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Pulmonology Exam > Pulmonary Pharmacology 1 > Flashcards

Pulmonary Pharmacology 1 Flashcards

1
Q

effects of B2 stimulation on the bronchial smooth muscles

A

relaxation of bronchial smooth muscles (bronchiole dilation)

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2
Q

general classes of meds used for COPD & asthma

A

*bronchodilators (ex. albuterol, salmeterol, formoterol)
*corticosteroids (ex. budesonide, fluticasone, beclomethasone, prednisone)
*leukotriene antagonists (ex. montelukast, zileuton)
*phosphodiesterase inhibitors (ex. roflumilast)
*Cromolyn
*biologic immunomodulators

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3
Q

bronchodilators - overview

A

*relax constricted airway smooth muscle and cause immediate reversal of airway obstruction
*3 main classes available:
1. beta2 adrenergic agonists
2. methlyxanthines
3. muscarinic cholinergic antagonists

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4
Q

bronchodilator: beta 2 adrenergic agonists - MOA

A

*stimulate adenylyl cyclase and increase cyclic adenosine monophosphate (cAMP) in smooth muscle cells
*increase in cAMP results in a powerful bronchodilator response
*results in rapid decrease in airway resistance

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5
Q

bronchodilator: beta 2 adrenergic agonists - 2 types

A
  1. short-acting (“reliever” - treat attack)
    -inhaled beta-agonists are most widely used and effective bronchodilators in the treatment of asthma
    -duration of action: ~3-4 hours
    -ex: ALBUTEROL
  2. long-acting (“controller” - prevent attack)
    -duration of action: > 12 hours
    -do not act quickly enough to be used to treat an attack
    -ex: SALMETEROL, FORMOTEROL
    -combination inhalers exist with corticosteroid
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6
Q

albuterol - drug class, MOA, & uses

A

*drug class: beta 2 adrenergic agonist
*MOA: stimulate adenylyl cyclase → increased cAMP → relaxation of bronchial smooth muscle (bronchodilation)
*uses: SHORT-ACTING; used to TREAT asthma attacks

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7
Q

salmeterol - drug class, MOA, & uses

A

*drug class: beta 2 adrenergic agonist
*MOA: stimulate adenylyl cyclase → increased cAMP → relaxation of bronchial smooth muscle (bronchodilation)
*uses: LONG-ACTING; used to PREVENT asthma attacks

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8
Q

formoterol - drug class, MOA, & uses

A

*drug class: beta 2 adrenergic agonist
*MOA: stimulate adenylyl cyclase → increased cAMP → relaxation of bronchial smooth muscle (bronchodilation)
*uses: LONG-ACTING; used to PREVENT asthma attacks

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9
Q

bronchodilator: beta 2 adrenergic agonists - ADEs

A

*unwanted effects are dose-related and due to stimulation of extrapulmonary beta receptors
*not common with inhaled therapy, but quite common with oral or IV administration
*example ADEs: skeletal muscle tremor, palpitations, tachyarrhythmias, restlessness, and hypokalemia

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10
Q

bronchodilator: methylxanthines (ex. Theophylline) - MOA, use, metabolism

A

*likely causes bronchodilation by inhibiting phosphodiesterase → increased cAMP levels; blocks actions of adenosine
*limited use clinically
*rapidly and completely absorbed
*eliminated by liver CP450 drug-metabolizing enzymes (esp. CYP1A2)
*factors affecting clearance: age, smoking, drug inducers or inhibitors

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11
Q

bronchodilator: methylxanthines (ex. Theophylline) - ADEs

A

*undesirable effects generally occur at higher serum levels (theophylline has a very narrow therapeutic window)
*overall, ADEs are cardiotoxicity and neurotoxicity
*ADEs include:
-headache
-nausea/vomiting
-diuresis
-CARDIAC ARRHYTHMIA

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12
Q

bronchodilator: muscarinic cholinergic antagonists - MOA

A

*blocks the effects of endogenous ACh at muscarinic receptors
*activity from inhibition of M3 subtype receptor
*PREVENTS CONSTRICTION of airway smooth muscle and prevents the increase in secretion of mucus that occurs in response to vagal activity
*useful in COPD > asthma

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13
Q

bronchodilator: muscarinic cholinergic antagonists - 2 types

A
  1. short-acting
    -relatively slow onset of bronchodilation
    -duration of action: 6-8 hours
    -often combined with short-acting beta2 agonist (albuterol)
    -ex: IPRATROPIUM
  2. long-acting
    -once-daily dosing
    -duration of action: 24+ hours
    -useful for COPD
    -ex: TIOTROPIUM, glycopyrrolate, umeclidium, aclidinium
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14
Q

bronchodilator: muscarinic cholinergic antagonists - ADEs

A

*generally well-tolerated
*dry mouth
*unpleasant bitter taste
*urinary retention in elderly patients (rare)

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15
Q

ipratropium - drug class, MOA, uses

A

*drug class: muscarinic cholinergic antagonist
*MOA: competitively blocks muscarinic receptors → prevents bronchoconstriction
*uses: SHORT-ACTING; often combined with albuterol

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16
Q

tiotropium - drug class, MOA, uses

A

*drug class: muscarinic cholinergic antagonist
*MOA: competitively blocks muscarinic receptors → prevents bronchoconstriction
*uses: LONG-ACTING; useful for COPD

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17
Q

why do we use ipratropium/tiotropium instead of atropine as our go-to anticholinergics for asthma/COPD?

A

*these drugs have much fewer ADEs compared to inhaled atropine because they are quaternary ammonium compounds with poor absorption and CNS penetration (i.e. less systemic effects)

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18
Q

methacholine

A

*analogue of acetyl choline, used for diagnosis
*produces smooth muscle CONTRACTION of the airways and increased tracheobronchial secretions
*Methacholine Challenge Test: to diagnose bronchial airway hyper-reactivity in patients who do not have clinically apparent asthma

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19
Q

corticosteroids in asthma - MOA

A

*alter gene expression → changes mRNA → changes in protein synthesis
*effects in asthma because they DOWNREGULATE INFLAMMATORY GENES (inhibit the synthesis of virtually all cytokines)
*biggest impact in asthma due to decreased infiltration of airways by lymphocytes, eosinophils, and mast cells
*this process takes time, so most effects of steroids are not seen instantly

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20
Q

inhaled corticosteroids for asthma

A

*quicker onset of action
*fewer side effects
*examples: BECLOMETHASONE, BUDESONIDE, ciclesonide, flunisolide, mometasone, and FLUTICASONE
*low dose steroid-beta-2 agonist combo now recommended as a “reliever”

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21
Q

systemic corticosteroids

A

*IV and oral forms
*slower onset of action
*more side effects
*examples: hydrocortisone, methylprednisolone, prednisone

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22
Q

inhaled corticosteroids - efficacy and toxicity

A

*efficacy of inhaled drug is dependent on:
-delivery to the lung
-residency time in the lung
-potency of the steroid

*systemic toxicity of inhaled drug is dependent on:
-delivery to non-lung areas with absorption
-metabolism of the drug

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23
Q

inhaled corticosteroids - ADEs

A

*dysphonia
*oropharyngeal candidiasis (use a spacer and rinse mouth after each use to avoid)
*slight increased risk of osteoporosis and cataracts with chronic use

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24
Q

oral corticosteroids - ADEs

A

*steroid withdrawal syndrome (must be reduced slowly)
*weight gain, increased appetite, fluid retention
*osteoporosis
*hyperglycemia
*immunosuppression

25
Q

issues associated with inhaled drugs

A

*getting it into the lungs and not the back of throat or outside air
*patient education is key - watch patient’s technique
*delivery devices - pharmacokinetics meets pharmaceutical science
*what if they can’t cooperate and/or use device?:
-nebulizer (requires equipment)
-oral therapy (often decreased efficacy and increased adverse effects)

26
Q

leukotriene antagonists (antileukotrienes) - MOA

A

*interfere with the synthesis or the action of the leukotrienes (block CysLT1 leukotriene receptors)
*do not provide much added benefit compared to beta2 agonists or corticosteroids

note - Cysteinyl-leukotrienes are produced in asthma

27
Q

leukotriene antagonists (antileukotrienes) - examples

A

*Montelukast
*Zileuton

28
Q

Montelukast - drug class, MOA

A

*drug class: leukotriene antagonists (antileukotrienes)
*MOA: interfere with the synthesis or the action of the leukotrienes (block CysLT1 leukotriene receptors)

29
Q

zileuton - drug class, MOA

A

*drug class: leukotriene antagonists (antileukotrienes)
*MOA: interfere with the synthesis or the action of the leukotrienes (block CysLT1 leukotriene receptors)

30
Q

leukotriene antagonists - uses

A

*especially good for aspirin-induced asthma and exercise-induced asthma

31
Q

leukotriene antagonists - ADEs

A

*rare hepatic dysfunction
*Churg-Strauss syndrome
*BLACK BOX WARNING FOR MONTELUKAST (neuropsychiatric events)

32
Q

Montelukast - black box warning ADE

A

*serious neuropsychiatric events (especially in young people):
-aggression, abnormal behavior, anxiety, suicidal ideation, depression, nightmare, anger, crying, insomnia
*avoid prescribing montelukast for patients with mild symptoms
*risks greater than benefits in many patients

33
Q

phosphodiesterase inhibitors/PDE4 inhibitors (Roflumilast) - MOA

A

*inhibits phosphodiesterase → increased cAMP (decreased degradation of cAMP) → bronchodilation and decreased airway inflammation

34
Q

Roflumilast - drug class, MOA, uses

A

*drug class: oral PDE-4 inhibitor (phosphodiesterase inhibitor)
*MOA: inhibits phosphodiesterase → increased cAMP → bronchodilation and decreased airway inflammation
*uses: used in COPD to reduce exacerbations

35
Q

phosphodiesterase inhibitors/PDE4 inhibitors (Roflumilast) - ADEs

A

*think GI and CNS:
-diarrhea
-nausea/vomiting
-decreased appetite
-depression
-insomnia
-anxiety

36
Q

cromolyn - MOA

A

*stabilizes mast cells, preventing their degranulation
*blocks release of histamine and slow-reacting substance of anaphylaxis

37
Q

cromolyn - uses, ADEs

A

*route: inhalation (nebulization)
*use: prevention of asthma exacerbations (seldom used now)
*well-tolerated

38
Q

omalizumab - drug class, MOA, uses

A

*drug class: anti-IgE monoclonal antibody (biologic immunomodulator)
*MOA: binds mostly unbound serum IgE and blocks binding to FceRI
*used in allergic asthma with increased IgE levels resistant to inhaled glucocorticoids and long-acting beta2 agonists

39
Q

biologic immunomodulator: anti-IgE monoclonal antibody

A

omalizumab

40
Q

biologic immunomodulator: anti-IL-5 monoclonal antibodies

A

-mepolizumab
-reslizumab
-benralizumab

41
Q

mepolizumab - drug class, MOA, uses

A

*drug class: anti-IL-5 monoclonal antibody
*MOA: antibody against IL-5; prevents eosinophil differentiation, maturation, activation, and survival (which is normally mediated by stimulation of IL-5)
*uses: maintenance therapy in severe eosinophilic asthma

42
Q

reslizumab - drug class, MOA, uses

A

*drug class: anti-IL-5 monoclonal antibody
*MOA: antibody against IL-5; prevents eosinophil differentiation, maturation, activation, and survival (which is normally mediated by stimulation of IL-5)
*uses: maintenance therapy in severe eosinophilic asthma

43
Q

benralizumab - drug class, MOA, uses

A

*drug class: anti-IL-5 monoclonal antibody
*MOA: antibody against IL-5 RECEPTOR; prevents eosinophil differentiation, maturation, activation, and survival (which is normally mediated by stimulation of IL-5)
*uses: maintenance therapy in severe eosinophilic asthma

44
Q

biologic immunomodulator: anti-IL-4 monoclonal antibody

A

dupilumab

45
Q

narcotic antitussives - MOA, examples

A

*MOA: not fully understood; might work centrally at the medullary cough center (nucleus tractus solitarius) and peripherally on the paratracheal ganglia
*examples: codeine, hydrocodone
*more effective than non-narcotic antitussives

45
Q

dupilumab - drug class, MOA, uses

A

*drug class: anti-IL-4 monoclonal antibody
*MOA: blocks IL-4 and IL-13 signaling by binding to IL-4 alpha receptor
*uses: effective for eosinophilic esophagitis, COPD with type II inflammation, and atopic dermatitis

46
Q

narcotic antitussives - ADEs

A

*sedation
*respiratory depression
*nausea
*vomiting
*constipation

47
Q

non-narcotic antitussives - examples

A

*dextromethorphan
*benzonatate

48
Q

dextromethorphan - drug class, MOA, ADEs

A

*drug class: non-narcotic antitussive
*MOA: suppresses the cough reflex and increases the cough threshold by direct action on the medullary cough center
*glutamate and N-methyl-D-aspartate (NMDA) receptor antagonism in the CNS at higher doses
*ADEs: well tolerated; at higher doses, hallucination, dystonia, fatigue, dizziness
*note - mild SSRI, so may have potential drug interactions, leading to serotonin syndrome

49
Q

benzonatate - drug class, MOA, ADEs

A

*drug class: non-narcotic antitussive
*MOA: acts peripherally by anesthetizing the stretch receptors located in the respiratory passages, lungs, and pleura
*may reduce cough reflex at its source
*ADEs: dizziness, dysphagia

50
Q

expectorants - goal, examples

A

*increase volume and/or hydration of secretions
*goal: produce a sufficient volume of mucus to enable it to be coughed up
*does not alter ciliary beat frequency or mucociliary clearance
*examples: hypertonic saline, guaifenesin

51
Q

expectorant: hypertonic saline - MOA, ADEs, info

A

*MOA: increases secretion volume and perhaps hydration
*info: aerosolized expectorant form; improves pulmonary function and reduces exacerbations in patients with cystic fibrosis
*ADEs: unpleasant taste, cough induction

52
Q

guaifenesin - drug class, MOA, ADEs

A

*drug class: expectorant
*MOA: may reduce bronchial sputum surface tension; can stimulate cholinergic pathway and increase mucus secretion from the airway submucosal glands
*ADEs: dizziness, headache, N/V

53
Q

mucolytics - goal, examples

A

*change the biophysical properties of secretions through degradation of mucin polymers, DNA, fibrin, or F-actin in airway secretion
*reduce the viscosity of sputum
*do not necessarily improve secretion clearance
*examples: N-acetylcysteine, dornase alfa

54
Q

N-acetylcysteine - drug class, MOA, info, ADEs

A

*drug class: mucolytic
*MOA: severs disulfide bonds linking mucin polymers; antioxidant and anti-inflammatory effects
*info: aerosolized form; rapidly inactivated and not found in airway secretions
*ADEs: unpleasant odor during administration

55
Q

dornase alfa - drug class, MOA, info, ADEs

A

*drug class: mucolytic
*MOA: proteolytic enzyme - hydrolyzes free DNA strands that are primarily from neutrophils entering airways as part of inflammatory response; reduces viscosity and adhesiveness of infected sputum
*info: aerosolized form; used in patients with CF
*ADEs: chest pain, pharyngitis, voice alterations

56
Q

decongestants - MOA, ADEs, examples

A

*MOA: alpha-1 agonists → vasoconstriction → decrease volume of nasal mucosa
*used to treat nasal congestion from colds or allergies
*ADEs: rebound congestion, minor increased BP
*examples: phenylephrine, pseudoephedrine, oxymetazoline, xylometazoline

57
Q

antihistamine MOA in “drying up your nose” in a viral illness

A

*work by blocking Ach receptors (not by blocking H1 receptors)

Pulmonology Exam (36 decks)

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