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Pharmacology > Respiratory (Exam 3) > Flashcards

Respiratory (Exam 3) Flashcards

1
Q

Outcome of smoking on public

A

Loss of tax dollars

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2
Q

Indications of human health

A

Life expectancy and infant mortality

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3
Q

Indications of human health vary greatly between…

A

Developed and developing countries

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4
Q

Lower respiratory tract

A

Includes trachea, bronchi, and alveoli in the lungs
Tuberculosis bacteria settle and cause infection

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5
Q

Upper respiratory tract

A

Includes nose, throat, and sinuses

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6
Q

Upper respiratory tract infections

A

Sinusitis, Allergic rhinitis, stridor, tonsillitis, influenza, croup, whooping cough

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7
Q

Lower respiratory infections

A

Acute bronchitis, pneumonia, SARS, tuberculosis

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8
Q

Structure and function of respiratory system

A

Surface area
Blood-gas barrier
Cell types

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9
Q

Largest surface area of the body?

A

Alveolar
Substantial surface for toxicant contact and absorption

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10
Q

Respiratory airways and alveolar epithelium are in…

A

direct contact with environmental toxicants in air

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11
Q

What separates the blood from contaminated environmental air?

A

Alveolar epithelium and capillary endothelium

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12
Q

Cells types involved in pulmonary toxicity

A

Type-I
Type-II
Clara cells
Alveolar macrophages
Endothelial cells

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13
Q

Normal lung

A

Thin walls in upper and lower airways allow normal exchange of gases between blood vessels and airspace

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14
Q

Diseased upper airway of lungs

A

Produces influx of inflammatory cells
Increased fibrosis
Constriction of bronchiolar airways

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15
Q

Diseased lower airway of lungs

A

Fibroblasts and mononuclear inflammatory cells lead to collagen deposits and thickening of lung walls

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16
Q

Clara cells

A

Non-ciliated rounded secretory cells
Target for pulmonary toxicants

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17
Q

How are Clara cells distinguished?

A

By smooth rounded “domes” which project into bronchiolar lumen

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18
Q

Function of Type I alveolar cells

A

Line alveolar spaces
Only barrier between air and capillary endothelium

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19
Q

Where are Clara cells located?

A

Only in small bronchioles

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20
Q

Functions of Type II alveolar cells

A

Synthesize surfactant
Serve as Stem cells for Type I alveolar epithelium
Form part of blood-gas barrier

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21
Q

Functions of alveolar macrophages

A

Phagocytosis
Fibrosis in lungs

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22
Q

How do alveolar macrophages lead to fibrosis?

A

When overload, they die and release acid hydrolases and phospholipases
These stimulate fibroblasts –> Fibrosis

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23
Q

How do Type II cells serve as stem cells?

A

Type I cells destroyed
Type II proliferate to cover alveolar surface

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24
Q

How many days to replace type I cells with type II?

A

2 days

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25
Q

Immature Type II cells

A

Cuboidal and transfer oxygen more slowly than type I

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26
Q

Functions of Clara cells

A

Secretions
Xenobiotic metabolism via CYP450

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27
Q

CYP450

A

Found in high concentration in Clara cells

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28
Q

Functions of endothelial cells (5)

A

Formation of blood-gas diffusion barrier
Maintenance of active transport
Uptake & metabolism of pesticides
Angiotensin I –> angiotensin II
Synthesis & metabolism of prostaglandins

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29
Q

Upper respiratory disorders

A

Allergies
Bronchitis

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30
Q

Obstructive Lung Diseases

A

Asthma
COPD
Cystic Fibrosis

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31
Q

Viruses of Upper Respiratory Tract (CRRABCHIP)

A

Coxsack
Rhinovirus
Respiratory Syncytial
Adenovirus
Bocavirus
Coronavirus
Herpesvirus
Influenza
Parainfluenza

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32
Q

Viruses of Lower Respiratory Tract (PRAMBIS)

A

Parainfluenza
Respiratory Syncytial
Adenovirus
Metapneumovirus
Bocavirus
Influenza
SARS-COV-2

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33
Q

How are upper respiratory disorders characterized?

A

By infection and hypersensitivity of specific areas

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34
Q

Symptoms of upper respiratory disorders

A

Runny nose
Sore throat
Cough
Breathing difficulty and lethargy

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35
Q

Asthma is triggered by

A

environmental variables
allergens, pollutants, exercise

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36
Q

Symptoms of asthma

A

shortness of breath
contraction of bronchiolar smooth muscle

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37
Q

Mechanisms of upper respiratory disorders

A

Swelling
Increased vascular permeability
Increased secretions

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38
Q

Mechanisms of Asthma

A

Activation of mast cells
Infiltration of eosinophils and helper T cells (TH2)

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39
Q

Which two disorders are characterized by chronic inflammation of airway?

A

Asthma
COPD

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40
Q

Symptoms of COPD

A

Shortness of breath
Progressive destruction of lung parenchyma of small airway

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41
Q

Mechanisms of COPD

A

Infiltration of Neutrophils, macrophages and cytotoxic T-cells

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42
Q

Respiratory Disease Controlling Agents

A

Meds used to relieve, treat, or prevent respiratory diseases such as asthma, chronic bronchitis, COPD, or pneumonia

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43
Q

Inhalation Respiratory Agents

A

Deliver meds directly to lungs
Meds act directly on lung tissues
Minimal systemic side effects

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44
Q

Cystic Fibrosis (CF)

A

Autosomal-recessive inherited disease

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45
Q

What does CF cause?

A

Defective Cl- secretion in the lung

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46
Q

What is defective CL- secretion caused by?

A

Mutations of the CFTR Cl- channel

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47
Q

Result of CFTR mutation

A

Thick dehydrated mucus and chronic bacterial infections

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48
Q

How many mutations in CFTR gene have been identified?

A

1600

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49
Q

Therapies for CF target…

A

downstream consequences that are secondary to loss of CFTR Cl- channel function

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50
Q

Goals of CF treatment

A

Prevent/control infections
Remove & loosen mucus
Treat/prevent intestinal blockage
Provide nutrition

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51
Q

CFTR modulators

A

Elexacaftor
Ivacaftor
Tezacaftor
Lumacaftor

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52
Q

Trikafta
(elexacaftor, ivacaftor, tezacaftor)

A

Approved for age 12 and older

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53
Q

Symdeko
(tezacaftor, ivacaftor)

A

Approved for age 6 and older

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54
Q

Orkambi
(lumacaftor, ivacaftor)

A

Approved for age 2 and older

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55
Q

Kalydeco
(Ivacaftor)

A

Approved for 6 months and older

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56
Q

CFTR modulator therapies correct…

A

malfunctioning protein made by CFTR gene

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57
Q

Do CFTR medications work for all CF patients?

A

NO!
Only for specific mutations

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58
Q

Precursor to Histamine

A

Histadine

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59
Q

Autacoids

A

Do NOT act on cholinoreceptors or adenoreceptors but have effects on smooth muscle

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60
Q

Most important amine autacoids

A

Histamine and serotonin

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61
Q

First generation H1 blocker

A

Diphenhydramine

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61
Q

Ergot alkaloids

A

Heterogeneous group of drugs that interact with serotonin, dopamine, and alpha receptors

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61
Q

Second generation H1 blocker

A

Cetirizine

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62
Q

H2 blocker

A

Cimetidine

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63
Q

5-HT1 agonist

A

Sumatriptan

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64
Q

5-HT4 partial agonist

A

Tegaserod

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65
Q

5-HT2 antagonist

A

Ketanserin

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66
Q

5-HT3 antagonist

A

Ondansetron

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67
Q

5-HT agonist in obesity

A

Lorcaserin

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68
Q

Classes of histamine receptors

A

H1-H4

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69
Q

Where are H1 and H2 receptors distributed?

A

Periphery and central nervous system

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70
Q

H1 receptors

A

Blocked selectively by classical ‘antihistamines’

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71
Q

Where are H1 receptors found?

A

Endothelial cells

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72
Q

Are H1 receptors direct or indirect vasodilators?

A

INDIRECT

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73
Q

Are H2 receptors direct or indirect vasodilators?

A

DIRECT

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74
Q

H2 receptors

A

stimulate gastric acid secretion

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75
Q

Where are H2 receptors found?

A

Gastric mucosa
Cardiac muscle
Mast cells
Brain

76
Q

H3 receptors are

A

presynaptic autoreceptors

77
Q

H3 receptors decrease…

A

release of histamine
PROMOTE SLEEP

78
Q

Where are H4 receptors expressed?

A

Cells of hematopoietic lineage

79
Q

What do H4 receptors do?

A

Mediate immune function

80
Q

Low affinity histamine receptors

A

H1 and H2

81
Q

High affinity histamine receptors

A

H3 and H4

82
Q

H1 partially selective antagonists or inverse agonists

A

Mepyramine
Triprolidine
Cetirizine

83
Q

H2 partially selective antagonists or inverse agonists

A

Cimetidine
Ranitidine
Nizatidine

84
Q

H3 partially selective antagonists or inverse agonists

A

Thioperamide
Iodophenpropit
Clobenpropit
Tiprolisant
Proxyfan

85
Q

H4 partially selective antagonists or inverse agonists

A

Thioperamide

86
Q

Distribution of H1 receptors

A

Smooth muscle
Endothelium
Brain

87
Q

Distribution of H2 receptors

A

Gastric mucosa
Cardiac muscle
Mast cells
Brain

88
Q

Distribution of H3 receptors

A

Presynaptic autoreceptor

89
Q

Distribution of H4 receptors

A

Eosinophils
Neutrophils
CD4 T cells

90
Q

H1 receptor antagonists

A

Competitive inhibition of H1 receptor in blood vessels of nasal mucosa

91
Q

1st Gen H1 receptor antagonists

A

Clemastine
Chlorpheniramine
Cyproheptadine
Diphenhydramine
Doxylamine
Hydroxyzine
Ketotifen
Promethazine

92
Q

2nd Gen H1 receptor antagonists

A

Terfenadine
Loratadine (Claratin)
Ceterizine (Zyrtec)

93
Q

3rd Gen H1 receptor antagonists

A

Desloratadine
Fexofenadine (Allegra)
Levocetirizine

94
Q

Which H1 receptor antagonists have anti-muscarinic effects?

A

1st Gens
Diphenhydramine
Bromopheniramine
Chlorpheniramine
Carbinoxamine

95
Q

Bronchiolar Smooth Muscle Relaxation Pathway

A

Epinephrine binds to B2-receptor, activates AC, ATP activates cAMP –> Protein Kinase A –> decrease in Ca+

96
Q

leukotrienes

A

slow reacting substance of anaphylaxis

97
Q

examples of leukotriene inhibitors

A

zileuton
montelukast
pranlukast
zafirlukast

98
Q

zileuton MOA

A

inhibitor of 5-lipoxygenase activity in LOX pathway

99
Q

Adrenergic alpha receptor agonists

A

Phenylephrine
Ephedrine
Psuedoephedrine

100
Q

montelukast/pranlukast/zafirlukast MOA

A

inhibit CYSLTR1 which is a target of cysteinyl leukotrienes

101
Q

Psuedoephrdrine is a _____ of ephedrine.

A

Stereoisomer

102
Q

why is zileuton least prescribed?

A

due to liver toxicity

103
Q

does the leukotriene receptor antagonists have toxicity?

A

little

104
Q

Ephedrine and Psuedoephedrine Pharmacodynamics

A

Mixed acting sympathomimetics
Increase NE release
a1 receptor agonist

105
Q

what happens when cysteinyl leukotrienes bind to CYSLTR1?

A

constriction of airway smooth muscle
increased vascular permeability
decreased mucocilliary clearance
mucus hypersecretion

106
Q

Phenylephrine

A

Selective a1 receptor agonist

107
Q

inhaled corticosteroid MOA

A

cortisol transported by glucocorticoid receptor and enters nucleus
GRE interacts with DNA and alters transcription

108
Q

Sympathomimetic Agents Actions

A

Decrease resistance to airflow by decreasing volume of nasal mucosa
Activation of alpha receptors that have erectile characteristics
Decrease mucous secretions

109
Q

examples of inhaled corticosteroids

A

beclomethasone
flunisolide
fluticasone
budesonide
mometasone

110
Q

where do inhaled corticosteroids bind?

A

glucocorticoid receptor

111
Q

when inhaled corticosteroids bind to the GR, what happens?

A

induction of anti inflammatory genes
inhibition of pro inflammatory genes
modification of cellular protein transcription

112
Q

when is peak action of inhaled corticosteroids?

A

hours to days

113
Q

are inhaled corticosteroids used for acute relief?

A

NO

114
Q

inhaled corticosteroid doses _____ and are initially used to cause _________ for airway clearance

A

vary

bursts

115
Q

most important action of inhaled corticosteroids

A

inhibition of the infiltration of asthmatic airways by lymphocytes, eosinophils, and mast cells

116
Q

Sympathomimetic Agents therapeutic applications

A

Used in OTC remedies for upper respiratory tract disorders

117
Q

therapeutic indications for inhaled corticosteroids

A

COPD and asthma

118
Q

short term adverse effects of inhaled corticosteroids

A

anaphylaxis (beclomethasone)
localized opportunistic infections
SOB
mood alterations
restlessness
dry mouth

119
Q

Ephedrine adverse effects

A

CNS effects
Tachycardia
Hypertension

120
Q

Pseudoephedrine adverse effects

A

less potent tachycardia
increased BP
CNS stimulation

121
Q

long term adverse effects of inhaled corticosteroids

A

moon face
fluid retention
weight gain
osteoporosis
glomerulonephritis

122
Q

mucokinetic therapy also known as

A

mucolytics
mucous controlling agents

123
Q

Phenylephrine adverse effects

A

Increased BP
Vasoconstriction

124
Q

example of mucolytics

A

n-acetylcysteine
Pulmozyme (dornase-a)

125
Q

Where is histaminergic system localized?

A

Posterior hypothalamus

126
Q

MOA of mucolytics

A

breaks down disulfide bonds in mucoproteins

127
Q

therapeutic indications for mucolytics

A

thins abnormally thick mucus in CF and pulmonary fibrosis

128
Q

adverse effects of mucolytics

A

wheezing
airway obstruction due to liquefaction of secretions
nausea and rhinorrhea
odor (hydrogen sulfide)
incompatibility with anti infective compounds

129
Q

Histamine acting via H1 or H3 receptors

A

Regulation of sleep-wakefulness

130
Q

omalizumab

A

recombinant, humanized mAB against human IgE
monoclonal antibody

131
Q

What induces wakefulness?

A

Histamine
H1 receptor agonists

132
Q

omalizumab MOA

A

binds to free IgE so they cannot bind to mast cell and cause inflammation/trigger an effect

133
Q

What promotes sleep?

A

H1 receptor antagonists

134
Q

Pulmozyme MOA

A

recombinant human deoxyribonuclease I (rhDNase)

135
Q

H3 receptor functions as…

A

Autoreceptor
Regulates synthesis/release of histamine

136
Q

rhDNAse

A

selectively cleaves DNA
hydrolyzes the DNA present in sputum/mucus of CF and reduces viscosity in lungs

137
Q

Histaminergic neurons display max activity during…

A

State of vigilance

138
Q

adverse effects of pulmozyme

A

pharyngitis
laryngitis
rash
chest pain

139
Q

dimetapp day vs dimetapp night

A

both have phenylephrine (decongestant)

day - brompheniramine (antihistamine) and dextromethorphan (cough suppressant)

night - diphenhydramine (antihistamine and cough suppressant)

140
Q

Histaminergic neurons cease activity during

A

NREM and REM sleep

141
Q

Classification of beta2 agonists

A

SABAs
LABAs
ultra-LABAs

142
Q

DayQuil vs nyquil

A

both - acetaminophen and dextromethorphan

day - phenylephrine

night - doxylamine

143
Q

Which class of beta2 agonists has shortest half life?

A

SABAs
Immediate symptomatic relief

144
Q

robitussin DM

A

dextromethorphan (antitussive) and guaifenesin (thins mucus)

145
Q

Prolonged duration of beta2 agonists is achievable by

A

decreasing susceptibility of agonists to COMT and MAOs

146
Q

Robitussin Max strength DM day vs night

A

both - dextromethorphan

day - guaifenesin

night - doxylamine

147
Q

Adrenergic beta receptor agonists

A

Bronchodilators dilate bronchi by direct action on adrenoreceptor on bronchial smooth muscle and relac muscle

148
Q

Benadryl allergy (my fav)

A

diphenhydramine (antihistamine)

149
Q

Benadryl Allergy Plus congestion

A

diphenhydramine (antihistamine)
phenylephrine (decongestant)

150
Q

Benadryl Itch Stopping Cream

A

diphenhydramine (antihistamine)
zinc (skin protectant)

151
Q

Benadryl itch cooling gel

A

camphor

152
Q

besides being an antihistamine, Benadryl is also classified as an

A

antitussive (cough suppressant)

because you can’t cough when your passed out cold!

153
Q

Non-selctive Adrenergic beta receptor agonists

A

Epinephrine
Isoproterenol

154
Q

Sympathomimetic agents therapeutics indication

A

Asthma

155
Q

Sympathomimetic agents adverse effects

A

Cardiovascular
Tachycardia
Hypertension
Somatic tremor
Nausea and insomnia

156
Q

Common SABAs

A

Salbutamol (albuterol)
Terbutaline
Levalbuterol
Pirbuterol

157
Q

Common LABAs

A

Salmeterol
Formoterol

158
Q

Common Ultra-LABAs

A

Indacaterol
Olodaerol
Vilanterol
Formoterol

159
Q

Bronchiolar Smooth Muscle Contraction Pathway

A

ACh binds to M2/M3 receptor to release PLC –> cleaved by PIP2 into DAG and IP3
DAG –> PKC
IP3 –> increases Ca+

160
Q

Anticholinergic Agents

A

Ipratropium
Tiotropium
Aclidinium

161
Q

Anticholinergic Agents MOA

A

Block M3 on bronchiolar smooth muscles and secretory tissues

162
Q

Anticholinergic Agents Therapeutic Indications

A

Asthma
COPD

163
Q

Anticholinergic Agents Adverse effects

A

Dry mouth
Ocular
Slow gastric emptying
tremors

164
Q

Antimuscarinic drugs are contraindicated…

A

in patients with glaucoma

165
Q

Methyl Xanthines

A

Theophylline
Aminophylline
Roflumilast

166
Q

Methyl Xanthines MOA

A

Phosphodiesterase inhibitors cause relaxation of smooth muscle and promotes dilation

167
Q

Methyl Xanthines Therapeutic indications

A

Asthma
COPD
Emphysema

168
Q

Methyl Xanthines Adverse Effects

A

Nausea
Tachycardia, increase CO
increase in TPR
CNS stimulation
Insomnia

169
Q

Roflumilast MOA

A

PDE4 inhibitors inhibit inflammatory cytokine and mediator release. Inhibits neutrophil chemotaxis activity
Promotes apoptosis

170
Q

Endothelins

A

Powerful vasoconstrictor produced in endothelial cells

171
Q

Pathway of Endothelins

A

Prepro ET (inactive) –> Big ET (inactive) –> ET (active)

172
Q

Enzymes in endothelins pathways

A

Furin-like protease
ECE-1 and ECE-2

173
Q

Most potent vasoconstrictor in cardiovascular system

A

Endothelin-1

174
Q

ET-1 and ET-2 act on

A

ETA and ETB

175
Q

ET-3 acts on

A

ETB

176
Q

ETA

A

Increases Ca+
Makes receptors more sensitive

177
Q

ETB

A

Clearance receptor
Increases NO

178
Q

Endothelin Receptor Antagonists

A

Bosentan
Ambrisentan
Macitentan

179
Q

Bosentan

A

Dual ETA and ETB antagonist

180
Q

Ambrisentan

A

Selective ETA antagonists

181
Q

Macitentan

A

Selective ETA antagonists

182
Q

Endothelin Receptor Antagonists adverse effects

A

Hypotension
Increased HR
Facial flushing
Edema, headaches

183
Q

Endothelin Receptor Antagonists to treat pulmonary artery hypertension

A

Used in conjunction with negative inotropic agents and direct vasodilators

184
Q

Endothelin Antagonists are contraindicated

A

in pregnancy

185
Q

Groups of Prophylactic bronchodilators

A

Cromolyn Sodium
Leukotriene Inhibitors

186
Q

Cromolyn Sodium

A

Low solubility, poorly absorbed
Must be inhaled

187
Q

Cromolyn Sodium has no effect on

A

airway smooth muscle tone

188
Q

Cromolyn Sodium is ineffective in

A

reversing bronchospasm

189
Q

Cromolyn Sodium is only of value when

A

taken prophylactically

190
Q

Cromolyn Sodium MOA

A

Alters function of delayed Cl- channels in cells
Inhibits cell activation

Pharmacology (16 decks)

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