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BM4 Part 1 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What type of drug is usually used as a short term asthma reliever?

A

Short-acting β agonist (e.g. salbutamol).

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2
Q

What causes atopic asthma reactions?

A

IgE mediated inflammation.

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3
Q

What is JVP measured for?

A

An indirect measure of pressure in the right atrium.

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4
Q

What can cause a raised JVP?

A

Heart failure
Fluid overload
Constrictive pericarditis
Cardiac tamponade

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5
Q

How is oxygen carried in the blood?

A

98.5 % bound to haemoglobin.
1.5 % directly dissolved in the plasma.

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6
Q

What are the 2 clinical measurements of oxygen, and what do they relate to?

A

PO2 - amount of oxygen directly dissolved in blood.
SO2 - proportion of Hb that is bound to oxygen (remember 50 % saturation means half of the total Hb has 4 oxygen molecules bound).

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7
Q

What factors can affect haemoglobin-oxygen affinity?

A

pH - low pH reduces affinity (Bohr effect).
Temperature - increased temperature reduces affinity.
2,3-BPG - reduces affinity.

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8
Q

What is 2,3-BPG?

A

2,3-bisphosphoglycerate - intermediate product of glycolysis.
Binds to haemoglobin and shifts to tense conformation thereby reducing oxygen affinity.

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9
Q

How does foetal haemoglobin differ from adult?

A

Adult = 2x alpha and 2x beta subunits.
Foetal = 2x alpha and2x gamma subunits.
Foetal has higher affinity for oxygen than adult enabling oxygen to be delivered across the placenta.

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10
Q

How is CO2 transported in the arteries and veins?

A

Arteries: 5% dissolved; 90% bicarbonate; 5% carbamino compounds.
Venous: 10% dissolved; 60% bicarbonate; 30% carbamino compounds.

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11
Q

How does CO2 form bicarbonate?

A

Diffuses down concentration gradient from tissues into RBCs. Carbonic anhydrase catalyses conversion to carbonic acid.
Then hydrolysed into H+ ions and bicarbonate where the H+ ions are bound by haemoglobin which buffers the process.
Reverse occurs in lungs also catalysed by carbonic anhydrase.

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12
Q

What is chloride shift?

A

The exchange of chloride for bicarbonate by carrier protein to allow bicarbonate to leave RBCs.

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13
Q

What are the 3 main homeostatic mechanisms regulating pH?

A
  1. Chemical acid-base buffer systems T
  2. Respiration (controlled by respiratory centre)
  3. The kidneys

First two can react within seconds to minutes whilst the kidneys take hours to days.

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14
Q

What are two minor pH buffering systems?

A
  1. Proteins - histidine residues on haemoglobin acts as proton acceptor.
  2. Phosphate - inorganic phosphate (HPO4)2- can reversible bind free protons (less of an impact as bicarbonate, but critical for buffering pH of urine).
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15
Q

What is tidal volume?

A

The volume of air that moves in or out of the lungs during normal respiration (normal = 7 mL/kg).

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16
Q

What is inspiratory reserve volume?

A

The extra volume of air that can be inspired with maximal effort after reaching the end of a normal, quiet inspiration.

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17
Q

What is expiratory reserve volume?

A

The extra volume of air that can be expired with maximum effort beyond the level reached at the end of a normal, quiet expiration.

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18
Q

What is residual volume?

A

The volume of air remaining in the lungs following maximum forceful expiration (normal = 1-1.2 L).

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19
Q

What is the vital capacity?

A

TV + IRV + ERV.
Maximum amount of air exhaled from full inspiration.

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20
Q

What is total lung capacity?

A

VC + RV.
The total volume of air in the lungs after a maximal inspiration.

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21
Q

What is pulmonary compliance?

A

The expandability of the lungs and chest wall.

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22
Q

What is pulmonary resistance?

A

The resistance of the airways to the movement of air through the tubes.

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23
Q

What can cause hypoxemia?

A

Low inspired PO2
Under ventilation
Ventilation/perfusion (V/Q) mismatch
Extra pulmonary shunt
Diffusion block

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24
Q

What does spirometry measure?

A

Airflow and volume of air moved in/out of the lungs.
Determines pulmonary compliance

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25
Q

What is forced vital capacity?

A

Volume of air expelled following forced maximal expiration.

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26
Q

What is FEV1?

A

Forced Expiratory Volume.
Volume of air expelled in one second of a forced expiration.

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27
Q

What are normal ranges for FVC, FEV1 and FEV1/FVC ratio?

A

FVC and FEV1 - 80-120% of predicted value.
FEV1/FVC ratio - > 70%.

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28
Q

What are the obstructive patterns in spirometry?

A

Reduced flow rates, normal lung volumes, low ratios.

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29
Q

Classifications of severity of obstruction dependent on FEV1% predicted.

A

> 80% : mild
50-79% : moderate
30-49% : severe
< 30% : very severe

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30
Q

What is required for COPD diagnosis?

A

FEV1/FVC ratio < 70% post bronchodilator (confirms persistent airflow obstruction).

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31
Q

When is reversibility considered in adults?

A

FEV1 improvement of 12% and 200 ml as a positive result following bronchodilation.

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32
Q

What are intrinsic causes of restriction?

A

Tuberculosis, pneuomonectomy or pneumonia.

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33
Q

What are extrinsic causes of restriction?

A

Scoliosis, pleural effusion, pregnancy, gross obesity, tumour, ascites, pain (e.g. pleurisy/rib fracture).

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34
Q

What are the restrictive patterns in spirometry?

A

Reduced lung volume, reduced flow rates but normal or slightly high ratios.

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35
Q

What is a peak flow measurement?

A

The fastest rate of airflow achieved in one forced expiration from maximum inhalation and is used to detect obstruction in the upper airway.

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36
Q

What is bronchial asthma?

A

Inflammatory condition of the airways characterised by bronchial hyper-responsiveness with reversible airway obstruction.

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37
Q

What causes airway obstruction in asthma?

A

Smooth muscle contraction, vascular congestion, oedema of the airway wall, mucus secretion and epithelial damage.

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38
Q

What is the most common primary lung tumour?

A

Carcinoma.

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39
Q

What are the main causes of lung cancer?

A

Smoking
Atmospheric pollution
Ionising radiation
Asbestos
Interstitial lung disease

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40
Q

What is the lamina propria?

A

Loose, connective tissue.
Richly vascularised network providing nutrients to the epithelium as well as mechanical support.
May contain glands.

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41
Q

What layers make up the pharynx?

A

Nasopharynx = respiratory epithelium
Oropharynx and laryngopharynx = stratified squamous non-keratinised epithelium
Lamina propria
Skeletal muscle

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42
Q

What cell types make up the larynx?

A

Mostly respiratory epithelium
Epiglottis and vocal folds = stratified squamous non-keratinised epithelium
Underneath = dense connective tissue

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43
Q

What are the layers of the trachea and primary bronchi?

A

Respiratory epithelium
Lamina propria
Submucosa
C-shaped hyaline cartilage
Trachealis muscle

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44
Q

What is the function of the submucosa layer?

A

Contains mucous and seromucous glands.
Seromucous glands secrete watery secretions to humidify inspired air.
Mucous glands secrete mucin and with goblet cells trap particles from the air.

45
Q

What are the layers of the intrapulmonary bronchi?

A

Respiratory epithelium
Muscularis mucosa (circular smooth muscle)
Submucosa
Irregular plates of hyaline cartilage distributed across entire circumference

46
Q

What are the layers of the bronchioles?

A

Simple cuboidal epithelium with no goblet cells. Contain interspersed club cells.
Elastin
Smooth muscle

47
Q

What cells make up the surface of the alveoli?

A

Simple squamous epithelium.

48
Q

What tissue type makes up the alveolar septa?

A

Connective tissue.

49
Q

Type I Pneumocysts

A

Very flat squamous cells
95% of alveolar surface

50
Q

Type II Pneumocysts

A

Cuboidal secretory cells
Secrete surfactant by exocytosis of lamellar bodies

51
Q

What is the function of surfactant?

A

Lines alveoli and decreases surface tension to prevent collapse.

52
Q

Dust Cells

A

Alveolar macrophages
Located in alveolar septa and air spaces
Phagocytose inhaled particulate matter and pathogens and contain lysosomes with hydrolytic enzymes.

53
Q

What cell type makes up the pleura?

A

Simple squamous epithelium (mesothelium) and connective tissue.

54
Q

Signs and symptoms of asthma.

A

Wheeze
Dyspnoea
Cough (may be nocturnal)
Chest tightness
Diurnal variation
Tachyonoea
Hyper inflated chest
Hyper-resonance on chest perfusion
Decreased air entry
Wheeze on auscultation

55
Q

Asthma investigations

A

Peak flow diary with diurnal readings and >20% variability
Total IgE and eosinophils raised
Chest x-ray excludes other causes
Spirometer FEV1/FVC <70% (reversible following bronchodilator)
FeNO >40 in adults, >35 in children

56
Q

Asthma management

A

Short acting beta 2 agonist (e.g. salbutamol)
Low dose inhaled corticosteroids (ICS)
Leukotriene receptor antagonist
Long acting beta 2 agonist (e.g. salmeterol)

57
Q

Asthma differentials

A

GORD/acid reflux
Churg-Strauss syndrome
Allergic bronchopulmonary aspergillosis

58
Q

Signs of severe asthma attack

A

Inability to speak in complete sentences
RR > 25
Peak flow 30-50% predicted
HR > 110

59
Q

Signs of life-threatening asthma attack

A

Peak flow <30% predicted
Silent chest
Altered consciousness
Bradycardia
Hypotension
Hypoxia
Cyanosis
Exhaustion

60
Q

What acute changes occur due to asthma?

A

IgE mediated mast cell degranulation
Th2 activation
Cytokine release
Eosinophil leukocyte recruitment

61
Q

What chronic changes occur due to asthma?

A

Epithelial damage
Thickening of the airway wall
Increased vascularity
Smooth muscle hypertrophy and hyperplasia
Mucous gland hyperplasia

62
Q

What causes airway obstruction in asthma?

A

Smooth muscle contraction
Vascular congestion
Oedema of the airway wall
Mucous secretion
Epithelial damage

63
Q

What is the clinical characterisation of asthma?

A

Bronchoconstriction that is episodic and reversible.

64
Q

What is the most common primary lung tumour?

A

Carcinoma

65
Q

What are the two divisions of carcinoma?

A

Non-small cell carcinoma (e.g. squamous cell carcinoma, adenocarcinoma)
Small cell carcinoma (‘oat cell’)

66
Q

What are the main causes of lung cancer?

A

Smoking
Atmospheric pollution
Ionising radiation
Asbestos (promoting role)
Interstitial lung disease

67
Q

What are the steps of lung cancer pathogenesis?

A

Squamous metaplasia (response to chronic irritation)
Dysplasia
In situ carcinoma
Invasive carcinoma

68
Q

What are the most common gene mutations in lung cancer?

A

KRAS
EGFR
TP53
p16/RB

69
Q

What cell type does adenocarcinoma occur in?

A

Glandular

70
Q

What are the two clinical entities of COPD?

A

Emphysema
Chronic bronchitis

71
Q

What are the main risk factors of COPD?

A

Current/former smokers
Age 35+

72
Q

What is emphysema?

A

Destructive process involving alveoli in which there is an abnormal increase in size of airspaces.

73
Q

What is a bulla?

A

Space > 1 cm

74
Q

What does air trapping cause?

A

‘Barrel chest’ and hyperinflation
Reduced alveolar surface area for gas exchange

75
Q

What is the clinical definition of chronic bronchitis?

A

Persistent or recurrent excess of bronchial secretion on most days for at least 3 months in the year, over at least two years.

76
Q

What are the clinical features of chronic bronchitis?

A

Cough - producing clear, white or purulent mucoid secretions
Especially purulent with infective exacerbations
Disease progression also leads to permanently purulent secretions
Overnight accumulation of secretions

77
Q

What is the pathogenesis of chronic bronchitis?

A

Irritants cause mucus hypersecretion
Increase in mucous goblet cells within epithelium
Up-regulation of mucin genes and epidermal growth factor

78
Q

What is the pathophysiology of emphysema?

A

Irritants cause increase in macrophages, therefore increasing neutrophils leading to increased elastase in the lungs.

79
Q

Pneumonia triad

A

Evidence of infection (fever, chills, leucocytosis)
Signs and symptoms localised to the RT (cough, sputum, SoB, chest pain etc)
New or changed infiltrate on CXR

80
Q

Differential diagnosis of CAP with abnormal CXR?

A

Aspiration pneumonitis
Pulmonary infarction
Acute exacerbation of pulmonary fibrosis
Acute exacerbation of bronchiectasis
Acute eosinophilic pneumonia
Hypersensitvity pneumonitis
Pulmonary vasculitis
Cocaine-induced lung injury (‘crack lung’)

81
Q

Differential diagnosis of CAP with normal CXR?

A

Acute exacerbation of COPD
Influenza
Acute bronchitis
Pertussis
Asthma with associated with viral syndrome to explain infectious symptoms

82
Q

What tests should be ordered for severe CAP?

A

Blood culture
Sputum culture
Influenza (during influenza season)
Urinary pneumococcal antigen
Urinary legionella antigen
Pleural fluid culture

83
Q

What system is used to determine the severity of pneumonia?

A

CURB-65
Confusion
Urea
RR
BP
>65 years

84
Q

Central trachea, decreased expansion, dullness to percussion, bronchial breathing, crackles, increased vocal resonance.

A

Consolidation

85
Q

Central or deviated trachea away, reduced expansion, stony dull to percussion, absent breath sounds, reduced vocal resonance.

A

Pleural effusion

86
Q

Trachea deviation toward, decreased expansion, dull to percussion, absent breath sounds, normal vocal resonance.

A

Lobar collapse
Lobectomy
Pneumonectomy

87
Q

Central trachea, decreased expansion, hyper-resonance to percussion, quiet breath sounds, reduced vocal resonance.

A

Pneumothorax

88
Q

Trachea deviation toward, decreased expansion, hyper-resonance to percussion, decreased/absent breath sounds, may get pleural click, reduced vocal resonance.

A

Tension pneumothorax

89
Q

Central trachea, reduced expansion, resonant/normal to percussion, expiratory wheeze or coarse crackles, reduced vocal resonance.

A

COPD/asthma

90
Q

Central trachea, reduced expansion, normal/dull to percussion, bronchial breathing, fine crackles, normal vocal resonance.

A

Fibrosis - usually bilateral.
If unilateral then tracheal deviation

91
Q

Where are the CO2 chemoreceptors situated?

A

Central - ventral surface of the medulla
Peripherally - carotid bodies

92
Q

What are peripheral chemoreceptors sensitive to?

A

CO2, H+ and O2 in the blood

93
Q

What are central chemoreceptors sensitive to?

A

CO2 that has crossed the BBB and dissociated into H+ in the CSF

94
Q

What is the PO2 in arteries and veins?

A

Arteries = 13.3 kPa
Veins = 5.3 kPa

95
Q

What can cause a right shift in the oxyhaemoglobin dissociation curve?

A

Increased 2,3 DPG
Increased H+ or CO2
Increased temperature

96
Q

What does a right shift in the oxyhaemoglobin dissociation curve cause?

A

Reduced affinity of Hb for O2

97
Q

What does a left shift in the oxyhaemoglobin dissociation curve cause?

A

Increased affinity of Hb for O2

98
Q

What can cause a left shift in the oxyhaemoglobin dissociation curve?

A

Decreased 2,3 DPG
Decreased H+ or CO2
Decreased temperature
HbF

99
Q

What are the criteria of Type 1 respiratory failure?

A

Low PaO2 (< 8 kPa)
Normal or low PaCO2

100
Q

What are the criteria of Type 2 respiratory failure?

A

Low PaO2 (< 8 kPa)
High PaCO2 (> 6 kPa)

101
Q

What causes Type 1 respiratory failure?

A

V/Q mismatch (e.g. impaired diffusion, shunt)

102
Q

What causes Type 2 respiratory failure?

A

Ventilation problem due to hypoventilation with or without V/Q mismatch (e.g. obstructive lung disease)

103
Q

What is the first line treatment for low severity CAP?

A

Amoxicillin; 500 mg; 3x daily; 5 days

104
Q

What is the first line treatment for moderate severity CAP?

A

Amoxicillin; 500 mg; 2x daily; 5 days
With (if atypical pathogens suspected):
Clarithromycin; 500 mg; 2x daily; 5 days
OR
Erythromycin (in pregnancy); 500mg; 4x daily; 5 days

105
Q

What is the first line treatment for high severity CAP?

A

Co amoxiclav; 500/125 mg, 3x daily oral; 1.2 g, 3x daily IV
With:
Clarithromycin; 500 mg, 2x daily; 5 days (oral or IV)
Erithromycin (in pregnancy); 500 mg; 4x daily; 4 days (oral or IV)

106
Q

What is the first line treatment for non-severe HAP?

A

Co-amoxiclav; 500/125 mg; 2x daily, 5 days (review)

107
Q

What is the first line treatment for severe HAP?

A

Pip/taz
Ceftazidime
Ceftriaxone
Cefuroxime
Meropenem
Ceftazidime with avibactam
Levofloxacin (safety issues)
Based on microbiological advice

108
Q

What antibiotic is added if MRSA is suspected for HAP?

A

Vancomycin or teicoplanin alongside IV antibiotic of choice from first line severe treatment

BM4 Part 1 (11 decks)

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