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.► ABORDAGEM SINDRÔMICA > Step Up - Diseases Of The Pulmonary System > Flashcards

Step Up - Diseases Of The Pulmonary System Flashcards

1
Q

Emphysema - Definition:

A

Pathologic:

–> Permanent enlargement of air spaces distal to terminal bronchioles due to destruction of alveolar walls.

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2
Q

4th leading cause of death in the US:

A

COPD

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3
Q

Role of tobacco in asthma:

A
  1. Incr. number of activated PMNs and macros.
  2. Inhibits alpha-1 antitrypsin.
  3. Free radicals –> Oxidative stress.
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4
Q

In COPD (FEV1, FVC):

A
  1. FEV1/FVC <0.80.
  2. FEV1 is decreased.
  3. TLC is incr.
  4. RV is incr.
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5
Q

Pink puffers:

A
  1. Thin - due to incr. energy expenditure during breathing.
  2. When sitting, patients tend to lean forward.
  3. Patients have a barrel chest (incr. AP diameter of chest).
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6
Q

Blue bloaters:

A
  1. Overweight and cyanotic (2o to hypercapnia and hypoxemia).
  2. Chronic cough and sputum production are characteristic.
  3. Signs of cor pulmonale may be present in severe long standing disease.
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7
Q

COPD - Signs:

A
  1. PROLONGED Forced expiratory time –> >6sec.
  2. End-expiratory wheezes on forced expiration.
  3. Decr. breath sounds.
  4. Inspiratory crackles.
  5. Tachypnea/tachycardia.
  6. Cyanosis.
  7. Hyperresonance on percussion.
  8. Signs of cor pulmonale.
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8
Q

The lower the FEV1, the more…?

A

Difficulty one has breathing.

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9
Q

COPD - Definitive diagnostic test:

A

Spirometry.

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10
Q

COPD - Diagnosis - FEV1:

A

If FEV1 is 70% of predicted value –> Mild disease.

If FEV1 is 50% of predicted value –> Severe disease.

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11
Q

To diagnose airway obstruction, one must have:

A
  1. Normal or Incr. TLC.

2. Decr. FEV1.

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12
Q

Key points in taking history of COPD patients - General:

A
  1. History of cardiopulmonary diseases.
  2. Smoking.
  3. FHx - COPD, Heart disease, asthma.
  4. Occupation - industrial dusts, fumes.
  5. History of respiratory infections.
  6. Pulmonary medications.
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13
Q

Key points in taking history of COPD patients - Pulmonary symptoms:

A
  1. Dyspnea - quantitative severity.
  2. Cough.
  3. Sputum production - quantity, quality, duration, hemoptysis.
  4. Pulm. medications.
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14
Q

Obstructive vs Restrictive lung disease - FEV1:

A

O –> Low.

R –> Normal or slightly low.

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15
Q

O vs R lung disease - FEV1/FVC:

A

O –> Low.

R –> Normal or high.

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16
Q

O vs R lung disease - Peak expiratory flow rate:

A

O –> Low.

R –> Normal.

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17
Q

O vs R lung disease - RV:

A

O –> High.

R –> Low, normal, or high.

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18
Q

O vs R lung disease - TLC:

A

O –> High.

R –> Low.

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19
Q

O vs R lung disease - Vital capacity:

A

O –> Low.

R –> Low.

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20
Q

COPD - Diagnosis - CXR:

A
  1. Low sensitivity - Only severe, advanced emphysema will show typical changes.
  2. Useful in ACUTE EXACERBATION to rule out complications such as pneumonia or pneumothorax.
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21
Q

COPD - Diagnosis - ABG:

A

Chronic pCO2 retention + decr. pO2.

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22
Q

How faster does FEV1 decline in smokers?

A

3-4fold the normal rate. –> If smoker quits, then same rate of someone WHO HAS NEVER SMOKED.

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23
Q

In COPD, respiratory symptoms improve within?

A

1yr of quitting.

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24
Q

Clinical monitoring of COPD patients entails the following:

A
  1. Serial FEV1 measurements - this has the highest predictive value.
  2. Pulse oximetry.
  3. Exercise tolerance.
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25
Q

COPD - Treatment:

A
  1. Bronchodilators (beta-2 agonists, anticholinergics).

2. Steroids + antibiotics for acute exacerbations.

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26
Q

COPD - O2 therapy:

A

Shown to improve survival and quality of life in patients with COPD + Chronic hypoxemia.

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27
Q

Criteria for continuous or intermittent long-term O2 therapy in COPD:

A
  1. PaO2 55mmHg OR,
  2. SaO2<88% either at rest or during exercise, OR,
  3. PaO2 55-59mmHg + polycythemia or evidence of cor pulmonale.
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28
Q

COPD - Treatment guidelines - Mild to moderate disease:

A
  1. Begin with a bronchodilator in a metered-dose inhaler (MDI) formulation - Anticholinergics or beta-agonists are first-line.
  2. Inhaled steroids may be used as well - Use LOWEST DOSE POSSIBLE.
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29
Q

COPD at night?

A

In many patients with COPD, O2 levels decrease during sleep. Look for and treat nocturnal hypoxemia, if present (eg, oxygen, CPAP).

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30
Q

COPD - Treatment guidelines - Severe disease:

A
  1. Medications as above.
  2. Continuous O2 therapy (if patient is hypoxemic).
  3. Pulmonary rehabilitation.
  4. Triple inhaler therapy (long-acting beta-agonist plus a long acting anticholinergic plus an inhaled steroid).
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31
Q

Acute COPD exacerbation - Definition:

A

A persistent incr. in dyspnea (not relieved with bronchodilators).

  • -> Incr. sputum + cough are common.
  • -> Acute COPD exacerbation can lead to acute respiratory failure requiring hospitalization, and possibly mechanical ventilation - potentially fatal.
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32
Q

What is one of the main precipitants of COPD exacerbations?

A

Pulm. infection.

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33
Q

COPD - Complications:

A
  1. Acute exacerbations - MCC are infection, non compliance with therapy, and cardiac disease.
  2. Secondary polycythemia (Ht>55% in men, >47% in women) - compensatory response to chronic hypoxemia.
  3. Pulm. HTN and cor pulmonale - may occur in patients with severe, long-standing COPD who have chronic hypoxemia.
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34
Q

If a patient presents with COPD exacerbation, the following steps are appropriate:

A
  1. CXR.
  2. Beta-2 agonist + anticholinergic inhalers.
  3. Systemic corticosteroids.
  4. Antibiotics.
  5. Supplemental O2.
  6. Non invasive positive pressure ventilation (NPPV) if needed.
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35
Q

Asthma - Characteristically defined by the triad:

A
  1. Airway inflammation.
  2. Airway responsiveness.
  3. REVERSIBLE airflow obstruction.
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36
Q

Asthma can begin at what age?

A

At ANY age.

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37
Q

Signs of acute severe asthma attacks:

A
  1. Tachypnea
  2. Diaphoresis.
  3. Wheezing.
  4. Speaking in incomplete sentences.
  5. Use of accessory muscles of respiration.
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38
Q

Sign of impending respiratory failure:

A

Paradoxic movement of the abdomen and diaphragm on inspiration.

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39
Q

Asthma - MC finding on physical exam:

A

Wheezing - during BOTH inspiration + expiration.

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40
Q

All that wheezes is NOT asthma:

A

Any condition that mimics large-airway bronchospasm can cause wheezing:

  1. CHF - Due to edema of airways and congestion of bronchial mucosa.
  2. COPD - Inflamed airways may be narrowed, or bronchospasm may be present.
  3. Cardiomyopathies, pericardial diseases can lead to edema around the bronchi.
  4. Lung cancer - due to obstruction of airways (central tumor or mediastinal invasion).
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41
Q

Asthma - Dyspnea is common when?

A

When the patient is exposed to rapid changes in temperatures and humidity.

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42
Q

Asthma - Diagnosis - What is required?

A

Pulmonary function tests –> Show obstructive pattern.

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43
Q

Asthma - What confirms diagnosis:

A

Spirometry before and after bronchodilators can confirm diagnosis by proving reversible airway obstruction.
–> If inhalation of a bronchodilator results in an increase in FEV1 or FVC by at least 12%, airflow obstruction is considered reversible.

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44
Q

PFTs in asthma:

A
  1. Decr. FEV1, decr. FVC, decr. FEV1/FVC.
  2. Incr. in FEV1>12% with albuterol.
  3. Decr. in FEV1>20% with methacholine or histamine.
  4. Incr. in diffusion capacity of lung for CO.
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45
Q

In the ED, when patient is SOB, what is the quickest method of asthma diagnosis:

A

Peak flow measurement (peak expiratory flow rate).

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46
Q

Bronchoprovocation test:

A
  1. May be useful when asthma is suspected but PFTs are non diagnostic.
  2. Measures ease with which airways narrow in response to stimuli.
  3. Measures lung function before and after inhalation of increasing doses of methacholine –> Hyperresponsive airways develop obstruction at lower doses.
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47
Q

Asthma - Diagnosis - Role of CXR:

A

Normal in mild cases - severe asthma reveals hyperinflation.
–> Only necessary in severe asthma to exclude other conditions (eg pneumonia, pneumothorax, pneumomediastinum, foreign body).

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48
Q

If PaCO2 is INCREASED in a patient with asthma, what happened?

A

Incr. PaCO2 is a sign of respiratory muscle fatigue or severe airway obstruction –> Intubation is REQUIRED.

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49
Q

Drugs to be avoided in asthmatics:

A

Beta-blockers.

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50
Q

Side effects of inhaled steroids:

A

Due to oropharyngeal deposition:

  1. Sore throat.
  2. Oral candidiasis (thrush).
  3. Hoarseness.
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51
Q

How to minimize inhaled steroid side effects?

A

Using a spacer with MDIs are rinsing the mouth after use.

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52
Q

For acute asthma exacerbation, test to order:

A
  1. PEF - Decr.
  2. ABG - Incr. A-a gradient.
  3. CXR - Rule out pneumonia, pneumothorax.
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53
Q

Complications of asthma:

A
  1. Status asthmaticus - does NOT respond to standard medications.
  2. Acute respiratory failure - due to muscle fatigue.
  3. Pneumothorax, atelectasis, pneumomediastinum.
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54
Q

Aspirin-sensitive asthma should be considered in?

A

Patients with asthma + nasal polyp.

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55
Q

Bronchiectasis - General features:

A

PERMANENT, abnormal dilation + destruction of bronchial walls –> Cilia are damaged - Onset usually in CHILDHOOD.

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56
Q

Bronchiectasis - What precipitates the disease?

A

Infection in a patient with airway obstruction or impaired defense or drainage mechanism.

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57
Q

Bronchiectasis - Cause?

A

The cause is found in <50% of patients.

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58
Q

Bronchiectasis - Common today?

A

Less common today, due to modern antibiotics.

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59
Q

Bronchiectasis - Etiology:

A
  1. CF - MCC of bronchiectasis - Accounts for half of all cases.
  2. Infection, humoral immunodeficiency (abnormal lung defense), airway obstruction.
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60
Q

Bronchiectasis - Diagnostic test of choice:

A

High-resolution CT scan.

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61
Q

Bronchiectasis - Other diagnostic tests:

A
  1. PFTs reveal an obstructive pattern.
  2. CXR is an abnormal finding in most cases, but findings are non specific.
  3. Bronchoscopy applies in certain cases.
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62
Q

Bronchiectasis - Treatment:

A
  1. Antibiotics for acute exacerbations - superimposed infections are signaled by change in quality/quantity of sputum, fever, chest pain, etc.
  2. Bronchial hygiene is very important:
    a. Hydration.
    b. Chest physiotherapy to help remove the mucus.
    c. Inhaled bronchodilators.
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63
Q

Main goal in treating bronchiectasis:

A

To prevent the complications of pneumonia + hemoptysis.

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64
Q

Main problem in CF:

A

Defect in chloride channel protein causes impaired chloride and water transport, which leads to excessively thick, viscous secretions in the respiratory tract, exocrine pancreas, sweat glands, intestines, and GUT.

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65
Q

CF - Typically results in:

A
  1. OBSTRUCTIVE lung disease.
  2. Chronic pulmonary infections (freq. Pseudomonas).
  3. Pancreatic insufficiency.
  4. Other GI complications.
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66
Q

CF - Treatment:

A
  1. Pancreatic enzyme replacement.
  2. Fat-soluble vitamin supplements.
  3. Chest physical therapy.
  4. Vaccinations (influenza and pneumococcal).
  5. Treatment of infections with antibiotics.
  6. Inhaled recombinant deoxy-ribonuclease (rhDNase) –> Breaks down the DNA in respiratory mucus that clogs the airways.
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67
Q

CF - Prognosis:

A

Median age of death is over 30 yrs.

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68
Q

Lung cancer - Risk factors:

A
  1. Cigarette smoking - accounts for >85% of cases –> LINEAR relationship.
  2. Passive smoke.
  3. Asbestos - synergistically with smoking.
  4. Radon - high levels found in basements.
  5. COPD - an independent risk factor after smoking is taken into account.
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69
Q

SCLC - Staging:

A

NOT with TNM:
A. Limited –> Confined to chest + supraclavicular nodes, but NOT cervical or axillary nodes.
B. Extensive –> Outside of chest + supraclavicular nodes (85%).

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70
Q

What is the main problem with lung cancer?

A

Signs + symptoms are generally NON specific for lung cancer, and by the time they are present, disease is usually widespread.

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71
Q

Superior vena cava syndrome in lung cancer patients:

A

Occurs in 5% of patients - Most commonly with SCLC.

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72
Q

Phrenic nerve palsy in lung cancer:

A
  1. Occurs in 1% of patients.
  2. Phrenic nerve courses through the mediastinum to innervate the diaphragm.
  3. Results in hemidiaphragmatic paralysis.
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73
Q

Recurrent laryngeal nerve palsy in lung cancer?

A
  1. Occurs in 3%.

2. Causes hoarseness.

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74
Q

Horner’s syndrome in lung cancer:

A

Due to invasion of CERVICAL SYMPATHETIC chain by an apical tumor.

  1. Unilateral facial anhidrosis (no sweating).
  2. Ptosis.
  3. Miosis.
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75
Q

Pancoast’s tumor:

A
  1. An apical tumor involving C8 and T1-T2 nerve roots –> Shoulder pain radiating down the arm.
  2. Usually SCC.
  3. Associated with Horner’s syndrome 60% of the time.
  4. Malignant pleural effusion - occurs in 10-15% of patients - Prognosis is very poor - equivalent to distal metastases.
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76
Q

Lung cancers - Paraneoplastic syndromes - Hypertrophic pulmonary osteoarthropathy:

A

Adenocarcinoma + SCC –> Severe long bone pain may be present.

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77
Q

Prognosis of small cell lung carcinoma:

A
  1. For limited disease –> 5yr is 10-15% –> Median survival is 15-20months.
  2. For extensive disease –> 5yr survival rate is 1-2% –> Median survival is 8-13 months.
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78
Q

Steps for lung cancer diagnosis:

A
  1. CXR.
  2. CT scan.
  3. Tissue biopsy to confirm diagnosis.
  4. Determine histologic type.
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79
Q

Lung cancer - Diagnosis - CXR may show what?

A

Pleural effusion –> Should be examined for malignant cells.

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80
Q

Lung cancer diagnosis - CT scan with IV contrast:

A
  1. For staging.
  2. Extent of local + distant metastases.
  3. Very accurate in revealing lymphadenopathy in mediastinum.
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81
Q

Lung cancer - Diagnosis - Cytological exam of sputum:

A
  1. Diagnoses central tumors (80%) but not peripheral lesions.
  2. Provides highly variable results; if negative and clinical suspicion is high, further tests are indicated.
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82
Q

Regardless of the findings of CXR and CT, what is required for definitive diagnosis of lung cancer?

A

Pathologic confirmation.

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83
Q

NSCLC - Treatment:

A
  1. Surgery.
  2. Radiation therapy is an important adjunct.
  3. Chemo is of uncertain benefit.
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84
Q

SCLC - Treatment:

A

Limited disease –> Combination of chemo + radiation therapy are used initially.
Extensive disease –> Chemo is used alone as initial treatment. If respond, prophylactic radiation decreases incidence of brain metastases and prolongs survival.

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85
Q

Solitary pulmonary nodule?

A

A single, well-circumscribed nodule seen on CXR (usually incidentally) with no associated mediastinal or hilar lymph node involvement.

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86
Q

Features that favor benign over malignant nodules:

A
  1. Age –> Over 50% chance of malignancy if patient is over 50.
  2. Smoking –> More likely to be malignant.
  3. Size of nodule –> The larger the nodule, the more likely to be malignant (small is 2cm).
  4. Borders - Malignant nodules have more irregular borders. Benign lesions have smooth/discrete borders.
  5. Calcification - Eccentric asymmetric calcification suggest malignancy. Dense central calcification suggests benign lesion.
  6. Change is size - enlarging suggests malignancy.
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87
Q

Low probability nodules - Do:

A

Serial CT scan.

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88
Q

Intermediate probability nodules smaller than 1cm - Do?

A

Serial CT scan.

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89
Q

Intermediate probability nodule 1cm or larger - Do:

A

PET scan. If positive, excise the nodule.

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90
Q

High probability nodule - Do:

A

Excision.

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91
Q

In the evaluation of solitary pulmonary nodule, what is very helpful?

A

Previous CXR.

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92
Q

Solitary pulmonary nodule - Testing:

A
  1. Flexible bronchoscopy - good for central lesions.
  2. Transthoracic needle biopsy.
  3. PET scan - determines whether content of lesion is malignant.
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93
Q

Mediastinal masses - MCC:

A

Metastatic cancer (especially from lung cancer).

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94
Q

Mediastinal masses - MCC according to location:

A
  1. Anterior mediastinum –> Thyroid, teratogenic tumors, thymoma, lymphoma.
  2. Middle mediastinum –> Lung cancer, lymphoma, aneurysms, cysts, Morgagni hernia.
  3. Posterior mediastinum –> Neurogenic tumors, esophageal masses, enteric cysts, aneurysms, Bochdalek’s hernia.
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95
Q

Mediastinal masses - Clinical features:

A
  1. Usually asymptomatic.
  2. When symptoms are present, they are due to compression or invasion of adjacent structures.
  3. Cough, sometimes hemoptysis.
  4. Chest pain, dyspnea.
  5. Postobstructive pneumonia.
  6. Dysphagia (compression of esophagus).
  7. SVC syndrome.
  8. Compression of nerves:
    a. Hoarseness (recurrent laryngeal nerve).
    b. Horner’s syndrome (sympathetic ganglia).
    c. Diaphragm paralysis (phrenic nerve).
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96
Q

Mediastinal masses - Diagnoses:

A
  1. Chest CT is test of choice.

2. Usually discovered incidentally on a CXR performed for another reason.

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97
Q

If CT suggests a benign mass and the patient is asymptomatic, what should be done?

A

Observation is appropriate.

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98
Q

Pleural effusions - When are they well tolerated?

A

If the patient has minimal lung compromise.

In the presence of lung disease –> May lead to respiratory failure.

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99
Q

Pleural effusion - Transudate - Etiology:

A
  1. CHF
  2. Cirrhosis
  3. PE
  4. Nephrotic syndrome
  5. Peritoneal dialysis
  6. Hypoalbuminemia
  7. Atelectasis
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100
Q

Pleural effusion - Exudate - Etiology:

A
  1. Bacterial pneumonia, TB.
  2. Malignancy, metastatic disease.
  3. Viral infection.
  4. PE.
  5. Collagen vascular diseases.
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101
Q

If an exudative effusion is suspected, perform the following tests on the pleural fluid:

A
  1. Differential cell count.
  2. Glucose.
  3. pH.
  4. Amylase.
  5. Triglycerides.
  6. Microbiology.
  7. Cytology.
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102
Q

Pleural effusion - MCC:

A

CHF

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103
Q

Pleural effusion - Etiology:

A
  1. CHF (MCC).
  2. Pneumonia (bacterial).
  3. Malignancies: lung (36%), breast (25%), lymphoma (10%).
  4. PE.
  5. Viral diseases.
  6. Cirrhosis with ascites.
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104
Q

Pleural fluid pearls - Elevated pleural fluid amylase:

A
  1. Esophageal rupture.
  2. Pancreatitis.
  3. Malignancy.
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105
Q

Pleural fluid pearls - Milky, opalescent fluid:

A

Chylothorax (lymph in the pleural space).

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106
Q

Pleural fluid pearls - Frankly purulent fluid:

A

Empyema (pus in the pleural space).

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107
Q

Pleural fluid pearls - Bloody effusion:

A

Malignancy.

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108
Q

Pleural fluid pearls - Exudative effusions that are primarily lymphocytic:

A

TB

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109
Q

Pleural fluid pearls - pH<7.2?

A

Parapneumonic effusion or empyema.

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110
Q

Pleural effusion - Clinical features - Symptoms:

A
  1. Often asymptomatic.
  2. Dyspnea on exertion.
  3. Peripheral edema.
  4. Orthopnea, paroxysmal nocturnal dyspnea.
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111
Q

Pleural effusion - Signs:

A
  1. Dullness to percussion.
  2. Decr. breath sounds over the effusion.
  3. Decr. tactile fremitus.
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112
Q

Pleural effusion - Diagnosis - CXR:

A

PA + Lateral - Look for:

  1. Blunting of the costophrenic angle.
  2. About 250mL (!) of fluid must accumulate before an effusion can be detected.
  3. Lateral decubitus films: More reliable than PA and lateral CXRs for detecting small pleural effusions.
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113
Q

Pleural effusion - Diagnosis - CT scan:

A

More reliable than CXR for detecting effusions.

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114
Q

Pleural effusion - Diagnosis - Thoracentesis:

A
  1. Useful if etiology is NOT obvious. Diagnosis in 75% of patients, and even when NOT diagnostic it provides important clinical information.
  2. Therapeutic - symptom relief.
  3. Send fluid –> 4 Cs –> Chemistry (glucose, protein), cytology, cell count (CBC with differential, and Culture.
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115
Q

Pleural effusion - Thoracentesis - Complication:

A

Pneumothorax –> Complication seen in 10-15% of thoracenteses, but it requires treatment with a chest tube in DO NOT perform if effusion is <10mm thick on lateral internal decubitus CXR.

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116
Q

Pleural effusion - Transudate - Treatment:

A
  1. Diuretics and sodium restriction.

2. Therapeutic thoracentesis - only if massive effusion is causing dyspnea.

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117
Q

Pleural effusions - Exudate - Treatment:

A

Treat underlying disease.

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118
Q

Pleural effusion - Parapneumonic effusion - Pleural effusion in the presence of pneumonia - Treatment:

A

A. Uncomplicated –> Antibiotics alone (in most cases).
B. Complicated effusions or empyema:
1. Chest tube drainage.
2. Intrapleural injection of thrombolytic agents (streptokinase or urokinase) - May accelerate drainage.
3. Surgical lysis of adhesions may be required.

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119
Q

Empyema can occur?

A

If exudative pleural effusions are left untreated.
–> Most cases occur as a complication of bacterial pneumonia, but other foci of infection can also spread to the pleural space (eg mediastinitis, abscess).

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120
Q

Empyema - Diagnosis:

A
  1. CXR

2. CT scan of the chest are the recommended tests.

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121
Q

Empyema - Treatment:

A
  1. Treat empyema with AGGRESSIVE drainage of the pleura (via thoracentesis) + antibiotic therapy.
  2. Infection is very DIFFICULT to eradicate, and recurrence is common, requiring repeated drainage.
  3. If empyema is severe and persistent, rib resection and open drainage may be necessary.
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122
Q

Pneumothorax - Definition:

A

Air in the normal AIRLESS pleural space.

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123
Q

Pneumothorax - 2 major categories:

A
  1. Spontaneous

2. Traumatic

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124
Q

Traumatic pneumothoraces are often iatrogenic. Always obtain a CXR after the following procedures:

A
  1. Transthoracic needle aspiration.
  2. Thoracentesis.
  3. Central line placement.
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125
Q

Spontaneous pneumothorax - Recurrence rate?

A

50% in 2 yrs.

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126
Q

Secondary (complicated) pneumothorax:

A
  1. Occurs as a complication of underlying lung disease, MC COPD.
  2. More life-threatening because of lack of pulmonary reserve in these patients.
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127
Q

1st step in treatment of spontaneous pneumothorax:

A

Supplemental O2 hastens the resorption of air in pleural space and is the first treatment.

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128
Q

Pneumothorax - Symptoms:

A
  1. Ipsilateral chest pain, usually SUDDEN in onset.
  2. Dyspnea.
  3. Cough.
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129
Q

Pneumothorax - Signs:

A
  1. Decr. breath sounds over the affected side.
  2. Hyperresonance over the chest.
  3. Decr. or absent tactile fremitus on affected side.
  4. Mediastinal shift TOWARD side of pneumothorax.
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130
Q

Pneumothorax - Diagnosis:

A

CXR confirms diagnosis - Shows the visceral pleural line.

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131
Q

Pneumothorax - Treatment of primary spontaneous pneumothorax:

A

A. If small and patient is asymptomatic:
–> Observation - should resolve spontaneously in approx. 10days.
–> Small chest tube (with 1-way valve) may benefit some patients.
B. If larger and/or patient is symptomatic:
–> Administration of supplemental O2.
–> Chest tube insertion to allow air to be released and lung to re-expand.

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132
Q

2o spontaneous pneumothorax - Treatment:

A

Chest tube drainage.

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133
Q

Tension pneumothorax - General features:

A
  1. 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 to escape.
  2. Accumulation of air under (positive) pressure in the pleural space collapses the ipsilateral lung and shifts the mediastinum AWAY from the side of the pneumothorax.
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134
Q

Tension Pneumothorax - Etiology:

A
  1. Mechanical ventilation associated with barotrauma.
  2. CPR.
  3. Trauma.
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135
Q

Tension pneumothorax - Clinical features:

A
  1. Hypotension - cardiac filling is impaired due to compression of the great veins.
  2. Distended neck veins.
  3. Shift of trachea AWAY from side of pneumothorax on CXR.
  4. Decr. breath sounds on affected side.
  5. Hyperresonance to percussion on side of pneumothorax.
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136
Q

Tension Pneumothorax - Treatment:

A

Must be treated as a MEDICAL EMERGENCY –> If the tension in the pleural space is NOT relieved, the patient is likely to die of hemodynamic compromise.
—> Immediately perform chest decompression with a large-bore needle (in the 2nd or 3rd intercostal space in the midclavicular line), followed by chest tube.

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137
Q

Malignant mesothelioma - Features:

A
  1. Most cases 2o to asbestos exposure.
  2. Dyspnea, weight loss, and cough are common findings.
  3. Bloody effusion is common.
  4. Prognosis is dismal (few month’s survival).
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138
Q

Are ALL mesotheliomas malignant?

A

NOT ALL mesotheliomas are malignant.

Benign mesotheliomas have an excellent prognosis (and are unrelated to asbestos exposure).

139
Q

ILD - Definition:

A

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

140
Q

If ILD is suspected ask the following:

A
  1. Medication history - some drugs are known to be toxic to lungs.
  2. Previous jobs, because occupational exposure is a cause of ILD (asbestos, silicone, beryllium, coal).
141
Q

How many causes of ILD have been identified?

A

Over 100.

142
Q

ILD - Classification:

A
  1. Environmental lung disease.
  2. ILD associated with granulomas.
  3. Alveolar filling disease.
  4. Hypersensitivity lung disease.
  5. Drug-induced.
  6. Miscellaneous.
143
Q

ILD - Clinical features - Symptoms:

A
  1. Dyspnea (at first with exertion, later at rest).
  2. Cough (nonproductive).
  3. Fatigue.
  4. Other symptoms may be present 2o to another condition (such as connective tissue disorder).
144
Q

ILD - Signs:

A
  1. Rales at the bases are common.
  2. Digital clubbing is common (especially with idiopathic pulmonary fibrosis).
  3. Signs of pulmonary HTN and Cyanosis in advanced disease.
145
Q

Honeycomb lung refers to?

A

A scarred shrunken lung and is an end-stage finding with POOR prognosis.
–> Air spaces are dilated, and there are fibrous scars in the interstitium. It can arise from many types of ILD.

146
Q

ILD - Diagnosis:

A
  1. CXR.
  2. High resolution CT.
  3. PFTs.
  4. O2 desaturation during exercise.
  5. Bronchoalveolar lavage (fluid for culture and cytology).
  6. Tissue biopsy.
  7. Urinalysis.
147
Q

ILD - PFTs:

A
  1. A restrictive pattern is noted: FEV1/FVC is INCREASED.
  2. All lung volumes are LOW.
  3. Both FEV1 and FVC are decreased, but the latter MORE so.
  4. Low diffusing capacity.
148
Q

ILD - Tissue biopsy:

A
  1. This is often required in patients with ILD.
  2. This can be done via fiberoptic bronchoscopy with transbronchial biopsy (a limited amount of tissue can be obtained, which limits its utility), open lung biopsy, or video-assisted thoracoscopic lung biopsy.
149
Q

ILD - Urinalysis:

A

If there are signs of glomerular injury (for Goodpasture, Wegener).

150
Q

Sarco - Target group:

A

75% of cases occur when individual is <40 years of age.

151
Q

Sarco - Prognosis:

A

Generally, carries a good prognosis in majority of patients.

–> Up to 2/3 of patients experience resolution/improvement of symptoms over several years.

152
Q

Sarco - Percentage that develops chronic disease:

A

20%.

153
Q

Sarco - Skin problems:

A

25% of cases:

  1. Erythema nodosum.
  2. Plaques, subcutaneous nodules, maculopapular eruptions.
154
Q

Sarco - Eyes:

A

25% of cases:

  1. Anterior uveitis (75%).
  2. Posterior uveitis (25%).
  3. Conjunctivitis.
155
Q

Sarco - Heart:

A

5%:

  1. Arrhythmias.
  2. Conduction disturbances, such as heart block.
  3. Sudden death.
156
Q

Sarco - Musculoskeletal:

A

25-50%:

  1. Arthralgias and arthritis.
  2. Bone lesions.
157
Q

Sarco - Nervous system:

A

5%:

  1. CN VII involvement (Bell’s palsy).
  2. Optic nerve dysfunction.
  3. Papilledema.
  4. Peripheral neuropathy.
158
Q

Sarco - Asymptomatic but have CXR findings:

A

10-20%.

159
Q

Sarco - MCC of death:

A

Cardiac disease - although it is NOT a common finding.

160
Q

Sarco - Hallmark:

A

Bilateral hilar adenopathy - Seen in 50% of cases.

161
Q

Sarco - Typical presentation:

A

Young patient with constitutional symptoms +

  1. Respiratory complaints.
  2. Erythema nodosum.
  3. Blurred vision.
  4. Bilateral hilar adenopathy.
162
Q

Sarco - ACE:

A

ACE is elevated in 50-80% of patients. (However, other pulmonary diseases may cause an elevation in this enzyme - Lacks sensitivity/specificity).

163
Q

Sarco - Calcium:

A

Hypercalcemia + Hypercalciuria.

164
Q

Sarco - Definitive diagnosis:

A

Requires TRANSBRONCHIAL biopsy.

165
Q

Sarco - Transbronchial biopsy:

A
  1. Non caseating granulomas.
  2. By itself is not diagnostic.
  3. Must be used in the context of clinical presentation.
166
Q

Sarco - PFTs:

A
  1. Decr. lung volumes (VC, TLC).
  2. Decr. DLco (diffusing capacity for CO).
  3. Decr. FEV1/FVC.
167
Q

Sarco - Staging - Stage I:

A

Bilateral hilar adenopathy without parenchymal infiltrates (highest rate of remission).

168
Q

Sarco - Stage II:

A

Hilar adenopathy + Parenchymal infiltrates.

169
Q

Sarco - Stage III:

A

Diffuse parenchymal infiltrates WITHOUT hilar adenopathy (least favorable prognosis).

170
Q

Sarco - Stage IV:

A

Pulmonary fibrosis with honeycombing + fibrocystic parenchymal changes.

171
Q

Sarco - Treatment:

A

Most cases resolve or significantly improve spontaneously in 2 years and DO NOT require treatment.
–> Systemic steroids are the treatment of choice. (Indications are unclear).

172
Q

Sarco - Treatment - If refractory to steroids?

A

Methotrexate.

173
Q

Histiocytosis X - What is it?

A

Chronic interstitial pneumonia caused by abnormal proliferation of histiocytes (related to Langerhans cells of the skin).

174
Q

Histiocytosis X - Most patients are:

A

Smokers.

175
Q

Histiocytosis X - Variants of the disease:

A
  1. Eosinophilic granuloma (localized to bone or lung).
  2. Letterer-Siwe disease.
  3. Hand-Schuller-Christian syndrome.
176
Q

Histiocytosis X - Common findings:

A
  1. Dyspnea.

2. Non productive cough.

177
Q

Histiocytosis X - Other possible manifestations:

A
  1. Spontaneous pneumothorax.
  2. Lytic bone lesions.
  3. DI
178
Q

Histiocytosis X - CXR and CT:

A

CXR –> Honeycomb appearance.

CT –> Cystic lesions.

179
Q

Histiocytosis X - Prognosis:

A

Highly variable - Steroids are sometimes effective.

–> Lung transplantation may be necessary.

180
Q

Wegener Granulomatosis - Gold standard for diagnosis:

A

Tissue biopsy - BUT if the patient tests positive for c-ANCA –> Likelihood of having this condition is high.

181
Q

Churg-Strauss affects nerves?

A

Yes - Systemic vasculitis.

182
Q

Classic CXR findings in environmental lung disease - Asbestosis:

A

Pleural plaques

183
Q

Classic CXR findings in environmental lung disease - Silicosis:

A

“egg shell” calcifications.

184
Q

Pneumoconiosis with incr. risk for TB:

A

Silicosis.

185
Q

Berylliosis - Chronic disease is similar to:

A

Sarco –> Granulomas, skin lesions, and hypercalcemia may be present.

186
Q

Berylliosis - Useful diagnostic blood test:

A

Beryllium lymphocyte proliferation test.

187
Q

Idiopathic pulmonary fibrosis (IPF) - General characteristics:

A
  1. Etiology unknown.
  2. More common in men + smokers.
  3. Devastating and unrelenting disease - Mean survival is 3-7yrs after 1st diagnosis.
188
Q

IPF - Diagnosis:

A

CXR –> Ground glass or honeycombed appearance - may be normal.
Definitive diagnosis –> Open lung biopsy, but this even yield non specific findings.
–> Other causes of ILD must be excluded.

189
Q

IPF - Treatment:

A
  1. Supplemental O2.
  2. Steroids +/- cyclophosphamide.
  3. Lung transplantation.
190
Q

Acute respiratory failure - General:

A

Results when there is inadequate oxygenation of blood or inadequate ventilation (elimination of CO2) or both.

191
Q

Severe hypercapnia (respiratory acidosis) - Complications:

A
  • -> Dyspnea + Vasodilation of cerebral vessels.
    1. Incr. intracranial pressure + papilledema.
    2. Headache.
    3. Impaired consciousness.
    4. Finally coma.
192
Q

General criteria to define acute respiratory failure:

A

HYPOXIA –> PaO250.

HYPERCAPNIA –> PaCO2>50.

193
Q

Structures/Systems essential for maintaining normal respiration:

A
  1. CNS –> Depression or insult - Drug OD, stroke, trauma.
  2. Neuromuscular disease.
  3. Upper airway obstruction.
  4. Thorax and pleura.
  5. Cardiovascular system and blood.
  6. Lower airway and alveoli.
194
Q

Acute respiratory failure - 2 major types (overlap often exists):

A
  1. Hypoxemic respiratory failure.

2. Hypercarbic respiratory failure.

195
Q

Hypoxemic respiratory failure:

A

Low PaO2 with PaCO2 that is either low or normal - present when O2 sat is 0.6.

196
Q

Hypoxemic respiratory failure - Etiology:

A
  1. ARDS.
  2. Severe pneumonia.
  3. Pulmonary edema.
197
Q

Hypoxemic respiratory failure - Major pathophysiologic mechanisms:

A
  1. V/Q mismatch.

2. Intrapulmonary shunting.

198
Q

Hypercarbic (ventilatory) respiratory failure:

A

A failure of alveolar ventilation.

199
Q

Hypercarbic (ventilatory) respiratory failure - Mechanism:

A

Either decr. in minute ventilation or an incr. in physiologic dead space –> CO2 retention –> Hypoxemia.

200
Q

Hypercarbic respiratory failure - Etiology:

A

May be caused by an underlying lung disease (COPD, asthma, CF, severe bronchitis).
–> May also occur in patients with no underlying lung disease –> Neuromuscular diseases, CNS depression, mechanical restriction of lung inflation, or ANY cause of respiratory fatigue(!).

201
Q

Ventilation vs Oxygenation:

A

Ventilation –> Monitored by PaCO2.
Oxygenation –> Monitored by O2 sat and PaO2.
–> These 2 are UNRELATED. SaO2 may be 100% with a very high PaCO2, and the patient can be in ventilatory failure!

202
Q

To determine the underlying mechanism of hypoxemia, 3 pieces of information are needed:

A
  1. PaCO2.
  2. A-a gradient.
  3. Response to supplemental O2.
203
Q

Pathophysiology of acute respiratory failure - General mechanisms:

A
  1. V/Q mismatch.
  2. Intrapulmonary shunting.
  3. Hypoventilation.
  4. Incr. CO2 production.
  5. Diffusion impairment.
204
Q

Pathophysiology of acute respiratory failure - V/Q mismatch:

A
  1. Typically leads to hypoxia WITHOUT hypercapnia (in fact, PaCO2 is often low or normal).
  2. MC mechanism of hypexemia (chronic lung disorder).
  3. Responsive to supplemental O2.
205
Q

Pathophysiology of acute respiratory failure - Intrapulmonary shunting:

A
  1. Little or no ventilation in perfused areas (due to collapsed or fluid-filled alveoli).
  2. Venous blood is shunted into the arterial circulation without being oxygenated.
206
Q

Intrapulmonary shunting - Etiology:

A
  1. Atelectasis or fluid buildup in alveoli (pneumonia or pulm. edema).
  2. Direct R–>L intracardiac blood flow in congenital heart diseases.
207
Q

Hypoxia due to a shunt is responsive to supplemental O2?

A

It is NOT responsive to supplemental O2.

208
Q

Acute respiratory failure - Signs:

A
  1. Inability to speak in complete sentences, use of accessory muscles of respiration.
  2. Tachypnea + Tachycardia.
  3. Cyanosis.
  4. Impaired mentation (due to fatigue or hypecapnia, or if cause of respiratory failure is CNS depression).
209
Q

Diagnosis of acute respiratory failure involves?

A
  1. ABG analysis.
  2. CXR or CT scan of the chest.
  3. CBC + metabolic panel.
  4. If cardiogenic pulm. edema is suspected –> Cardiac enzymes.
210
Q

Acute respiratory failure - ABG analysis:

A

May confirm diagnosis and help determine severity of condition.

  1. Hypoxemia –> Mechanisms include V/Q mismatch/ Intrapulm. shunting/ Hypoventilation.
  2. Hypercapnia –> Hypoventilation (secondary to a variety of causes).
  3. Arterial pH –> Respiratory acidosis –> Hypercapnia is present.
211
Q

Acute respiratory failure - Treatment:

A
  1. Treat underlying disorder - Bronchodilators, steroids, antibiotics.
  2. Supplemental O2 if patient is hypoxemic.
  3. Apply NPPV only for CONSCIOUS patients.
  4. Intubation + mechanical ventilation may be needed in both types of respiratory failure.
212
Q

Hypoxemic respiratory failure - Supplemental O2:

A

Use the lowest concentration of O2 that provides sufficient oxygenation to avoid O2 toxicity, which is due to free radical production.

213
Q

Hypercarbic respiratory failure - Supplemental O2:

A

Traditionally –> High concentration of O2 can cause retention of CO2, especially in COPD patients –> Hypoxia drives breathing.
Validity of this theory has come into question, however.

214
Q

Techniques to improve tissue oxygenation:

A
  1. Incr. FiO2.
  2. Incr. PEEP.
  3. Extend inspiratory time fraction.
  4. Decubitus, upright, or prone positioning bronchodilation.
  5. Improve O2 delivery - Incr. CO or incr. Hb.
  6. Decr. O2 requirements: decr. work of breathing, fever, agitation.
  7. Remove pulmonary vasodilators (eg nitroprusside).
215
Q

NPPV stands for:

A

Noninvasive positive pressure ventilation.

216
Q

NPPV is indicated in?

A

Impending respiratory failure in an attempt to avoid intubation and mechanical ventilation.

217
Q

ARDS - Pathophysiology:

A

Massive intrapulmonary shunting of blood is a key event in ARDS.

  • -> Severe hypoxemia with NO improvement on 100% O2.
  • -> Shunting is 2o to widespread atelectasis, collapse of alveoli, and surfactant dysfunction.
218
Q

Remember the following when examining a patient with ARDS:

A
  1. Physical findings are usually nonspecific.
  2. Because the patient is usually intubated and on a ventilator, decr. unilateral breath sounds may be due to endotracheal tube being in the right main bronchus or possibly pneumothorax.
  3. Look for potential sources of sepsis and check for any signs of infection: acute abdomen, IV lines, wounds, decubiti, etc.
  4. Keep in mind that cardiogenic pulm. edema has to be distinguished from ARDS - Look for signs of volume overload, CHF, JVD, edema, and hepatomegaly.
219
Q

ARDS - Diagnosis - What to do:

A
  1. CXR - Show diffuse bilateral pulm. infiltrates.
  2. ABG.
  3. Pulm. artery catheter –> PCWP –> Most useful in differentiating ARDS from cardiogenic pulm. edema.
  4. Bronchoscopy with bronchoalveolar lavage.
220
Q

ARDS - Treatment:

A
  1. Oxygenation - Try to keep SaO2 >90%.
  2. Mechanical ventilation with PEEP is usually required.
  3. Fluid management.
  4. Treat the underlying cause, eg infection.
  5. Do not forget to address the patient’s nutritional needs.
221
Q

ARDS - Complications:

A
  1. Permanent lung injury.
  2. Complications associated from mech. ventilation.
  3. Line-associated infections.
  4. Renal failure.
  5. Ileus, stress ulcers.
  6. Multiple organ failure.
  7. Critical illness myopathy.
222
Q

Pulm. HTN - Definition:

A

Mean pulm. arterial pressure >25mmHg at rest or 30mmHg during exercise.

223
Q

PHTN - Classification from pathophysiologic standpoint:

A
  1. Passive type - Resistance to pulm. venous drainage.
  2. Hyperkinetic type.
  3. Obstructive type.
  4. Obliterative type.
  5. Vasoconstrictive type.
  6. Incr. intrathoracic pressure.
224
Q

PHTN - Classification from an anatomic standpoint:

A
  1. Post capillary causes.

2. Mixed capillary and precapillary causes.

225
Q

PHTN - Symptoms:

A
  1. Dyspnea on exertion.
  2. Fatigue.
  3. Chest pain - exertional.
  4. Syncope - exertional (with severe disease).
226
Q

PHTN - Signs:

A
  1. Loud pulmonic component of the 2nd heart sound (P2) and subtle lift of sternum (sign of RV dilation) –> May be the ONLY findings and still the patient may have a DEVASTATING disease.
  2. When RV failure occurs –> Corresponding signs/symptoms.
227
Q

PHTN - Diagnosis:

A
  1. ECG –> Right ventricular hypertrophy –> Right axis deviation + Right atrial abnormality.
  2. Echocardiogram:
    a. Dilated pulm. artery.
  3. Dilation/Hypertrophy of RA and RV.
  4. Abnormal movement of IV septum (due to incr. RV volume.
  5. Right heart catheterization –> incr. pulmonary artery pressure.
228
Q

Primary PHTN - Target:

A

Young-middle aged females.

229
Q

Primary PHTN - Prognosis:

A

The prognosis is poor - Mean survival is 2-3yrs from the time of diagnosis.

230
Q

Primary PHTN - Diagnosis:

A
  1. Cardiac catheterizatio –> establishes the diagnosis.
  2. CXR shows enlarged pulm. arteries, enlarged RV, and CLEAR lung fields.
  3. PFTs show a restrictive pattern.
  4. ECG shows RIGHT axis deviation + RV hypertrophy.
231
Q

Cor pulmonale - Is MV stenosis a cause?

A

NO - The definition does NOT encompass any of the causes of PHTN due to LV disease (such as mitral stenosis or L–>R shunt).

232
Q

Death due to cor pulmonale:

A

Many COPD patients die of RV failure 2o to chronic PHTN.

Many deaths due to PE result from acute PHTN + RV failure.

233
Q

Cor pulmonale - Etiology:

A
  1. It is most commonly 2o to COPD.
  2. Recurrent PE.
  3. ILD.
  4. Asthma.
  5. CF.
  6. Sleep apnea.
  7. Pneumoconioses.
234
Q

Cor pulmonale - Clinical features:

A
  1. Decr. in exercise tolerance.
  2. Cyanosis + digital clubbing.
  3. Signs of RV failure: hepatomegaly, edema, JVD.
  4. Parasternal lift.
  5. Polycythemia is often present if COPD is the cause.
235
Q

Cor pulmonale - Diagnosis:

A
  1. CXR –> Enlargment of RA, RV, pulm. arteries.
  2. ECG –> Right axis deviation, P pulmonale (peaked P waves), RV hypertrophy.
  3. Echocardiogram –> RV dilation, but normal LV size and function. Useful in excluding LV dysfunction.
236
Q

Cor pulmonale - Treatment:

A
  1. Treat underlying disorder.
  2. Use diuretics cautiously because patients may be preload-dependent.
  3. Apply continuous long-term O2 if the patient is hypoxic.
  4. Administer digoxin only if there is coexistent LV failure.
  5. A variety of vasodilators have been studied - no definitive improvement has been shown with their use.
237
Q

Upper extremity DVT indicates:

A

Rare –> IVDA.

238
Q

Other sources of emboli to the lung:

A
  1. Fat embolism (long bone fractures).
  2. Amniotic fluid embolism (during or AFTER delivery).
  3. Air embolism (trauma to thorax).
  4. Septic embolism (IVDA).
  5. Schistosomiasis.
239
Q

Complications in patients with PE who survive the initial event include:

A
  1. Recurrent PE.

2. PHTN (up to 2/3 of patients).

240
Q

PE - 2 important studies to know:

A

JAMA 1990 –> The prospective investigation of pulmonary embolism diagnosis (PIOPED) is a landmark study –> Guides treatment is V/Q is performed.
JAMA 2006 –> The Christopher Study –> Guides treatment if spiral CT is performed.

241
Q

Risk factors for DVT/PE:

A
  1. Age >60yrs.
  2. Malignancy.
  3. Prior history of DVT, PE.
  4. Hereditary hypercoagulable states (factor V Leiden, protein C and S deficiency, antithrombin III def.)
  5. Prolonged immobilization or bed rest, long-distance travel.
  6. Cardiac disease, especially CHF.
  7. Obesity.
  8. Nephrotic syndrome.
  9. Major surgery, especially pelvic surgery (orthopedic procedures).
  10. Major trauma.
  11. Pregnancy, estrogen use (OCPs).
242
Q

When PE is undiagnosed, mortality approaches:

A

30%. A significant number of cases are undiagnosed (as many as 50%).

243
Q

When PE is diagnosed, mortality is … in the first 60min.

A

10%.

244
Q

Of those who survive the initial PE, approx. … of patients will DIE of a recurrent PE if left untreated.

A

30%.

245
Q

Most death in PE patients:

A

Are due to recurrent PE within the first few hours of the initial PE.

246
Q

PE - Treatment with anticoagulants decreases the mortality to:

A

2-8%.

247
Q

PE symptoms - Frequencies per the PIOPED.

A
  1. Dyspnea 73%.
  2. Pleuritic chest pain 66%.
  3. Cough 37%.
  4. Hemoptysis 13%.
  5. Only 1/3 of patients with PE will have signs/symptoms of a DVT.
  6. Syncope seen in large PE.
248
Q

PE signs - Frequency per the PIOPED study:

A
  1. Tachypnea 70%.
  2. Rales 51%.
  3. Tachycardia 30%.
  4. S4 24%.
  5. Incr. P2 23%.
  6. Shock with rapid circulatory collapse in massive PE.
  7. Other signs: low grade fever, decr. breath sounds, dullness on percussion.
249
Q

Workup of PE - It is often difficult to definitively diagnose or rule out PE. The following tests provide adequate basis for treating PE with anticoagulation:

A
  1. Intraluminal filling defects in central, segmental, or lobular pulm. arteries on helical CT (or high probability with a scan) and clinical suspicion.
  2. DVT diagnosed with US and clinical suspicion.
  3. Positive pulm. angiogram (definitively proves PE).
250
Q

Workup of PE - The following can essentially rule out PE:

A
  1. Low probability V/Q scan (or normal helical scan) and low clinical suspicion.
  2. Negative pulmonary angiogram (definitive).
  3. Negative d-dimer assay + low clinical suspicion.
251
Q

Diagnosis of PE - Methods:

A
  1. ABG
  2. CXR
  3. Venous duplex US
  4. V/Q scan
  5. Helical (spiral) CT scan of the chest with IV contrast.
  6. Pulm. angiography (gold).
  7. D-dimer assay.
252
Q

Tension pneumothorax - Clinical features:

A
  1. Hypotension - cardiac filling is impaired due to compression of the great veins.
  2. Distended neck veins.
  3. Shift of trachea AWAY from side of pneumothorax on CXR.
  4. Decr. breath sounds on affected side.
  5. Hyperresonance to percussion on side of pneumothorax.
253
Q

Tension Pneumothorax - Treatment:

A

Must be treated as a MEDICAL EMERGENCY –> If the tension in the pleural space is NOT relieved, the patient is likely to die of hemodynamic compromise.
—> Immediately perform chest decompression with a large-bore needle (in the 2nd or 3rd intercostal space in the midclavicular line), followed by chest tube.

254
Q

Malignant mesothelioma - Features:

A
  1. Most cases 2o to asbestos exposure.
  2. Dyspnea, weight loss, and cough are common findings.
  3. Bloody effusion is common.
  4. Prognosis is dismal (few month’s survival).
255
Q

Are ALL mesotheliomas malignant?

A

NOT ALL mesotheliomas are malignant.

Benign mesotheliomas have an excellent prognosis (and are unrelated to asbestos exposure).

256
Q

ILD - Definition:

A

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

257
Q

If ILD is suspected ask the following:

A
  1. Medication history - some drugs are known to be toxic to lungs.
  2. Previous jobs, because occupational exposure is a cause of ILD (asbestos, silicone, beryllium, coal).
258
Q

How many causes of ILD have been identified?

A

Over 100.

259
Q

ILD - Classification:

A
  1. Environmental lung disease.
  2. ILD associated with granulomas.
  3. Alveolar filling disease.
  4. Hypersensitivity lung disease.
  5. Drug-induced.
  6. Miscellaneous.
260
Q

ILD - Clinical features - Symptoms:

A
  1. Dyspnea (at first with exertion, later at rest).
  2. Cough (nonproductive).
  3. Fatigue.
  4. Other symptoms may be present 2o to another condition (such as connective tissue disorder).
261
Q

ILD - Signs:

A
  1. Rales at the bases are common.
  2. Digital clubbing is common (especially with idiopathic pulmonary fibrosis).
  3. Signs of pulmonary HTN and Cyanosis in advanced disease.
262
Q

Honeycomb lung refers to?

A

A scarred shrunken lung and is an end-stage finding with POOR prognosis.
–> Air spaces are dilated, and there are fibrous scars in the interstitium. It can arise from many types of ILD.

263
Q

ILD - Diagnosis:

A
  1. CXR.
  2. High resolution CT.
  3. PFTs.
  4. O2 desaturation during exercise.
  5. Bronchoalveolar lavage (fluid for culture and cytology).
  6. Tissue biopsy.
  7. Urinalysis.
264
Q

ILD - PFTs:

A
  1. A restrictive pattern is noted: FEV1/FVC is INCREASED.
  2. All lung volumes are LOW.
  3. Both FEV1 and FVC are decreased, but the latter MORE so.
  4. Low diffusing capacity.
265
Q

ILD - Tissue biopsy:

A
  1. This is often required in patients with ILD.
  2. This can be done via fiberoptic bronchoscopy with transbronchial biopsy (a limited amount of tissue can be obtained, which limits its utility), open lung biopsy, or video-assisted thoracoscopic lung biopsy.
266
Q

ILD - Urinalysis:

A

If there are signs of glomerular injury (for Goodpasture, Wegener).

267
Q

Sarco - Target group:

A

75% of cases occur when individual is <40 years of age.

268
Q

Sarco - Prognosis:

A

Generally, carries a good prognosis in majority of patients.

–> Up to 2/3 of patients experience resolution/improvement of symptoms over several years.

269
Q

Sarco - Percentage that develops chronic disease:

A

20%.

270
Q

Sarco - Skin problems:

A

25% of cases:

  1. Erythema nodosum.
  2. Plaques, subcutaneous nodules, maculopapular eruptions.
271
Q

Sarco - Eyes:

A

25% of cases:

  1. Anterior uveitis (75%).
  2. Posterior uveitis (25%).
  3. Conjunctivitis.
272
Q

Sarco - Heart:

A

5%:

  1. Arrhythmias.
  2. Conduction disturbances, such as heart block.
  3. Sudden death.
273
Q

Sarco - Musculoskeletal:

A

25-50%:

  1. Arthralgias and arthritis.
  2. Bone lesions.
274
Q

Sarco - Nervous system:

A

5%:

  1. CN VII involvement (Bell’s palsy).
  2. Optic nerve dysfunction.
  3. Papilledema.
  4. Peripheral neuropathy.
275
Q

Sarco - Asymptomatic but have CXR findings:

A

10-20%.

276
Q

Sarco - MCC of death:

A

Cardiac disease - although it is NOT a common finding.

277
Q

Sarco - Hallmark:

A

Bilateral hilar adenopathy - Seen in 50% of cases.

278
Q

Sarco - Typical presentation:

A

Young patient with constitutional symptoms +

  1. Respiratory complaints.
  2. Erythema nodosum.
  3. Blurred vision.
  4. Bilateral hilar adenopathy.
279
Q

Sarco - ACE:

A

ACE is elevated in 50-80% of patients. (However, other pulmonary diseases may cause an elevation in this enzyme - Lacks sensitivity/specificity).

280
Q

Sarco - Calcium:

A

Hypercalcemia + Hypercalciuria.

281
Q

Sarco - Definitive diagnosis:

A

Requires TRANSBRONCHIAL biopsy.

282
Q

Sarco - Transbronchial biopsy:

A
  1. Non caseating granulomas.
  2. By itself is not diagnostic.
  3. Must be used in the context of clinical presentation.
283
Q

Sarco - PFTs:

A
  1. Decr. lung volumes (VC, TLC).
  2. Decr. DLco (diffusing capacity for CO).
  3. Decr. FEV1/FVC.
284
Q

Sarco - Staging - Stage I:

A

Bilateral hilar adenopathy without parenchymal infiltrates (highest rate of remission).

285
Q

Sarco - Stage II:

A

Hilar adenopathy + Parenchymal infiltrates.

286
Q

Sarco - Stage III:

A

Diffuse parenchymal infiltrates WITHOUT hilar adenopathy (least favorable prognosis).

287
Q

Sarco - Stage IV:

A

Pulmonary fibrosis with honeycombing + fibrocystic parenchymal changes.

288
Q

Sarco - Treatment:

A

Most cases resolve or significantly improve spontaneously in 2 years and DO NOT require treatment.
–> Systemic steroids are the treatment of choice. (Indications are unclear).

289
Q

Sarco - Treatment - If refractory to steroids?

A

Methotrexate.

290
Q

Histiocytosis X - What is it?

A

Chronic interstitial pneumonia caused by abnormal proliferation of histiocytes (related to Langerhans cells of the skin).

291
Q

Histiocytosis X - Most patients are:

A

Smokers.

292
Q

Histiocytosis X - Variants of the disease:

A
  1. Eosinophilic granuloma (localized to bone or lung).
  2. Letterer-Siwe disease.
  3. Hand-Schuller-Christian syndrome.
293
Q

Histiocytosis X - Common findings:

A
  1. Dyspnea.

2. Non productive cough.

294
Q

Histiocytosis X - Other possible manifestations:

A
  1. Spontaneous pneumothorax.
  2. Lytic bone lesions.
  3. DI
295
Q

Histiocytosis X - CXR and CT:

A

CXR –> Honeycomb appearance.

CT –> Cystic lesions.

296
Q

Histiocytosis X - Prognosis:

A

Highly variable - Steroids are sometimes effective.

–> Lung transplantation may be necessary.

297
Q

Wegener Granulomatosis - Gold standard for diagnosis:

A

Tissue biopsy - BUT if the patient tests positive for c-ANCA –> Likelihood of having this condition is high.

298
Q

Churg-Strauss affects nerves?

A

Yes - Systemic vasculitis.

299
Q

Classic CXR findings in environmental lung disease - Asbestosis:

A

Pleural plaques

300
Q

Classic CXR findings in environmental lung disease - Silicosis:

A

“egg shell” calcifications.

301
Q

Pneumoconiosis with incr. risk for TB:

A

Silicosis.

302
Q

Berylliosis - Chronic disease is similar to:

A

Sarco –> Granulomas, skin lesions, and hypercalcemia may be present.

303
Q

Berylliosis - Useful diagnostic blood test:

A

Beryllium lymphocyte proliferation test.

304
Q

Idiopathic pulmonary fibrosis (IPF) - General characteristics:

A
  1. Etiology unknown.
  2. More common in men + smokers.
  3. Devastating and unrelenting disease - Mean survival is 3-7yrs after 1st diagnosis.
305
Q

IPF - Diagnosis:

A

CXR –> Ground glass or honeycombed appearance - may be normal.
Definitive diagnosis –> Open lung biopsy, but this even yield non specific findings.
–> Other causes of ILD must be excluded.

306
Q

IPF - Treatment:

A
  1. Supplemental O2.
  2. Steroids +/- cyclophosphamide.
  3. Lung transplantation.
307
Q

Acute respiratory failure - General:

A

Results when there is inadequate oxygenation of blood or inadequate ventilation (elimination of CO2) or both.

308
Q

Severe hypercapnia (respiratory acidosis) - Complications:

A
  • -> Dyspnea + Vasodilation of cerebral vessels.
    1. Incr. intracranial pressure + papilledema.
    2. Headache.
    3. Impaired consciousness.
    4. Finally coma.
309
Q

General criteria to define acute respiratory failure:

A

HYPOXIA –> PaO250.

HYPERCAPNIA –> PaCO2>50.

310
Q

Structures/Systems essential for maintaining normal respiration:

A
  1. CNS –> Depression or insult - Drug OD, stroke, trauma.
  2. Neuromuscular disease.
  3. Upper airway obstruction.
  4. Thorax and pleura.
  5. Cardiovascular system and blood.
  6. Lower airway and alveoli.
311
Q

Acute respiratory failure - 2 major types (overlap often exists):

A
  1. Hypoxemic respiratory failure.

2. Hypercarbic respiratory failure.

312
Q

Hypoxemic respiratory failure:

A

Low PaO2 with PaCO2 that is either low or normal - present when O2 sat is 0.6.

313
Q

Hypoxemic respiratory failure - Etiology:

A
  1. ARDS.
  2. Severe pneumonia.
  3. Pulmonary edema.
314
Q

Hypoxemic respiratory failure - Major pathophysiologic mechanisms:

A
  1. V/Q mismatch.

2. Intrapulmonary shunting.

315
Q

Hypercarbic (ventilatory) respiratory failure:

A

A failure of alveolar ventilation.

316
Q

PE - ABG:

A

NOT diagnostic for PE.

  1. PaO2 and PaCO2 are low (the latter due to hyperventilation) and pH is high –> Typically, there is a respiratory alkalosis.
  2. A-a gradient is usually elevated.
317
Q

PE - CXR:

A
  1. Atelectasis or pleural effusion amy be present.
  2. Main usefulness is in excluding alternative diagnoses.
  3. Classic radiographic signs such as Hampton’s hump or Westermark’s sign are rarely present.
318
Q

PE - Venous duplex US of the lower extremities:

A
  1. If there is a positive result, treat with IV anticoagulation (heparin).
  2. Very helpful when positive, but of little value when negative (occur in 50% of patients with proven PE).
319
Q

Source of embolus in PE is often…?

A

NOT identified, even at autopsy (either because the entire thrombus embolized, or because the remainder of the thrombus lies in a vein that is NOT identified).

320
Q

PE - Initial study of choice:

A

CT-PA (Spiral CT of the chest with IV contrast).
–> Good sensitivity + specificity.
Can visualize very small clots (as small as 2mm).
Replaced V/Q scan.

321
Q

If CTPA is negative for PE, and clinical probability of PE is high, there is a … incidence of PE.

A

5%.

322
Q

CTPA cannot be performed in patients with significant … because of the IV contrast that is required.

A

Renal insufficiency.

323
Q

CTPA - Sensitivity and specificity:

A

Sensitivity is 85% –> So it can miss up to 15%.

Specificity is over 95%.

324
Q

Modified Wells criteria:

A
  1. Symptoms/Signs of DVT –> 3pts.
  2. Alternative diagnosis less likely than PE –> 3pts.
  3. Heart rate >100beats/min –> 1.5pts.
  4. Immobilization (>3d) or surgery in previous 4 weeks –> 1.5pts.
  5. Previous DVT or PE –> 1.5pts.
  6. Hemoptysis –> 1pt.
  7. Malignancy –> 1pt.
325
Q

Gold standard for PE diagnosis:

A

Pulmonary angiography, BUT it is invasive. Rarely performed due to 0.5% mortality.

326
Q

PE diagnosis - D-dimer assay:

A
  1. D-dimer –> Specific fibrin degradation product.
  2. Fairly sensitive test (90-98%). If NORMAL and clinical suspicion is low –> PE is unlikely.
  3. Specificity is LOW (!).
327
Q

PE treatment - Initial step:

A

Supplemental O2 to correct hypoxemia –> Severe hypoxemia or respiratory failure requires intubation + mechanical ventilation.

328
Q

Acute anticoagulation therapy in PE:

A

Heparin to prevent another PE, and further clot formation.
Start IMMEDIATELY on a basis of clinical suspicion. Do NOT wait for studies to confirm PE if clinical suspicion is high.
ALSO start WARFARIN at same time –> Goal is INR of 2 to 3.

329
Q

Contraindications to heparin:

A
  1. Active bleeding.
  2. Uncontrolled HTN.
  3. Recent stroke.
  4. HIT.
330
Q

Thrombolytic therapy in PE:

A

There is NO evidence that thrombolysis improves mortality rates in patients with PE. Therefore, its use is NOT well defined at this point.

331
Q

Thrombolysis in PE - When to consider?

A
  1. Patients with massive PE who are hemodynamically unstable (persistent hypotension).
  2. Patients with evidence of RH failure (thrombolysis can reserve this).
332
Q

Why PE and DVT are problematic for physicians:

A
  1. Clinical findings are sometimes subtle in both.
  2. Non invasive imaging tests do not always detect either condition.
  3. Anticoagulation carries significant risk.
333
Q

When do we use a therapeutic INR between 2.5-3.5?

A

Usually it is between 2-3. Notable exceptions:

  1. Prosthetic valves.
  2. Prophylaxis of recurrent MI.
  3. Antiphospholipid antibody syndrome.
334
Q

PE treatment - IVC filter - Indications:

A
  1. Contraindication to anticoagulation in a patient with documented DVT or PE.
  2. A complication of current anticoagulation.
  3. Failure of adequate anticoagulation as reflected by recurrent DVT or PE.
  4. A patient with low pulm. reserve who is at high risk for death from PE.
335
Q

Aspiration pneumonia develops in … of patients who aspirate, usually … after aspiration.

A

40%. 2-4days.

336
Q

Pulmonary aspiration - Predisposing factors:

A
  1. Reduced level of consciousness (eg seizures, stroke, sedating drugs).
  2. Alcoholism.
  3. Extubation (impaired pharyngeal or laryngeal function).
  4. Excessive vomiting, ileus.
  5. Tube feeding, tracheostomy tubes.
  6. Anesthesia/surgery.
  7. Neuromuscular diseases.
  8. Esophageal disorders (achalasia, GERD, cancer).
337
Q

Pulmonary aspiration - What if initially silent?

A

It may be initially silent, with development of acute respiratory failure with no obvious cause.

338
Q

Pulmonary aspiration - Fever?

A

May or may not be present.

339
Q

Pulmonary aspiration - Sign?

A

May lead to obstruction of the airways with localized wheezing.

340
Q

Pulmonary aspiration - Diagnosis:

A

Findings on CXR are variable and resemble infiltrates that mimic bacterial pneumonia.
–> Atelectasis and local areas of collapse may also be present.

341
Q

Pulmonary aspiration - Treatment:

A
  1. If aspiration was witnessed –> ABCs (airway, breathing, circulation), supplemental O2, supportive measures.
  2. If aspiration is SUSPECTED –> Give antibiotics (penicillin G, clindamycin) - Controversial.
  3. If OBSTRUCTION –> Early bronchoscopy.
  4. Prevention is critical in HIGH risk patients.
342
Q

Aspiration can lead to … if untreated:

A

Lung abscess.
Poor oral hygiene predisposes to such infections.
–> Foul smelling sputum often indicates such infections.

343
Q

Depending on patient presentation, any of the following tests may be helpful in distinguishing between lung and heart disease:

A
  1. CXR.
  2. Sputum Gram stain + culture.
  3. PFTs.
  4. ABGs.
  5. ECG.
  6. Echocardiogram.
344
Q

Chronic bronchitis - Definition:

A

Clinical:

–> Chronic cough productive of sputum for at least 3 months per year for at least 2 consecutive years.

.► ABORDAGEM SINDRÔMICA (41 decks)

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