Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pathophysiology Test 3 > conditions caused by pulmonary disease and the diseases themselves > Flashcards

conditions caused by pulmonary disease and the diseases themselves Flashcards

1
Q

what is hypercapnia?

A

increase in co2 in arterial blood

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

what is the most common cause of hypoxemia?

A

ventilation-perfusion abnormalities

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

what would lead to V/Q abnormalities?

A

decreased ventilation
decreased perfusion

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

what does decreased ventilation
and decreased perfusion lead to?

A

impaired gas exchange at the alveoli

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

what is a pleural abnormality also called?

A

pneumothorax

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is a pneumothorax?

A

presence of o2 in the pleural space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is primary pneumothorax also called?

A

spontaneous

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

when does a primary pneumothorax occur?

A

unexpectedly in healthy adults

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

what causes a secondary pneumothorax?

A

disease
trauma
injury
a condition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is a open pneumothorax?

A

Air that is drawn into the pleural space during inspiration is forced back out during expiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is a tension pneumothorax?

A

Site of pleural rupture acts as a one-way valve, permitting air to enter on inspiration but preventing its escape by closing up during expiration

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

what type of pneumothorax if life threatening?

A

tention pneumothorax

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

how do you treat a tension pneumothorax?

A

put in a chest tube

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what can tension pneumothorax lead to?

A

lung collapse

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

what is restrictive lung disorder?

A

decrease compliance in lung tissue

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

what effect do restrictive lung disorders have?

A

-Decreased compliance of lung tissue
-More effort needed during inspiration
-Increase respiratory rate
-Decreased tidal volume - hard to expand the lungs to get in air

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is the term for collapse of lung tissue (alveolar)?

A

atelectasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is compression atelectasis?

A

External compression on the lung

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is absorption atelectasis?

A

-Gradual absorption of air from obstructed or hypoventilated alveoli
-Alveoli begin to collapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is surfactant impairment?

A

Decreased production or inactivation of surfactant. Surface tension created by fluids. Surfactant is produced by cells and is necessary. Increased surface tension results in lungs collapsing

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

what are the manifestations of surfactant impairment?

A

dyspnea and cough

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

how do you treat surfactant impairment?

A

Prevention - Deep breathing for absorption atelectasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is pore of Kohn and how is it caused?

A

-deep breath
causes inspired air to flow between alveoli through the pore of Kohn to ventilate an alveoli from the other one.

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

what is the effect on V/Q of blocked alveolus?

A

decreased ventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What happens to the vessels that perfuse the affected areas (the collapsed alveoli)?
they are restricted
26
what is atelectasis triggered by?
hypoxemia
27
what is pulmonary fibrosis?
-restrictive lung disorder excessive amounts of fibrous or connective tissue in the lung
28
what happens to the lung in pulmonary fibrosis?
it becomes stiff and difficult to ventilate -lung compliance decreases
29
what does pulmonary fibrosis lead to?
hypoxemia-vasoconstiction- increase TPR-hypertrophy cells in RV- decrease in contractility- RSHF- peripheral edema
30
what are the causes of pulmonary fibrosis?
-idiopathic: no specific cause -inhalation of various substances
31
what is pulmonary edema?
build up of fluid in the lungs or interstitial spaces
32
what is effected when pulmonary edema occurs?
gas exchange (decreases)
33
what disturbances lead to pulmonary edema?
increase in BHP decreases in BOP increase in capillary permeability
34
what is the most common cause of pulmonary edema?
Left side heart disease
35
what are the other causes of pulmonary edema?
liver disease infectous processes
36
what are the manifestations of pulmonary edema?
dyspnea orthopnea hypoxemia increased work of breathing
37
what is obstructive pulmonary disease?
-Airway obstruction is worse with expiration (vs restrictive was inspiration) -More force or more time is required to expire a given volume of air; emptying the lungs is slowed
38
what are the signs and symptoms of obstructive pulmonary disease?
wheezing and dyspnea
39
what are the manifestations of obstructive pulmonary disease?
-Increased work of breathing -ventilation-perfusion (V/Q) mismatching -decreased forced expiratory volume in one second (FEV1 ), -increased residual volume (RV)
40
what are the obstructive pulmonary diseases?
asthma chronic bronchitis emphysema COPD
41
what is asthma?
Chronic inflammatory disorder of the bronchial mucosa
42
what are the causes of asthma?
reversible bronchial hyperresponsiveness (excessive constriction of bronchial tissue) - variable airflow obstruction
43
when do 1/2 of the cases of asthma develop?
during childhood
44
what is a familial disorder with over 100 genes identified?
asthma
45
what is the hygiene hypothesis?
Lack of early childhood exposure to various agents that are necessary for immune system development
46
what increases the risk of developing asthma?
Allergen exposure, urban residence, air pollution, tobacco smoke, infection
47
what happens in the early asthmatic response?
-Antigen exposure activates antigen-presenting cells -Interleukin 4 (IL-4) stimulates production of antigen-specific IgE -Immunoglobulin E (IgE) causes the mast cells to degranulate, releasing a large number of inflammatory mediators -IL-5 stimulates the activation of eosinophils, which contributes to increased bronchial hyperresponsiveness, fibroblast proliferation, epithelial injury, and airway scarring.
48
what happen when Immunoglobulin E (IgE) causes the mast cells to degranulate, releasing a large number of inflammatory mediators in the early asthmatic response?
- vasodilation – increased capillary permeability – mucosal edema – tenacious mucous secretion – bronchial smooth muscle contraction (bronchospasm)
49
what happens in the last asthmatic response?
Air trapping Decrease oxygen and increase co2 Hyperinflation distal to obstructions Increased work of breathing RV increases FEV1 decreases Ventilation is impaired (decrease in V/Q)
50
how does air trapping effect oxygen and co2 levels?
Decrease oxygen and increase co2
51
what does increased work of breathing cause?
dyspnea
52
what are the clinical manifestations of asthma?
Asymptomatic between attacks Chest constriction expiratory wheezing Dyspnea nonproductive coughing prolonged expiration Increased RV Decreased FEV
53
what is the mildest/intermittent treatment for asthma?
short acting beta agonist inhalers - bronchodilators (albuterol)
54
what is the treatment for persistent asthma?
anti inflammatory medications and inhaled corticosteroids
55
what should be monitored while giving treatments for asthma?
gas exchange and airway obstruction in response to therapy
56
what are the other treatments for asthma?
-Antihistamine -Leukotriene antagonists (prevents mast cell degranulation) -Reduction of asthma exacerbations (avoiding triggers) - immunotherapy -Monoclonal antibodies to IgE
57
what is chronic bronchitis?
Hypersecretion of mucus (from the cells) therefore there is more mucus in the bronchioles
58
what do the bronchioles look like in chronic bronchitis?
Thicker tissue, mucous, smaller lumen size
59
what classifies someone having chronic bronchitis?
Chronic productive cough that lasts at least 3 months of the year and for at least 2 consecutive years
60
what is the pathophysiology of chronic bronchitis?
-Inspired irritants increase mucus production Increase size and number of mucous glands mucus is thicker than normal -bronchial edema -Hypertrophied bronchial smooth muscle -Airways collapse early in expiration, trapping gas in the lung
61
hat effect does the pathophysiology of chronic bronchitis have on oxygen and co2 levels in the blood?
Decreased oxygen, increase co2 Hypoxemia and hypercapnia
62
what are the clinical manifestations chronic bronchitis?
-Decreased exercise tolerance -Wheezing and shortness of breath -Productive cough (“smoker’s cough”) becomes copious -FEV1 is decreased because there is an obstruction -RV is increase -Polycythemia -RHF and peripheral edema
63
why would chronic bronchitis cause polycythemia?
Increase in EPO - tissue hypoxia Secondary polycythemia
64
what are the treatments for chronic bronchitis?
Smoking cessation - diseases progression can be halted Bronchodilators Expectorants Chest physical therapy Antibiotics Steroids mechanical ventilation if needed Oxygen therapy
65
what is emphysema?
Abnormal permanent enlargement of the air sacs (alveoli) in your lungs, accompanied by the destruction of the alveolar walls (without obvious fibrosis)
66
what can emphysema lead to physically?
-Loss of elastic recoil - not doing as much expanding or contracting -Walls are destroyed and broken down -One large compartment, not small ones -Reduces surface area of alveolar walls. -With the big spaces, there is less surface area (Surface area required for gas exchange) -Reduced surface area - less O2 can reach the blood stream
67
what is the cause of primary emphysema?
Inherited deficiency of the enzyme α1 -antitrypsin
68
what does a deficiency of the enzyme α1 -antitrypsin do?
-neutrophil elastase breaks down elastin, which contributes to elasticity of the lungs -Result is breakdown of alveolar walls and their elasticity
69
what are the causes of secondary emphysema?
-Main cause: smoking -Possible contributors: Air pollution Occupational exposure - dust Childhood respiratory infections
70
what are the pathological effects of emphysema?
-Increased FRC, RV, and TLC (everything you could expire) -Opened up more space, but it does not provide the surface area for gas exchange
71
what are the clinical manifestations of emphysema?
-Dyspnea on exertion -Later progresses to marked dyspnea, even at rest -Little coughing and very little sputum -Thin (extra energy expenditure from labrador breathing) -Rapid breathing with prolonged expiration -Barrel chest -Forward lean with arms extended and braced on knees when sitting
72
what are the treatments for emphysema?
-Smoking cessation -Oxygen -Inhaled bronchodilators -Oral steroids and antibiotics -Inhaled anticholinergic agents and beta agonists -Inhaled corticosteroids -Pulmonary rehab -Improved nutrition -Breathing techniques (Exhale through pursed lips to help prevent expiratory airway collapse)
73
what is COPD?
Chronic Obstructive Pulmonary Disease (Chronic bronchitis plus emphysema)
74
what is the third leading cause of death in the United States and the sixth leading cause of death worldwide
COPD
75
is COPD damage reversible?
no
76
what is COPD associated with?
an abnormal inflammatory response to noxious particles or gasses
77
what are the risk factors for COPD?
-Tobacco smoke -Occupational dusts and chemicals -Indoor air pollution from biomass fuel used for cooking and heating -Outdoor air pollution -Genetic susceptibilities (Inherited mutation in the alpha-1 antitrypsin)

Pathophysiology Test 3 (4 decks)

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