Respiratory Flashcards
1
Q
What are the structures in the upper respiratory tract?
A
Nose and nasal cavity
Paranasal sinuses
Pharynx
Larynx
2
Q
What are the structures in the lower respiratory tract?
A
Trachea
Bronchi and small bronchioles
Lungs and alveoli
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
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
5
Q
What are the paranasal sinuses?
A
The air containing cavities in the skull
Lined with mucous membrane
There are 4
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
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
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
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
10
Q
True of False: the cause of laryngitis is not only due to inflammation
A
True, laryngitis can arise from vocal cord strain
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
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
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
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
15
Q
What is pleurisy?
A
inflammation of the lungs
16
Q
What are the ribs and diaphragm covered by?
A
parietal pleura
17
Q
What is the space between the lungs and ribs called?
A
pleural cavity
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
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
20
Q
What do alveolar macrophages do?
A
They are the janitors of the alveoli and bronchioles
Carbon, dust, etc
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
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
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)
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
25
What are the two pathways of blood supply? Explain
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
26
What is the conducting system are the sites in the conducting system?
All sites involved in conducting air into the lungs
Nose, nasal, cavity, pharynx, larynx, trachea, bronchi, bronchiole, terminal bronchioles
27
What is the respiratory zone (or lung parenchyma) and what structures does this contain?
Where gas exchange occurs
Respiratory bronchioles, alveolar ducts, alveolar sacs, alveoli
28
What is respiration and what does it include?
The exchange of gases between the atmosphere, blood, and cells
Pulmonary ventilation
external respiration
internal respiration
29
What is pulmonary ventilation, external respiration, internal respiration?
Pulmonary ventilation = breathing (ins. +exp.)
external respiration = lung and pulmonary action
internal respiration= tissues taking up oxygen
30
Explain inspiration pulmonary ventilation
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
31
Why is it harder to breath at high altitudes?
There is less atmospheric pressure with higher altitude
32
What structures help in expanding or contracting the thorax?
External intercostal muscles
33
What is quiet inspiration?
An active process representing normal breathing
Involves the diaphragm and the intercostal muscles
34
What is forces inspiration?
used in times of extra oxygen need such as exercise
Involves the accessory muscle of inspiration : Sternocleidomastoids, scalenes, pectoralis minor
35
What is quiet expiration?
a passive process
diaphragm relaxes and raises upwards
36
What is forced expiration?
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
37
What is external respiration?
exchange of gases between blood and external environment
CO2 removed and O2 gained thru diffusion
38
Where does external respiration occur?
At the alveoli's capillary memb
39
What must be balanced for proper external respiration?
Exchange of gas and blood supply
40
What are other requirements for external resp.?
must be enough air in the alveoli, blood flow in the capillaries, and hemoglobin to carry the oxygen
41
What is special about external respiration?
Can compensate for minor imbalances via bronchoconstriction or vasoconstriction of the pulmonary arteries
ex) asthma attack
42
What is ventilation mismatch?
When ventilation and blood flow are not in an optimal ratio of 0.8 or 80%
occurs in severe lung diseases
43
What are two anatomical causes of ventilation mismatch? What do mismatches lead to?
Obstruction in the lungs and capillary obstruction
Lead to hypoxemia
44
What is internal respiration ?
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
45
What is eupnea?
normal breathing patterns
46
what is apnea?
breathing that stops
47
What is dyspnea?
shortness of breath
48
What is tachypnea?
rapid breathing
(distress not exercise-induced)
49
What is costal breathing?
forced inhalation (using accessory msucles)
50
What is diaphragmatic breathing?
using abdominal muscles to breath
51
What is type 1 respiratory failure?
The inability of lungs to preform adequate gas exchange
52
What are the potential causes of Typ1 resp failure?
Lung disorder (asthma , COPD)
Pneumonia
Pulmonary- edema, fibrosis, embolism, HTN
53
What does Type 1 resp failure lead to?
hypoxemia
O2 saturation falls to below 90%
CO2 levels remain normal or can be low
54
What does a person with hypoxemia look like?
Drowsy, shortness of breath, fast HR, confusion, cyanosis
55
What is type 2 respiratory failure?
Occurs when breathing is not sufficient tot rid the body of CO2
sometimes called ventilatory failure
CO2 excretion less than CO2 production
56
What are the potential causes of Type 2 respiratory failure?
Decreased CNS drive, impaired neuromuscular fxn, chronic bronchitis or COPD, excessive inspiratory load
57
What does type 2 respiratory failure lead to?
hypercapnia = too much CO2
58
What can type 2 respiratory failure eventually lead to?
hypoxemia, CNS depression, respiratory acidosis
59
What are used to determine acid-base balance? What is this useful to us?
Arterial blood gases
They help us determine the causes of respiratory issues
60
What is blood ph controlled by?
the action of the lungs and the kidneys
61
What is PaCO2?
The pressure or tension exerted by dissolved CO2 gas in blood
62
What is PaO2?
Indicates the level of oxygenation of arterial blood
63
What is metabolic?
refers to a disorder from an alteration in HCO3
influenced by the kidney
64
What is respiratory?
refers to a disorder form an alteration in CO2
influenced by the lungs
65
Explain hypoventilation using gaseous terms
lungs expel CO2, so increase in CO2 -> acid buildup
hypercapnic
blood pH decrease(s)
chronic asthma, chronic COPD
66
Explain hyperventilation using gaseous terms
lungs get rid of CO2
Increase in pH due to alkaline levels
ex) acute asthma attack or panic attack
67
What is respiratory compensation?
lungs can modulate how much CO2 is retained or excreted
68
What is metabolic compensation?
the kidneys can modulate how much HCO3 is retained or excreted
69
What are the four disturbances of acid/base?
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
What are the two main lung tests for lung fxn?
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
What is FEV1 and FVC?
forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC)
72
What is tidal volume?
normal breathing
73
What is residual volume?
the air that you cannot get out no matter how hard you exhale
74
What is inspiratory reserve volume?
Inhale as much as physically possible
75
What is expiratory reserve volume?
the amount of air that is exhaled
76
What does the FEV1/FVC ratio tell us?
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
What does spirometery tell us?
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
What changes occur in the respiratory system when fitness improves?
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
Why do people who smoke have poor exercise tolerance?
Nicotine causes bronchoconstriction
Lung fibrosis (poor elasititicy)
XS mucous secretion
inhibited cilia
destruction of elastic fibers
80
What are the age-related impacts on lung function?
respiratory tissues and chest wall becomes more rigid
weak respiratory muscles
vital capacity gradually decreases
macrophages activity decreases
cilia are less active
81
What is asthma?
A chronic inflammatory disorder
82
What is asthma characterized by?
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
true of false: childhood asthma is not the #1 chronic condition in Canada in children
false, most diagnosed by age 5
leading cause of ER hospitalizations of children
84
What is the etiology and risk factors for people with asthma?
genetic predisposition
hygiene hypothesis
atopic vs non-atopic
gender
maternal factors
perinatal factors
factors during childhood
factors during adulthood
85
Explain the genetic predisposition of asthma
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
What is the hygiene hypothesis?
Limited exposure to normal environment stimuli may cause the allergic immunologic system to develop more than the system to fight infection
87
Based on the hygiene hypothesis, what makes children at a lower risk for developing asthma?
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
What can be said about atopic responses and asthma?
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
What is the impact of sex on asthma?
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
Explain the maternal factors for asthma
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
What are the perinatal factors for asthma?
Pre-eclampsia - high bp, kidney dysfunction at week 20
prematurity
C-section increases the risk of asthma
Breastfeeding
Vit D supplementation
92
What are the factors during childhood for asthma?
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
What are factors during adulthood for asthma?
Obesity
tobacco smoke
occupational exposures
rhinitis (chronic version)
94
What are the triggers of asthma?
Irritants - perfumes
Respiratory tract infxn
weather
stress
hormonal fluxt
gastro-esophageal reflux disease
Meds (ASA,NSAIDS, BB)
sulfites - found in food preservatives
95
What are the three hallmarks of asthma pathology?
bronchial hyper-reactivity
bronchial inflammation
airway obstruction (bronchoconstriction, mucous plugs)
96
Explain bronchial hyper-reactivity
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
What are the mediators that are released and their fnx?
histamines - increase tissue permeability
leukotrienes - contraction in bronchioles
cytokines - cell signaling for inflammation
TNF-a - mediators for cell signaling
98
Explain allergen induced bronchoconstriction
Mast-cell mediators bind to smooth muscle, causing bronchoconstriction
99
Explain non-allergen bronchoconstriction
Irritants, exercise, cold air, NSAIDs/ASA, stress
100
What are the three mechanism for bronchoconstriction?
Spasmodic state due to the PNS releasing Ach
inflammation of the bronchi
XS mucous production
101
What is the early phase rxn of bronchial inflammation?
occurs within several minute of exposure/inhalation of allergen
Mast cells release mediators - hist and leuko act v quick
-> bronchospasm and constriction
102
What is the late phase rxn of bronchial inflammation?
Occurs in hours
Cytokines and TNF-a recruit inflammatory cells
Continued bronchospasms and constriction
Inflammation builds
hyper-responsiveness increases
103
What does continued inflammation eventually lead to?
Airway remodeling (can be irreversible; increases airflow limitations and exacerbation of previous processes)
104
What are the pathologic changes of airway remodeling?
Vascular dilation
edema
subepithelial fibrosis
inflammatory cell infiltration
smooth muscle hypertrophy - leads to more bronchoconstriction
mucous gland hypertrophy
sub-basement membrane thickening
105
What is the clinical presentation of airway remodeling?
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
What is the definition of asthma control?
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
What are the lung function test results characterized by asthma?
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
What is asthma exacerbation and what can you expect to see?
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
What is the feedback loop in asthma exacerbation?
Inflammation -> increased bronchial hyper-responsiveness -> increased infiltration of allergic and inflammatory mediators -> bronchoconstriction and obstruction (air-trapping) -> inflammation
110
What can occur to the patient if asthma exacerbation treatment is delayed?
Cardiac arrest
Respiratory failure
Hypoxemia
Pneumothorax (collapsed lung, there is leakage of air between the lung and the chest, increased pressure in lungs)
111
What are the complications of asthma exacerbation?
Airway remodeling
Fatigue
Underperformance at work or school
Inability to exercise
Frequent hospitalizations
Pneumonia and influenza
GERD
Sleep apnea
112
What is a chronic respiratory condition characterized by?
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
What are some stats for COPD?
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
What are the causes and risk factors of COPD?
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
What are the cardinal sx of COPD?
Dyspnea = shortness of breath
Chronic cough
Sputum production
116
What is emphysema and what can it lead to?
Airway collapse due to loss of lung recoil caused by alveolar wall destruction
Can lead to:
Air trapping
impaired gas diffusion
Lung hyperinflation
117
What is emphysema caused by?
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
What is chronic bronchitis?
Chronic inflammation of the bronchioles
119
What resutls from chronic bronchitis?
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
See the clinical presentation of Emphysema vs Chronic bronchitis
See the slide
121
Name some differences between asthma and COPD
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
What are the predictors of mortality in COPD?
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
What are the common comorbitidites of COPD?
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
What are the differences between a reliever and a controller?
Relievers - drugs stop symptoms very quickly, taken when needed
Controllers - target anti-inflammatory symptoms, taken chronically, everyday
125
What are examples of relievers, controllers, exacerbations, and novel therapy?
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
What are SABAs? Provide examples
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
What is the MOA of SABAs?
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
What are the secodnary effects of SABA?
Reduced mediator release from mast cells
reduced microvascular leakage after exposure to mediators
enhances mucociliary clearance
reduces neurotransmission of cholinergic nerves
129
What are the side effects of SABA?
Cardiovascular stimulation:
tachycardia, palpitations, dizziness, tremor
- tolerance typically develops - overstimulation leads to down regulation
130
Are SAMAs commonly used in asthma? What is their place in therapy? Provide an example
No, they are used as an add-on during asthma attacks
They work by causing smooth muscle relaxation and bronchodilation to "rescue"
Ipratropium
131
What is the MOA of SAMAs?
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
What are the side effects of SAMAs?
Cough, headache, dizziness, dry mouth
Drug interaction with other anticholinergic drugs, combined net effect of anti-cholinergic effects
133
What are inhaled corticosteroids?
The first-line controller medication
No immediate effect, takes weeks to months to max effect
134
What do inhaled corticosteroids do?
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
What are some examples of inhaled corticosteroids?
Beclomethasone, budesonide, Ciclesonide, Fluticasone, Mometasone
136
What is the MOA of inhaled corticosteroids?
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
What are some of the cellular changes that occur from inhaled corticosteroids?
Decrease the numbers of eosinophils, cytokines, mast cells, macrophages (cytokines), dendritic cells, mediators, mucus secretion
138
What are the side effects of inhaled corticosteroids?
Oral thrust
Hoarseness of voice
High does long term lead to:
Adrenal suppression
Increase glucose levels
pneumonia
Osteoporosis
139
What is a drug interaction with inhaled corticosteroids?
Desmopressin and ICS lead to hyponatremia risk
140
What are LABAs?
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
What are two examples of LABAs?
Salmeterol and formoterol (the latter can be used as a reliever too because it works fast)
142
What are leukotriene receptor antagonists?
Oral controller medication in very mild asthma
May be added to ICS/ LABA
Possible role in exercise-induced asthma
143
What is an example of a leukotriene receptor antagonist?
Montelukast, blocks leukotriene receptors
144
What is the MOA of leukotriene antagonists?
Cysteinyl-leukotriene receptors cause mucous secretion, bronchoconstriction and eosinophil recruitment when activated
Montelukast antagonizes this receptor, preventing these effects
145
What are the side effects and drug interactions of leukotriene antagonists?
Minimal side effects
No drug interactions
146
What is theophylline?
A rare oral last-line controller medication
Limited use due to difficult dosing, toxicity potential, and more effective agents
147
How does theophylline cause bronchodilation?
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
What are the side effects and drug interactions of theophylline?
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
What are biologics?
New injectable agents that directly target the allergic response or inflammatory mediators.
Reserved for last line use
150
What are some exampels of biologics?
MAB's
Omalizumab, Mepolizumab, dupilumab
151
What is used to treat COPD?
SABAs and LABAs (same as asthma)
they are dosed on a schedule and not as needed
152
Ture or false: SAMAs and LAMAs are effective in COPD
True, they are slightly more effective than SABA and LABAs
153
What are the short and long acting anti-muscarinic?
Short: ipratropium
Long: A,T, C, G -ium
154
What is the main difference in ICS for COPD?
They are utilized in end-stage COPD
155
What are the combinations of inhalers that exist?
LABA/LAMA
SAMA/SABA
LABA/ ICS
LAB/LAMA/ ICS
