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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
Terbutaline administration route:
1) Inhalation 2) PO 3) SC
26
B2 adrenergic agonist indication:
Asthma tx
27
What is the DOC for acute asthmatic attacks?
Albuterol (via inhalation)
28
What is the DOCs for severe asthmatic attacks?
1) Terbutaline SC INJ | 2) Epinephrine (+ corticosteroids)
29
When using B2 agonists, why is co-administration with corticosteroids/anti-inflammatory agents recommended?*****
To prevent development of desensitization and promote B2 agonists efficacy
30
Name 3 AEs of B2 agonists
1) B1 receptors on heart may get stimulated at high doses --> tachycardia 2) Skeletal muscle tremor 3) Tolerance
31
Name 1 DI with B2 agonists
1) B-blockers (eg: propranolol) for HTN or other cardiac conditions
32
Name a drug example for the class Methylxanthines
Theophylline
33
Theophylline MOA (3)
- Phosphodiesterase inhibited --> cAMP levels increase to relax airway - Adenosine receptors inhibited --> bronchiole smooth muscle contraction, histamine release - Stimulates diaphragmatic muscle contractility
34
Theophylline route of admin:
- Aerosol (safest) | - Other routes can have adverse effects on heart and CNS
35
Theophylline indication:
- 2nd DOC for acute asthmatic attacks (used when pt has developed sensitization or is on a B-blocker) - COPD - May reverse steroid insensitivity
36
Theophylline PK:
- Narrow therapeutic window - PK = unpredictable - Give under supervision!
37
Name 3 common SEs of theophylline:
Headache, insomnia, tremors
38
Name 5 serious SEs of theophylline:
anaphylactic shock, N/V, fever, seizures, stimulates heart
39
Theophylline DI:
can result in toxic concentrations bc metabolized by CYP450
40
Theophylline caution:
If given with B2 agonists, cardiovascular effects are increased
41
Name 2 anticholinergics (Achgics):
1) Ipratropium (short-acting) | 2) Tiotropium (long-acting)
42
Achgics MOA:
1) Blocks muscarinic receptors to prevent broncho constriction and mucus secretion 2) No effects on inflammation!!!
43
Achgics administration route:
aerosol
44
Ipratropium indication (3):
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
Ipratropium AE:
well-tolerated, but may cause atropine like effects when used excessively
46
Ipratropium caution (2):
1) Glaucoma | 2) Urinary retention
47
What are leukotrienes?
Products of arachidonic acid metabolism
48
What is the role of LTC4, LTD4?
- Bronchconstriction - Increased bronchial reactivity - Mucosal edema - Mucus secretion
49
What are leukotriene modifiers?
Drugs that inhibit leukotriene synthesis and block receptors they act upon
50
What is the enzyme that converts arachidonic acid to leukotrienes?
Lipooxygenase
51
Name a leukotriene synthesis inhibitor (LSI):
Zileuton
52
LSI MOA:
Inhibits 5-lipooxygenase
53
LSI administration route:
PO qid
54
LSI Indication:
- Persistent asthma in adults - ASA induced asthma - Exercise and antigen induced bronchospasm prevention
55
LSI AEs:
Hepatotoxicity (management: liver enzyme levels monitoring)
56
LSI DIs:
``` CYP450 inhibitor (drug metabolism is interfered- theophylline, warfarin) ```
57
Name 2 leukotriene receptor blockers (LRB):
1) Zafirlukast | 2) Montelukast
58
LRB MOA:
1) Selective + reversible CysLT1 receptor inhibitors --> leukotriene induced bronchoconstriction/edema inhibition 2) Prevents chemotactic infiltration of neutron/basophils
59
Zafirlukast administration route:
PO BID
60
Zafirlukast indication:
- Mild to moderate asthma (but less effective than corticosteroids)
61
Zafirlukast CI:
Children ≤ 8 years old
62
Zafirlukast AE:
- Headache - GI - Hepatotoxicity (management: liver enzyme levels monitoring)
63
Zafirlukast DI:
Inhibits CYP450
64
Montelukast administration route:
PO OD
65
Montelukast indication:
- Persistent asthma in children and adults (less effective than corticosteroids)
66
Montelukast CI:
Children ≤ 6 years old
67
Montelukast DI:
Inhibits CYP450
68
Montelukast AE:
Heptatoxicity
69
Anti-inflammatory agents (AIA) MOA:
Reduce inflammation, edema, and mucus production to reduce asthma attacks and COPD flares/progression
70
Name 4 classes of AIA
1) Corticosteroids 2) Mast cell blockers 3) Anti-IgE monoclonal anti-body 4) LK modifiers
71
What is the role of glucocorticoids in the body?
Regulation of glucose metabolism
72
What is the role of mineralocorticoids in the body?
Regulate salt and water balance
73
Methylprednisone administration route:
IV (indicated in severe exacerbations)
74
Prednisone administration route:
PO (indicated in severe exacerbations)
75
Corticosteroids MOA:
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
Corticosteroid preferred mode of administration:
aerosol (to limit systemic SEs)
77
Corticosteroid indication:
First-line tx for anti-infammatory conditions for all ages
78
Common + reversible AE of corticosteroids:
1) Thrush 2) Hoarseness 3) Whole list on Slide 47
79
Common + permanent AE of corticosteroids (3):
1) osteoporosis 2) cataracts in adults 3) growth retardation in children
80
Chronic use of corticosteroids can result in what?
Suppression of adrenal glands and endogenous production of corticosteroids
81
How can the AE of corticosteroids be reduced?
Via alternate day tx for oral medication + morning administration***
82
Name 2 drugs under the class of mast cell blockers (MCB):
1) Cromolyn Sodium | 2) Nedocromil
83
MCB MOA:
Inhibits release of mediators from mast cells by blocking ion-channels (Ca, Cl) needed for degranulation --> regular use reduces bronchial hyperactivity
84
MCB administration:
Aerosol (BID-QID)
85
MCB indication:
- mild-mod asthma - anti-inflammatory DOC for allergic asthma in children 2-3 y/o - prevention in exercised induced asthma
86
List 2 disadvantages of MCB:
1) less potent than inhaled glucocorticoids in controlling asthma 2) Needs 4-6 week trial period to determine efficacy
87
Name an anti-IgE monoclonal antibody:
Omalizumab
88
IgE monoclonal antibody MOA:
Selectively binds human free IgE
89
IgE monoclonal antibody indication:
Allergic asthma (acute and prolonged)
90
IgE monoclonal antibody administration route:
SC INJ
91
IgE monoclonal antibody AE:
Anaphylaxis
92
Tx plan
Slides 55-58

Pharmacology (9 decks)

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