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2a > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What are the main URTI syndromes?

A
  • Common cold (rhinitus, sinusitis)
  • Sore throat ( pharyngitis, tonisllitis)
  • Influenza
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2
Q

Main features of viral URTIs?

A
  • Sore throat
  • Cough
  • Otalgia
  • Blocked nose and rhinorrhoea
  • Mild fever
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3
Q

Main viral causative organisms of common cold?

A
  • Rhinoviruses
  • Corona viruses (!)
  • Other: Coxsackie viruses, echoviruses, parainfluenza, RSV, influenza C
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4
Q

Main viral causative organisms of pharyngitis/tonsillitis?

A
  • Adenoviruses
  • Epstein-Barr virus
  • Other: Influ A,B,C, parainfluenza virus
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5
Q

Main viral causative organisms of influenza?

A
  • Influenza A and B
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6
Q

What are the main syndromes of LRTIs?

A
  • Croup - laryngotracheobronchitis
  • Acute bronchitis
  • Chronic bronchitis
  • Bronchiolitis
  • Pneumonia
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7
Q

Main viral causative organisms of Croup?

A
  • Parainfluenza virus

- Other: Influ A and B, RSV, Coxsackie

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8
Q

Main viral causative organisms of Acute bronchitis?

A
  • Adenoviruses

- Other: RSV, rhinoviruses, measles virus, influ a and b

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9
Q

Main viral causative organisms of chronic bronchitis?

A
  • RSV
  • Rhinoviruses
  • Parainfluenza viruses
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10
Q

Main viral causative organisms of bronchiolitis?

A
  • RSV
  • Adenoviruses
  • Other: Parainfluenza
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11
Q

Main viral causative organisms of pneumonia?

A
  • Adenoviruses
  • Influ A and B
  • Measles virus
  • VZV
  • CMV
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12
Q

What is flu?

A
  • An acute respiratory illness caused by infection with influenza viruses
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13
Q

Different types of influenza virus?

A

A - Affects all sorts of animals. Causes severe and extensive outbreaks and pandemics.

B - Causes sporadic, less severe, outbreaks. Eg care homes, garrisons

C - Relatively minor disease

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14
Q

Symptoms of flu?

A
  • Upper and/or lower resp tract symptoms
  • Fever
  • Headache
  • Myalgia
  • Weakness
  • Risk of 2ndary bacterial pneumonia
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15
Q

What is pneumonia?

A
  • Inflammation of the lung parenchyma
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16
Q

Causes of pneumonia?

A
  • bacterial pneumonia (common)
  • viral
  • fungal
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17
Q

Main bacteria causing pneumonia?

A
  • Streptococcus pneumoniae
  • Haemophilus influenzae
  • Staphylococcus aureus
  • Mycoplasma pneumoniae
  • Legionella pneumophilia
  • Klebsiella pneumoniae
  • Pneumocystis jiroveci
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18
Q

Features of pneumococcal pneumonia?

A
  • 80% of cases
  • Ass w/ : High fever, rapid onset, pleuritic chest pain, herpes labialis
  • Vaccine available
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19
Q

Who does haemophilus influenzae commonly affect?

A
  • Pt with COPD
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20
Q

When does S. Aureus pneumonia commonly occur?

A
  • Often occurs in patients following influenza infection
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21
Q

What are the features of mycoplasma pneumonia?

A
  • One of the atypical pneumonias
  • Often presents with a dry cough and atypical chest signs/XR findings
  • Autoimmune haemolytic anaemia and erythema multiforme may be seen
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22
Q

Features of legionella pnia?

A
  • Atypical

- Hyponatraemia and lymphopenia common

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23
Q

Who often gets klebseilla pneumonia?

A

Alcoholics

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24
Q

What are the features of pneumocystis pneumonia?

A
  • Typically seen in HIV patients

- P/w: Dry cough, exerise-induced desaturations, absence of chest signs

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25
Q

What is idiopathic interstitial pneumonia?

A
  • Group of non-infective causes of pneumonia
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26
Q

Which groups are at risk of pneumonia?

A
  • Infants and the elderly
  • COPD and other chronic lung disease (CF, bronchiectasis)
  • Immunocompromised
  • Nursing home residents
  • Impaired swallow
  • Diabetes
  • Congestive heart disease
  • Lifestyle: smokers, alcoholics, drug users
  • Iatrogenic - eg long term steroids
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27
Q

Symptoms of pneumonia?

A
  • Cough
  • Sputum
  • Dyspnoea
  • Chest pain - may be pleuritic
  • Fever
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28
Q

What are the signs of pneumonia?

A
  • Signs of systemic inflam response: Fever, tachycardia
  • Reduced O2 sats
  • On exam:
    • Reduced breath sounds
    • Bronchial breathing
    • Crackles/ consolidation
    • +/- wheeze
    • Dull to percussion
    • decreased air entry
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29
Q

Pneumonia investigations?

A
  • CXR: Shows consolidation
  • Bloods:
    • FBC - neutrophilia in bacterial infections
    • U&E
    • CRP
  • ABG
  • Blood and sputum cultures
  • CRP monitoring for admitted pts
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30
Q

Management principles for pneumonia?

A
  • Antibiotics

- Supportive care: O2, IV fluids

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31
Q

What is risk tool for pneumonia?

What is it made up of?

A 
CURB-65
Confusion (AMT<8/10)
Urea >7
Resp rate >30
Blood pressure <90 sys and/or <60dia
>65

0 low risk
1-2 intermediate
3-4 high risk

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32
Q

Other markers of severe pneumonia?

A
  • CXR – more than one lobe involved
  • PaO2 <8 kPa
  • Low albumin
  • White cell count <4x10^9 or >20x10^9
  • Blood culture positive
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33
Q

Treatment of low-severity CAP ?

A
  • Amoxicillin first line
  • If allergic give - macrolide (azith, clarith, erith) or tetracycline
  • 5days course
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34
Q

Moderate severity CAP tx?

A
  • Dual abx therapy with amoxicillin and a macrolide

- 7-10day course

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35
Q

High severity CAP tx?

A
  • Consider Co-Amoxiclav and a macrolide
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36
Q

Indications for pneumocooccal vaccine?

A
  • > 65 years
  • Splenic dysfunction
  • Immunocompromised
  • Chronic medical condition
  • Protects against invasive pneumococcal disease but not pneumonia
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37
Q

Most common infecting organisms in HAP?

A
  • Gram negative enterobacteria
  • Staph Aureus
  • Also: Pseudomonas, Klebsiella, Bacterioles, Clostridia
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38
Q

How is HAP managed?

A
  • Aminoglycoside antibiotic (eg. gentamycin, neomycin)

- + Antipseudomonal penicillin IV or 3rd gen cephalosporin

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39
Q

What is aspiration pneumonia?

A
  • Pneumonia that develops as a result of foreign materials gaining entry to the bronchial tree
  • Usually oral or gastric contents such as food and saliva
  • Depending on the acidity of the aspirate, a chemical pneumonitis can develop, as well as bacterial pathogens adding to the inflammation
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40
Q

Causes of aspiration pneumonia?

A 
Impaired swallow:
- Neuro disease: MND, MG, bulbar palsy, huntingtons
- Stroke
- MS
- Intoxication
- Oesophageal disease: Achalasia, reflux
Iatrogenic cause:
- Intubation
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41
Q

Risk factors for asp pnia?

A
  • Poor dental hygeine
  • Swallowing difficulties
  • Prolonged hospitalization or surgical procedures
  • Impaired consciousnes
  • Impaired mucociliary clearance
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42
Q

Bacteria often found in aspiration pneumonia?

A
  • S Pneumonia
  • S Aureus
  • Haem Influenzae
  • Pseudomonas aerugionsa
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43
Q

Treatment of aspiration pneumonia?

A
  • IV cephalosporin

- + IV metronidazole

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44
Q

What is bronchitis?

A
  • Inflammation of the mucous membrane in the bronchial tubes

- Typically causes bronchospasm and coughing

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45
Q

Cause of bronchitis?

A
  • Usually viral

- can be bacterial: H. Influenzae, S. Pneumoniae

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46
Q

How does bronchitis present?

A
  • Cough can be productive or non-productive
  • SOB and often wheeze
  • May be fever but no systemic signs of infection
  • Wheeze but no signs of focal consolidation
  • May cause acute exacerbations of COPD or asthma
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47
Q

Management of bronchitis?

A
  • Usually none especially if viral
  • Amoxicillin, doxycycline or clarithromycin- options if ill or chronic lung disease and purulent sputum
  • Augmentin (smokers or COPD but not initial NICE recommendations for COPD)
  • Manage exacerbation of COPD/asthma with steroids and increased inhalers
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48
Q

What is COPD?

A
  • Airflow obstruction > FEV1/FVC ratio of <0.7
  • Due to combination of:
    1) Airway damage (bronchitis)
    2) Parenchymal damage (emphysema)
  • Damage is a result of chronic inflammation
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49
Q

Causes of COPD?

A
  • Smoking
  • Alpha-1-antitrypsin deficiency
  • Air pollution/exposure to pollutants at work eg: Coal, cadmium, cotton, cement, grain
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50
Q

Why does alpha-1-antitrypsin defiency cause COPD?

A
  • A1AT is a protease inhibitor
  • Proteases are involved in structural changes and breakdown of lung tissue that results in emphysema
  • A1AT is also inactivated by cigarette smoke - so smoking causes a similar effect to the deficiency
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51
Q

2 phenotypes of COPD?

A
  • Blue bloaters
  • Pink puffers

Most will be combination of both

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52
Q

What are blue bloaters?

A
  • Predominantly chronic bronchitis (airway inflammation)
  • Hypoventilation and cyanosis
  • Cough
  • Phlegm
  • Cor pulmonale
  • Resp failure
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53
Q

What are pink puffers?

A
  • Predominantly emphysema
  • Weight loss
  • Breathlessness
  • Maintained pO2
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54
Q

Main presentation of COPD?

A
  • Cough: productive (clear/white thick sputum)
  • Dyspnoea
  • Wheeze

Smoker
Elderly

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55
Q

Clinical signs of COPD?

A
  • Cyanosis
  • Signs of CO2 retention - flap, confusion
  • Barrel shaped, hyperinflated chest
  • Raised JVP, ankle swelling, cor pulmonale
  • Reduced chest expansion and air entry
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56
Q

What is Cor Pulmonale?

A

increased resistance in the blood vessels in the right side of the heart due to pulmonary hypertension/increased pulmonary resistance – causing symptoms of RHF

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57
Q

Investigations for ?COPD

A
  • Post bronchodilator spirometry to show FEV1/FVC below 0.7
  • CXR: Hyperinflation, bullae, flat hemidiaphragm
  • FBC
  • BMI
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58
Q

Management of COPD?

A 
General:
 - Smoking cessation
 - Annual influenza vaccine
 - One off pneumococcal vaccine
Bronchodilator therapy
 - SABA or SAMA - 1st line
 - Next step up is ?steroids
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59
Q

What features suggest COPD steroid responsiveness?

A
  • Hx of asthma
  • History of atopy
  • Raised eosniphils
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60
Q

Treatment offered if they have steroid responsive features?

A
  • ICS + LABA

- If still breathless: triple therapy of ICS+LABA+LAMA

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61
Q

Treatment offered if they DONT have steroid responsive features?

A
  • LABA and LAMA
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62
Q

Features and management of cor pulmonale?

A 
Features:
 - Peripheral oedema
 - Raised JVP
 - systolic parasternal haeve
 - Loud P2
Management:
 - Use a loop diuretic for oedema
 - Consider LTOT
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63
Q

What can improve survival in stable COPD pts?

A
  • Smoking cessation
  • LTOT
  • Lung volume reduction surgery
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64
Q

Who should be assessed for LTOT?

A
  • Very severe airflow obstruction (FEV1 < 30% predicted
  • Cyanosis
  • Polycythaemia
  • Peripheral oedema
  • Raised jugular venous pressure (sign of cor pulmonale)
  • Oxygen saturations <92 OA
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65
Q

How to assess for LTOT?

A

Measuring 2 ABGs on 2 occasions

At least 3 weeks apart

In patients with stable COPD on optimal management

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66
Q

Target O2 sats for COPD pt on oxygen therapy?

A

88-92%

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67
Q

Features of acute exacerbation of COPD?

A
  • Increase in sx above and beyond normal day to day variation for 2 days
  • Moderate needs tx
  • Severe needs admission
  • Associated with poor QoL and poor prognosis
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68
Q

Common infective organisms of AEofCOPD?

A
  • haemophilus influenzae
  • Streptococcus pneumoniae
  • Moraxella catarrhalis
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69
Q

Management of AEofCOPD?

A
  • Increase freq of bronchodilator use - consider nebs
  • Give prednisolone 30mg daily for 7-14 days
  • Oral abx only if clinical signs of pneumonia or purulent sputum
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70
Q

What is asthma?

A

A chronic inflammatory condition of the airways secondary to hypersensitivity

The symptoms are variable and recurring and manifest as reversible bronchospasm resulting in airway obstruction

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71
Q

3 pathological characteristic features of asthma?

A
  • Airflow limitation
  • Airway hyper-responsiveness to a range of stimuli
  • Inflammation of the bronchi
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72
Q

Risk factors/causes of asthma?

A
  • Persona/Fhx of atopy
  • Antenatal: Maternal smoking and Viral infection during pregnancy
  • Low birth weight
  • Not being breastfed
  • Maternal smoking around child
  • Exposure to high conc of allergens (house dust mite etc)
  • Air pollution
  • Hygeine hypothesis - reduced exposure to infectious agents
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73
Q

What medication may patients with asthma be sensitive to?

A

Aspirin

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74
Q

2 phenotypes of asthma?

A

1) Eosinophillic:
- Non atopic
- Atopic - fungal allergy, pets, occupation, common aeroallergens
2) Non-eosinophillic
- Non smoking
- Smoking associated
- obesity related

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75
Q

What monoclonal antibody can be used to treat eosinophillic asthma?

A
  • Anti-IgE > Omalizumab
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76
Q

Presentation of asthma?

A
  • Cough - often worse at night or in morning
  • Dyspnoea
  • Wheeze
  • Chest tightness
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77
Q

What triggers asthma symptoms?

A
  • Allergens
  • Infections
  • Menstrual cycle
  • Exercise
  • Cold air
  • Laughter/other emotions eg. stress, anger
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78
Q

Signs of asthma?

A
  • Expiratory wheeze on auscultation

- Reduced peak expiratory flow rate

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79
Q

RCP3 questions for assessing asthma severity?

A
  • Recent waking in the night?
  • Usual asthma symptoms in the day?
  • Interference with ADLs?
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80
Q

Investigations for asthma?

A

Spirometry:

  • FEV1
  • FVC
  • FEV1 significantly reduced, FVC normal, ratio <70%
  • Bronchodilator reversibility test >12%

Fractional exhaled nitric oxide (FeNO)

CXR - rule out lung Ca in elderly/smokers

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81
Q

Step up management steps for asthma?

A

1) SABA
2) Not controlled on previous step OR newly-diagnosed with symptoms ≥ 3x week or night time waking – SABA and low-dose ICS
3) SABA + low-dose ICS + leukotriene receptor antagonist (LTRA)
4) SABA + low-dose ICS + LABA (+/- LTRA depending on response)
5) SABA +/- LTRA. Switch ICS/LABA for low dose ICS MART
6) SABA +/- LTRA + medium dose ICS MART, or consider changing back to a fixed-dose ICS and separate LABA
7) SABA +/- LTRA + one of the following:
- Increase ICS to high-dose only, as fixed regime not part of MART
- A trial of additional drug – e.g. LAMA or theophylline
- Seek advice from healthcare professional with expertise in asthma

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82
Q

What is maintenance and reliever therapy (MART)?

A

A form of combined ICS and LABA treatment
In which a single inhaler, containing both ICS and a fast-acting LABA, is used for both daily maintenance therapy and the relief of symptoms as required

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83
Q

Classifying acute asthma attack: MODERATE

A
  • PEFR 50-75% best/predicted
  • Speech normal
  • RR <25/min
  • Pulse <110bpm
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84
Q

Classifying acute asthma attack: SEVERE

A
  • PEFR 33-50% best or predicted
  • Cant complete sentences
  • RR > 25/min
  • Pulse >110bpm
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85
Q

Classifying acute asthma attack: LIFE-THREATENING

A
  • PEFR <33% best or predicted
  • Oxygen sats <92%
  • Silent chest, cyanosis, or feeble resp effort
  • Bradycardia, dysrhythmia or hypotension
  • Exhaustion, confusion or coma
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86
Q

Escalatory steps to managing acute SEVERE asthma attack?

A

1) Oxygen
2) Salbutamol nebulisers
3) Ipratropium bromide nebulisers
4) Hydrocortisone IV OR Oral Prednisolone
5) Magnesium Sulphate IV
6) Aminophylline/IV salbutamol

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87
Q

Manageing mild-moderate asthma attack?

A

Beta 2 agonist via spacer (for a child < 3 years use close fitting mask)
1 puff every 30-60 seconds up to a maximum of 10 puffs
If symptoms are not controlled, repeat and refer to hospital

Give steroid for 3-5days.

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88
Q

What is bronchiectasis?

A

Permanent dilatation of the airways, secondary to chronic infection of inflammation

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89
Q

Causes of bronchiectasis?

A
  • Post infective - TB, measles, pertussis, pneumonia
  • Cystic fibrosis
  • Bronchial obstruction - lung cancer, foreign body
  • Immune deficiency - selective IgA, hypogammaglobulinaemia
  • Allergic bronchopulmonary aspergillosis
  • Ciliary dyskinetic syndromes (Kartageners, Youngs)
  • Yellow nail syndrome ( Pleural effusion+Lymphoedema+Yellow nails)
  • Post radiotherapy
  • CTD
  • IBD
  • Post-transplant
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90
Q

What are features of Kartageners syndrome?

A

Aka Primary ciliary dyskinesia
Pathogenesis - dynein arm defect results in immotile cilia

Features:

  • Dextrocardia or complete situs inversus
  • Bronchiectais
  • Recurrent sinusitis
  • Subfertility (decreased sperm motility and defective ciliary action in fallopian tubes)
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91
Q

How does bronchiectasis come about?

A
  • Microbial insult + defect in host response
  • Leads to resp tract infection > bronchial inflammation > resp tract damage
  • Leads to progressive lung disease
  • Failure of mucociliary clearance and immune function
  • Bronchitis > Bronchiectasis > Fibrosis
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92
Q

Most common infecting orgaisms isolated from bronchiectasis pts?

A
  • Haem influenza (most common)
  • Pseudomonas Aeruginosa
  • Klebsiella spp.
  • Streptococcus pneumonia
  • Also: Moraxella cattarhalis, S. Aureus
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93
Q

Symptoms of bronchiectasis?

A
  • Cough: Copious sputum, foul smelling, green/yellow, can be non-productive in 5%
  • Recurrrent exacerbations w/ long recov time
  • weight loss
  • Dyspnoea
  • Deterioration in control of prev stable lung condition
  • Haemoptysis
  • Chest pain
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94
Q

Signs of bronchiectasis?

A
  • Finger clubbing
  • Crepitations
  • Bronchial breath sounds
  • (rarely pyrexial)
95
Q

What respiratory diseases cause clubbing?

A 
ABCDEF
A - Abcess
B -Bronchiectasis
C - Cys Fibrosis
D - DONT say COPD
E - Empyeme
F - Fibrosis
96
Q

What other diseases cause clubbing?

A 
CLUBBING
C – Cyanotic heart disease
L – lung diseases
U – Ulcerative colitis + Crohn’s (IBD)
B – Biliary cirrhosis
B – Birth defects
I – infective endocarditis
N - Neoplasm (Lung Ca, mesothelioma)
G - I malabsorption (coeliac disease)
97
Q

Investigations for bronchiectasis?

A
  • Spirometry - obstructive pattern shown
  • Sputum culture
  • CXR
  • High res CT scan (97%sens,99%spec)
  • In younger pt w/ no smoking history do immunology, sweat test for CF and ciliary ix
  • Bronchoscopy
98
Q

Management of bronchiectasis

A
  • Find and tx underlying cause: immune deficiency, CF etc
  • Physical training
  • Postural drainage
  • Abx for exacerbations and long term if severe
  • Bronchodilators
  • Immunisations - flu+pneumococcal
  • Surgery in selected cases - eg localised cases
99
Q

What is respiratory failure?

A

Inadequate gas exchange by the respiratory system
Meaning that arterial oxygen dioxide or both cannot be kept at normal levels

Type 1 – hypoxia
Type 2 – hypoxia plus hypercapnia

100
Q

What is difference between central and peripheral resp failure?

A

Central = Problem with brain/chemoreceptors

Peripheral = Problems with lungs/muscles

101
Q

Causes of hypoventilation?

A 
OHS (obesity hypoventilation system)
Hypothyroidism
Respiratory muscle weakness
Post-sedation
REM sleep
Loop diuretics causing metabolic alkalosis
102
Q

Causes of hyperventilation?

A 
Hyperthyroidism 
Post cortical CVA (a stroke)
Liver cirrhosis 
Metabolic acidosis 
Anxiety and stress (common cause)  overriding of normal drives by ‘emotional centres’, reticular activation centre and sympathetic nerves
103
Q

What is Extrinsic Allergic Alveolitis?

A

AKA Hypersensitivity pneumonitis

  • Condition caused by hypersensitivity induced lung damage due to a variety of inhaled organic particles
  • Thought to be largely caused by immune-complex mediated tissue damage (type III hypersensitivity)
  • Delayed hypersensitivity (type IV) thought to play a role
104
Q

Examples of EAA?

A
  • Bird fanciers’ lung - avian proteins
  • Farmers lung - spores ofSaccharopolyspora rectivirgula
  • Malt workers’ lung -Aspergillus clavatus
  • Mushroom workers’ lung - thermophilic actinomycetes
105
Q

How does EAA present?

A
  • Can be acute (4-8hrs after exposure) or chronic
  • SOB
  • Dry cough
  • Fever
106
Q

Investigations for EAA?

A
  • CXR: Upper/midzone fibrosis
  • CT scan: May see ‘ground glass’ appearance ass w/ hypersensitivity
  • Bronchoalveolar lavage - lymphocytosis
  • Blood - no eosinophilia
107
Q

What is occupational lung disease?

A

A response to inhaling some kind of trigger at work.

  • Fume
  • Dust
  • Gas/Vapour
  • Mist/Aerosol
108
Q

By what mechanisms can occupational lung diseases occur?

A
  • Direct injury: Acute irritant asthma, pulmonary oedema
  • Infection: Silicotuberculosis
  • Allergy: Asthma, EAA
  • Chronic inflammation: COPD, bronchitis
  • Destruction of lung tissue: Emphysema
  • Lung or pleural fibrosis: Asbestos related disease
  • Carcinogenesis: Lung cancer, mesothelioma
109
Q

Effects of occupational lung disease?

A
  • May be immediate or after a latent interval of months, years or decades
  • Variable depending on indivudual susceptibility
  • May occur whilst still at work or after retirement
  • Effects range from mild to v severe
110
Q

What is occupational asthma?

A

Definition in 90% of cases – asthma induced by allergy to an agent inhaled at work

Definition in 10% of cases – asthma induced by massive accidental irritant exposure at work (direct airway injury)

111
Q

Occupations associated with occupational asthma?

A
  • Farmers
  • Bakers
  • Factory workers
  • Painters
112
Q

Chemicals associated with occupational asthma?

A
  • Isocyanates
  • Platinum salts
  • Soldering flux resin
  • Flour
113
Q

How does occupational asthma present?

A
  • Pt concerned work worsening asthma
  • Sx better at weekends/when away
  • SOB
  • Tachypnoea
  • Cough
114
Q

Investigations for occupational asthma?

A
  • Serial PEF at work and away
  • Spirometry
  • Immunology
115
Q

What is interstitial lung disease?

A

Disease of the alveolar/capillary interface

116
Q

What are the 5 major groups of causes of interstitial lung disease?

A

1) Ass w/ systemic disease
2) Caused by environmental triggers
3) Granulomatous disease
4) Idiopathic
5) Other

117
Q

Which systemic diseases can cause ILD?

A
  • Any rheumatological contion: SLE, RA, seronegative spondyloarthropathies
  • Vasculitis
  • Vascular - AVMs
118
Q

Which environmental triggers can cause ILD?

A
  • Drugs
  • Fungal
  • Dusts
119
Q

Which granulomatous diseases can cause ILD?

A
  • Sarcoidosis

- Wegeners

120
Q

What are the main idiopathic causes of ILD?

A

1) IPF (idiopathic pulmonary fibrosis)
2) NSIP (non-specific interstitial pneumonia)
3) DIP (desquamative interstitial pneumonia)
4) COP (cryptogenic organising pneumonia)

121
Q

What are the other main causes of ILD?

A

LAM – lymphaniolyomyomatosis

  • ‘Benign’ proliferation of lymphatic smooth muscle cells
    - Leads to lung cysts, respiratory failure, pneumothorax, chylous pleural effusion
  • Often presents in pregnancy – hormonal influences
  • Treated with hormonal manipulation – rapamycin, transplant

Eoisinophilic pneumonia

122
Q

What diseases causing ILD predominantly affect upper zones of lungs?

A 
C – Coal worker’s pneumoconiosis
H – Histiocytosis/ hypersensitivity pneumonitis (EAA)
A – Ankylosing spondylitis
R – Radiation
T – Tuberculosis
S – Sarcoidosis/ silicosis
123
Q

What diseases causing ILD predominantly affect lower zones of lungs?

A
  • Idiopathic pulmonary fibrosis
  • Most CTD
  • Drug induced - amiodarone, bleomycin, methotrexate
  • Asbestosis
124
Q

Symptoms of ILD?

A
  • Cough
  • SOB
  • Constitutional symptoms

PMH of lung problems
Drugs, occupation, pets, smoking

125
Q

Signs of ILD?

A
  • Clubbing
  • Fine end inspiratory crepitations
  • Skin, eye, joint sx
126
Q

Investigations for OLD?

A
  • CXR
  • Pulm function tests - restrictive pattern, reduced gas transfer, low/normal PaO2
  • Blood tests
  • High res CT
  • Broncho-alveolar lavage
127
Q

Treatment of ILD?

A
  • manage underlying cause

- May response to steroids

128
Q

What is idiopathic pulmonary fibrosis?

A

Chronic lung condition characterised by progressive fibrosis of the interstitium of the lungs.
50-70yrs. 2x more common in men.

129
Q

Risk factors for IPF?

A
  • Smoking
  • Infectious agents: CMV, Hep C, EBV
  • Dust exposure (metals, woods)
  • Antidepressants (imipramine)
  • Chronic aspiration
  • Genetics
130
Q

Features of IPF?

A
  • Progressive exertional dyspnoea
  • Bibasal crackles on auscultation
  • Dry cough
  • Clubbing
131
Q

Investigations for IPF?

A
  • Spirometry: Restrictive disease (normal/decreased FEV1, decreased FVC, normal/increased FEV1/FVC ratio)
  • Transfer factor (TLCO): reduced due to imparied gas exchange
  • Imagine
    • Bilateral intersitial shadowing
    • Honeycombing/ground glass appearance
  • ANA and RhF
132
Q

How is IPF managed?

A
  • Pulm rehab
  • Pirfenidone (antifibrotic)
  • Supportive: O2, transplant, GORD, Cough,
133
Q

Treatment of acute exacerbations of IPF?

A
  • Broad spec abx (tazocin often)
  • Steroids
  • Oxygen
  • ?Ventilator
134
Q

What is sarcoidosis?

A
  • Multisystem disorder of unknown aetiology
  • Characterised by non-caseating granulomas
  • More common in young adults
  • More common in people of african descent
  • Predominantly lymph nodes and lungs
135
Q

How does sarcoidosis present?

A
  • Can be asymptomatic in 50%
  • Non specific constitutional symptoms: fever, fatigue, cachexia, lack of energy
  • Specific features by body systems
136
Q

Chest features of sarcoidosis?

A

Symptoms: Cough, breathlessness, wheeze
Signs: Wheeze, fine crackles, bilateral hilar lymphadenopathy

137
Q

Skin features of sarcoidosis

A
  • Erythema nodosum: Big blotchy tender lumps affecting mainly shins
  • Waxy maculopapular lesions
  • Lupus pernio
  • Scars on skin: due to granuloma infiltration
138
Q

Eye manifestations of sarcoidosis?

A
  • Anterior uveitis
  • Posterior uveitis
  • Conjunctival nodes
  • Lacrimal gland enlargement
  • Heefordts syndrome
139
Q

What is Heerfordts syndrome?

A
  • Parotid gland enlargement
  • Facial palsy
  • Anterior uveitis
  • Fever
140
Q

Bone manifestations of sarcoidosis?

A
  • Arthralgia

- Bone cysts

141
Q

Metabolic features of sarcoidosis?

A
  • Hypercalcaemia
142
Q

Liver manifestations of sarcoidosis?

A
  • Granulomatous hepatitis

- Hepatosplenomegaly

143
Q

What are the neurological manifestations of sarcoidosis?

A
  • Meningeal inflammation
  • Seizures
  • Mass lesions: Granulomata
  • Hypothalamic pituitary infiltration
  • Mononeuropathy
144
Q

Cardiac manifestations of sarcoidosis?

A
  • RARE
  • Ventricular arrhytmias
  • Condcution defects
  • Cardiomyopathy w/ cardiac failure
145
Q

Syndromes associaed with sarcoidosis?

A

Lofgren’s syndrome - an acute form of the disease characterised by bilateral hilar lymphadenopathy (BHL), erythema nodosum, fever and polyarthralgia. It usually carries an excellent prognosis

Mikulicz syndrome - enlargement of the parotid and lacrimal glands due to sarcoidosis, tuberculosis or lymphoma

Heerfordt’s syndrome – parotid enlargement, fever and uveitis

146
Q

Diagnosis of sarcoidosis?

A
  • Clin features
  • Radiology
  • Biopsy
147
Q

What will be raised in sarcoidosis?

A
  • Serum ACE

- Calcium

148
Q

Management of sarcoidosis?

A
  • Steroids
  • Start with oral prednisolone
  • Wean off when can.
149
Q

What is Langerhans cell histiocytosis?

A
  • Rare condition associated with abnormal proliferation of histiocytes
  • Typically presents in childhood with bony lesions
  • Granulomatous disease
150
Q

Features of LCH?

A
  • Bone pain – typically in the skull or proximal femur
  • Well-defined ‘punched out’ osteolytic lesions seen on skull
  • Cutaneous nodules
  • Recurrent otitis media/mastoiditis
  • Tennis racket shaped Birbeck granules on electromicroscopy

Pulmonary LCH – isolated smoking related disease, probably different aetiology

151
Q

What is acute respiratory distress syndrome?

A

ARDS aka Acute lung injury

  • May be caused by direct lung injury or occur secondary to severe systemic illness
  • Lung damage and release of inflammatory mediators cause increased capillary permeability and non-cardiogenic pulmonary oedema
  • Often accompanied by multiorgan failure
  • Mortality of 40%
  • Significant morbidity in those who do survive
152
Q

Pulmonary causes of ARDS?

A
  • Pneumonia
  • Gastric aspiration
  • Inhalation of damaging agent eg. smoke, poison
  • Injury
  • Vasculitis
  • Contusion
153
Q

Other causes of ARDS?

A
  • Obstetric events (eclampsia, amniotic fluid embolus)
  • Drugs/toxins (aspirin, heroin)
  • Shock
  • Septicaemia
  • Haemorrhage
  • Multiple transfusions
  • DIC
  • Pancreatitis
  • Acute liver failure
  • Head injury
  • Trauma
  • Malaria
  • Burns
  • Fat embolism
154
Q

Clinical features of ARDS?

A
  • Acute onset
  • Severe symptoms
  • Dyspnoea
  • Tachypnoea
  • Tachycardia
  • Bilateral lung crackles
  • Cyanosis
  • Peripheral vasodilation
155
Q

ARDS investigations?

A
  • Bloods: FBC, U&E, LFT, clotting
  • Amylase: Pancreatitis is a cause
  • Blood cultures
  • ABG - low paO2
  • CXR: bilateral pulm infiltrates
  • Pulmonary artery catheter
156
Q

Diagnostic criteria for ards?

A

1) Acute onset - within 1 week of known risk factor
2) Pulmonary oedema - bilateral infiltrates on CXR, not fully explained by effusions, lobar/lung collapse or nodules
3) Non-cardiogenic
4) Hypoxaemia - pO2/FiO2 <40kPa

157
Q

Management of ARDS?

A
  • Admit to ITU
  • Oxygenation/ventilation to treat hypoxaemia
  • Tx of underlying cause
  • Nutritional support: Enteral, high fat antioxidant forumulations
  • Prone positioning and muscle relaxants
158
Q

What is mesothelioma?

A
  • Cancer of the pleura
  • Commonly associated with asbestos exposure
  • Rarely metastasises
  • Long latency
  • Rapidly progressive and incurable pleural effusion
  • Progressive breathlessness, chest pain, weight loss
  • Average survival 8-14months
159
Q

Causes of mesothelioma?

A
  • Exposure to asbestos
  • Blue asbestos (crocidolite) is most dangerous
  • Long latent period after exposure 30-40yrs
  • More common on men by 3x
160
Q

How does mesothelioma present?

A
  • Progressive shortness of breath
  • Chest pain
  • Pleural effusion
  • Constitutional symptoms: W loss, fever, night sweats, lymphadenopathy
  • Abdo bain, palpable chest masses
  • SVCO
  • Presents like any lung cancer
161
Q

Which other tumours can affect pleura?

A

Malignant: Mesothelioma, Primary lymphoma, Pleural Thymoma, Pleura sarcoma

Benign: Fibrous

162
Q

How is mesothelioma investigated?

A
  • CXR
  • High res CT scan
  • Pleural fluid aspiration - straw or blood stained
  • Pleural biopsy for histology
163
Q

Management of mesothelioma?

A
  • Palliative chemotherapy
  • May be surgical and radiotherapy role
  • Financial compensation for diagnosis
  • Median survival 8-14months
164
Q

What is TB?

A

An infective disease which can be pulmonary or extra-pulmonary.
Caused by Mycobacterium Tuberculosis or Mycobacterium Bovis.

165
Q

What are mycobacteria?

A

Aerobic, non-spore forming, non-motile bacteria with high content of high molecular weight lipids in its cell wall

Slow growing – takes 15-20 hours to double, so takes 3-8 weeks to grow on solid media

166
Q

Risk factors for TB?

A
  • Foreign born (eg Sub-saharan Africa)
  • HIV+ve
  • IVDU
  • Homeless
  • Alcoholic
  • Prisons
167
Q

How does TB spread?

A
  • Spread in aerosol droplets
168
Q

What is primary TB?

A
  • A non-immune host who is exposed to M. tuberculosis may develop primary infection of the lungs
  • A small lung lesion known as a Ghon focus develops, of tubercle-laden macrophages
  • The combination of a Ghon focus and hilar lymph nodes is known as a Ghon complex
  • In immunocompetent people the lesion initially usually heals by fibrosis.
  • Those who are immunocompromised may develop disseminated disease (miliary tuberculosis).
169
Q

What is secondary TB?

A
  • If the host becomes immunocompromised the initial infection may become reactivated
  • Reactivation generally occurs in the apex of the lungs and may spread locally or to more distant sites
  • Possible causes of immunocompromise include:
    Immunosuppressive drugs including steroids
    HIV
    malnutrition
170
Q

Where else other than lungs can secondary TB occur?

A
  • Central nervous system (tuberculous meningitis - the most serious complication)
  • Vertebral bodies (Pott’s disease)
  • Cervical lymph nodes (scrofuloderma)
  • Renal
  • Gastrointestinal tract
  • GU tract
  • Bones and joints
  • Pericarditis
171
Q

Clinical features of TB?

A
  • Weight loss and night sweats
  • Low grade fever
  • Anorexia
  • Malaise
  • Cough >3weeks
  • Maybe haemoptysis
172
Q

Symptoms specific to primary TB disease?

A
  • Chest pain and dyspnoea
  • Upper lobe consolidation - dull apex with bronchial breathing
  • Compression by LN causing collapse, cough etc
  • Features of cell mediated immunity
173
Q

Possible features of secondary TB?

A
  • Asymptomatic, presenting as nodules, fibrosis or cavity on CXR
  • Systemic presentation
  • Haemoptysis
  • Pneumonic presentation
  • Pleurisy
174
Q

Extra-pulmonary TB features?

A

Systemic features: Weight loss, low grade fever, anorexia, night sweats, malaise

Lymph node TB: Swelling +/- discharge

Bone TB: Painful/swollen joints, Potts disease

Abdo TB: Ascities, abdominal lymph nodes, sx of malabsorption

GU TB: Epididymitis, urinary freq, dysuria, haematuria

TB Meningitis: Normal meningtis sx, CSF sample +++ glucose and protein

175
Q

How is TB diagnosed?

A
  • Ziehl Neelsen stain for AFB
176
Q

What culture medium is needed and how long to grow?

A

Solid media: Lowenstein-Jensen or Middlebook 7H12 agar. 3-8weeks.

Liquid media: Middlebook 7H12. 1-3weeks.

177
Q

X-ray features of TB?

A

1 - consolidation
2 - cavitation
3 - calcification
4 - pleural effusion

178
Q

Treatment of active TB?

A

RIFAMPICIN 6/12
ISONIAZID 6/12
PYRAZINAMIDE 2/12
ETHAMBUTOL 2/12

179
Q

Treatment of latent TB?

A

3 months of Isoniazid and Rifampicin

Give Pyridoxine to prevent peripheral neuropathy.

180
Q

Side effects of rifampicin?

A
  • Stains body secretions/urine orange
  • Induces liver enzymes
  • Flu like sx
181
Q

Side effects of isoniazid?

A
  • Polyneuropathy (prevent by giving Pyridoxine)
  • Hepatitis
  • Haemolytic anaemia
182
Q

Side effects of pyrazinamide?

A
  • Hepatitis
  • Hyperuricaemia and gout
  • Rash and arthralgia
183
Q

Side effects of ethambutol?

A
  • Optic neuritis
184
Q

How to screen for TB?

A
  • Mantoux test

- Interferon gamma blood test

185
Q

What is pulmonary hypertension?

A

Resting mean pulmonary artery pressure of >25mmHg

Can be primary (PAH) or secondary

186
Q

What is PAH?

A

Diagnosed when there is raised resting pulmonary artery pressure in the absence of underlying chronic lung disease

187
Q

What diseases may pulmonary hypertension occur secondary to?

A
  • Left heart disease: Valvular, systolic dysfunction, diastolic dysfunction
  • Lung disease and/or hypoxia: COPD, obstructive sleep apnoea, lung fibrosis
  • Thromboembolic occlusion of proximal or distal pulmonary vasculature
  • Multifactorial: Myeloproliferative disorders, sarcoidosis, glycogen storage disease
188
Q

What are the causes of PAH?

A
  • Hereditary – 10% cases inherited in AD fashion
  • Idiopathic (no cause identified)
  • Inflammatory conditions - Systemic sclerosis, systemic lupus erythematosus, rheumatoid arthritis
  • Recreational drugs - long term use of cocaine and amphetamines
  • Anorexigenic drugs – (suppress appetite) – fenfluramine
  • HIV infection
  • Portal hypertension (portopulmonary hypertension)
  • Congenital heart disease with systemic to pulmonary communication (atrial septal defect ventricular septal defect)
  • Schistosomiasis
  • Chronic haemolytic anaemia
  • Pulmonary veno-occlusive disease
189
Q

What protein plays a role in PAH?

A

Endothelin

190
Q

How does PAH present?

A
  • Classically: Progressive exertional dyspnoea
  • Plus lethargy and fatigue
  • Other possible symptoms: Exertional syncope, exertional chest pain, peripheral oedema, weakness, abdo pain
191
Q

Signs on exam of PAH?

A
  • Oedema
  • Cyanosis
  • Right ventricular heave
  • Loud P2
  • Raised JVP with prominent a waves
  • Tricuspid regurgitation
192
Q

Investigations of PAH?

A
  • Aim is to confirm presence of pulm htn and show cause
  • CXR: Enlarged proximal pulmonary arteries
  • ECG: RVH and P pulmonale
  • ECHO: RV dilatation and/or hypertrophy
  • TFTs to rule out hypothyroid
  • Autoimmune screening
  • Routine biochemistry
193
Q

How is P-pulmonale seen on ECG?

A

Right atrial enlargement.

Seen as tall, peaked P wave on ECG.

194
Q

Management of PAH?

A
  • Tx of underlying cause
  • Oxygen
  • Anticoagulation
  • Following this: Acute vasodilator therapy
195
Q

What are the features of Wegeners/GPA?

A
  • High incidence of upper airways involvement (nasal crusting, destruction)
  • Endobronchial involvement
  • Cavitating nodules
  • C-ANA, anti-PR3+ve
  • See MSK
196
Q

Features of churg-strauss?

A
  • High incidence of upper airway involvement (polyps, sinusitis)
  • V high incidence of preceding asthma
  • Ground glass, consolidation, bronchial wall thickening
  • Peripheral eosinophilia
  • P-ANCA, anti-MPO +ve
197
Q

Features of Goodpastures syndrome?

A
  • Antibodies form to basement membrane (type 4 collagen)
  • Largely affects the kidneys and the lungs because basement membranes are very important in these organs
  • Presents with cough, haemoptysis, and tiredness followed by acute glomerulonephritis
  • Can cause intrapulmonary haemorrhage so can produce diffuse infiltrates on the CXR
  • Treatment – corticosteroids (to suppress the immune system)
198
Q

How to classify pleural effusions?

A

Transudative (<30g/L protein)
- Often caused by organ failure (esp. renal failure/nephrotic syndrome)

Exudative (>30g/L protein)
- Anything that affects the structure or causes increased permeability of membranes. Inflammation and CTD disorders.

199
Q

Causes of transudative pleural effusion?

A
  • Heart failure
  • Hypoalbuminaemia (liver disease, nephrotic, malabsorption)
  • Hypothyroidism
  • Meigs syndrome
  • Renal failure
  • Nephrotic syndrome
  • Liver cirrhosis
200
Q

Causes of exudative pleural effusion?

A
  • Infection: pneumonia (most common), TB, subphrenic abcess
  • Autoimmune/Inflam/CTD: RA, SLE
  • Neoplasia: Lung cancer, mesothelioma, metastases from other sites
  • Pancreatitis
  • Pulm embolism
  • Dresslers syndrome
  • Yellow nail syndrome
  • Traumatic: haemothorax, chylothorax
201
Q

Presenting symptoms of pleural effusion?

A
  • Dyspnoea
  • Cough - non-productive
  • Chest pain
  • Weight loss
202
Q

Signs of pleural effusion?

A
  • Dullness too percussion
  • Reduced breath sounds
  • Reduced chest expansion
  • Reduced tactile vocal fremitus
203
Q

Investigating pleural effusion?

A
  • PA CXR in all pt
  • USS- to visualise and aspirate
  • Contrast CT
  • Pleural aspiration
204
Q

What do you test pleural fluid for?

A
  • pH
  • Protein
  • LDH
  • Cytology
  • Microbiology
205
Q

What criteria is used to differentiate between transudative or exudative effusion?

A

LIGHTS criteria.
Exudate likely if one of following met:
- Pleural fluid protein/serum protein >0.5
- Pleural fluid LDH/serum LDH >0.6
- Pleural fluid LDH >2/3 the upper limits of normal serum LDH

206
Q

What may low glucose in pleural fluid aspiration point to?

A

RA

TB

207
Q

What may raised amylase in pleural fluid point to?

A

Pancereatitis

Oesophageal perforation

208
Q

What may heavy blood staining mean in pleural fluid?

A

mesothelioma
pulm embolsim
TB

209
Q

Treatment of pulmonary effusions?

A
  • Simple: observe and follow up
  • If complicated/empyema: Drainage, fibrinolytics, surgery
  • Tx of underlying cause
  • Drain exudates
  • Transudate resolve if cause resolved
210
Q

When is a chest drain indicated for pleural effusion?

A
  • Malignant and symptomatic
  • empyema/complicated parapneumonia
  • traumatic haemothorax
  • Post-op
  • Ventilated pt
  • Site
211
Q

How to manage recurrent pleural effusions?

A
  • Recurrent aspiration
  • Pleurodesis
  • Indwelling pleural catheter
  • Drug management for sx
212
Q

What is pleural infection?

A

All patients with a pleural effusion in association with sepsis or a pneumonic illness require diagnostic pleural fluid sampling

if the fluid is purulent or turbid/cloudy a chest tube should be placed to allow drainage
if the fluid is clear but thepH is less than 7.2 in patients with suspected pleural infection a chest tube should be placed

213
Q

Whaat is a pneumothorax?

A
  • Air in the pleural space
  • Leading to partial or complete collapse of the lung
  • Occurs spontanenously or 2ndary to chest trauma
  • A ‘tension pneumothorax’ is rare unless pt on NIV or a ventilator
  • In this situation (tension pneumo) the pleural tear acts as a one-way valve through which air passes during inspiration but is unable to exit on expiration. The lung will then flatten because the pressure in the pleural space is greater than the pressure inside the lung
214
Q

Causes of pneumothorax?

A

Traumatic: Penetrating injuries, eg stab, RTA, rib fractures

Spontaneous:

  • Primary (incl. Marfans) - Primary spontaneous pneumothorax
  • Secondary - COPD, pulm fibrosis
  • Infections - pneumocystis pneumonia, TB
  • Catamenial - w/ menstruation

Iatrogenic: pacemakers, central lines, ventilation

215
Q

Who gets affected by pneumothorax?

A
  • Men 6x more than women

- Often pt tall and thin

216
Q

Clinical presentation of pneumothorax?

A
  • Sudden onset of unilateral pleuritic chest pain

- Breathlessness

217
Q

Signs of pneumothorax?

A
  • Reduced breath sounds
  • Hyper resonant percussion on exam
  • Pallor
  • Tachycardia
  • Tachypnoea
  • Sweating
  • Reduced chest expansion on side of lesion
  • Low o2
  • low BP
218
Q

How to dx pneumothorax?

A
  • Hx and exam and signs
  • Chest XR - see air in pleural cavity
  • Tension pneumothorax = clin diagnosis
219
Q

Treatment of tension pneumothorax?

A
  • NEedle decompression and chest tube insertion
220
Q

What is a bronchial carcinoma?

A
  • Malignant neoplasm of lung arising from epithelium of bronchus or bronchiole
  • Accounts for 95% of primary lung tumours
  • 3:1 male to female
221
Q

Classifications of lung cancer>

A

SCLC - 15% of cases, worse prognosis

NSCLC
- Squamous, adenocarcinoma, large cell, alveolar cell, bronchial adenoma

222
Q

Causes of lung cancer?

A

Smoking = most common cause

Higher incidence in urban than rural areas

Passive smoking

Environmental – radon exposure, asbestos, polycyclic aromatic hydrocarbons and ionising radiation

Occupational – arsenic, chromium, nickel, petroleum products and oils

Host factors – pre-existing lung disease e.g. PF, HIV infection, Genetic factors

223
Q

Characteristics of squamous cell cancer?

A
  • Most present as obstructive lesion leading to infection
  • Occasionally cavitates
  • Local spread is common
  • Widespread metastases occur late
  • Typically central
  • Associated with parathyroid hormone-related protein (PTHrP) secretion  hypercalcaemia
  • Strongly associated with finger clubbing
  • Hypertrophic pulmonary otseoarthropathy (HPOA)
224
Q

Features of large cell lung cancer?

A
  • Metastasize early
  • Typically peripheral
  • Anaplastic, poorly differentiated tumours with a poor prognosis
  • May secrete beta-HCG
225
Q

Features of adenocarcinoma of lung?

A
  • Most common lung cancer associated with asbestos exposure, although the majority of patients who develop lung adenocarcinoma are smokers
  • Proportionately more common in non-smokers
  • Usually occurs peripherally
  • Local and distance metastases
226
Q

Features of small cell lung cancer?

A
  • Usually central
  • Arise from APUD cells:
    • Amine – high amine content
    • Precursor uptake – high uptake of amine precursors
    • Decarboxylase – high content of the enzyme decarboxylase
  • Association with ectopic ADH and ACTH secretion
    • ADH – hyponatraemia
    • ACTH – Cushing’s syndrome
    • ACTH secretion can cause bilateral adrenal hyperplasia, the high levels of cortisol can lead to hypokalaemic alkalosis
  • Lambert-Eaton syndrome – antibodies to voltage gated calcium channels causing myasthenic like syndrome
227
Q

Management of small cell lung cancers?

A

Usually metastatic disease by time of diagnosis (much poorer prognosis than non-small cell)

Patients with very early stage disease (T1-2a, N0, M0) are now considered for surgery.

However, most patients with limited disease receive a combination of chemotherapy and radiotherapy

Patients with more extensive disease are offered palliative chemotherapy

228
Q

4 main ways in which lung cancers can present?

A

1) Local effects of a tumour within a bronchus
2) Spread within the chest
3) Metastatic disease
4) Non-metastatic manifestations

229
Q

Clinical features of lung cancer, due to local effects?

A
  • Cough
  • Chest pain
  • haemoptysis
  • Breathlessness
  • Dysphagia
  • Wheeze
  • Hoarse voice
  • Recurrent infections
230
Q

Effects of lung cancer spreading to chest?

A

Pancoast’s tumour - Spread to involve the brachial plexus causes pain in the shoulder and inner arm (shoulder pain, parasthesia)

Horner’s syndrome – Spread to the sympathetic ganglion (HS marked by a contracted pupil, drooping upper eyelid, inability to sweat on the side of face where the damage is)

Hoarseness and a “bovine cough” – bovine cough = where they sound like there hooting/blowing air out without being able to make the proper rumbling cough sound. This is caused by spread to the recurrent laryngeal nerve.

Involvement of the oesophagus, heart or SVC – causes upper limb oedema, facial congestion and distended neck veins (increased JVP)

231
Q

Where do lung cancer metastise to?

A
  • LN
  • Bone
  • Brain
  • Liver
  • Adrenal glands
232
Q

Investigating lung cancer?

A

CXR

CT

Bronchoscopy

PET scanning

233
Q

Management of nsclc?

A
  • MDT approach to care
  • Surgery can be curative – around 20% suitable for surgery
  • Mediastinoscopy performed prior to surgery as CT does not always show mediastinal lymph node involvement
  • Radiotherapy – curative or palliative
  • Poor response to chemotherapy – given in advanced disease, improves median survival from 6 to 10 months
234
Q

What cancers spread to lung?

A 
Breast
colorectal
prostate
kidney - RENAL CELL CARCINOMA is most common to present as pulm mets.
melanoma
thyroid
lymphoma

2a (7 decks)

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