguishing asthma vs COPD?

A
  • As part of spirometry,reversibility testingmay be completed that assesses spirometry measurements following inhalation of a bronchodilator (e.g. beta-agonist).
  • COPD is characterised by limited reversibility post-bronchodilator, which helps differentiate it from asthma.
  • Reversibility is a hallmark of asthma.
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74
Q

Features supportive of COPD (versus asthma) include:

A
  • Smoker or ex-smoker
  • Symptoms in older adults(> 35 years old)
  • Chronic productive cough
  • Persistent/progressive breathlessness
  • Night time waking with symptoms uncommon
  • Variability uncommon(diurnal or day-to-day)
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75
Q

COPD staging

A
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76
Q

Ix of COPD?

A
  • pulse oximetry
  • ABG - if hypoxia or hypercapnia suspected
  • ECG(if cor pulmonale suspected)
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77
Q

Bloods for COPD?

A
  • Full blood count: important to assess for anaemia and polycythaemia
  • Alpha-1 antitrypsin levels
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78
Q

CXR for COPD?

A
  • Hyperexpanded
  • Flattened hemidiaphragms
  • Hypodense
  • Saber-sheath trachea
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79
Q

CT scan for COPD?

A
  • if alt diagnosis suspected - bronchiectasis, fibrosis
  • lung cancer suspected
  • echo if CP suspected
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80
Q

Management of COPD - lifestyle?

A

smoking cessation

  • NRT
  • smoking cessation services

vaccination

  • seasonal influeza vaccine and pneumoccal vaccine
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81
Q

Pulm rehab in COPD?

A
  • MDT programme
  • long term lung conditions like COPD
  • involvesexercise training, health education, and breathing techniques
  • Nutritional education and behavioural techniques are also utilised.
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82
Q

Self management plans in COPD?

A
  • helping patients manage their symptoms including how to manage exacerbations
  • education + providing patients with a rescue pack pf ab and steroids
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83
Q

MRAs in COPD?

A
  • prevent activation of muscarinic receptors by ACh
  • prevents airway smooth muscle contraction and causes bronchodilation.
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84
Q

LABA?

A

salmetrol

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85
Q

SAMA =

A

ipatropium

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86
Q

LAMA =

A

tiotropium

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87
Q

ICS =

A

beclomethasone

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88
Q

trimbow inhaler =

A

formoterol/glycopyrronium/beclometasone

LABA-LAMA-ICS

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89
Q

stepwise management of COPD?

A
  • 1: SABA or SAMA
  • 2) LAMA + LABA if no evidence of steroid responsiveness
  • or LABA + ICS of steroid responsiveness if asthmatic features
  • 3) triple therapy (LABA + LAMA + ICS)
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90
Q

Oral therapies in COPD - theophylline?

A
  • theophylline - some bronchodilator action through inhibition of phosphodiesterase.
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91
Q

Oral therapies in COPD - mucolytics?

A
  • mucolytics - can be used in patients with a chronic productive cough to reduce frequency of cough and sputum production (e.g. carbocisteine).
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92
Q

oral therapies in COPD - ab?

A
  • antibiotics - for acute exacerbations. May be used prophylactically e.g. azithromycin
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93
Q

surgical intervention for COPD?

A
  • Lung reduction surgery
  • Bullectomy
  • Lung transplantation
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94
Q

Ix for COPD?

A
  • CXR
  • ABG
  • ECG
  • bloods - FBC, U&Es, CRP
  • cultures - blood if pyrexial
  • theophylline levels
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95
Q

Managing acute COPD exacerbations involves (4)

A
  • oxygen
  • bronchodilators
  • steroids
  • ab
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96
Q

COPD AE - oxygen?

A
  • Venturi mask
97
Q

COPD AE - bronchodilators?

A
  • usually as nebulisers
  • salbutamol: 2.5mg nebulised
  • ipatropium (muscarinic antagonist)
98
Q

steroids in COPD AE?

A

prednisolone 30 mg once daily should be given for 5 days unless there is a significant contraindication

99
Q

Ab in COPD AE?

A
  • typically doxyclcine or co-amoxiclav
100
Q

complications of COPD?

A
  • Respiratory failure
  • Pneumonia: often recurrent
  • Pneumothorax: rupture of bullous disease
  • Polycythaemia or anaemia
  • Depression
101
Q

Resp symptoms pathway

A
102
Q

NSCLC types?

A
  • Adenocarcinoma
  • squamous cell
  • large cell
103
Q

SCLC?

A
  • undifferentiated
  • usually in the central airways
  • 10-20% of lung cancer
104
Q

Which type of LC is rare in non smokers?

A

SCLC

105
Q

adenocarcinomas?

A
  • Malignant epithelial neoplasm
  • Gland formation
106
Q

adenocarcinomas are ? tumours

A

peripheral

107
Q

which type of cancer is the most common in non smokers?

A
  • adeno
  • they make up 40% of LC overall
108
Q

squamous cell cancer?

A
  • plemorphic squamous cells
  • Keratin (individual cells or keratin pearls) and intercellular bridges
109
Q

SCC arise in ?

A
  • arise centrally in larger bronchi
  • often metastasizes to locoregional lymph nodes - paticularly the hilar nodes
  • usually cavitates
110
Q

initial Ix of LC?

A
  • CXR
  • spirometry
  • bloods - BCP and clotting
111
Q

General features of LC?

A
  • tiredness
  • weight loss
  • decreased appetite
  • fever
112
Q

Resp symptoms of LC?

A
  • cough
  • haemoptysis
  • breathlessness
  • wheeze
  • stridor
  • chest pain
113
Q

Hypercalcaemia from LC?

A

non small cell( Squamous)

114
Q

Small cell cancer paraneoplastic syndromes?

A
  • SIADH
  • ectopic ACTH
  • eaton lambert
115
Q

neuro neoplastic syndromes?

A
  • Horners- Pancoast tumour
  • Ptosis, miosis, anhydrosis
  • fitting - brain mets and low sodium
116
Q

examination findings in LC?

A
  • wheeze
  • dullness - effusion
  • signs of SVCO
  • lymph nodes - neck or axilla
117
Q

LC RF?

A
  • Smoking
  • Asbestos
  • Radon Gas
  • Family History
118
Q

Ix of LC?

A
  • CXR
  • CT
  • PET-CT
  • bronchoscopy
  • EUS
119
Q

risks of bronchoscopy?

A
  • bleeding
  • infection
  • pneumothorax
  • air embolus
120
Q

EBUS?

A
  • similar to bronchoscopy
  • under sedation
  • minimally invasive
121
Q

Risks of EBUS?

A
  • bleeding
  • infection
  • pneumothorax
122
Q

mediastinoscopy?

A
  • gold standard
  • large biopsies
  • invasive
  • under general anaesthetic
123
Q

other signs of lung cancer?

A
  • an effusion
  • deviated trachea
  • enlarged liver due to mets
  • cachexia
  • signs of SVCO
124
Q

Metastatic LC?

A
  • lymphadenopathy
  • effects of spread to brain, bone, adrenal and liver
125
Q

Mets LC acronym?

A

Brain
Bone
Adrenal
Liver
Lung - other

126
Q

importance of obtaining a histological diagnosis?

A
  • to distinguish primary from secondary cancer
  • molecular testing to ascerrtain suitability for targeted treatments e.g. TKIs
127
Q

lingula atelectasis

A
128
Q

pleural effusion from LC

A

meniscus from fluid line

129
Q

TNM staging - N

A
130
Q

M staging

A
131
Q

EGFR Mutation?

A
  • freq of 10-15% in NSCLC
  • sensitive to small molecule tyrosine kinase inhibitor - TKI - erlotinib, gefitinib
132
Q

pleural effusion =

A
  • imbalance between the formation and removal of pleural fluid
133
Q

transudative pleural effusion ?

A
  • ↑ Hydrostatic pressure
  • ↓ Colloid osmotic pressure
134
Q

exudative pleural effusion?

A
  • ↑ Pleural permeability.
  • ↓ Absorption of pleural fluid by lymphatics
135
Q

what causes transudative pleural effusion?

A
  • congestive cardiac failure
  • liver cirrhosis
  • nephrotic syndrome
136
Q

exudate pleural effusion causes?

A
  • infection
  • PE
  • neoplastic
  • TB
  • asbestos related diseases including mesothelioma
137
Q

malignant pleural effusion?

A
  • metastatic LC
  • MM
  • Metastatic (non-lung) cancer - kidney, breast, CRC, oesophagus, pancreas
138
Q

imaging the pleura

A
  • CXR
  • thoracic US
  • CT/ PET CT
  • MRI
139
Q

Diagnostic pleural aspiration ?

A
  • indicated for pleural effusions that have no clear cause or do not resolve with appropriate treatment e.g. diuretics
140
Q

straw coloured pleural effusion?

A

non specific

141
Q

blood stained aspirated pleural effusion =

A

malignancy or PE

142
Q

haemorrhagic aspirated pleural effusion =

A

haemothorax

143
Q

frank pus in the pleural effusion?

A

empyema

144
Q

pH indicating empyema?

A

<7.2

145
Q

malignant pleural effusion?

A
  • common causes: bronchogenic carcinoma, mesothelioma, metastatic disease
146
Q

high polymorphs in pleural effusion?

A

empyema

147
Q

high lymphocytes in pleural effusion?

A

Lymphoma, TB, RA

148
Q

high oesinophils in pleural effusions?

A

Haemothorax, Pneumothorax

149
Q

glucose in pleural effusion?

A
  • <3.3mmol in
  • empyema
  • RA
  • SLE
  • malignancy
150
Q

amylase in pleural effusion?

A
  • pancreatitis
  • oesophageal perf
151
Q

Adenine deaminase in PE?

A
  • TB
152
Q

malignant pleural effusion management ?

A
  • chest drain and talc pleurodesis
  • Medical thoracoscopy and talc pleurodesis
  • Surgical VATS
  • Indwelling pleural catheter
153
Q

exudative stage of pleural effusions?

A
  • sterile pleural fluid accumulates in pleural space
  • Pleural fluid originates in lung interstitial spaces and in capillaries of visceral pleura due to increased permeability.
  • effusions resolve with ab therapy
154
Q

fibropurulent stage of pleural effusions?

A
  • Bacterial invasion of the pleural space occurs → accumulation of neutrophils, bacteria and cellular debris
  • Deposition of fibrinà loculations
  • Pleural fluid pH <7.2 , glucose levels ↓,
155
Q

organization stage of pleural effusions?

A
  • fibroblasts grow into the exudates from both the visceral and parietal pleural surfaces
  • They produce an inelastic membrane called pleural peel.
  • Thick pleural fluid
156
Q

Ix of pleural effusions?

A
  • diagnosis: CXR, thoracic US, CT
  • Blood cultures, pleural fluid sampling/drainage (chest drain insertion)
157
Q

PE - intrapleural thrombolytic agent?

A

rtPa and Dnase

158
Q

Spontaneoys pneumothorax

A
159
Q

pneumothorax =

A
  • air in pleural cavity
  • Primary spontaneous pneumothorax
  • Secondary pneumothorax
  • Iatrogenic pneumothorax
160
Q

safe triangle in a pneumothorax

A
161
Q

XR of a pneumothorax?

A
  • silhouette sign - normally recognisable tissue boundaries are lost
  • lobar collapse - the air in the alveolar tissue makes the lungs less dense than the soft tissue structures that lie adjacent
162
Q

cancer clinical nurse specialists?

A
  • see people before, at the time of and after diagnosis
  • provide continuing support
  • facilitate communication between the secondary care team (including the multidisciplinary team), the person’s GP, the community team and the person with lung cancer
  • help people access advice and support whenever they need it
163
Q

lung cancer referral criteria?

A
164
Q

urgent CXR for suspected LC?

A
165
Q

How many new LC cases a year?

A
  • 50k new cases every year, 35k deaths/ year
  • most common cause of cancer deaths per year - 21%
166
Q

LC is the ? most common cancer in the UK

A

3rd

167
Q

proportion of LC cases caused by smoking?

A

80%

168
Q

promoting quitting tobacco?

A
  • raising public awareness of harm caused by smoking and second hand smoking
  • provide info on how people who smoke can reduce risk of illness and death by using 1 or more medicinally licensed nicotine containing products
  • Provide information on using medicinally licensed nicotine-containing products
  • awarness of local smokeless tobacco sensation
169
Q

excisional biopsy =

A

When an entire lump or suspicious area is removed

170
Q

incisional biopsy =

A

orcore biopsysamples a portion of the abnormal tissue without attempting to remove the entire lesion or tumor.

171
Q

FNA?

A
  • provides cellular specimen
  • freq used for carcinomas
172
Q

core biopsy?

A
  • allow for tumour structural examination
  • frequently used for soft tissue sarcoma
  • 85-95% accuracy in diagnosis
173
Q

incisional biopsies?

A
  • small surgical incision carefully placed to access tumour without contamination of critical structures
174
Q

excisional biopsy?

A
  • small superficial soft tissue masses
175
Q

process of biopsy?

A
  • samples are received in a fixative solution which halts the autolysis process
  • Processing” is the term used to describe the removal of water from tissues and its
  • gradual replacement with molten paraffin wax.
  • tissues embedded in a wax block
  • cutting sections
176
Q

Stage 1 NSCLC Tx?

A
  • Has not spread to lymph nodes or distal organs
  • Surgery to remove part or all of the lung
  • May have chemotherapy, immunotherapy or targeted cancer drugs after
177
Q

Stage 2 NSCLC Tx?

A

*Some may have neoadjuvant therapy prior to surgery
*Surgery to remove part or all of the lung
* May have chemotherapy combined with immunotherapy or targeted drug Osimertinib (if tumour is positive for EGFR mutation)

178
Q

drug for EGFR positive LC?

A

Osimertinib

179
Q

Stage 3 NSCLC Tx?

A

*Neoadjuvant therapy
*Surgery to remove part or all of the lung
* Adjuvant treatment

180
Q

stage 4 NSCLC Tx?

A
  • Control cancer as long as possible and help to reduce symptoms
181
Q

LC referral guidelines

A
182
Q

pulm complications of cocaine toxicity?

A
  • Pulmonary complications of cocaine toxicity include pulmonary edema, pulmonary hemorrhages, pulmonary barotrauma, foreign body granulomas, cocaine related pulmonary infection, asthma
183
Q
A
184
Q

cannabis use and LC?

A
  • cannabis use increases risk of lung cancer - smoking marijuana leads to 4x the deposition of tar compared to cigarette smoking
  • lack of research on link between cannabis and lung cancer though
185
Q

stopping smoking - support?

A
  • behavioural support
  • medically licensed products:
  • bupropion
  • NRT
  • vareniciline
  • nicotine containing e-cigarettes
  • telephone quitlines
186
Q

methods of preventing uptake of smoking ?

A
  • national campaigns to prevent uptake in young people under 18
  • denormalise smoking - news articles, posters, brochures, digital media
  • school based interventions - smoking prevention activities
  • peer led interventions in school
187
Q

side effects of chemo?

A
  • N&V
  • fatigue
  • hair loss
  • peripheral nerve damage
  • sore mouth and throat
188
Q

side effects of radiotherapy?

A
  • reddening/ darkening of skin
  • tiredness
  • breathlessness and cough
  • difficulty swallowing
  • chest pain/ discomfort
189
Q

side effects of surgery for LC?

A
  • pneumothorax
  • pain
  • DVTs
  • breathing problems
190
Q

apical lung tumours (Pancoast tumours)?

A
  • typically NSCLC
  • compression of brachial plexus
  • produce upper limb paraesthesia or weakness
  • Horners syndrome - ptosis, miosis, facial anhidrosis
191
Q

Pancoast tumours - compression of (3)

A
  • phrenic nerve
  • recurrent laryngeal
  • SVC
192
Q

PT - phrenic nerve compression?

A
  • Compression on the phrenic nerve, leading toparalysisof theipsilateral hemidiaphragm, can cause further respiratory compromise.
193
Q

PT - reccurent laryngeal nerve compression?

A

hoarse voice

194
Q

SVCO

A
  • Compression of the superior vena cava(SVC obstruction) can cause facial plethora
  • prominence of facial and/or upper limbs veins, and respiratory compromise (Pemberton’s sign).
195
Q

PNS - PTH?

A
  • Squamous cell lung cancers can produceparathyroid hormone-related peptide(PTHrP),
  • which can mimic the function of parathyroid hormone (PTH), leading to clinical featuresofhypercalcaemia.
196
Q

PNS - osteoarthropathy?

A

Adenocarcinoma can causehypertrophic osteoarthropathythat can present withclubbing,joint pain, andbone pain.

197
Q

PNS - ADH?

A

Small cell lung cancers can produceanti-diuretic hormone(ADH) that can lead tosyndrome of inappropriate antidiuretic syndrome secretion(SIADH), resulting inhyponatraemia.

198
Q

PNS - cushings?

A
  • SCLC -> ACTH production -> Cushings
199
Q

Lambert-Eaton syndrome?

A
  • Antibodies against thepresynaptic calcium channel of the neuromuscular junctioncan also be produced by small cell lung cancers,
  • resulting in aLambert-Eaton syndrome, which can present withproximal muscle weakness.
200
Q

aetiology of LC?

A
  • smoking - 80-90% of cases
  • asbestos exposure - strongly associated with mesothelioma but also linked to adenocarcinoma of the lung
  • radon gas - occurs from uranium
201
Q

NSCLC form ?% of LC

A

80-85%

202
Q

most common form of LC?

A

Adeno - around 38%

203
Q

which type of cells are affected in adenocarcinomas?

A
  • musus secreting
  • tends to occur in lung peripheries
204
Q

second most common form of LC?

A

Squampus cell carcinomas

205
Q

SCC?

A
  • typically occurs in the central parts of the lungs
  • can present w pneumonia secondary to obstructed bronchus
206
Q

most common cause of SCC?

A

smoking

207
Q

histopathology of SCC?

A
  • histopathology classicly shows kertain
208
Q

Large cell cancer?

A
  • undifferentiated neoplasms
  • account for 5% of lung cancers
  • metastasise early
209
Q

SCC tend to metastasise?

A

late

210
Q

SCLC nature?

A
  • fast doubling time, aggressive nature and early mets
211
Q

type of cell affected in SCLC?

A
  • SCLC is a cancer of the APUD cells, a neuroendocrine cell found in the lungs.
  • It occurs almost exclusively in smokers.
212
Q

LC presentation

A
  • Freq asymptomatic
  • when symptomaic, cough, malaise and weight loss predominate
  • haemoptysis
  • features of SVC obstruction or paraneoplastic syndrome
213
Q

What can you get w LC?

A
  • Hypertrophic pulmonary osteoarthropathy(HPOA)
  • Signs of pleural effusion
214
Q

signs of pleural effusion?

A
  • reduced breath sounds
  • reduced VF
  • stony dull percussion
215
Q

SVCO?

A
  • A tumour may cause compression of the superior vena cava.
  • This causes engorgement of vessels in the neck and face, shortness of breath and a ‘fullness’ of the head.
216
Q

Pancoast tumour ?

A
  • tumour of the pulm apex
  • may spead to brachial plexus, cervical sympathetic trunk and stellate ganglion, subclavian vein
217
Q

mets from LC?

A
  • Bone: bone pain, raised ALP
  • Brain: focal and non-focal neurology
  • Liver: abnormal LFTs
  • Adrenal glands: though a common site of metastasis, normally asymptomatic
218
Q

hypercalcaemia in LC can be from?

A
  • can be due to bony mets or tumour secretion of Parathyroid hormone-related protein (PTHrP) or Calcitriol
219
Q

Hypercalcaemia mneumonic?

A
  • stones - renal calculi
  • bones - bone pain
  • groans - abd pain
  • thrones - polyuria
  • psychiatric moans - signs if altered mental status
220
Q

lambert eaton syndrome characterised by?

A

both proximal and ocular muscle weakness.

221
Q

hypertrophic osteoarthropathy?

A
  • This syndrome is characterised by clubbing and periostitis.
  • It features a symmetrical, painful arthropathy affecting the distal joints.
222
Q

2 week referral for LC

A
  • unexplained haemoptysis and aged over 40
  • Patients with evidence of SVCO or stridor require an urgent referral and emergency admission to hospital for further review.
223
Q

Bloods in LC?

A
  • Deranged liver function tests (LFTs) should prompt suspicion of liver metastasis.
  • Calcium (measured in the bone profile) can be elevated in patients with malignant hypercalcaemia or bony metastasis.
  • FBC
  • U&Es
  • LFTs
  • Bone profile
224
Q

Signs of lung cancer on CXR include:

A
  • Focal lesion
  • Pleural effusion
  • Widened mediastinum (indicative of enlarged nodes)
225
Q

CT findings in LC?

A
  • Typical findings are a solitary pulmonary nodule with irregular or spiculated (looks like spikes coming out of the surface of the lesion).
  • It may also show lymph node involvement or invasion.
226
Q

Other scans in LC?

A
  • PET-CT - help w staging
  • CT/MRI brain - to exclude cerebral mets
227
Q

Bronchoscopy in LC?

A
  • bronchoscopy - It allows for visualisation of the airways and any lesions that may be impinging or invading them.
  • It also allows for washings/brushings to be taken for cytological analysis
228
Q

Lung function tests in LC?

A
  • allows clinicians to estimate if the patient will have sufficient residual lung capacity following a wedge resection (a wedge of the lung with tumour removed), a lobectomy (an entire lobe is removed) or pneumonectomy (removal of a whole lung).
  • This is of particular importance in patients with pre-existing lung disease (e.g. emphysema) as they will already have reduced lung function.
229
Q

different staging systems for LC?

A
  • NSCLC - TNM
  • SCLC - VALSG
230
Q

management of LC?

A
  • surgical resection
  • VATS - key-hole procedure, requires deflation of the lung
  • thoracotomy - large incision, open procedure
231
Q

Radiotherapy in LC?

A
  • It can be used with radical intent (i.e. potentially curative) as an alternative to surgery in early-stage NSCLC.
  • It can also be used as a combination with chemotherapy (that can follow surgery) or alone for both NSCLC and SCLC.
232
Q

Chemotherapy in LC?

A
  • can be used for NSCLC and for SLCLC
233
Q

SACT in LC?

A
    • Systemic anti-cancer therapy(SACT): these are specific therapies used in non-squamous NSCLC (i.e. adenocarcinoma, large cell undifferentiated)
  • for patients w certain mutations like EGFR
234
Q
A
235
Q

EGFR-TK inhibitors?

A

afatinib, erlotinib and gefitinib.

236
Q

ALK inhibitors?

A

crizotinib, ceritinib and alectinib.

237
Q

NSCLC Tx?

A
  • Surgical resection (normally lobectomy) is the treatment of choice in those where it is potentially curative (e.g. stage I-II).
  • Radical radiotherapy can be used where surgery is not suitable
  • Adjuvant chemotherapy is used in comb w surgery or given as a palliative therapy to improve survival in advanced disease
238
Q

SCLC Tx?

A
  • Surgical resection is only an option in early disease,
  • Generally, treatment consists of chemotherapy (often cisplatin-based) and/or radiotherapy with the goal of extending survival and reducing symptoms.
239
Q
A
240
Q
A

Year 3 (45 decks)

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