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Pharmacology Test #3 > Asthma > Flashcards

Asthma Flashcards

1
Q

What are the goals of the treatment of Asthma?

A

Reduce Impairment

Reduce Risk

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2
Q

How do you reduce impairment in asthmatic patients?

A

Prevent chronic/troubling symptoms

Require infrequent (< 2 days/wk) inhaled SABA for quick relief of symptoms

Maintain normal pulmonary function

Maintain normal activity levels

Meet pts/families expectations of satisfactory care

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3
Q

How do you reduce risks in asthmatic patients?

A

Prevent recurrent exacerbations

Minimize ED visits/hospitalizations

Prevent loss of lung function

Prevent reduced lung growth (kids)

Provide optimal pharmacotherapy w/ minimal or no adverse effects of therapy

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4
Q

How is asthma treatment broken down?

A

3 different age groups:

0 - 4 yo (< 5 yo)

5 - 11 yo

≥ 12 yo

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5
Q

What is step 1 treatment of asthma?

A

Short-Acting Bronchodilators –> Short-acting β2-Agonist (SABA)

Short-Acting Bronchodilators –> Anticholinergics

Short-Acting Bronchodilators –> Combo

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6
Q

What is the mode of action of SABAs?

A

Binds to β-receptors in lung –> smooth muscle relaxation

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7
Q

How long is the onset of action for SABAs?

A

~ 5 min

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8
Q

What are the adverse effects of SABAs?

A

Dose-dependent heart palpitations

Anxiety

Tachycardia

Tremor

**Rare = hypokalemia/hypomagnesemia

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9
Q

What if a patient is using their SABA > 2 days/week?

A

Need to increase/begin long-term control meds

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10
Q

Name the common SABAs (generic name) their duration of action and dosage forms available

A

Albuterol = 5 - 8 hrs –> MDI, nebulizer, tablet, syrup

Levalbuterol = 5 - 8 hrs –> MDI, nebulizer

Pirbuterol = 5 hrs –> MDI

Metaproterenol = 2 - 6 hrs –> tablets, syrup

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11
Q

Are anticholinergics a preferred agent for treatment of asthma?

A

No

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12
Q

What is the mode of action of anticholinergics?

A

Inhibits cholinergic and muscarinic receptors in bronchial smooth muscle –> bronchodilation

Decrease vagal tone

Antisecretory properties

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13
Q

What is the onset of action of anticholinergics?

A

5 - 15 minutes (short-acting)

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14
Q

What are the adverse events of anticholinergics?

A

Dry mouth

Respiratory secretions

Increased wheezing in some

Less cardiac stimulation than SABAs (warning found in pt w/ COPD)

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15
Q

What is the anticholinergic that is commonly used to treat asthma and how is it given?

A

Ipratropium **only to pts ≥ 12 yo

MDI, nebulizer

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16
Q

What are the drugs that make up short-acting bronchodilator combo?

A

Albuterol

Ipratropium

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17
Q

How is the short-acting bronchodilator combo given?

A

MDI

Nebulizer

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18
Q

What is the step 2 treatment of asthma?

A

Low-Dose Inhaled Corticosteroids

Mast Cell Stabilizers

Leukotriene Receptor Antagonists

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19
Q

What is the preferred step 2 treatment for asthma?

A

Low-dose inhaled corticosteroids

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20
Q

What is the mode of action of low-dose inhaled corticosteroids?

A

Decrease # and activity of inflammatory cells

Enhance effect of β-adrenergic drugs

Inhibit bronchoconstrictor mechanisms

Direct smooth muscle relaxation

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21
Q

What are the adverse effects of inhaled corticosteroids?

A

Cough/dysphonia = most common

Oral thrush if pt doesn’t rinse mouth after use

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22
Q

What are the adverse effects of high dose inhaled corticosteroids?

A

Adrenal Suppression

Osteoporosis

Skin Thinning

Easy Bruising

Cataracts

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23
Q

What are the adverse effects of low-medium dose inhaled corticosteroids?

A

Growth Suppression (kids) –> minor 1-2 cm TOTAL through adult hood

Altered Growth Velocity

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24
Q

Name the common inhaled corticosteroids and their delivery system

A

Budesonide = DPI; nebulizer

Fluticasone = HFA, DPI

Mometasone = DPI

Ciclesonide = HFA

Beclomethasone = HFA

Flunisolide = HFA

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25
Q

What are the important clinical pearls for budesonide?

A

Only steroid available via nebulizer

Requires less coordination d/t DPI device

DPI particles = larger –> requires good inspiratory flow rate

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26
Q

What are the important clinical pearls for fluticasone?

A

High potency (2nd generation)

Similar efficacy/adverse events to other agents

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27
Q

What are the important clinical pearls for mometasone?

A

High potency (2nd generation)

Similar efficacy/adverse events to other agents

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28
Q

What are the important clinical pearls for ciclesonide?

A

Converted to active metabolite in lungs

Low systemic bioavailability –> good tolerability

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29
Q

What are the important clinical pearls for beclomethasone?

A

Multiple puffs needed @ each dose

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30
Q

What are the important clinical pears for flunisolide?

A

Available March 2014

Used to be Aerobid

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31
Q

What is the mode of action of mast cell stabilizers?

A

Stabilize mast cells

Blockade of Cl- Channels

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32
Q

When would you use mast cell stabilizers to treat asthma?

A

Preventative therapy priorto exercise or unavoidable exposure to known allergens

**anti-inflammatory properties

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33
Q

What are the 2 mast cell stabilizers, and what is their available forms?

A

Cromolyn = MDI, Nebulizer

Nedocromil = MDI

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34
Q

Why wouldn’t you use mast cell stabilizers to treat asthma?

A

Has excellent safety profile BUT questionable efficacy

Cough

Irritation

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35
Q

What is the mode of action of leukotriene receptor antagonists?

A

Interfere w/ pathway of luekotriene mediators (released from mast cells, eosinophils, basophils)

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36
Q

What else would you use with leukotriene receptor antagonists?

A

Inhaled Corticosteroids

**not preferred to LABAs for pt 12+ yo

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37
Q

What asthma symptom does luekotriene receptor antagonists help with?

A

Attenuate exercise induced bronchospasm (EIB)

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38
Q

What are the adverse effects of luekotriene receptor antagonists?

A

No specific effects have been ID’d BUT want to monitor liver enzymes

Cases of reversible hepatitis

Rarely irreversible hepatic failure –> death/liver transplantation

Depression/suicidal ideation in kids

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39
Q

What are the 2 leukotriene receptor antagonists used to treat asthma?

A

Montelukast

Zafirlukast

40
Q

What is the mode of action of Zileuton?

A

5-lipoxygenase inhibitor

**similar to leukotriene receptor antagonists BUT blocks above enzyme not receptor

41
Q

What are the adverse effects of zileuton?

A

Elevation of liver enzymes

Rare –> reversible hepititis (2-4%) and hyperbilirubinema

Drug interactions –> inhibits metabolism of warfarin/theophylline

**not preferred over leukotriene receptor antagonists

42
Q

When do you want to take zafirlukast?

A

1 hour before or 2 hours after meals (food decreases bioavailability)

43
Q

What CYP is does Zafirlukast interact w/?

A

CYP 2C9 is a substrate AND inhibitor

**will increase levels of warfarin

44
Q

What is the mode of action of theophylline?

A

Mild-Moderate Bronchodilator

Non-selective phosphodiesterase inhibitor

45
Q

What must you do in pts taking theophylline?

A

Monitor serum theophylline concentrations

**wide inter patient variability, and narrow therapeutic window

46
Q

What are the adverse affects of a usual dose of theophylline?

A

Insomnia

Gastric upset

Aggravation of ulcer/reflux

Increase hyperactivity in some kids

Difficult urination in elderly males who have prostatism

47
Q

What are the signs of theophylline toxicity?

A

Tachycardia

Nausea/Vomitting

Tachyarrhythmias

Central nervous system stimulation

Headache

Seizures

Hematemesis

Hyperglycemia

Hypokalemia

48
Q

What are the 2 CYPs that metabolize theophylline?

A

CYP1A2

CYP3A4

49
Q

What compounds will increase theophylline clearance?

A

Smoking (by 40% –> induces 1A2 activity) –> polycyclic aromatic hydrocarbons NOT nicotine

Phenytoin

Phenobarbital

Rifampin

50
Q

What compounds will decrease theophylline clearance?

A

Macolides = erythromycin/clarithromycin
(↓ clearance 25-50%)

Fluoroquinolone antibiotics = Ciprofoxacin
(↓ clearance 25-50%)

Cimetidine (↓ clearance 25-60%)

51
Q

What is step 3 treatment of asthma?

A

Increase Inhaled Corticosteroid Dose (to medium dose)

OR

Low-Dose Inhaled Corticosteroid Dose + Long-Acting β2-Agonist (LABA)

52
Q

What is the preferred step 3 treatment?

A

Medium Dose Inhaled Corticosteroids

53
Q

Besides the medium dose inhaled corticosteroids, or adding a LABA what are some other alternative treatments?

A

Low-dose inhaled corticosteroids (+):

Leukotriene Receptor Antagonist

Theophylline

Zileuton

54
Q

What is the mode of action of LABAs?

A

Tail binds to β-receptor @ exosite –> prevent molecule from dissociating from receptor

Head attaches to same spot as SABA

Continually attaches/detaches

Causes bronchodilation

**SHOULD NOT BE USED AS MONOTHERAPY!

55
Q

What are the adverse effects of LABAs?

A

Tachycardia

Tremor

Hypokalemia

Unexpected bronchospasms

Hyperresponsiveness

Binding to Heart β2-receptors –> pulse/BP; prolong QTC interval in overdose

56
Q

What are the block box warning on LABAs?

A

Increased risk of severe asthma exacerbation and asthma related death w/ regular use

Study in UK found non-statistical increase in asthma related death w/ use of salmeterol vs albuterol **not reproduceable

57
Q

What are the combo products of LABA & inhaled corticosteroids and what mode of dosage is available?

A

Fluticicasone/salmeterol = DPI

Budesonide/formoterol = MDI

Mometasone/formoterol = BID SPECIFICIALLY EVERY 12 hr

58
Q

What is the preferred step 4 treatment of asthma?

A

Medium dose inhaled corticosteroid + LABA

59
Q

What are the alternate step 4 treatments of asthma?

A

Medium dose inhaled corticosteroid (+):

Leukotriene Receptor Antagonist

Theophylline

Zileuton

OR

Long-acting anticholinergic

60
Q

What is the name of the long acting anticholinergic used in step 4 treatment of asthma?

A

Tiotropium

61
Q

What is the preferred step 5 treatment of asthma?

A

High-dose inhaled corticosteroid + LABA

AND

Consider Omalizumab (pts w/ allergies)

62
Q

What is the preferred step 6 treatment of asthma?

A

High-dose inhaled corticosteroid + LABA + oral corticosteroid

AND

Consider Omalizumab (pts w/ allergies)

63
Q

When is Omalizumab recommended?

A

Pts w/ allergies and severe persistent asthma inadequately controlled on high dose ICS + LABA

64
Q

Who is Omalizumab treatment approved in?

A

Approved in pts 12+ w/ proven allergies to: dust mites, cockroach, cat, dog

65
Q

What is the mode of action of Omalizumab?

A

Recombinant DNA-derived humanized monoclonal antibody (IgE type)

Binds to portion of IgE antibody –> prevent binding to receptors on mast cells/basophils

Decrease in release of allergen response mediators

66
Q

What are the adverse effects of Omalizumab?

A

Urticaria/anaphylaxis (.1%)

Anaphylaxis (.2%)

Injection site pain/bruising (up to 20%)

Malignancies –> 0.5% BUT twice as likely as placebo

67
Q

When do most incidences of anaphylaxis in response to Omalizumab injection?

A

Within 2 hr of injection

After first 3 injections

**some outside of these time periods

68
Q

How is Omalizumab given?

A

Subcutaneous injection

69
Q

What are the oral corticosteroids given to treat asthma?

A

Methylpredinisolone

Prednisolone

Prednisone

70
Q

What are the adverse effects of short term oral systemic corticosteroids?

A

Reversible abnormalities in glucose metabolism

Increased Appetite

Fluid retention

Weight gain

Mood alteration

Hypertension

Peptic ulcers

Aseptic necrosis = rare

71
Q

What are the adverse effects of long term oral systemic corticosteroids?

A

Adrenal axis suppression

Growth suppression

Dermal thinning

Hypertension

Diabetes

Cushing’s Syndrome

Cataracts

Muscle Weakness

Impaired Immune Function = rare

72
Q

What are the medical conditions that can be worsened w/ the use of oral systemic corticosteroids?

A

Herpes virus infection

Varicella

TB

HTN

Peptic ulcer dz

DM

Osteoporosis

73
Q

When are short term bursts of oral systemic corticosteroids effective?

A

Establishing control when initiating therapy

Period of gradual deterioration

74
Q

When don’t you need to taper pts off oral systemic corticosteroids?

A

Courses < 1 week

75
Q

Do you need to taper pts off 7 - 10 day courses of oral systemic corticosteroids?

A

Not if they are on inhaled corticosteroids

76
Q

When do you want to taper older pts off oral systemic corticosteroids?

A

Courses > 5 days

77
Q

When do you want to taper younger pts off oral systemic corticosteroids?

A

> 3 - 5 days

78
Q

What are the nonpharmacologic treatments of asthma?

A

Avoid Triggers

Remove Carpets

Encase Mattresses/Pillows

Vacuum

Windows Closed

Air Filters

Allergen-Free Zone

Discuss goals

Develop Pt Care Plan (including self-monitoring)

79
Q

What is the first line treatment of exercise-induced bronchospasms?

A

SABAs

5-30 min before exercise

Helpful for 2-3 hrs in 8-% of pts

80
Q

What is the second line treatment of exercise-induced bronchospasms?

A

Leukotriene Receptor Antagonists

**Need to administer way ahead of time

81
Q

What is the last line treatment of exercise-induced bronchospasms?

A

Cromolyn

**Not as effective as SABAs

82
Q

What are the non-pharmacological techniques to manage exercise-induced bronchospasms?

A

Warm-up period before exercise (reduce degree)

Mask/Scarf over mouth –> attenuate cold-induced EIB

83
Q

What are the signs/symptoms of mild asthma exacerbation?

A

Dyspnea only w/ activity (assess tachypnea in young kids

PEF ≥ 70%

84
Q

How do you treat mild asthma exacerbation?

A

@ Home

Prompt relief w/ SABA

Possible short course of oral systemic corticosteroids

85
Q

What are the signs and symptoms of moderate asthma exacerbation?

A

Dyspnea interferes w/ or limits usually activity

PEF 40-69% predicted or person best

86
Q

How do you treat moderate asthma exacerbation?

A

Office/ED Visit

Relief from frequent SABA

Oral systemic corticosteroids; symptoms may last 1 - 2 days after treatment

87
Q

What are the signs and symptoms of severe asthma exacerbation?

A

Dyspnea @ rest

Interferes w/ conversation

PEF < 40% predicted or personal best

88
Q

How do you treat severe asthma exacerbation?

A

Require ED visit –> likely hospitalization

Partial relief from frequent SABA

Oral systemic corticosteroids; symptoms may last > 3 days after treatment

Adjunctive therapies = helpful

89
Q

What are the signs and symptoms of life threatening asthma exacerbation?

A

Too dyspneic to speak

Perspiring

PEF < 25% predicted or personal best

90
Q

How do you treat life threatening asthma exacerbation?

A

Require ED/hospitalization; possible ICU

Minimal/no relief from frequent inhaled SABA

Intravenous corticosteroids

Adjunctive therapies are helpful

91
Q

What is a condition that is frequently associated with Asthma (not including allergies, atopy)?

A

GERD

75% have GERD

Twice as likely to have GERD

92
Q

How do asthma/gerd effect each other?

A

GERD can worsen Asthma

Asthma and Asthma meds can worsen GERD

93
Q

What can the treatment of GERD do to asthma?

A

Relieve Asthma Symptoms

94
Q

What can acid flow from GERD do?

A

Injury to lining of throat, airways, lungs –> injury and cough

95
Q

What does acid in the esophagus do to the nerves?

A

Trigger nerve reflex –> narrow airway (prevent acid from entering) –> SOB

Pharmacology Test #3 (6 decks)

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