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Respiratory Flashcards

1
Q

What is acute bronchitis?

A

a self-limiting lower respiratory tract infection

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2
Q

What is the difference between bronchitis and pneumonia?

A

Bronchitis refers to infections causing inflammation in bronchial airways, whereas pneumonia denotes infection in the lung parenchyma resulting in consolidation of the affected segment or lobe.

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3
Q

What criteria is used for diagnosing acute bronchitis?

A

Criteria by MacFarlane for acute bronchitis:

(a) An acute illness of <21 days
(b) Cough as the predominant symptom
(c) At least 1 other lower respiratory tract symptom:
a. Sputum production
b. Wheezing
c. Chest pain
(d) No alternative explanation for symptoms

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4
Q

What are the main causes of bronchitis?

A 
o	Viral (90%)
Influenza type A & B
Parainfluenza
Adenovirus
RSV
Rhinovirus
Coronavirus 
o	Bacterial
o	Environmental
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5
Q

Presentation of bronchitis

A
  1. Cough +/- sputum production that resolves in 2-3 weeks
  2. Symptoms of preceding or simultaneous URTI
  3. Malaise
  4. Chest pain
  5. Mild dyspnoea
  6. Auscultation – may be clear / rhonchi, wheezing
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6
Q

Ix for acute bronchitis

A

Clinical diagnosis but may use pulmonary function tests / CXR / CRP to rule out asthma / pneumonia.

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7
Q

Tx for acute bronchitis

A

No treatment necessary usually, may need antipyretic & SABA

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8
Q

What is asbestosis?

A

diffuse interstitial fibrosis of the lung because of exposure to asbestos fibres.

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9
Q

Name types of pneumoconiosis

A

Asbestosis
Siderosis (iron)
Silicosis (silica)
Farmer’s lung (hay dust)

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10
Q

what is the pathophysiology of asbestosis?

A

o Inhalation of airborne asbestos fibres into alveoli, causes inflammation and fibrosis of pleural parenchyma which has carcinogenic effects
o Disease progress is more rapid in smokers due to impaired mucociliary clearance
• There is a long latency period from exposure to asbestos.
• Fibrotic changes in the lungs.

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11
Q

What are the pleural abnormalities seen in asbestosis?

A

o Plaques +/- calcification
o Diffuse pleural thickening
o Benign pleural effusions
o Rounded atelectasis (atelectasis = a complete or partial collapse of the entire lung or lobe of the lung)

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12
Q

What occupations can lead to asbestos exposure?

A
  1. Shipping
  2. Plumbing
  3. Roofing
  4. Insulation
  5. Heat resistant clothing
  6. Brake lining
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13
Q

What is the presentation of asbestosis?

A
  • Long latency period
  • Exertional dyspnoea
  • Dry cough&raquo_space;> productive cough
  • Digital clubbing
  • Bilateral fine, basal end-inspiratory crepitations
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14
Q

Ix for abestosis

A

CXR
CT chest
Pulmonary function tests = restrictive pattern of disease
Bronchoalveolar lavage = microscopic asbestos bodies

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15
Q

CXR changes with asbestosis

A

a. Lower zone linear interstitial fibrosis
b. Diffuse bilateral infiltrates predominantly in the lower lobes
c. Progressively involves the entire lung
d. Pleural thickening
e. Rounded atelectasis
f. Pleural effusions

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16
Q

Mx of asbestosis

A

No curative treatment
o Oxygen therapy / pulmonary rehabilitation
o No smoking
o Immunisation against influenza and pneumococcal pneumonia
o Antimicrobial treatment of respiratory infections
o Pleural decortication / lung transplant
o Palliative care in advanced disease

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17
Q

Complications of asbestosis

A
  1. Mesothelioma = malignant tumour that develops from mesothelial cells
  2. Bronchogenic carcinoma
  3. Laryngeal cancer
  4. Pulmonary HTN
  5. Cor pulmonale
  6. R sided HF
  7. Progressive respiratory failure
  8. Caplan syndrome = RA + pneumoconiosis
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18
Q

What is asthma?

A

chronic inflammatory airway disease characterised by bronchial hyper-responsiveness, episodic acute asthma exacerbations and reversible airflow obstruction.

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19
Q

What are the 3 characteristic features of asthma?

A

o Bronchoconstriction = smooth muscles of the bronchi contract causing a reduction in the diameter of the airways
o Reversible airway obstruction = usually responds to bronchodilators e.g., salbutamol
o Hypersensitivity = can triggered by environmental factors

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20
Q

What is the pathology of asthma?

A

Acute (30 min)
o Mast cell degranulation = histamine release
o Bronchoconstriction, mucus plugs and mucosal swelling
Chronic (12 hours)
o T helper cells release IL-3,4,5 causing mast cell, eosinophil, and B cell recruitment
o Airway remodelling

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21
Q

what are the different types of asthma?

A

ALLERGIC ASTHMA (extrinsic asthma) – most common type of asthma, begins with intermittent symptoms in childhood and is usually associated with atopy.

NON-ALLERGIC ASTHMA (intrinsic asthma) – uncommon type of asthma that’s not related to atopy and is typically associated with a poor response to standard treatment.

Subtypes / variants:
o Exercise induced asthma
o Adult onset asthma – poor response to standard treatment
o Cough variant asthma – predominant symptom is chronic dry cough

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22
Q

Triggers for asthma

A

o Allergic asthma:
 Atopy
 Environmental allergens – pollen, dust mites, domestic animals, mould spores, flour dust

o	Non-allergic asthma:
	Viral RTI
	Cold air
	Physical exertion / laughter
	GORD
	Chronic sinusitis / rhinitis
	Aspirin/NSAIDs/b-blockers
	Stress
	Irritant induced asthma
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23
Q

Risk factors for asthma

A 
o	Family history 
o	Atopic history 
o	History of allergies
o	Low socioeconomic status 
o	Childhood second hand exposure to smoke
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24
Q

Presentation of asthma

A
  1. Episodic symptoms
  2. Diurnal variability – typically worse at night
  3. Dry cough with wheeze and SOB
  4. Chest tightness
  5. Bilateral widespread polyphonic end expiratory wheeze heard by a healthcare professional
  6. Prolonged expiratory phase on auscultation
  7. Hyperresonance to lung percussion
  8. History of atopic conditions
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25
Q

How is asthma diagnosed?

A

Diagnosis made based on a combination of the following:

o Presence of more than one variable symptom of wheeze, cough, breathlessness and chest tightness

o Personal/family history of other atopic conditions

o The results of fractional exhaled nitric oxide testing (in over 17s, >40 parts per billion is a positive result, used to confirm eosinophilic airway inflammation)

o Results of objective tests to detect airway obstruction, when the person is symptomatic:
 Spirometry
• FEV1/FVC ratio <70%, reduced
• FVC normal
• FEV1 significantly reduced
 Bronchodilator reversibility
• Improvement of FEV1 of >12% + increase in volume of >200ml following SABA or corticosteroids = positive result
• In children, just FEV1 >12% = positive result
 Variable peak expiratory flow (PEF)
• >20% variability after monitoring twice daily for 2-4 weeks = positive result

o Direct bronchial challenge test with histamine or methacholine (specialist centres)

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26
Q

How are children under 5 diagnosed with asthma?

A

use clinical judgement as child can’t perform objective tests

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27
Q

What do the British thoracic society SIGN guidelines say for initiating asthma tx?

A

o High probability of asthma = try treatment
o Intermediate probability of asthma = perform spirometry with reversibility testing
o Low probability of asthma = consider referral and investigation for other causes

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28
Q

What is FVC?

A

forced vital capacity = measures the amount of gas expelled when a person takes a deep breath and then forcefully exhales maximally and as rapidly as possible

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29
Q

What is FEV?

A

forced expiratory volume = amount of air expelled during specific time intervals of the FVC test

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30
Q

What is FEV1?

A

the volume exhaled in the first second. Healthy individuals can exhale 80% of the FVC in one second.

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31
Q

What do you see on spirometry for obstructive disease?

A

decrease in both FEV1 and FEV1/FVC ratio

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32
Q

what do you see on spirometry for restrictive disease?

A

normal FEV1/FVC ratio

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33
Q

Red flag symptoms that suggest another diagnosis than asthma

A

o Prominent systemic features e.g., myalgia, fever, weight loss
o Unexpected clinical findings e.g., crackles, finger clubbing, cyanosis, cardiac disease, monophonic wheeze, stridor
o Persistent non-variable breathlessness
o Chronic sputum production
o Unexplained restrictive spirometry
o CXR shadowing
o Marked blood eosinophilia

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34
Q

Asthma differentials

A 
o	Bronchiectasis 
o	COPD
o	Ciliary dyskinesia
o	CF
o	Foreign body aspiration 
o	GORD
o	HF
o	Interstitial ling disease e.g., asbestosis
o	Lung Ca
o	Pertussis
o	PE
o	TB
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35
Q

NICE guidelines for asthma management

A
  1. SABA PRN for infrequent wheezy episodes
    • regular low dose inhaled corticosteroid
    • oral montelukast (oral leukotriene receptor antagonist)
    • LABA and continue only if the patient has a good response
  5. Consider changing to a maintenance and reliever therapy (MART) regime
  6. Increased inhaled corticosteroid to moderate dose
  7. Consider increasing the inhaled corticosteroid to high dose or oral theophylline or an inhaled LAMA (tiotropium)
  8. Refer to specialist
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36
Q

Try draw out NICE ladder for asthma

A

See notes

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37
Q

Additional management for asthma patients

A
  • Everyone should have an individual asthma self-management programme
  • Yearly flu jab
  • Yearly asthma review
  • Advise exercise and avoid smoking
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38
Q

What is a SABA? Give an example, how it works, when its used and the side effects

A

Short acting beta 2 adrenergic receptor agonist (SABA)

Salbutamol

Reliver or rescue medication used PRN for acute exacerbations

Dilation of bronchial smooth muscles

Tremor
Arrhythmias
Tachycardia 
Hyperglycaemia
Hypokalaemia
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39
Q

What is an ICS? Give an example, how it works, when its used and the side effects

A

Inhaled corticosteroid (ICS)

Beclometasone
Fluticasone
Mometasone

Maintenance or preventer used regularly
Don’t take full effects until they’ve been used for 1 week

Oral thrush
Hoarse/croaky voice 
Cough
Nosebleeds
Stunted growth in children
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40
Q

What is a LABA? Give an example, how it works, when its used and the side effects

A

Long acting beta 2 adrenergic receptor agonist (LABA)

Salmeterol

Longer action than SABA, for long term maintenance therapy (taken every day regardless of symptoms)

Dilation of bronchial smooth muscles

Tremor
Arrhythmias 
Tachycardia
Hyperglycaemia
Hypokalaemia
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41
Q

What is a LAMA? Give an example, how it works, when its used and the side effects

A

Long acting muscarinic antagonist (LAMA)

Tioptropium

Blocks parasympathetic nervous system to cause bronchodilation

Dry mouth
Constipation
Urinary retention

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42
Q

Give an example leukotriene receptor antagonist, how it works, when its used and the side effects

A

Leukotriene receptor antagonist

Montelukast

Prevents leukotrienes binding to receptors and causing bronchoconstriction/ inflammation

Oral URTI
Pharyngitis
Headache
Fever

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43
Q

What monitoring is required for theophylline?

A

Need to monitor plasma theophylline as it has a narrow therapeutic window, checked 5 days after starting and 3 days after dose changes

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44
Q

What is MART?

A

Maintenance and reliever therapy (MART)

Low dose ICS and LABA combined

Single inhaler for preventer and reliever

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45
Q

Give example oral corticosteroids, when they are used in asthma and the side effects

A

Methylprednisolone
Prednisolone

For severe persistent asthma

Cushings
Osteoporosis
Reduced growth 
Thin skin 
Immunosuppression 
Cataracts
Oedema 
Suppressed HPA axis
Teratogenic
Emotional disturbance
Rise in BP
Obesity
Increased hair growth 
Diabetes
Striae
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46
Q

What is an acute exacerbation of asthma?

A

rapid deterioration of symptoms, could be triggered by any of the typical asthma triggers such as infection, exercise, or cold weather.

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47
Q

Presentation of acute asthma

A
  • Progressively worsening SOB
  • Use of accessory muscles
  • Tachypnoea
  • Symmetrical expiratory wheeze on auscultation
  • Chest sounds tight on auscultation, with reduced air entry
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48
Q

How is acute asthma graded

A

Moderate
Severe
Life threatening

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49
Q

What is moderate acute asthma

A

o PEFR 50-75% predicted

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50
Q

What is severe acute asthma?

A

o PEFR 33-50% predicted
o Respiratory rate >25
o Heart rate >110
o Unable to complete sentences

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51
Q

What is life threatening acute asthma

A 
o	PEFR <33%
o	Sats <92%
o	Becoming tired 
o	No wheeze, this occurs when the airways are so tight that there is no air entry at all. ‘Silent chest’
o	Haemodynamic instability – shock
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52
Q

What are the ABG results seen In acute asthma?

A

respiratory alkalosis due to tachypnoea causing CO2 drop.

A normal pCO2 or hypoxia is concerning as it means the person is tiring = life threatening asthma.

Respiratory acidosis due to high CO2 = very bad sign

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53
Q

How is the patient monitored during an acute asthma attack?

A 
o	RR
o	Respiratory effort
o	Peak flow
o	O2 saturations 
o	Chest auscultation
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54
Q

Mx of acute asthma

A
  1. Moderate
    o Nebulised short acting beta 2 agonist (salbutamol) – repeated as often as required : WATCH THEIR SERUM POTASSIUM (salbutamol = hypokalaemia)
    o Nebulised ipratropium bromide
    o Steroids – oral prednisolone / IV hydrocortisone (continue for 5 days)
    o Abx if bacterial infection
  2. Severe
    o Oxygen
    o Aminophylline infusion
    o IV salbutamol
  3. Life threatening
    o IV magnesium sulphate infusion
    o Admission ITU/HDU
    o Intubation
55
Q

What is asthma COPD overlap syndrome and what should you expect?

A

Symptoms of both asthma and COPD

Significantly worse respiratory symptoms, poorer quality of life and increased risk of exacerbations/hospital admissions

56
Q

What is bronchiectasis?

A

permanent dilation of the airways secondary to chronic infection or inflammation.

57
Q

causes of bronchiectasis

A
  • Post infective – TB, measles, pertussis, pneumonia
  • Cystic fibrosis
  • Bronchial obstruction e.g., lung cancer, foreign body
  • Immune deficiency – selective IgA, hypogammaglobinaemia
  • Allergic bronchopulmonary aspergillosis
  • Ciliary dyskinetic syndrome – Kartagener’s syndrome, Young’s syndrome
  • Yellow nail syndrome
58
Q

Symptoms of bronchiectasis

A
  • Cough
  • Sputum production (daily)
  • Crackles, high pitched inspiratory squeaks and rhonchi
  • Dyspnoea
  • Fever
  • Fatigue
  • Haemoptysis
  • Weight loss
  • Pleuritic chest pain
  • Rhinosinusitis
59
Q

Ix for bronchiectasis

A 
CXR
Chest CT
Sputum culture and sensitivities 
FBC
Spirometry
60
Q

CXR signs for bronchiectasis

A

o Tram track opacities
o Air fluid levels
o Ring shadows
o Dilated rhonci and bronchioles

61
Q

CT chest signs of bronchiectasis

A

o Thickened, dilated airways
o Air fluid levels
o Cysts

62
Q

Mx for bronchiectasis

A
  1. Influenza and pneumococcal vaccine
  2. Pulmonary rehabilitation
  3. Stop smoking
  4. Airway clearance therapy
  5. Inhaled bronchodilator – salbutamol
  6. Nebulised hypertonic saline
  7. Abx for acute exacerbations
63
Q

What is bronchiolitis?

A

inflammation and infection in the bronchioles, the small airways of the lungs. Childhood disease.

64
Q

causes of bronchiolitis

A

respiratory syncytial virus (RSV) [Other causes – mycoplasma and adenoviruses]

65
Q

When do patients get bronchiolitis and what age are they?

A

Common in the winter in children under 1 year (most common in children <6 months old)

66
Q

Pathology of bronchiolitis

A

: small size of airways in children means that a small amount of inflammation and mucus in the airway can cause great effect on the infants ability to circulate air to the alveoli = wheeze and crackles.

67
Q

Symptoms of bronchiolitis

A
  • Coryzal symptoms (URTI) – snotty nose, sneezing, mucus in throat, watery eyes
  • Signs of respiratory distress
  • Dyspnoea
  • Heavy laboured breathing
  • Tachypnoea
  • Poor feeding
  • Mild fever (under 39)
  • Apnoeas
  • Wheeze and crackles on auscultation
  • Grunting
  • Stridor
  • Course of infection = URTI with coryzal symptoms, half get better and half get worse. Chest symptoms develop 1-2 days later, most fully recover in 2-3 weeks.
68
Q

Signs of respiratory distress in a child

A 
Raised respiratory rate 
o	Accessory muscle use 
o	Intercostal and subcostal recessions 
o	Nasal flaring 
o	Head bobbing 
o	Tracheal tugging 
o	Cyanosis – due to low oxygen saturation 
o	Abnormal airway noises
69
Q

Reasons to admit a child with bronchiolitis

A
  • <3 months old
  • Pre-existing condition – prematurity, Down’s syndrome, cystic fibrosis
  • 50-75% or less of their normal milk intake
  • Clinical dehydration
  • Respiratory rate above 70
  • Oxygen sats below 92%
  • Moderate to severe respiratory distress = deep recessions, head bobbing
  • Apnoeas
  • Parents not confident in managing at home / difficulty accessing medical help from home
70
Q

Mx for bronchiolitis

A
  • Supportive
  • Adequate intake – oral, NG or IV fluids
  • Saline nasal drops and nasal suctioning
  • Supplementary oxygen
  • Ventilatory support: high flow oxygen, CPAP, intubation and ventilation
  • PALIVIZUMAB – monoclonal antibody against RSV, given as a monthly injection to prevent bronchiolitis in high risk children (ex-premature/congenital heart disease)
71
Q

complication of bronchiolitis

A
  • Increased risk of viral induced wheeze during childhood
72
Q

Definition of COPD

A

non reversible long-term deterioration in air flow through the lungs caused by damage to lung tissue, which is almost always the result of smoking.

73
Q

Presentation of COPD

A
  • Long term smoking
  • Chronic SOB
  • Cough
  • Sputum production
  • Wheeze
  • Recurrent respiratory infections – particularly in winter
  • DOES NOT CAUSE CLUBBING. Haemoptysis and chest pain is unusual
74
Q

Grading used for dyspnoea in COPD

A
  • Grade 1 – breathless on strenuous exercise
  • Grade 2 – breathless on walking up hill
  • Grade 3 – breathless that slows walking on the flat
  • Grade 4 – stop to catch breath after walking 100m on flat
  • Grade 5 – unable to leave house due to breathlessness
75
Q

Diagnosis of COPD

A
  1. Clinical presentation
  2. Spirometry:
    o Obstructive = FEV1/FVC <70%
    o No dramatic response to reversibility testing
  3. CXR – to exclude lung cancer
  4. FBC – polycythaemia or anaemia
  5. BMI to assess later weight loss
  6. Sputum culture
  7. ECG and echocardiogram
  8. CT thorax – to exclude fibrosis, lung cancer and bronchiectasis
  9. Serum alpha-1 antitrypsin – if there’s deficiency = early onset and more severe disease
  10. Transfer factor for carbon monoxide (TLCO) – decreased in COPD (indication of disease severity & raised in asthma)
76
Q

Grading system for severity of COPD

A

Severity grading by FEV1:

  • Stage 1 = FEV1 >80% of predicted
  • Stage 2 = FEV1 50-79% of predicted
  • Stage 3 = FEV1 30-49% of predicted
  • Stage 4 = FEV1 <30% of predicted
77
Q

Long term management of COPD

A

1) SABA = salbutamol OR SAMA = ipratropium bromide
2) If they do not have asthmatic or steroid responsive features = LABA and LAMA e.g., ellipta, ultibro breezhaler and duaklir genuair
3) If they have asthmatic/steroid responsive features = LABA and ICS e.g., fostair, Symbicort, Seretide
4) LABA + LAMA + ICS = trimbo, trelegy ellipta

5) Other options:
a. Nebulisers – salbutamol/ipratropium
b. Oral theophylline
c. Oral mucolytic therapy e.g., carbocisteine
d. Long term abx e.g., azithromycin
e. Long term oxygen therapy at home

78
Q

When should a COPD patient have oxygen at home?

A

if chronic hypoxia, polycythaemia, cyanosis or heart failure secondary to pulmonary HTN (cor pulmonale)

79
Q

Other management for COPD

A
  • Stop smoking

- Pneumococcal and influenza vaccine

80
Q

What is an exacerbation of COPD?

A

acute worsening of symptoms e.g., cough, SOB, sputum production and wheeze. Usually triggered by viral or bacterial infection.

81
Q

Ix for exacerbation of COPD

A 
-	ABG = 
o	Raised pCO2 = respiratory alkalosis
o	Raised bicarbonate as they chronically retain CO2 so the kidneys produce more bicarbonate to compensate 
-	CXR
-	ECG
-	FBC
-	U&E
-	Sputum culture
-	Blood culture
82
Q

How is oxygen therapy used in COPD?

A
  • Venturi masks are used to give oxygen as they can deliver a specific percentage concentration – some oxygen leaks out the side of the mask and normal air can be inhaled alongside the oxygen
  • Venturi masks deliver:
    o 24% blue
    o 28% white
    o 31% oxygen
    o 35% yellow
    o 40% red
    o 60% green
  • If retaining CO2, aim for 88-92% on sats titrated on venturi mask
  • If not retaining CO2 and normal bicarbonate, aim for >94% sats
83
Q

Treatment for COPD exacerbation

A
  1. If they can be treated at home:
    a. Prednisolone 30mg OD 7-14 days
    b. Regular inhalers or home nebulisers
    c. Abx if infection
  2. In hospital
    a. Nebulised bronchodilators e.g., salbutamol and ipratropium
    b. Steroids (IV hydrocortisone or oral prednisolone)
    c. Abx if infection
    d. Physiotherapy to clear sputum
  3. Severe cases
    a. IV aminophylline
    b. NIV
    c. Intubation and ventilation – ITU/HDU
    d. Doxapram – respiratory stimulant where NIV/intubation isn’t indicated
84
Q

Causes of clubbing

A 
Hereditary clubbing 
Cyanotic heart disease
Infective endocarditis
Cystic fibrosis
TB
Inflammatory bowel disease
Liver cirrhosis
85
Q

Definition of cystic fibrosis

A

autosomal recessive disorder causing increased viscosity of secretions (e.g., in the lungs and pancreas). Due to a defect in the cystic fibrosis transmembrane conductase regulator gene (CFTR) on chromosome 7, which codes a cAMP-regulated chloride channel.

86
Q

Genetic inheritance of CF

A
  1. Autosomal recessive genetic condition
  2. Genetic mutation on cystic fibrosis transmembrane conductance regulatory gene
  3. Chromosome 7
  4. Most common mutation = delta-F508 mutation
  5. The gene codes for cellular channels – particularly chloride channels
  6. 1 in 25 are carriers of the mutation
  7. 1 in 2500 children have CF
87
Q

Features of CF

A
  • Thick pancreatic and biliary secretions that cause blockage of the ducts = lack of digestive enzymes e.g., pancreatic lipase
  • Low volume thick airway secretions that reduce airway clearance = bacterial colonisation and susceptibility to airway infections
  • Congenital bilateral absence of vas deferens in males = healthy sperm but no way of ejaculating healthy sperm causing male infertility
88
Q

How do children with CF present?

A
  1. Screened at birth with newborn blood spot test
  2. Meconium ileus – meconium is stuck in the bowel causing obstruction = no meconium passed, abdominal distention and vomiting
  3. Childhood = recurrent LRTI, failure to thrive or pancreatitis
89
Q

Symptoms of CF

A
  • Chronic cough
  • Thick sputum production
  • Recurrent RTI
  • Loose, grey stools (steatorrhoea) due to a lack of lipase enzymes
  • Abdominal pain and bloating
  • Salty taste when kissing the child
  • Failure to thrive
  • Nasal polyps
  • Finger clubbing
  • Crackles and wheeze on auscultation
  • Abdominal distention
90
Q

Diagnosis of CF

A

1) Newborn blood spot testing

2) Sweat test = gold standard
o Pilocarpine applied to skin, electrodes either side and small current is passed causing the skin to sweat
o Sweat is absorbed with lab gauze and tested for chloride concentration
o CF = chloride concentration >60 mmol/L

3) Genetic testing for CFTR gene – amniocentesis or chorionic villous sampling or after birth blood test

91
Q

Bacterial colonisation of the lungs in CF - what bacteria?

A
  • Staphylococcus aureus – long term prophylactic flucloxacillin
  • Pseudomonas aeruginosa – difficult to get rid of, can become resistant to multiple abx. Increases morbidity and mortality. Children with CF to avoid others with CF to prevent spread of pseudomonas aeruginosa. Tx: long term nebulised tobramycin and oral ciprofloxacin.
  • Haemophilus influenza
  • Krebsiella pneumoniae
  • E coli
  • Burkhodheria cepacia
92
Q

Mx for CF

A
  • Chest physiotherapy – multiple times daily to clear mucus
  • Exercise
  • High calorie diet – due to malabsorption
  • CREON tablets – for pancreatic insufficiency
  • Prophylactic flucloxacillin – for staph aureus colonisation
  • Treat chest infections
  • Bronchodilators
  • Nebulised DNase (dornase alfa) – easier to clear respiratory secretions
  • Nebulised hypertonic saline
  • Vaccinations – pneumococcal, influenza and varicella
  • Lung transplantation
  • Liver transplantation
  • Fertility treatment
  • Genetic counselling
93
Q

Monitoring for CF

A
  • Respiratory colonisation
  • Diabetes
  • Osteoporosis
  • Vitamin D deficiency
  • Liver failure
94
Q

Average life expectancy for people with CF

A

47

95
Q

what is interstitial lung disease?

A

conditions that affect the lung parenchyma causing inflammation and fibrosis.

96
Q

how is interstitial lung disease diagnosed?

A

high resolution CT chest = ground glass appearance. Can do lung biopsy if diagnosis unclear

97
Q

mx interstitial lung disease

A
  • Remove/treat underlying cause
  • Home oxygen if chronically hypoxic
  • Stop smoking
  • Physiotherapy and pulmonary rehabilitation
  • Pneumococcal and influenza vaccines
  • Advanced care planning / palliative care
  • Lung transplant
98
Q

name 6 types of interstitial lung disease

A 
Idiopathic pulmonary fibrosis
Drug induced pulmonary fibrosis
Secondary pulmonary fibrosis
Hypersensitivity pneumonitis
Crytogenic organising penumonia
Asbestosis
99
Q

what is pulmonary fibrosis?

A

replacement of normal elastic lung tissue with scar tissue that is stiff and doesn’t function effectively

100
Q

What is idiopathic pulmonary fibrosis, the symptoms and tx?

A

Progressive pulmonary fibrosis with no clear cause

SOB
Dry cough
Clubbing
Bibasal fine inspiratory crackles

Pirfenidone
Nintedanib

101
Q

Drugs that cause drug induced pulmonary fibrosis

A
  • Amiodarone
  • Cyclophosphamide
  • Methotrexate
  • Nitrofurantoin
102
Q

Conditions that cause secondary pulmonary fibrosis

A
  • Alpha 1 antitripsin deficiency
  • RA
  • SLE
  • Systemic sclerosis
103
Q

What is hypersensitivity pneumonitis and what are some types?

A

Type III hypersensitivity reaction to environmental allergens that causes parenchymal inflammation

Examples:

  • Bird fanciers lung
  • Farmers lung
  • Mushroom workers lung
  • Malt workers lung
104
Q

What is cryogenic organising pneumonia, the symptoms, ix and tx?

A

bronchiolitis obliterans

Focal area of inflammation of the lung tissue

SOB
Cough
Fever
Lethargy
Focal consolidation on CXR

Need lung biopsy (gets mistaken for pneumonia)

Tx = systemic corticosteroids

105
Q

What is influenza?

A

seasonal influenza, outbreaks occur in the winter. It’s an RNA virus. There are 3 types: A, B and C (A and B are most common).

106
Q

Presentation of influenza

A
  • Fever
  • Coryzal symptoms
  • Lethargy and fatigue
  • Anorexia
  • Muscle and joint aches
  • Headache
  • Dry cough
  • Sore throat
107
Q

Diagnosis of influenza

A
  • Clinical diagnosis

* Viral nasal or throat swabs for PCR analysis

108
Q

Mx of influenza

A
  • Public health monitor case numbers
  • Self care, adequate fluids and rest
  • If at risk of complications (start within 48 hrs of symptom onset) =
    o Oral oseltamivir 5 days
    o Inhaled zanamivir 5 days
  • Can give oseltamivir and zanamivir to high risk patients after exposure as prophylaxis
109
Q

complications of influenza

A
  • Otitis media, sinusitis and bronchitis
  • Viral pneumonia
  • Secondary bacteria pneumonia
  • Worsening COPD and HF
  • Febrile convulsions in young children
  • Encephalitis
110
Q

how are children vaccinated against influenza

A
  1. It’s given intranasally
  2. First dose is given at 2-3 years old, then annually after that
  3. It’s a live vaccine
  4. More effective than injectable vaccine
  5. Only children aged 2-9 years that haven’t had a vaccine before need 2 doses
111
Q

CI for the influenza vaccine in children

A
  • Immunocompromised
  • Aged <2 years
  • Current febrile illness or blocked nose
  • Current wheeze
  • Egg allergy
  • Pregnancy/breastfeeding
  • Child is taking aspirin e.g., for Kawaski disease – risk of Reye’s syndrome (swelling of liver and brain)
112
Q

How are adults vaccinated against influenza

A
  1. Inactivated vaccine
  2. Can get fever and malaise – lasts for 1-2 days
  3. Stored at 2-8 degrees, shielded from light
  4. Cis: egg hypersensitivity
  5. Takes 10-14 days for antibodies to reach protective levels
113
Q

Which adults get the influenza vaccine

A
  • Over 65s
  • Chronic respiratory disease
  • Chronic heart disease
  • Chronic kidney disease
  • Chronic liver disease
  • Chronic neurological disease
  • DM
  • Immunosuppressed
  • Asplenia or splenic dysfunction
  • Pregnant women
  • > 40 BMi
  • Health and social care staff
  • People in long stay residential care homes
  • Carers
114
Q

What types of cancer can lung cancer be?

A
  1. Small cell lung cancer – 20%
  2. Non-small cell lung cancer – 80%
    a. Adenocarcinoma (most common) – seen in non-smokers
    b. Squamous cell carcinoma
    c. Large cell carcinoma
    d. Other types
115
Q

What is associated with small cell lung cancers?

A

contain neurosecretory granules that release neuroendocrine hormones = paraneoplastic syndromes.

116
Q

Presentation of lung cancers

A
  • SOB
  • Cough
  • Haemoptysis
  • Finger clubbing (squamous cell carcinoma)
  • Recurrent pneumonia
  • Weight loss
  • Lymphadenopathy – often supraclavicular nodes
  • Fixed monophonic wheeze
117
Q

Extra pulmonary manifestations of lung cancer (general)

A
  • Recurrent laryngeal nerve palsy – hoarse voice
  • Phrenic nerve palsy – diaphragm weakness = SOB
  • Superior vena cava obstruction – facial swelling, difficulty breathing and distended neck veins
    o Pemerton’s sign = raising hands over the head causes facial congestion and cyanosis = medical emergency
118
Q

Extra pulmonary manifestation of pancoast tumours

A
  • Horner’s syndrome – ptosis, anhidrosis and miosis (Pancoast tumour in pulmonary apex compressing the sympathetic ganglion)
119
Q

Extra pulmonary manifestations of SCLC

A
  • SiADH – hyponatraemia (ectopic ADH from SCLC)
  • Cushing’s syndrome (ectopic ACTH from SCLC)
  • Limbic encephalitis – short term memory impairment, hallucinations, confusion and seizures (SCLC causes autoantibodies against tissues in the brain: anti-Hu antibodies)
  • Lambert-Eaton myasthenic syndrome – proximal muscle weakness, intraocular muscle weakness = diplopia, ptosis, pharyngeal muscle weakness = slurred speech and dysphagia & autonomic dysfunction (dry mouth, blurred vision, impotence & dizziness) – SCLC causes autoantibodies against voltage gated calcium channels on presynaptic terminals in motor neurones.
120
Q

Extra pulmonary manifestations of adenocarcinoma in the lungs

A
  • Gynaecomastia
121
Q

Extra pulmonary manifestation of squamous cell carcinoma in the lungs

A
  • Hypercalcaemia (ectopic PTH from squamous cell carcinoma)
122
Q

When to do a 2 week wait referral for CXR to look for lung cancer

A
  • Clubbing
  • Lymphadenopathy (supraclavicular or persistent abnormal cervical nodes)
  • Recurrent or persistent chest infections
  • Raised platelets = thrombocytosis
  • Chest signs of lung cancer
-	Or in over 40’s: 2+ unexplained symptoms in non-smokers/1+ unexplained symptom in smoker –
o	Cough
o	SOB
o	Fatigue 
o	Chest pain 
o	Weight loss
o	Loss of appetite
123
Q

Ix for lung cancer

A
  1. CXR
  2. Staging CT CAP (contrast enhanced)
  3. PET-CT
  4. Raised platelets on bloods
  5. Bronchoscopy with endobronchial ultrasound (EBUS) & biopsy
  6. Histological diagnosis – bronchoscopy or percutaneous biopsy
124
Q

CXR signs seen in lung cancer

A

o Hilar enlargement
o Peripheral opacity – visible lesion in lung field
o Pleural effusion – usually unilateral in cancer
o Collapse

125
Q

Tx for non small cell lung cancer

A

o Surgery
o Radiotherapy
o Chemotherapy – in addition to surgery/radiotherapy or palliative

126
Q

Tx for small cell lung cancer

A

o Chemotherapy
o Radiotherapy
o Worse prognosis
o Endobronchial treatment with stents or debulking to relieve obstruction

127
Q

Surgeries to remove lung cancers

A
  1. Options to remove tumour:
    a. Segmentectomy or wedge resection
    b. Lobectomy – absent breath sounds in one zone
    c. Pneumonectomy (entire lung) – no breath sounds on one side
  2. Types of surgery
    a. Thoracotomy – open surgery with an incision and separation of the rib cage to assess the thoracic cavity
    b. Video assisted thorascopic surgery – minimally invasive keyhole surgery
    c. Robotic surgery
128
Q

Thoracotomy incisions (3)

A

a. Anterolateral thoracotomy – front and side
b. Axillary thoracotomy – axilla
c. Posterolateral thoracotomy – incision around the back and side (most common)

129
Q

What is OSA

A

caused by collapse of the pharyngeal airway. It is characterised by episodes of apnoea during sleep, where the person stops breathing periodically for up to a few minutes. The partner usually reports this happening, and the patient is unaware of the episodes.

130
Q

RFs for OSA

A
  • Middle age
  • Male
  • Obesity
  • Alcohol
  • Smoking
131
Q

symptoms of OSA

A
  • Episodes of apnoea during sleep (reported by their partner)
  • Snoring
  • Morning headache
  • Waking up unrefreshed from sleep
  • Daytime sleepiness
  • Concentration problems
  • Reduced oxygen saturation during sleep
  • Hypertension,
  • heart failure
  • increase the risk of myocardial infarction and stroke.
132
Q

Scoring system for sleepiness due to OSA

A

Epworth Sleepiness Scale
The Epworth Sleepiness Scale is used to assess symptoms of sleepiness associated with obstructive sleep apnoea.
- Daytime sleepiness
- Occupation / driving
- Asks how likely you are to sleep in certain situations

133
Q

Mx of OSA

A
  • referral to an ENT specialist or a specialist sleep clinic to perform sleep studies
  • correct reversible risk factors by advising them to stop drinking alcohol, stop smoking and lose weight
  • continuous positive airway pressure (CPAP) machine that provides continuous pressure to maintain the patency of the airway
  • Surgery = significant surgical reconstruction of the soft palate and jaw. The most common procedure is called uvulopalatopharyngoplasty (UPPP).
134
Q

Ix and mx for coal workers pneumoconiosis

A

Coal workers pneumoconiosis – coal dust particles cause fibrosis

Investigations:

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

Management:

  • Avoid exposure to coal dust and other respiratory irritants (e.g. Smoking).
  • Manage symptoms of chronic bronchitis
  • Patients may be eligible for compensation via the Industrial Injuries Act.

Finals Revision (18 decks)

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