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Pharm Exam 5 -- Smooth Muscle, GI and OTC > Smooth Muscle (pt 1/4) Asthma > Flashcards

Smooth Muscle (pt 1/4) Asthma Flashcards

1
Q

What are the clinical characteristics of asthma?

A

-Small, inflamed internal lumen.
-Increased mucus production.
-Recurrent bouts of SOB, chest tightness, coughing and wheezing

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2
Q

What is the pathophysiology of Asthma?

A

-Widespread, reversible narrowing of the bronchial airways
-Significant bronchial responsiveness to inhaled stimuli

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3
Q

What is the pathology of Asthma?

A

-Lymphocytic and eosinophilic inflammation of the bronchial mucosa
-“Remodeling” of the bronchial mucosa: Hyperplasia of the cells of the airway walls
- Overproduction of mucus

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4
Q

Describe Mild Asthma

A

-Occasional
-Occurs on exposure to allergens or certain pollutants (pet dander)
-During exercise
-Triggered by viral URI

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5
Q

Describe Severe Asthma

A

-Frequent
-Associated with wheezing and dyspnea
-Often at night
-Chronic airway narrowing with chronic respiratory impairment
-Regular overproduction of mucus. End up on multi-agent treatments (PO and rescue)

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6
Q

Explain the effects of Volatile Agents on Asthma.

A

-1st exposure to gases can trigger an event and cause bronchoconstriction. Once gas circulates, goes to bloodstream, then we get bronchodilation.

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7
Q

T/F: Volatiles are irritants to lung tissue.

A

True, and effects are more profound in patients with irritated tissues (asthma, COPD).

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8
Q

Will Volatiles help in a true, complete bronchospasm?

A

If you aren’t moving air, volatiles won’t help.
1) Off of vent and bag them
2) Epi ?

If you can’t move air, deepening the gas may help but probably doesn’t.

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9
Q

In asthma, exposure to an allergen causes the synthesis of what?

A

IgE, which binds to Mast Cells in the airway mucosa.

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10
Q

What occurs on re-exposure to the allergen?

A

Antigen-antibody interaction on mast cell surfaces triggers release of mediators of anaphylaxis.

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11
Q

What are the mediators of anaphylaxis?

A

Histamine, tryptase, prostaglandin D2 (PGD2), leukotriene C4, and platelet-activating factor (PAF) = all inflammatory agents. Inflammation is occurring.

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12
Q

What do the mediators of anaphylaxis (histamine, PGD2, leukotriene) cause to happen in the body?

A

Contraction of the airway smooth muscle, causing the immediate fall in FEV1(25%)

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13
Q

Re-exposure to allergen also causes the synthesis and release of a variety of cytokines (cytokines are coming from mast cells and t-lymphocytes), such as?

A

-Interleukins 4 & 5
-granulocyte-macrophage colony-stimulating factor (GM-CSF)
-Tumor Necrosis Factor (TNF)
-Tissue Growth Factor (TGF)

Released from T-cells and mast cells

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14
Q

What do these cytokines do that are released on re-exposure to an allergen?

A

These cytokines in turn attract and activate eosinophils and neutrophils, which go on to create products that further the immune response.

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15
Q

What are the products created by cytokine attraction and activation of eosinophils and neutrophils?

A

-Eosinophil Catonic Protein (ECP)
-Major Basic Protein (MBP)
-proteases
-platelet-activating factor (PAF)

(Immune response)

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16
Q

What do the products of eosinophils and neutrophils (ECP, MBP, proteases, and PAF) cause?

A

These mediators cause the edema, mucus hypersecretion, smooth muscle contraction, and increase in bronchial reactivity (more intensive narrowing) associated with the late asthmatic response indicated by a second fall in FEV1 3-6 hours after the exposure.

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17
Q

What does increasing cAMP do in relation to Asthma?

A

Increases bronchodilation.

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18
Q

What two categories of drugs increase cAMP?

A

-Beta 2 Agonists
-PDE-Inhibitors (Theophylline or Aminophylline)

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19
Q

How do Beta 2 Agonists increase cAMP?

A

Increase the rate of synthesis of cAMP by adenylyl cyclase (AC)

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20
Q

How do Phosphodiesterase (PDE)-Inhibitors (Theophylline or Aminophylline) increase cAMP?

A

Interrupt the breakdown of cAMP (slow the rate of degredation). PDE is the enzyme that breaks down cAMP. Allows more to be available.

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21
Q

What is the other way that PDE-Inhibitors can decrease bronchoconstriction?

A

Theophylline (PDE-Is) also are Adenosine receptor inhibitors. (Adenosine receptors normally = bronchoconstriction). Inhibiting adenosine receptor promotes bronchodilation.

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22
Q

How does antagonization of M3 receptors in the lung tissue affect asthma?

A

-M3 receptors are in lung tissue
-Antagonizing M3 causes bronchodilation
-M3 normally = bronchoconstriction
-Use Muscarinic antagonists to alleviate bronchoconstriction

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23
Q

Explain the effects of Epinephrine and asthma.

A

-Can be given many different routes (IV, INH, SQ)
-Stimulates α & β1
-Problematic adverse effects: Tachycardia, Arrythmias, and Angina
-Useful in anaphylaxis
-Displaced by β2 selective agents in Asthma therapy

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24
Q

Explain the effects of Ephedrine and asthma.

A

-A sympathomimetic
-Compared to Epi: Longer DOA, oral availability, ⬆CNS effects, ⬇ potency
-Displaced by β2 selective agents in Asthma therapy

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25
Q

Explain the effects of Isoproteronol and Asthma.

A

-Potent bronchodilator
-1960s in the UK
-⬆ in asthma related mortality
-Attributed to cardiac arrhythmias from high dose inhaled isoproteronol

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26
Q

What are the long acting (12+ hrs) B2 agonists used in asthma treatment?

A

-Salmeterol
-Formeterol
-Indacaterol (COPD) only

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27
Q

Explain the effects of long acting B2 agonists on asthma.

A

-Highly lipid soluble
-Synergistic with corticosteroids
-No anti-inflammatory effects
-Cannot be used as monotherapy
-BBW for inc risk of death/near death from an asthma attack, especially in AAs.

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28
Q

What is the BBW associated with long-acting B2 agonists?

A

BBW for inc risk of death/near death from an asthma attack, especially in African Americans.

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29
Q

What kind of drug is Albuterol?

A

Beta 2 selective (not specific. Prefers B2)

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30
Q

What is the overall goal with the use of Albuterol in Asthma?

A

To relax airway smooth muscle and promote dilation.

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31
Q

What is the physiology behind the relaxing effects of Albuterol?

A

-Inhibits bronchoconstricting mediators from mast cells
-Inhibits microvascular leakage (decreasing edema)
-Increases mucociliary transport via increased ciliary activity (increases removal of mucus)
-Stimulates adenylyl cyclase, increasing cAMP

Interrupt the cascade of events to promote bronchodilation.

32
Q

What are the different routes of Albuterol?

A

PO, MDI, Nebulized

33
Q

What form of Albuterol is a larger molecule, so you can give a bigger dose?

A

Nebulized form is a larger molecule, can give a bigger dose than the MDI

34
Q

How long does the bronchodilation last from Albuterol?

A

Short-lived bronchodilation (DOA 3-4 hrs). May have to use multiple times/day

35
Q

What are the systemic effects associated with Albuterol?

A

-Increases shunt (perfusion without ventilation)
-Tachycardia (hits some B1s)
-Vasodilation (B2 mediated)
-Arrhythmias (B1)
-Tremors
-Can cause Hypokalemia (Activates Na/K Pump. Can be used in tx of HyperK+)

36
Q

Which method of delivery provides the best local effect on airway smooth muscle with the least systemic toxicity?

A

Inhalational Therapy

37
Q

What percentage of the total dose of INH therapy is deposited in the mouth or pharynx?

A

80-90%

38
Q

How is absorption in the bronchi increased with INH therapy?

A

Absorption in the bronchi is increased with slow full breath followed by 5 sec of breath holding
-Have to seal lips, breathe in, have to hold lungs to disperse it throughout lung tissues and get down deep in lungs.

39
Q

Describe the proper technique for use of a MDI.

A

Patients are supposed to exhale, place lips around MDI, draw tidal breath in, squeeze, and then hold breath.

40
Q

What drugs are the Methylxanthines?

A

-Theophylline
-Aminophylline
-Theobromine
-Caffeine

41
Q

Which methylxanthine is no longer popular due to:
1) safer INH Beta2 agonists & INH anti-inflammatory agents
2) Narrow therapeutic index - measured trough levels (decreases compliance)

A

Theophylline

42
Q

Which methylxanthine is less potent than theophylline and has a short 1/2 life?

A

Aminophylline

43
Q

What is the MOA of the Methylxanthines (-phylline drugs)

A

-PDE-Is: inc cAMP by decreasing its degradation. (dilation)
-Inhibiting PDE also decreases release of cytokines and chemokines, therefore decreasing immune cell activation
-Inhibition of cell surface adenosine receptors (relaxation)
-Enhancement of histone deacetylation (researching this - blocks inflammatory genes)

44
Q

What does inhibition of Cell Surface Adenosine receptors do?

A

-Relaxation of airway smooth muscle
-Inhibits histamine release

45
Q

What are the respiratory effects associated with the Methylxanthines?

A

-Bronchodilation
-Inhibit antigen induced release of histamine
-Inhibition of inflammatory response

46
Q

What are the CNS effects associated with the Methylxanthines?

A

-Mild cortical arousal
-⬆ alertness
-Deferral of fatigue
-Nervousness, anxiety
-Tremor & HA
-Medullary stimulation*
-Convulsions* & Death*

47
Q

What are the CV effects associated with the Methylxanthines?

A

-(+) Chronotropy = Tachycardia
-(+) Inotropy = ⬆BP, ⬆SVR, & ⬆CO
-Adenosine receptor antagonism
-⬆ in SNS catecholamine release
-⬆cAMP = ⬆ Ca2+
-Decrease blood viscosity
-Potential for arrhythmias

48
Q

What are the GI/GU/Endo effects associated with the Methylxanthines?

A

-Stimulate secretion of gastric acid
-Stimulate digestive enzymes
-Weak diuretics (not therapeutic)
-Anorexia, N/V, ABD pn

49
Q

What are the skeletal muscle effects associated with the Methylxanthines?

A

Improve contractility & reverse fatigue of the diaphragm in patients with COPD

50
Q

What are the toxic effects from high doses or ODs of Methylxanthines?

A

Medullary stimulation
Convulsions & Death

51
Q

Which methylxanthine is more effective on smooth muscle, and which is more effective on neural tissues?

A

Theophylline = smooth muscle
Caffeine = neural tissues

52
Q

What are the pharmacokinetics of Methylxanthines?

A

-Slightly water soluble
-Well absorbed
-Narrow therapeutic window
-Requires blood draws to monitor therapeutic levels
-⬆ provider workload
-Patient compliance issue
-Metabolized in the liver
-Plasma clearance varies
-PO/IV
-Tolerance does not develop
-Adverse effects (esp CNS) may limit the dosing
-Improves long-term control of asthma, When taken as the sole maintenance treatment, or When added to inhaled corticosteroids.

53
Q

What are the anti-muscarinics used in the treatment of Asthma?

A

-Ipatropium Bromine
-Atropine
-Tiotropium

54
Q

What is the MOA of anti-muscarinics used in the tx of asthma?

A

-Competitively inhibits Ach at the M3 of the ANS
-Blocks airway smooth muscle contraction
-Blocks the ⬆ of mucous secretion that occurs with vagal stimulation

55
Q

What is the overall effect of the use of anti-muscarinics in Asthma?

A

Bronchodilation

56
Q

What is unique about the Inhalational form of anti-muscarinics in the tx of asthma?

A

-Does NOT enter the CNS
-Poorly absorbed into the circulation
-Don’t have to worry about systemic SLUDGE effects (poorly absorbed into the circulation)
-Can be used if intolerant to B2 agonists
-Adjunct therapy for asthma exacerbation (used in combo therapy).
-Enhances effects of Albuterol in acute, severe attacks
-NOT an anti-inflammatory med.
-Blocks Smooth muscle contraction and mucus production only

57
Q

What are the 3 corticosteroids you need to know?

A

-Prednisone (PO/IV)
-Beclomethasone
-Budesonide

58
Q

What is the MOA for corticosteroids in Asthma?

A

-Broad, anti-inflammatory.
-Inhibit production of cytokines,
-Block lymphocytes, eosinophils, and mast cells from infiltrating the airways (!!)
-Block chemical mediators of asthma
-Doesn’t directly relax sm, but decreases bronchial reactivity. Not working on cAMP, but working on inflammatory immune response.
-Potentiates Beta agonists. Given in combo with Albuterol.

59
Q

What are the pharmacodynamics associated with the use of Corticosteroids?

A

-↓bronchial reactivity
-Effective only as long as they are taken
-↓ Contraction of the engorged vessels in the bronchial mucosa
-Taper oral doses slowly to avoid adrenal insufficiency
-Oropharyngeal candidiasis (thrush - risk with INH form. Use mouthwash)

Blocks swelling & immune response to increase lumen size.

60
Q

What are the effects associated with Corticosteroids?

A

-Systemic effects are worse in PO Form
-↓ the frequency of asthma exacerbations if taken regularly
-↓ airway reactivity & ↑ quality of life
-Severe adverse effects when taken chronically
-Reserved for urgent treatment
-INH/aerosols are the best way to avoid the adverse effects
-↑risk of cataracts & osteoporosis in adults with long term usage
-Slow the rate of growth in children

61
Q

What are Leukotrienes?

A

Mediators associated with bronchoconstriction.
-Antagonism = bronchodilation.

62
Q

What is the MOA of the Leukotriene-Receptor Antagonists (Montelukast aka Singulair)?

A

-LDT4 Receptor Antagonist
-Oral therapy for pts whose symptoms persist more than 2X a week or awaken from sleep by asthma more than 2X a month
-Widely used in the treatment of children with asthma in the US (age 6 and older)
-Improve asthma control
-Decrease exacerbations
-Once a day dosing (increased compliance)

PO is easier for kids than multiple INH doses/day.

63
Q

Use of ____ or more canisters of an inhaled B agonist per month is the marker of increased risk of asthma fatality.

A

2

64
Q

What are Beta 2 Agonists used for in the treatment of Asthma?

A

-Rescue inhaler
-Lone therapy for someone with mild asthma
-Supplementation required for severe asthma (corticosteroid)

IF….additional treatment is needed
-Symptoms require “rescue” therapy more than twice a week OR
-Nocturnal symptoms occur more than twice a month OR
-FEV1 is less than 80% predicted

65
Q

How is Theophylline used in the treatment of Asthma?

A

-Reserved for patients who are poorly controlled with inhaled anti-inflammatory agent (pulmicort) and PRN Beta2 Agonist (Albuterol)
-Aminophylline: safer profile.

66
Q

How are Anti-muscarinics (Ipratropium Bromide) used in the treatment of Asthma?

A

Largely used as an alternative for patients intolerant to Beta2 Agonists

67
Q

How are Corticosteroids used in the treatment of Asthma?

A

Inhaled corticosteroids are started IF:
-Significant airflow obstruction persists despite bronchodilator therapy (urgent)

In severe asthma, standard inhaled corticosteroid may not be enough
-Double the dose of corticosteroid?
OR combine with another drug:
-Theophylline
-Montelukast (Singulair)
-Long acting Beta2 receptor agonist

68
Q

What makes up a Combo Inhaler?

A

Corticosteroid + Long Acting B2 Agonist

69
Q

What are the advantages of Combo Inhalers?

A

-Convenient
-Effective: Prompt improvement in pulmonary function
-Decrease asthmatic exacerbations

70
Q

What are the disadvantages of Combo Inhalers?

A

-Mild-mod asthma should be treated with low-dose INH corticosteroid alone
-If NOT well controlled, the possible ⬆ in the risk of asthma fatality should be discussed in presenting options for treatment (Higher INH corticosteroid vs. adding long acting β2 agonist)
-BBW

71
Q

What is the BBW associated with Combo Inhalers

A

Mild-mod asthma should be treated with low-dose INH corticosteroid alone due to increased risk of death with combo therapy.

72
Q

When might additional treatment for asthma be required?

A

IF….additional treatment is needed
-Symptoms require “rescue” therapy more than twice a week OR
-Nocturnal symptoms occur more than twice a month OR
-FEV1 is less than 80% predicted

73
Q

When might a standard inhaled corticosteroid not be enough, and what can you do about it?

A

In severe asthma patients

If the standard inhaled corticosteroid is not enough with the beta agonist, you can
1. double the dose of the steroid
2. Add another agent
- Methylxanthines – theophylline
- Leukotriene receptor antagonist – Singulair
- Long acting beta two agonist

74
Q

What makes up Advair?

A

flucticasone + salmetrol

75
Q

What makes up Symbicort

A

budesonide + formeterol

Pharm Exam 5 -- Smooth Muscle, GI and OTC (10 decks)

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