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Pulmon USMLE
| Question | Answer |
|---|---|
| types of pathologies of COPD (2) and their locations | centrilobar (prox acini and upper lungs); panlobar (in prox and distal acini, lung bases) |
| types of pathologies of COPD (2) and the pts they're seen in | centrilobar-in smokers, panlobar-in AAT defic |
| two clinical types of COPD (hint: blue, pink), and by what means are they diagnosed | chronic bronchitis (clinical dx) and emphysema (pathol diagnosis) (although often substantial overlap) |
| pathophysiol/dx of chronic bronchitis | clinical diagnosed as chronic, productive cough >3mo/yr for >2yr |
| pathophysiol of emphysema | destruction of alveolar walls, leading to enlargement of alv spaces terminal bronchioles |
| characteristics of pink puffer patients, dz | dz=emphysema; thin barrel chest, lean forward in distress using access mscls to breathe; tachypnic, long expir through pursed lips |
| characteristics of blue bloater patients, dz | dz=chronic bronchitis; overwgt, cyanotic (chronic hypoxemia and hypercapnia); cough w sputum; RR nml or sl incrs in no distress |
| pathology of emphysemic pts | desctruction of alveoli from incrsd protease (elastase), or decrsd AAT |
| pathology of chronic bronchitis | excess mucus production, enlarged mucus glands and smooth muscle hyperplasia |
| risks for COPD | smoke (90%), AAT (and worse w smoking), chronic asthma |
| PFTs showing obstruction | decrsd FEV/FVC (<0.75 and severe when <0.5); incrsd TLC, FRC, decrsd VC [air trapping able to use less of lungs]; prolonged forced expir time |
| at what peak flow would suspect obstruction and order PFTs | if <350L/min |
| when do you measure AAT | if emphysema less than or eq 50yo, in patient or family |
| for COPD what measure should you monitor | FEV1 |
| Rx tx for COPD | 1) b2 ag (albut) inhalor, or longer acting salmeterol; 2) anithcol (ipratropium Br) inhalors; 3) steroids (budenoside, fluticasone) inhalors; 4)oral theophylline (controversial) may help mucocilliary clearance and respir drive but narrow therapeutic index |
| what's theophylline used for? | oral theophylline (controversial) may help mucocilliary clearance and respir drive but narrow therapeutic index |
| when give suppl O2 to COPD pt | if despite max med therapy PaO2<55; O2 sat <88 (rest or exercise), OR PaO2 55-59 but also have polycythemia or cor pulmonale |
| what preventative measures should COPD pts take (hint vacc, overall health) | stop smoking! Will slow the decline in fxn, also vaccine for flu and S Pneu |
| what commonly causes COPD exacerb | infxns, incl S Penu, H Flu, Mycopla Pneu and Moraxella [Secretes says H Flu and Moraxella key causes PNA in COPD] |
| how tx COPD exacerb | 1) bronchodilators +/- antichol, 2) if hospitaliz IV steroids (methylpred), taper w oral prednisone (not inhaled), 3) Abx: azithro or levofloxacine, 4) suppl O2 (+/- CPAP or BIPAP) |
| 2 types of asthma and when present | extrinsic-atopy, produce IgE to antigens, present young; intrinsic-no atopy or environmental triggers |
| triggers for asthma | pollens/dust/mold, animals/cockroaches, smoke, meds, cold air, exercise, viral |
| clinical present of asthma and timing of when sympt present | intermittent wheezing (MC finding), SOB, cough, chest tightness, usu within 30 min of trigger; sympt are worse at night |
| 3 other causes of wheezing besides asthma | CHF (edema of airways), COPD, lung cancer |
| what reqd to dx asthma; specific cut offs | PFT showingobstruction and that this obstruction is reversible (w bronchodilators); FEV1/FVC <0.75 and b2 causes an incrs in FEV1 or FVC by at least 12% |
| what are nml peak flow rates for an adult | nml male 450-650 L/min, female 350-500 [but depends on age and hgt] |
| what level of peak flow rate shows mild, mod-severe, and severe impairment | mild=>300, mod-severe 100-300, and severe <100 |
| describe a bronchoprovocation test | measure PFT before and after difft doses of methacholine (muscarinic agonist in parasymp nervous system); if asthma will develop obstruct at lower doses |
| when is a bronchoprovocation test used | when PFT w b2 are inconclusive |
| how tx asthma | 1) b2 agonist (albuterol or salmeterol; 2) steroids inhalors; 3) montelukast-leukotriene modifiers (not as strong as steroids), 4) cromolyn/nedocromil (only prophylaxis) |
| what does cromolyn do? How is it used? | prevents rel of histamine from mast cells, used in prophylaxis for asthma |
| how tx acute asthma (hospitalization) | 1) b2 agonist (albuterol); 2) steroids IV; [3) theophylline, IV Mg], 4) supplemental O2, 5) Abx if severe or suspect infection |
| what should look for on Head and neck exam in Asthmatic | nasal polyps--ASA-sensitive asthma (should also avoid NSAIDs in these pts) |
| how does bronchiectasis present | cough w large amts of mucupurulent, foul smelling sputum, dysphagia, hemptysis (usu self-limited), recurrent/persistent PNA |
| causes of bronciectasis (3) | 1) CF (50%), 2) infxn, 3) immune defic |
| pathology of bronchiectasis | permanent dilation and destruction of bronchial walls |
| tx bronchiectasis | Abx for acute exacerbations |
| types of lung cancer: names, % occurrence (5) | 1) small cell lung cancer (25%); 2-5=non-small cell lung cancer (75%): 2) squamos cell (30%), 3) adeno (35%, MC), 4) large cell (5-10%), 5) bronchoalveolar |
| which lung cancers tend to present centrally? Peripherally? | central=SCLC, SCC; peripheral=adeno and large cell |
| key features and presentation of SCLC incl paraneoplastic and cxns | widespread, distant mets early (often even at time of dx); paraneoplastic incl: SiADH, ACTH, Eaton-Lambert; SVC syndrome |
| which paraneoplastic syn are assoc w which lung cancers | SCLC: SiADH, ACTH, Eaton-Lambert; SCC: PTH, |
| how does SCC lung cancer present | centrally, can be w cavitation, airway involvement (obstruction, PNA), Pancoast |
| features of adeno lung cancer: how presents, pt type, assoc | often peripheral, can be w pleural involvement, less assoc w smoking, can be assoc w pul scars and fibrosis |
| describe Pancoasts syn | superior sulcus apical tumor, shoulder pain and upper extrem wknss |
| describe Horner's syn | unilateral ptosis, myosis, anhidrosis from cervical symp chain involvement from apical lung tumor |
| which nerves can be involved in lung cancer, how does that present | Laryngeal (hoarseness), phrenic (diaphragm paralysis) |
| tx of lung cancer | NSCLC: surgery if no mets outside the chest + radiation (+/- chemo); SCLS: chemo (radiation can help if dz limited), surgery not helpful bc unresectable |
| dx of lung cancer | 1) CXR, 2) CT (for staging), 3) bx for histol type (via bronchoscopy or transthoracic CT guided) |
| factors that make solitary lung nodule more likely to be malignant | 1) >50yo, 2) smoking, 3) >3cm, 4) irregular or speculated margin w stippled or eccentric Ca++ (v central laminated Ca++) |
| causes of mediastinal mass | MC is metastic cancer, esp lung |
| list anterior mediastinal masses (4) | thyroid, teratogenic, thymoma, lymphoma |
| list middle mediastinal masses (5) | lung cancer, lymphoma, aneurysm, cyst, Morgagni hernia |
| list posterior mediastinal masses (5) | neurogenic, esophageal, enteric cyst, aneurysm, Bochdalek |
| symptoms of mediastinal masses | (due to invasion, compression of surrounding) cough, chest pain, dyspnea, obstruct PNA, compression of nerves (hoarseness, diaphragm paralysis, Horners) |
| cut offs for exudative v transudative | exudative: Protein (pl/serum) > 0.5; LDH (pl / serum) > 0.6; LDH > 2/3 upper limit nml serum |
| describe pathology of a transudative pl effusion v exudative | transudative: increase P or decrsd plasma oncotic; exudative: incrsd perm of pl surface |
| list causes of transudative pl eff (5) | CHF (MC), cirrhosis, nephrotic, hypoalbuminemia, atelectasis (PE can be either) |
| list causes of exudative pl eff (4) | bac PNA/TB, cancer (lung>breast>lymphoma), viral infxn, collagen vascular disease (PE can be either) |
| tx for 2 types of pl eff | transudative: diuretic and Na restriction; exudative: tx underlying (ie for paraPNA pl effusion Abx alone) |
| dx (incl specific tests) for pl eff | 1) CXR, 2) thoracentesis order 4 Cs chemistry (glu, protein, LDH, pH), cytology (malignancy), cell count (CBC + diff), culture |
| what are the specific CXRs that can be ordered for pl eff and what do they tell you, incl vol of pl eff | 1) A/P blunting of costophrenic angle if >250ml; 2) lateral decubitus can see smaller pl eff and will indicate if loculated |
| order CXR to check for PTX after which procedures | transthoracic needle aspiration, thoracentesis, central line placement |
| 2 types of spontaneous PTX and who they occur in | 1) primary/simple: no lung dz, rupture of subpleural blebs occurs in tall, lean young males; 2) secondary/complicated: lung dz, usu COPD, but also asthma, ILD, cancer, CF, TB |
| clinical findings of PTX | decrsd breath sounds, hyperresonance, mediastinal shift TOWARD affected |
| clinical findings of tension PTX | decrsd breath sounds, hyperresonance, trachea shift AWAY affected; hypotension and distended neck veins |
| tx spont PTX; chance of recurrence | if small just observe and should resolve in 10d (or sm chest tube); supp O2 can help w resorption; in simple 50% recurrence in 2 yrs |
| how might malignant mesothelioma present, assoc w, px | bloody pl effusion, most due to asbestos and poor px [although benign ones not assoc w asbestos and not poor px] |
| tx tension PTX | don't get CXR, immed decompression w large bore needle (2 or 3rd intercostal space at midclavicular) or chest tube |
| describe pathology of inflamm lung dz (ILD) | inflamm process of alveolar wall leading to irrevers fibrosis and impaired gas exchange |
| clinical findings of ILD | dyspnea, cough (non productive), rales at base |
| general dx w/u for ILD | 1) CXR (usu non specific), 2) CT, 3) PFT (show restrictive), 4) tissue bx (usu reqd for dx) |
| describe general problem in sarcoid, who it affects, general prognosis | noncaseating granulomas in mltpl organs; often AA women <40; 2/3 improve sympt and 20% have chronic dz |
| key features of sarcoid [not incl labs or imaging] | erythema nodosum (25%), uveitis (blurred vision, 25%), arthralgia/arthritis (25-50%), heart rhythm, malaise F, wgt loss, [[bilateral hilar adenopathy (50%)]] |
| staging of CXR in sarcoid and which best/worst px | I: hilar adenopathy w/o parenchymal infiltrate (most likely remission); II: hilar adenopathy w/ parenchymal infiltrate; III: diffuse infiltrate w/o hilar adenopathy (worst px); IV: pul fibrosis w honeycombing |
| dx of sarcoidosis | 1) CXR for bilateral adenopathy, 2) ACE incrsd in serum (in other lung dzs also), 3) incrsd Ca++ in blood and urine, 4) PFTs decrsd lung vol, DLCO, and FEV/FVC, 5) **transbronchial bx nec for definit dx: noncaseating granulomas w correct clinical picture |
| tx sarcoid | most resolve/improve within 2 yrs and don't need tx; systemic steroids used if sympt/active lung dz, deteriorating PFTs, heart rhythm, severe eye/skin [use MTX if refractory to steroids] |
| name 4 granulomatous ILD | 1) sarcoid, 2) histiocytosis X, 3) Wegeners, 4) Churg-Strauss |
| describe pathology and imaging of Histiocytosis X and who it appears in | prolifer of histiocytes, usu in smokers, CXR: honeycomb, CT: cystic lesions |
| describe problem in Wegeners, clinical presentation, dx, tx | necrotizing granulomatous vasculitis in lung and kidney; present w upper and lower respir infxn, pul nodules, GN; dx: cANCA (although bx gold std); tx: immunosupp and glucocorticoids |
| describe problem in Churg Strauss, clinical presentation, dx, tx | granulomatous vasculitis in pts w asthma, pul infiltrate, rash, eosinophilia; dx: + pANCA, tx: glucocorticoids |
| name 4 environmental ILDs | coal workers, asbestosis, silicosis, beryllosis |
| which of the 4 environmental ILDs have a tx | only beryllosis (glucocorticoid for acute and chronic dz); coal workers, asbestosis, and silicosis don't have tx |
| which environmental ILD can look like sarcoid, in what manner? | chronic beryllosis can get granulomas, skin lesions, incrsd Ca++ |
| which environmental ILD usu appears in upper lobes? Lower lobes? | upper=silicosis, lower lobes=asbestosis |
| what does asbestos put pt at risk for | bronchogenic cancer (smoking makes worse), malignant mesothelioma |
| hazy infiltrates, bilateral linear opacities--which environmental ILD? What else might be on the CXR? | asbestosis, might also see pleural plaques |
| egg shell calcifications on CXR suggests | silicosis |
| compare silicosis and asbestosis on CXR | silicosis: localized and nodular peribronchial fibrosis in upper lobes; asbestosis: diffuse interstitial w hazy infiltrates, lienar opacities +/ pl plaques in lower lobes |
| which environmental ILD has a serum dx test? What is it? | beryllosis; beryllium lymphocyte prolifer test |
| occupations at risk for silicosis | mining, stone cutting, glass |
| farmer's lung, bird breeder's lung, and moldy sugar cane are all what type of ILD | hypersensitivity pneumonitis |
| clinically how does hypersensitivity pneumonitis present (sympt) | flu like F, chills, cough, dyspnea |
| mech of eosinophilic PNA, CXR, tx | Eos accumulate in lung, present w F and eos in blood, CXR=peripheral infiltrates; tx: glucocorticoids (although can be relapse after off steroids)--note some overlap w Churg Strauss |
| how does Goodpasteurs present | hemoptysis and dyspnea w GN |
| type of hypersensitivity in Goodpasteurs | II |
| tx for Goodpasteurs | plasmaphoresis, cyclophosphamide, steroids |
| describe pulmonary alveolar proteinosis: pathology, CXR, dx, tx | (rare) accum of surfactant-like proteins and phsopholipids in alveoli; CXR: ground glass bilateral infiltrates look like bat; bx for dx; lung lavage for tx although granulocyte colony stim factor being tried **don't give steroids--at risk for infxn |
| describe pt pop and clinical presentation of idiopathic pul fibrosis (IPF) | more common in men and smokers, progressive dyspnea and nonproductive cough |
| CXR, dx, tx of IPF | CXR can be nml or show ground glass or honeycomb; dx is r/o others (bx can give dx or be nonspecific); tx: give suppl O2, steroids +/- cyclophosphamide |
| features, CXR, and tx of cryptogenic organizing pneumonitis (COP) | features like infxs PNA w cough, dyspnea, flu; CXR: bilateral patchy infiltrates; tx: steroids but relapse can occur |
| timing, clinical presentation, CXR/CT, and tx of radiation pneumonitis | (see in 5-15% of pts), acute 1-6mo, chronic 1-2y; clinical: low F, cough, dyspnea, pl chest pain, hemoptysis; CXR=nml, CT=diff infiltrate; tx=steroids |
| describe 2 types of respir failure and the cut offs | 1) hypoxia: PaO2 <60, PaCO2 >50; 2) hypercapnia PPCo2 >50 |
| 3 mechanisms of hypoxemia and how to tell them apart | 1) A-a nml=hypoventilate; 2) if both PaCO2 and A-a incrsd: V/Q mismatch or shunt; if PaO2 improves w suppl O2 then its V/Q mismatch |
| what monitor to tell ventilation status? How change on mech vent? | PaCO2: to decrs incrs RR or TV |
| what monitor to tell oxygenation status? How change on mech vent? | O2 sat, PaO2: to decrs PaO2 decrs FiO2 or PEEP [or time inspir?] |
| what's the eqn for minute ventilation | RR*TV |
| how does hypercapnia affect CNS | causes vasodilation of cerebral vessels, incrsd ICP, papilledema, impaired consciousness, coma |
| causes of acute respir failure (CNS, neuromuscl, respir, CVS) | CNS, neuromusc: MG, Guillan-Barre, ALS; respir: upper airway obstruct, thorax (scoliosis, hemothorax), lower airway (asthma, COPD, PNA, ARDS); CVS: CHF, PE, anemia |
| what do PaO2 and PaCO2 look like in V/Q mismatch, how can dx and tx? | [MC mech of hypoxemia] low PaO2 w nml or low nml PaCO2; respond to suppl O2 |
| describe mech and PaO2 and PaCO2 values for intrapul shunt | collapsed or fluid filled alveoli, atelectasis not responsive to suppl O2; hypovent leads to incrsd PaO2 and decrsd PaO2 |
| describe progression of hypercarbic (ventilatory) respir failure | decrsd minute ventilation or incrsd dead space leads to CO2 retention and then hypoxemia |
| sepsis, DKA, hyperthermia can lead to what type of respir failure? How? | the incrsd CO2 leads to hypercapnic respir failure |
| describe patholphys of ARDS | diff inflamm (but not infxs) process in both lungs involving systemic PMN activ; massive shunting from atelectasis, interstitial edema, lung collapse leads to stiff lungs (incrsd work of breathing), incrsd A-a and diff gas exchange; incrsd dead space |
| what condition must ARDS be differentiated from? How are they difft and how differentiate? | pul edema, exc in ARDS the cause isn't incrsd P but incrsd perm of alveoli; differentiate by PCWP |
| possible causes of ARDS | sepsis (MC), aspiration, severe trauma, Rx, toxins, CPB |
| clinical dx of ARDS | progressive hypoxemia refractory to O2 suppl; PaO2:FiO2 >200; bilateral diffuse pul infiltrate on CXR; no evidence of CHF w PCWP < or = 18mmHg |
| tx of ARDS, incl preferred method of feeds | keep O2 sat >90% using mech vent w PEEP (opens collapsed alveoli), avoid vol overload (PCWP 12-15); treat underlying causes; tube feeds preferred over TPN |
| indications for starting on vent (4) | 1) respir distress (incrsd RR) or respir fatigue, 2) inability to protect airway, 3) significant hypoxemia (PaO2<70) or hypercapnia (PaCO2>50); respir acidosis (pH<7.2) w hypercapnia, 4) metabolic acidosis if pt can't compensate w hypervent |
| where should ET tube appear on CXR | 3-5 cm above carina |
| describe assisted controled vent | back up minute ventilation (predetermined RR and TV), once pt starts a breath machine delivers a TV, pt can breathe over this RR but ea breath over would get that TV |
| describe SIMV vent setting | synch intermittent mandat vent (SIMV): pts can breathe alone above RR w/o help from machine (so TV of those breaths aren't determined); mandatory breath is sync'c w spontaneous breath |
| describe CPAP setting on mech ventilators | provide positive P during inspir and expir, but no volume (otherwise pt breathes on own) |
| pressure support vent | used during weaning trials, pressure is only delievered when pt initiates a breath |
| what nml values for minute ventilat, how titrate on mech vent | titrate minute ventilation for PaCO2; usu TV=8-10 ml/kg (but lower COPD and ARDS); RR=10-12 |
| how titrate FiO2 on mech vent | start 100%, quickly decrs to minimum where PaO2 >50 and O2 Sat>90; should be <0.6 to avoid oxygen toxicity; if FiO2 0.5 isn't enough can try adding PEEP and CPAP |
| what's normal I/E | 1 to 2 |
| what are nml values PEEP, how does effect CVS? | nml 2.5-10 (used ARDS mostly); does decrs venous return and incrs pul vascular resistance by incrs intrathoracic P |
| define cut offs for pul HTN | mean pul artery P>25 at rest, 30 during exercise |
| describe causes of pulHTN | block pul v drain (ie MS); incrsd BF (ie L-R shunt); resistance of large pul art (PE, PA stenosis); resist in pul arterioles (1ry pul HTN, CREST, coll vascular dz); vasoconstrict w hypoxia; incrsd intrathoracic P w vent; incrsd blood visc polycy vera |
| dx of 1ry pul HTN | dx of exclusion (no cardiac or pul dz) w cardiac cath to dx |
| present of 1ry pul HTN | usu young or middle aged woman |
| tx of 1ry pul HTN | pul vasodilators: IV prostacyclins (epoprostenol), CCB; anticoag w warfarin INR 2 |
| define cor pulmonale and common causes | RVH and eventual failure from pul HTN 2ry to pul dz (not LV failure); MC: COPD, also PE, ILD, asthma, CF, sleep apnea, pneumoconiosis |
| special feature on ECG indicating cor pulmonale | P pulmonale waves (peaked P waves), also see RAD and RVH |
| what to note abt diuretics and cor pulmonale | pts may be preload dependent, so be careful w diuretic use |
| risks for PE (10) | >60, cancer, hypercoag (factor V Leiden, prot C, S defic, anti thrombin III defic), immobilization, cardiac dz esp CHF, obesity, nephrotic, surgery (esp ortho), trauma, preg and OCP |
| MC source of clot for PE | lower extremity DVT, esp above the knee ileofemoral |
| types of clot in PE (6) | thrombo embolus (MC), fat (long bone fx), amniotic fluid, air embolism, septic (IV drug), schistomiosis |
| under what conditions should you treat for PE (3) | 1) CT shows PE and clinical suspicion, 2) DVT by US and clinical suspicion, 3) positive pul angiogram |
| what rules out PE | 1) low prob V/Q scan and low clinical suspicion; 2) negative pul angiogram, 3) negative D dimer and low clinical suspicion |
| details on heparin tx of PE | bolus + cont IV for 5-10d, goal INR 1.5-2.5; LMWH has more bioavailabilit and lower cxns |
| when is heparin for PE contraindicated | active bleeding, uncontrolled HTN, recent stroke, HIT |
| how tx PE longterm | oral warfarin, INR 2-3 |
| what thrombolytic agents can be used for PE; when use? | streptokinase or tissue plasminogen activator (tPA); used in massive PE in pts hemo unstable or if evidence of RV failure |
| what part of lung most at risk for pul aspiration | R lung, esp lower seg RUL and upper seg of RLL |
| 3 main causes of hemoptysis | MC=bronchitis, if F, N/S think TB, if renal think Goodpasteurs |
| what vol is considered massive hemoptysis; MC cause; key action | 600ml in 24hr, bronchiectasis, key protect airway |
| to evaluate hemoptysis--initial imaging | CXR and bronchoscopy (+/- CT) |
| cut off for home O2 | O2 sat <=88% |
| amt pH should change if PaCO2 changes | as PaCO2 decrsd 10mmHg, pH decrs 0.08 |
| describe DLCO test | pt breathes a certain amt of CO, measure how much gets into pul capillary blood |
| causes of high DLCO (4) | asthma, obesity, L-R shunt, pul hemorrh |
| causes of low DLCO (4) | emphysema, sarcoid, interstitial fibrosis, pul vascul dz |
| what's nml V/Q | 0.8 |
Created by:
ehstephns
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