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196 Cards in this Set
- Front
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Alveolar wall destruction in COPD hypothesis
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Alveolar wall destruction due to imbalance between proteases (mainly elastase) and antiproteases in the lung - aided by oxidant-antioxidant imbalance
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Extrinsic asthma
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Initiated by a type I hypersensitivity reaction - induced by exposure to an extrinsic antigen
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Instrinsic asthma
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Initiated by diverse, nonimmune mechanisms, aspirin, pulmonary infections, cold
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Model for allergic asthma
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Inhaled allergen - Th2 response - IgE production and eosinophil recruitment
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Curschmann spiral
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Asthma - papanicolaou stain - large spiral found in lavage fluid
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Charcot-Leyden crystals
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Asthma - Collections of crystalloid made up of eosinophil membrane protein
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The most dangerous particle size in pneumoconiosis is:
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1.0 - 5.0 micrometers
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Most prevalent chronic occupational disease worldwide:
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Silicosis
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The most common manifestation of asbestos exposure
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Pleural Plaques
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Most common cause of lower respiratory tract infection:
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Influenza virus
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The major cause of croup (laryngotracheobronchitis):
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Human Parainfluenza Virus
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Seal bark cough
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Think Croup (Human Parainfluenza Virus)
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Virus that peaks in late autumn through winter; children 1-4 with peak at 2 years, more common in boys
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Human Parainfluenza Virus
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The major lower respiratory tract pathogen of infants worldwide
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Respiratory Syncytial Virus
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Premature infants are especially susceptible to severe disease by this virus that can cause bronchitis, bronchiolitis, and pneumonia
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Respiratory Syncytial Virus
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Similar clinical and epidemiological spectrum as Respiratory Syncytial Virus
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Metapneumovirus
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2 viruses that have peak incidence at 2 months of age; spread within hospitals via respiratory droplets
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Respiratory Syncytial Virus and Metapneumovirus
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Sin Nombre virus with deer mouse/cotton rat vector; 50% fatality rate
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Hantavirus Pulmonary Syndrome
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The attachment protein in influenza viruses that is responsible for membrane fusion, antibody neutralization, and RBC agglutination
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Hemagglutinin (H or HA)
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Active enzyme in influenza viruses that removes sialic acid residues from glycoproteins
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Neuraminidase (N or NA or sialidase)
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For influenza viral clearance the immune system has to target:
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Response to Hemagglutinin and Neuraminidase (H and N)
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16 distinct H, 9 distinct N for this many potential combinations:
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144 combinations
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The most common current human influenza strains
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H3N2 and H1N1
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Traditionally the only human flu viruses
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H1, 2, 3 and N1, 2 (H5N1 bird flu)
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Core proteins in influenza viruses responsible for typing into A, B, and C groups
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S-Ag (soluble antigen) also known as ribonucleoprotein antigen (RNP)
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Genome ssRNA, 8 segments, enveloped, each segment = 1 gene, functional nucleus required for replication
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Influenza A, B, C
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Influenza type that can cause epidemics, worldwide pandemics
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Influenza type A
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Minor epidemics of influenza
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Influenza type B
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Accounts for most fatalities from Influenza Virus
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Secondary bacterial pneumonia
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Classic diagnostic test for Influenza virus
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Hemagglutination-inhibition test
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Small changes in hemagglutinin and/or neuraminidase - due to mutation
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Antigenic drift
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Major change in most all antigenic determinants of hemagglutinin and/or neuraminidase
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Antigenic shift
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Influenza antigenic variation due to mutation
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Antigenic drift
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Influenza antigenic variation due to intragenomic or intergenomic recombination
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Antigenic shift
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Antiviral drugs that target Influenza type A only, minimally therapeutic, interfere with uncoating (M2 matrix); not effective against H1N1
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Amantadine and Rimantidine
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Therapeutic antiviral drugs for Influenza that inhibit viral neuraminidase
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Zanamivir, Oseltamivir, and Peramivir
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An atypical pneumonia due to different pattern of features think these 2 causative agents
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Mycoplasma pneumoniae or Chlamydia pneumoniae
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Smallest and simplest known bacterium
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Mycoplasma pneumoniae
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Atypical pneumonia, lacks cell walls, requires cholesterol, infects mucous membranes
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Mycoplasma pneumoniae
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Slow onset of fever, headache, malaise and nonproductive cough; primary presentation is tracheobronchitis or bronchiolitis
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Atypical pneumonia think Mycoplasma pneumoniae or Chlamydia pneumoniae
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Cold agglutinins
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Mycoplasma pneumoniae
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Treat Mycoplasma pneumoniae with:
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Doxycycline or erythromycin
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Similar disease to Mycoplasma pneumoniae with 75% of young adults demonstrating Ab to this organism
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Chlamydia pneumoniae
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Chlamydia pneumoniae exists in 2 forms
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Elementery body (infectious) and Reticulate body (noninfectious)
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Isolation using McCoy cell line and staining with specific antibody; treat with tetracycline
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Chlamydia pneumoniae
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Ornithosis
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Chlamydia psittaci, think bird droppings
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Plague
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Yersinia pestis
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Tularemia
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Francisella tularensis
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Counterstain with fuchsin; infects amoeba in natural environments; smokers and elderly predisposed
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Legionella pneumophila
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Virulence factors for Legionella pneumophila
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Cytotoxin, hemolysin, endotoxin, beta-lactamase
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Organisms are inhaled from contaminated water source; Pontiac Fever
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Legionella pneumophila
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Virulence factor of Legionella pneumophila that interferes with oxygen-dependent processes of phagocytosis
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Cytoxin (Dot/Icm proteins)
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Prevention of Legionella pneumophila
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Eliminate organism from water supply, heat to above 60 C, chlorine
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The bacteria release a toxin that binds to the receptors of the host cell. 7 of these bind together and attract either Lethal Factor or Edema Factor
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Anthrax
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Highest mortality of anthrax when:
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Inhaled
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Large, gram-positive rod, nonmotile, sensitive to penicillin, central and subterminal spores
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Bacillus anthracis
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Community-Acquired pneumonia - 3 weeks to 2 months
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Chlamydia trachomatis, Bordetella pertussis, Staphylococcus aureus, Parainfluenza, and Strept. pneumonia
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Community-Acquired pneumonia - birth - 20 days
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Group B Streptococci (Streptococcus agalactiae)
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Community acquired pneumonia- 2 months - 4 years
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Respiratory Syncytial Virus
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Community acquired pneumonia- 5 -15 years
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Chlamydia pneumoniae, Mycoplasma pneumoniae, Mycobacterium tuberculosis, parainfluenza virus, strept. pneumoniae
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Pneumonia that occurs within 48 hours after hospital admission
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Hospital-Acquired Pneumonia
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Most common core pathogens for hospital-acquired pneumonia
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Non-severe: enteric gram-negative rods; moderate to severe: pseudomonas aeruginosa and Acinetobacter sp.
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Patients breath and sputum may have a putrid odor
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Aspiration Pneumonia
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Gram positive branching rod with pneumonia; sulfur granules
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Actinomyces israelii
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Caused by an infection that spreads from the lung and leads to an accumulation of pus in the pleural space
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Empyema
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Gram positive branching, filamentous bacteria found in the soil that can be treated with sulfonamides
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Nocardia asteroides
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HLA-BW15
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Single gene in chromosome 17 may account for 7x increased susceptibility for TB
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Tubercles in the lung and caseous material or calcified lesions in lymph nodes
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Ghon complex
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Macrophages contribute to the symptoms of TB via these 2 factors:
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Interleukin-1 and Tumor Necrosis Factor
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In TB - Interleukin-1
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Mediator of fever
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In TB - Tumor Necrosis Factor
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Interferes with lipid metabolism and leads to severe weight loss
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Tuberculosis most commonly affects this part of the lung
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Upper lobes
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Symptoms of TB
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Persistant cough, purulent sputum containing blood, chest pain, and breathlessness; fever, sweating, lethargy, and weight loss
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Has to do with mycolic acid in cell wall - characteristic of TB
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Acid Fast
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A drug is ineffective for TB when
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More than 1% of mycobacteria are resistant
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Gold standard test for TB
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Purified Protein Derivative - positive if 10 mm or more erythema after 48 hours
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QuantiFeron
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New TB Gold Test: blood mixed with TB antigens - amount of interferon-gamma measured
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Bacillus Calmette-Guerin vaccine
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Vaccine for TB - strain of M. bovis
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Prevent TB by taking this vitamin
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Vitamin D
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TB like symptoms - HIV really susceptible - may lead to increased resistance to M. tuberculosis
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MAI Complex (Mycobacterium avium - intracellulare)
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How does alveolar wall destruction occur in COPD?
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Protease-antiprotease theory: due to imbalance between proteases (mainly elastase) and antiproteases/in the lung
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Protease-antiprotease imbalance and oxidant-antioxidant imbalance
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Think COPD - two are additive with both contributing to tissue damage
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Recurrent episodes of wheezing, breathlessness, chest tightness and cough especially at night and/or early morning
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Asthma
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Classifications of asthma
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Mild intermittent, mild, moderate, and severe persistant
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Asthma initiated by a type I hypersensitivity reaction induced by exposure to an antigen
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Extrinsic Asthma
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Asthma initiated by diverse, nonimmune mechanisms; aspirin, pulmonary infections,cold; inhaled irritants, stress, exercise
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Intrinsic Asthma
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3 Major etiologic factors of asthma:
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Genetic predisposition (Type I hypersensitivity), Acute and chronic airway inflammation, bronchial hyperresponsiveness
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Immediate response vs. late phase reaction in asthma
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Acute think mast cells going crazy with stimulation of subepithelial vagal receptors; late phase mediated by leukocytes
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Curschmann spiral and Charcot-Leyden crystals
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Think Asthma
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Most dangerous particle size to inhale
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1 - 5 micrometers; may reach terminal small airways/alveoli
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Non-neoplastic lung reaction to inhalation of mineral dusts
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Pneumoconiosis
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Findings in coal workers
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Asymptomatic anthracosis, simple Coal Workers' Pneumoconiosis, complicated CWP/Progressive Massive Fibrosis (PMF)
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Most innocuous coal-induced lung lesion; also seen in city dwellers/tobacco smokers
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Anthracosis
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Most prevalent chronic occupational disease worldwide
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Silicosis - crystalline forms much more fibrogenic
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Accumulation of carbon in the lungs from inhaled smoke or coal dust
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Anthracosis
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2 forms of asbestos
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Serpintine and Amphibole (which is more pathogenic and associated with mesothelioma)
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Which is worse in asbestos - long thin fibers or short thick ones
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Long thin; 8 micrometers and thinner than .5 micrometers worse
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Most common manifestation of asbestos exposure
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Pleural plaques (do not contain asbestos bodies) on the pleural surface of the diaphragm
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Ferruginous body
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Asbestos fiber becomes coated with Fe and calcium - ingestion by macrophages
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Heart Failure cells
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Hemosiderrin-laden macrophages seen with pulmonary edema/congestion
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Pulmonary emobolus that settles at the bifurcation of the main pulmonary artery
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Saddle Embolus
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Pulmonary pressure is 1/4 of systemic levels
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Pulmonary hypertension
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With Pleural effusions; low protein content
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Transudate
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With pleural effusions; high protein content
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Exudate
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First line anti-TB drugs
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StRIPE: Streptomycin, Rifampin, Isoniazid, Pyrazinamide, Ethambutol
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Drug used for asymptomatic or latent TB
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Isoniazid (INH)
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TB drug with bimodal distribution; is a prodrug
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Isoniazid (INH)
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Adverse effects of Isoniazid (INH)
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Can inhibit metabolism of drugs, potentially fatal hepatitis, and peripheral neuropathy and CNS toxicity
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Most important risk factor for hepatitis with patients on Isoniazid
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Age
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How does Isoniazid cause peripheral neuropathy and CNS toxicity
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Causes vitamin B6 (pyridoxine) deficiency
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TB drug used for latent infection in meningococcal epidemics
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Rifampin
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Adverse effects of Rifampin
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Potent CYP450 inducer!, rash, fever, abdominal pain, hepatitis (rare), flu-like syndrome, red-orange color to bodily fluids
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TB drug in which you see harmless red-orange color in urine, tears, sweat, etc.
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Rifampin
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You have flu-like syndrome when taking Rifampin unless you:
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Administer the drug more that twice weekly
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Expensive TB drug for infected HIV patients treated concurrently with NNRTIs or PIs
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Rifabutin
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Most hepatotoxic of the first line therapy drugs for TB - can cause hyperuricemia
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Pyrazinamide
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Only first line TB drug that is bacteriostatic
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Ethambutol
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Adverse effects of Ethambutol
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Optic neuritis and hyperuricemia
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IM only TB drug that is reserved for more serious TB infections
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Streptomycin
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Adverse effects of Streptomycin
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Ototoxicity and nephrotoxicity
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Therapy regimen for general population with active TB infection
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RIPE for 2 months, then RI for 4 months
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Therapy regimen for general population with active TB infection with resistance to Isoniazid
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RPE for 6 months
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Occurs when gas exchange becomes significantly impaired leading to respiratory muscle fatigue
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Respiratory Failure
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2 types of respiratory failure
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Hypoxemic and Hypercarbic
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Clinical signs of respiratory failure (4)
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Tachypnea, Accessory muscle use, Paradoxical respirations, Decreased respiratory rate and apnea
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Abdominal contents rise up and into chest during inspiration and outwards during respiration = failure/fatigue of diaphragm
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Paradoxical Respirations
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5 pathologic mechanisms for hypoxemia
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Low inspired oxygen, hypoventilation, low V/Q, Right to left shunt, Diffusion impairment
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The amount of O2 an individual requires to burn one millimole of carbohydrate, fat, and protein
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Respiratory Quotient (RQ) = 0.8
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Cause left shift in O2 disassociation curve
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Decreased temp, 2,3 DPG, and H+; CO
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Cause right shift in O2 disassociation curve
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Increased temp, 2,3 DPG, and H+
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5 variables to know with ventilators
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Rate, Tidal Volume, FiO2, Positive end expiratory pressure, pressure support if indicated
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3 forms for ventilator Pressure Control
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Assist Control (A/C), Synchronized intermittent manditory ventilation, pressure support ventilation
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Machine breath or patient breath always same amount of tidal volume
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Assist Control (A/C)
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Set number of breaths receive fixed tidal volume
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Synchronized Intermittent Manditory Ventilation
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Generally no set rate or tidal volume - statistically the most successful weaning mode for ventilation
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Pressure Support
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RR x VT =
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Minute ventilation
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Vasopressor agents available
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Dopamine, Norepinephrine, Epinephrine, Phenylephrine, Vasopressin
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Indicated when volume resuscitation fails to restore adequate arterial pressure/organ perfusion
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Usage of vasopressors
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Vasopressor that increases GFR, renal blood flow and Na+ excretion
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Dopamine
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Vasopressor at lower doses beta agonist, higher doeses alpha agonist
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Epinephrine
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Vasopressor for increased mean arterial pressure in shock despite Dopamine; mainly alpha-1 agonist
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Norepinephrine
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Vasopressor that is a direct vasoconstrictor without inotropic or chronotropic effects
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Vasopressin
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Spirometery before and after bronchodilator showing an increase in FVC or FEV1 of 12%
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Asthma
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Can use this test to check for underlying asthma that may not be symptomatic at the moment
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Methacholine challenge with a drop in FEV1 of 20%
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Asthma with daytime symptoms less than or equal to 2 days a week and less than or equal to 2 nights a month
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Mild intermittent - no medications needed
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Asthma with daytime symptoms more than twice a week but less than once a day or symptoms more than 2 nights a month
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Mild Persistant - low dose inhald corticosteroids
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Asthma with daily daytime symptoms or symptoms more than 1 night a week
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Moderate Persistant - inhaled corticosteroids and long-acting B2 agonist
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Asthma with continual symptoms or frequent nighttime symptoms
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Severe Persistant - inhaled corticosteroids, long acting B2 agonist, and Corticosteroid tablets
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Never use these drugs as a mono therapy for asthma
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Long acting B agonists
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Persistent progressive asthma attack despite appropriate interventions
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Status Asthmaticus
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Definition of Asthma Control
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Use of rescue inhaler > 2 times a week; noctural inhaler > 2 times a month; use of more than 2 canisters of rescue inhaler a year
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Taken for chronic rhinitis has been shown to reduce asthma inflammation
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Intranasal steroids
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Sampters Triad
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Asthma, aspirin allergy, and nasal polyps
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Churg-Strauss Syndrome stages
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Prodromal phase, Eosinophilic Phase, Vasculitic phase
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Use this drug with patients with moderate and severe persistant asthma with IgE > 30 and positive RAST or skin testing
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Omalizumab
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The diagnosis of COPD requires a spiometry reading of:
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Post bronchodilator; FEV1/FVC less than 70%
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X-ray findings of COPD:
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Flat diaphragms, retrosternal air, decreased vascularity, hyperlucency
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60% of COPD exacerbations can progress to:
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Bacterial infection - give antibiotics
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Oxygen qualifications for the standard patient
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Oxygen saturation of 88% or less - PaO2 of 55 mmHg or less
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Oxygen qualifications for patients with heart disease, cor pulmonale, and/or peripheral edema
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Oxygen saturation of 89% or less - PaO2 or 59 mmHg or less
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Poses a strong risk factor for early onset emphysema
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Alpha-1 Antitrypsin Deficiency
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Acute lower respiratory tract infection - acute infection of the pulmonary parenchyma
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Pneumonia
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Gold standard for diagnosing pneumonia
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The presence of an infiltrate on plain chest radiograph
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Most common bacteria pathogen for pneumonia
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Streptococcus pneumoniae
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CURB-65 uses 5 prognostic variables for determining the treatment plan for pneumonia patient
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Confusion, Urea (> 7 mmol), Respiratory rate >30, BP (systolic <90, systolic <60), Age >65
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Measures both ventilated and unventilated areas of the lungs - good for COPD
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Plethesmography
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4 parts to pulmonary function testing
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Spirometry, flow volume loops, lung volumes, and diffusion
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20% of all pulmonary embolisms are caused because of this congential issue
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Factor V Leiden
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Gold standard for diagnosing pulmonary embolus
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Pulmonary angiogram
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"Traditional" treatment of DVT
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IV bolus followed by continuous infusion of Unfractionated heparin and daily dose of Warfarin (Coumadin)
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Indicated for Heparin-induced thrombocytopenia
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Hirudin and Argatroban
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Goal INR
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2 - 3
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If the reason for the thromboembolus is obvious the treatment should be
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Coumadin for 3 months
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In most cases the VTE is without an obvious cause so the treatment is:
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Coumadin for 6 months
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If the reason for the VTE was an ongoing disease the treatment is:
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12 months to lifetime Coumadin
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Acute Lung Injury is characterized by 3 clinical features:
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Bilateral radiographic infiltrates, PaO2/FiO2 between 201 and 300 mmHg, no evidence for elevated left atrial pressure
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Acute Lung Injury with worse hypoxia with a PaO2/FiO2 of 200 mmHg or less
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Acute Respiratory Syndrome
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The A-a gradient should not be any more than:
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Patient age/4 + 2.5
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Temporary absence of cessation of breathing during sleep
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Sleep Apnea
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A temporary decrease in inspiratory airflow that is out of proportion to the individual's effort or metabolic needs
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Hypopnea
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Most common place of obstruction in sleep apnea
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Nasopharynx at the level of the soft palate
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Clinical risk factors for Sleep Apnea (4)
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Neck size > 17 inches, Epworth Sleep score > 10, Mallampati score of 3+, history of apnea, heavy snoring/gasping
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With Obstructive Sleep Apnea you have an increased risk of (4)
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Stroke, Hypertension, Depression, and Mortality
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Modafinil
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Drug that can be used to help Obstructive Sleep Apnea
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The gold standard and last resort in the treatment of Obstructive Sleep Apnea
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Tracheostomy
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2 parts of lung parenchyma
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Parenchymal interstitium and loose binding connective tissue
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Tissue infiltration by monocytes and lymphocytes and noncaseating granulomas which mainly affect the lungs and lymphatics
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Sarcoidosis
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If you want the location of the hemoptysis and location of lymph node involvement run this test
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CT Scans
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Violaceous indurating skin lesion affecting chiefly the nose and facial skin
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Lupus pernio
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Inhalation and deposition of coal dust into the lungs
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Pneumoconiosis
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Coal macules that reach 2 cm or greater in size
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Progressive Massive Fibrosis
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In Progressive Massive Fibrosis the macules can cavitate and produce black fluid
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Melanoptysis
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3 Major Disease of COPD
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Emphysema, Chronic Bronchitis, and Asthma
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Get the Pneumovax at ages
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50 and 65
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Test to diagnose Sleep Apnea
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Polysomnogram (PSG)
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May hear "Velcro" rales - generally in inspiration; many have a dry spasmodic cough
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Interstitial Lung Diseases
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