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97 Cards in this Set
- Front
- Back
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composition of surfactant
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dipalmitoyl phosphatidocholine
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what in amniotic fluid is indicitive of fetal lung maturaty
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lecithin to sphingomyelin ration of >2
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aspiration of something while standing goes where
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lower portion of R inferior lobe
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aspiration of something while supine goes where
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superior portion of R inferior lobe
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aspiration of something while laying on R side goes where
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R middle lobe or posterior segment of R upper lobe
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relation of pulm artery in relation to each lung hilus
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Right anterior, Left superior
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muscles of forced inspiration (3)
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external intercostals, scalenes, SCMs
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muscles of forced expiration (5)
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rectus abdominus, internal and external obliques, transversus abdominus, internal intercostals
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residual volume
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air in lung after max expiration, cannot be measured on spirometry
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expiratory reserve volume
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air that can still be breathed out after normal expiration
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inspiratory reserve volume
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air in excess of tidal volume that moves into lung on max inspiration
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vital capacity
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tidal volume plus both the inspiratory and expiratory reserve volumes
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functional residual capacity
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volume in lungs after normal expiration (= to RV plus ERV)
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inspiratory capacity
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IRV plus tidal volume
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total lung capacity
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IRV + TV + ERV + RV
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where is the most functional dead space in a healthy lung
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apex
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which form of Hb dominates in the periphery
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T (taut) form, allows for release of O2 and binding of CO2
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where on Hb does CO2 bind
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binds to AA's on the globin chains, NOT to heme
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which form of Fe in heme binds O2
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reduced state, Fe+2
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O2 content of blood
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content = (1.34 x Hb x %sat) + dissolved O2
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alveolar gas equation
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PAO2 = PIO2 - (PACO2/R) R=resp quotient = CO2 produced/O2 consumed usually approx: 150-PACO2/.8
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A-a gradient
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PAO2-PaO2, usually 10-15
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hypoxemia vs hypoxia
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hypoxemia is decr PaO2 and hypoxia is decr delivery of O2 to tissues
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how is CO2 transported from tissues to lungs and how do you eventually breath it off
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CO2 formed in the tissues diffuses into RBCs from venous blood, in the RBC it combines with H2O to form H2CO3 (carbonic anhydrase) which dissociates to H+ and HCO3; HCO3- leaves the RBC in exchange for Cl- and is transported to the lungs; H+ in the RBC is buffered by deoxy-Hb; in the lungs, HCO3 enters the RBC in exchange for Cl-, recombines with H+ (which is released as Hb binds O2) to from H2CO3 which decomposes to CO2 which can diffuse out of the cell
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PaO2, O2 sat and O2 content in person in chronic altitude
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decr PaO2, decr O2 sat but normal O2 content due to incr Hb
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up to what point in the respiratory tree does pseudostratified ciliated columnar extend and goblet cells
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columnar cells: up to the respiratory bronchioles; goblet cells present up to terminal bronchioles
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respiratory zone
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respiratory bronchioles, alveolar ducts, aveoli
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clara cells
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nonciliated, contain secretory granules, inhibit PMN recruitment
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lamellar bodies
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found in type II, contain surfactant
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blood supply to nasal cavity
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sphenopalatine artery, branch of maxillary
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bronchopulmonary segement
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tertiary bronchus and 2 arteries in the center (bronchial and pulmonary), veins and lymph drain around the borders
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why do aspirated things go to right lung
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R main stem bronchus is more upright and wider
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at what levels do the IVC, esophagus, vagus, aorta, thoracic duct and azygois vein penetrate the diaphragm
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IVC: 8; esophagus and vagus: 10; aorta, thoracic duct, azygous vein: T12
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physiologic dead space calc
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VD=VT x (PaCO2-PeCO2)/PaCO2; VT is tidal vol, PeCO2 is expired air PCO2
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why does fetal Hb bind O2 more tightly
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has a decr affinity for 2,3-BPG
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met-Hb
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has Fe+3 so it doesn't bind O2 well; causes a decr in O2 saturation but NO CHANGE in PaO2, has incr affinity for CN-; treatment is methylene blue; L shifts O2-Hb curve
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treatment of CN- poisoning
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give nitrites to oxidize Hb to metHb which binds CN-, use thiosulfate to bind this which forms thiocyanate which is renally excreted
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CO poisoning
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CO binds with 200X greater affinity to Hb, decr O2 saturation but PaO2 is normal, red pigment produced masks cyanosis, inhibits the ETC, HA usually first symptoms, L shift of curve, give 100% O2
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in normal health, which gases are perfusion limited
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O2, CO2, N2O; means that gas equilibrates early along the length of the CAP
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which gases are diffusion limited
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CO, (also O2 in emphysema or fibrosis); means that gas does not equilibrate by the time blood reachs the end of the CAP
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normal pulm artery pressure, pulm HTN
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normal is 10-14, HTN is >25
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primary pulmonary HTN
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due to inactivating mutation of BMPR2 gene, leads to idiopathic pulmonary endothelial dysfunction with medial hypertrophy, intimal fibrosis, W>M, poor prognosis
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pulmonary vasc resistence equation
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PVR = [P(pulm artery) - P(LA)]/CO
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what happens to PaO2 with chronic lung dz
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PaO2 decr, as you become hypoxic, blood in your lungs is shunted to areas with better ventilation, but this shunt can lead to decr O2 extraction from the inhaled air and hence a decr in PaO2 occurs
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tissues most affected by O2 eprivation
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neurons, watershed areas, subendocardium, renal cortex and medulla (esp straight segment of PT and Na/2Cl/K channel in the thick ascending loop)
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3 general causes of incr A-a gradient
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V/Q mismatch, diffusion limitation (fibrosis), R to L shunt
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pt has low PaO2, you give 100% O2, it doesn't improve
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airway obstructing leading to a shunt (ventilation defect); most common in kids is hyaline memb, adults is ARDS
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pt has low PaO2, you give O2, it improves some
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perfusion defect (ex: pulm emboli), incr in dead space
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complicance vs. elasticity
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complicance refers to inspiration, elasticity refers to expiration (elastic fibers apply radial traction to keep open aveoli)
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RV, FVC, FEV1, FVC and FEV1/FVC in obstructive lung dz
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incr RV, big decr FEV1, decr FVC, decr FEV1/FVC (hallmark), V/Q mistmatch
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Reid index
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gland depth/total thickness of bronchial wall; >50% in chronic bronchitis
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chronic bronchitis
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persistant cough for >3 consecutive months in >2 years, mucus hypersecretion in the large bronchioles, can have airway obstruction in smaller airways, assoc with smoking; early cyanosis/hypoxmia, late dyspnea
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emphysema
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incr lung compliance due to destrc of alveolar walls (and assoc BVs), have early dyspnea and hyperventilation so they maintain normal blood gases at first and thus have late onset cyanosis (eventually BVs are destroyed as well and decr in gas exchange occurs)
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CXR in emphysema
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hyperluscent lungs, long heart, low diaphragms
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centri vs. pan vs. paraseptal emphysema
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centriacinar: upper lobes, assoc with smoking, affects resp bronchioles but can eventaully extend distally to affect acini; panacinar: due to a-1 antitrypsin def, affects lower lobes, affects the respiratory bronchiole distal; paraseptal: assoc with bullae which can rupture and cause pneumothorax, usually in young males, not obstructive usually
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FVC, TLC, FEV1/FVC ratio in restrictive lung dz
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FVC and TLC are decr; while both FEV1 and FVC are decr, most of the FVC is exhaled in the first second so the ratio of FEV1/FVC is >80%
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hallmark of restrictive lung dz
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decr compliance (which then requires more work to breathe and hence patients have dyspnea)
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2 most common causes of restrictive lung dz
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pneumoconioses (coal miners, silicosis, absestosis) and sarcoidosis
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key perpetrator in pneumoconioses
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alveolar macrophage, as it ingests the particles it realeases mediators which cause lung injury and fibrosis
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Farmers and Silo fillers lung
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can be causes of obstructive lung disease; farmers is due to hypersensitivity to thermphilic actinomycetes; silo fillers is hypersensitivity to gas from fermentation
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at what time in fetal development is surfactant made abundantly by the type II pneumocytes
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after 35 weeks
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neonatal resp distress syndrome
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surfactant def causes atelectasis, also there is incr permeability which causes hyaline membrane; is a ventilation defect which leads to shunting (this also incr risk of patent PDA)
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baby with neonatal resp distress, give O2, what is side effect
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may develop retinal damage
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common causes of ARDS (7)
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trauma, burns, sepsis, shock, gastric aspiration, acute pancreatitis, amniotic fluid emboli
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what causes the damage in ARDS
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PMN substances which are toxic to alveolar walls, also ROS, activation of coag cascade; leads to alveolar damage which leads to incr permeability which leads to formation of intra-alveolar hyaline membrane
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treatment for sleep apnea
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1. weight loss 2. CPAP 3. surgery
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sleep changes in sleep apnea
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decr stage 1, delta and REM sleep
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ex of synergysm in lung pathology
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absestosis and smoking, incr risk of bronchogenic CA (not mesothelioma)
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location of lesions in absestosis and other pneumoconiosis
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absestosis: lower lobes; others affect upper lobes
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absestos exposure incr your risk for what
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1. bronchogenic CA 2. mesothelioma
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2 major causes of spontaneous pneumothorax
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secondary to trauma (scuba, other) or lung pathology (ex: ruptured sub-pleural bleb)
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what happens to the diaphragm on the side with a pneumothorax (non-tension)
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it rises up into the empty space
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tension pneumo
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ex: secondary to knife injury to lungs; causes a tear with a flap, as you inhale it opens and as you exhale it closes, continues to trap air and incr volume, pressure atelectasis pushes the trachea away from the lesion and depresses the disphragm
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most common met to lung
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breast
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SVC syndrome
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can occur with lung CA, esp small cell; CA knocks off SVC, causes back up into the venous system and dural sinuses, presents with blurry vision and HA; associated with mediastinal mass
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Pancoasts tumor
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CA that appears in the posterior apex of the lung, can affect the cervical symp plexus and causes Horners; can also hit brachial plexus; may present with shoulder pain; SCC most likely
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Horners
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ptosis, miosis, anhidrosis
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SCC of lung
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central mass, arising from bronchus, cavitates, assoc with smoking, can secrete PTHrp, 2nd most common
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adenoCA of lung
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coin like lesion in periphery, most common CA in non-smokers, has early mets (brain most common), may develop near old scar; most common; can be mucin producing
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small cell CA
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undifferentiated, presents centrally, early mets, ectopic ADH or ACTH, Lambert Eaton, assoc with smoking; neoplasm of neuroendocrine (small blue cells), highly malignant
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which lung CA assoc with Lambert Eaton
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small cell CA; blocks Ca channels in presynaptic terminals, preventing ACh release
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4 causes of bronchopneumonia and description
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S. aureus, H. flu, Klebsiella, S. pyogenes; acute inflammatory infiltrates from bronchioles into adjacent alveoli; patchy distribution involving >1 lobe
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pain from mediastinal and diaphragmatic parietal pleura carried by what
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phrenic
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J-receptors
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located in the alveolar walls, close to CAPs, engorgement of the CAPs (like in left heart failure) stimualtes the J receptors which cause rapid shallow breathing
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P50
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PP gas required to achieve 50% saturation
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findings in pulmonary HTN
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SM hyperplasia/hypertrophy, atherosclerosis of main elastic pulm arteries, incr P2 heart sound; leads to severe resp distress, RVH and death
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3 things on which PaO2 is depenent on
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%O2 in inpired air, atmospheric pressure and normal O2 exchange
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sign of lung maturity in fetus
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lectithin (phosphatidylcholine) to sphingomyelin (phospholipid) ratio > 2; test is to mix a sample of amniotic fluid with alcohol and see if foam generates
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X-ray of ARDS
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fluffy infiltrates
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minute ventilation vs. alveolar ventilation
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minute (includes dead space): TV X breaths.min; alveolar: (TV-dead space) X breaths per min
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most common lesion associated with absestos exposure
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benign fibrous plaque on pelura, not mesothelioma precursor
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where in the lung do pneumoconeosis vs. aspestos affect
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pneumo: upper lungs; aspestos: lower
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where does lung CA often met to
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adrenals; can cause Addisons
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large cell CA
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peripheral lesion, highly anaplastic and undifferentiated, early mets, invasion of pleura common
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4 causes of atypical pneumonia and treatement choices
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mycoplasma, legionella, chlamydia, viruses (RSV, adenovirus); treat bacterial causes with macrolide or tetracylcine
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causes of lung abscesses
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often due to S. aureus or anaerobes; due to bronchial obstruction or aspiration
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treatment for liver abscess
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clindamycin, will also cover anaerobics
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