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221 Cards in this Set
- Front
- Back
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What is the stem cell of leukocytes?
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Hematopoeitic Stem Cell
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Which leukocytes are myeloid?
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Erythrocytes, platelets, eosinophils, basophils, neutrophils, monocytes
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Which leukocytes are lymphoid?
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B cells, T cells, NK cells, NKT cells
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Where are lymphocytes activated?
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Peripheral lymphoid tissue
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What does TLR2 detect?
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Bacterial peptidoglycan, lipoprotein, lipotechoic acid (PAMPs)
HMGB1 (DAMP) |
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What does TLR4 detect?
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LPS, fungal mannans, viral envelope protein (PAMPs)
HMGB1 (DAMP) |
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What does RAGE detect?
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HMGB1
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What detects HMGB1?
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TLR2, TLR4, RAGE
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Which cells express innate immune response receptors?
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Macrophages, Dendritic Cells, Lymphocytes, Epithelial Cells, Endothelial Cells
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What does TLR1 detect?
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Bacterial peptidoglycan, lipoprotein, lipotechoic acid
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What does TLR6 detect?
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Bacterial peptidoglycan, lipoprotein, lipotechoic acid
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What does TLR-5 detect?
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Bacterial flagella
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What detects bacterial flagellin?
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TLR5
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What detects bacterial peptidoglycan, lipoproteins, and lipotechoic acid?
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TLR1, TLR2, TLR6
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What detects LPS, fungal mannans, and viral envelope proteins?
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TLR4
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What does TLR3 detect?
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ssRNA, unmethylated CpG dinucleotides
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What does TLR7 detect?
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ssRNA, unmethylated CpG dinucleotides
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What does TLR8 detect?
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ssRNA, unmethylated CpG dinucleotides
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What does TLR9 detect?
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ssRNA, unmethylated CpG dinucleotides
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What detects bacterial nucleic acids (e.g. ssRNA, unmethylated CpG dinucleotides)?
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TLR3, TLR7, TLR8, TLR9
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What does TLRs recognizing PAMPs or DAMPs lead to?
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TFs: NFkB and IRF3
Expression of: Cytokines (TNFa, IL-1, IL-12) Chemokines (IL-8) Endothelial adhesion molecules (E-selectin) Antiviral cyotkines (IFNa, IFNb) |
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Which cells secrete TNFa?
What are its effects on target cells? |
Secreted by: Macrophages, DCs, T Cells
Epithelial Cells - produce Defensins, Selectins, Integrin-L, Chemokines Neutrophils - Activate, produce Defensins Hypothalamus: Fever Liver: Synthesize of acute phase proteins Fat, Muscle: Catabolism (cachexia) Bone marrow: WBC release Many cell types: Apoptosis Nerves: pain |
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Which cells secrete IL-1?
What are its effects on target cells? |
Secreted by: Macrophages, DCs, Endothelial cells, some Epithelial cells
Epithelial Cells - produce Defensins, Selectins, Integrin-L, Chemokines Hypothalamus: Fever Liver: Synthesis of acute phase proteins T cells: Th17 differentiation Mast cells: Histamine release Basophils: Histamine release Bone marrow: WBC release |
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Which cells secrete IL-4?
What are its effects on target cells? |
Secreted by: Th2 cells
B cells - IgE class-switching |
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Which cells secrete IL-5?
What are its effects on target cells? |
Secreted by: Th2, Mast cells
Eosinophils - activate B cells - growth, Ig secretion |
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Which cells secrete IL-6?
What are its effects on target cells? |
Secreted by: Macrophages, Endothelial cells, T cells
Liver - Synthesize acute phase proteins B cells - Proliferation of plasma cells T cells - Th17 differentiation Hypothalamus - Fever |
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Which cells secrete IL-8?
What are its effects on target cells? |
Secreted by Macrophages, Epithelial cells, Endothelial cells
Mast Cells - Histamine release Basophils - Histamine release Leukocytes - Chemotaxis |
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Which cells secrete IL-10?
What are its effects on target cells? |
Secreted by: Macrophages, DC, Treg cells
Macrophages: reduce IL-12 secretion, reduce expression of MHC II and co-stimulators DC: reduce IL-12 secretion, reduce expression of MHC II and co-stimulators |
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Which cells secrete IL-12?
What are its effects on target cells? |
Secreted by: DCs, Macrophages
NK - produce IFNg, increased cytotoxic activity T cells - produce IFNg, increased cytotoxic activity, Th1 differentiation |
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Which cells secrete IL-13?
What are its effects on target cells? |
Secreted by: Th2 cells
B cells - IgE class-switching |
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Which cells secrete IFNa/b?
What are its effects on target cells? |
IFNa secreted by: DC, Macrophages
IFNb secreted by: Fibroblasts All cells - Antiviral state, increased MHC I expression NK cells - Activate |
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Which cells secrete IFNg?
What are its effects on target cells? |
Secreted by: NK, Th1 cells
Macrophages - activate B cells - IgG class-switching T cells - Th1 differentiation |
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Which cells secrete TGFb?
What are its effects on target cells? |
Secreted by: Treg, platelets, macrophages
Fibroblasts - recruitment, collagen synthesis, myofibroblast phenotype Macrophages - recruitment B cells - Class-switching to IgA T cells - Th17 and Treg differentiation Angioblasts - angiogenesis Blocks plasminogen inhibitor, collagenase |
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What causes defective leukocyte recruitment to sites of infection and increased susceptibility to infections?
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Inherited deficiencies in integrins and selectins (Leukocyte Adhesion Deficiencies)
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What is the result of inherited deficiencies in integrins and selectins (Leukocyte Adhesion Deficiencies)?
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Defective leukocyte recruitment to sites of infection and increased susceptibility to infections
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What is are the 2 roles of NK cells?
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Kill infected cells
Produce IFNg to activate macrophages |
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How are uninfected host cells protected from NK cells?
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Uninfected host cells express MHC I, which sends an inhibitory signal to NK cells. Even if uninfected cells express the activating ligand for NK cells, the MHC I inhibition overpowers the activation.
Infected host cells express less MHC I and more activating ligand for NK cells. |
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How does Pneumococcus evade the innate immune system?
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Pneumococcus produces a capsular polysaccharide which inhibits phagocytosis
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Which organism evades the innate immune system by resisting phagocytosis and how?
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Pneumococcus produces a capsular polysaccharide which inhibits phagocytosis
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Which organism produces a capsular polysaccharide and how does that allow it to evade the innate immune system?
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Pneumococcus produces a capsular polysaccharide which inhibits phagocytosis
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How does Staphylococci evade the innate immune system?
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Staphylococci produces catalase which breaks down ROS intermediates, thus inhibiting destruction in phagolysosomes
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Which organism evades the innate immune system by inhibiting destruction in phagolysosomes and how?
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Staphylococci produces catalase, which breaks down ROS intermediates, thus inhibiting destruction in phagolysosomes
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Which organism produces catalase and how does that allow it to evade the innate immune system?
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Staphylococci produces catalse which breaks down ROS intermediates, thus inhibiting destruction in phagolysosomes
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Which organisms evade the innate immune system by blocking complement activation and how?
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Neisseria meningitides produces sialic acid which inhibits C3 and C5 convertases
Streptococcus produces M protein which blocks C3 binding to bacteria and C3b binding to complement receptors |
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How does Neisseria meningitides evade the innate immune system?
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Neisseria meningitides produces sialic acid which inhibits C3 and C5 convertases.
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How does Streptococcus evade the innate immune system?
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Streptococcus produces M protein which inhibits C3 binding to bacteria and C3b binding to complement receptors
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Which organism produces sialic acid and how does that allow it to evade the innate immune system?
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Neisseria meningitides produces sialic acid which inhibits C3 and C5 convertases.
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Which organism produces M protein and how does that allow it to evade the innate immune system?
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Streptococcus produces M protein which inhibits C3 binding to bacteria and C3b binding to complement receptors
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How does Pseudomonas evade the innate immune system?
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Pseudomonas produces modified LPS which resists the action of antimicrobial peptide antibiotics
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Which organism produces modified LPS and how does that allow it to evade the innate immune system?
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Pseudomonas produces modified LPS which resists the action of antimicrobial peptide antibiotics
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Which organism evades the innate immune system by resisting antimicrobial peptide antibiotics?
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Pseudomonas produces modified LPS which resists antimicrobial peptide antibiotics
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Which innate and adaptive immune systems do blood-borne pathogens activate?
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Complement system, which activates the humoral immune response
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Which innate and adaptive immune systems do intracellular and phagocytosed pathogens activate?
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IL-12 production by macrophages, which activates the cell-mediated immune response
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Describe cross-presentation and its function in the immune system.
How is this different from normal presentation. |
Cross-presentation is when peptides from phagocytosed proteins are presented on MHC I molecules. This allows CD8 CTL to bind to the MHC I and activate.
Usually phagocytosed proteins are degraded in the phagolysosome and presented on MHC II molecules while cytosolic proteins are degraded in the proteasome and presented on MHC I. |
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How are peptides loaded onto MHC I?
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Proteins are produced in the cytoplasm and degraded by the proteasome. TAP1/2 transport the peptides into the rER where they are loaded onto MHC I molecules.
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How are peptides loaded onto MHC II?
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Proteins are phagocytosed and degraded in the phagolysosome into peptides. These peptides are sequestered into an endosome. The secretory vesicle containing MHC II then fuses with the endosome. The peptides displace the invariant chain from MHC II with the help of HLA-DM.
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What are the genes which code for MHC I?
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HLA-A, HLA-B, HLA-C
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What do HLA-A, HLA-B, and HLA-C code for?
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MHC I
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What do HLA-DP, HLA-DQ, and HLA-DR code for?
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MHC II
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What are the genes which code for MHC II?
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HLA-DP, HLA-DQ, HLA-DR
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What does HLA-DM do?
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Assists in loading of peptides onto MHC II, displacing the invariant chain
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What does CD1b/d do?
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Presents bacterial lipids to NKT cell's invariant a/b TCR
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What does FcRn do?
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Transports maternal IgG across the placenta and recycles IgG, increasing its serum half-life.
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How many signals are required for production of IgM by B cells?
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Only 1. After binding to antigen and endocytosing it, the B cell enters the cell cycle, proliferates, expresses more B7 and cytokine receptors, and expresses low level IgM.
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Which chains of the TCR and Ig have VDJ recombination?
Which chains of the TCR and Ig have VJ recombination? |
B chain of TCR and H chain of Ig have VDJ recombination.
A chain of TCR and L chain of Ig have VJ recombination. |
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What is the order of events in VDJ recombination?
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D joins J
V joins DJ |
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Describe the selection of T cells in the thymus after they have rearranged their TCR genes
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T cell progenitors arise in the bone marrow and travel to the thymus. In the thymus, they undergo positive and negative selection as well as death by neglect.
T cells which bind weakly to MHC I:self with their TCR:CD8 receptors mature into CD8 CTLs. T cells which bind weakly to MHC II:self with their TCR:CD4 receptors mature into Th cells. This is positive selection. T cells which bind strongly to MHC I:self or MHC II:self are destroyed. This is negative selection. T cells which do not bind to MHC I:self or MHC II:self do not receive survival signals. This is death by neglect. |
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What does bradykinin do during inflammation?
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Increase vascular permeability
Vasodilation Bronchoconstriction (asthmatics) Elicit pain |
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What does C3a do during inflammation?
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Increase vascular permeability
Chemotaxis Histamine release |
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What does C5a do during inflammation?
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Increase vascular permeability
Chemotaxis Histamine release |
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What does histamine do during inflammation?
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Increase vascular permeability
Vasodilation |
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What does serotonin do during inflammation?
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Increase vascular permeability
Vasodilation |
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What does low dose PAF do during inflammation?
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Increase vascular permeability
Vasodilation Chemotaxis |
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What does high dose PAF do during inflammation?
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Increase vascular permeability
Vasoconstriction Bronchoconstriction Chemotaxis |
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What does PGE2 do during inflammation?
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Vasodilation
Pain Fever Chemotaxis |
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What do Leukotrienes C,D,E do during inflammation?
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Increase vascular permeability
Vasoconstriction (transient) Chemotaxis |
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What does NO do during inflammation?
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Vasodilation
Tissue destruction |
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What does C3b do during inflammation?
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Opsonization
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What does FcIg do during inflammation?
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Opsonization
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What do N-formylated peptides do?
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Chemotaxis
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What does Leukotriene B4 do during inflammation?
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Chemotaxis
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What does Thromboxane A2 do during inflammation?
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Induce platelet aggregation
Vasoconstriction |
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What does PGI2 do during inflammation?
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Vascular Permeability
Vasodilation Inhibit platelet aggregation |
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What do lysozymes from leukocytes do during inflammation?
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Destroy tissues
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What do CSFs do during inflammation?
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Increase WBC production in bone marrow
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Which cytokine is required for granuloma formation?
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TNFa
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Which cells are always present in wound healing?
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Angioblasts
Fibroblasts Mast cells Macrophages |
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What is does TNFa do during inflammation?
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Fever
Pain WBC release from bone marrow |
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What does IL-1 do during inflammation?
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Histamine release
Fever WBC release from bone |
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What do deficiencies in C5-C8 lead to?
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Increased susceptibility to recurrent infections, especially Neisseria.
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What deficiency leads to increased susceptibility to Neisseria infections?
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C5-C8 deficiencies
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What does a deficiency in C3 lead to?
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Serious recurrent infections from pyrogenic and Gm- bacteria
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What do deficiencies in C1, C2, and C4 lead to?
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Autoimmune diseases which resemble Systemic Lupus Erythematous and increased susceptibility to bacterial infections.
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What deficiency leads to serious recurrent infections by pyrogenic and Gm- bacteria?
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C3 deficiency
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What deficiencies lead to autoimmune diseases resembling Systemic Lupus Erythematous?
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C1, C2, C4 deficiencies
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What deficiencies lead to increased susceptibility to bacterial infections?
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C1, C2, C4 deficiencies
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What is the function of C1 INH?
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C1 INH inhibits C1s and C1r protease activity
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What protein inhibits C1s and C1r protease activity?
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C1 INH
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What is the function of Factor I?
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Factor I cleaves C3b and C4b
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Which protein cleaves C3b and C4b?
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Factor I cleaves C3b and C4b
(Cofactors: Factor H, C4BP) |
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What is the function of Factor H?
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Dissociates alternative C3 convertase subunits (C3bBbC3b)
Factor I cofactor |
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Which proteins are cofactors for Factor I?
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Factor H
C4BP |
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Which protein dissociates alternative C3 convertase subunits C3bBbC3b?
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Factor H dissociates alternative C3 convertase subunits (C3bBbC3b)
It is also a cofactor for Factor I |
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What is the function of C4BP?
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C4BP dissociates classical C3 convertase subunits (C4bC2aC3b)
It is also a cofactor for Factor I |
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Which protein dissociates classical C3 convertase subunits (C4bC2aC3b)?
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C4BP dissociates classical C3 convertase subunits (C4bC2aC3b)
It is also a cofactor for Factor I |
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What does DAF do?
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Causes dissociation of C3 convertase subunits
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What molecule causes dissociation of C3 convertase subunits?
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DAF
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What does CD59 do?
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CD59 blocks C9 and the MAC
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Which protein blocks C9 and the MAC?
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CD59 blocks C9 and the MAC
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What does a deficiency in C9 lead to?
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Nothing
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What does a deficiency in C1 INH lead to? What are the symptoms?
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Hereditary angioneurotic edema
Large amounts of vasoactive peptides lead to systemic edema and possible obstruction of passage of air through the larynx. |
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What leads to a Hereditary angioneurotic edema? What are the symptoms?
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Deficiencies in C1 INH
Widespread activation of vasoactive peptides leads to systemic edema and possible obstruction of passage of air through the larynx. |
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What does a deficiency in DAF lead to?
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Paroxysmal Nocturnal Hemoglobulinuria
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What does a deficiency in CD59 lead to?
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Paroxysmal Nocturnal Hemoglobulinuria
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What leads to Paroxysmal Nocturnal Hemoglobulinuria?
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Deficiencies in CD59 and DAF
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What does Silver Stain show?
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Fungi
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How do you visualize fungi on LM?
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Silver stain (better)
PAS |
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How do you visualize amyloid on LM?
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Congo Red
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How do you visualize glycogen and basement membranes on LM?
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PAS
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What causes fibrinoid necrosis?
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Malignant hypertension
Autoimmune disorder Vasculitis |
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What are the causes of macrovesicular fatty changes?
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EtOH abuse, DM, starvation, obesity, protein malnutrition, toxins, hypoxia
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What are the four primary causes of fatty changes?
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Increased synthesis of FFA and TG (alcohol)
Increased FFA uptake (hepatic catabolism in starvation or DM, increased fat ingestion) Decreased FA oxidation (hypoxia, anemia) Decreased synthesis and/or export of apolipoproteins (some drugs/toxins, nutrition deficiency) |
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What are the causes of microvesicular fatty changes?
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Late pregnancy, drugs/toxins, Reye Syndrome when children take acetyl salicylic acid during febrile illnesses
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What causes pink droplets to accumulate in renal tubules?
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Glomerular disease leads to increased protein filtration, tubule cells increase reabsorption
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What are the four major causes of protein accumulations?
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1. Synthesis >> degradation/removal
2. Defect in folding/transport/secretion --> accumulation of abnormal/normal protein 3. Defective enzyme --> substrate accumulation 4. Undigestible exogenous substrate accumulates |
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What are Russel bodies and what causes them?
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Hyaline inclusions caused by an excessive production of a normal protein such as Ig production in plasma cells
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What protein deficiency can lead to emphysema or cirrhosis?
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Alpha-1-antiprotease deficiencies.
Alpha-1-antiprotease helps counterbalance the proteolytic activity of neutrophils, especially in the lung. |
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What can alpha-1-antiprotease deficiencies lead to?
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Emphysema or cirrhosis.
Alpha-1-antiprotease helps counterbalance the proteolytic activity of neutrophils, especially in the lung. |
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What are Mallory Bodies, and what causes them?
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Mallory bodies, also known as alcoholic hyalin, are irregular cytoplasmic inclusions in hepatocytes made up of cytokeratin IFs + HSPs.
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What are Lewy bodies and what disease process are they associated with?
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Lewy bodies are intracellular hyaline inclusions that accumulate in damaged neurons in patients with parkinsons disease
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What is hemosiderin?
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storage form of iron
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What is hemosiderosis?
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Short term accumulation of iron in the form of hemosiderin
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What is hemochromatosis?
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chronic total body iron overload
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What does hemochromatosis cause?
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Iron catalyzes the formation of free radicals which typically damage the pancreas, heart, and liver, leading to DM, heart failure, and cirrhosis + increased risk of hepatocellular carcinoma.
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What can cause glycogen accumulation?
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Genetic diseases cause defects in glycogen metabolism or synthesis, know as glycogen storage diseases.
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What are heart-failure cells?
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Macrophages eat extravasated red blood cells in the lungs which accumulate due to left-sided heart failure.
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Which accumulation can lead to a brownish skin discoloration? Why?
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Hemochromatosis. Iron deposition and increased melanin production, typically also associated with DM since iron destroys pancreas, known as "bronze diabetes."
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What are the primary and secondary causes of hemochromatosis?
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Primary: autosomal recessive disorder in regulation of intestinal iron absorption
Secondary: RBC disorders, chronic blood transfusions, anything else |
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Which form of bilirubin is water-soluble?
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Bilirubin is conjugated to glucuronide in the liver and becomes water soluble for excretion in bile.
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What is chronic obstruction of bile flow know as? What can it lead to?
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Cholestasis
Biliary cirrhosis |
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What causes copper accumulation?
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Autosomal recessive defect in copper excretion in the bile: Wilson's Disease.
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What does copper accumulation lead to?
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cirrhosis (liver accumulation)
motor dysfunction (brain accumulation) |
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Name two examples of interstitial accumulations
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Amyloidosis
Pathological calcification |
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Describe AL?
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Primary amyloidosis
Amyloidosis caused by Amyloid Light Chain Immunoglobulin. Plasma cell neoplasms cause this. |
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Where is AL usually found?
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Heart, GI, Resp, nerves, skin, tongue.
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Describe AA?
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Amyloidosis caused by Amyloid Associated precursor serum Amyloid A protein, an APP secreted by the liver.
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In what conditions is AA usually observed?
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Chronic inflammatory conditions
Rheumatoid arthritis Inflammatory bowel disease Ankylosing spondylitis TB |
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Where are AA deposits usually found?
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kidney, liver, spleen, lymph nodes, adrenal glands, thyroid
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Describe Amyloid Beta
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b-Amyloid associated with alzheimers and Down's syndrome
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In which form of calcium deposition are serum calcium levels normal?
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Dystrophic
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Where does dystrophic calcification occur?
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Injured or necrotic tissues due to normal serum calcium levels.
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In which form of calcium deposition are serum calcium levels high?
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Metastatic
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Where does metastatic calcification occur and why?
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Interstitial tissues of kidneys, lungs, gastric mucosa, and blood vessels where tissues lose protons and become more basic.
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Lymphangitis
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Infection of lymph vessels
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Lymphadenitis
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Infection of lymph nodes
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Infection of lymph vessels
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Lymphangitis
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Infection of Lymph nodes
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Lymphadenitis
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Protein content/SG of exudate?
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>1.5gm/dL
>1.015 |
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Protein concentration/SG of transudate?
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0-1.5g/dL
1.010-1.015 |
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Protein content of transudate vs exudate?
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Transudate: albumin
Exudate: all |
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Possible places for fibrinous exudate?
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Heart: pericarditis
Appendix: appendicitis |
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What facilitates expression of P- and E-selectins?
What do they bind to? |
TNFa, IL-1
Sialylated Lewis-X on surface of WBC |
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What causes Leukocyte Adhesion Deficiency 1?
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Mutation in b-chain of integrin
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Mutation in b-chain of integrin leads to what disorder?
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Leukocyte Adhesion Deficiency 1
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What causes Leukocyte Adhesion Deficiency 2?
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Mutation in selectin receptor
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Mutation in selectin receptor leads to what disorder?
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Leukocyte Adhesion Deficiency 2
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What is required for exudate formation?
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Increased vascular permeability
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What does Chediak-Higashi syndrome cause?
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Defects in PMN phagolysosome
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Which cell uses myeloperoxidase?
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PMNs
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Which change in vascular flow and vessel caliber is transient and may not always take place?
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Initial vasoconstriction of arterioles
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What causes the first invariable event of inflammation?
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Vasodilation of arterioles and their dependent microvascular beds, leading to hyperemia.
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What causes heat and redness?
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Vasodilation leads to hyperemia
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What causes swelling, pain, and loss of function?
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Actin filaments in venules and capillaries contract, increasing vascular permeability and causing exudation which can press against nerves.
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Describe the immediate transient pattern of increased vascular permeability
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Chemical mediators cause small to medium sized post-capillary venules to vasodilate
Begins immediately, lasts 30-60 minutes. |
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Describe the immediate sustained pattern of increased vascular permeability
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Direct injury to endothelium leads to sloughing and increased vascular permeability. All levels of microcirculation are affected.
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In which pattern of increased vascular permeability are only small to medium sized post-capillary venules affected?
How is it mediated? |
Immediate transient
Chemical mediators |
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In which pattern of increased vascular permeability are all levels of microvasculature affected?
How is it mediated? |
Immediate sustained
Endothelial damage |
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Describe the delayed, prolonged pattern of increased vascular permeability
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Sunburn, thermal injury, X-ray, UV radiation, bacterial toxins, or delayed hypersensitivity reactions lead to vasodilation of venules and capillaries.
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In which pattern of increased vascular permeability are venules and capillaries affected?
How is it mediated? |
Delayed prolonged
Sunburn, thermal injury, X-ray or UV radiation, bacterial toxins, or delayed hypersensitivity (also direct damage to endothelium) |
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What does IL-8 do during inflammation?
|
Histamine release
Chemotaxis |
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How do macrophages degrade pathogens?
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Lactoferrin
Lysozyme (muramidase) NO |
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What causes cyclic neutropenia, what are the symptoms, and what is the treatment?
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Inherited mutations in neutrophil elastase lead to recurring 3-6 day periods of neutropenia every 3 weeks. It is treated with CSF.
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What causes chronic granulomatous disease?
What is the mechanism of disease? |
X-linked or autosomal recessive disorders lead to NADPH oxidase deficiencies, which make cells (macrophages, PMNs) unable to undergo a respiratory burst.
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What does a deficiency in NADPH oxidase lead to?
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Macrophages and PMNs are unable to undergo a respiratory burst. This leads to Chronic Granulomatous Disease.
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What is the compensatory mechanism for myeloperoxidase deficiency? Which cells would be affected?
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PMNs increase their formation of H2O2.
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What can lead to leukocyte defects?
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Chediak-Higashi Syndrome
Adhesion defects: -Hemodialysis Chemotaxis defects: -Malignancy -Burns -Diabetes Phagocytosis and Killing defects: -Leukemia -Anemia -Sepsis -Malnutrition |
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What does PGF do during inflammation?
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Anti-inflammatory
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Which cells have increased levels of alpha-1-antiprotease? What is a possible outcome of this phenomenon?
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Giant cells have increased levels of alpha-1-antiprotease, which may make them important in management of chronic inflammation.
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Which forms of acute inflammation contain lymphocytes?
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viral hepatitis
viral myocarditis |
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Which forms of chronic inflammation contain PMNs?
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osteomyelitis
actinomycosis |
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What does Eosinophilic Cationic Protein do?
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Stimulate HA synthesis
Inhibit T cell proliferation |
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What does Eosinophilic Peroxidase do?
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Kills cells
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What does Eosinophil-derived Neurotoxin do?
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Ribonuclease activity damages neurons
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What does Major Basic Protein do?
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Comes from eosinophils, destroys epithelium
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What is the difference between effector memory and central memory T cells?
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Effector memory T cells:
-migrate to peripheral tissues -CCR7(-) -become effector T cells after exposure to antigen Central memory T cells: -recirculate through lymph nodes -CCR7(+) -reactivate more slowly |
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Which cells are required for memory?
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CD4 T cells
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How will a deficiency in MHC II lead to compromised immune function?
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CD4 T cells must see antigen presented on MHC II in order to create immunological memory. Without MHC II, CD4 T cells cannot be activated, thus B cells cannot receive activation signals.
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Where are plasma and memory B cells generated?
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Germinal centers of lymphoid follicles from activated B cells. Plasma cells do not appear to give rise to memory cells
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What mIg molecules do memory B cells express?
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IgA, IgG, IgE
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What is the order of Ig isotypes?
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M D G E A
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Where do plasma cells usually reside?
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Bone marrow
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Where do memory B cells usually reside?
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circulating in the spleen, blood, and tissue
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Which adhesion molecule do memory B cells express?
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CD27
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Which adhesion molecules allow naive B and T cells to enter lymph nodes?
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CCR7 and L-selectin CD62L
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Why must conjugated vaccines be used for children under two years of age?
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Children's immune systems are not good at developing T-independent thymus responses.
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What are conjugated vaccines?
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Conjugated vaccines are bacterial capsular polysaccharides attached to protein. This allows children's immune systems to bind to the polysaccharide (or protein) and present the protein to CD4 T cells, thus creating an immunological response to capsular polysaccharides.
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What sort of Ig response do conjugated vaccines elicit?
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anti-capsular polysaccharide IgG
anti-conjugated protein IgG |
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What is an example of a conjugated vaccine?
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H. influenzae
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A wedge-shaped blood supply is known as what sort of organization?
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Hilar
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Name 6 causes of cirrhosis
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Hemachromatosis
Cholestasis Wilson Disease EtOH HBV HCV |
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Identify the following cells as permanent, labile, or stable:
Surface epithelia Mucosal lining of all excretory ducts Hematopoeitic stem cells Liver cells Kidney cells Vascular endothelium Neurons Cardiac muscle Smooth muscle Skeletal muscle Bone Cartilage Connective tissue |
Surface epithelia: labile
Mucosal lining: labile HSC: labile Hepatocytes: stable Kidney cells: stable Vascular endothelium: stable Neurons: permanent Cardiac muscle: permanent Smooth muscle: stable Skeletal muscle: permanent Bone: stable Cartilage: stable Connective tissue: stable |
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What occurs within the first 0-24 hours of primary union wound healing?
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Clot forms, dehydrates, becomes scab
PMNs appear, basal epithelial cells proliferate, fibroblasts proliferate |
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What occurs within 24-48 hours of primary union wound healing?
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Epithelial cells migrate, establishing epidermal continuity and secreting a proteolytic enzyme.
Scab falls off. Fibroblasts proliferate. |
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At what time period is epidermal continuity established during healing by first intention?
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24-48 hours
Epidermal continuity Scab falls off Fibroblasts proliferate |
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What occurs by day 3 of primary union wound healing?
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Macrophages have replaced PMNs
Granulation tissue appears Collagen (I, III) synthesized at wound margins Epithelial proliferation leads to epidermal thickening |
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What occurs by day 4 of primary union wound healing?
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Proliferated fibroblasts move into the wound area and produce procollagen and fibronectin
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What occurs by day 5 of primary union wound healing?
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Incisional space filled with granulation tissue, collagen bridges the area.
Epidermis of normal thickness, redundant epithelial cells undergo remodeling. Keratinization occurs |
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What occurs by day 7 of primary union wound healing?
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Collagen (I, III) synthesis is at a maximum. Actin fibrils begin to condense in fibroblasts
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What occurs by day 9 of primary union wound healing?
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Abundant ECM
Fibroblasts become myofibroblasts |
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What occurs by day 14 of primary union wound healing?
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New vessels disappear, leukocyte infiltration and edema diminish.
Tissue appears paler. Wound contraction occur and fibroblasts undergo apoptosis |
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What occurs by one month of primary union wound healing?
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The epithelium is completely intact and remodeled and cellular connective tissue comprises the area.
Overproduction of collagen can lead to keloid formation |
