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Clinical Physiology > Respiratory disorders > Flashcards

Respiratory disorders Flashcards

1
Q

What was the Bhopal disaster (1984)?

A

A leak and failing of a safety valve in a Bhopal pesticide plant that released a methyl isocyanate (MIC) gas into the air, killing thousands of humans and animals and exposing more than half a million people

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2
Q

What were the early respiratory effects of the Bhopal methyl isocyanate exposure (0 to 6 months)?

A
  • Respiratory distress
  • Pulmonary oedema
  • Pneumonitis
  • Pneumothorax
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3
Q

What were the late respiratory effects of the Bhopal methyl isocyanate exposure (6 months onwards)?

A
  • Obstructive and restrictive airway disease
  • Decreased lung function
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4
Q

What lines the inside of the trachea?

A

Epithelium with cilia to get rid of mucus

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5
Q

What is the result of functioning ciliated epithelium in the trachea?

A

Mucus is carried back up to the pharynx by the cilia then swallowed

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6
Q

List and briefly describe the roles of four mechanisms that protect the respiratory system

A
  • Epiglottis - stops food entering the respiratory system
  • Epithelium - mucus
  • Immune system - tonsils, macrophages in the lungs
  • Pleura - double membrane around the lungs
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7
Q

Out of the bronchi, bronchioli, and alveoli, which has the most connective tissue?

A

Bronchi

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8
Q

Out of the bronchi, bronchioli, and alveoli, which has the least connective tissue?

A

Alveoli

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9
Q

Which lung has a superior lobe, middle lobe, and inferior lobe?

A

Right

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10
Q

Describe the two phases of pulmonary ventilation

A
  • Inspiration
    • ​Air is drawn into lungs
    • Active (diaphragm, intercostals)
  • Expiration
    • ​Air is expelled from lungs
    • Passive (recoil of elastic structures in thorax and lung)
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11
Q

Neurologically, what controls respiration?

A

The inspiratory and expiratory neurones in the medullary respiratory control centre in the medulla oblongata, as well as peripheral chemoreceptors in carotid and aortic bodies, and central chemoreceptors in the medulla.

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12
Q

What is hypercapnia and what are the effects?

A

Excess CO2 which lowers blood pH, usually caused by hypoventilation due to respiratory depression or a mechanical obstruction

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13
Q

What is hypocapnia and what are the effects?

A

Excess HCO3 (bicarbonate) which increases blood pH, usually due to hyperventilation

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14
Q

Describe what happens on a cellular level after contracting rhinovirus

A
  • Within 15min rhinovirus binds to a cell adhesion molecule (ICAM) on respiratory epithelial cells
  • The binding triggers RNA release from the virus into the host cell
  • The virus replicates and spreads
  • Lytic virus destroys cells and triggers an immune reaction, i.e. chemokines/cytokines
  • Symptom onset usually within 48 hours
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15
Q

What is H5N1?

A

Influenza A

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16
Q

What is antigenic shift?

A

Combining of two or more viruses, resulting in more cell surface molecules (antigens) and therefore a ‘stronger’ virus

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17
Q

What is antigenic drift?

A

Natural mutations over time which may not be recognised by the immune system or prevented by vaccination

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18
Q

What can cause pneumonia, and which is the most common?

A
  • Bacteria (most common)
  • Viruses
  • Fungi
  • Parasites
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19
Q

How is pneumonia dx?

A

Bacteria in sputum and chest x-ray. Pt may also have pleurisy (inflammation of the pleura)

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20
Q

True or false: pneumonia is the leading cause of death amongst infectious diseases

A

True

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21
Q

List some symptoms of pneumonia

A
  • SOB
  • Fatigue
  • Coughing
  • Fever
  • Confusion (elderly)
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22
Q

Differentiate between obstructive and restrictive respiratory disorders

A

Obstructive: cannot exhale (asthma/chronic bronchitis/emphysema)

Restrictive: cannot inhale, lungs cannot expand (alveolitis/lung section removal)

Note that cystic fibrosis is both obstructive and restrictive

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23
Q

What lung volumes make up the vital capacity?

A

Inspiratory reserve volume (3L, maximal air able to be inhaled), tidal volume, and expiratory reserve volume (1L, maximal air that can be exhaled)

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24
Q

What is total lung capacity, and what is its average volume?

A

Vital capacity and residual volume, average of 5.8L

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25
Q

What is the definition of vital capacity?

A

The amount of air that can be exhaled after a maximal inhalation

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26
Q

What is minute ventilation?

A

Tidal volume x breaths per minute

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27
Q

What does spirometry measure?

A

The volume of air in L moving in and out of the lungs, and the flow rate by which the air is moving in L per second

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28
Q

What is forced expiratory volume (FEV1)?

A

Maximal amount of air able to be exhaled in the first second after a deep inhalation

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29
Q

What is FEV1/FVC?

A

The % of FVC that is expelled in the first second

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30
Q

What is indicated by a reduced FVC, FEV1, and FEV1/FVC?

A

Obstructive respiratory disorder

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31
Q

What is indicated by reduced FVC but normal FEV1/FVC?

A

Restrictive respiratory disorder

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32
Q

What is peak inspiratory flow (PIF)?

A

The fastest flow rate recorded during inhalation

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33
Q

What is peak expiratory flow (PEF)?

A

The fastest flow rate recorded during exhalation

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34
Q

What is FEF25-75%?

A

The flow rate of air coming out of the lungs during the middle portion of a forced expiration

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35
Q

What spirometry parameter is often first affected when someone develops respiratory disease?

A

FEF25-75%

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36
Q

What is FEF25-75% below 50% of average indicative of?

A

Obstructive respiratory disorder (trouble breathing out quickly)

37
Q

What is FEF25-75% above 130% of average indicative of?

A

Restrictive respiratory disorder (breathing out too quickly)

38
Q

What is air trapping?

A

Increased residual volume, resulting in a barrel chest

39
Q

What is a respiratory shunt?

A

O2 from alveoli does not reach lung capillaries because alveoli are closed off; blood returns to the heart without being properly oxygenated

40
Q

Give a general description of major obstructive airway diseases

A

Lower airway narrowing leads to expiratory flow limitation, gas trapping, and hyperinflation of the lungs

41
Q

Differentiate between asthma and COPD

A
  • Asthma
    • Intermittent and reversible airway obstruction
    • Caused by airway inflammation and bronchial smooth muscle contraction primarily due to mediators released from mast cells and eosinophils
  • COPD
    • Progressive and primarily irreversible airways narrowing caused by airway narrowing and loss of lung elasticity
    • Most commonly due to smoking-induced activation of airway neutrophils
42
Q

Contrast the histopathology of asthma and COPD

A
  • Alveolar disruption - increased in COPD
  • Mast cells - increased and activated in asthma
  • Eosinophils - increased in asthma
  • Neutrophils - increased in COPD
43
Q

What occurs at the cellular level during an asthma exacerbation?

A

Mast cells empty out too much histamine, causing oedema, airway constriction, and excess mucus production, resulting in airway obstruction

44
Q

How is asthma an obstructive airway disorder?

A

It is hard to breathe in because there is air in the lungs, so more pressure is needed; it is harder still to breathe out as more pressure is needed to force air out of closed airways

45
Q

How does asthma effect spirometry graphs?

A
46
Q

Describe what happens in an asthma exacerbation

A
  • Pt cannot get enough O2 into the blood and starts to hyperventilate, developing hypocapnia and respiratory alkalosis
  • If not relieved the airways close and prevent the pt exhaling sufficient CO2, leading to respiratory acidosis and eventual LOC
47
Q

What are the three components of an asthma exacerbation?

A

Bronchospasm, the ‘late phase’, and airway hyperresponsiveness

48
Q

Describe asthmatic bronchospasm

A
  • Early and prominent in allergic asthma
  • Small airway narrow due to smooth muscle contraction
  • Closure begins to occur during expiration, trapping gas and initiating hyperinflation
49
Q

Describe the asthmatic ‘late phase’

A
  • Airway inflammmation developing a few hours after bronchospasm (note that respiratory infections may bypass the acute bronchospasm phase)
  • Airway obstruction continues
  • Cough with sputum develops
50
Q

Describe asthmatic airway hyperresponsiveness

A
  • Asthmatics become wheezy in response to stimuli that have little effect on others
  • Inhaled metacoline or histamine can be used to measure degree of AHR by determining the inhaled concentration that gives rise to a 20% decrease in FEV1
51
Q

Describe the involvement of mast cells in asthma

A
  • Plentiful in walls of airways and alveoli, free in lumen
  • Activation is main cause of bronchospasm in allergen-provoked asthma
  • Surface of cell has large number of receptors that bind IgE
  • Hypersensitive, within 30s of activation they degranulate and release histamine
  • Granules also contain protease tryptase that can cause epithelial cells to detach
52
Q

Describe the involvement of histamine in asthma

A
  • Acts directly on H1 receptors on bronchial smooth muscle to cause contraction
  • Acts on H1 receptor of endothelial cells to cause vascular permeability
  • Acts on H2 receptor of goblet cells to increase mucus production

Note: antihistamines will block the processes initiated by mast cell release of histamine as they antagonise the histamine receptor

53
Q

Describe the involvement of eosinophils in asthma

A
  • Freely distributed with mast cells in sub-mucosa
  • Principle cell involved in the late phase response
  • Release lipid mediators (leukotrienes) that prolong bronchoconstriction
54
Q

How do beta2 receptor agonists assist asthma?

A

Beta2-adrenergic receptor increases cAMP in bronchial smooth muscle cells which decreases calcium levels, relaxing bronchial smooth muscle and dilating the airways

55
Q

Bronchitis, emphysema, and COPD are all ____ disorders

A

Obstructive

56
Q

What is bronchitis, and what is its characteristic symptom?

A

Inflammation of the mucous membranes of the bronchi; hypersecretion of mucous (productive cough) is a defining feature

57
Q

What causes acute bronchitis?

A

Virus, e.g. influenza

58
Q

What causes/is associated with chronic bronchitis?

A

Smoking is associated with bronchiolar fibrosis and goblet cell hyperplasia (mucous plugging)

59
Q

List symptoms of severe bronchitis

A
  • Hypoxaemia
  • Decreased haemoglobin saturation (not delivering sufficient O2 to alveoli while also trapping stale air), resulting in cyanosis
  • Hypercapnia (not breathing out enough CO2) leading to carbonic acid formation
  • Respiratory acidosis (raised blood pH), with renal compensation resulting in elevated bicarbonate
  • Hypoxic pulmonary vasoconstriction (constriction of lung capillaries due to lack of O2 in the area, supposedly negating the need for perfusion; increases pulmonary artery pressure and overloads the right side of the heart)
  • RVF (common long term complication)
  • Systemic oedema (classic sign)
60
Q

What is the rx for bronchitis?

A
  • Bronchodilators
  • Inhaled steroids
  • O2 (in severe cases)
61
Q

What is emphysema?

A

Enlargement and decreased number of alveoli, resulting in a decreased surface area for gas exchange, as well as low elasticity and high compliance making it harder to breathe without recoil and with potential for alveoli to collapse

62
Q

List the symptoms of emphysema

A
  • Tachypnoea (compensates for reduced gas exchange)
  • Hypoxaemia (though normoxia is maintained by increased minute ventilation in early stages [pink puffers])
  • Hypercapnia (may be hypo in early stages ∵ increased ventilation rate)
  • Peripheral oedema due to pulmonary hypertension (∵ hypoxia-induced vasoconstriction)
  • Cor pulmonale (∵ pulmonary hypertension), aka RVF
63
Q

What is the role of α1-anti-trypsin (α1-AT)?

A

α1-AT protects cells from neutrophil elastase which destroys the elasticity of alveoli

64
Q

What causes α1-AT deficiency?

A

It is an autosomal recessive disorder caused by mutations in the SERPINA1 (pre-protein) gene which regulates α1-AT expression

65
Q

What is the prognosis for people with α1-AT deficiency?

A

Pts develop emphysema between 20-50 years of age, and ~15% also develop cirrhosis of the liver

66
Q

What is the effect of cigarette smoke on the function of α1-AT?

A

Inhibitory; cigarette smoke causes oxidation of an amino acid residue in the α1-AT protein at the site where it binds to elastase, which is important for its ability to inhibit elastase activity. Excessive elastase release from neutrophils in response to smoking is not regulated by α1-AT, and the result is accumulation of damage to alveolar elastin.

<em><strong>TL;DR</strong>: neutrophils secrete an enzyme (elastase) that destroys the elasticity of alveoli. α1-AT protects cells from this, but cigarette smoke blocks this action (note the persistent presence of neutrophils is due to repeated inflection/inflammation)</em>

67
Q

What is the rx for α1-AT deficiency?

A
  • No cure; symptom mx only (lifestyle changes, mx RVF)
  • O2
  • Bulectomy (remove bullae [fused alveoli])
68
Q

Give a general description of restrictive airway diseases

A

Cannot fill lungs; restriction of lung expansion

69
Q

What can cause restrictive airway diseases?

A
  • Removal of part of lung
  • Alveolitis, interstitial fibrosis (inflammation in respiratory membrane with fibrosis)
  • Problem with pleura or thorax
70
Q

What are the general symptoms of restrictive airway disease?

A
  • Hypoxia
  • All lung capacities are decreased
  • Residual volume is decreased
71
Q

What is the result of a thicker interstitium ∵ interstitial fibrosis?

A

Poor diffusion ∴ blood is not properly oxygenated

72
Q

Do the symptoms of interstitial fibrosis improve or worsen during exercise? Why?

A

Worsens during exercise ∵ it doesn’t help to increase breathing rate

73
Q

Describe the spirometry of a person with restrictive airways

A
  • Restrictive ventilatory pattern with reduced FVC and FEV1
  • FEV1/FVC ratio is generally unaffected and is often increased (>100%, ∵ increased elastic recoil produces normal to increased expiratory flow rate when adjusted for lung volume)
74
Q

What is chronic interstitial disease?

A

A heterogenous group of disorders, many idiopathic, with chronic involvement of pulmonary connective tissue

75
Q

Anatomically, what is principally involved in chronic interstitial disease?

A

The most peripheral and delicate interstitium of the alveolar wall

76
Q

What is the hallmark feature of chronic interstitial disease?

A

Reduced compliance (more pressure required to inflate lungs due to stiff fibrosis), resulting in dyspnoea. Damage to alveolar epithelium and interstitial vasculature produces abnormalities in the ventilation-perfusion ration, resulting in hypoxia.

77
Q

List four forms of chronic interstitial disease

A
  • Idiopathic pulmonary fibrosis
  • Non-specific interstitial pneumonia
  • Crypotogenic organising pneumonia
  • Pneumoconiosis
78
Q

Describe the development of idiopathic pulmonary fibrosis

A

Alveolitis leads to fibrosis; believed to be ∵ repeated cycles of inflammation and epithelial injury

Abnormal epithelial repair at sites of damage/inflammation gives rise to hyperactivated fibroblast and myofibroblast proliferation, causing excessive collagen deposition.

79
Q

What is interstitial fibrosis also known as?

A

‘Honeycomb lung’ as alveoli are stuck open (∴ no air trapping)

80
Q

What is pneumoconiosis?

A

Non-neoplastic lung reaction to inhaled mineral dust/chemical fumes

81
Q

List three types of pneumoconiosis and their causes

A
  • Coal dust (coal worker’s pneumoconiosis/black lung)
  • Silica (silicosis)
  • Asbestos (asbestosis, not to be confused with mesothelioma)
82
Q

What is asbestos?

A

Crystalline hydrated silicates with a fibrous geometry

83
Q

Occupational exposure to asbestos was linked to what complications?

A
  • Parenchymal interstitial fibrosis (asbestosis)
  • Pleural effusions
  • Localised fibrous plaques in the pleura
  • Longer term lung cancer
  • Mesothelioma (pleural or peritoneal)
84
Q

Describe the role of macrophages in relation to asbestosis

A
  • Key component of the pathogenesis as they attempt to phagocytose the fibres
  • Macrophages that have engulfed asbestos form asbestos bodies. These differentiate the honeycomb appearance from that of idiopathic pulmonary fibrosis
  • Asbestos promotes generation of free radicals (mutagenic), and may also bind to toxins like tobacco smoke
85
Q

What is the effect of smoking on the health impacts of inhaled mineral dust?

A

Tobacco smoke worsens the effect of all inhaled mineral dust, especially asbestos

86
Q

What does DLCO mean?

A

Diffusion capacity of lung carbon monoxide

87
Q

Describe a DLCO test

A

The pt takes a deep breath of air containing a portion of carbon monoxide (CO), holds the breath for 10s, then breathes out. CO has a higher affinity than O2 in the blood, ∴ there is a strong drive for CO to go from alveoli to blood. CO is measured in exhaled air as a proxy for transfer across the alveolar capillary membrane

<strong>TL;DR</strong>: if too much CO is exhaled it indicates impaired gas exchange

88
Q

Describe the results of a DLCO test for a pt with a) interstitial fibrosis, b) emphysema, and c) chronic bronchitis

A
  • Interstitial fibrosis - decreased (fibrotic destruction of capillary beds)
  • Emphysema - decreased (proportional to disease progression, reflecting loss of alveoli and ∴ capillaries)
  • Chronic bronchitis - normal (alveolar-capillary bed is preserved beneath the obstruction)
89
Q

List the mx options for chronic interstitial fibrosis

A
  • No fully effective rx (symptom delay only)
    • Inhaled steroids
    • Immunomodulators (reduce inflammation)
    • Surgery (removal of badly affected areas)

Clinical Physiology (11 decks)

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