Respiratory Disorders: Emphysema Flashcards

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1
Q

What is emphysema?

A

Destruction of alveolar walls and capillary beds

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2
Q

Alveolar wall and capillary are involved with __________ _________

A

capillary exchange or GE

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3
Q

What 2 things can destruction of alveolar wall and capillary cause?

A
  1. l/o compliance

2. enlarged distal airspaces

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4
Q

How does l/o compliance impact filling/emptying of alveoli?

A

l/o compliance–> decrease elastic tissue and recoil of alveoli–> increase residual volume –> filling/emptying of alveoli is impacted

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5
Q

Elastic tissue provides _____ and recoil ______ out the ____

A

compliance

pushes

air

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6
Q

How are enlarged distal airspaces formed?

A

by destroying wall of adjoining millions of little alveoli–> fewer and larger alveoli are created–> decrease SA for GE

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7
Q

Etiology of Emphysema (2)

A
  1. smoking

2. genetic deficiency of alpha-1 anti-trypsin (~1%)

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8
Q

What is Trypsin? Function

A

enzyme that breakdowns protein in the gut and aging structures for regeneration of tissue

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9
Q

Alpha-1 is the _____

A

subclass

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10
Q

Alpha-1 Anti-trypsin Function? What does it protect the lung from?

A

oppose the breakdown of proteins so useful tissues are not excessively broken down

It protect the lung from breakdown

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11
Q

What happens in deficient alpha-1 anti-trypsin?

A

Trypsin are freely breaking down functional tissues of the walls of alveoli and capillaries

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12
Q

Patho: Alpha-1 anti-trypsin regulates ______. Why must be regulated? What happens if there is deficient alpha-1 anti-trypsin?

A

proteases–> breaks down structural proteins

Proteases must be regulated otherwise it continuously break down protein structures

If there is a deficient of alpha-1 anti-trypsin–>proteases fxn freely and cause destruction of lung structures (alveoli, bronchi, etc)

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13
Q

Patho: Deficiency of alpha-1 anti-trypsin is damaging to the ____ and cause what (2)?

A

lungs

  1. irreversible destruction resulting in distended air spaces where there is no GE
  2. air become trapped in alveoli–> increase work of breathing
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14
Q

Patho: What are 2 effects of smoking in Emphysema?

A
  1. inhibits alpha-1 antitrypsin –> regulation of proteases is lost causing destruction in lung
  2. attracts inflm cells–> releasing more proteases and cause inflammatory damage –> more destruction
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15
Q

Patho: How do proteases impair ventilation?

A

proteases destroy alveolar walls –> alveoli merge –> decrease SA–> distended air space develop–> ventilation impaired

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16
Q

d/t damage, air coming in move into spaces between _______ creating large ______ of ___ between _______. This is also known as ______ _____.

A

alveoli

pockets

air

alveoli

dead space

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17
Q

In dead space, there is no ____ ______, and air will not _____ or _____ the pocket or within alveoli. What result from this?

A

GE

leave or enter

increase respiratory effort (increase work of breathing) d/t compromised GE and ventilation

18
Q

What membrane surrounds the lung and which airspaces are pushed into?

A

pleural membrane

19
Q

Patho: Destruction of capillary causes ____ ______.

A

impaired perfusion

20
Q

Give an example of a physiological dead space in the respiratory tract?

A

trachea

21
Q

Which variable of V:P ratio is compromised? How is perfusion impacted?

A

both ventilation and perfusion

b/c capillaries are damaged

22
Q

In destructions of capillaries, which is associated with the capillaries?

A

terminal a/w

23
Q

Fig. 29.11: In a view of the right lung with emphysema, what are the black areas of the lungs? What are they referred as?

A

Black area = collection of air trapped in alveoli

referred to as blebs or bullae

24
Q

Whats the difference between bullae and bleb?

A

Bullae are large collection of air trapped in dead space

Bleb is a small collection

25
Q

Fig. 29.11: What is the acinus?

A

the functional unit of gas exchanging structure of the lung distal to the terminal bronchiole

26
Q

Fig. 29.11: What does the acinar consist of? Explain in right order.

A

respiratory bronchioles–> alveolar ducts–> alveolar sacs–> alveoli

27
Q

Fig. 29.11: What is centrilobular emphysema? What part of the acinus is damaged?

A

destruction in the terminal and respiratory bronchioles

proximal acinar

28
Q

Fig. 29.11: What is panacinar emphysema? What is another name for it?

A

the acinus is uniformly damaged (everything distal to the respiratory bronchioles)

panlobular

29
Q

Fig. 29.10: Smoking inhibits ____ ____-______ and attracts ________ ____ and favours the recruitment of which 2 defense cells?

A

alpha-1 anti-trypsin and inflm cells

favours the recruitment of macrophages and neutrophils (and elastase)

30
Q

Fig. 29.10: As a result of decreased ___ ___-______, proteases are free to cause damage specifically the _____ tissue. What kind of protease cause this damage?

A

elastic tissues

elastase

31
Q

Manifestations of Emphysema (10)

A
  1. dyspnea
  2. cough
  3. activity intolerance
  4. xs sputum prod.
  5. wheezing and crackles
  6. hypoxemia and hypercapnia
  7. barrel chest (emphysema)
32
Q

Several mnfst are following an initially ________ onset

A

insidious

33
Q

What cause dyspnea in emphysema?

A

prob w/ ventilation and GE–> hypoxemia–> hypoxia –> dyspnea

34
Q

What triggers the cough? How is it described?

A

inflm –> xs mucus secretion–> exudate –> irritation of alveoli and a/w–> trigger coughs

productive and dry at times

35
Q

Why is there activity intolerance? How is it displayed? When age is this mnfst most pronounced?

A

d/t lack of oxygen in cells to metb and produce ATP –> inadequate energy

difficulty getting up a flight of stairs and bus

50-60–> seek medical attention

36
Q

What contribute to xs sputum (2). What is this function?

A

continuous prod. of mucus and exudate from inflm

to clear the a/w and alveoli

37
Q

Wheezing and crackles are caused by _____ ____ in ______ ____. Wheezing is a result of compromised ______. Crackles are ____ d/t air passing over ______ in resp tract.

A

forceful air

narrow tubes

a/w

wet

fluids

38
Q

What is hypoxemia and hypercapnia? What lab values is used?

A

hypoxemia = deficiency of O2

hypercapnia = build up of CO2

ABGs changes in gas levels

39
Q

What is a barrel chest? Causes (2)

A

chest become fixed in an inspiratory position b/c air is trapped between alveoli

increase respiratory effort and use of accessory muscles

40
Q

Give 5 examples of accessory muscles?

A
  1. sternocleidomastoid
  2. scalene muscles
  3. Pectoralis major and minor
  4. Latissimus Dorsi
  5. Serratus Anterior
41
Q

What does APD and TD stand for and what is the ratio normally and in barrel chest? Explain location.

A

APD = anteroposterior diameter –> vertical, front to back

TD = transverse diameter –> horizontal side to side

Normal = APD:TD –> 1:2

Barrel Chest = APD is equal or twice the size of TD –> 1:1 or 2:1