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Pharmacology > Asthma/COPD > Flashcards

Asthma/COPD Flashcards

1
Q

What is COPD?`

A

Slowly progressive airway obstruction due to chronic inflammation

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2
Q

Name 3 clinical sx of COPD:`

A

1) cough
2) mucus hypersecretion
3) SOB

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3
Q

Name 2 disorders of COPD:

A

1) chronic bronchitis

2) emphysema

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4
Q

What is emphysema?

A

Alveolar structure destruction –> airway collapse during expiration

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5
Q

What is asthma?

A

Chronic inflammatory disorder of the airways (recurring episodes of hyper-responsiveness to stimuli that cause bronchoconstriction)

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6
Q

Name 4 clinical sx of asthma:

A

1) recurring cough episodes
2) wheezing
3) chest tightness
4) SOB

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7
Q

What are 2 types of triggering stimuli for asthma?

A

1) extrinsic (allergenic)

2) intrinsic (non-allergenic)

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8
Q

Pathophysiology of extrinsic asthma:

A

external stimuli trigger plasma cells to produce antigen specific IgE ABs –> allergen+IgE complex bind to mast cells –> mast cell degranulation

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9
Q

What part of the allergen induces IgE production?

A

Glycoproteins on the allergen are recognized as antigens by immune cells

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10
Q

Name examples of non-allergic triggers for asthma:

A

anxiety, stress, cold/dry air, smoke, exercise, viruses

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11
Q

Pathophysiology of intrinsic asthma:

A

Unknown
Possible mechanisms:
1) autonomic regulation of airway functions = abnormal (increased responsiveness)
2) innate immune system is involved

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12
Q

Name 6 direct triggers of mast cell degranulation:

A

1) opiates
2) contrast media
3) hyper osmolality
4) venoms
5) toxins
6) neuropeptides

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13
Q

What are 4 stages involved in airway hyper responsiveness and remodelling?

A

1) fibrosis
2) muscle hypertrophy/hyperplacia
3) angiogenesis
4) mucus hypersecretion

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14
Q

Describe fibrosis involved in airway remodelling:

A

Inflammation damages epithelial cells –> nerve cells are exposed and activated –> scar tissue (elasticity is lost)

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15
Q

Describe the hypertrophy involved in airway remodelling:

A

muscles are working over time –> muscles become bigger and take up more space (less space is available for air exchange)

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16
Q

What are bronchodilators?

A

Agents that interact with smooth muscle cells that line the airway and relax smooth muscles

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17
Q

Name 4 classes of bronchodilators:

A

1) B-adrenergic
2) Methylxanthines
3) Anticholinergics
4) Leukotriene modifiers

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18
Q

How does the sympathetic nervous system affect the bronchiole airway?

A

adrenaline/epinephrine act on B2-adrenergic receptor –> bronchodilation

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19
Q

How does the parasympathetic nervous system affect the bronchiole airway?

A

Ach act on muscarinic receptor (M3) –> bronchoconstriction + increased secretion

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20
Q

Name 2 short acting B2 adrenergic agonists

A

1) Albuterol/Salbutamol

2) Terbutaline

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21
Q

Name 1 long acting B2 adrenergic agonist

A

1) Salmeterol (12 hours)

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22
Q

B2 adrenergic agonist MOA:

A

Stimulates adenylyl cyclase –> cAMP formation increases –> airway smooth muscle relaxation

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23
Q

What is the usual B2 adrenergic agonist administration route?

A

Inhalation (bc want direct access to lungs and prevent systemic effects)

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24
Q

Albuterol administration route:

A

1) Inhalation

2) PO

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25
Q

Terbutaline administration route:

A

1) Inhalation
2) PO
3) SC

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26
Q

B2 adrenergic agonist indication:

A

Asthma tx

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27
Q

What is the DOC for acute asthmatic attacks?

A

Albuterol (via inhalation)

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28
Q

What is the DOCs for severe asthmatic attacks?

A

1) Terbutaline SC INJ

2) Epinephrine (+ corticosteroids)

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29
Q

When using B2 agonists, why is co-administration with corticosteroids/anti-inflammatory agents recommended?*****

A

To prevent development of desensitization and promote B2 agonists efficacy

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30
Q

Name 3 AEs of B2 agonists

A

1) B1 receptors on heart may get stimulated at high doses –> tachycardia
2) Skeletal muscle tremor
3) Tolerance

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31
Q

Name 1 DI with B2 agonists

A

1) B-blockers (eg: propranolol) for HTN or other cardiac conditions

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32
Q

Name a drug example for the class Methylxanthines

A

Theophylline

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33
Q

Theophylline MOA (3)

A
  • Phosphodiesterase inhibited –> cAMP levels increase to relax airway
  • Adenosine receptors inhibited –> bronchiole smooth muscle contraction, histamine release
  • Stimulates diaphragmatic muscle contractility
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34
Q

Theophylline route of admin:

A
  • Aerosol (safest)

- Other routes can have adverse effects on heart and CNS

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35
Q

Theophylline indication:

A
  • 2nd DOC for acute asthmatic attacks (used when pt has developed sensitization or is on a B-blocker)
  • COPD
  • May reverse steroid insensitivity
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36
Q

Theophylline PK:

A
  • Narrow therapeutic window
  • PK = unpredictable
  • Give under supervision!
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37
Q

Name 3 common SEs of theophylline:

A

Headache, insomnia, tremors

38
Q

Name 5 serious SEs of theophylline:

A

anaphylactic shock, N/V, fever, seizures, stimulates heart

39
Q

Theophylline DI:

A

can result in toxic concentrations bc metabolized by CYP450

40
Q

Theophylline caution:

A

If given with B2 agonists, cardiovascular effects are increased

41
Q

Name 2 anticholinergics (Achgics):

A

1) Ipratropium (short-acting)

2) Tiotropium (long-acting)

42
Q

Achgics MOA:

A

1) Blocks muscarinic receptors to prevent broncho constriction and mucus secretion
2) No effects on inflammation!!!

43
Q

Achgics administration route:

A

aerosol

44
Q

Ipratropium indication (3):

A

1) COPD + chronic bronchitis
2) Acute asthma attacks in children, adults, and pts who cannot tolerate B agonists
3) Severe asthma attacks (when used with B agnostic - bc enhances bronchodilation of B agnostic)

45
Q

Ipratropium AE:

A

well-tolerated, but may cause atropine like effects when used excessively

46
Q

Ipratropium caution (2):

A

1) Glaucoma

2) Urinary retention

47
Q

What are leukotrienes?

A

Products of arachidonic acid metabolism

48
Q

What is the role of LTC4, LTD4?

A
  • Bronchconstriction
  • Increased bronchial reactivity
  • Mucosal edema
  • Mucus secretion
49
Q

What are leukotriene modifiers?

A

Drugs that inhibit leukotriene synthesis and block receptors they act upon

50
Q

What is the enzyme that converts arachidonic acid to leukotrienes?

A

Lipooxygenase

51
Q

Name a leukotriene synthesis inhibitor (LSI):

A

Zileuton

52
Q

LSI MOA:

A

Inhibits 5-lipooxygenase

53
Q

LSI administration route:

A

PO qid

54
Q

LSI Indication:

A
  • Persistent asthma in adults
  • ASA induced asthma
  • Exercise and antigen induced bronchospasm prevention
55
Q

LSI AEs:

A

Hepatotoxicity (management: liver enzyme levels monitoring)

56
Q

LSI DIs:

A 
CYP450 inhibitor
(drug metabolism is interfered- theophylline, warfarin)
57
Q

Name 2 leukotriene receptor blockers (LRB):

A

1) Zafirlukast

2) Montelukast

58
Q

LRB MOA:

A

1) Selective + reversible CysLT1 receptor inhibitors –> leukotriene induced bronchoconstriction/edema inhibition
2) Prevents chemotactic infiltration of neutron/basophils

59
Q

Zafirlukast administration route:

A

PO BID

60
Q

Zafirlukast indication:

A
  • Mild to moderate asthma (but less effective than corticosteroids)
61
Q

Zafirlukast CI:

A

Children ≤ 8 years old

62
Q

Zafirlukast AE:

A
  • Headache
  • GI
  • Hepatotoxicity (management: liver enzyme levels monitoring)
63
Q

Zafirlukast DI:

A

Inhibits CYP450

64
Q

Montelukast administration route:

A

PO OD

65
Q

Montelukast indication:

A
  • Persistent asthma in children and adults (less effective than corticosteroids)
66
Q

Montelukast CI:

A

Children ≤ 6 years old

67
Q

Montelukast DI:

A

Inhibits CYP450

68
Q

Montelukast AE:

A

Heptatoxicity

69
Q

Anti-inflammatory agents (AIA) MOA:

A

Reduce inflammation, edema, and mucus production to reduce asthma attacks and COPD flares/progression

70
Q

Name 4 classes of AIA

A

1) Corticosteroids
2) Mast cell blockers
3) Anti-IgE monoclonal anti-body
4) LK modifiers

71
Q

What is the role of glucocorticoids in the body?

A

Regulation of glucose metabolism

72
Q

What is the role of mineralocorticoids in the body?

A

Regulate salt and water balance

73
Q

Methylprednisone administration route:

A

IV (indicated in severe exacerbations)

74
Q

Prednisone administration route:

A

PO (indicated in severe exacerbations)

75
Q

Corticosteroids MOA:

A

1) Blocks release of arachidonic acid (LK production)
2) Increase sensitivity of B adrenergic receptors and prevent their desensitization
3) Prevents long-term changes in airway structure and function

76
Q

Corticosteroid preferred mode of administration:

A

aerosol (to limit systemic SEs)

77
Q

Corticosteroid indication:

A

First-line tx for anti-infammatory conditions for all ages

78
Q

Common + reversible AE of corticosteroids:

A

1) Thrush
2) Hoarseness
3) Whole list on Slide 47

79
Q

Common + permanent AE of corticosteroids (3):

A

1) osteoporosis
2) cataracts in adults
3) growth retardation in children

80
Q

Chronic use of corticosteroids can result in what?

A

Suppression of adrenal glands and endogenous production of corticosteroids

81
Q

How can the AE of corticosteroids be reduced?

A

Via alternate day tx for oral medication + morning administration***

82
Q

Name 2 drugs under the class of mast cell blockers (MCB):

A

1) Cromolyn Sodium

2) Nedocromil

83
Q

MCB MOA:

A

Inhibits release of mediators from mast cells by blocking ion-channels (Ca, Cl) needed for degranulation –> regular use reduces bronchial hyperactivity

84
Q

MCB administration:

A

Aerosol (BID-QID)

85
Q

MCB indication:

A
  • mild-mod asthma
  • anti-inflammatory DOC for allergic asthma in children 2-3 y/o
  • prevention in exercised induced asthma
86
Q

List 2 disadvantages of MCB:

A

1) less potent than inhaled glucocorticoids in controlling asthma
2) Needs 4-6 week trial period to determine efficacy

87
Q

Name an anti-IgE monoclonal antibody:

A

Omalizumab

88
Q

IgE monoclonal antibody MOA:

A

Selectively binds human free IgE

89
Q

IgE monoclonal antibody indication:

A

Allergic asthma (acute and prolonged)

90
Q

IgE monoclonal antibody administration route:

A

SC INJ

91
Q

IgE monoclonal antibody AE:

A

Anaphylaxis

92
Q

Tx plan

A

Slides 55-58

Pharmacology (9 decks)

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