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Pulmonary_Board_Revie  - Welcome to the Texas Medical Center
 

Pulmonary_Board_Revie - Welcome to the Texas Medical Center

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    Pulmonary_Board_Revie  - Welcome to the Texas Medical Center Pulmonary_Board_Revie - Welcome to the Texas Medical Center Document Transcript

    • Pulmonary Board Review<br />Pulmonary function tests: <br />TLC- total lung capacity<br />VC- vital capacity<br />RV- residual volume<br />IC- inspiratory capacity<br />FRC -functional residual volume<br />IRV- inspiratory reserve volume<br />TV—total lung capacity<br />ERV—expiratory reserve volume<br />FVC- forced vital capacity<br />FEV1- forced expiratory volume at one second<br />FEV1/FVC <br />FEV 25-50%<br />Intra-thoracic obstruction<br />Extra-thoracic obstruction<br />Diffusion capacity<br />Increased or decreased diffusion capacity<br />Alveolar hemorrhage<br />Early pulmonary edema<br />polycythemia <br />left to right cardiac shunt<br />pregnancy<br />Diffusion capacity/alveolar volume<br />6 second expiration<br />12% (200ml) improvement with bronchodilators<br />Methacholine challenge. FEV1 decreases by 20%<br />Good negative predictive value<br />Positive in asthma, COPD, viral illness, smoking, allergic rhinitis<br />Asthma<br />Cough, shortness of breath, chest tightness, intermittent symptoms<br />Cough variant asthma<br />Bimodal distribution<br />Airway obstruction, inflammation and hyper-responsiveness<br />Airway eosinophilia<br />Infiltration of inflammatory cells, denudation of epithelium, subepithelial fibrosis, mucous gland hyperplasia, increase smooth muscle mass, goblet cell hyperplasia<br />Airway remodeling<br />Wheezing on exam.<br />No wheezing on exam during status asthmaticus<br />If CO2 rises or ph lowers, time to intubate<br />Normal DLCO<br />Clinical definitions:<br />Mild intermittent asthma<br /><2 times per week, <2 per month nocturnal symptoms<br />Mild persistent asthma<br />>2 times per week<1 time per day, >2 per month nocturnal symptoms<br />Moderate persistent<br />Daily symptoms, daily use of bronchodilators, > 1 time per week nocturnal symptoms<br />Severe persistent<br />Continual symptoms, limited activity<br />Peak flow measurements<br />Worse at night, peak flows at the lowest in the am<br />Adjunct therapies<br />Allergic rhinitis treatment<br />Allergy meds<br />Nasal steroids<br />Anti-reflux meds<br />Occupational asthma<br />Recurrent symptoms while in working environment<br />Allergic sensitization or non allergic mechanisms<br />Hundreds of agents have been identified<br />Flour-byssinosis<br />RADS<br />No history of asthma, exposed to high levels of respiratory irritants<br />Allergic bronchopulmonary aspergillosis<br />wheezing<br />Humoral and cellular immune reaction to aspergillus fumigates<br />Bronchiectasis<br />Pulmonary infiltrates<br />Pulmonary fibrosis<br />Positive skin test for aspergillus<br />Elevated IGE levels<br />Serum precipitants <br />Steroids/antifungals<br />Churg-strauss vasculitis<br />Small vessel necrotizing vasculitis<br />“uncovered” in patients with asthma on leukotriene inhibitors and tapering off steroids<br />Exercise induced asthma/exercise induce urtacaria<br />Cold dry air<br />Exercise tolerance test reveals decrease in FEV1 with exercise<br />Aspirin sensitive asthma<br />Severe asthma with nasal polyps exacerbated by aspirin or NSAIDS<br />Treatment<br />Short acting β agonists<br />Inhaled corticosteroids<br />Long acting β agonists<br />Increased inhaled corticosteroids<br />Cromolyn<br />Leukotriene modifiers<br />Theophylline<br />Anti-IgE antibody<br />Omalizumab (Xolair)<br />Vocal cord dysfunction<br />Flutter waves on PFT’s<br />Obstructive lung disease<br />COPD/emphysema/chronic bronchitis/obliterate bronchiolitis/asthmatic bronchitis<br />GOLD guidelines<br />Airflow limitation which is not fully reversible<br />Smoking association<br />Air pollution/exposure to dust and chemicals/cooking/heating<br />Prevalence 6.9% for mild COPD<br />Prevalence 6.6% for moderate COPD<br />Screen for α-1 antitrypsin (AAT): younger, family occurrence, liver disease<br />ZZ alleles severely deficient<br />smoking cessation decrease the rate of decline of the FEV1<br />inflammatory response<br />chronic hyper-secretion of mucus, bronchial gland hypertrophy and goblet cells, ciliary dysfunction<br />loss of alveolar attachments and loss of elasticity, small airway collapse, loss of tethering<br />FEV1 does not correlate with symptoms<br />BODE<br />Body mass index/air flow obstruction/dyspnea/exercise capacity index (6 minute walk distance)<br />Correlates with survival<br />More than 75% of COPD patients have some reversibility with bronchodilators in FEV1<br />52% of non responders with change reversibility on the next set of PFT’s<br />Dynamic hyperinflation occurs with exercise, increases dyspnea<br />Flattened diaphragm. Increased retrosternal airspace. Increase A-P diameter<br />ABG to assess for hypercapnea and hypoxemia<br />Normal 6 minute walk distance is 500-600m. assess for hypoxemia<br />Screen for alpha-1 antitrypsin deficiency<br />Smoking cessation is the most effective intervention to reduce risk of developing COPD and stop progression<br />Only oxygen therapy and smoking cessation improve survival<br />Short-acting β-agonist, long acting β-agonists<br />SMART trial (salmeterol in asthma)<br />Short-acting anti-cholinergics, ipratropium<br />Long acting anti-cholinergics, triotropium<br />Theophylline (methylxanthines)<br />Inhaled corticosteroids does not affect the yearly decline in lung function<br />Inhaled corticosteroids decreases the rate of exacerbations<br />Inhaled CS and long acting beat agonist combined decline in quality of life and health status and rate of acute exacerbations is reduced, improvement of lung function and alleviation of Dyspnea<br />Oral CS not recommend for long term maintenance<br />Influenza and pneumococcal vaccine recommended<br />Weekly infusions of α-1 antitrypsin purified protein<br />Antibiotics for exacerbations<br />n-acetylcysteine (mucomyst) does not decrease the number of exacerbations<br />cough has a significant airway protective effect<br />leukotriene modifiers not recommended in COPD unless patient also has allergic rhinitis or asthma, but 1 study showed used acutely decrease the number of returns to ER within 30 days<br />oxygen for >15 hrs per day increases survival<br />P02 <55mmHg and sat <88% with or without hypercapnea<br />Or PaO2 >55mmHg but <60mmHg or sat >89% with evidence of pulmonary hypertension, peripheral edema suggesting right heart failure or polycythemia with Hct >55%<br />Nocturnal oxygen supplement<br />CPAP for nocturnal hypercapnea <br />Pulmonary rehabilitation—exercise training, nutrition counseling and education<br />Bullectomy<br />Lung volume reduction surgery (NETT)<br />Low FEV1 and low DLCO worse mortality<br />Predominant upper lobe bullae and low baseline line exercise function, improved function and survival<br />Lung transplant. Refer when FEV1<35%. PaO2 55-60 and PCO2 >50<br />COPD exacerbations<br />Increase in dyspnea, sputum production and sputum volumes<br />Many causes for exacerbations<br />Antibiotics therapy decrease hospitalization time<br />Bacteria: strep pneumo, H flu, Moraxella, Klebsiella, Pseudomonas, atypical (Chlamydia, legionella)<br />Systemic steroids<br />Bronchodilator therapy<br />Non-invasive positive pressure ventilation<br />Deceases rate of intubation by 28%, length of stay and in-hospital mortality (10%)<br />pH 7.25-7.35, CO2>45 and RR >25. Expect to see improvement by 10 in CO2 by 2-3 hrs<br />Intubation and Mechanical ventilation<br />Severe dyspnea, hemodynamic instability, impending respiratory arrest, life-threatening hypoxemia, sever acidosis (ph<7.25) and hypercapnea >60)<br />Discharge criteria:<br />Use of beta agonist no more than q 4hrs<br />Ability to walk across the room<br />Ability to eat and sleep without frequent awakenings by dyspnea<br />Stable clinical status and ABG for 24 hrs<br />Understanding by the patient and care givers the correct use of inhalers<br />Follow-up and home care arrangements<br />Sleep medicine<br />Obstructive sleep apnea<br />Absence of airflow for 10 seconds despite persistence of respiratory effort with desaturation of 4%<br />Oxygen saturation occurs after the obstruction<br />Terminates with snore and arousal<br />Hypopnea is decreased airflow of 30% lasting 10 seconds with 4% desaturation<br />Degree classified by AHI (apnea-hyponea index)<br />Mild 5-15<br />Moderate 16-30<br />Severe >30<br />Estimated prevalence is 24% of middle aged men and 9% of middle aged women<br />Epworth scale is an estimate of daytime sleepiness (>10 indicates sleepiness)<br />Incidence increases with neck circumference and increase in BMI<br />Increased risk with craniofacial abnormalities (enlarged tonsils too)<br />Incidence increases with age, women after menopause, hypothyroidism<br />Associated with increase risk of stroke, hypertension, MI, CHF and metabolic syndrome<br />Increases driving and work-related accidents due to sleepiness<br />Loss of upper airway tone<br />Complain of daytime sleepiness, fatigue, snoring, am headaches, dry mouth, witnessed apneas, gasping for breath<br />Evaluate with nocturnal polysomnography<br />Treatment with positive airway pressure, CPAP, BiPAP, weight loss<br />Adequate sleep hygiene, avoid sleeping on back<br />No driving or operating machinery until treated<br />CPAP improves quality of life, cognitive function, and daytime sleepiness<br />Improves mortality, blood pressure and cardiac function<br />Improve compliance with heated humidifier, appropriate mask selection<br />AutoPAP<br />Surgical procedures: tonsillectomy, uvulopalatopharyngoplasty (UPP), genioglossal or mandibular advancement, tracheostomy<br />Oral devices: tongue retaining devices, or mandibular advancement<br />modafinil<br />Central Sleep apnea<br />Carbon dioxide threshold, high ventilator response<br />“unmasked” by treatment of OSA with CPAP<br />Associated with congestive heart failure (EF<40%) and strokes<br />Insomnia, poor sleep quality, daytime sleepiness and fatigue<br />Treat underlying illness<br />Cheyne-stokes respiration, periodic breathing<br />BiPAP, oxygen<br />Obestity hypoventilation (pickwickian syndrome)<br />Increased CO2, decreased O2 due to hypoventilation. Chemoreceptors in brain are reset and less responsive to elevated CO2<br />Medroxyprogesterone, acetazolamide<br />Associated with OSA but not always (10-20%)<br />Oxygen desaturation during REM sleep (hypoventilation) in COPD patients<br />Neuromuscular diseases: muscular dystrophy, myotonic dystrophy, amyotrophic lateral sclerosis, post polio syndrome, myasthenia gravis<br />Restrictive lung disease, interstitial lung disease, kyphoscoliosis, obesity<br />Nocturnal respiratory impairment can precede daytime abnormalities<br />REM-related hypoventilation<br />Upright to supine reduction by >25% in vital capacity indicates diaphragmatic weakness<br />Non-invasive positive pressure ventilation<br />Narcolepsy<br />Excessive daytime sleepiness<br />Abdnormalities in REM sleep<br />Diagnosis with normal nocturnal PSG followed by abnormal MSLT (multiple-sleep latency test)<br />Short mean sleep latency and 2 or more SOREM’s (sleep onset REM’s)<br />Decreased hypocretin in CSF<br />HLA DR-4 associate<br />Cataplexy with excitement, laughing, hyponogogic hallucinations, sleep paralysis<br />Scheduled daytime naps recommened<br />CNS stimulants, modafinil<br />Rest leg syndrome diagnosised with URGE criteria<br />an urge to move the limbs with or without sensations <br />improvement with activity <br />worsening at rest <br />worsening in the evening or night<br />Peridoic limb movement disorder<br />Rhythmic movements of arms or legs during sleep<br />REM-behavior disorder<br />Associated with Parkinson’s disease<br />High altitude pulmonary edema<br />Sleeping at high altitude is associated with greater hypoxemia and crescendo-decrescendo breathing pattern followed by hypopnea or apnea<br />Increased ventilator response to hypoxia <br />Patients complain of frequent arousals and poor sleep quality.<br />Prevent by gradual ascent, acetazolamide, low dose hypnotics<br />Acute altitude sickness (mountain sickness) (18-40%)<br />Occurs with in 4-36 hours of ascent to 2000m (6500ft)<br />Headache, loss of appetite, nausea, vomiting, weakness, malaise, difficulty sleeping<br />Neurologic abnormalities can occur (HACE)<br />Resolves spontaneously in 2-5 days, worse the first night<br />Slow ascent, rest, acetazolamide, dexamethasone, if symptoms don’t reverse, have to descend <br />High-Altitude Pulmonary edema (HAPE) (.01%)<br />Occur 2-4 days after ascent.<br />Dyspnea, dry cough, worsening hypoxemia, frothy blood tinged sputum, fever, mental status changes, death<br />x-ray changes consistent with pulmonary edema<br />rate of ascent, male gender, physical activity, individual susceptibility<br />blunted ventilator response to hypoxia, accentuated pulmonary vasoconstrictor response to hypoxia, reduced vital capacity, leads to increase pulmonary pressures<br />inflammatory response, high pulmonary pressures and leakage of high protein fluid into alveoli<br />nifedipine is effective at treating along with descent and oxygen<br />air travel<br />commercial jets pressurized to 8000ft, leads to alveolar PO2 of 15% of inspired oxygen at sea level<br />with COPD patients, goal is PaO2 >50 mmHg<br />formula to predict the PaO2<br />Pulmonary Hypertension<br />Secondary, associated and primary<br />Pulmonary venous hypertension<br />Left atrial or ventricular disease (systolic or diastolic dysfunction)<br />Left-sided valvular disease<br />Pulmonary hypertension due to chronic hypoxemia<br />COPD/emphysema<br />Interstitial lung disease/Idiopathic pulmonary fibrosis<br />Sleep-disordered breathing<br />Alveolar hypoventilation disorders<br />Chronic exposure to high altitude<br />Pulmonary hypertension due to thrombotic or embolic disease<br />Chronic thrombo-embolic disease<br />Tumor, parasite, foreign material emboli<br />Sickle cell disease<br />Sarcoidosis, histiocytosis X, LAM (lymphangioleiomyomatosis)<br />Extensive compression of pulmonary arteries—tumor, adenopathy, fibrosisng mediastinisis<br />Pulmonary venous or capillary disease<br />Pulmonary veno-occlusive disease<br />Pulmonary capillary hemangiomatosis<br />Associated diseases:<br />Collagen vascular diseases (scleroderma, lupus)<br />Congenital systemic to pulmonary shunts<br />Portal hypertension<br />HIV infection<br />Drugs (Phen-Fen, rapseed oil)<br />Most common cause of pulmonary hypertension is left heart disease. Must be ruled out by right heart cath<br />Additional screening tests for diagnosis of pulmonary HTN<br />PFT’s<br />V/Q followed by pulmonary angiogram<br />High resolution CT chest<br />Serologic screening tests for HIV, sickle cell, collagen vascular disease<br />Polysomnography (sleep study)<br />Echocardiogram with bubble study (contrast, agitated saline)<br />Pathophysioloy of Pulmonary arterial hypertension<br />Narrowing of lumen of the small pulmonary arteries resulting in increased vascular resistance and pulmonary artery pressure<br />Vasoconstriction of the pulmonary arteries, proliferation of the cellular elements within the arterial wall obliteration of the vascular lumen. Plexiform lesions<br />Inability to recruit vessels during exercise leading to increased pulmonary pressures. Right heart unable to maintain cardiac output during exercise causing progressive Dyspnea, dizziness, syncope. Eventually right failure, dilation, arrhythmias<br />Familial PAH associated with the bone morphogenic protein receptor 2 (BMPR2).<br />93% of cases are sporadic form<br />Therapies<br />Oxygen<br />Coumadin, no randomized control trials, historical controls suggest improved survival<br />Digoxin for RV failure, not validated<br />Prostacyclin analogs<br />Epoprostenol (flolan)<br />Treprostinil (remodulin)<br />Iloprost (ventavis)<br />Endothelin-1 Receptor Antagonist<br />Bosentan (tracleer) A and B receptor<br />Ambrisetan (letairis) A receptor<br />Phosphodiesterarse Inhibitors<br />Sildenafil (Revatio)<br />Tadafinil <br />Increases NO by decreasing the degradation of cyclic guanosine 3’-5’ monophosphate (cGMP)<br />Diurectics, low dose<br />Atrial septostomy<br />Lung transplant<br />Per NIH registry of PAH patients in the 1980’s, the median survival was 2.8 years<br />Poor prognosis:<br />Advanced NYHA functional class<br />Poor exercise tolerance (6 minute walk distance)<br />Elevated right atrial pressure and pulmonary artery pressure<br />Increase PVR, decrease cardiac index<br />Chronic thrombo-embolic disease<br />Most patients lung perfusion returns to normal or near normal. <br />Some (4%) develop CTEPH<br />Proximal involvement of the pulmonary arteries may cause elevated pulmonary vascular resistance, cor pulmonale and right ventricular dysfunction<br />Exercise tolerance decreases and may have dizziness or syncope as the RV fails.<br />Obstruction of the vasculature not longer resembles a blood clot, it an organized web with extensive scarring. Walls become thicken and progressively narrowed. Angio shows tapering of vessels with luminal irregularities<br />Risk factors: previous PE, younger age, large perfusion defect, idiopathic PE<br />V/Q scan for diagnosis, followed by pulmonary angiography for confirmation and to evaluate if<br />Echo to evaluate RV dysfunction and pulmonary HTN<br />Pulmonary thromboendarteretomy in specific centers<br />Pulmonary Malignancies<br />Mesothelioma<br />Cancer of the pleura and peritoneum (90%/10%)<br />Estimated 3000 cases/year<br />5-6 more common in men<br />Long latency period (40 years)<br />Strong asbestosis exposure (90%)<br />Increased risk with incrased exposure<br />Ship building, (navy ship yards) Sand balsting, house building/destruction, mines, factories<br />Asbestosis increases risk of bronchogenic cancer<br />Smoking plus asbestosis 40-fold increases risk of bronchogenic cancer<br />Smoking does not increase the risk of Mesothelioma<br />Chest pain, shortness of breath, pleural effusion, pleural thicking, malais, weight loss<br />Surgical biopsy for diagnosis<br />Pleural biopsy is usually inadequate tissue<br />Placing of chest tube never finishes draining effusion and tumor will grow out the chest tube or biopsy site<br />VATS 80% positive, open thoractomy 90%<br />Distinguish from adenoca—negative PAS satin for mucin, negative TTF-1<br />Mature mestothelial cells<br />Poor respone to chemotherapy, radiation therapy. Extrapleural pneumonectomy<br />Survival 10% at 2 years<br />Solitary Pulmonary nodule<br />Single discrete intrapulmonary density less than 3 cm in diameter completely surrounded by normal aertated lung<br />Bronchogenic CA, mets to the lung, granulomas, benign lung tumors, AVM’s, COP, pulmonary infarcts<br />Estimated changes of malignancy based on size, age, smoking history, previous malignancies, nodule characteristics (Fleischer’s Recommnedation)<br />Malignant nodules have speculated margins, little or no calcifications, doubling times 30-500 days<br />Old films are key: benign lesions have either very long double times (200 years) or very short (30 days)<br />Benign lesions have smooth margins, central, diffuse or laminated calcifications<br />PET scan show uptake in >90% of malignant nodules >1cm in size, but can be false negative in bronchoaveloar carcinoma and false positive in inflammatory lesions<br />Initial evaluation: monitor with serial radiographs if low concern for cancer vs attempted transthoracic needle aspiration (must be >1cm). transbronchial biopsies unrealiable. Or surgical resection/biopsy.<br />Assess comorbidities. Lung function test. If possible straight to resection/lobectomy<br />Bronchogenic cancer<br />Second most common cancer, but the most common cause of cancer death.<br />Overall survival is 14-16% at 5 years. Not much improved from 20 years ago<br />80-90% related to cigarette smoking<br />Smoking cessation reduces risk to near baseline risk at 10 years<br />Other risk: second hand smoke, radon, asbestos, age and COPD<br />Screening by sputum cytology and chest radiography in the 1980’s failed to show reduction in lung cancer mortality. Increased detection<br />CT scan increases detection but also causes increased cost and morbitity for work up for bening lesions. Has not shown improvement in survival benefit<br />85% are non-small cell type. (adenoca, Squamous cell ca, large cell/undifferentiated)<br />15 % small cell type. 70% metastatic at the time of diagnosis.<br />Asymptomatic in only 5-15% of patinents<br />Present with cough (most common), dyspnes, chest pain, and Hemoptysis (indicates endobronchial component)<br />1/3 present with features suggestive of metastatic disease (bone pain, headache)<br />10% present with paraneoplastic syndromes: SIADH, clubbing, hypercalcemia, ACTH, hypertrophic osteoarthropathy<br />Diagnosis with bronchoscopy if central lesions (up to 90%), TTNA if peripheral (50-90%), sampling a metastatic sites: lymph nodes, pleural fluid. Most easily accessible site. Mediastinoscopy or surgical biopsy/resection<br />Staging<br />CT scan of chest, abdomen (liver and adrenals), bone scan, MRI of brain<br />Mediastinal biopsy of enlarged lymph nodes >1cm or distant sites<br />PET scan, not readily available at all sites, so not uniformly recommended<br />Resectability?<br />Operability? Nutrition, performace status, PFT’s<br /> Metastatic to lung: lbs kg<br />Thyroid: teeny tiny nodules, calcify<br />Breast: nodules, pleural effusions<br />Renal: pleural effusions, bloody, large masses, endobronchial mets<br />Melanoma: hemorrhagic nodules, hemoptysis<br />Colon, to liver first<br />Lymphoma: lymphadenopathy, or nodules<br />Osteosarcoma: large calcified mets<br />Lymphangitic carcinomatosis<br />Benign neoplasm of the lung<br />Hamartoma<br />Normal tissue in abnormal place<br />Cartilage, fat, fibromyoid stroma<br />Very slow growing, eccentric “popcorn” calfications<br />