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49 Cards in this Set
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20-year-old female college student presents to the clinic with complaints of cough for the past 3 months. She admits to occasional nocturnal cough and chest tightness. Over-the-counter cough medications had no impact on symptoms. She has no past medical or surgical history. She does not smoke, drink alcohol, or use illicit drugs. Her only medication is an oral contraceptive. She has no known drug allergies. On physical examination, she appears anxious; respiratory rate is 20 breaths per minute; BP 120/70 without change during respiration; and there is no cyanosis. Neck is supple with no masses, thyromegaly, jugular venous distension; or stridor. Heart has normal S1 and physiologically-splitting S2. There are no murmurs or rubs. Lungs reveal fine end-expiratory wheezing with scattered rhonchi and no rales. The peak expiratory flow rate (PEFR) is 62% predicted and the forced expiratory volume in the first second (FEV1) is 65% predicted. Peripheral blood eosinophil count is 1,500/mm3. She is given albuterol via a metered-dose inhaler and is observed for 30 minutes in the examination room. She feels subjectively improved and repeat pulmonary function tests reveal PEFR 70% predicted and FEV1 80% predicted.
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asthma
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What is asthma?
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chronic inflammatory disorder of airways in which many cells/cellular elements play a role (eosinophils, macrophages, Tcells)
inflammation causes recurrent episodes of coughing (night or early morning), wheezing, SOB, and chest tightness variable airway obstruction that's reversible (spontaneously or w/ treatment) |
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How do you establish diagnosis of asthma?
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history, physical, and spirometry demonstrate:
1. episodic symptoms of airflow obstruction or hyper-responsiveness 2. obstruction is reversible 3. alternative diagnoses are excluded (asthma treatments are very different from other diseases) |
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How do you establish airflow obstruction?
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A. peak flow meters
advantages-simple to perform; inexpensive; allows patient to monitor and treat symptoms at home disadvantages-patient dependent; errors in estimating lung function; misses mild disease; can't differentiate obstructive vs restrictive defects B. spirometry-more accurate and reliable; can distiguish b/t obstructive vs restrictive defects C. reversibility determined after inhalation of SABA; increase in FEV1>200ml and >12% from baseline indicates reversibility |
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How do you classify asthma severity?
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based on symptoms and lung function
A. Intermittent symptoms-<2 days/week night awakenings-<2x/month SABA use-<2 days/week interference w/ activity-none FEV1/FVC-normal (>70%) B. mild symptoms->2/week, not daily night awakenings: 3-4/month SABA use->2/week, not daily, not >1/day interference w/ activity-minor FEV1/FVC: normal C. moderate symptoms-daily night awakenings->1/week, not nightly SABA use-daily interference w/ activity-some FEV1/FVC-reduced <5% D. severe symptoms-throughout day night awakenings-nightly SABA use->1/day interference w/ activity-extreme FEV1/FVC-reduced >5% |
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How do you assess asthma control?
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same way as asthma classification (symptoms and lung function)
A. well-controlled: correlates w/ intermittent asthma B. not well-controlled: correlates to a combined mild/moderate asthma C. very poorly controlled-correlates to severe asthma |
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Describe the step wise approach in asthma treatment and treatment goal
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treatment goal-stabilize and maintain long term normal lung function by managing symptom triggers w/ least amount of meds (minimize side effects)
Step 1-SABA as needed Step 2-low dose inhaled corticosteroids (ICs) Step 3-low dose ICs and LABA or medium dose ICs Step 4-medium dose ICs and LABA Step 5-high dose ICs and LABA (consider omalizumab for patients w/ allergies) Step 6-high dose ICs, LABA, and oral corticosteroid (consider omalizumab) smoking cessation is key component of asthma control and prevention of asthma exacerbations |
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Describe the principles of step wise therapy
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a. long term conrol-ICs are best
b. SABA use-for acute symptoms and exacerbations and intermittant asthma c. patients w/ persistant asthma-use both SABA and ICs (SABA overuse-->inflammation; ICs often underused since patients don't feel immediate relief) d. addling LABA-improves lung function > increasing ICs; don't use alone |
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Describe stepping up, stepping down, and follow up in asthma treatment
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step up if not controlled; if very poorly controlled, consider stepping up 2 steps or adding oral corticosteroids
before increasing drugs, consider other causes (environmental, poor adherence, comorbidities) follow up: 2-6 weeks if not controlled; 3-6 months when controlled step down therapy w/ well-controlled asthma >3 months; watch out for relapse w/ reduction of ICs |
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Describe the risk factors for asthma exacerbations and asthma related deaths
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previous severe exacerbation (intubation, ICU admission)
>2 hospitalizatioin or >3 ED visits in 1 year use >2 SABA cannisters/month difficulty perceiving airway obstruction or worsening symptoms low socioeconomic status drug use psychosocial problems or psychiatric disease comorbidities (CVD, chronic lung disease) |
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How do you classify the severity of asthma exacerbations?
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A. mild
dyspnea only w/ activity PEF (FEV1)->70% B. moderate dyspnea limits usual activity PEF: 40-70% predicted C. severe dyspnea at rest; interferes w/ conversation PEF-<40% D. life threatening too dyspneic to speak; perspiring PEF-<25% |
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Describe the treatment of asthma exacerbations
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A. mild-SABA; possible oral corticosteroids (OCs); home care
B. moderate-same as above; may require office or ED visit C. severe-usually requires hospitalization; SABA, OCs, adjunctive therapies helpful D. life threatening-requires hospitalizatioin (possible ICU); minimal relief w/ SABA; IV corticosteroids; adjunctive therapies |
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Describe what happens to arterial blood gases in asthma exacerbation
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early stage-mild hypoxemia and respiratory alkalosis
severe stage-PaCO2 increases (hypercapnia); patient unable to blow off CO2 through airway obstruction; pH normalizes Loss of consciousness or other altered mental statusw/ PH normalizing and dyspnea w/ rest/conversation is very bad sign |
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A 72-year-old male is evaluated in the clinic for progressive dyspnea on exertion and has had two unscheduled visits in the past 6 months for “bronchitis.” He smoked 2 packs of cigarettes for over 50 years (100 year + pack history). On physical examination, respiratory rate is 22 breaths per minute; BP is 150/90 (Stage I HTN) with no change during respiration. He is thin, acyanotic, and is barrel-chested; breath sounds are diminished in all fields. FEV1 does not improve with inhaled albuterol.
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COPD
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Wha'ts the definition of COPD?
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preventable and treatable disease w/ extrapulmonary effects
airflow limitation is not fully reversible airflow limitation is progressive and associated w/ abnormal inflammatory response of lung to noxious particles or gases a. chronic bronchitis-chronic cough for >3 months in 2 successive years w/ other causes of cough ruled out b. emphysema-abnormal permanent enlargement of air spaces distal to terminal bronchioles accompanied by destruction of their walls w/out obvious fibrosis |
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Describe the pathogenesis of COPD
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cigarette smoke-->lung inflammation-->oxidative stress and proteinases-->COPD pathology
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What are the risk factors for developing COPD?
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A. exposures
1. cigarette smoking** 2. dust/chemicals 3. pollution 4. bronchopulmonary infections 5. socioeconomic status B. host factors 1. genetic: alpha-1 antitrypsin deficiency 2. airway hyper-responsiveness 3. gender 4. age 5. nutrition 6. co-morbidities (lung cancer, CAD, depression, osteoporosis) |
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Describe the natural history of COPD and compare smoker w/ nonsmokers
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FEV1 begins to decline in healthy nonsmokers at age 25
rate of decline is steepr for smokers than nonsmokers upon smoking cessation, rate of decline parallels rate of decline of nonsmokers (no recovery, but matches progression rate); this is true no matter how long someone has been smoking |
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Describe clinical features in history of COPD
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>20 pack/year smoking history
productive cough or acute chest illness in 5th decade; w/ disease progression, intervals b/t acute exacerbations become shorter dyspnea on exertion in 6th or 7th decade low volume sputum production occurring mostly in morning |
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Describe the physical exam features of COPD
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early-slowed expiration and wheezing on forced expiration
disease progression-hyperinflation, increased AP diameter of chest, flattened diaphragm; accessory muscles used in breathing; decreased heart and breath sounds end stage-positional modification to relieve dyspnea (leaning forward); cyanosis large tender liver indicates right heart failure blue bloater-typical chronic bronchitis appearance pink puffer-typical emphysema appearance new class-atypical appearance (model) |
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Describe the diagnostic evaluations of COPD
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1. PFT-necessary for diagnosis, determining severity of airflow obstruction and prognosis; FEV1/FVC makes diagnosis; FEV1 classifies severity; not useful as a screening tool
2. Imaging a. chest x-ray-poor sensitivity (50%); shows low, flat diaphragm; heart appears long and narrow, cor pulmonale CT-better sensitivity/specificity for emphysema; differentiates centriacinar (caused by smoking) vs panacinar (alpha1-antitrypsin deficiency-younger patients) ABG |
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What findings predict airflow obstruction?
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>55 pack year smoking history
wheezing on auscultation self-reported wheezing history and physical exams are generally poor predictors |
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What are the prognosis factors of COPD?
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smoking history
age FEV1 severity of hypoxemia CO2 retention reversibility of airway obstruction (favorable prognostic factor) |
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Describe the GOLD classification of COPD
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for all stages, FEV1/FVC<70%
Stage I (mild): FEV1>80% predicted Stage II (moderate): FEV1 50-80% Stage III (severe): FEV1 30-50% Stage IV (very severe): FEV1 <30% or <50% w/ chronic respiratory failure |
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Describe the goals of treatment and treatment by severity of disease
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goals-reduce lung function decline, hospitalization, and mortality; prevent and treat exacerbation; relieve dyspnea; improve exercise tolerance and quality of life
stage 1-SABA when needed 2-add LABA and rehabilitation 3-add inhaled glucocorticosteroids 4-add long term O2; consider surgical treatment |
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Describe the pharmacological managment of COPD
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a. bronchodilators (beta 2 agonists or anticholinergics-tiotropium) are central to symptomatic management; ok to use LABA alone in treatment of COPD
b. inhaled corticosteroids (ICs)-reduces inflammation, exacerbations, and progression of symptoms; side effects include dysphonia, oral thrush, and increased risk of pneumonia c. monotherapy-tiotropium, LABAs, or ICs are recommended in symptomatic patients w/ FEV1<60% as a good place to start (combination therapy can be used but not proven to be better) |
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Describe non-pharmalogical, non-surgical management of COPD
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A. O2 therapy-improves long term survival in hypoxemic patients; improves secondary polycythemia, wasting, cor pumonale, cardiac function, neuropychological function, exercise performance, and activities of daily living
b. pulmonary rehab (exercise training)-improves exercise tolerance, symptoms of dyspnea and fatigue (not mortality); recommended in symptomatic patients w/ FEV1<50% |
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Describe surgical procedures for COPD
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lung reduction-effective in reducing symptoms; indicated when FEV1<45%, PaO2>45, PaCO2>60
lung transplant-increasing incidence; indicated in patients <64yo w/ low exercise tolerance, and FEV1 and DLCO both <20% |
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Describe the mangement of COPD exacerbations
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most common causes of exacerbations are infections and air pollutions; patients w/ clinical signs of airway obstruction should be treated w/ antibiotics
systemic steroids improve symptoms and lung function non-invasive intermittant positive pressure ventilation (BiPAP)-improves blood gases and pH, reduces in hospital mortality, decreases need for mechanical ventilation and length of hospital stay |
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A 59-year-old male presents with persistent cough, dyspnea, wheezing, and increasing sputum production over the past 3 months. He states he presented one month ago to a walk-in clinic where he was presumptively diagnosed with asthma and was treated with inhaled albuterol, inhaled budesonide, and montelukast. He reports occasionally coughing up blood. He admits to a 40-pack-year smoking history. Lungs reveal scattered rhonchi localizing over the left hemithorax and diminished breath sounds at the left base.
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lung caner
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What is lung cancer?
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Uncontrolled growth of malignant cells lungs and tracheo-bronchial tree
esult of repeated carcinogenic irritation causing increased rates of cell replication Proliferation of abnormal cells leads to hyperplasia, dysplasia or carcinoma in situ African american men have highest incidence and mortality; women more likely to develop lung cancer than men w/ same smoking habits |
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What causes lung cancer?
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Radiation Exposure-radiation therapy increases risk of obtaining a primary lung cancer (for mastectomy, Hodgkin lymphoma)
Smoking-tobacco use is leading cause of lung cancer; Risk related to age of smoking onset, amount smoked, gender, product smoked, depth of inhalation Environmental/ Occupational Exposure-Asbestos; Radon; Passive smoke |
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What are the histologic cell types of lung cancer (in order of prevalence)?
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Adenocarcinoma (most common)
Squamous cell carcinoma Small cell carcinoma Large cell carcinoma |
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What does cancer metastasize to? What symptoms would indicate metastasis?
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a. Lymph nodes-lymphadenopathy of supraclavicular, axillary, cervical nodes
b. Brain-focal neurologic defects c. Liver-jaundice, ascites, RUQ pain/tenderness; AST/ALT elevated d. Adrenal glands-most common site of metastasis (40%); hyper/hypotension, cushing syndrome (small cell carcinoma) e. Bones-pain, elvated alkaline phosphatase and Ca f. Paraneoplastic syndrome (elevated endocrine hormones)-associated w/ small cell carcinoma |
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What are methods used to diagnose and stage lung cancer?
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History and Physical exam
Diagnostic tests-Chest x-ray; Biopsy (bronchoscopy, needle biopsy, surgery) Staging tests-CT chest or abdomen; Bone scan; Bone marrow aspiration; PET scan |
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Describe syndromes and associated symptoms of regional metastasis of lung cancer
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Esophageal compression-dysphagia
Laryngeal nerve paralysis-hoarseness Symptomatic nerve paralysis-Horner’s syndrome Cervical/thoracic nerve invasion-Pancoast syndrome Lymphatic obstruction-pleural effusion Vascular obstruction-superior vena cava syndrome Pericardial/cardiac extension-effusion, tamponade |
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Describe lab testing for cancer
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Liver function test-suggestive of liver metastasis
Hypercalcemia-suggestive of bone metastasis Elevation of alkaline phosphatase-suggestive of bone or liver metastasis Anemia-suggestive of metastatic disease No tumor markers exist for non-small cell lung cancer |
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Describe the imaging studies done in lung cancer
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A. CT scan of chest-characterizes primary tumor & defines its relationship to chest wall and mediastinum; identify mediastinal lymph nodes that are enlarged for possible malignant involvement; detects contralateral lung, chest wall or abdominal lesions that are suspicious for metastasis; assists in staging of lung CA
B. Positron emission tomography (PET)-functional imaging study in which cells metabolize glucose and concentrate radioactive label material w/in the cell; malignant cells metabolize glucose more rapidly than normal cells distinguishes benign vs malignant lesions better than CT scan; good negative predictive value C. MRI-helpful when brain metastasis, adrenal metastasis, mediastinal invasion, chest wall invasion or spinal cord invasion is suspected |
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Describe tissue sampling (biopsy) in lung cancer
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Non small cell or small cell lung cancer can't be diagnosed or accurately staged noninvasively (tissue is required)
Sampling primary tumor is diagnostically only; biopsying possible metastatic sites can be diagnostic and provide additional staging information important to differentiat b/t small cell and non small cell (need to do before cancer can be staged and treated) Non-Surgical Approach-Needle Biopsy; Bronchoscopy; Endobronchoscopic ultrasound Surgical Approach-Cervical mediastinoscopy; Anterior mediastinotomy; Thoracoscopy |
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Describe staging and treatment associated w/ lung cancer
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A. TMN staging based upon Tumor characteristics (T); presence/absence of regional lymph node metastasis (N); Presence or absence of distant metastasis (M)
B. Staging and treatment of non small cell carcinoma Stage Ia/b-tumor found only in lung; surgery IIa/b-tumor has spread to lymph nodes associated w/ lung; surgery IIIa-tumor has spread to tracheal lymph nodes, chest wall, and diaphragm; chemotherapy followed by radiation or surgery IIIb-tumor has spread to lymph nodes in opposite lung or in neck (infiltrated major vessels); combo chemo and radiation IV-tumor has spread beyond chest; chemo and palliative care prognosis-generally decreases w/ stage progression (IV and IIIb are flipped in pathological staging) |
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Describe small cell lung carcinoma
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Small Cell lung carcinoma (SCLC)-distinguished from non-small cell lung cancer by its rapid doubling time and early development of widespread metatses (70% metastasis by time of diagnosis)
Highly responsive to chemotherapy & radiotherapy; usually relapses & become refractory to treatment within 1-2 yrs (poor prognosis) |
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Describe the clinical presentation of small cell lung carcinoma
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Typically arises in the central airways; large hilar mass with bulky mediastinal lymphadenopathy
Limited Stage-tumor involvement of 1 lung, mediastinum and supraclavicular lymph nodes or encompassed in single radiotherapy port (prognosis is 15-20 months) Extensive Stage-tumor has spread beyond one lung, mediastinum, and supraclavicular lymph nodes Common distant sites of metastases are adrenals, bone, liver, bone marrow, and brain (prognosis is 8-12 months) |
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4. A 60-year-old female presents with complaints of a purulent, productive cough and shortness of breath that has become progressively worse over the past several months. She admits to intermittent episodes of blood-streaked sputum. She denies fever or chills. Her past medical history is unremarkable and she takes no medication. She smoked 1 pack per day of cigarettes for the past 30 years. Her physical examination reveals scattered rhonchi. PFTs reveal an FVC of 79% predicted; FEV1 45% predicted; and FEV1/FVC of 45% with no improvement following bronchodilator. Sputum culture reveals normal respiratory tract flora.
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bronchiecstasis
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Define bronchiecstasis
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irreversible dilation and destruction of one or more bronchi w/ inadequate clearance and pooling of mucus in airways
characterized by persistent microbial infection and inflammatory response divided into disorders associated w/ cystic fibrosis or non-cystic fibrosis |
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Describe the clinical history and physical exam findings of bronchiecstasis
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classic presentation is cough and daily production of large amount of sputum for months-years; hemoptysis; dyspnea and wheezing; pleuritic chest pain
smoking is not a cause (most patients have never smoked); most common in elderly women physical finding are nonspecific (rales/crackles and wheezing) |
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Describe how to differentiate bronchiecstasis from COPD
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a. History-nonsmoker, large mucous production
b. Microbes-psuedomonas, h. flu, atypical (mycobacterium avium, etc) cause infection c. Chest x-ray: presence of infiltrates, mucous plugging, scarring |
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Describe the pathophysiology of bronchiecstasis
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result of infectious insult, impaired drainage, airway obstruction, or defect in host defense
diffuse presentation-involves much of both lungs; often accompanied by other sinopulmonary diseases (sinusitis, asthma) focal presentation-luminal blockage by foreign body, broncholith, or slow growing tumor (benign); extrinsic narrowing due to enlarged lymph nodes; displacement of airway after lobar resection (surgical procedure; recurrent pneumonias are often associated |
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Describe the diagnostic tests used in bronchiectasis
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A. lab tests-CBC w/ differential; measure Igs IgG, IgM, and IgA; sputum culture-smear for bacteria, mycobacteria, and fungi
B. imaging high resolution CT-best tool for definitive diagnosis (97% sensitivity) C. pulmonary function test-shows airflow limitation w/ reduced FEV1 amd normal FVC; indicates airways are blocked by mucus |
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Describe the management of bronchiectasis
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A. acute exacerbations-difficult to differentiate from normal disease process (look for symptoms of infection); treat w/ early antibiotic therapy (flouroquinolones); if no improvement, do sputum culture
B. bronchopulmonary hygiene-enhancing removal of secretions (chest clapping, inflatable vest, mechanical vibration); oral device applies positive end expiratory pressure to maintain open airways; adequate hydration; nebulization w/ saline or acetylcysteine; bronchodilators (beta 2 agonists, anticholinergics, ICs) C. Surgery-localized disease (focal disease); lung transplant |
