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230 Cards in this Set

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  • Back
What kind of biopsy is needed to dx sarcoid when infiltrates are obvious on CXR? How about when hilar adenopathy is the only finding?
Transbronchial biopsy.

Otherwise, open lung biopsy
What is the alveolar gas equation?
PAO2 = (Pb-Ph20)*FiO2 - PaCO2/0.8
What are the 6 causes of hypoxemia?
V/Q mismatch, shunt, dec ventilation, dec diffusion, high altitudes and low mixed venous O2
What causes V/Q mismatch?
Obstructive lung disease, alveolar disease, ILD, PH, PE
What causes shunting?
ARDS or PNA (perfusion of non-ventilated alveoli), intracardiac shunt and vascular shunt
A-a gradient is present in which of the causes of hypoxemia? Which one is it not present in?
It's present V/Q, shunt, decreased SVO2, and decreased diffusion.

It is not present in hypoventilation and high altitude.
What is a normal A-a gradient? What's a rule of thumb to calculate expected? What about to calculate actual?

When can you see a normal A-a gradient in a patient who is hyperventilation?
5-15; expected is 0.3*age
-to calculate actual, do 150-(PaO2 +1.25*PaCO2)

You can see it in a patient with significant PE who is hyperventilating.
What is DO2 equal to?
CO X 1.34 X Hgb X SaO2 (Not PaO2)
What is SaO2 dependent on? What factor(s) hugely shifts it to the right?
tap tap tap shifts right. temperature, acidosis, phosphorous (inc phosphorous causes inc 2,3 dpg). SaO2 vs PaO2 - so decreased affinity for O2 promoting offloading to tissues.

CO and methemoglobinemia (iron goes from ferrous to ferric in hgb so it can't pick O2 up) hugely shifts it to the right.
What are exam signs of methemoglobinemia?
perioral and peripheral cyanosis, fatigue and dyspnea, coma/death
How do you treat methemoglobinemia?
100% O2, remove cause, and methylene blue
When is the normal oximeter inaccurate?
With either CO or methemoglobinemia
What is the Bohr effect?
Local acidosis causes release of O2 to the tissues
What is the net effect of systemic acidosis on oxygen saturation?
Lowers it (less O2 pickup at lung but inc delivery at tissue which dampens the negative effect)
What is the first PFT parameter to decrease in ILD or PAH?
How do you differentiate emphysema from chronic bronchitis?
Low DLCO vs normal DLCO
For lung volumes, what is abnormal in terms of percentages?
< 80% and > 120%
What is the PFT test used for ILD? What is airway obstruction defined as?
TLC is used for ILD. FEV1/FVC < 70% (normal is 80%)
What does obstruction look like on a flow-volume loop?
Scooping of the tracing in the latter half of expiration. Also overall it is left shifted (x-axis is going 5-->0) and smaller width and height.
What does restrictive disease look like on flow-volume loop?
Right-shifted (again x-axis going from 5-->0) but otherwise the similar to normal
What are the reasons for why bronchodilator test is done?
To see if beta agonist treats obstruction, and also to see if the current regimen is optimally treating the patient (so do not withhold medication in this case)
What is methacholine challenge for?
People with normal spirometry and PFTs, and intermittent asthma-like symptoms to look for bronchial hyperreactivity -often done in w/u for a chronic cough or cold air-induced exercise related bronchospasm
For pre-op, who gets PFT's and ABGs? What to look for?
If surgery is close to diaphragm (e.g. gallbladder) or if they have moderate lung disease - look for FEV1 < 1L or elevated PCO2 for stratifying high risk patients.
How do you determine if lung disease is restrictive by PFT's? Once you do that, what is the next step in ddx?
First look at TLC (<80%). If it is, next check DLCO to see if it is proportional or disproproportionately low to decreased TLC. This will tell you if it is extrathoracic or intrathoracid.
What is a complication of CABG to suspect if patient 2 days afterwards has new orthopnea? How to check for this?
Bilateral diaphragmatic paralysis 2/2 cold cardioplegia. Look for extrathoracic restrictive lung disease on PFT's.
Is silica a cause of asthma? How about unvented gas stoves?
No not silica

Yes unvented gas stoves release NO2 which worsens asthma
What is considered a positive bronchodilator response (seen in asthma dx)?

What is considered diagnostic for exercise induced bronchospasm on PFT's?
>12% FEV1 increase, or 200mL at least

Exercise-induced bronchospasm will have decrease 10% in FEV1 after exercise (or methacoline if cold air, etc induced))
Who should have peak flows monitored in asthmatic population?
patients with moderate to severe disease
How many days a week can you use albuterol before you're classified as having poor control of asthma?
>2 days a week
What should you use steroids in asthma exacerbation? How many hours before you see the antiinflammatory effects (as opposed to the initial bronchodilator effect)?
Use steroids when peak flow is < 80% after 3 Rx's of albuterol.

Steroids will take antiinflammatory effect only after 6 hours
What is the difference between ipratropium and tiotropium?
Ipratropium is short acting and spiriva is long-acting. Only ipratropium is used in asthma (per guidelines should only be used in ED).
For inhaled steroids, what is the difference in the dose response curve between mild asthma and severe asthma?
In mild asthma the dose response curve is flattened, so that low doses are just as effective as higher doses.
Besides more efficacy what is another benefit of spacer?
Spacers filter larger particles and reduce the amount of drug stays in oropharynx thereby reducing systemic side effects.
Which steroid is okay in pregnancy?
When in the treatment guidelines is LABA's recommended?
Only after inhaled steroids aren't enough (SABA should be 1st line in general). LABA should never be used alone, but instead wiht ICS.
What does cromolyn sodium do and when do you use it? Are there any side effects? How long does it take to take effect?
Cromolym sodium is a mast cell stabilizer and has no side effects. It takes several weeks to work properly, does not work in acute exacerbations. Should be used after SABA, ICS, LABA
When is monteleukast used?

What about theophylline- Is it good for acute exacerbation? How about for chronic?
It is never the preferred agent - for exercise-induced bronchospasm SABA is preferred.

Theophylline is not recommended for acute treatment of exacerbation because it has a narrow therapeutic index and increased risk of toxicity. For chronic treatment, yes as an adjunct to inhaled corticosteroids (but theophylline + ICS is less powerfull than LABA + ICS).
What are symptoms of theophylline toxicity?

What drugs increase toxicity?

What drugs will theophylline itself decrease the level of?
Nausea and vomiting, headache, tremulousness. Can have seizures, arrhythmias.

Cipro, Clarithro, allopurinol, MTX, propanolol, verapamil, estrogens.

Will decrease levels of phenytoin and lithium if co-administered.
What is omalizumab and what is it for?
Omalizumab is an anti-IgE ab that blocks IgE receptors on mast cells, basophils.

It is for patients with asthma and severe uncontrolled asthma already on optimal therapy (LABA+ICS).
When to use FEV1/PEF in terms of evaluating initially and later on?
Use FEV1 only in initial evaluation. PEF can be used later on for determining control of symptoms.
When do you give oral steroids to a patient with acute asthma exacerbation at any level?
Inhaled SABA x 3 treatments and if PEF is still < 80%, give oral steroids
What home PEF flow should trigger ED visit asap?

What ED PEF should trigger ipratropium addition to SABA?

What ED PEF after treatment is OK to discharge home with?
<50% of predicted or personal best

PEF < 40% in ED indicates that ipratropium should be added to SABA

PEF > 70% -- d/c home with SABA, OCS and follow-up
What to do with ventilation in asthma exacerbation intubation?

What to do with RR, Vt and flows rate?
Permissive hypocapnea to prevent autopeep. Focus on O2 sat of 90% and instead pH can be 7.2-7.25.

low RR, small Vt, high flow on inspiration -- all for decreasing autoPEEP.
Is obstruction in COPD reversible or irreversible? What is the FEV1/FVC ratio?
irreversible. FEV1/FVC < 70%
What are the symptoms and term applied to large airway damage?

What does small airway damage cause?

What does alveolar damage cause?
Cough and mucus - chronic bronchitis.

Airflow obstruction causing hyperinflation

Impaired cas exchange (emphysema)
How is alveolar damage different by etiology of obstructive disease?
In smoking-related COPD the alveolar damage (emphysema) is in bronchioles only or across lung.

In alpha1 antitrypsin deficiency it is across the lung, usually lower lungs.
What is chronic bronchitis defined as?
Productive cough for 3 consecutive months for at least years.
What does clubbing signify in a patient with COPD?
COPD alone does not cause clubbing. Look for lung cancer.
What are the GOLD criteria?
Management of COPD by FEV1, after having FEV1/FVC < 70% diagnosis. FEV1 >80%, 50-70%, 30-50%, and <30%.
What is the BODE index?
It incorporates pulmonary and extrapulmonary manifestations on survival.

BMI, Obstruction degree, Dyspnea, Exercise capacity
What is the best prognosticator in COPD?
What is the best predictor of FEV1?
Pack-years of cigarette smoking
At what point does PaO2 fall in COPD by FEV1?
When FEV1 is less than 50% predicted.
At what point by FEV1 does CO2 retention occur?
FEV1 less than 25% of predicted (PaO2 therefore falls first, then PCO2)
Who should get screened for AAT deficiency?
White patients with COPD less than 45 years
What should you be careful not to miss in a patient billed as COPD exacerbation?
How can spirometry or PEF be used in COPD exacerbation?
It should not be used in exacerbation.
When are antibiotics beneficial in chronic bronchitis?
Only if increased dyspnea, cough and sputum are present.
Does pulmonary rehab improve mortality in COPD?
No it does not (only oxygen, lung volume reduction surgery and smoking cessation)
How do you diagnose AAT deficiency?
Check serum level of alpha1 antitrypsin and genetic testing of Pi locus
How do you treat AAT deficiency?
Weekly IV alpha1 antiprotease infusions (pooled human AAT), also treat COPD symptomatically.

If very severe - lung transplantation. Also the IV infusion does not effect liver disease.
What is recombinant DNase and when should it be used?
Aerosolized recombinant DNase should be used to treat bronchiectasis only when it is caused by CF - it can cause harm in other causes.
What is CF secondary to?
Mutation of CFTR gene on chromosome 7, which regulates Na/Cl transporter. Transporter normally brings in Na and brings out Cl.
What are signs of CF?
hx of recurrent sinusitis, nasal polyps, weight loss, chronic productive cough. infertility in males.
What kinds of organisms are seen in sputum of patients with CF?
GNR's and weird organisms ((eg Burkholderia, Alcaligenes), also Asperillus and MAI.
What will sweat chloride test show in CF? What if patient has a strong clinical history and the sweat chloride test is normal?
elevated concentrations of chloride in sweat (although not intuitive based on cursory knowledge of what CFTR does).

if it is normal but you are still suspicious then do the nasal potential difference test, genetic analysis.
In addition to pulmonary toilet what else are options for CF management?
Recombinant human DNase (protease) and inhaled hypertonic saline.

Also b/l lung transplantation is an option.
How should causes of ILD be categorized?
Occupational/environmental; idiopathic; and other
What are the categories of occupational/environmental ILD?
1)hypersensitivity, 2) organic dust (byssinosis), and 3) inorganic dust (asbestosis, silicosis, coal workers' pneumoconiosis, and berylliosis)
What is the pathology and what are the causes of hypersensitivity pneumonitises?

What is the typical presentation?
Pathology- it is granulomatous reaction to organic antigens

Causes include- farmer's lung (moldy hay), pet birds, grain dust (grain elevator), isocyanates, air conditioning systems, and crack cocaine.

patient presents with recurrent or persistent PNA's w/hx of exposure to one of the antigens. (but also on ddx is sarcoid and COP and eosiniophilic pna)
How can hypersensititivy pneumonitis be differentiated from sarcoidosis?
BAL shows lymphocytosis in both, but CD4:CD8 ratio of <1. vs sarcoid CD4:CD8 is >4:1.
What is acute rx for hypersensititivy pneumonitis?
What is byssinosis and how does it present?
Byssinosis is caused by inhalation of cotton, flax or hemp dust. Not immune-related.

Progresses from occasional chest tightness to Monday chest tightness.
What does asbestos exposure cause on CXR?
bilateral, middle-thorax thickening (spares costophrenic angles) - these are benign plaques.

also pleural effusions (benign also)- vary from serous to bloody, +/- eos, and occur early in the exposure history.
What do malignant mesotheliomas arise from?
What is the latency period?
Is smoking a risk factor? What is the prognosis?
Asbestos exposure (not necessarily asbestosis). Latency period can be several decades.

No smoking association. Usually rapidly fatal.
What is asbestosis? Exposure history and latency period?

Is smoking a risk factor?
The pulmonary disease- parenchymal fibrosis, develops mostly in the bases.

Happens with a decade of exposure, and decades of latency period.

Smoking is not a RF for asbestosis, but it has synergy in development of squamous and adenocarcinoma (but not SCLC or LCLC).
What is the most prevalent occupational disease in the world? What are RF's? What is the latency?
Silicosis- years of exposure to crystalline silica - as in mining, glassmaking, ceramics, sandblasting, brick yards.

Latency is 2-3 decades.
What is the association between silica and TB?

Silica and cancer?
Silica ingested by alveolar marcophages render them ineffective - so a +PPD in these patients makes the dx of latent TB infection and should be treated regardless of age.

All patients with suspected silicosis should have yearly TB skin tests and screening.

Silica is considered a carcinogen.
What does silicosis look like on CXR?
Upper lung (vs asbestosis which involves lower lung).

Small calcified nodules in upper lung (ddx = TB, coal worker's pneumoconiosis and berylliosis), also hilar LAD (hilar eggshell calcification).
If patient with silicosis rapidly worsens what do you do?
Think TB
What does coal workers' pneumoconiosis look like on CXR? what is on the ddx for this?

what can they present with?
Upper lung fiield nodules - similar to silicosis, berylliosis, TB.

melanoptysis (coughing up black soot).
What do you suspect in a patient with coal workers' pneumoconiosis who then develops peripheral lung nodules? Any further workup?
suspect Caplan syndrome (massive coal workers' pneumoconiosis) -- check rheumatoid factor, bc it is associated with seropositive RA
What is RF for berylliosis?

What does it look like on CXR?
Working in high-tech electronics, alloys, ceramics, pre-WW II fluorescent light manufacturing.

Hilar LAD looks like sarcoidosis, also upper lobe (like silicosis, TB and coal workers' pneumoconiosis)
How can you diagnosis berylliosis?

Any treatment?
History, positive beryllium lymphocyte transformation test, lung bx showing noncaseating granulomas

Yes, berylliosis can be treated- steroids +/- methotrexate
What are the 2 most prominent idiopathic ILD's?
What does early IPF look like on HRCT? Late IPF?
early- ground glass
late- honeycombing
What does a low DLC signify in IPF?
It portends PAH and poor prognosis.
What is the association between clubbing and emphysema? clubbing and sarcoidosis?
Almost never seen with either one!
What is treatment for IPF?

how to see if there is any improvement with treatment?
Steroids +/- cytoxan, azathioprine. Can consider single-lung transplant.

Objectively measuring PFT's/DLCO, ABG w/exercise-related A-a gradient.
What is the typical presentation of COP (cryptogenic organizing pneumonia)? How to definitively diagnose COP?

How does it differ from IPF in presentation, management, and prognosis?
Insidious onset (weeks-months) of cough, fever, dyspnea, malaise, myalgias. would need open lung bx to definitively dx COP.

Multiple courses of abx w/o effect.

IPF onset is more insidious than COP (>6 months in IPF), there is no fever in IPF, and patients don't look acutely ill in IPF. CXR in COP is patchy infiltrates, whereas it is diffuse in IPF.

Management of COP- treat with steroids (not abx) and slow taper over 1 year. Prognosis is very good.
How many patients with rheumatoid arthritis get ILD? What is the most common lung problem seen in patients with RA?
> 1/3 of patients with RA will get ILD

The most common lung problem in RA is pleurisy +/- exudative pleural effusion +/- necrobiotic nodules in upper lung zones.
What else can cause ILD besides RA itself, in patients with RA?
Treatments for RA including gold and MTX.
What can cause COP?
50% are idiopathic. Other 50% are assoc with toxic fume inhalation, drug exposure (eg amio, bleo, carbamazepine, nitrofurantoin, dilantin, penicilliamine, sulfasalazine), infection, connective tissue disease.
What else can cause pleuritis?

What about scleroderma? How does lung disease differ in scleroderma vs CREST?
SLE, along with diaphragmatic weakness and hemoptysis.

There is no pleuritis with scleroderma. Scleroderma causes ILD and PAH. CREST causes just PAH and not ILD.
Is there an increased risk of lung ca with any of the connective tissue diseases?
Yes, increased risk of bronchogenic carcinoma with RA and scleroderma.
What are CXR findings for sarcoidosis? How does it change with severity? PFT's in sarcoidosis?
b/l hilar LAD +/- reticulonodular or alveolar infiltrates. The bilateral hilar lymphadenopathy disapperars as sarcoidosis progresses. PFT's are very variable.
Are there any skin findings that can be seen with sarcoidosis? What is it called when you have this and what does it imply?
Yes- erythema nodosum. Sarcoid with erythema nodosum is called Lofgren syndrome and has a good prognosis.
What is the natural course of sarcoidosis and what is management of it?
Natural course of sarcoidosis is that 3/4 patients will recover without treatment.

Can use steroids (inhaled or systemic) for severe lung symptoms or extrapulmonary symptoms.
What is histiocytosis X? Biggest risk factors for this?

How is this ILD different from other ILD's?
Also called Langerhans cell granulomatosis or eosinophilic granuloma. It is a form of ILD.

All patients are smokers. As opposed to most other ILD's, patients have normal or increased lung volume.
What are complications of eosinophilic granuloma?

What is it called when a group of these complications exist (and what are these complications)?
The granulomas can cause lytic bone lesions and DI (by involving posterior pituitary), honeycombing in upper lung fields, and also pneumothorax.

Hand-Schuller-Christian syndrome- eosinophilic granulomatosis causing lytic bone lesions, DI, and exophtalmus.
What is LAM on CXR and who does it occur in? What are these patients at risk for? What disease is LAM associated with?
LAM occurs only in premenopausal women. It has honeycombing diffusely (vs in upper lung fields only like in eosinophilic granuloma)

Chylous pleural effusions and pneumothorax.

It is associated with tuberous sclerosis.
What disease is associated with necrotizing granuloma? What are diagnostic tests for it?
Wegener granulomatosis (GPA)

Dx with c-ANCA and anti-PR3. Confirm with biopsy of nasal membrane or open lung biopsy (not kidney bc not always specific or sensitive).
What is the natural course of Wegener and how do you treat it? Prognosis with treatment?
Natural course is death within 2 years.

Treat with cytoxan and steroids for at least 6 months - can induce remission. Can do MTX for maintenance.
What is lymphomatoid granulomatosis? What does biopsy show? What is natural course of it and what is treatment?
It is like Wegener's but mainly only affects lungs (no sinuses, rarely kidneys). Biopsy shows a neroctic vasculitis.

50% will progress to histiocytic lymphoma.

Treat with cytoxan and steroids.
What is the differential for a necrotizing vasculitis on biopsy? Necrotizing granuloma?
Lymphomatoid granulomatosis and Churg-Strauss syndromes.

What is presentation of Churg-Strauss? What else is on ddx? What is treatment?
Necrotizing vasculitis with eos, and peripheral eos, hx of asthma. Asthmatic presents with progressive worsening and eosinophilia. Could be unmasked if they were given monteleukast and no steroids.

Also consider ABPA for this presentation.

Treatment is steroids.
What is the only ILD-causing vasculitis that is not granulomatous? Which vasculitidis that cause ILD are granulomatous?
Polyarteritis nodosa.

GPA, lymphomatoid granulomatosis, Churg-Strauss are all granulomatous.
What is PAN associated with? What is the presentation?

What diagnostic measures are available?

How do you treat it?
chronic hepatitis B.

Presents with constitutional symptoms +/- cough, skin nodules, abdominal pain, tender testicles

Dx with p-ANCA, anti-MPO, and non-granulomatous vasculitis by biopsy. Angiogram that shows aneurysms in small and medium sized BV's could be enough too.

Treat with cytoxan + prednisone and treat hep B
What is the ddx for eosinophilia?
parasite, asthma, ILD's (including eosinophlic pna, ABPA, and Churg-Strauss)
What are the eosinophilic ILD's?

What are 3 presentations (and their associated hallmarks) of eosinophilic pna?
Eosinophilic ILD's are eosinophilic PNA (Loeffler's, acute eosinophilic PNA, chronic eosinophilic PNA), Churg-Strauss, and ABPA

Loeffler syndrome 2/2 Ascaris (or Strongyloides, hookworms)- will see migratory CXR infiltrates.

Acute eosinophilic pna- acute, febrile, looks like ARDS. unknown cause.

chronic eosinophilic pna- most common. subacute with cough, wheezing, low-grade fever. assoc with asthma. it is the photograph negative of pulmonary edema. very high ESR.
How do you treat:
Loeffler syndrome?
Acute eosinophilic pna?
Chronic eosinophilic pna?
Loeffler syndrome- albendazole +/- steroids

Acute eosinophilic pna- ventilatory support and steroids

chronic eosinophilic pna- long-term steroids
What is ABPA 2/2 to? Who gets it?
allergic rxn to aspergillus.

patients with asthma and CF can get it. (so if you see progressively woresning asthmatic think ABPA vs Churg-Strauss).
What is seen with ABPA on labs and imaging?
eos (like churg-strauss) and look for Aspergillus in sputum cx. Also can do Aspergillus antigen skin prick test and hten measure total IgE and Aspergillus IgG and IgE

Imaging shows "fingers-in-glove" appearing central infiltrate.
How do you treat ABPA?
Itraconazole +/- steroids.
What is alveolar proteinosis secondary to? What organisms are associated with infections in this?

Who gets it and what is the presentation? Dx? Rx?
Defective alveolar macrophages causing a buildup of pulmonary surfactant.

PNA's 2/2 to nocarida, mycobacteria, or fungus.

middle-aged males presenting with indolent cough, constitutional symptoms, hypoxemia w/shunt. Dx with biopsy.

Treatment with whole lung lavage +/- GM-CSF for new macrophages.
What is typical Goodpasture's presentation? what is seen on pathology?
Hemoptysis preceding renal abnormalities.

See linear deposition of IgG and C3 in alveoli and glomerular BM's.
How do you treat Goodpasture syndrome? What about for severe pulmonary hemorrhages?
Treat with immunosuppressives and plasmapheresis.

Nephrectomy may treat severe pulmonary hemorrhages.
What is the usual way to diagnose interstitial lung disease? What about for interstitial pneumonitis?
Bronchoscopy with transbronchial biopsy.

For interstitial pneumonitis best way is thorascopic bx / open lung bx.
What are the 3 broad categories of diseases that can cause pulmonary hemorrhage?

What 4 autoimmune diseases are assocaited with pulmonary hemorrhage? What other conditions can cause pulmonary hemorrhage?
Autoimmune, cardiopulm, and infection.

Goodpasture, GPA, SLE, idiopathic pulmonary hemorrhage.

Cardiopulm causes: pulm AV malformations, aortic aneurysm, mitral stenosis.

infection: bronchitis, bronchiectasis, TB, abscess, aspergilloma, chemo
What are WHO groups for PH?
Group 1- PAH (idiopathic and immune mediated)

Group 2- 2/2 Left heart
Group 3- assoc with lung (COPD, ILD)
Group 4- chronic VTE
Group 5- multifactorial, mechanical obstruction
What to look for in PFT's in patients with PH?
Low DLCO = poor prognosis. Other PFT parameters are normal.
Who gets anticoagulated in PH?
idiopathic PAH and group 4 (2/2 chronic VTE)
What are medication options in PAH? Anything to watch out for with them?
endothelin receptor antagonists (bosentan)


prostaglandin (epoprostenol)- exhibit tachyphylaxis and need to slowly ramp up dosing over time

PDE-5 inhibitors (revatio)
What is the usual cause of PE in hospitalized patients?
inadequate DVT prophylaxis
What do pleurisy and friction rubs tell you about a PE?
likely not massive- these findings tell you it is 2/2 to a distal vessel blockage near the pleura.
What combination of findings is specific for a massive PE?
cyanosis, S3/S4 gallop, increased P2
What does superficial migratory thrombophlebitis suggest? How about thrombophlebitis in unusual places (eg arms and trunk)
Malignancy for both
Where is Hampton hump seen on CXR in PE? What is Westermark sign?
Hamptom hump is wedge-shaped defect just above the diaphragm

Westermark sign is lack of vasculature in area downstream of the embolus.
In Wells Criteria for PE, what are the 2 most important factors? What are the other ones?
2 most important are clinical signs of DVT and alternative dx is less likely.

The other criteria are tachy, immobilization/surgery recently, prior DVT/PE, hemoptysis, and malignancy
Who should get pulmonary angiography?
Reserved for cases with inconclusive results from CT/PE and V/Q scan, negative DVT workup, but still a high clinical suspicion
Does it matter what type of heparin is used for PE?
Yes, lovenox is better because of lower risk of major bleeding (however should still give UFH if high risk bleeder) and reaches therapeutic state the fastest. Also lower risk of osteoporosis.
What is the mechanism of action of lovenox? UFH?
Lovenox inactivates factor Xa only.

UFH binds antithrombin making it more effective in inactivating thrombin and factor Xa.
How do you treat HIT type II?
Stop heparin and use a direct thrombin inhibitor (eg lepirudin, bivalirudin, argatroban) and coumadin when plt count recovers.
Contraindication to lepirudin?
CKD. le-pee-ru-din shouldn't be given to patients who can't pee
What does fondaparinaux do? Advantage? Contraindication? Drawbacks?
Factor Xa inhibitor.

subQ injection once daily, and no HIT.

Contraindication- CKD

Drawbacks- can't monitor and no antidote
How long should overlap period be when bridging to coumadin?
4-5 days, with therapeutic INR x 2 days
What does fat emboli present with? In what context does it occur?
It presents with the triad of dyspnea, confusion and petechiae (neck, axillae, eyes)

Will occur w/in 3 days of femur fx, after CPR, or with sickle cell bone-occlusive crisis.
Light criteria for exudate?
protein > 0.5 or LDH > 0.6 ( or > 200)
What size of pleural effusion will require therapeutic thoracentesis in the setting of PNA?
What features of pleural effusion require chest tube +/- surgical intervention?
complicated pleural effusion- loculation, pH<7.2, glucose<60, postive gram stain/cx
What are the most common malignant pleural effusions 2/2 to?

What if you suspect it is 2/2 to pleural malignancy- what to do?
Lung > breast > lymphoma.

If pleural malignancy, cytology of effusion fluid is as good as pleural biopsy. If cytology negative do thorascopy (not pleural biopsy).
What does a grossly hemorrhagic pleural effusion in a patient cause consideration for?
How do you diagnose TB etiology of pleural effusion?
ADA, interferon assa, and TB DNA PCR from pleural fluid along with cultures etc. If negative do a pleural biopsy (unlike the workup for malignancy - pleural biopsy for malignancy is not used).
How does WBC count help with exudative pleural effusion?
>1,000 think exudate
>10,000 think complicated parapneumonic effusion
>100,000 think empyema
What is the definition of hemothorax and what is it secondary to?
Hemothorax is grossly bloody effusion with hematocrit ratio > 0.5.

Think trauma.
What does a very low pleural fluid glucose suggest (< 30)?
Rheumatoid arthritis (vs 80 in TB, 60 in cancer, empyema)
What are causes of a chylous effusion?
TG elevated - malignancy and trauma

Beware of pseudochylous effusion where cholesterol is elevated but not TG- think chronic inflammation like TB, RA
What is a Pott puffy tumor?
Sign of osteomyelitis of the frontal bone in sinusitis - a pale, cool edematous area over the forehead.
What is Lemierre syndrome? What organism?
Thrombophlebitis of the jugular vein 2/2 adjacent tonsillar abscess. anaerobic sepsis.
What characteristics of a sputum sample are needed in order for it to be adequate for diagnosing PNA organism?
<10 epithelial cells per low-powered field, and >25 PMN's
What scores on the PNA severity index (PSI) require admission?

What is CURB-65 and what score should be admitted?
PSI stages 4 and 5 (based on exam, comorbidities, age, labs).

curb-65 score > 1 admitted:
Uremia (BUN>18)
RR > 30
BP Systolic < 90 or diastolic < 60
65yo or older
What type of PNA are patients with cattle or sheep exposure more likely to get?
Coxiella burnetii (Q fever)
What do you use for outpatient Rx for CAP? What if the patient has any RF's for drug-resistant Strep pneumo?
Azithro/clarithro or doxycycline.

If RF's for DRSP (olrd, hx of recent abx, immunosuppressed, DM, COPD, CHF), use levaquin or augmentin + azithro.
How should you treat non-ICU inpatient CAP?

How about ICU CAP?
Use levaquin or augmentin + azithro/doxi.

In ICU, would use ceftriaxone + levaquin/azithromycin. Change if MRSA/Pseudomonas suspected.
In pneumococcal PNA, what complications are associated with increased mortality?
Multilobar disease, bacteremia, and WBC < 6,000 are associated with increased mortality.
Who gets the pneumococcal vaccince?
People >65yo, smokers, or chronic disease.

Give the booster vaccine once to patients over 65yo if >5 years have passed since initial vaccination when they were less than 65.
In pneumococcal PNA, what complications are associated with increased mortality?
Multilobar disease, bacteremia, and WBC < 6,000 are associated with increased mortality.
Who gets the pneumococcal vaccince?
People >65yo, smokers, or chronic disease.

Give the booster vaccine once to patients over 65yo if >5 years have passed since initial vaccination when they were less than 65.
What does S pneumo look like on gram stain? H. influenzae?
S. pneumo- lancet-shaped gram positive diploccoi

H. flu- pleomorphic gram negative coccobacilli
What is a presentation in which to suspect Staph aureus PNA?
A resolving case of influenza that worsens with new dyspnea and cough (suprainfection).
What can you use to treat MSSA PNA? MRSA PNA?
MSSA PNA can be treated with nafcillin (beta-lactam). MRSA PNA should be treated with vanc or linezolid - not daptomycin.
What is the bulging fissure sign? What do you see currant jelly sputum in?
Bulging fissure sign on CXR (bowing fissure with consolidation), as well as currant jelly sputum are seen in Klebsiella PNA.
What bacteria is associated with PNA in COPD patients only? What is seen on sputum culture?
Moraxella catarrhalis. Gram negative cocci.
Why are atypical organisms of CAP called atypical? How do you diagnose?

What are examples of atypical organisms?
They are not identifiable by Gram stain and are resistant to beta-lactam abx. Dx bacteria with IgM titers (except Legionella)

Mycoplasma pneumoniae, Chlamydophila pneumoniae, Legionella pneumophila, endemic fungi and viruses
What does mycoplasma PNA present with?
Insidious PNA but extrapulm manifestations too (hemolytic anemia, erythema multiforme, arhtritis, confusion)
What does Chlamydophila pna present with that is unique?
Sore throat --> 2 weeks later with PNA and horse voice
How do you treat severe legionella pna? What does it present with?
Azithro or quinolones in addition to rifampin.

Legionella prsents with h/a, diarrhea, confusion --> pulm symptoms. Can see hyponatremia and hypophosphatemia.
What are skin findings associated with coccidioides? How do you diagose it? Treatment?
Erythema nodosum and erythema multiforme

Diagnose with KOH smear, fungal culture, serum ab.

Treatment- commonly self-limted. if hemoptysis or CXR abnormal then diflucan or ampho
How do you treat histoplasmosis? What if patient has HIV?
Itraconazole or ampho.

If HIV then treat with chronic suppresion with itraconazole.
How do you diagnose blastomycosis? Treatment? What if patient has HIV?
KOH prep shows broad-base budding yeast. Treat with observation or itraconazole or ampho.

If HIV then treat with chronic itraconazole like in histoplasmosis.
Which endemic fungal disease causes hilar adenopathy, focal infiltrates and nodules?
Which patients are at increased risk for complications from H1N1?
Young people and pregnant women
What is the most common cause of lung abscess?
Aspiration of organisms from the oropharynx
What is the classic CXR for miliary TB?
faint and diffuse reticulonodular infiltrate (nodules are 1mm)
What is the role of PPD test in patients who have had the BCG vaccine?
Mantoux test should still be given bc the vaccine was probably given very long time ago
What proportion of patients with active TB and negative PPD?

How long does PPD take to react after TB exposure? Does a control test help to rule out false negative PPD in suspicion of anergy?

Up to 10 weeks

No it does not - can still have false neg PPD despite neg control. Therefore there is no role for it.
Who has 5mm threshold for positive PPD? Who has 15mm? 10mm?
5mm for HIV, pos CXR, severely immunocomp, close contacts.

15mm if no RF's

10mm for everyone else
What is the booster effect in TB testing? What does 'new converter' refer to? How to avoid mixing these two up?

If given >10mm induration increase, How does management of new converter differ from booster effect?
Booster effect refers to retesting with a 2nd PPD some time after the 1st PPD in patients who develop no induration (no induration bc T cells have bad memory). Can last for several months even.

New converter refers to new positive PD: >10mm increase within 2 years

Avoid mixing the 2 by retesting a non-responder in a week to establish new baseline. (2 step regimen at first screening)

Management is the same - treat for LTBI. The difference is that the risk of reactivation TB w/in the next 2 years is much higher in new converter.
Which of the TB drugs cannot be used in pregnancy?
Pyrazinamide (PZA)
How do you treat LTBI?
INH x 9 months or if intolerant, Rifampin x 4 months
What is treatment for active TB?

What if patient has HIV on HAART?
-2 months with 4 drug Rx (can use 3 drugs (INH, rifampin, PZA) only if there is a very slight prevalence of MDR pathogen)
-4 months with INH+rifampin

If on HAART, give rifabutin instead of rifampin.
When is vit B6 needed with TB meds?

What if patient with active TB cannot take PZA?

What if patient with active TB cannot take INH?
If regimen contains INH.

If they cannot take PZA then give INH and rifampin for a total of 9 months, not 6 months (2+7 instead of 2+4).

If no INH, give 3 drugs for 6 months total, or rifampin + ethambutol for 12 months.
Which TB drug causes decreased visual acuity and decreased color perception? Reversible?
Ethambutol - reversible
What do you do if a healthy patient had a sputum sample growing non-TB mycobacteria?

What is the treatment for non-TB mycobacteria?

Treatment is clarithro, ethambutol, rifampin (but guided by susceptibilities) for months.
What type of organism is associated with cutaneous infections at surgical sites of immunocompetent patients?
Non-TB mycobacteria - after plastic surgery for example with exposure to sand and water.
What is the only screening required with active TB regimen?

What are effects of streptomycin?
Ethambutol needs eye screening

Streptomycin is an aminoglycoside- ototoxicity and nephrotoxicity.
What kinds of infections do patients with organ transplant patients get?
Same as patients with T-cell defects.

First month- nosocomial infections
Months 1-4- PJP (PCP), CMV, Mycobacteria
>4 months- PJP, fungus, virus
What is the most common cause of post-transplant fever 2 months after transplant? What does it cause? Diagnosis? Management?
CMV infection- causes pneumonitis, hepatitis, adrenalitis causing AI

Dx with seeing inclusion bodies on BAL or tissue sample

Rx with ganciclovir (+ IVIG in BMT patients)
Who gets steroids in PJP? Benefit?
PaO2 < 70 or A-a gradient > 35 -- reduces respiratory failure and mortality
Who gets invasive pulmonary aspergillosis? What is the presentation? What helps to diagnose this but what do you need to be careful with in one of these tests?
Patients who are immunocompromised.

Acute or indolent sxs, can see hemoptysis with fungal ball

Diagnose with 1) HRCT of chest - see halo sign (early evidence of pulmonar infarct) and
2) galactomannan (seen in Aspergillosis cell walls- but beware zosyn contains galactomannan and give false positive)
How do you treat invasive pulmonary aspergillus infections?
What if there is aspergilloma?
Sinus disease?
Use voriconazole.

If aspergilloma - surgery

If ABPA- itraconazole and steroids.

sinus disease- surgery and any antifungal
What is next step of management if crypto is found in sputum?
lumbar puncture
Who gets nocardia infections? What should you be aware of as potential complications?
T-cell deficient patients and pulmonary alveolar proteinosis.

Be aware of brain abscesses and subc spread.

Treat with sulfonamides.
What is mucormycosis called now and who gets it?
It's not called zygomycosis

Leukemia and DM/DKA patients get it.
What drug causes hypersensitivy interstitial pneumonitis?
What is the prognosis with gold-induced lung disease?
It is reversible- just stop the drug.
What drugs have dose-related pulmonary effect?
Bleomycin and amiodarone
What exacerbates bleomycin lung toxicity?
Uremia, supplemental O2 and XRT
What to do with pulmonary hemorrhage in AML?
May be 2/2 AML but also rule out aspergillus.
What is characteristic of radiation changes on imaging?
You will see sharp boundaries corresponding to field of radiation exposure.
What is PaO2/FiO2 in ALI? ARDS?
300; 200
What acid-base disturbance should you look for in a patient who is having difficulty weaning off a vent?
Alkalemia - decreases respiratory drive
What is the role of PEEP in focal lung disease?
It can decrease PaO2. Therefore only use PEEP in diffuse lung disease.
What is refeeding sydrome secondary to? What if you see heart and respiratory failure (what is the cause)?
Dramatic increase in circulating insulin levels - swift uptake into cells of glucose, K+, Phos, Mg.

Severe hypophos can cause CHF, respiratory failure
What is the formula for SVR?
(MAP-CVP) * 80 / CO
What is the danger with cardiac advancement of Swan Ganz catheter in patient with hx of LBBB?
Can cause RBBB resulting in complete block (transient)
What is the cure rate of uvulopalatopharyngoplasty in OSA?

In whom is it most effective?

Best in young, thin patients with mild to moderate OSA.
What is the role of modafanil (provigil)?
If patient is getting daytime sleepiness espite receiving full therapy.
What is obesity hypoventilation syndrome?
BMI > 35 and PCO2 > 45 while awake.
How should patients with OSA sleep?
not supine
What is the ddx for Cheyne-Stokes breathing?
Central sleep apnea/CNS disease, high altitudes for the 1st time, CHF
How d you treat central sleep apnea?
Avoid CNS depressants, weight loss. can try nighttime O2, acetazolamide (causes metabolic acidosis), can use CPAP
When do nocturnal O2 desaturations occur without apnea?
COPD, kyphoscoliosis, and muscular dystrophy
What type of lung cancer is asbestos associated with?
both adenocarcinoma and squamous. (and mesothelioma)
What are risk factors for lung cancer in addition to smoking? Whoi s most affected by 2nd hand smoke?
-uranium and nickel mining, -chromium and arsenic
-radon in underground miners.
-atmospheric pollution.

second hand smoke (>25 PY's) in people < age 20.
What is metastatic potential of adenocarcinoma? large cell? squamous cell cancer? Radiographic features of squamous cell?
Adenocarcinoma usually metastasizes early especially CNS, adrenals and bones.

Large cell will spread to CNS and mediastinum.

Squamous does not spread early. It is usually central and most likely lung cancer to cavitate.
What are the paraneoplastic syndromes associated with small cell lung cancer?
siADH, ectopic ACTH production, and LEMS
What impacts the management of solitary lung nodule when discovered?
Size and risk for lung cancer
What does calcification of a solitary pulmonary nodule suggest?
that it is benign (popcorn = hamartoma, etc).
How often should a lung nodule be followed?
If calcified and low risk, follow q3 months for 2 years.

If high risk- FNA/bronch/open lung biopsy.

If > 1cm -- can use PET scan
What paraneoplastic syndromes occur in squamous cell ca of lung?
What paraneoplastic syndrome is seen in all NSCLC?
Hypertrophic pulmonary osteoarthropathy (HPO) -- clubbing and new bone formation on long bones (painful ankles)
What comes first in staging lung cancer, imaging or tissue biopsy?
If effusion is present in suspected lung ca, is it effective to get the fluid? What to do if it comes back negative?
Yes - submit a 2nd sample if 1st is negative for malignancy.
How does post-resection XRT help in NSCLC management?
Reduces rate of local recurrence but not survival.
What lung cancer is associated with gynecomastia?
Large cell lung ca
Which cancers causes SVC syndrome?
Most are caused by small cell or squamous cell lung ca (also lymphoma, metastic tumors)
Anterior mediastinal mass ddx?

Middle mediastinal mass?

Posterior mediastinal mass?
Anterior: Thymoma, thyroid tumor, teratoma, PTH tumor, testicular met

Middle: lymphoma, cysts

Posterior: neurogenic, esophageal lesions
BAL showing increased lymphocytes? Increased eosinophils?
Hypersensitivity pneumonitis and sarcoidosis.

Increased eos- acute and chronic eosinophilic PNA, Churg Strauss, Loffler syndrome, parasite, TB, drug rxn, malignancy
Inclusion bodies seen on BAL cells in what disease?

Turbid, PAS-positive material on BAL?

Langerhans cells on BAL?

Foamy changes with lamellar inclusions on BAL?

hyperplastic pneumocytes on BAL?
CMV pneumonia

PAS-positive in alveolar proteinosis.

Langerhans cells in histiocytosis x (eosinophilic granulomatosis)

Foamy changes w/lamellar inclusions- amiodarone induced disease

hyperplastic- seen in cytotoxic lung injury