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Internal Medicine EOR > Pulmonology > Flashcards

Pulmonology Flashcards

1
Q

What is acute bronchitis?

A

cough > 5 days with or without sputum production, lasts 2-3 weeks

  • chest discomfort
  • shortness of breath
  • +/- fever
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2
Q

What is the etiology of acute bronchitis?

A

viruses (most common)

-cannot distinguish acute bronchitis from URTI in the first few days

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3
Q

What are the labs for acute bronchitis?

A

labs not indicated, unless pneumonia suspected (HR>100, RR >24, T>38, rales, hypoxemia, mental confusion, or systemic illness) - CXR

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4
Q

What is the tx for acute bronchitis?

A

antibiotic not recommended - mostly viral

  • symptomatic-based treatment NSAIDs, ASA, Tylenol, and/or ipratropium
  • cough suppressants - codeine-containing cough meds
  • bronchodilators (albuterol)
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5
Q

What is the presentation of asthma?

A

most often young patients present with wheezing and dyspnea often associated with illness, exercise and allergic triggers
-airway inflammation, hyperresponsiveness, and reversible airflow obstruction

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6
Q

How do you diagnosis with asthma?

A

diagnosis and monitor with peak flow

  • PFT’s: greater than 12% increase in FEV1 after bronchodilator therapy
  • FEV1 to FVC ratio <80% (you would expect the amount of air exhaled during the first second (FEV1) to be the greatest amount
  • in asthma, since there is an obstruction (inflammation) you will have a decreased FEV1 and therefore a reduced FEV1 to FVC ratio
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7
Q

What is the tx for mild intermittent asthma?

A

less than 2 times per week or 3-night symptoms per month

-step 1: short acting beta2 agonist (SABA) prn

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8
Q

What is the tx for mild persistent asthma?

A

more than 2 times per week or 3-4 night symptoms per month

-step 2: low-dose inhaled corticosteroids (ICS) daily

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9
Q

What is the tx for moderate persistent asthma?

A

daily symptoms or more than 1 nightly episode per week

  • step 3: low dose ICS + long acting beta2 agonist (LABA) daily
  • step 4: medium-dose ICS + LABA daily
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10
Q

What is the tx for severe persistent asthma?

A

symptoms several times per day and nightly

  • step 5: high-dose ICS + LABA daily
  • step 6: high-dose ICS + LABA + oral steroids daily
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11
Q

What is acute treatment for asthma?

A

oxygen, nebulized SABA, ipratropium bromide, and oral corticosteroids

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12
Q

What is forced vital capacity?

A
  • forced expiratory volume (FEV) measures how much air a person can exhale during a forced breath
  • the amount of air exhaled may be measured during the first (FEV1), second (FEV2), and/or third seconds (FEV3) of the forced breath
  • forced vital capacity (FVC) is the total amount of air exhaled during the FEV test
  • you would expect the amount of air exhaled during the first second to be the greatest amount
  • in asthma, since there is an obstruction (inflammation) you will have a decreased FEV1 and therefore a decreased FEV1 to FVC ratio
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13
Q

What is bronchiectasis?

A

a condition in which the lungs’ airways become dilated and damaged, leading to inadequate clearance of mucus in airways

  • mucus builds up and breeds bacteria, causing frequent infections
  • a common endpoint of disorders that cause chronic airway inflammation (CF, immune defects, recurrent pneumonia, aspiration, tumor)
  • 1/2 of cases are due to cystic fibrosis
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14
Q

What are the symptoms of bronchiectasis?

A

include a daily cough that occurs over months or years and production of copious foul-smelling sputum, frequent respiratory infections

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15
Q

How is bronchiectasis dx?

A

CXR=linear “tram track” lung markings, dilated and thickened airways - “plate-like” atelectasis; CT chest = gold standard
-crackles, wheezes, purulent sputum

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16
Q

What is the tx for bronchiectasis?

A

ambulatory oxygen, aggressive antibiotics for acute exacerbations, CPT (chest physiotherapy = bang on the back); eventual lung transplant

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17
Q

What is a carcinoid tumor?

A

a tumor arising from neuroendocrine cells = leading to excess secretions of serotonin, histamine, and bradykinin

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18
Q

What are the characteristics of carcinoid tumor?

A
  • common primary sites include GI (small and large intestines, stomach, pancreas, liver), lungs, ovaries, and thymus
  • carcinoid syndrome (the hallmark sign) is actually quite rare and occurs in approximately 5% of carcinoid tumors and becomes manifest when vasoactive substances from the tumors enter the systemic circulation escaping hepatic degradation
  • carcinoid syndrome = diarrhea, shortness of breath, flushing, itching
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19
Q

How is carcinoid tumor dx?

A

octreotide scan, urine for 5-hydroxyindoleacetic acid (5-HIAA), serum niacin, CT scan to locate tumor

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20
Q

What is the tx for carcinoid tumor?

A

is by surgical excision and carries a good prognosis

  • the lesions are resistant to radiation therapy and chemotherapy
  • octreotide - a somatostatin analog which binds the somatostatin receptors and decreases the secretion of serotonin by the tumor
  • niacin supplementation
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21
Q

What is chronic obstructive pulmonary disease?

A

a chronic inflammatory lung disease that causes obstructed airflow from the lungs due to loss of elastic recoil and increasing airways resistance

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22
Q

What are the characteristics of chronic obstructive pulmonary disease?

A
  • includes emphysema and chronic bronchitis = both usually coexist with one being more dominant
  • damage to the lungs from COPD can’t be reversed
  • 30 pack-year history = low dose chest CT
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23
Q

What are the risk factors of chronic obstructive pulmonary disease?

A
  • cigarette smoking/exposure is the most important risk
  • alpha 1 antitrypsin deficiency = genetic and linked to COPD in patients <40 y/o (protects elastin in lungs from damage by WBCs)
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24
Q

What is emphysema?

A
  • exposure to irritants (eg cigarette smoke) - degrades elastin in alveoli, airways - lose elasticity - low pressure during expiration pulls walls of alveoli inward - collapse - air-trapping distal to collapse - septa breaks down - neighboring alveoli coalesce into larger air spaces - decreased surface area available for gas exchange
  • loss of elastin - lungs more compliant (lungs expand, hold air)
  • alveolar air sacs permanently enlarge, lose elasticity - exhaling is difficult
  • DOE = hallmark symptom
  • hyperinflation of lungs + hyperresonance to percussion, decreased/absent breath sounds, decreased fremitus, barrel chest (increased AP diameter), quiet chest, pursed-lip breathing
  • individuals are able to oxygenate blood (pink) but they have to purse their lips to do so (puffers) = Pink Puffers
  • pursing lip increases pressure in airway - keeps the airway from collapsing - weight loss
  • barrel chest due to air trapping and hyperinflation of lungs
  • CXR reveals loss of lung markings, hyperinflation, increased anterior-posterior diameter
  • PETs show FVC decreases (esp. FEV1) + increased TLC (due to air trapping)
  • ABG/labs: respiratory alkalosis, mild hypoxemia, normal CO2
  • cachectic with pursed-lip breathing - “pink puffers”
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25
Q

What is chronic bronchitis?

A

defined as a chronic cough that is productive of phlegm occurring on most days for 3 months of the year for 2 or more consecutive years without an otherwise-defined acute cause

  • exposure to irritants (e.g cigarette smoke) - hypertrophy/hyperplasia of bronchial mucous glands, goblet cells in bronchioles, cilia less mobile - increased mucus production, less movement - mucus plugs - obstruction in bronchioles - air trapping - productive cough
  • rales (crackles), rhonchi, wheezing, signs of cor pulmonale (peripheral edema, cyanosis)
  • ABGs: respiratory acidosis (arterial PCO2>45 mmHg, bicarbonate >30 mEq/L)
  • PET’s: FEV1/FVC ratio less than 0.7
  • increased TLC (air trapping)
  • chest radiography: peribronchial and perivascular markings
  • increased HGB and HCT are common because of the chronic hypoxic state
  • pulmonary HTN with RVH, distended neck veins, hepatomegaly
  • obese and cyanotic = blue bloaters
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26
Q

What are the diagnostic studies for chronic obstructive pulmonary disease?

A
  • PFTs/spirometry = gold standard diagnosis COPD
  • FEV1 = important factor of prognosis and mortality (<1 L = increased mortality)
  • obstruction: decreased FEV1, decreased FVC, decreased FEV1/FVC
  • hyperinflation: increased lung volumes: increased RV, TLC, RV/TLC, increased FRC (functional residual capacity)
  • CXR/CT scan
  • emphysema: hyperinflation: flat diaphragm, increased AP diameter, increased vascular markings, enlarged right heart border
  • ECG: cor pulmonale: RVH, RAE, RAD, r-sided heart failure (due to longstanding pulmonary hypertension), MAT, hypertension
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27
Q

What are the clinical therapeutics for chronic obstructive pulmonary disease?

A

-smoking cessation = single most important step
-bronchodilators: combo therapy (Beta2 agonist + anticholinergic = greater response than used alone - tx of choice in stable COPD with resp. symptoms
-short acting (SAMA) or long-acting (LAMA) muscarinic agent (also known as an anticholinergic agent): tiotropium (spiriva) inhaled long-acting; ipratropium (atrovent)
-ipratropium preferred over short-acting B2 agonist in COPD
s/e: dry mouth, thirst, blurred vision, urinary retention, difficulty swallowing, mydriasis
-contraindications: glaucoma, BPH
-short acting (SABA) or long-acting (LABA) beta 2 agonist: albuterol, terbutaline, salmeterol (long-acting)
-s/e: B1 cross-reactivity, tachycardia/arrhythmias, muscle tremor, CNS stimulation
-contraindications: severe CAD; caution in pt. with DM (hyperglycemia), hyperthyroid)
-theophylline: only used in refractory cases bc narrow therapautic index - monitor serum levels to prevent nausea, palpitations, arrhythmias, seizures from toxic levels; higher doses needed in smokers and coffee drinkers - don’t initiate in acute exacerbation
-+/- inhaled glucocorticoids: inhaled corticosteroids not considered monotherapy
-s/e: osteoporosis, thrush
-oxygen: only medical therapy proven to decrease mortality (decreases pulmonary hypertension/cor pulmonale by decreasing hypoxia-mediated pulmonary vasoconstriction)
-long-term oxygen therapy in all patients with COPD who have chronic hypoxemia defined as resting PaO2 <55 mmHg or SaO2 <89

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28
Q

What is the tx for stage I for chronic obstructive pulmonary disease?

A

mild

  • FEV1 >80%
  • bronchodilators prn short-acting/decrease risk factors
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29
Q

What is the tx for stage 2 for chronic obstructive pulmonary disease?

A

moderate

  • FEV1 50-80%
  • above + long-acting dilator
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30
Q

What is the tx for stage 3 for chronic obstructive pulmonary disease?

A

severe

  • FEV1 30-50%
  • above + pulm rehab; inhaled steroids if increased exacerbations
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31
Q

What is the tx for stage 4 for chronic obstructive pulmonary disease?

A

very severe

  • cor pulmonale, right heart failure, resp failure, FEV1 <30%
  • above + O2 therapy
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32
Q

What is the health maintenance for chronic obstructive pulmonary disease?

A
  • control triggers: pollutants, bronchospasm, cardiopulmonary disease, meds (decongestants, B blockers, sedative)
  • infections: bronchitis and pneumonia
  • prevention of exacerbations: SMOKING CESSATION
  • vaccinations: pneumococcal and influenza every fall
  • pulmonary rehab: improves the quality of life, dyspnea, and exercise intolerance
  • surgery: lung reduction surgery - improves dyspnea by removing damaged lung; lung transplant
  • azithromycin has anti-inflammatory properties in the lung
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33
Q

What is cor pulmonale?

A

right ventricular enlargement and eventually failure secondary to lung disorder that causes pulmonary artery HTN

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34
Q

What is the etiology of cor pulmonale?

A

COPD (most common), pulmonary embolism, vasculitis, asthma, ILD, acute respiratory distress syndrome

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35
Q

What is the physical exam of cor pulmonale?

A

lower extremity edema, neck vein distention, hepatomegaly, parasternal lift, tricuspid/pulmonic insufficiency, loud S2

36
Q

How is cor pulmonale dx?

A
  • the diagnosis of cor pulmonale is usually made with an echocardiogram that shows evidence of increased pressure in the pulmonary arteries and right ventricle
  • follow up tests can be done to identify the underlying cause, for example, spirometry can be done to look for chronic lung disease
  • the gold standard diagnostic test to directly measure pulmonary pressures and assess for response to vasodilating medications is a right heart catheterization
37
Q

What is the tx for cor pulmonale?

A

diagnose and treat the underlying condition before cardiac structure change becomes irreversible
-diuretics not helpful, may be harmful

38
Q

What is hypoventilation syndrome?

A

may be secondary to several mechanisms, including central respiratory drive depression (drugs - narcotics, benzodiazepines, neurologic disorders - multiple sclerosis, etc.), neuromuscular disorders (ALS, myasthenia gravis, etc.), chest wall abnormalities, obesity hypoventilation, and COPD

39
Q

What are the characteristics of hypoventilation syndrome?

A
  • obesity hypoventilation syndrome (OHS), also known as Pickwickian syndrome, is a condition in which severely overweight people fail to breathe rapidly or deeply enough, resulting in low oxygen levels and high blood carbon dioxide (CO2) levels
  • s/s: sluggish/sleepy during day
  • sequalae: pulmonary hypertension, cor pulmonale, secondary erythrocytosis
40
Q

How is hypoventilation syndrome dx?

A

PFTs, sleep studies, CXR, arterial blood gas, serum bicarb

41
Q

What is the treatment of hypoventilation syndrome?

A

lifestyle, healthy weight, physical activity, CPAP, tracheostomy
-sleep apnea fails into this category

42
Q

What is idiopathic pulmonary fibrosis?

A

a type of lung disease that results in scarring (fibrosis) of the lungs for an unknown reason

43
Q

What are the characteristics of idiopathic pulmonary fibrosis?

A
  • over time, the scarring gets worse and it becomes hard to take in a deep breath and the lungs cannot take in enough oxygen
  • etiology unknown: MC of all interstitial lung diseases
  • in order to be considered “idiopathic”, you must rule out other common causes such as drugs (amiodarone), and environmental or occupational exposures
  • non-idiopathic: smoking, viral infections, environmental (silica, hard metal dust), medications, genetics, XRT, GERD
  • physical exam: inspiratory crackles
44
Q

How is idiopathic pulmonary fibrosis dx?

A

CXR shows fibrosis

  • CT chest: diffuse patchy fibrosis with pleural based honeycombing
  • PFTs = restrictive (decreased lung volume, normal/increased FEV1/FVC ratio)
45
Q

How is idiopathic pulmonary fibrosis tx?

A

few effective treatment options other than a lung transplant
-corticosteroids, O2

46
Q

What is pneumoconiosis?

A

any fibrosis of the lung tissues with a known cause - usually from prolonged environmental or occupational contact

47
Q

What is Coal Worker’s?

A

coal mining; complication = progressive massive fibrosis

-CXR: small nodular opacities in upper lung fields

48
Q

What is Silicosis?

A

mining, sandblasting, stone, quarry work; increased risk TB and progression to massive fibrosis
-CXR: small rounded opacities throughout the lung, hilar lymph nodes may be calcified - “eggshell” calcifications

49
Q

What is Asbestos?

A

insulation, demolition, shipbuilding, construction; complication = mesothelioma
-CXR: interstitial fibrosis, thicken pleura, calcified plaques appear on diaphragms or lateral chest wall

50
Q

What is Berylliosis?

A

high tech field, nuclear power, ceramics, aerospace, electrical plants, foundries; requires chronic steroids
-CXR: diffuse infiltrates and hilar adenopathy

51
Q

What are the s/sx of pneumoconiosis?

A

SOB + nonproductive cough + chronic hypoxia, cor pulmonale

52
Q

How is pneumoconiosis dx?

A

CXR: interstitial fibrosis

-PFTs = reduced lung volume - restrictive dysfunction and reduced diffusing capacity

53
Q

What is the tx for pneumoconiosis?

A

primarily supportive = oxygen, vaccinations (pneumococcal, flu) and rehab

  • steroids to relieve chronic alveolitis
  • smoking cessation = synergistically linked to lung cancer
54
Q

What is viral pneumonia?

A

adults = flu = MC cause; kids = RSV; comes on fast

  • Dx: CXR = bilateral interstitial infiltrates; rapid antigen testing for flu, RSV nasal swab, cold agglutinin titer negative
  • Tx: flu with Tamiflu (A and B) if sx began <48 hrs; symptomatic tx = beta 2 agonists, fluids, rest
55
Q

What is bacterial pneumonia?

A

fever, dyspnea, tachycardia, tachypnea, cough, +/- sputum

  • dx: patchy, segmental lobar, multilobar consolidation; blood cultures x2, sputum gram stain
  • tx: outpatient = doxy, macrolides; inpatient = ceftriaxone + azithromycin/respiratory FQs
56
Q

What is fungal pneumonia?

A

common in immunocompromised pt (AIDs, steroid use, organ transplant)

57
Q

What is coccidiodes (valley fever)?

A

non-remitting cough/bronchitis non-responsive to conventional tx

  • fungal inhalation in western states; test with EIA or IgM and IgG
  • tx: fluconazole/itraconazole
58
Q

What is pulmonary aspergillosis?

A

usually those with healthy immune systems

-tx: fluconazole/itraconazole

59
Q

What is cryptococcus?

A

found in soil; can disseminate and = meningitis

  • lumbar puncture for meningitis
  • tx: amphotericin B
60
Q

What is histoplasma capsulatum?

A

pulmonary lesions that are apical and resemble cavitary TB; worsening cough and dyspnea, progression to disabling respiratory dysfunction; no dissemination

  • bird or bat droppings (caves, zoo, bird); Mississippi ohio river valley
  • signs: mediastinal or hilar LAD (looks like sarcoid)
  • Tx: amp B
61
Q

What is PJP (pneumocystis jiroveci)?

A
  • common in HIV patients with CD4 count <200

- XR: diffuse interstitial or bilateral perihilar infiltrates

62
Q

How is PJP dx?

A

bronchoalveolar lavage PCR, labs, HIV test; low O2 sat despite supplemental oxygen

63
Q

What is the tx of PJP?

A

bactrim and steroids; pentamidine for allergy

-prophylaxis for high risk pt with Cd4 <200 = daily bactrium

64
Q

What is CURB65?

A

estimates mortality of community-acquired pneumonia to help determine inpatient vs outpatient treatment

  • confusion, urea >7, RR >30, SBP <90 OR DBP <60, age >65
  • 0-1 = low risk, consider home tx
  • 2 = probable admission vs close outpatient management
  • 3-5 admission, manage as severe
65
Q

What is pulmonary hypertension?

A

blood pressure in the lugs is usually very low 15/5

-in pulmonary hypertension, the pressure increases > 25 mmHg at rest

66
Q

What are the characteristics of pulmonary hypertension?

A
  • usually caused by an underlying disorder (constrictive pericarditis, mitral stenosis = MC, LV failure, mediastinal disease compression pulmonary veins)
  • mitral stenosis: mitral valve = tight so blood can’t pass into left ventricle = pressure backs up to lungs
  • when the right heart can’t pump against vascular resistance = right heart failure = cor pulmonale
67
Q

What is the presentation and physical exam of pulmonary hypertension?

A
  • presentation: dyspnea on exertion, fatigue, chest pain, edema
  • physical exam: loud pulmonic component of second heart sound (P2); jugular venous distention; ascites; hepatojugular reflux; lower limb edema
68
Q

How do you dx pulmonary hypertension?

A

a right heart catheterization (gold standard) - most accurate measure of pressures

  • CXR:
  • enlarged pulmonary arteries
  • lung fields may or may not be clear, dependent on the underlying cause
  • Echocardiogram:
  • increased pressure in pulmonary arteries, right ventricles - dilated pulmonary artery
  • dilation/hypertrophy of right atrium, right ventricle
  • large right ventricle - bulging septum
  • ECG - right heart strain pattern: T wave inversion in right precordial (V1-V4), and inferior leads (II, III, aVF)
69
Q

What is the tx for pulmonary hypertension?

A

identify and treat the underlying cause

  • pulmonary hypertension secondary to left ventricular failure - optimize left ventricular function
  • diuretics (cautiously - individuals may be preload dependent)
  • digoxin
  • anticoagulants
  • cardiogenic pulmonary arterial hypertension
  • relax smooth muscle (promote vasodilation), reduce vascular remodeling, improve exercise capacity with prostanoids, phosphodiesterase inhibitors, endothelin antagonists
  • pulmonary arterial hypertension
  • endothelin receptor antagonists
  • prostanoids
70
Q

What are the two major categories of lung cancer?

A
  • small cell lung cancer (SCLC), about 15% of cases (poor prognosis)
  • non-small cell lung cancer (NSCLC), about 85% of cases, four subtypes include adenocarcinoma, squamous cell carcinoma, large cell carcinoma and carcinoid tumor
71
Q

What is small cell lung cancer?

A

(15% of cases) - 99% smokers, does not respond to surgery and metastases at presentation

  • location: (central mass), very aggressive
  • treatment: combination chemotherapy needed
  • paraneoplastic syndrome: Cushing’s, SIADH
72
Q

What is non-small cell?

A

(85% lung cancer cases)

  • adenocarcinoma
  • squamous cell (central mass)
  • large cell
  • carcinoid tumor
73
Q

What is adenocarcinoma?

A

most common (peripheral mass), 35-40% of cases of lung cancer

  • most common
  • associated with smoking and asbestos exposure
  • location: periphery
  • paraneoplastic syndrome: thrombophlebitis
74
Q

What is squamous cell?

A

(central mass) with hemoptysis, 25-35% of lung cancer cases

  • location: central
  • may cause hemoptysis
  • pareneoplastic syndrome: hypercalcemia
  • elevated PTHrp
75
Q

What is large cell?

A

fast doubling rates - responds to surgery rare (only 5%)

  • location: periphery 60%
  • paraneoplastic syndrome: gynecomastia
76
Q

What is carcinoid tumor (1-2%?

A

lack glandular and squamous differentiation

  • a tumor arising from neuroendocrine cells - leading to excess secretion of serotonin, histamine, and bradykinin
  • GI tract carcinoid tumor may metastasize to lung (CA of appendix = MC; appendix - liver - lung)
  • presentation: hemoptysis, cough, focal wheezing, recurrent pneumonia
  • carcinoid syndrome = cutaneous flushing, diarrhea, wheezing, hypotension (telltale sign)
  • adenoma = MC type (slow-growing, rare)
77
Q

What is the tx for non-small cell?

A

can be treated with surgery

  • treatment depends on staging:
  • stage 1-2 surgery
  • stage 3 Chemo then surgery
  • stage 4 palliative
  • carcinoid tumors are treated with surgery
78
Q

What is the tx for small cell?

A

CAN NOT be treated with surgery will need chemotherapy

  • associated manifestations:
  • superior vena cava syndrome (facial/arm edema and swollen chest wall veins)
  • pancoast tumor (shoulder pain, Horner’s syndrome, brachial plexus compression)
  • Horner’s syndrome (unilateral miosis, ptosis, and anhidrosis)
  • Carcinoid syndrome (flushing, diarrhea, and telangiectasia)
79
Q

What is sarcoidosis?

A

chronic autoimmune inflammatory disease in which small nodules (granulomas) develop in lungs, lymph nodes, and other organs, increased ACE levels + bilateral hilar adenopathy
-pulmonary manifestations (most common); skin = 2nd most; skin and lymph = mot common areas

80
Q

What are the symptoms of sarcoidosis?

A
  • symptoms vary, depending on the organs affected - fever, weight loss, arthralgias, erythema nodosum = initial presenting sx
  • Lupus pernio (chronic, violaceous, raise plaques and nodules commonly found on cheeks, nose, eyes) = pathognomonic for sarcoid and most specific physical exam finding
81
Q

How is sarcoidosis dx?

A

chest radiograph: bilateral hilar lymphadenopathy, reticular infiltrates

  • hypercalcemia; ACE levels 4x normal, elevated ESR
  • biopsy of peripheral lesions or fiber optic bronchoscopy for central pulmonary lesions
  • biopsy = non-caseating granulomas
82
Q

What is the tx for sarcoidosis?

A

steroids = 90% respond to steroid

  • methotrexate, other immunosuppressive meds
  • serial PFTs to assess disease progression/guide treatment
  • ACE-I for periodic HTN

prognosis depends on disease severity; spontaneous improvement common
-pulmonary fibrosis = leading cause of death

83
Q

What is pulmonary nodules?

A

< 3 cm = nodules, >3 cm = mass

  • found on CXR = get CT
  • if suspicious = biopsy (ill-defined lobular or spiculated suggests cancer)
  • not suspicious = < 1 cm monitor at 3 cm, 6 mo, yearly for 2 yr (calcification, smooth well defined edges = benign
84
Q

What are the radiographic characteristics that help to define the malignant potential of solitary pulmonary nodules?

A
  • growth rate determined by comparison of previous CXR or CT
  • the lesion that hasn’t grown in >2 yr = benign
  • double from 21-40 days = malignant
  • small (< 1 cm) monitor at 3, 6 mo then yearly for 2 yr
  • calcification suggests benign especially if central, concentric, popcorn
  • margins that are spiculated or irregular = CA
  • diameter <1.5 cm strongly suggests benign; diameter >5.3 cm strongly suggests CA
85
Q

What is the tx for pulmonary nodules?

A

management depends on radiographic findings

-if malignant = biopsy

Internal Medicine EOR (10 decks)

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