hsci 334 COPD

COPD

also known as chronic airflow limitation/obstruction, chronic

obstructive airway disease, chronic obstructive lung disease; mainly in airways or lung parenchyma

airflow

COPD is a group of disorders that disrupt what

bronchial asthma

emphyseam and chronic bronchitis are a type of COPD. what is not a type of COPD

16 million

how many Americans are affecte by COPD

4th

COPD are the ____ most common cause of death in the US

disability causing disorders worldwide

COPD is ranked among top 20 what

• bronchi

• bronchioles

• parenchyma

what does smoking affect

mucus glands

when smoking, there’s an increased number and size of what

mucus

smoking results in excess what

thickened wall

smoking results in a __________ from glands and inflammatory cells (macrophages, neutrophils, T-cells)

airway diameter

thickened bronchi wall reduces _____ and mucus, further compromising the flow

inflammatory

what type of cell release contributes to damage in the tissue

cilia

cigarette smoke causes structural changes in ________

mucociliary clearance

cigarette smoke causes structural changes in cilia, reducing _______

less than 2mm diameter

what size are bronchioles

(of the bronchi)

• inflammation

• fibrosis

• narrowing

what’s believed to be responsible for COPD

parenchyma

affected _____ from smoking eventually results in emphyseama development

Protease-antiprotease hypothesis

• Connective tissue of alveolar walls destroyed by proteolytic enzymes from inflammatory cells

• Break down structural protein elastin; neutrophils release neutrophil elastase, elastase inhibited by α1-antitrypsin, balance required to prevent destruction of alveolar walls

matrix metalloproteinases

from macrophages & neutrophils

• Proteolytic enzymes able to break down alveolar wall structure

elastase

α-1 antitrypsin inhibits which substance?

slide 6

slide 7

tar phase

semi-liquid particles from 0.1-1μm diameter & increase quickly via

coagulation. Exert local effect

• contains nicotine, tar, PAHs

gas phase

llonger-lived gas components cause local & systemic effects

• CO, ROS, HCN, Carbonyls (formaldehyde, acrolein, etc.)

• Exposure from direct inhalation and inflammatory processes in lungs

• Superoxide, hydrogen peroxide, hydroxyl radicals

RNS

what species include nitric oxide, nitrogen dioxide, peroxynitrite

peroxynitrite

very unstable & highly reactive

• May form from reaction of superoxide and nitric oxide

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genetic factors

what may contribute to development of COPD

deficiency of serum protein α₁-antitrypsin

what is the most established genetic factor for COPD development

deficency of serum  α₁-antitrypsin

• Impaired secretion by liver – remains in globules and may cause liver disease

• Frequently develops early – 3rd or 4th decade of life

Partially genetic bronchial hyperresponsiveness

what’s another genetic factor that may contribute to COPD development

• coal dust exposure in coal miners

• farmers: organic dust, ammonia from livestock, endotoxins

• biomass smoke

• outdoor air pollution

what are some occupational exposures that can lead to COPD

1/2

how much of the world’s population uses solid cooking fuel

true

true or false: women are often highly exposed to biomass smoke

biomass smoke exposure

• includes exposure to wood, animal dung, cropresidues, mixtures

• often burned in poorly ventilated stoves

• high lvsl of fine particulate matter generated

vehicle exhaust and industry

outdoor air pollution mainly comes from

PM_2.5

which particulate matter levels are mainly driven by meterology (weather) instead of local soruces and may also be from the tens to hundreds of μg/m3

PM₁₀ and PM_2.5

cases of COPD are associated with with PMs

PM₁₀

which particulate matter is deposited throughout airways, getting trapped in mucus of larger areas (nose, trachea, etc)

PM_2.5

which particulate matter is beyond airways to reach centriacinar region (can reach smaller bronchioles and penetrate into alveolar region, causing damage)

panacinar

emphyseam type: fairly uniform involvement of acinus past terminal

bronchiole (resp bronchioles, alveolar ducts, alveolar sacs)

• relative diffuse damage

• lower lobes usually more involved than upper

• usual type in those with α1-antitrypsin deficiency

panacinar

in which emphyseama type are the lower lobes more involved than upper

panacinar

which emphyseam type is more common in people with α1-antitrypsin deficiency

centrilobular

emphyseama types: dilation of proximal acinus (resp bronchiole)

• More irregular involvement

• Usually involves the upper lobes+

• Most often seen in smokers

centrilobular

what type of emphyseama is most often seen in smokers

centrilobular

what type of emphyseama is going to mostly involve the upper lobes

panacinar

which type of emphyseama is less compliant and ventilated, but has uniform air distribution

centriacinar

which emphyseama type has a larger dead space

terminal bronchiole

obstruction of _______ underventilates alveolia

hyperinflation

severe COPD may result in ________ at rest; “barrel chest”

hyperinflation

Inability to completely exhale from limited expiratory flow

• Decreased elastic recoil, shortening of vertical diaphragm muscles so less energy (mechanical disadvantage)

• Diaphragm not able to generate as much pressure

PM_2.5

Which airborne particles are able to reach the centriacinar region of the respiratory system?

increased anterior to posterior dimension

what does the term “barrel chest” refer t

decreased elastic recoil → decreased dirivng pressure during expiration

what is the main issue in emphyseamas

airways collapsible

what emphyseama abnormality involves:

• alveolar destruction, lading to less radial traction on airways

• expiration places increased pressure, more likely to collapse

decrease in elastic recoil

what emphyseama abnormality invovles:

• resisting expansion less; greater volumer for any transpulmonary pressure

• increased TLC resulting in smaller opposing action of muscles

• increased FRC as chest wall recoil favored

• increased RV as airways are prone to collapse

true

true or false: in chronic bronchitis, decreased size of airway does not necessarily correlate with amount of obstrution present

decreased

in chronic bronchitis, is expiratory flow rate (FEV₁/FEV) usually increased or decreased

false

true or false: in chronic bronchitis, TLC is usually abnormal

true

true or false: in chronic bronchitis, FRC and RV may be increased as narrow ariways cause air trapping

cough

in chronic bronchities, increased mucus glands seccrete mucus, resulting in ______ and septum production

chronic bronchitis

in ___________, either inflammation/fibrosis in the small airway or parenchyma; small airway involvement with mild case, severe obstruction with emphysema

type A (pink puffer)

presentation of COPD:

• Arterial PO2 preserved reasonably well

• Dyspnea and high minute volume with patient working hard to bring in air “puffing”

• Gas exchange abnormalities not major feature, so no significant

hypoxia

• Pulmonary htn or elevated hematocrit not seen

type B (blue bloater)

presentation of COPD:

• Major problem with gas exchange

• Cyanosis from severe hypoxemia

• Frequently obese, may have peripheral edema from right

ventricular failure

• Primary chronic bronchitis

• V/Q mismatch

• Pulmonary htn, cor pulmonale, ploycythemia common