Chronic obstructive pulmonary disease (COPD)

Question 1

what is COPD?

Answer 1

-acute, recurrent & chronic obstructiion of airways

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

Question 2

with COPD the disease is ________ but the obstruction is not

Answer 2

chronic

Question 3

what is the parenchyma

Answer 3

alveolar tissue

Question 4

what are the two diseases that are part of COPD

Answer 4

• chronic bronchitis

- emphysema

Question 5

COPD may also co-exist with

Answer 5

asthma

Question 6

what is compliance?

Answer 6

ease at with which we breathe in and out

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

Question 7

what is the etilogy and risks for copd?

Answer 7

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

Question 8

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

Answer 8

smoking

Question 9

what is a1 anti-trypsin

Answer 9

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

Question 10

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

Answer 10

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.

Question 11

what are the three mechanisms of airflow obstruction in copd?

Answer 11

• 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

Question 12

what is chronic bronchitis

Answer 12

Inflammation causing obstruction of airway

Question 13

what is chronic bronchitis due to

Answer 13

smoking and recurrent infection

Question 14

how does chronic bronchitis present

Answer 14

chronic productive cough

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

Question 15

how does the chronic bronchitis chronic productive cough have to present

Answer 15

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

Question 16

chronic bronchitis affects _____ airway 1st then _______ airway later

Answer 16

large airway first then smaller airway later

Question 17

what happens to large airways in chronic bronchitis ?

Answer 17

• large airway affected first

- hypertrophy of submucosal glands causing an increase in mucus secretion

Question 18

what happens in the smaller airways in chronic bronchitis?

Answer 18

• smaller airways affected after large airways

- increase in golbet cells therefore an increase in mucus secretion

Question 19

Patho of chronic bronchitis

Answer 19

• 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)

Question 20

what is hypoxia and what is hypoxemia

Answer 20

hypoxia=deficencey in 02 systemically in tissues

hypoxemia= hypoxia in arterial blood gases (ABGS)

Question 21

mnfts of chronic bronchitis

Answer 21

• 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

Question 22

what is Emphysema?

Answer 22

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

Question 23

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

Answer 23

enlarged distal spaces & loss of compliance

Question 24

Etiology of emphysema?

Answer 24

• smoking

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

Question 25

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

Answer 25

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

Question 26

what is the patho of emphysema

Answer 26

-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

Question 27

what is dead space

Answer 27

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

Question 28

bullae

Answer 28

pockets of air trapped in between the alveloli

Question 29

blebs

Answer 29

smaller areas of air trapped in between the alveoli

Question 30

what are the mnfts of emphysema?

Answer 30

- dyspnea - increased ventilatory (respiratory effort) - barrel chest

Question 31

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

Answer 31

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

Question 32

diagnosing COPD?

Answer 32

-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

Question 33

treatment of COPD?

Answer 33

- 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

Question 34

what is an antagonsit and what is an agonist

Answer 34

antagonist --antagonizes someone so opposes | agonist--facilitates or helps

Question 35

the drugs for treating COPD are ?

Answer 35

stage based

Question 36

what do beta adrenergic agonsits do?

Answer 36

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

Question 37

what do anticholinergics do?

Answer 37

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

Question 38

what is theophylline and what is it other properties

Answer 38

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