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213 Cards in this Set
- Front
- Back
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strongest known risk factor for development of TB
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HIV
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patient is infected with TB with no previous history of exposure
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primary tuberculosis
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patient is infected with TB with known history of previous exposure
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secondary tuberculosis
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Ghon focus is seen in what part of the lungs
why |
middle/lower lobes due to increased blood flow - primary tuberculosis
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Fibrocaseous cavitary lesion is seen in what part of the lungs
why |
upper lobes due to increased oxygen tension - secondary tuberculolsis
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sites of extrapulmonary tuberculosis
what leads to this |
meningitis, Pott's disease, lymphadenitis, renal, intestinal
due to secondary tuberculosis |
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how is TB spread
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breathing infectious particles
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two ways secondary TB can occur
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reinfection of the lung
reactivation from old infection |
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most common cause of secondary TB in the U.S.
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reactivation of old TB infection
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where do the TB bacilli replicate
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intracellularly in the macrophages
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What makes up the Ghon complex
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parenchymal lesion usually in the lower lobes - Ghon focus
enlarged caseous Hilar lymph nodes draining the parenchymal focus |
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Four potential fates once the TB organism has made their way into the lung
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1. initial host response completely kills all bacilli
2. organisms grow immediately causing primary tuberculosis 3. Bacilli become dormant, latent infection 4. latent organisms can grow, resulting in reactivation tuberculosis |
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Associated with negative tuberculin skin test
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host immune response completely wipes out TB bacilli
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suggests failure of both innate and adaptive immunity
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primary tuberculosis
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two major forms of primary tuberculosis
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progressive lung disease
miliary TB |
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adaptive immunity was successful in that the bacilli cannot cause disease but what can happen
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reinfection can occur leading to secondary TB
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associated with positive tuberculin skin test
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latent infection
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partially successful adaptive immunity
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latent organisms can become reactivated to cause secondary TB
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what is associated with reactivation TB
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immunosupression (especially HIV) is a major risk factor
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dissemination of TB bacilli through the body via the blood
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Miliary TB
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characteristics of miliary TB
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failure of immunity leading to multiplying of bacilli in Hilar lymph nodes
caseous nodes discharge infective particles to efferent lymphatics, which drain to venous system carry to lungs and may enter systemic circulation |
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associated with a Ghon focus, caseous hilar lymphadenitis, and tubercles though the lung
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Miliary TB
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result from reinfection or reactivation from previous TB infection
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secondary TB
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where do dormant bacilli establish themselves
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high oxygen tension areas such as upper lobes of lungs
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predisposes one to extrapulmonary TB
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cavity formation from secondary TB infection
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unique feature of secondary TB
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cavity formation
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allow TB bacilli to multiply masively extracellularly and have propensity to rupture into airways
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Cavity formation
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associated with Bird and Bat dropping in the MidWest
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Histoplasma Capsulatum
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associated with thick capsule, seen with India Ink
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Cryptococcus neoformans
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associated with Southwest Desert and spherules full of endospores
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Coccidiodes immitis
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collapse lung tissue caused by external pressure
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compression atelectasis
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collapse of lung tissue caused by removal of air from obstructed or hypoventilated alveoli
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absorption atelectasis
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Ways to get compression atelectasis
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external pressure from tumor, air, fluid, or abdominal distention
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ways to get absorption atelectasis
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removal of air from obstructed or hypoventilated alveoli
inhalation of concentreated oxygen or anesthetic agents |
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common atelectasis after surgery
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absorption atelectasis
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most common postoperative complication
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fever
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4 ways to get postoperative fever
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Wind - atelectasis
Wound - wound infection Water - urinary infection Walk - thrombophlebitis |
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3 ways why there is increased likelihood of postoperative atelectasis
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shallow breathing
relunctance to change position production of viscous secretions that form mucous plug |
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prevention of postoperative atelectasis
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deep breathing - permits colateral ventilation through pores of Kohn
frequent position changes early ambulation - walking |
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two most important capillary net filtration forces
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capillary hydrostatic
capilly oncotic |
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what is important in maintaining oncotic pressure
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integrity of the capillary membrane
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why is there a difference in hydrostatic pressure between parietal and visceral pleura
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parietal is supplied by systemic circulation
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why is there a negative intrapleural pressure
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opposing forces of the chest wall wanting to move outward from lung wanting to move toward hillus
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4 ways pleural effusions take place and causes
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1. increased capillary hydrostatic pressure - CHF
2. decreased capillary oncotic prssure - liver failure, protein loss 3. occluded pleural lymphatics - cancer 4. loss of capillary membrane integrity - infection, cancer, inflammation |
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differentiate transudate and exudate
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transudate is plasma with low protein concentration, while exudate contains plasma proteins, platelets, WBCs
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reasons why exudate is seen in pleural effusion
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capillary protein leak from damaged epithelium - trauma, tumor, inflammation
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diagnostic testing to distinguish transudate from exudate
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exudate if:
1. pleural fluid protein/serum protein ratio greater than 0.5 2. pleural fluid LDH/serum LDH ratio greater than 0.6 3. pleural fluid LDH greater than two third the upper limits of normal of the serum LDH |
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presence of air or gas in the pleural space caused by rupture in the visceral pleura or parietal pleura
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pneumothorax
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what happens to the lung in a case of a pneumothorax
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collapses toward the hilum because the negative pressure is destroyed
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what are the two types of pneumothoraxes
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spontaneous
traumatic |
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differentiate primary and secondary spontaneous pneumothorax
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primary - no previous lung disease, results from a rupture of subpleural bleds in the apices usually
secondary - occurs with associated underlying lung disease - asthma |
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pneumothorax with pressure in the pleural space exceeding the astmospheric pressure during expiration
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tension pneumothorax
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problems resulting from tension pneumothorax
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displaces the mediatinum and can progress to cardiogenic shock
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excess fluid withing the blood vessels resulting in increased hydrostatic pressure
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pulmonary congestion
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fluid leaving the blood vessels and collecting in the alveoli
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pulmonary edema
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Sepsis
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SIRS in response to a confirmed infectious process
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what is the worst effect of sepsis
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the body's own response to the infection
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Acute respiratory distress syndrome (ARDS)
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severe, bilateral acute lung injury resulting in altered pulmonary vascular permeability
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characteristics of ARDS pathologically and clinically
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pathologically - diffuse damage to alveolar walls
clinically - acute respiratory failure |
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what predisposes patients to ARDS
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sepsis (especially gram negative)
multiple trauma |
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differentiate initial and progressive symptoms/signs of ARDS
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initially - dyspnea and tachypnea, but chest radiograph is normal
progresses to cyanosis and hypoxemia and there is diffuse bilateral infiltrates on x-ray |
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what causes pulmonary edema in ARDS patients
specify two different mechanisms |
injury to the alveolocapillary memebrane due to massive inflammatory response by the lungs:
directly - aspiration of highly acidic gastric contents or inhalation of toxic gases indirectly - chemical mediators released in response to systemic disorders |
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what two things are damaged in the acute stage of ARDS and what is the result
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capillary endothelium - vascular leaking
alveolar apithelium - cell sloughing and loss of surfactant |
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what does pulmonary edema result in with ARDS
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reduced lung compliance
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organized stage of ARDS
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recovery due to type II cell proliferation causing fibrosis
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morphology associated with ARDS
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some alveoli are collapsed - atelectasis
some alveoli are distended due to alveoli containing, debris, desquamted cells, and hyaline membranes |
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3 pathophysiologic problems with ARDS
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1. alveolocapillary diffusion abnormality - membrane is thickened due to edema or fibrosis
2. V/Q mismatch from inadequate ventilation 3. shunt when ventilation is so severely affected that hypoxemia doesn't respond to supplemental oxygen concentration |
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occurs when ventilation is so severely affected that hypoxemia does not respond to increases in supplemental oxygen
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shunt
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most important predictors of mortality in ARDS
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infection
MODS |
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3 different clinical stages of ARDS
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acutely - edema fills the lung interstitium but not the alveoli, hypoxemia due to an alveolocapillary diffusion abnormality
subsequently - alveoli are now beginning to fill with edema, hypoxemia due to V/Q mismatch secondary to inadequate ventilation shunt - alveoli are so filled with edema that signficant portion of pulmonary capillary bed is never exposed to oxygen, hypoxemia becomes unresponse to oxygen therapy |
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patients presents with dyspnea, tachypnea, and pleuritic pain
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pulmonary embolism
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what test is used to rule-out a PE
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D-dimer, high sensitive
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what test is used to rule-in PE
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spiral CT w/ pulmonary angiogram, highly specific
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why do a low percentage of emboli cause pulmonary infarctions
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double blood supply to the lungs
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differentiate the V/Q mismatches found in PE vs. ARDS
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PE - high V/Q mismatch due to decreased flow
ARDS - low V/Q mismatch due to decreased ventilation |
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most common cause of high V/Q
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pulmonary embolus
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heart problem that results from pulmonary embolism
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RV hypertrophy/failure, needed to generate increased systolic pressure in excess of 50 mmHg
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4 underlying mechanisms of secondary pulmonary hypertension and causes
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1. elevated LV filling pressure - LV dysfunction, mitral/aortic valve disease
2. increased flow through the pulmonary circulation - VSD, PDA 3. obliteration or obstruction of pulmonary vascular bed - PE, collagen vascular disease 4.. hypoxic vasoconstriction - COPD, obstructive sleep apnea |
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differentiate reversible and irreversible pulmonary hypertrophy
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reversible - muscularis thicking (medial hypertrophy)
irreversible - intimal fibrosis leading to narrowing of the lumen |
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cor pulmonale
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hypertrophy and dilation of RV
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common abnormality in preterm infants from reduced surfactant
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respiratory distress syndrome of the newborn
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primary cause of RDS
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surfactant deficiency
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what happens with less surfactant production
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increased surface tension and increased tendency for the alveoli to collapse if have smaller radius
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morphology of RDS
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atelectasis
hyaline membrane |
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why don't some newborns present with RDS immediately after birth
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because some have bordeline surfactant level
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lab testing for fetal maturity
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lecithin/sphingomyelin ratio - risk of RDS is low when L/S is greater than 2
phosphatidylglycerol level - increased associated with less RDS risk lamellar body count - direct measurement of surfactant production by type II pneumocytes |
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direct measure of the surfactant production by the type II pneumocytes
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Lamellar body count
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when do lecithin concentration begin to increase
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about 32 weeks gestation
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why causes the hyaline membrane in RDS
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combination of fibrin in the edema fluid and the necrotic cells leads to the characteristic hyaline membrane
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treatment of RDS
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exogenous surfactant
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disease associated with decreased surfactant, inflammation, pulmonary edema, and hyaline membrane
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respiratory distress syndrome of the newborn
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defined as the presence of productive cough that does not result from a medically discernible cause
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chronic bronchitis
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how long do the symptoms need to be present for chronic bronchitis to be diagnosed
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half the time for 2 years
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what does chronic irritation in chronic bronchitis lead to
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hypersecretion of mucous
hypertrophy of mucous glands goblet cell metaplasia bronchiolitis |
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what do microbiologic infections do in chronic bronchitis
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they do not initiate bronchitis but appear to maintain the condition
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the main problem in chronic bronchitis
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mucous plugging of the airways
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Reid Index
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ratio of thickness of mucous gland layer to the thickness of the wall
normally the ratio if less than 0.5, but increased in patients with chronic bronchitis |
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what does mucous plugs and narrowed airways cause in chronic bronchitis
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air trapping and hyperinflation
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abnormal permanent enlargement of the air spaces distal to the terminal bronchioles accompanied by destruction of their walls
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emphysema
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centriacinar emphysema
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central or proximal parts of the acini, formed by respiratory bronchioles, are affected while distal alveoli are spared
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associated with cigarette smoking and pronouned in the upper lobes
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centriacinar emphysema
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panacinar emphysema
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acini are uniformly enlarged from the level of the respiratory bronchioles to the terminal blind alveoli
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associated with a1-protease inhibitor deficiency and occurs mostly in the lower lobes
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panacinar emphysema
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distal acinar epmhysema is present with preserved pulmonary function
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apical emphysema that causes spontaneous pneumothorax
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pathogenesis of emphysema
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smoking leads to increaed elastase production from PMNs and decreased anti-protease inhibitors resulting in destruction of the alveolar walls
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why is hyperinflation present in emphysema
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loss of elastic recoil due to increased elastase production causing expiration to become difficult
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associated with: blue bloater, blood is not oxygenated, and cor pulmonale more common
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chronic bronchitis
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associated with: no trouble with oxygenation, pink puffer, and less cor pulmonale until later in the course
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emphysema
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what two ways does tobacco smoke lead to airway obstruction, air trapping, and frequent infections
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continual bronchial irritation and inflammation - hypersecretion of mucous
breakdown of elastin from increased elaste and API deficiency - destruction of alveolar septa (walls) |
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three major causes of death in COPD
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1. RHF - more common in chronic bronchitis
2. respiratory acidosis and coma 3. massive collapse of lung secondary to pneumothorax |
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pathogenesis of asthma
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exposure to triggers leads to inflammatory cell infiltration, which is TH2 mediated, causing hyperresponsiveness leading to bronchoconstriction
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two inflammatory cells that play an important role in asthma
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mast cells
eosinophils |
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link between antigenic triggers and inflammation
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TH2 mediated
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differentiate asthma and chronic bronchitis
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asthma is reversible due to having triggers
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morphology of asthma
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exudates containing eosinophils in lumen of small brochus
thickened epithelial basement membrane smooth muscle wall hypertrophy |
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abnormal dilation of the large conduction airways
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bronchiectasis
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causes of bronchiectasis
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bronchial obstruction leading to atelectasis and diminished elastic forces holding airways taut
inflammatory process from infection |
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most common cause of bronchiectasis
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cystic fibrosis
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where are the most severe changes of bronchiectasis seen
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large airways of the lober lobes
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clinical manifestations of bonchiectasis
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production of voluminous amounts of purulent sputum
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the most common cause for pulmonary hypertension
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COPD
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associated with ground glass appearance on x-ray
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interstitial lung disease
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interstitial lung disease
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diffuse chronic inflammation and fibrosis of alveolar interstitium with sparing of bronchioles and bronchi
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most important of the known origins of ILD
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environmental disease because it's the most treatable
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differentiate percentage of known and unknown origins of ILD
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known - 1/3
Unknown - 2/3 |
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examples of unknown origins of ILD
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idiopathic pulmonary fibrosis
collagen vascular disease lupus sarcoidosis |
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characterize the three stages of pathology for ILD
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early stage - active alveolitis with minimal alveolar fibrosis
advanced disease - minimal alveolitis with widespread alveolar fibrosis and destruction progressive - end stage lung disease with honeycomb appearane |
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association of honeycomb appearance
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end-stage lung disease from progressive ILD
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what is needed to be intact in order for repair of alveolar to occur in ILD
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basement membrane
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pathogenesis of ILD
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1. initial stimulus causing injury to epithelial/endothelium
2. alveolitis results from release of cytokines into the alveolar interstitium 3. repair process occurs which can either repair completely or chronically cause significant fibrosis and end-stage lung disease |
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non-neoplastic lung reaction to inhalation of organic or mineral dust, chemical fumes, or vapors
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pneumoconioses
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extrinsic allergic alveolitis from repeated inhalation of a variety of small organic particles
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hypersensitivity pneumonitis
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differentiate acute reaction and re-exposed individual with hypersensitivity pneumonitis
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acute reaction - occurs 4 to 8 hours after exposure in the absence of repeated exposure with spontaneous recovery: present with dyspnea, cough, chills, fever, myalgias
re-exposed individual presents with breathlessness, dyspnea with exertion, and cough |
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differentiate simple coal worker's pneumoconiosis and progressive massive fibrosis
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simple CWP - patients presents with cough, black sputum, but no significant dysfunction
PMF - severe fibrosis with disabling respiratory symptoms and may eventually get pulmonary HTN and cor pulmonale |
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two examples of mineral dust exposure resulting in pneumoconiosis
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carbon dust
silica particles |
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pathology seen in CWP
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aggregates of coal macule with small focal lesions of macrophage accumulation with surrounding collagen fibrosis
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associated with a chest radiograph with dense pinpoint nodulation in the upper lobes
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chronic simple silicosis
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associated with chest radiograph with bilateral progressive mass opacification greater than 1 cm in the upper third of the lungs
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progressive massive fibrosis in silicosis
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diseases associated with patients in the insulation industry, shipyards, or construction
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asbestos-related diseases
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what are the 4 diseases associated with asbestos exposure
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1. benign pleural disease
2. asbestosis 3. lung cancer 4. mesothelioma |
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fibrohyaline plaques found on the parietal pleura, with no loss of lung function
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benign pleural disease
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fibrosing alveolitis involved in the base of the lungs with presence of numberous iron-staining bodies
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asbestosis
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increased risk of developing lung cancer if lifelong smoker with asbestos exposure
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70-fold risk increase
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differentiate malignant and benign mesothelioma
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benign - focal type that is unrelated to asbestos
malignant - diffuse type with 70% of the cases attributable to asbestos |
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multisystem disorder of unknown etiology characterized by presence of non-caseating epitheloid granulomas
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Sarcoidosis
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what cells are involved in the central compact zone of granuloma in sarcoidosis
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macrophages
epithelioid cells giant cells CD4+ lymphocytes |
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disease associated with the persistence of activated monocytes/macrophages and CD4+ lymphocytes in the alveolar interstitium
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sarcoidosis
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normal amount of alveolar macrophages and lymphocytes
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>85% alveolar macrophages
<15% lymphcotyes both are not activated |
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differentiate the amount of alveolar macrophages and lymphocytes in a person with sarcroidosis
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increased number of both with >15% being lymphocytes
both are activated decreased peripheral amount of CD4+ lymphocytes |
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why would a person with sarcoidosis look like they have AIDS
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decreased number of peripheral CD4+ lymphocytes
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Is elevated ACE a good diagnositc tool for sarcoidosis
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No, elevated in only 80% of patients and not specific for sarcoidosis
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etiology of sarcoidosis
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young, black, female,
involves lung in over 90% of patients up to 30% present with extrapulmonary disease hypercalcemia up to 10% die from their disease |
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in what patients can miliary TB occur
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more common in secondary TB
can occur in primary TB in children or immunosuppressed patients |
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how can transverse ulceration of intestinal TB occur
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from the patients swallowing own infected sputum after coughing it up into the mouth
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pulmonary sequestration
what is the result |
a lobe of lung supplied form the aorta instead of a branch of the pulmonary artery and is not connected to the bronchial tree
-results in frequent recurrent pneumonias |
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why does pulmonary hypertension develop in chronic bronchitis
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because mucous obstructs bronchi and the distal alveoli are not ventilated resulting in unoxygenated blood causing pulmonary arteriole spasm
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Goodpasture syndrome
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antibody directed against antigen in basement membrane of glomerulus and alveolus
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centrally located tumor with strong association with smoking and marked male predominance
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squamous cell carcinoma
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tumor recognized by formation of keratin
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squamous cell carcinoma
well differentiated carcinoma - formed pearls moderate to poorly differentiated - individual cell keratinization (majority) |
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peripherally located tumor with weak association with smoking, most common carcinoma in women, increasing in frequency
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adenocarcinoma
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carcinoembryonic antigen positive
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adenocarcinoma
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recognized by formation of glands and mucin production
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adenocarcinoma
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tumor with high association with smoking and is poorly differentiated squamous cell or adenocarcinoma
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large cell anaplastic carcinoma
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centrally located tumor with high association with smoking and a distinct cell type that arises from Kulchitsky cells
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small cell anaplastic carcinoma
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tumor with distinctive cytology with tightly packed, small nuclei with stippled chromatin and extensive crush artifact
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small cell anaplastic carcinoma
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associated with endocrine effects such as ACTH and ADH production
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small cell anaplastic carcinoma
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highly malignant tumor that is almost always disseminated at times of diagnosis
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small cell anaplastic carcinoma
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tumors that are variants of adenocarcinoma and arise from Clara cells
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bronchioalveolar carcinoma
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associated with coughing up copious amounts of mucous and may mimick pneumonia on CXR
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bronchioalveolar carcinoma
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most common site of hematogenous spread of metastatic primary lung cancers
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BLAB - brain, liver, adrenals, bone
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tumor of large bronchi that may protrude into the lumen, occurs in young to middle aged adults, no relationship to smoking, and arise from Kulchitsky cells
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carcinoid tumor
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most common tumor in the lung, well demarcated peripheral lung nodule
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hamartoma
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fibrochondrolipoma within the lung
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hamartoma
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commonly found in the larynx or trachea of children, may cause obstructive symptoms
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papilloma
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radioactive substances associated with lung cancer
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uranium
radon gas |
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10-30 year latent period between exposure and development of lung cancer
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asbestos exposure
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metals associated with lung cancer
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BANIC - beryllium, arsenic, nickel, iron, chromate
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centrally located tumors
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squamous cell carcinoma
small cell anaplastic carcinoma |
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peripherally located tumors
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adrenocarcinoma
large cell anaplastic carcinoma |
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diffusely located tumors
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bronchioalveolar carcinom
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most frequent cause of death in lung cancer
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pneumonia
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4 results from direct invasion of lung carcinoma
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1. malignant pleural effusion
2. superior vena cava syndrome 3. pancoast tumor 4. recurrent laryngeal nerve |
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associated with ipsilateral ptisosi, miosis, and anhidrosis or atrophy of hand muscles
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pancoast tumor
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small cell or squamous cell carcinoma of the right mainstem bronchus resulting in what
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superior vena cava syndrome
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endocrine dysfunction resulting from paraneoplastic syndrome
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small cell - ACTH and ADH
squamous - parathormone 5-OH tryptamine (serotonin) - carcinoid |
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carcinoma associated with Eaton-Lambert syndrome and peripheral neuropathy and myopathy
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small cell carcinoma
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solitary fibrous tumor
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benign
purely fibrous localized proliferation of the pleura well demarcated not associated with asbestos exposure |
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diffuse mesothelioma
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strong association with asbestos exposure
diffuse thickening of the pleura highly malignant no effective treatment |
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two classical patterns of involvement by pneumonia
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lobar pneumonia
bronchopneumonia |
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organism rapidly spreads throughout the entire lobe or segment and generate an exudative response that fills up alveoli
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lobar pneumonia
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classical organisms associated with lobar pneumonia
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strep pneumo
klebsiella pneumo |
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characteristics of bronchopemonia
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bronchiolitis
more damage, necrosis, and scarring more common than lobar pattern - especially in hospitalized patients |
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associated with lobar pneumonia and occurs when defense barriers are breached such as following viral infection, aspiration, alcohol
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strep pneumo
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capsule prevents phagocytosis because of inhibition of production of C3b by alternative pathway
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strep pneumo
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associated with pleuritis, pleural effusion, pyothorax, and empytema
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strep pneumo
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major cause of fatal pneumonia and meningitis in children
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hemophilus influenzae
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associated with pneumonia, otitis media, and second most common bacterial cause of acut exacerbation of COPD
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M.catarrhalis
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most commonly occurs in infants less than 2 years
causes bronchial ulceration and abscesses common problem in cystic fibrosis and nosocomial infection of debeilitated |
staph aureus
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associated with pneumatoceles that can break and drain into the airway causing cavitation, pleural effusion, and abscesses
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staph aureus
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nosocomial infection in already ill patient, especially if on ventilator
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klebsiealla pneumoniae
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associated with lobar pattern, mucoid secretions, mostly macrophages, bronchopleural fistula, micro-abscess with cavitation
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klebsiella pneumoniae
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associated with immunosuppressive therapies, liberal use of broad-spectrum antibiotics, and AIDS
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opportunistic pneumonias caused by gram-negative bacteria
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bronchopneumonia in otherwise normal patients having GI or urological surgery
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E. coli
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most often seen in burns, cystic fibrosis, and immunocompromised patients, often superinfections occur
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pseudomonas aeruginosa
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acquired directly from water/aerosols, necrosis may be prominent which often leads to fibrosis of affected areas of lung
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legionella pneumophil
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extensive infiltration of alveolar walls by plasma cells and lymphocytes
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pneumocystic jeroveci
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debilitated patient with bronchopneumonia with only few neutrophils but much fibrin and edema fluid
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strep pyogenes
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classical cause of streptococcal pneumonia in newborn
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strep agalactiae
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symptoms similar to respiratory distress of newborn except newborn is often full term
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strep agalactiae
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commensural of oral cavity which are aspirated in debilitated patients
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streptococci, fusobacteria, bacteroides
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bilateral, necrotizing bronchopneumonia with abscesses
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anaerobic organisms
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most common malignancy in the lung
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metastatic cancer from elsewhere (other lung, colon, breast, prostate). features s number of small tumor nodules of about the same size scattered throughout the lungs
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associated with bubbly pink exudate in the alveoli and silver stain showing fungi
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pneumocystis jeroveci
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