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Step 1. 1.3.13
Respiratory I
| Question | Answer |
|---|---|
| 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. |
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