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140 Cards in this Set
- Front
- Back
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What is COPD?
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A lung condition characterized by airflow limitation that is not fully reversible. A progressive disease, often caused by an abnormal inflammatory response leading to systemic effects. Includes chronic bronchitis and emphysema. Alteration in function and structure of large airways, small airways, and parenchyma
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What is the most important risk factor for COPD?
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Cigarette smoking, especially 20+ pack years. Other factors: occupational exposure, passive smoking, air pollution, genetics
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How does COPD develop?
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Cigarette smoke (or other factor) activates alveolar macrophages and epithelial cells. Cytokines, chemokines are released, inflammatory cells accumulate, epithelial and endothelial cell death occurs, loss of normal clearance combined with release of proteinase leads to destruction of the lung structure
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What are some cellular changes that occur in COPD in the large airways?
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Globlet cells increase in size, number, and output – so lots of mucus. Squamous metaplasia – from loss of cilated cuboidal epithelium, increased risk of cancer; and Neutrophil influx.
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What are some cellular changes that occur in COPD in the small airways?
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Globlet cell metaplasia; Clara cells replaced by monocytes – loss of surfactant, destruction of elastic fibers; Smooth muscle hypertrophy – overall effect is narrowing of diameter, mucus, inflammation, fibrosis, +/- hyperreactivity
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What alveolar changes occur in COPD?
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Macrophages accumulate in bronchioles, resulting in release of elastolytic proteinases, perforation of the terminal airway walls, ineffective repair of elastin; Perforations enlarge and coalesce --> emphysema.
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Define emphysema
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Abnormal permanent enlargement of airspaces distal to terminal bronchioles – no fibrosis visible to the naked eye and there are three types.
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What are the three types of emphysema?
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Centriacinar, Panacinar, Mixed
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What is centracinar emphysema?
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Large airspaces affecting upper lobes in a focal pattern
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What is panacinar emphysema?
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Large airspaces evenly distributed within and across acinar units, especially in lower lobes – particularly common in alpha-1 trypsin deficiency.
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What are the systemic effects of COPD?
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Systemic inflammatory response continues, characterized by increased resting energy expenditure and poor utilization of nutrients – comorbidities develop like heart disease, osteoporosis, diabetes,
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What is the general presentation of emphysema?
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Cough, sputum production, dyspnea on exertion
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How is emphysema diagnosed?
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Attention to SH, FH, ROS (morning headache); Physical exam – initially normal, increased expiratory phase, signs of hyperinflation, late findings of cyanosis, cachexia, cor pulmonale, clubbing of digits
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What laboratory/test findings will there be with emphysema?
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FEV1 and FVC, FEV1/FVC ratio, evaluate lung capacity, FRC, RV. Hematocrit may be elevated (polycythemia to maximize air exchange), EKG changes (late) may show diffuse low voltage and right axis deviation; Radiography
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What are some x-ray characteristics of emphysema?
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Flattening of diaphragm, hyperinflation of the lungs
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What are some CT characteristics of COPD?
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Destruction of matrix with coalescence of airspaces, leading to an overall reduced surface area for gas exchange. Also increased AP diameter.
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How is COPD managed?
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Stabilize the disease – cease smoking, supplemental oxygen for resting SpO2 < 88%; Symptom control –pharmacologic – GOLD criteria for staging and therapy – non-pharmacologic.
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What are the GOLD criteria for COPD?
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There are four stages – mild, moderate, severe, very severe – depends on FEV1/FVC and FEV1
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What is stage I: Mild COPD? How is it managed at that level?
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FEV1/FVC < 70%; FEV1 > 80% predicted; Active reduction of risk factors, influenza vaccine – add short acting bronchodilator when needed.
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What is stage II: Moderate COPD? How is it managed at that level?
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FEV1/FVC < 70%; 50% < FEV1 < 80% predicted; Active reduction of risk factors, influenza vaccine – add short acting bronchodilator when needed. Add regular treatment with one or more long-acting bronchodilators (when needed), add rehabilitation.
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When is spirometry tested?
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When they are stable – NOT when they are having an exacerbation.
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What is stage III: severe COPD? How is it managed at that level?
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FEV1/FVC < 70%; 30% < FEV1 < 50% predicted; Active reduction of risk factors, influenza vaccine, add short-acting bronchodilator (when needed), add regular treatment with one or more long-acting bronchodilators (when needed); add rehabilitation; Add inhaled glucocorticosteroids if repeated exacerbations.
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What is stage IV: very severe COPD? How is it managed at that level?
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FEV1/FVC < 70%; FEV1 < 30% or FEC1 < 50% predicted plus chronic respiratory failure; Active reduction of risk factors, influenza vaccine, add short-acting bronchodilator (when needed), add regular treatment with one or more long-acting bronchodilators (when needed); add rehabilitation; Add inhaled glucocorticosteroids if repeated exacerbations. Add long term oxygen if chronic respiratory failure. Consider surgical treatments.
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What are some non-pharmacologic ways to approach COPD?
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Annual flu vaccine, pneumovax, pulmonary rehabilitation, lung volume reduction surgery, lung transplantation
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What is Alpha-1 Antitrypsin Deficiency?
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Genetic cause of C OPD – positive Pi*ZZ alleles (normal is Pi*MM). Young patients (40s), strong family history of early onset COPD, can occur in non-smokers, accounts for 1-2% of severe COPD cases. Screen for other environmental exposures.
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What are the characteristics of Alpha-1 Antitrypsin Deficiency-type COPD?
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Predominantly affects the lower lobes, a panacinar pattern of emphysema. Spirometric findings, perform blood testing to confirm diagnosis, and treat with appropriate GOLD treatment, plus IV infusion of alpha-1 antitrypsin or Lung Volume Reduction Surgery (LVRS)
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For what group of COPD patients is Lung Volume Reduction Surgery an option?
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Alpha-1 Antitrypsin Deficiency-type COPD
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What causes acute exacerbations of COPD?
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Precipitated by viruses, bacteria, exposures to pollutants – may see evidence of infection on CXR. Marked by increases in dyspnea, cough, sputum changes; Degree of impairment determines treatment.
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What is the AECOPD treatment?
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Nebulized bronchodilators
Parenteral steroids Antibiotics, usually empiric Oxygen supplementation to maintain SpO2 > 90% NIPPV vs IPPV |
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How many deaths from COPD are due to respiratory failure?
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1/3 of deaths
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What is the current goal of COPD treatments?
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It is thought that treating the underlying inflammatory condition will halt or reverse disease, as well as comorbidities
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What are two processes of inflammation in COPD?
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Small airway disease (airway inflammation, remodeling)
Parenchymal destruction (loss of alveolar attachments, decreased elastic recoil) |
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Which two diseases are commonly included within COPD?
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Emphysema
Chronic bronchitis Most patients exhibit both |
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What are the three kinds of chronic bronchitis?
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Simple chronic bronchitis
Chronic asthmatic bronchitis Obstructive chronic bronchitis |
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Describe simple chronic bronchitis.
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Cough with sputum, no significant obstruction
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Describe chronic asthmatic bronchitis
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Hyperreactive airways, intermittent bronchospasm, wheezing
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Describe obstructive chronic bronchitis.
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Heavy smokers - chronic airflow obstruction, emphysema
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What are some of the epidemiological facts about COPD?
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12-24 million cases; #4 cause of death
85-90% of cases from cigarettes 2nd leading cause of disability |
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What groups are more likely to suffer alpha-1 antitrypsin deficiency, and for what percent of COPD cases does it account?
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1-2 percent of COPD cases
Genetic predisposition in Caucasian individuals |
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What are alpha-1-protease inhibitors?
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Serine protease inhibitors or SERPINS
Produced by liver, circulate in blood, prevent proteolysis by elastase (Anti-Elastase); Polymorphic, deficiency leads to emphysema, metabolically active site can be oxidized by cigarette smoke and pharmaceutical industry produces anti-proteinases. |
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What is the normal purpose of Alpha-1 Antitrypsin?
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Alpha-1 Antitrypsin inhibits elastase released during phagocytosis, thus preventing the elastase from damaging lung tissue.
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Describe the protease-antiprotease theory.
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Neutrophils and macrophages accumulate in alveoli - possibly attracted by nicotine, ROS - and as a result, more elastase is released and alpha-1 antitrypsin levels are not sufficient to prevent damage.
Leukocytes are activated, secrete elastase, ROS from smoke inhibits alpha-1 antitrypsin. ROS use up antioxidants like superoxide dismutase, glutathione. Promotes tissue destruction. |
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What are gross pathological findings in patients with alpha-1 antitrypsin deficiency and emphysema?
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Basilar panacinar emphysema with alveolar septal destruction and airspace enlargement seen on light microscopy.
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How does the mutation which causes alpha-1 antitrypsin deficiency produce problems?
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Alpha-1 antitrypsin is poorly made and polymerize in cytoplasmic globules in hepatocytes. The accumulation of these globules appears to damage the liver.
The absence of functioning alpha-1 antitrypsin in the lungs results in unchecked destruction of lung tissue by elastases released by macrophages and neutrophils in response to normal infections/damage. |
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What are the general types of presentations of alpha-1 antitrypsin deficiency?
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Simple alpha-1 antitrypsin deficiency - no other complications
Alpha-1 antitrypsin deficiency with COPD Alpha-1 antitrypsin deficiency with Liver disease Or...Alpha-1 antitrypsin deficiency with COPD AND Liver disease. |
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Describe Bronchiectasis.
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Affects medium-sized airways (segmental and sub-segmental bronchi) - permanent dilatation, includes destruction and inflammation.
Tends to occur in older patients, 2/3 are female - also in infants/toddlers after severe lung infection or in CF |
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What is the macroscopic appearance of Bronchiectasis?
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Always dilated
Filled with purulent material Eventually there is fibrous replacement of cartilage, muscle, elastic tissue Three patterns |
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What are the three patterns of bronchiectasis?
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Cylindrical
Varicose Saccular |
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Describe cylindrical bronchiectasis.
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Uniformly dilated and ends abruptly at secretory plug
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Describe varicose bronchiectasis.
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Irregular pattern, beads on a string
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Describe saccular bronchiectasis.
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Ballooned at periphery with blind sacs and lack of recognizable bronchial structures distal to sacs.
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What is a characteristic of bronchiectasis on CXRs?
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Tram tracks
Saccular lesions |
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What is a characteristic of bronchiectasis on CTs?
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Mucus plugs
Beads on a string, white patches Saccular lesions |
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How does bronchiectasis appear microscopically?
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Neutrophil infiltration
Ulcerated bronchial wall Squamous metaplasia Mucus gland hyperplasia Increased vascularity of bronchial wall with anastamoses of bronchial and pulmonary arterial circulations |
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How does bronchiectasis typically progress?
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Neutrophils invade, cause inflammation
Infectious organisms move in Infection and inflammation injure the epithelium Decreased mucociliary clearance allows further infection Destructive cycle repeats |
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What are some inciting events for bronchiectasis?
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Severe lung infections
Endobronchial obstructions (foreign body aspiration, external compression, tumor, impacted secretions) Impairment of defense mechanisms (panhypogammaglobulinemia, CF, primary ciliary dyskinesia, acquired immune deficiencies) Toxic exposures (ammonia inhalation, aspiration injury) Non-infectious cases (yellow nail syndrome, AAT deficiency) |
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How does bronchiectasis typically present?
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Cough (insidious vs non-resolving following infection)
Purulent sputum Hemoptysis Non-specific - fatigue, weight-loss, myalgias |
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What characteristics of bronchiectasis may be present in a physical exam?
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Physical exam typically normal
Abnormal findings over affected areas - crackles, ronchi, wheezes Clubbing Cor pulmonale |
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What laboratory and imaging studies can diagnose bronchiectasis?
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Spirometry may reveal obstruction with reversibility
Sputum contains neutrophils, multiple pathogens Plain film often non-diagnostic - tram-tracks, ring shadows CT is gold standard |
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What common pathogens cause bronchiectasis?
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Pseudomonas aeruginosa (mucoid type in CF patients, associated with worse quality of life, and faster progression)
Haemophilus influenzae Adenovirus RSV Aspergillus Bordetella pertussis Staphylococcus aureus Klebsiella Tuberculosis, other Mycobacteria |
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How is bronchiectasis treated?
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Antibiotics during acute episodes - 10-14 days, empiric treatment, cultures
Facilitate drainage - mucolytics, bronchodilators, pulmonary toilet Surgical resection possible in several localized disease Embolization vs resection for massive hemoptysis |
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What are the effects of S-ANS stimulation of the lungs?
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T1-T6
Increased thickness of secretions Vasoconstriction of lung tissue Bronchiolar dilation |
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What are the effects of P-ANS stimulation of the lungs?
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Vagus nerve
Thins secretions Increases production of mucus Bronchiolar constriction |
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Where are Chapman's points relating to the respiratory tract (bronchiectasis)?
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Anterior along lateral sternal border in interspaces 3, 4, 5
Posterior along lateral spinous process of T2, 3, 4 |
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What are some structural findings associated with bronchiectasis (Osteopathic Correlates)?
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Increased A-P diameter (altered rib mechanics)
Overuse of accessory muscles of respiration - secondary cervical dysfunction, scalene hypertrophy can cause neurovascular compromise to upper extremities Flattened diaphragm |
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What is the osteopathic treatment approach to bronchiectasis?
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Prevent facilitated segments
Attention to cranial base Improve chest cage motion - rib raising (1-6), re-doming of diaphragm Improving lymphatic drainage - open thoracic inlets, local and systemic lymphatic pumps |
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What are the three types of Atelectasis?
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Resorption
Compression Contraction |
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Describe Resorption Atelectasis.
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Bronchial obstruction by mucus plugs, foreign body, or endobronchial tumor.
Mediastinum shifts TOWARD the atelectasis Reversible |
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Describe Compression Atelectasis.
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Fluid, tumor, air in pleural cavity (tension pneumothorax)
Abnormal elevation of diaphragm Mediastinum shifts AWAY from the affected lung Reversible |
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Describe Contraction Atelectasis
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Localized or generalized fibrotic changes in the pleura or lung prevent full expansion
Irreversible |
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How does the ratio of FEV1/FVC change in obstructive lung diseases? Restrictive lung diseases?
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Restrictive lung diseases - FEV1 and FVC decrease proportionally, so same ratio
Obstructive lung diseases - The ratio decreases |
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What are the clinical features of COPD?
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Insidious beginning
Takes 30 years to kill - exception, asthma Progressive dyspnea is most important symptom Clinical manifestations appear after 1/3 of functioning lung parenchyma is destroyed (exception, wheezing) Wheezing, coughing, expectoration in varying proportions depending on the type of COPD. |
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What is small airway disease?
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Common in smokers
Airways <2-3 mm diameter affected The earliest manifestation of COPD Infection does not play a primary role |
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How does small airway disease develop?
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Small airways are normally tethered by the elastic recoil of the lung parenchyma
Loss of elastic tissue in the walls of alveoli surrounding respiratory bronchioles reduces radial traction Respiratory bronchioles collapse during expiration, resulting in functional airflow obstruction despite the absence of mechanical obstruction. |
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What is the clinical definition of chronic disease bronchitis?
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Persistent cough with sputum production for at least 3 months in at least 2 consecutive years in the absence of any other identifiable disease
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What are some histologic/pathologic characteristics of globlet cell hyperplasia?
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Normal globlet cell : ciliated cell = 1:20 (1:5?)
Globlet cell hyperplasia Hypertrophic muscle Mucous gland hypertrophy Usually stained blue, also an increased basement membrane. |
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What are some histological/pathological features of chronic bronchitis acute exacerbation?
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PMNs
Thick bronchial walls Chronic inflammation Erosion of the walls Within the walls, hyperemic - many capillaries, lymphocytes |
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What is the cause of Cystic Fibrosis?
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CFTR gene mutation on chromosome 7 - 1300+ mutations have been identified.
Results in cAMP-dependent chloride channels (cystic fibrosis transmembrane conductance regulators, CFTRs) are defective, epithelial membranes are relatively impermeable to Cl- and secretory process is impaired. |
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What are some clinical manifestations of Cystic Fibrosis, from normal to most severe?
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Normal
Azoospermia Sinusitis, absent vas deferens Mild lung disease, polyposis, pancreatic insufficiency Bronchiectasis, pancreatic insufficiency, male infertility Meconium ileus, pancreatic insufficiency, mild lung disease Classic Cystic Fibrosis - Bronchiectasis, pancreatic insufficiency, male infertility, hepatic cirrhosis |
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What are some clinical features of Kartagener syndrome?
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Primary ciliary dyskinesia
Situs inversus (organ locations are reversed), bronchiectasis, sinusitis, infertility Autosomal recessive |
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Which type of emphysema is the most common?
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Centracinar emphysema - over 95% since they are caused by smoking.
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What are some histological characteristics of centracinar emphysema?
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Lots of black pigment - central star regions
Inflammation around bronchi and bronchioles Distal acinus may become involved, differentiation will become difficult |
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What are some histological characteristics if alpha-1 antitrypsin deficiency?
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Digested PAS, granules - liver tissue
In lungs - megakaryocytes and neutrophils |
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What lung problem is most associated with distal acinar (parseptal) emphysema?
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Spontaneous pneumothorax in younger patients
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Describe irregular emphysema.
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Associated with scarring
Acinus is irregularly involved May be the most common form of emphysema, foci are usually asymptomatic and clinically insignificant so underdiagnosed. |
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What is bullous emphysema?
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Descriptive term for large subpleural blebs or bullae (>1 cm in diameter in the distended state)
Can occur in any form of emphysema Represents localized accentuations of emphysema Occurs near the apex, sometimes in relation to old scars Rupture of the bullae may give rise to pneumothorax |
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What is compensatory emphysema?
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Hyperinflation emphysema
Dilation of alveoli but no destruction of septal walls in response to loss of lung substance elsewhere Results from hyperexpansion of the residual lung surgical removal of a diseased lung or lobe |
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What is congenital lobar overinflation?
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Apparent at birth
Probably results from hypoplasia of bronchial cartilage Sometimes associated with other congenital cardiac and lung abnormalities |
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What is obstructive overinflation?
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1. Lung expands because air is trapped within it
2. Causes: Subtotal obstruction by a tumor or foreign object 3. Mechanisms: Ball-valve action of the obstructive agent; air enters on inspiration but cannot leave on expiration Ventilation through collaterals may bring in air from behind the obstruction (pores of Kohn and canals of Lambert) Can be a life-threatening emergency, if the affected portion distends sufficiently to compress the remaining normal lung |
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What is senile emphysema?
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Age-related loss of lung mass (atrophy)
Affects the entire lung but is often more pronounced in the upper lobes |
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Who is at risk for interstitial emphysema?
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COPD patients (combination of coughing and bronchiolar obstruction produces sharply increased pressures within the alveolar sacs)
Children with whooping cough and bronchitis Patients with airway obstruction by blood clots or foreign bodies Artificially ventilated patients (premature infants and neonates with hyaline membrane disease have a particularly high risk because of their delicate lung structure) |
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What causes interstitial emphysema?
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Alveolar tears
Chest wounds that allows air to be sucked in Fractured ribs that punctures the lung Inhalation of irritant gases |
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What is the definition of Asthma?
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Asthma is a disease characterized by
increased irritability of the tracheobronchial tree with intermittent paroxysmal narrowing of the airways, which may reverse spontaneously or a result of treatment |
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Be familiar with the following classifications of asthma...
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Intrinsic
Extrinsic Steroid-dependent Steroid-resistant Seasonal Exercise-induced Drug-induced Occupational Asthmatic bronchitis Allergic bronchopulmonary aspergillosis |
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What are Curschmann spirals?
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Coiled strands of mucus in bronchoalveolar lavage specimen from an asthma patient.
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What are some histological characteristics with Asthma?
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Massive eosinophilia
Macrophages Charcot-Leyden crystals (in BAL) Tenacious mucus Increased smooth airway muscle Inflammatory infiltrates and edema in bronchial wall Enlarged mucus glands Mast cells |
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What are some differences between obstructive and restrictive lung diseases (besides the obvious)?
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Obstructive: Decreased tissue mass, irregular thin-walled spaces
Restrictive: Increased tissue mass, irregular thick-walled spaces |
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What is Lipoid pneumonia?
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Also known as "Golden" pneumonia
Exogenous - large lipid droplets, from occupational exposure or intentional inhalation of fat droplets... Endogenous - fine lipid vacuoles - seen in COP/BOOP and amiodarone toxicity |
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What is pulmonary alveolar proteinosis?
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Accumulation of surfactant in alveoli and bronchioli - typical in all forms of PAP.
Three types: acquired, congenital, secondary |
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Describe acquired pulmonary alveolar proteinosis.
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Autoimmune due to anti-granulocyte-macrophage colony-stimulating factor (GM-CSF). May recur after transplantation.
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Describe congenital pulmonary alveolar proteinosis.
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Rare cause of immediate-onset neonatal respiratory distress - fatal in 3-6 months without transplantation. Mutations in multiple genes encoding SP-B, SP-C, and ABCA3
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Describe secondary pulmonary alveolar proteinosis.
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Hematopoietic disorders, malignancies, immunodeficiency disorders, lysinuric protein intolerance, acute silicosis and other inhalation syndromes.
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What is pulmonary venoocclusive disease (PVOD)?
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Underdiagnosed
Usually pt is diagnosed with pulmonary arterial hypertension - but CXR and CT scan raise suggestion of pulmonary edema. Diagnosed with that, but ECG or right-side heart catheterization reveals pulmonary hypertension. About 5-20% of cases are idiopathic (PAH) Equal in men and women Characterized by occlusion or narrowing of the pulmonary veins and venules by collagen-rich, fibrous tissue Clinical manifestations are similar to primary PAH: Dyspnea on exertion, fatigue, and cough with development of right-sided heart failure as the disease progresses Grim prognosis: fatal within 2 years of diagnosis without lung transplant |
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What is lymphangio-leiomyomatosis?
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Sporadic (women 20-40 yo) or LAM associated with tuberous sclerosis.
Proliferation of smooth muscle in bronchiolar walls, alveolar septa, lymphatics, and perivascular spaces Obstruction of small airways Cyst formation leading to rupture and spontaneous pneumothorax Obstruction of lymphatics leading to chylous pleural effusion Associated with agiomyolipomas of the kidney Fatal without lung transplantation |
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What are the histological and morphological characteristics of lymphangio-leiomyomatosis?
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Cystic lung parenchyma with proliferation of spindle cells along interstitium and enlarged alveoli. Immunhistochemical studies reveal positive staining for HMB45, Desmin and alpha-SMA, but are negative for CD31 and CD34. Similar spindle cell proliferation was seen also in lymph nodes.
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What complications are associated with lung transplants?
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Postoperative complications - anastomotic dehiscence
Vascular thrombosis Primary graft dysfunction Pulmonary infections - same as lung infections in immunocompromised patients |
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Describe acute rejection in lung transplants.
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Nonspecific symptoms - fever, dyspnea, cough, and infiltrates in chest films
Morphological features - inflammatory infiltrates (lymphocytes, plasma cells, few neutrophils and eosinophils), around small vessels, in the submucosa of airways Diagnosis by transbronchial biopsy |
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Describe chronic rejection in lung transplants.
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At least half of all lung transplant patients develop rejection within 3-5 years
Manifested by cough, dyspnea, irreversible decrease in LFTs Morphologies - patchy bronchiolitis obliterans, w/ or w/o active inflammation, bronchiectasis and pulmonary fibrosis in long-standing cases. Diagnosis by thoracoscopic biopsy. |
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What is a solitary pulmonary nodule?
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Aside from the obvious...
35% of nodules on adults are malignant The older the patient, the more likely it is cancer. < 35 yo = 1% malignant > 50 yo = 50% malignant *Find old CXRs!* |
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What is included in a differential diagnosis for a solitary pulmonary nodule?
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Primary malignancy
Metastatic malignancy Benign neoplasm Localized infection Wegener granulomatosis Rheumatoid nodule Vascular malformation Bronchogenic cyst Amyloidoma |
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How do you evaluate a solitary pulmonary nodule?
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Complete history, including smoking and occupational history
Physical exam with careful palpation of lymph nodes: supra-clavicular, axillary, cervical Routine lab studies CT scan PET scan |
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What radiographic criteria would reliably predict a benign lesion?
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Lack of growth over 2 years
Calcification of a certain type: popcorn, bulls eye, multiple punctate foci, dense central nidus |
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What is the benefit to having old CXRs?
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Normally patients are checked every 3-6 months for at least 2 years if there is a nodule that cannot be determined to be bad
Increase in size or change in shape - full evaluation - is lesion respectable? Patient operable? Needle biopsies. Old CXRs help establish a history for the nodule. |
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Without old CXRs, what diagnostic tests should be done?
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CT to look for calcification not seen on CXR
PET scan - if negative and patient under 35, non-smokers can be followed every 3 months. Patients over 35 need tissue Dx. |
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What percentage of lung cancer cases are not caused by smoking?
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15% - mostly in women
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What is the 5 year survival rate for people with lung cancer?
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15%
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How is Lung Cancer screened?
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CXR - no impact on mortality from screening
Spiral CT - more sensitive than CXR, often false positives 25-75%; Trial ongoing to see how good it is. |
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What are the risk factors for lung cancer?
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Cigarette smoking
Second-hand smoke Radon gas Asbestos Metals Various industrial carcinogens Family history Other diseases Previous lung cancer Asbestos exposure is in heavy smoker increases risk to 50-90x that of smoking alone. |
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What are some symptoms of lung cancer?
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Fatigue
Cough Dyspnea Anorexia, weight loss Chest pain Other pain Hemoptysis Osteoarthropathy Hoarseness Clubbing Wheezing Dysphagia Asymptomatic - 5-15% |
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What are some paraneoplastic syndromes associated with lung cancer?
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Anorexia, cachexia, weight loss, fever, suppressed immunity, others of unknown origin
Endocrine syndromes - most common is HYPERcalcemia Skeletal/connective tissue - pulmonary osteoarthropathy, clubbing Migratory thrombophlebitis - Trousseau's syndrome - poor prognostic sign Neurologic - myopathic - Eaton-Lambert, neuropathies, polymyositis |
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What is Schamroth's sign?
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When the backs of the terminal segments of two digits are placed together, in normal fingers there will be a gap at the nailbed.
In individuals with clubbing there is no gap. |
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To where may lung cancer spread?
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WIthin thorax or to regional lymph nodes
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What symptoms/conditions may result from metastasis of primary lung cancer?
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Chest pain
Dyspnea (phrenic nerve paralysis, bronchial obstruction) Cough/dyspnea (tracheal obstruction) Dysphagia (esophageal dompression) Hoarseness (recurrent laryngeal nerve injury) Horner's syndrome (sympathetic nerve paralysis) Superior vena cava syndrome - constricted by the cancer, so have them move their arm up it should further constrict it. May also see diffuse capillary breakage. |
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How do you treat SVC syndrome? How urgent is it?
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It may cause laryngeal or cerebral edema, an urgent to emergent situation
Rapid diagnosis Quickly treated with diuretics and steroids Radiation therapy, stenting, anticoagulation |
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What is the effect of metastasis of lung cancer to the CNS? Bones? Bone marrow? Liver?
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CNS: seizure, headache, neurologic deficit
Bone: pain, pathologic fracture Bone marrow: anemia, pancytopenia Liver: biliary obstruction (pain, jaundice), liver failure (rare) |
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What are the major types of lung cancer?
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Small cell carcinoma - 18%
Epidermoid (SCC) - 29% Adenocarcinoma - 32% Large cell carcinoma - 9% All others (carcinoid, sarcoma, etc) - 12% |
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What is resectability? Operability?
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The chance a tumor can be removed by a surgical procedure
Can the patient withstand the surgical procedure (cardiopulmonary functions) |
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What are the TNM staging?
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Stage I, II and some IIIA can be resected
Stage IIIB and stage IV generally not resectable |
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What divides tumors from being surgically curable or not surgically curable?
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T4 - tumor invides mediastinum, heart, great vessels, malignant effusion
M1 - distant metastases N3 - metastasis to contralateral mediastinal, contralateral hilar, ipsilateral, or contralateral scalene or supraclavicular nodes. Determine staging with PET/CT, mediastinoscopy (right) or mediastinotomy (left) |
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Describe small cell lung cancer?
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Usually extensive upon presentation
Extremely rare to find a very small early SCLC Staging - limited - confined to one hemithorax and regional lymph nodes (30%) or extensive - all others. |
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How are NSCLC treated?
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Dependent on stage - surgery, radiation therapy, chemotherapy
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How is SCLC treated?
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Limited stage - combine chemo and radiation therapy
Extensive stage - combination chemo All - prophylactic brain radiation |
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What is the prognosis for NSCLC?
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Complete resection in N0 disease - 60-80% 5 year survival
Stage I or II who are irradiated - 20% 5 year survival rate |
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What is the prognosis for SCLC?
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Untreated limited stage - median survival 12 weeks
With chemo - median survival 18 months Extensive stage with treatment - median survival 9 months |
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So, what are some characteristics of metastatic lung cancer? Treatment? Survival?
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With a known extrathoracic neoplasm: assume a SPN is a lung cancer
Tumors that are metastatic to the lung, when the lung is the sole site, can often be resected with resultant disease free interval >1 year, some with 5 year survival of 20-30% Osteogenic sarcoma- repeated thoracotomies often required |
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What is the difference between ALI and ARDS?
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ALI - oxygen concentration ratio is <300 mmHg
ARDS - oxygen concentration ratio is <200 mmHg |
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How is the oxygen concentration ratio measured?
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ABG
PaO2 preferred |
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What are the most common causes of ARDS/ALI?
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Sepsis, Trauma, Aspiration
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How do you search for the cause of ARDS/ALI?
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Systematically review events immediately preceding onset of respiratory distress
Look for drugs, administration of blood products, contrast media, overlooked portal of entry for air embolism, recent neurological events such as seizures |
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What are the three phases of ARDS?
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Exudative
Proliferative/Organizing Fibrotic |
