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Question 1
What is a Metered-Dose Inhaler (pMDI)?
pressurized inhaler that propels drugs from canister with the aid of a propellant
Question 2
What is the purpose of a Spacer Chamber in inhalation therapy?
To increase the percentage of drug inhaled into the lower airways, especially useful in children.
Question 3
What are Dry Powder Inhalers typically used for?
used for drugs given every day, especially for peptides and proteins like insulin
Question 4
What is the difference between a metered-dose inhaler and a dry-powder inhaler?
MDI: delivers aerosolized drug to the lungs DPI: delivers powdered medications to the lungs
Question 5
How does a nebulizer work?
changes liquid drug to mist delivers to the lungs over a period of time (between 10-20 minutes)
Question 6
What is the preferred route of inhalation for medication delivery?
Inhalation route with small particle size
Question 7
What percentage of inhaled medication is absorbed by the lungs?
10%–20%
Question 8
What is the oral route of administration?
Generally reserved for patients unable to use inhalers.
Question 9
What is the parenteral route of administration?
IV mainly for severely ill patients due to fast onset and inability to absorb drugs from the GI tract
Question 10
parasympathetic innervation in the tracheobronchial tree?
Bronchoconstriction
Question 11
Sympathetic innervation in the tracheobronchial tree?
Bronchodilation
Question 12
What are the two zones of the tracheobronchial tree?
Conducting Zone and Respiratory Zone
Question 13
what respiratory structures are in the conducting zone
trachea, bronchi, bronchioles, terminal bronchioles
Question 14
what respiratory structures are in the respiratory zone
respiratory bronchioles, alveolar ducts, alveolar sacs
Question 15
What is the definition of asthma?
Chronic inflammatory disorder caused by excessive airway hyperresponsiveness in response to triggers
Question 16
What is the role of Ach in asthma?
• Ach binds to airway muscarinic receptors • triggers smooth muscle contraction and mucus secretion
Question 17
What happens in the early phase of asthma
• allergen triggers IgE-mediated mast cell degranulation • histamine release • bronchospasm, vasodilation, wheezing, airway inflammation
Question 18
What happens in the later phase of asthma
• activated lymphocytes, release cytokines • recruit other proinflammatory cells • airway hyperresponsive, edema, mucus secretion
Question 19
What is the mechanism of extrinsic (allergic) asthma?
Type I hypersensitivity reaction
Question 20
How is acute asthma divided into phases?
Early phase: histamine derived, bronchoconstriction and edema Late phase: inflammatory mediator derived, mucus secretion
Question 21
What is the epidemiology of intrinsic asthma?
More frequent in adults, occurring after the age of 30 years.
Question 22
What is the mechanism of intrinsic asthma?
Due to nonallergic causes.
Question 23
What are the triggers of intrinsic asthma?
Smoking, chronic bronchitis, respiratory infections, air pollutants, cold air, and exercise.
Question 24
What are the classifications of asthma
• mild intermittent • mild persistent • moderate persistant • severe persistant
Question 25
occurrence of mild intermittent asthma?
Symptoms less than twice a week
Question 26
Classification for asthma with symptoms between once a day and twice a week?
Mild persistent
Question 27
What are the three main categories of asthma management as shown in the slide?
• Bronchodilators • Anti-inflammatory • Inflammation pathway Leukotriene modifiers
Question 28
What are the types of Anti-inflammatory Meds?
Steroids Biologics: Anti-IgE Anti-IL-5 Prophylatic Lipoxygenase inhibitor Leukotriene antagonists Phosphodiesterase inhibitors
Question 29
What are the three therapeutic goals of asthma therapy?
1. Decrease intensity and frequency of asthma 2. prevent asthma exacerbation 3. minimize limitations in daily activity
Question 30
What does the Global Initiative for Asthma (GINA) recommend for asthma patients?
patients should receive treatment with long-term controller and reliever meds
Question 31
What are bronchodilators?
Meds that relax the muscles in the airways, making it easier to breathe
Question 32
What are the types of bronchodilators?
• Short-acting β2-adrenoceptor agonists (SABAs) • Long-acting β2-adrenoceptor agonists (LABAs) • Muscarinic Antagonists • Methylxanthines
Question 33
β2 agonists MOA
activate β2 adrenergic receptors, ↑ cAMP levels → ↓ calcium availability → bronchodilation
Question 34
What are some examples of SABAs?
Albuterol Levalbuterol
Question 35
onset and duration of Short-acting β2-adrenoceptor agonists?
fast onset of action (1-5 min) short duration (4-6 hours)
Question 36
Onset and duration of LABAs
onset: slower duration: 12 hours
Question 37
What are some examples of LABAs?
Salmeterol Formoterol
Question 38
Muscarinc Antagonist meds
Ipratropium Tiotropium
Question 39
Muscarinic Antagonist MOA
Competitive antagonist for Ach-mediated bronchoconstriction at M3 receptors ↓ mucus secretion
Question 40
What are the main types of controller medications for anti-inflammatory agents?
Examples include corticosteroids and nonsteroidal anti-inflammatory drugs (NSAIDs)
Question 41
Methylxanthines medication
theophylline
Question 42
Methylxanthines: Theophylline MOA
poorly understood PDE inhibitor → ↑ cAMP → ↓ calcium → bronchodilator effect
Question 43
Steroid drugs
Beclomethasone Fluticasone Budesonide
Question 44
Steroid MOA
increase production of inflammatory cytokines
• inhibit phospholipase A2 → inhibit arachidonic acid + products • ↓ inflammatory cells and ↓ mucus production • suppress airway inflammation; not a cure
directly kill pathogens in the airway
cause bronchodilation by directly relaxing bronchial smooth muscle
Question 45
Biologics: Anti-IgE drug
Omalizumab
Question 46
Biologics: Anti-IgE MOA
blocks binding of IgE to mast cells → Prevents degranulation → ↓ eosinophils + inflammatory mediators
Question 47
Biologics: Anti-IL-5 Drug
Benralizumab
Question 48
Biologics: Anti-IL-5 Drug
block IL 5 action → reduce the inflammatory response
Question 49
Prophylatic Drug
Cromolyn
Question 50
Cromolyn MOA
stabilize mast cells → inhibits degranulation + release of histamine
Question 51
Lipoxygenase inhibitor drug
Zileuton
Question 52
Lipoxygenase inhibitor MOA
Selective inhibitor of 5- lipoxygenase → prevents conversion of arachidonic acid to leukotrienes
Question 53
Leukotriene antagonist drugs
Montelukast Zafrilukast
Question 54
Leukotriene antagonist MOA
blocks leukotriene receptors → prevent response to leukotriene mediators
Question 55
Treatment strategy for Well Controlled asthma
1. Low dose ICS/LABA, PRN 2. low dose ICS daily Reliever: SABA
Question 56
Treatment strategy for partly controlled asthma
3. low dose ICS/LABA daily Reliever: SABA
Question 57
Treatment strategy for poorly controlled asthma
4. medium dose ICS/LABA, daily 5. High dose: ICS/LABA daily + LAMA, + biologics Reliever: SABA
Question 58
Treatment strategy • low COPD • few symptoms
SABA, SAMA, LABA, LAMA choose one
Question 59
Treatment strategy • low COPD • more symptoms
LABA or LAMA
Question 60
Treatment strategy • high COPD • few symptoms
LAMA
Question 61
Treatment strategy • high COPD • more symptoms
LAMA or LAMA + LABA or LABA + ICS
Question 62
Phosphodiesterase inhibitor med
Roflumilast tablet
Question 63
Phosphodiesterase inhibitors MOA
inhibit PDE4 → accumulation of cAMP
Question 64
Antihistamine drugs
Cetirizine Loratadine
Question 65
Antihistamine MOA
2nd Gen compete w/ histamine for receptor binding sites
Question 66
α-adrenergic agonists meds
Pseudoephedrine Oxymetazoline
Question 67
α-adrenergic agonists MOA
Stimulates α-adrenergic receptors in nasal arterioles → local vasoconstriction
Question 68
What are some examples of intranasal corticosteroids?
Fluticasone triamcinolone
Question 69
What are the side effects of opioids in patients with asthma?
Bronchospasm due to histamine release
Question 70
What are the side effects of opioids and sedatives?
Respiratory depression
Question 71
What side effect can anticholinergic agents cause?
Mild xerostomia
Question 72
Mechanism of aspirin induced asthma
Aspirin inhibits COX1 → prevents prostaglandin production → more leukotrienes (inflam. mediators) → smooth muscle contraction