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Step 1. 1.3.13

Respiratory I

QuestionAnswer
What are the conducting zones of the respiratory system? nose, pharynx, trachea, bronchi, bronchioles, terminal bronchioles
In what part of the conducting zones is cartilage found? only in trachea and bronchi
What is the function of the conducting zone? brings air in and out, warms, humidifies and filters. anatomic dead space. alls contain SMM
What does the respiratory zone of the respiratory sx consist of? What is its fx? respiratory bronchioles, alveolar ducts and alveoli.participates in gas exchange
Where are pseudostratefied ciliated columnar cells and goblet cells found in the respiratory system? pseudostratefied ciliated columnar ce;lls extend to the respiratory bronchioles( macrophages clear debris in alveoli). goblet cells extend only to bronchi
What is the function of ciliated cells in the respiratory system? mucus secretions swept out of lungs toward mouth
What are Type I pneumocytes? Where are they found? 97% of alveolar surface. line the alveolic. squamous with very thing cytoplasm for optimal gas exchange
What are type II pneumocytes? Where are they found? secrete pulmonary surfactant (dipalmitoyl phosphatidylcholine) which decr alveolar surface tension. cuboidal and clustered. also serve as precursors to type I and type II cells.
What type of pneumocytes proliferate in lung damage? type II
What are Clara cells? nonciliated; columnar with secretory granules. secrete component of surfactant. degrade toxins, act as reserve cells
What ratio indicates fetal lung maturity? lecithin to sphingomyelin ration of >2.0 in amniotic fluid
What are the lobular structures of the right and left lung? right has 4 lobes, left has 2 + lingula which is a homologue of the right middle lobe
What is the more common lung site for an inhaled foreign body? Why? Right because it has a wider right main stem bronchus and more vertical
What is the relation of the pulmonary artery to the bronchus at the hilum in the right vs left lungs? RALS: Right anterior, Left: PA is superior superior
Where would you expect to find an aspirated peanut while upright vs while supine? aspirate upright: lower portion of right inferior lobe. aspirate supine: superior portion of right inferior lobe
Where does IVC perforate the diaphragm? T8
Where does the esophagus and vagus nerve perforate the diaphragm? T10
Where does the aorta, thoracic duct, and azygous vein penetrate? T12
What nerve roots and nerve innervate the diaphragm? C3,4,5 (phrenic n.). C3,4,5 keep diaphragm alive
Where might diaphragmatic pain be referred to? shoulder
What is a mnemonic for the levels of penetration of structures going thru the diaphragm? I (IVC) ate (8) ten (10) eggs ( esophagus) at (aorta) 12.
What are the muscles used in inspiration and expiration during quiet breathing? inspiration: diaphragm, expiration is passive
What are the accessory muscles of inspiration used in exercise? external intercostals, Scalenes, sternomastoids
What are the accessory muscles of expiration used during exercise? rectus abdominus, internal and external obliques, transversus abdominus, internal intercostals
What makes surfactant and what is its role? produced by type II pneumocytes: decr alveolar surface tension, incr compliance, decr work of inspiration
What is the chemical composition of surfact? Under what condition is it deficient? made of dipalmitoyl phosphatidylcholine (lecithin) is defienct in neonatal RDS
How do you calculate respiratory collapsing pressure? P=2(surface tension)/radius
What is the tendency to happen in the lungs on expiration? Why? tendency to collapse due to decr radius according to Laplace's law
What are 5 major lung products? 1. surfactant 2. prostaglandins 3. histamine 4. angiotensin converting enzyme 5. kallikrein
What is the role of histmine produced by the lungs? incr bronchoconstriction
What is the role of ACE produced by the lung? converts angiotensin I to II, inactivates bradykinin( ACE I incr bradykinin and cause cough and angioedema)
What is the role of the kallikrein produced by the lung? activates bradykinin
What is residual volume (RV)? air in lung after maximal expiratioonm. cant be measured on spirometry
Vital capacity includes all volumes but what? not the residual volume
What is the expiratory reserve volume (ERV)? air that can still be breathed out after normal expiration
What is a tidal volume (TV)? What is normal? air that moves into lung with each quiet respiration. typically about 500mL
What is an inspiratory reserve volume (IRV)? air in excess of tidal volume that moves into lung on maximum inspiration
How is vital capacity calculated? TV+IRV+ERV
What is functional residual capacity and how is it calculated (FRC)? volume in lungs after normal inspiration. RV+ERV
How do you calc ulate inspiratory capacity? IRV + TV
How do you calculate totoal lung capacity? TLC= IRV + TV +ERV+RV
How do you calculate physiological dead space? Vd=Vt x [(PaCO2-PeCO2)/ PaCO2)]. (Taco, Paco, Peco, Paco) (Vt is tidal volume, PaCO2= arterial PCO2, PeCO2= expired air PCO2)
What is the definition of physiological deadspace? = anatomical deadspace of the conducting airways + the functional dead space of the alveoli. volume of inspired air not taking part in gas exchange
What physiological space in a healthy lung is the largest contributor to physilogical dead space? apex of healthy lung
What is the natural tendency of the lungs and chest wall? lungs want to collapse, chest wants to spring out
How is the inward and outward pull balanced at FRC? What is the system P? inward pull of lungs is balanced by outward pull of the cheat wall and system pressure is atm
What determines the combined volume of chest wall and lungs? their elastic properties
What are the airway and alveolar pressures at FRC? What is the intrapleural pressure? airway and alveoli=0. intrapleural= negative (prevents a pneumothorax)
What is compliance in the lungs? When is it decr? change in lung volume for a given change in P. decr in pulmonary fibrosis, insufficient surfactant, and pulmonary edema.
What is the composition of normal Hb? 4 polypeptide units, 2 alpha and 2 beta
What are the 2 forms of Hb? 1. T(taut)= low O2 affinity 2. R(relaxed) form which binds O2 w high affinity
What are the cooperativity and allostery properties of Hb? positive cooperativety and negative allostery (accounts for simgloid shaped O2 dissociation curve), unlike myoglobin
What types of things favor the T form of Hb? incr Cl-, H+, Co2, 2,3-BPG and temp favor T form over R ( shifts dissociation curve to the right, leading to incr O2 unloading)
What is the composition of fetal Hb and how does it compare to adult? 2 alpha and 2 gamma subunits. lower affinity for 2,3BPG than adult (HbA) so higher O2 affinity
What is the general effect of Hb modifications? lead to tissue hypoxia and decr O2 content
What is methemaglobin? oxidized form of hemoglobin (ferric, Fe3+, that does not bind O2 as readily, but has incr affinity for CN-
What state is iron in in normal Hb? 2+
How do you tx methemoglobinemia? methylene blue
How do you treat cyanide poisoning? What is the mech? use nitrites to oxidize Hb to methemoglobin which binds CN allowing cytochrome oxidase to function. use thiosulfate to bind this cyanide forming thiocyanate which is renall secreted
What is carboxyhemoglobin? form oh Hb bound to CO in place of O2, causes decr in O2 binding capacity with left shift in dissociation curve. decr O2 unloading in tissue
Which has a greater affitinity for Hb, O2 or CO? CO
Why is the dissociation curve sigmoidal for Hb? Why isnt it for myoglobin? due to positive cooperativity (each O2 bound makes the next easier). Myoglobin doesnt have it
What is the implication if the Hb dissociation curve shifts to the right? decr affinity of Hb for O2. facilitates unloading to tissue
What is the effect of an incr or decr in all factors except pH on the Hb dissociation curve? incr= shift of curve to the right. decr = shift of curve to left
Where is the curve of HbF compared to HbA? fetal Hb has higher affinity than adult so it is left of the left
What factors cause a RIGHT shift in the Hb dissociation curve? Mnemonic? CBEAT: CO2, BPG (2,3 BPG), exercise, acid/altitude, Temp
What happens to Hb saturatuon at any given O2 in the presence of CO? incr due to positive cooperativity
What are the normal properties of the pulmonary circulation? How do PO2 and PCO2 affect it? normally low resistance and high compliance. PO2 and PCO2 have opposite effects on pulmonary and systemic circulations.
How does the body react to a decr in PAO2? causes hypoxic vasoconstriction that shifts blood away from a poorly ventilated area of the lung to well ventilated regions
How are O2, CO2, and N2) limited normally? What does that mean? perfusion limited. gas equilibrates along whole length of capullary
What is the only way to incr diffusion of a perfusion limited gas? only if blood flow incr
How is O2 in emphysema or fibrosis or CO limited? What does that mean? diffusion limited. gas does not equilibrate by the time blood reaches the end of the capillary.
Wnder what 2 condtions is O2 diffusion limited? emphysema or fibrosis
What are the major conseqences of pulmonary HTN? cor pulmonale and RV failure (JVD, edema, hepatomegaly)
How do you calculate diffusion of a gas? Vgas= A/T x Dk(P1-P2) where A= area, T= thickness and Dk(P1-P2) approximately = the diff in partial pressures.
What factors in the diffusion equation are affected by emphysema vs pulmonary fibrosis? A is decr in emphysema. T is incr in pulmonary fibrosis
What is normal pulmonary artery P? How is pulmonary HTN defined? norm: 10-14 mmHg, PulmHTN: >25mmHg or >35mmHg during exercise
What are the lung results of pulmonary HTN? atherosclerosis, medial hypertrophy, intimal fibrosis of pulmonary arteries
What might cause a primary pulmHTN? due to inactivating of BMPR2 gene (normally functions to inhibit vascular SMM proliferation). poor prognosis
What are some major causes of secondary pulmHTN? COPD, mitral stenosis, recurrent thromboemboli, AID, L to R shunt, sleep apnea or living at high altitdue
How can COPD cause pulmHTN? destruction of lung parenchyma
How can mitral stenosis cause pulmHTN? incr resistance--> incr pressure
How does recurrent thrombosis cause pulmHTN? decr crossectional area of pulmonary vascular bed
How does an AID lead to pulmHTN? systemic sclerosis. or inflammation-->intimal fibrosis-->medial hypertrophy
How can a L to R shunt cause pulmHTN? incr shear stress= endothelial injury
How might sleep apnea or living at high altitiude cause pulmHTN? hypoxic vasoconstriction
What is the natural course of pulmHTN? severe respiratory distress-->cyanosis and RVH---> death from decompensation or cor pulmonale
How do you calculate pulmonary vascular resistance? PVR= P pulm a- P L atrium/cardiac output
How do you calculate resistancE? R=8(nu)l/pi r^4: where nu = viscosity of blood, l is the vessel length, and r is the vessel radius
How do you calculate the O2 content of the blood? O2 content= (O2 binding capacity x %saturation) + dissolved O2
How much O2 can 1 g of Hb bind? What is the normal amount of Hb in the blood? 1 g Hb can bind 1.34 mL O2. normal Hb amount is 15 g/ dL
What Hb levels are seen in cyanosis? if deox Hb > 5 g/dL
What is the normal O2 binding capacity? 20.1mL O2/dL
What is the relation of O2 content, saturation and PaO2 as Hb decr? O2 content decr as Hb does, but saturation and Pa O2 do not
What happens to Pa O2 in chronic lung disease? Why? decr because of physiological shunt decr the O2 extraction ratio
What is the effect of exercise on venous PO2? decr
How do you calculat oxygen delievery to tissues? COxoxygen content of blood
What is the alveolar gas equations? PA02=PIO2'PaCO2/R. Normally approximated to: PAO2= 150-PaCO2/0.8. where PAO2= alveolar, PIO2=inspired, PaCO2=arterial R= respiratory quotient (Co2pproduced/ O2 consumed)
How do you calculate the A-a gradient? What is normal? PAO2-PaO2. normally = 10 - 15 mm Hg
When might the A-a gradient be incr? hypoemia, shunting, V/Q mismatch, fibrosis (impairs diffusion)
What is the A-a gradient in high altitude or hypoventilation? normal
What hypoxia and ischemia is seen at high altitude? decr CO and impeded arterial flow
What hypoxia and ischemia is seen in hypoventialation? see hypoxemia and reduced venous drainage
What is the A-a gradient seen in a V/Q mismathc, diffusion limitation, R to L shunt? incr A-a gradient
What might cause a V/Q mismatch? anemia
What might cause a diffusion limitation A-a gradient incr? cyanide poisoning
What might cause a R to L shunt incr A-a gradient? CO poisoning
What is ideal V/Q ratio? 1, ideally ventillation and perfusion are exactly linked
What is V/Q at the lung apexes vs the base of the lung? Apex= 3 ( wasted ventilation). Base= 0.6 (wasted perfusion)
Where are ventilation and perfusion the highest? at base of lung
What happens to V/Q in exercise? How? incr CO causes vasodilation of apical capillaries resulting in a V/q that approaches 1
What types of organisms flourish in the apex of the lungs? TB, those that thrive in O2
What does a V/Q approaching 0 mean? What does 100% O2 do? airway obstruction ( shunt). in a shunt 100% O2 wont improve PO2
What does a V/w appraoching infinity mean? What does 100% O2 do? blood flow obstruction (physiologic dead space) assuming <100% dead space, 100% O2 improves PO2
What is the properties of PA, Pa, and Pv in zone 1 ,2 , 3 of lungs? Zone 1: PA>Pa>Pv. Zone 2: Pa>PA>Pv. Zone 3: Pa>Pv>PA
What 3 forms is CO2 transported? 1. HCO3 (90%) 2. bound to Hb at N terminus of globulin (NOT heme) as carbaminohemoglobulin. CO2 bindinf favors the taut form. 3 dissolved CO2
What is the Haldane effect? in lungs, oxygenation of Hb promotes dissociation of H+---> shift equilibrium toward CO2 formation. so CO2 is release from RBCs
What happens to CO2 binding in the periphery? incr H+ from tissue metabolism shifts equilibrium to the right, unloading O2 (Bohr effect). the majority is carried as bicarbonate in the blood
How is CO2 transported as HCO3? CO2 from peripheral tissue enters the RBC converted by carbonic anhydrase to HCO3 which is exchange extracellularly for Cl-
How does high altitude effect ventilation? acute incr in ventialation, decr PO@, PCO2, chronic incr in ventialtion
What happens to erythropoetin in high altitude? incr in hematocrit and hemoglobin (chronic hypoxia)
What happens to 2,3BPG at high altitude? Why? incr. binds to Hb so it releases more O2
What cellular changes are seen at high altitude? incr mitochondria
What happens renally at high altitude? incr excretion of HCO3 to compensate for resp alkalosis. can augment with acetazolamide
What happens to the RH at high altitude? chronic hypoxic pulmonary vasoconstriction results in RVH
What are 7 major body responses to exercise? 1. incr CO2 production 2. incr O2 consumption 3. incr vent rate to meet demad 4. V/Q ratio from apex to base more uniform 5. incr pulmonary blood flow due to incr cardiac output 6. decr pH during strenuous exercise (lactic acidosis) 7. incr venous CO2
What happens to PaO2 and PaCO2 in exercise? no change in PaO2 or PaCO2, but incr in venous CO2 content
What are 6 types of emboli? FATBAT: Fat, air, thrombus, bacteria, amniotic fluid, tumor.
What might cause a fat embolus? bone fractures or liposuction
What can amniotic fluid emboli cause? DIC esp post partum
What are the sx of pulmonary embolism? CP, tachypnea, dyspnea
Where do most pulmonary emboli arise from? deep leg veins
What is the imaging test of choice for a PE? helical CT
What are the 3 major predisposing factors for deep venous thrombosis? (Virchow's triad) 1. stasis 2. hypercoagulability ( defect in cascade. 3. endothelial damage (exposed collagen triggers clotting cascade)
What is Homans' sign? dorsiflexion of foot causes a tender calf muscle. could be sign of DVT.
How do you prevent/tx DVT? heparin
What is obstructive lung disease (COPD)? What might be seen in lung volumes? obstuction of airflow results in air trapping in lungs. airways close prematurely at high lung volumes causing incr RV and decr FVC.
What PFTs might be seen in COPD? very decr FEV1, decr FVC leading to decr FEV1/FVC ration which is the hallmark. also see V/Q mismatch
What is the pathology of chronic bronchitis COPD? hypertrophy of mucus secreting glands in the bronchioles
What is the Reid index? gland depth/total thcikness of the bronchiole wall. in COPD. Reid index >50%
What are the sx and findings of chronic bronchitis? productive cough for > 3 consecutive months in >2 years. disease of small airways. Findings: wheezing, crackles, cyanosis (early onset due to shunting). late onset dyspnea. "blue bloaters"
What pathology is seen in emphysema "pink puffers" barrel chest"? enlargement of air spaces and decr recoil resulting from destruction of the alveolar wall. incr compliance
What enzyme has incr activity in emphysema? elastase
What happens to compliance in emphysema? incr due to loss of elastic fibers.
How does a person with emphysema breath out? Why? exhalation through pursed lips to incr airway pressure and prevent airway collapse during respiration
What is the pathology of asthma? bronchial hyperresponsiveness causes reversible bronchoconstriction. SMM hypertrophy and Curschmann's spirals (shed epithelium from mucous plugs)
What can trigger asthma? viral URIs, allergens, stress
How do you test for asthma? methacholine challenge test
What are the key findings in asthma? cough, wheezing, tachypnea, dyspnea, hypoxemia, decr I/E ration, pulsus paradoxus, mucus plugging
What is seen in pathology of bronchiectasis? chronic necrotizing infection of bronchi-->permanently dilated airways, purulent sputum, recurrent infection, hemoptysis
What are some key associations of bronchiectasis? What can it lead to? assoc: bronchial obstruction, poor ciliary motility (smoking), Kartagener's syndrome. can lead to aspergillosis
What happens to lung volumes and PFTs in restrictive lung disease? decr FVC and TLc. PFTs: FEV1/FVC >80%
What are 2 types of poor breathing mechanics (peripheral hypoventilation) leading to restrictive lung disease? 1. poor muscular effort ( polio, myasthenia gravis) 2. poor structural appratus ( scoliosis, morbid obesity)
How do interstital lung disease cause restrictive lung disease? decr the diffusing capacity
Where is the disease in neonatal respiratory distress syndrome? disease of the hyaline membranes
What are 3 types of pneumoconioses? coal miner's, silicosis, abestosis
What are some key findings in sarcoidosis? bilateral hilar lymphadenopathy, noncaseating granulomas, incr ACE and Ca++
What happens in idopathic pulmonary fibrosis? repeated cycles of lung injury and wound healing with incr collagen
What drugs might cause restrictive lung disease? bleomycin, busulfan, amiodarone
What is seen in Coal miner's pneumoconioses? What part of the lung does it affect? associated with coal mines. can result in cor pulmonale, Caplan's syndrome ( RA involvement). affects upper lobes
What types of work are associated with sillicosis? foundries, sandblasting, mines
What is the pahogensis of silicosis? macrophages respond to silica and release fibrogenic factors leading to fibrosis. silica might disrupt and impair macrophages or phagolysossomes, incr susceptability to TB
What part of the lungs does silicosis affect and what key feature is seen at hilar LN? affects upper lobes, see "eggshell" calcification of hilar LN
What types of work is abestosis associated with? shipbuilding, roofing, plumbing
What is seen in abestosis and what does it incr the risk of? see "ivory white" calcified pleural plaques, associated with incr risk of bronchogenic carcinoma and mesothelioma
What part of the lungs does abestosis affect? lower lobes
What are abestosis bodies? golden brown fusiform rods resembling dumbelss. located inside macrophages
What is the pathophysiology of neonatal distress styndrome? surfactant deficiency leading to incr surface tension, resulting in alveolar collapse. Surfactant made after 35w gestation by type II pneumocytes.
What is seen in the lecithin to sphingomyelin ratipo in neonatal respiratory distress syndrome? < 1.5 in neonatal respiratory distress syndrome
What circulatory problem can neonatal respiratory distress syndrome cause? peristently low O2 can lead to PDA
What might heppen if a baby with NRDS was given supplemental O2? could cause retinopathy of prematurity
What is the major component of surfactant? dipalmitoyl phosphatidylcholine
What are the major RF for neonatal respiratory distress syndrome? prematurity, maternal DM (due to elevated insulin), C section (decr release of fetal glucocorticoids)
What is the tx for neonatal respiratory distress syndrome? maternal steroid before birth, artificial surfactant for infant, thyroxine
What are some causes of acute respiratory distress syndrome (ARDS)? trauma, sepsis, shock, gastric aspiration, uremia, acute pancreatitis, or amniotic fluid embolism
What is the mech of acute respiratory distress syndrome (ARDS)? diffuse alveolar damage-->incr in alveolar capillary permeability--> protein leakage into alveolar which leads to hyaline membrane formation
What cuases the initial damage of acute respiratory distress syndrome (ARDS)? due to release of neutrophilic substances toxic to the alveolar wall, activation of the coagulation cascade, and oxygen drived free radicals
What is FEV1/FVC normally, in obstructive lung diease and in restrictive? norm= 80%, < 80% in obstructive lung disease. in both restr and obstr, FEV1 and FVC are reduced but FEV1 is much more reduced in obstructive resultign in the decr ratio
What happens to TLC in restrictive lung disease? decr
What is the difference in lung volumes obstructive vs restrictive? obstructive> normal (incr TLC, FRC, RV) > restrictive.
What is sleep apnea? person stops breathing for 10 seconds while sleeping
What is the difference b/w central sleep apnea vs obstructive sleep apnea? central= no effort, obstructive= respiratory effort against obstruction
What are some associations of sleep apnea? obesity, loud snoring, systemi pulmHTN, arryhtmias, and sudden death. individulas migh be chronically tired.
What is the effect of sleep apnea on EPO? apnea-->hypoxia-->incr EPO--> incr eryhtrocytosis
What breath sounds, resonance, fremitus, and tracheal deviation might be seen in a bronchial obstruction? Breath sounds: absent or decr over affected area, decr resonance, decr fremitus, tracheal deviation toward side of lesion
What breath sounds, resonance, fremitus might be heard in a pleural effusion? decr breath sounds over effusion, dullness on resonance, decr fremitus
What breath sounds, resonance, fremitus in a lobar pneumonia? may have bronchial breath sounds over lesion, dullness on resonance, incr fremitus
What breath sounds, resonance, fremitus, and tracheal deviation might be seen in a tension pneumothorax? decr breaht sounds, hyperresonant, absent fremitus, deviation is away from the side of the lesion
What breath sounds, resonance, fremitus, and tracheal deviation might be seen in a spontaneous pneumothorax? decr breath sounds, hyperrresonant, decr fremitus, tracheal deviation is toward the side of the lesion
What is the leading cause of cancer death? lung cancer
What is the presentation of lung cancer? cough, hemoptysis, bronchial obstruction, wheezing, pneumonic coin lesion on CXR or noncalcified nodule on CT
What is the most common cause of lung cancer? metastases from breast, colon, prostate, bladder
Where does primary lung cancer metastasize to? adrenals, brain (epilepsy), bone (pathological fracture), liver (jaundice, hepatomegaly)
What is a mnemonic for the major complications of lung cancer? SPHERE: SVC syndrome, Pancoast tumor, Horner's syndrome, Endocrine (paraneoplastic), recurrent laryngeal sx (hoarseness), Effusions (pleural or pericardial)
What is the location and histology of small cell (oat cell) carcinoma of the lung? What is its origin? central, enoplasm of neuroendocrine Kulchitsky cells--->small and dark blue
What are the general characteristics of small cell carcinoma of the lung? undifferentiated and very aggressive. can produce ACTH or ADH. responsive to chemotherapy but inoperable
What AID might small cell lung carcinoma lead to? Lambert-Eaton syndrome (autoAb against Ca++ channels)
What is the location and origin or bronchial and bronchioloalveolar adenocarcinoma? peripheral. clara cells-->type II pneumocytes. see multiple densities on CXR
Where does a bronchial adenocarcinoma grow? develops in site of a previous pulmonary inflammation or injury( most common lung cancer in nonsmokers and females)
Where does a bronchoalveolar adenocarcinoma develop? What does it present like and what can it lead to? not associated with smoking, grows along airways and can present like pneumonia. can result in hypertropic osteoarthropathy
What is the location and histology of squamous cell carcinoma of the lung? central. keratin pearls and intracellular bridges
What are the general characterisitcs of squamous cells carcinoma of the lung? hilar mass, cavitation and clearly linked to smoking. parathyroid like activity--->PTHrP
What is the location and histology of large cell carcinoma of the lung? peripheral, pleomorphic giant cells with leukocyte fragments in the cytoplasm
What are the general characteristics of large cell carcinoma of the lung? highly anaplastic, poor prognosis, doesnt respond to chemotherapy and is removed surgically
What are the major complications produced by a carcinoid tumor of the lung? secretes serotonin and can cause carcinoid syndrome ( flushing, diarrhea, wheezing, salivation). can cause fibrous deposits on RH valves leading to tricuspid insufficiency, pulmonary stenosis, RHF
What is the location and histology of mesothelioma? pleural. see Psammoma bodies
What can mesothelioma cause? caused by abestosis. results in hemmorrhagic pleural effusions and pleural thickening
What is a Pancoast tumor? carcinoma in apex of lung that can affect cervical sympathetic plexus causing Horner's syndrome.
What is Horner's syndrome? ptosis, miosis, anhidrosis
What is superior vena cava syndrome? obstruction of SVC can impair blood drainage from the head (facial plethora), neck (JVD), and edema of upper extermities. usually caused by neoplasm or thromboses
How might SVC syndrome present and whan can it lead to? can rais ICP which presents with Ha and dizziness and can incr risk of aneurysm or rupture of cranial arteries
What organisms tend to cause a lobar pneumonia? pneumococcus, klebsiella
What is seen in a lobar pneumonia? intra-alveolar lavage--> consolidation, might invovle whole lung
What organisms tend to cause a bronchopneumonia? S. aureus, H. flu, Klebsiella, S. pyogenes
What is seen in a bronchopneumonia? acute inflammatory infiltrates from bronchioles into adjacent alveoli; patchy distrobution involving >1 lobes
What organisms tend to cause an interstitial (atypical) pneumonia? viruses (RSV, adenoviruses), mycoplasma, legionella, Chlamydia
What is seen in a interstitial pneumonia? diffuse patchy inflammation localized to interstital areas at alveolar walls. more than 1 lobe invovled. generally a more indolent course than bronchopneumonia
What is a lung abscess? localized collection of pus within parenchyma
What can cause a lung abscess? bronchial obstruction (canceR), aspiration of stomach ( alcoholics, epileptics)
What is a key CXR finding in a lung abscess? air-fluid levels
What organisms cause lung abscesses? often due to S aureus or anaerobes (bacteroides, fuscobacterium, peptostreptococcus)
What is hypersenstivity pneumonitis and who gets it? mixed type II/IV hypersensitivity rreaction to environmental Ag-->dyspnea, cough, CP, HA
Who gets hypersensitivity pneumonitis? farmers and those exposed to birds
What is seen in a transudative pleural effusion and what might cause it? decr protein content. due to CHF, nephrotic syndrome, or hepatic cirrhosis
What is seen in an exudative pleural effusion? What might cause it?> incr protein content, cloudy. due to malignancy, pneumonia, collagen vascular disease, trauma( occurs in states of incr vascular permeability). MUST be drained
What is senn in a lymphatic pleural effusion? aka chylothorax. milky appearing with incr triglycerides
What is the presentation of a pneumothorax? unilateral CP and dyspnea and unilateral cheast expansion, decr tactile fremitus, hyperesssonance, diminished breath sounds
What is seen in a spontaneous pneumothorax and who gets it? Where is the trachea? accumulation of air in the pleural space. occurs in tall, thin, young males b/c of rupture of apical blebs. trachea deviates to the affected side
What is seen in a tension pneumothorax? Where does the trachea deviate? usually occurs in setting of trauma or lung infection. air is capable of entering pleural space but not leaving. trachea deviates away from affected lung
What is the class/mech of diphenhydramine, dimenhydrinate, chlorpheniramine? 1st gen reversible inhibitors of H1, receptors
What are the clinical uses of diphenhydramine, dimenhydrinate, chlorpheniramine? allergy, motion sickness, sleep aid
What are the major SE of diphenhydramine, dimenhydrinate, chlorpheniramine? sedation, antimuscarinic, anti alpha adrenergic
What is the class/mech of loratidine, fexofenadine, desloratidine, cetirizine? 2nd gen reversible H1 histamine receptor blockers
What is the clinical use of loratidine, fexofenadine, desloratidine, cetirizine? allergy
What are the major SE of loratidine, fexofenadine, desloratidine, cetirizine? less sedation than first gen b/c decr CNS entry. can still have antimuscarinic, anti alpha adrenergic
What 2 pathways mediate bronchoconstriction? inflammatory proccesses and sympathetic tone
What is the class and mech of isoproterenol? non specific Beta agonist, relaxes bronchial SMM via beta 2
What is the major SE of isoproterenol? causes tachycardia via Beta 1 receptor
What is the class of albuterol and salmeterol? Beta 2 agonists
What is the clinical use of albuterol? for acute exacerbation of asthma
What is the clinical use of salmeterol? long acting agent for prophylaxis
What is a major SE of salmeterol? tremor, arrythmias
What is the class and mech of theophylline? methylxanthine which inhibits phosphodiesterase, decr cAMP hydrolysis. usuage limited due to limited theapeutic index
What are the major SE of theophylline? cardiotoxicity, neurotoxicity, metabolized by p-450. blocks actions of adenosine
What is the class and mech of ipratropium? competitive block of muscarinic receptors preventing bronchoconstriction. also used for COPD
What is the mech and use of cromolyn? prevents release of mediators from mast cells. effective only as prophylaxis agisnt asthma, not for acute attack. rarely has any SE
What is the class and mech of beclomethasone and predisone? corticosteroids which inhibit synth of cytokines. inactivate NF-kappaB which induces production of TNF-alpaha.
What is the use of beclomethasone, predisone? 1st line for chronic asthma
What is the mech/class of zileuton? anti leukotriene for athma. 5 lipoxygenase pathway inhibitor which blocks conversion of arachidonic acid to leukotrienes
What is the mech/class of zafirlukast, montelukast? when are they especially useful? block leukotriene receptors. esp good for aspirin induced asthma
What is an expectorant? removes excess sputum, does not surpress cough relfex
What is the class of guaifenesin? expectorant
What is the class n acetylcysteine? mucolytic- can loosen mucous plugs in Cf pt, also an antidote for acetaminophe OD
What is the mech and use of bosetan? used to tx pulmonary HTN. competitively antagonizes endothelin 1 receptors, decr pulmonary vascular resistance
What is the use and mech of dextromethrorphan? antitussive (antagonizes NDMA receptors), synthetic codeine analog. mild opioid effect if used in excess. mild abuse potential
What id given for an OD of dextromethorphan? naloxone
What is the mech of pseudoephedrine, phenylephrine? sypathomimetic alpha agonist npon persecription nasal decongestant
What is the clinical use of pseudoephedrine, phenylephrine? reduces hyperemia, edema, and nasal congestion. opens obstructed eustachian tubes. pseudoephedrine also used as stimulant
What are the major SE of pseudoephedrine, phenylephrine? HTN, can also cause CNS stim/ anxiety (esp pseudoephedrine)
What is the mech/use of methacholine? muscarinic receptor agonist. used in astma challenge test.
Created by: tjs2123