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60 Cards in this Set

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ASA/Samter's triad

asthma




nasal polys




aspirin use




avoid aspirin or NSAIDs




tx with leukotriene inhibitors

Drugs to avoid in asthmatics

especially with nasal polys:




aspirin




NSAIDs




color agents such as tartrazine




b-antagonists




may worsen symptoms

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

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)

Intrinsic asthma

50% of pts




non allergic




nonimmunological stimuli:


infections


irritating inhalants


cold air


exercise


emotional upset




atacks are severe and prognosis is poor

Extrinsic asthma

20% of pts




allergic




immune mediated -> IgE elevated




fam hx of allergies




allergic rhinitis, urticaria, eczema




better prognosis

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%

Nocturnal asthma

most likely moderate persistent form so need to use long-acting b-2-agonist (eg salbutamol) + glucocorticoids

Bronchial thermoplasty

applies radiofrequency waves to the airways during bronchoscopy to decrease large airway smooth muscle mass




maybe helpful in severe asthma

Postnasal drip

most common cause of chronic cough

Lofgren's syndrome

presentation of acute sarcoidosis with:




arthritis


hilar adenopathy


erythema nodusum




DO NOT BX

Sarcoidosis imaging

obtain CXR (PA & lateral views):


find b/l hilar enlargement




CT:


reticular nodular disease with b/l hilar adenopathy

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

DDx with sarcoidosis

Tb


lymphoma (Hodgkins)


SLE or other vascular dz


fungal infection


Berylliosis

Gold standard for sarcoidosis dx

bronchoscopy with bx in pt with active sxs


non-caseating granulomas, AFB - & cx -

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



PFT obstructive vs restrictive dz

Obstructive --> FEV1/FVC is down




Restrictive --> FEV1/FVC is normal to high

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

W/u of suspected sarcoidosis

CXR --> CT


PFT


CBC


BMP


UA


EKG


Optho exam


PPD and/or IFN-g release assay

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 +

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 +

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

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

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

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%

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

Direct observed therapy programs

state sponsored prgms that follow pts to ensure they take their drugs over long periods of time like in Tb

Sites of Tb dz

lungs (80-85%)


pleura


CNS


lymphatic system


GU tract


bones and joints


peritoneum

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

Dx of pleural Tb

pleural fluid stain/cx


adenosine deaminase


Tb PCR


Quantiferon Gold


pleural bx (gold standard)

Tb meningitis

lymph predominance


protein is high


glucose is slightly low




gives mix of bacterial and viral meningitis




devastating esp in children

Side effects of Tb drugs

isoniazid- peripheral neuropathy, hepatotoxicity




rifampin- hepatoxicity




ethambutol- gout, optic neuritis (do not use in kids)




pyrazinamide- gout

Asbestos testing findings

CXR:


calcified pleural plaques, rounded atelectasis




PFT:


restrictive pattern




definitive dx is via bronchoscopy with bx

Asbestosis

common environmental cause of ILD




mineral silicate fibers lodged in lungs that are phagocytosed by macrophages




inflammatory process leading to fibrosis

Occupations assoc with asbestosis

construction worker


automobile repair


insulation


textiles


mining


milling


ship building

Long term asbestosis consequences

honeycombing --> end stage dz




increased risk of bronchogenic carcinoma




mesothelioma but not as much as lung cancer

Sitting tripod position

when someone sits sitting fwd with hands on knees




think COPD

Physical findings of obstructive dz

increased antero-posterior diameter




hyper-resonance to percussion




increased S2 --> secondary to pulm HTN

Chief complaints in emphysema vs chronic bronchitis

emphysema --> SOB




chronic bronchitis --> productive cough

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

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

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

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)

Vaccines for COPD

pneumococcal vaccine (booster q5 yrs)




annual influenza vaccine

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

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

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

Diagnostic test for sleep apnea

split night nocturnal polysomnography with CPAP titration with apnea hypopnea index >15

Tx for obstructive sleep apnea

behavioral modification for weight loss




nasal CPAP (O2 w/o pressure is useless)




oral appliances




hypoglossal nerve stimulator




surgery

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

Lung cancer on CT

>3cm lesion on CT is worrisome for lung cancer




non-calcified lesion

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

Granuloma description on CT

centrally calcified and smooth border

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

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

Two common heritable causes of PE

Factor V Leiden




Prothrombin gene mutation

Most common signs of PE

tachypnea and tachycardia




dyspnea




pleuritic chest pain




cough, calf, or thigh pain or swelling

D-dimer testing

increases are positive tests




very sensitive for detection of thromboembolic


dz




good for low risk pts

LE U/S or doppler U/S

sometimes used for DVT detection




is an adjunct test so never first line

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