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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

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2
Q

what is the most common cause of hypoxemia?

A

ventilation-perfusion abnormalities

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3
Q

what would lead to V/Q abnormalities?

A

decreased ventilation
decreased perfusion

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4
Q

what does decreased ventilation
and decreased perfusion lead to?

A

impaired gas exchange at the alveoli

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5
Q

what is a pleural abnormality also called?

A

pneumothorax

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6
Q

what is a pneumothorax?

A

presence of o2 in the pleural space

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7
Q

what is primary pneumothorax also called?

A

spontaneous

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8
Q

when does a primary pneumothorax occur?

A

unexpectedly in healthy adults

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9
Q

what causes a secondary pneumothorax?

A

disease
trauma
injury
a condition

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10
Q

what is a open pneumothorax?

A

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

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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

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12
Q

what type of pneumothorax if life threatening?

A

tention pneumothorax

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13
Q

how do you treat a tension pneumothorax?

A

put in a chest tube

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14
Q

what can tension pneumothorax lead to?

A

lung collapse

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15
Q

what is restrictive lung disorder?

A

decrease compliance in lung tissue

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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

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17
Q

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

A

atelectasis

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18
Q

what is compression atelectasis?

A

External compression on the lung

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19
Q

what is absorption atelectasis?

A

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

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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

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21
Q

what are the manifestations of surfactant impairment?

A

dyspnea and cough

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22
Q

how do you treat surfactant impairment?

A

Prevention - Deep breathing for absorption atelectasis

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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.

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24
Q

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

A

decreased ventilation

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25
Q

What happens to the vessels that perfuse the affected areas (the collapsed alveoli)?

A

they are restricted

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26
Q

what is atelectasis triggered by?

A

hypoxemia

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27
Q

what is pulmonary fibrosis?

A

-restrictive lung disorder
excessive amounts of fibrous or connective tissue in the lung

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28
Q

what happens to the lung in pulmonary fibrosis?

A

it becomes stiff and difficult to ventilate
-lung compliance decreases

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29
Q

what does pulmonary fibrosis lead to?

A

hypoxemia-vasoconstiction- increase TPR-hypertrophy cells in RV- decrease in contractility- RSHF- peripheral edema

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30
Q

what are the causes of pulmonary fibrosis?

A

-idiopathic: no specific cause
-inhalation of various substances

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31
Q

what is pulmonary edema?

A

build up of fluid in the lungs or interstitial spaces

32
Q

what is effected when pulmonary edema occurs?

A

gas exchange (decreases)

33
Q

what disturbances lead to pulmonary edema?

A

increase in BHP
decreases in BOP
increase in capillary permeability

34
Q

what is the most common cause of pulmonary edema?

A

Left side heart disease

35
Q

what are the other causes of pulmonary edema?

A

liver disease
infectous processes

36
Q

what are the manifestations of pulmonary edema?

A

dyspnea
orthopnea
hypoxemia
increased work of breathing

37
Q

what is obstructive pulmonary disease?

A

-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
Q

what are the signs and symptoms of obstructive pulmonary disease?

A

wheezing and dyspnea

39
Q

what are the manifestations of obstructive pulmonary disease?

A

-Increased work of breathing
-ventilation-perfusion (V/Q) mismatching
-decreased forced expiratory volume in one second (FEV1 ),
-increased residual volume (RV)

40
Q

what are the obstructive pulmonary diseases?

A

asthma
chronic bronchitis
emphysema
COPD

41
Q

what is asthma?

A

Chronic inflammatory disorder of the bronchial mucosa

42
Q

what are the causes of asthma?

A

reversible bronchial hyperresponsiveness (excessive constriction of bronchial tissue)
- variable airflow obstruction

43
Q

when do 1/2 of the cases of asthma develop?

A

during childhood

44
Q

what is a familial disorder with over 100 genes identified?

A

asthma

45
Q

what is the hygiene hypothesis?

A

Lack of early childhood exposure to various agents that are necessary for immune system development

46
Q

what increases the risk of developing asthma?

A

Allergen exposure, urban residence, air pollution, tobacco smoke, infection

47
Q

what happens in the early asthmatic response?

A

-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
Q

what happen when Immunoglobulin E (IgE) causes the mast cells to degranulate, releasing a large number of inflammatory mediators in the early asthmatic response?

A
  • vasodilation
    – increased capillary permeability
    – mucosal edema
    – tenacious mucous secretion
    – bronchial smooth muscle contraction (bronchospasm)
49
Q

what happens in the last asthmatic response?

A

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
Q

how does air trapping effect oxygen and co2 levels?

A

Decrease oxygen and increase co2

51
Q

what does increased work of breathing cause?

A

dyspnea

52
Q

what are the clinical manifestations of asthma?

A

Asymptomatic between attacks
Chest constriction
expiratory wheezing
Dyspnea
nonproductive coughing
prolonged expiration
Increased RV
Decreased FEV

53
Q

what is the mildest/intermittent treatment for asthma?

A

short acting beta agonist inhalers - bronchodilators (albuterol)

54
Q

what is the treatment for persistent asthma?

A

anti inflammatory medications and inhaled corticosteroids

55
Q

what should be monitored while giving treatments for asthma?

A

gas exchange and airway obstruction in response to therapy

56
Q

what are the other treatments for asthma?

A

-Antihistamine
-Leukotriene antagonists (prevents mast cell degranulation)
-Reduction of asthma exacerbations (avoiding triggers) - immunotherapy
-Monoclonal antibodies to IgE

57
Q

what is chronic bronchitis?

A

Hypersecretion of mucus (from the cells) therefore there is more mucus in the bronchioles

58
Q

what do the bronchioles look like in chronic bronchitis?

A

Thicker tissue, mucous, smaller lumen size

59
Q

what classifies someone having chronic bronchitis?

A

Chronic productive cough that lasts at least 3 months of the year and for at least 2 consecutive years

60
Q

what is the pathophysiology of chronic bronchitis?

A

-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
Q

hat effect does the pathophysiology of chronic bronchitis have on oxygen and co2 levels in the blood?

A

Decreased oxygen, increase co2
Hypoxemia and hypercapnia

62
Q

what are the clinical manifestations chronic bronchitis?

A

-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
Q

why would chronic bronchitis cause polycythemia?

A

Increase in EPO - tissue hypoxia
Secondary polycythemia

64
Q

what are the treatments for chronic bronchitis?

A

Smoking cessation - diseases progression can be halted
Bronchodilators
Expectorants
Chest physical therapy
Antibiotics
Steroids
mechanical ventilation if needed
Oxygen therapy

65
Q

what is emphysema?

A

Abnormal permanent enlargement of the air sacs (alveoli) in your lungs, accompanied by the destruction of the alveolar walls (without obvious fibrosis)

66
Q

what can emphysema lead to physically?

A

-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
Q

what is the cause of primary emphysema?

A

Inherited deficiency of the enzyme α1 -antitrypsin

68
Q

what does a deficiency of the enzyme α1 -antitrypsin do?

A

-neutrophil elastase breaks down elastin, which contributes to elasticity of the lungs
-Result is breakdown of alveolar walls and their elasticity

69
Q

what are the causes of secondary emphysema?

A

-Main cause: smoking
-Possible contributors:
Air pollution
Occupational exposure - dust
Childhood respiratory infections

70
Q

what are the pathological effects of emphysema?

A

-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
Q

what are the clinical manifestations of emphysema?

A

-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
Q

what are the treatments for emphysema?

A

-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
Q

what is COPD?

A

Chronic Obstructive Pulmonary Disease (Chronic bronchitis plus emphysema)

74
Q

what is the third leading cause of death in the United States and the sixth leading cause of death worldwide

A

COPD

75
Q

is COPD damage reversible?

A

no

76
Q

what is COPD associated with?

A

an abnormal inflammatory response to noxious particles or gasses

77
Q

what are the risk factors for COPD?

A

-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)

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