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Pharm Block 1 > Respiratory Pharmacology > Flashcards

Respiratory Pharmacology Flashcards

1
Q

What are the major classes of bronchodilator drugs?

A

1) βeta2 agonists (short and long acting)
2) Anticholinergics
3) Anti-inflammatory

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2
Q

What are examples of short and long acting Beta2 agonist bronchodilators?

A

1) Short acting => Albuterol (rescue)

2) Long acting => Salmeterol (used for maintenance)

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3
Q

What is an example of an anticholinergic bronchodilator?

A

Ipratropium bromide/Tiotropium br.

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4
Q

What is an example of an anti-inflammatory bronchodilator?

A

Glucorticosteroids

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5
Q

Give the brief summary of Beta 2 agonist action on smooth muscle

A

βeta2 agonist binds to beta2 receptor which via G protein stimulates adenylyl cyclase —> increases cAMP–> protein kinases -> reduces [Ca 2+]i —> relaxes smooth muscle

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6
Q

What are the additional actions of Beta 2 agonists a part from bronchodilation/relaxation?

A
  1. Enhance mucociliary clearance
  2. Decrease microvascular permeability
  3. Suppress mediator release from inflammatory cells
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7
Q

Describe the systemic pharmacokinetics of beta 2 agonists.

A

Systemic:

1) Reasonable oral absorption (especially in children/elderly –> liquid/tablet)
- Variable- presystemic metabolism
2) Metabolism COMT/MAO
3) Bioavailability 15-70%
4) T1/2 –> 6-8h

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8
Q

Describe the inhaled pharmacokinetics of beta 2 agonists (i.e. albuterol).

A
  • 8-15% of dose reaches systemic circulation
  • Low systemic concentrations (MDI - 90 mcg Alb = Cmax 1-2 mcg/L)
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9
Q

Describe the oral pharmacodynamics of beta 2 agonists.

A

Onset 30-60 min: peak 1-3 h., duration 6-8h

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10
Q

Describe the inhaled pharmacodynamics of beta 2 agonists (albuterol).

A
  • Onset: 15-30 min duration 4-6 h
  • Metabolism COMT/MAO
  • βeta2 selectivity reduced at high doses
  • Tolerance/tachyphylaxis => tendency to become desensitized (increase dosage)
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11
Q

What are the cardiovascular adverse effects of beta 2 agonists?

A
  • Tachycardia, palpitations, flushing
  • Exacerbation of angina/arrhythmias
  • Vasodilates Pulm Art -> V/Q mismatch
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12
Q

What are the CNS adverse effects of beta 2 agonists?

A
  • Tremor/Anxiety
  • Headache
  • Insomnia
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13
Q

What are the metabolic adverse effects of beta 2 agonists?

A
  • Hypokalemia => especially important in patients with cardiac/arrhythmia issues
  • Hyperglycemia
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14
Q

When do most adverse effects of beta 2 agonists occur?

A

Toxicity/adverse effects generally happen when given at milligram dosages (in contrast to microgram)

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15
Q

What is the mechanism of action of salmeterol?

A

lipophilic arm of salmeterol binds more readily and longer (at multiple sites that can alternate)
-> binds at an active and exosite

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16
Q

Why should long acting beta 2 agonist be used with glucosteroids?

A

Maintenance beta 2 agonist should be used with steroids to reduce the chance/number of sudden death syndrome.

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17
Q

Describe the pharmacodynamics of anti-cholinergics (ipatromium).

A

Slower rate of onset

Not as much bronchodilation as albuterol

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18
Q

Describe the pharmacokinetics of inhaled ipatromium.

A
  • 8-15 % of dose reaches bronchi
  • < 1% of dose reaches systemic circulation
  • Inactive metabolites in urine
  • Duration of action 6-8 h
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19
Q

What are the adverse effects associated with ipatromium?

A
  • Bitter taste –> compliance (adherence) issues
  • ACh effects: rare and mainly at high doses
  • Drying of secretions does not occur
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20
Q

What is the major pro/con of tiotropium?

A

Tiotropium pro => longer acting (~ 24h) dry powder

con => ACh effects seen in patients with severe renal impairment

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21
Q

What is an example of inhaled corticosteroid?

A

Fluticasone

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22
Q

What are some examples of systemic inhaled corticosteroids?

A

Hydrocortisone; Prednisone; Methylprednisolone

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23
Q

What are the indications for systemic use of corticosteroids in asthma?

A

1) Acute severe asthma

2) Chronic maintenance therapy

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24
Q

What are the indications of inhaled use of corticosteroids in asthma?

A

1) Prophylaxis in mild/moderate or refractory asthma

2) Combined with systemic steroids in chronic asthma–> reduces systemic dose

25
What enzymes do corticosteroids inhibit and what is the overall effect?
Inhibits enzymes producing PGs, LTs and TX e.g. PLA2 via lipocortin, COX-2. => anti-inflammatory mechanism
26
What mediators do corticosteroids block in gene transcription? What is the overall effect
1) Inhibits gene transcription of pro-inflammatory cytokines e.g. IL-1,TNF-alpha,GM-CSF, IL-3,4,5 & 6 2) Directly counteracts the positive effects of several cytokines on transcription factors AP-1 and NF-KB => anti-inflammatory mechanism
27
What enzymes do corticosteroids induce and what is the effect?
Induce enzymes e.g. ACE and NEP which degrade bradykinin (can lead to bronchoconstriction/cough) and tachykinin => anti-inflammatory mechanism
28
What sort of receptor transcription do corticosteroids increase? What is the overall effect?
Increases βeta2 receptor transcription => anti-inflammatory
29
Corticosteroid inhibition of TNF has what effect?
Inhibition of TNF reduces cell trafficking and reduces expression of cell adhesion molecules => anti-inflammatory
30
Corticosteroids induce apoptosis in what kinds of cells?
Induces apoptosis in eosinophils | => anti-inflammatory effect
31
How do corticosteroids inhibit plasma exudation?
Inhibits plasma exudation from venules by synthesis of an antipermeability factor- vasocortin
32
Describe the pharmacokinetics of corticosteroids.
``` MDI Rx: ~ 10% dose -->bronchi ~ 90% --> oropharynx and swallowed Metabolism – hepatic CYP3A Low systemic concentrations - Half life of 2 hrs ```
33
What are the local adverse effects of corticosteroids?
- Thrush (C. Albicans) 10-15% of patients | - Hoarse voice
34
What are the acute systemic adverse effects of corticosteroids?
1) CNS-insomia/psychosis 2) Metabolic => hyperglycemia and Na/water retention 3) Signs of suppressed immune system (infection) - Bruising/purpura 4) Acute proximal myopathy
35
What are the chronic systemic adverse effects of corticosteroids?
``` 1) HPA (hypothalamic-pituitary-adrenal)-axis suppression => adrenal suppression 2) Cushingnoid appearance 3) Hypertension 4) Opportunistic infection 5) Peptic ulcer 6) Osteoporosis 7) Posterior cataracts 8) Inhibition of bone growth (children) 9) Pancreatitis 10)Aseptic necrosis (femoral head) ``` *Don't need to memorize all, just understand that corticosteroids can be toxic
36
What are 3 major classes of anti-inflammatory drugs to treat asthma/COPD/allergic rhinitis?
1) Leukotriene antagonists 2) Cromokalim derivatives 3) Histamine pharmacology
37
What is an example of a leukotriene antagonist?
Montelukast
38
What are the major properties of leukotrienes (i.e. why are they bad?)?
- Bronchoconstrict - Increase vascular permeability --> edema - Increase mucus secretion => decreased mucociliary clearance - Stimulate phospholipase A2 - Release prostaglandins and thromboxanes - Increase cellular infiltrate into the airways
39
What is the mechanism of action of montelukast?
- Competitive inhibitor at the Cys LT1 receptor - Plasma concentrations => LTD4 decreases in airway conductance - Blocks PAF induced airway hyper-responsiveness - Attenuates response to inhaled antigens & cold air
40
What are the indications for Montelukast?
- Prophylactic and chronic maintenance therapy - Often used in combination with other anti-asthma Rx - Useful for aspirin induced asthma * Effective and safe in children * Not as good a bronchodilator as βeta2 agonists
41
Describe the pharmacodynamics of Montelukast.
- Bronchodilatation within 1-2 h | - Duration of receptor blockade 10-14 h
42
Describe the pharmacokinetics of Montelukast.
- Good oral absorption-Tmax 3-4 h. - Food decreases bioavailability by 40% - T1/2 = 3-6 hours (maybe 20 hours in elderly) - Hepatic metabolism - CYP3A /2C9
43
What are the major adverse effects of Montelukast?
Overall well tolerated: - GI; nausea and vomiting - CNS; mild headaches - Hepatitis; transaminitis (reversible) - Churg-Strauss vasculitis ?
44
What are pertinent drug-drug interactions with Montelukast?
CYP 450 inducers reduce AUC by 40%
45
What are the major second line anti-asthma drugs?
- Anti-histamines (H1blockers) => Fexofenadine - Steroid sparing=> Methotrexate, Azathioprine (6-MP) - Monoclonal antibody=> Omalizumab
46
How does Omalizumab work (10-12k/yr)?
Anti-IgE monoclonal antibody | - given subcutaneously every 2-3 weeks (some hypersensitivity problems)
47
What are some adverse effects of Omalizumab?
- Hypersensitivity - Possible long term toxicity - Rashes/urticaria - Gastrointestinal upsets
48
What drugs are contraindicated in ASthamtic patients?
- Beta antagonists (blockers); propanolol > metoprolol = > will exacerbate bronchoconstriction - Cholinergic agonists; e.g. carbachol - Adenosine => acute broncospasm - Aspirin & NSAIDs (2-7% asthmatics) * ACE-inhibitors (ie lisinopril) => dry cough
49
What are the major types of therapy for allergic rhinitis?
1) Reduce exposure to allergens 2) Oral anti-histamine (Anti-H1) 3) Topical disodium cromoglycate 4) Topical glucocorticosteroids - “Xnase” 5) Topical ipratropium bromide 6) Immunotherapy and desensitization
50
What are the uses of Disodium Cromoglycate (Cromolyn)?
- Allergic rhinitis and conjunctivitis - Prophylaxis in exercise induced asthma (No MDI in US) - Mastocytosis (mast cell disease-esp children)
51
What is the mechanism of action of disodium cromoglycate (Cromolyn)?
- Inhibits chloride channels and calcium flux --> reduces release of preformed cytokines from T cells and eosinophils - Suppresses effects of kinins on inflammatory cells
52
What are the adverse effects of Disodium Cromoglycate (Cromolyn)?
* Generally very well tolerated | - Nasal stinging, Headache, nausea
53
Describe the pharmacokinetics of H1 receptor antagonists.
- Well absorbed orally - Diphenhydramine T1/2 = 6-8h; Fexofenadine T1/2 = 25h. - Hepatic metabolism by CYP3A. - Enters CSF/CNS well => induces drowsiness due to anti-cholinergic and anti-serotonin components
54
What are the uses/indications for H1 receptor antagonists?
- Allergic reactions, allergic rhinitis, - “cold” remedies - Anti-emetics and anti-motion sickness
55
Describe the pharmacodynamics of H1 receptor antagonists.
Competitive inhibition at H1 receptors. (H1 receptors couple to IP3 and increase Ca2+)
56
What are the major adverse effects of H1 receptor antagonists?
1) CNS: Drowsiness, sedation, confusion, esp. 1st gen. drugs 1st gen. are anti-5HT1 and anti-cholinergic 2) Headaches; GI disturbances (constipation) Second generation: 1) No ACh. effects, less drowsiness, headaches & GI disturbance
57
What are the drug-drug interactions/contraindications for H1 receptor antagonists?
- Inhibitors of metabolism -->Prolong QTc --> VT | - PD interaction: Increased sedation with e.g. EtOH
58
What are special considerations for patients on H1 receptor antagonists?
First generation agents not used in the elderly | => confusion, hallucinations, sedation

Pharm Block 1 (16 decks)

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