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Biology 253 > Respiratory Disorders: COPD > Flashcards

Respiratory Disorders: COPD Flashcards

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1
Q

What is COPD?

A

Persistent widespread inflm of the a/w, parenchyma, and vasculature

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2
Q

How does inflm lead to obstruction in the a/w?

A

inflm–> exudate produced in lumen of a/w–> obstruction in a/w–> increase prod. of mucus from cells lining the a/w

xs mucus and exudate cause more obstruction and serious consequences

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3
Q

T or F: COPD is recurrent throughout lifetime and persist through life

A

T

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4
Q

If recurs, a/w obstruction is ____ but not _____

A

acute, persistent

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5
Q

T or F: COPD is a combination of disease

A

T

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6
Q

COPD includes _____ _______ and/or _______ and may be accompanied by ______

A

chronic bronchitis

emphysema

asthma

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7
Q

Is asthma preventable?

A

almost completely preventable–> YES

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8
Q

What is the parenchyma?

A

parenchyma = epithelial cells involved in gaseous exchange @ alveolar level

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9
Q

What is the vasculature?

A

vessels involved in gaseous exchange eg. pulmonary capillaries

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10
Q

Etiology/Risks of COPD (4)

A
  1. smoking
  2. ageing
  3. recurring infections
  4. alpha-1 anti-trypsin deficiency (genetic)
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11
Q

Etiology: What % of COPD is linked to smoking? How does smoking cigs cause COPD (4)?

A

80-90% of COPD is linked to smoking

smoking cigs contain irritants which increase mucus secretion, destroy cilia, produce chronic coughing, and induce inflm

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12
Q

Explain the 4 effects of cigarette smokes in COPD in details.

A
  1. irritants in cig smokes increase mucus production –>overwhelms of the cilia –> unable to sweep up harmful debris–> impede GE
  2. irritants in cig smokes damage cilia
  3. irritants in cig smokes induce chronic coughing
  4. Irritants in cig smokes induce inflm in resp tissues —> damage a/w and walls between alveoli–> decrease fxn of alveoli
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13
Q

Is chronic coughs beneficial? why?

A

NOOOOOOO

constant repetitive coughing damage the lining of a/w

coughing shoots 100km/hr of air damaging tissues w/ this force

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14
Q

Etiology: How does ageing contribute to COPD? (3)

A

d/t

  1. degenerative change of tissues
  2. decrease elasticity
  3. decrease compliance
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15
Q

Compliance is ________ proportional to elasticity. What does this mean? What happens if elasticity decrease?

A

inversely

one variable increase and other decrease

compliance increases

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16
Q

What is the definition of compliance?

A

the ease in which we fill and empty the lungs during breathing

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17
Q

What happens if there is too much or too little elasticity? How does elasticity relate to recoil? What happens if there is too much compliance

A
  1. lungs cannot fill or empty completely
  2. little elasticity = less recoil
    more elasticity = more recoil
  3. more compliance = less elasticity (air remain in the lungs) = more work of breathing
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18
Q

Etiology: How does recurrent infections contribute to COPD?

A

there is chronic hypersecretion of mucus + coughing + inflm damage

infection–> inflm–> tissue damage

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19
Q

Etiology: What percentage of alpha-1 anti-trypsin deficiency applies to COPD?

A

1% of people with COPD –> not a great risk from genetic perspective

20
Q

Fig 29-7: What % is a severe compromised lumen? How? How is it simulated?

A

70-90% lumen compromised

d/t damage of the a/w resulting in hypertrophy

Simulated as trying to breathe from a straw

21
Q

Fig 29-7: What happens when 50% of lumen is compromised?

A

wall of lumen is normal and elasticity is normal BUT it is filled w/ mucus –> only 1/2 amount of air can be carried or lungs is inflated 50% d/t hypersec of mucus

22
Q

Fig 29-7: What happens when there is a loss of elastic tissue?
A = there is some degree of ____________ a/w and _________ decrease

A

compromised

compliance

23
Q

Diagnosis of COPD (4)

A
  1. hx and px
  2. labs: CBC, CRP, and ABGs
  3. Pulmonary function test (PFT)
  4. Chest X-Ray (CXR)
24
Q

What is assessed in COPD? (5)

A
  1. breath sounds
  2. SOB
  3. accessory muscle use
  4. ventilation issues
  5. arms propped on table to help ease of breathing
25
Q

What is used during PFT?

A

spirometry

26
Q

What is identified during PFT?

A

cause of obstruction (CB, emphysema, and asthma)

27
Q

What is FVC?

A

forced vital capacity = total volume maximally and forcefully exhaled

28
Q

What is FEV1?

A

forced expiratory volume = volume of air forcefully exhaled in one second

29
Q

In COPD, do FVC and FEV1 increase or decrease? In a normal person?

A

both decrease

Healthy person should exhale at least 80% total vital capacity in one second

30
Q

What is the total volume and tidal volume?

A

normal volume of air when no extra effort is used

31
Q

What is found on CXR (3)? It is taken on _____ and ______ and compared

A
  1. consolidation
  2. damaged in lungs
  3. decreased volume of lungs

taken on inhalation/exhalation and compared

32
Q

Treatment of COPD (5)

A
  1. manage prognosis
  2. drugs
  3. vaccines
  4. cessation of smoking
  5. avoid a/w irritants
33
Q

Drugs are _____ based

A

staged

34
Q

Damage in lung tissue decrease in ____ min of quitting smoking

A

20 minutes

35
Q

What are 3 examples of a/w irritants?

A
  1. cigarette smoke irritants
  2. smoke fires
  3. strong odours
36
Q

Manage prognosis by ________ modifications

A

lifestyle

37
Q

Drugs: begin with least _____ and least ____ ______.

A

expensive and SE

38
Q

What drugs are given in early stage? “B-adrenergic agonists” are ________. What is given in early stage that is more advanced?

A

short acting beta agonists (SABA) and anticholinergics

bronchodilators

Inhaled steroids

39
Q

What is the MOA of SABA?

A

stimulate beta-2 adrenergic receptors in lungs –> activating adenylate cyclase to produce cyclic adenosine monophosphate (cAMP)–> triggers relaxation of bronchial smooth muscles

40
Q

What is the MOA of anticholinergics?

A

bronchodilators that act by blocking acetylcholine receptors on the bronchi tree so PNS is not activated to release ACh –> results in bronchodilation

41
Q

Classification of inhaled steroids used in advanced early stage? How? Function (3)

A

inhaled steriods –> long acting beta agonists

directly in respiratory tract

  1. decrease inflm by decreasing mediators released
  2. limiting WBS activity
  3. increase responsiveness of bronchial smooth muscle to B-agonists
42
Q

What drugs are given in the late stage? What is it prescribed with?

A

Long acting beta agonist (LABA) prescribed w/ glucocorticoids

43
Q

Give an Example of LABA? Fxns (2)? Which function is it used for?

A

Xanthine Derivatives –> THEOPHYLLINE

Function:
1. cause bronchodilators by increasing levels of cAMP to trigger smooth muscle relaxation

  1. anti-inflm properties –> not solely for this fxn but is beneficial to COPD to tx inflamed a/w
44
Q

What happens when adrenaline binds to beta receptors in a/w?

A

stimulates the beta-1 and beta-2 receptors and increase HR, CO, contractile force of heart, cause bronchodilation, and raise BG.

45
Q

What vaccines are used prophylactically? (2)

A

pneumococcal vaccine and flu shots

to prevent complications and prevent pneumonia caused by this virus

Biology 253 (39 decks)

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