Chronic Obstructive Pulmonary Disease Flashcards Preview

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Flashcards in Chronic Obstructive Pulmonary Disease Deck (31)
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obstructive lung disease resulting from cigarette smoking and other toxic chemicals

airflow limitation that is not fully reversible, usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases

third leading cause of death in adults in the US, increasing in prevalence


causal risk factors of COPD

cigarette smoking

occupational exposures

genetic risk (alpha-1-antitrypsin deficiency)


genetic factors that predispose COPD

alpha-1-antitrypsin deficiency - PiZZ or PiMZ + smoking

single nucleotide polymorphisms - Type IV collagen alpha3, solute carrier familly 11 member 1 (SLC11A1), interleukin-1B

MMP-9 and CCL-1 increase severity and exacerbation risk


alpha-1-antitrypsin deficiency

coded by single gene on chromosome 14

PiZZ patients are severely deficient

PiSZ, Pi null-null, and Pi null-Z are also deficient

normal phenotyp eis PiMM

cigarette smoking is the most important risk factor

increased risk of cirrhosis and lung cancer as well


mechanisms of airflow obstruction in COPD

1) loss of tethering of airways due to emphysema - alveolar destruction resulting in decreased elastic recoil and airway collapse

2) remodeling of the small airways which causes plugging

3) increased mucous secretion which decreases the internal airway caliber and increases


inflammatory cells involved in COPD

epithelial cells and alveolar macrophages activate fibroblasts,CD8+ lymphocytes, neutrophils, and monoytes

COPD is a nuetrophilic disease


alveolar macrophages in COPD

orchestrate much of the inflammatory process

release mediators that attract neutrophils, monocytes, and CD8+ lymphocytes

release elastolytic enzymes and generate ROS


neutrophils in COPD

attracted by IL-8, LTB4 from macrophages and PMNs

release ROS and MPO which contribute to ongoing inflammatory response

serine proteases lik eneutrophil elastase contribute to destruction of th elung parenchyma

increased numbers of sputum neutrophils are associated with declining lung function


CD8+ lymphocytes in COPD

found in the airway walls, vessels, and lymph nodes of smokers with COPD

increased number associated with worse lung function

suggest that an antigenic process in the lung leads to abnormal inflammatory responses

perpetuate the inflammatory response by releasing chemoattractants


changes in the large airways in COPD

leads to chronic bronchitis

neutrophils in sputum

squamous metaplasia of epithelium, no basement membrane thickening

increased macrophages

increased CD8+ lymphocytes

mucous gland hyperplasia

goblet cell hyperplasia

mucous hypersecretion


changes in the small airways in COPD

remodeling of the airways

inflammatory exudate in lumen

disrupted alveolar attachments

thcikened wall with inflammatory cells - macrophages, CD8+ cells, fibroblasts

peribronchial fibrosis


changes in lung parenchyma in COPD


alveolar wall destruction

loss of elasticity

destruction of pulmonary capillary bed

increased number of inflammatory cells - macrophages, CD8+ lymphocytes


Describe the flow-volume and volume-time cirves in COPD.

flow-volume curve more concave, can't reach the same peak outflow

volume-time curve flatter and takes longer to get closer to FVC


Mechanisms of Airflow Limitation in COPD

mucus hypersecretion (luminal obstruction)

disrupted alveolar attachments (emphysema)

mucosal and peribronchial inflammation and fibrosis (obliterative bronchiolitis


GOLD classification of mild COPD

FEV1/FVC < 70%

FEV1 >/= 80% predicted


GOLD classification of moderate COPD

FEV1/FVC < 70%

FEV1 between 50% and 80%


GOLD classification of severe COPD

FEV1/FVC < 70%

between 50% and 30%


GOLD classification of very severe COPD

FEV1/FVC < 70%

FEV1 < 30% predicted


maximal inspiration and expiration in COPD

IC is decreased, RV is increased, FRC is increased


respiratory response to exercise in COPD

Lungs stay overinflated, more volume and less inspiration each breath

Can breath up to TLC, everything is shifted upward, IC is smaller

RR goes up

EELV goes up, dynamic lung hyperinflation, IC goes down


grade 0 mMRC dyspnea

breathless with strenuous exercise


grade 1 mMRC dyspnea

short of breath when hurrying onf the level or walking up a slight hill


grade 2 mMRC dyspnea

walk slower than people of the same age level because of breathlessness

have to stop for breath when walking at my own pace on the level


grade 3 mMRC dyspnea

stop for breath after walking about 100 meters of after a few minutes on the level


grade 4 mMRC dyspnea

too breathless to leave the house

breathless when drssing or undressing


treatment options for COPD

long acting beta agonists (can be used safely by itself) - salmeterol or formoterol

ultra long-acting beta-agonist - indacaterol

long-acting anti-muscarinic - tiotropium

beta agonist + inhaled corticosteroid - salmeterol + fluticasone or formoterol + budesonide


definition of a COPD exacerbation

an event in the natural course of the disease characterized by a change in the patient's baseline dyspnea, cough, and/or sputum that is beyond normal day-to-day variations, is acute in onset, and may warrant a change in regular medication in a patient with underlying COPD


consequences of COPD exacerbations

faster decline in lung function

poorer quality of life

higher mortality

greater airway inflammation


COPD exacerbation treatment


inhaled bronchodilators

systemic corticosteroids


ventilatory support (either NIV or intubation)


Describe the progression of disease in COPD.

lung inflammatory cells present in greater numbers due to smoking or other toxic chemicals, release of toxic oxygen species

activation of NF-kB and increase in TNF alpha and IL-8 lead to neutrophil recruitment

what results is bronchitis, mucus hypersescretion, bronchospasm, destruction of alveolar walls, and small airway remodeling resulting in peribronchiolar fibrosis and formation of airway lymphoid follicles

decrease in anti-proteases lead to lung damage