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PHAR 123* > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What are the structures in the upper respiratory tract?

A

Nose and nasal cavity
Paranasal sinuses
Pharynx
Larynx

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2
Q

What are the structures in the lower respiratory tract?

A

Trachea
Bronchi and small bronchioles
Lungs and alveoli

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3
Q

What are the main fxns of the nose and nasal cavity?

A

Airway for respiration
Moistens and warms air
Filters the inhaled air
Contains olfactory receptors (for smell)
Involved in speech

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4
Q

What is said about the mouth as an air passageway?

A

The mouth is a shorter passageway
No moistening
More efficient to get the air
ex) swimming

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5
Q

What are the paranasal sinuses?

A

The air containing cavities in the skull
Lined with mucous membrane
There are 4

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6
Q

What are the functions of the paranasal sinuses?

A

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

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7
Q

What is the pharynx and what are the structures within the pharynx? What do these structures do?

A

The upper part of the throat

Nasopharynx (nasopharyngeal and tubal tonsil)
- simply an air passageway
- closes when swallowing

Oropharynx (palatine and lingual tonsils)
- Food and air passageway
- epiglottis closes during inspiration to prevent aspiration

Laryngopharynx
- connects the throat to the esophagus
- extends to branching of respiratory (layrngela) and digestive (esophageal) pathways

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8
Q

What does the larynx do?

A

Connects the laryngopharynx to the trachea
Contains the vocal cords
Thyroid gland sits on the outside of the larynx

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9
Q

What are the main functions of the larynx?

A

Protective fxn

Aids in coughing and other reflexes
Prevents food and fluid from entering the lungs

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10
Q

True of False: the cause of laryngitis is not only due to inflammation

A

True, laryngitis can arise from vocal cord strain

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11
Q

What do the bronchi and the bronchioles do?

A

They contain mucus and cilia to remove contaminants
Can constrict or dilate to modify airflow

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12
Q

What are the level categorization of bronchi?

A

Primary is the closest to the esophagus
secondary is branches from the primary
tertiary branch from the secondary
the terminal bronchioles are respiratory and they are at the very end

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13
Q

How many lobes are in the right and left lung?

A

Right has three; left has two
The left has two to make space for the heart

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14
Q

Explain the surface structures of the lungs

A

There are oblique and horizontal fissures present
They are also covered by visceral pleura

Pleura help with inspiration and expiration

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15
Q

What is pleurisy?

A

inflammation of the lungs

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16
Q

What are the ribs and diaphragm covered by?

A

parietal pleura

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17
Q

What is the space between the lungs and ribs called?

A

pleural cavity

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18
Q

What are in alveoli? How many are on the respiratory bronchioles?

A

Type 1 cells (squamous epithelium)
Type 2 cells (cuboidal epithelium)
- contain lamellar bodies that secrete surfactant
Alveolar macrophages

There are millions on the bronchioles

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19
Q

Why are surfactants important?

A

They are a fatty substance that decreases alveolar surface tension and helps prevent alveolar collapse
Otherwise they would stick together

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20
Q

What do alveolar macrophages do?

A

They are the janitors of the alveoli and bronchioles

Carbon, dust, etc

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21
Q

Explain the gas exchange that occurs in the capillaries that surround the alveoli

A

CO2 diff out of the blood and into the alveoli for exhalation
O2 diff out of the alveoli and into the blood

Alv type 1 cell -> alveolar basement memb -> capillary basement memb, capillary endothelial cells

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22
Q

How is the respiratory membrane affected in chronic bronchitis? emphysema?

A

Bronchitis: xs mucus and inflammation at the bronchioles
reduced airflow

emphysema: cells are not affected
thin alveolar walls and less elastic

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23
Q

What is compliance and the consequences of poor compliance?

A

Stretching that governs inhalation
There would be a problem getting air in
(restrictive disease)

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24
Q

What is elasticity and the consequences of poor elasticity?

A

Facilitates expiration; it is the recoil and the spring back

CO2 air would be trapped and it can’t get out
Seen in asthma and COPD

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25
Q

What are the two pathways of blood supply? Explain

A

Pulmonary vessels:
Responsible for gas exchange
Deoxygenated blood arrives thru pulmonary artery from RV
Arrives at respiratory membrane and becomes oxygenated
Pulmonary veins return oxygenated blood to LA

Bronchial vessels :
Come form systemic circulation
oxygenates the lung tissue itself

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26
Q

What is the conducting system are the sites in the conducting system?

A

All sites involved in conducting air into the lungs

Nose, nasal, cavity, pharynx, larynx, trachea, bronchi, bronchiole, terminal bronchioles

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27
Q

What is the respiratory zone (or lung parenchyma) and what structures does this contain?

A

Where gas exchange occurs

Respiratory bronchioles, alveolar ducts, alveolar sacs, alveoli

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28
Q

What is respiration and what does it include?

A

The exchange of gases between the atmosphere, blood, and cells

Pulmonary ventilation
external respiration
internal respiration

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29
Q

What is pulmonary ventilation, external respiration, internal respiration?

A

Pulmonary ventilation = breathing (ins. +exp.)
external respiration = lung and pulmonary action
internal respiration= tissues taking up oxygen

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30
Q

Explain inspiration pulmonary ventilation

A

Air is pulled into the lings when the alveolar pressure is less than the atmospheric pressure
Air is pushed out of the lungs when alveolar pressure is greater than atmospheric pressure
Pressure is controlled by the contraction and relaxation of the diaphragm

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31
Q

Why is it harder to breath at high altitudes?

A

There is less atmospheric pressure with higher altitude

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32
Q

What structures help in expanding or contracting the thorax?

A

External intercostal muscles

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33
Q

What is quiet inspiration?

A

An active process representing normal breathing
Involves the diaphragm and the intercostal muscles

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34
Q

What is forces inspiration?

A

used in times of extra oxygen need such as exercise
Involves the accessory muscle of inspiration : Sternocleidomastoids, scalenes, pectoralis minor

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35
Q

What is quiet expiration?

A

a passive process
diaphragm relaxes and raises upwards

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36
Q

What is forced expiration?

A

Uses obliques and intercostals to contract inwards to help force the air out (make smaller pressurized compartment)
Activated when air movement out of the lungs is impeded

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37
Q

What is external respiration?

A

exchange of gases between blood and external environment
CO2 removed and O2 gained thru diffusion

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38
Q

Where does external respiration occur?

A

At the alveoli’s capillary memb

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39
Q

What must be balanced for proper external respiration?

A

Exchange of gas and blood supply

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40
Q

What are other requirements for external resp.?

A

must be enough air in the alveoli, blood flow in the capillaries, and hemoglobin to carry the oxygen

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41
Q

What is special about external respiration?

A

Can compensate for minor imbalances via bronchoconstriction or vasoconstriction of the pulmonary arteries
ex) asthma attack

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42
Q

What is ventilation mismatch?

A

When ventilation and blood flow are not in an optimal ratio of 0.8 or 80%

occurs in severe lung diseases

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43
Q

What are two anatomical causes of ventilation mismatch? What do mismatches lead to?

A

Obstruction in the lungs and capillary obstruction

Lead to hypoxemia

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44
Q

What is internal respiration ?

A

Exchange of gases between blood and cells:
oxygen carried by hemoglobin to systemic circulation
reaches capillaries of various tissues
oxygen diffuses in to cells’ CO2 diffuses in to blood
oxygen then used cellular respiration

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45
Q

What is eupnea?

A

normal breathing patterns

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46
Q

what is apnea?

A

breathing that stops

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47
Q

What is dyspnea?

A

shortness of breath

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48
Q

What is tachypnea?

A

rapid breathing
(distress not exercise-induced)

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49
Q

What is costal breathing?

A

forced inhalation (using accessory msucles)

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50
Q

What is diaphragmatic breathing?

A

using abdominal muscles to breath

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51
Q

What is type 1 respiratory failure?

A

The inability of lungs to preform adequate gas exchange

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52
Q

What are the potential causes of Typ1 resp failure?

A

Lung disorder (asthma , COPD)
Pneumonia
Pulmonary- edema, fibrosis, embolism, HTN

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53
Q

What does Type 1 resp failure lead to?

A

hypoxemia

O2 saturation falls to below 90%
CO2 levels remain normal or can be low

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54
Q

What does a person with hypoxemia look like?

A

Drowsy, shortness of breath, fast HR, confusion, cyanosis

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55
Q

What is type 2 respiratory failure?

A

Occurs when breathing is not sufficient tot rid the body of CO2
sometimes called ventilatory failure

CO2 excretion less than CO2 production

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56
Q

What are the potential causes of Type 2 respiratory failure?

A

Decreased CNS drive, impaired neuromuscular fxn, chronic bronchitis or COPD, excessive inspiratory load

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57
Q

What does type 2 respiratory failure lead to?

A

hypercapnia = too much CO2

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58
Q

What can type 2 respiratory failure eventually lead to?

A

hypoxemia, CNS depression, respiratory acidosis

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59
Q

What are used to determine acid-base balance? What is this useful to us?

A

Arterial blood gases
They help us determine the causes of respiratory issues

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60
Q

What is blood ph controlled by?

A

the action of the lungs and the kidneys

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61
Q

What is PaCO2?

A

The pressure or tension exerted by dissolved CO2 gas in blood

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62
Q

What is PaO2?

A

Indicates the level of oxygenation of arterial blood

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63
Q

What is metabolic?

A

refers to a disorder from an alteration in HCO3

influenced by the kidney

64
Q

What is respiratory?

A

refers to a disorder form an alteration in CO2

influenced by the lungs

65
Q

Explain hypoventilation using gaseous terms

A

lungs expel CO2, so increase in CO2 -> acid buildup
hypercapnic
blood pH decrease(s)

chronic asthma, chronic COPD

66
Q

Explain hyperventilation using gaseous terms

A

lungs get rid of CO2
Increase in pH due to alkaline levels

ex) acute asthma attack or panic attack

67
Q

What is respiratory compensation?

A

lungs can modulate how much CO2 is retained or excreted

68
Q

What is metabolic compensation?

A

the kidneys can modulate how much HCO3 is retained or excreted

69
Q

What are the four disturbances of acid/base?

A

respiratory acidosis - low pH, normal HCO3, increased PaCO2, resp. kidneys relase bicarb into the blood
respiratory alkalosis - increased pH, normal HCO3, decrease PaCO2, kidneys retain bicarb (decrease in HCO3)
metabolic acidosis - decrease in pH, decrease in HCO3, normal PaCO2, lungs remove CO2
metabolic alkalosis - increase pH, Increased HCO3, normal PaCO2, Lungs retain CO2

70
Q

What are the two main lung tests for lung fxn?

A

Spirometry - measures how much air you can move in and out of the lungs, assess person’s pulmonary performance

Peak-flow meter - for asthma patients, used to compare current results to personal best

71
Q

What is FEV1 and FVC?

A

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

72
Q

What is tidal volume?

A

normal breathing

73
Q

What is residual volume?

A

the air that you cannot get out no matter how hard you exhale

74
Q

What is inspiratory reserve volume?

A

Inhale as much as physically possible

75
Q

What is expiratory reserve volume?

A

the amount of air that is exhaled

76
Q

What does the FEV1/FVC ratio tell us?

A

helps us differentiate between restrictive and obstructive lung disease

Obstructive give us a low ratio, and normal FVC
restrictive gives us normal ratio, and also low FVC

*look at the chart in notes

77
Q

What does spirometery tell us?

A

help us determine the reversibility of an airway obstruction in asthma patients
If FEV1 increases after 10-15minutes using a bronchodilator, then obstruction is present

78
Q

What changes occur in the respiratory system when fitness improves?

A

Lungs can accommodate high volumes of air
Increased diffn of resp gases
Strengthens cilia and diaphragm
Strengthens other muscles of inspiration and expiration
VO2 max increases

79
Q

Why do people who smoke have poor exercise tolerance?

A

Nicotine causes bronchoconstriction
Lung fibrosis (poor elasititicy)
XS mucous secretion
inhibited cilia
destruction of elastic fibers

80
Q

What are the age-related impacts on lung function?

A

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

81
Q

What is asthma?

A

A chronic inflammatory disorder

82
Q

What is asthma characterized by?

A

paroxysmal (sudden intensification of sx)or persistent symptoms
Dyspnea, wheezing , cough, chest tightness, sputum production - different from each person
airway is hyper-responsiveness to a variety of stimuli

83
Q

true of false: childhood asthma is not the #1 chronic condition in Canada in children

A

false, most diagnosed by age 5
leading cause of ER hospitalizations of children

84
Q

What is the etiology and risk factors for people with asthma?

A

genetic predisposition
hygiene hypothesis
atopic vs non-atopic
gender
maternal factors
perinatal factors
factors during childhood
factors during adulthood

85
Q

Explain the genetic predisposition of asthma

A

Many genes influence asthma
some may be predisposing to atopy = tendency of developing allergic disease
Genes involved in the severity of the asthma (airway hyper-responsiveness)
genes related to the response to therapy/ how well tx will work

86
Q

What is the hygiene hypothesis?

A

Limited exposure to normal environment stimuli may cause the allergic immunologic system to develop more than the system to fight infection

87
Q

Based on the hygiene hypothesis, what makes children at a lower risk for developing asthma?

A

Exposed to high levels of bacteria or endotoxin
have older siblings
have early enrollment into child care
experience exposure to cats and dogs early on
exposure to fewer antibiotics

88
Q

What can be said about atopic responses and asthma?

A

They can result in asthma
The greater the person’s sensitization, the high er the likelihood of asthma
there can be high levels of IgE found
allergens include: dust mites, fungi, indoor and outdoor animals

89
Q

What is the impact of sex on asthma?

A

Childhood asthma is more common in males
When 20-40, prevalence is equal among the sexes
After age 40, females are more likely to have asthma

90
Q

Explain the maternal factors for asthma

A

Increasing the maternal age means that there is a lower risk of asthma
Mother’s diet during preg is important -> vitamin D decreases; high omega 6 and low omega 3 increase asthma
Maternal asthma control
prenatal exposure to maternal smoking
acetaminophen, antibiotics, and acid supressors in mother

91
Q

What are the perinatal factors for asthma?

A

Pre-eclampsia - high bp, kidney dysfunction at week 20
prematurity
C-section increases the risk of asthma
Breastfeeding
Vit D supplementation

92
Q

What are the factors during childhood for asthma?

A

These are viral infections that are predictors for asthma in later life (include rhinovirus and resp syncytial virus)

Medication use in infancy (acet, ibu, AB)

Air pollution
Tobacco smoke exposure
obesity

93
Q

What are factors during adulthood for asthma?

A

Obesity
tobacco smoke
occupational exposures
rhinitis (chronic version)

94
Q

What are the triggers of asthma?

A

Irritants - perfumes
Respiratory tract infxn
weather
stress
hormonal fluxt
gastro-esophageal reflux disease
Meds (ASA,NSAIDS, BB)
sulfites - found in food preservatives

95
Q

What are the three hallmarks of asthma pathology?

A

bronchial hyper-reactivity
bronchial inflammation
airway obstruction (bronchoconstriction, mucous plugs)

96
Q

Explain bronchial hyper-reactivity

A

Begins with the sensitatzation to an allergen

Allergen exposure leads to production of IgE anitbodies
-IgE regulated by Th2 cells
- in sensitized individuals th2 cells are over-expressed and theyr are activated by dendritic cells

IgE bind to mast cells, which releases mediators

97
Q

What are the mediators that are released and their fnx?

A

histamines - increase tissue permeability
leukotrienes - contraction in bronchioles
cytokines - cell signaling for inflammation
TNF-a - mediators for cell signaling

98
Q

Explain allergen induced bronchoconstriction

A

Mast-cell mediators bind to smooth muscle, causing bronchoconstriction

99
Q

Explain non-allergen bronchoconstriction

A

Irritants, exercise, cold air, NSAIDs/ASA, stress

100
Q

What are the three mechanism for bronchoconstriction?

A

Spasmodic state due to the PNS releasing Ach
inflammation of the bronchi
XS mucous production

101
Q

What is the early phase rxn of bronchial inflammation?

A

occurs within several minute of exposure/inhalation of allergen
Mast cells release mediators - hist and leuko act v quick
-> bronchospasm and constriction

102
Q

What is the late phase rxn of bronchial inflammation?

A

Occurs in hours
Cytokines and TNF-a recruit inflammatory cells
Continued bronchospasms and constriction
Inflammation builds
hyper-responsiveness increases

103
Q

What does continued inflammation eventually lead to?

A

Airway remodeling (can be irreversible; increases airflow limitations and exacerbation of previous processes)

104
Q

What are the pathologic changes of airway remodeling?

A

Vascular dilation
edema
subepithelial fibrosis
inflammatory cell infiltration
smooth muscle hypertrophy - leads to more bronchoconstriction
mucous gland hypertrophy
sub-basement membrane thickening

105
Q

What is the clinical presentation of airway remodeling?

A

Intermittent episodes of wheezing, cough, dyspnea
Chest tightness and chronic cough in some
sx often worse at night or upon waking
Prescence of repeatable triggers
possible signs of atopy

106
Q

What is the definition of asthma control?

A

Day time symptoms 2 or less days per week
Night time symptoms less than 1 night per week and mild
Normal physical activity and no absence of work
Exacerbations should be mild and infrequent
The need for a reliever (SABA or bud/form) should be two or less doses per week

107
Q

What are the lung function test results characterized by asthma?

A

FEV1/FVC < 0.7
Significant reversibility of post-bronchodilator challenge (>12%)

Sensitive to bronchoprovocation testing, where you give the pt a cholinergic agent and you’ll see bronchoconstriction

108
Q

What is asthma exacerbation and what can you expect to see?

A

Status asthmaticus

Episodes of worsening asthma sx, lung fxn, and hyper-responsiveness
Very common in those with underutilized anti-inflammatory therapy
Can progress without tx and become life-threatening
This is the most common reason for hospitalizations in asthmatics
Unresponsive to bronchodilator tx alone
Must be intensively treated promptly - think ER situation

109
Q

What is the feedback loop in asthma exacerbation?

A

Inflammation -> increased bronchial hyper-responsiveness -> increased infiltration of allergic and inflammatory mediators -> bronchoconstriction and obstruction (air-trapping) -> inflammation

110
Q

What can occur to the patient if asthma exacerbation treatment is delayed?

A

Cardiac arrest
Respiratory failure
Hypoxemia
Pneumothorax (collapsed lung, there is leakage of air between the lung and the chest, increased pressure in lungs)

111
Q

What are the complications of asthma exacerbation?

A

Airway remodeling
Fatigue
Underperformance at work or school
Inability to exercise
Frequent hospitalizations
Pneumonia and influenza
GERD
Sleep apnea

112
Q

What is a chronic respiratory condition characterized by?

A

Persistent sx (unlike asthma)
Condition gets worse over time
Airflow limitation and narrowing airways
Chronic inflammation Mucociliary dysfxn
Mix of Obstructive bronchiolitis and emphysema

113
Q

What are some stats for COPD?

A

85% of deaths caused by continued smoking or exposure
4th leading cause of death in Canada, increasing
3rd leading cause of death worldwide
5% of canadians over 35 years old

114
Q

What are the causes and risk factors of COPD?

A

Exposure to particles
- Cigarette smoking is the most prominent cause
- General air quality and pollution

Airway responsiveness
- Higher responsiveness increases COPD risk

Genetic polymorphisms
- Matric Metalloproteinases XS
- Alpha-1 antitrypsin deficiency

Old age - due to particle exposure over time

115
Q

What are the cardinal sx of COPD?

A

Dyspnea = shortness of breath
Chronic cough
Sputum production

116
Q

What is emphysema and what can it lead to?

A

Airway collapse due to loss of lung recoil caused by alveolar wall destruction

Can lead to:
Air trapping
impaired gas diffusion
Lung hyperinflation

117
Q

What is emphysema caused by?

A

An imbalance between proteolysis and anti-proteolysis in the lungs

Elastase (prod by neutrophils and macrophages) is the main enzyme responsible for proteolysis in the lungs. This enzyme targets elastic tissues.
Elastase irreversibly inhibited by alpha-1-antitrypsin

MMP also involved

118
Q

What is chronic bronchitis?

A

Chronic inflammation of the bronchioles

119
Q

What resutls from chronic bronchitis?

A

Increased ox stress and inflammatory hypersecretions
Increase in goblet cells -> mucous hypersecretion (prod cough)
Hyperplasia or submucosal mucous glands
Ciliary dysfxn
Fibrosis and thickening of bronchiole walls
edema and smooth muscle contraction

120
Q

See the clinical presentation of Emphysema vs Chronic bronchitis

A

See the slide

121
Q

Name some differences between asthma and COPD

A

Asthma: usually less than 40 years old, smoking worsens control, infrequent sputum production, often allergies, intermittent symptoms, disease is stable, spirometry normalizes with reversibility, bronchodilators as needed

COPD: usually older than 40 years, more than 10 pack-years, infrequent allergies, symptoms feature progressive worsening, spirometry may improve but never normalizes, regular bronchodilators use is necessary

122
Q

What are the predictors of mortality in COPD?

A

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

123
Q

What are the common comorbitidites of COPD?

A

Lung cancer (Most common 6-13X time more than normal)
CVD (HF, Arrythmias, Peripheral artery disease, HTN, Ischemic heart disease)
Sleep apnea
Metabolic syndrome
Osteoporosis (due to low weight, smoking, low vit D)

124
Q

What are the differences between a reliever and a controller?

A

Relievers - drugs stop symptoms very quickly, taken when needed
Controllers - target anti-inflammatory symptoms, taken chronically, everyday

125
Q

What are examples of relievers, controllers, exacerbations, and novel therapy?

A

Reliever: Short-acting beta-adrenergic agonists (SABA), Short-acting muscarinic antagonist (SAMA)
Controller: Inhaled corticosteroids (ICS), Long-acting beta-adrenergic agonists (LABA) , Leukotriene receptor antagonist (LTRA), Theophylline (rarely used)
Exacerbations: Oral steroids
novel therapy: biologics

126
Q

What are SABAs? Provide examples

A

the most used agents in asthma, for relief
they act promptly to cause bronchial smooth muscle relaxation and bronchodilation -> “rescue” mediation

Ex) Salbutamol/albuterol (B2 selective), terbutaline, epinephrine (non-selective)

127
Q

What is the MOA of SABAs?

A

Binds to the B2 receptors in the lung to cause:

  1. Hyperpolarization of Ca2+ activated K+ channels in the airways
  2. Stimulation of ATP-> cAMP -> removal of calcium from the muscle, which prevents contraction
128
Q

What are the secodnary effects of SABA?

A

Reduced mediator release from mast cells
reduced microvascular leakage after exposure to mediators
enhances mucociliary clearance
reduces neurotransmission of cholinergic nerves

129
Q

What are the side effects of SABA?

A

Cardiovascular stimulation:
tachycardia, palpitations, dizziness, tremor

  • tolerance typically develops - overstimulation leads to down regulation
130
Q

Are SAMAs commonly used in asthma? What is their place in therapy? Provide an example

A

No, they are used as an add-on during asthma attacks
They work by causing smooth muscle relaxation and bronchodilation to “rescue”

Ipratropium

131
Q

What is the MOA of SAMAs?

A

Ach in lungs cause bronchoconstriction and increased mucous secretion, causing inflammation

Ipratropium is a competitive antagonist of endo Ach at muscarinic receptors
Inhibits bronchial smooth muscle constriction mediated by physiological pathway

topical, so there is minimal abs

132
Q

What are the side effects of SAMAs?

A

Cough, headache, dizziness, dry mouth

Drug interaction with other anticholinergic drugs, combined net effect of anti-cholinergic effects

133
Q

What are inhaled corticosteroids?

A

The first-line controller medication
No immediate effect, takes weeks to months to max effect

134
Q

What do inhaled corticosteroids do?

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

135
Q

What are some examples of inhaled corticosteroids?

A

Beclomethasone, budesonide, Ciclesonide, Fluticasone, Mometasone

136
Q

What is the MOA of inhaled corticosteroids?

A

Enter the target cells in the lung and bind to glucocorticoid receptors (GRs)
Then they into the nucleus of the cell and bind to coactivators to inhibit histone acetyltransferase (HAT) and increase Histone deacetylase 2 (HDAC2)

HAT acetyls inflammatory proteins; HDAC2 deacetylates inflammatory proteins
Net effect to decrease inflammation

137
Q

What are some of the cellular changes that occur from inhaled corticosteroids?

A

Decrease the numbers of eosinophils, cytokines, mast cells, macrophages (cytokines), dendritic cells, mediators, mucus secretion

138
Q

What are the side effects of inhaled corticosteroids?

A

Oral thrust
Hoarseness of voice

High does long term lead to:
Adrenal suppression
Increase glucose levels
pneumonia
Osteoporosis

139
Q

What is a drug interaction with inhaled corticosteroids?

A

Desmopressin and ICS lead to hyponatremia risk

140
Q

What are LABAs?

A

Common controller medications
Added after a corticosteroid
Less rapid acting that short-agents, but long lasting
Same MOA, side effects and drug interactions as SABAs

141
Q

What are two examples of LABAs?

A

Salmeterol and formoterol (the latter can be used as a reliever too because it works fast)

142
Q

What are leukotriene receptor antagonists?

A

Oral controller medication in very mild asthma
May be added to ICS/ LABA
Possible role in exercise-induced asthma

143
Q

What is an example of a leukotriene receptor antagonist?

A

Montelukast, blocks leukotriene receptors

144
Q

What is the MOA of leukotriene antagonists?

A

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

Montelukast antagonizes this receptor, preventing these effects

145
Q

What are the side effects and drug interactions of leukotriene antagonists?

A

Minimal side effects
No drug interactions

146
Q

What is theophylline?

A

A rare oral last-line controller medication
Limited use due to difficult dosing, toxicity potential, and more effective agents

147
Q

How does theophylline cause bronchodilation?

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

148
Q

What are the side effects and drug interactions of theophylline?

A

Significant cardiac toxicity - tachycardia, arrhythmias
Significant GI side effects - Nausea, heartburn, diarrhea

Drug interactions:
3A4 substrate and 1A2 substrate
inhibitors will increase conc of theophylline

149
Q

What are biologics?

A

New injectable agents that directly target the allergic response or inflammatory mediators.
Reserved for last line use

150
Q

What are some exampels of biologics?

A

MAB’s
Omalizumab, Mepolizumab, dupilumab

151
Q

What is used to treat COPD?

A

SABAs and LABAs (same as asthma)
they are dosed on a schedule and not as needed

152
Q

Ture or false: SAMAs and LAMAs are effective in COPD

A

True, they are slightly more effective than SABA and LABAs

153
Q

What are the short and long acting anti-muscarinic?

A

Short: ipratropium
Long: A,T, C, G -ium

154
Q

What is the main difference in ICS for COPD?

A

They are utilized in end-stage COPD

155
Q

What are the combinations of inhalers that exist?

A

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

PHAR 123* (11 decks)

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