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42 Cards in this Set

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inflammation sentries
fibroblasts, endothelial cells, dendritic cells, mast cells, macrophages--release chemokines and whatnot
chemokines
small molecular wight peptides secreted by resident macrophages, fibroblasts, endothelial cells which attract and activate neutrophils, monocytes, and lymphocytes. i.e IL8
site of entry for cells and plasma proteins at the site of tissue injury
post capillary venules
exudate
protein rich fluid that egresses into tissue thanks tue increased permeability of post capillary venules in inflammation
transudate
low in protein and cells and results from increased hydrostatic pressure (heart failure) or low oncotic pressure (liver, kidney disease)
causes of pain in inflammation
nerve injury, locally produced cytokines like bradykinin
Source of histamine
mast cells, platelets
source of bradykinin
plasma cleavage product of high molecular with kininogen HMWK
stasis (inflammation)
slow flow that allows phagocytes to attach to vessel wall, results from increasing viscosity secondary to loss of plasma
PMN description; source, lifetime, function, granule types
1) produced in marrow 2) viable less than 24 hours after migration to injury 3) major cell in acute inflammatory response 4) primary cell against bacteria 5) two granule types: azurophil and secondary
contents of azurophil granules
proteases, myeloperoxidase, lysozyme
contents of specific (secondary) granules
lysozyme, lactoferrin
mediators of adhesion of neutrophils to vessel wall
histamine, complement products (C5a), TNF, IL1, IL8
transmigration, definition, causes
passage of activated phagocytes thru vessel wall, promoted by gradients of chemotactic substances like C5a, LTB4 (lipoxygenase pathway metabolite of arachidonic acid), F-met leu phe (bacterial cell wall peptide), IL8
phagocytosis opsonins
Fc portion of immunoglobulin, C3b, Mannose
Products released by phagocytes
Lysosomal producsts such as elastase, lysosome, collagenase; Nitric oxide; oxygen derived metabolites (i.e. HOOH), HO, superoxide o2-, hypochloruos acid (HOCL)
Means of activation of complement
1) Classic pathway via Cl binding to Fc portion of IgG or IgM, 2) Alternate pathway by bacterial surfaces which stabilize C3b hiding it from serum proteases like factors H and I
Function of C5a
1) vasodilation and increased blood flow, 2) causes phagocytes to produce adhesive surface molecules that allow them to stick to endothelial cells 3) chemotactic peptide for phagocytes, enhances production of mxygen derived metabolites
C3a function
vasodilaation and increased blood flow
C3b function
opsonin
major cell types involved in chronic granulomatous inflammation
mononuclear phagocyts and CD4 T cells
Types of macrofages
1) mobile macrophages, migrate into tissue in response to chemotactic substances 2) splenic macrophages 3) kupffer cells (hepatic macrophages) 4) alveolar macrophages 5) osteoclasts, 6) microglial cells
CD4 T cell role in granulomatous infections
produce cytokines like interferon gamma to activate macrophages to kill phagocytized bugs, other CD4 TH1 cytokines drive granuloma formations to keep bug in jail
Stages of streptococcus pneumonia infection
1) complement activation predominately by the alternate pathway 2)C3a & C5a --> local vasodilation and vascular permeability-->exudate 4) at 7 days adaptive immune response w/ IgM and IgG-->classic pathway complement activation--> better opsonisation
Stages of pulmonary TB
1) TB evade intitial inflammatory respnse and PMNs 2) TB multiply in macrophages and travel to lymph nodes 3) Over 2-3 weeks sensitized TH1 CD4 cells specific for TB multiply in lymph nodes and migrate to infected sites 4) produce lymphokines like macrophage activating factor/INF-g/macrophage chemotactic factor-->intracellular killing of TB
coaches (granulomas)
sensitized TH1 lymphocytes surrounding granuloma
mechanism of fever production
IL1, TNF, IL6 produced by macrophages, endothelial cells, fibroblasts, keratinocytes, lymphocytes,--> cause hypothalamic synthesis of PGE2 raises thermal set point cause vasoconstriction, and shivering (heat conservation and production)
Systemic manifestations of inflamation
1 fever,
2 anemia,
3 neutrophilia,
4 somnolence-malaise, muslce breakdown--wasting--cachexia--anorexia
5 shock, disseminated intravascular coagulation
cause of anemia in inflammation
decreased erythropoiesis probably due to TNF, interferon, and/or IL1
Cause of neutrophelia in inflammation
GM-CSF (granulocyte monocyte-colony stimulating factor) produced by epidermal cells, endothelial cells, and fibroblkasts --> increased production of PMNs and macrophages; parasitic infections -->eosinophilia from (IL5, GM-CSF)
Somnolence, malaise cause in inflammation
IL-1, TNF
Muscle breakdown, wasting, cachexia, anorexia in inflammation
IL1--> proteolysis thru prostaglandin E2 generation; IL1 decreases appetite by unknown mechanism. IL1 and TNF inhibit enzymes for trigylceride synthesisi
Shock cause in inflammation
Massive release of TNF, induces vasodilation and myocardial depression
Dissemincated intravascular coagulation causes in inflammation
TNF activates endothelial cells to convert them from a surface which inhibits coagulation to one that promotes clotting; small clots form--consuming clotting factors whle blocking tissue perfusion
immunodeficiencies that cause susceptibilty to bacterial infection
1) few phagocytes (neutropenia) 2) Leukocyte adhesion deficiency 3) antibody deficiency 4) complement C3 deficiency 5) Slow PMN's and macrophages--alcoholic liver disease 6) asplenia
cause of neutropenia
2ndary to chemotherapy
causes of antibody deficiency
x-linked agammaglobulinemia rare congenital cause of antibody deficiency 2) acquired antibody deficiency in patients with two B cell malignancies, multiple myeloma and chronic lymphocytic leukemia
Complement C3 deficiency causes
congenital C3 deficiency (rare); liver disease (C3 production in liver)
Slow PMNs and macrophage cause
alcoholic liver disease
Asplenia relevence to pneumococcal infection
30% pts w/ pneumococcal pneumonia get bugs in blood, splenic macrophages filter them. Asplenia --> may die quickly from overwhelming infection
Causes of susceptibility to TB
1) Not enough CD4 T cells (AIDS, immunosuppressive therapy) 2) geriatric CD$ T cells ; 3) too few macrophages from chemotherapy 4) macrophages not activated (corticosteroid therapy paralyxzes macrophages)
Outcomes from inflammatory response, examples
Resolution (pneumococcal pneumonia--macrophages clean debris); 2) scarring, damage (damage from superoxides and enzymes, IL1 and TNF stimulate collagen production--in cystic fibrosis persistant pulmonary inflamation makes destruction of airways) 3) cancer. chronic unresolved infections (osteomyelitis), or infections w/ parasites (Schistosoma Japonicum) may lead to cancer-->superoxides and free radicals damage DNA