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Human Pathophysiology: Final > Respiratory System II > Flashcards

Respiratory System II Flashcards

1
Q

What are some causes of airway narrowing?

A
  • smooth muscle constriction
  • plugging of the airway
  • edema of the airway wall
  • loss of the retractive forces of the lung parenchyma
  • loss of tethering
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2
Q

How does airway narrowing affect the body?

A

airway narrows –> increased Raw (airway resistance) –> more difficult for respiratory muscles to move air in and out of the lungs (need to generate more pressure)

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3
Q

How is Raw and radius related?

A

R is proportional to 1/r^4

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4
Q

What is the easiest way to measure airway narrowing?

A

comparing te FEV1 (forced expiratory volume in 1 sec) to the forced vital capacity (the total amount of air a person can breath out). If the ratio FEV1/FVC is

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5
Q

What factors affect lung volume?

A
  • age
  • sex
  • height
  • weight
  • ethnic origin
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6
Q

What is FRC?

A

functional residual capacity - the volume in your lungs at the end of a breath when you are completely relaxed (tendency of chest wall to recoil outwards exactly matches inward recoil)

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7
Q

What is TLC?

A

total lung capacity - the total amount of air in your lungs at the end of a maximal inspiratory effort (overall size of the lung)

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8
Q

What is RV?

A

residual volume - the volume of air in your lungs at the end of a maximal expiratory effort

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9
Q

What is VC?

A

vital capacity - the difference between TLC and RV; primarily determined by overall thoracic size

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10
Q

What is the formula for VC?

A

VC = (5.2 * height) - (X*age) - (Y)

X = 0.022 (male) or 0.018 (female)
Y = 3.6 (male) or 4.36 (female)
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11
Q

Definition: airway narrowing that reverses either spontaneously or after drug treatment; increased airway responsiveness; airway inflammation

A

asthma

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12
Q

How is asthma diagnosed?

A

A bronchodilator is administered to increase FEV1. A greater than 15% increase is indicative of asthma.

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13
Q

What causes bronchoconstriction during asthma?

A

mainly caused by smooth muscle constriction but also by mucous plugging and airway edema

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14
Q

What is airway hyperresponsiveness?

A

increased airway narrowing in response to contractile agonists that cause constriction of airway smooth muscle; sometimes used to diagnose asthma

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15
Q

What does the severity of asthma correlate with?

A

PD20, or the provocative dose of asthmatic agent that is required to cause a 20% decrease in FEV1.

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16
Q

What is allergic airway inflammation characterized by?

A

T-lymphocytes (CD4 and CD8) and eosinophils

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17
Q

How do eosinophils contribute to asthma?

A
  • contain granule proteins that can damage epithelium and make it more leaky to allergens
  • promote contraction of smooth muscle
  • recruit more eosinophils
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18
Q

How do lymphocytes contribute to asthma?

A
  • produce cytokines which promote eosinophils proliferation

- promote IgE formation

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19
Q

What are common symptoms of asthma?

A
  • cough
  • SOB
  • chest tightness
  • wheezing
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20
Q

What are some characteristics of asthma (histology)?

A
  • airway smooth muscle thickening
  • mucous plugs in airway lumens
  • presence of inflammatory cells
  • disrupted epithelium (sub epithelial fibrosis)
  • basement membrane thickening
  • airway wall edema
  • increased numbers of blood vessels in airway wall
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21
Q

How does asthma affect pulmonary function?

A
  • TLC is normal
  • FRC and RV are increased
  • pulmonary resistance is increased
  • lung stiffness is low or normal
  • airway obstruction is caused by smooth muscle constriction and plugging
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22
Q

How does asthma affect blood gases?

A
  • PaO2 is low (V/Q mismatch)
  • PaCO2 can sometimes be low (hyperventilation due to anxiety, if its increased, its usually a sign of ventilatory failure)
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23
Q

What are he epidemiology stats of asthma?

A
  • affects 5-10% of Americans
  • more prevalent in urban than rural settings
  • incidence/severity has doubled in last 20 yrs
  • more severe among AA than europeans
  • mortality rates have been increasing but still rare
  • leading cause of pediatric hospitalizations
  • leading serious chronic illness in children
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24
Q

How are allergies and asthma associated?

A

In people with allergies, IgE antibodies (made by B lymphocytes) recognize allergens. IgE binds to mast cells and then allergens. The mast cell degranulates and releases histamine and leukotrienes into extracellular fluid (bronchoconstrictors) as well as cytokines. Asthmatics and people with allergies have high levels of IgE in their blood.

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25
Q

What are the most common allergens in the US?

A
  • house dust mite
  • cockroach
  • cat
  • fungi
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26
Q

What happens what an asthmatic inhales an allergen?

A

Early Response: within minutes, a rapid drop in FEV1 occurs, which resolves in 1 hour; caused by products released from mast cells to narrow airways

Late Response: 4-6 hours later there is another drop in FEV1 which takes longer to resolve. It results from an influx of inflammatory cells into the airway due the mast cell response. These cells also release products that cause smooth muscle contraction and edema of the airway wall.

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27
Q

What are some triggers for asthma

A
  • allergens
  • exercise
  • hyperventilation of cold air
  • emotions
  • pollution
  • cigarette smoke
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28
Q

What are some things that can cause asthma?

A
  • pathophysiology not well understood still; origins appear to arise in early childhood
  • genetic: genes that regular IgE and cytokines
  • environmental: exposure to allergens/pollution/cigaretter smoke/viruses/obesity
  • viral illnesses during childhood can contribute
  • exposure to allergens to which the individual is allergic too
  • obesity
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29
Q

What are some ways to treat asthma?

A
  • corticosteroid type drugs: reduce inflammation by preventing the production and action of cytokines and other inflammatory mediators
  • beta-agonists drugs: act on beta-adrenergic receptors (target of adrenaline) to relax airway smooth muscle
  • leukotriene synthesis inhibitors and receptor antagonists: prevents the synthesis or action of leukotrienes (bronchoconstrictor)
  • anti-IgE (omalizumab): binds and removes IgE from circulation
  • allergen avoidance: self explanatory
  • education: self-assessment and consultation with a physician are important in managing asthma
30
Q

What is the hygiene hypothesis?

A

The theory that recent increases in asthma prevalence are because of cleaner environments, increased vaccinations and increased use of antibiotics; develop fewer childhood illnesses.

31
Q

How does the hygiene hypothesis theory explain the increasing prevalence of asthma?

A
  • stimulation with endotoxin –> immature T cells receive signals that cause the immune system to develop in such a way that they become optimized for fighting infections.
  • this type of T cell is termed a Th1 cell and produces cytokines like IFNgamma
  • if no such signals are ever received by the developing immune system, the T cells develop along a line in which the T cells produce cytokines of the Th2 type (IL-4, IL-5, IL-13)
  • this results in B cells of the class that generate IgE and predisposes one to the development of allergies; these cytokines can also act on eosinophils.
32
Q

What are some of the epidemiology stats of COPD?

A
  • 5th leading cause of death in the US
  • 2nd leading cause of disability
  • smoker’s disease
  • consists of two diseases: chronic bronchitis and emphysema; many show characteristics of both
33
Q

What are some other consequences of smoking?

A
  • heart disease
  • CAD
  • stroke
  • cancer
34
Q

What are some of the consequences of passive smoking in children?

A
  • children born to mothers who smoked have an average birth weight that is 200g less than normal and lower lung size
  • children whose parents smoke are more susceptible to asthma, bronchitis, pneumonia, and have a lower lung size/function than normal
35
Q

__% of coronary deaths can be attributed to smoking. __% of cancer deaths can be attributed to smoking. Smoking can all cause ____ and _____.

A

30
30
ulcers
periodontal disease

36
Q

Smoking is responsible for ___ of all fire-related deaths.

A

1/4

37
Q

On average, ___ minutes of life is lost for every cigarette smoked.

A

5.5

38
Q

What happens during emphysema?

A

alveolar walls are destroyed –> causes enlarged air spaces –> small airspaces are narrowed/ thin walled, may be reduced –> decrease in total surface area of the lungs

39
Q

What is panacinar emphysema?

A

when the central part of the acinus (respiratory bronchioles) are mainly affected

40
Q

What is pan lobular emphysema?

A

when the whole acinus is destroyed

41
Q

What is the most commonly affected part of the lung in emphysema?

A

the apex

42
Q

What happens during chronic bronchitis?

A

hypertrophy of mucus glands –> goblet cell metaplasia –> inflammation of small airways and glands –> mucus in airway can occlude lumen –> airway wall edema/thickened epithelium

43
Q

What is the main cause of chronic bronchitis?

A

chronic inflammation resulting from inhaled particles and/or chemical present in smoke

44
Q

How does the inflammatory reaction contribute to chronic bronchitis?

A

influx and activation of phagocytic cells –> released proteases and oxygen radicals –> destruction of extracellular matrix/tissue/mucous glands/cilia –> decreased mucociliary clearance –> increased infections (further agitates the condition)

45
Q

What is one special case where emphysema is NOT caused by smoking? Explain pathophysiology.

A

alpha-1-antitrypsin deficiency:

mutation in gene coding for the enzyme –> inability to secrete the enzyme –> low levels of alpha-1-antitrypsin in blood and airway lavage fluid –> early onset emphysema

46
Q

What parts of the lungs does alpha-1-antitrypsin deficiency affect first?

A

lower lobes

47
Q

What are the signs and symptoms of emphysema?

A
  • dyspnea at rest, exaggerated by exercise
  • think, barrel chest (“pink puffer”)
  • wheeze on expiration
48
Q

What are the signs and symptoms of chronic bronchitis?

A
  • dyspnea on exertion but NOT at rest
  • cough
  • sputum (purulent)
  • cyanosis (deoxyhemoglobin > 5g/100ml)
  • frequent respiratory infections
  • pops and rales
49
Q

How does emphysema affect pulmonary function?

A
  • increased TLC, RV, and FRC
  • decreased FEV1
  • airway closure
  • decreased FEV1/FVC
  • uneven ventilation
  • airway obstruction due to loss of elastic recoil
50
Q

How does chronic bronchitis affect pulmonary function?

A
  • normal TLC, increased RV
  • decreased FEV1
  • airway closure
  • decreased FEV1/FVC
  • uneven ventilation
  • airway obstruction due to mucus plugging, airway edema, and smooth muscle contraction
51
Q

What is FVC?

A

forced vital capacity - the amount of air one can breath out in one breath

52
Q

How does FEV1 change with age for a non smoker? For a smoker?

A

There is a gradual decline with age in all patients, however, smokers decline much faster.

53
Q

What happens to FEV1 when a smoker stops smoking?

A

They revert to the rate of loss of function of a non-smoker but they never regain the function they have lost.

54
Q

What constitutes as a disability from a low FEV1?

A

When the patient has difficulty doing even minor tasks such as walking down the hall with major breathlessness

55
Q

What are some genetic factors that increase chances of COPD?

A
  • familial association of low FEV1

- genes associated with COPD

56
Q

What are some genes associated with COPD?

A
  • alpha-1-antitrypsin
  • microsomal epoxide hydrolase
  • glutatione-S-transferase
  • hemoxygenase 1
  • TNF-alpha
57
Q

What does microsomal epoxide hydrolase do?

A

degrades chemicals in cigarette smoke

58
Q

What does glutatione-S-transferase do?

A

degrades chemicals in cigarette smoke

59
Q

What does hemoxygenase-1 do?

A

its an antioxidant

60
Q

What does TNF-alpha do?

A

is an inflammatory gene

61
Q

How does emphysema affect blood gases?

A
  • PaO2 is low but not very low
  • “pink puffers” increase their ventilation
  • PaCO2 is normal
62
Q

How does chronic bronchitis affect blood gases?

A
  • PaO2 is low (very low)
  • PaCO2 is high
  • “blue bloaters” hyperventilate and have a blunted ventilatory response to CO2
63
Q

How and why does emphysema cause changes in the blood gases?

A
  • decreased PaO2 is a results of V/Q mismatch

- blood and air are going unevenly to different parts of the lung; in emphysema both are affected

64
Q

How and why does chronic bronchitis cause changes in the blood gases?

A

it causes abnormal distribution of ventilation due to differences in the resistance of different parts of the lung

65
Q

How does chronic bronchitis cause hypoventilation?

A
  • it may increase the cost of breathing and make it equal to O2 flux
  • compensation in the CSF such that the pH in normal there despite a high PaCO2
  • kidneys may also compensate by altering excretion of buffering ions, thus decreasing pH despite a high PaCO2
66
Q

How does increasing PaO2 in chronic bronchitis patients affect their ventilation?

A

It causes them to stop breathing. In healthy patients, RR is dependent on PaCO2. However, in patients with chronic bronchitis, RR is dependent on PaO2 because they lost their sensitivity to PaCO2. If you increase O2 levels, then their body thinks that O2 levels are too high and slows down/stops breathing.

67
Q

What are some consequences of low PaO2?

A
  • polycythemia: decrease PaO2 –> increased erythropoietin in kidney –> increased RBC production in bone marrow
  • hypoxic pulmonary vasoconstriction (in chronic bronchitis) –> increased pulmonary artery pressure –> increased load on right heart –> right heart hypertrophy (cor pulmonale) –> right heart failure and death
  • loss of pulmonary capillary bed (in emphysema) –> increased pulmonary artery pressure
  • cyanosis (deoxyhemoglobin > 5g/100ml) due to low oxygen and increased RBCs
68
Q

How do you treat chronic bronchitis?

A
  • stop smoking
  • bronchodilators/anticholinergics
  • increasing use of corticosteroids (still being studied)
  • lung transplant surgery (not recommended)
69
Q

How does indoor air pollution cause emphysema?

A
  • in some parts of the world, cooking and heating are done using solid fuels –> increases levels of particulate air pollution
  • increases risk of COPD 3-fold (especially in women and children) and accounts for 1/4th of COPD deaths worldwide
  • also increases risk of respiratory infections
70
Q

How do corticosteroids help asthmatics?

A
  • reduce inflammation
  • improve lung function and symptoms
  • decrease airway hyperresponsiveness
  • reduce exacerbations
  • must be taken regularly regardless of symptoms
  • not immediately effective
71
Q

What are the effects of leukotrienes?

A
  • very potent constrictors of airway smooth muscle
  • mucus hypersecretion
  • edema formation
  • eosinophil chemoattraction
72
Q

What are some of the benefits of anti-IgE therapy?

A
  • reduces corticosteroid requirements
  • reduces symptom scores
  • reduces rescue medication use
  • improves lung function
  • reduces exacerbations

Human Pathophysiology: Final (6 decks)

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