Pulmon USMLE
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| types of pathologies of COPD (2) and their locations | centrilobar (prox acini and upper lungs); panlobar (in prox and distal acini, lung bases)
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| types of pathologies of COPD (2) and the pts they're seen in | centrilobar-in smokers, panlobar-in AAT defic
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| 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)
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| pathophysiol/dx of chronic bronchitis | clinical diagnosed as chronic, productive cough >3mo/yr for >2yr
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| pathophysiol of emphysema | destruction of alveolar walls, leading to enlargement of alv spaces terminal bronchioles
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| 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
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| 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
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| pathology of emphysemic pts | desctruction of alveoli from incrsd protease (elastase), or decrsd AAT
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| pathology of chronic bronchitis | excess mucus production, enlarged mucus glands and smooth muscle hyperplasia
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| risks for COPD | smoke (90%), AAT (and worse w smoking), chronic asthma
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| 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
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| at what peak flow would suspect obstruction and order PFTs | if <350L/min
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| when do you measure AAT | if emphysema less than or eq 50yo, in patient or family
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| for COPD what measure should you monitor | FEV1
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| 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
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| what's theophylline used for? | oral theophylline (controversial) may help mucocilliary clearance and respir drive but narrow therapeutic index
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| 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
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| 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
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| 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]
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| 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)
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| 2 types of asthma and when present | extrinsic-atopy, produce IgE to antigens, present young; intrinsic-no atopy or environmental triggers
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| triggers for asthma | pollens/dust/mold, animals/cockroaches, smoke, meds, cold air, exercise, viral
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| 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
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| 3 other causes of wheezing besides asthma | CHF (edema of airways), COPD, lung cancer
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| 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%
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| what are nml peak flow rates for an adult | nml male 450-650 L/min, female 350-500 [but depends on age and hgt]
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| what level of peak flow rate shows mild, mod-severe, and severe impairment | mild=>300, mod-severe 100-300, and severe <100
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| 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
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| when is a bronchoprovocation test used | when PFT w b2 are inconclusive
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| 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)
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| what does cromolyn do? How is it used? | prevents rel of histamine from mast cells, used in prophylaxis for asthma
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| 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
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| what should look for on Head and neck exam in Asthmatic | nasal polyps--ASA-sensitive asthma (should also avoid NSAIDs in these pts)
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| how does bronchiectasis present | cough w large amts of mucupurulent, foul smelling sputum, dysphagia, hemptysis (usu self-limited), recurrent/persistent PNA
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| causes of bronciectasis (3) | 1) CF (50%), 2) infxn, 3) immune defic
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| pathology of bronchiectasis | permanent dilation and destruction of bronchial walls
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| tx bronchiectasis | Abx for acute exacerbations
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| 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
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| which lung cancers tend to present centrally? Peripherally? | central=SCLC, SCC; peripheral=adeno and large cell
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| 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
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| which paraneoplastic syn are assoc w which lung cancers | SCLC: SiADH, ACTH, Eaton-Lambert; SCC: PTH,
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| how does SCC lung cancer present | centrally, can be w cavitation, airway involvement (obstruction, PNA), Pancoast
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| 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
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| describe Pancoasts syn | superior sulcus apical tumor, shoulder pain and upper extrem wknss
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| describe Horner's syn | unilateral ptosis, myosis, anhidrosis from cervical symp chain involvement from apical lung tumor
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| which nerves can be involved in lung cancer, how does that present | Laryngeal (hoarseness), phrenic (diaphragm paralysis)
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| 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
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| dx of lung cancer | 1) CXR, 2) CT (for staging), 3) bx for histol type (via bronchoscopy or transthoracic CT guided)
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| 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++)
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| causes of mediastinal mass | MC is metastic cancer, esp lung
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| list anterior mediastinal masses (4) | thyroid, teratogenic, thymoma, lymphoma
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| list middle mediastinal masses (5) | lung cancer, lymphoma, aneurysm, cyst, Morgagni hernia
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| list posterior mediastinal masses (5) | neurogenic, esophageal, enteric cyst, aneurysm, Bochdalek
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| symptoms of mediastinal masses | (due to invasion, compression of surrounding) cough, chest pain, dyspnea, obstruct PNA, compression of nerves (hoarseness, diaphragm paralysis, Horners)
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| cut offs for exudative v transudative | exudative: Protein (pl/serum) > 0.5; LDH (pl / serum) > 0.6; LDH > 2/3 upper limit nml serum
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| describe pathology of a transudative pl effusion v exudative | transudative: increase P or decrsd plasma oncotic; exudative: incrsd perm of pl surface
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| list causes of transudative pl eff (5) | CHF (MC), cirrhosis, nephrotic, hypoalbuminemia, atelectasis (PE can be either)
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| list causes of exudative pl eff (4) | bac PNA/TB, cancer (lung>breast>lymphoma), viral infxn, collagen vascular disease (PE can be either)
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| tx for 2 types of pl eff | transudative: diuretic and Na restriction; exudative: tx underlying (ie for paraPNA pl effusion Abx alone)
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| 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
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| 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
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| order CXR to check for PTX after which procedures | transthoracic needle aspiration, thoracentesis, central line placement
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| 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
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| clinical findings of PTX | decrsd breath sounds, hyperresonance, mediastinal shift TOWARD affected
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| clinical findings of tension PTX | decrsd breath sounds, hyperresonance, trachea shift AWAY affected; hypotension and distended neck veins
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| 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
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| 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]
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| tx tension PTX | don't get CXR, immed decompression w large bore needle (2 or 3rd intercostal space at midclavicular) or chest tube
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| describe pathology of inflamm lung dz (ILD) | inflamm process of alveolar wall leading to irrevers fibrosis and impaired gas exchange
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| clinical findings of ILD | dyspnea, cough (non productive), rales at base
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| general dx w/u for ILD | 1) CXR (usu non specific), 2) CT, 3) PFT (show restrictive), 4) tissue bx (usu reqd for dx)
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| 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
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| 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%)]]
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| 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
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| 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
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| 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]
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| name 4 granulomatous ILD | 1) sarcoid, 2) histiocytosis X, 3) Wegeners, 4) Churg-Strauss
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| describe pathology and imaging of Histiocytosis X and who it appears in | prolifer of histiocytes, usu in smokers, CXR: honeycomb, CT: cystic lesions
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| 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
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| describe problem in Churg Strauss, clinical presentation, dx, tx | granulomatous vasculitis in pts w asthma, pul infiltrate, rash, eosinophilia; dx: + pANCA, tx: glucocorticoids
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| name 4 environmental ILDs | coal workers, asbestosis, silicosis, beryllosis
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| 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
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| which environmental ILD can look like sarcoid, in what manner? | chronic beryllosis can get granulomas, skin lesions, incrsd Ca++
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| which environmental ILD usu appears in upper lobes? Lower lobes? | upper=silicosis, lower lobes=asbestosis
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| what does asbestos put pt at risk for | bronchogenic cancer (smoking makes worse), malignant mesothelioma
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| hazy infiltrates, bilateral linear opacities--which environmental ILD? What else might be on the CXR? | asbestosis, might also see pleural plaques
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| egg shell calcifications on CXR suggests | silicosis
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| 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
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| which environmental ILD has a serum dx test? What is it? | beryllosis; beryllium lymphocyte prolifer test
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| occupations at risk for silicosis | mining, stone cutting, glass
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| farmer's lung, bird breeder's lung, and moldy sugar cane are all what type of ILD | hypersensitivity pneumonitis
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| clinically how does hypersensitivity pneumonitis present (sympt) | flu like F, chills, cough, dyspnea
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| 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
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| how does Goodpasteurs present | hemoptysis and dyspnea w GN
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| type of hypersensitivity in Goodpasteurs | II
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| tx for Goodpasteurs | plasmaphoresis, cyclophosphamide, steroids
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| 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
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| describe pt pop and clinical presentation of idiopathic pul fibrosis (IPF) | more common in men and smokers, progressive dyspnea and nonproductive cough
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| 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
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| 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
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| 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
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| describe 2 types of respir failure and the cut offs | 1) hypoxia: PaO2 <60, PaCO2 >50; 2) hypercapnia PPCo2 >50
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| 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
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| what monitor to tell ventilation status? How change on mech vent? | PaCO2: to decrs incrs RR or TV
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| what monitor to tell oxygenation status? How change on mech vent? | O2 sat, PaO2: to decrs PaO2 decrs FiO2 or PEEP [or time inspir?]
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| what's the eqn for minute ventilation | RR*TV
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| how does hypercapnia affect CNS | causes vasodilation of cerebral vessels, incrsd ICP, papilledema, impaired consciousness, coma
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| 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
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| 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
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| 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
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| describe progression of hypercarbic (ventilatory) respir failure | decrsd minute ventilation or incrsd dead space leads to CO2 retention and then hypoxemia
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| sepsis, DKA, hyperthermia can lead to what type of respir failure? How? | the incrsd CO2 leads to hypercapnic respir failure
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| 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
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| 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
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| possible causes of ARDS | sepsis (MC), aspiration, severe trauma, Rx, toxins, CPB
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| 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
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| 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
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| 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
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| where should ET tube appear on CXR | 3-5 cm above carina
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| 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
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| 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
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| describe CPAP setting on mech ventilators | provide positive P during inspir and expir, but no volume (otherwise pt breathes on own)
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| pressure support vent | used during weaning trials, pressure is only delievered when pt initiates a breath
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| 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
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| 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
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| what's normal I/E | 1 to 2
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| 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
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| define cut offs for pul HTN | mean pul artery P>25 at rest, 30 during exercise
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| 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
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| dx of 1ry pul HTN | dx of exclusion (no cardiac or pul dz) w cardiac cath to dx
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| present of 1ry pul HTN | usu young or middle aged woman
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| tx of 1ry pul HTN | pul vasodilators: IV prostacyclins (epoprostenol), CCB; anticoag w warfarin INR 2
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| 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
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| special feature on ECG indicating cor pulmonale | P pulmonale waves (peaked P waves), also see RAD and RVH
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| what to note abt diuretics and cor pulmonale | pts may be preload dependent, so be careful w diuretic use
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| 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
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| MC source of clot for PE | lower extremity DVT, esp above the knee ileofemoral
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| types of clot in PE (6) | thrombo embolus (MC), fat (long bone fx), amniotic fluid, air embolism, septic (IV drug), schistomiosis
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| 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
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| 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
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| 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
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| when is heparin for PE contraindicated | active bleeding, uncontrolled HTN, recent stroke, HIT
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| how tx PE longterm | oral warfarin, INR 2-3
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| 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
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| what part of lung most at risk for pul aspiration | R lung, esp lower seg RUL and upper seg of RLL
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| 3 main causes of hemoptysis | MC=bronchitis, if F, N/S think TB, if renal think Goodpasteurs
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| what vol is considered massive hemoptysis; MC cause; key action | 600ml in 24hr, bronchiectasis, key protect airway
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| to evaluate hemoptysis--initial imaging | CXR and bronchoscopy (+/- CT)
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| cut off for home O2 | O2 sat <=88%
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| amt pH should change if PaCO2 changes | as PaCO2 decrsd 10mmHg, pH decrs 0.08
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| describe DLCO test | pt breathes a certain amt of CO, measure how much gets into pul capillary blood
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| causes of high DLCO (4) | asthma, obesity, L-R shunt, pul hemorrh
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| causes of low DLCO (4) | emphysema, sarcoid, interstitial fibrosis, pul vascul dz
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| what's nml V/Q | 0.8
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To hide the entire table, click on the "Hide All" button.
You may also shuffle the rows of the table by clicking on the "Shuffle" button.
Or sort by any of the columns using the down arrow next to any column heading.
If you know all the data on any row, you can temporarily remove it by tapping the trash can to the right of the row.
To hide a column, click on the column name.
To hide the entire table, click on the "Hide All" button.
You may also shuffle the rows of the table by clicking on the "Shuffle" button.
Or sort by any of the columns using the down arrow next to any column heading.
If you know all the data on any row, you can temporarily remove it by tapping the trash can to the right of the row.
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Created by:
ehstephns
Popular Midwifery sets