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PHARM 123 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

List the parts of the upper respiratory tract

A

nose
nasal cavity
paranasal sinuses
pharynx
larynx

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2
Q

List the parts of the lower respiratory tract

A

trachea
bronchi and smaller bronchioles
lungs
alveoli

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3
Q

What is the purpose of the nose and nasal cavity?

A

provides airway for resp
moistens and warm air
filters inhaled air
contains olfactory receptors
involved in speech

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4
Q

What is the purpose of paranasal sinuses?

A

air containing cavities in the skull
lined with mucous membrane

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5
Q

What is the function of paranasal sinuses?

A

decrease weight of skull
increase resonance of voice
buffer against facial trauma
insulates sensitive structures from rapid temperature fluctuations
humidifies and heats air
immunological defense

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6
Q

What is the purpose of nasopharynx?

A

simply an air passageway
closes while swallowing
contains nasopharyngneal and tubal tonsil

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7
Q

What is the purpose of oropharynx?

A

food and air passageway
epiglottis closes during inspiration to prevent aspiration
contains palatine and lingual tonsils

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8
Q

What is the purpose of laryngopharynx?

A

connects throat to esophagus
extends to branching of respiratory and digestive pathways

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9
Q

What is the purpose of larynx?

A

connects the laryngopharynx to the trachea
contains vocal folds
thyroid glands sits on the outside of the larynx

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10
Q

What is the main function of larynx?

A

protection
aids in coughing and other reflexes
prevents food/fluid from entering lungs

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11
Q

What is the breakdown of bronchi and smaller bronchioles?

A

primary bronchi
secondary bronchi
tertiary bronchi
terminal –> respiratory bronchioles

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12
Q

What is the purpose of bronchi and smaller bronchioles?

A

contains mucus and cilia to remove contaminants
can constrict or dilate to modify airflow

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13
Q

How many lobes are on each lungs?

A

right lung contains three lobes
left has two lobes

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14
Q

What is visceral pleura?

A

it covers the lungs

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15
Q

What is the parietal pleua?

A

it covers the ribs and diaphragm

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16
Q

What the space between lungs and ribs?

A

pleural cavity

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17
Q

What is the breakdown of alveoli?

A

type I cells
type II cells

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18
Q

What is types I cells?

A

squamous epithelium

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19
Q

What is types II cells?

A

cuboidal epithelium
contain lamellar bodies for surfactant secretion

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20
Q

What is alveolar macrophages?

A

the janitor of the alveoli and bronchioles

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21
Q

What are pathway of cells in the alveoli?

A

alveolar type I cell –>
alveolar basement membrane –>
capillary basement membrane –>
capillary endothelial cells

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22
Q

What is the purpose of alveoli?

A

capillaries surround the alveoli to facilitate gas exchange
CO2 is diffused out of the blood and into the alveoli for exhaustion
O2 diffuses out of the alveoli and into the blood

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23
Q

What governs how well the lungs/alveoli can inflate and deflate?

A

Compliance and elasticity

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24
Q

What is the two pathways of blood supply?

A

pulmonary vessels
bronchial vessels

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25
Q

What is the purpose of pulmonary vessels?

A

responsible for gas exchange
deoxygenated blood arrives through pulmonary artery from the right ventricle
arrives at resp membrane and becomes oxygenated
pulmonary veins return oxygenated blood to left atrium

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26
Q

What is the purpose of bronchial vessels?

A

come from systemic circulation
oxygenates the lung tissue itself

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27
Q

What is conducting system?

A

includes all sites involved in conducting air into the lungs

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28
Q

What is the respiratory zone?

A

consists of where gas exchange occurs

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29
Q

List where the respiratory zones are?

A

respiratory bronchioles
alveolar ducts
alveolar sacs
alveoli

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30
Q

What is respiration?

A

the exchange of gases between the atmosphere, blood and cells
cells continually use O2 and release CO2

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31
Q

What is the stages of respiration?

A

pulmonary ventilation
external respiration
internal respiration

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32
Q

Explain inspiration

A

air is pulled into the lungs when alveolar pressure < atmospheric pressure
air is pushed out of the lungs when alveolar pressure > atmospheric pressure
pressure is controlled by contraction or relaxation of the diaphragm

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33
Q

What does the external intercostal muscles do?

A

aid in expanding or contracting thorax

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34
Q

Define quiet inspiration

A

an active process representing normal breathing
involves diaphragm and intercostal muscles

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35
Q

Define forced inspiration

A

used in times of extra need
sternocleidomastoids, scalenes, pectoralis minor used

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36
Q

Define quiet expiration

A

a passive process
diaphragm relaxes and raises upwards

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37
Q

Define forced expiration

A

uses obliques and intercostals to contract inwards to help force air out
activated when air movement out of the lungs impeded

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38
Q

What is external respiration?

A

exchange of gases
CO2 removed O2 gained
occurs via diffusion

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39
Q

What is a normal partial pressure oxygen gradient?

A

Alveolar space = 100 mgHg
deoxygenated blood = 40 mgHg

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40
Q

Normal partial pressure carbon dioxide gradient?

A

alveolar space = 40 mmHg
deoxygenated blood = 45 mgHg

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41
Q

ventilation - perfusion mismatch

A

can occur in severe lung disease
- ventilation and blood flow are not at an optimal ratio

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42
Q

Ventilation and Perfusion Matching

A

exchange of gas and blood supply must be balanced for poper external respiration
must be enough air in the alveoli, bloodflow in the capillaries and hemoglobin to carry oxygen

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43
Q

V/Q mismatch can lead to

A

hypoxemia

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44
Q

Define eupnea

A

normal, good healthy unlabored breathing

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45
Q

Define apnea

A

potentially serious sleep disorder in which breathing repeatedly stops and starts

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46
Q

Define tachypnea

A

abnormally rapid breathing

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47
Q

define costal breathing

A

a mode of breathing that requires contraction of the intercostal muscles

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48
Q

Define diaphragmatic breathing

A

an exercising technique to help strengthen your diaphragm and fill your lungs with air more efficiently

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49
Q

Define of type 1 respiratory failure

A

the inability of lungs to perform adequate gas exchange
can lead to hypoxemia

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50
Q

What are some potential causes of type 1 resp failure?

A

lung disorder
pneumonia
pulmonary edema, fibrosis, embolism, hypertension

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51
Q

What is hypoxemia?

A

Oxygen saturation falls <90%
CO2 levels remain normal or can be low

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52
Q

What is type 2 respiratory failure?

A

also called ventilatory failure
it occurs when breathing is not sufficient to rid the body of CO2
leads to hypercapnia

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53
Q

What are potential causes of Type 2 resp failure?

A

decreased CNS drive
impaired neuromuscular function
chronic bronchitis or COPD
excessive inspiratory load

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54
Q

What are arterial blood gases used for?

A

determine acid-base balance which helps determine causes of resp issues
blood ph controlled by action of the lungs and kidneys
useful to diagnosis the underlying cause of a breathing disorder

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55
Q

What is PaCO2

A

pressure or tension exerted by dissolved CO2 gas in blood

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56
Q

What is PaO2

A

indicates the level of oxygenation of arterial blood

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57
Q

What is respiratory compensation?

A

lungs can modulate how much CO2 is retained or excreted

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58
Q

What is metabolic compensation?

A

kidneys can modulate how much HCO3 is retained or excreted

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59
Q

What is disturbances of respiratory acidosis

A

have acidic
normal HCO3
high PaCO3

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60
Q

What is disturbances of respiratory alkalosis?

A

have basic
normal HCO3
low PaCO3

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61
Q

What is the disturbances of metabolic acidosis?

A

have acid
low HCO3
normal PaCO3

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62
Q

What is the disturbance of metabolic alkalosis?

A

have acid
high HCO3
normal PaCO3

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63
Q

What are the two main tests for lung function?

A

Spirometry
Peak flow meter

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64
Q

Explain what a spirometry

A

a spirometry objectively assesses an individual’s pulmonary performance
measures how much air you can move in and out of lungs

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65
Q

Explain how a peak flow meter works?

A

utilized in people with asthma
used by an individual to compare current results to personal best

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66
Q

What does spirometry measure?

A

Lung volume
lung capacity
airflow measures

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67
Q

List the factors of lung volume

A

tidal volume
inspiratory reserve volume
expiratory reserve volume
residual volume

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68
Q

List the factors of lung capacity

A

total lung capacity
functional residual capacity
vital capacity

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69
Q

List the factors of airflow measures

A

forced expiratory volume in 1 second (FEV1)
forced vital capacity (FVC)
FEV1/FVC ratio

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70
Q

What does the FEV1/FVC tell us?

A

helps differentiate between restrictive and obstructive lung disease

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71
Q

What ratio shows obstructive lung disease?

A

low FEV/FVC, normal FVC

72
Q

What ratio shows restrictive lung disease?

A

normal FEV1/FVC ratio but low FVC

73
Q

What is spirometry is used to determine?

A

reversibility of airway obstruction
test repeated 10-15 m after inhaling a bronchodilator
if FEV1 increases, obstruction is present

74
Q

What improves as fitness does

A

lungs can accommodate higher volumes of air
increased diffusion of resp gases
strengthen cilia and diaphragm
strengthens other muscles of inspiration/expiration
VO2 max increases

75
Q

People who smoke have poor exercise tolerance for many reasons

A

nicotine causes bronchoconstriction
lung fibrosis
excess mucous secretion
inhibited cilia
destruction of elastic fibers

76
Q

What is age-related impact on lung function

A

respiratory tissues and chest wall becomes more rigid
weak resp muscles
vital capacity gradually decreases
macrophages activity decreases
cilia less active

77
Q

What are the characteristics of asthma?

A

paroxysmal or persistent symptoms
dyspnea, wheezing, cough, chest tightness sputum production
airway hyper-responsiveness to a variety of stimuli

78
Q

What is the epidemiology of asthma?

A

over 3 million canadians have it
canada has one of the highest rates in the world

79
Q

How many people with asthma do not have it under control?

A

6 out of 10

80
Q

What are some of the risk factors of asthma?

A

genetic predispoition
hygiene hypothesis
atopic vs no atopic
gender
maternal factors
perinatal factors
factors during childhood
factors during adulthood

81
Q

Explain genetic predisposition

A

development of asthma –> pre-disposing to atopy
severity of condition –> airway hyperresponsiveness
response to therapy

82
Q

What are some factors that childs who had lower risk of asthma?

A

are exposed to high levels of bacteria or endotoxin
have older siblings
have early enrollment into child care
experience exposure to fewer antibiotics

83
Q

Explain atopic vs non-atopic

A

allergic responses can result in asthma
the greater an individual’s sensitization, the higher the likelihood of asthma
high levels of IgE found
exposure to high levels of allergenes increase likelihood of asthma

84
Q

Explain the etiology factor of sex

A

childhood asthma has a greater prevalence in males
equal around 20-40
more females at the age of 40 and above

85
Q

How does maternal factors affect asthma?

A

increasing maternal age –> lower risk of asthma
diet during pregnancy can also be a factor

86
Q

What perinatal factors increase the chance of having asthma?

A

pre-eclampsia
prematurity
mode of delivery (C section)
lack of vitamin D supplementation

87
Q

What factors during childhood increase the odds of having asthma?

A

viral infections predictive of asthma later in life
use of medication in infancy
air pollution
tobacco smoke exposure

88
Q

What factors during adulthood increase the odds of having asthma?

A

obesity
tobacco smoke
occupational exposures
rhinitis

89
Q

List some asthma triggers

A

irritants
respiratory tract infections
weather
stress
hormonal fluctuations
GERD
medications
sulfites

90
Q

List the hallmarks of asthma

A

bronchial hyperreactivity
bronchial inflammation
airway obstruction

91
Q

What is the physiology of bronchial hyper-reactivity?

A

begins with sensitization to an allergen
allergen exposure –> production of specific IgE antibodies

92
Q

What is regulate for IgE?

A

They are regulated by Th2 cells
it is overexpressed in sensitized individuals (this is activated by dendritic cells)

93
Q

What does IgE is bind to?

A

mast cells
subsequent exposure to allergen –> binds to iGE antibody on mast cell –> release of mediators

94
Q

List some mediators that are released

A

histamine
leukotrienes
cytokines
tumor necrosis factor alpha (TNF-a)

95
Q

List non allergen induced

A

irritants
exercise
cold air
NSAIDs or ASA
stress

96
Q

What is three mechanisms that mast cell mediators?

A

spasmodic state
inflammation of bronchi
excessive mucous production

97
Q

Explain spasmodic state

A

from the parasympathetic nervous system releasing acetylcholine

98
Q

How does allergen induced bronchoconstriction?

A

mast cell mediators bind to smooth muscle, causing bronchoconstriction

99
Q

Explain early phase reaction of physiology of bronchial inflammation

A

occurs within several minutes of inhalation of allergens
mast cells release mediators –> histamine and leukotrienes acts quickly
leads to bronchospasm and constriction

100
Q

Explain late phase reaction of physiology of bronchial inflammation

A

occurs within hours
cytokines and TNF-a recruit inflammatory cells
continued bronchospasm and constriction
inflammation builds
hyper responsiveness increases

101
Q

Explain the physiology of airway remodeling

A

remodeling is irreversible
increases airflow limitations and exacerbation of previous processes

102
Q

List pathologic changes in the airways remodeling

A

vascular dilation
edema
subepithelial fibrosis
epithelial damage
inflammatory cell infiltration
smooth muscle hypertrophy
mucous gland hypertrophy
sub basement membrane thickening

103
Q

What is the clinical presentation of asthma?

A

intermittent episodes of wheezing, cough and dyspnea
chest tightness and chronic cough in some
symptoms often worse at night or upon waking
presence of repeatable triggers
possible signs of atopy

104
Q

What is lung function testing results of asthma?

A

FEV1/FVC <0.7 is diagnostic of asthma
significant reversibility post bronchodilator challenge
sensitive to bronchoprovocation testing

105
Q

What is complicated asthma called?

A

Status asthmaticus (asthma exacerbation)

106
Q

Describe the symptoms of complications of asthma

A

episode of worsening asthma symptoms, lung function and hyperresponsiveness
most common in those with underutilized anti-inflammatory therapy

107
Q

Explain the feedback loop of asthma exacerbation

A

inflammation –> increased bronchial hyperresponsiveness –> increased inflitration of allergic and inflammatory mediators –> bronchoconstriction and obstruction –> inflammation

108
Q

What happens if asthma treatment is delayed?

A

cardiac arrest
respiratory failure
hypoxemia
pneumothorax

109
Q

What are complications are asthma?

A

airway remodeling
fatigue
underperformance at work/school
inability to exercise
frequent hospitalization
pneumonia and influenza
GERD
sleep apnea

110
Q

Define COPD

A

chronic respiratory condition characterized by
persistent symptoms
airflow limitation and narrowing airways
chronic inflammation
mucociliary dysfunction
mix of obstructive bronchiolitis and emphysema

111
Q

What is the epidemiology?

A

affects 5 % of canadians >35 years old
85% of COPD deaths mainly caused by continued smoking or exposure
4th leading cause of death in Canada
3rd leading cause death world wide

112
Q

Risk Factors of COPD

A

exposure to particles
airway responsiveness
genetic polymorphisms
old age

113
Q

Explain the risk factor of exposure to particles

A

cigarette smoking most prominent cause
general air quality and pollution

114
Q

Explain the risk factor of airway responsiveness

A

higher responsiveness increase COPD risk

115
Q

Explain the risk factor of genetic polymorphisms

A

matrix metalloproteinases (MMPs) excess
alpha 1 antitrypsin deficiency

116
Q

Define Emphysema

A

refers to airways collapse due to loss of lung recoil caused by alveolar wall destruction
caused by an imbalance between proteolysis and anti-proteolysis in the lungs

117
Q

Define Elastase

A

the main enzyme responsible for proteolysis in lungs

118
Q

What produces elastase?

A

neutrophils and macrophages

119
Q

What irreversibly inhibits elastase?

A

alpha-1-antitrypsin

120
Q

What does emphysema lead to?

A

air trapping
impaired gas diffusion
lung hyperinflation

121
Q

Define Chronic Bronchitis

A

chronic inflammation of the bronchioles

122
Q

What are the changes caused by chronic bronchitis?

A

Increased oxidative stress and inflammatory mediators
Increase in goblet cells  mucous hypersecretion
Hyperplasia of submucosal mucous glands
Ciliary dysfunction
Fibrosis and thickening of bronchiole walls
Edema and smooth muscle contraction

123
Q

What are the two forms of clinical presentation?

A

pink puffer
blue bloater

124
Q

What are symptoms of emphysema?

A

Shortness of breath
Barrel chest
Enlarged lungs
Weight loss
Pink skin
Accessory muscle use
Pursed lip breathing
Hypoxemia/co2

125
Q

What are symptoms of chronic bronchitis?

A

Shortness of breath
Chronic productive cough
Excessive mucous production
Wheezing
Pulmonary hypertension (due to alveolar hypoxia shunting blood to healthy alveoli)
Weight gain
Peripheral edema
Cyanosis
Hypoxemia
Hypercapnia (resp acidosis)
Right-sided heart-failure
Fluid retention

126
Q

What is the nickname for emphysema?

A

pink puffer

127
Q

what is the nickname for chronic bronchitis

A

blue bloater

128
Q

Are emphysema and chronic bronchitis on a spectrum or two sides of it?

A

They represent extremes, mixed type presentation is more likely

129
Q

What is COPD prognosis?

A

COPD is progressive; cannot halt decline of lung function and FEV1
Depends on severity of disease, management of comorbidities, level of fitness

130
Q

What are predictors of mortality?

A

Low FEV1 and rate of decline
Continued smoking
Low BMI (<21)
Increased airway bacterial load
Rate of exacerbations
Decreased exercise capacity
Males
Emphysema predominant
Development of comorbidities

131
Q

Common Comorbidities for COPD

A

Lung cancer
Cardiovascular disease
Ischemic heart disease
Heart failure (cor pulmonale)
Arrhythmias
Peripheral artery disease
Hypertension
Sleep apnea
Metabolic syndrome
Osteoporosis

132
Q

What are the broad categories of asthma treatment?

A

reliever
controller
exacerbations
novel therapy

133
Q

List the relivers

A

SABA
SAMA

134
Q

List the controllers

A

ICS
LABA
LTRA
theophylline

135
Q

List exacerbations

A

oral steroids

136
Q

Explain short acting beta adrenergic agonists

A

most used agent in asthma
act promptly to cause bronchial smooth muscle relaxation and bronchodilation

137
Q

Example of SABA

A

salbutamol

138
Q

SABA MOA

A

binds to B2 receptor in lungs causing
Hyperpolarization of calcium-activated potassium channels in airways
Stimulation of ATP  cAMP  removal of calcium from muscle

139
Q

Key side effects SABA

A

Cardiovascular stimulation central to side effects

Tachycardia
Palpitations
Dizziness
Tremor

140
Q

SAMA

A

not commonly used for astham
useful add on during asthma attacks

141
Q

SAMA acts

A

promptly to cause smooth muscle relaxation and bronchodilation -

142
Q

Example of SAMA

A

iprtropium

143
Q

SAMA MOA

A

Acetylcholine in lungs causes bronchoconstriction and increased mucous secretion
Increased in states of inflammation
Ipratropium is a competitive antagonist of endogenous acetylcholine at muscarinic receptors

144
Q

AE for SAMA

A

cough
headache
dizziness
dry mouth

145
Q

DI for SAMA

A

anti choliergic load

146
Q

Inhaled corticosteroids

A

commonly used first line controller medication

147
Q

Examples of IC include

A

Beclomethasone ● Fluticasone
Budesonide ● Mometasone
Ciclesonide

148
Q

Benefits of IC

A

Directly reduces inflammation
Improves symptoms
Improves long-term outcomes
Reduces asthma mortality and frequency and severity of attacks
Reduces airway remodeling and airway hyper-reactivity

149
Q

MOA of IC

A

Enters target cells in the lung and binds to Glucocorticoid Receptors (GRs)
Then moves into nucleus of cell  binds to coactivators to inhibit histone acetyltransferase (HAT) and increase Histone deacetylase 2 (HDAC2)

HAT acetylates inflammatory proteins
HDAC2 deacetylates inflammatory proteins

150
Q

AE for IC

A

oral thrush
hoarseness of voice

151
Q

AE for high dose long term IC

A

Adrenal suppression
Increased glucose levels
Pneumonia
Osteoporosis

152
Q

DI for IC

A

desmopression –> hyponatremia risk

153
Q

LABA

A

commonly used controller medication

154
Q

Examples of LABA

A

salmeterol
formoterol

155
Q

LABA MOA

A

have the same MOA, AE, SI as SABA

156
Q

LRA

A

oral controller medication used in very mild asthma

157
Q

Example of LRA

A

montelukast

158
Q

MOA of LRA

A

Cysteinyl-Leukotriene receptors cause mucous secretion, bronchoconstriction and eosinophil recruitment when activated

Montelukast antagonizes this receptor, preventing these effects

159
Q

AE for LRA

A

minimal side effects

160
Q

DI for LRA

A

none

161
Q

Theophylline

A

rarely used oral last line

162
Q

Negatives for Theophylline

A

use limited by difficult dosing, toxicity potential and more effective agents

163
Q

Things that theophylline causes

A

Inhibition of phosphodiesterase  increases cAMP
Antagonizing adenosine receptors  prevents release of histamine and leukotrienes
Increasing interleukin 10 levels (anti-inflammatory)
Preventing creation of pro-inflammatory mediators

164
Q

AE of theophylline

A

Significant cardiac toxicity
Tachycardia
Arrhythmias

Significant GI side effects
Nausea
Heartburn
Diarrhea

165
Q

DI for theophylline

A

Theophylline is a 3A4 substrate and 1A2 substrate
Any inhibitor will increase concentrations of theophylline

166
Q

Explain biologics as a treatment for asthma

A

new injectable agents that directly target the allerguc response or inflammatory mediators

167
Q

Biologics include

A

MAB’s
Omalizumab
Mepolizumab, reslizumab, benralizumab
Dupilumab

168
Q

Omalizumab

A

inhibits IgE

169
Q

Dupilumab

A

inhibits interleukin 4 and 13

170
Q

Mepolizumab, reslizumab, benralizumab

A

inhibits interleukin -5

171
Q

COPD Treatment Categories

A

main therapy
sever disease
exacerbations
rarely used

172
Q

SABA /LABA in COPD

A

slightly less effective in COPD

173
Q

SAMA and LAMA in COPD

A

utlized more in COPD
same as asthma

174
Q

Examples of LAMA

A

Tiotropium
Aclidinium
Glycopyrronium
Umeclidinium

175
Q

IC for COPD

A

main difference used in end stage COPD

176
Q

Inhalers are often in combinations

A

LABA / LAMA
SAMA / SABA
LABA / ICS
LABA / LAMA / ICS

177
Q

List different inhaler devices

A

Metered-dose inhalers (MDIs)
Dry powder inhalers
Turbuhaler
Discus
Handihaler
Soft-mist inhalers

PHARM 123 (4 decks)

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