COPD Flashcards by Jessica Mangan

1 cause of COPD

cigarette smoking

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A heredity deficiency of _____ may result in early onset and severe COPD.

alpha-1 antitrypsin

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polymorphisms

genes that code for TNF, surfactant, proteases and antiproteases

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airway inflammation and obstruction of the major and small airways
chronic productive cough for at least 3 consecutive months over 2 consecutive years

chronic bronchitis

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Loss of lung elasticity & abnormal enlargement of the airspaces distal to the terminal bronchioles with destruction of the alveolar walls & capillary beds

emphysema

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permanent dilation of the bronchi and bronchioles
caused by destruction of the muscle and elastic supporting tissue due to vicious cycles of infection & inflammation

bronchiectasis

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onset of COPD

occurs midlife

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clinical features of COPD

persistent or worsening dyspnea, chronic cough

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pathologic changes in COPD

squamous metaplasia of epithelium, parenchymal destruction, mucus gland metaplasia & enlargement

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a respiratory disorder largely caused by smoking, characterized by progressive, partially reversible airway obstruction and lung hyperinflation, systemic manifestations, and increasing frequency and severity of exacerbations.

COPD

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occurs with emphysema due to protease mediated degradation of connective tissue elements in the lungs.

loss of lung elastic recoil

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occurs due to an imbalance between the lung’s repair and defense mechanisms.

Peribronchiolar fibrosis

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contributes to airway remodeling

fibrosis of the small airways

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the persistent changes that occur within the structural components of the airways in response to inflammation.

airway remodeling

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mucus hyperplasia and increased expression of mucin genes results in…

increased airway secretions

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due to hyperactivity of the bronchi with bronchoconstriction due to persistent inflammation

increased tone in airway smooth muscle

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first feature of chronic bronchitis

hypersecretion in the large airways

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airway obstruction causes….

ventilation-perfusion mismatch, hypercapnia, and hypoxemia.

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cor pulmonale

enlargement of the right ventricle

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enzymes that digest proteins

proteases

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Characterised by a breakdown of elastin in the alveolar septa and bronchial walls as well as breakdown of alveolar and bronchial wall components by proteases

emphysema

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where are proteases released from?

neutrophils, alveolar macrophages and other inflammatory cells

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____ contributes to air trapping.

decreased elastic recoil in bronchial walls

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septal destruction in the alveoli destroys portions of the pulmonary capillary bed causing ______.

ventilation-perfusion mismatch and hypoxemia.

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the action of elastin is normally inhibited by ____

alpha-1-antitrypsin

the most serious a1-antitrypsin deficiency is caused by ___

PIZ variant which is found in 5% of the population

what is the most common form of emphysema?

Centriacinar emphysema

- the destruction is confined to the terminal and respiratory bronchioles. - upper parts of the lung

centriacinar emphysema

- there is involvement of the peripheral alveoli and later the more central bronchioles. - lower parts of the lung

panacinar emphysema

this form of emphysema is more common in individuals with inherited a1-antitrypsin deficiency

panacinar emphysema

appearance of barrel chest is due to

air trapping

expanded thorax results in

decreased tidal volume, hypoventilation and hypercapnia

____ is a central feature of COPD

inflammation

leads to damage & remodeling of the lung parenchyma -> airflow limtiation

inflammation

___ immunity activated at all stages of COPD

innate

____ immunity activated in more severe disease

adaptive

____ mediate both types of immunity

cytolines

___ likely link innate and adaptive immunity in COPD

dendritic cells

what are the most important inflammatory cells in COPD?

neutrophils, macrophages and CD8+ T lymphocytes

what are the most important proteases involved in emphysema?

Elastases, cathepsins and matrix metalloproteinases

secrete inflammatory mediators that active neutrophils and CD8+ T lymphocytes.

macrophages

secrete inflammatory mediators that active neutrophils and CD8+ T lymphocytes.

TNF-a

activates macrophages to secrete inflammatory cytokines, chemokines and matrix metalloproteinase.

IL-B

s a link between innate and acquired immunity and stimulates C-reactive protein release from the liver.

IL-6

is newly described pro-inflammatory cytokine and is correlated with disease severity.

IL-32

- belongs to the IL-7 family - plays a role in dendritic cell programming by stimulating specific chemokines which then attract T helper lymphocytes and cytotoxic T lymphocytes

Thymic stromal lymphopoeitin (TSLP)

induce leukocyte chemotaxis specifically promoting neutrophil activation and migration.

Chemockines, growth factors, anti-inflammatory cytokines

It plays an important role in regulating energy and is decreased in persons with COPD.

leptin

An elevated ____ during exacerbations is correlated with the severity of exacerbations

serum amyloid A

increased ____ has been linked to health and exercise capacity and appears to be a significant predictor of BMI.

CRP

may be caused by disturbances in ventilation, gas exchange or ventilation-perfusion relationships as well as increase work of breathing or diseases that damage the lung parenchyma.

dyspnea

occurs as breathing with effort depletes energy stores.

fatigue and exercise intolerance

is a reflex that is stimulated in COPD by excessive secretions and/or inhaled irritants

cough

is caused by inflammation in the airways

sputum production

occurs as air passes through narrowed airways

wheezing

often seen due to prolonged expiratory phase.

hypoventilation

may be present related to inadequate gas exchange in COPD.

hypoxemia

helps to prevent expiratory airway collapse.

pursed lip breathing

is caused by hypoxemia.

cyanosis

are caused by abnormal secretions, mucus or fluid in the airways.

crackles

usually associated with upper airway obstruction

inspiratory wheezing

usually associated with lower airway obstruction

expiratory wheezing

indicates more advanced disease

FEV1 <80%

not always reduced in early stages of COPD

FVC

confirms airflow limitation

FEV1/FVC post-bronchodilatory <0.70

main pharmacological therapy for COPD

bronchodilators

decrease bronchoconstriction by reducing muscle tone and glandular mucus.

inhaled anticholingeric

It is important to identify the _____ names and what they are prior to administering

generic

can also be used especially in patients with significant mucus hypersecretion.

mucolytics

third line treatment

methylxanthines

the only intervention shown to slow the rate of lung function decline.

smoking cessation

COPD Flashcards

(71 cards)