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clinical medicine

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Question
Answer
asthma   chronic inflammatory disorder of the airways  
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atopy   complex interaction between multiple genes and environmental factors, leading to IgE mediated response to allergens  
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asthma clinical findings   cough, sob, wheezing, tachypnea, use of accessory muscles, wheezing, prolonged expiratory phase, agitation, cyanosis  
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differential of cough and wheezing in children   CRADLE (cystic fibrosis, respiratory TI, aspiration, dyskinetic cilia, lung and airwary malformation, edema chf)  
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asthma evolution   plasma cells in lung overreact and tell mast cells about it, in chronic esosinophils degranulate causing airway damage and eventually remodeling-fibrinoblasts lay down collagen  
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inhaled corticosteroid benefits   sx diminish and improve gradually, decreases use of rescues, lung function improves, occurrence of exacerbations reduce  
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COPD   many diseases characterized by chronic airflow obstruction  
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less than 0.7   post BD- fev1/fvc of_______ confirms COPD  
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Suspect COPD in patients over 40 with   Dyspnea, chronic cough, chronic sputum production, exposure history, family history of COPD  
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Obstruction (PFT)   FEV1 is reduced out of proportion to total volume of forced exhalation (FVC) Ratio of FVV1:FVC is reduced 70%  
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GOLD staging   Gold 1- mild FEV1 >80% Gold 2- mod 50%<FEV1<80% Gold 3- Severe 30%<FEV1<50% Gold 4- very severe FEV1<30%  
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COPD risk factors   Smoking, exposure to products of combustion, occupational dusts/fumes/vapors, airway hyper reactivity, genetics  
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COPD airflow obstruction   Largely determined by resistance in small airways (airway remodeling, loss of elastic recoil, lumenal obstruction with mucous, bronchiolar lumenal narrowing  
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COPD hyperinflation   Obstruction increases end expiratory volume (Increases elastic recoil, increases expiratory flow, mechanical disadvantage, positive alveolar pressure must be overcome to breath)  
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COPD V/Q mismatch   variable from one pt to another, loss of hypoxic vasoconstriction, major determinant of decreases pao2  
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COPD decreased diffusing capacity   loss of alveolar capillary bed, extent proportional to severity of emphysema  
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COPD alveolar hypoventilation   Adaptive response to increase WOB, increase paco2 decrease pao2  
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Pink Puffer   emphysema predominates, less alveolar surface are for gas exchange, hyperventilate to compensate, ABG normal  
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Blue Bloater   Chronic bronchitis, alveolar space intact but airways obstructed, decrease ventilation, V/Q mismatch, air trapping, hypercanpia (CO increase)  
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COPD exacerbations   amplification of baseline airway inflammation, precipitated by infections environmental pollutants smoking, major determinant of outcomes in pts  
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COPD tx, FEV1 >60% and no sx   no pharm or a saba  
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COPD tx, FEV1 <60%   saba, laba, ics, pulm rehab, oxygen, azithromycin  
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COPD exacerbation causes   infections (most common), environmental pollution, unknown  
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Pulmonary Hypertension pathology   small pulmonary arteries, vasoconstriction vascular remodeling  
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Pulmonary Hypertension diagnosis   right heart cath, mean pulmonary artery pressure of greater than 25mmHg or mean pulmonary capillary wedge pressure of less than 15mmHg  
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Pulmonary Hypertension symptoms   dizziness +/- syncope SOB chest pain ascities edema fatigue  
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mTB bacteria   aerobic, nonmotile, bacillus with waxy lipid-rich outer wall (acid fast staining)  
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mTB pathogenesis   TB hits alveoli, macrophages engulf, transport to hilar lymphnodes, CD4 Tcells try to kill create caseous granulomas  
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Primary TB   refers to 1st exposure to inhaled infectious particles followed by flu-like illness, spread controlled sub pleural granulomas form, remain stable and no further spreading  
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Latent TB Infection   mTB survive for decades in walled off lesions, not infectious, risk of reactivation  
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Reactivated TB causes   Immune deficiency, AIDs, Immune modulated agents (occurs in 10-15% of pts half within 2 yrs of primary disease)  
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Reactivated TB symptoms   worsen over months, cough with sputum, low grade fever, weight loss, fatigue, hemoptosis and pleuritic pain (severe disease)  
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Miliary TB   initial exposure to mTB fails to incude cell-mediated immunity  
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Miliary TB physical exam   chronically ill-appearing, LAD choroid TB in eyes (dx with transbronchial biopsy)  
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Screening for TB   PPD (purified protein derivative) or interferon gamma release assay (IGRA)  
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Treating TB   RIPE (rifampin, isoniazid, pyrazinamide, ethambutol) and vit b6  
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Fungal Pneumonia at risk populations   neutropenics, lupus/RA, organ transplant recipients  
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Histoplasmosis   transmitted by airborne spores inhaled from contaminated soil, primarily lungs and lymph chains (bat guano and chicken droppings)  
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Histobelt   southern Ohio, Missouri, Tennessee, Arkansas, Kentucky, Illinois  
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Histo symptoms   fever, fatigue, weight loss, hepatosplenomegaly, cough and dyspnea for greater than one month recurrent pneumonia  
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Histo dx testing   urine histo ag or blood/BM cx  
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Histo, coccidiodomycosis, and blasto treatment   liposomal amphotericin and itraconazole  
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Coccidiodomycosis geographic   american southwest, mexico  
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Coccidiodomycosis   transmitting by inhaling c immitis or c posadasil, 1-4 weeks of mild flu like illness, pleuritic chest pain resolves in a few weeks  
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Coccidiodomycosis DX   IgM/IgG serologies, fungal comp fix panel, tissue biopsy  
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Blastomycosis geographic   along mississippi, north, Canadian border  
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Blastomycosis   least common, can infect lungs skin and bone  
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Ubiquitous fungi   cryptococcus neoformans, aspergillosis  
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Cryptococcus neoformans   more commonly meningitis, yeast, mostly infect immunocompromised  
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cryptococcus neoformans sx   fever, weight loss, malaise, pleuritic pain, cough, wheeze, hemoptysis  
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Cryptococcus neoformans dx test   serum cryptococcal  
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Crytococcus neoformans tx   liposomal amphotercin, fluconazole  
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Aspergillosis   mostly infects immunocompromised (leading cause of death in acute leukemia, bone marrow transplant)  
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Aspergillosis dx   culture, serum galactomannan level, X-ray (solitary/multiple nodules, cavitary lesions) CT (halo sign, crescent sign)  
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Aspergillosis treatment   empiric, surgical excision, once diagnosis is established variconazole and caspofungin  
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Normal pulmonary defense   mucociliary clearance, cough and gag reflex, innate flora of oropharynx  
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Pneumonia pathophysiology   inhalation of pathogen, macrophages overwhelmed, inflammatory mediators  
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Phases of pneumonia   edema, red hepatization, gray hepatization, resolution  
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CAP pathogen   strep pneumo (most common) H flu, M cat, M pneumo, RSV  
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MRSA risk factors (pneumonia)   recent illness, flu, esrd, pleural effusion, multifocal infiltration, recent antibiotics, IVDA  
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Pneumonia typical   acute, thick brown yellow sputum, productive cough, high fever shaking chills, consolidation on cxr  
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Pneumonia atypical   gradual, clear sputum, low grade fever, no infiltrates  
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Pneumonia physical exam   inspiration crackles, bronchial breath sounds, dull to percussion, e to a changes  
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CURB 65   confusion, uremia, rr (>30), bp (<90/<60), 65yo  
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Acute bronchitis   inflammation of tracheobronchial tree, cough 1-3 weeks duration, usually viral  
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DVT   thrombus usually found in the lower extremities, pelvic veins, and upper extremities  
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PE   obstruction of the pulmonary artery or its branches by material (fat, air, tumor, or thrombus)  
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Virchows triad (DVT)   venous stasis, venous injury, hyper-coagulability  
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Cause of death for PE   r ventricle after load increases, rv dilates, rv dysfunction, rv ischemia, rv failure  
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PE "the great masquerader"   non-specific symptoms, tachy, elevated neck veins, loud p2, pleural rub, humans sign (swollen, warm, erythematous)  
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PE EKG   sinus tach, RBBB, right axis deviation, P wave pulmonale, new a fib, rt ventricle strain  
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Wells criteria   clinical prediction model for PE  
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Gold standard for PE diagnosis   pulmonary angiogram  
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Massive PE   PE with systolic BP less than 90mmHg  
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Submassive PE   PE with RHF with normal BP  
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Small Cell carcinoma   extremely rapid growth, central location, almost always smokers, crush artifact  
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Non-small cell carcinoma   squamous cell carcinoma, adenocarcinoma, large cell  
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Squamous cell carcinoma   most common with hemoptysis, central location, exfoliates, aggressive  
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Adenocarcinoma   Most common lung cancer, slow growing, peripheral location, "scar" tumor, more common in non smokers  
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Large cell carcinoma   Poorly differentiated, peripheral, rapid growth  
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Cancer clinical presentation   constitutional symptoms most common, other symptoms related to local tumor growth, local spread, metastasis  
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Pancoast tumor   superior sulcus tumor, compresses brachial and cervical nerve roots, manifests as horners syndrome, anhydrosis, or arm pain  
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Paraneoplastic syndrome   endocrine hormone secretion, clubbing, anorexia, weigh loss/ cachexia, fever  
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Gold standard for cancer diagnosis   Surgical lung biopsy  
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TNM system   Tumor size and invasion, lymph Nodes, Metastasis  
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Stage 1   no lymph nose involvement, surgical removal  
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Stage 2 and 3   lymph nodes involved, larger tumor, multiple lung tumors, surgery radiation and chemo  
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Small cell carcinoma staging   limited or extensive both bad  
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Visceral pleura   adheres to lung, covers each lobe, gets blood from the brachial artery, limited lymphatic drainage, no innervation  
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Parietal pleura   adheres to chest wall, blood from systemic capillary, lymphatic drainage, innervated  
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Pleural effusion cause   excess production of fluid, decreased drainage  
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Pleural effusion classification   transudative, exudative  
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Transudative pleural effusion   disorder of hydrostatic or oncontic or hydrostatic forces, fluid seeps from vessels  
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Exudative pleural effusion   Disorder of inflammation, fluid exudes through wide gaps between cells, rich in cells and protein  
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Lights criteria   protein/serum protein ratio >0.5 LDH/serum LDH ratio >0.6 LDH> 2/3 the upper limit of normal serum  
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Treatment of exudative pleural effusion   bacterial infections (empyema) and malignancy need chest tube, chronic can lead to fibrosis, the rest of pts you drain or do surgically debride  
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Treatment of transudative pleural effusion   no chest tube needed, treat underlying cause, can do a thoracentesis to help with dyspnea  
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Pneumothorax physical exam   chest pain, dyspnea, hyperresonant, diminished tactile fremitis, decreased breath sounds  
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Pneumothorax Xray   peripheral absence of lung markings and the presence of a pleural stripe  
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Pneumothorax classifications   spontaneous, traumatic, tension  
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Primary Spontaneous   no underlying lung disease, peak incidence in the 3rd decade of life  
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Blebs   physical stress can cause small patches of irregular architecture which can rupture spontaneously  
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Secondary spontaneous   pneumothorax in a lung with underlying disease  
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Traumatic pneumothorax   penetrating chest injury, blunt chest injury, iatrogenic (healthcare on purpose or an oops)  
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Tension pneumothorax   Rapid accumulation of air in the pleural space, rise in pleural pressure, pressure can reduce blood flow, decrease CO, shock and death  
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Tension pneumothorax exam   low bp, absent/decreased breath sounds, hyperresonant, tracheal deviation  
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Tension pneumothorax treatment   needle decompression, chest tube  
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Pleuritis   pleural inflammation  
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Restriction causes   P (pleural) A (alveolar) I (interstitial) N (Neuromuscular) T(thoracic cage abnormalities)  
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Interstitial lung disease   diseases of the alveoli and interstitum  
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Usual Interstitial Pneumonia   most common idiopathic interstitial pneumonia, worst prognosis, does not respond to anti-inflammatory tx  
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Idiopathic Granulomatous   Sarcoidosis, second most common ILD, frequently a multi system disease  
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Sarcoidosis diagnosis and treatment   transbronchial biopsy to find granulomas, treat with corticosteroids  
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ILD Granulomatous   Chronic beryllium disease, hypersensitivity pneumonitis  
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ILD non-granulomatous   autoimmune disease, occupational exposure, drugs, radiation  
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