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MBChB 3 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Why do we measure lung function?

A

Evaluation of the breathless patient.
-screening for COPD or occupational lung disease
-lung cancer-fitness for treatment
-pre-operative assessment
-disease progression and treatment response
monitoring of drug treatment
pulmonary complications of systemic disease

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2
Q

Potential pitfalls of spirometry?

A
  • Appropriately trained technician
  • Effort and technique dependent
  • Patient frality
  • Pain, patient too unwell
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3
Q

What is tidal volume?

A

During normal quiet breathing the amount of air that moves in and out of the lungs with each breath. Normally 500ml.

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4
Q

What is inspiratory reserve volume?

A

The volume of air that can be inspired beyond the tidal volume.

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5
Q

What is the expiratory reserve volume?

A

The volume of air that can be expired after a tidal expiration.

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6
Q

What is the residual volume?

A

Volume of air (approx. 1200ml) that remains in the lungs after the most strenuous expiration. The residual volume prevents atelectasis.

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7
Q

What is the vital capacity?

A

The total amount of exchangeable air. VC=TV+IRV+ERV.

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8
Q

What is total lung capacity?

A

The sum of all lung volumes and is normally around 6L in males.

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9
Q

What is FEV1?

A

Forced expiratory volume in one second. The maximal volume of gas, which can be expired from the lungs in the first second of a forced expiration from full inspiration.

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10
Q

What is FVC?

A

Forced vital capacity. Maximal volume of gas, which can be expired from the lungs during a forced expiration from full inspiration.

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11
Q

What is the FEV1/FVC(%)?

A

Proportion of the FVC, which can be expelled during the first second of expiation-expressed as a percentage. Derived by calculating FEV1/FVC x 100. If less than 70=obstructive airflow.

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12
Q

What is the peak expiratory flow?

A

The maximum expiratory flow that can be sustained for a minimum of 10msecs.

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13
Q

What is ventilation?

A

Refers to the movement of gas into and out of the alveoli. Expressed as V.

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14
Q

What is perfusion?

A

Refers to the blood flow through the pulmonary capillaries. Expressed as Q.

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15
Q

What is COPD?

A

Chronic obstructive pulmonary disease. Largely irreversible airflow obstruction, includes emphysema and chronic bronchitis. Smokers disease. Alveolar destruction.

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16
Q

What is asthma?

A

Recurrent reversible airflow obstruction due to inflammatory changes in the airways. Bronchial hyper-reactivity. Causes wheezing, coughing, hyperinflation.

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17
Q

What are xanthines?

A

Bronchodilators. Narrow therapeutic window, many drug interactions. Cause cause cardiac dysrhythmias and seizures. Use of xanthines has declined, but still used in lower doses for anti-inflammatory effects.

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18
Q

What is mild COPD?

A

> 80% FEV1

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19
Q

What is moderate COPD?

A

50-80% FEV1

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20
Q

What is severe COPD?

A

30-50% FEV1

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21
Q

What is very severe COPD?

A

<30% FEV1

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22
Q

In reversibility testing, what is suggestive of asthma?

A

After having given salbutamol, 15% AND 400ml reversibility of FEV1.

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23
Q

Obstructive lung disease

A

FEV1/FVC ratio less than 70%. Asthma and COPD.

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24
Q

Restrictive lung disease

A

FEV1 and FVC reduced but FEV1/FVC ratio over 70 (normal). Causes interstitial lung disease, obesity, chest wall abnormality.

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25
Q

What are causes of obstructive lung disease?

A

Asthma and COPD

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26
Q

What are causes of restrictive spirometry disease?

A

Interstitial lung disease, chest wall abnormality, previous pneumonectomy, neuromuscular disease, obesity, poor effort/technique.

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27
Q

What is sarcoidosis?

A

A multi or single organ disease of unknown aetiology which is characterised by ‘non-necrotising Granulomatous inflammation’. Diagnosis of exclusion.

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28
Q

What are the lung signs of sarcoidosis?

A

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

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29
Q

What causes pulmonary fibrosis?

A

Smoking, radiation, post infection, drugs, other chronic conditions eg. RA.

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30
Q

Idiopathic pulmonary fibrosis

A

Age>50, M:F 2:1, progressive breathlessness, bibasilar crackles, clubbing, peripheral interstitial pattern. Subpleural honeycombing. Hacking dry cough, fatigue and weakness, appetite and weight loss.

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31
Q

What is a ‘fibroblastic focus’?

A

Histological feature of UIP (usual interstitial pneumonia). Temporal heterogeneity is also a feature.

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32
Q

Smoking predisposes you to what types of lung cancer?

A

Squamous and small cell lung cancer.

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33
Q

Signs and symptoms of lung cancer

A

Cough, haemoptysis, SOB, chest pain, weight loss, general malaise.

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34
Q

How do you measure transfer factor in the lungs?

A

Single breath of a very small concentration of carbon monoxide (CO has a very high affinity to Hb). Measure concentration in expired gas to derive uptake in the lungs.

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35
Q

What affects ‘transfer factor’?

A

Alveolar surface area, pulmonary capillary blood volume, haemoglobin concentration, ventilation perfusion mismatch.

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36
Q

When is ‘transfer factor’ reduced?

A

In emphysema, interstitial lung disease, pulmonary vascular disease and anaemia (increased in polychthaemia.

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37
Q

What are the 2 ways to measure residual volume?

A

Cannot be measured by spirometry.

1) Helium dilution (inspire known quantity of inert gas).
2) Body plethysmography (respiratory manoevures in a sealed box lead to changes in air pressure-can derice lung volumes).

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38
Q

What is oximetry?

A

Non-invasive measurement of saturation of haemoglobin by oxygen.

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39
Q

What are the main causes of hypoxaemia?

A
  • Hypoventilation eg. drugs, neuromuscular disease.
  • Ventilation/perfusion mismatch eg. COPD, pneumonia
  • Shunt eg. congenital heart disease
  • Low inspired oxygen
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40
Q

What is a ‘shunt’?

A

An extreme form of V/Q mismatch where blood bypasses the lungs entirely. Does not correct with oxygen administration.

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41
Q

What is the treatment for exacerbation of COPD?

A

O-Oxygen-24% aiming for SpO2 of 88-92%
N-Nebulised salbutamol and ipratropium bromide
A-Amoxicillin (oral)
P-Predinosolone

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42
Q

Definition of respiratory failure

A

PO2 less than 8kPa at sea level.

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43
Q

What is Cor Pulmonale?

A

Clinical syndrome of right sided heart failure secondary to lung disease and salt and water retention leading to peripheral oedema. Treatment is diuretics to control peripheral oedema.

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44
Q

What are the signs of Cor Pulmonale?

A

Peripheral oedema, raised jugular venous pressure, a systolic parasternal heave, loud pulmonary second heart sound.

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45
Q

What are the effects of cigarettes smoking on the respiratory system?

A
  • Cilial motility is reduced
  • Airway inflammation
  • Hypertrophy of Goblet cells
  • Increased protease activity, decreased anti-proteases
  • Oxidative stress
  • Squamous metaplasia=higher risk of lung cancer.
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46
Q

What is chronic bronchitis?

A

Clinical syndrome of COPD. The production of sputum on most days for at least 3 months in at least 2 years.

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47
Q

What is emphysema?

A

Abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles.

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48
Q

Centri-acinar emphysema

A

Damage around respiratory bronchioles. More in the upper lobes.

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49
Q

Pan-acinar emphysema

A

Uniformly enlarged from the level of terminal bronchiole distally. Can get large bullae. Associated with alpha1 anti-trypsin deficiency.

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50
Q

What are the 3 types of emphysema?

A

1) Centriacinar (causes airflow obstruction)
2) Panacinar (causes airflow obstruction)
3) Paraseptal (doesn’t cause airflow obstruction)-can lead to pneumothorax.

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51
Q

What is the mechanism of airflow obstruction in COPD?

A

Loss of elasticity and alveolar attachments due to emphysema-airways collapse on expiration. Causes air trapping and hyperinflation- increased work of breathing- breathlessness.

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52
Q

Type 2 respiratory failure

A

Blue bloater-low respiratory drive. Low oxygen, high Co2. Cyanosis, warm peripheries, flapping tremor, right heart failure.

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53
Q

Type 1 respiratory failure

A

Pink puffer-high respiratory drive. Low O2 and low CO2. Pursed lip breathing, uses accessory muscles, wheeze, tachypnoea, desaturates on exercise.

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54
Q

What are dermatophytes?

A

Fungi that cause common infections of skin, nails and hair. Only colonise keratinised areas.

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55
Q

Name some systemic fungal infections

A

1) Fungal meningitis (Crytococcus neoformans)
2) Aspergillosis of the lungs (Aspergillus fumigatus)
3) Pneumocystis pneumonia (pneumocystis jiroveci)

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56
Q

What causes fungal meningitis?

A

Crytococcus neoformans

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57
Q

What can Aspergillus fumigatus cause?

A

1) Allergic bronchopulmonary aspergillosis (ABPA)
2) Invasive pulmonary aspergillosis (IPA)
3) Aspergilloma

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58
Q

What is the treatment for pneumonia caused by Pneumocystis jiroveci?

A

Trimethoprim-sulfamethoxazole.

59
Q

What is the largest class of antifungal agents?

A

‘Azoles’ eg. Miconazole and Clotrimazole. Many applications.

60
Q

MOA of ‘Azoles’

A

Azoles are inhibitors of 14-methlysterol alpha-demethylase. This is important enzyme in the ergosterol pathway. Ergosterol is a key component of fungal plasma membrane.

61
Q

MOA of Amphotericin B

A

Forms a channel in the fungal membrane leading to leakage of intracellular cations. Does this by binding to ergosterol and intercalating into cell membrane. Hydrophobi side of amphotericin B interacts with ergosterol.

62
Q

Amphotericin B

A

Anit-fungal agents. Has to be given IV, at high levels interact with cholesterol. Best given as ambisome- part of a liposome. Allows better movement through body and reduced toxicity.

63
Q

MOA of amoxicillin

A

Inhibits bacterial cell wall synthesis.

64
Q

MOA of clarithryomycin

A

Bacteriostatic drug inhibiting protein synthesis.

65
Q

MOA of doxycyline

A

Bacteriostatic drug-inhibits action of amino acids to growing peptide.

66
Q

MOA of corticosteroids in an asthma attacke

A

Bind to activated glucocorticoid receptors to suppress multiple pro-inflammatory genes that are activated in asthmatic airways reversing histone acetylation.

67
Q

MOA of B2 agonist

A

Bronchodilator. Acts on B2 receptors to stimulate adenyl cyclase to increase intracellular cAMP-relaxation of bronchial smooth muscle.

68
Q

MOA of anti-muscarinics eg. Ipatropium bromide

A

Bronchodilator. Inhibition of cholinergic M1 and M3 receptors in the lung-reduction in cGMP and inhibition of parasympathetic-mediated bronchoconstriction.

69
Q

MOA of methylxanthines eg. Theophylline

A

Non-selective inhibition of phosphodiesterase-increased intracellular cAMP-bronchial smooth muscle relaxation. Immunomodulatory action-improved mucociliary clearance and anti-inflammatory effect.

70
Q

MOA of leukotriene receptor antagonists eg. Motelukast

A

Bind with high affinity to cysteinyl leukotriene receptor (CysLT1) inhibiting action of LTD4 in smooth muscle cells of the airway and airway macrophages-reduced airway oedema and smooth muscle contraction.

71
Q

Obstructive sleep apnoea defintion

A

Recurrent episodes of partial or complete upper (pharyngeal) airway obstruction during sleep, intermittent hypoxia and sleep fragmentation.

72
Q

Obstructive sleep apnoea syndrome

A

Manifests as excessive daytime sleepiness.

73
Q

What is retrognathia?

A

A type of malocclusion which refers to an abnormal posterior positioning of the maxilla or mandible, particularly the mandible, relative to the facial skeleton and soft tissues.

74
Q

Symptoms of OSA

A

Snorer, witnessed apnoeas, disruptive sleep, unrefreshed sleep, daytime tiredness, fatigue, low mood, poor concentration.

75
Q

Assessment of OSA

A

Weight, BMI, BP, neck circumference (>40cm), craniofacial appearance (posterior mandible, small jaw?), tonsils, nasal patency.

76
Q

What is the mallampati score?

A

Used to assess ease of intubation in a patient or to assess for OSA.
Class I-Complete visualisation of soft palate.
Class II-Complete visualisation of uvula.
Class III- Visualisation of bottom of uvula.
Class IV-Soft palate not visible at all.

77
Q

Define apnoea

A

Cessation, or near cessation of airflow leading to a 4% oxygen desaturation lasting more than or equal to ten seconds.

78
Q

Define hypopnoea

A

Reduction of airflow to a degree insufficient to meet the criteria for an apnoea.

79
Q

Define respiratory effort related arousals

A

Arousals associated with a change in airflow that does not meet the criteria for apnoea or hypopnea.

80
Q

Apnoea-hypopnoea index (AHI)

A

Calculated by adding the number of apnoeas and hypopnoeas and dividing the total sleep time (in hours). AHI> or equal to 15 suggests OSA. Or 5-15 with compatible symptoms.

81
Q

Oxygen-desaturation index

A

Number of times per hour of sleep that the SpO2 falls more than or equal to 4% from baseline.

82
Q

CPAP

A

Continuous Positive Airways Pressure. Treatment for OSA. Splints airway open, stops snoring and sleep fragmentation. A mask over the nose gently directs air into the throat to keep the airway open.

83
Q

What causes bilateral hilar adenopathy?

A

1) Sarcoidosis
2) Lymphoma
3) TB
4) Malignancy

84
Q

What are the 3 causes of a ‘white out’ on CXR?

A

1) Pleural effusion
2) Pneumonectomy
3) Lung collapse

85
Q

What is a pneumothorax?

A

Air within the plural cavity. Can be traumatic, iatrogenic or spontaneous.

86
Q

Causes of traumatic pneumothorax

A
  • Stabbing

- Fractured rib

87
Q

Causes of iatrogenic pneumothorax

A

Normally heals in 72 hours

  • CT guided lung biopsy
  • Pleural aspiration
88
Q

Spontaneous pneumothorax

A

Primary-young patient, no underlying lung disease

Secondary- underlying lung disease (COPD, cystic fibrosis).

89
Q

How do you manage a tension pneumothorax?

A

Immediately insert venflon 2nd intercostal space midclavicular line to relieve pressure.

90
Q

Tension pneumothorax

A

A medical emergency. Leads to increased intrapleural pressure-venous return is impaired, cardiac output and blood pressure falls. Can lead to cardiac arrest without intervention.

91
Q

Pathophysiology of primary pneumothorax

A

Development of subpleural blebs/bullae at apex of lung. Spontaneous rupture leads to tear in visceral pleura. Air flows from airways to pleural space down a pressure gradient. Elastic lung then collapses.

92
Q

When would you consider surgical pleurodesis to treat a pneumothorax?

A

If it is the 2nd pneumothorax on the same side or first contralateral event.

93
Q

Risks factors for lung cancer

A

Smoking, environmental tobacco smoke, ionising radiation (radon, uranium), air pollution, asbestos, fibrosing conditions of the lungs, human papilloma virus.

94
Q

Signs and Symptoms of lung cancer

A

Cough, haemoptysis, SOB, chest pain, weight loss/anorexia, malaise.

95
Q

Central lung cancer signs

A

Haemoptysis, bronchial obstruction -SOB, retention pneumonia, and cough.

96
Q

Peripheral lung cancer signs

A

May have few symptoms, pain if pleura or chest wall involved.

97
Q

Where can lung cancer spread to locally?

A

Pleura, hilar lymph nodes, adjacent lung tissue, pericardium, mediastinum.

98
Q

If you get lung cancer spread to the mediastinum, what can happen?

A

Superior vena cava obstruction, recurrent laryngeal nerve, phrenic nerve.

99
Q

Small cell carcinoma of the lung

A

Most aggressive form of lung cancer, metastasises early and wide. Often initially response so chemo but often relapse. Oval to spindle shaped cells, scant cytoplasm, nuclear moulding.

100
Q

What are the types of non-small cell carcinoma?

A
  • Squamous cell carcinoma
  • Adenocarcinoma
  • Large cell carcinoma
  • Other
101
Q

Squamous cell carcinoma of the lung

A

Arises centrally from major bronchi. Slow growing and metastasises late. May undergo cavitation and block bronchi leading to retention pneumonia or collapse. A malignant epithelial tumour showing keratinization and/or intercellular bridges.

102
Q

Define ‘lepidic’

A

Lepidic growth adenocarcinoma is defined as tumor cells proliferating along the surface of intact alveolar walls without stromal or vascular invasion pathologically.

103
Q

Adenocarcinoma of the lung

A

Common tumour in females. Also seen in non-smokers. 2/3 arise peripherally, sometimes in relation to scarring.. Can be glandular, solid, papillary or lepidic, mucin production.

104
Q

Large cell caricnoma

A

Diagnosis of exclusion. An undifferentiated malignant epithelial tumour that lacks the cytological features of SCLC and glandular or squamous differentiation.

105
Q

Carcinoid tumour

A

Tumour of neuroendocrine cells. Central or peripheral. Typical or atypical. Can metastasise but much better prognosis than other conventional lung cancers.

106
Q

Name some molecular targets identified for lung cancer treatment.

A

EGFR, 4-Anaplastic lymphoma kinase fusion gene, PDL1

107
Q

Deletions in what exon are commonly associated with good response to EGFR inhibitors in lung cancer treatment?

A

Exon 19

108
Q

How do you test for ALK fusion?

A

FISH or IHC for protein product.

109
Q

What is mesothelioma?

A

Primary pleural tumour (also occurs in peritoneum, pericardium, tunica vaginalis of testes). Almost always due to asbestos exposure.

110
Q

What is a ‘Pack year’ in relation to cigarettes?

A

1 pack year= 20 cigarettes/day for 1 year.

111
Q

You would consider the diagnosis of COPD in people over 35 years old, smoker and ex-smokers with:

A
  • Exertional breathlessness
  • Regular sputum production
  • Wheeze
  • Chronic cough
  • Frequent winter ‘bronchitis’
112
Q

What signs on COPD might you see on a CXR?

A

Hyperinflation of lungs (more anterior ribs on show), flattened hemidiaphragms, bullae, pruned blood vessels-large proximal vessels. Heart can look longer and thinner due to increased intrathoracic pressure.

113
Q

What is polycythaemia?

A

An abnormally increased concentration of haemoglobin in the blood, either through reduction of plasma volume or increase in red cell numbers. It may be a primary disease of unknown cause, or a secondary condition linked to respiratory or circulatory disorder or cancer. Can been seen in COPD if chronic hypoxaemia.

114
Q

What is a Ghon complex?

A

Calcified areas of the lungs seen on chest x-ray, typical of TB.

115
Q

Which of the antibiotic used in TB can cause visual disturbance?

A

Ethambutol can cause visual disturbance and deterioration.

116
Q

What are the clinical components of COPD?

A

Chronic bronchitis and emphysema.

117
Q

What is chronic bronchitis?

A

Production of sputum on most days for at least 3 months in at least 2 years (when other causes of chronic cough have been excluded).

118
Q

What is emphysema?

A

Abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles.

119
Q

Pink puffer

A

High respiratory drive, low PaO2 and low PaCO2, type 1 respiratory failure. Pursed lip breathing, uses acessory muscles.

120
Q

Blue bloater

A

Low respiratory drive, Low PaO2 and high PaCO2, type 2 respiratory failure. Confusion, drowsiness, cyanosis. Loss of central sensitivity to CO2 and reliance on hypoxic drive to stimulate breathing.

121
Q

What is the definition of an exacerbation of COPD?

A

Sustained worsening of the patients symptoms from their usual state which is beyond day-to-day variations, and is acute in onset. Commonly reported symptoms are worsening breathlessness, cough, increased sputum production and change in sputum colour. The change in these symptoms often necessitates a change in mediation.

122
Q

What are the clinical signs of pleural effusion?

A
  • Decreased breath sounds
  • Stony dull to percussion
  • Decreased tactile or vocal fremitus
123
Q

CXR appearance of pleural effusions

A

Need >300ml of fluid to be present to see on CXR. Uniformly white appearance. Blunting of costophrenic and cardiophrenic angles. A meniscus at upper edge.

124
Q

When is long-term oxygen therapy appropriate for a COPD patient?

A

Based on ABGs. PaO2 of less than 7.3 if they are well- indication for LTOT. Have to be a non-smoker for at least 3 months. or PaO2 of 7.3-8.0kPa AND any of secondary polycythaemia, nocturnal hypoxaemia, peripheral oedema, pulmonary hypertension.

125
Q

What are features of a life threatening asthma attack?

A 
PEF <33% best or predicted
SpO2 <92%
PaO2 <8kPa
Normal PaCO2 (4.6-6kPa)
Silent chest
Cyanosis
Poor respiratory effort
Arrhythmia
Exhaustion, altered conscious level
126
Q

What is asthma?

A

A chronic inflammatory condition of the airways that causes recurrent episodes of wheezing, breathlessness, chest tightness and cough, particularly at night and/or early morning. These symptoms are usually associated with widespread but variable bronchoconstriction and airflow limitation that is at least partly reversible, either spontaneously or with treatment.

127
Q

What are the key features of asthma?

A
  • Increased airways hyper-responsiveness to a variety of stimuli resulting in episodic bronchoconstriction
  • Inflammation of the bronchial walls
  • Increased mucus secretion
128
Q

Atopic asthma

A

Extrinsic asthma. Usually starts in childhood. Atopic individuals have a raised total serum IgE and the presence of specific IgE against common aeroallergens.

129
Q

Non-atopic asthma

A

Intrinsic asthma. Often starts in middle age- possible triggers include respiratory viruses and air pollutants.

130
Q

Causes and triggers of asthma

A

Environmental exposure to allergen, occupational sensitisers, viral infections, atmospheric pollution, drugs, irritant vapours and fumes, exercise, cold air.

131
Q

Pathological features in asthmatic airways

A 
Increased airway inflammatory cells
Plasma exudation
Oedema
Smooth muscle hypertrophy
Mucus plugging
Shedding of epithelium
132
Q

What is ‘stridor’?

A

A high-pitched, wheezing sound caused by disrupted airflow.

133
Q

Serum osmolal gap=

A

measured osmolality- calculated osmolality

134
Q

Calculated osmolality=

A

2 x (Na+ + K+) + urea + glucose (all in mmol/L)

135
Q

Respiratory acidosis

A

pH less than 7.35 with a PaCO2 greater than 45mmHg.

136
Q

Respiratory alkalosis

A

pH greater than 7.45 with a PaCO2 less than 35mmHg,

137
Q

Metabolic acidosis

A

pH of less than 7.35 and a bicarbonate level of less than 22mEq/L.

138
Q

Metabolic alklaosis

A

pH greater than 7.45 and bicarbonate greater than 26mEq/L.

139
Q

PaO2

A

Partial pressure of oxygen that is dissolved in arterial blood. Normal range is 80 to 100mmHg.

140
Q

SaO2

A

Arterial oxygen saturation. Normal range is 95-100%.

141
Q

PaCO2

A

Amount of carbon dioxide dissolved in arterial blood. Normal range is 35 to 45mmHg.

142
Q

HCO3

A

Calculated value of the amount of bicarbonate in the bloodstream. Normal range is 22-26mEq/litre.

143
Q

What is bilateral hilar adenopathy and what causes it?

A

Bilateral enlargement of the lymph nodes of pulmonary hila. Caused by sarcoidosis, lymphoma, TB, malignancy.

144
Q

What is Golden S Sign?

A

Golden S-sign is seen on both PA chest radiographs and on CT scans. It is named because this sign resembles a reverse S shape, and is therefore sometimes referred to as the reverse S-sign of Golden. Typical of right upper lobe collapse.

MBChB 3 (13 decks)

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