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54 Cards in this Set
- Front
- Back
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What are the 3 ways that macrophages persist during chronic inflammation?
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1)continued recruitment of monocytes
2)local proliferation of macrophages 3)immobilization of macrophages (cytokines that tell them to stick around) |
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Are mast cells found in acute or chronic infection?
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both, they express on surface receptor for Fc portion of IgE
-bound IgE ab's recognize antigen and cell degranulates |
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What role do eosinophils have in chronic infection?
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-they are involved in immune reactions mediated by IgE and parasitic infections
-they are phagocytic and undergo activation -their granules contain Major basic protein which is toxic to parasites and lyses mammalian cells |
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In what condition do neutrophils persist for many months into chronic inflammation?
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osteomyelitis
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Name the 6 major diseases that cause granuloma formation.
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TB, leprosy, syphilis, cat-scratch disease, sarcoidosis (this is a disease of exclusion, it is diagnosed only when all others have been ruled out), and Crohn disease (IBD, immune reaction against intestinal bacteria, self-antigens)
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What are the 2 types of giant cells?
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1)langerhans type giant cell with many nuclei arranged peripherally
2)foreign body type giant cell with many nuclei arranged haphazardly |
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What are the granulomas called in TB?
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tubercles (they are caseating granulomas usually)
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What are the functions of complement products (C5a, C3a, C4a) in acute inflammation?
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they are plasma protein derived and function in leukocyte chemotaxis and activation, vasodilation (mast cell stimulation)
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What is the function of kinins in acute inflammation?
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plasma protein derived, made in liver, causes increased vascular permeability, sm. mm. contraction, vasodilation, and pain
-mostly bradykinin responsible for these actions |
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What action does serotonin have in acute inflammation?
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-same actions as histamine
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What role does histamine play in acute inflammation?
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comes from mast cells, causes dilation of arterioles and increases vascular permeability of venules via H1 receptor
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What 2 molecules are produced from prostaglandins?
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prostacyclins and thromboxane
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Which AA metabolites cause vasodilation?
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PGI2 (prostacyclin), prostaglandins
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Which AA metabolites cause vasoconstriction?
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thromboxane A2, leukotrienes C, D and E
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Which AA metabolites cause increased vascular permeability?
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leukotrienes C, D, and E
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Which AA metabolites cause chemotaxis and leukocyte adhesion?
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leukotriene B, HETE
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What are the effects of Platelet activating factor?
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has multiple inflammatory effects, vascular and cellular,
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What is the role of NO in inflammation?
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it is produced by endothelial cells mostly
-dual actions in inflammation, causes vasodilation, reduces platelet aggregation and adhesion, inhibits some mast cell actions, and inhibits leukocyte recruitment |
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What is the role of TNF and IL1 in inflammation?
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produced in activated macrophages, play a role in fever and systemic effects of inflammation, stimulate expression of endothelial adhesion molecules and secretion of other cytokines, activate leukocytes, procoagulants, increased collagen synthesis and proliferation, increase sleep, increase acute phase protein production, leukocytosis, decreased appetite
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What is the role of chemokines in inflammation?
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stimulate leukocyte movement and directed movement (chemotaxis)
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What is the role of substance P in inflammation?
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transmits pain signals, poweful mediator of increased vascular permeability
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What are the 2 big players in complement system and what are their effects?
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C3a and C5a and this system provides protection against microbial agents
-can lead to cell lysis by MAC complex or biological effect of proteolytic fragments of complement, recruitment and activation of leukocytes, enhanced phagocytosis, etc.. |
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How is the superoxide radical produced?
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by incomplete reduction of O2 during ox. phos., also by phagocyte oxidase in leukocytes
-acts close to site of production |
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How is the superoxide radical inactivated?
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coversion to H202 and O2 by superoxide dismutase
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How is hydrogen peroxide produced?
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generated by SOD from O2- and by oxidases in peroxisomes
-can act distant from site of production |
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How is H2O2 inactivated?
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conversion to H20 and O2 by catalase in peroxisomes, glutathion peroxidase (cytosol, mito.)
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How is OH- produced?
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generated from H2O by hydrolysis (from Fenton rxn, radiation, etc.)
-most reactive oxygen derived free radical |
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How is OH- inactivated?
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conversion to H2O by glutathione peroxidase
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How is ONOO- produced?
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interaction of a superoxide radical with NO in many cell types
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How is ONOO- inactivated?
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conversion to HNO2 by peroxiredoxins (cytosol, mito.)
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What is the functions of epidermal growth factor (EGF)?
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-shares a common receptor with TGF-alpha
-stimulates cell division by binding to receptor (EGRF) tyrosine kinase receptor -main receptor is calld ERB B1 -mutations and amplifications in cancers of head, neck, breast, etc.. |
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What is the function of TGF-alpha?
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causes cells to divide, actions similar to EGF
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What is the function of hepatocyte growth factor (HGF)?
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-causes cell division on most epithelial cells and hepatocytes
-receptor is c-MET which is frequently over-expressed in human tumors |
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Describe the function of VEGF.
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-plays a role in vasculogenesis and angiogenesis
-promotes angiogenesis in tumors, chronic inflammation, healing of wounds -signals through tyrosine kinase receptors |
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Describe the function of platelet derived growth factor (PDGF).
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-causes migration and proliferation of fibroblasts, sm. mm. cells and monocytes
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What is the function of fibroblast growth factors (FGFs)?
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functions is angionenesis, development of sk. mm. and lung maturation, wound repair, and hematopoiesis
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What is the function of TGF-beta?
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stimulates proliferation of fibroblasts and sm. mm. cells
-anti-inflammatory effects -inhibits growth of most epithelial cell types -blocks cell cycle by increasing expression of cell-cycle inhibitors, loss of receptor often in human tumors, provides proliferative advantage to tumor cells |
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What 2 cytokines play a role in liver regeneration?
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IL6 and TNF
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What cytokines play a role in wound healing?
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IL1 and TNF
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What is osteopontin?
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it promotes fibrosis during wound healing
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In what tissues is telomerase present?
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germ cells, stem cells, and cancer cellst
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What are the 2 most notable opsonins?
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c3b and IgG
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What are some examples of growth factor mediated pathologic hyperplasia?
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1)wound healing producing excessive scar-hypertrophic scar or keloid (excess collagen produced by fibroblasts)
2)viral warts-HPV of squamous cells promotes growth via cell cycle inhibitors (E6, E7) 3)psoriasis-overgrowth of the epidermal squamous cells due to inflammatory cytokines |
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What are warts?
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they are hyperplastic epidermis due to growth factors elaborated by HPV
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What are some examples of pathologic devervation atrophy?
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1)hereditary sensory motor neuropathy
-Charcot marie tooth (genetic defect in myelin leads to neuron loss) 2)Spinal mm atrophy (hereditary defect leads to loss of motor neurons) 3)encephalitis (CNS infection) damages ant. horn cells; Polio and west nile virus |
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What is the mechanism of atrophy?
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net loss of intracellular protein:decreased synthesis, increased degradation
-degradation via ubiquitin-proteasome path (accel. in longstanding infection) -autophagy of cytoplasmic organelles to yield energy or rectly damaged structure (residual bodies/lipofuscin accumulation) |
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What are the 3 pathways of cell death?
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1)necrosis-always pathologic
2)apoptosis-can by physiologic or pathologic 3)autophagy-regulated by autophage genes (Atgs), usually occurs as a result of nutrient depletion |
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How are necrotic cells degraded?
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1)autolysis-enzymes intrinsic to injured cell
2)lysosomal enzymes from immigrant leukocytes of the inflammatory response |
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Describe the morphology of the nuclei in necrotic cells.
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there will be non-specific breakdown of DNA
1)karyolysis-fading of nuclei 2)nuclear pyknosis-shrinkage and increased basophilia (also seen in apoptosis) 3)karyorrhexis-fragmentation of pyknotic nucleus (also seen in apoptosis) |
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What are the main causes of septic shock?
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-mainly gram positive bacteria
-can also be caused by gram negative bacilli, fungi, viruses |
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What is the pathogenesis of septic shock?
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response of innate immune system to overwhelming dose of microbial constituents
-leads to systemic vasodilation and pooling of blood in the periphery |
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What are the steps in apoptosis?
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-phagocytic recognition by macrophages of neighboring cells
-phosphatidylserine moves to cell surface and is recognized by receptor on phagocytic cell -apoptotic cell may be coated by complement and there will be rapid disappearance of apoptotic cell |
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What molecules play a role in the extrinsic apoptotic pathway?
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Fas/FasL:membrane protein of T lymphs binds to Fas on target cell and eliminates self reactive lymphs
TNF binding to receptor may lead to apoptosis in inflammatory condition through death domain (Note: can also lead to cell survival by activating transcription factor NF-KB which then increases transcription of Bcl2 family) -death domains involved in both |
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Which proteins are sensors for the instrinsic apoptotic pathway?
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BH3 (bim, bid, and bad)
-they activate Bax, Bak to open channel and release cytochrome c -p53 also upregulates Bax if damage is sensed in DNA |
