Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology > Drugs for Asthma/COPD > Flashcards

Drugs for Asthma/COPD Flashcards

1
Q

What is COPD?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are some symptoms of COPD?

A

cough
mucus hypersecretion
dyspnea (shortness of breath)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are 3 causes of COPD?

A

smoking
air pollution
occupational exposures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what occupations are a risk factor for CODP?

A

firefighters

construction workers exposed to asbestos and other chemicals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is chronic bronchitis? emphysema?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are the alveoli?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is asthma?

A

a chronic inflammatory disorder of the airways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are some symptoms of asthma?

A

recurring episodes of cough
wheezing
tight chest
dyspnea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

is asthma damage reversible? COPD?

A

asthma - yes

COPD - no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what symptoms are amenable to drug therapy?

A

excessive airway smooth muscle tone
inflammation
mucus plugging
pulmonary edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what class of drug targets airway muscle tone? give examples

A

bronchodilators

beta-adrenergic agonists, methylxanthines, anticholinergics, leukotriene modifiers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what class of drug targets inflammation? give examples

A

anti-inflammatory agents

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are bronchodilators?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what regulates the airway smooth muscle?

A

autonomic nervous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what system causes bronchodilation? bronchoconstriction?

A

dilation - SNS

constriction - PNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what electrolyte is related to bronchodilation and constriction?
high levels of this electrolyte causes dilation or constriction? low levels?

A

intracellular calcium
high levels = constriction
low levels = dilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

how does calcium cause bronchodilation or contriction?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is the process that leads to bronchoconstriction?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is the process that leads to bronchodilation?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

name 3 examples of beta2-adrenergic agonists?

A

albuterol (salbutamol)
terbutaline (short acting)
salmeterol (long acting)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what is the MoA for beta agonists?

A

stimulate adenylyl cyclase thereby increase the formation of cAMP which acts to relax the airway smooth muscle leading to bronchodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is the typical administration for beta agonists? what other forms could they be found in?

A

inhalation
albuterol/terbutaline - tablet form as well
terbutaline can be given SC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what is the indication for beta agonists? which is the drug of choice?

A

treatment of asthma
inhaled albuterol DoC for acute attacks
SC terbutaline or epinephrine for severe attacks along with corticosteroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what can be administered with beta-agnists and why?

A

corticosteroids

improve efficacy of beta agonists and prevent development of tolerance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what are some adverse effects of beta agonists?

A

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
Q

what are some drug interactions with beta agonists?

A

not effective on patients taking propanolol (beta blocker) for hypertension

38
Q

what is an example of a methylxanthine?

A

theophylline

39
Q

what is the MoA of theophylline?

A

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
Q

what is the route of administration for theophylline?

A

aerosol; other routes adversely affect the heart

41
Q

what is the indication for theophylline?

A

second line treatment in acute asthma attacks

used in COPD

42
Q

why is theophylline second line?

A

narrow therapeutic window; given under supervision

43
Q

what are some adverse effects of theophylline?

A

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
Q

what are two drugs classified under anticholinergics?

A

ipratropium (short acting)

tiotropium (long acting)

45
Q

what is the MoA of anticholinergics?

A

blocks muscarinic receptors, preventing bronchoconstriction and mucus secretion; no effect on inflammation

46
Q

what is the route of administration for anticholinergics?

A

aerosol

47
Q

what is the indication for ipratropium?

A

treatment of COPD and chronic bronchitis

treatment of acute asthma attacks in children, adults, and those that are intolerant of beta-agonists

48
Q

what can ipratropium be used with and why?

A

beta agonists
enhance the bronchodilation produced by beta agonists
can be an effective treatment of severe asthma attacks

49
Q

what are some side effects of ipratropium?

A

generally well tolerated, but excessive use may cause dry mouth, dilated pupils, tachycardia, etc

50
Q

which type of patients should use caution with ipratropium?

A 
glaucoma patients (increased intraocular pressure)
prostatic hypertrophy patients (urinary retention)
51
Q

what are leukotrienes? what do they do?

A

inflammatory mediators that are products of arachidonic acid metabolism
cause bronchoconstriction, increased bronchial reactivity, mucosal edema, and mucus secretion

52
Q

what do leukotriene modifiers do?

A

inhibit the synthesis of leukotrienes and block the receptors that leukotrienes act upon

53
Q

what is an example of a leukotriene synthesis inhibitor?

A

zileuton

54
Q

how does zileuton work?

A

inhibits 5-lipoxygenase, which is an enzyme that catalyzes the formation of leukotrienes from arachidonic acid

55
Q

what is the route of administration for zileuton?

A

oral

administered QID

56
Q

what is the indication for zileuton?

A

treatment of persistent asthma in adults
ASA induced asthma
prevents exercise and antigen-induced brochospasm
good for intrinsic asthma treatment

57
Q

what are some side effects of zileuton?

A

possible hepatotoxicity

liver enzyme levels should be checked periodically

58
Q

what are two drug combination concerns for zileuton? why?

A

theophylline - may promote theophylline toxicity

warfarin - zileuton inhibits CYP450 which may interfere with the metabolism

59
Q

what are two examples of leukotriene receptor blockers?

A

zafirlukast

montelukast

60
Q

what is the MoA for leukotriene receptor blockers?

A

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
Q

what is the route of administration for zafirlukast?

A

orally

administered BID

62
Q

what is the indication for zafirlukast?

A

used for the treatment of mild-mod asthma
less effective than corticosteroids
should not be administered to children under 8 y.o

63
Q

what are some side effects of using zafirlukast?

A

headache, GI disturbance
inhibits CYP450 which may interfere with the metabolism of other drugs (like zileuton)
possible hepatotoxicity

64
Q

what is the route of administration for montelukast?

A

oral

administered OD

65
Q

what is the indication for montelukast?

A

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
Q

what are some drug interactions and adverse effects with montelukast?

A 
inhibits CYP450 (same as zileuton)
possible hepatotoxicity
67
Q

what do anti-inflammatory agents do?

A

prevent the production, release and/or actions of inflammatory mediators

68
Q

what are four classes of anti-inflammatory agents?

A

corticosteroids
mast cell blockers
anti-IgE monoclonal-antibody
leukotriene modifiers

69
Q

what are corticosteroids?

A

steroid hormones produced in the adrenal cortex

70
Q

what are the functions of glucocorticoids and mineralocorticoids?

A

gluco - regulate glc metabolism

mineral - regulates salt and water balance

71
Q

name 7 corticosteroids? what is the route of admin for each?

A 
inhaled (preferred):
beclometasone
flunisolide
fluticasone
budesonide
mometasone
IV: methylprednisolone
oral: prednisone
72
Q

what is the MoA for corticosteroids?

A

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
Q

what is the indication for corticosteroids?

A

aerosol ones used in moderate cases of asthma and COPD

first line of anti-inflammatory drugs for all ages

74
Q

what are some adverse effects associated with corticosteroids?

A

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
Q

what is a concern with corticosteroids?

A

25% of asthma patients have resistance to corticosteroids

76
Q

name 2 mast cell blockers

A

cromolyn sodium

nedocromil

77
Q

what is the MoA of mast cell blockers?

A

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
Q

what is the route of administration for mast cell blockers?

A

aerosol BID-QID

79
Q

what are the indications for mast cell blockers?

A

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
Q

what are some adverse effects of mast cell blockers?

A

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
Q

name 1 anti-IgE monoclonal antibody

A

xolair (omalizumab)

82
Q

what is the MoA for xolair?

A

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
Q

what is the indication for xolair?

A

allergic asthma; recommended in mod-severe asthma not controlled by inhaled corticosteroids in those over 12y.o

84
Q

what is the route of administration for xolair?

A

SC injection

85
Q

what is an adverse effect of xolair?

A

may cause anaphylaxis

86
Q

what are 5 goals of therapy for asthma/COPD?

A

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
Q

what is the general outline for asthma treatment based on severity?

A

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
Q

what is the general outline for COPD treatment based on severity?

A 
mild = bronchodilators as needed
mod = bronchodilators and anti-inflammatory drugs
severe = antibiotics (prevent pneumonia), bronchodilators, anti-inflammatory drugs and oxygen therapy

Pharmacology (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions