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52 Cards in this Set
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- Back
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Polymorphonuclear leukocytes:
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neutrophils
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Mononuclear cells (of wbc) include:
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lymphocytes, plasma cells, monoctyes/Mphages
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Some of the sources of inflammation:
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Microbial infection, necrotic tissue, physical agents, foreign bodies, immune reactions, trauma, chemical agents
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Acute inflmmation depends on this immune system, which last about this long
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Acute inflammation relies on innate system and last about a week.
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Intracellular bacteria control relies on these innate and adaptive components:
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Innate: NK and macrophage (induced by NK to kill internal bacteria); Adpative: Cell mediated immunity
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Chronic infection features and immune type:
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Chronic infections last weeks to years; patients shows fever, fatigue and weight loss; tissue damage and scarring results; the ADPATIVE system is responsible.
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The six types of general tissue response to infection include:
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Acute/suppurative, mononuclear/interstitial, granulomatous, cytopathic/cytoproliferative, eosinophilia, necrosis
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What does pus contain:
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viable and dying WBC (mostly neutrophils), liquified tissue & cellular debris
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what does purulent and pyogenic mean?
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Purulent: pus containing; pyogenic: pus producing
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Acute/suppurative inflammation immune system and organism involved?
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Acute inflammation involves innate system fighing extracellular bacteria/fungi
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Why does some tissues thicken (ie. Appendix) in inflammation?
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edema from fluid and inflammatory cells cause tissue to thicken
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Three possible outcomes of acute inflammation
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Normal healing (usual); tissue destruction/necrosis (abscess formation); Progress to chronic inflammation
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Abscess definition and common microbe causing it?
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Abscess: a localized collection of pus from acute inflammation tissue necrosis; commonly caused by Staphylococci, Klebsiella
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Two possible outcomes of abscess?
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Drainage or being surround by a vascularized fibrous wall.
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What kind of cells are in the center of abscess usually?
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PMNs
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What's the result of a acute inflammaion in neutropenic host?
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masses of bacteria may form.
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Mononuclear/Interstitium inflammation inflammatory infiltrate and microbes responsible?
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lymphocytes, plasma cells, monoctyes/Mphages; intracellular bacteria/virus/parasites, spirochetes, and ANY persistent microbes.
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Mononuclear inflammation in lungs can be demonstrated as this:
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widened lung interstitium
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Viral pneumonia creates this tissue response:
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mononuclear inflammation
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Mononuclear inflammation can be seen as both ___ and ___, each involving these cells?
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mononuclear inflammation can be both acute (NK cells) and chronic (lymphcytes)
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Granuloma inflammation's time course & features
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Granuloma inflammation is chronic featuring, epithelioid histiocytes.
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Epithelioid formation? & function?
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Type IV hypersensitivity, CD4 cells/IFN-gamma assisted activation of histiocytes; fused epithelioid form giant cells; functions to wall off infection
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Microbes eliciting granulomatous inflammation:
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Intracelluar: poor digestible/soluable microbes, those resistant to eradication (***TB***); Extracellular: some fungi/worms
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What forms a granuloma?
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Epithelioid and giant cells forming center; mononuclear cell can form rim
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Necrosis types:
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Liquefactive necrossi (pus, abscess center); Caseous necrosis (dead cells and granular debris)
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Granuloma (espeicaially with Caseous necrosis) in lungs indicate what?
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TB
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Instead of forming granulomas, patients with defective CD4+ cells has:
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macrophages filled with bacteria, no walling off, wide spread infection
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Cytopathic -Cytoproliferative Changes: causes and 3 signs
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Cytopathic: virus induced; causes viral inclusions (CMV); cell fusion (measle); Epithelia proliferation (HPV)
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Cytopathic changes from CMV and Herpes:
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CMV (nuclear & cytoplasmic inclusion); Herpes (nuclear inclusions)
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Eosinophilic inflammation:
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Helminthic parasite induced MBP release from eosinophils
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Necrosis tissue reaction:
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Wide necrosis with few inflammation signs.
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Staph
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Staph. aureus lab ID:
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Gram + forming staphyle (like grape bunch); colonies soft, and convex round on agar; range of color; catalase +; coagulase +, beta-hemolytic
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What are used to distinguish Staph aureus and epidermidis?
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Coagulase (aureus +), mannitol, beta hemolysis (aureus)
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Staphylococcus epidermidis features:
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Coagulase -, skin flora; catheter or device related infection (biofilms); and UTI
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Three methods for geneotyping Staph. aureus:
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Pulse field gel electrophoresis (PFGE); Multilocus sequence typing (MLST); Staphylococcal protein A typing (spa-typing)
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S. aureus' most generally three types of clinicla manifestations:
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1. Superficial lesion (abscesses & wound infection, scalded skin, pustule, impetigo) 2. Systemic (pneumonia, bacteremia, mastitis, osteomyelitis) 3.Toxin-mediated (toxic shock, food poisoning)
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What's S. aureus' temporal virulence factor expression regulator?
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Accessory Gene Regulator (AGR); as density grows, decreases surface protein, increases secreted proteins.
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Three types of S. aureus virulence factors:
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Attachment (Clumping factor, Sdr, Fibronectin binding protin); Evasion of host defence (Protein A, lipase, V8 serine protease); Invasion (alpha/beta hemolysin)
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Alpha hemolysin's importance to S. aureus?
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Hla punches hole in RBC membrane, found to be needed for S. aureus action; can also lyse PMNs
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S. aureus immunity:
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none successful so far.
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S. aureus toxic shock syndrome symptoms:
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Desquamation, fever, hypotention, weakness.
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Two types of superantigens of S. aureus:
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Toxic shock superantigen and enterotoxins
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Staphylococcus aureus epidemiology:
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10-14% anterior nares colonization, skin and hands contaminated as well; transient and chronic carriers; chronic carriers as recurrent boils and are sources of innosocomial infection. Mupirocin can rid carriage.
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What's the number one US nosocomial pathogen?
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MRSA
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Methicillin resistance: genetics, mechanism, other consequences?
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Methcillin resistance coded by mecA gene on the mobile element of SCCmec; mecA codes alternative PBP; Resistant to ALL beta-lactams and often multi drug resistant.
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How is SCCmec spread between S. aureus?
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via Phages carrying SCCmec
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Nosocomial MRSA resistance and sensitivity?
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Alll beta-lactam resistant; 50% vancomycin sensitive
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Vancomycin resistance genetics:
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vanA operon on plasmid responsible.
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Community MRSA: featuers and genetics:
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Mostly causing abscesses, less resisitant, Panton Valentine Leukotoxin +, Type IV SCCmec responsible.
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TSST 1 may cause what symptom?
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Rash
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