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BIo 253 > Chronic obstructive pulmonary disease (COPD) > Flashcards

Chronic obstructive pulmonary disease (COPD) Flashcards

1
Q

what is COPD?

A

-acute, recurrent & chronic obstructiion of airways

d/t chronic inflm of airway, parenchyma (alveolar tissuse) & vasculature (capillaries surronding alveoli)

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2
Q

with COPD the disease is ________ but the obstruction is not

A

chronic

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3
Q

what is the parenchyma

A

alveolar tissue

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4
Q

what are the two diseases that are part of COPD

A
  • chronic bronchitis

- emphysema

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5
Q

COPD may also co-exist with

A

asthma

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6
Q

what is compliance?

A

ease at with which we breathe in and out

if there is more competent tissue in lungs more elasticity & more compliance

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7
Q

what is the etilogy and risks for copd?

A
  • smoking (80%-90%)
  • recurrent resp infections (not a common cause)
  • ageing
  • genetic deficiency of a1 antitrypsin
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8
Q

what is the most common cause of copd causing (80-90%)

A

smoking

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9
Q

what is a1 anti-trypsin

A

tyrpsin is an enzyme that breaks down proteins, anti therefor inhibits this enzyme

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10
Q

what is the problem with cigarette smoke and why is it so damaging?

A

cigarette smoke contains a variety of irritants, an cause production of too much mucus from irritants, impedes cillliary function. irritants cause coughing–to much coughing is injurious. Irritants are going to cause inflm and tissue damage.

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11
Q

what are the three mechanisms of airflow obstruction in copd?

A
  • obstruction of airway caused by hypertrophy of bronchial wall
  • inflammation & hypersecretion of mucus causing obstruction
  • loss of elastic fibres that hold airway open causing obstruction
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12
Q

what is chronic bronchitis

A

Inflammation causing obstruction of airway

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13
Q

what is chronic bronchitis due to

A

smoking and recurrent infection

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14
Q

how does chronic bronchitis present

A

chronic productive cough

has to be more than 3 months a yr in 2 consecutive years

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15
Q

how does the chronic bronchitis chronic productive cough have to present

A

has to last for more than 3 months in a yr 2 consecutive years

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16
Q

chronic bronchitis affects _____ airway 1st then _______ airway later

A

large airway first then smaller airway later

17
Q

what happens to large airways in chronic bronchitis ?

A
  • large airway affected first

- hypertrophy of submucosal glands causing an increase in mucus secretion

18
Q

what happens in the smaller airways in chronic bronchitis?

A
  • smaller airways affected after large airways

- increase in golbet cells therefore an increase in mucus secretion

19
Q

Patho of chronic bronchitis

A
  • excessive quantities of mucus obstruct airways
  • mucus is moist, warm, full of nutrients ideal for bacteria growth
  • excess mucus –impaired mucociliary defenses–infection —bronchial walls inflm & thickenend— lumen obstruction (mucus&inflm)– airway collapse– air trapped in parts of lung— decrease in alveolar ventilation(air in & out) causing a ventilation perfusion imbalance cause hypoxemia (decrease of 02 in arterial blood)
20
Q

what is hypoxia and what is hypoxemia

A

hypoxia=deficencey in 02 systemically in tissues

hypoxemia= hypoxia in arterial blood gases (ABGS)

21
Q

mnfts of chronic bronchitis

A
  • resp fx impaired: hypoxemia & hypercapina(increase in c02 levels in the blood)
  • dyspnea
  • activity tolerance
  • increase in sputum
  • wheezing (narrowing of airways)
  • crackles (wet crackles because of mucus & exudate there, when air moves through fluid(exudate/mucus sounds of crackles)
  • mucus provides ideal place for infection- recurrent infection is a mnfts
22
Q

what is Emphysema?

A
  • destruction of alveolar walls & capilllary beds causing:
  • enlarged distal spaces
  • loss of compliance
23
Q

Emphysema is the destruction of alveolar walls & capillary beds which causes

A

enlarged distal spaces & loss of compliance

24
Q

Etiology of emphysema?

A
  • smoking

- genetic deficiency of a1 antitrypsin (accounts for less than 1%)

25
Q

what is the problem with a genetic deficency of a1 antitrypsin?

A

a1 antitrypsin is an inhibitor of trypsin(enzyme), this enzyme is an example of protease it breaks down proteins and this is happening outside of digestive tract so causing tissue damage by breaking down proteins in tissues, a1 antitrypsin regulates so that enzyme not reacting when it doesnt need to

26
Q

what is the patho of emphysema

A

-a1 antitrypsin protects lung
-smoking: smoking inhibits a1 antitrypsin(causing enzymes to break down proteins and then tissues)
smoking also brings about inflammatory cells b/c injurious (attracts inflm cells)
-an increase in protease(not regulated) this causes destruction of alveolar walls, then alveoli merge which causes a decrease in surface area
-then there is permanant distended air spaces which causes ventilation to be impaired
-there is air trapped between alveoli which causes an increase in dead space then there is an increase in work of breathing

27
Q

what is dead space

A

where there is no gas exchange, capillary wall destroyed causing impaired perfusion, there will then be a ventilation perfusion imbalance (both will be impaired)

28
Q

bullae

A

pockets of air trapped in between the alveloli

29
Q

blebs

A

smaller areas of air trapped in between the alveoli

30
Q

what are the mnfts of emphysema?

A
  • dyspnea
  • increased ventilatory (respiratory effort)
  • barrel chest
31
Q

what is the difference between a normal chest and a barrel chest?

A

normal has a transverse diameter:anterior posteiror diameter of 2:1
barrel chest has a transverse diameter: anterior posterior diameter of 1:2 or 1:1

32
Q

diagnosing COPD?

A

-history, physical exam
-chest x-ray
-pulm fx tests (spirometery) lung volume,tidal volume
pulmonary fx tests give significant information on how compromised pts lungs are)
-labs start with basic and then move to specialised

33
Q

treatment of COPD?

A
  • limit progression: no smoking, avoid airway irritants
  • vaccines (flushot, pneumococcal)
  • drugs (stage based)
  • short acting beta adrenergic agonists & anticholinergics
  • inhaled steroids
  • long acting beta adrenergic agonists (b agonists)
  • theophylline (potent bronchodilator)
  • other physiotherapy for mucus & mucolytics
34
Q

what is an antagonsit and what is an agonist

A

antagonist –antagonizes someone so opposes

agonist–facilitates or helps

35
Q

the drugs for treating COPD are ?

A

stage based

36
Q

what do beta adrenergic agonsits do?

A

beta adrenergic agonists facilitates the action of Adrenalin (ephinephrine) facilitate the binding of beta relaxes muscles & brings about bronchodilation

37
Q

what do anticholinergics do?

A

cholinergic -refers to acetylcholine, preventing acetylcholine, bidning of acetylcholine to smooth muscles causes vasoconstriction, anti is conteracting blocking acetlycholine causing bronchodilation

38
Q

what is theophylline and what is it other properties

A

is a potent bronchodilator, additional propertys is that it is anto-inflmmatory will not use solely as anti -inlm b/c there are better drugs but is a bonus because there is inflm with COPD

BIo 253 (60 decks)

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