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Block 2: Pharmacology > Lecture 5 > Flashcards

Lecture 5 Flashcards

1
Q

(Useful Drugs)
B2 Agonist?

A

-Albuterol
-Salmeterol

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2
Q

(Useful Drugs)
Leukotriene Antagonist?

A

Montelukast

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3
Q

(Useful Drugs)
Muscarinic Antagonist?

A

-Ipratropium
-Tiotropium

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4
Q

(Useful Drugs)
Inhaled Corticosteroid?

A

Fluticasone

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5
Q

(Useful Drugs)
Monoclonal Anti-IgE antibody?

A

Omalizumab

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6
Q

(Useful Drugs)
Rescue?

A

-Albuterol
-Ipratropium
-Tiotropium

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7
Q

(Useful Drugs)
Control?

A

-Salmerterol
-Montelukast
-Fluticasone
-Omalizumab
-Ipratropium
-Tiotropium

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8
Q

(Useful Drugs)
Asthma?

A

-Ipratropium
-Tiotropium
-Montelukast
-Omalizumab

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9
Q

(Useful Drugs)
COPD?

A

-Ipratropium
-Tiotropium

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10
Q

(Useful Drugs)
Asthma and COPD (BOTH)?

A

-Albuterol
-Salmeterol
-Flucticasone

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11
Q

(Lung Disease)
Increased airway resistance (obstructive lung disease)?

A

-Decreased airflow (zones 0-10, increased resistance) (decreased elasticity)
-Airflow is limited during expiration (hard to get air out, people often hyperinflated)
-Decreased L-CW compliance (restrictive lung disease) (parenchyma fibrosis)

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12
Q

(Lung Disease)
Increased airway resistance (obstructive lung disease)?

A

-Decreased airflow (zones 0-10, increased resistance) (decreased elasticity)
-Airflow is limited during expiration (hard to get air out, people often hyperinflated)
-Decreased L-CW compliance (restrictive lung disease) (parenchyma fibrosis)

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13
Q

Obstructive Lung Diseases?

A

-Asthma
-Chronic Obstructive Pulmonary Disease

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14
Q

(Obstructive Lung Diseases)
Asthma?

A

Spasmodic contraction of smooth muscle in bronchi

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15
Q

(Obstructive Lung Diseases)
COPD?

A

-Bronchitis (inflammation of bronchi and bronchioles (increased mucus))
-Emphysema (alveolar destruction)
-Combination
(Bronchitis (mucus) + Emphysema (loss of alveolar))

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16
Q

Resistance to airflow in?

A

Conducting Zone (only conducting airway has smooth muscle)

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17
Q

Respiratory Zone is mainly for?

A

Gas Exchange

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18
Q

Conducting Zone is mainly for?

A

Resistance

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19
Q

Further down Airway there is an?

A

Increase in cross-sectional area

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20
Q

Further down Airway there is an?

A

Increase in cross-sectional area

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21
Q

Factors that Determine Airway Resistance?

A

(SALE)
-Structure of airways
-Airway smooth muscle contraction
-Lumen obstruction (mucus)
-Elasticity of lung parenchyma

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22
Q

(Airway smooth muscle contraction)
When receptors activate, they will increase in?

A

Intracellular Ca2+ (Gq) causes smooth muscle contraction

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23
Q

(Airway smooth muscle contraction)
No change in alveoli because?

A

Alveoli do not have smooth muscle

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24
Q

Autonomic Control of Airway Resistance?

A

1) Provides reflex arc for airway constriction following inhalation of irritants
2) Provides airway dilation during exercise

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25
Q

(Autonomic Control of Airway Resistance)
Provides reflex arc for airway constriction following inhalation irritants?

A

Irritant –> afferent –> medulla –> Para –> constriction to remove irritant

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26
Q

(Autonomic Control of Airway Resistance)
Provides airway dilation during exercise?

A

-Decreased parasympathetic influence
-Increased circulation epinephrine (no direct sympathetic innervation of airway smooth muscle in humans) –> bronchial dilation

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27
Q

(Airway Diameter Depends on Retractile Force of Tissue Surrounding Airways in Lung Parenchyma)
As Lung expands, retractile force on airways?

A

Increase
(as lung expands alveoli pull on airway to keep it open, if we destroy alveoli there is nothing to keep airway from collapsing (emphysema))

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28
Q

(Spirometry)
Breathing normal?

A

vt

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29
Q

(Spirometry)
After inhaling, there’s still air in lungs?

A

IRV

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30
Q

(Spirometry)
After exhaling, there’s still air left in lungs?

A

FRC

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31
Q

(Spirometry)
FRC includes the air you can exhale out forcefully?

A

ERV

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32
Q

(Spirometry)
Air left in your lungs no matter how hard you try to breath out?

A

RV

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33
Q

(Spirometry)
Total amount you can breathe in?

A

IC

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34
Q

(Spirometry)
All air you can force in and out (inhale and exhale as fast as you can) (IC + ERV)?

A

FVC

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35
Q

(Spirometry)
TLC?

A

Total Lung Capacity

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36
Q

(Spirometry)
FRC?

A

Functional Residual Capacity

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37
Q

(Spirometry)
IRV?

A

Inspiratory Reserve Capacity

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38
Q

(Spirometry)
ERV?

A

Expiratory Reserve Capacity

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39
Q

(Spirometry)
FVC?

A

Forced Vital Capacity

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40
Q

(Spirometry)
RV?

A

Residual Volume

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41
Q

(Spirometry)
IC?

A

Inspiratory Capacity

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42
Q

(Spirometry)
Vt?

A

Tidal Volume

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43
Q

(Spirometry)
VC?

A

Vital Capacity

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44
Q

(Volume-Time Curves)
FEV1?

A

Forced Expired Volume in 1 second

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45
Q

(Volume-Time Curves)
FVC?

A

Inhaled deep + Exhale deep

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46
Q

(Volume-Time Curves)
With COPD it’s hard to?

A

Get air out and it will take longer, this will decrease FEV/FVC

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47
Q

(Volume-Time Curves)
COPD will ___ FEV?

A

Decrease FEV

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48
Q

(Obstructive Lung Disease)
Emphysema?

A

-Airspace enlargement destruction (alveoli)
-Decreased FEV1
-Decreased FVC
-Decreased FEV1/FVC ratio
-Decreased elastic recoil reduces structural support for bronchioles. This bronchioles collapse (increase resistance)

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49
Q

(Obstructive Lung Disease)
Chronic Bronchitis?

A

-Mucus gland hyperplasia and hyper secretion, bronchiole fibrosis
-Decreased FEV1
-Decreased FVC
-Decreased FEV1/FVC ratio
-Increased resistance due to clogged bronchioles

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50
Q

(Obstructive Lung Disease)
Asthma?

A

-Smooth muscle hyperplasia/spasmodic contraction, mucus, inflammation, AHR
-Decreased FEV1
-Decreased FVC
-Decreased FEV1/FVC ratio
-Increased resistance due to contracted bronchioles and bronchi

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51
Q

(Obstructive Lung Disease)
All will ___ FEV but all for different reasons?

A

Decrease FEV

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52
Q

(Obstructive Lung Disease)
FVC will decrease only with?

A

Severe Disease

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53
Q

(Obstructive Lung Disease)
FVC will decrease only with?

A

Severe Disease

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54
Q

Reversible Airway Obstruction (Bronchospasm)?

A

Asthma is a common chronic disorder of airways that is complex and characterized by variable and recurring symptoms, airflow obstruction (bronchospasm), bronchial hyperresponsiveness, and an underlying inflammation

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55
Q

Spirometry: Assessment of asthmatic airway obstruction (bronchospasm)?

A

-“Hallmark” of asthma: reversibility with bronchodilator
-Airway obstruction may be absent between “attacks”

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56
Q

Measuring Airway Responsiveness?

A

-We don’t want to drop too much and kill someone. So, we look at the amount of methacholine to drop FEV by 20%
-If 0.3 mg/mL of methacholine causes a drop of FEV by 20% = severe asthma

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57
Q

Measuring Airway Responsiveness?

A

-We don’t want to drop too much and kill someone. So, we look at the amount of methacholine to drop FEV by 20%
-If 0.3 mg/mL of methacholine causes a drop of FEV by 20% = severe asthma

58
Q

Asthma - Link to Allergy?

A

-Allergen Sensitization
-Allergen-induced mast cell activation
(allergen detected, presented to T-cell by APC. T-cell instructs by B-cell to produce IgE. Circulating IgE binds to mast cell to release its granules with inflammatory agents)

59
Q

(Remodeling of Lung in Severe Asthma)
Severe Asthmatic Lung?

A

-Epithelial damage
-Goblet cell hyperplasia
-Smooth muscle hypertrophy and hyperplasia
-Basement membrane thickening
-Collagen deposition
-Submucosal fibrosis
-Angiogenesis
-Mucus plug formation

59
Q

(Remodeling of Lung in Severe Asthma)
Severe Asthmatic Lung?

A

-Epithelial damage
-Goblet cell hyperplasia
-Smooth muscle hypertrophy and hyperplasia
-Basement membrane thickening
-Collagen deposition
-Submucosal fibrosis
-Angiogenesis
-Mucus plug formation

60
Q

(Role of Vagal Nerve in Respiratory Diseases)
Vagal Afferent?

A

Sensory nerves that are activated by inflammation, irritants and pollutants

61
Q

(Role of Vagal Nerve in Respiratory Diseases)
Vagal Efferent?

A

Parasympathetic nerves (cholinergic) innervating smooth muscle and mucosal glands

62
Q

(Role of Vagal Nerve in Respiratory Diseases)
Activation of sensory nerves causes CNS reflexes?

A

-Cough
-Dyspnea
-Bronchospasm (para)
-Hypersecretion (para)

63
Q

(Role of Vagal Nerve in Respiratory Diseases)
Asthmatic subjects are?

A

Hyperreflexive to inhaled irritants

64
Q

(Chronic Obstructive Pulmonary Disease - Smoking)
Progressive decrease in lung function?

A

(clinically relevant in aged population)
-Decreased FEV1
-Limited reversibility

65
Q

(Chronic Obstructive Pulmonary Disease - Smoking)
Presenting symptoms?

A

-Cough
-Dyspnea (SOB)

66
Q

(Chronic Obstructive Pulmonary Disease - Smoking)
Lung Function?

A

-Decreased airflow
-Hyperinflation

67
Q

(Chronic Obstructive Pulmonary Disease - Smoking)
Worse with exercise?

A

Exercise Tolerance Test (6 minute walk)

68
Q

(Chronic Obstructive Pulmonary Disease - Smoking)
Exacerbations (infections) and Airway?

A

Hyperactivity (limited)
(different than asthma)

69
Q

(Chronic Obstructive Pulmonary Disease - Smoking)
People with COPD tend to?

A

Die from bacterial infection

70
Q

(Chronic Obstructive Pulmonary Disease - Smoking)
If you start smoking?

A

-FEV will decrease
-By time 60 cannot breathe out

71
Q

(Chronic Obstructive Pulmonary Disease - Smoking)
Neutrophilia?

A

Neutrophil elastase, matrix metalloproteinases, reactive oxygen species –> tissue destruction

72
Q

(Chronic Obstructive Pulmonary Disease - Smoking)
Neutrophils will get rid of?

A

Damaged cells but in the process they damage normal cells

73
Q

(Chronic Obstructive Pulmonary Disease - Smoking)
Neutrophilia (examples of work)?

A

-Remodeling
-Smooth muscle metaplasia
-Goblet cell metaplasia
-Fibrosis
-Cell death
-Increase Resistance
(Decrease Airflow)
-Decrease Elastic Recoil
-Decrease Gaseous Exchange

74
Q

Chronic Bronchitis?

A

(blue boaster)
Excessive mucus production, fibrosis of bronchioles

75
Q

Fibrosis/Mucus Blockage?

A

Increases Resistance and Decreases Airflow

76
Q

Lack of Ventilation?

A

Hypoxia (blue), edema (bloater)
(mucus stuck in conducting airway so no O2 delivery)

77
Q

Emphysema?

A

(pink puffer)
Parenchymal/Alveolar damage

78
Q

Decrease Alveoli Structure = ?

A

-Decrease Elastic Recoil and Decrease Structural Support (Bronchiole collapse)
-Leads to Increase Resistance and Decreased Airflow

79
Q

Lack of Perfusion = only?

A

Mild Hypoxia (pink)

80
Q

Bronchiole Collapse = ?

A

Hard to Breathe (puffer)

81
Q

Bronchiole Collapse = ?

A

Hard to Breathe (puffer)

82
Q

(Chart)
Asthma?

A

-Usually <40 years (children)
-No History Required
-Common (IgE) (allergy)
-Episodic drop in FEV1
-Increase resistance reversible with B2 agonist
-Increased Hyperactivity
-Frequent family history
-Cough (often dry)
-Eosinophils, Mast Cells, Basophils
-CD4+, Th2 cells, B cells

83
Q

(Chart)
COPD?

A

-Usually >40 years
->10 pack years of smoking
-No correlated with allergies
-Chronic drop in FEV1
-Minimal increase resistance reversible with B2 agonist
-Small increase in hyperactivity
-Cough (often wet)
-Neutrophils, Macrophages
-CD8+, Tcyt cells

84
Q

Bronchitis?

A

Gap is filled with mucus

85
Q

Asthma?

A

Gap closed with bronchoconstriction

86
Q

Emphysema?

A

Lost structural support, bronchi collapse

87
Q

Bronchitis, Asthma, and Emphysema all?

A

Increase Resistance

88
Q

Bronchitis, Asthma, and Emphysema all?

A

Increase Resistance

89
Q

(Obstructive Disease Pharmacological Treatments)
Primarily concerned with increasing?

A

Airflow/decreasing resistance

90
Q

(Obstructive Disease Pharmacological Treatments)
Actively cause bronchodilation (beta-adrenoceptor agonists) B2?

A

Albuterol, Salmetrol

91
Q

(Obstructive Disease Pharmacological Treatments)
Inhibit specific inflammatory mediators (leukotriene and muscarinic antagonists)?

A

Montelukast, Ipratopium, Tiotropium

92
Q

(Obstructive Disease Pharmacological Treatments)
Reduce inflammation (corticosteroids)?

A

Fluticasone

93
Q

(Obstructive Disease Pharmacological Treatments)
Prevent inflammation (anti-IgE antibodies (for asthma only))?

A

Omalizumab

94
Q

(Obstructive Disease Pharmacological Treatments)
Some are used for?

A

Rescue from a respiratory attack, some are used for control of symptoms

95
Q

3 Things for Patient Education?

A

1) Lifestyle changes (quit smoking)
2) Compliance
3) Control of Environment (allergens, mold, pollutants)

96
Q

(B Adrenoceptor Agonists)
B2 selective ligands?

A

Albuterol, Salmeterol (inhalation, oral)

97
Q

(B Adrenoceptor Agonists)
MOA?

A

-Activation of B2 adrenoceptors on bronchial smooth muscle (increase cAMP) –> relaxation –> bronchodilation

98
Q

(B Adrenoceptor Agonists)
Therapeutic Uses?

A

-Short-acting (albuterol) (rescue for asthma and COPD)
-Long-acting (LABA) (salmeterol)
(control for asthma and COPD)
-Salmeterol (everyday use)

99
Q

(B Adrenoceptor Agonists)
Side Effect?

A

Tachycardia
(B2 also in Heart and these drugs are not completely B1 inactive)

100
Q

(B Adrenoceptor Agonists)
Asthma Attack?

A

Give Albuterol

101
Q

(B Adrenoceptor Agonists directly relax Bronchial Smooth Muscle)
MOA?

A

(increase cAMP –> relaxation –> bronchodilation)
1) Facilitates sequestration of Ca2+
2) Inactivates MLCK
3) Inactivates MLC20

102
Q

(B Adrenoceptor Agonists directly relax Bronchial Smooth Muscle)
PKA inhibits?

A

Kinase

103
Q

(B Adrenoceptor Agonists directly relax Bronchial Smooth Muscle)
Myosin light chain phosphatase, dephosphorylate myosin?

A

No cont.

104
Q

(Cysteinyl Leukotrienes)
Originally known as slow reacting substances of anaphylaxis de novo synthesis occurs in?

A

Mast cells and basophils following allergen-binding IgE de novo synthesis also in eosinophils and neutrophils

105
Q

(Cysteinyl Leukotrienes)
Pharmacology?

A

-G protein coupled receptors CysLT1 and CysTL2
-Both are Gq coupled - phospholipase C activation –> IP3 and DAG production, increase Ca2+ and PKC
-All cysteinyl leukotrienes are effective at both receptors

106
Q

(Cysteinyl Leukotrienes)
Receptor Expression?

A

Bronchial smooth muscle (CysLT1)
(causes contraction –> bronchospasm)
(increase hyperplasia)

107
Q

(Cysteinyl Leukotrienes)
LTD has?

A

Highest Concentration

108
Q

(Leukotriene Antagonist)
Montelukast given?

A

Oral

109
Q

(Leukotriene Antagonist)
Montelukast MOA?

A

-CysTL1 antagonist
-Prevents Sys-LT-induced bronchospasm, decrease immune cell infiltration, no decrease AHR, very mild reversal of remodeling

110
Q

(Leukotriene Antagonist)
Montelukast Therapeutic Uses?

A

-Control for asthma
-Not for COPD because you don’t produce LT

111
Q

Leukotriene Antagonist is a ___ for asthma?

A

Control

112
Q

Muscarinic Antagonists?

A

-Ipratopium bromide (non-selective)
-Tiotropiumbromide (M1, M3 but not M2 inhibitor) - quaternary amine derivates of atropine (quart can’t move = less SE)

113
Q

(Muscarinic Antagonists)
Given?

A

Inhalation

114
Q

(Muscarinic Antagonists)
MOA?

A

-Blocks acetylcholine-induced activation of muscarinic receptors on: (airway smooth muscle (M3) - decrease bronchospasm) (epithelial mucosal glands (M3) - decrease mucus secretion)

115
Q

(Muscarinic Antagonists)
Therapeutic Uses?

A

-Rescue for asthma
-Control for COPD

116
Q

(Muscarinic Antagonists)
Therapeutic Uses?

A

-Rescue for asthma
-Control for COPD

117
Q

Inhaled Corticosteroids?

A

Analogs of corticosterone, steroid hormone (adrenal cortex) ex. Budesonide, Fluticasone

118
Q

(Inhaled Corticosteroids)
Given?

A

Nasal or Inhalation

119
Q

(Inhaled Corticosteroids)
MOA?

A

Anti-inflammatory, decrease infiltration of eosinophils/basophils/mast cells, mild reversal of remodeling

120
Q

(Inhaled Corticosteroids)
Therapeutic Uses?

A

-Control for asthma (inhalation, nasal)
-Control for COPD - limited relief

121
Q

(Corticosteroid: Mechanism of Action)
In multiple cell types including?

A

Epithelial cells, lymphocytes, granulocytes, mast cells, smooth muscle, dendrites cells and fibroblasts

122
Q

(Corticosteroid: Mechanism of Action)
Steroid molecule binds to?

A

Cytoplasmic glucocorticoid receptor (GR), dimerizes, enters nucleus, binds to DNA at specific sites (glucocorticoid response elements):
(decrease pro-inflammatory protein production)
(increase anti-inflammatory protein production)

123
Q

(Corticosteroid: Mechanism of Action)
Modulation of Protein expression is?

A

Slow-onset (>12 hours)

124
Q

(Corticosteroid: Mechanism of Action)
Slow Onset?

A

Not a rescue drug

125
Q

(Corticosteroid: Mechanism of Action)
Decrease de novo transcription of?

A

Pro-inflammatory proteins: cytokines (ex. IL-4 and IL-5) and chemokine

126
Q

(Corticosteroid: Mechanism of Action)
Increase transcription of IkB?

A

A potent anti-inflammatory protein that inhibits NFkB (pleiotropic gene transcription factor which produces TNFa, iNOS, COX2, adhesion molecules, IL-2)

127
Q

(Corticosteroid: Mechanism of Action)
Inhibits AP-1?

A

Pleotropic gene transcription factor which produces collagenase, IL-2

128
Q

(Corticosteroid: Mechanism of Action)
Increase transcription of?

A

-B2, Adrenoceptor
-Lipocortin 1 (inhibitor of PLA2)

129
Q

(Corticosteroid: Mechanism of Action - Asthma)
Asthma?

A

-Steroids decrease airway eosinophilia
-Steroids decrease IgE production from B cells and inhibit mast cell degranulation

130
Q

(Corticosteroid: Mechanism of Action - Asthma)
COPD?

A

-Corticosteroids have little effect on neutrophilic
-Corticosteroids may increase lung defense against neutrophil elastase
-Corticosteroids may decrease activity of neutrophil-derived metalloproteinases
-Corticosteroids have no effect on MORTALITY

131
Q

(Corticosteroid: Mechanism of Action - Asthma)
COPD?

A

-Corticosteroids have little effect on neutrophilic
-Corticosteroids may increase lung defense against neutrophil elastase
-Corticosteroids may decrease activity of neutrophil-derived metalloproteinases
-Corticosteroids have no effect on MORTALITY

132
Q

Corticosteroid: Side Effects?

A

Due to GR signaling/MR signaling (mineralocorticoid/aldosterone)/both in multiple tissues

133
Q

Corticosteroid Inhalation Side Effects?

A

-Inhalation decreases systemic effects
-Increases risk of infection (oropharyngeal candidiasis)
(COPD: bacterial lung infection - pneumonia)

134
Q

Corticosteroid Oral (systemic) Side Effects?

A

-Hyperglycemia
-Dyslipidemia
-Hypertension
-Osteoporosis
-Cataracts
-Glaucoma
-Teratogenic

135
Q

(Anti-IgE Antibodies)
Omalizumab given?

A

Subcutaneous injection

136
Q

(Anti-IgE Antibodies)
Omalizumab?

A

Monoclonal antibody (IgE)

137
Q

(Anti-IgE Antibodies)
Omalizumab MOA?

A

-Binds to free IgE (Fc region), promotes destruction
-Decreases IgE from binding to FCeR1 and FCeR2
-Decreases expression of FCeR1 on mast cells/basophils
-Decreases allergen-induced IgE crosslinking on mast cells/basophils

138
Q

Anti-IgE Antibodies MOA?

A

-Prevents allergen-induced bronchospasm, decreased immune cell infiltration, decreased exacerbations, no decreased AHR, effect on remodeling is unclear

139
Q

Anti-IgE Antibodies Therapeutic Uses?

A

Control for severe, steroid-resistant asthma

140
Q

Anti-IgE Antibodies Rate of Onset?

A

-Circulating IgE destroyed in hours/days
-Takes more than a week for mat cell-attached IgE to reduce

141
Q

Anti-IgE Antibodies _____ only?

A

Control only

Block 2: Pharmacology (5 decks)

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