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STEP2 > Pulmonology > Flashcards

Pulmonology Flashcards

1
Q

Describe the presentation, associated findings, diagnosis, and treatment of chronic asthma.

A
  • presents as wheezing with acute onset of dyspnea, cough, and chest tightness which are often worse at night
  • associated with sensitivity to aspirin, nasal polyps, and atopy
  • use spirometry showing a 12% rise in FEV1 following bronchodilator administration if patients are symptomatic
  • use methacholine challenge showing a 20% decrease in FEV1 if patients are asymptomatic
  • the mainstays of treatment are SABA, ICS, and then a LABA (salmeterol or formoterol)
  • use tiotropium, omalizumab, montelukast, theophylline, and cromolyn salts as alternative therapy
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2
Q

What spirometry findings are consistent with asthma?

A
  • FEV1/FVC decreased
  • FEV1 increases more than 12% with bronchodilators
  • DLCO normal or slightly increased
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3
Q

What is the difference between diagnosing chronic asthma and an acute asthma exacerbation.

A
  • for chronic asthma diagnosis, use spirometry if symptomatic and methacholine challenge if asymptomatic
  • for acute exacerbation with current dyspnea, use peak flow or ABG
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4
Q

What is the difference between tiotropium and ipratropium?

A

both are muscarinic antagonists but tiotropium has a longer duration of action than ipratropium

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5
Q

List the class of agent each of the following asthma medications belongs to:

  • albuterol
  • cromolyn salt
  • ipratropium
  • tiotropium
  • salmeterol
  • formoterol
  • budesonide
  • montelukast
  • omalizumab
A
  • albuterol: SABA
  • cromolyn salt: mast cell stabilizer
  • ipratropium: short acting muscarinic antagonist
  • tiotropium: long acting muscarinic antagonist
  • salmeterol: LABA
  • formoterol: LABA
  • budesonide: ICS
  • montelukast: leukotriene receptor antagonist
  • omalizumab: anti-IgE
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6
Q

How is acute asthma exacerbation diagnosed and treated?

A
  • because patients will be short of breath, spirometry can’t be performed
  • instead the diagnosis is made with peak flow or ABG
  • treat with oxygen, albuterol, iptratropium, oral steroids, and magnesium
  • monitor for a rise in PaCO2, which suggests impending respiratory collapse and the need for intubation
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7
Q

What is the key indicator that a patient with an asthma exacerbation may need intubation?

A

a rising PaCO2, which suggests impending respiratory failure

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8
Q

Describe the pathogenesis, presentation, diagnosis, and treatment of COPD.

A
  • in most cases tobacco smoke causes destruction of elastin in the lungs which is responsible for lung compliance and recoil during exhalation
  • presents with dyspnea, barrel-chest, and weight loss
  • the best initial test is CXR; the most accurate is PFTs; echo will show evidence of chronic right heart strain
  • only smoking cessation, oxygen therapy, and influenza and pneumococcal vaccinations improve mortality
  • LAMAs are the mainstay of symptomatic therapy; SABAs, ICS, and LABAs are also used
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9
Q

Describe the PFT results consistent with COPD.

A
  • FEV1 less than 80% predicted
  • FEV1/FVC less than 70% predicted
  • no bronchodilator or methacholine response
  • decreased DLCO
  • increased TLC
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10
Q

What are the indications of oxygen therapy in those with COPD? What other interventions improve mortality?

A
  • use oxygen for those with PaO2 less than 55 or SaO2 less than 88%
  • as well as for those with PaO2 less than 60 or SaO2 less than 90% who have evidence of right heart strain (pHTN, elevated Hct, or RA/RV hypertrophy)
  • vaccination for influenza and pneumococcus as well as smoking cessation also improve mortality
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11
Q

How are acute COPD exacerbations treated?

A
  • bronchodilators like albuterol and ipratropium
  • oral corticosteroids
  • antibiotics, primarily azithromycin
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12
Q

Describe the etiology, presentation, diagnosis, and treatment of bronchiectasis.

A
  • most cases are due to CF; others are secondary to infection and immune deficiency
  • presents with dyspnea, wheezing, hemoptysis, and high volume purulent sputum production
  • the best initial test is CXR showing dilated, thickened bronchi; the most accurate is CT showing the same
  • treat with chest physiotherapy; use azithromycin for exacerbations; use Dornase alfa for cases secondary to cystic fibrosis
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13
Q

Describe the pathophysiology, presentation, diagnosis, and treatment of allergic bronchopulmonary aspergillosis.

A
  • it is a hypersensitivity of the lungs to fungal antigens almost exclusive to those with a history of atopy
  • presents with recurrent episodes of brown-flecked sputum, transient CXR infiltrates, cough, wheezing, and hemoptysis
  • diagnosis with skin reactivity to Aspergillus antigens, peripheral eosinophilia, and elevated serum IgE
  • treat with oral steroids, itraconazole, and omalizumab
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14
Q

Describe the pathogenesis, presentation, diagnosis, and treatment of cystic fibrosis.

A
  • due to autosomal recessive CFTR gene mutations that impair chloride transport and lead to thickened secretions, which damage the pancreas, sinuses, intestines, GU tract
  • presents with chronic lung disease and recurrent pulmonary infections with Staph and Pseudomonas
  • sinus pain, nasal polyps, meconium ileum, pancreatic insufficiency, recurrent pancreatitis, distal intestinal obstruction, biliary cirrhosis, and infertility are also seen
  • the most accurate test is sweat chloride greater than 60; genotyping is likely to miss many mutations
  • treat with antibiotics, vaccination, bronchodilators, recombinant DNase and lung transplantation
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15
Q

Why are most patients with cystic fibrosis infertile?

A
  • most males have azoospermia and some lack vas deferens

- in females, chronic lung disease alters menstruation and thickened cervical mucus blocks sperm entry

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16
Q

What is the most common organism responsible for pneumonia in patients with cystic fibrosis?

A
  • S. aureus predominates early in life

- Pseudomonas predominates later on

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17
Q

How are CAP and HAP defined?

A
  • CAP is pneumonia with onset before hospitalization or within 48 hours of admission
  • HAP is pneumonia with onset more than 48 hours after admission or within 90 days of a prior hospitalization
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18
Q

What is unique about the population affected by and the presentation of each of the following CAP pathogens:

  • Strep pneumo
  • Hib
  • S. aureus
  • Klebsiella
  • Anaerobes
  • Mycoplasma
A
  • Strep pneumo is the most common cause of CAP
  • Hib is most commonly seen in patients with COPD
  • S. aureus is a common cause of secondary pneumonia
  • Klebisella is seen in alcoholics and diabetics and presents with “currant jelly” sputum due to necrosis
  • Anaerobes are seen in those with poor dentition and those who aspirate, presenting with a foul-smelling sputum
  • Mycoplasma is seen in young, healthy patients
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19
Q

What are the agents responsible for atypical pneumonia? What does this mean?

A
  • Mycoplasma, viruses, Coxiella, PJP, and chlamydia

- these are not visible on Gram stain or cultural on standard agar and tend to cause bilateral interstitial infiltrates

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20
Q

What is the best method for diagnosing pneumonia?

A
  • the best initial test is a CXR looking for lobar consolidation or bilateral infiltrates
  • sputum sample with gram stain and culture is the best diagnostic test though it lacks sensitivity
  • in some cases, there is a place for thoracentesis looking for empyema or a BAL
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21
Q

What is unique about the diagnosis for the following causes of community-acquired pneumonia:

  • Legionella
  • Mycoplasma
  • Pneumocystis jiroveci
A
  • Legionella: use a urine antigen or culture on yeast-charcoal agar
  • Mycoplasma: use PCR and look for cold agglutinins
  • Pneumocystis jiroveci: perform a bronchoalveolar lavage because other methods are unlikely to identify the organism and identification is critical to guide therapy
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22
Q

Under what circumstances would you perform a thoracentesis, chest tube placement, or bronchoscopy in those with community-acquired pneumonia?

A
  • thoracentesis for new, large effusions, looking for empyema
  • chest tube for empyemas which act like abscesses and will improve more rapidly with drainage
  • BAL for those in the ICU for whom sputum didn’t yield an etiology and empiric treatment isn’t working; and for those in whom PCP is the presumed diagnosis
23
Q

Describe the empiric treatment of community-acquired pneumonia.

A

> outpatient treatment for previously healthy patients and no antibiotics in the past 3 months: macrolide or doxycycline
outpatient treatment for patients with comorbidities or antibiotics in the past 3 months: respiratory fluoroquinolone
inpatient treatment indicated for 2 or more points on CURB65: respiratory fluoroquinolone or ceftriaxone plue azithromycin

24
Q

Which patients with CAP should be hospitalized and what treatment should they receive?

A

hospitalize if they meet two of the CURB65 criteria:
- confusion
- uremia
- respiratory distress
- BP low
- age over 65
treat with a respiratory fluoroquinolone or ceftriaxone blue azithromycin

25
Q

How are community-acquired, hospital-acquired, and ventilator-associated pneumonias treated?

A
  • CAP as outpatient: macrolide or doxycycline unless they’ve had antibiotics in the last 90 days, then use a respiratory fluoroquinolone
  • CAP as inpatient for CURB65: respiratory fluoroquinolone or ceftriaxone plus azithromycin
  • HAP: antipseudomonal cephalosporin, antipseudomonal penicillin, or carbapenem
  • VAP: combination of antipseudomonal cephalosporin, penicillin, or carbapenem; plus an amino glycoside or fluoroquinolone; plus a MRSA agent like vanc or linezolid
26
Q

Describe the etiology, presentation, diagnosis, and treatment of lung abscesses.

A
  • typically due to an anaerobes after a large-volume aspiration and inadequate treatment
  • presents as a chronic infection developing over weeks with large-volumes of foul-smelling sputum
  • CXR is the best initial test, but biopsy and culture is most accurate
  • treat with clindamycin or penicillin
27
Q

Describe the presentation, diagnosis, and treatment for PCP.

A
  • presents in patients with CD4 counts less than 200 not on bactrim prophylaxis
  • presents with dyspnea, dry cough, and fever like other atypical pneumonias; notably LDH is always elevated
  • the best initial test is a CXR or ABG looking for an increased A-a; then move to sputum culture; most accurate is BAL
  • bactrim is first-line for treatment as well as prophylaxis and steroids are added for PaO2 less than 70 or A-a greater than 35
  • switch to clindamycin plus primaquine or to pentamidine for bactrim myelosuppresion
28
Q

What are alternatives to bactrim for PCP prophylaxis and treatment? What would be an indication for these?

A
  • switch from bactrim if it causes myelosuppression
  • for prophylaxis use dapsone or atovaquone
  • for treatment use clindamycin plus primaquine or use pentamidine
29
Q

Describe the presentation, diagnosis, and treatment of active TB in a symptomatic patient.

A
  • presents with fever, cough, hemoptysis, weight loss, and night sweats in a patient with risk factors
  • the best initial test is a chest x-ray then three sputum acid-fast stains are needed to fully exclude TB; pleural biopsy is the most accurate test
  • treat with two months of RIPE therapy followed by four months of rifampin and isoniazid
  • add steroids to reduce the risk of constrictive pericarditis in those with pericardial involvement and neurologic complications in those with meningitis
  • treatment should be under direct observation to ensure compliance
30
Q

When is TB treatment extended beyond the typical six months?

A

for those with any of the following:

  • osteomyelitis
  • miliary TB
  • meningitis
  • pregnancy (due to contraindications to pyrazinamide)
  • cavitary lesions
31
Q

Describe the adverse effects and management of the TB drugs.

A
  • all are capable of causing a transaminitis, but shouldn’t be stopped unless enzymes are 3-5 times the upper limit of normal
  • rifampin causes a benign red discoloration of body secretions
  • isoniazid causes peripheral neuropathy treated with B6
  • pyrazinamide causes hyperuricemia but is only stopped if symptomatic
  • ethambutol causes optic neuritis and color vision change and the dose should be decreased for those in renal failure
32
Q

What is considered a positive PPD?

A
  • greater than 15mm in the general population
  • greater than 10mm in those recent immigrants, prisoners, healthcare workers, close contacts of someone with latent TB
  • greater than 5mm in those with HIV, chronic steroid use, close contacts of someone with active TB, abnormal calcifications on CXR, and organ recipients
33
Q

When are PPD and interferon gold testing useful?

A

only for asymptomatic paints at increased risk; those with symptoms or abnormal chest x-rays should have sputum cultures performed

34
Q

How is a positive PPD or interferon gold test managed?

A
  • these patients should have a CXR to exclude active disease
  • then be given 9 months of isoniazid or 12 weeks of isoniazid and rifapentine
  • importantly, previous BCG vaccination has no impact on management and a positive PPD still warrants this workup
35
Q

How should a patient who received the BCG vaccine and now has a positive PPD be managed?

A
  • the BCG vaccine has no impact on management

- use CXR to exclude active disease and then initiate 9 months of isoniazid

36
Q

Describe the diagnosis of TB in patients with and without symptoms.

A
  • for those without symptoms but who have risk factors, perform a PPD or interferon gold test
  • if patients have symptoms or have a positive PPD/interferon gold test, the best initial step is a CXR
  • if the CXR excludes active TB, start 9 months of isoniazid for those with a positive PPD/interferon gold and workup those with symptoms for other causes
  • if CXR demonstrates finings consistent with TB, perform 3 sputum cultures to exclude disease
37
Q

Describe the presentation, diagnosis, and treatment of MAC.

A
  • presents as pneumonia in patients with COPD
  • patients may be colonized so only treat if patients have repeat positive cultures, respiratory symptoms, and an abnormal CXR
  • do so with azithromycin, rifampin, and ethambutol
38
Q

How are solitary pulmonary nodules managed?

A
  • those that are likely benign (less than 1cm and in a non-smoker less than 30 years old) can be watched
  • those with characteristics of intermediate risk can undergo sputum cytology which is highly specific
  • those with high malignant risk or positive cytology should have biopsy/resection
39
Q

Coal Worker’s Pneumoconiosis

A
  • an interstitial lung fibrosis due to chronic exposure to carbon dust, which is engulfed by alveolar macrophages, inducing fibrosis
  • leads to “black lung” and diffuse fibrosis that tends to affect the upper lobes more
  • is associated with rheumatoid arthritis as part of Caplan syndrome
40
Q

Silicosis

A
  • an interstitial lung fibrosis due to chronic exposure to silica, which is engulfed by alveolar macrophages, inducing fibrosis
  • seen in sandblasters and silica miners
  • fibrotic nodules appear in the upper lobes of the lung and may resemble TB
  • also increases the risk for TB as silica impairs phagolysosome formation in macrophages
41
Q

Berylliosis

A
  • an interstitial lung fibrosis due to chronic exposure to beryllium, which is engulfed by alveolar macrophages, inducing fibrosis
  • seen in those that work in the aerospace industry or who mine beryllium
  • noncaseating granulomas can be found in the lung, hilar lymph nodes, and systemic organs (don’t confuse with sarcoidosis)
  • increases the risk for lung cancer
42
Q

Describe the presentation, diagnosis, and treatment of interstitial pulmonary fibrosis.

A
  • presents with dyspnea, fine crackles, a loud P2, clubbing of the fingers, and restrictive pattern of PFTs
  • the best initial test is a radiograph followed by a CT, which show honeycombing; the most accurate test is a lung biopsy
  • most cases are untreatable, but patients with a white blood cell infiltrate should undergo a trial of steroids; if steroids work, switch to azathioprine for long-term control
43
Q

Describe the pathophysiology, presentation, diagnosis, and treatment of hypersensitivity pneumonitis.

A
  • an exaggerated immune response to repeated exposure to antigens such as bird droppings, mold, or fungi in the lungs
  • presents with cough and dyspnea as well as systemic symptoms of fever, chills, rash, and malaise; these have an onset within hours of exposure and resolve within a couple of days of avoidance
  • best initial test is a CXR or CT showing bilateral hazy opacities
  • treat with steroids and avoidance to prevent progression to interstitial pulmonary fibrosis
44
Q

Describe the presentation, diagnosis, and treatment of sarcoidosis.

A
  • presents in young, African American women with shortness of breath, fine rales, erythema nodosum, and lymphadenopathy
  • PFTs show a restrictive lung disease and there can also be involvement of the facial nerve, heart, eyes, parotids
  • the best initial test is CXR looking for hilar adenopathy; the most accurate is lymph node biopsy finding non-caseating granulomas
  • will also find elevated ACE level, hypercalcemia, and a higher CD4/CD8 ratio on BAL
  • treat with steroids
45
Q

For the following tests, what is the most common result and what is the most common abnormality in those with pulmonary embolism:

  • physical exam
  • ECG
  • CXR
  • ABG
  • V/Q
  • CTA
A
  • physical exam: clear lungs, tachycardia, tachypnea
  • ECG: usually sinus tach; most common abnormality is non-specific ST changes; may see signs of right heart strain
  • CXR: usually normal; atelectasis is the most common abnormality; wedge-shaped infarcts are possible
  • ABG: hypoxia and respiratory alkalosis
  • V/Q: areas of ventilation without perfusion
  • CTA: vascular filling defect
46
Q

Describe the appropriate workup and treatment for pulmonary embolism.

A
  1. if low probability, start with D-dimer to rule it out
  2. otherwise, start with an ECG, ABG, and CXR
  3. if consistent with PE, start therapy with heparin while completing the rest of the workup
  4. get a CTA unless patient is pregnant or has a contraindication to contrast, then use a V/Q scan
  5. start patient on long-term anticoagulation plan after the diagnosis is made
47
Q

What is the role of the following in diagnosing PE:

  • D-dimer
  • LE doppler
  • Angiogram
A
  • D-dimer: sufficient to rule out PE
  • LE doppler: sufficient to diagnose PE and begin treatment without getting a V/Q scan or CTA
  • Angiogram: most accurate but high mortality, so not used
48
Q

What are the treatment options of PE?

A
  • thrombolytics are given in the acute setting for hemodynamically unstable patients or those with acute RV dysfunction
  • the preferred long-term treatment is initiation of a NOAC like rivaroxaban or apixaban
  • LMWH enoxaparin can be started and followed with warfarin as an alternative
  • IVCs are placed when patients have contraindications to AC, recurrent emboli while on appropriate AC, or right ventricular dysfunction with enlarged RV on echo
49
Q

Describe the definition, etiology, presentation, diagnosis, and treatment of pulmonary hypertension.

A
  • defined as a pulmonary artery pressure above 25/8
  • can be idiopathic in young females but more often secondary to any disease that causes chronic hypoxia
  • presents with dyspnea, syncope, chest pain, and a wide split S2
  • CXR or CT is the best initial test showing dilation of proximal pulmonary arteries and narrowing/pruning of distal vessels
  • right heart catheter is the most accurate; ECG shows right-axis deviation and right-heart hypertrophy
  • treat with vasodilators: epoprostenol (prostacyclin), bosentan (endothelin antagonist), sildenafil, or CCBs
50
Q

Describe the pathophysiology, presentation, diagnosis and treatment of obstructive sleep apnea.

A
  • obesity leads to pharyngeal stenosis and cessation of breathing during sleep; this contributes to nocturnal hypoxia and thus pulmonary hypertension
  • presents with cognitive dysfunction, depression, headache, hypertension, and ED
  • diagnose with polysomnography
  • treat with weight loss and CPAP
51
Q

How does central differ from obstructive sleep apnea?

A

central is secondary to a diminished respiratory drive from stroke, heart failure, or opiates and is unique in that apneic episodes are accompanied by a lack of abdominal and thoracic movement

52
Q

Describe the pathophysiology of obesity hypoventilation syndrome.

A
  • a form of sleep apnea seen in the obese
  • excess weight reduces respiratory rate, which increases PaCO2 and decreases PaO2 during sleep
  • PaCO2 remains elevated during the waking hours with a corresponding compensatory metabolic alkalosis
  • PaO2 is normal during the day but nocturnal hypoxia contributes to systemic and pulmonary hypertension, arrhythmias, polycythemia, and sudden death
53
Q

For ARDS, give the following:

  • definition
  • pathogenesis
  • etiology
A
  • defined as a PaO2/FiO2 < 300
  • diffuse damage to the alveolar-capillary interface allows protein-rich fluid to leak into the alveoli, which combines with necrotic epithelial cells to form hyaline membranes
  • secondary to sepsis, aspiration, lung trauma, near-drowning, burns, and pancreatitis
  • the diagnosis is made with CXR or CT showing white out and airbronchograms; importantly, the edema is not cardiogenic so PCWP is normal
  • treat with PEEP

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