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Pharmacology > Lecture 9 (Pulm)- Exam 5 > Flashcards

Lecture 9 (Pulm)- Exam 5 Flashcards

1
Q

What are the bronchodilators (4)?

A
  • Beta 2 agonists
  • Antimuscarinics
  • Leukotriene antagonists
  • Methylxanthines
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2
Q

Asthma at a glance

  • What first happens? What is the downfall?
A

Excessive Th2 response against specific antigens
* Triggers presented to Th2 cells
* Release cytokines

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3
Q

What are the two types of cytokines released in ashma?

A

IL-4
* IgE released->coats mast cells ->releases histamine, prostaglandin, leukotriene

IL-5
* Eosinophils released -> cytokines -> leukotriene

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4
Q

What is the result from all the cytokines released from asthma?

A

Results in airway spasm and increased mucous production
* Airways narrowed

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5
Q

COPD at a glance

  • What happens in chronic bronchitis?
  • What happens in emphysema?
  • Most patients have what?
A

Chronic bronchitis
* Increased mucous production
* Airway obstruction (dt mucous)

Emphysema
* Excessive elastases
* Destruction of alveolar walls that causes air trapping and impaired gas exchange (bc less alv walls so decrease SA)

Most patients have combined disease

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6
Q

COPD

  • What are the two ways that causes obstruction of airflow?
  • What is it triggered by?
A
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7
Q

Sympathetic Nervous system - Beta receptors
* Found where?
* What is the normal physiology of beta receptors?
* What are the two types of beta receptors?

A
  • Found on multiple different target organs
  • Normal physiology: norepinephrine and epinephrine stimulate beta receptors during a flight or fight situation
  • Beta-1 and beta-2 receptors
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8
Q

Where is beta 1 receptors?

A

Heart

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9
Q

What happens when you stimulate beta 1?

A
  • Increase HR (conduction) = Increased blood pressure
  • Increased contractility = Increased SV=increase CO = Increase BP

CO=SV x HR
BP=CO x SVR

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10
Q

What happens when beta 1 is blocked?

A
  • Decrease HR and contractility
  • Decrease oxygen demand
  • Decrease blood pressure
  • Decrease conduction effects

CO=SV x HR
BP=CO x SVR

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11
Q

Where are beta 2 receptors located?

A

lungs

two lungs

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12
Q

What happens when you stimulate beta 2 receptors?

A

Bronchodilation

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13
Q

What happens when you block the beta 2 receptors?

A

Bronchoconstriction

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14
Q

Beta-2 agonists
* Bind to what? where?
* What is the primary effect (what activates, increases, decreases and happens)?

A

Bind to beta-2 receptors in the lungs

Primary Effect:
* Activates adenylyl cyclase
* Increase cAMP production and smooth muscle relaxation
* Decrease calcium release
* Decrease contraction of smooth muscle in airway
* Bronchodilation

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15
Q

Beta-2 agonists
* What is the secondary effects? (stimulates, decreases)

A
  • Stimulate mast cells to decrease inflammatory mediators: Leukotrienes, prostaglandins
  • Decrease inflammation, swelling, irritation
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16
Q

What are the overall effects of beta 2 receptors?

A
  • Bronchodilation
  • Increase bronchiole diameter
  • Increased oxygen delivery to lungs
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17
Q

What are the Short Acting (SABAs) drugs? (3)

A
  • Albuterol - inhaled
  • Levalbuterol - inhaled
  • Terbutaline – IV / SC

LAT

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18
Q

Short Acting (SABAs)
* What is the onset?
* What is the duration?
* What type of therapy? ⭐️

A
  • Onset: 2 to 5 minutes
  • Duration: 2 to 4 hours
  • Rescue therapy
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19
Q

Long Acting (LABAs)
* What are the drugs? (5)

A
  • Salmeterol
  • Formoterol
  • Arformoterol
  • Indacaterol
  • Olodaterol

I FASO

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20
Q

Long Acting (LABAs)
* What is the onset?
* What is the duration?
* What type of therapy?

A
  • Onset: 15 to 30 minutes
  • Duration: 12 hours
  • Controller therapy-> schedule basis even when no sxs
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21
Q

Albuterol:
* What are the two dosage forms?
* What are the usualy dose range for mild symtom control (both forms)?
* What is the usual dose range for exacerbations (both forms)?

A
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22
Q

Levalbuterol:
* What are the two dosage forms?
* What is the usual dose range for mild symotoms control?
* What is not recommended for?

A
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23
Q

A word about levalbuterol

  • What is the mixture of albuterol?
  • What is the mixture of levalbuterol? When was it approved by FDA?
A
  • Albuterol = 1:1 mixture of the R and S albuterol enantiomers (mirror images)
  • Levalbuterol = R-enantiomer only->More active enantiomer
    * 1999
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24
Q

Levalbuterol:
* Marketed as what?
* What is the problem?
* What is the bottom line?

A
  • Marketed STRONGLY for equal efficacy with less adverse effects
  • Problem: $$$$
  • Bottom line: equivalent doses = equivalent efficacy = equivalent adverse effects
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25
Q

LABA – asthma related deaths

When do you see LABA-asthma related deaths?
* What is it associated with?
* Monotherapy contraindicated for what?
* Not used for what?

A

LABAs associated with increased asthma-related deaths when NOT used in combination with inhaled corticosteroids (ICS)
* Associated with lethal arrythmias
* Monotherapy contraindicated for asthma (not COPD)
* NOT used for rescue therapy

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26
Q

LABA
* Available as what?

A

Available as combination products with inhaled corticosteroids and long-acting antimuscarinics (LAMAs)

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27
Q

What are the Beta 2 adverse effects?

A

Secondary to beta-1 and beta-2 stimulation
* Tachycardia
* Palpitations
* Tremors
* Nervousness
* Dizziness
* Hyperactivity
* Insomnia
* Headache
* Decreased potassium

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28
Q

Parasympathetic nervous system (PSN) –muscarinic receptors
* Where are the different receptors?

A

Receptors found in brain (M1), heart (M2), smooth muscles (M3)

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29
Q

Parasympathetic nervous system (PSN) – muscarinic receptors
* What is the normal airway pathophysiology?

A
  • Acetylcholine is released during rest and digest times
  • Binds to muscarinic M3 receptors causing physiologic smooth muscle contraction
  • Decreases airway diameter
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30
Q

Parasympathetic nervous system (PSN) – muscarinic receptors
* What is the hypothesis?

A

Hypothesis: upregulation of PSN involved in the underlying pathophysiology of asthma

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31
Q

Muscarinic antagonists
* What do they bind to?
* What does it prevent (2)?
* Less effective and more effective for what diseases?

A
  • Bind to muscarinic M3 receptors located in airways
  • Prevents binding of acetylcholine
  • Prevents vasoconstriction
  • Less effective for asthma
  • More effective for COPD
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32
Q
  • What is the short acting muscarinic anatagonists?
  • What is the onset and duration?
A
  • Ipratropium
  • Onset: 15 minutes
  • Duration: 4 to 8 hours
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33
Q
  • What are the long acting muscarinic antagonist?
  • What is the onset and duration?
  • What are the other long acting LAMAs?
A
  • Tiotropium MC
  • Onset: 15 minutes
  • Duration: 24 hours
  • Others: Umeclidinium, Aclidinium, Glycopyrronium, Revefenacin
34
Q

What are the adverse effects of muscarinic antagonists? What is a CL?

A

Adverse effects:
* Minimal systemic absorption – few adverse effects

Anticholinergic
* Dry mouth (MC)
* Dizziness
* Headache
* Cough

CI: narrow angle glaucoma

Past question on anticholinergic SE: Mydriasis

35
Q

Ipratropium:
* What are the dosage forms (2)?
* What are the dose ranges for maintenance use?
* What are the dose ranges for exacerbations?

A
36
Q

Tiotropium:
* What are the dosage forms?
* What is the dose range for maintenance use?
* What is not recommended?

A
37
Q

Leukotriene (LT) antagonists
* What is the normal leukotriene pathophysiology?

A
  • Bind to LT receptors on bronchial smooth muscle and cause bronchoconstriction
    * LTC4, LTD4, LTE4 strongest bronchoconstrictors
  • Bind to receptors on mucous glands to increase mucous production
38
Q
A
39
Q

What are the different leukotriene antagonists?

A
  • Leukotriene receptor antagonists
  • Leukotriene synthesis inhibitors
40
Q

Leukotriene receptor antagonists
* What is the MOA?
* What are drug names? (route, used as what, Best for what?

A
41
Q

Leukotriene receptor antagonists: Montelukast, zafirlukast
* What are the adverse effects?

A
42
Q

Leukotriene synthesis inhibitor
* What is the MOA?
* What is the drug name? (what is the route, used for, best for?)

A
43
Q

What is the adverse effects of leukotriene synthesis inhibitor, zileuton?

A
  • Hepatotoxicity
  • CYP34A inhibitor
44
Q

Leukotriene antagonists- Montelukast
* What is the adult dose?
* What is the pediatric dose?
* What are the warnings?

A
45
Q

What are the warnings for zarfirlukast and zileuton?

A
46
Q

methylxanthines- theophylline
* What is the MOA?

A

Non-selective phosphodiesterase inhibition in bronchial smooth muscles
* Inhibits cAMP break down
* Vasodilation

Inhibits adenosine receptors
* Smooth muscle relaxation

47
Q

methylxanthines- theophylline
* What type of agent?
* Narrow or wide therapeutic index?
* Requires what?

A
  • Oral agent
  • Narrow therapeutic index
  • Requires therapeutic drug monitoring
48
Q

What are the ADRs of methylxanthines (Theophylline)?

A
  • Nausea
  • Arrhythmias and seizures
  • Metabolized by CYP450 enzymes
49
Q

Adenosine
* What is the normal physiologic effects (4)?
* What happens when there is inhibition of adenosine?

A
50
Q

METHYLXANTHINES- Roflumilast:
* What is the MOA? (hint: enxyme inhibitor and decrease pro-inflam mediators)

A

Selective PDE4 enzyme inhibitor (lung)
* Increased cAMP concentration
* Bronchodilation
Decreases pro-inflammatory mediators
* Suppression of cytokine release
* Inhibition of neutrophil infiltration
* Attenuates pulmonary remodeling and mucociliary malfunction

oral tables

51
Q

Methylxanthines-Roflumilast
* What are the adverse reactions?(7)

A
52
Q

Corticosteroids
1. Enter what? What does it inhibit
2. What does it decrease the synthesis of?
3. Down regulate what?
4. Inhibit what?
5. Decrease the production of what?
6. What does it further decrease?

A
53
Q

Explain how inhale corticosteroids work in terms of absorption, local/systemic effects?

A
54
Q

Inhaled Corticosteroids (ICS)
* What do you want?

A

Localized action and decreased systemic side effects
* Do not want systemic

55
Q

Fill in for how much medicine is deposited in lungs:

Fluticasone
* F. furoate (Ellipta) -
* F. propionate (Flovent) –

Budesonide -
Beclomethasone –
Mometasone –

A

Fluticasone
* F. furoate (Ellipta) - 80%*
* F. propionate (Flovent) – 20%*

Budesonide - 5 to 30%*
Beclomethasone – 50 to 60%*
Mometasone – 11%*

Higher the number= increase systemic issues

56
Q

Local adverse effects of ICS:
* What does it depend on?
* What are the SE? (3)

A
57
Q

What are the systemic adverse effects of ICS? (4)

A
58
Q

Measures to reduce ICS systemic effects

  • What should you step down to?
  • Optimize what? (2)
  • What does the pt need to do after each dose?
  • What should you add?
  • Maximize what?
  • Avoid what?
A
  • Step down to lowest possible dose
  • Optimize compliance
  • Optimize delivery – spacer devices
  • Rinse and spit after each use
  • Add LABA for steroid sparing per guidelines
  • Maximize nonpharmacologic therapy
  • Avoid drug interactions
59
Q

Systemic corticosteroids
* What is it severed for? (3)

A
  • Asthma / COPD exacerbations
  • Severe disease not controlled by other agents
  • Lowest dose for shortest interval
60
Q

Systemic corticosteroids:
* What are the short term adverse effects?(8)

A
61
Q

What is a common combo to increase pt compliance?

A

LABA/ICS combo

62
Q

Metered Dose Inhalers (MDI)
* What type of inhalers?
* What surrounds it?
* What does it require?
* What is recommended for ALL patients?
* Improves what?
* What is it avaiable for?

A
  • Aerosol inhalers
  • Canister inside plastic case
  • Require good technique and coordination
  • Spacers recommended for ALL patients
  • Improves lung deposition
  • Available for all inhaled medication types
63
Q

Spacers
* What does it increase?
* What does it decrease?
* Easier or harder?
* Help who?
* Technique depends on what?

A
  • Increase lung deposition up to 50% (increase systemic effects)
  • Decrease oral deposition (decrease candida infections)
  • Easier to use when severely symptomatic
  • Help young children use MDIs
  • Technique depends on patient age and spacer type (mask vs mouth piece)
64
Q

Dry powder inhalers
* Deliver medication where?
* No what?
* What does it require?
* What is not needed?
* What does technique include?
* _ tracker

A
  • Deliver medication directly into lungs
  • No propellant (Safe for environment)
  • Breath actuated and require minimal hand-lung coordination (follow instructions+ deep breath)
  • No spacer required (easy)
  • Technique includes deep quick breath
  • Inhaler tracker

LONG ACTING

65
Q

What are the disadvantages of dry powder inhalers (3)?

A
  • Not for small children (age varies)
  • Not for patients with decreased inspiratory effort
  • Susceptible to humidity (cause clumping)
66
Q

What are the examples of dry powder inhalers?

A

Turbuhalers, Accuhalers, Ellipta inhaler

67
Q

Dry powder capsule inhalers
* What are they?
* Same technique as what?
* Requires what?
* Less susceptible to what?

A
  • Inhalant capsules or cartridges
  • Same technique as DPI
  • Requires capsule loading prior to each dose
  • Less susceptible to humidity
68
Q

Soft mist inhaler (Respimat)
* How does it work?
* What is needed for proper use?
* What id not required?
* What is a pro?

A
  • Liquid medication converted to a fine mist which is inhaled
  • Some coordination required for proper use
  • No spacer required
  • Compact, easy to carry
69
Q

Soft mist inhaler (Respimat)
* How does it compare to an MDI?
* What is required?

A
  • Less oral deposition compared to an MDI
  • Some strength and coordination required to assemble
70
Q

Which inhaler requires assemble?

A

Soft mist inhaler (Respimat)

71
Q

Nebulizers
* What are the pros? (3)

A
  • No coordination required (just breathing in)
  • Ideal for patients who cannot use an inhaler (used in elderly dt decrease dexterity)
  • May offer benefit during severe exacerbation of asthma or COPD
72
Q

Nebulizers
* what are the cons? (6)

A
  • Time to set up
  • Time to deliver medications
  • Not as portable
  • Requires energy source
  • Cost
  • Limited medications
73
Q

Mast cell stabilizers
* What is the MOA?

A

Stabilize the mast cell membrane and inhibit the release of inflammatory mediators
* Prostaglandins and leukotrienes

74
Q

Mast cell stabilizers
* What are the medications?
* how does it work?
* What is it used for?
* Inferior to what?

A
  • Nedocromil / cromolyn
  • Inhaled; work locally on lung tissues
  • Use: long-term prophylaxis
  • Inferior to ICS; use uncommon

Safe / well tolerated

75
Q

What drug is Anti-IgE antibody?

A

Omalizumab (Xolair)

76
Q

Omalizumab (Xolair)
* Monoclonal anti-IgE antibody approved for what?
* What is the MOA?
* What is does that result in?
* What does it decrease in 8-12 weeks?

A
  • Monoclonal anti-IgE antibody approved for use in asthma not controlled by inhaled or systemic corticosteroids
  • Binds to the Fc portion of IgE preventing stimulation of Fc€R1receptors on mast cells and basophils
  • Results in decreased release of inflammatory mediators when exposed to an allergen
  • Decreases expression of Fc€R1 receptors on submucosal mast cells (8-12 weeks)
77
Q

Omalizumab
* What is the dose determined by?
* What is an example?

A

Determined by baseline serum IgE levels and weight

EX: Pretreatment IgE ≥ 30 to 100 units/mL
* 30 to 90 kg: 150 mg SQ Q 4weeks
* > 90 kg: 300 mg SQ Q 4 weeks

78
Q

What are the adverse effects of Omalizumab? (3)

A
  • Increased risk of infection
  • Pain at injection site
  • Limited by cost
79
Q

Anti-IL5
* What is the MOA?

A
  • Monoclonal antibody that inhibits binding of IL5 to eosinophils
  • Prevents eosinophil differentiation and activation
80
Q

Anti-IL5
* What are the two meds that reduce eosinophil survival?
* What is the route?
* Indicated for what?
* Limited by what?

A
  • Reduces eosinophil survival
    * Mepolizumab (Nucala)
    * Reslizumab (Cinqair)
  • SC injection
  • Indicated for severe asthma
  • Limited by cost
81
Q

Anti-IL4
* What is the MOA?

A
  • Monoclonal antibody that binds and inhibits the IL-4α receptor
  • Blocks IL-4 and IL-13 signaling; prevents cytokine release
  • Decreases IgE synthesis
82
Q

Anti-IL4
* What is the drug name?
* What is the route?
* Decreases what?
* _ sparing
* Limited by what?

A

Dupilumab (Dupixent)
* SC administration
* Decreases asthma exacerbation rates by 50%
* Steroid sparing
* Limited by cost

Pharmacology (14 decks)

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