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Therapeutics > EX. 3 - Asthma > Flashcards

EX. 3 - Asthma Flashcards

1
Q

Episodic bronchospasm resulting form an exaggerated bronchoconstrictor response to various stimuli

A

Asthma

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2
Q

Asthma is an - of the bronchi

A

Inflammation

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3
Q

Episodic bronchospasm causes

A

Dyspnea, cough, and wheezing

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4
Q

Asthma affects -% of adults and -% of children

A

5% adults
7-10% children
(Over 3,000 fatalities a year)

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5
Q

Types of asthma

A

Extrinsic (allergic/classical)
Intrinsic

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6
Q

Extrinsic asthma:

A

Hypersensitivity rxn induced by exposure to an extrinsic antigen (dust, mold, pollen)
Commonly associated w/other allergy in patient/family members
Onset - early in life
Elevated serum IgE levels and eosinophil count
Driven by TH2 subset of CD4+T cells

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7
Q

Intrinsic asthma

A

Nonimmune triggering mechanism (ex. aspirin, viral infection, cold, psychological stress, exercise)
No personal or family history of allergy
Serum IgE levels - normal

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8
Q

Two phases of extrinsic asthma attacks

A

Acute bronchoconstriction
(immediate; 30-60 min)
Sustained bronchoconstriction:
(Late; 4-8 hours later after immediate response)

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9
Q

Acute bronchoconstriction

A

Immediate asthmatic response (IAR)
Occurs after sensitization
Mediated by IgE, produced in response to exposure of foreign particles
(IgE binds to FcER-1 on mast cells in the airway mucosa

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10
Q

Re-exposure to the allergen triggers the release of mediators from the mast cells in a process called

A

mast cell degranulation

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11
Q

Mast cells release

A

Histamine
Tryptase
Leukotrienes (LTC4 and LTD4)
Prostaglandin D2 (PGD2)

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12
Q

Mediators of acute bronchoconstriction cause

A

Smooth muscle contraction and vascular leakage

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13
Q

Sustained Bronchoconstriction

A

Late asthmatic response (LAR)
(3-6hrs after acute)
Caused by Activation of TH2 cells and cytokine production

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14
Q

Activation of TH2 cells in sustained bronchoconstriction

A

Ex. IL5, IL9, IL13
Attract and activate eosinophils
Stimulate mucus hypersecretion by bronchial epithelial cells
Stimulate IgE production by B lymphocytes

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15
Q

Activation of eosinophils

A

Release major basic protein, (MBP), eosinophil cationic protein (ECP) peroxidase, - causes tissue damage

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16
Q

Epithelium remodeling

A

Hyperplasia
Hypersecretion

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17
Q

Basement membrane remodeling

A

Thickening

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18
Q

Smooth muscle remodeling

A

Hypertrophy

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19
Q

Pharm treatments in asthma

A

Sympathomimetics
ICs’s
(^^MOST COMMON^^)
Leukotriene pathway inhibitors
Methylxanthine drugs
Antimuscarinic Agents
Cromolyn and Nedocromil
Monoclonal antibodies

20
Q

Sympathomimetics are - while ICS’s are -

A

Relievers, controllers

21
Q

Sympathomimetics mechanism

A

Binds to B2 adrenergic receptors in the bronchial smooth muscle
Increases the cAMP concentration -> relax the muscle cellsS

22
Q

Types of sympathomimetics

A

-Nonselective
Epinephrine (IV inject. after severe attack)
-B selective (also affects heart - B1)
Isoproterenol (displaced by B2 selective drugs)
-B2 selective
Most common
Short and long acting agonists

23
Q

B2 Selective agonist SAR

A

Bulky N subs-> B2 selective
Subs in the phenyl ring -> B2 selective and resistant to COMT
Mostly racemic -R active

24
Q

B2 Selective agonists Toxicities

A

Tachycardia, arrhythmias (less)
Skeletal muscle tremors
Induction of tachyphylaxis - reduction in the bronchodilator response upon regular uses

25
Q

SABA vs LABA use

A

SABA - PRN for acute attacks
LABA - additional therapy for patients currently using inhaled glucocorticoids
NOT for acute attacks, but regular daily use
No anti-inflam action (black box warning)
Comonly combined with corticosteroids

26
Q

Metoproterenol

A

SABA
Resorcinol analogue of isoproterenol
Somewhat B2 selective
LEAST POTENT B2 AGONIST
5-min onset, 4hr duration
Good oral bioavailability

27
Q

Terbutaline

A

SABA
N-t-butyl analogue of metapro
Greater B2 selectivity
3-fold greater potency than metaproterenol at B2 receptors
Good oral bioavailability

28
Q

Albuterol

A

SABA
most widely used
Resistant to COMT
5-min onset, 4-8hr duration of action when inhaled
Levalbuterol is R-isomer
(Greater potency, more expensive)

29
Q

Pirbuterol

A

Analogous to albuterol except the pyridine ring
Comparable duration of action as albuterol
Less potent than albuterol

30
Q

Salmeterol

A

LABA
-Available as powder
Greater lipid solubility; dissolve in cell membranes
20-minute onset and 12hr duration of action

31
Q

Formoterol

A

LABA
-Available as powder
-More rapid onset than salmeterol with a comparable duration of action
Resistant to COMT and MAO

32
Q

Inhaled corticosteroids (ICSs)

A

Maintenance therapy for persistent asthma
Not curative
“controller”
Effective only so long as they are taken

33
Q

_ or _ corticosteroids are reserved for severe cases

A

Oral or systemic

34
Q

_ is the most effective way to minimize the systemic adverse effects

A

Inhaled corticosteroids

35
Q

ICs’s Adverse effects:

A

Candidiasis - can be treated with topical clotrimazole
Can be reduced by having patients gargle water and expectorate after each inhaled treatment
Ciclesonide - 21 ester prodrug, associated with less candidiasis
Hoarseness - direct effect of corticosteroids on the vocal cords
Long term - use may increase the risk of osteoporosis and cataracts
In children, I cm reduction in the growth only for the first year

36
Q

Produced form arachidonic acid by 5-lipoxygenase
Involved in many inflammatory diseases and in anaphylaxis
LTB4 - potent neutrophil chemoattractant
LTC and LTD4 - responsible for many symptoms of asthma, such as bronchoconstriction, increased bronchial reactivity, mucosal edema, and mucus hypersecretion

A

Leukotrienes

37
Q

Improve asthma control and reduce the frequency of asthma exacerbations
Not as effective as inhaled glucocorticoids
Effective when taken orally, easier than inhalation for children
Reduce significantly the response to aspirin in aspirin-induced asthma (5-10% of asthma patients)

A

Leukotriene pathway inhibitors

38
Q

Zileuton

A

Leukotriene pathway inhibitor
5-lipoxygenase inhibitor
Racemic mix
N-hydroxy group is essential for inhibitory activity
Good oral bioavailability
Alternative to LABA in addition to ICS
NOT for acute asthma attack
Requires periodic monitoring of liver

39
Q

Monetlukast

A

Blocks the binding of LTC4, LTD4, and LTE4 to the receptor
Once a day dosing
Good oral bioavailable
Reduces the frequency of asthma exacerbations
Little toxicity

40
Q

Theophylline (most effective; more specific for smooth muscle)
Theobromine
Caffeine
Once a mainstay for asthma tx, replaced by B2
Still used in some countries due to low cost

A

Methylxanthine drugs

41
Q

Methylxanthine MOA

A

Inhibition of phosphodiesterases (PDE3 and PDE4)-> increase in the cellular cAMP concentration -> bronchodilation and suppression of histamine release
Block the action of adenosine, which causes bronchoconstriction and the release of histamine
Histone deacetylation, which suppresses inflammatory gene expression

42
Q

Toxicity of Methylxanthine drugs

A

Nausea, vomiting, tremulousness, arrhythmias
Narrow therapeutic index

43
Q

“Anticholinergic agents”
MOA:
Stimulation of cholinergic (parasympathetic) nerves causes bronchoconstriction and mucus secretion
Antimuscarinic drugs competitively inhibit the action of acetylcholine at muscarinic receptors
Clinically valuable patients who are intolerant of inhaled B agonists

A

Antimuscarinic agents

44
Q

Ipratropium

A

Antimuscarinic agent
Bronchodilator
Quaternary amine derivative of atropine
Poorly absorbed into the circulation after inhaled
Minimal oral bioavailability
Relatively free of systemic atropine-like effects

45
Q

Cromolyn and nedocromil
Once widely used for asthma management, especially in kids
Inhibit mast cell degranulation
No direct bronchodilator action; should be used prophylactically (daily dosing)
Poorly absorbed in the systemic circulation; little toxicity; not as potent as glucocorticoids
Current use; allergic rhino conjunctivitis eye drops

A

Mast cell Stabilizers

46
Q

Omalizumab
Recognizes the portion of IgE binding to its receptor (FCER-I and FCER-2) on immune cells
Inhibits IgE binding to mast cells
Reserved for patients with severe asthma and allergic sensitization

A

Anti-IgE monoclonal antibody

47
Q

IL-5 release from TH2 cells attracts and activates eosinophils
Anti-IL-5 monoclonal antibodies (Mepolizumab and Reslizumab)
Anit-IL-5 receptor monoclonal antibody Benralizumab
Used as a maintenance therapy of severe asthma in patients with an eosinophilic phenotype

A

Anti-IL-5 Therapy

Therapeutics (61 decks)

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