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Drugs for Asthma/COPD Flashcards

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1
Q

What is COPD?

A

slowly progressive airway obstruction due to chronic inflammation
includes chronic bronchitis and emphysema

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2
Q

what are some symptoms of COPD?

A

cough
mucus hypersecretion
dyspnea (shortness of breath)

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3
Q

what are 3 causes of COPD?

A

smoking
air pollution
occupational exposures

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4
Q

what occupations are a risk factor for CODP?

A

firefighters

construction workers exposed to asbestos and other chemicals

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5
Q

what is chronic bronchitis? emphysema?

A

CB: inflammation of bronchi
E: destruction of alveolar structure, airways collapse during expiration (irreversible)

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6
Q

why is chronic inflammation a problem?

A

creates mucus layer, plugging the airway
edema caused by inflammation also narrows the airway
leads to difficulty breathing

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7
Q

what are the alveoli?

A

little sacs with a honeycomb structure (high SA) that are highly vascularized and function for air exchange

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8
Q

what is asthma?

A

a chronic inflammatory disorder of the airways

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9
Q

what are some symptoms of asthma?

A

recurring episodes of cough
wheezing
tight chest
dyspnea

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10
Q

what is asthma characterized by?

A

recurring episodes of hyper-responsiveness to stimuli that causes bronchoconstriction
triggering stimuli characterized as extrinsic (allergenic) or intrinsic (non-allergenic)

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11
Q

how does the airway of an asthmatic patient look different compared to healthy bronchi?

A

smooth muscles are tightened
inflammation in brochial tubes and increased mucus secretion
air trapped in alveoli

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12
Q

is asthma damage reversible? COPD?

A

asthma - yes

COPD - no

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13
Q

what 4 complications could occur if asthma is not treated and chronic inflammation of the airways occur?

A

1) fibrosis (scar tissue) - affects elasticity of bronchi (need high elasticity)
2) muscle hypertrophy/hyperplacia (increased muscle thickness) - due to hyperventilation/gasping - reduces airway
3) angiogenesis
4) mucus hypersecretion

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14
Q

what symptoms are amenable to drug therapy?

A

excessive airway smooth muscle tone
inflammation
mucus plugging
pulmonary edema

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15
Q

when would we not want to suppress a cough?

A

if the cough is productive, good idea to try and get the mucus out of the airway

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16
Q

what is extrinsic asthma?

A

“Allergen-induced”
external stimuli such as environmental allergens (dust, mold, pollen, animal dander, foods) trigger plasma cells to produce antigen specific IgE antibodies
IgE and/or antigens binding to mast cells resulting in degranulation and release of inflammatory mediators

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17
Q

What is intrinsic asthma?

A

“Non-allergenic asthma”
Symptoms triggered by non allergenic factors (anxiety, stress, cold/dry air, exercise, viruses)
Abnormalities in the autonomic regulation of airway functions suggested to increase responsiveness; innate immune system involved and role of adaptive immune system remains elusive

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18
Q

how does stress/anxiety lead to asthma? cold/dry air? smoke?

A 
s/a = CNS mediated Ach release
air = stimulate sensory receptors
smoke = inhaled irritatn, triggers innate immune response
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19
Q

what is the pathophysiology of asthma?

A

1) allergen binds to both mast cell (IgE receptors?) and macrophages
2a) mast cell induces release of: histamine, leukotrienes, prostaglandins, and platelet activating factors leading to an acute response within minutes (bronchoconstriction)
2b) antigen binds to T cell which releases cytokines and chemokines or leukotrienes
3b1) cytokines and chemokines act on basophils and eosinophils which release other inflammatory mediators that cauuse prolonged response hours after acute reaction (vasodilation, mucus secretion, edema, bronchoconstriction) - leads to chronic inflammation
3b2) leukotrienes act on plasma cell, releasing IgE which acts on mast cell causing further inflammatory mediator release

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20
Q

inflammation of the airways ultimately causes shedding of epithelial cells. what are 3 consequences of this?

A

1) lack of protective barrier, allowing inhaled irritants and allergens to penetrate
2) exposes sensory nerves, which activation (release of neuropeptide substance B) leads to..
3) microvascular leaks and edema, and further inflammation stimulates Ach release from cholinergic reflex and leads to bronchoconstriction

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21
Q

the drugs for asthma and COPD can be divided based on what two things? name the subcategories for each

A

1) based on treatment strategies (controllers, relievers)

2) based on targets (airway muscle tone, inflammation)

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22
Q

what class of drug targets airway muscle tone? give examples

A

bronchodilators

beta-adrenergic agonists, methylxanthines, anticholinergics, leukotriene modifiers

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23
Q

what class of drug targets inflammation? give examples

A

anti-inflammatory agents

corticosteroids, mast cell stabilizers, anti-IgE monoclonal-antibody, leukotriene modifiers

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24
Q

what are bronchodilators?

A

agents that interact with smooth muscle cells lining the airways (bronchiole) and relax smooth muscles

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25
what regulates the airway smooth muscle?
autonomic nervous system
26
what system causes bronchodilation? bronchoconstriction?
dilation - SNS | constriction - PNS
27
what electrolyte is related to bronchodilation and constriction? high levels of this electrolyte causes dilation or constriction? low levels?
intracellular calcium high levels = constriction low levels = dilation
28
how does calcium cause bronchodilation or contriction?
dilation - decreased levels of calcium works with adenylate cyclase and cAMP to cause bronchial dilation constriction - increased levels work with Ach to cause bronchial constriction
29
what is the process that leads to bronchoconstriction?
1) Ach binds to M3 muscarinic receptor and activation Gq 2) PLC activation leads to increased DAG and IP3 hydrolysis 3) Increased cytoplasmic calcium 4) calcium-calmodulin activates myosin (phosphorylation of light chains) via MLCK (myosin light chain kinase) 5) myosin binds to actin - actin slide past myosin 6) contraction occurs as long as calcium is present Note: adenosine also increases calcium levels via PLC activation by the A1 receptor
30
what is the process that leads to bronchodilation?
1) activation of beta2 receptor, GPCR 2) activation of Gs 3) activation of adenylyl cyclase 4) ATP is converted to cAMP, leading to PKA activation - promotion of SR calcium pumps decreases cytoplasmic calcium - inhibition of MLCK prevent myosin binding to actin 5) dilation and relaxation occurs
31
name 3 examples of beta2-adrenergic agonists?
albuterol (salbutamol) terbutaline (short acting) salmeterol (long acting)
32
what is the MoA for beta agonists?
stimulate adenylyl cyclase thereby increase the formation of cAMP which acts to relax the airway smooth muscle leading to bronchodilation
33
what is the typical administration for beta agonists? what other forms could they be found in?
inhalation albuterol/terbutaline - tablet form as well terbutaline can be given SC
34
what is the indication for beta agonists? which is the drug of choice?
treatment of asthma inhaled albuterol DoC for acute attacks SC terbutaline or epinephrine for severe attacks along with corticosteroids
35
what can be administered with beta-agnists and why?
corticosteroids | improve efficacy of beta agonists and prevent development of tolerance
36
what are some adverse effects of beta agonists?
at higher doses, beta1 receptors can get stimulated leading to tachycardia skeletal muscle tremor tolerance may develop with very frequent use also induces insulin release
37
what are some drug interactions with beta agonists?
not effective on patients taking propanolol (beta blocker) for hypertension
38
what is an example of a methylxanthine?
theophylline
39
what is the MoA of theophylline?
main mechanism: inhibits adenosine receptor in CNS and elsewhere (adenosine cause contraction of isolated bronchial smooth muscle and provoke release of histamine from mast cells) other mech: at high concentrations inhibit phosphodiesterase resulting in an increase in cAMP; cAMP relaxes airway Can also stimulate the contractility of diaphragm muscles
40
what is the route of administration for theophylline?
aerosol; other routes adversely affect the heart
41
what is the indication for theophylline?
second line treatment in acute asthma attacks | used in COPD
42
why is theophylline second line?
narrow therapeutic window; given under supervision
43
what are some adverse effects of theophylline?
common: headache, insomnia, tremors serious: anaphylactic shock, N/V, stimulates heart, fever, seizures metabolized by CYP450 enzymes - drug interactions may result in toxic concentrations
44
what are two drugs classified under anticholinergics?
ipratropium (short acting) | tiotropium (long acting)
45
what is the MoA of anticholinergics?
blocks muscarinic receptors, preventing bronchoconstriction and mucus secretion; no effect on inflammation
46
what is the route of administration for anticholinergics?
aerosol
47
what is the indication for ipratropium?
treatment of COPD and chronic bronchitis | treatment of acute asthma attacks in children, adults, and those that are intolerant of beta-agonists
48
what can ipratropium be used with and why?
beta agonists enhance the bronchodilation produced by beta agonists can be an effective treatment of severe asthma attacks
49
what are some side effects of ipratropium?
generally well tolerated, but excessive use may cause dry mouth, dilated pupils, tachycardia, etc
50
which type of patients should use caution with ipratropium?
``` glaucoma patients (increased intraocular pressure) prostatic hypertrophy patients (urinary retention) ```
51
what are leukotrienes? what do they do?
inflammatory mediators that are products of arachidonic acid metabolism cause bronchoconstriction, increased bronchial reactivity, mucosal edema, and mucus secretion
52
what do leukotriene modifiers do?
inhibit the synthesis of leukotrienes and block the receptors that leukotrienes act upon
53
what is an example of a leukotriene synthesis inhibitor?
zileuton
54
how does zileuton work?
inhibits 5-lipoxygenase, which is an enzyme that catalyzes the formation of leukotrienes from arachidonic acid
55
what is the route of administration for zileuton?
oral | administered QID
56
what is the indication for zileuton?
treatment of persistent asthma in adults ASA induced asthma prevents exercise and antigen-induced brochospasm good for intrinsic asthma treatment
57
what are some side effects of zileuton?
possible hepatotoxicity | liver enzyme levels should be checked periodically
58
what are two drug combination concerns for zileuton? why?
theophylline - may promote theophylline toxicity | warfarin - zileuton inhibits CYP450 which may interfere with the metabolism
59
what are two examples of leukotriene receptor blockers?
zafirlukast | montelukast
60
what is the MoA for leukotriene receptor blockers?
selective reversible inhibitors of the cysteinyl leukotriene-1 (CysL1) receptor, thereby preventing leukotriene induced bronchoconstriction and airway wall edema also prevents chemotaxis (infiltration of neutrophils and eosinophils)
61
what is the route of administration for zafirlukast?
orally | administered BID
62
what is the indication for zafirlukast?
used for the treatment of mild-mod asthma less effective than corticosteroids should not be administered to children under 8 y.o
63
what are some side effects of using zafirlukast?
headache, GI disturbance inhibits CYP450 which may interfere with the metabolism of other drugs (like zileuton) possible hepatotoxicity
64
what is the route of administration for montelukast?
oral | administered OD
65
what is the indication for montelukast?
modestly effective in the treatment of persistent of asthma in children and adults less effective than corticosteroids should not be administered to children under 6 y.o
66
what are some drug interactions and adverse effects with montelukast?
``` inhibits CYP450 (same as zileuton) possible hepatotoxicity ```
67
what do anti-inflammatory agents do?
prevent the production, release and/or actions of inflammatory mediators
68
what are four classes of anti-inflammatory agents?
corticosteroids mast cell blockers anti-IgE monoclonal-antibody leukotriene modifiers
69
what are corticosteroids?
steroid hormones produced in the adrenal cortex
70
what are the functions of glucocorticoids and mineralocorticoids?
gluco - regulate glc metabolism | mineral - regulates salt and water balance
71
name 7 corticosteroids? what is the route of admin for each?
``` inhaled (preferred): beclometasone flunisolide fluticasone budesonide mometasone IV: methylprednisolone oral: prednisone ```
72
what is the MoA for corticosteroids?
block the release of arachidonic acid hence the production of leukotrienes increases the sensitivity of beta adrenergic receptors and prevents their desensitization prevents long term changes in airway structure and function
73
what is the indication for corticosteroids?
aerosol ones used in moderate cases of asthma and COPD | first line of anti-inflammatory drugs for all ages
74
what are some adverse effects associated with corticosteroids?
aerosol well tolerated; may cause oral thrush and hoarseness chronic use may result in suppression of adrenal glands (reduce dose gradually) may increase risk of osteoporosis and cataracts in adults; growth retardation in children (reduce growth hormone levels) loss of glucose in diabetic patients (increased gluconeogenesis, insulin resistance)
75
what is a concern with corticosteroids?
25% of asthma patients have resistance to corticosteroids
76
name 2 mast cell blockers
cromolyn sodium | nedocromil
77
what is the MoA of mast cell blockers?
poorly understood; inhibit release of mediators from mast cells and inhibit NT release from nerve endings (inhibits mast cell degranulation by blocking Cl/Ca channels essential for degranulation
78
what is the route of administration for mast cell blockers?
aerosol BID-QID
79
what are the indications for mast cell blockers?
treatment of mild-mod asthma (cromolyn = all ages; nedocromil = use in pts over 12y.o) does not reverse an ongoing bronchoconstriction, but regular use reduces bronchial hyperreactivity and inhibits phase 1 and 2 asthma attack trial period of 4-6 wks required to determine drug efficacy less potent than inhaled glucocorticoids in controlling asthma anti-inflammatory drug of choice for treatment of allergenic asthma in children; also helpful to prevent exercise induced asthma
80
what are some adverse effects of mast cell blockers?
generally well tolerated throat irritation, cough, dry mouth serious SEs: (rare) tight chest and wheezing less than 2% of pts experience reversible dermatitis, myositis (muscular inflammation), gastroenteritis
81
name 1 anti-IgE monoclonal antibody
xolair (omalizumab)
82
what is the MoA for xolair?
prevents IgE binding to cell and reduces IgE levels. Both first and second phase (acute and prolonged) of bronchoconstriction reduced targets free IgE and IgE bound to B cells, not IgE bound to mast cell, basophils, or dendritic cells
83
what is the indication for xolair?
allergic asthma; recommended in mod-severe asthma not controlled by inhaled corticosteroids in those over 12y.o
84
what is the route of administration for xolair?
SC injection
85
what is an adverse effect of xolair?
may cause anaphylaxis
86
what are 5 goals of therapy for asthma/COPD?
1) maintain normal activity levels 2) maintain near normal pulmonary function rates 3) prevent troublesome symptoms - cough, breathlessness at night or during exertion 4) avoid adverse effects of medications 5) avoid drug interactions
87
what is the general outline for asthma treatment based on severity?
when symptoms are very mild (less than 2 episodes per week) or before that, just use non pharms when it reaches mild (>2 episodes per week), add beta-agonist on add needed bases as severity increases to moderate (>6 episodes/week) add inhaled glucocorticoid for daily use when symptoms become severe (continuous) need additional therapy such as prednisone, long acting bronchodilators, anti-IgE monoclonal antibody
88
what is the general outline for COPD treatment based on severity?
``` mild = bronchodilators as needed mod = bronchodilators and anti-inflammatory drugs severe = antibiotics (prevent pneumonia), bronchodilators, anti-inflammatory drugs and oxygen therapy ```

Pharmacology (9 decks)

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