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S2 Case 3 - asthma & COPD > Pathophysiology + Pharmacology of Asthma > Flashcards

Pathophysiology + Pharmacology of Asthma Flashcards

1
Q

What is asthma?

A

Recurrent + reversible (in short term) obstruction to airways in response to stimuli

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2
Q

What are the causes of asthma attack?

A

Allergens
Exercise
Respiratory infections
Smoke, dust, environmental pollutants

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3
Q

Describe structure of smooth muscle in airways in acute asthma

A

Contraction of smooth muscle
Mucus hypersecretion
Air inflammation

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4
Q

What are the symptoms of acute asthma?

A

Dyspnoea
Wheezing
Coughing

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5
Q

What is dyspnoea?

A

Loss of breath

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6
Q

What hypersensitivity reaction is sensitisation of asthma?

A

Type I

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7
Q

Describe what happens in sensitisation to asthma

A

IL-4 stimulates production of IgE by B cells + activate mast cells
IL-13 stimulate mucus secretion from bronchial submucosal glands
+ stimulate IgE by B cells + activate mast cells
IL-5 activates locally recruited eosinophils

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8
Q

What is basic immediate response?

A

Bronchospasm

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9
Q

What is basic delayed response?

A

Inflammatory reaction

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10
Q

Describe immediate phase

A

Bronchoconstriction
Increased mucus production
Vasodilation
Release of mediators

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11
Q

Describe delayed phase

A

Recruitment of leukocytes + T cells by cytokines, produced by mast cells
Release of mediators of inflammation

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12
Q

Describe the immediate response on re-exposure to antigen

A

Antigen binds to IgE-IgE receptor complex
Cross links IgE receptors
Stimulates Ca2+ entry into mast cells evoking …
Release of histamine + leukotrienes = smooth muscle contraction
Release of eosinophils that attract cells causing inflammation

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13
Q

What are the effects of mast cell mediators?

A

Bronchospasm
Increased vasodilation
Mucus production
Recruit mediator-releasing cells

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14
Q

What are examples of mast cell mediators?

A

Histamine + leukotrienes

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15
Q

Describe what happens in late phase

A

More pro-inflammatory mediators released =
Eosinophil major basic protein = epithelial damage + airway constriction
Cytokines = contribute to amplification of inflammation

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16
Q

Describe chronic asthma

A

Increased smooth muscle
Accumulation of interstitial fluid
Increased mucus
Exposed sensory nerve endings

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17
Q

How do you diagnose?

A

Demonstrate increased airflow obstruction (spirometry)
Wheezing
Eosinophil count in blood test
Allergy tests

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18
Q

What does parasympathetic intervention do?

A

Worsen symptoms of asthma

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19
Q

Describe what happens in parasympathetic intervention

A

IP3 increases = Ca2+ increases
= bronchoconstriction + increased mucus

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20
Q

What does sympathetic innervation?

A

Improve symptoms

21
Q

Describe what happens in sympathetic intervention

A

Adrenaline acts on beta-2 receptors = bronchodilation

22
Q

What does chromolyn do?

A

Prevents mast cells from exploding

23
Q

What treatments are used for immediate phase (bronchospasm)?

A

Bronchodilators
- Beta-2 agonists
- Muscarinic antagonists
- Xanthines

24
Q

Describe what beta-2 agonists do in immediate phase

A

Direct action on beta-2 receptors on smooth muscle
= smooth muscle relaxation
Decrease mucus

25
Q

How are beta-2 agonists given?

A

Inhalation

26
Q

What are the 2 types of beta-2 agonists (inhaler)?

A

Short acting = salbutamol
Long acting = salmeterol

27
Q

What are the side effects of beta-2 agonists?

A

Tolerance
Tremor

28
Q

Describe the action of salbutamol on beta-2 receptors

A

Stimulation receptors
= activation of adenalyl cyclase
+ increase cAMP + PKA activation
= smooth muscle relaxation

29
Q

Describe what muscarinic antagonists do in immediate phase

A

Dilate bronchi
Decrease mucus

30
Q

Describe how muscarinic antagonist dilate bronchi

A

Block Gq signalling pathway
= increased Ca2+ conc

31
Q

What is an example of muscarinic antagonists?

A

Ipratropium

32
Q

Describe how ipratropium is used

A

Inhalation

33
Q

Why can ipratropium not cause many side effects?

A

NOT well absorbed so doesn’t get into circulation

34
Q

What do xanthines do in immediate response?

A

Bronchodilation
Anti-inflammatory properties

35
Q

Describe how xanthines cause bronchodilation

A

Block phosphodiesterase
= increase cAMP = bronchodilation

36
Q

What is an example of xanthine?

A

Theophylline

37
Q

What is the problem with theophylline?

A

Narrow therapeutic window

38
Q

What are the side effects of theophylline?

A

HR change
Arrhythmias
CNS stimulation
GI disturbances

39
Q

What treatments are involved in the inflammatory phase?

A

Glucocorticoids

40
Q

Describe what glucocorticoids do in the inflammatory response

A

Inhibit transcription of phospholipase A2
= decrease production of inflammatory mediators

41
Q

What are examples of glucocorticoids?

A

Beclomethasone = inhalation
Prednisolone = orally (short term)
Hydrocortisone = injection

42
Q

What are examples of glucocorticoids?

A

Oral candidiasis
Cushing like syndrome

43
Q

What does sodium cromolyn do?

A

Prevents the release of histamine + inflammatory mediators

44
Q

What do cysteinyl-leukotriene receptor antagonists do?

A

Block leukotrienes induced bronchospasm

45
Q

What are cysteinyl-leukotriene receptor antagonists effective for?

A

Mild persistent asthma

46
Q

What is an example of cysteinyl-leukotriene receptor antagonists?

A

Montelukast

47
Q

Why can’t propanolol be used to treat hypertension with patients with asthma?

A

Because beta 1 + 2 blockers = beta-2 blocked = bronchospasm

48
Q

Why can ACE inhibitor captopril not be used in patients with asthma?

A

Induce cough

49
Q

Why can NSAIDs precipitate asthma?

A

= in aspirin = COX1/2 blocked = increase leukotriene generation

S2 Case 3 - asthma & COPD (25 decks)

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