Asthma & COPD Flashcards

(68 cards)

1
Q

Define Asthma

A

Reversible increases in airway resistance involving bronchoconstriction and inflammation

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2
Q

What is the effect of Asthma on measures of lung function?

A

Reversible decreases in FEV1:FVC (<70-80%)

Variations in PEF, improving w/ B2 agonist (morning dipping)

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3
Q

Describe the parasympathetic control of bronchial calibre

A

ACh - muscarinic M3 receptors

Bronchoconstriction AND increased mucus

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4
Q

Describe the sympathetic control of bronchial calibre

A

Circulating adrenaline - B2 adrenoceptors
Relaxation of bronchial SM
Sympathetic fibres release NA - B2 adrenoceptors
Inhibit mucus secretion
Decrease PNS activity

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5
Q

What factors lead to an asthmatic attack?

A

Genetic predisposition, provoked by:

  • Allergens
  • Cold air
  • Viral infections
  • Smoking
  • Exercise
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6
Q

What are the two phases of an asthmatic attack?

A

Early (immediate)
Late
Sometimes just one or the other

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7
Q

What are the clinical features of Asthma?

A
Wheezing
Breathlessness
Tight chest
Cough
Decreases in FEV1, reversed by B2 agonist
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8
Q

What are Spasmogens?

A
Factors released from mast cells
Stimulate bronchospasm (early)
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9
Q

What are Chemotaxins?

A
Factors released from mast cells
Stimulate inflammation (late)
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10
Q

What type of cell releases Spasmogens/Chemotaxins?

A

Mast cells (mononuclear)

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11
Q

Describe the time course of an asthmatic attack?

A

Early phase - 1 hour after stimulus, large drop in PEF followed by quick improvement
Late phase - 3-8 hours, gradual drop in PEF

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12
Q

What are the five Spasmogens involved in an asthmatic attack?

A

Histamine
Prostaglandin D2
Leukotrienes C4 & D4
Platelet Activating Factor (PAF)

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13
Q

How are Spasmogens produced?

A

Arachidonic acid separated from membrane by PLA2
Leukotrienes produced by LOX
Prostaglandins by COX

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14
Q

What are the two Chemotaxins involved in an asthmatic attack?

A

Leukotriene B4

Platelet Activating Factor (PAF)

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15
Q

How do Chemotaxins lead to the late phase of an asthmatic attack?

A
Attract leukocytes (esoinophils + mononuclear cells)
Leads to inflammation + airway hyper-reactivity
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16
Q

What are the two types of therapy for Asthma?

A

Bronchodilators

Preventative

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17
Q

What is the purpose of Bronchodilators?

A
Reverse bronchospasm (early phase)
RAPID RELIEF
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18
Q

What is the 1st choice Bronchodilator?

A

Salbutamol

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19
Q

What is Salbutamol?

A

B2 adrenoceptor agonist

Increases FEV1

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20
Q

How does Salbutamol work?

A

Acts on B2 adrenoceptors to increase cAMP`

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21
Q

How are B2 agonists given?

A

Inhalation

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22
Q

What is the problem with long term use of B2 agonists?

A

Prolonged use leads to receptor down-regulation

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23
Q

What are LABAs?

A

Long acting beta agonists (SALMETEROL)

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24
Q

What are LABAs used for?

A

Long term prevention/control (ie. overnight)

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25
What are the 2nd choice Bronchodilators?
Xanthines (THEOPHYLLINE)
26
How do Xanthines work?
Phosphodiesterase inhibitors - elevate cAMP
27
How are Xanthines given?
Oral/i.v.
28
What are the problems with Xanthines?
Narrow therapeutic index Large range of interactions Removed by hepatic metabolism Hypokalaemia (esp. w/ B2 agonists)
29
What are the 3rd line Bronchodilators?
Muscarinic receptor antagonists
30
What are the two common Muscarinic receptor antagonists?
Ipratropium (short acting, t.d.s.) | Tiotropium (long acting, o.d.)
31
How do Muscarinic receptor antagonists work?
Block parasympathetic bronchoconstriction
32
How are Muscarinic receptor antagonists given?
Inhalation - prevents antimuscarinic side effects
33
How are Muscarinic receptor antagonists mainly used?
Little value in asthma | Widely used in COPD
34
What are the four types of preventative medication?
Corticosteroids Steroids Cromones Leukotriene Receptor Antagonists (LTRAs)
35
How do Corticosteroids work?
Anti-inflammatory | Activation of intracellular receptors - altered gene transcription (decreased cytokines) - production of lipocortin
36
What are the two main Corticosteroids?
Beclometasone (inhalation) | Prednisolone (oral)
37
How does Lipocortin have it's positive effect?
Inhibits PLA2 | Decreased production of Leukotrienes/Prostaglandins
38
How do steroids work?
Given w/ B2 agonists | Reduce receptor down regulation
39
What are the side effects of steroids?
Inhalation - Throat infections, hoarseness | Oral administration - Adrenal suppression, diabetes, osteoporosis, immunosuppression
40
How should patients be counselled to take inhaled steroids?
Rinse out mouth after inhalation | Use spacer
41
How do Cromones work?
Poorly Uncertain MoA -reduce reflexes of sensory nerves? -reduce PAF/cytokine release?
42
What is the main Cromone used clinically?
Sodium Cromoglicate
43
How do LTRAs work?
Antagonise actions of LTs
44
What is the main LTRA used clinically?
Montelukast
45
What is the first stage of treating asthma?
Occasional bronchodilator (SABA)
46
What is the second stage of treating asthma?
SABA + regular inhaled steroid
47
What is the third stage of treating asthma?
Step 2 + LABA (or LTRA/Xanthine)
48
What is the fourth stage of treating asthma?
Step 3 + Increase dose of inhaled steroid
49
What is the fifth stage of treating asthma?
Step 4 + Add oral steroid
50
What is the management of acute asthma?
Oxygen (40-60%) Nebulised SABA (salbutamol/terbutaline) Oral prednisolone/i.v. hydrocortisone
51
What steps should be added to normal management when treating an acute, life-threatening attack?
Nebulised ipratropium s. c. SABA i. v. aminophylline (if patient not on Xanthine) i. v. magnesium sulphate
52
Define COPD
Chronic Obstructive Pulmonary Disease | Combination of Chronic Bronchitis + Emphysema
53
Describe Chronic Bronchitis
Increased mucus Airway obstruction Intercurrent infections
54
Describe Emphysema
Destruction of alveoli
55
What is the effect of COPD on measures of lung function?
FEV1 reduced | Little variation in PEF
56
Describe Mild COPD
FEV1 60-80% of predicted, smoker's cough, little/no breathlessness
57
Describe Moderate COPD
FEV1 59-40% of predicted, breathless on mild exertion, possibly wheezing + cough
58
Describe Severe COPD
FEV1 <40% of predicted, breathless on mild exertion/rest, wheeze +cough
59
What is the main structure of treatment in COPD?
Smoking cessation | Regular bronchodilators
60
What is the baseline treatment for COPD?
SABA or Short acting antimuscarinic
61
If the FEV1 is >50% in a COPD patient how should treatment be modified?
Add LABA or Long acting antimuscarinic (in place of SA)
62
If the FEV1 is <50% in a COPD patient how should treatment be modified?
Add LABA + inhaled steroid | Replace SA antiM with LA antiM
63
What is the final stage of treatment for severe COPD?
LA antiM + LABA + inhaled steroid
64
What role do antibiotics play in treating COPD?
Antibiotics for intercurrent infections | Patients given antibiotics to have for start of exacerbation
65
What are the clinical signs of an exacerbated chest infection?
2 of: | Purulent sputum, increased sputum, breathlessness
66
What role does oxygen therapy play in treating COPD?
Severe disease | 24-28% Ox for 15hrs/day
67
How should NSAIDs be used in asthma?
AVOIDED | Provoke asthma, increase LT production
68
How should B-blockers be used in asthma/COPD?
AVOIDED | ccause bronchospasm