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Pulmonology Flashcards

1
Q

How are the diagnoses of emphysema and chronic bronchitis made?

A
  • emphysema is a pathologic diagnosis defined as the permanent enlargement of air spaces distal to the terminal bronchioles due to destruction of alveolar walls
  • chronic bronchitis is a clinical diagnosis defined by a chronic productive cough for at least 3 months per year for at least 2 consecutive years
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2
Q

Describe the mechanism by which smoking leads to emphysema.

A

the smoke activates PMNs and macrophages responsible for the production of elastase, inhibits a1-antitrypsin, and increases oxidative stress

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3
Q

What are the signs and symptoms of COPD?

A
  • the classic symptoms includes some combination of dyspnea, cough, and sputum production
  • signs include prolonged expiratory time, end-expiratory wheezes, decreased breath sounds, tachypnea and tachycardia, cyanosis, use of accessory respiratory muscles, and signs of cor pulmonale
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4
Q

What is the classic clinical picture of a patient with emphysema?

A

these patients are “pink puffers”

  • they tend to be thin due to the increased energy used to breath but have a barrel chest
  • they tend to lean forward as they breath with pursed lips
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5
Q

What is the classic clinical picture of a patient with chronic bronchitis?

A

these patients are “blue bloaters”

  • they tend to be overweight and cyanotic
  • they present with more cough and sputum production that emphysema patients
  • the respiratory rate is normal or slightly increased
  • often exhibit signs of cor pulmonale in severe disease
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6
Q

What is the difference between a1-antitrypsin deficiency and tobacco smoke-induced emphysema?

A
  • those with a1-antitrypsin deficiency typically have a panlobular emphysema with a predilection for the lung bases
  • cases due to smoking typically are a centrilobular emphysema with a predilection for the lung apices
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7
Q

How is COPD screened, diagnosed, and staged?

A

screening using peak expiratory flow rate
- a rate less than 350 L/min indicates a need for PFTs

diagnosed using PFTs

  • the primary criteria is an FEV1/FVC < 0.7
  • supportive findings include an increased TLC and residual volume but reduced tidal volume

GOLD staging is based on the FEV1 alone

  • FEV1 greater than 80% predicted is mild disease
  • FEV1 between 50-80% predicted is moderate
  • between 30-50% is severe and less than 30% is very severe
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8
Q

What are the expected findings on an arterial blood gas in a patient with COPD?

A

a chronic respiratory acidosis with metabolic alkalosis as compensation

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9
Q

The single most important intervention in those with COPD is what?

A

smoking cessation

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10
Q

Describe four test results consistent with a diagnosis of COPD.

A
  • PFTs showing FEV1/FVC less than 0.7
  • CXR showing hyperinflation, flattened diaphragm, and diminished vascular markings
  • reduced a1-antitrypsin levels
  • ABG showing a compensated respiratory acidosis with chronic hypoxemia
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11
Q

Describe the general approach to managing COPD and acute exacerbations.

A

chronic therapy

  • smoking cessation is the single most important intervention, slowing the rate of decline
  • oxygen therapy has been shown to improve survival and quality of life for patients with COPD and chronic hypoxemia
  • initiate inhaled anticholinergics and B2-agonists for symptomatic relief
  • pulmonary rehabilitation including education, exercise, and physiotherapy
  • annual flu vaccinations and vaccination against Strep pneumonia every 5-6 years for those over 65

exacerbations

  • combined inhaled B2-agonsits and anticholinergics
  • systemic corticosteroids (usually IV methylprednisolone)
  • antibiotics (azithromycin or doxycycline)
  • supplement oxygen to keep saturation between 90-93%
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12
Q

For which group of COPD patients with long-term oxygen therapy shown to improve survival?

A

for those with a PaO2 less than 55 mmHg or SaO2 less than 88% at rest or on exertion and those with a PaO2 between 55-59 mmHg who have signs of cor pulmonale or polycythemia

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13
Q

What are the four major complications of COPD?

A
  • acute exacerbations
  • secondary polycythemia
  • pulmonary hypertension
  • cor pulmonale
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14
Q

What are the three most common triggers of an acute COPD exacerbation?

A

infection, medication non-compliance, and cardiac disease

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15
Q

COPD

A
  • a combination of emphysema and chronic bronchitis
  • defined as a dilation of air sacs due to alveolar wall destruction or a chronic productive cough for 3 months in at least 2 consecutive years
  • the typical symptoms are dyspnea, cough, and sputum production; other signs include expiratory wheezes, a prolonged expiratory phase, poor aeration, tachypnea, and signs of cor pulmonale
  • screen using peak flow, diagnose based on a FEV1/FVC less than 0.7, and stage based on FEV1
  • manage disease with smoking cessation, inhaled anticholinergics, inhaled B2-agonists, and long-term oxygen therapy
  • manage acute exacerbations by adding a systemic corticosteroid and antibiotics (azithromycin or doxycycline)
  • complications include acute exacerbation, pulmonary hypertension, cor pulmonale, and secondary polycythemia
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16
Q

What triad defines asthma?

A
  • airway inflammation
  • airway hyperresponsiveness
  • reversible airflow obstruction
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17
Q

What is the difference between extrinsic and intrinsic asthma?

A
  • extrinsic is more common and occurs in atopic patients

- intrinsic are cases not related to atopy or environmental triggers

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18
Q

If an asthmatic comes in with an acute attack, what are two key signs of impending respiratory failure?

A
  • paradoxical movement of the abdomen and diaphragm on inspiration
  • a normal or high PaCO2
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19
Q

Describe the clinical features of asthma.

A
  • characterized by intermittent SOA, wheezing, chest tightness, and cough
  • symptoms usually occur within 30 minutes of exposure to triggers
  • and symptoms are usually worse at night
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20
Q

What are some causes of wheezing other than asthma?

A

any condition that mimics large-airway bronchospasm

  • CHF due to edema of airways
  • COPD due to inflammation of airways
  • cardiomyopathies and pericardial disease that lead to edema around bronchi
  • lung cancer
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21
Q

What PFTs are characteristic of asthma?

A
  • decreased FEV1, FVC, and FEV1/FVC
  • increase in FEV1 more than 12% following albuterol
  • decrease in FEV1 more than 20% following methacholine or histamine challenge
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22
Q

What ABG values are consistent with asthma?

A

most often they have hypoxemia driving hypocarbia

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23
Q

What is salmeterol?

A

a LABA

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24
Q

What is the benefit of cromolyn sodium for asthmatics?

A

it is prophylactic and reduces the likelihood of an attack before a predictable trigger exposure

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25
Q

If a patient with asthma presents with an acute exacerbation, what tests should you perform?

A
  • peak flow (decreased)
  • ABG (increased A-a gradient)
  • CXR (rule out pneumonia or pneumothorax)
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26
Q

What is aspirin sensitive asthma and what clinical findings would suggest this diagnose?

A
  • it is a form of aspirin in which aspirin or NSAIDs may cause a severe systemic reaction
  • most patients have asthma and nasal polyps
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27
Q

What are the first three lines of treatment for acute asthma exacerbation?

A
  • inhaled B2-agonsit
  • IV corticosteroids
  • IV magnesium
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28
Q

Bronchiectasis

A
  • a permanent dilation and destruction of bronchial walls with chronic inflammation, airway collapse, and ciliary loss/dysfunction, leading to impaired secretion clearance
  • causative inflammation may be due to recurrent infections, cystic fibrosis, primary ciliary dyskinesia, autoimmune disease, humoral immunodeficiency, or airway destruction
  • presents with chronic cough, large amounts of mucopurulent foul-smelling sputum, dyspnea, hemoptysis, and recurrent/persistent pneumonia
  • complications include hypoxemia with cor pulmonale and secondary amyloidosis
  • diagnosed by high-resolution CT and PFTs will reveal an obstructive pattern
  • treatment involves antibiotics for acute exacerbations, hydration, chest physiotherapy, and inhaled bronchodilators
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29
Q

What are the most common causes of bronchiectasis?

A
  • recurrent infections
  • cystic fibrosis
  • primary ciliary dyskinesia
  • autoimmune disease or humoral immunodeficiency
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30
Q

Which lung cancer has the lowest associated with smoking?

A

adenocarcinoma, a non-small cell lung cancer

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31
Q

List three major risk factors for lung cancer.

A
  • smoking
  • asbestos exposure (synergistic with smoking)
  • radon
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32
Q

How does lung cancer often present?

A
  • local manifestations include cough, hemoptysis, obstruction, wheezing, dyspnea, and postobstructive pneumonia
  • anorexia, weight loss, and weakness are common
  • local invasion leads to superior vena cava syndrome, phrenic nerve palsy, laryngeal nerve palsy and hoarseness, horner syndrome, and pancoast tumor
  • malignant pleural effusion
  • a wide variety of paraneoplastic syndromes including ectopic ADH, ACTH, PTH-like hormone production; hypertrophic pulmonary osteoarthropathy; eaton-lambert syndrome; and digital clubbing
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33
Q

What is superior vena cava syndrome?

A
  • a complication of locally invasive lung cancer caused by obstruction of the superior vena cava
  • presents with facial fullness, facial and arm edema, dilated veins over the anterior chest, arms, and face, and JVD
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34
Q

What is a pancoast tumor?

A
  • a superior sulcus tumor which involves C8-T2

- causes shoulder pain which radiates down the arm, upper extremity weakness, and sometimes Horner syndrome

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35
Q

What paraneoplastic syndromes are common in lung cancer?

A
  • SIADH, ectopic ACTH secretion, and Eaton-Lambert syndrome with small cell carcinomas
  • PTH-like hormone secretion and hypertrophic pulmonary osteoarthropathy with squamous cell carcinoma
  • hypertrophic pulmonary osteoarthropathy with adenocarcinoma
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36
Q

What is the key difference between small cell and non-small cell lung cancer?

A

it is a tissue diagnosis, but the key difference is that small cell are rarely amenable to resection and non-small cell are more readily amenable

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37
Q

What tests might the workup for lung cancer involve?

A
  • CXR is the most important for diagnosis
  • CT with contrast is useful for staging and revealing lymphadenopathy in the mediastinum
  • cytologic examination o the sputum for central tumors
  • fiberoptic bronchoscope for larger central tumors
  • trans thoracic needle biopsy for more peripheral lesions
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38
Q

How is lung cancer typically treated?

A
  • for non-small cell, surgery is usually accompanied by radiation therapy
  • for small cell, systemic chemotherapy with prophylactic radiation to prevent brain metastases is preferred
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39
Q

What is the typical location and a unique feature about the following lung cancers:

  • squamous cell
  • adenocarcinoma
  • large cell carcinoma
  • small cell carcinoma
A
  • squamous is usually central, has cavitation on CXR, and is associated with PTHrH production and hypertrophic pulmonary osteoarthropathy
  • adenocarcinoma is often peripheral, is the least associated with smoking, and is associated with hypertrophic pulmonary osteoarthropathy
  • large cell are usually peripheral
  • small cell are usually central, tend to narrow bronchi by extrinsic compression, and are associated with SIADH, ectopic ACTH secretion, and Eaton-Lambert syndrome
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40
Q

What are possible causes of a solitary, benign lung nodule?

A
  • infectious granuloma
  • bronchogenic carcinoma
  • hamartoma
  • bronchial adenoma
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41
Q

What features of a lung nodule are more suggestive of benign than malignant origin?

A
  • younger age
  • absence of smoking history
  • nodule smaller than 1 cm
  • smooth, regular, discrete borders
  • dense, central calcification (as opposed to eccentric, asymmetric calcification)
  • stable in size or growth over a period of days which would suggest an infectious or inflammatory process
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42
Q

If one discovers a solitary pulmonary nodule on CXR, describe the process of working this up.

A
  • if an old CXR is available and shows no change in size for more than 2 years, stop the workup and follow yearly
  • if the nodule is new, hasn’t been stable that long, or films aren’t available, perform a CT with thin sectinos
  • if the CT is benign, follow every three months, but if the CT is suspicious, perform a biopsy
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43
Q

What are the most likely causes of a mediastinal mass?

A
  • anterior (4Ts): thyroid, teratogenic tumors, thymoma, and terrible lymphoma
  • middle: lung cancer, lymphoma, aneurysms, cysts, Morgagni hernia
  • posterior: neurogenic tumors, esophageal masses, enteric cysts, aneurysms, Bochdalek hernia
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44
Q

What is the pathophysiology of a transudative versus exudative effusion?

A
  • transudative are those due to either elevated capillary pressure in visceral or parenteral pleura or due to decreased plasma oncotic pressure
  • exudative are those caused by increased permeability of pleural surfaces or decreased lymphatic flow from pleural surface because of damage to pleural membranes or vasculature
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45
Q

What causes a transudative pleural effusion and what are possible etiologies?

A

elevated capillary pressure or decreased oncotic pressure

  • CHF
  • cirrhosis
  • pulmonary embolism
  • nephrotic syndorme
  • peritoneal dialysis
  • hypoalbuminemia
  • atelectasis
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46
Q

What causes an exudative pleural effusion and what are possible etiologies?

A

increased permeability of pleural membranes or vasculature

  • bacterial pneumonia, viral infection, or TB
  • malignancy
  • pulmonary embolism
  • collagen vascular disease
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47
Q

How is an exudative effusion differentiated form a transudative one through labs?

A

exudative effusions meet at least one Light’s criteria

  • pleural protein/serum protein > 0.5
  • pleural LDH/serum LDH > 0.6
  • LDH > two thirds the upper limit of normal serum LDH
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48
Q

What are the clinical features of a pleural effusion?

A
  • for the most part, without pre-existing lung disease, pleural effusions are well-tolerated clinically
  • when symptomatic, it presents with dyspnea on exertion, peripheral edema, orthopnea, and paroxysmal nocturnal dyspnea
  • signs include dullness to percussion, decreased breath sounds over the effusion, and decreased tactile fremitus
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49
Q

What are the following characteristics of a pleural effusion indicative of:

  • elevated pleural fluid amylase
  • milk, opalescent fluid
  • frankly purulent fluid
  • bloody
  • predominately lymphocytic exudative effusions
  • pH less than 7.2
A
  • elevated pleural fluid amylase: esophageal rupture, pancreatitis, or malignancy
  • milk, opalescent fluid: chylothorax (lymph in the space)
  • frankly purulent fluid: pus in the pleural space
  • bloody: malignancy
  • predominately lymphocytic exudative effusions: TB
  • pH less than 7.2: parapneumonic effusion or empyema
50
Q

What is a parapneumonic effusion?

A

a non-infected pleural effusion secondary to bacterial pnuemonia

51
Q

What is an empyema?

A

pus in the pleural fluid indicative of a complicated parapneumonic effusion that has become infected

52
Q

What is the best way to diagnose a pleural effusion? What is the volume threshold at which one is detectable?

A
  • about 250 mL of fluid is needed before a CXR will detect it
  • lateral decubitus films are more reliable than an AP film and help determine if the fluid is free flowing or loculated
  • a CT is more sensitive than a CXR
  • thoracentesis can play a therapeutic or diagnostic role once a pleural effusion has been diagnosed
53
Q

What is the feared complication of a thoracentesis? How do we guard against this?

A

pneumothorax, which is why we never perform a thoracentesis if the effusion is less than 1 cm thick on lateral internal decubitus CXR

54
Q

How are pleural effusions treated?

A
  • transudative effusions are treated with diuretics, sodium restriction, and therapeutic thoracentesis for symptomatic cases
  • exudative are treated by treating the underlying disease (bacterial pneumonia, TB, viral infection, malignancy, PE, or collagen vascular disease)
55
Q

Empyema is a complication of which type of pleural effusion?

A

usually an exudative one, complicating a bacterial pneumonia

56
Q

Pneumothorax

A
  • defined as air in the normally airless pleural space
  • can be divided into those that are traumatic and spontaneous, which are further divided as simple (occurring without underlying lung disease) and complex (secondary to an underlying lung disease)
  • traumatic tend to be iatrogenic (e.g. thoracentesis); simple spontaneous tend to be due to rupture of air-filled sacs on the lung at the apices in tall, lean, young men; complex spontaneous usually complicate COPD, asthma, interstitial lung disease, neoplasms, CF, or TB
  • presents with ipsilateral, abrupt onset chest pain, dyspnea, cough, decreased breath sounds over the affected side, hyper-resonance, decreased tactile remits, and mediastinal shift toward the side of the pneumothorax
  • diagnosed with CXR
  • primary spontaneous are treated with observation if small and asymptomatic, O2 and needle aspiration or chest tube if larger or symptomatic; chest tube for secondary spontaneous
57
Q

Tension Pneumothorax

A
  • an accumulation of air within the pleural space such that tissues surrounding the opening into the pleural cavity act as valves, allowing air to enter but not escape
  • this positive pressure accumulates and collapses the ipsilateral lung and shifts the mediastinum away
  • may be due to mechanical ventilation and barotrauma, CPR, or trauma
  • presents with hypotension as cardiac filling is impaired due to compression of the great veins, distended neck veins, shifted trachea, decreased breath sounds, and hyper resonance
  • treat with immediate chest decompression
58
Q

What is the usual cause of death in those with a tension pneumothorax?

A

hemodynamic compromise as the great veins are compressed, cardiac filling is impaired, and hypotension ensues

59
Q

What is the common presentation of malignant mesothelioma?

A
  • usually have a history of asbestos exposure
  • present with dyspnea, weight loss, and cough
  • effusion is typically bloody
60
Q

What is interstitial lung disease?

A

an inflammatory process involving the alveolar wall, resulting in fibroelastic proliferation and collagen deposition that can lead to irreversible fibrosis, distortion of lung architecture, and impaired gas exchange

61
Q

Which drugs are most known for causing interstitial lung disease?

A

amiodarone, nitrofurantoin, bleomycin, phenytoin, and illicit drugs

62
Q

What are the clinical features of interstitial lung disease?

A
  • dyspnea, unproductive cough, and fatigue

- rales, digital clubbing, signs of pulmonary hypertension, and cyanosis

63
Q

How is interstitial lung disease diagnosed?

A
  • CXR findings are usually nonspecific, diffuse changes including reticular, reticulonodular, ground glass, or honecombing
  • CT is better able to asses the extent of fibrosis
  • PFTs demonstrate a restrictive pattern
  • desaturation with exercise
  • tissue biopsy is often required and can be done via fiberoptic bronchoscopy, open lung biopsy, or video-assisted thoracoscopic lung biopsy
64
Q

What PFTs are consistent with a restrictive lung disease?

A

all lung volumes are decreased, the FEV1/FVC ratio is increased, and the DLCO is diminished

65
Q

What are the most common causes of clubbing?

A
  • pulmonary disease
  • congenital heart disease
  • bacterial endocarditis
  • biliary cirrhosis
  • inflammatory bowel disease
66
Q

Interstitial Lung Disease

A
  • an inflammatory process that involves alveolar walls, resulting in fibroelastic proliferation and collagen deposition
  • these changes contribute to irreversible fibrosis, distortion of lung architecture, and impaired gas exchange
  • causes include pneumoconiosis, sarcoidosis, histiocytosis X, wegener granulomatosis, churg-strauss syndrome, good pasture disease, alveolar proteinosis, hypersensitivity and eosinophilic pneumonitis, or drug-induced by amiodarone, nitrofurantoin, bleomycin, etc.
  • presents with dyspnea, unproductive cough, fatigue, rales, digital clubbing, cyanosis, and other signs of pulmonary hypertension
  • CXR findings are diffuse and non-specific, CT gives a better estimation of the degree of fibrosis, PFTs show a restrictive pattern, and a tissue biopsy is often needed
  • treatment varies based on the etiology
67
Q

Sarcoidosis

A
  • a systemic disease of noncaseating granulomas
  • classically seen in African American females
  • granulomas are most commonly found in the hilar lymph nodes and lungs, contributing to a restrictive lung disease, but can be found in any tissue
  • presents with constitutional symptoms, dry cough, dyspnea, erythema nodosum, anterior uveitis, blurred vision, arrhythmias or conduction disturbances, bell palsy
  • diagnosis is supported by bilateral hilarity adenopathy on CXR, skin anergy, elevated ACE, hypercalcemia and hypercalciuria, restrictive PFTs
  • definitive diagnosis is made by trans bronchial biopsy which finds noncaseating granulomas
  • most cases solve spontaneously within 2 years but steroids or methotrexate may be required
68
Q

Why does sarcoidosis present with hypercalcemia and hypercalciuria?

A

because the granulomas have 1-alpha hydroxyls activity and activate vitamin D

69
Q

Describe the typical presentation and lab findings for someone with sarcoidosis.

A
  • presents with constitutional symptoms, dry cough, dyspnea, erythema nodosum, anterior uveitis, blurred vision, arrhythmias or conduction disturbances, bell palsy
  • diagnosis is supported by bilateral hilarity adenopathy on CXR, skin anergy, elevated ACE, hypercalcemia and hypercalciuria, restrictive PFTs
  • definitive diagnosis is made by trans bronchial biopsy which finds noncaseating granulomas
70
Q

Histiocytosis X

A
  • a chronic interstitial pneumonia caused by an abnormal proliferation of histiocytes
  • variants include eosinophilic granuloma affecting the bone and lungs and Letterer-Siwe disease or Hand-Schuller-Christian syndrome, which are systemic
  • almost all patients are cigarette smokers
  • presents with dyspnea and nonproductive cough; occasionally spontaneous pneumothorax, lytic bone lesions, and diabetes insidious
  • CXR shows honeycombing and CT shows cystic lesions
  • may require corticosteroids or lung transplantation
71
Q

Wegener Granulomatosis

A
  • a necrotizing granulomatous vasculitis
  • typically affects the vessels of the lungs, kidneys, and upper airway, making it a cause of interstitial lung disease
  • presents with upper and lower respiratory infections, glomerulonephritis, and pulmonary nodules
  • diagnosis is made based on tissue biopsy and the presence of c-ANCA
  • treated with immunosuppression
72
Q

What diseases are characterized by the presence of c-ANCA and p-ANCA?

A
  • cANCA: wegener granulomatosis

- pANCA: Churg-Strauss syndrome or Goodpasture syndrome

73
Q

Churg-Strauss Syndrome

A
  • a small vessel necrotizing, granulomatous vasculitis with eosinophilia
  • affects the heart and lungs in particular causing an interstitial lung disease
  • presents with asthma, skin nodules or purpura, and peripheral neuropathy
  • diagnosed based on the presence of pANCA and eosinophilia
74
Q

What is a pneumoconiosis?

A

an interstitial lung fibrosis due to chronic exposure to specific small particles, which induce macrophage activity

75
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 which causes a restrictive lung disease
  • is associated with rheumatoid arthritis as part of Caplan syndrome
76
Q

Asbestosis

A
  • an interstitial lung fibrosis due to chronic exposure to asbestosis, which is engulfed by alveolar macrophages, inducing fibrosis
  • seen in construction workers, plumbers, and shipyard workers
  • fibrosis of the lung and pleura affects the lower lobes more than the upper
  • “ivory white” calcified plaques can be seen on CXR on the pleura and on the top of the diaphragm which are pathognomonic
  • increased risk for bronchogenic lung cancer and mesothelioma
77
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
  • causes a localized and nodular peribronchial fibrosis, more so in the upper lobes than lower
  • presentation includes dyspnea and restrictive pulmonary abnormalities
  • may resemble, but also increases the risk for, TB
78
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)
  • diagnosed by a beryllium lymphocyte proliferation test
  • treat with glucocorticoids
  • increases the risk for lung cancer
79
Q

Compare the populations, lesion distribution, and risks/complications for the four major pneuomconioses.

A
  • coal workers: coal miners, diffuse lung fibrosis, risk for RA
  • silicosis: sandblasters, fibrotic nodules in upper lobes, risk for TB
  • berylliosis: aerospace workers, systemic granulomas, risk for cancer
  • asbestosis: plumbers/construction workers/shipyard workers, fibrosis of lung and pleura, risk for bronchogenic carcinoma and malignant mesothelioma
80
Q

Hypersensitivity Pneumonitis

A
  • an interstitial lung disease associated with hypersensitivity
  • inhalation of an antigenic agent induces an immune-mediated pneumonitis and chronic exposure may lead to restrictive lung disease
  • may be induced by moldy hay, avian droppings, moldy sugar cane, compost material, and other organic dusts
  • presents with flu-like features in the acute form including fever, chills, cough, and dyspnea; the chronic form is more insidious
  • serum IgG and IgA to the inhaled antigen is the hallmark finding for diagnosis
  • treat with glucocorticoid
81
Q

Pulmonary Alveolar Proteinosis

A
  • an alveolar filling disease causing interstitial lung disease
  • caused by an accumulation of surfactant-like protein and phospholipids in the alveoli
  • presents with dry cough, dyspnea, hypoxia, and rales
  • CXR has a ground glass appearance with bilateral alveolar infiltrates in a bat-wing distribution
  • lung biopsy is required for diagnosis
  • treat with lung lavage and granulocyte colony-stimulating factor; do not give steroids as patients are at increased risk for infection
82
Q

A CXR with ground glass appearance with bilateral alveolar infiltrates in a bat-wing distribution?

A

pulmonary alveolar proteinosis, a alveolar filling disease causing an interstitial lung disease

83
Q

Idiopathic Pulmonary Fibrosis

A
  • an interstitial lung diseasing causing restrictive deficits
  • more common in men and in smokers
  • presents with gradual onset dyspnea and unproductive cough with a progressive and unrelenting course
  • diagnosed based on CXR with ground glass or honeycombed appearance with open lung biopsy to confirm
  • there is no effective treatment but supplemental oxygen, corticosteroids, and lung transplant are used
84
Q

Radiation Pneumonitis

A
  • an interstitial pulmonary inflammation characterized by alveolar thickening and pulmonary fibrosis
  • the acute form presents 1-6 months after radiation and the chronic develops 1-2 years after
  • morbidity and mortality are related to the irradiated lung volume, dose, patient status, and concurrent chemo
  • presents with low-grad fever, cough, chest fullness, dyspnea, pleuritic chest pain, hemoptysis, and acute respiratory distress
  • CXR is usually normal and so a CT scan is the best study
  • treat with corticosteroids
85
Q

What are the two major goals of mechanical ventilation?

A

maintain alveolar ventilation and correct hypoxemia

86
Q

On CXR, where should the tip of an ET tube be located?

A

approximately 2-5 cm above the carina

87
Q

What are the consequences of high and low static airway pressures when mechanical ventilation is used?

A
  • low: underinflation and atelectasis

- high: overinflation and barotrauma

88
Q

Describe assist control ventilation.

A
  • guarantees a backup minute ventilation but lets the patient initiate breaths at a faster rate if desired
  • can be volume or pressure targeted (give the pressure needed to elicit a particular volume with risk for barotrauma or give a set pressure with risk of under inflation)
  • all breaths are supported by the ventilator unlike synchronous intermittent mandatory ventilation
89
Q

Describe synchronous intermittent mandatory ventilation.

A
  • patients can breathe on their own above the mandatory rate without help from the ventilator
  • the ventilator steps in and supports breathing if the desired rate is not achieved spontaneously
90
Q

What is the difference between assist control ventilation and synchronous intermittent mandatory ventilation?

A

both set a minimum respiratory rate but assist control ventilation supports every breath while synchronous intermittent mandatory ventilation assists only the additional breaths required to meet the minimum threshold, not spontaneous breaths

91
Q

What is pressure support ventilation?

A

that which provides a constant, baseline PEEP in addition to an inspiratory pressure to support each patient-triggered breath (no set minimum)

92
Q

What is the difference between CPAP and pressure support ventilation?

A

pressure support provides the same baseline PEEP as CPAP but also provides an inspiratory pressure to support each patient-initiated breath

93
Q

What is BiPAP?

A

a form of ventilation similar to pressure support ventilation in that it delivers a set inspiratory pressure and a constant PEEP but does so with a face or nasal mask rather than intubation

94
Q

What ventilation parameters affect PaCO2 and which affect PaO2?

A
  • PaCO2 is affected by minute ventilation (tidal volume and respiratory rate)
  • PaO2 is affected by the FiO2 and PEEP
95
Q

What risks are associated with high levels of PEEP during ventilation?

A
  • risk of barotrauma, including pneumothorax or pneumomediastinum
  • decreased cardiac output secondary to increased intrathoracic pressure and decreased venous return
96
Q

What complications are typical of most forms of ventilation?

A
  • anxiety, agitation, and discomfort requiring sedation and analgesia
  • difficulty managing tracheal secretions
  • ventilator-associated pneumonia
  • barotrauma
  • tracheomalacia
  • laryngeal damage during intubation
97
Q

What is tracheomalacia?

A

a softening of the tracheal cartilage which can be a complication of mechanical ventilation

98
Q

What are the two most common manifestations of barotrauma sustained during mechanical ventilation?

A
  • pneumothorax

- pneumomediastinum

99
Q

Why is hypercapnia a problem?

A

because it can lead to dyspnea and vasodilation of cerebral vessels with a corresponding increase in ICP, with subsequent papilledema, headache, impaired consciousness, and coma

100
Q

What are the general criteria for acute respiratory failure?

A
  • hypoxia defined as PaO2 less than 60 despite FiO2 greater than 0.6 or
  • hypercapnia defined as PaCO2 more than 50
101
Q

What are possible causes of acute respiratory failure?

A
  • CNS depression or insult
  • neuromuscular diseases like MG, polio, Guillain-Barre
  • upper airway obstruction
  • thoracic problems like kyphoscoliosis, flail chest, or hemothorax
  • CHF, valvular disease, PE, and anemia
  • lower airway abstruction including asthma, COPD, pneumonia, and ARDS
102
Q

What are possible causes of hypoxemic respiratory failure and hypercapnic respiratory failure?

A
  • hypoxemic: process that involve the lung itself as in ARDS, pneumonia, pulmonary edema; VQ mismatch and intrapulmonary shunting
  • hypercapnic: failures of alveolar ventilation due to decreased minute ventilation or increased physiologic dead space as in COPD, asthma, CF, severe bronchitis, neuromuscular diseases, CNS depression, mechanical restriction of lung inflation, or respiratory fatigue in prolonged hyperventilation in DKA
103
Q

How are patients with acute respiratory failure and hypoxemia evaluated?

A
  • first measure a PaCO2
  • if elevated, the etiology is related to hypoventilation; measure the A-a gradient - if normal, hypoventilation alone accounts for the hypoxemia, but if elevated, another mechanism must be present
  • if PaCO2 is normal, measure the A-a gradient - if normal, low inspired PaCO2 is the cause of hypoxemia but if elevated you must ask if the lowered PaO2 improved with supplemental O2
  • if it does not improve, there is a shunt and if it does improve, there is a VQ mismatch
104
Q

What is pulmonary shunting?

A

a state in which there is little or no ventilation of perfused areas, so venous blood is shunted into the arterial circulation without being oxygenated

105
Q

Describe the difference in presentation between a VQ mismatch and a shunt.

A
  • both present with hypoxemia, normal PaCO2, and elevated A-a gradient
  • a VQ mismatch (ventilation without perfusion) typically leads to hypoxia without hypercapnia that responds to supplemental O2
  • a shunt (perfusion without ventilation) typically leads to hypoxia without hypercapnia that does not respond to supplemental O2
106
Q

What would cause hypoxemia with a normal A-a gradient?

A
  • low inspired PO2

- hypoventilation

107
Q

Diffusion impairment such as interstitial lung disease causes what kind of hypoxemia?

A

hypoxemia without hypercapnia

108
Q

ARDS

A
  • neutrophil activations in the systemic or pulmonary circulations induces damage to the alveolar-capillary interface
  • this allows protein rich fluid to leak into the alveoli, which combines with necrotic epithelial cells to form hyaline membranes
  • widespread atelectasis, collapse of alveoli, interstitial edema, and surfactant dysfunction secondary to this lung fluid then contribute to a shunt
  • the shunt is responsible for hypoxemia refractory to oxygen supplementation, without hypercarbia, and an increased A-a gradient
  • causes include SPARTAS: sepsis (most common risk factor), pancreatitis/pneumonia, aspiration, uremia, trauma, amniotic fluid embolism, shock
  • presents with dyspnea, tachypnea, tachycardia, hypoxemia not responsive to supplemental oxygen, diffuse bilateral pulmonary infiltrates on CXR, a respiratory alkalosis followed by respiratory acidosis as the work of breathing increases (possibly complicated by metabolic acidosis if septic), and normal PCWP less than 18
  • the Berlin criteria require acute onset of less than 1 week, bilateral infiltrates seen on chest imaging, pulmonary edema not explained by fluid overload or CHF (PCWP < 18), and hypoxemia refractory to oxygen therapy
  • treat with oxygenation using a high PEEP and low tidal volumes; avoid fluid overload while treating the underlying disease
  • may be complicated by permanent scarring, barotrauma, nosocomial pneumonia, line-associated infections, renal failure
109
Q

What is the most common cause of ARDS?

A

sepsis

110
Q

Explain the pathophysiology of ARDS.

A
  • neutrophil activations in the systemic or pulmonary circulations induces damage to the alveolar-capillary interface
  • this allows protein rich fluid to leak into the alveoli, which combines with necrotic epithelial cells to form hyaline membranes
  • widespread atelectasis, collapse of alveoli, interstitial edema, and surfactant dysfunction secondary to this lung fluid then contribute to a shunt
  • the shunt is responsible for hypoxemia refractory to oxygen supplementation, without hypercarbia, and an increased A-a gradient
111
Q

Pulmonary Hypertension

A
  • defined as a mean pulmonary arterial pressure greater than 25 mmHg at rest
  • may be due to resistance in the pulmonary venous system as seen in left heart failure, mitral stenosis, and atrial myxoma; hyperkinetics as in left-to-right cardiac shunts; obstruction as in PE or pulmonary artery stenosis; vascular obliteration as in collagen vascular disease; or pulmonary vasoconstriction as in chronic hypoxemia, COPD, and OSA
  • presents with dyspnea, fatigue, exertional chest pain, a loud pulmonic heart sound, parasternal heave, and eventually signs and symptoms of right sided heart failure
  • diagnosis is made by a right heart catheterization; an ECG may show RV hypertrophy, a CXR may showed enlarged pulmonary arteries, and an echo may show abnormal movement of the inter ventricular septum due to increased right ventricular volume
  • treat with inhaled phosphodiesterase inhibitors like sildenafil, oral CCBs, prostacyclin like epoprostenol, and endothelia receptor antagonists like bosentan
  • many patients require home oxygen, diuretics, and inotropes
112
Q

Describe the different mechanisms that can contribute to pulmonary hypertension.

A
  • resistance in the pulmonary venous system as seen in left heart failure, mitral stenosis, and atrial myxoma
  • hyperkinetics as in left-to-right cardiac shunts
  • obstruction as in PE or pulmonary artery stenosis
  • vascular obliteration as in collagen vascular disease
  • pulmonary vasoconstriction as in chronic hypoxemia, COPD, and OSA
113
Q

Primary Pulmonary Hypertension

A
  • defined by MAP > 25 mmHg
  • idiopathic but classically seen in young adult females
  • associated with inactivating mutations of MBPR2, which leads to proliferation of vascular smooth muscle
  • presents with dyspnea on exertion and right ventricle hypertrophy
  • atherosclerosis of the pulmonary trunk, fibrosis of the intima of pulmonary arteries, and plexiform lesions are often seen with long-standing disease
114
Q

Cor Pulmonale

A
  • defined as right ventricular hypertrophy with eventual RV failure resulting from pulmonary hypertension secondary to pulmonary disease
  • it does not include any of the causes of pulmonary hypertension due to heart disease
  • it is most often secondary to COPD but can also be due to PE, interstitial lung disease, asthma, CF, sleep apnea, and pneumoconioses
  • presents with exercise intolerance, cyanosis, digital clubbing, signs of right ventricular failure, and parasternal heave
  • CXR shows enlargement of the RA, RV, and pulmonary arteries; ECG shows right axis deviation, peaked P waves, and right ventricular hypertrophy; echo show right ventricular dilatation but normal left ventricular size and function
  • treat with diuretics cautiously because these patients may be preload-deponent
115
Q

Pulmonary Embolism

A
  • emboli most often come from a lower extremity DVT, including the iliofemoral vein; upper extremity DVT may be a source in IV drug users; they can also come from long-bone fractures, amniotic fluid, etc.
  • these block a portion of the pulmonary vasculature and lead to increased pulmonary vascular resistance, pulmonary artery pressure, and right ventricular pressure
  • they also create dead space in which there is ventilation without perfusion; the resulting hypoxemia and hypercarbia drive tachypnea and a respiratory alkalosis
  • usually asymptomatic but recurrences may lead to chronic pulmonary hypertension and cor pulmonale
  • symptoms include dyspnea, pleuritic chest pain, cough, hemoptysis, and syncope; signs include tachypnea, rales, tachycardia, an S4 heart sound, and increased P2
  • a CTA is the diagnostic test of choice but a VQ scan may be used if a CTA cannot as in renal failure patients; venous duplex ultrasound of the lower extremities, blood gases, D-dimer, and CXR may all be helpful
  • if CTA is equivocal, the risk of anticoagulation is high, or the patient is unstable, perform a pulmonary angiography
  • treat with supplemental oxygen, acute anticoagulation therapy with heparin, long-term anticoagulation with warfarin, and thrombolytic therapy with streptokinase or tPA
116
Q

What happens to the A-a gradient in those with a PE?

A

the gradient is usually elevated

117
Q

What is considered a therapeutic INR?

A

between 2-3

118
Q

Which segments of the lungs are most at risk during an episode of aspiration?

A

the lower segments of the right upper lobe and the upper segments of the right lower lobe

119
Q

How does aspiration pneumonitis present?

A
  • at the extreme it may present with acute onset or delayed onset of ARDS
  • otherwise it may develop with delayed respiratory dysfunction including cough, SOA, fever, tachypnea, hypoxemia, and frothy sputum
  • it may later be complicated by an aspiration pneumonia
120
Q

What are the most common causes of acute dyspnea? What are other causes of dyspnea?

A
  • CHF exacerbation, pneumonia, bronchospasm, PE, or anxiety are most common
  • can also be due to MI, pericarditis, arrhythmia, obstructive luge disease, PE, ARDS, pleural effusion, pneumothorax, upper airway obstruction, ILD, chest wall abnormalities, medications, DKA, GERD, and neuromuscular disease
121
Q

What two things cause paroxysmal nocturnal dyspnea and how?

A
  • left sided ventricular failure because at night, when supine, there is increased preload and worsening of pulmonary edema
  • COPD because at night there is an increase in airway secretions that can form an airway obstruction
122
Q

Hemoptysis

A
  • defined as an expectoration of blood with more than 600 mL defining massive hemoptysis
  • most common causes are bronchitis, idiopathic, bronchogenic carcinoma, TB, and pneumonia; bronchiectasis and bleeding diathesis are the most common causes of massive hemoptysis
  • history, CXR, bronchoscopy, and CT may all be helpful in diagnosis
  • during management, protection of the airway is very important; otherwise, suppress cough, correct bleeding diathesis, and treat any other cause

IM (13 decks)

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