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586 Cards in this Set
- Front
- Back
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What are indicators of severe asthma attack?
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Normal to inc pCO2 levels, speech difficulty, diaphoresis, altered sensorium, cyanosis, "silent" lungs. pCO2 is normally dec due to hyperventilation so inc pCO2 indicates severe airway obstruction (air trapping) and/or respiratory muscle fatuge. Typical findings in asthma attack that aren't indicative of severe attack: dec pO2, tachypnea, inc work of breathing, hyperinflation, tachycardia
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What is Light's criteria for fluid classification?
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Exudative pleural effusion if any one of following are present: 1. Pleural:serum protien >0.5 2. Pleural:serum LDH >0.6 3. Pleural LDH >2/3 of upper limit of normal for serum LDH. If all neg, transudative
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When do you see exudative pleural effusion with pleurla fluid acidosis (pH <7.2) and low pleural fluid glucose (<60)?
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Pts with complicated parapneumonic effusion, rheumatoid pleurisy, drug-induced lupus, TB, and malignancy
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What is complicated parapneumonic effusion? How do you treat it and what can it lead to?
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Involves peresistent bacterial invasion into pleural space which decreases pleural fluid glucose (<60) and increases LDH (from lysis of neutrophils). Culture usually neg and effusion resolves with abx as bacterial can be cleared easily from pleural space. Complicated effusions can progress to empyema which is FRANK PUS in pleural space requiring chest tube drainage.
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What are causes of drug-induced lupus?
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Hydralazine procainamide, INH
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What type of pleural effusions are caused by heart failure?
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Bilateral, transudative with normal pleural fluid pH and normal pleural glucose
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What type of pleural effusion does hypoalbuminemia cause?
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Bilateral, transudative (due to proteinuria or cirrhosis)
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What type of pleural effusions do PE cause? How can you differentiate form parapneumonic effusions?
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Exudative (75%) or transudative (25%). Pleural fluid pH and glucose are usually normal (whereas in parapneumonic effusions pH and glucose are low)
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What is the risk of reactivation of TB in HIV pts? How does it present and what does CXR look like?
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10% per year risk. Fever, night sweats, wt loss, fatigue, pleuritic pain, chronic cough, hemoptysis. CXR: apical cavitary lesion
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Where is the inital infection of TB in lung on CXR? What about after reactivation?
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Initially, peripheral pulmonary focus of infection with mediastinal or hilar LAD on CXR and asymptomatic; primary site of infection (Ghon focus) remains as calcified granuloma. Ractivation (esp common if immunosuppressed) causes apical cavitary pulmonary lesion (aerobic, apex has highest oxygen tension)
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What is seen on PE of postnasal drip?
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Cobblestoning of nasal mucosa
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What is CXR of GERD?
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Normal; symptoms worse 30min after meals or when recumbent
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What are symptoms of coccidiodomyocosis and where is it found?
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Southwest US, soil-borne. Flu-like illness with dyspnea and slightly productive cough. varying lung findings
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What are symptoms of PCP PNA and what see on CXR?
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Fever, dyspnea, nonproductive cough. CXR: "ground glass" infiltrate
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What is cough of CHF like? What will PE and CXR show?
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Chronic nonproductive cough that is worse when lying flat. Bibasilar rales on lung exam and pleural effusions on CXR
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What is the best way to evaluate undiagnosed pleural effusion? ****
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Thoracentesis (to determine if exudate or transudate), unless pt has clear-cut evidence of CHF. It is a bedside, minimally invasive procedure that permits fluid to be rapidly sampled, visualized, examined microscopically, and quantified. Provides info to make a decision in 90% of cases. If shows exudative, need further diagnostic workup
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What is a pleural effusion and what is the workup?
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Excess quantity of fluid in pleural space. First step - determine cause. Start with determining of fluid is transudative or exudateive. Do this with diagnostic thoracentesis except which classic s/s of CHF (where trial of diuretic warranted)
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What type of pleural effusion is caused by malignancy?
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Exudative, thoracentesis may also show malignant cells
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What are the 3 main causes of malignant pleural effusions (what type of cancers)?
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Lung, breast, lymphoma
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What is the next step in dx of malignancy if have pleural effusion and thoracentesis with pleural fluid cytoplogy does give diagnosis?
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Bronchoscopy
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What do pts with CHF exacerbation present with?
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Fluid overload (wt gain), pedal edema, crackles at both lung bases with rales and dullness to percussion (LVF causes fluid to pool in dependent areas of heart), PND, orthopnea, DOE, can have bibasilar infiltrates on CXR
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What population is MC to have sarcoidosis in the US?
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Young to middle aged African American females
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What are s/s of sarcoidosis?
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Insidious-onset dyspnea and dry cough in absence of constitutional symptoms. Typically affects skin (protean manifestations, most commonly erythema nodosum) and eyes (uveitis - 1/4 pts will have anterior uveitis with variable severity), can also affect liver, kidneys, heart
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What is pulmonary sarcoidosis look like on CXR and PE?
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Interstitial inflammation that can progress to fibrosis. Dry rales on PE, CXR shows bilateral hilar LAD and diffuse interstitial infiltrates.
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How does idiopathic pulmonary fibrosis present?
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Insidiously with progressive dyspnea on exertion and dry, nonproductive cough. "Velcro-like" inspiratory crackles
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What is ankylosing spondylitis? How can it cause lung disease?
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HLA-B27 assoc spondyloarthropathy somtimes accompanied by anterior uveitis. Costovertebral joint inflammation with subsequent fusion can cause a restrictive lung pattern (due to difficulty in chest wall expansion). Back pain is usual presenting symptom
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What type of reaction is Aspirin sensitivity syndrome, what causes it, what are clues to diagnosis and how is it treated?
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Pseudo-allergic reaction resulting from aspirin-induced Prostaglandin/Leukotriene misbalance in susceptible individuals - ASA is a COX1 and COX2 inhibitor; arachidonate diverges from blocked COXs to a 5-lipoxyganse pathway and accumulatino of LT and changed PG/LT balance triggers reactions. Clues to dx: ASA ingestion, persistent nasal blockage, episodes of bronchoconstriction Tx: avoid NSAIDs and use of Leukotriene receptor antagonists (drug of choice). Other tx include topical corticosteroids and aspirin desensitization therapy
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What is the effect of flattening of diaphragm in pts with COPD?
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Causes inc work of breathing (makes it more difficult to decrease intrathoracic pressure during inhalation and thus inc work of breathing
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What are the lung volume changes in COPD?
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Inc TLC, inc FRC, inc RV -> hyperinfilation and diaphragm flattening
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What does hyperinflation of lungs do in COPD?
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preserves max expiratory airflow bc higher lung volume increases elastic recoil pressure and enlarged airwasy decreases overall airway resistance.
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What does lung volume reduction surgery due?
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Reduces lung volume in COPD via excision of emphysematous tissue -> inc diaphragm length and return its curvature. Also thought to dec FRC and improve interplay between diaphragm, chest, and abd walls, inc exercise capacity, and reduce work of breathing
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What happens to pulmonary compliance in COPD?
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Increased due to loss of alveolar and elastic tissue (restrictive lung disease has dec lung complaine)
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What changes in airflow in COPD?
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Significant airflow limitation with reduced inspiratory and expiratory flow rates
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What is the first step to determining cause of pleural effusion (unless know it is CHF)?
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Pleural fluid analysis - Light's criteria. Pleural:serum protein >0.5, Pleural:serum LDH >0.6, Pleural fluid LDH >2/3 upper limit of normal for serum LDH (just need 1 of 3 for exudative effusion; if all 3 neg it is transudate)
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What are causes of exudative effusions?
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Infection (PNA, TB), malignancy, PE, CT diseases, iatrogenic (ex: drug-induced lupus)
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What are S/S of PE?
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Dyspnea, tachypnea, pleuritic chest pain, resp alkalosis and widened alveolar-arterial oxygen gradient due to ventilation/perfusion mismatch.
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What does CXR of PE show?
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Normal or evidence of atelectasis and/or pleural effusion.
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What is the gold standard test for PE? What is the diagnostic test of choice?
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Gold standard: pulmonary angiography. helical CT is diagnostic TOC
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What cause pleural effusions on CHF?
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inc intravascular hydrostatic pressure. Transudative, bilateral effusions with few RBC and WBC and glucose concentration = to serum
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What causes pleural effusions in hypoalbuminemia?
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Dec intravascualr oncotic pressure. Transudative, bilateral effusions with few RBC and WBC and glucose concentration = serum
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What can parapneumonic pleurla effusions lead to if untreated?
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Pulmonary abscess -> empyema with frank pus in infiltrate
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What does malignant pleural effusion show?
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Turbid or bloody exudates with L predominance of WBC fractionand many RBC. Glucose in pleural fluid is variable
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What is the typical presentation of sleep apnea syndrome?
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Moderately obese middle aged man complianing of daytime somnolence, morning headaches, inc fatigability, loud snorer. Often mild HTn often seen which usually improves with treatment of sleep apnea
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What is first step in sleep apnea treatment?
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Start with: Wt reduction, avoidance of sedatives and alcohol, and avoidance of supine posture during sleep. Other tx: uvulopalatopharyngoplasty and nasal CPAP during sleep
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What is standard diagnostic method for sleep apnea?
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Polysomnography
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What do steroids do to labs?
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Glucocorticoids cause neutrophilia by increasing bone marrow release and mobilizing the marginated neutrophil pool. Eosinophils and lymphocytes are decreased.
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What would hypersensitivity reaction do to WBC?
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Inc eosinophils
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What are pts with Hodgkin's lymphoma at risk for later down the line? Who is at most risk?
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Secondary malignancies form chemo and/or radiation, esp those treated before age 30. Breast and lung cancers are most common.
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What are pts treated with radiation at risk for in terms of lung disease? When does it occur?
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Radiation-induced lung fibrosis. Typically presents as dyspnea 4-24mo after therapy.
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What will fungal PNA in immunosuppressed present with?
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Fevers, chills, wt loss, cough.
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In pts with fungal PNA who have aspergillus fungal ball on CXR, what was usually preceding the fungal ball?
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Preexisting cavitary lesion
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What are the s/s and CXR of pulmonary TB?
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Progressive fever, chills, cough, hemoptysis, wt loss. CXR: cavitary lesions
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Whast is the MC SE of inhaled corticosteroid therapy?
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Oropharyngeal thrush (high doses can lead to inc systemic absorption and can produce adrenal suppression, cataract formation, dec growth in chidlren, interference with bone metabolism, and purpura but those are dose-dependent and only occur at high doses over long periods of time)
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What test can be used to differentiate asthma from COPD?
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Bronchodilator response test (demonstrates reversibility of airway obstruction). Both asthma and CPD are chronic inflammatory diseases of the respiratory tract. Bronchodilator response test measures FEV1 before and after bronchodilator (usually b2 agonist). Significant improvement in FEV1 after bronchodilator administration (15% or greater) indicates reversibility of obstruction (more common in asthma). There is a subset of pts with COPD who also show positive bronchodilator response.
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Besides bronchodilator response, what other PFT test can help differentiate COPD from asthma?
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Low DLCO in COPD
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What is CXR in asthma?
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Almost all pts is normal except hyperinflation in acute exacerbations
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What is bronchoscopy used for?
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Bronchial washings (PCP infection) and bx of endobronchial and perihilar masses
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What immunologic test is useful in dx bronchopulmonary aspergillosis if index of suspicion is high?
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Serum IgE
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What is nocturnal pulse oximetry used for?
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Diagnosing noctural desaturation, esp in pts with sleep apnea
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What are common SE of b2 agonists?
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Reduce serum K levels by driving K into cells. Can result in muscle weakness, arrhythmias, and EKG changes. Also, tremor, headaches, palptations
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What is peak expiratory flow rate used for?
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Evaluating severity of asthma attack and monitoring respiratory movement
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When are chest x-rays most useful in asthma pts?
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When foreign body aspiration or underlying PNA are suspected
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What does EMG measure? When is it useful in evaluating muscle weakness?
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Electrical activity of muscle fibers. Useful in evaluaiton of muscle weakness due to neuropathic or myopathic conditions.
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What are the 4 categories of asthma severity and what are they determined by?
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intermittent, mild persistent, moderate persistent, severe persistent. Determined by frequency of pts daytime symptoms, nighttime awakenings, use of short-term b2 agonists, and PFTs
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What is the criteria for the 4 categories of asthma severity?
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Intermittent: day symptoms/beta agonists <= 2x/wk, nightime awakenings <=2x/mo, normal baseline FEV1 and FEV1/FVC and no limitations on daily activities. Mild persistent: symptoms >2days/wk but not daily, nightime 3-4x/mo, minor limitation on activities, normal PFTs. Moderate persistent: daily symptoms, weekly nighttime awakenings, moderate limitations on activities, FEV1 60-80% predicted. Severe persistent: symptoms throughout day, frequent nighttime, extremely limited activity, FEV1<60% predicted
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What is the appropriate therapy for the different categories of asthma severity?
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Intermittent: short-acting b2 agonist. Mild persistent: add low dose inhaled steroid. Moderate persistent: add LABA. Severe: high dose inhaled steroids, can add oral steroids as well.
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What is empyema and what causes it?
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Empyema = infection in pleural space. Can occur from parapneumonic effusiosn and also as a result of contamination of the pleural space by rupture of a lung abscess, bronchopleural fistula, penetrating truam, thoracotomy, and infection from hepatic or subphrenic abscess or from ruptured viscus (esophagus) and also have hemothorax bc residual blood in chest is a great medium for growth of bactera
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How do pts with empyema present? How dx?
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Low-grade fever, dx with CT scan
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When do you do surgery on empyema?
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WHen it is localized, complex, and has a thick rim - surgery is only option
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What is the tx of recent onset noncomplex empyema without thick rim with loculation?
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Fibrinolytic therapy (streptokinase or urokinase)
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When are abx useful in empyema?
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When it is early. If subacute or complex, abx don't work well, always need drainage
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What should you do when empyema fails to be drained by single chest tube?
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Can place another one in case the first one is blocked, but for complex empyema that can be hard and may need CT or US guidance and usually wont work if there is a thick peel present
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What is the cause of low glucose concentration in exudative effusions?
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High metabolic activity of WBC (and/or bacteria) in pleural fluid.
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What glucose concentration suggests empyema or rheumatic infusion? What about malignancy, lupus, esophageal rupture, or TB?
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Pleural glucose <30: empyema or rheumatic effusion. 30-50: malignancy, lupus, esophageal rutpure, TB
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How do inflammatory conditions cause pleural effusions?
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By increasing pleural membrane and capillary permeability
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What is the mechanism of transudative pleural effusions?
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Inc capillary hydrostatic pressure
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What is the theory behind right-sided pleural effusions in cirrhosis (hepatic hydrothroax)
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Inc permeability of R hemidiaphragm
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What type of pleural effusions are usually caused by cirrhosis?
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Transudative
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When do you see high amylase in pleural effusions?
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Esophageal rupture
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What is diagnostic of respiratory acidosis?
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Acidosis with high CO2 and normal/elevated bicarb
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How can seizure cause respiratory acidosis?
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Post-ictal can be hypoventilating -> hypoventilation induced hypoxia -> respiroatry acidosis
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What type of acidosis is lactic acidosis?
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Metabolic (low bicarb)
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What is the most common acid-base disturbance in PE?
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Respiratory alkalosis due to hyperventilation as pt tries to overcome hypoxia and V/Q mismatching. Would have low pCO2 on ABG
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What is the MC acid-base disturbance in renal failure?
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Metabolic acidosis due to inadequate excretion of metabolically-producing acids (sulfates, phosphates). It is a chronic problem often compensated by a mild respiratory acidosis -> ABC has low bicarb and low pCO2
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What type of acid-base disturbance does vomiting cause?
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Metabolic alkalosis due to loss of acid gastric secretions
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When should suspect alpha-1 antitrypsin deficiency?
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Non-smoking adults <45yo with panlobular emphysema on CXR. Also at risk for liver disease (neonatal hepatitis, cirrhosis, and/or liver failure)
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What is the pathopysh of alpha-1 antitrypsin deficiency?
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It is an enzyme that counteracts neutrophil elastase. In AAT deficiency, uninhibited elastase causes bullous changes in lungs -> classic CXR pattern is emphysematous changes in the lower lobes. The involvement is panlobular (vs centrilobular in smoking-induced). Can also cause liver disease
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What is the next step in suspicion for lung disease being high but CXR non-dx?
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CT
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What will PFTs in emphyseam show?
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Dec FEV1/FVC ratio, inc TLC, dec DLCO
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What is the first choice for inpt tx of CAP? Outpt?
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Inpt: Newer antipneumonal quinolones like levofloxacin or moxifloxacin (cipro doesn't have good strep coverage and doesn't cover atypical organisms). Outpt: Azithromycin or doxycycline
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How do you decide if pt with CAP needs to be admitted?
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Pneumonia Severity Index clinical rediction rule (stratifies adults with radiographic evidence of PNE into 5 classes for risk of death from all causes within 30d of presentations - based on medical history, PE, Labs, Radiographic findings)
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What is MCC of lobar CAP?
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Pneumococcus. Other causes: H. flu, Moraxella, etc.
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What is Bactrim DOC for?
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Uncomplicated cystitis and sinusitis
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When do you use vancomycin in PNA?
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Noscomial
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WHen do you use clindamycin in PNA?
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If suspicion for aspiration PNA (recent stroke, hx of unconsciousness (heavy alcohol user), recent sedation for procedures (endoscopy, etc))
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How can increase O2 in vent settings?
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Inc FiO2 or adding PEEP. Should add PEEP before FiO2 bc of risk of pulmonary O2 toxicity and bc want to keep FiO2 <40%
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How can dec CO2 in vent settings?
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Inc TV or RR
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What is the pathophys of ARDS?
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Diffuse injury to pulmonary capillary endotehlium and alveolar epithelium that results in leakage of protein-rich fluid into alveolar and interstitial spaces. Protein, cellular debris, and pulmonary surfacant in edema fluid aggregate within alveolar spaces to form hyaline membranes that themselves predispose to alveolar collapse and impaired pulmonary gas exchange
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What does ARDS do to O2 and how can fix it with vent settings?
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ARDS causes hypoxemia refractory to high inspired O2 concentrations. Adequate oxygenation in ARDS often requires PEEP.
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What is the criteria for long-term O2 therapy in COPD pts?
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1. All COPD pts with PaO2 <55mmHg or SaO2 <88% on room air. 2. Pts with cor pulmonale, evidence of PHTN or Hct <55% should be started on home O2 even when PaO2 is 56-69 with SaO2 >89%. 3. Home O2 can also be used in pts whose resting awake PaO2 >60 with SaO2 >90% if become hypoxic during exercise or sleep. Dosing: maintian >90% SaO2 during sleep, normal walking, and at rest. Survival benefits significant when O2 used for minimum of 15hrs per day
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What is the algorithm for the approach to pt with suspected PE?
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1. Stabilize with O2 and IVF 2. Contraindications to antigoactulation? If yes, do diagostic test to evaluate for PE and if positive, consider IVF (if neg, nothing needed) If no contraindications to anticoagulation, assess clinical suspicion for PE - if unlikely, do diagnostic test for PE first. If likely, assesss clinical suspicion with Modified wells and start anticoagulation now and get diagnostic test (if positive, continue anticoag and consider surgery or thrombolytics if indicated and stop anticoagulation if negative). 3717, 485039
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What should be your first step in pt with high clincal suspicion for PE?
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Start early empiric anticoagulation prior to pursuing confirmatory testing (LMWH or unfractionated heparin)
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What is diagnostic evaluation for PE?
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CT angiogram of chest in pts with stable creatinine and no contrast allergy
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When is D-dimer useful in PE?
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inital screening to exclude PE in pts with unlikely PE. Poor specificistiy and PPV but good sensitivity and NPV
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Why is a lower extremity doppler not helpful in pt with high clinical suspicion of PE?
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Bc doesn't rule out pt (could have a dislodged clot)
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What is the mainstay of symptom management in COPD?
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Inhaled anti-muscarinic (anti-cholinergic) agents - and when combined with short acting beta-agonists have greatest symptom relief
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What are the only proven therapies to prolong survival in pts with COPD?
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Smoking cessation, supplemental O2, and lung reduction surgery
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What are alpha blockers used for?
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BPH, HTN
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When are BB stafe in COPD and asthma?
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When COPD and asthma are mild-moderate
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When are dopamine agonists used?
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To treat parkinsons, prolactinomas, restless leg
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What are some alpha 2 agonists and what are they used for?
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Clonidine and methyldopa - HTN. Dexmedetomidine - ICU for sedation
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What is the lung exam findings in lung consolidation?
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Bronchial breath sounds (full expiratory wheeze), dullness to percussion, inc fremitus, bronchophony, egophony, and whispered pectoriloquy
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What is PE of PTX?
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Hyperresonance to percussion, dec/absent breath sounds, dec/absent fremitus, transmitted voice sounds
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What is PE of pleural effusion?
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Fluid in pleural space blocks sound transmission from air-filled lungs -> dullness to percussion, dec breath sounds, dec tactile fremitus, dec transmitted airway sounds
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What are PE findings in emphysema?
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Lung hyperinflation and airspace enlargement -> diffusely hyperresonant to percussion, breath sounds dec, fremitus and voice sounds dec, wheezing
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What are PE findings in asthmatics?
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Wheezing
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What happens to A-a gradient in interstitial lung disase?
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Increases due to dec diffusing capacity and V/Q mismatch
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What are the changes in lung volumes in restrictive lung disease?
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TLC, FRC, RV are all reduced. Flow volumes are also reduced by the ratio of FEV1/FVC is either normal or increased as alveolar fibrosis increases elastic recoil. Usually causes hypoxemia more than hypercarbia until late stages.
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How do pts with idiopathic pulmonary fibrosis present?
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It is a restrictive lung disease of unkown etiology. Chronic inflammation of alveolar walls -> progressive widespread fibrosis and destruction of normal lung architecture. Chronic progressive dyspnea, nonproductive cough, digital clubbing. Dry, end-inspiratory crackles. CXR: dec lung volumes, airway fibrosis giving "honeycomb" pattern, pulmonary vascular congstion most evident in hilum
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What is the MCC of daytime sleepiness in US?
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OSA - transient upper airway obstruction due ot poor pharyngeal muscle tone; pt continues to contract the diaphragm in an attempt to breathe, but airflow is impeded by upper airway obstruction
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What are risk factors for OSA?
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Obesity, tonsillar hypertrophy, hypothyroidism. Men > Women.
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What are symptoms and PE of OSA?
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Daytime sleepiness, morning headaches, impotence, poor judgement, dperession. Bed partners kept awake by snoring. PE: obseity, inc soft tissue in oropharynx. Labs: erythrocytosis
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What are complications of chronic OSA?
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Pulmonary HTN, RVF
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What is narcolepsy and what are symptoms?
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Poorly regulated REM sleep. Excessive daytime sleepiness, cataplexy, sleep attacks, pynagognic/hypnopompic hallucinations, sleep paralysis
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What is obesity hypovntilation syndrome? What ares symptoms and complications? How different from OSA?
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aka Pickwickian Syndrome; occurs when obesity impedes the expansion fo the chest and abd wall during breathing -> inc respiratory work and dec respiratory drive. Underventilation of the lungs during all hours -> chronically inc PaCO2 and reduced PaO2 (different from OSA which doesn't have chronic ABG changes). Eventually (same as OSA), get polycythemia, PHTN, RVF. Often have concomitant OSA
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What is central sleep apnea and how is it different OSA?
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Central sleep apnea occurs when the pt's central drive to initiate breaths is absent (so it is a neurologic rather than mechanical problem)
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What should suspect in pt with fever, foul-smelling productive cough after EGD or other instrumentation of upper airway or esophagus? How tx?
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Anaerobic lung infection. Tx with clindamycin
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What type of pneumonia does aspiration cause? What are symptoms?
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Anaerobic -> foul smelling sputum, fever, malaise
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Who are at inc risk for aspiration PNA?
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Poor dentition, recent EGD/upper airway instrummentation, alcoholics, dementia/AMS pts
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When dose aspiration PNA occur in lungs?
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dependent lung zones - posteiorr semgents of upper lobes (recumbent) and uperior and basilar segments of the lower lobes (standing)
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What kind of PNA is doxycycline good for?
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outpt CAP treatment where macrolide resistance is supected
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What does cipro cover?
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Gram neg but not anaerobic or most gram positive
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What is DOC for PCP?
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TMP-SMX - effective against many gram neg and gram pos agents but doesn't provide significant anaerobic coverage
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What does amp/gent combo cover and what is it used for?
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Gram neg anaerobes. Used for abd infections in combo with metronidazole
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What is the algorithm for evaluation of subacute and chronic cough?
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Subacute (3-8 weeks) or chronic (>8 weeks) cough -> History and physical -> (a) pt taking ACEI - stope ACEI (b) suspect postnasal drip, asthma, or GERD - treat etiology and if persistent cough, get CXR (c) suspect pulmonary parynchymal disease or no obvious etiology - CXR (d) purulent sputum, smoker, or immunocompromised - get CXR - if normal, consider empiric abx and if peristsent cough, evaluate and treat for asthma, GERD, non-asthmatic eosinophilic bronchitis, and chronic sinusitis. If CXR in these cases is normal, start on empiric oral 1st gen antihistmaine for post-nasal drip +/l nasal steroid or nasal antihistamine
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What are the 3 main causes of chronic cough in nonsmokers without pulmonary disease? How manage?
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Post-nasal drip (upper airway cough syndrome), GERD, asthma. If clear history of one of these, treat and stop ACEI if taking it
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How to treat post-nasal drip
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Empirically with oral first-gen antihistamien (ex: chlorpheniramine) or combo antihistmaine-decongestant (bromphiramine and pseudoephedrine). If pts dont' respond after 2-3 weeks, may require further investigation (sinus imaging, PFGs, CT of chest) and empiric sequential therapy for GERD, cough-variant asthma, chronic sinusitis, and non-ashtmatic eosinophilic bronchitis
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When is CXR indicated in chronic cough pt?
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pts without a clear etiology or with possible pulmonary parenchymal disease, immunocompromised condition, purulent sputum, or smoking history
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What will a fixed upper airway obstruction do to the lung flow curve?
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Dec air flow rate during inspiration (bottom line), active expiration, and passive expiration (top line)
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What is the treatment for anaphylaxis?
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Epi, systemic corticosteroids, antihistamines
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What are the airflow changes in asthma?
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Intrapulmonary obstruction - bronchosconstription decreases airflow during the passive phase of exhalation, causing flow-volume loops to have a "scooped out" pattern on exhalation
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What kind of flow pattern does PTX cause?
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PTX decreas ventilation of one hemithorax, causing a restrictive pattern on flow-volume testing.
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Does panic attack change flow rates?
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no
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What are criteria for ARDS?
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acute onset respiratory distress in setting of predisposing condition (sepsis, PNA, etc), PaO2/FiO2 ratio <200, bilateral infiltrates on CXR, and normal PCWP
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What are the most common causes of ARDS?
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sepsis, PNA, aspiration, toxic ingestions, truama, burns, alcoholism increaess risk, acute pancreatitis (15%)
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What is the pathophys of ARDS?
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Release of inflammatory mediators as a result of local or distant tissue injury. These inflammatory mediators cause alveolar damage, increased alveolar capillary permeability, and leakage of proteinaceous fluid into the alveoli.
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What are teh s/s of ARDS, what does ABG and CXR show?
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Acute onset tachypnea, tachycardia, fever, dyspnea. ABG: hypoxemia. CXR: biltateral infiltrates.
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How can differentiate ARDS from cardiogenic pulmonary edema?
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Both will have bilateral infiltrates on CXR and hypoxemia. So, use PCWP: <18 (normal) suggests ARDS whil >18 (abnormal) suggests cardiogenic pulmonary edema
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What do disease processes that cause edema or pulmonary fibrosis do to lung compliance?
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Decrease it (tx with PEEP)
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When do you see inc LVEDP?
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CHF caused by HTN or hypertrophic CM
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What happens to A-a gradient in ARDS?
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increased bc of shunting. (in contrast, hypoventilation and dec FiO2 cause hypoxemia with normal A-a gradient)
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Where is Legionella found? What does it cause? What are s/s, PE, CXR? What does gram stain look like? Dx? What treat with?
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Intracellular gram neg organism found in cooling towers and water supplies, relatively common cause (2-10%) of CAP, linked to cruise sips, hotel water supplies, travel. Distinguish from other causes of CAP by: high grade fever (>39), GI symptoms, neurologic symptoms. PE: rales. CXR: focal lobar pneumonia. Gram stain: Gram neg rod but stains poorly bc primarily intracellular - but showing many neutrophils and no organisms is characteristic. Dx: culure bacteria on charcoal agar and/or urine antigen testing. Tx: macrolides (azithro) or newer gen fluroquinolones (levoquin)
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What is fluconazole used to treat?
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anti-fungal, can tx pulmoanry cryptococcal infeciton
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How is mechanical ventilation managed in pt with ARDS?
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Provides oxygenation by increasing FiO2 and providing PEEP to prevent alveolar collapse. The first step in inital ventilator management of ARDS is usually to decrease the FiO2 to relatively non-toxic levels (once adequate PaO2) - PEEP may need to be increased as needed to maintain adequate oxygenation after FiO2 lowered
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How is the diagnosis of upper-airway cough syndrome confirmed?
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Elimination of nasal discharge and cough with use of H1 histamine receptor antagonists (ex: chlorpheniramine - in addition to blocking H1 histamine receptors, chlorpheniramine exhibits anti-inflammatory effects by blocking histamine release from mast cells and limiting the secretory response to inflammatory cytokines)
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What is upper-airway cough syndrome?
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Caused by rhinosinus conditions including allergic, perennial nonallergic, and vasomotor rhinitis; acute nasopharyngitis; and sinusitis. Cough is caused by mechanical stimulation of the afferent limb of the cough relfex in the upper airway in these conditions
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How does acid reflex cause chronic cough? How is it treated?
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Acid reflux can irritate the cough reflex and is a common cause of chronic cough. EMpiric therapy of GERD includes dietary and lifestyle modifications and PPIs, which suppress stomach acid secretion.
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How does asthma cause chronic cough and how do you treat?
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Variable and recurring symptoms, airflow obstruction, bronchial inflammation, and airway hyperreactivity. Empiric treatment involves inhaled corticosteroids, which reduce airway inflammatio, and beta-adrenergic agonists, which dilate bronchial smooth muscle.
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How do ACEI cause chronic dry cough?
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(5-20%). ACE inhibition causes dec degradation of bradykinin and substance P -> accumulation of these causes cough. Only improves with discontinuation of ACEI
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What is the most common cause of death from envenomation?
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Bee stings
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How do you first treat anaphylactic shock?
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Any cause should promptly be treated with IM epinephrine to acutely prevent respiratory distress and circulatory collapse
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What are the s/s of anaphylaxis and what causes it? How do you treat it?
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Hives, flushing, pruritis, swollen lips/tongue after allergic exposure that can cause either respiratory distress (dyspnea, wheezing, stridor, hypoxia) or hypotension. Usulaly have piror exposure to the offending agent (most commonly bee stings, food, meds) -> therefore, they have preformed IgE to cause type 1 HSR with widespread histmaine-mediated peripheral vasodilation, hypotension, and ultimately circulatory collapse. It is a medical emergency. 1st step in tx: IM epi. If doesn't respond, can give IV epi. Other therapies as adjuncts to epi: H1 antihistamines (for skin symptoms - pruritis, hives) but don't help respiratory symptoms or shock. Nebulized bronchodilators (albuterol) can be given if have persistent bronchospasm after getting epi, but doens't prevent or relieve upper airway mucosal edema or shock. Steroids - no immediate effect but can prevent relapse and can be given after epi
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Why is IM epi used as first line in anaphylaxis?
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Higher plasma and tissue levels than subQ. Epi has both alpha nad beta adrenergic effects to inc vasoconstriciton and bronchial SM relaxation, decrease vascular permeability, and inc bronchodilation to offset the primary pathophysiologic disturbances in anaphylaxis. IF symptoms are severe or pt doesn't respond to IM epi, can give IV
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When is dopamine effective in shock?
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"cold" septic shock (hypotension, low SVR, hypoperfusion of extremities cool to touch). Dopamine at low doses acts on D1 receptors to vasodilate and improve renal flow. Higher doses act on b1 and alpha adrenergic receptors to inc CO and vasoconstriction
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What are the complications of ventilation with a high PEEP?
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Alveolar damage, tension PTX, hypotension. Delivery of high pressure ventilation can rupture fragile lung parenchyma -> PTX which can lead to compression of mediastinum and impraired RV filling -> hypotension, tachycardia
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How does tension PTX present?
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Sudden onset SOB, hypotension, tachycardia, tracheal deviation, unilateral absence of breath sounds
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How does PEEP help in ARDS?
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helps maintain airway pressures above atmospheric pressure at the end of expiration to counteract alveolar collapse and inc FRC and dec work of breathing.
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How do pts with atelectasis present?
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Cough, dyspnea, dec O2 saturation
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What are classic findings of PE?
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Sudden onset SOB, pleuritic CP, hypoxia, tachypnea, tachycardia
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What is the mechanism of exudative and transudative pleural effusion?
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Exudative: inc capillary permeability (which allows protein and LDH to pass into pleural fluid). Transudative: inc hydrostatic or dec oncotic pressure
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What are causes of exudative pleural effusions?
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Infection, autoimmune disease (ex: sarcoid, RA), neoplasm, sometimes PE
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What is common cause of transudative pleural effusion with dec plasma oncotic pressure?
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Liver failure
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What is a common cause of elevated hydrostatic pressure and transudative pleural effusion?
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CHF
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Is PHTN itself often assoc with pleural effusions?
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No - but can be secondary to PE (usually transudative in this case)
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What symptoms should raise suspicion for OSA?
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Snoring, daytime sleepiness, apneic episodes during sleep. HTN, heart disease, cor pulmonale, impotence, depression and accidents are risks/complications assoc with OSA
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How dx OSA?
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Nocturnal polysomnography
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What are risk factors for OSA?
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most common in middle-aged men. Obesity, abnormalities of upper airway (tonsillar hypertrophy, excessive soft tissue, micrognathia)
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What are CNS stimulants used to treat in sleep disorders?
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(ex: methylphenidate). Narcolepsy
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When can surgery for OSA be considered?
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Only when CPAP, oral appliances, and wt loss have been proven ineffective
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What is the dexamethasone suppresion test used for?
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To diagnose cushings syndrome
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When is a D-dimer helpful in excluding pulmonary venous thromboembolism?
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in low risk pts, negative D-dimer helpful. But positive D-dimer is far from diagnostic and must be followed by more specific studies
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What is D-Dimer?
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Fibrin degradation product elevated in presence of blood clots and a number of inflammatory conditions
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What would ECHO show in large PE?
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Pulmonary PHTN and/or evidence of right heart strain (but only in large PEs)
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What are classic CXR findings in pts with PE?
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Often have normal CXR, but classic findings include pleural-based densities representing lung infarction (Hampton's hump) and a prominent central pulmonary artery with local oligemia (Westermark's sign)
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How useful is venous US for diagnosing proximal deep vein thromboses?
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Both sensitive and specific, but only 70% of pts with PE have detectable DVT so a normal venous US of legs can't exlude PE
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What is the classic (but very uncommon) EKG in PE?
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S1Q3T3 (S wave in lead I, Q wave in lead III and T wave inversion in lead III)
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What is the definition of pulmonary HTN?
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Mean pulmonary arterial pressure >25mmHg at rest or 30mmHg with exercise). It is seen following hte narrowing of precapillary vessels, the loss of the pulmonary capillary bed, or passive backpressure from the post-capillary vessels from any cause
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What are the 5 classifications of pulmonary HTN?
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1. Assoc with disorders of respiratory system, hypoxemia, or both 2. Due to pulmonary venous HTN (LV disease, MV disease, or pulmonary veno-occlusive disease) 3. Following chronic thromboembolic diseae 4. Primary PHTN, pulmonary HTN assoc with vasculopathy 5. Due to disorders directly affecting the pulmonary vasculature (pulmonary capillary hemangiomatosis). But note taht features of PHTN are the same regardless of underlying cause (s/s)
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What are common clinical features of PHTN?
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Dypsnea, weakness, fatigue are early complaints. May be followed by CP, hemoptysis, syncope, or hoarseness (due to compression of recurrent laryngeal nerve). RVF develops late in the disease and manifests with RV heave, JVD, tender hepatomegaly, ascites, eema, etc.
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What does CXR of PHTN show?
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Enlargement of pulmonary arteries with rapid tapering of the distal vessels (pruining) and enlargement of RV.
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What can EKG show in PHTN?
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R-axis deviation, which is secondary to RV strain and hypertrophy due to PHTN.
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What does untreated PHTN eventually lead to?
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Cor pulmonale
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When do you most often see primary PHTN? How does it present and what do CXR and EKG show?
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middle-aged adults. Presents with exertional breathlessness and clear lungs. CXR: enlargement of pulmonary arteries with tapering of the distal vessels (pruning) and enlargement of the RV.
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What are the 2 lung diseases that are very common in pts with long smoking hx
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Chronic bronchitis and emphysema/COPD (10-15% of smokers develop COPD, but 80-90% of pts with COPD are smokers)
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What are the only 2 treatments taht dec mortality in COPD pts?
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Smoking cessation, home O2 therapy
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When are long acting beta-agonists used in pts with COPD?
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More advanced disease
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When are systemic steroids useful in COPD?
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Short term basis during acute exacerbations
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What is the MCC of superior vena cava syndrome?
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Malignancy - lung cancer (esp small cell) and non-hodgkin's lymphoma. Other possible causes: fibrosing mediastinitis (secondary to histoplasmosis or TB) or thrombosis secondary to indwelling central venous devices
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When suspect SVC syndrome, what is next test?
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CXR - can identify cause in >80% of cases. Follow-up with Chest CT and histology to determine tumor type and guide therapy
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What are the s/s of SVC syndrome?
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Obstruction of SVC impedes venous return from the head, neck, and arms to the heart. S/S: dyspnea, venous congestion, swelling of head, neck, and arms
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When is upper extremity US doppler indicated?
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Unexplained unilateral arm swelling
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When is 24-hr urinary protein excretion helpful?
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Assessing for nephrotic syndrome
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What is the most likely cause of acute-onset cough produtive of yellow, blood-tinged suputum in a young afebrile pt with no smoking history
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Hemoptysis in this cause is likely due to acute bronchitis - this dx supported by lack of history and PE supportive of more serious condition and by no maliase and sore throat and no fever
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What usually causes acute bronchitis and how do you treat?
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MC is viral -> no abx. CLose obstervation and follow up
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When is CT of chest in pts with hemoptysis indicated?
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When PE, mass lesions, bronchiectasis, or vascular malformations are suspected
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When are sputum gram stain and culture, acid fast stain, and cytology useful?
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Gram stain and culture: PNA. AFB stain: TB. Cytology: pulmonary malignancy
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When is bronchoscopy indicated in hemoptysis?
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Recurrent episodes to assess for mass lesions of airway and in cases where diagnosis is unclear with high-res CT
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What are COPD exacerbations classically caused by?
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URT infection (bacterial or viral) and may be preceded by cough and fever. Present with cough and SOB
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What are PE and ABG findings in COPD exacerbation?
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Bilateral wheezes, accessory respiratory muscle use, and prolonged expiratoyr phase and ABG findings of respiratory acidosis and hypoxia, hypercapnea
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What does CHF exacerbation present like?
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Exertional dyspnea, orthopnea, and chronic nonproductive cough. Gallops on cardiac auscultation, bibasilar crackles with basilar dullness to percussion, peripheral edema, and signs of fluid overlad. Hypoxemia with respiratory alkalosis (vs acidosis in COPD exacerbation) with widened A-a gradient
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What happens to ABG and A-a gradient in PE?
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Hypoxemia and respiratory alkalsosi with widened A-a gradient (like CHF exacerbation)
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What does ARDS clinically manifest as (s/s, PE, CXR)
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Acute onset marked respiratory distress with tachypnea. Rales throughout lung fields, hypoxemia is severe and unresponsive to supplemental oxygen. CXR: diffuse bilateral interstitial and alveolar infiltrates.
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What type of ventilation can panic attacks be assoc with and what does ABG show?
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Hyperventilation leading to sensation of faintness. ABG shows hypercapnia and alkalosis but no hypoxia
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What kind of pulmonary edema is ARDS?
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non-cardiogenic - release of inflammatory mediators causes inc alveolar capillary permeability and resultant pulmonary edema.
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What are the criteria for dx ARDS?
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acute dyspnea, an inciting condition, bilateral infiltrates on CXR, PCWP <18, PaO2/FiO2 <200
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What are some causes of ARDS?
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Sepsis, severe bleeding, trauma, toxic injury
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How can differnetiate cardiogenic vs non-cardiogenic pulmonary edema using PCWP?
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PCWP >18 suggests pulmonary edema secondary to impaired LV function. PCWP <18 suggest snon-cardiogenic (ex: ARDS)
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How does idiopathic pulmonary fibrosis present? CXR?
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Gradual onset cough, dyspnea, crackles, clubbing. CXR: dec lung volumes and interstitial prominence, esp at bases.
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What happens to PCWP in fluid overload in CHF?
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INcreases bc pulmonary edema accumulates as a result of congestion and elevated hydrostatic pressure rather than from inc alveolar capillary permeability
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What is the background story of most cases of active TB in US?
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Pts who immigrated to US from endemic geographic regions
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How does reactivation of TB present?
|
Chronic low-grade fever, night sweats, wt loss, productive cough with blood-tinged sputum CXR: Apical cavitary lesion
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What is smoking a risk factor for?
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Occlusive arterial disease, various forms of cancer including squamous and small cell lung as well as pancreatic cancer and cancers of upper aerodigestive tract
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What is Hep C a risk factor for?
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Hepatocellular carcinoma, cirrhosis, lichen planus, porphyria cutanea tarda, cyroglobulinemia, glomerulonephritis
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What is included in ddx of recurrent bacterial infections in adult pt? What is workup?
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Recurrent bacterial infections is highly suggestive of immunodeficiency with involvement of humoral immunity. Selective Ig deficiency that includes IgA or IgG is possible. Dx: quantitiative measurement of serum Ig levels
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What is methacholine challenge used for?
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to Dx asthma
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How does a pt with hypercapnic respiratory failure due to COPD maintain a normal pH?
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Kidneys increase bicarb retention to compenstae for inc pCO2. Importantly, pts don't typically normalize or overcorrect their pH
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What is minut ventilation?
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TV x RR = MV.
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What happens to dead space in COPD?
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Increased
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What happens to pulmonary vasculature when have alveolar hypoxia?
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Pulmonary vasoconstriction -> normalizes shunting and V/Q mismatching in lung
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What is the purpose of shift of bicarb out of and chloride into RBC?
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Carbon dioxide transport
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What type of tumors cause both inc AFP and HCG?
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Nonseminoatmous germ cell tumors - don't have to just be in testicles, can present in other parts of body as well (HCG elevated in both seminomatous and nonseminomatous germ cell tumors, but nonseminomatous also produce AFP). Can start therapy without tissue bx
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What are benign teratomas?
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Includes tissue from all 3 germ layers and doesn't produce tumor markers
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How do pericardial cysts present?
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Most are asymptomatic
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What are thymomas commonly assoc with?
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Myasthenia gravis, pemphigus
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What is the tumor marker for HCC?
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AFP
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What is a choriocarcinoma?
|
Form of gestational trophoblastic disease that classically occurs in setting of molar pregnancy. HCG levels are very high
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What is the pathophys of massive/submassive PE?
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Massive PE -> RV outflow obstruction, inc RV pressure -> RV hypokinesis and dilation -> dec RV CO and septal deviation toward LV -> dec LV preload and CO -> dec coronary perfusion and dec RV myocardial supply -> RV ischemia and infarction -> RV hypokinesis and dilation (cycle). Also, RV outflow obstruction and inc RV pressure causes inc RV wall tension and inc RV myocardial O2 demand, resulting in RV ischemia and infarction
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What are the s/s of massive PE?
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Low arterial perfusion (hypotension, syncope) and acute dyspnea, pleuritic CP, tachycardia. PE can show an accentuated pulmonic component of the second herat sound and elevated central venous pressure (ex: high JVP)
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What are predictive factors of poor surivival in pts with PE?
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RV dysfunction, elevated BNP and troponin levels
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What will see on PE in pts with acute AR (ex: as a complication of MI) and cardiogenic shock?
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Flash pulmonary edema with crackles on exam
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What can see in acute massive PE on EKG?
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New RBBB, RV strain pattersn
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What type of cancers do you usually see maligant pericardial effusions in?
|
Lung cancers
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What does TPTX look like on PE?
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Hypotension, elevated JVP, dec breath sounds in that hemithorax
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What should do to treat pts with DVT in whom anticoagulation is contraindicated?
|
IVC filter to prevent PE (while there is some debate about their long-term effectiveness, they have been proven to prevent PE in pts with DVT in the acute setting)
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What are the contraindications to anticoagulation?
|
Recent surgery, hemorrhagic stroke, bleeding diathesis, active bleeding, history of complications from anticoagulation (ex: HIT)
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How are most pts with DVT treated?
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Acutely with heparin and then managed with warfarin over long term to prevent PE
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What is the first line treatment for isolated exercise-induced asthma?
|
Short acting beta adrenergic agonists administered 20min before exercise. (LABA can be used in children or in athletes who engage in athletic events throughout the day)
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What is the trigger of exercise-induced asthma?
|
High minue ventilation of dry, cold air which stimulates mast cell degranulation and airway constriction
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When are daily oral steroids indicated in asthma?
|
Only in severe persistent (continuous daytime symptoms, frequent nighttime symptoms, FEV1 <60% of predicted)
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When are daily steroid inhalers indicated in asthma?
|
They are the preferred treatment for mild persistent asthma, which is characterized by more than 2 episodes per week and more than 2 nighttime episodes per month
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When is oral theophylline used in asthma?
|
Can be used as an alternative tx for any form of asthma other than mild intermittent
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When are ipratropium inhalers used in asthma?
|
When combined with beta-adrenergic agonists for additive bronchodilator effect. Ipratropium is more effective in pts with COPD than asthma
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What is the recommended therapy for acute bacterial exacerbation of COPD?
|
Supplemental O2, inhaled bronchodilators (b2 agonists and anticholinergics), broad spectrum abx, 2 week steroid taper, somking cessation
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Why are steroids useful in COPD exacerbation?
|
Proven to shorten hospital stay and prolong intervals between exacerbations. Likely beneficial bc they reduce inflammation and reacive edema in the bronchial mucosa.
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Why should be careful in givin O2 to chronically hypoxic pts?
|
Can suppress hypoxia-fueled respiratory drive
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What is airway obstruction in COPD mainly due to?
|
Infections/inflammatory mucosal edema, bronchial SM hypertrophy and bronchial submucosal gland hyperplasia
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What are aminophylline and methylxanthines and what do they do for asthma?
|
Bronchodilators
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What are cromolyn sodium and luekotriene inhibitors useful for in asthma?
|
Acute exacerbations but not first line
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What is the formula for ventilation?
|
RR x TV
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What is the change in ventilation that causes respiratory alkalosis?
|
Hyperventilation
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What is the management of pt that is mechanically ventilated with respiratory alkalosis?
|
If tidal volume is appropriate, then dec RR (reductions in TV can trigger inc ventilatory rate which can worsen the situation)
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What is assist-control mode of mechanical ventilation?
|
Delivers a predetermined TV with every breath. Inspiratory cycles can be initiated by the pt, but if the pt fails to breathe at a set minimum rate, then the ventilator will deliver the TV on its own.
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What should tidal volume be?
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~6mL/kg of ideal body weight
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How does bronchodilator therapy help pts with obstructive lung disease?
|
Helps conduct inspired air from trachea to alveoli
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What is incentive spirometry used for?
|
To prevent atelectasis in bed-bound pts, esp after surgery
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What is chest physiotherapy used for?
|
PNA or atelectasis to loosen and promote expectoration of secretions. Pts with bronchiectasis require long-term chest physiotherapy
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When is tracheostomy indicated?
|
If prolonged intubation is foreseen or if pt has difficulty miantaining airway patency and/or managing airway secretions following weaning from mechanical ventilation
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What is aspirgilloma and what do you see on PE and CXR?
|
Fungal infection with coarse fragmented septae. Hyphae typically seen. CXR: crescent radiolucency next to a rounded mass. Cavity lersions can form bc of destruction of the underlying pulmonary parenchyma and debris and hyphae may oalesce and form a fungus ball which lies free in the cavity and moves around with positional change
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Why do lung abscesses occur and who do they occur in? What do you see on CXR and how do you treat?
|
Infection behind a blocked bronchus. Usually due to anaerobes, may be assoc with alcohol abuse or aspiration. Pt appears sick with elevated WBC. CXR: Air fluid level. Mgt: abx, postural drainage, bronchoscopy. The incidence is decreasing with use of abx
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What can see on EKG in PE?
|
RVH, RBBB, right axis deviation, T wave inversions in anterior leads
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What does CXR show in PE?
|
Can be normal or show dec pulmonary vascular markngs or enlarged R descending pulmonary artery
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What is the most common fungal infection in the US?
|
Histoplasmosis
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What kind of an infection is histoplasmosis and how do you get it? What are complications and how is it treated? CXR?
|
Yeast infection, acquired by inhalation. Usually resolves without treatment. Calcified nodes in lung, mediastinum, spleen, and liver may occur. CXR: central or target calcification, solitary nodule may be seen. Can occasionally get mediastinal LN enlargement with lymphogenous reaction to Histoplasma. No cavitary lesions
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What is bronchiectasis? How do you dx and tx?
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Infection of bronchial wall and surrounding lung with sufficient severity to cause destruction and dilation of airways. Usually basal segments of lower lobes infected. Dx: CT scan. Tx: stop smoking, postural drainage, bronchodilator therapy, abx
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What is the algorithm for solitary pulmonary nodule (<3cm)
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If high malignancy risk (older age, smoking, corona radiate or spiculated appearance of nodule, history of cancer, irregular borders, poorly defined) -> surgical excision. If intermediate probability and <1cm get serial CT scans but of >1cm get FDG-PET scan (18-fluorodeoxyglucose positron emission tomography) and if suspicious for malignancy do surgical excision and if not, serial CT scans. If low risk for malignancy, get serial CT scans (4252)
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What is the cause of the majority of benign nodules presenting as solitary pulmonary nodules
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Infectious granulomas (histoplasmosis, coccidio, TB)
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What are the most common bugs to cause acute exacerbation of COPD?
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Strep pneumo, H flu, M catarrhalis
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In pt with suspected bacterial PNA, what is first step and when should give abx?
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CXR. Start abx asap without waiting for sputum gram stain or cultures to come back
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When is bronchoscopy useful in respiratory infections?
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PCP PNA, fungal infections
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What type of PNA does mycoplasma cause?
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Atypical - fever, dry cough, bilateral perihilar infiltrates. No serology needed - empiric abx cover it (azithro, levo)
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What does bronchiectasis look like on CT?
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Dilated bronchi with thickened walls
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How do pts with bronchiectasis present and what is a potential complication?
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Chronic productive cough often treated with repeated courses of abx (similar to COPD bc abnormal airways cause obstructive signs and symptoms. Can have hemoptysis sometimes to the point of requiring bronchial artery embolization
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What pulmonary complication are bullae assoc with?
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Pneumothorax
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What are the manifesations of sarcoidosis?
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Lungs: bilateral hilar adenopathy, interstitial infiltrates. Eyes: anterior uveitis (iridocyclitis or iritis), posterior uveitis. Rediculoendothelial: peripheral LAD, hepatomegaly, splenomegaly. MSK: acute polyarthritis (esp ankle joints), chronic arthritsi with periosteal bone resorption. CNS/endocrine: central DI, hyperCa. Lofgren's syndrome: erythema nodosum, hilar adenopathy, migratory polyarthralgias, fever
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What is the pathophys of sarcoidosis?
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Chronic multisystem d/o due to noncaseating granulomatous inflammaiton deposited into various organs
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Who is more common to have sarcoid and what are s/s?
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Young adults, 3-4x more common in blacks, F>M. Frequently detected incidentally on CXR but can show s/s such as cough, dyspnea, fever, malaise, wt loss. Mainly involves lungs. ACEI and Ca are often elevated
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How dx sarcoidsois?
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Definitively with mediastinoscopy/bronchoscopy for tissue bx. Symptomatic pts treated with steroids
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What are the medium-sized vasculitises?
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Polyarternitis nodosa, Kawasaki, primary CNS vasculitis
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When do you see pulmonary venous congestion on CXR?
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CHF (also see cardiomegaly, cephalization of pulmoanry vessels with prominent vascular markings, Kerley B lines, pleural effusions.
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What is asbestosis?
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Pneumoconiosis resulting from inhalation of particles involved in industrial processes.
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What are s/s of asbestosis, what do PFTs show, and what does imaging show?
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Progressive dyspnea, clubbing, end-inspiratory crackles. PFTs: RESTRICTIVE lung disease pattern with dec LV, dec DLCO, normal FEV1/FVC ratio. Imaging: pleural plaques
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What are the clinical features of asbestosis?
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Prolonged asbestos exposure (shipyard, mining and construction workers, pipe fitters), symptoms develop >20rs after initial exposure, progressive dyspnea (over months) bibasilar end-inspiratory fine crackles and clubbing, inc risk for malignancies (lung cancer, malignant mesothelioma)
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What is the diagnostic evaluation of asbestosis?
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History and clinical findings (ex: pleural plaques on chest imaging virtually pathognomonic), interstital fibrosis on imaging or histology and/or PFTs with restrictive pattern, exclusion of other diseases
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What is PCWP?
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Indicator of L arterial pressure. Elevated PCWP in setting of dyspnea confirms cardiac origin.
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What are the changes in RV in different lung disorders?
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(amt of air remaining after max exhalation). Inc in obstrucitve lung disease (asthma, COPD, bronchiectasis) and normal or decreased in restrictive lung diseases
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What is a normal FEV1/FVC ratio?
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>80%. Normal in restrictive lung disease (although FEV1 and FVC on their own may be reduced), reduced in obstructive
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What are the cirteria for long-term supplemental O2 therapy?
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PaO2 <55, SaO2 <88%, erythrocytosis (Hct >55%), evidence of cor pulmonale
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What is hypersensitivity pneumonitis? What are s/s and management? What does CXR show?
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Inflammation of lung parenchyma caused by antigen exposure (commonly aerosolized bird droppings ad molds assoc with farming). Acute episodes present with cough, breathlessness, fever, malaise within 4-6hrs of antigenic exposure. Chronic episodes can cause wt loss, clubbing, honeycombing of the lung. Management: avoidance of responsible antigen CXR: ground glass opacity or "haziness" of lower lung fields.
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What is the main complication of hypersensitivity pneumonitis?
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Progressive pulmonary fibrosis
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In pt with acute exacerbation of COPD refractory to standard initial managment of aerosolized bronchodilators but is not crashing - what should do next?
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Non-invasive postitive pressure ventilatoin before going to intubation. NIPPV has dec complications that are hallmakr of intubation, including infections. NIPPV recommended in pt with respiratory distress with pH <7.35 or PaCO2 >45 or RR >25. But, contraindicated in pts that are septic, hypotenisve, or dysrhythmic
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What are the changes in ascultation, tactile fremitus, percussion, and mediastinal shift in consolidation of lung?
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Crackles/bronchial breath sounds/bronchophony, egophony, pectoriloquy; inc TF at consolidation site; dullness to percussion; no mediastinal shift
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What are the changes in auscultation, tactile fremitus, percussion, and mediastinal shift in pleural effusion?
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Dec BS, dec TF, dullness to percussion, mediastinal shift away from effusion (in large effusion)
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WHat are changes in auscultation, tactile fremitus, percussion, and medistinal shift in COPD?
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Dec BS, dec TF, hyperresonant to percussion (esp if large bullae), no mediastinal shift
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What are changes in auscultation, tactile fremitus, percussion, and mediastinal shift in pneumothorax?
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Dec BS, dec TF, hyperresonant to percussion, mediastinal shift away from PTX of tension, no shift if small
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What type of organism is Klebsiella?
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Encapsulated gram neg bacillus
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What is Friedlander's pneumonia?
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Klebsiella pneumonia -most frequently affects the upper lobe and produces currant jelly-like suputum with tissue necrosis and early abscess formation and fulminant course. Common in alcoholics, grows as mucoid colonies
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What are the common gram neg bacteria that cause pneumonia?
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E. coli, Klebsiella, Pseudomonas, Enterobacter, Proteus, Serratia, Acinetobacter. Rare in healthy indivutals and usally occur in infants, elderly, alcoholics, immunocompromised pts (esp with neutropenia). Usually colonize oropharynx then microaspiration of upper airway secretions
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What does gram stain of mycoplasma PNA show?
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Sparse bacteria, mix of PMNs and mononuclear cells, clumps of desquamated respiratory epithelial cells.
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What type of bacteria is pseudoomas and what does it cause?
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Gram neg bacillus, very common cause of nosocomial infection. Generally seen in pts with CF, neutropenia, advanced AIDS, bronchiectasis, and pneumonias acquired in ICU. It is encapsulated
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How does CHF exacerbation cause its symptoms?
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CHF -> tachypnea as LV dysfunction allows fluid to pool in the lungs -> pleural effusion and hypoxemia due to reduced ventilation. Tachypnea causes hypocapnia and respiratory alkalosis
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What are PE findings of CHF exacerbation?
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Fluid overload, S3 and S4 gallops, cardiomegaly, bibasilar crackles, dec breath sounds if have pleural effusions, can have wheezing (cardiac asthma)
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What are blood gas findings of CHF exacerbation?
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Hypoxia, hypocapnia, respiratory alkalosis (vs COPD which has resp acidosis with hypercapnia)
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What tests can help distinguish COPD vs CHF exacerbation?
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BNP, PCWP (high in CHF, nL in COPD)
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What does ABG and A-a gradient show in PE?
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Hypoxemia, resp alkalosis, wide A-a gradient
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What is PE of PTX?
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Hyperresonance to percussion, dec tactile and vocal fremitus, dec/absent preath sounds on affected side
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What is the formula for peak airway pressure (max prssure measured as tidal volume is being delivered)
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Peak airway pressure = resistive pressure + plateau pressure. Plateau pressure (pressure measured during an inspiratory hold maneuver when pulmonary airflow and therefore resistive pressure are 0; it represents the sum of the elastic pressure and the PEEP; elastic pressure = lung elastance x volume of gast delivered (elastic recoil is inversely related to lung compliance -> elastic pressure = TV/compliance); dec compliance (ex: pulmonary fibrosis) causes stiffer lungs and therefore stiffer lungs and higher elastic pressure. 4713
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What does inc peak pressure assoc with an unchanged plateau pressure suggest?
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Pathologic processes causing inc airway resistance such as bronchospasm, mucus plug, or ET tube obstruction 4713
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What does elevation of both peak and plateau pressures suggest?
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Process causing dec pulmonary compliance, such as pulmonary edema, atelectasis, PNA, or R mainstem bronchus 4713
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How do you measure expiratory muscle strength?
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Using forced VC and max expiratory pressure
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What does the end-expiratory hold maneuver measure?
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auto-PEEP (intrinsic PEEP) - useful in obstructive lung diseases where the alveoli can't empty completely, resulting in higher than normal end-expiratory pressures
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What is the goal INR for warfarin for idiopathic VTE or afib?
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2-3 (provides adequate anticoagulation without excessive risk of bleeding)
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What should pts with DVT be treated with?
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Acutely with heparin - then continue with warfarin for at least 3mo in pts with reversible risk factor and 6-12mo in pts with idiopathic DVT
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How does warfarin work?
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Inhibits vit K-dependent coag factors (II, VII, IX, X) of the extrinsic clotting pathway (reflected in PT)
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What is the goal INR in pts with prosthetic heart valves?
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2.5-3.5
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When is the bleeding risk for warfarin significantly increased?
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when INR >4
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What are signs of R mainstem bronchus intubation?
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Asymmetric chest expansion during inspiration and markedly dec or absent breath sounds on the L side; fix by repositioning ET tube back slightly to move the tip between the carina and vocal cords. Relatively common complication.
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What are s/s of cardiac tamponade?
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Hypotension, distended neck veins, pulsus paradoxus, muffled heart sounds
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When do you use chest tube, needle thoracostomy, tension PTX, pericardiocntesis?
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CT: PTX, hemothorax, empyema, malignant effusion. Needle thoracostomy: emergency for PTX; pericardiocentesisi: cardiac tamponade or large pericardial effusion
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What are the effects of Goodpastures disease and who is it common in? How do you dx?
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Most common in young males; lungs (cough, dyspnea, hemoptysis), kidneys (nephritic range proteinuria, acute renal failure, dysmorphic red cells/RBC casts on UA); systemic symptoms are uncommon (fever, wt loss, arthralgia. Dx: renal bx showing linear IgG Ab (they are Ab to the alpha-3 chain of type IV collagen, a protien expressed most strongly in the glomuar and alveolar BM) along the basement membrane on immunofluorescence.
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How can TB and amylodiosis cause kidney symptoms?
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TB: dysuria, hematuria. Secondary amyloidosis: nephrotic range proteinuria
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What are s/s of endocarditis?
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Almost all have prominent systemic symptoms (feer, chills, dyspnea, sweats, weakness) + new onset heart murmur, Osler's nodes, Roth's spots, Janeway lesions, splinter hemorrhages. Can have septic emboli to almost any organ, causing a range of organ symptoms
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What is cor pulmonale?
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RHF due to pulmonary disease (MC COPD but less commonly pneumoconiosis, pulmonary fibrosis, kyphoscolisois, primary PHTN, recurrent PE)
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What are signs of RHF?
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JVD, right-sided S3, RV heave, hepatomegaly, ascites, dependent edema
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If dyspnea were caused by LV falure, what would you see on PE and CXR?
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Rales/crackles + signs of significant pulmonary congestion in CXR
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WHat are the common symptoms of compensated cor pulmonary related to pulmonary disorder?
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Chronic cough, exertional dyspnea, wheezing, fatiguability. When pulmonary disease severe enough to cause RV dysfunciton, signs of R-sided heart failure develop (JVD, R-sided S3, RV heave, hepatomegaly, ascites, dependent edema). CXR: prominent RV and pulmonary artery in addition to any lung disease that can be visualized
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What does alcoholic cirrhosis look like on exam?
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Small, firm fibrosed liver (rather than hepatomegaly)
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What will mets to the liver look like on PE?
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Uusally irregular hepatomegaly (if it does cause hepatomegaly)
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What are pts with acute-on-chronic resp failure that are treated with high-flow supplemental O2 at risk for?
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Worsening hypercapnia and CO2 narcosis (due to combo of reduced alveolar ventilation, inc dead space ventilation causing ventilation-perfusion mismatch, and dec Hb affinity for CO2. Goal oxyHb saturation is 90-94% (not >95%)
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What is the effect of excess O2 therapy in COPD pts in terms of inc dead space?
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At baseline: poorly ventilated and low-oxygen areas (dead space) of the lung, localized vasoconstriction directing blood to higher ventilation/perfusion. WIth excess oxygen: vasodilation that redirects blood flow to poorly ventilated areas, dec CO2 excretion, worsened V/P mismatch 4718
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What is the effect of excess O2 therapy in COPD pts in terms of Haldane effect?
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At baseline: inc deoxygenated Hb with inc CO2 affinity; inc CO2 lung excretion. With excess O2: Inc oxyenated Bc with dec CO2 affinity; dec CO2 excretion leading to hypercapnia 4718
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What is the effect of excess O2 therapy in COPD pts in terms of dec minute ventilation?
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At baseline: shift in respiratory drive from hypercapnic to hypoxic. With excess O2: acute inc in O2 can blunt hypoxic respiratoyr drive 4718
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What are the clinical effects of acute hypercapnia?
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Dec level of consciousness, dec seizures threshold, dec myocardial contractility.
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What does acute hypercapnia due to cerebral vasculature?
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Causes cerebral vasodilation and increases cerebral blood flow
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What type of acidosis is more common in COPD?
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Respiratory
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What are most subarachnoid hemorrahges caused by?
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Ruptured aneurysm or bleeding form intracranial vascular malformations. Presents with severe HA, nausea, vomiting
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What is protocol for acute venous thromboemboli?
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Start with combo of heparin (LMWH or unfractionated) and warfarin and after 5 days, d/c warfarin if INR is therapeutic. Warfarin should be continued for at least 6mo for first time clot (after second time, antigoaculation for life)
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How does heparin work in venous thromboebolism management?
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several functions in acute setting: first, retards additional thrombus formation by binding to antithrombin III and enhancing its activity. This helps stabilize, but not lyse, the clot. Second, provides anticoagulaiton until warfarin achieves therapeutic levels. Warfarin inhibits vit K dependent clotting factors, but the firs tto be affected are protein C and S, which are actually anti-thrombotic - so, in the absence of a second anticoagulatn, warfarin may initiaily be thrombogenic.
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What does R cath in pts with massive PE show?
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Elevated R arterial and pulmonary artery pressures with normal PCWP . Depending on the size of embolus, PE can occlude part of the pulmonary artery to increase R atrial, RV, and pulmonary artery pressures -> hyperdynapic LV function with inc CI. However, PCWP and SVR are generally not affected. Massive PE usually causes RA pressure >10 and pulmonary artery puressure >40
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What would cardiac tamponade do to parameters of R heart cath?
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inc RA pressure, pulmonary artery pressure, and PCWP bc of constriction
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What are the parameters of R heart cath in hypovolemic shock?
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Low intravascualr volume -> dec RA, RV, pulmonary artery, and PCW pressures. SVR increased to maintain adequate perfusion to vital organs
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What changes in PCWP, CO, SVR in LAD MI with severe LV damage?
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Inc PCWP, dec CO, inc SVR
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What changes in R heart cath will you see in septic shock?
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Dec RA, pulmonary artery, PCW pressures. CO increased to miaintain adquate tissue perfusion. Distributive shock leading to peripheral vasodilation adn dec SVR. Early stages will be warm and flushed, later cold and clammy
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How does bronchiectasis usually present and how is it different from chronic bronchitis. How dx bronchiectasis?
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Cough, mucopurulent sputum, hemoptysis that often response to abx (in contrast, pts with chronic bronchitis complain of NON-purulent expectoration) Dx: CXR is often abnormal but not sufficient for diagnosis. High-resolution CT scan is definitive for diagnosis (CXR findings vary from linear atelectasis to clearly visible dilated and thickened airways whereas CT findings show airway dilation, bronchial thickening, lack of airway tapering)
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What are the causes of bronchiectasis?
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Inherited or acquired. CF is the most common cause of inherited; an infectious insult damages the mucociliary clearance mechanism, which leads to airway obstrucitonand dilation, mucus plugging, and suppuration. Impaired host defense, such as in pts with hypogammaglobulinemia or immunosuppression, also contributes to the disease process. Smoking greatly increases the likelihood of bronchiectasis
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What are bronchoscopy and alveolar lavage useful for?
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Dx of PCP and certain cancers. Rigid bronch can be occasionally used to control massive hemoptysis
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What are PFTs useful for?
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Establishing baseline for restrictive and obstructive lung diseases.
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What does bronchiectasis show on PFTs?
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Obstructive lung pattern with dec DLCO (PFTs should be used for disease progression not diagnosis in bronchiectasis)
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What are the 2 most common symptoms of PE?
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acute onset SOB and pleuritic CP (73, 66%), hemoptysis (20%), leg symptoms (<30%).
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What are the common PE findings of PE?
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Tachypnea, tachycardia, low grade fever (70, 30, 15%)
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What are CXR findings of PE (if present)?
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Hampton's hump, estermark's sign
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What are PE findings of TPTX?
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unilateral absence of breath sounds, tracheal deviation, hypotension
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What does PE show in mitral stensois?
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mid-diastolic rumble and opening snap at apex
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What are s/s of GERD?
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symptoms worse after meals, exercise, or lying down
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What is first step in management when suspect GED?
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Trial of PPI can be both diagnostic and therapeutic
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How common is GERD in asthma pts?
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Up to 75% of asthma pts have GERD (maybe be the primary trigger of asthma)
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What is PE findings of GERD?
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obesity, hoarseness, erythematous pharynx and larynx
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When is fluticasone used in asthma?
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Inhaled glucocorticoid -> persistent asthma (>2 symptoms per week). Prevents inlfammation and bronchial hyperresponsiveness
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What is theophyllline and when is it used?
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Methylxanthine phosphodiesterase inhibitor that causes bronchodilation. Limited use bc of SE profile but occasionally used in persistent asthma
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When are oral steroids used in asthma?
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Severe persistent asthma and emergency for asthma attacks
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When does empyema most commonly occur?
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in setting of untreated PNA due to baterial seeding of a pleural effusion. Inflammation and collection of pus in pleural cavity leads to formation of a loculatd, abnormally contoured effusion with adjacent pulmonary consolidation
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What is an empyema? What organisms cause it?
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Intrapleural colleciton of pus (purulent pleural effusion). Caused by Strep pneumo, Staph aureus, Klebsiella (same as PNA). A mized aerobic and anaerobic bacterial population supersedes as the infected pleural effusion progresses to empyema - this is one reason why empyema often unresponsive to abx that normally are used to treat CAP
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How do pts with empyema present?
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fever, cough (productive or nonproductive), SOB, often have pleuritic CP.
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What are CXR findings of empyema?
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Free-flowing (early) and loculated (late) pleural effusion and lung consoidation with air bronchograms. Effusion (opacity) typically has an abnormal contour
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What is the treatment of empyema?
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Drainage and abx
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When does bronchopleural fistula occur?
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Typically following surgical procedures involving the bronchi such as pneumonectomy, but can result from recurrent PTX or sequel of infeciton. CXR would show air in pleural space
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How can differentiate lunga abscess from empyema?
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Absecess will have discrete abscess cavity on CXR
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What are radiologic signs of pulmonary infarction?
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Pleural effusion on affected side as well as wedge-shaped opacity in infarcted segment (Hampton's hump)
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What is choriocarcinoma, when does it occur?
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Metastatic form of gestational trophoblatic disease. Can occur after molar pregnancy (50%), abortion (25%) or normal gestation (25%). Lungs are most frequent site of metastatic spread
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What should suspect in pts that are postpartum with pulmonary symptoms and multiple nodules on CXR? What test can you do to help confirm dx?
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Choriocarcinoma. Elevated HCG helps confirm.
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How does gestational trophoblastic disease (GTD) present?
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All forms of GTD tend to present with irregular vaginal bleeding, enlarged uterus, and pelvic pain. Irregular vaginal bleeding beyond 8 weeks post-partum is abnormal and should raise suspicion for GTD. Maligannt forms include invasive gesatinoal trohoblatic neoplasm (GTN) and choriocarcinoma. Either can arise after normal pregnancy, but GTN is almost always only locally invasive whereas choriocarcinoma is highly metastatic (MC to the lungs -> chest pain, dyspnea, hempytosis (sometimes).
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What is the most common cause of pleural effusion?
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CHF (inc hydrostatic pressure leads to transudation of fluid across the visceral pleura into the pleural space). Usually transudative effusion
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What is pH of pleural fluid useful for?
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The determination of pH is important in parapneumonic effusions where a value of <7.2 requires a chest tube aspiration to prevent empyema. Normal pleural fluid is 7.64. <7.3 indicates pleural inflammation. 7.35 consistent wtih transudative pleural effusion
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What does glucose of <60 in pleural fluid favor?
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Parapneumonic effusion, TB, or rheumatoid arthritis.
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When do you see high amylase in pleural fluid?
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Pancreatitis-assoc effusion or esophageal rupture
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Where are bronchogenic cysts usually found? THymomas? Neurogenic tumors?
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Bronchogenic cysts: middle mediastinum. Thymoma: anterior mediastinum. Neurogenic tumors: posterior mediastinum
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What are middle mediastinal masses?
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bronchogenic cysts (benign), tracheal tumors, pericardial cysts, lymphomas, LN enlargement, aortic aneurysms of the arch
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When should suspect thymoma?
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When see anterior mediastinal mass in young male or female. 20% of pts with myasthenia gravis have them.
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What are the anterior mediastinal masses?
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Thymoma, restrosternal thyroid, teratoma, lymphoma. If large, can cause chest heaviness or discomfort
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What are neurogenic tumors of the mediastinum and at what location are they in mediastinum?
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Posterior mediastinum. Meningocele, enteric cysts, lymphomas, diaphragmatic hernias, esophageal tumors, aortic aneurysms. MRI is best test for these
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Where are esophageal leiomyomas located?
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Posterior mediastinum. They are submucosal and usually asymptomatic, only producing symptoms when >5cm. Only large tumors should be removed
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What is the development of clubbing and sudden-onset joint arthropathy in chronci smoker suggestive of? What is next step in management?
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Hypertrophic osteoarthropathy. Often assoc with lung cancer -> CXR indicated to rule out malignancy or other lugng pathology. HOA is a condition where digial clubbing is accompanied by sudden-onset arthropathy, commonly affecting wrist and hand joints. Hypertrophic pulmonary osteoarthropathy is a subset of HOA where clubbing and arthropathy are attributable to underlying lung disease like lung cancer, TB, bronchiectasis, or emphysema
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What is the other name for Granulomatosis with polyangiitis and what is it/how does it present?
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Wegner's. Triad of systemic vasculitis, upper and lower airway granulomatous inflammation, and glomerulonephritis. Nasal cartilage destruction and vasculitic cutaneous lesiosn (tender nodules, palpable purpura, ulcerations) are common external manifestations. Disese onset usually around age 40, M=W. URT most commonly affected. Granulomatous inflammation in nasopharynx causes epistaxis, purulent rhinorrhea, otitis, sinusitis, and, over time, saddle nose deformity due to destruction of nasal cartilage. Cutaneous manifestations are varied and include painful subcuaneous nodules, palpable purpura, and/or pyoderma gangrenosum-like lesions
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What is workup for Wegener's (granulomatosis with polyangiitis)? Tx?
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positive c-ANCA due to ab against proteinase-3 and elevated CRP. UA: RBC casts, proteinuria, sterile pyuria if glomerulonephritis is present. Tx: cytotoxic agents such as cyclophosphamide
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What are cutanous findings of TB?
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Can have scrofuloderma overlying infected LN, a facial eruptoin known as lupus vulgaris and others.
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When do you see nasal destruction in TB/leprosy?
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More often in leprosy than TB
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What are clinical mainfestations of pulmonary AV malformations?
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Range from asymptomatic to causative of severe respiratory distress and massive hemoptysis in stances of rupture.
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What pts are predisposed to aspiration PNA?
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Impaired consciousness, advanced dementia, and other neurologic disorders are predisposed to aspiration PNA due to impaired epiglottic function
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What are the usual etiologic factors of aspiration PNA?
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Aerobic oral flora (viridans strep)
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What lung problems can advanced GERD cause?
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Aspiration of gatric content, bronchoconstriciton, and PNA
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How do pts with ARDS present?
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Dypsnea, tachypnea, hypoxemia, bilatearl alveolar infiltrates on CXR
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What sound vent settings be for pts with ARDS?
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PEEP and low TV (PEEP improves oxygenation by preventing alveolar collapse at the end of expiration which increases the FRC and decreases the work of breathing. Can go up to 15 on PEEP.
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Do you want to give lots of IVF in ARDS?
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No, bc in ARDS leaky alveolar capillaries causes pulmonary edema. Excessive IVF administration would increase hydrostatic pressure and worsen pulmonary edema. Thus, IVF must be used sparingly in these pts
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When are PRBC transfusions beneficial in ARDS?
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Hb <9 is shown to improve outcome
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Where do you see blastomycosis?
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Pulmnary fungal infection found in Great Lakes, Mississippi, and Ohio River basins (Wisconsin has the highest infection rate)
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What are the s/s of systemic blastomycosis?
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Pulmonary manifestastions (productive cough, fever), can also have systemic symptoms like night sweats, wt loss. Can also have ulcerated skin lesions and bone lesions
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How do you treat blastomycoiss?
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Intraconazole or Ampho B
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Where can disseminated TB affect?
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Peritoneum, cervical LN, eyes, bones, skin
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What are risk factors for TB?
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Immigration, homelessness, alcoholism, immunosuppression, working in healthcare field
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How does sarcoidosis present?
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Asymptomatically or with fever, cough, wt loss, arthrits. CXR: bilateral hilar adenopathy with interstitial infiltrates. Erythema nodosum (tender red nodules on shins) are typicla skin manifestations
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Who gets osteosarcomas and where is most affected?
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Adolescents. Distal femur most common. Presents with soft tissue mass and localized pain without systemic symptoms
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Where do you find coccidiodomycosis and how does present?
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SW US. Fever, cough, nith sweats. Extrapulm manifestations in skin, meninges, skeleton
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What does asbestos exposure put you at risk for?
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Malignancy (both bronchogenic carcinoma and pleural mesothelioma, but bronchogenic more common), pulmonary fibrosis, pleural plaques
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Who is at risk for asbestosis?
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Mining, shipbuilding, insulation, pipe work.
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What are the s/s of asbestosis?
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Dyspnea without cough or sputum production is most common. Bibasilar end-expiratory crackles and clubbing in 40-50% with advanced disase. CXR: interstital abnormalities in lower lung fields consistent with pulmonary fibrosis; pleural plaques in 50% on CXR (helps distinguish from other causes of pulmonary fibrosis) Symptoms usually develops 20-30yrs after initial exposure.
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WHo is at risk for PCP PNA and what do you see on CXR?
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Immunocomproimised. CXR: bilteral diffuse interstitial infilrtartes. Incubation 4-8 weeks, aireborne
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What are s/s of PCP PNA?
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Dypsnea, fever, nonproductive cough, tachypnea, tachycardia, cyanosis with minmal chest findings. Can disseminate out of lung - MC sites are LN, spleen, liver, BM
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What does Aspergillosis look like on CXR?
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Solid mass surrounded by a radiolucent crescent (crescent sign, Monod's sign)
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Can candida cause PNA?
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no - esophagitis, endocarditis, endophthalmitis, hepatosplenic disease, meningitis, vaginitis
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What does V/Q scan show for PE?
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Area of perfusion defect without ventilation defect (mismatched defect) - but this classic finding is present in <50% of PEs! Inconclusive findings include several small perfusion defects or matched ventilation/erpfusion defect. (area of ventilation defect wihtout perfusion defect is more suggestive of a respiratory problem)
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What are the S/S of PE?
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Dypsnea, tachypnea, normal lung exam, R axis deviation on EKG.
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What is test of choice for PE?
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CT angiography. If contrast allergy or renal insufficiency, can do V/Q scan
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In a pt with PNA, what causes desat when shfiting position?
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When the consolidated lung segment is placed in the dependent position, can increase R->L shunt. Proper oxygenation of blood requires balance between ventilation and perfusion. In normal persion, both ventilation and perfusion are greatest at the lung bases (most dependent regions of the lungs) and least at the apices. WHen lying on R or L side, the dependent lung gets the greatest ventilation and perfusion. in consolidated lung segments the alvoeli are filled with exudate and do not participate in pulmonary gas exchnage, so their ventilation is eessentially 0 (ie blood perfusing consolidated ares is not oxygenated). Positions that increase the proportion of pulmonary blood flow passing thorugh such segments decreases the patient's oxygen saturation (R->L shunt).
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What do you see on PE in pt with PNA?
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Dec breath sounds and inc fremitus over consoldation
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What is dead space? Does PNA incrase dead space? What pathologic condition can inc dead space?
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Volume of inhaled air not available for gas exchange. As a consolidated lob can't fill with inhaled air, it doesn't inc the physicioloci dead space. An example of a situation that would cause hypoxia due ot inc dead space would be a PE, where the lung is properly ventilated, but segments of the lung are not perfused
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What should you do if you suspect ACEI causing chronic cough?
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D/c drug. Only if cough persists should get CXR
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What is hypoxia in pts with PNA seconary to?
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Alveolar and interstitial inflammation, which causes areas of V/Q mimatch -> inc in A-a gradient
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What happens to PCWP in left atrial hypertension?
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Increases. LA hypertension typically due to LV failure but also may result from MV disease.
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Can you get a murmur from fever and hypoxemia?
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Yes, because causes hyperkinetic state
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How do obstructive lung diseases and obesity hypoventilation sydnrome cause hypoxia?
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Secondary to alveolar hypoventilation
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What happens to lung compliance in COPD?
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increases. LA hypertension typically due to LV failure but also may result from MV disease.
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What are components of teh wells criteria and points? What does it mean?
|
Hemoptysis, cancer 1 point. Previous PE or DVT, HR >100, recent surgery/immobliziation 1.5 points. Clinical signs of DVT, most likely dx 3 poitns. >4 PE likely, <= 4 PE unlikely.
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What is diagnostic strategy in suspected PE?
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PE unlikely (modified wells) -> D-dimer - if <500, no PE. If >500, do CT angio. If PE likely with modified wells, go straight to CT
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How does the kidney compensate for respiratory alkalsois?
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Preferentially excretes bicarb into the urine -> inc urine pH. Specifically, the kidneys retain inc amts of H+ (protons) and excrete increased amounts of bicarb in an attempt to normalize pH.
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What is the formula for ventilation?
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Vent = TV x RR. Hyperventilation (caused by inc RR or RV) results in excessive CO2 losses and resp alkalosis. Hypoventilation (casued by dec TB and/or RR) causes CO2 retention and resp acidosis.
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How does kidney compensate for resp or metabolic acidosis?
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Low urine bicarb excretion
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What does high aldo do to cation losses?
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Inc aldo causes inc H+ and K+ losses in the urine and serum alkalosis. "Contraction alkalosis" occurs in states of intracellular volume contraction, where inc aldo functions to restore intravascular volume but also causes inc urinary proton loss.
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What are causes of high serum AG?
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Metabolic acidosis resulting from DKA, renal failure, lactic acidosis, methanol, ethylene glycol, and salicylate poisoning
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What is the work-up for incidental discovery of pulmonary nodule on CXR?
|
1st step - obtain any preiovus radiographic lung images. Absence of growth over time rules out malignancy. If not available, then assign nodule as either low, intermediate, or high probability of malignancy based on clinical and radiographic data (clinically favoring malignancy: >50yo, hx smoking, wt loss, previous malignancy. radiographic favoring malignancy: large size, low density, spiculated borders, absence of calcifications). Low probability followed by serial high resolution chest CT. Intermediate are furher investigated with PET scan and/or bx. High: removed surgically
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When is bronchoscopy used for tissue sample?
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Best for centrally located lesions (can look at peripheral with CT)
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What is the pathophys and PFT changes in COPD?
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Progressive expiratory airflow limitation which causes air trapping, dec VC, inc TLC, inc FRC, inc TLC. FEV1 disproportionately decreasd compared to VC. (FEV1/FVC <0.7). Alveolar-capillary membrane (site of gas exchange) destroyed in COPD -> inc lung distinsibility and compliance
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What conditions have respiratory muscle fatigue?
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Botulism, Gullian-Barre, ALS, myasthenia gravis
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What is the algorithm for management of asthma exacerbation in ED?
|
Initially assess: History and PE (accessory muscle use, RR, HR, ascultation), PEF or FEV1, O2 sat. If mild to moderate exacerbation (FEV1 or PEF >40%) -> Oxygen until O2 sat >90%, inhaled SABA up to 3 doses/hr, systemic corticosteroids if no response or if recent oral steroid use. If mod-severe (FEV1 or PEF <40%) -> O2 until sat >90%, high dose SABA + ipratropium neb every 20min or continuously for 1 hr, systemic corticosteroids. If impending or actual resp arrest -> intubation with 100% O2, nebulized SABA+ipratropium, IV steroids, consider IV magnesium, then admit to ICU 4706
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Why can asthma pts go into impending respiratory failure?
|
Acute asthma exacerbation increases respiratory drive and hyperventilation, leading to dec arterial partial pressure of CO2 (PaCO2) -> if PaCO2 elevated or even normal, suggests dec respiratory drive (likely due to respiratory muscle fatigue). Other clinical s/s of poor respiratory drive: dec breath sounds, absent wheezing, AMS, marked hpoxia with cyanosis
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Are IV abx indicated in acute asthma exacerbations?
|
no bc viral infections are most common trigger. If ahve fever with infiltrate on CXR may suggest bacterial cause and need for abx. Note: WBC count in asthma exacerbation usually due to acute stress, not specific for infection
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Should use theophylline or aminophylline (mehtylxanthines) in asthma attack?
|
No - no additional benefit to SABAs alone
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Any role for systemic epi in asthma attacks?
|
No - but yes for bronchospasm assoc with anaphylaxis
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How does Legionella present and how is it differnet from other bacterial pneumonias?
|
Similar presentation to bacterial pneumonias, but also has prominent GI symptoms (diarrhea), hyponatremia, and LFT abnormlaities.
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How do you dx and tx legionella?
|
Many cases are diagnosed with a urinary antigen test, although attempts at culture may also be done. Treatment usually with a quinolon or macrolide antibiotic.
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Who is H. flu PNA more common in?
|
It is a common cause of CAP and also more common in COPD
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Who usually gets mycoplasma infections?
|
teens and twenty year olds
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Who is Moraxella catarrhalis PNA more assoc with?
|
COPD
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When do you usually see staph aureus PNA?
|
After recent influenza infection
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What is the most common cause of pulmonary complications in pt with systemic sclerosis?
|
Interstitial fibrosis
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What pulmonary cancer is increased in systemic sclerosis?
|
bronchogenic carcinoma
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Where are DVTs usually located in the legs?
|
Proximal deep leg veins are most common source of symptomatic PE (iliac, femoral, popliteal) bc of their large caliber and proximity to the lungs. Less common: calf veins, renal veins, pelvic veins, upper extremity veins, R heart
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What are thrombi originating form the renal veins most commonly assoc with?
|
pts with nephrotic sydnrome (prevalence of PE in pts with nephrotic syndrome is 10-30%)
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What should you suspect in COPD pts with catastrophic worsening of their respiratory sytmpoms?
|
Secondary PTX usually due to dilated alveolar blebs that rupture air into the pleural space, generally in the upper lobes. Smoking also markedly increases risk of PTX. PTX pts typically present with acute onset CP and SOB; breath sounds markedly reduced and chest is hyperresonant to percussion.
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When would you suspect diffuse alveolar obstruction in acute exacerbation of COPD?
|
Pts who complain of inc production of purulent sputum. Lung exam will show diffuse rhonchi and wheezing. Tend to occur more gradually than PTX. PaCo2 increased
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Why are pts with COPD at inc risk of PNA?
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Due to inc inflammatory infiltrates
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How do pts with PNA present?
|
CP, breathlessness, cough with sputum, fever. PE: infiltrated lung, crackles, bronchial breath sounds.
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How can differnetiate a COPD exacerbation from acute pulmonary edema seen in acute CHF?
|
Coarse crackles bilaterally on PE is more consistent with CHF, while wheezes are more commonly heard in COPD (although can hear wheezes with CHF - cardiac wheezing)
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What is the difference between OSA and obseity hypoventilation syndrome?
|
OSA - only hypoventilate at night (causing transient hypoxia and hypercarbia that resolves during wakefulness), whereas in OHVS they do not have the respiratory mechanics to allow them to resume normal ventilation during wakefulness and therefore develop chronic respiratory failure
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What are consequences of obesity hypoventilation syndrome? Also, what happens to bicar/Cl balance?
|
Pulmonary hypertension with cor pulmonale, secondary erythrocytosis, hypoxia, choric hypercapnia (due to persistent hypoventilation) and respiratory acidosis. In a compensatory effort to maintain normal pH, the kidney increases bicarb retention and decreases chloride reabsorption.
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What is the differential for obstructive pattern on PFTs (FEV1/FVC <70% predicted) based on DLCO?
|
Low DLCO: emphysema. nL: chronic bronchitis. Inc: asthma
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What is the differential for restrictive pattern on PFTs (FEV1/FVC >70% of predicted but FVC <80% of predicted) based on DLCO?
|
Low DLCO: interstitial lung disease, sarcoidosis, asbestosis, heart failure. NL: MSK deformity, neuromuscular disease. High: morbid obesity
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What is the differential for normal spirometry on PFTs based on DLCO?
|
Low DLCO: anemia, PE, PHTN. High DLCO: pulmonary hemorrhage, polycythemia
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What does DLCO measure?
|
Carbon monoxide diffusing capacity of the lung - measures the lung's ability to transfer gas to the blood. CO uptake is influenced by the diffusion capacity of the alveolar capillary membrane and the binding of CO and Hb. A normal DLCO indicates intact alveolar and capillary structure
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What is the difference between the 2 main subtypes of COPD?
|
Predominant emphysema: generally thin with severe dyspnea, hyperinflated chest, dec vascular markings, DEC DCLO (due to alveolar destruction), moderate O2 desat. Predominant chronic bronchitis: chronic productive cough >= 3mo over 2 consecutive years not due to other causes (ex: bronchiectasis). Due to hypersecretion of mucus and structural changes in the tracheobronchial tree after prolonged exposure to nonspecific irritants. Usually presents with prominent bronchovascular markings, mildly flattened diaphragm, and NORMAL DLCO
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What type of emphysema is typical for alpha-1-antitrypsin deficiency?
|
Panacinar (centriacinar more characteristic of smoking-induced)
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What are the risk factors for aspiration PNA?
|
1. Altered consciousness - seizures, alcoholism, drug overdose, CVA 2. Dysphagia: esophageal reflux, diverticula, obstruction. 3. Neurologic disorder: advanced dementia, Parkinsonism, myasthenia. 4. Sedation prior to procedures such as bronchoscopy, intubation, EGD
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What are signs of aspiration PNA (as opposed to other types of PNA)?
|
Foul-smelling sputum and RLL PNA
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What are recurrent PNA in the same anatomical location a red flag for?
|
Bronchial obstruction due to an underlying abnormality - most concerning is bronchogenic carcinoma (other causes: 1. Local anatomic obsturction (including carcinoma): bronchial compression due to mediastinla adenopathy or vascular anomaly or intrinsic bronchial obstruction due to bronchiectasis, retained foreign body, or bronchial stenosis or 2. Recurrent aspiration from seizures, ETOH/drug use, or GERD/dysphagia/achalasia)
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What are recurrent PNA in different regions of the lung concerning for?
|
Sinopulmonary disease (ex: CF, immotile cilia), noninfectious (vasculitis, bronciolitis obliterans with organizing PNA), immunodeficiency (ex: HIV, leukemia, dec Igs)
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|
What is the best way to visualize underlying lung parenchymal abnormalities including lung cancer?
|
CT of chest. Bronchoscopy is invasive and generally reserved for pts with masses documented by CT scan - it would be the next step in pt with neg CT and high suspicion for endobronchial obstruction or if see central mass on CT can do bronchoscopy to directly observe and bx lesion (but if more peripheral lesion, CT-guided biopsy is preferred)
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What is the protocol for treatment of acute DVT?
|
Combo warfarin and heparin for 1st 5 days, then d/c heparin if INR is therapeutic. Warfarin should be continued for at least 6mo in most pts with a first-time clot. A progressing clot in a pt with sub-therapeutic INR requires bridigng heparin until the INR is therapeutic. (DVT management is divided into acute anticoagulation adn clot stabilization, chronic anticoagulation and treatment of DVT-related complications. Initial clot stabilization by heparin is mandatory. Heparin further retards thrombus formation by binding to ATIII and enhancing its activity - heparin stabilizes but doesn't lyse the existing clot. Next, long-term anticoag with warfarin is necessary - warfarin inhibits activation of Vit K dependent clotting factors II, VII, IX, and X but unfortunately takes at least 4-5d for level to become therapetuic. Lastly, pts with new DVT should wear compression stockings to reduce risk of post-phlebitic syndrome, a potentially devastating complication).
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What should do with a pt with a propagating DVT in setting of sub-therapeutic warfarin?
|
Tx like new, unstable clot - heparin + warfarin until INR therapeutic, then can d/c heparin
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When are thromboltyics indicated in venous clots?
|
Hemodynamically significant PE (not routinely for DVTs)
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When are IVC filters used?
|
In pts with lower extremity DVT where anticoagulation contraindicated or failed (recurrent/extending DVT with therapeutic INR)
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|
Besides cancer, what can asbestos exposure lead to?
|
Pneumoconiosis and pulmonary fibrosis (restrictive lung disease)
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How do you use spirometry to differentiate different types of lung diseases?
|
1. Low FEV1/FVC -> obstructive. Do bronchodilator challenge - if inc in FEV1 then asthma, if no change, then COPD. 2. Normal or high FEV1/FVC but low FVC -> restrictive. Then look at DLCO - if low, interstitial lung disease/sarcoid/asbestosis/CHF. If normal, then due to chest wall weakness (low DLCO indicated imparied diffusion across the alveolar-epithelial membrane)
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How do normal lungs sound?
|
Resonant to percussion, auscultation reveals vesicular breath sounds (quiet inspiratory phase, almost inaudible expiratory phase).
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How do consolidated lungs sound?
|
Dullness to percussion. Sound conduction thru the consolidated region will result in bronchial breath sounds, which are louder and have a more prominent expiratory component - BUT, this only holds true if the airway is patent!! If airways are blocked, the breath sounds over the consolidated lung tissue will be decreased! Increased sound transmissin over the consolidated lung region can also be assessed by asking the pt to say the letter E and listening - if sounds like an A with a nasal or bleating quality, this is called egophaony and suggests consolidation. Crackles are also often heard
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How does a pleural effusion sound on lung exam?
|
Dec movement of ipsilateral chest wall, dullness to percussion, and dec breath sounds. Can sometimes hear egophony at fluid level due to transmission of breath sounds thru collapsed lung tissue
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What are lung exam findings in PTX?
|
Hyperresonance on percussion and dec breath sounds on that side
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How does emphysema sound on lung exam?
|
Hyperresonance to percussion bilaterally. Breath sounds are vesicular and the intensity of breath sounds is significantly decreased. May hear wheezing
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How do pts with interstitial lung disease present on lung exam?
|
Resonant on percussion and have vesicular breath sounds. Fine crackles are herad at end of inspiration
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What will you hear on lung exam with mucous plugging?
|
Dec airflow in the affected part of the bronchial tree -> collapse of downstream lung parenchyma -> no breath sounds in affected area
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What is the problem in high altitude and how are A-a graident and PaCO2 changed and does it correct with supplemental O2?
|
Reduced inspired O2 tension. Normal A-a gradient and PaCO2, corrects with supplemental O2
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What is the problem with respiration in CNS depression and how are A-a graident and PaCO2 changed and does it correct with supplemental O2?
|
Hypoventilation. Normal A-a gradient, increased PaCo2. Corrects with supplemental O2
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What is the problem with respiration in interstitial lung disease and how are A-a graident and PaCO2 changed and does it correct with supplemental O2?
|
Diffusion limitation. Inc A-a gradient, normal PaCO2. Corrects with Supplemental O2
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What is the problem with respiration in intracardiac shunts or extensiv ARDS? How are A-a gradient and PaCO2 changed and does it correct with supplemental O2?
|
Shunting. Inc A-a gradient, normal PaCO2. Does NOT correct with supplemental O2
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What is the problem with respiration in obstructive lung diseases, atelectasis, pulmonary edema, and PNA? How do A-a gradient and PaCO2 change? Does it correct with supplemental O2?
|
V/Q mismatch. Inc A-a gradient, normal or inc PaCO2. Corrects with supplemental O2
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What does A-a gradient measure? What are causes of elevation?
|
degree of alveolar O2 transfer to blood. If elevated, due to diffusion limitation (ex: interstitial diseases), V/Q mismatch (ex: pulmonary edema, PNA, obstructive lung disease, atalectasis) or shunts (ex: intracardiac shunts).
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How do you calculate A-a gradient and what is normal?
|
A-a g = PAO2 - PaO2. Normal is <15 and increases with age, but >30 is elevated at any age. PAO2 = (FiO2 x (Patm-PH2O)) - (PaCO2/R)
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What does V/Q mismatch mean?
|
Imbalance of blood flow and ventilation -> dec PaO2. When ventilation obstructed and blood flow unchanged (ex: emphysema), there is a dec in O2 and an inc in CO2. When blood flow excessive relative to ventilation (ex: pulmonary edema, PNA, atelectasis), there is a dec in O2.
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How does pulmonary edema change lung compliance?
|
Decreases it
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How does COPD change lung compliance and A-a gradient?
|
increases lung compliance, increases A-a gradient
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Why does shunt cause high A-a gradient and low PaO2 that doesnt' correct with supplemental O2?
|
Bc a shunt bypasses blood flow around ventilated alveoli to prevent gas exchange in the blood. Also, a large L->R intracardiac shunt will lower compliance by increasing pulmonary blood flow, elevating pulmonary arterial and/or venous pressures, and causing fluid leakage into interstitium and alveoli
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How does ARDS change lung compliance?
|
Causes poorly aerated lung that is stiff and less compliant
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What does pulmonary edema do to A-a gradient and lung compliance?
|
increases it due to V/Q mismatch. Excessive fluid reduces lung compliance by preventing some alveoli from fully expanding. Supplemental O2 usually corrects the hypoxemia, V/Q mismatch, and A-a gradient
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What type of vasculitis is Wegener's (Granulomatossi with polyangiitis), how do pts present, dx, tx? Who is it common in?
|
Small and medium-sized vessels. Presentation: glomerulonephritis (renal insufficiency, microscopic hematuria, RBC cases (RPGN) and upper and lower respiratory tract disease (upper: bloody/purulent nasal discharge, oral ulcers, sinusitis; lower: dyspnea, cough, hemoptysis), systemic sypmtoms like fever, wt loss, fatigue. CXR: nodular densities and alveolar/pleural opacities. Dx: if suspect, shoudl get c-ANCA test (pos in >90%) then bx of active site (preferably nasopharyngeal) makes definitive dx. Tx: corticosteroids and cytotoxic agents. Highest incdence in whites 30-50yo
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|
What is serum AFP used as a tumor marker for?
|
hepatcellular carcinoma, testicular cancer
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How do pts with TB present, what does CXR look like?
|
cough, hemoptysis, dyspnea, fever, wt loss, night sweats. CXR: lower lobe infiltrates in primary TB and apical infiltates in reactivation disease
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|
When is ESR of greatest clinical utility?
|
Dx of temporal arteritis/polymyalgia rheumatica. It is non-speciifc in many other diseases
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What are causes of hemoptysis?
|
Pulmonary (MC): bronchitis, PE, bronchiectasis, lung cancer. Cardiac: MS/acute pulmonary edema. Infectious: TB, lung abscess. Hematologic: coagulopathy. Vascular: AV malformation. Systemic diseases: Wegener's granulomatosis, Goodpastures, SLE, vasculitis
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What is the definition of chronic bronchitis and what is the MC cause?
|
Chronic producive cough for 3mo in 2 successive years. Cigarette smoking is the leading cause.
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What is bronchiectasis? How can differentiate from chronic bronchitis?
|
Irreversibel dilation and destruction of bronchi resulting in chronic cough and inadequate mucus clearance. Compared to chronic bronchitis, bronchiectasis is more likely assoc with history of recurrent respiratory tract infections and chronic cough with daily production of copious MUCOPURULENT SPUTUM. PE: findings of crackles, rhonchi, and wheezing are more common in bronciectasis than chronic cough
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How do pts with lung abscess present?
|
Fever, chills, purulent expectoration
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How does mitral stenossi cause hemoptysis?
|
Produces acute pulmonary edema
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What is a more common cause of hemoptysis - chronic bronchitis or TB?
|
Chronic bronchitis
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|
How does the kidney compensate for respiratory alkalosis and what does it result in in the urine?
|
Preferentially excretes bicarb into the urine, resulting in alkalinized urine. Specifically, the kidneys retain increased amounts of H+ and excrete inc amounts of bicarb.
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What are mechanically ventilated pts at risk for in terms of ventilation?
|
Both forced hyper and hypoventilation. Ventilation = TVxRR. Hyperventilation (caused by inc TV or RR) results in excesive CO2 losses and respiratory alkalosis, while hypoventilation (caused by dec TV and/or RR) results in CO2 retention and respiratory acidosis
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|
What is the most common inherited disorder causing hypercoagulability?
|
Factor V Leiden. Predisposes to thromboses, esp DVT of lower extremities. It is the result of a point mutation in a gene coding for teh caogulation factor V. As a result, Factor V becomes resistant to inactivation by protein C, which is an important counterbalance factor in the hemostatic cascade. Prevalence as high as 5-6% of population.
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What is the definition of obesity hypoventilation syndrome? What does ABG show and what are some potential therapies?
|
Severe obesity (>150% of ideal body weigh) and alveolar hypoventilation during wakefulness. Classically show extreme obesity, thick neck, hypersomnolence. EKG: distant heart sounds, low voltage QRS, poor qualtiy CXR. ABG: hypercapnia, hypoxemia, respiratory acidosis as a consequence of dec lung compliance. Therapies: wt loss, ventilator support, O2 therapy, progestins (respiratory stimulant)
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What causess the derangement of ABC in obesity hypoventilation syndrome?
|
Dec chest wall compliance, which leads to inc work of breathing. Eventually, the work of breathing becomes so high that CNS chemoreceptors establish a higher pCO2 set-point, causing resultant hypoventilation, hypercapnia, and hypoxemia.
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|
How does atypical PNA present?
|
More indolent course (low-grade fever, longer symptoms before seek medical attention), non-productive cough, and with higher incidence of extrapulmonary manifestations (headache, sore throat, skin rash) than pyogenic PNA. CXR: findings may be out of proportion to findings on PE.
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What are causes of atypical pneumonia? What is most common cause? How can distinguish different causes?
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Mycoplasma pneumoniae, CHlamydia pneumoniae, Legionella, Coxiella, and influenza. Mycoplasma most common cause in ambulatory setting. Erythema multiforme typical of Mycoplasma (also, no cell wall -> no gram stain).
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What is the MCC of CAP requiring hospitalization?
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Pneumococcus. Cough - rusty colored sputum
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What will Hemophilus influenza show on gram stain?
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Small gram neg rods
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How does influenza usually present?
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Cough, fever, HA, myalgias. Onset often sudden, tends to occur in outbreaks
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How can distinguish Legionella from other causes of PNA? How is it spread? Who is more susceptible? How can make dx?
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Causes extrapulmonary symptoms (ex: GI - diarrhea). Environmental water sources are often involved in spread. MC in elderly pts and smokers. Urine Legionella Ag test helpful in dx
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What is the MC presenting symptom of EBV infection? What are other symptoms?
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(momnonucleosis). Sore throat MC, can also have fatigue, malaise, HA, abd pain.
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What is a complication of a pulmonary neoplasm in the superior sulcus?
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Apical lung tumor in this location can cause compression of the sympathetic trunk (Horner's syndrome), the brachial plexus (Pancoast syndrome -> pain, paresthesias, and/or weakness of R arm. Specifically, shoulder pain radiating to arm in ulnar distribultion caused by tumor invasion of C8 and T1), the R recurrent laryngeal nerve (hoarse voice), and the SVC (SVC syndrome).
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How does Aspergillomas present? Dx?
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Hemoptysis, fever, wt loss, chronic cough. Mass usually mobile and moves with position. Dx: finding of hyphae in specimen.
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Where do carcinoid tumors usually present?
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Centrally located, easily visible with bronchoscope. Slowly growing and have best prognosis of all lung cancers. Rare to ahve carcinoid syndrome.
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What are s/s of cryptogenic organizing PNA? CXR?
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Dry cough and systemic symptoms that last for months. CXR: bilateral ground glass infiltrates
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What are symptoms and CXR of lung abscess?
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Thick-walled cavitary lesions on CXR. Affected pts have cough, hempotysis, fever, production of purulent sputum
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What would aortic arch aneurysm show on MRI?
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Fusiform dialtion of ascending aorta and arch which projects to L within the chest
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What should you suspect in new clubbing in pt with COPD?
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Lung cancer. Finger clubbing is NOT a feature of simple COPD and in fact the apeparance of fingernail clubbing strongly suggests lung maliganncy. Clubbing is thickening of the nail bed that causes a dec in the angle between the nail bed and the nail fold. In severe clubbing, the terminal parts of the fingers and toes appear swollen like drumsticks
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What are condiitions assoc with fingernail clubbing?
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Pulmonary HTN, hypoxemia due to congenital herat disease. Also, lungabscesses, bronchiectasis, CF, interstitial lung disease, sarcoidosis, lung malignancy. COPD rarely assoc unless have malignancy
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What are risk factors for GERD?
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Obesity, supine position soon after large meal, laryngitis, change in voice quality.
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What are s/s of GERD?
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Heartburn, regurgitation, dysphagia, CP, laryngitis, change in voice quality, noctural respiratory smptoms taht can exacerbate asthma
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How common is GERD in asthma?
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Very common - up to 30-90% of pts wtih asthma can ahve it. GERD cand exacerbate airlfow obstruction in ashtmatics by increasing vagal tone, heightened bronchial reactivity, and microaspiration of gastric contents into the upper airway.
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What is treatment of GERD in pts with asthma?
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Initial treatment includes lifestyle modifications such as elevating the head of the bed, dietary changes, and wt loss. Treatment with PPI can improve PEF in pts with asthma, noctural respiratory symptoms, and GERD.
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When does aspirin-exacerbated respiratory disase occur and how does it present?
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Occurs in pts with asthma and chronic rhinosinusitis. Symptoms: worsenign of asthma and nasal congestion 30min-3hrs after ingestion of NSAIDs
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How does ACEI cause cough?
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Accumulation of kinins, substance P, prostaglandin, and thromboxane. Occurs within several weeks of initiating ACEI
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What do you need to rule out in pt with sudden onset of severe SOB?
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Upper airway obstrction (esp if also have difficulty swallowing).
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How do pts with laryngeal edema usually present? What are some other signs?
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Acute-onset dyspnea. Usually there is an identifiable precipitating event (ex: peanut ingestion in pt with history of peanut alleriges). More common in pts with food allergies and urticaria. PE: stridor and harsh respiratory sounds from trachea. Usually no wheezing.
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How do pts with eosinophilic PNA present?
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Gradual onset. Usually present with asthma-like symptoms ongoing for several days. PE: diffuse wheezing and fine inspiratory crackles suggestive of bronchial and interstitial involvement. Peripheral eosinophilia also present
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How does leukocytoclastic vasculitis present?
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Prominent cutaneous manifestations. (Pulmonary infiltrates and pleural effusions can occur but symptoms are relatively slow to evolve)
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What organs does CF usually affect?
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Respiratory tract, sinuses, pancreas, intestines, reproductive systems secondary to abnormal secretions. Recurrent pulmonary infections and bronchiectasis are commonly seen in the lungs. Dec exocrine function of the panreas leads to fat malabsorption.
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When is CF dx?
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Most think of CF as a disease diagnosed in early childhood, but there are a considerable number of milder cases which have a later initial presentation in teens or twenties.
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What is the cause of CF?
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Mutation in the chloride transporter protein CFTR. This mutation leads to abnoramlly thick secretions which can affect the respiratory tract, sinuses, pancreas, intestines, and reproductive systems
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What are the lung findings in CF?
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Chronic cough with frequent exacerbations due to superimposed infection. Most pts develop bronchiectasis, which can predispose to hemoptysis
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What are pancreatic findings of CF?
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Involvement of the pancreas commonly manifests as dec exocrine function leading to fat malabsorption with bloating and greasy, floating stools. CT: atrophic pnacreas with calcificatios is consistent with chronic pancreatisi (possible manifestation of CF)
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What causes Kartagener's syndrome?
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Abnormal ciliary funciton - can present with sinus and respiratory symptoms as well as infertility
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How do pts with primary phagocytic defects usually present?
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Recurrent skin infections with bacteria such as staph aureus
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What do pts with selective IgA deficiency present with?
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Problems with immunity at the mucosal surfaces - predisposed to recurrent pulmonary infections as well as GI manifestations such as celiac or IBD
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When is bronchoalveolar lavage most useful?
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In evaluation of suspected malignancy and opportunistic infection. >90% sens and specific for PCP. Less useful in evaluating for other forms of interstitial lung disease such as interstitial pulmonary fibrosis, sarcoidosis, and CT diseases
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What are s/s of PCP PNA?
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CD4 <200 in HIV. Non-productive cough, progressive dyspnea, wt loss, tahcypnea. CXR: vary - some are normal, classic appearance is biltareal intersitial and/or alvoelar infiltrates.
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How do you dx PCP PNA?
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definitive dx before drug therapy is highly preferable, bc definitive dx has been tied to better clinical outcomes. Sputum induciton with hypertonic saline is 1st-line method bc minimally invasive. But, only 50% sensitive. When sputum induction doesn't confirm dx, BAL is performed (>90% sens/spec)
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How do you diagnose sarcoidosis?
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No definitive test. Dx requires compatable clinical and radiographic features, exclusion of alternative dx, and histopathologic demonstration of noncaseating granulomas. Transbornchial bx used to demonstrate histopathology.
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How do you diagnose interstitial fibrosis and interstitial lung disease caused by rheumatoid arthritis?
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Lung biopsy
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What is the MCC of mitral stenosis? How does it present and what are complications?
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MC cause: rheumatic heart disease (usually occurs in childhood but can happen at any age; latent period of several years befor symptom onset (usually 4th-5th decade of life) . S/S: gradual and progressively worsening dyspnea on exertion or orthopnea, hemoptysis (due to pulmonary edema); symptoms usually precipitated by exercise or conditions causing tachycardia (ex: fever, anemia, pregnancy). Afib is a common complication (bc MS causes eventual backflow of blood in LA -> elevated L atrial and pulmonary vascular pressures -> over years casues LA enlargement) and can cause rapid decompensation in previously asymptomatic pts. Longstanding MS can cause severe LA enlargement leading to elevation of L main bronchus on CXR. LA enlargement can also compress recurrent laryngeal nerve to cause persistent cough or hoarse voice. 70% get Afib
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What are PE findings of mitral stenosis?
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Loud 1st heart sound, opening snap after S2 (best heard at apex), low-pitched diastolic rumble best heard at cardiac abpex (pt lying on L side in held expiration)
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What are complications of acute pericarditis?
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Pericardial effusion and tamponade with symptoms of progressive dyspnea, orthopnea, and enlarged cardiac silhouette
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How does interstitial lung disease present and what are CXR findings?
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Progressive dyspnea, persistent cough (and can also cause atrial arrhythmias (MAT, frequent PACs) causing palpitations. CXR: inc reticular or nodualr intesritial markings without L mainstem bronchus displacement.
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Where do you find Histoplasmosis? How does it usually present? How is it contracted?
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Common and usually asymptomatic infection in endemic areas like Mississippi and Ohio River valleys and Central America. Usually found in soil with a high concentration of bird or bat guano droppings. Infection contracted by inhalation of spores or mycelial fragments. Infection very common in endemic areas and most people are infected before adulthood. <5% have symptomatic disease - extent is determined by amount of exposure and immunity of the host. Symptomatic infection: elf-limiting fever, chills, non-productive cough. CXR: patchy lobar or multinodular lobar infiltrates. Chronic cavitary pulmonary histoplasmosis is a progressive, fatal form of histo that usually develops in older COPD pts. Disseminated histo seen in immunocompromised adults and young children.
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How is dehydration a risk factor for venous thrombosis?
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Due to hemoconcentration
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What are s/s of PE?
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Sudden-onset pleuritic chest pain, cough, dyspnea, hemoptysis, tachycardia. Hemoptysis is due to pulmonary infarction. Common to also have low-grade fever and mild leukocytosis
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What will cehst CT show in PE?
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Characteristic wedge-shaped pleural-based opacification that is likely to occur distal to a completely occluded pulmonary artery. If contrast-enhanced, can usually see pulmonary artery filling defects.
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What are s/s of CPE on CXR?
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Hampton's hump.
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Are HIV pts at inc risk of pulmonary TB?
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Yes
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How will lung cancer look on CT?
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Rounded or spiculated mass
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How dos nonallergic rhinitis (aka vasomotor rhinitis) usually present? How do dx and treat?
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One of the chronic rhinitis symptoms (nasal congestion, rhinorrhea, sneezing, post-nasal drainage) without a specific etiology. Routine allergy testing not necessary prior to initiating empiric treatment. Depending on severity of symptoms, should treat with intranasal antihistamine (first gen H1 antihistamiens - rately respond to antihistamines that don't have anticholinergic properties), intranasal glucocorticoid, or combination of therapy
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How are the clinical features and treatment of allergic and nonallergic rhinitis different?
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Nonallergic rhinitis: nasal congestion, rhinorrhea and/or post-nasal drainage with later onset (>20yo) and can't identify clear trigger. Symptoms throughout year, sometimes worsen with change of seasons. Nasal mcosa - normal or erythematous Less commonly assoc with asthma, allergic disorders (eczema) or fhx of allergic disorders. Allergic rhinorrhea: more prominent EYE symptoms, watery rhinorrhea and/or sneezing, earlier age of onset, usually identifiable trigger (animals, environmental exposure), usually seasonal but can be throughout year. Nasal mucosa - normal, pale blue, or pallor. More commonly assoc with allergic disorders (ex: eczema),a shtma, and eustachian tube dysfunction. Tx: nonallergic with topical intranasal antihistamines or intranasal glucocorticoids for mild symptoms, combo therapy for moderate-severe. Allergic: avoid allegen, topical intranasal glucocorticoids are first line.
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How can simply distinguish nonallergic from allergic rhinitis?
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Predominant nasal congestion/stuffiness, post-nasal drip (dry cough), no specific identifiable triggers in non-allergic (allergic have predominant eye sypmtoms, itching, sneezing, with identifiable triggers in most cases)
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What will nasal cytology show in nonallergic rhinitis?
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Predominant eosinophils and inc mast cells (nasal cytology not ncessary for dx of NAR)
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How are serum IgE levels different in allergic rhinitis vs nonallergic?
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Elevated in allergic, normal in NAR
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What is the usual cause of parapneumonic effusions? How can dx? What are s/s?
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Pneumonia. CT scan will identify the fluid. Fluid may be sterile in initial stages and resovle with abx therapy, but in a few cases, pt will have continued elevated temp, pleuritic CP, dyspnea.
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What is an indication of chest tube placement in parapneumonic effusion?
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PH <7.2 almost always indcative of empyema and indicates removal of fluid by thoracostmy. Glucose of <60 also an indication
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What conditions have low pleural fluid glucose?
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Rheumatoid arthritis, TB, empyema, malignancy esophageal rupture
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When is LDH elevated?
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MI, cirrhosis, generalized ischemia
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When are L's in pleural space elevated?
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TB effusions or lymphomas
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How is active TB treated?
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4 drug therapy
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What is bronchiectesis and what is seen on CT?
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Progressive bronchial dilation, cyst formation, poor mucus clearance, secretion pooling that results form severe, repeated airway inflammation. CT: bronchial thickening
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What is allergic bronchopulmonary aspergillosis (ABPA), who gets it, and how present?
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A hypersensitivity reaction to Aspergillus colonization of the bronchi. Most commonly in pts with asthma or CF and presents with fever, malaise, productive cough, eosinophilia, and hemoptysis
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How are acute exacerbations of COPD treated?
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Combo of inhaled/nebulized bronchodilators and systemic steroids (most commonly used parental steroid is methylprednisone). In terms of abx, there is some role (gatifloxacin, clarithromycin, etc if have fever, WBC count elevation, infiltrate on CXR)
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What is N-acetylcysteine and what is its role in COPD exacerbation?
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Mucolytic agent. No longer used in exacerbation of COPD bc can worsen bronchospasm
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Should you use amionphylline in acute COPD exacerbation?
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Proven to be inferior to combo fo bronchodilator and corticosteroids for treatment of acute COPD exacerbation
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What change in A-a gradient is seen in PE?
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Elevated A-a gradient (caused by any process taht results in impaired gas exchage)
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What are causes of inc A-a graient?
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Interstitial disease, processes taht result in V/Q mismatching (PE, PNA, atelectasis, etc)
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What is hemithorax opacification on CXR often due to?
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Secondary to very large pleural effusion or complete collapse of a lung, possibly secondary to a mucus plug in mainstem bronchus. Tracheal deviation will help distinguish between the 2.
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What happens to PaCO2 in COPD?
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Dec PaCO2 due to inc in ventilation. If have elevated PaCO2, very concerning for developing respiratory failure.
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How does theophylline toxicity manifest?
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CNS STIMULATION (HA, insomnia, seizures), GI disturbances (nausea, vomiting), and CARDIAC TOXICITY (arrythmias). Inhibition of cytochrome oxidase system by other meds (cimetidine, cipro, erythromycin, clarithromycin, verapamil), diet, or underlying disease (cirrhosis, cholestasis, respiratory infections with fever) can alter its narrow therapeutic window. Toxicity can occur form accumulation by reduced clearance or decreased metabolism due to saturation of metabolic pathways.
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How do pts with pheo present?
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Headache, sweating, tachycardia, paroxysmal HTN
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