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SP Pharm > pulm > Flashcards

pulm Flashcards

1
Q

why is the respiratory system a good system for drug delivery?

A

rapid and efficient

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2
Q

how are drugs administered through the respiratory system?

A

aerosol

and drugs are smoked

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3
Q

what is an aerosol?

A

suspension of liquid or fine particles in air

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4
Q

what is the advantage of an aerosol?

A

drugs can be delivered to the site of action with limited systemic effects

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5
Q

is it possible for an aerosol produce significant systemic effects?

A

yes…think about meth or crack that gets smoked, addicts use the tissues of the lungs to get the drug to their brains

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6
Q

most drugs that have rapid onset also have what?

A

short half life….meth is an exception. rapid onset, long half life

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7
Q

what do pulmonary drugs target?

A

lungs, but can still have systemic effects

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8
Q

how are aerosols delivered? (methods)

A

nebulizers
dry powder inhaler (DPI)
metered dose inhaler (MDI)

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9
Q

what does a nebulizer do?

A

turns a liquid into a fine mist

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10
Q

what are the common problems with aerosol therapy?

A
  1. difficult to determine if the correct dose is given
  2. can alter breathing pattern
  3. drugs can end up in oral mucosa, not lungs
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11
Q

what are the features of asthma?

A

airway inflammation
airway hyperresponsiveness
bronchoconstriction
hyper secretions of mucus

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12
Q

what is atopy?

A

inherited predisposition to allergic diseases such as asthma, allergic rhinitis, or eczema

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13
Q

atopy is the underlying factor in what?

A

almost all asthma in children

most asthma in adults

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14
Q

based on the drawing on slide 8, what are some features of an inflamed airway?

A
  1. smooth muscle layer widened due to edema
  2. more mucus on the surface of the airway
  3. plasma leakage
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15
Q

what are the goals of asthma therapy?

A
  • end acute bronchial constriction
  • reduce inflammation
  • reduce hypersecretions of mucus
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16
Q

what is the overarching def. of COPD?

A

chronic obstructive pulmonary disease

-lung condition with non-reversible airflow limitation

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17
Q

what are 2 examples of COPD?

A

chronic bronchitis

emphysema

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18
Q

what are the treatment goals of COPD?

A

reduce inflammation
relieve bronchoconstriction
reduce risk or treat infection (infection control)
control cough

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19
Q

what type of drug is used for acute bronchoconstriction?

A

beta 2 adrenergic agonists

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20
Q

how do beta 2 adrenergic agonists work to reduce bronchoconstriction?

A

stimulate beta 2 receptors found in the smooth muscle of the bronchi and bronchioles, causing the muscles to relax

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21
Q

what type of drug delivery is aerosol?

A

parenteral

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22
Q

what are some side affects of beta 2 agonists?

A

tachycardia
nervousness
shaking

severe effects, pulmonary edema, myocardial infarction, cardiac arrhythmia.

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23
Q

what is a drug that stimulates beta 1 and beta 2 receptors?

A

don’t know…find out

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24
Q

What is the advantage of selective β-2 agonists vs. non-selective agents?

A

don’t know…find out

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25
Q

what drug provides rapid therapeutic effect in the event of acute bronchoconstriction?

A

epinephrine (racemic)

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26
Q

epinephrine can also be used to treat what?

A

bronchiolitis
RSV
status asthmaticus

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27
Q

what is status asthmaticus?

A

severe, prolonged asthma that is unresponsive to standard drug treatment.

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28
Q

describe the series of events that beta 2 agonists precipitate

A

Stimulation of β-2 receptors increases activity of adenylcyclase enzyme

Increase in adenylcyclase activity increases production of intracellular cyclic AMP

The increase of cyclic AMP activates protein kinase A

Protein kinase A inhibits phosphorylation of myosin

Decrease of phosphorylation of myosin lowers intracellular ionic Ca++ concentrations=
relaxation of the bronchioles

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29
Q

stimulation of beta 2 receptors causes an increase in what type of activity?

A

activity of adenylcyclase enzyme

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30
Q

what does the induction of adenylcyclase cause?

A

increase in production of intracellular cyclic AMP

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31
Q

what does an increase of cyclic AMP cause?

A

activation of protein kinase A

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32
Q

what does protein kinase A do?

A

inhibits phosphorylation of myosin and lowers intracellular calcium concentrations that results in relaxation of bronchioles

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33
Q

how long does an ultra short acting beta 2 agonist work?

A

2-3 hours

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34
Q

how long does a short acting beta 2 agonist last?

A

3-6 hours

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35
Q

how long does an intermediate beta 2 agonist last?

A

8 hours

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36
Q

how long does a long acting beta 2 agonist last?

A

12 hours

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37
Q

Why is tachycardia observed if these agents are selective for β-2 receptors?

A

don’t know…vagus nerve suppression maybe???

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38
Q

what it is a mirror image of a molecular compound called?

A

what is a R-Enantiomer?

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39
Q

what is the R-Enantiomer of albuterol?

A

levabuterol

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40
Q

why use the R-Enantiomer of albuterol (levabuterol)?

A

beta 2 selective drugs are usually a mixture of R and S isomers (enantiomers). only the R isomer activates the beta 2 receptors

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41
Q

what type of isomer activates the beta 2 receptors?

A

only R isomers

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42
Q

what type of beta 2 agonist is highly selective and has a long duration of action?

A

formoterol

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43
Q

explain how formoterol works

A
  • highly lipophilic
  • enters plasma membrane in form of depot
  • gradually released into aqueous phase to activate B2 receptors=long duration
44
Q

what type of activity is not demonstrated by salmeterol?

A

aqueous phase activity

45
Q

what can happen in short acting beta 2 agonists are overused?

A

tolerance because b2 receptors may become unresponsive to stimulation

46
Q

how can tolerance to short acting beta 2 agonists be reversed?

A

use of inhaled corticosteroids

47
Q

do long acting beta 2 agonists carry a risk of tolerance?

A

no

48
Q

beta 2 agonists cause bronchodilation, while anticholinergics ______________.

A

anticholinergics inhibit bronchoconstriction and decrease mucus secretions

49
Q

how does an inhaled anticholinergic work?

A

decreased cGMP formation
decreased cGMP=decreased smth ms contractility
=inhibition of bronchoconstriction and mucus secretion

50
Q

what does an inhaled anticholinergic do at the receptor level?

A

blocks muscarinic cholinergic receptors

non-specific anticholinergic

51
Q

inhaled anticholinergic are used for the symptomatic relief of what condition?

A

COPD

52
Q

what are the side effects of inhaled anticholinergics?

A 
dry mouth
nervousness
GI upset
headache
worsening narrow-angle glaucoma
prostatic hypertrophy
53
Q

what type of drugs blocks M receptors in the lungs?

A

atropine derivatives

54
Q

2 things about tiotropium (Spiriva)

A

longer-acting

structural analog of ipratropium bromide

55
Q

why does tiotropium (Spiriva) have a long-acting effect?

A

slow dissociation rate from M receptors

56
Q

what drug has been FDA approved for maintenance of COPD?

A

tiotropium (Spiriva)

57
Q

what are the primary actions of inhaled corticosteroids in the lungs? 4

A

suppresses airway inflammation
decreases mucous cell secretions
reduces edema
assists with repair of damaged epithelium

58
Q

how do inhaled corticosteroids work?

A

increases number and sensitivity of beta 2 receptors leading to increased effectivenesss of beta 2 agonist agents

59
Q

In most acute severe asthma attacks, IV administration of corticosteroids offers__________over PO dosing (and what is PO dosing?)

A

little advantage

PO=per os or oral

60
Q

how long will full action of systemic corticosteroids will take?

A

48-72 hrs

61
Q

how long should oral corticosteroids should be taken for?

A

7-10 days with doses titrated down; should not discontinue rapidly.

62
Q

what is the advantage to inhaled corticosteroids compared to systemic corticosteroids?

A

even at high doses, inhaled corticosteroids do not appear to cause significant adverse effects while long-term systemic corticosteroid treatment is associated with serious adverse effects

63
Q

long-term systemic corticosteroid treatment is associated with what serious adverse effects?

A 
adrenal gland atrophy
peptic ulcers
hyperglycemia
osteopenia and osteoporosis
aseptic necrosis of the hip
immune suppression
64
Q

long-term systemic corticosteroid treatment is associated with what unpleasant side effects?

A

moon face and weight redistribution

thin skin/acne/fatigue/GI disturbance

65
Q

what is an advantage of fluticasone propionate (Flovent)?

A

the bioavailability of fluticasone is minimal outside of the airway

66
Q

why is the bioavailability of fluticasone minimal outside of the airway?

A

it is subject to rapid liver inactivation (CYP450 3A4 pathway) and the metabolite that is produced is largely inactive and has limited affinity for the glucocorticoid receptor

67
Q

what are some inhaled medications that contain both corticosteroid and a bronchodilator

A

advair diskus contains fluticasone and salmeterol

symbicort contains budesonide and formoterol

68
Q

what is the name of the bronchodilators that are related to caffeine?

A

methylxanthines

69
Q

what are the effects of methylxanthines?

A

bronchodilation
inhibit pulmonary edema
increase cilia activity

70
Q

how do methylxanthines inhibit pulmonary edema?

A

by decreasing vascular permeability

71
Q

what are the side effects of methylxanthines?

A

increases cardiac output
peripheral vasodilation
diuretic effect
CNS stimulation

72
Q

how are methylxanthines administered?

A

orally (PO) and IV

73
Q

why has use of methylxanthines decreased?

A

narrow margin of safety and drug toxicity/adverse side effects

74
Q

why must serum levels be monitored when administering methylxanthines?

A

don’t know

75
Q

how are mast cell stabilizers used?

A

prophylaxis to prevent acute asthma attacks

76
Q

what drug is an immunosuppressant monoclonal antibody?

A

omalizumab

77
Q

how do mast cell stabilizers work?

A

inhibit release of histamine from mast cells

78
Q

what is the half life of a mast cell stabilizer?

A

2.5 hours so must be used long term to be of significant benefit

79
Q

what are leukotrienes?

A

strong chemical mediators of bronchoconstriction and mucous secretion

80
Q

how are leukotrienes formed?

A

formed by the lipoxygenase pathway of arachidonic acid metabolism in response to cellular injury

81
Q

2 examples of opioid antitussive

A

codeine

hydrocodone bitartrate

82
Q

what are leukotriene modifiers?

A

drugs that counteract the effects of leukotrienes

83
Q

what are leukotriene modifiers used for?

A

long-term treatment of asthma and allergies

84
Q

how does zileuton work?

A

reduces formation of leukotrienes

85
Q

how do monelukast and zariflukast work?

A

block leukotriene receptors

86
Q

how does omalizumab work

A

binds to immunoglobulin E, preventing IgE attachment to mast cells and basophils

this in turn prevents the release of pro-inflammatory and pro-allergic substances

87
Q

who gets prescribed omalizumab?

A

patients with severe, persistent asthma, which cannot be controlled even with high doses of corticosteroids

88
Q

how are mucolytics and expectorants are used ?

A

to reduce the viscosity of bronchial mucous and aid in its removal

89
Q

example of OTC mucolytic/expectorant?

A

guaifenesin

90
Q

what is an antitussive?

A

reduces cough reflex

91
Q

how are most antitussives used?

A

in combination with other agents such as a mucolytic/expectorant

92
Q

what happens in RDS?

A

condition where the lungs are not producing surfactant

93
Q

who is most at risk for RDS?

A

premature infants

94
Q

how does surfactant work in the lungs?

A

forms a thin layer on the inner surface of the alveoli allowing the lung to remain open during respiration

95
Q

what cells produce surfactant?

A

type II alveolar cells

96
Q

what is RSV?

A

Respiratory Syncytial Virus

a virus that normally affects infants and young children

97
Q

how is RSV treated?

A 
non-selective β-adrenergic drugs
selective β-adrenergic drugs
oxygen
ribavirin
supportive care
98
Q

how can RSV be prevented?

A

monthly injection consisting of RSV antibodies can be given during peak RSV season to reduce the risk of infection

99
Q

what is anaphylaxis?

A

A severe, sometimes life-threatening allergic reaction to a variety of agents

100
Q

what agents can cause anaphylaxis?

A

1- Foods: nuts, shellfish, milk, and eggs
2- Stinging insects: honeybees, wasps
3- Medications e.g. Penicillins

101
Q

what are the symptoms of anaphylaxis?

A

Flushing, urticaria, pruritis, bronchospasm, cramping, hypotension

102
Q

anaphylaxis treatment

A

epinephrine

103
Q

how does epinephrine work?

A
  • alpha agonist activity: Increased peripheral vascular resistance, reverse vascular permeability
  • beta agonist activity: Bronchodilatation, positive ionotropic effect
104
Q

look at slide 40 extra credit

A

look at slide 40 extra credit

105
Q

what type of drug stimulates bronchodilation

A

beta 2 agonists

106
Q

what type of drug inhibits bronchoconstriction?

A

anticholenergic

107
Q 
what is the effect of each?
Beta 2 agonist
anticholinergics
corticosteroids
leukotriene modifiers
A

Beta 2 agonist=asthma, causes bronchodilation by stimulation of B2 receptors
Anticholinergics=COPD, inhibits bronchoconstriction by blocking/inhibition of M receptors
Corticosteroids=increases number and sensitivity of beta 2 receptors leading to increased effectiveness of beta 2 agonist agents
leukotriene modifiers=asthma and allergies, counter affect leukotrienes

SP Pharm (10 decks)

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