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Pharm Y2S2 > Respiratory > Flashcards

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
Q

What is cystic fibrosis?

A

Defective gene leading to cystic fibrosis transmembrane regulator (apical chloride channel) mutations
Leading to mucus build up to to impact on fluid secretion

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26
Q

What features of the respiratory organs help to protect and prevent collapse?

A

Lungs surrounded by individual pleural sacs
Inner side attached to lungs via connective tissue
Outer side attached to diaphragm and thoracic wall

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27
Q

What is the thoracic wall made up of?

A

Spinal cord
Ribs
Intercostal muscles

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28
Q

What is pneumothorax?

A

Pleural sac broken due to puncture of chest wall allowing air to enter, lungs recoil and collapse

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29
Q

In which diseases can spontaneous pneumothorax occur?

A

Pneumonia

Emphysema

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30
Q

What is the treatment for minor pneumothorax?

A

X-ray monitoring
Absorption of air
Needle and chest tube insertion

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31
Q

What is the treatment for major pneumothorax?

A

Surgery to repair puncture

Removal of lung

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32
Q

Describe stage 1 of the asthma treatment pathway.

A

Occasional use of short acting beta agonist when required

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33
Q

Describe stage 2 of the asthma treatment pathway.

A

Use of SABA when required

Addition of low dose inhaled corticosteroid as preventer

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34
Q

Describe stage 3 of the asthma treatment pathway.

A

Use of SABA when required
Low dose inhaled corticosteroid as preventer
Addition of long acting beta agonist

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35
Q

Describe add ons at stage 4 of asthma treatment pathway.

A 
Medium ICS dose
Continuation of LABA if benefit seen
Trial one of:
- leukotriene antagonist
- Theophylline
- LAMA
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36
Q

What are the add ons at stage 5 of the asthma treatment pathway?

A 
High dose ICS
Addition of fourth drug:
-leukotriene antagonist
- theophylline
- beta agonist tablet
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37
Q

What is added at stage 6 of the asthma treatment pathway?

A

Continued use of oral steroids at lowest effective dose alongside high dose ICS

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38
Q

What are the symptoms of an acute asthma exacerbation?

A 
Cyanosis
Drowsiness/unconsciousness
Tachycardia
Severe dyspnoea
PEF <50%
Respiratory rate >25
Oxygen sats <92%
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39
Q

What is the treatment for an acute asthma exacerbation in hospital?

A

Ipratropium nebulisers 500mcg every 4-6 hours
Single dose IV magnesium sulphate
IV aminophylline/salbuatmol
Oxygen 40-60%

40
Q

What is the standard dose of oral steroids in acute asthma?

A

40-50mg daily for 5 days

41
Q

What is the MOA of beta-2 adrenoceptor agonists?

A

Mimic adrenaline to increase cAMP levels causing relaxation of smooth muscle

42
Q

Give examples of short acting beta agonists and their onset/duration of action.

A

Salbutamol, terbutaline
Onset of 1-5 minutes
Duration of 4-6 hours

43
Q

Give examples of long acting beta agonists and their onset/duration of action.

A 
Formeterol
Onset 1-3 minutes
Salmeterol
Onset 10-20 minutes
Duration of 12 hours
44
Q

Give side effects of beta-agonists.

A

Fine tremor
Headache
Tachycardia

45
Q

What is the MOA of corticosteroids?

A

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
Q

Give examples of inhaled corticosteroids.

A

Beclomethasone

Budesonide

47
Q

Give examples of oral corticosteroids.

A

Prednisolone

48
Q

Give examples of IV corticosteroids.

A

Hydrocortisone

49
Q

What are the criteria for corticosteroid indication.

A

Exacerbation in the last 2 years
Using SABA at least twice weekly
Waking with symptoms once per week

50
Q

What are the side effects of corticosteroids?

A 
Oral candidiasis
Hoarseness
Adrenal suppression
Skin thinning
Cushing's
51
Q

What is the MOA of leukotriene antagonists?

A

Antagonise broncho-constriction, reducing mucus secretion and airway oedema

52
Q

Give examples of leukotriene antagonists.

A

Montelukast

Zafirlukast

53
Q

What are the side effects of leukotriene antagonists?

A

Abdominal pain
Thirst
Headache

54
Q

What are methylxanthines?

A

PDE inhibitors that prevent the breakdown of cAMP, preventing broncho-constriction

55
Q

Give examples of methylxanthines.

A

Theophylline

Aminophylline

56
Q

Why are leukotriene antagonists not 1st choice drugs in asthma? Give two reasons

A

Not as effective as beta-agonists

Side effect of thirst can increase risk of bedwetting in children

57
Q

Why are methylxanthines not 1st choice drugs in asthma?

A

Narrow therapeutic window of 10-20mg/L

58
Q

What are the side effects of methylxanthines with a dose over 20mg/L?

A

Insomnia
Arrhythmia
Hyperglycaemia
Convulsions

59
Q

What are PDE4 inhibitors?

A

Reduce production of matrix metallaproteinase, enhancing effects of beta-2 agonists

60
Q

Give an example of a PDE4 inhibitor.

A

Roflumilast

61
Q

When are PDE4 inhibitors indicated?

A

Severe persistent COPD associated with chronic bronchitis

62
Q

What are the side effects of PDE4 inhibitors?

A

Diarrhoea
Abdominal pain
Unexplained weight loss

63
Q

What is the mechanism of action of monoclonal antibodies in asthma?

A

Inhibit IgE binding to mast cell receptors, thus reducing inflammation

64
Q

Give an example of monoclonal antibodies used in asthma. What is the regimen?

A

Omalizumab SC every 2-4 weeks

Discontinued after 16 weeks if no adequate response is seen

65
Q

Give examples of immunosuppressants that may be used by specialists in asthma.

A

Cyclosporin
Methotrexate
Gold

66
Q

What are analeptics?

A

Stimulate chemoreceptors in carotid and aortic bodies to increase respiratory work rate

67
Q

Give an example of an analeptic.

A

Doxapram

68
Q

When are analeptics used?

A

Post-operative respiratory depression
Ventilatory failure in COPD
Apnoea in neonates

69
Q

Why is caffeine useful in respiratory disease?

A

It is a phosphodiesterase inhibitor, increasing levels of cAMP and promoting effects of beta-adrenoceptors

70
Q

What are cromones? Give an example.

A

Nedocromil

Mast cell stabilisers, work to reduce inflammation

71
Q

What is the role of carotid and aortic chemoreceptors?

A

Activated by increased carbon dioxide levels in the blood increasing respiratory rate and workload

72
Q

What is the normal level of carbon dioxide in ventilation?

A

40mmHg

73
Q

What is the role of acetylcholine at M3 receptors in respiration?

A

Increases intracellular calcium ion levels
Interaction with calmodulin activates myosin light chain kinase
Kinase phosphorylates myosin leading to contraction

74
Q

What occurs upon activation of beta-2 adrenoceptors?

A

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
Q

What is allergic asthma?

A

Hyper-responsiveness to stimulus causing broncho-constriction and mucus secretion that is reversible

76
Q

Give examples of triggers of asthma.

A 
Stress
Cold
Allergens
Exercise
Infection
77
Q

How do dust mites cause allergic asthma?

A

Release of casts, secretions and enzymes

78
Q

What occurs in the initial phase of asthma?

A

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
Q

What occurs in the late phase of asthma?

A

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
Q

What is intrinsic asthma?

A

Occurs later in life due to precipitating factors such as inhalation of irritants or pollutants
Chronic and persistent symptoms

81
Q

What is the cause and action of COPD?

A

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
Q

What causes damage in COPD?

A

Inflammation is sustained and causes tissue damage and systemic effects
MMPs destroy elastin fibres causing proteolytic degredation

83
Q

What is COPD characterised by?

A

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
Q

What are the risk factors of COPD?

A

Smoking
Age
Alpha-1 antitrypsin deficiency
Occupation

85
Q

What does COPD present with?

A

Exertional breathlessness
Chronic cough
Regular sputum production
Wheeze

86
Q

What is the BODE index?

A 
Measure of COPD based on:
BMI
Obstruction
Dyspnoea
Exercise capacity
87
Q

What are the side effects of anti-muscarinics?

A

Dry mouth
Urinary retention
Blurred vision

88
Q

How can methylxanthines improve COPD symptoms?

A

Strengthen diaphragm

Increase mucociliary clearance

89
Q

What are mucolytics used for?

A

Reduce mucus viscosity making it easier to clear and reducing obstruction

90
Q

When is oxygen given in COPD?

A

Long term where FEV1 <35% and oxygen sats <92%

24-28% oxygen given >15 hours per day

91
Q

What are the common causes of infective exacerbations of COPD?

A

Streptococcus pneumoniae

Haemophilus influenzae

92
Q

What is the first line treatment of infective exacerbations of COPD?

A

Amoxicillin 500mg
OR tetracycline 100mg with 200mg doxycycline stat
Given alongside 30mg prednisone for 7-14 days

93
Q

What is the second line treatment of infective exacerbations of COPD?

A

Broad spectrum cephalosporin or macrolide

94
Q

What is hypercapnia?

A

Abnormally high carbon dioxide levels

95
Q

What is cor pulmonale?

A

Right side heart failure due to pulmonary hypertension

96
Q

What is polycythaemia?

A

Increase in RBCs due to chronic hypoxia, increasing blood viscosity

Pharm Y2S2 (26 decks)

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