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60 Cards in this Set
- Front
- Back
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ASA/Samter's triad |
asthma nasal polys aspirin use avoid aspirin or NSAIDs tx with leukotriene inhibitors |
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Drugs to avoid in asthmatics |
especially with nasal polys: aspirin NSAIDs color agents such as tartrazine b-antagonists may worsen symptoms |
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Respiratory acidosis in asthma |
normally asthma attack means pt is breathing rapidly --> blow off CO2 leading to resp alkalosis if attack is very severe, then can get muscle fatigue leading to a mild resp acidosis resp acidosis in asthmatic is ominious sign --> may eventually require intubation |
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Asthma exacerbation |
nebulizer treatment with short act acting b-agonist-2 (albuternol) can add short acting anti-cholinergics (eg ipratropium) supplement with O2 & consider non-invasive PEEP IV glucocorticoids (total of 10-14 days, some of which can be PO) |
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Intrinsic asthma |
50% of pts non allergic nonimmunological stimuli: infections irritating inhalants cold air exercise emotional upset atacks are severe and prognosis is poor |
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Extrinsic asthma |
20% of pts allergic immune mediated -> IgE elevated fam hx of allergies allergic rhinitis, urticaria, eczema better prognosis |
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Asthma and PFTs |
shows obstructive pattern improvement with bronchodilator by 12% in FEV1 or FVC if PFT is normal and still considering asthma --> challenge with methacholine or cold air or exercise will decrease FEV1 and/or FVC by >20% |
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Nocturnal asthma |
most likely moderate persistent form so need to use long-acting b-2-agonist (eg salbutamol) + glucocorticoids |
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Bronchial thermoplasty |
applies radiofrequency waves to the airways during bronchoscopy to decrease large airway smooth muscle mass maybe helpful in severe asthma |
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Postnasal drip |
most common cause of chronic cough |
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Lofgren's syndrome |
presentation of acute sarcoidosis with: arthritis hilar adenopathy erythema nodusum DO NOT BX |
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Sarcoidosis imaging |
obtain CXR (PA & lateral views): find b/l hilar enlargement CT: reticular nodular disease with b/l hilar adenopathy |
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Sarcoidosis presentation |
polyarthralgia visual changes (uveitis) erythema nodosum b/l hilar adenopathy can have elevated Ca due to overactivation of vit D PPD & IFN-g release assay r/o latent Tb |
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DDx with sarcoidosis |
Tb lymphoma (Hodgkins) SLE or other vascular dz fungal infection Berylliosis |
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Gold standard for sarcoidosis dx |
bronchoscopy with bx in pt with active sxs non-caseating granulomas, AFB - & cx - |
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PFT in sarcoidosis |
Restrictive pattern: FEV1 & FVC are down FEV1/FVC is normal or high TLC and DLCO are down w/no bronchodilator response PFT can be done to track dz |
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PFT obstructive vs restrictive dz |
Obstructive --> FEV1/FVC is down Restrictive --> FEV1/FVC is normal to high |
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Sarcoidosis tx |
oral corticosteroids if symptomatic if pt is found to have b/l hilar adenopathy w/no other sxs --> DO NOT BX OR TREAT |
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W/u of suspected sarcoidosis |
CXR --> CT PFT CBC BMP UA EKG Optho exam PPD and/or IFN-g release assay |
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PPD interpretation |
only done in NON-SYMPTOMATIC PTS high risk --> >5mm is + immunocompromised including HIV+ steroid use organ transplant contact with active Tb moderate risk --> >10mm is + healthcare workers diabetes renal dz lung dz silicosis foreigners or works with foreigners low risk --> 15mm is + |
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Next step with PPD+ |
Need to r/o active infection CXR (primary Tb affects lower lobes, reactivated Tb affects upper lobes) LFT (bc the Tb drugs are hepatotoxic) Never give PPD again, once it's + |
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Active Tb management |
hospt with isolation tx with 4 drug regimen for 2 months isoniazid + vit B6 rifampin ethambutol pyrazinamide then isoniazid + rifampin for an additional 4 months depending on sensitivities each new active case must be reported to health dept |
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Latent Tb management |
no need for hospitalization or testing of contacts tx with isoniazid and vitamin B6 for 9 months & check LFT q2-3 months (gold standard) OR isoniazid & B6 for 6 months depending on drug toxicity & compliance OR rifampin for 4 months for those who cant take isoniazid OR weekly rifapentine + isoniazid for 3 months |
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Amnestic PPD response |
if elderly pt was infected with Tb many decades ago, PPD may falsely be - Perform two step testing: Do PPD and if -, repeat PPD in 2 weeks |
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IFN-g release assay |
now is gold standard but usually only done when PPD is equivocal can do with someone with AIDS no cross-reactivity with BCG QuantiFERON Tb Gold incubate blood with 2 Tb Ags & this stimulates IFN-g release that is measured by ELISA T-Spot test sensitivity and specificity >95% |
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PPD conversion risk |
only 10% of pts who convert will develop active Tb those who do develop active Tb, will occur within 2 yrs of PPD conversion |
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Direct observed therapy programs |
state sponsored prgms that follow pts to ensure they take their drugs over long periods of time like in Tb |
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Sites of Tb dz |
lungs (80-85%) pleura CNS lymphatic system GU tract bones and joints peritoneum |
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Tb terminology |
Ghon focus- primary lesion usually subpleural Ghon complex- involves infection of adjacent lymphatics and hilar lymph nodes Ranke complex- when Ghon complex undergoes fibrosis and calcification |
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Dx of pleural Tb |
pleural fluid stain/cx adenosine deaminase Tb PCR Quantiferon Gold pleural bx (gold standard) |
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Tb meningitis |
lymph predominance protein is high glucose is slightly low gives mix of bacterial and viral meningitis devastating esp in children |
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Side effects of Tb drugs |
isoniazid- peripheral neuropathy, hepatotoxicity rifampin- hepatoxicity ethambutol- gout, optic neuritis (do not use in kids) pyrazinamide- gout |
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Asbestos testing findings |
CXR: calcified pleural plaques, rounded atelectasis PFT: restrictive pattern definitive dx is via bronchoscopy with bx |
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Asbestosis |
common environmental cause of ILD mineral silicate fibers lodged in lungs that are phagocytosed by macrophages inflammatory process leading to fibrosis |
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Occupations assoc with asbestosis |
construction worker automobile repair insulation textiles mining milling ship building |
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Long term asbestosis consequences |
honeycombing --> end stage dz increased risk of bronchogenic carcinoma mesothelioma but not as much as lung cancer |
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Sitting tripod position |
when someone sits sitting fwd with hands on knees think COPD |
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Physical findings of obstructive dz |
increased antero-posterior diameter hyper-resonance to percussion increased S2 --> secondary to pulm HTN |
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Chief complaints in emphysema vs chronic bronchitis |
emphysema --> SOB chronic bronchitis --> productive cough |
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PFT findings for COPD |
dec FEV1 (most important indicator for COPD) dec FVC dec FEV1/FVC dec DLCO incr TLC incr RV incr FRC PFT may not be accurate in acute exacerbation, should wait until patient is back to baseline |
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Modifications that extend life in COPD |
smoking cessation home O2 if: PaO2 <55 or O2 sat <88% cor pulmonale and PaO2 <60 consider 6 min walk test for desat on exertion lung transplant |
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Tx of COPD |
inhaled bronchodilators are cornerstone of tx --> anticholinergics (eg ipratropium or tiotropium) & b-agonist are second line severe COPD, can consider inhaled corticosteroids |
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Tx for acute exacerbation of COPD |
O2 to maintain sat ~90% --> DO NOT GIVE TOO MUCH O2 inhaled bronchodilators --> ipratropium Abx --> azithro + ceftriaxone or fluoroquinolone Sputum Cx and gram stain (Legionella urinary Ag if considering atypical bacteria) corticosteroids (IV to oral) |
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Vaccines for COPD |
pneumococcal vaccine (booster q5 yrs) annual influenza vaccine |
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Smoking changes in lungs |
abnormalities in ciliary movement hyperplasia of mucous-secreting glands inhibition of alveolar macrophages release of proteolytic enzymes from neutrophils inhibition of anti-proteolytic enzymes |
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Alpha-1 antitrypsin |
anti-trypsin --> enzyme responsible for inhibition of trypsinase and elastinase in lungs def causes severe panacinar emphysema consider in young pts with obstructive dz involving bases of lungs and liver abnormalities |
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Emphysema |
loss of airway elastic recoil and caliber resulting in collapse during forced expiration results in prolonged expiratory phase, incr residual capacity, and air trapping with increases in lung volume results in increased work of breathing as tidal breathing takes place on less compliant part of pressure/volume curve |
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Diagnostic test for sleep apnea |
split night nocturnal polysomnography with CPAP titration with apnea hypopnea index >15 |
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Tx for obstructive sleep apnea |
behavioral modification for weight loss nasal CPAP (O2 w/o pressure is useless) oral appliances hypoglossal nerve stimulator surgery |
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DDx for lung nodule on CXR |
malignancy: bronchogenic ca pulm metastases carcinoid tumor benign dz: granulomas benign tumor (hamartoma) resolving infarction rheumatoid and vasculitic nodule AV malformation trauma rounded atelectasis |
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Lung cancer on CT |
>3cm lesion on CT is worrisome for lung cancer non-calcified lesion |
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Low risk patients for lung cancer |
<40 yo Nonsmoker or quit >15 yrs ago nodule <3 cm calcified lesion tx with repeat imagining in 3-6 months |
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Granuloma description on CT |
centrally calcified and smooth border |
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Gold standard test for PE |
CT angiography dont do if pt is allergic to contrast, have renal failure, or is pregnant if cant do CT angio then do V-Q scan |
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Tx of initial PE |
tx with LMW heparin first then start coumadin once dx is made continue both until INR is therapeutic or after 5-7 days, stop LMWH tx with coumadin for 6 months |
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Two common heritable causes of PE |
Factor V Leiden Prothrombin gene mutation |
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Most common signs of PE |
tachypnea and tachycardia dyspnea pleuritic chest pain cough, calf, or thigh pain or swelling |
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D-dimer testing |
increases are positive tests very sensitive for detection of thromboembolic dz good for low risk pts |
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LE U/S or doppler U/S |
sometimes used for DVT detection is an adjunct test so never first line |
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PE in lung |
large thrombi can lodge at bifurcation of main pulm art or lobar branches smaller thrombi continue traveling distally and are more likely to produce pleuritic chest pain, by initiating an inflammatory response ~10% of PE can cause pulm infarction |
