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A13THP @ UoN > Asthma & COPD > Flashcards

Asthma & COPD Flashcards

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
Q

What are the 2nd choice Bronchodilators?

A

Xanthines (THEOPHYLLINE)

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26
Q

How do Xanthines work?

A

Phosphodiesterase inhibitors - elevate cAMP

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27
Q

How are Xanthines given?

A

Oral/i.v.

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28
Q

What are the problems with Xanthines?

A

Narrow therapeutic index
Large range of interactions
Removed by hepatic metabolism
Hypokalaemia (esp. w/ B2 agonists)

29
Q

What are the 3rd line Bronchodilators?

A

Muscarinic receptor antagonists

30
Q

What are the two common Muscarinic receptor antagonists?

A

Ipratropium (short acting, t.d.s.)

Tiotropium (long acting, o.d.)

31
Q

How do Muscarinic receptor antagonists work?

A

Block parasympathetic bronchoconstriction

32
Q

How are Muscarinic receptor antagonists given?

A

Inhalation - prevents antimuscarinic side effects

33
Q

How are Muscarinic receptor antagonists mainly used?

A

Little value in asthma

Widely used in COPD

34
Q

What are the four types of preventative medication?

A

Corticosteroids
Steroids
Cromones
Leukotriene Receptor Antagonists (LTRAs)

35
Q

How do Corticosteroids work?

A

Anti-inflammatory

Activation of intracellular receptors - altered gene transcription (decreased cytokines) - production of lipocortin

36
Q

What are the two main Corticosteroids?

A

Beclometasone (inhalation)

Prednisolone (oral)

37
Q

How does Lipocortin have it’s positive effect?

A

Inhibits PLA2

Decreased production of Leukotrienes/Prostaglandins

38
Q

How do steroids work?

A

Given w/ B2 agonists

Reduce receptor down regulation

39
Q

What are the side effects of steroids?

A

Inhalation - Throat infections, hoarseness

Oral administration - Adrenal suppression, diabetes, osteoporosis, immunosuppression

40
Q

How should patients be counselled to take inhaled steroids?

A

Rinse out mouth after inhalation

Use spacer

41
Q

How do Cromones work?

A

Poorly
Uncertain MoA
-reduce reflexes of sensory nerves?
-reduce PAF/cytokine release?

42
Q

What is the main Cromone used clinically?

A

Sodium Cromoglicate

43
Q

How do LTRAs work?

A

Antagonise actions of LTs

44
Q

What is the main LTRA used clinically?

A

Montelukast

45
Q

What is the first stage of treating asthma?

A

Occasional bronchodilator (SABA)

46
Q

What is the second stage of treating asthma?

A

SABA + regular inhaled steroid

47
Q

What is the third stage of treating asthma?

A

Step 2 + LABA (or LTRA/Xanthine)

48
Q

What is the fourth stage of treating asthma?

A

Step 3 + Increase dose of inhaled steroid

49
Q

What is the fifth stage of treating asthma?

A

Step 4 + Add oral steroid

50
Q

What is the management of acute asthma?

A

Oxygen (40-60%)
Nebulised SABA (salbutamol/terbutaline)
Oral prednisolone/i.v. hydrocortisone

51
Q

What steps should be added to normal management when treating an acute, life-threatening attack?

A

Nebulised ipratropium

s. c. SABA
i. v. aminophylline (if patient not on Xanthine)
i. v. magnesium sulphate

52
Q

Define COPD

A

Chronic Obstructive Pulmonary Disease

Combination of Chronic Bronchitis + Emphysema

53
Q

Describe Chronic Bronchitis

A

Increased mucus
Airway obstruction
Intercurrent infections

54
Q

Describe Emphysema

A

Destruction of alveoli

55
Q

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

A

FEV1 reduced

Little variation in PEF

56
Q

Describe Mild COPD

A

FEV1 60-80% of predicted, smoker’s cough, little/no breathlessness

57
Q

Describe Moderate COPD

A

FEV1 59-40% of predicted, breathless on mild exertion, possibly wheezing + cough

58
Q

Describe Severe COPD

A

FEV1 <40% of predicted, breathless on mild exertion/rest, wheeze +cough

59
Q

What is the main structure of treatment in COPD?

A

Smoking cessation

Regular bronchodilators

60
Q

What is the baseline treatment for COPD?

A

SABA or Short acting antimuscarinic

61
Q

If the FEV1 is >50% in a COPD patient how should treatment be modified?

A

Add LABA or Long acting antimuscarinic (in place of SA)

62
Q

If the FEV1 is <50% in a COPD patient how should treatment be modified?

A

Add LABA + inhaled steroid

Replace SA antiM with LA antiM

63
Q

What is the final stage of treatment for severe COPD?

A

LA antiM + LABA + inhaled steroid

64
Q

What role do antibiotics play in treating COPD?

A

Antibiotics for intercurrent infections

Patients given antibiotics to have for start of exacerbation

65
Q

What are the clinical signs of an exacerbated chest infection?

A

2 of:

Purulent sputum, increased sputum, breathlessness

66
Q

What role does oxygen therapy play in treating COPD?

A

Severe disease

24-28% Ox for 15hrs/day

67
Q

How should NSAIDs be used in asthma?

A

AVOIDED

Provoke asthma, increase LT production

68
Q

How should B-blockers be used in asthma/COPD?

A

AVOIDED

ccause bronchospasm

A13THP @ UoN (19 decks)

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