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Phase 3 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

How would you classify obstructive lung disease using spirometry?

A

FEV1/FVC ratio < 70%

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2
Q

Describe how the severity of COPD is measured.

A

By % predicted FEV1 post bronchodilator

  • Mild > 80%
  • Moderate 50-80%
  • Severe 30-50%
  • Very severe <30%
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3
Q

How would you distinguish between COPD and asthma using spirometry?

A
  • Give salbutamol inhaler and spirometry readings taken before and after
  • 15% and 400ml FEV1 reversibility suggests asthma
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4
Q

Aside from reversibility seen in spirometry, how else would you investigate asthma?

A
  • PEFR – look for diurnal variation, response to inhaled corticosteroid,
  • Spirometry – before and after a trial of inhaled local corticosteroid
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5
Q

How would restrictive lung disease present in spirometry?

A
  • FEV1 and FVC reduced

- FEV1/FVC ratio > 70%

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6
Q

List some causes of restrictive lung disease.

A
  • Interstitial lung disease
  • Kyphoscoliosis/chest wall deformity
  • Previous pneumoectomy
  • Neuromuscular disease
  • Obesity
  • Low effort/technique
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7
Q

What methods are used to measure lung volume?

A
  • helium dilation

- body plethysmography

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8
Q

Describe the changes in lung volume seen in obstructive and restrictive disease.

A

obstructive: increased RV and RV/TLC ratio
restrictive: lung volume decreased

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9
Q

Discuss the usage of transfer factor and what it is affected by.

A
  • single breath of very small conc. of CO
  • measure conc. in expired gas to derive uptake in lungs
  • affected by: alveolar surface area, pulmonary capillary volume, Hb conc, V/Q mismatch
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10
Q

In which conditions is transfer factor reduced?

A
  • emphysema
  • interstitial lung disease
  • pulmonary vascular disease
  • anaemia
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11
Q

What must you be aware of when giving oxygen to patients with acute asthma, COPD or hypoventilation?

A

their O2 stats will now appear normal

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12
Q

Name causes of hypoxaemia.

A
  • hypoventilation e.g. drugs, neuromuscular disease
  • ventilation/perfusion mismatch e.g. COPD, pneumonia
  • shunt e.g. CHD
  • low inspired oxygen e.g. altitude, flight
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13
Q

What is a ‘shunt’?

A

extreme form of V/Q mismatch where blood bypasses the lungs altogether

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14
Q

Describe how you would identify a V/Q mismatch.

A
  • alveolar oxygen equation: PaO2 = FiO2 - (1.25 x PaCO2)
  • measure pO2 of blood
  • difference between calculated alveolar and arterial pO2
  • > 4kPa suggests V/Q mismatch
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15
Q

Describe the acid-base differences between acute respiratory acidosis and compensated acidosis.

A
  • acute: increased pCO2, normal HCO3-, increased H+

- compensated: increased pCO2, increased HCO3-(renal compensation), normal H+

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16
Q

Define COPD.

A
  • characterised by airflow obstruction

- usually progressive, not fully reversible

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17
Q

What are some causes of COPD?

A

smoking, environmental pollution, occupational dusts, alpha 1 anti-trypsin deficiency

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18
Q

Describe the effects of cigarette smoking on the airways.

A
  • cilia motility reduced
  • airway inflammation
  • mucus and goblet cell hypertrophy
  • increased protease action and decreased anti-protease inhibition
  • squamous hyperplasia -> risk increased of lung Ca
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19
Q

Define emphysema.

A

abnormal permanent enlargement of airspaces distal to terminal bronchioles

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20
Q

Define chronic bronchitis.

A

the production of sputum on most days for at least 3 months in at least 2 years - other causes of cough must be excluded

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21
Q

Discuss the pathology of bronchitis.

A
  • increased epithelial mucous cells
  • squamous metaplasia
  • mucus gland hyperplasia
  • neutrophil and CD8+ lymphocyte infiltration
  • loss of interstitial support
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22
Q

Differentiate between bronchitis and bronchiolitis.

A
  • bronchitis: larger airways >4mm diameter - inflammation leads to scarring and thickening of airways
  • bronchiolitis: 2-3mm, early feature of COPD
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23
Q

What are the cells and components that lead to the inflammation seen in bronchitis?

A
  • macrophages, CD8 and CD4 T lymphocytes, neutrophils
  • TNF, IL8, neutrophil elastase, proteinase 3, elastase, MMP, ROS
  • chemoattractant substances in cigarette smoke
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24
Q

Describe the mechanisms that lead to airway obstruction.

A
  • loss of elasticity and alveolar attachments due to emphysema: airways collapse on expiration, airtrapping and hyperinflation, increased work of breathing, breathlessness
  • goblet cell metaplasia with mucus plugging of lumen
  • inflammation of airway wall
  • thickening of bronchiolar wall: smooth muscle hypertrophy and peribronchial fibrosis
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25
Q

How is COPD diagnosed?

A 
CLINICAL PRESENTATION
Consider COPD diagnosis for people who are over 35 and smokers/ex-smokers with any of:
- exertional breathlessness
- chronic cough
- regular sputum production
- frequent winter 'bronchitis'
- wheeze

SPIROMETRY
- obstructive pattern: FEV1/FVC ratio <70%

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26
Q

Briefly describe the treatment of COPD.

A
  1. Inhaled bronchodilators
    - SABA: salbutamol - SAMA: ipatropium bromide
    - LABA: salmeterol - LAMA: tiotropium
  2. Inhaled corticosteroids
    - beclomethasone
    - oxygen therapy
  3. Oral theophyllines
  4. Mucolytics - carbocysteine
  5. Nebulised therapy
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27
Q

What is the mechanism of action of beta-adrenergic bronchodilators?

A

Relaxes bronchial smooth muscle, inducing bronchodilation. Inhibit pro-inflammatory cytokine release from mast cells and TNF-α release from monocytes, reducing airway inflammation. Increase mucus clearance from the airways by stimulating cilia action.

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28
Q

Describe the mechanism of action of beclomethasone.

A

Anti-inflammatory effect on the airways.
Decrease formation of pro-inflammatory cytokines.
Up-regulates beta-2-adrenoreceptors in airways.

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29
Q

Discuss respiratory failure in COPD in regards to pink puffers and blue bloaters.

A

PINK PUFFERS

  • high respiratory drive
  • type 1 RF: PaO2 down, PaCO2 down
  • pursed lip breathing
  • using accessory muscles
  • wheeze
  • indrawing of intercostals
  • tachypnoea

BLUE BLOATERS

  • low respiratory drive
  • type 2 RF: PaO2 down, PaCO2 up
  • cyanosis
  • warm peripheries
  • bounding pulse
  • flapping tremor (CO2 retention)
  • confusion, drowsiness
  • right heart failure
  • oedema, raised JVP
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30
Q

Describe the differences between asthma and COPD.

A

Inflammation agents:

  • asthma: CD4+ T lymphocytes, eosinophils, lymphocytes
  • COPD: CD8+ T lymphocytes, macrophages, neutrophils

Asthma has a sensitising agents whereas COPD has a noxious agent.
Asthma is reversible whereas COPD is not.
COPD is seen nearly always in smokers/ex-smokers whereas it is less common in asthma.
Asthma symptoms <35 y/o.
Chronic productive cough in COPD.
Persistent and progressive SOB in COPD, whereas variable in asthma.
Diurnal or day-to-day variation of symptoms in asthma, whereas COPD has less variation

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31
Q

What is cor pulmonale?

A

a clinical syndrome of RHF secondary to lung disease and salt and water retention leading to peripheral oedema

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32
Q

What are the 4 signs of cor pulmonale?

A
  1. Peripheral oedema
  2. Raised JVP
  3. Systolic parasternal heave
  4. Loud pulmonary second heart sound
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33
Q

How is cor pulmonale treated?

A

diuretics to control oedema

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34
Q

What metabolic disturbances are seen in compensated metabolic acidosis?

A

increased H+, decreased HCO3-, decreased pCO2

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35
Q

Which acid/base disorder causes decreased H+, increased HCO3- and increased pCO2?

A

compensated metabolic alkalosis

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36
Q

Describe the metabolic disturbances seen in compensated respiratory alkalosis.

A

decreased H+, decreased pCO2, decreased HCO3-

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37
Q

What are the normal ranges in the blood for:

  1. H+
  2. pH
  3. pCO2
  4. pO2
A
  1. 36-43 nmol/L
  2. 7.35-7.45
  3. 4.6-6.0 kPa
  4. 10.5-13.5 kPa
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38
Q

How is anion gap measured? What is the normal range?

A

[Na+] - ([Cl-] + [HCO3-])

Normal = 8-16 nmol/L

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39
Q

What is the clinical use of anion gap? Describe the importance of results of raised and normal anion gap.

A

Clinical use is in DDx of metabolic acidosis.
Raised = renal failure, DKA, lactic acidosis, toxins
Normal = renal tubular acidosis, diarrhoea, carbonic anhydrase inhibitors, ureteric diversion

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40
Q

When is non-invasive ventilation used in COPD?

A
  • COPD exacerbation with persistent hypercapnic RF

- respiratory acidosis or if acidosis persists despite maximal medical therapy

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41
Q

Describe the benefits of non-invasive ventilation in COPD.

A
  • reduces resp. rate
  • improves dyspnoea and gas exchange
  • lowers mortality
  • reduces need for ventilation
  • reduces length of hospital stay
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42
Q

Define allergy.

A
  • immune system mediated intolerance

- must have a trigger e.g. cats, birds

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43
Q

Define asthma. List some triggers.

A

reversible airflow obstruction involving airway inflammation

triggers - cold air, exercise, cats, night time

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44
Q

What are the clinical features of asthma?

A

cough, wheeze, hyperreactivity, hypersensitivity, breathlessness, exercise intolerance

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45
Q

Describe the pathological and physiological changes that occur in asthmatic patients.

A 
pathological = inflammation, scabby epithelium, thickened BM, thickened SM, mast cells releasing histamine in SM
physiological = yellow mucus, repair pathways, non-elastic airways, hyperresponsiveness, hypersensitivity
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46
Q

Discuss the pathophysiology of asthma.

A

Airway allergy drives eosinophilic inflammation
- activation of IL-5, TSLP, IL-13 - activate mast cells, lymphocytes, macrophages

Cytokines drive allergic airways inflammation/remodelling:

  • TNFa, TGFb, VEGF, IL-13
  • angiogenesis, epithelial cell damage, fibrosis, smooth muscle hypertrophy
  • becomes less sensitive to asthma treatment over time
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47
Q

What drug treatments are available in asthma?

A 
bronchodilators
corticosteroids
anti-leukotriene receptor drugs
anti-IgE biologic therapies
anti-IL-5 therapy
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48
Q

What is the other name for extrinsic allergic alveolitis?

A

hypersensitivity pneumonitis

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49
Q

List some types of EAA.

A

bird fancier’s lung, mushroom worker’s lung, farmer’s lung, malt worker’s lung, cheese washer’s lung, humidifier lung

50
Q

Describe the clinical features of acute EAA.

A

onset within 4-6 hours of exposure, wheeze, cough, fever, chills, headache, myalgia, malaise, fatigue, may last several days

51
Q

What changes are seen in the lungs in acute EAA?

A
  • thickening of septae
  • filling of alveolus with fluid (consolidation)
  • zonal distribution
  • fine reticulation
52
Q

How is EAA identified?

A

each type of EAA has a specific antibody that can be measured in serum e.g. avian precipitans (bird fancier’s lung) which leads to immune complex formation, chronic cell death and inflammation

53
Q

What changes are seen in the lungs with chronic exposure EAA?

A

FIBROSIS - interstitial scarring from chronic tissue remodelling
EMPHYSEMA - interstitial destruction from neutrophilic enzyme release
- bronchiocentric pattern
- foamy macrophages in alveolar spaces
- NNGI

54
Q

Describe the consequences of chronic exposure EAA.

A
  • reduced O2 transport into blood - measure by CO gas transfer during full PFTs
  • dispace shadowing on CXR
55
Q

How would you manage EAA?

A
  • avoid allergy triggers
  • corticosteroids
  • oxygen supplementation
56
Q

What is obstructive sleep apnoea?

A

recurrent episodes of partial or complete upper airway obstruction during sleep, intermittent hypoxia and sleep fragmentation

57
Q

Describe the mechanism by which obstructive sleep apnoea manifests and its consequences.

A
  • pharyngeal narrowing - airway collapses, stopping air from traveling to and from the lungs
  • negative thoracic pressure
  • arousal
  • sleep disruption = sleepiness, decreased quality of life, RTAs
  • blood pressure surge = MI, stroke
58
Q

What are the symptoms of OSA?

A
  • snoring
  • witnessed apnoeas
  • disrupted sleep: nocturia/choking/dry mouth/sweating
  • unrefreshed sleep
  • daytime somnolence
  • fatigue/low mood/poor concentration
59
Q

What investigations are carried out in OSA?

A
  • limited polysomnography
  • full polysomnography
  • TOSCA (transcutaneous oxygen saturations and carbon dioxide assessment)
60
Q

Describe the differences between

  1. apnoea
  2. hypopnoea
  3. respiratory effort related arousals.
A
  1. cessation or near-cessation of airflow, 4% oxygen desaturation lasting >10s
  2. reduction in airflow to a degree insufficient to meet criteria for an apnoea
  3. arousals associated with a change in airflow that does not meet above criteria
61
Q

What is AHI? And how is it used to diagnose OSA?

A

number of apnoea’s + hypopnoea’s, divided by total sleep time (in hours)
normal < 5
OSA > 15

62
Q

What are the consequences if OSA is left untreated?

A
  • hypertension
  • right heart strain
  • poor concentration
  • 4x more likely to have RTA
63
Q

How is OSA treated?

A

treat the symptomatic i.e. OSAS (manifests in daytime sleepiness)

  • weight loss, avoid triggers, treat underlying conditions
  • continuous positive airways pressure
  • mandibular advancement device
  • sleep position trainers
64
Q

What is a pneumothorax?

A

air within the pleural cavity - any breach of pleural space leads to collapse of the elastic lung

65
Q

What are the symptoms and signs of a pneumothorax?

A
  • pleuritic chest pain
  • breathlessness
  • respiratory distress
  • reduced air entry on affected side
  • decreased vocal resonance
  • tracheal deviation if tension
66
Q

List the DDx of pneumothorax.

A

pneumonia, PTE, MSK pain

67
Q

How does a tension pneumothorax develop?

A
  • ‘one way valve’ leads to increased intrapleural pressure
  • venous return impaired and so CO and BP fall
  • PEA arrest without intervention
68
Q

What is the immediate management of a tension pneumothorax?

A

insert venflon 2nd IC space midclavicular line to relieve pressure

69
Q

What are the different types of pneumothorax?

A
  1. traumatic e.g. stabbing, fractured rib
  2. iatrogenic e.g. CT guided lung biopsy
  3. spontaneous
    - primary - no underlying disease
    - secondary - underlying lung disease
70
Q

Describe the pathophysiology of primary pneumothorax.

A
  • development of subpleural bullae at lung apex
  • microscopic emphysema below surface of visceral pleura
  • spontaneous rupture leads to tear in visceral pleura
  • air flows from airways into pleural space
  • elastic lung collapses
71
Q

By what mechanisms can secondary pneumothorax develop?

A
  • inherent weakness in lung tissue e.g. emphysema
  • increased airway pressure e.g. asthma
  • increased lung elasticity e.g PF
72
Q

Aside from venflon insertion what other methods of management for pneumothorax are there?

A
  • intercostal drain with underwater seal
  • video assisted thoracic surgery if not resolved in 5 days
  • talc pleurodesis
  • pleural abrasion
  • surgical pleurodesis
73
Q

Discuss the aetiology of lung cancer.

A

SMOKING, passive smoking, ionising radiation, pollution, asbestos, fibrosis, HPV, genetics

74
Q

What are the signs and symptoms of lung cancer?

A

cough, haemoptysis, SOB, chest pain, weight loss, malaise

75
Q

Where might a lung cancer spread and how would it manifest?

A

LOCAL

  • pleura = haemorrhagic effusion
  • hilar lymph nodes
  • adjacent lung tissue = large blood vessel, haemoptysis
  • pericardium = effusion
  • mediastinum = SVC obstruction (oedema of face and arms, raised JVP, dilated veins on chest wall), recurrent laryngeal n, phrenic n
  • pancoast tumour = brachial plexus, Horner’s syndrome

DISTANT

  • haematogenous = liver, bone, brain, adrenal
  • lymphatic = cervical
76
Q

Discuss some of the non-metastatic effects of lung cancer.

A
  • ACTH secretion - adrenal hyperplasia, increased cortisol, Cushing’s
  • ADH secretion - water retention, dilutional hyponatraemia (SIADH)
77
Q

Describe the histological appearance of a small cell carcinoma.

A
  • oval to spindle shaped cells
  • inconspicuous nucleoli
  • scant cytoplasm
  • nuclear moulding
  • apoptotic bodies
78
Q

Which is the most aggressive form of lung cancer?

A

small cell carcinoma - metastasises early and widely

79
Q

Describe the appearance of non-small cell squamous carcinoma.

A
  • malignant epithelial tumour showing keratinisation and/or intracellular bodies
  • tend to arise centrally from major bronchi
80
Q

Which type of NSCLC produces mucin and appears glandular, solid, papillary or lepidic?

A

adenocarcinoma

81
Q

What is a carcinoid tumour?

A

tumour of neuroendocrine cells

82
Q

Describe a large cell lung carcinoma.

A

undifferentiated malignant epithelial tumour that lacks cytological features of SCLC and glandular or squamous differentiation

83
Q

What is a mesothelioma and what is its most common cause?

A

primary pleural tumour due to asbestos exposure

84
Q

Where do metastases to the lungs commonly arise?

A

breast, colorectal, kidneys, head and neck, testicular, bones, sarcoma, melanoma, thyroid

85
Q

Discuss the target therapies for lung cancer.

A
  1. Epidermal growth factor receptor e.g. cetuximab and erlotinib
  2. ALK-EML4 fusion gene e.g. crizotinib
  3. PDL1 e.g. nivolumab
86
Q

What is sarcoidosis?

A

multisystem inflammatory disease of unknown aetiology that predominantly affects lungs and intrathoracic lymph nodes - NON-NECROTISING GRANULOMATOUS INFLAMMATION

87
Q

Describe the clinical presentation of sarcoidosis.

A

5%: asymptomatic
45%: systemic e.g. fever, anorexia, fatigue, night sweats
50%: dyspnoea on exertion, cough, chest pain, haemoptysis, wheeze

88
Q

What are the 4 classes of sarcoidosis seen in CXR?

A
  1. bilateral hilar lymphadenopathy without infiltration
  2. bilateral hilar lymphadenopathy with infiltration
  3. infiltration alone
  4. fibrotic bands, bullae, hilar retraction, bronchietasis, diaphragmatic tenting
89
Q

What is idiopathic pulmonary fibrosis?

A

the clinical manifestation of the pathological diagnosis of usual interstitial pneumonia

90
Q

What are the signs and symptoms of IPF?

A
  • progressive breathlessness
  • bibasilar crackles and clubbing
  • hacking dry cough
  • appetite and weight loss
  • fatigue and weakness
  • subpleural honeycombing
91
Q

List 6 causes of PF with an example of each.

A
  1. occupation/environmental e.g. asbestos, HSP
  2. drug induced e.g. amiodarone
  3. connective tissue disease e.g. lupus
  4. primary diseases e.g. sarcoidosis
  5. idiopathic (25%)
  6. genetics
92
Q

How is pulmonary fibrosis diagnosed?

A

high resolution CT

93
Q

Discuss the pathophysiology of pulmonary fibrosis.

A
  • cause e.g. genetics, idiopathic, environment
  • repetitive alveolar epithelial injury
  • altered alveolar microenvironment
  • dysregulated repair
  • loss of epithelial cells
  • accumulation of mesenchymal cells
  • fibrosis
94
Q

Miconazole, ketaconazole and clotrimazole are examples of what type of drug? And how do they work?

A
  • azoles - antifungals
  • inhibitors of 14-methylsterol a-demethylase which produces ergosterol which is an essential part of the fungal plasma membrane
95
Q

Describe the mechanism of action of amphotericin B.

A
  • exploits presence of ergosterol

- forms a pore in fungal membranes -> leakage of intracellular cations

96
Q

Which fungal pathogen is commonly associated with meningitis and secondary infection with HIV?

A

cryptococcus neoformans

97
Q

Aspergillus fumigatus is a type of fungus. Which disease does it cause associated with asthma and CF? And how is it treated?

A

allergic bronchopulmonary aspergillosis

prednisolone

98
Q

What 3 diseases does aspergillus fumigatus cause?

A

allergic bronchopulmonary aspergillosis
invasive pulmonary aspergillosis
aspergilloma

99
Q

Define aspergilloma. How is it managed?

A

a fungal ball that develops in an area of past lung disease or lung scarring e.g. TB
no treatment unless bleeding occurs then surgery

100
Q

Describe the management of asthma exacerbation.

A
  • high flow oxygen
  • nebulised bronchodilators
  • oral prednisolone
  • oral doxycycline
  • IV magnesium
  • discussion with ITU
  • consider IV aminophylline infusion
101
Q

What are the side effects associated with B2 agonists?

A

tremor, low K+, high glucose, flushing, increased HR, arrhythmias

102
Q

Describe the mechanism of action of antimuscarinics.

A

inhibits cholinergic M1 and M3 receptors

inhibits parasympathetic mediated bronchoconstriction

103
Q

List the side effects of antimuscarinics.

A

blurry vision, dry mouth, urinary retention, nausea, constipation

104
Q

How does aminophylline work?

A
  • non-selective inhibition of phosphodiesterase
  • increased intracellular cAMP
  • bronchial SM relaxation
  • increased mucus clearance
  • anti-inflammatory effect
105
Q

Describe how corticosteroids work in lung disease.

A

bind to activated glucocorticoid receptors to suppress multiple pro-inflammatory genes at are activated in asthmatic airways by reversing histone acetylation

106
Q

Which drug is useful for prophylaxis of exercise-induced asthma? How does it work?

A

leukotriene receptor antagonists

  • bind to CysLT1 inhibiting action of LTD4 in SM cells of airway macrophages
  • decreased airway oedema and smooth muscle contraction
107
Q

What are the two biologic therapies currently available in asthma?

A
  1. Omalizumab: anti-IgE antibody for severe persistent allergic asthma
  2. Mepolizumab: anti-IL5 antibody for severe refractory eosinophilic asthma
108
Q

Which drug is used additionally in COPD to decrease viscosity of mucus and therefore decreased exacerbations?

A

carbocysteine

109
Q

What is a pleural effusion?

A

accumulation of abnormal volume of fluid in the pleural space > 15ml

110
Q

How is a pleural effusion seen on CXR?

A

blunting of costophrenic margin

111
Q

List the clinical signs of pleural effusion.

A
  • decreased chest expansion
  • decreased tactile vocal fremitus
  • stony dull percussion
  • quiet breath sounds
112
Q

Discuss the mechanisms by which pleural effusions develop.

A
  • imbalance between pleural fluid production and absorption
  • increased hydrostatic pressure (CCF)
  • decreased osmotic pressure (hypoalbuminaemia)
  • increased vascular permeability (pneumonia)
113
Q

What is the immediate management if the effusion is seen to be bilateral?

A

treat the cause (usually obvious), no need to sample initially

114
Q

Heart failure causes right or left pleural effusions?

A

right

115
Q

How would you investigate a unilateral pleural effusion?

A
  • always consider pleural infections: sepsis? empyema? needs sampling and drainage
  • if not sepsis: contrast CT chest/abdo/pelvis, consider breast/gynae malignancy, asbestos, TB?
116
Q

Differentiate between transudate and exudate pleural effusions.

A
  • protein > 30g/l in exudate (transudate normal)
  • pleural/serum lactate dehydrogenase ratio >0.6 in exudate = Light’s criteria (transudate normal)
  • transudate bilateral, exudate unilateral
  • transudate clear, exudate clear, cloudy or bloodstained
117
Q

What are the common causes of transudate and exudate pleural effusions?

A
  • transudate: cardiac failure, cirrhosis, nephrotic syndrome, hypoalbuminaemia
  • exudate: bacterial pneumonia, malignancy, mesothelioma, TB
118
Q

Describe the management of pleural malignancy effusions.

A

drain to dryness once and discharge
medical pleurodesis
thoracoscopic pleurodesis
indwelling pleural catheter

119
Q

What test results would show the presence of a complex parapneunomic effusion?

A

pH < 7.2, LDH > 1000, glucose < 2.2, located on US

120
Q

What is the management plan of an empyema?

A

small bore chest drain, sterile saline flushes, IV antibiotics, DVT prophylaxis, fibrinolytics

Phase 3 (10 decks)

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