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Bio 253 > Chronic Obstructive Pulmonary Disease > Flashcards

Chronic Obstructive Pulmonary Disease Flashcards

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Biology 101 flashcards
1
Q

T or F:

COPD is largely preventable.

A

T

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2
Q

Description of COPD:

5

A
  • Serious and prevalent
  • Life threatening with complications
  • Progressive
  • Chronic, widespread
  • Acute, recurrent
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3
Q

What conditions are included in COPD?

A
  • Chronic bronchitis

- Emphysema

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4
Q

Can COPD co-exist with asthma?

A

Yerp

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5
Q

What are the Et/risks for COPD?

A
  • Smoking (80-90%)
  • Aging
  • recurrent respiratory infcts
  • Genetic deficiency of alpha 1 anti-trypsin
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6
Q

Why is smoking a risk actor for COPD?

5

A

The irritants in cigarette smoke have several damaging effects:
- They increase mucus secretion -> too much can
obstruct
- Damages cilia
- Causes coughing, damaging if persistent
- Inflm -> tissue damage
- Damage to the walls of capillaries and alveoli

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7
Q

Why is aging a risk factor for COPD?

A

Because as the elastic tissue in the lungs degenerates with age, their ability to recoil is impeded

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8
Q

What is compliance? How does this relate to COPD?

A

This refers to the ease with which the lungs are filled and emptied. In COPD, the compliance of the lungs is decreased.

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9
Q

What is chronic bronchitis?

A

Chronic inflm and obstruction of an airway.

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10
Q

For bronchitis to be considered chronic, how long must the productive cough be present?

A

For >3 consecutive months in 2 consecutive years

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11
Q

Where does chronic bronchitis generally take place?

A

In large airways

- eg trachea, bronchi

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12
Q

What causes obstruction in the airways during chronic bronchitis?

A
  • Hypersecretion of mucus
  • Hypertrophy of submucosal glands
    • Protective at first but will result in obstruction
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13
Q

Eventually, bronchitis will reach the small airways. What will happen here?
(4)

A

There will be an increase in goblet cells and mucus, causing obstruction. There will also be inflm and fibrosis.

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14
Q

T or F:

Chronic bronchitis is not an infct.

A

T

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15
Q

Overview of the patho of chronic bronchitis:

A

Increased mucus secretion -> compromised mucociliary defenses -> infct -> airways become inflmed -> obstruction and airway collapse -> air gets trapped in parts of the lung -> decreased alveolar ventilation

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16
Q

What is the average L/min for ventilation in the lungs?

A

~4.2 L/min

17
Q

What is the average L/min for perfusion in the lungs?

A

~5.5 L/min

18
Q

What is the ventilation:perfusion ration?

A

~0.8

19
Q

If your ventilation:perfusion ratio is less than 0.8, are you at risk for?

A

Hypoxemia, which will lead to hypoxia

20
Q

What is the major problem happening in emphysema?

A

The walls of the alveoli and capillaries are damaged

  • loss of compliance
  • Stretched out airways
21
Q

What is the Et of emphysema?

A
  • Smoking

- Genetic deficiency of alpha 1 anti-trypsin (~1%)

22
Q

What is the role of a1 anti-trypsin? How does this relate to emphysema?

A

To regulate proteases. This opposes the action of trypsin, which is to breakdown proteins. If there is a deficiency of a1 anti-trypsin, the levels of trypsin increase and can cause major damage to functional cells.

23
Q

How does smoking contribute to emphysema?

A
  • Inhibits a1 anti-trypsin = unregulated enzymes
  • Attracts inflm cells = increased amount of trypsin =
    more structural damage
24
Q

Patho of emphysema:

A

Proteases destroy alveolar walls -> alveoli merge -> decreased surface area -> less area for diffusion/gas exchange

25
Q

What happens as a result of air becoming trapped between alveoli?

A

This increases dead space -> more effort is required to breathe (accessory muscle must be used)

26
Q

Perfusion is impeded by:

A

The destruction of the capillaries by trypsin

27
Q

What are “blebs”?

A

Small pockets of dead space filled with air, pushes against the pleura.

28
Q

What are “bullae”?

A

A large pocket of dead space filled with air, pushes against the pleura.

29
Q

Initially, the mnfts for COPD are_______.

A

Insidious

30
Q

Mnfts of COPD:

A
  • Dyspnea
    • Initially only on exertion
    • As COPD progresses, with rest as well
  • Cough
  • Activity intolerance
    • Impeded gas exchange, decreases ATP production
  • Extremely increased amount of sputum
  • Wheezing and crackles
  • Impaired respiratory Fx
    • Hypoxemia and hypercapnia
  • Barrel chest (emphysema)
31
Q

Upon viewing your pneumonia patient’s chest xray, what abnormal results will you see?

A
  • Buildup of fluid

- Consolidation

32
Q

What is an example of a pulmonary fx test that might be run to Dx a COPD patient?

A

A spirometry test.

33
Q

What changes must be made to limit the progression of COPD?

A
  • Overall healthy lifestyle (diet, activity, etc.)
  • Absolutely NO smoking
  • Avoid respiratory irritants
34
Q

COPD Tx:

What is a short acting beta adrenergic agonist?

A
  • A med that will bind to the receptors that adrenaline normally would
  • Causes bronchodilation by relaxing smooth muscle
35
Q

COPD Tx:

What is an anticholinergic?

A
  • Opposes the normal action of adrenaline at receptors

- Causes bronchodilation

36
Q

COPD Tx:

After treating COPD with short acting drugs, what are 3 other drugs you would consider giving?

A
  • Inhaled steroids, O2
  • Inhaled long acting beta agonists
  • Theophylline
37
Q

What is theophylline?

A
  • 2 forms: short and long acting
  • Potent bronchodilator
  • Anti-inflm
38
Q

Which vaccines should be given to patients with a Hx of COPD?

A

Trick question: all of them!

But in this situation: flu and pneumococcal vaccine

Bio 253 (44 decks)

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