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Pharm Fall '24 > Test 3 - Asthma and Bronchodilators (10/14 & 10/16) > Flashcards

Test 3 - Asthma and Bronchodilators (10/14 & 10/16) Flashcards

1
Q

factors affecting ventilation

A
  1. airway resistance

Airway diameter
-contraction and relaxation of smooth muscle
-ANS input

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2
Q

where is the greatest resistance in the airway

A

medium bronchi

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3
Q

Why do smokers cough in the mornings?

A

bc the cilia is damaged so they cough to try to get the shit up

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4
Q

Obstructive airway disorders lead to ______

A

hyper-reactive airway.

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5
Q

Obstructive disorders discussed in class

A
  1. asthma
  2. chronic bronchitis
  3. emphysema
  4. COPD
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6
Q

what is the most common chronic disease in children?

A

obstructive disorders (asthma)

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7
Q

what is the histamine challenge?

A

spray a little histamine into airway and checking forced expiratory volume.

normal people will have a drop.

asthmatics will have a significant drop.

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8
Q

why are asthma cases increasing?

A

Suspects.
1. second hand smoke
2. worsening air quality
3. hygiene hypothesis

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9
Q

what is the hygiene hypothesis. how can we counteract this?

A

we all wanted to be clean and wash our hands so our immune system doesn’t react to pathogens like normal. starts to react to our own autoantigens.

according to Dr T. get a dog.

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10
Q

Symptoms of asthma

A
  1. Wheezing
  2. Breathlessness
  3. chest tightness
  4. coughing (more at night)
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11
Q

what is asthma? what cells are involved

A

airway inflammation - obstruction.

WBC, epithelial cells

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12
Q

describe the smooth muscle walls in an asthmatic pt.

A

even in relaxed state they are inflamed and thickened

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13
Q

Air trapping in alveoli can lead to _____

A

emphysema

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14
Q

In asthma we have increased responsiveness of _____ and ____ to various stimuli

A

trachea; bronchi

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15
Q

What causes the widespread narrowing of airways in asthma? (3)

A
  1. contraction of airway smooth muscle
  2. mucosal thickening
  3. mucous plugs formed and thicken
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16
Q

symptoms of Croup. what can cause it. what can we give?

A

following viral infection. Seal like barking cough. nebulized epi

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17
Q

symptoms of COPD

A

chronic bronchitis + emphysema.
chronic productive cough that lasts for at least 3 months of the year and for at least 2 consecutive years

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18
Q

Symptoms of bronchitis

A

Inflammation of bronchioles

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19
Q

Alveolar walls in emphysema

A

Permanent enlargement of alveolar walls. loss of elasticity

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20
Q

What is FEV1 checking for? how is it done? what will we see in asthma pts?

A

Bronchial hyperreactivity test.

Inhaling increasing concentrations of histamine or methacholine and then forced expiration volume over 1 second.

significant fall in forced expiratory volume

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21
Q

what is PEF?

A

Peak expiratory flow
-maximum flow of forced expiration

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22
Q

(asthma treatment) what will we give for contraction of smooth muscle. what will we give for edema and cellular infiltration.

A
  1. beta adrenergic agonists (beta 2 specific)
  2. anti-inflammatory agents
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23
Q

what types of asthma are there?

A

Intrinsic - genetic factors

Atopic (extrinsic) - type 1 hypersensitivity reactions

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24
Q

What happens during a second time we are introduced to an allergin?

A

the b memory cells will recall the allergen and Mast cells degranulate and produce histamines

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25
Q

What happens during the first exposure to an allergen?

A
  1. breath in allergen
  2. dendritic cells (antigen presenting cell) - process and break up allergen and present it on the surface with MHC2 receptor and migrates to the closest lymph node
  3. MHC2 receptor is presented to a T Cell - T cell releases interleukin 4 which activates B cells
  4. B cells activated and produce antibodies/
  5. B cells turn into plasma cells (antibody producing factories) and B memory cells (will cause significant reaction the next time allergen is encountered)
  6. IgE will bind to surface of mast cells
  7. Mast cells become sensitized once IgE sticks to them
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26
Q

What is dupixent? who is it used for?

A

Blocks interleukin 4 from binding to the B cell. used for asthma and allergy

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27
Q

Early mediators are responsible for the early reaction. They diffuse through the cell wall and cause what?

A

muscular contraction and vascular leakage and immediate bronchoconstriction

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28
Q

What is a slower mediator that is released from mast cells (after histamine) in early stages of asthma and the effect

A
  1. Leukotrienes: bronchospasm. Enhances histamine effects
  2. Prostaglandins D2: Proinflammatory. Potent bronchconstricting agent

Both are GPCR

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29
Q

What is the immediate mediator that is released following an allergy response? What does it cause?

A

Histamine.
Induces smooth muscle contraction and bronchospasms

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30
Q

The eosinophil and neutrophil release a number of different substances called

A

Proteases.

They break down proteins holding cells together and they can infiltrate into smooth muscle and cause contraction.

but this causes swelling of the tissues because now its leaky

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31
Q

What draws in the eosinophil and the neutrophil?

A

The release of cytokines from T cells

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32
Q

what role does mucus have?

A

defense against irritants and microorganisms

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33
Q

Mucus is produced by ____

A

goblet and epithelial cells

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34
Q

What happens to the mucus viscosity in asthma?

A

it is increased

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35
Q

What is the sympathetic effect on airway diameter?

A

relaxes bronchiolar smooth muscle (B2 receptor)

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36
Q

What is the parasympathetic effect on airway diameter?

A

Contracts bronchiolar smooth muscle ( M3 receptor).

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37
Q

How is our normal resting tone of airway smooth muscle maintained?

A

Parasympathetic, vagus nerve

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38
Q

In the CNS the vagal afferent is responsible for what?

A

Sensory. inhaled irritant

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39
Q

In the CNS the efferent vagus is responsible for what?

A

Release ACh. bind to M3. will constrict the smooth muscle in the airway

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40
Q

in sympathetic response we get more of an effect from ____

A

circulating catecholamines (epi).

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41
Q

Do we get help from alpha blockers during an asthma attack?

A

no, the major resistance airways have alpha adrenergic receptors. activation produces bronchoconstriction. so we want beta 2 to relax

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42
Q

What can cause an asthma attack

A
  1. allergens
  2. respiratory infections
  3. irritants
  4. certain meds
  5. exercise
  6. GERD
  7. anxiety/stress/scared
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43
Q

What are the 2 categories for treatment for reactive airway diseases.

A

Short term relievers (sympathomimetics)

long-term controllers (corticosteroids)

44
Q

when do we use a short term reliever vs a long term controller?

A

Short term- during an asthma attack

long term- to prevent an asthma attack

45
Q

What are the 3 sub categories for the short term bronchodilators for asthma?

A

-beta agonists (specifically 2)
-anti muscarinic
-methylxanthines

46
Q

What are the 2 subcategories for long term anti-inflammatory agents for asthma

A

-steroids
-antibodies

47
Q

what are the two mechanisms for the leukotriene antagonists for the long term treatment of asthma?

A

-Inhibit 5 Lipoxygenase
-inhibit receptor binding

48
Q

Short term asthma treatment: Sympathomimetics.
beta agonists have what affect?

A

relax airway smooth muscle.

-inhibit substance from mast cells
-increases mucociliary transport

49
Q

Sympathomimetics toxic effects

A

skeletal muscle tremor

50
Q

Terbutaline, albuterol, metaproterenol, pirbuterol and salmeterol are examples of what?

A

Beta 2 agonists (bronchodilators)

51
Q

Epinephrine for asthma. What receptor? what is the effect?

A

affects beta 1 and 2.
-bronchodilation (B2)
-tachycardia, arrythmias, worsening of angina (B1)

52
Q

epi can stimulate alpha adrenergic receptors and cause what

A

constriction of arterioles and decreased laryngeal edema

53
Q

isoproterenol in asthma

A

potent bronchodilator. strictly beta

its a sympathomimetic

54
Q

SABA and LABA

A

short acting beta agonist
long acting beta agonist

55
Q

Primary short acting beta 2 agonist for asthma?

A

Albuterol

56
Q

beta 2 selective drug used for asthma. what does it cause?

A

albuterol.
bronchodilation.

Terbutaline (IV)

57
Q

Salmeterol and formoterol for asthma, what receptor? action?

A

Long acting beta 2 agonist. duration 12 hours.

58
Q

sympathomimetic agents are usually delivered via _____ because it has _____

A

oral inhalation. greatest airway effects.

59
Q

when we use oral inhalation how much medication do we actually get?

A

10-20%

60
Q

Methylxanthines: theophylline, theobromine, caffeine. what affect do these have for asthma? why aren’t they that great?

what is the main one?

A

Inhibit phosphodiesterase. slight anti inflammatory.

not that great bc they are non medicines. coffee, tea and chocolate

Theophylline

61
Q

How does theoohylline work?

A

PDE inhibitor. breaks down cAMP.

decrease bronchial tone

62
Q

Ipratroprium bromide is a muscarinic antagonist used for what? how does it work

A

COPD. decrease in bronchial tone

63
Q

Atropine is a muscarinic antagonist used for ____.

A

COPD

64
Q

What methylxanthine is used for COPD? what is a special consideration?

A

Purified theophylline. have to monitor for toxicity for purified version (the med itself, not the tea)

65
Q

Atropine, ipratropium bromide and tiotropium are what kind of meds and what are they used to treat? Short acting or long acting?

A

Short term relievers. Muscarinic antagonist (anticolinominetic). COPD

66
Q

Why would we use ipratropium bromide over atropine for COPD

A

its more selective for the lungs and longer acting.

67
Q

Tiotropium is most useful for what? what kind of med is it?

A

COPD. muscarinic antagonist

68
Q

Corticosteroids are used for ______ and it has an ________ effect. Are these short term or long term?

A

Asthma
anti-inflammatory
long term

69
Q

what type of corticosteroids do we like to use primarily?

A

Inhaled

70
Q

True/False: COPD is less responsive to corticosteroids

A

True

71
Q

Steroids are ____ soluble

A

lipid

72
Q

where are glucocorticoids produced?

A

adrenal cortex

73
Q

Glucocorticoids inhibit immune response by _____

A

blocking transcription/translation

74
Q

Where is the receptor for the corticosteroid?

A

in the cytoplasm

75
Q

What happens after the corticosteroid binds to the receptor?

A

migrates into the nucleus itself where it selectively binds to different genes with GRE (glucocorticoid response elements). Will only bind to genes that have the GRE.

76
Q

The GRE (glucocorticoid response element) can be a _____ or a _____.

A

Silencer (shut down production of genes) or enhancer (increase production of genes)

77
Q

What will happen when the corticosteroid binds to the GRE?

A

Increase in annexin-1

Increase in secretory leukoprotease inhibitor

Increase in IL-10

Inhibit NFkB

78
Q

What effect does an increase in annexin-1 have?

A

it will suppress phospholipase A2.

suppresses overall pathway for inflammation

79
Q

what effect does an increase in secretory leukoprotease inhibitors have?

A

blocks protease enzymes that are produced by WBC from a secondary allergen response

80
Q

What effect does an increase in IL-10 have following glucocorticoid administration?

A

its an immunosuppressive cytokine. anti inflammatory

81
Q

what effect would we see from a decrease in NFkB following glucocorticoid administration?

A

repressing the pro inflammatory cytokine

82
Q

What are the negatives to corticosteroids

A

-increase osteoporosis with long term
-slow the rate of growth in children
-orophanyngeal candidiasis (inhaled)

83
Q

what are the positives for corticosteroids?

A

-reduce bronchial activity
-increases airway caliber
-reduce frequency of asthmatic exacerbations
-improve quality of life

84
Q

What is the most effective route of administration for corticosteroids?

A

Aerosol

85
Q

Long term use of corticosteroids (inhaled)

A

-reduces symptoms
-improves pulmonary function
-reduces need for oral steroids
-reduces bronchial reactivity

86
Q

How do Anti-IgE monoclonal antibodies work? short term or long term?

A

Long term. target IgE that binds to mast cells and keep them from degranulating.

87
Q

Xolair would be an example of what? how is it used (short term/long term)

A

Anti-IgE monoclonal antibody. long term controller

88
Q

Leukotriene pathways inhibitors work by what?

A

interrupting synthesis pathway.

89
Q

How can leukotriene pathway inhibitors interrupt synthesis pathway?

A
  1. inhibit 5-lipoxygensase
  2. inhibit binding to receptor
90
Q

Montelukast is a leukotriene pathway inhibitor. How does it work?

A

inhibits binding to the receptor.

91
Q

In a secondary response, leukotriene’s cause what?

A
  1. bronchoconstriction
  2. increase bronchial reactivity
  3. mucosal edema
  4. mucus hypersecretion
92
Q

Clinical pharmacology for mild asthma

A

beta 2 agonists PRN (rescue inhaler)

93
Q

Clinical pharm for mod asthma (nocturnal symptoms)

A

Anti-inflammatory
-inhaled corticosteroids
-oral leukotriene receptor antagonist

94
Q

For frequent symptoms as asthma what would we use?

A

inhaled corticosteroids

95
Q

Clinical pharm for severe symptoms or airway obstruction

A

-oral corticosteroids
-switch to inhaled (over time)
-anti-IgE antibody

96
Q

What are the 5 steps for asthma progression

A
  1. symptoms <2X/month
  2. symptoms >2X/month (not daily)
  3. symptoms most days
  4. symptoms most days + low lung function
  5. uncontrolled symptoms
97
Q

For step 1 asthma what is the short term reliever and long term controller

A

Short- Short acting beta 2 agonist (SAB2A)
Long- Low dose inhaled corticosteroid

98
Q

For step 2 asthma what is the short term reliever and long term controller

A

Short: short acting B2 agonist (SAB2A)
Long: low dose ICS, formoterol. Alt: leukotriene receptor antagonist

99
Q

For step 3 asthma what is the short term reliever and long term controller

A

Short: ICS/formoterol
long: Low dose ICS-LABA, leukotriene receptor antagonist

100
Q

For step 4 asthma what is the short term reliever and long term controller

A

Short: ICS/formoterol
Long: medium dose ICS-LABA add tiotropium or leukotriene receptor antagonist

101
Q

For step 5 asthma what is the short term reliever and long term controller

A

Short: ICS/formoterol
Long: High dose ICS-LABA, oral corticosteroids (short course), refer to specialist, add tiotropium, anti-IgE mab

102
Q

For COPD we want to use meds that do what? what is the standard treatment?

A

Give us a more prolonged opening of the airway.
Long acting beta agonist (LABA) and long acting muscarinic antagonist (LAMA)

103
Q

What drug/class of meds are used for both asthma and COPD?

A
104
Q

What are the Drug/class used in asthma?

A
105
Q

Which ones are used for COPD

A
106
Q

COPD meds are often ____

A

Combination of different drugs.
Ex. Trelegy has
-Fluticasone (anti-inflammatory)
-anticholinergic
-beta 2 agonist (rol)

107
Q

Severe acute attacks

A

-oxygen
-frequent or continuous inhalation of beta-2 agonist
-systemic steroids (prednisone)
-Intubate

Pharm Fall '24 (7 decks)

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