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60 Cards in this Set

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ASA/Samter's triad


nasal polys

aspirin use

avoid aspirin or NSAIDs

tx with leukotriene inhibitors

Drugs to avoid in asthmatics

especially with nasal polys:



color agents such as tartrazine


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:


irritating inhalants

cold air


emotional upset

atacks are severe and prognosis is poor

Extrinsic asthma

20% of pts


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:


hilar adenopathy

erythema nodusum


Sarcoidosis imaging

obtain CXR (PA & lateral views):

find b/l hilar enlargement


reticular nodular disease with b/l hilar adenopathy

Sarcoidosis presentation


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


lymphoma (Hodgkins)

SLE or other vascular dz

fungal infection


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






Optho exam

PPD and/or IFN-g release assay

PPD interpretation


high risk --> >5mm is +

immunocompromised including HIV+

steroid use

organ transplant

contact with active Tb

moderate risk --> >10mm is +

healthcare workers


renal dz

lung dz


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




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)


isoniazid & B6 for 6 months depending on drug toxicity & compliance


rifampin for 4 months for those who cant take isoniazid


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%)



lymphatic system

GU tract

bones and joints


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


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


calcified pleural plaques, rounded atelectasis


restrictive pattern

definitive dx is via bronchoscopy with bx


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





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


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


DDx for lung nodule on CXR


bronchogenic ca

pulm metastases

carcinoid tumor

benign dz:


benign tumor (hamartoma)

resolving infarction

rheumatoid and vasculitic nodule

AV malformation


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


pleuritic chest pain

cough, calf, or thigh pain or swelling

D-dimer testing

increases are positive tests

very sensitive for detection of thromboembolic


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