Block 1 - Asthma + COPD Pharmacology Flashcards

1
Q

What are examples of the relievers?

A
  1. SABA
  2. Systemic steroids
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2
Q

What are SABAs used for?

A

Relieves acute symptoms associated with asthma or COPD (rescue)

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3
Q

What are systemic steroids used for?

A

for moderate to severe acute exacerbations, but can be used for severe asthma as controller

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4
Q

Why are nonselective sympathomimetic bronchodilators not used has often for exacerbations?

A

Contains a, b1, and b2 activity leading to numerous ADRs (injection or nebulizer)

Undergoes COMT metabolism

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5
Q

What are examples of b nonselective?

A

isoproterenol (isuprel)

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6
Q

List some isoproterenol (isuprel) characteristics?

A
  1. IV prep only
  2. Good for bronchial relaxation but cardiac effects due to b1 activity
  3. Positive chronotropic and inotropic actions on heart
  4. Primarily for cardio stimulatory effects
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7
Q

What do B2-agonists achieve?

A
  1. Relaxes bronchial airways smooth muscle directly and by raising cAMP that inhibits contraction
  2. Stabilizes mast cells by inhibiting mediators suppressing parasympathetic ganglionic activity
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8
Q

What is the difference between nonselective b and selective b2 agonists?

A

Non: cardiac stimulation, causing palpitations, tachycardia, headache, flushed skin
Sel: limits cardiac stimulation but not absolute selectivity, increases HR with increasing dose

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9
Q

What are examples of SABAs?

A
  1. Albuterol (Proventil, Ventolin)
  2. Levalbuterol (Xopenex)
  3. Terbuline Sulfate
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10
Q

What are the ADRs of b2 agonists (SABA)?

A

Albuterol (Ventolin, Proventil)
Levalbuterol (Xopenex)

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11
Q

What is the relations between albuterol and levalbuterol?

A

Albuterol: GOLD standard, racemic mixture, oral and inhalation
Levalbuterol: R enantiomer, inhaler and nebulizer

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12
Q

What is the GOLD standard b agonist?

A

Albuterol (Ventolin, Proventil)

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13
Q

What are the benefits of using SABA (albuterol and levalbuterol)?

A
  1. Relaxes bronchial airways
  2. 2 min onset
  3. Inhaled med -> enhanced therapy -> rapid onset with fewer ADRs
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14
Q

What are the disadvantages of using SABA (albuterol and levalbuterol)?

A
  1. > 1 canister/month means inadequate control of disease
  2. PRN not for chronic use
  3. Can have CV effect, fine muscle tremors, anxiety, restlessness, tachyphylaxis
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15
Q

In what occasions would you use terbutaline sulfate instead of albuterol/levalbuterol?

A
  1. status asthaticus
  2. tocolysis (uterine contraction)
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16
Q

What are the categories of controller therapies?

A
  1. Anti inflammatory medications
  2. Long acting bronchodilators
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17
Q

What are categories of anti inflammatory meds?

A
  1. inhaled glucocorticosteroids
  2. oral glucocorticoids
  3. leukotriene receptor antagonists
  4. Cromolyn
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18
Q

What are categories of long acting bronchodilators?

A
  1. LABAs
  2. Ipratropium
  3. Tiotropium
  4. Theophylline
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19
Q

What are the benefits of using ICS?

A
  1. preferred treatment alone or in combo for all persistent asthma
  2. potent and safe
  3. reduces asthma symptoms
  4. reduces dependence on SABAs
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20
Q

What is the MOA for ICS?

A
  1. Suppresses IL and CK
  2. Reduces eosinophil infiltration and function
  3. Inhibits macrophages and release of the chemical mediators of inflammation
  4. Increases B2 receptors
  5. Binds to intracellular GCR to regulate gene transcription within target cells
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21
Q

What are the main ICS?

A
  1. Budesonide (Pulmicort)
  2. Ciclesonide (Alvesco)
  3. Mometasone (Asmanex Twisthaler)
  4. Beclomethasone diproprionate (Beclovent, Vanceril)
  5. Fluticasone propionate (Flonase)
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22
Q

Why is fluticasone propionate a good ICS?

A

Drug undergoes rapid metabolism where derivative has 1/2000 affinity for GR than FP overcoming potential ADRS

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23
Q

What are the physiological effects of GC?

A
  1. Regulates carb, protein, and lipid metabolism
  2. Maintenance of fluid and electrolyte balance
  3. Preservation of normal function of systems
  4. Preservation of homeostasis
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24
Q

What are examples of systemic steroids?

A

Prednisone or Prednisolone

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25
Q

When would you prescribe someone a systemic steroid?

A
  1. Rescuer for acute asthma
  2. Severe persistant asthma that is uncontrolled (chronic use)
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26
Q

What are the side effects of ICS?

A
  1. Deposition in mouth and throat may promote oral candidiasis (rinse mouth after use)
  2. Mild reversible increases in glucose, decreased potassium, fluid retention, and HTN
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27
Q

What are the side effect of short term systemic steroid use?

A

Reversible increases in glucose, decreased potassium, fluid retention, and HTN

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28
Q

What are the side effect of long term systemic steroid use?

A
  1. growth and immune suppression
  2. iatrogenic Addision’s syndrome (must taper)
  3. Iatrogenic cushing syndrome
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29
Q

What are the symptoms of iatrogenic cushing syndrome?

A
  1. lipid tissue redistribution
  2. fragile skin and easy bruising
  3. Mask of infection
  4. Mental
  5. metabolic disturbances (hyperglycemia, steroid diabetes, osteoporosis, water and salt retention, potassium wasting)
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30
Q

What is the cause and effects of secondary adrenal insufficiency?

A
  1. Rapid withdrawn from exogenous steroids due to chronic inhibitor of AcTH release in pituitary

Results:
1. Decrease in ACTH
2. Weakness and fatigue
3. Addisonian crisis
4. Hypoglycemia
5. Hypotension

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31
Q

What are examples of LABAs for Asthma and COPD?

A

Salmeterol (Serevent)
Formoterol (Foradil)
Arformoterol (Brovana)

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32
Q

What is the onset of salmeterol?

A

15-30 minutes

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33
Q

What should be prescribed in concurrence with LABA?

A

ICS

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34
Q

Why should are shouldn’t Salmeterol be used as a resume inhaler?

A
  1. Not PRN
  2. Slow onset of action 15-30 min
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35
Q

What are the combo products with salmeterol?

A

With fluticasone as Advair diskus or HFA

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36
Q

What are the benefits of using formoterol and arformoterol?

A
  1. Onset is minutes
  2. Effective over nocturnal asthma
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37
Q

What are the combos with formoterol or arformoterol?

A
  1. Budesonide (symbicort)
  2. Mometasone (Dulera)
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38
Q

What are the ultra labas and what are they primarily used for?

A

Treatment for COPD but some are approved for asthma

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39
Q

What ultra labas are approved for asthma?

A

Vilanterol + Fluticasone (Breo Ellipta)
Vilanterol + umeclidinium + fluticasone (Trilogy)

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40
Q

What do antimuscarinics mainly treat?

A

COPD or serve persistant asthma

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41
Q

Describe the MOA of antimuscarinics?

A
  1. ACh causes bronchoconstriction (M3 receptors) and an increase in secretion predominately in large and medium sized airways
    2.
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42
Q

Why are antimuscarinics used for COPD?

A
  1. Airways are narrow in COPD therefore the vagal cholinergic tone has a greater effect on airway resistance
    2, Muscarinic receptor antagonists block the parasympathetic cholinergic induced bronchoconstriction and reduces mucus hyper secretion
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43
Q

What are examples of antimuscarinics for COPD?

A
  1. Ipratropium
  2. Tiotropium
  3. Aclidinium
  4. Umeclidinium
  5. Glycopyrrolate
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44
Q

Which antimuscarinics are for bronchospasm?

A
  1. Ipratropium (Atrovent)
  2. Tiotropium (Spiriva)
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45
Q

Why would we use ipratropium for COPD?

A
  1. quat amine ensures poor absorption and fewer ADRs
  2. Doesn’t impede mucociliary clearance of mucous, avoiding accumulation
    3.
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46
Q

Why is tiotropium a little better than ipatropium

A
  1. Longer duration, QD
  2. Selectivity for M1 and M3 receptors
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47
Q

What are dosages of spiriva?

A

Handihaler COPD: 18mcg QD
Respimat COPD: 2.5 mcg QD
Respimat Asthma: 1.25 mcg QD

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48
Q

How does Aclidinium BR (tudorza Pressair) differ from ipatropium or tiotropium?

A
  1. Muscarininc antagonist for COPD management
  2. Antagonizes M2 and 3 receptors
  3. rapidly hydrolyzed in plasma leading to lower systemic exposure and reduced ADRs
  4. Used twice daily
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49
Q

What are common ADRS with antimuscarinics?

A
  1. Dry mouth (inhaled)
  2. Pharyngitis (inhaled)
  3. Gastroenteritis (systemic or swallowing)
  4. Headache (systemic or swallowing)
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50
Q

Who are contraindicated when using antimuscarinics?

A

BPH, urinary retention, closed angle glaucoma

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51
Q

What are the delivery options of asthma meds?

A
  1. Dry powder inhaler
  2. Metered dose inhalers
  3. Nebulizers
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52
Q

What is the most effective particle size for asthma inhalers?

A

1-5 µm

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53
Q

What are spacers?

A

help patients who have difficulty with technique, thus increasing response and reducing potential side effects

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54
Q

What are nebulizers?

A

uses compressed air machine to deliver medicine as an inhaled mist

good for younger children, older adults, are severe asthma episodes

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55
Q

What is the MAO of leukotrienes?

A
  1. Increase vascular permeabiliuty
  2. Increase bronchiolar smooth muscle contraction
  3. Increase mucus secretions
  4. Augment neutrophils and eosinophils migration
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56
Q

How are leukotrienes synthesized?

A
  1. Lipoxygenase Pathway produces the leukotrienes
  2. Leukotriene inflame airways in asthma causing anaphylactic shock
    3, Cysteinyl leukotriene receptors CysLT1 and CysLT2 are present on mast cells, eosinophil, and endothelial cells.
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57
Q

What is the MAO of zileuton (zyflo)?

A

5-lipoxygenase (enzyme) inhibitor

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58
Q

What are warning that is associated with zyflo?

A

Inhibits metabolism of theophylline and warfarin, requires montioring

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59
Q

What are the leukotriene receptor antagonists?

A

Zafirlukast (Accolate)
Montelukast (Singulair)

60
Q

What is the MAO of leukotriene receptor antagonist?

A

Inhibits the CysLT1 Leukotriene receptor reducing albuterol use

Attenuates the late response to inhaled allergen and post-allergen induced bronchospasms

61
Q

What is the warnings associated with leukotriene receptor antagonists?

A

Increases warfarin half-life and must be monitored

Increased risk of serious neuropsychiatric events, including suicide and suicide attempts seen with use of montelukast

62
Q

What is the treatment for managing atopy?

A

Omalizumab (Xolair)

63
Q

What is the MOA of omalizumab (xolair)

A
  1. Forms complexes with free IgE, inhibiting IgE binding to mast cells and basophils, decreasing mediator release
  2. Down regulates high-affinity IgE receptor (FcεRI) expression on mast cells, dendritic cells, and basophils
  3. Inhibits activation of IgE already bound to mast cells, preventing degranulation
  4. Attenuates early and late phase airway responses to allergen and suppresses accumulation of eosinophils in the airways
64
Q

What is the dosing and pricing of omalizumab (xolair)?

A

SC 2-4 weeks
Cost is dose dependent and reserved for patients with atopy

65
Q

What biologics are used for eosinophilic asthma?

A

Benralizumab (Fasenra)
Mepolizumab (Nucala)
Reslizumab (Cinqair)

66
Q

What are eosinophils and its relationship to asthma?

A

Key effector cell in the pathogenesis of allergic inflammation

67
Q

What is the function of IL5?

A

regulates proliferation, maturation, migration, and effector functions of eosinophils

68
Q

What biologic targets eosinophils’ receptor?

A

Benralizumab (Fasenra)

69
Q

What biologic targets IL5?

A

Mepolizumab (Nucala)
Reslizumab (Cinqair)

70
Q

What biologics are used for severe prednisone dependent eosinophilic asthma?

A

Mepolizumab (Nucala)
Reslizumab (Cinqair)

71
Q

What are the benefits of using mepolizumab or reslizumab?

A
  1. Reduce 50% of exacerbations
  2. Improves lung function
  3. Reduces eosinophils
  4. No severe side effects
72
Q

What is the MAO of benralizumab (fasenra)?

A
  1. It binds with high specificity to interleukin-5 receptor-α on eosinophils and basophils
  2. Binds with increased affinity to Fc receptors on immune effector cells through the Fc region of benralizumab
  3. This results in increased antibody-dependent cell-mediated cytotoxicity and death of eosinophils and basophils via apoptosis (programmed cell death)
73
Q

What is the general effectiveness ranking of anti-IL5s?

A

Mepolizumab > Reslizumab > Benralizumab

74
Q

What biologic targets IL4Ra?

A

Dupilumab (Dupixent):

75
Q

What is the MOA of dupilumab (dupixent)?

A

Fully human monoclonal antibody that targets IL4Ra receptors for IL4 and 13

76
Q

What are examples of ultra LABAs?

A
  1. Vilanterol
  2. Indacaterol (Arcata Neohaler)
  3. Olodaterol (Striverdi Respimat)
77
Q

Why doesn’t antimuscarinic have no effect on pulmonary vessels?

A

Pulmonary vessels are nor innervated

78
Q

Why is inhalation an effective delivery method for asthma?

A
  1. localized site of action
  2. rapid onset
  3. reduces systemic absorption and ADRs
79
Q

What is TSLP?

A

An epithelial cytokine that is at the top of the inflammatory cascade that drive immune response using APC (dendritic cells) implicated in asthma

80
Q

What drug blocks TSLP?

A

Tezepelumab (Tezspire)

81
Q

How is tezepelumab benefit patients with severe asthma?

A
  1. blocks TSLP from binging to APCs
  2. Allows fewer exacerbations, lung function, improving health quality
82
Q

Describe the MOAs of biologics for severe asthma

A
  1. TSLP inhibition (Tezepelumab)
  2. IL4 and 13 inhibition (Dupilumab)
  3. IgE suppression (Omalizumab)
  4. IL5 inhibition (Mepolizumab, Reslizumab, Benralizumab)
83
Q

Why is theophylline not 1st line therapy for asthma?

A

Other meds are more effective, mild to moderate bronchodilation and anti- inflammatory, narrow TI

84
Q

Describe the levels of theophylline toxicity?

A

<15mcg/mL: uncommon ADRs
>20mcg/mL: n/v, diarrhea, ha, insomnia, CNS effects
>35 mcg/mL: hyperglycemia, hypotension, arrhythmias, tacky, seizures, death

85
Q

What are some counseling points for xanthine bronchodilators?

A
  1. Don’t interchange brands w/o consulting physician
  2. smoking may alter and lower blood levels
  3. Don’t crush or chew
86
Q

What are the main combos for asthma?

A
  1. Advair Diskus (fluticasone + salmeterol)
  2. Symbicort - budesonide + formoterol
  3. Dulera - mometasone + formoterol
  4. Breo Ellipta - fluticasone and vilanterol
  5. Trelegy Ellipta - fluticasone, umeclidinium and vilanterol
  6. Combivent - albuterol + ipratropium
  7. DuoNeb - ipratripium + albuterol
  8. Stiolto Respimat - tiotropium + olodaterol
  9. Bevespi aerospace - glycopyrrolate + formoterol
  10. utibron neohaler - glycopyrrolate + indaceterol
  11. anoro elliptia - umeclidinium + vilanterol
87
Q

What are the benefits of having asthma combo meds?

A

Increased therapeutic results in general

88
Q

What is status asthmaticus?

A

Failure of outpatient therapies, PFR=<60%

89
Q

What are the symptoms of status asthmaticus?

A
  1. SOB
  2. Chest tightness
  3. Anxious
  4. W/C
  5. Tachypnea
  6. Tachycardia
  7. Cyanosis
90
Q

What are the labs for status asthmaticus?

A

PEF: <40%
FEV1 <40%
O2: <90%
Altered blood gases

91
Q

What are the treatments for status asthmaticus?

A
  1. O2
  2. SABA (albuterol or terbutaline)
  3. Oral or systemic IV CS
92
Q

What are the key indicators of COPD?

A
  1. Chronic cough
  2. Chronic sputum
  3. Risk factors (smoking)
  4. Acute bronchitis
  5. Dyspnea
93
Q

What is the treatment goals for COPD?

A
  1. Reduce symptoms (improve lung function)
  2. Reduce risks (limit exacerbations, prevent progression, reduce morbidity and mortality)
94
Q

What are inhaler options for COPD?

A
  1. SA AND LA MA
  2. SABA
  3. LABA
95
Q

What are combo options for COPD?

A
  1. SABA + ANTICHOLINERGICS
  2. LABA, LAMA, ICS
96
Q

What are some bronchodilators used for COPD?

A
  1. Antimuscarinics (Ipratropium, tiotropium)
  2. SABA (Albuterol)
  3. LABA (Salmeterol, formetarol)
  4. PDE4i (Roflumilast)
  5. Methylxanthines (Theophylline)
97
Q

Why are ICS not used for COPD?

A

COPD is not an immunological response and experience no inflammation

98
Q

What is Group A COPD patients prescribed?

A

Bronchodilators

99
Q

What is Group D COPD patients prescribed?

A

LABA, LAMA, ICS

100
Q

When would PDE4i be prescribed?

A

Add on for chronic bronchitis and severe airflow restrictions

101
Q

What are examples of ultra LABAs?

A
  1. Vilanterol
  2. Indacaterol (Arcata Neohaler)
  3. Olodaterol (Striverdi Respimat)
102
Q

Why doesn’t antimuscarinic have no effect on pulmonary vessels?

A

Pulmonary vessels are nor innervated

103
Q

Why is inhalation an effective delivery method for asthma?

A
  1. localized site of action
  2. rapid onset
  3. reduces systemic absorption and ADRs
104
Q

What gives antimuscarinics poor systemic absorption?

A

Quat amine

104
Q

List the types of 2nd gen antihistamines?

A
  1. Piperazines (Cetiratize -Zyrtec)
  2. Piperidines
105
Q

What is Group B COPD patients prescribed?

A

LABA or LAMA

105
Q

List the types of 2nd gen antihistamines?

A
  1. Piperazines (Cetiratize -Zyrtec)
  2. Piperidines:
    Desloratidine (Clarinex)
    Fexofenadine (Allegra)
    Levocetirizine (Xyzal)
    Loratidine (CLaritin)
    Olopatadine (Patanol)
106
Q

What is Group C COPD patients prescribed?

A

LAMA

106
Q

List the types of 2nd gen antihistamines?

A
  1. Piperazines (Cetiratize -Zyrtec)
  2. Piperidines:
    Desloratidine (Clarinex)
    Fexofenadine (Allegra)
    Levocetirizine (Xyzal)
    Loratidine (CLaritin)
    Olopatadine (Patanol)
107
Q

What is the treatment options for moderate to severe COPD?

A

Require combo therapies, LAMA+LABA

107
Q

List the types of 2nd gen antihistamines?

A
  1. Piperazines (Cetiratize -Zyrtec)
  2. Piperidines:
    Desloratidine (Clarinex)
    Fexofenadine (Allegra)
    Levocetirizine (Xyzal)
    Loratidine (CLaritin)
    Olopatadine (Patanol)
108
Q

What are the therapeutic options for bronchodilators?

A

LAMA, LAMA+LABA (CAT>20), or ICS+LABA (if eosinophils≥300)

108
Q

List the types of 2nd gen antihistamines?

A
  1. Piperazines (Cetiratize -Zyrtec)
  2. Piperidines:
    Desloratidine (Clarinex)
    Fexofenadine (Allegra)
    Levocetirizine (Xyzal)
    Loratidine (CLaritin)
    Olopatadine (Patanol)
109
Q

What do you do with asthma+COPD overlap

A

ICS w/ LABA and/or LAMA
Never treat asthma alone w/o ICS
Start with LABA and/or LAMA w/o ICS

110
Q

What are the consequences of COPD exacerbations?

A
  1. Negative impact of life
  2. impact on lung function
  3. Increased economic cost
  4. Increased mortality
  5. Accelerated lung decline
111
Q

How do you manage COPD exacerbations?

A
  1. medical intervention
  2. SABA w/ or w/o SAMA
  3. Noninvasive intermittent positive pressure ventilation
  4. long term o2 use
112
Q

What are allergies?

A

Body producing IgE that binds to the allergen releasing histamines as an reaction

112
Q

List the types of 2nd gen antihistamines?

A
  1. Piperazines (Cetiratize -Zyrtec)
  2. Piperidines:
    Desloratidine (Clarinex)
    Fexofenadine (Allegra)
    Levocetirizine (Xyzal)
    Loratidine (CLaritin)
    Olopatadine (Patanol)
113
Q

What are the symptom of allergies?

A
  1. Itchy eyes
  2. Sneezing
  3. Runny nose
  4. Rashes
  5. tired
  6. Hives
114
Q

What are the signs of food allergies?

A
  1. Stomach cramp
  2. Vomiting
  3. Diarrhea
115
Q

What are the signs of insect allergies?

A
  1. Swelling
  2. Redness
  3. Pain
116
Q

What are the treatment options for allergic rhinitis?

A
  1. Avoid allergen
  2. Antihistamins
  3. Steroids
  4. Immunotherapy
117
Q

What is the MAO of antihistamine?

A

Competitive H1 receptor antagonist

118
Q

What are the therapeutic uses for antihistamines?

A

Allergies, insomnia, rash, nausea, vomiting

119
Q

Describe characterics of H1 receptors?
Location, type, effect, treatment, antagonist

A
120
Q

What are the characteristics of 1st gen antihistamine?

A
  1. More sedating due to CNS penetration
  2. Greater anticholinergic effect -> antiemetic
121
Q

What are examples of 1st gen H1 receptor antagonist

A
  1. Ethanolamines (Diphenhydramine - Benadryl)
  2. Alkylamines (Chropheniramine - Chlor-Trimeton)
  3. Piperazines (Hydroxyzine - Vistaril)
  4. Tricyclic (Promethazine - Phenergan)
122
Q
A
123
Q

How does 2nd gen antihistamine differ from 1st gen?

A
  1. Greater effect on peripheral H1 receptors and not central
  2. Charged so doesn’t cross the BBB
  3. Fewer anticholinergic actions and ADRs
124
Q

What are the systemic ADRs of INCS?

A
  1. Budesonide (Rhinocort)
  2. Ciclesonide (Omnaris)
  3. Beclomethasone (Beconase AQ)
  4. Triamcinolone (Nasocort)
  5. Mometasone (Nasonex)
  6. Fluticasone (Flonase)
125
Q

What are the characteristics of cromolyn sodium?

A
  1. Inhibits IgE mediator release of mast cells blocking Cl-
  2. Modulates eosinophilic recruitment
  3. Inhibits bronchospasm
126
Q

Why doesn’t antimuscarinic have no effect on pulmonary vessels?

A

Pulmonary vessels are nor innervated

127
Q

What are examples of ultra LABAs?

A
  1. Vilanterol
  2. Indacaterol (Arcata Neohaler)
  3. Olodaterol (Striverdi Respimat)
128
Q

Why is inhalation an effective delivery method for asthma?

A
  1. localized site of action
  2. rapid onset
  3. reduces systemic absorption and ADRs
129
Q

What are the risks of using combo ICS with LABA for COPD?

A

Increased risk of pneumonia

130
Q

What gives antimuscarinics poor systemic absorption?

A

Quat amine

131
Q

Describe the uses of GC for COPD?

A

Effects in COPD are significantly more modest compared to asthma

132
Q

When should you use start acting bronchodilators?

A

Albuterol, ipratropium: PRN

133
Q

When should you use long acting bronchodilators?

A
  1. Maintenance
134
Q

When should you consider ICS for COPD?

A
  1. ≥2 moderate exacerbations
  2. > 300 eosinophils
  3. Asthma concurrent
135
Q

When should you be against ICS for CODP?

A
  1. pneumonia events
  2. <100 eosinophils
  3. History of mycobacterial infection
136
Q

Whar is the MAO of Roflumilast (Daliresp)?

A
  1. PDE4 INHIBITOR
  2. Increases cAMP in lungs -> decreasing cell type activity associated with COPD
137
Q

What are the characteristics of Roflumilast?

A
  1. Not a direct bronchodilator
  2. Extensive metabolism of Phase 1 and 2 (conjugations) -> active metabolite
  3. Common ADRs
  4. 15-18% reduction of exacerbations
138
Q

What are the most common cause of COP exacerbations?

A
  1. viral Urti
  2. bronchitis
  3. air pollution
139
Q

What are the ADRs of antihistamines?

A
  1. Sedation
    2., Dizziness
  2. Tinnitus
  3. Blurred vision
  4. Euphoria
  5. Anxiety
  6. Insomnia
  7. Tremor
  8. N/v
  9. Dry mouth and cough
140
Q

What are the local ADRs of INCS?

A

1 Nasal burning, stinging
2. Sneezing
3. Throat irritation
4. Dry nose

141
Q

What are the systemic ADRs of INCS?

A

HA, n/v, dizziness