Respiratory Flashcards

1
Q

What is an average tidal volume?

A

500mL

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2
Q

What is a normal vital capacity?

A

4.8L

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3
Q

What is the residual volume of the lungs?

A

1.2L

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4
Q

What is vital capacity?

A

Total volume of air possible to expire?

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5
Q

Define residual volume.

A

Volume of the lungs with no air

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6
Q

How do you work out total lung volume?

A

Vital capacity + residual volume

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7
Q

How do you calculate minute ventilation?

A

Tidal volume x respiratory rate

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8
Q

How do you calculate alveolar ventilation?

A

(tidal volume - dead space) x respiratory rate

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9
Q

What is the normal volume of anatomic dead space in the lungs?

A

150mL

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10
Q

What is FVC?

A

Forced vital capacity, the maximum volume exhaled

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11
Q

What is FEV1?

A

Forced expiratory volume within 1 second, should be 80% of FVC

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12
Q

What findings in lung function tests are indicative of obstructive lung disease?

A

Reduced FEV1 due to increased resistance, less than 80% of FVC

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13
Q

What findings in lung function tests are indicative of restrictive lung disease?

A

FEV1 and FVC reduced but with FEV1 over 80% of FVC

Vital capacity reduced due to lack of elasticity

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14
Q

What is lung compliance?

A

The ease with which lungs and thorax expand

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15
Q

What results in high compliance?

A

Old age, emphysema

Small increase in TP, large increase in volume due to loss of elastic recoil

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16
Q

What results in low compliance?

A

Oedema, fibrosis, pneumonia

Large increase in TP, small increase in volume due to increased collagen expression and inflammation

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17
Q

What is newborn respiratory distress syndrome?

A

Occurs in premature babies, type II cuboid cells are underdeveloped reducing surfactant secretion, causing alveolar collapse on expiration

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18
Q

What conditions can cause alveolar collapse on expiration?

A

Arthritis
Ankylosing spondylitis
Due to reduced spinal cord/rib articulation

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19
Q

What is emphysema?

A

Degeneration of alveolar, bronchiole walls and capillaries due to proteolytic attack by leukocyte proteases, increasing alveolar dead space.

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20
Q

List the 4 main conducting airways.

A

Trachea
Bronchi
Bronchioles
Terminal bronchioles

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21
Q

List the 3 main respiratory airways.

A

Respiratory bronchioles
Alveolar ducts
Alveolar sacs

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22
Q

What is the opening of the larynx?

A

Glottis, covered by the epiglottis

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23
Q

What are the roles of the conducting airways?

A

Low resistance pathway for air flow
Warms and moistens air to increase efficiency
Defence against infection

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24
Q

What are the features of the respiratory tract that defend against infection?

A

Macrophages
Cilia
Mucus secretion and escalator
Movement of chloride ions out of cells

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25
What is cystic fibrosis?
Defective gene leading to cystic fibrosis transmembrane regulator (apical chloride channel) mutations Leading to mucus build up to to impact on fluid secretion
26
What features of the respiratory organs help to protect and prevent collapse?
Lungs surrounded by individual pleural sacs Inner side attached to lungs via connective tissue Outer side attached to diaphragm and thoracic wall
27
What is the thoracic wall made up of?
Spinal cord Ribs Intercostal muscles
28
What is pneumothorax?
Pleural sac broken due to puncture of chest wall allowing air to enter, lungs recoil and collapse
29
In which diseases can spontaneous pneumothorax occur?
Pneumonia | Emphysema
30
What is the treatment for minor pneumothorax?
X-ray monitoring Absorption of air Needle and chest tube insertion
31
What is the treatment for major pneumothorax?
Surgery to repair puncture | Removal of lung
32
Describe stage 1 of the asthma treatment pathway.
Occasional use of short acting beta agonist when required
33
Describe stage 2 of the asthma treatment pathway.
Use of SABA when required | Addition of low dose inhaled corticosteroid as preventer
34
Describe stage 3 of the asthma treatment pathway.
Use of SABA when required Low dose inhaled corticosteroid as preventer Addition of long acting beta agonist
35
Describe add ons at stage 4 of asthma treatment pathway.
``` Medium ICS dose Continuation of LABA if benefit seen Trial one of: - leukotriene antagonist - Theophylline - LAMA ```
36
What are the add ons at stage 5 of the asthma treatment pathway?
``` High dose ICS Addition of fourth drug: -leukotriene antagonist - theophylline - beta agonist tablet ```
37
What is added at stage 6 of the asthma treatment pathway?
Continued use of oral steroids at lowest effective dose alongside high dose ICS
38
What are the symptoms of an acute asthma exacerbation?
``` Cyanosis Drowsiness/unconsciousness Tachycardia Severe dyspnoea PEF <50% Respiratory rate >25 Oxygen sats <92% ```
39
What is the treatment for an acute asthma exacerbation in hospital?
Ipratropium nebulisers 500mcg every 4-6 hours Single dose IV magnesium sulphate IV aminophylline/salbuatmol Oxygen 40-60%
40
What is the standard dose of oral steroids in acute asthma?
40-50mg daily for 5 days
41
What is the MOA of beta-2 adrenoceptor agonists?
Mimic adrenaline to increase cAMP levels causing relaxation of smooth muscle
42
Give examples of short acting beta agonists and their onset/duration of action.
Salbutamol, terbutaline Onset of 1-5 minutes Duration of 4-6 hours
43
Give examples of long acting beta agonists and their onset/duration of action.
``` Formeterol Onset 1-3 minutes Salmeterol Onset 10-20 minutes Duration of 12 hours ```
44
Give side effects of beta-agonists.
Fine tremor Headache Tachycardia
45
What is the MOA of corticosteroids?
Bind glucocorticoid receptors to dissociate heat shock proteins and allow receptors to travel to the nucleus where they bind to DNA blocking genes that code for cytokines for inflammation.
46
Give examples of inhaled corticosteroids.
Beclomethasone | Budesonide
47
Give examples of oral corticosteroids.
Prednisolone
48
Give examples of IV corticosteroids.
Hydrocortisone
49
What are the criteria for corticosteroid indication.
Exacerbation in the last 2 years Using SABA at least twice weekly Waking with symptoms once per week
50
What are the side effects of corticosteroids?
``` Oral candidiasis Hoarseness Adrenal suppression Skin thinning Cushing's ```
51
What is the MOA of leukotriene antagonists?
Antagonise broncho-constriction, reducing mucus secretion and airway oedema
52
Give examples of leukotriene antagonists.
Montelukast | Zafirlukast
53
What are the side effects of leukotriene antagonists?
Abdominal pain Thirst Headache
54
What are methylxanthines?
PDE inhibitors that prevent the breakdown of cAMP, preventing broncho-constriction
55
Give examples of methylxanthines.
Theophylline | Aminophylline
56
Why are leukotriene antagonists not 1st choice drugs in asthma? Give two reasons
Not as effective as beta-agonists | Side effect of thirst can increase risk of bedwetting in children
57
Why are methylxanthines not 1st choice drugs in asthma?
Narrow therapeutic window of 10-20mg/L
58
What are the side effects of methylxanthines with a dose over 20mg/L?
Insomnia Arrhythmia Hyperglycaemia Convulsions
59
What are PDE4 inhibitors?
Reduce production of matrix metallaproteinase, enhancing effects of beta-2 agonists
60
Give an example of a PDE4 inhibitor.
Roflumilast
61
When are PDE4 inhibitors indicated?
Severe persistent COPD associated with chronic bronchitis
62
What are the side effects of PDE4 inhibitors?
Diarrhoea Abdominal pain Unexplained weight loss
63
What is the mechanism of action of monoclonal antibodies in asthma?
Inhibit IgE binding to mast cell receptors, thus reducing inflammation
64
Give an example of monoclonal antibodies used in asthma. What is the regimen?
Omalizumab SC every 2-4 weeks | Discontinued after 16 weeks if no adequate response is seen
65
Give examples of immunosuppressants that may be used by specialists in asthma.
Cyclosporin Methotrexate Gold
66
What are analeptics?
Stimulate chemoreceptors in carotid and aortic bodies to increase respiratory work rate
67
Give an example of an analeptic.
Doxapram
68
When are analeptics used?
Post-operative respiratory depression Ventilatory failure in COPD Apnoea in neonates
69
Why is caffeine useful in respiratory disease?
It is a phosphodiesterase inhibitor, increasing levels of cAMP and promoting effects of beta-adrenoceptors
70
What are cromones? Give an example.
Nedocromil | Mast cell stabilisers, work to reduce inflammation
71
What is the role of carotid and aortic chemoreceptors?
Activated by increased carbon dioxide levels in the blood increasing respiratory rate and workload
72
What is the normal level of carbon dioxide in ventilation?
40mmHg
73
What is the role of acetylcholine at M3 receptors in respiration?
Increases intracellular calcium ion levels Interaction with calmodulin activates myosin light chain kinase Kinase phosphorylates myosin leading to contraction
74
What occurs upon activation of beta-2 adrenoceptors?
Stimulates adenylyl cyclase, increasing production of cAMP Protein kinase A activates to phosphorylate proteins acting to reduce intracellular calcium Reduces activity of MLCK, causing relaxation of airway muscles
75
What is allergic asthma?
Hyper-responsiveness to stimulus causing broncho-constriction and mucus secretion that is reversible
76
Give examples of triggers of asthma.
``` Stress Cold Allergens Exercise Infection ```
77
How do dust mites cause allergic asthma?
Release of casts, secretions and enzymes
78
What occurs in the initial phase of asthma?
Occurs abruptly due to spasm Allergen interacts with mast cell IgE releasing histamine, leukotriene B4 and prostaglandin D2 Interleukins, TNF and macrophage proteins also released into airway Chemotaxins attract eosinophils to trigger late phase
79
What occurs in the late phase of asthma?
Allergens interact with dendritic and CD4 cells leading to ThO cell development, leading to Th2 clones B cells produce IgE IL-5 activates eosinophils Cytokines induce IgE receptor expression Eosinophils release cysteine leukotrienes, interleukins and toxic proteins which cause damage to epithelium Inflammatory mediators include adenosine, NO and neuropeptides
80
What is intrinsic asthma?
Occurs later in life due to precipitating factors such as inhalation of irritants or pollutants Chronic and persistent symptoms
81
What is the cause and action of COPD?
Exposure to irritants causing epithelial cells to release factors activating neutrophils CD8, B cell and macrophage accumulation accumulation Inflammatory cascade causes mediator release- TNF, interferon, MMP, interleukins
82
What causes damage in COPD?
Inflammation is sustained and causes tissue damage and systemic effects MMPs destroy elastin fibres causing proteolytic degredation
83
What is COPD characterised by?
Airflow obstruction that is not fully reversible Does not changed markedly over several months but progressive in the long term FEV1/FVC ratio <70%
84
What are the risk factors of COPD?
Smoking Age Alpha-1 antitrypsin deficiency Occupation
85
What does COPD present with?
Exertional breathlessness Chronic cough Regular sputum production Wheeze
86
What is the BODE index?
``` Measure of COPD based on: BMI Obstruction Dyspnoea Exercise capacity ```
87
What are the side effects of anti-muscarinics?
Dry mouth Urinary retention Blurred vision
88
How can methylxanthines improve COPD symptoms?
Strengthen diaphragm | Increase mucociliary clearance
89
What are mucolytics used for?
Reduce mucus viscosity making it easier to clear and reducing obstruction
90
When is oxygen given in COPD?
Long term where FEV1 <35% and oxygen sats <92% | 24-28% oxygen given >15 hours per day
91
What are the common causes of infective exacerbations of COPD?
Streptococcus pneumoniae | Haemophilus influenzae
92
What is the first line treatment of infective exacerbations of COPD?
Amoxicillin 500mg OR tetracycline 100mg with 200mg doxycycline stat Given alongside 30mg prednisone for 7-14 days
93
What is the second line treatment of infective exacerbations of COPD?
Broad spectrum cephalosporin or macrolide
94
What is hypercapnia?
Abnormally high carbon dioxide levels
95
What is cor pulmonale?
Right side heart failure due to pulmonary hypertension
96
What is polycythaemia?
Increase in RBCs due to chronic hypoxia, increasing blood viscosity