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MS2 Respiratory > 9/22- Pharmacology of Obstructive Lung Diseases > Flashcards

9/22- Pharmacology of Obstructive Lung Diseases Flashcards

1
Q

What are the main pathologic features in obstructive lung diseases?

A
  • Bronchoconstriction
  • Increased airway inflammation
  • Increased mucus production
  • Airway Remodeling
  • Parenchymal lung destruction (emphysema)
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2
Q

Describe PS bronchial autonomic innervation

  • NT
  • Mechanism
  • End result
A

Parasympathetic

  • NT: ACh
  • Binds muscarinic M3 receptors (cholinergic) on sm cells within bronchial walls
  • End result: constricts the airways
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3
Q

Describe sympathetic bronchial autonomic innervation

  • NT
  • Mechanism
  • End result
A
  • NT: catecholamines
  • Binds adrenergic receptors
  • Airway sm cells express B2 adrenergic receps mainly (expressed elsewhere too, but mostly on smooth muscles)
  • End result: bronchodilation
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4
Q

Overview of Medications for Asthma - Ant-inflammatories - Bronchodilators - Others

A

Anti-inflammatories:

  • Inhaled Corticosteroids
  • Antileukotrienes
  • Cromones
  • Theophylline (?)

Bronchodilators

  • Short and Long-acting ß-agonists
  • Short-acting Anticholinergic ICS/LABA

Combination

Anti IgE

(Thus, you can see that bronchodilation may be achieved by promoting sympathetic stimulation or blocking PS)

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5
Q

Overview of Medications for COPD:

  • Ant-inflammatories
  • Bronchodilators
  • Others
A

Anti-inflammatories:

  • Inhaled Corticosteroids
  • Roflumilast Bronchodilators
  • Short and Long-acting ß-agonists
  • Short and Long-acting

Anticholinergics

  • Theophylline
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6
Q

What method of administration is preferred for bronchodilators?

A

Inhalation

  • Can be given systemically if really severe/can’t inhale
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7
Q

What is the benefit of combining bronchodilators in COPD?

A
  • May improve efficacy
  • May decrease the risk of side effects compared with increasing the dose of a single bronchodilator
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8
Q

Provide examples of classes of bronchodilators?

A
  • Beta 2 agonists
  • Anticholinergics
  • Methylxanthines
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9
Q

How do the following effect bronchodilation?

  • Beta agonists
  • Muscarinic antagonists
  • Theophylline
A
  • Beta agonists: activation of AC -> more cAMP -> bronchodilation
  • Muscarinic antagonists: block ACh activation of bronchoconstriction
  • Theophylline: blocks PDE, increasing cAMP levels (by preventing cAMP -> AMP degradation) and blocks adenosine (?)
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10
Q

In addition to relaxing airway sm, what other functions to B2 agonists have?

A
  • Inhibition of plasma exudation and airway edema
  • No effect on chronic inflammation
  • Don’t want too use to frequently (bad outcomes), so used to supplement long-acting treatment
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11
Q

Provide example drugs for short and long-acting B2 agonists?

(Don’t need to remember drug names at this point)

A

Short

  • Albuterol
  • Pirbuterol

Long

  • Salmeterol
  • Formoterol
  • Indacaterol
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12
Q

Describe short-acting beta agonists

  • Onset
  • Duration
  • Frequency
A

(Albuterol is the most commonly used rescue inhaler)

  • Onset: rapid, within 10-15 min
  • Duration: max 4-6 hrs
  • Most effective when used on “as-needed” basis, or “rescue”
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13
Q

Describe long-acting beta agonists

  • Duration
  • Frequency
  • Effects
A

(Salmeterol and formoterol)

  • Similar to short-acting, but longer duration: 12 hrs
  • Dosed 2x/day
  • Variable effects on exercise, exacerbation, QOL
  • Should only be used as add-on to ICS (immunocorticosteroids?) in asthma
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14
Q

Recommendations on use of LABAs in Asthma?

A

Not recommended as monotherapy for long-term control

  • Consider as adjunctive therapy in patients aged >5 years who require more than a low-dose ICS
  • Consider adding an LTRA in patients aged >5 years

Not recommended for treatment of acute symptoms

May be used before exercise to prevent EIB

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15
Q

How to anticholinergics function to alleviate asthma and COPD (mechanism/targeted pathology)?

A
  • Block vagal pathways-decreases vagal tone
  • Blocks reflex bronchoconstriction caused by inhaled irritants
  • Role in asthma is less clear (than in COPD) may have added benefit in combination with beta2-agonists in acute asthma
  • Delivered locally, but may be associated with systemic effects (since cholinergic): most common = dry mouth
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16
Q

Provide examples of short and long acting anticholinergics (don’t memorize names)?

A
  • Ipratropium: slow onset (30 min)
  • Tiotropium: bronchodilation, long acting (24 hrs)

Overall, slower than B2 agonists, which is why the latter are preferred in rescue situations

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17
Q

What drug is included in the class of methylxanthines?

A

Theophylline

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18
Q

Describe Theophylline

  • Functions
  • Mechanism
  • Duration
  • Dosing
  • Metabolism
  • Toxicity
A
  • Bronchodilator (mild-moderate) with questionable anti-inflammatory properties
  • Mechanism uncertain (probably PDE inhibition)
  • Long acting dosage form
  • Very narrow therapeutic window (get ASEs easily!)
  • Recommended serum concentration = 5-8 ug/mL; dose varies person to preson
  • Metabolism: liver

Toxicity:

  • GI (most common): irritation, burning, nausea
  • CNS stimulation: tremors
  • Tachyardia
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19
Q

T/F: Theophylline has numerous drug-drug/disease-drug interactions?

A

True

20
Q

What drugs/diseases may increase metabolism of Theophylline (decrease levels)?

A
  • Cigarette smoking
  • Young age
  • Hyperthyroidism
  • Barbiturates
  • Phenytoin (ex: if someone stops smoking, may have super high theophylline levels)
21
Q

What drugs/diseases may decrease metabolism of Theophylline (increase levels)?

A
  • Liver disease
  • CHF
  • Older age
  • Viral infections
  • Febrile illness
  • Macrolide antibiotic
  • Cimetidine
  • Quinolone antibiotics
  • Propranolol
  • Allopurinol
22
Q

What are classes of anti-inflammatory agents used in asthma/COPD treatment?

A
  • Inhaled Corticosteroids
  • Leukotriene Modifiers
  • Mast-cell stabilizers (Cromones)
  • Anti Ig-E therapy (severe allergic asthma)
23
Q

Describe inhaled corticosteroids

  • Systemic effect
  • Effects of chronic use
  • Frequency
  • Not used in what situations
  • When to use in asthma
  • When to use in COPD
A
  • Potent local anti-inflammatory with minimal systemic toxicity
  • Chronic use decreases airway hyper-responsiveness
  • A “preventer”, not a “reliever”
  • Daily regularly scheduled - Generally not used in acute exacerbations
  • Asthma: 1st line in daily asthma management!
  • COPD: Reserved for more moderate-severe disease with frequent exacerbation
24
Q

What are the cellular effects of corticosteroids?

A

Inflammatory cell effect

  • Decrease numbers of eosinphils (apoptosis), mast cells, and dendritic cells
  • Decrease cytokine release by T lymphocytes and macrophages

Structural cell effect

  • Decrease cytokines/mediators of ep cells
  • Decrease endo cell leak
  • Decrease B2 receps and cytokines in airway SM
  • Decrease mucus secretion
25
Q

What are the beneficial effects of inhaled corticosteroids that make them the first-line therapy for persistent asthma?

A

(1st line therapy even in mild persistent disease)

  • Reduce asthma symptom severity
  • Improve quality of life
  • Improve pulmonary function
  • Reduce rescue inhaler use
  • Reduce exacerbations/ hospitalizations/ ?mortality
  • Reduce bronchial hyperreactivity
  • Slow deterioration of lung function
  • ? May prevent airway remodeling

Basically: improve lung function and symptoms and health status, decrease exacerbations; decrease mortality

  • Significant anti-inflammatory effects
26
Q

What are some safety/risk considerations of inhaled corticosteroids?

A
  • Small risk for topical adverse events at recommended dosage
  • New formulations have lower systemic bioavailability and higher topical potency

Reduce potential for adverse events by:

  • Using spacer and rinsing mouth
  • Using lowest dose possible
  • Using in combination with long-acting beta2-agonists
27
Q

What are the beneficial effects of inhaled corticosteroids that make them somewhat effective in COPD? Negatives?

A
  • Modest effect on long-term deterioration in lung function (limited because COPD involves neutrophilic inflammation)
  • Significant decrease in exacerbations
  • Improvement in quality of life
  • Modest effect on mortality
  • Recommended by guidelines for severe disease and in patients with recurrent exacerbations

BUT: Increase risk of pneumonia

28
Q

When should oral corticosteroids be used?

A

Acute exacerbation of asthma and COPD

  • Role in chronic, daily management is limited
  • Minimize use!
29
Q

What are some side effects of oral corticosteroids?

A

(Not uncommon)

  • Osteoporosis
  • Glaucoma
  • Diabetes
  • Adrenal suppression
  • Skin fragility, bruising
30
Q

What are the most active leukotrienes in asthma (and COPD?) treatment?

A
  • LTC4
  • LTD4
  • LTE4

(- LTB4- more neutrophilic infiltrate?)

31
Q

What are the effects of leukotrienes that are blocked by leukotriene modifiers?

A

Leukotriene modifiers block:

  • Plasma exudation
  • Bronchoconstriction
  • Mucus secretion
32
Q

What is the main unique benefit of leukotriene modifiers?

A

They are safe

  • Used more in kids to avoid steroid use?
33
Q

What are the classes of leukotriene modifiers?

A

5-lipoxygenase (5-LO) inhibitors

  • Zileuton (rarely used; liver tox)

LT-receptor antagonists

  • Zafirlukast
  • Montelukast
34
Q

What are characteristics of Zileuton

  • Class/mechanism of action
  • Pros/cons
A
  • 5-LO synthesis inhibitor
  • Con: significant drug interactions with other meds that are metabolized in the liver
35
Q

What are characteristics of Zafirlukast and Montelukast

  • Class/mechanism of action
  • Duration
  • Frequency
  • Pros/cons
A
  • LTE4, C4, D4 receptor antagonists
  • Longer acting than Zileuton
  • 1-2 daily doses
36
Q

T/F: Leukotriene modifiers typically have a uniform level of effectiveness in all pts? Explain

A

False

  • Fewer than 1/2 are positive responders; should be discontinued if no response within 1 mo
  • Uncovering of Churg-Strauss syndrome seen
37
Q

What drug is anti-IgE?

A

Omalizumab

38
Q

When should anti-IgE treatment (Omalizumab) be considered?

A

Moderate to severe persistent asthma when concomitant allergy seems important in the causation or provocation of the asthmatic process

39
Q

What are methods of drug delivery? Most common?

A
  • Metered Dose Inhalers (most common)
  • Nebulizers
  • Dry Powder Inhalers
  • Oral Pills
  • Used for leukotriene modifiers
  • Not liked for beta agonists
  • Intravenous medications
40
Q

Pros/cons of metered dose inhalers (MDI)?

A
  • Most commonly used method of drug delivery for lung diseases
  • Technique of use is most important to achieve optimal effect
  • Only 10-30% of each puff deposits in lung

Pros:

  • Convenience
  • Wide safety margin
  • Effective in microgram doses
  • Spacers increase effectiveness

Cons:

  • Improper technique common (at about 50%)
  • Can be overused
41
Q

Optimal particle size for metered dose inhalers?

A

2-5 um

  • Too large: systemic absorption if swallowed
  • Too small: none/minimal clinical effect; systemic absorption
42
Q

Describe nebulization

  • Medication format
  • Comparison to MDI
  • Pros
A
  • Medications are a mist (not liquid); more easily inhaled into lungs
  • Has been found to be equivalent drug delivery to using MDI with spacer

Pros:

  • Much higher doses can be delivered
  • Does not require patient coordination
  • Method of choice in ERs
43
Q

Describe dry powder inhalers

  • Activated by what?
A
  • Deliver medication to the lungs as patients inhale through the device.
  • Do not contain propellants or any other ingredients– only the medication
  • Breath-activated
44
Q

What respiratory medications are delivered orally?

A
  • Theophylline
  • Oral steroids
  • Leukotrienes
  • B-2 agonists: not as good a delivery method for this class because higher doses are required which cause higher side effects and less bronchodilation
45
Q

How is COPD graded?

A
  • Severity, risk, lung function

Grade A

  • Mild-moderate stage with minimal symptoms
  • 0-1 exacerbations/yr

Grade B

  • Mild-moderate stage with severe symptoms
  • 0-1 exacerbations/yr

Grade C

  • Severe-very severe with minimal symptoms
  • 2+ exacerbations/yr

Grade D

  • Severe-very severe with severe symptoms
  • 2+ exacerbations/yr
46
Q

What is PDE4 inhibitor used for?

A

COPD (recently approved)

  • Blocks PDE4 in neutrophils
  • Possible effect on neutrophilic inflammation
  • Approved for severe COPD pts (history of exacerbation)
  • Potential adverse effects: diarrhea, weight loss

MS2 Respiratory (26 decks)

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