Internal Medicine Rotation

Internal Medicine Rotation: Pulmonology (PEARLS)

You have completed internal medicine EOR topics:

Acute/chronic bronchitis
Patient will present as → a 23-year-old-female  with a one-week history of cough productive of whitish sputum. This was preceded one week prior by a URI. She denies chills, night sweats, shortness of breath, or wheeze. Temperature is 99.9°F (37.7°C).

Acute Bronchitis

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

  • Chest discomfort
  • shortness of breath
  • +/- fever

Etiology - viruses (most common). Cannot distinguish acute bronchitis from URTI in the first few days

Labs not indicated, unless pneumonia suspected (HR >100, RR >24, T >38°C, rales, hypoxemia, mental confusion, or systemic illness) → CXR

Treatment: Antibiotics not recommended—mostly viral

  • Symptomatic-based treatment NSAIDs, ASA, Tylenol, and/or ipratropium
  • Cough suppressants—codeine-containing cough meds
  • Bronchodilators (albuterol)
Patient will present as → a 5-year-old boy who is brought to the emergency department by his parents for a cough and shortness of breath. He has a past medical history of eczema and seasonal rhinitis. On physical exam, you note a young boy in respiratory distress taking deep slow breaths to try and catch his breath. He has diminished breath sounds in all lung fields with prolonged, expiratory wheezes.

Presentation: Most often young patients present with wheezing and dyspnea often associated with illness, exercise, and allergic triggers

  • Airway inflammation, hyperresponsiveness, and reversible airflow obstruction

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

Treatment guidelines:

Mild Intermittent: Less than 2 times per week or 3-night symptoms per month

  • Step 1: Short-acting beta2 agonist (SABA) PRN

Mild Persistent: More than 2 times per week or 3-4 night symptoms per month

  • Step 2: Low-Dose inhaled corticosteroids (ICS) daily

Moderate Persistent: 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

Severe Persistent: Symptoms several times per day and nightly

  • Step 5: High-Dose ICS +LABA daily
  • Step 6: High-Dose ICS +LABA +oral steroids daily

Acute treatment: Oxygen, nebulized SABA, ipratropium bromide, and oral corticosteroids

Making Sense of Forced Vital Capacity

  • 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 reduced FEV1 to FVC ratio.

Patient will present as → a 25-year-old cystic fibrosis patient complaining of chronic, frequent coughing productive of yellow and green sputum. She recently recovered from a Pseudomonas spp. pneumonia requiring hospitalization. On physical examination, you notice foul breath, purulent sputum, and hemoptysis along with a CXR demonstrating dilated and thickened airways with “plate-like” atelectasis (scarring).

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

DX: CXR = linear “tram track” lung markings, dilated and thickened airways – plate-like” atelectasis; CT chest = gold standard

    • Crackles, wheezes, purulent sputum

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

Carcinoid tumor
Patient will present with → a 43-year-old man who comes to the emergency department because of a 3-week history of episodic cutaneous flushingdiarrhea, and wheezing. He has a past medical history of hypertension and type 2 diabetes mellitus. His temperature is 36.6°C (97.9°F), pulse is 125/min, respirations are 30/min, and blood pressure is 90/60 mm Hg. Pulmonary examination shows diffuse wheezes in both lung fields. Cardiac examination shows a prominent “v” wave of the jugular vein and a 1/6 holosystolic murmur best heard on the left lower sternal border. Abdominal examination shows hyperactive bowel sounds.

A tumor arising from neuroendocrine cells → leading to excess secretion of serotoninhistamine, and bradykinin

  • Common primary sites include GI (small and large intestines, stomach, pancreas, liver), lungs, ovaries, and thymus
    • The most common site of a neuroendocrine (carcinoid) tumor to metastasize to is the liver
    • Carcinoid tumor of the appendix is the most common cause. The appendiceal cancer travels from the appendix then to the liver where it metastasizes to the lungs
  • Usually asymptomatic until liver metastasis; symptoms develop occasionally
    • GI tract tumor→ hormone secretion → enter into enterohepatic circulation → liver inactivates hormones → no symptoms
    • Liver tumor → hormone secretion → released into circulation + liver dysfunction → symptoms
  • Carcinoid syndrome (the hallmark sign) = Cutaneous flushing, diarrhea, wheezing and low blood pressure is actually quite rare and occurs in ~ 5% of carcinoid tumors and becomes manifest when vasoactive substances from the tumors enter the systemic circulation escaping hepatic degradation.
  • The syndrome includes flushing, ↑ intestinal motility (diarrhea), itching and less frequently, heart failure, vomiting, bronchoconstriction, asthma, and wheezing
    • ↑ Serotonin leads to collagen fiber thickening, fibrosis = heart valve dysfunction → tricuspid regurgitation, pulmonary stenosis/bronchoconstriction, and wheezing
    • ↑ Histamine and bradykinin = vasodilation and flushing
    • ↑ serotonin synthesis → ↓ tryptophan → ↓ niacin/B3 synthesis = pellagra


CT-Scan to locate the tumors

    • Octreoscan → radiolabeled somatostatin analog (octreotide) binds to somatostatin receptors on tumor cells
    • Urinalysis → elevated 5-hydroxyindoleacetic acid (5-HIAA) → is the main metabolite of serotonin and is used to determine serotonin levels in the body
    • Pellagra (niacin/B3 deficiency) - ↑ serotonin synthesis → ↓ tryptophan → ↓ niacin/B3 synthesis
    • Chest X-Ray shows low-grade CA seen as pedunculated sessile growth in the central bronchi
    • Bronchoscopy- pink/purple central lesion, well-vascularized

Treatment is by surgical excision and carries a good prognosis

  • The lesions are resistant to radiation therapy and chemotherapy
  • Octreotide - a somatostatin analog that binds the somatostatin receptors and decreases the secretion of serotonin by the tumor
  • Niacin supplementation
Chronic obstructive pulmonary disease (COPD)
Patient will present as → a 56 yo female with shortness of breath, as well as a productive cough that has occurred over the past two years for at least three months each year. She is a heavy smoker. Physical exam reveals a respiratory rate of 32, slightly labored breathing, and a temperature of 98.9FHer SpO2 is 90% while receiving oxygen via nasal cannula at 2 Lpm. (chronic bronchitis) 

Chronic obstructive pulmonary disease ( COPD ) is a chronic inflammatory lung disease that causes obstructed airflow from the lungs due to loss of elastic recoil and increasing airways resistance

  • Includes emphysema and chronic bronchitis ⇒ both usually coexist with one being more dominant
  • Damage to the lungs from COPD can't be reversed
  • Risk factors:
    • Cigarette smoking/exposure is the most important risk
    • Alpha 1 antitrypsin deficiency = genetic and linked to COPD in patients < 40y/o (protects elastin in lungs from damage by WBCs)
  • 30 pack-year history = low dose chest CT


  • Exposure to irritants (e.g. 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 lips increases pressure in the airway → keeps the airway from collapsing → weight loss
    • Barrel chest due to air trapping and hyperinflation of lungs
  • CXR reveals loss of lung markingshyperinflation, increased anterior-posterior diameter
  • PFTs show FVC decreased (esp. FEV1) + increased TLC (due to air trapping) 
  • ABG/ labs: respiratory acidosis, mild hypoxemia, normal CO2
  • Cachectic with pursed-lip breathing ⇒ “pink puffers”

Chronic Bronchitis:

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)
  • PFT's: FEV1/FVC ratio of less than 0.7
    • Increased TLC (air trapping)
  • Chest radiograph: peribronchial and perivascular markings
  • ↑ HGB and HCT are common because of the chronic hypoxic state
  • Pulmonary HTN with RVH, distended neck veins, hepatomegaly
  • Obese and cyanotic = blue bloaters

Diagnostic Studies:

  • 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, decreased vascular markings; bullae
    • Chronic bronchitis: 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

Clinical Therapeutics:

  • Smoking cessation = the single most important step
  • Bronchodilators: combo therapy β2 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 agonists: 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 due to narrow therapeutic index – monitor serum levels to prevent nausea, palpitations, arrhythmias, and seizures from toxic levels; higher doses needed in smokers and coffee drinkers- don’t initiate in acute exacerbation
  •  +/- inhaled glucocorticoids: inhaled corticosteroids are 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%
Stage PFT %  predicted Therapy
I: mild FEV1 > 80% Bronchodilators prn short-acting /decrease risk factors
II: moderate FEV1 50-80% Above + long-acting dilator
III: severe FEV1 30-50% Above + pulm rehab; inhaled steroids if increased exacerbations
IV: very severe Cor pulmonale, right heart failure, resp failure, FEV1 <30% Above + O2 therapy

Health Maintenance:

  • Control triggers: pollutants, bronchospasm, cardiopulmonary disease, meds (decongestants, B blockers, sedative)
  • Infections: bronchitis and pneumonia
  • Prevention of exacerbations: SMOKING CESSATION
  • Vaccinations: pneumococcal vaccine and influenza vaccine
  • 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
Cor pulmonale
Patient will present as → 65 y/o with 3 days of progressive dyspnea and purulent sputum production. The patient takes albuterol and tiotropium bromide for moderate COPD. His PMH is relevant for a 40 pack-year smoking history, type II DM, hyperlipidemia, and coronary artery stenting 2 years ago. PE shows barrel-shaped chest, inspiratory crackles, hepatojugular refluxpulsus paradoxus, and ventricular gallop. His temperature is 38.1°C (100.5°F), his pulse is 130/min, respirations are 28/min, blood pressure is 130/84 mmHg, and pulse oximetry on room air shows an oxygen saturation of 86%.

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


  • 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.

TX: Diagnose and treat the underlying condition before cardiac structure change becomes irreversible

    • Diuretics are not helpful! May be harmful
Hypoventilation syndrome Hypoventilation syndrome 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

  • 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
  • Sequelae: pulmonary hypertension, cor pulmonale, secondary erythrocytosis

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

TX: lifestyle, healthy weight, physical activity, CPAP, tracheostomy

  • Sleep apnea falls into this category
Idiopathic pulmonary fibrosis
Patient will present as → a 55-year-old female who is a current smoker presents with a 9-month history of respiratory symptoms, including dyspnea on exertion, thoracic pain, and dry cough, which were preceded by a pulmonary infection. On auscultation, you hear inspiratory crackles. Pulmonary function tests (PFTs) show only mild impairment of vital capacity with decreased lung volume and a normal to increased FEV1/FVC ratio.

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

  • 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), medication, genetics, XRT, GERD
  • Physical exam: Inspiratory crackles

DX: CXR shows fibrosis

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

Tx: Few effective treatment options other than a lung transplant

  • corticosteroids, O2
Patient will present as → a 53-year-old man presents to the office complaining of progressive dyspnea over the past few years. History reveals that he has worked in construction for the past 20 years demolishing and refurbishing old buildings. He rarely uses any protective breathing equipment. Physical examination demonstrates an afebrile man in mild respiratory distress with inspiratory crackles. The chest x-ray reveals a reticular linear pattern with basilar predominanceopacities, and honeycombing. (asbestosis)

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

  • Coal worker’s: coal mining; complication = progressive massive fibrosis
    • CXR: small nodular opacities in upper lung fields
  • Silicosis: 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
  • Asbestos: insulation, demolition, shipbuilding, construction; complication = mesothelioma
    • CXR: interstitial fibrosis, thickened pleura, calcified plaques appear on diaphragms or lateral chest wall
  • Berylliosis: high tech field, nuclear power, ceramics, aerospace, electrical plants, foundries; requires chronic steroids
    • CXR: diffuse infiltrates and hilar adenopathy

S/SX: SOB + nonproductive cough + chronic hypoxia, cor pulmonale

DX: CXR: interstitial fibrosis

  • PFTs = reduced lung volumes - restrictive dysfunction and reduced diffusing capacity

Tx: primarily supportive ⇒ oxygen, vaccinations (pneumococcal, flu) and rehab

  • Steroids to relieve chronic alveolitis
  • Smoking cessation = synergistically linked to lung cancer
Pneumonia (viral, bacterial, fungal, human immunodeficiency virus-related)
Patient will present as → a 71-year-old male who was admitted to the acute care hospital two days following a massive CVA with a possible brainstem infarct. Because he was also experiencing secondary respiratory failure, he was intubated and placed on mechanical ventilation. He was subsequently transferred to the neurointensive care unit where he was stabilized. His present vital signs are respiratory rate 14 (ventilator rate), temperature 100.4 F. His SpO2 is 95%. His rating on the Glasgow Coma Scale is 5.

Viral: 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

Bacterial: 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

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

  • Coccidioides (valley fever); non-remitting cough/bronchitis non-responsive to conventional tx
    • Fungal inhalation in western states; test with EIA for IgM and IgG
    • Tx: fluconazole/itraconazole
  • Pulmonary aspergillosis: usually those with healthy immune systems
    • Tx: fluconazole/itraconazole
  • Cryptococcus: found in soil; can disseminate and ⇒ meningitis
    • Lumbar puncture for meningitis
    • Tx: amphotericin B
  • Histoplasma capsulatum: 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

HIV: PJP (pneumocystis jiroveci)

  • Common in HIV patients with CD4 count <200
  • XR: diffuse interstitial or bilateral perihilar infiltrates

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

Tx: Bactrim and steroids; pentamidine for allergy

  • Prophylaxis for high risk pt with CD4 <200 = daily Bactrim

CURB65: 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
Pulmonary hypertension
Patient will present as → a 43-year-old woman with a history of COPD presents to the office with worsening dyspnea, especially at rest. She also complains of dull, retrosternal chest pain. On examination, she has persistent widened splitting of S2. Radiographic findings (seen here) demonstrate peripheral “pruning” of the large pulmonary arteries.

Blood pressure in the lungs is usually very low 15/5. In pulmonary hypertension, the pressure increases > 20 mmHg at rest

  • 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
  • Presentation: Dyspnea on exertion, fatigue, chest pain, edema
  • Physical Exam: Loud pulmonic component of second heart sound (P2); Jugular venous distension; Ascites; Hepatojugular reflux; Lower limb edema

Diagnose with 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
    • Dilatation/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)

TX: 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
Pulmonary neoplasm
Patient will present as → a 65-year-old woman with a 40 pack-year history of smoking presents with a 7 kg weight loss over the last 3 months and recent onset of streaks of blood in the sputum. PE reveals a thin, afebrile woman with clubbing of the fingers, an increased anteroposterior diameter, scattered and coarse rhonchi and wheezes over both lung fields, and distant heart sounds.

Lung cancer is classified into 2 major categories

  • 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

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

  • Location: (central mass), very aggressive
  • Treatment: Combination chemotherapy needed
  • Paraneoplastic syndromes: Cushing's, SIADH

⇒ Non-Small Cell  (85% lung cancer cases)

  • Adenocarcinoma - most common (peripheral mass), 35-40% of cases of lung cancer
    • Most common
    • Associated with smoking and asbestos exposure
    • Location: Periphery
    • Paraneoplastic syndrome: Thrombophlebitis
  • Squamous cell (central mass) with hemoptysis, 25-35% of lung cancer cases
    • Location: central
    • May cause hemoptysis
    • Paraneoplastic syndrome: hypercalcemia
    • Elevated PTHrp
  • Large cell - fast doubling rates - responds to surgery rare (only 5%)
    • Location: Periphery 60%
    • Paraneoplastic syndrome: Gynecomastia
  • Carcinoid tumor (1-2%): lack glandular and squamous differentiation
    • A tumor arising from neuroendocrine cells leading to excess secretion of serotoninhistamine, 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)


Non-Small Cell 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

Small Cell: 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)
Patient will present as → a 30-year-old African American female with a cough, fever, and generalized body aches. You order a CXR which shows bilateral hilar adenopathy.

Chronic autoimmune inflammatory disease in which small nodules (granulomas) develop in lungs, lymph nodes, and other organs↑ ACE levels + Bilateral hilar adenopathy

  • Pulmonary manifestations (most common); skin = 2nd most; skin and lymph = most common areas
  • 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

DX: 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

TX: 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 nodules
Patient will present as → a 35-year-old female who was found to have a small (2.5 cm) pulmonary lesion on chest radiograph found incidentally after a screening exam for a positive PPD at work. The patient has no significant past medical history and is asymptomatic.

Pulmonary nodules: < 3 cm = nodule; >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 mo, 6 mo, then yearly for 2 yr (calcification, smooth well defined edges = benign)

Radiographic characteristics help define the malignant potential of solitary pulmonary nodules

  • 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

Tx: management depends on radiographic findings

  • If malignant ⇒ biopsy!
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