Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PHAR123 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What makes up the upper respiratory tract?

A

nose and nasal cavity
paranasal sinuses
pharynx
larynx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What makes up the lower respiratory tract?

A

trachea
bronchi and smaller bronchioles
lungs and alveoli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

True or false: the left lung contains three lobes

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

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

A

lungs: visceral pleura
ribs and diaphragm: parietal pleura

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the respiratory zone?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is respiration?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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>

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What can ventilation and perfusion mismatch lead to?

A

hypoxemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is Type 1 respiratory failure?

A

inability of lungs to perform adequate gas exchange
leads to hypoxemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What are the potential causes of Type 1 respiratory failure?
lung disorder (asthma, COPD) pneumonia pulmonary-edema, fibrosis, embolism, hypertension
26
What is Type 2 respiratory failure?
sometimes called ventilatory failure breathing is not sufficient to rid the body of CO2 CO2 excretion
27
What are the potential causes of Type 2 respiratory failure?
decreased CNS drive impaired neuromuscular function chronic bronchitis or COPD excessive inspiratory load
28
What are arterial blood gases?
used to determine acid-base balance, which helps determine the cause of respiratory issues blood pH controlled by lungs and kidney
29
What would the pH value be for acidosis? What about alkalosis?
normal=7.40 acidosis=<7.35 alkalosis=>7.45
30
What are the two systems of compensation for acid-base balance?
respiratory compensation -lungs modulate how much CO2 is retained/excreted metabolic compensation -kidneys modulate how much HCO3 is retained/excreted
31
What would happen during respiratory acidosis?
pH is lowered HCO3 is normal PaCO2 is increased compensation: kidneys release HCO3
32
What would happen during respiratory alkalosis?
pH is raised HCO3 is normal PaCO2 is lowered compensation: kidneys retain HCO3
33
What would happen during metabolic acidosis?
pH is lowered HCO3 is lowered PaCO2 is normal compensation: lungs remove CO2
34
What would happen during metabolic alkalosis?
pH is raised HCO3 is raised PaCO2 is normal compensation: lungs retain CO2
35
What are the two main lung function tests?
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
36
What are the lung volumes?
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
37
What are the lung capacities?
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
38
What is the use of FEV1/FVC ratio?
differentiate between restrictive and obstructive lung disease -obstructive=low FEV1/FVC, normal FVC -restrictive=normal FEV1/FVC, low FVC
39
What would one predict to see happen with the respiratory system as fitness improves?
lungs can accommodate higher volumes of air increased diffusion of respiratory gases strengthens cilia and diaphragm strengthens other respiratory muscles VO2 max increases
40
What are the many reasons that smokers have poor exercise tolerance?
nicotine causes bronchoconstriction lung fibrosis excess mucous secretion inhibited cilia destruction of elastic fibers
41
What is the age-related impact on lung function?
respiratory tissues and chest wall become more rigid weak respiratory muscles VC decreases macrophage activity decreases cilia less active
42
What is asthma?
chronic inflammatory disorder characterized by: -paroxysmal or persistent symptoms -dyspnea, wheezing, cough, chest tightness, sputum -airway hyper-responsiveness
43
What are the risk factors/etiology for asthma?
genetics hygiene hypothesis atopic vs non-atopic gender maternal factors perinatal factors factors during childhood factors during adulthood
44
How can genes be involved in asthma?
development of asthma-->pre-disposing to atopy severity of condition-->airway hyper-responsiveness response to therapy
45
What is the hygiene hypothesis?
limited exposure to normal environmental stimuli may cause the allergic immunologic system to develop more than the system to fight infection
46
Why is atopy linked to asthma?
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
47
Describe the impact of gender on the development of asthma.
childhood asthma has higher prevalence in males equal from age 20-40 age 40: females>males
48
Describe the impact of maternal factors on the development of asthma.
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
What are the perinatal factors that can effect the risk of asthma development?
pre-eclampsia prematurity mode of delivery (caesarean) breastfeeding vit D supplementation
50
What are some childhood factors that can increase the risk of asthma development?
viral infections (RSV, HRV) medication use in infancy (acet, ibu, antibiotics) air pollution tobacco smoke exposure obesity
51
What are some adulthood factors that can increase the risk of asthma development?
obesity tobacco smoke occupational exposure rhinitis
52
What are the many triggers of asthma?
irritants resp tract infections weather stress hormonal fluctuations GERD medication (ASA/NSAIDs, beta-blockers) sulfites
53
What are the hallmarks of asthma pathology?
bronchial hyper-reactivity bronchial inflammation airway obstruction (bronchoconstriction, mucous plug)
54
What is the physiology of bronchial hyper-reactivity?
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
What is the physiology of bronchoconstriction?
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
What is the physiology of bronchial inflammation?
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
What does continued bronchial inflammation eventually lead to?
airway remodelling
58
What is the physiology of airway remodelling?
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
True or false: airway remodelling is irreversible
true
60
What is the clinical presentation of asthma?
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
What is the definition of controlled asthma, with regards to daytime symptoms, nighttime symptoms, and need for a reliever?
daytime symptoms <2 days/week nighttime symptoms <1 night/week and mild need for a reliver <2 doses/week
62
What would be the lung function testing results of an asthmatic? (FEV1/FVC, bronchodilator challenge, bronchoprovocation testing)
FEV1/FVC: <0.7 bronchodilator challenge: significant reversibility post-test (>12%) bronchoprovocation: sensitive to the testing
63
What is status asthmaticus?
severe exacerbation -episodes of worsening asthma symptoms, lung function, and hyper-responsiveness
64
Which group of patients is status asthmaticus most commonly seen in?
those with under-utilized anti-inflammatory therapy
65
True or false: status asthamticus can progress without treatment and become life-threatening, it also the most common cause for hospitalizations in asthmatics
true
66
What would be the treatment for status asthmaticus?
*unresponsive to bronchodilator treatment alone* must be intensively treated promptly
67
Aside from status asthmaticus, what are the many other complications of asthma?
airway remodelling fatigue underperformance at work/school inability to exercise frequent hospitalizations pneumonia and influenza GERD sleep apnea
68
How is COPD characterized?
chronic respiratory condition characterized by: -persistent symptoms -airflow limitation and narrowing airways -chronic inflammation -mucociliary dysfunction -mix of chronic bronchitis and emphysema
69
What is COPD a "mix" of?
obstructive bronchiolitis (chronic bronchitis) emphysema
70
What is the etiology and risk factors for COPD?
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
What are the cardinal symptoms of COPD?
dyspnea chronic cough sputum production
72
What is emphysema?
refers to airway collapse due to loss of lung recoil by alveolar wall destruction leads to: -air trapping -impaired gas diffusion -lung hyperinflation
73
What is the cause of emphysema?
imbalance between proteolysis and anti-proteolysis in the lungs
74
What is the main enzyme responsible for proteolysis in the lungs?
elastase -produced by neutrophils and macrophages -irreversibly inhibited by alpha-1-antitrypsin MMP also involved
75
What are the several changes that chronic bronchitis can cause to the bronchioles?
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
True or false: COPD is progressive and you cannot halt the decline of lung function and FEV1
true
77
What is the biggest predictor of mortality from COPD?
low FEV1 and rate of decline
78
What are common comorbidities with COPD?
lung cancer cardiovascular disease sleep apnea metabolic syndrome osteoporosis
79
For asthma, what are classes of drugs used for the following: relievers, controllers, exacerbations, novel therapy
relievers: SABA, SAMA controllers: ICS, LABA, LTRA, Theophylline exacerbations: oral steroids novel therapy: biologics
80
What is the most used agents in asthma?
short-acting beta-adrenergic agonists
81
What are the B2 selective, and non-selective SABAs?
B2 selective: salbutamol, terbutaline non-selective: epinephrine
82
What is the MOA of SABAs?
binds to B2 receptors in the lung, causing: -hyperpolarization of Ca-activated K channels -stimulation of ATP-->cAMP-->removal of calcium from muscle
83
What are the secondary effects that could occur from the MOA of SABAs?
reduce mediator release from mast cells reduces microvascular leakage after exposure to mediators enhances mucociliary clearance reduces neurotransmission of cholinergic nerves
84
What are the key side effects of SABAs?
cardiovascular stimulation -tachycardia -palpitations -dizziness -tremor *SABAs are inhaled to reduce risk of these side effects*
85
True or false: tolerance does not generally develop to the side effects of SABAs
false
86
When are SAMAs typically used in asthma?
add-on during asthma attacks acts promptly to cause smooth muscle relaxation+bronchodilation
87
What is an example of a SAMA?
ipratropium
88
What is the MOA of SAMAs?
ACh in lungs causes bronchoconstriction and increased mucous secretion ipratropium is a competitive antagonist of endogenous acetylcholine at muscarinic receptors
89
What are the key side effects of SAMAs?
cough headache dizziness dry mouth
90
What are the key drug interactions associated with SAMAs?
anti-cholinergic load
91
What are they key drug interactions with SABAs?
beta-blockers QTC prolongation loops and thiazides
92
What is the commonly used first-line controller medication for asthma?
inhaled corticosteroids -do not work for rapid symptom relief (weeks-months to max effect)
93
What are the many benefits of ICS as a controller for asthma?
directly reduces inflammation improves symptoms improves long-term outcomes reduces asthma mortality and frequency+severity of attacks reduces airway remodeling and hyper-reactivity
94
What are the ICS used for asthma control?
beclomethasone ciclesonide budesonide fluticasone mometasone
95
What is the MOA of ICS?
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
What are the actions of HAT and HDAC2?
HAT: acetylates inflammatory mediators HDCAC2: deacetylates inflammatory proteins
97
What are the key side effects of ICS?
common: -oral thrush (wash mouth after use) -hoarseness of voice high doses long term: -adrenal suppression -increased glucose levels -pneumonia -osteoporosis
98
What is the important drug interaction to keep in mind with ICS?
desmopressin-->hyponatremia risk
99
Describe the use of LABAs in asthma.
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
What are the LABAs?
formoterol salmeterol
101
Describe the use of LTRAs in asthma.
oral controller for very mild asthma may be added to ICS/LABA possible role in exercise-induced astham
102
What is the only LTRA?
montelukast
103
What is the MOA of LTRAs?
cysteinyl-leukotriene receptors cause mucous secretion, bronchoconstriction and eosinophil recruitment when activated LTRA antagonizes this receptor
104
What are the side effects and drug interactions of LTRAs?
none for both
105
What is a rarely used oral last-line controller medication for asthma?
theophylline -difficult dosing, toxicity, better agents
106
How does theophylline cause bronchodilation?
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
What are they key side effects of theophylline?
cardiac toxicity: tachycardia, arrythmias GI effects: nausea, heartburn, diarrhea
108
What are the important drug interactions associated with theophylline?
theophylline is a CYP 3A4 and 1A2 substrate -any inhibitor will increase theophylline levels
109
What is the last-line treatment of asthma?
biologics -targets allergic response or inflammatory mediators
110
For COPD, what are the classes of drugs used for the following: main therapies, severe disease, exacerbations, rarely used
main therapies: SABA/LABA, SAMA/LAMA severe disease: ICS exacerbations: oral steroids, antibiotics rarely used: methylxanthines (theophylline)
111
True or false: SABA/LABA are more effective than SAMA/LAMA in COPD
false SABA/LAMA are slightly less effective
112
What is the only difference in SABA/LABA use in COPD as opposed to asthma?
given scheduled in COPD, not as needed
113
True or false: SAMA/LAMA are utilized more in COPD
true
114
What are some LAMAs?
tiotropium aclidinium glycopyrronium umeclidinium
115
What is the difference in ICS usage in COPD as opposed to asthma?
utilized in end-stage COPD

PHAR123 (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions