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57 Cards in this Set

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1. Define emphysema
2. What causes centrilobular emphysema? Where does it occur?
3. What causes panlobular emphysema? Where does it occur?
1. Permanent enlargement of air spaces distal to terminal bronchioles due to destruction of alveolar walls.
2. Smoking; proximal acini; upper lung zones.
3. Alpha-antitrypsin def.; proximal+distal acini; lung bases.
Pathogenesis of chronic bronchitis?
Excess mucus production narrows the airways (productive cough). Inflammation/scarring in airways, hyperplasia/hypertrophy of mucus glands/goblet cells, smooth muscle hyperplasia, squamous metaplasia and loss of cilia.
1. What defines mild obstructive disease?
2. What defines severe obstructive disease?
3. What devise can be used to screen for obstruction? What value indicated further PFT's'?
1. FEV1 70%
2. FEV1 < 50%
3. Peak flow meter: peak expiratory flow < 350 L/min.
Treatment of COPD:
1. First line drugs?
2. When would budesonide or fluticasone indicated?
3. Do corticosteroids improve PFTs?
1. Combination of albuterol and ipratropium. Salmeterol (long-acting) for patients requiring frequent use.
2. Inhaled corticosteroids (anti-inflammatory) are reserved when symptoms aren't controlled by bronchodilators.
3. No. No improvement in pulmonary function.
1. What is the criteria for continuous or intermittent long-term oxygen therapy in COPD?
2. Does oxygen improve survival in patients with COPD and chronic hypoxemia?
1. PaO2 < 55 mmHg OR
O2 sat < 88% OR
PaO2 55-59 mmHg + polycythemia (Hct > 55%) or cor pulmonale OR
Resting PaO2 > 60 mmHg w/ SaO2 > 90% but hypoxic at sleep.
2. Yes. Prevents pulmonary HTN and cor pulmonale.
Exacerbation of COPD:
1. What are the main precipitants?
2. What are some treatment options?
1. S. pneumonia, H. influenza, M. pneumonia, M. catarrhalis, and viruses.
2. IV methylprednisolone (taper with oral prednisone on clinical improvement), antibiotics (axithromycin/levofloxacin), keep O2 above 90%, NPPV (BIPAP or CPAP).
1. Triad of asthma?
2. Wheezing on inspiration of expiration?
3. Signs of acute severe asthma attack?
1. Airway inflammation, airway hyperresponsiveness, reversible airflow obstruction.
2. Both!
3. Tachypnea, diaphoresis, INCOMPLETE SENTENCES, us of accessory muscles, paradoxic movement of abdomen on inspiration (sign of resp failure).
1. An increase in FEV1 by how much after the inhalation of a bronchodilator indicates reversible obstructive airway disease?
2. What peak flow indicated mild, moderate and severe disease?
3. What is used in a bronchoprovocation test?
1. 12%
2. Mild > 300, 100-300, severe < 100.
3. Methacholine.
1. During acute exacerbation what sign indicates decomensation and the requirement of intubation?
2. Peak flow is < 60% of predicted. What do you do?
1. Normal or high CO2 levels.
2. PF < 60% of predicted indicates severe exacerbations. Treatment: inhaled B2-agonist, corticosteroids (IV or oral + inhaled during tapering schedule), 3rd line: theophyllin/IV Mg, keep O2 > 90%.
Define the asthma term and treatment:
1. Mild intermittent.
2. Moderate persistent.
3. Severe persistent.
All patients should have short acting B2-agonists. Long term treatment:
1. Symptoms 2 or more / week. None.
2. Daily symptoms; frequent exacerbations. Daily inhaled corticosteroids OR cromolyn/nedocromil OR methylxanthine OR antileukotriene.
3. Continual symptoms, limited physical activity. Daily inhaled corticosteroids (high dose) + long acting B2-agonists OR methylxanthine and systemic corticosteroids.
1. When are montelukast-leukotriene modifiers indicated?
2. Cromolyn/nedocromil: how do they work? Used in adults or children?
1. Prophylaxis of mild exercise induced asthma.
2. Inhibit release of mediators from mast cells; prophylaxis; used in children.
Patient presents with mucopurulent, foul-smelling sputum and a chronic cough. CT shows dilated airways extending to the lung periphery.
1. MCC of this disease.
2. Goal of treatment.
Bronchiectasis (permanent, abnormal dilation and destruciton of bronchial walls, damaged cilia).
1. CF make up half of all cases. Other: ciliary dyskinesia, infection: TB, adeno, S. aureus, H. influenza.
2. Prevent complications of pneumonia and hemoptysis.
CF: (AR - 3 nucleotide deletion on chr. 7 (phenylalanine), damaged CFTR).
1. Whats the screen for infants?
2. What indicates a positive sweat test?
1. Trypsin levels. Karotyping.
2. > 60 mmol/L
Solitary Pulmonary Nodule on CXR:
1. Best indication that a lesion is benign?
2. If benign, next appropriate management?
3. Chance of malignancy if patient is over 50?
4. If lesion is highly suspicious of malignancy, next step?
5. If suspicion is intermediate, next step?
1. Previous CXR showing a lesion stable for 2 years.
2. CXR or CT every 3 months then every 6 months.
3. 50%
4. Surgical resection.
5. Transthoracic needle biopsy or fiberoptic bronchoscopy.
Identify the follow lung cancers:
1. 50-75% of patients have metastases at presentation.
2. Can be associated with pulmonary scars/fibrosis.
3. SIADH syndrome.
4. Eaton-Lambert.
5. Cavitation on CXR.
6. Central located.
1. Small cell: 20-25% of lung ca.
2. Adenocarcinoma
3/4. Small cell (ectopic ACTH).
5. Squamous CC.
6. SCC and small cell.
Name the structure damaged in the following lung cancer scenarios:
1. Hemidiaphragmatic paralysis.
2. Facial fullness, arm edema, JVD, dilated veins over anterior chest.
3. Anhidrosis, ptosis, miosis.
4. Hoarseness.
5. Shoulder pain radiating down arm + Horner's.
1. Phrenic nerve.
2. Superior vena cava syndrome: SCLC, mediastinal tumor.
3. Cervical sympathetic chain invasion.
4. Recurrent laryngeal nerve palsy.
5. Pancoast tumor (SCC normally). Invasion of brachial plexus (mostly C8, T1-T2).
Factors that favor malignant solitary pulmonary nodule?
Age > 50
Size > 3.0 cm
Steady growth
Nodule grossly irregular or speculated margin
Stippled or eccentric pattern of calcification (benign: central laminated calcification).
Diagnoses of lung cancer:
1. Most important radiologic study?
2. What is a CT scan useful for?
3. When should a biopsy be performed on intrathoracic lymphadenopathy?
1. CXR.
2. Staging, revealing lymphadenopathy in mediastinum.
3. Always.
Mediastinal masses. Name the common cause of:
1. Anterior
2. Middle
3. Posterior
1. Thyroid, teratogenic tumors, thymoma, Hodgkins lymphoma.
2. Lung ca, lymphoma, aneurysms, cysts, Morgagni hernia (trans colon + omentum).
3. Neurogenic tumors (neuroblastoma, ganglioneuroma), esophageal masses, cysts, aneurysms, Bochdalek's hernia (post. diaphragm defect).
Pleural effusion:
1. Causes of transudative.
2. Causes of exudative..
1. CHF, cirrhosis, PE, nephrotic syndrome, peritoneal dialysis, hypoalbuminemia, atelectasis.
2. Pneumonia (bacterial), TB, malignancy, viral infection, PE, collagen vascular diseases, pancreatitis, trauma.
Test to identify exudative pleural effusions.
If exudative, what other info is helpful?
Protein (pleural) / protein (seurm) > 0.5
LDH (pleural) / LDH (seurm) > 0.6
LDH > 2/3rds the upper limit of normal serum LDH
If exudative: CBC, glucose, pH, amylase, TG's, microbiology, cytology.
Pleural effusion:
1. How much fluid must accumulate to be detected on CXR?
2. What indicates complicated pleural effusion?
3. Next best step in complicated pleural effusion?
1. 250 mL
2. pH < 78, purulent, decrease glucose, polyorganisms.
3. Chest tube.
Pleural fluid pears:
1. Elevated amylase
2. Milky, opalescent fluid
3. Frankly purulent fluid
4. Bloody effusion
5. Lymphocytic predominant effusion
6. pH < 7.2
1. Esophageal rupture, pancreatitis, malignancy.
2. Chylothorax: lymph in pleural space.
3. Empyema
4. Malignancy
5. TB
6. parapneumonic or empyema
If pleural fluid glucose < 60, rule out....?
Rule out rheumatoid arthritis. Other causes: TB, esophageal rupture, malignancy, lupus.
Treatment of pleural effusion:
1. Transudative
2. Exudative
3. Parapneumonic
4. Complicated effusion
Thoracentesis drainage for relief of large effusions
1. Diuretics, sodium restriction.
2. Treat underlying disease.
3. Antibiotics.
4. Chest tube drainage, intrapleural thrombolytics, surgical lysis of adhesions.
MCC of:
1. Traumatic pneumothoraces
2. Spontaneous pneumothorax
1. Iatrogenic: transthoracic needle aspiration, throacentesis, central line placement.
2. Primary simple - ruptured subpleural bleb (tall, lean men...not very distressed).
Secondary (complex) - complication of COPD, asthma, neooplasm, etc. (very distressed...little pulmonary reserve).
34 yr old African American women has a dry cough, malaise, weight loss, and noncaseating granulomas in her lungs. Name other findings in the follow organs that she may have:
1. Skin
2. Eyes
3. Heart
4. Musculoskeletal
5. Nervous system
1. Lupus pernio (violaceous cheeks), erythema nodosum.
2. Anterior uveitis - ophotphobia, eye pain, decreased acuity.
3. Conduction disturbances, heart-block.
4. Arthralgias.
5. CN VII - Bell's paly
1. Hallmark on CXR?
2. Skin test?
3. Elevated enzymes?
1. Bilateral hilar adenopathy.
2. Skin anergy.
3. ACEi, 1-alpha-hydroxylase (therefore increase vitamin D).
Diagnose these patients. All have chronic interstitial pneumonia with cells that are CD1 positive +
1. < 2yrs, eczematous rash, lytic lesion in long bones.
2. Adult cigarette smoker with dyspnea, nonproductive cough.
3. Fever, rash on scalp, triad: lytic bone, diabetes insipidus, exophthalmos.
Histiocytosis X
1. Letterer-Siwe (systemic)
2. Eosinophilic granuloma (localized - lung).
3. Hands-Shuller-Christian
Patient has recurrent URTI and LRTI, a saddle nose, and glomerulonephritis.
1. Whats the pathogenesis?
2. Antibodies present?
3. Treatment?
4. Renal biopsy H&E shows?
Wegener's granulomatosis
1. Necrotizing granulomatous vasculitis.
2. c-ANCA.
3. Coritcosteroids and cyclophosphamide.
4. Cresentic
Patient with allergic rhinitis, asthma, pulmonary infiltrates, rash, and eosinophilia. +pANCA. Diagnosis?
Churg-Strauss. Vasculitis may involve skin, muscle, and nerve lesions.
Pneumoconiosis. Affect of the following on risk of lung cancer and TB:
1. Coal worker's (CWP)
2. Asbestosis
3. Silicosis
4. Beryliosis
1. nil nil
2. Increase lung ca, nil
3. Increase of both
4. Increase lung ca.
1. Most common lung lesion due to asbestosis.
2. Predilection for upper or lower lobes?
3. MC lung ca associated with?
1. Benign pleural plaques.
2. Lower.
3. Bronchogenic > mesothelioma.
Silicosis pneumonconiosis:
1. Upper or Lower lobes?
2. CXR finding?
1. Upper lobes.
2. Egg shell calcification of hilar lymph nodes.
What antibodies are elevated in hypersensitivity pneumonitis?

What causes Farmer's lung?
Serum IgG and IgA to the inhaled antigen (NOT IgE).

Thermophilic actinomycosis.
Middle aged male smoker with gradual onset of progressive dyspnea and dry cough. CXR shows honeycombed appearance. All other causes of ILD are excluded. Treatment?
Idiopathic pulmonary fibrosis. Mean survival 2-7 years. Supplemental oxygen and corticosteroids (1 year) may help, but lung transplantation is the only curative treatment.
Acute respiratory failure:
1. Define hypoxia (quantitatively)
2. Define hypercapnia (quantitatively)
3. How do you calculate PAO2?
1. PaO2 < 60 mmHg and PaCO2 > 50 mmHg
2. PaCO2 > 50 mmHg
3. PACO2 = %O2(713) - PaCO2/.8
1. Define minute ventilation.
2. How does one decrease PaCO2?
3. In a ventilated patient, how does one decrease PaO2?
1. RR*VT
2. Increase RR or tidal volume (VT)
3. Decrease FiO2 or decrease PEEP
1. Quantitatively (O2 sat), what is hypoxemic respiratory failure?
2. What is the main pathophysiological mechanism?
1. Low PaO2, low/normal PaCO2. Present when O2 saturation is < 90% despite FiO2 > 0.6
2. V/Q mismatch.
What mechanism of hypoxemia are the follow patients suffering from:
1. Normal PaCO2, Normal A-a gradient.
2. PaCO2 is elevated. A-a gradient is normal.
3. Normal PaCO2. Elevated A-a. Improvement with O2.
4. Normal PaCO2. Elevated A-a. No improvement with O2.
1. Low inspired PaO2.
2. Hypoventilation.
3. V/Q mismatch (perfusion defect).
4. Shunt.
What is NPPV and when should it be used?
Noninvasive positive pressure ventilation. Not sued for life support ventilation, only to support the patient's own spontaneous breathing. Patient must be neurologically intact, awake and cooperative. Most successful with hypercarbic respiratory failure (COPD). Two options BIPAP and CPAP via nasal or full-face mask.
Causes of ARDS
Sepsis, aspiration of gastric contents, severe trauma, femur fracture, pancreatitis, massive transfusion, near-drowning, drug overdose (heroin), intracranial HTN, cardiopulmonary bypass, amniotic fluid embolism, DIC.
Patient in the emergency department has hypoxemia that is refractory to oxygen therapy PaO2/FiO2 < 200, CXR shows bilateral pulmonary infiltrates. How could one rule out CHF?
PCWP < 18 mmHg in ARDS and > 18 mmHg in cardiogenic pulmonary edema.
Describe the principles of the following mechanical ventilator settings:
1. Assisted controlled (AC)
2. Synchronous intermittent mandatory ventilation (SIMV)
4. Pressure-support ventilation
1. Predetermined tidal volume given when patient initiates a breath. Predetermined rate if patient doesn't initiate.
2. Predetermined tidal volume and predetermined rate, but patient can breathe on own above minimum rate.
3. Set pressure, not volume.
4. Set pressure only given during a breathe.
NIPPV is contraindicated in:
Sepsis, hypotension, dysrhythmias.
Key parameters in mechanical ventilation:
1. Minute ventilation is (RR*VT) is altered in response to?
2. What should FiO2 start at? This should be titrated to maintain what PaO2 (or O2 sat)?
3. What parameter is altered to avoid oxygen toxicity? Safe level?
1. PaCO2 changes.
2. 100% then titrate to PaO2 >50-60 or O2 >90%.
3. FiO2 < 0.6 is generally safe.
Key parameters in mechanical ventilation:
1. What should I:E ratio be?
2. Advantages of PEEP.
3. Disadvantages of PEEP.
4. Appropriate initial setting for PEEP.
1. Inspiratory/expiratory ratio - 1:2
2. Increase compliance and oxygenation, prevent alveolar collapse/atelectasis.
3. Barotrauma, decrease venous return.
4. 2.5-10 cm H2O.
Mechanical ventilation:
1. Agent used for anxiety, agitation, discomfort.
2. Prolonged presence of an endotracheal tube can result in?
3. How does one prevent #2?
4. GI side effects of intubation?.
1. Benzo's. Other: opioids, propofol.
2. Tracheomalacia - tracheal cartilage softening.
3. Tracheostomy if ventilator-dependent > 2 weeks
4. Stress ulcers, cholestasis.
Define, quantitatively, pulmonary HTN.
Mean arterial pressure > 25 mmHg at rest or 30 during exercise.
Primary pulmonary hypertension:
1. Definition
2. Mean survival time from diagnosis
3. Treatment
1. Diagnosis of exclusion; absence of diseases of heart or lung.
2. 2-3 years
3. IV prostacyclins (epoprostenol, PGI), CCB's lower vascular resistence. Perform a vasodilator trial before long term treatment. Warfarin with INR 2.0.
55 yr old smoker presents with decreased exercise tolerance, cyanosis, digital clubbing, hepatomegaly, JVD. Investigations reveal polycythemia, ECG with RAD + RVH. Diagnosis?
Cor pulmonale: most commonly secondary to COPD. Other: PE, ILD, asthma, CF, apnea, pneumoconioses.
61 yr old female (BMI 30) who underwent pelvic surgery 2 days prior has dyspnea, pleuritic chest pain, and a cough. She has tachypnea and rales. What are some complications of her condition?
1. Death: mortality of diagnosed PE is 10% in first hour. Of those who survive, 30% will die of a recurrent PE if left untreated.
2. Recurrences are common which can lead to chronic pulmonary HTN and cor pulmonale.
1. PaO2 and PaCO2
2. A-a gradient
3. CXR
1. Both low
2. Elevated
3. Normal
Modified Wells Criteria (PE)
3.0 - Symptoms/signs of DVT
3.0 - Alternative diagnosis less likely
1.5 - HR > 100 bpm
1.5 - Immobile/surgery previous 4 weeks
1.5 - Previous DVT or PE
1.0 - Hemoptysis
1.0 - Malignancy
Workup in patient with suspected PE.
1. Clinical decision rule < 4: do D-dimer. If normal - no PE. If abnormal do CT.
2. Clinical decision rule > 4: do CT.
3. CT will indicated: no PE, PE, inconclusive.
4. Inconclusive/contraindication to CT - do leg ultrasound: DVT - treat. No DVT - V/Q or arteriogram.
1. When is pulmonary angiography indicated?
2. D-dimer is sensitive or specific?
1. When noninvasive testing is equivocal, high risk of anticoagulation, patient is hemodynamically unstable and embolectomy may be required.
2. Sensitive.
Treatment for PE
Day 1: heparin to achieve aPTT 1.5-2.5. Warfarin to achieve INR 2-3.
Day 5: stop heparin infusion.
3-6 months: stop warfarin.