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158 Cards in this Set
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Pores of Kohn
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connections between alveoli that allow passage of bacteria and exudates
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Heart failure cells
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RBCs that leak through alveoli in lung ingested by macrophages ---
seen in pulmonary and hemodynamic edema |
hemosiderin-laden macrophages; seen in hemodynamic edema
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brown induration
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is fibrosis and hemosiderin pigmentation of the lungs due to long standing pulmonary congestion (chronic passive congestion)
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Types of lung injuries that are sudden and acute in nature
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Acute lung injuries, Adult Respiratory Distress, neonatal Respiratory Distress
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What can cause ALI
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1)Pulmonary Edema
2) Hemodynamic Edema 3) Alveolar Injury |
acute lung injury
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Kulchitzky cells
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ECL cells (5HT2)
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pink frothy sputum
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ALI caused by Pulmonary Edema
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crackles and pulmonary BP or >25mmHg
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ALI caused by pulmonary edema
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What other pathologies can cuase pulmonary edema?
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CHF or parenchymal damage
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Most common cause of hemodynamic edema
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Left heart failure and volume overload such as anemia
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Key difference between ALI caused by hemodynamic edema and Alveolar Injury
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In Alveolar Injury, pulmonary hydrostatic pressure is normal
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Pnemonia MOA to cause edema
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alveolar injury
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same as septicemia
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ARDS MOA to cause edema
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alveolar or microvascular injury
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Mortality rate of ARDS
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40%
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Characterization of ARDS (What is ARDS?)
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-abrupt onset of HYPOXEMIA without heart failure
- with diffuse pulmonary infiltrates (bilaterally) |
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What is ARDS caused by?
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neutrophil injury due to conditions such as:
septic shock, DIC, pneumonia, toxins/smoke inhalation, aspirated vomit |
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What will oxygen therapy do to ARDS patients?
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MULTIORGAN FAILURE because ventilation can physically stress parenchyma and MAKE HYPOXEMIA WORSE
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what is acute interstitial pneumonia?
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idiopathic ARDS
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heavy, firm, red, boggy lungs
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morphology of diffuse alveolar damage (DAD)
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not caused by heart condition but looks like a heart!
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findings associated with ALI
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DAD
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DAD likes ALI
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DAD Acute phase:
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Congestion, Hyalinized Membrane, Inflammatory cells, Interstitial edema, Type II pneumocyte damage
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DAD likes to CHIIT (chat) for ONE WEEK
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DAD Proliferative phase
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Hyperplasia of Type II and fibroblasts
Interalveolar fibrosis Thickening of septae |
HIT
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Transcription factor responsible for activation of neutrophils in ARDS
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Nf-KB which causes cytokine expression by lymphocytes and therefore ACTIVATION OF NEUTROPHILS
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Decreased bronchoalveolar urokinase plasminogen activator-mediated fibrinolysis causes what?
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hyaline membrane formation in DAD
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How is hypoxemia caused in ALI?
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perfusion/ventilation mismatching
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NRDS
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neonatal respiratory distress syndrome
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Predisposing factors for NRDS
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C-section, Male baby, Gestational age, Diabetes
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CMGD
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clinical presentation of NRDS
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sudden cessation of respiratory function unresponsive to O2
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Cause of atelectasis in NRDS
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deficiency of surfactant
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it decreases surface tension in alveoli to prevent atelectasis during expiration
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What appears 3-4 hrs after NRDS babies?
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hyaline membranes due to destruction of Type II pneumocytes and fibroblast proliferation
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retrolental fibroplasia
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Retinopathy of prematurity - caused by upregulated VEGF due to hypoxia in NRDS
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causes angiogenesis and retinal vessel proliferation
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bronchopulmonary dysplasia
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decrease in alveolar septation
- at least 28 days O2 therapy in infant beyond 36 week's gestation |
reversible
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NRDS at risk for what other complications
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patent ductus arteriosis
Intraventricular brain hemorrhage Necrotizing enterocolitis |
PIN
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Types of Obstructive lung diseases
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Bronchitis (chronic)
Asthma Bronchiectasis Emphysema |
OLD: BABE
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Hallmark of OLD PFTs
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decreased FEV1/FVC ratios
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blue bloater
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BB is Bronchitis
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pink puffers
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emphysema
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hypertrophy of mucus glands, wheezing, crackles, cyanosis
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Chronic bronchitis
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enlargement of air spaces, dyspnea, increased elasetase activity
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Elastase = Emphysema
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bronchial hyperresponsiveness
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asthma
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chronic necrotizing infection of bronchi causing dilated airways, purulent sputum, and hemoptysis
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bronchiectasis
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Obstructive vs Restrictive lung diseases
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increase RESISTANCE vs REDUCED EXPANSION (lower TLC)
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PEople that get emphysema
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smoking black women
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How is emphysema an OLD?
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destruction of elastic tissue causes collapse of lung framework
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Type of emphysema caused by smokers
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centriacinar (affects the parts the smoke goes to most)
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Type of emphysema caused by a1 antitrypsin deficient ppl
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panacinar (entire acinar) by the bases and lower lobes
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what type of emphysema affects distal to acinar and adjacent to pleura
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distal acinar
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may cause spontaneous pneumothorax
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distal acinar emphysema
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irregular emphysema presents how?
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asymptomatic, its just space enlargement with fibrosis
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Microscopic presentation of emphysema
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Destroyed alveoli, > spaces with blebs and bullae
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cor pulmonale
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pulmonary HTN that causes right ventricular hypertrophy
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Clinical definition of chronic bronchitis
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productive cough for at least 3 mo in 2 consecutive years with no other etiology
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Measurement used in chronic bronchitis pts
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Reid index; ratio of mucus gland thickness to epithelial wall
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Reid index of 0.4
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normal; bronchitis is > 0.5
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Theorites of COPD pathogenesis
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1) protease-antiprotease imbalance theory
2) oxidant-antioxidant imbalance theory |
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Asthma definition
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chronic inflammatory disorder of the airways that causes episodic, reversible bronchoconstriction due to hypersensitvity to stimuli
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Atopy:
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genetic predisposition to Type I hypersensitivity rxns
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non-atopic
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sensitivity to inhaled antigen without other evidence of atopy
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Phases of Atopic asthma
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1) IgE mediated within minutes
2) late phase reaction in hrs mediated by leukocytes |
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Asthma triggered by respiratory tract infection
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non-atopic asthma
- hyperirritability of bronchial tree |
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nasal polyps pt has:
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aspirin-sensitive asthma
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Microscopic presentation of mucus plugs
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Curshmann spirals and Charcot-Leyden crystals
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what do asthmatics have elevated in their blood?
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eosinophils
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Irreversible dilation of brionchi and bronchial
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bronchiectasis
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what conditions does the diagnosis of bronchiectasis require
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obstruction AND infection (either one can cause the other)
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what can cause bronchiectasis
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congenital, infection, postinfection, obstruction
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How does cystic fibrosis cause bronchiectasis
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lack of Cl transport causes accumulation of thick secretions that block airways; infection is secondary
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Triad of bronchiectasis, situs inversus, and sinusitus?
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Kartagener syndrome (occurs in 50% of primary ciliary dyskinesia)
dyenine deficincy causes lack of ciliary mvnt; infection is secondary -- this causes bronchiectasis |
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areas of lung most likely to have bronchiectasis
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lower lobes
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Microscopic morphology of bronchiectasis
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desquamation, ulceration, abcesses, fibrosis
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clinical features of bronchiectasis
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hemoptysis, cough, paroxysmal orthopnea
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What is pneumoconioses?
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non-neoplastic lung reaction to inhaled inorganic and organic particulates
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What are the ABC's of pneumoconioses pathogenesis?
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Amount
Boyancy Chemical properties |
ABCs are what development of a pneumoconiosis depends on
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What are the DEF's of dust retention in the lungs?
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Dust concentration
Exposure duration Fectiveness of clearance mechanisms |
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most dangerous particle sizes that lead to pneumoconiosis
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1-5 micrometers
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Pneumoconiosis caused by smaller particles cause what?
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acute lung injuries (becasue it can reach alveoli)
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Pneumoconiosis caused by larger particles cause what?
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interstitial fibrosis (it gets stuck in central bronchioles)
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What is anthracosis?
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the accumulation of carbon-laden macrophages in subpleural lymphatics
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What is CWP caused by?
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silica in coal dust
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What is simple vs complicated CWP?
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simple : macules and nodules
complicated: fibrosis and scars |
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10% of patients with simple CWP progress to this
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Pulmonary Massive Fibrosis which can lead to worse things
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What can silicosis lead to but NOT COAL DUST?
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silicosis can lead to TB and cancer
no evidence of that with coal dust |
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Most prevalent chronic occupational disease worldwide
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silicosis
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Implicated in silicosis
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crystalline forms of silica
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morphology of silica pathogenesis
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nodules: concentric layers of hyalinized collagen with silica particles that appear in upper lung
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chest X rays showing fine reticulonodular pattern in upper zones:
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silicosis
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PFTs in patients with silicosis
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pretty normal
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serpentine
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most common form of asbestos (silica fibers)
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amphibole
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pathogenic form of silica fibers (asbestos) that cause mesothelioma
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increasing doses of amphiboles and chryostiles cause what?
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higher incidence of asbestos-related diseases EXCEPT mesothelioma
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dose-independent asbestos disease
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mesothelioma
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acts as both tumor initiator and promoter
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asbestos
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mesothelioma and smoking?
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risk of mesothelioma not increased by cigarette smoking
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how do you differentiate diffuse interstitial fibrosis from other ILDs
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asbestos bodies
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what are pleural plaques?
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dense collagen found on parietal pleura without asbestos bodies (asymptomatic)
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what are ILDs?
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lung diseases where there is:
Interstitial inflammation Granulation Fibroses |
there are 7 subtypes of this!
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Symptoms of ILD
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Dyspnea
Dry cough Collagen vascular Diseases Clubbing of fingers |
DDCC
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basilar velcro rales without wheezing or chest pain
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ILD
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common causes of ILD
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Drug induced
Idiopathic Collagen vascular disease Enviro/job related Diffuse alveolar damage progession and other |
DICED
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ILD radiographic pattern
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reticular pattern and honeycombing
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most important radiologic method for evaluating pts with ILD
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High Resolution CT scan
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What is seen in HRCT in ILD patients?
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ground class, honeycombing, consolidation
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What PFT results are expected in those with ILD?
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same with restrictive lung diseases:
low volume, proportionally decreased flow BUT ALSO reduced diffusion capacity for carbon monoxide |
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DLCO
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diffusion capacity for carbon monoxide, decreased in ILD.
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why is DLCO reduced in ILD pts?
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thickened interstitium due to fibrosis and V/Q mismatch
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Diagnosis of usual interstitial pneumonia or idiopathic pulmonary fibrosis?
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diffuse, bilateral, patchy, TEMPORALLY heterogenous fibrosis histological pattern
after all other ILD etiologies are exhausted |
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What areas are affected by idiopathic pulmonary fibrosis?
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subpleural and paraseptal areas alternating with normal lung
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Definite treatment for idiopathic pulmonary fibrosis?
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lung transplant
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What factors contribute to idiopathic pulmonary fibrosis?
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chronic epithelial cell stress which causes:
-surfactant protein C abnorm -ABCA3 abnormalities - active fibrosis - high and long TGF-B induced cytokine signaling |
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Histologic pattern shows temporally homogeneous inflammation or fibrosis
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non-specific interstitial pneumonia
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Why is it important to temporally distinguish ILDS?
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non-spec IP has a much better outcome that IPF
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Cellular pattern seen in non-spec IP?
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mild interstitial chronic inflammation,
Type II pneumo hyperplasia, preserved lung architecture |
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pertinent negative finding in non-specific interstitial pneumonia?
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absence of fibroblastic foci and honeycombing (the fibrosis is so mild and diffuse, not patchy)
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Treatment of non specific interstitial pneumonia?
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corticosteroids
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Histologic pattern of organizing pneumonia?
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excessive proliferations of granulation tissue within small ariways and alveolar ducts
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radiographic findings of organizing pneumonia:
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CXR: consolidation
HrCT: condolidation both subpleural distribution |
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pertainent negatives in organizing pneumonia
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no interstitial fibrosis, granulation, etc... its ALL in the ALVEOLI
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What is COP?
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crytogenic organizing pneumonia, has better outcome than OP due to secondary conditions
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Seen exclusively in current or recent heavy smokers
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respiratory bronchiolitis ILD
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What is respiratory brionchiolitis?
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ILD with chronic bronchiolitis and pigmented carbon
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radiographic findings of resp bronchiolitis?
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CXR:bronchial wall thickening, patches of ground glass.
HRCT: centrilobular opacities, ground glass |
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mean age of respiratory bronchiolitis onset?
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36, younger than all other ILDS. stop smoking and :)
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Intra-alveolar mononuclear cell infiltration without prominet dense fibrosis or honeycombing
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desquamative interstitial pneumonia (much like OP without fibrosis)
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CXR/HRCT of DIP
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LOWER lung zon ground glass and reticular patterns
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Pertainant negatives of DIP
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no dense or heavy interstitial stuff, only mild
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What is sarcoidosis?
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a (non-caseating) granulomatous disease of unknown etiology
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What are common CXR findings in sarcoidosis?
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hilar and mediastinal lymph node enlargement;
may or may not have nodular patters within interstitium. |
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What is a protean?
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the idea that some diseases such as sarcoidosis display a wide variation of clinical phenotypes, probs becasue of genetic differences
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Sarcoidosis has strong link to what?
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HLA-DRB1
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pathogenesis of sarcoidosis?
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immune system dysregulation mediated by Th1
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Typical sarcoidosis patient
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20-40, any age/sex but BW in US
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What is hypersensitivity pneumonitis?
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type II and type IV hypersensitivity inflam response to inhaled organic antigens.
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CXR findings in hypersensitivity pneumonitis?
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first, Consolidation, then ground glass, then reticular formation ( in alphabetical order)
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Treatment for hypersensitivity pneumonitis?
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remove antigen and give corticosteroids
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What is eosinophilic pneumonia?
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a histologic pattern with immense eosinophilic infiltration
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what does peripheral blood eosinophilia and pulm radiographic infiltrates mean?
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not necessarily EP! could be other things...
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EP CXR/HRCT:
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bilat consolidation within subpleural lung periphery
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Treatment for EP?
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corticosteroids
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proliferation of langerhans cell infiltrates?
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pulm langerhans cell histiocytosis (histiocytosis X)
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lung affected by PLCH CXR findings:
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diffuse, bilateral stellate nodules with upper and middle lung zones affected
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classic finding in langerhans cells
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birbeck granules
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people commonly affected by PLCH:
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20-40 yr old males, rarely blacks!
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treatment of PLCH?
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corticosteroids
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main factor for PLCH?
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smoking
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What histologic finding occurs when alveolar macrophages lose the ability to clear out surfactant?
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Pulmonary Alveolar Proteinosis
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What is found in PAP CXR and HRCT?
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CXR: perihilar and lower lung consolidation (where it accumulates)
HRCT: crazy paving pattern |
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2 things that cause acquired PAP
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1) Anti GM-SCF which inhibits the activity of GM-CSF
2) mutation of GM-CSF 3) mutation of GM-CSF receptor genes |
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What does GM-CSF do
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stimulates alveolar macrophages to clear surfactant
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Treatment for PAP
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whole lung lavage
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histologic pattern seen in chronic radiation pneumonitis
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DAD with type 2 pneumocytes and fibroblasts
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pulmonary patterns seen in patients with collagen vascular diseases:
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the interstitial ones: NSIP, UIP, vasculitis, OP, bronchiolitis
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Dual supply of lungs:
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pulm arteries that accommodate all cardiac output per beat; bronchiole arteries that get supply from aorta or intercostals
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What are most emboli made of?
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thrombi
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Most common preventable cause of death in hospitalized pts?
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pulmonary emoblism
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Most pulmonary emboli come from where?
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DVT
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What are the two consequences of pulmonary emboli?
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respiratory compromise due to unperfused area; hemodynamic compromise due to increased resistance, causing PULMONARY HTN/EDEMA/RHF
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Result of saddle emboli?
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death or cor pulmonale
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Result of smaller pulmonary emboli?
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infarct or hemorrhage
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