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PHAR123 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What makes up the upper respiratory tract?

A

nose and nasal cavity
paranasal sinuses
pharynx
larynx

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2
Q

What makes up the lower respiratory tract?

A

trachea
bronchi and smaller bronchioles
lungs and alveoli

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3
Q

What is the role of the nose and nasal cavity?

A

provides airway for respiration
moistens and warms air
filters inhaled air
contains olfactory receptors
involved in speech

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4
Q

What are the possible functions of the paranasal sinuses?

A

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

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5
Q

What are all the segments of the pharynx?

A

nasopharynx (air passageway, closes while swallowing)
oropharynx (food+air passageway, epiglottis closes during inspiration)
laryngopharynx (connects throat to esophagus)

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6
Q

What are the roles of the larynx?

A

connects laryngopharynx to the trachea
contains vocal folds
thyroid gland sits on the outside of the larynx
MAIN FUNCTION IS PROTECTIVE
-aids in coughing
-prevents food/fluid from entering lungs

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7
Q

What is the order of bronchi? What is their role?

A

primary bronchi–>secondary bronchi–>tertiary bronchi–>terminal–>respiratory bronchioles
mucus and cilia to remove contaminants
constrict or dilate to modify airflow

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8
Q

True or false: the left lung contains three lobes

A

false
two lobes due to the heart
right lung has three lobes

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9
Q

What covers the lungs? What about the ribs and diaphragm?

A

lungs: visceral pleura
ribs and diaphragm: parietal pleura

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10
Q

What are the different types of alveolar cells and what do they secrete?

A

type 1 (squamous epithelium) and type 2 (cuboidal epithelium)
-type 2 contain lamellar bodies for surfactant secretion
alveolar macrophages are janitors of alveoli and bronchioles

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11
Q

Describe gas exchange at the alveoli.

A

occurs at alveolar-capillary membrane
CO2 diffuses out of blood into alveoli for exhalation
O2 diffused out of alveoli into the blood

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12
Q

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

A

compliance: governs inspiration, stretchability]
elasticity: governs exhalation, recoil

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13
Q

Describe the two pathways of lung blood supply.

A

pulmonary vessels:
-responsible for gas exchange
-deoxygenated blood arrives through pulmonary artery from
the right ventricle
-arrives at respiratory membrane and becomes oxygenated
-pulmonary veins return oxygenated blood to left atrium
bronchial vessels:
-come from systemic circulation
-oxygenates the lung tissue itself

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14
Q

What is the conducting system?

A

includes all sites involved in conducting air into the lungs
nose–>nasal cavity–>pharynx–>larynx–>trachea–>bronchi–>bronchioles–>terminal bronchioles

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15
Q

What is the respiratory zone?

A

consists of where gas exchange occurs
respiratory bronchioles, alveolar ducts, alveolar sacs, alveoli

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16
Q

What is respiration?

A

exchange of gases between the atmosphere, blood, and cells
-pulmonary ventilation
-external respiration
-internal respiration

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17
Q

Describe pulmonary ventilation.

A

air in when alveolar pressure<atmospheric>atmospheric pressure
pressure controlled by contraction/relaxation of diaphragm
external intercostals expand/contract thorax</atmospheric>

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18
Q

Differentiate between quiet inspiration and forced inspiration.

A

quiet inspiration
-active process representing normal breathing
-internal intercostals and diaphragm
forced inspiration
-times of extra need
-sternocleidomastoids, scalenes, pectoralis minor

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19
Q

Differentiate between quiet expiration and forced expiration.

A

quiet expiration
-passive process
-diaphragm relaxes and moves up
forced expiration
-obliques and intercostals to contract inwards to force air out
-activated when air movement out of the lungs impeded

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20
Q

What is external respiration?

A

exchange of gases between blood and external environment
-CO2 removed, O2 gained
-occurs via diffusion
-occurs at alveoli-capillary membrane

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21
Q

What can ventilation and perfusion mismatch lead to?

A

hypoxemia

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22
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
-O2 diffuses into cells; CO2 diffuses into blood
-oxygen then used for cellular respiration

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23
Q

Define the following: eupnea, apnea, dyspnea, tachypnea, costal breathing, diaphragmatic breathing

A

eupnea: normal breathing pattern
apnea: breathing that stops
dyspnea: shortness of breath
tachypnea: rapid breathing
costal breathing: forced inhalation, use of accessory muscles
diaphragmatic breathing: deep breathing using diaphragm

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24
Q

What is Type 1 respiratory failure?

A

inability of lungs to perform adequate gas exchange
leads to hypoxemia

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25
Q

What are the potential causes of Type 1 respiratory failure?

A

lung disorder (asthma, COPD)
pneumonia
pulmonary-edema, fibrosis, embolism, hypertension

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26
Q

What is Type 2 respiratory failure?

A

sometimes called ventilatory failure
breathing is not sufficient to rid the body of CO2
CO2 excretion<CO2 production
leads to hypercapnia (may eventually lead to hypoxemia, CNS depression, respiratory acidosis)

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27
Q

What are the potential causes of Type 2 respiratory failure?

A

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

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28
Q

What are arterial blood gases?

A

used to determine acid-base balance, which helps determine the cause of respiratory issues
blood pH controlled by lungs and kidney

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29
Q

What would the pH value be for acidosis? What about alkalosis?

A

normal=7.40
acidosis=<7.35
alkalosis=>7.45

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30
Q

What are the two systems of compensation for acid-base balance?

A

respiratory compensation
-lungs modulate how much CO2 is retained/excreted
metabolic compensation
-kidneys modulate how much HCO3 is retained/excreted

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31
Q

What would happen during respiratory acidosis?

A

pH is lowered
HCO3 is normal
PaCO2 is increased
compensation: kidneys release HCO3

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32
Q

What would happen during respiratory alkalosis?

A

pH is raised
HCO3 is normal
PaCO2 is lowered
compensation: kidneys retain HCO3

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33
Q

What would happen during metabolic acidosis?

A

pH is lowered
HCO3 is lowered
PaCO2 is normal
compensation: lungs remove CO2

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34
Q

What would happen during metabolic alkalosis?

A

pH is raised
HCO3 is raised
PaCO2 is normal
compensation: lungs retain CO2

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35
Q

What are the two main lung function tests?

A

spirometry
-measures how much air you can move in and out
peak-flow meter
-utilized in people with asthma
-compare current results to personal best

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36
Q

What are the lung volumes?

A

tidal volume: air exhaled during normal respiration
IRV: maximum air inhaled above TV
ERV: maximum air exhaled below TV
residual volume: air remaining after maximal expiration

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37
Q

What are the lung capacities?

A

TLC: sum of all 4 volumes, total volume of air at maximal inspiration
VC: volume of air at end of maximal inhalation
FRC: volume of air at end of normal expiration

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38
Q

What is the use of FEV1/FVC ratio?

A

differentiate between restrictive and obstructive lung disease
-obstructive=low FEV1/FVC, normal FVC
-restrictive=normal FEV1/FVC, low FVC

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39
Q

What would one predict to see happen with the respiratory system as fitness improves?

A

lungs can accommodate higher volumes of air
increased diffusion of respiratory gases
strengthens cilia and diaphragm
strengthens other respiratory muscles
VO2 max increases

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40
Q

What are the many reasons that smokers have poor exercise tolerance?

A

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

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41
Q

What is the age-related impact on lung function?

A

respiratory tissues and chest wall become more rigid
weak respiratory muscles
VC decreases
macrophage activity decreases
cilia less active

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42
Q

What is asthma?

A

chronic inflammatory disorder characterized by:
-paroxysmal or persistent symptoms
-dyspnea, wheezing, cough, chest tightness, sputum
-airway hyper-responsiveness

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43
Q

What are the risk factors/etiology for asthma?

A

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

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44
Q

How can genes be involved in asthma?

A

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

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45
Q

What is the hygiene hypothesis?

A

limited exposure to normal environmental stimuli may cause the allergic immunologic system to develop more than the system to fight infection

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46
Q

Why is atopy linked to asthma?

A

allergic responses can result in asthma
greater an individuals sensitization, the higher the likelihood of asthma
higher levels of IgE found
exposure to high levels of allergens increases likelihood of asthma

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47
Q

Describe the impact of gender on the development of asthma.

A

childhood asthma has higher prevalence in males
equal from age 20-40
age 40: females>males

48
Q

Describe the impact of maternal factors on the development of asthma.

A

increasing maternal age–>lower risk of asthma
diet during pregnancy (vit D, high omega 6 vs low omega 3)
maternal asthma control
prenatal exposure to maternal smoking
medication use

49
Q

What are the perinatal factors that can effect the risk of asthma development?

A

pre-eclampsia
prematurity
mode of delivery (caesarean)
breastfeeding
vit D supplementation

50
Q

What are some childhood factors that can increase the risk of asthma development?

A

viral infections (RSV, HRV)
medication use in infancy (acet, ibu, antibiotics)
air pollution
tobacco smoke exposure
obesity

51
Q

What are some adulthood factors that can increase the risk of asthma development?

A

obesity
tobacco smoke
occupational exposure
rhinitis

52
Q

What are the many triggers of asthma?

A

irritants
resp tract infections
weather
stress
hormonal fluctuations
GERD
medication (ASA/NSAIDs, beta-blockers)
sulfites

53
Q

What are the hallmarks of asthma pathology?

A

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

54
Q

What is the physiology of bronchial hyper-reactivity?

A

begins with sensitization to an allergen
-allergen exposure–>production of IgE antibodies
-IgE production regulated by Th2 cells
-Th2 over-expressed in sensitized individuals
IgE antibodies then bind to mast cells
-release of mediators
various mediators released
-histamines, LT, cytokines, TNF-a

55
Q

What is the physiology of bronchoconstriction?

A

allergen induced bronchoconstriction
-mast cell mediators bind to smooth muscle
non-allergen induced (irritants, exercise, cold air, NSAIDs/ASA, stress)
occurs through three mechanisms:
-spasmodic state
-inflammation of bronchi
-excessive mucous production

56
Q

What is the physiology of bronchial inflammation?

A

early phase reaction
-within several minutes of inhalation of allergen
-mast cells release mediators
-leads to bronchospasm and constriction
late phase reaction
-within hours
-cytokines and TNF recruit inflammatory cells
-continued bronchospasm and constriction
-inflammation builds
-hyper-responsiveness increases

57
Q

What does continued bronchial inflammation eventually lead to?

A

airway remodelling

58
Q

What is the physiology of airway remodelling?

A

increases airflow limitations and exacerbation of other asthma hallmarks
pathologic changes:
-vascular dilation
-edema
-subepithelial fibrosis
-epithelial damage
-inflammatory cell infiltration
-smooth muscle hypertrophy
-mucous gland hypertrophy
-sub-basement membrane thickening

59
Q

True or false: airway remodelling is irreversible

A

true

60
Q

What is the clinical presentation of asthma?

A

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

61
Q

What is the definition of controlled asthma, with regards to daytime symptoms, nighttime symptoms, and need for a reliever?

A

daytime symptoms <2 days/week
nighttime symptoms <1 night/week and mild
need for a reliver <2 doses/week

62
Q

What would be the lung function testing results of an asthmatic? (FEV1/FVC, bronchodilator challenge, bronchoprovocation testing)

A

FEV1/FVC: <0.7
bronchodilator challenge: significant reversibility post-test (>12%)
bronchoprovocation: sensitive to the testing

63
Q

What is status asthmaticus?

A

severe exacerbation
-episodes of worsening asthma symptoms, lung function, and
hyper-responsiveness

64
Q

Which group of patients is status asthmaticus most commonly seen in?

A

those with under-utilized anti-inflammatory therapy

65
Q

True or false: status asthamticus can progress without treatment and become life-threatening, it also the most common cause for hospitalizations in asthmatics

A

true

66
Q

What would be the treatment for status asthmaticus?

A

unresponsive to bronchodilator treatment alone
must be intensively treated promptly

67
Q

Aside from status asthmaticus, what are the many other complications of asthma?

A

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

68
Q

How is COPD characterized?

A

chronic respiratory condition characterized by:
-persistent symptoms
-airflow limitation and narrowing airways
-chronic inflammation
-mucociliary dysfunction
-mix of chronic bronchitis and emphysema

69
Q

What is COPD a “mix” of?

A

obstructive bronchiolitis (chronic bronchitis)
emphysema

70
Q

What is the etiology and risk factors for COPD?

A

exposure to partic;es
-cigarette smoking most prominent cause
-general air quality and pollution
airway responsiveness
-higher responsiveness=increased risk
genetic polymorphisms
-matrix metalloproteinases excess
-alpha-1 antitrypsin deficiency
old age

71
Q

What are the cardinal symptoms of COPD?

A

dyspnea
chronic cough
sputum production

72
Q

What is emphysema?

A

refers to airway collapse due to loss of lung recoil by alveolar wall destruction
leads to:
-air trapping
-impaired gas diffusion
-lung hyperinflation

73
Q

What is the cause of emphysema?

A

imbalance between proteolysis and anti-proteolysis in the lungs

74
Q

What is the main enzyme responsible for proteolysis in the lungs?

A

elastase
-produced by neutrophils and macrophages
-irreversibly inhibited by alpha-1-antitrypsin
MMP also involved

75
Q

What are the several changes that chronic bronchitis can cause to the bronchioles?

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
ALL OF THE FOLLOWING LEAD TO NARROWING OF SMALL AIRWAYS AND OBSTRUCTION

76
Q

True or false: COPD is progressive and you cannot halt the decline of lung function and FEV1

A

true

77
Q

What is the biggest predictor of mortality from COPD?

A

low FEV1 and rate of decline

78
Q

What are common comorbidities with COPD?

A

lung cancer
cardiovascular disease
sleep apnea
metabolic syndrome
osteoporosis

79
Q

For asthma, what are classes of drugs used for the following: relievers, controllers, exacerbations, novel therapy

A

relievers: SABA, SAMA
controllers: ICS, LABA, LTRA, Theophylline
exacerbations: oral steroids
novel therapy: biologics

80
Q

What is the most used agents in asthma?

A

short-acting beta-adrenergic agonists

81
Q

What are the B2 selective, and non-selective SABAs?

A

B2 selective: salbutamol, terbutaline
non-selective: epinephrine

82
Q

What is the MOA of SABAs?

A

binds to B2 receptors in the lung, causing:
-hyperpolarization of Ca-activated K channels
-stimulation of ATP–>cAMP–>removal of calcium from muscle

83
Q

What are the secondary effects that could occur from the MOA of SABAs?

A

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

84
Q

What are the key side effects of SABAs?

A

cardiovascular stimulation
-tachycardia
-palpitations
-dizziness
-tremor
SABAs are inhaled to reduce risk of these side effects

85
Q

True or false: tolerance does not generally develop to the side effects of SABAs

A

false

86
Q

When are SAMAs typically used in asthma?

A

add-on during asthma attacks
acts promptly to cause smooth muscle relaxation+bronchodilation

87
Q

What is an example of a SAMA?

A

ipratropium

88
Q

What is the MOA of SAMAs?

A

ACh in lungs causes bronchoconstriction and increased mucous secretion
ipratropium is a competitive antagonist of endogenous acetylcholine at muscarinic receptors

89
Q

What are the key side effects of SAMAs?

A

cough
headache
dizziness
dry mouth

90
Q

What are the key drug interactions associated with SAMAs?

A

anti-cholinergic load

91
Q

What are they key drug interactions with SABAs?

A

beta-blockers
QTC prolongation
loops and thiazides

92
Q

What is the commonly used first-line controller medication for asthma?

A

inhaled corticosteroids
-do not work for rapid symptom relief (weeks-months to max
effect)

93
Q

What are the many benefits of ICS as a controller for asthma?

A

directly reduces inflammation
improves symptoms
improves long-term outcomes
reduces asthma mortality and frequency+severity of attacks
reduces airway remodeling and hyper-reactivity

94
Q

What are the ICS used for asthma control?

A

beclomethasone
ciclesonide
budesonide
fluticasone
mometasone

95
Q

What is the MOA of ICS?

A

enters target cell in the lungs and binds to glucocorticoid receptors
-then moves into nucleus–>binds to coactivators to inhibit
histone acetyltransferase (HAT) and increase histone
deacetylase 2 (HDAC2)

96
Q

What are the actions of HAT and HDAC2?

A

HAT: acetylates inflammatory mediators
HDCAC2: deacetylates inflammatory proteins

97
Q

What are the key side effects of ICS?

A

common:
-oral thrush (wash mouth after use)
-hoarseness of voice
high doses long term:
-adrenal suppression
-increased glucose levels
-pneumonia
-osteoporosis

98
Q

What is the important drug interaction to keep in mind with ICS?

A

desmopressin–>hyponatremia risk

99
Q

Describe the use of LABAs in asthma.

A

commonly used for control
added after ICS
less rapid acting than short-acting agents but lasts longer
same MOA, side effects, and drug interactions as SABAs

100
Q

What are the LABAs?

A

formoterol
salmeterol

101
Q

Describe the use of LTRAs in asthma.

A

oral controller for very mild asthma
may be added to ICS/LABA
possible role in exercise-induced astham

102
Q

What is the only LTRA?

A

montelukast

103
Q

What is the MOA of LTRAs?

A

cysteinyl-leukotriene receptors cause mucous secretion, bronchoconstriction and eosinophil recruitment when activated
LTRA antagonizes this receptor

104
Q

What are the side effects and drug interactions of LTRAs?

A

none for both

105
Q

What is a rarely used oral last-line controller medication for asthma?

A

theophylline
-difficult dosing, toxicity, better agents

106
Q

How does theophylline cause bronchodilation?

A

inhibition of phosphodiesterase–>increases cAMP
antagonizing adenosine receptors–>prevents histamine and leukotriene release
increases IL 10 levels (anti-inflammatory)
creation of pro-inflammatory mediators

107
Q

What are they key side effects of theophylline?

A

cardiac toxicity: tachycardia, arrythmias
GI effects: nausea, heartburn, diarrhea

108
Q

What are the important drug interactions associated with theophylline?

A

theophylline is a CYP 3A4 and 1A2 substrate
-any inhibitor will increase theophylline levels

109
Q

What is the last-line treatment of asthma?

A

biologics
-targets allergic response or inflammatory mediators

110
Q

For COPD, what are the classes of drugs used for the following: main therapies, severe disease, exacerbations, rarely used

A

main therapies: SABA/LABA, SAMA/LAMA
severe disease: ICS
exacerbations: oral steroids, antibiotics
rarely used: methylxanthines (theophylline)

111
Q

True or false: SABA/LABA are more effective than SAMA/LAMA in COPD

A

false
SABA/LAMA are slightly less effective

112
Q

What is the only difference in SABA/LABA use in COPD as opposed to asthma?

A

given scheduled in COPD, not as needed

113
Q

True or false: SAMA/LAMA are utilized more in COPD

A

true

114
Q

What are some LAMAs?

A

tiotropium
aclidinium
glycopyrronium
umeclidinium

115
Q

What is the difference in ICS usage in COPD as opposed to asthma?

A

utilized in end-stage COPD

PHAR123 (15 decks)

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