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Pulmon USMLE

QuestionAnswer
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 on 2010-12-06



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