Respiratory System III Flashcards

1
Q

What is a restrictive pulmonary disease characterized by?

A

A decreased TLC by %20 or more from predicted

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2
Q

What happens during pulmonary edema?

A
  • fluid backs up into interstitial space is usually cleared by the lymphatic system
  • if it becomes too much for the lymphatic system, the fluid builds up in the interstitial spaces around airways and blood vessels and can eventually start to leak into the alveoli
  • -fluid in alveoli impacts diffusion and can lead to a shunt; can also interfere with surfactant function and impair lung inflation
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3
Q

How does heart disease cause pulmonary edema?

A

myocardial infarction/hypertensie left ventricular failure –> increase left atrial pressure –> increase pressure in pulmonary vein –> increase Pcap –> increased fluid flux across endothelium

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4
Q

What else, aside from a heart condition, can cause increased Pcap?

A

excessive saline/plasma/blood infusions

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5
Q

How is pulmonary edema due to increased Pcap self-limiting?

A

as fluid leaks out, the proteins in the capillary become concentration and oncotic pressure increases –> fluid gets pulled back into capillary

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6
Q

How does increase capillary permeability occur and how does it contribute to pulmonary edema?

A

inhaled or circulating toxins –> integrity of endothelial barrier is destroyed –> proteins leak into interstitial space –>capillary oncotic pressure decreases –> fluid leaks into interstitial space (NOT SELF LIMITING, VERY DANGEROUS)

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7
Q

What are the symptoms of pulmonary edema?

A
  • dyspnea
  • cough (nonproductive in early stages, pink foam in advanced stages)
  • cyanosis
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8
Q

How does pulmonary edema affect pulmonary function?

A
  • PV curve is shifted downward and to the right
  • resistant to flow through airways increases (fluid surrounds airways and isolates them from retractive forces of parenchyma)
  • TLC, VC, and FRC decrease
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9
Q

How does pulmonary edema affect blood gases?

A
  • If only interstitial edema is present: little change in PaO2 despite increase in barrier to diffusion
  • If alveolar edema is present: decrease in PaO2 (due to shunt); PaCO2 remains normal/drops because ventilation increases due to low PaO2 or stimulation of lung receptors by high transpulmonary pressures (stiffer lung –> greater pressures for ventilation)
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10
Q

What causes idiopathic pulmonary fibrosis (diffuse interstitial pulmonary fibrosis)?

A

an immunological reaction due to some kind of toxic insult to lungs causes non-uniform thickening of the interstitium of the alveolar walls

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11
Q

Describe the pathogenesis of idiopathic pulmonary fibrosis.

A

inflammatory response –> infiltration with lymphocytes and plasma cells –> fibroblast lay down collagen (scarring)

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12
Q

Who is most affected by idiopathic pulmonary fibrosis?

A

middle-aged to older adults; genetic component

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13
Q

What are the symptoms of idiopathic pulmonary fibrosis?

A
  • dyspnea, especially upon exercise
  • rapid shallow breathing
  • unproductive cough
  • disease often progresses to respiratory failure
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14
Q

How is idiopathic pulmonary fibrosis treated?

A

currently there is not treatment

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15
Q

How does idiopathic pulmonary fibrosis affect pulmonary function?

A
  • TLC, VC, and FRC decrease
  • airway caliber is normal, FEV1/FVC are high
  • PV curve shifts downward and to the right
  • increased collagen/scarring reduces distensibility of the lung
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16
Q

How does idiopathic pulmonary fibrosis affect gas exchange?

A
  • PaO2 is reduced - mild at rest (results from V/Q mismatch), more severe upon exercise (diffusion impairment)
  • PaCO2 is low due to increased ventilation due to low PaO2
17
Q

How do diseases of the chest wall and neuromuscular disease affect lung volumes?

A

increased stiffness in the chest wall or inability of respiratory muscles to contract strongly (either due to nerve or muscle damage) can decrease lung volume

18
Q

What are the epidemiological stats for obesity?

A
  • prevalence has doubled over the last 2 decades
  • 30% of Americans are obese, another 35% are overweight
  • increasing prevalence in children
  • increasing prevalence worldwide
  • abdominal fat is the greatest problem
19
Q

How does obesity affect pulmonary mechanics?

A
  • FRC decreases due to increased chest wall stiffness
  • TLC is normal but RV may increase due to airway closure
  • compliance of lung is reduce
  • increased pulmonary resistance (Raw) and decreased Gaw (lung volume)
  • increased airway responsiveness
20
Q

How is Gaw related to Raw?

A

Gaw = 1/Raw

21
Q

How does breathing compare between normal and obese individuals?

A

obese patients breath at a lower tidal volume and higher frequency to reduce the work of breathing

22
Q

How does obesity affect blood gases?

A

PaO2: usually low due to low lung volume and airway obstruction (shunt)
PaCO2: usually normal; VE increases to maintain normal PaCO2

23
Q

Does obesity increase incidence of asthma or COPD?

A

asthma: increased incidence/prevalence; worsens with weight gain
COPD: emphysema patients are usually lean but chronic bronchitis is associated with obesity

24
Q

What happens during sleep apnea?

A

muscles relax during sleep –> tongue and soft palate fall back against throat –> obstruction –> hypoxemia –> arousal (can occur as many as 50 times/hr

25
Q

What are the outcomes of sleep apnea?

A
  • excessive daytime sleepiness
  • headaches upon awakening
  • depression
  • hypertension
  • cardiovascular disease
  • stroke
26
Q

How does obesity aggravate/contribute to sleep apnea?

A

fat deposition in the soft palate, uvula, neck area, and pharynx lead to increased risk of obstruction

27
Q

What is obesity hypoventilation syndrome (Pickwickian syndrome)?

A

blunting of chemoreceptor sensitivity leads to hypoventilation when awake

28
Q

How does obesity contribute to pulmonary hypertension?

A

airway closure –> low PAO2 levels –> constriction of pulmonary arterioles (hypoxic pulmonary vasoconstriction)

*may also increase interstitial edema, promoting airway obstruction