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OPT Respiratory I

atelectasis (collapsed lung) loss of lung volume caused by inadequate expansion of airspaces
resorption atelectasis an obstruction prevents air from reaching distal airways; often after anesthesia and mucous plugs
compression atelectasis accumulation of blood, fluid or air in pleural cavity, causing the lung to collapse; after effusions and CHF
contraction atelectasis fibrotic changes in the lungs or pleura; irreversible
acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) continuum of respiratory failure; symptoms include dyspnea, hypoxemia (decreased arterial oxygen pressure), and absence of left heart failure -{most common cause of noncardiogenic pulmonary edema} -caused by either {direct injury} or {indirect injury}
ARDS pathogenesis neutrophils thought to play an important role
diffuse alveolar damage histologic manifestation of ARDS
acute phase stage of diffuse alveolar damage; capillary congestion, necrosis and collection of neutrophils -{hyaline membranes} form
hyaline membranes protein-rich edematous fluid mixed with necrotic epithelial cells
organizing phase phase of diffuse alveolar damage; proliferation of type II pneumocytes and phagocytosis of hyaline membranes
diffuse interstitial fibrosis may occur after the acute phase of diffuse alveolar damage; compromises lung function
obstructive disease limitation of airflow from increased resistance due to obstruction -includes emphysema, chronic bronchitis, asthma and bronchiectasis
restrictive disease reduced expansion of lung parenchyma and decreased total lung capacity; both chronic and acute forms -includes ARDS, idiopathic pulmonary fibrosis (IPF), pneumoconiosis and sarcoidosis
chronic obstructive pulmonary disease (COPD) usually a combination of chronic bronchitis and emphysema {major etiologic factor is cigarette smoking}
emphysema anatomic entity restricted to the acini; abnormal, permanent enlargement of the airspaces
centriacinar emphysema central/proximal parts of the acinus is affected (aka the respiratory bronchioles) but the distal alveoli are unaffected -more common in upper part of lungs and seen as a consequence of {cigarette smoking}
panacinar emphysema effects the entire acinus in the lower parts of the lungs; often due to {alpha1-antitrypsin deficiency}
distal acinar emphysema effects the distal acinus, adjacent to the pleura; can cause spontaneous pneumothorax
irregular emphysema acinus is irregularly involved; associated with scarring after inflammatory diseases
protease-antiprotease imbalance hypothesis theory of emphysema pathogenesis; people with alpha1-antitrypsin deficiencies develop emphysema because their elastic tissue is destroyed
oxidant-antioxidant imbalance hypothesis theory of emphysema pathogenesis; oxidative injury recruits neutrophils and inactivates antiproteases
'pink puffers' describes clinical course of emphysema; no bronchitic component, barrel chest with dyspnea and hyperventilation but normal gas levels
'blue bloaters' describes clinical course of emphysema; history of bronchitis, patients are hypoxic and cyanotic
chronic bronchitis clinical presentation of persistent cough for 3 months in 2 consecutive years; due to hyper secretion of mucous from metaplastic transformation of mucin-secreting goblet cells
asthma episodic, reversible bronchospasm from and exaggerated bronchconstrictor response
atopic asthma asthmatic episode initiated by type I IgE-mediated hypersensitivity reaction to an antigen; most common type, hereditary, and driven by TH2 subset of CD4 T cells
non-atopic asthma triggering mechanism of asthmatic episode is not immune; no family history and normal IgE levels
airway remodeling persistent inflammation that leads to structural changes in bronchial walls; hypertrophy of bronchial smooth muscle and mucous glands, increased vascularity and collagen deposition -pathogenesis of atopic asthma
status asthmaticus sudden asthma attack that does not respond to therapy and persists for days to weeks
bronchiectasis permanent dilation of bronchi and bronchioles due to chronic necrotizing infections
predisposing conditions to bronchiectasis: 1. bronchial obstruction 2. congenital/hereditary conditions 3. necrotizing/suppurative pneumonia
chronic restrictive (interstitial) lung diseases hallmark is reduced compliance so breathing takes more effort -includes IPF, the pneumoconiosis, and sarcoidosis
idiopathic pulmonary fibrosis (IPF) patchy but progressive interstitial fibrosis causes hypoxia and cyanosis; breathing sounds like velcro crackling
pneumoconioses group of diseases caused by inhaling irritants, allergens or toxic aerosols; particles 1-5 micrometers are most damaging -{pulmonary alveolar macrophage is key cellular element in initiation and perpetuation of lung injury and fibrosis}
Caplan syndrome coexistence or rheumatoid arthritis with one of the pneumoconiosis; forms nodular lesions
coal workers' pneumoconiosis (CWP) spectrum of lung findings in coal workers -{does not increase risk of lung cancer in non-smokers}
anthracosis pigment accumulation in CWP without cellular reaction
simple CWP cellular accumulation of macrophages with little dysfunction -contains coal macule and nodules
coal macule dust-laden macrophage
coal nodule dust-laden macrophage with network of collagen fibers surrounding
complicated CWP / progressive massive fibrosis (PMF) extensive fibrosis and compromised lung function
silicosis inhalation of crystalline silica; carcinogenic and predisposes to tuberculosis
acute silicosis shortly after exposure to high levels of silica; develops quickly
chronic silicosis silica exposure over a prolonged time with formation of fibrotic nodules; latency period before onset
complicated silicosis progression of chronic silicosis with coalescence of nodules into hard scars; progresses to PMF
asbestosis marked by diffuse pulmonary interstitial fibrosis, indistinguishable from other fibrotic lung diseases -progresses to CHF, cor pulmonale and death
serpentine asbestosis with curly, flexible fibers
amphibole asbestosis with straight, stiff fibers; more pathogenic and predisposes to {malignant mesothelioma}
asbestos bodies distinguishes asbestosis; asbestos fibers coated in iron-containing proteinaceous fluid left from macrophage that tried to engulf it
pleural plaques asymptomatic plaques of dense collagen
sarcoidosis multisystem, idiopathic disease with {non-caveating granulomas in tissues and organs} -higher prevalence in non-smokers
bilateral hilar lymphadenopathy major manifestation of sarcoidosis
death from sarcoidosis due to: 1. progressive pulmonary fibrosis 2. cor pulmonale
Created by: Alexandra Arnold Alexandra Arnold