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SYSTEMIC PHARMACOLOGY > Respi - asthma > Flashcards

Respi - asthma Flashcards

1
Q

causes of asthma

A
  • chronic airway inflammation
  • hyperresponsiveness of the airway
  • recurrent reversible airway obstruction
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2
Q

2 main groups of anti-asthma drugs

A
  1. prevention (controller) - anti-inflammatory drugs

2. provide relief - bronchodilators

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3
Q

6 groups of anti-inflammatory (control) anti-asthma drugs

A

[NIL]

  • inhaled corticosteroids (ICS)
  • inhaled Na cromoglygate
  • leukotriene receptor antagonist (LTRA)
  • anti-IgE
  • anti-IL-5R
  • anti-IL-4R
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4
Q

ICS drug

A

fluticasone - has high receptor binding affinity

-sonide/ -solide

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5
Q

ICS MOA

A
  • Decrease secretion of inflammatory cells (T cells, mast cells, macrophages, eosinophils) in airways
  • Decrease epithelial cell shedding
  • Decrease macrophage phagocytosis and cytokine production and proteases
  • Decrease PLA2, COX II, 5-LOX (inflammatory enzymes), increase annexins = downregulate leukotriene expression
  • Increase airway SM b-receptors
  • reduce plasma exudate/mucus secretion
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6
Q

ICS indication

A

nocturnal asthma
1st line asthma prophylaxis
reduce long term asthma complications like airway remodeling

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7
Q

ICS ADR

A

oropharyngeal candidiasis (candida infection) and irritation
dysphonia (hoarseness of voice)
- fluticasone: adrenal suppression

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8
Q

leukotriene modifiers (receptor antagonists) drugs

A

(-lukast)

  • montelukast
  • zafirlukast
  • zileutone
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9
Q

montelukast and zafirlukast MOA

A

inhibit LTC4/LTD4

  • inhibits bronchoconstriction,
  • hyper-responsiveness,
  • mucosal edema,
  • mucus hypersecretion,
  • SM hyperplasia
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10
Q

montelukast target receptor and indications

A

competitive antagonist of CysLT1 (cysteinyl leukotriene)
indications:
- prophylaxis + chronic treatment
- aspirin/ exercise induced asthma
(aspirin induced: aspirin inhibits AA -> prostaglandin, so AA -> LTA4 -> LTC4 -> asthma)
ORAL

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11
Q

montelukast ADR

A

psychological: agitation, hallucination, depression

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12
Q

Na cromoglycate MOA

A

inhibit mast cell degranulation (IgE mediated) -> prevent release of inflammatory cells (histamine, prostaglandins, leukotrienes)

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13
Q

Na cromoglycate clinical use

A

paeds asthma

prophylaxis for asthma & allergic rhinitis/ conjuctivitis

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14
Q

Na cromoglycate ADR

A

throat irritation, dryness, cough

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15
Q

Omalizumab (anti-IgE mAb) MOA

A

attacks Fc portion of IgE antibodies

  • binds to IgE
  • decrease expression of receptors
  • decrease mediator release
  • decrease inflammatory response and possible exacerbation
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16
Q

Omalizumab clinical use + method

A

allergic asthma, allergic rhinitis

injection every 2-4wks

17
Q

Anti-IL-5R (-zumab) and anti-IL-4R (dupilumab) clinical use + method

A

severe asthma

subcutaneous injection

18
Q

6 groups of bronchodilators (beta agonists) as asthma RELIEVERS

A
  • non-selective (1-3hrs)
  • short acting: SABA (4-6hrs)
  • long acting: LABA (12hrs)
  • long acting for COPD (24hrs)
  • methylxanthine: theophylline
  • muscarinic antagonists: SAMA (3-5hrs)/ LAMA (24hrs)
19
Q

non-selective drug

A

epinephrine

20
Q

SABA drug

A

salbutamol

21
Q

salbutamol

A

rapid onset

hydrophilic

22
Q

LABA drugs + clinical use

A

(-terol)
- salmeterol
- formoterol* - preferred choice (faster onset of action)
long term maintenance of asthma (esp nocturnal asthma)

23
Q

formoterol

A

rapid onset

amphiphilic

24
Q

salmeterol

A

slow onset - less useful for emergency use

lipophilic - slowly bind and release

25
Q

LABA drug for COPD

A

indacaterol

26
Q

beta agonists ADR

A 
decrease muscle contraction: tremors, cramps
peripheral vasodilation 
palpitations and tachycardia
hypokalemia, hyperglycemia
LABA: asthma related mortality
27
Q

theophylline MOA

A
  • inhibits PDE + blocks adenosine - increase cAMP -> relaxation
  • release of epinephrine
  • anti-inflammatory effects
    but not as effective as a bronchconstrictor
28
Q

theophylline clinical use + method

A

add on to inhaled beta agonists + ICS (inhaled corticosteroids)
nocturnal bronchospasm
COPD: improve lung fn
Oral/IV

29
Q

theophylline ADR

A

narrow therapeutic range - be careful esp DDIs
GI: n/v, anorexia
CNS: anxiety, tremors
CVS: arrhythmia

30
Q

muscarinic antagonists drugs

A

SAMA: short acting - ipratropium bromide
LAMA - tiotropium
(-tropium)

31
Q

ipratroprium bromide MOA + method

A

inhibit m3 receptors = decrease inflammation
decrease bronchospasms and mucus secretion
less effective as a bronchodilator
inhaled, does not cross BBB
also used as a mucoregulator

32
Q

ipratropium clinical use

A

add on to beta agonists + IHC
alternative for those intolerant to b agonists
COPD - bronchodilator effect

33
Q

tiotropium clinical use

A

severe asthma

COPD - more potent than SAMA for COPD

34
Q

MA ADR

A

dry mouth
urinary retention in elderly
(paradoxical) bronchospasm - supposed to decrease

SYSTEMIC PHARMACOLOGY (22 decks)

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