ALS Lecture 7 - Pharmacology of Airways Obstruction DONE Flashcards

(46 cards)

1
Q

classic asthma starts in

A

childhood

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2
Q

classic asthma gives

A

bronchoconstriction

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3
Q

classic asthma has a

A

double reaction

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4
Q

1st asthma response

A

starts after 15mins of allergen, ends in ~15mins without treatment

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5
Q

2nd asthma response

A

75% is late reaction, more difficult to treat

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6
Q

asthma is characterised by

A

eosinophils

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7
Q

label the diagram of asthma pathophysiology

A

done

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8
Q

asthma pathophysiology (5 steps)

A
  1. IgE directed against allergen
  2. IgE produced by B lymphocyte, sticks onto mast cells
  3. degranulation of mast cells and inflammatory mediators
    4, bronchospasm, vasodilation, mucus secretion, oedema
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9
Q

asthma inflammation causes

A

mucus plugs to block airways

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10
Q

asthma histology of airway

A

filled with mucus, nuclei of inflammatory cells

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11
Q

eosinophils stain and how up

A

pink, stained with eosin

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12
Q

asthma medication types (5)

A

SABA, LABA, corticosteroids (inhaled), leukotriene receptor antagonist, combination inhalers

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13
Q

bronchoconstriction is mediated by

A

smooth muscle contraction, beta agonists reverse this

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14
Q

action of beta receptors on smooth muscle (3 steps)

A
  1. stimulated
  2. release cAMP
  3. relax smooth muscle
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15
Q

label the diagram of montelukast combined with a steroid affects the dual pathways of inflammation

A

done

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16
Q

short acting beta agonist (SABA) example

A

Salbutamol, 4-5hrs

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17
Q

long acting beta agonist (LABA) example

A

Salmetrol, Formoterol, 12-24hrs

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18
Q

leukotriene receptor antagonist MOA (2 steps)

A
  1. block leukotriene receptors

2. stop eosinophil recruitment

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19
Q

leukotriene receptor antagonist example

20
Q

antimuscarinics MOA (3 steps)

A
  1. blocks activity of muscarinic ACh receptor

2. bronchial dilation, decreased secretions

21
Q

long-acting muscarinic antagonist example

22
Q

methylxanthines act as

A

bronchodilators, relax smooth muscle

23
Q

methylxanthines are used in

24
Q

methylxanthines MOA (5 steps)

A
  1. inhibits phosphodiesterase which usually degrades cAMP
  2. increased cAMP
  3. activates PKA
  4. inhibits TNF-alpha, leukotriene synthesis
  5. reduces inflammation and innate immunity
25
methylxanthine example
theophylline
26
label the diagram of MOA of steroids
done
27
steroids are very effective at getting rid of _______ as they ____ ______
eosinophils, cause apoptosis
28
corticosteroids MOA (5 steps)
1. attaches to and activates receptor 2. receptor forms dimer 3. dimer acts on DNA 4. up regulates beta-receptor gene = more beta receptors 5. down regulating cytokine genes = less inflammation
29
only ____ inflammation responds to _____
eosinophilic, steroids
30
oral steroids used to be given but
give lots of side effects
31
side effects of oral steroids
cushing's syndrome
32
50-70% of inhaled steroids end up
in stomach
33
inhaled steroids don't give side effects as they are
metabolised on first pass through liver so don't get into systemic circulation
34
if patient is non-responsive to steroids, this may be due to (3)
poor compliance, poor technique, misdiagnosis
35
label the diagram of omalizumab
done
36
omalizumab blocks
IgE
37
IL-5 from innate lymphocyte also calls in
eosinophils
38
IL-5 blockers are injectable treatments used in _____ _____ with _____ _____
severe asthmatics, eosinophilic reaction
39
label the diagram of IL-5 blockers
done
40
label the triangle
done
41
copd includes
emphysema, chronic bronchitis
42
2 phenotypes of COPD patients
- pink puffers, mostly emphysema | - blue bloaters, mostly chronic bronchitis, neutrophilic inflammation so no steroid respsonse
43
eosinophilic bronchitis responds to
steroids
44
label the spirometry graph
done
45
to differentiate between eosinophilic and neutrophilic airway inflammation, look at the
full blood count
46
blood eosinophils above ___ indicate ______ ______ ______
0.3, steroid responsive disease