Cardinal sign of Inflammation
- Rubor ( redness)
- Calor heat
- Dolor pain
- Tumor Sweeling
- Functional Loss
what is the purpose and molecules activities of inflammation
- localize and eliminate cell injury and bring back to normality
- vascular changes
- and chemical mediator like cytokine
what immune molecules is involved in ACUTE inflammation
what immune molecules is involved in CHRONIC inflammation
monocyte macrophages and lymphocytes
How does acute inflammation happen ?
- vascular changes
- cellular changes
- termination of acute response
- consequence of acute response
Inflammatory response steps?
- Recognize injurious agaent
- Recruit WBC
- Remove Agent
- Regulate response
- Resolution /Repair
Hydrostatic pressure and oncotoic
- pressure that pushes fluid out
- Oncotic keeps it in
what clinical correlate of increased hydrostatic pressure? decrease oncotic pressure?
- Hydro- localized edems
- oncotic pressure- generalized edema
what is transudate? what's in it?
- What happens when there is disequilibrium btwn hydrostatic and oncotic pressure
- low protein, sg, cell material
what happens to hydro static pressure when there is vasodilation.
what are the origins of histamine?
Anaphylatoxins ( C5a, C3a, neuropeptides and cytokines) and mast cells also store and release it
Which is Nitric oxide produced and what does it do?
made from endothelial cells and it does vascular permeability
what is ( are) the principal mediator for vasodilation ?
Histamine and Prostaglandins
what is ( are) the principal mediator for vascular permeability ?
- Histamine serotonin
- C3a C5a
what is ( are) the principal mediator for chemotaxis, leukocyte recruitment, and activation?
- TNF and IL-1
- C3a C5a
- Luekotriene B4
what is ( are) the principal mediator for fever ?
what is ( are) the principal mediator for pain ?
- Substance p
what is ( are) the principal mediator for tissue damage ?
- Lysosomal enzymes for leukocytes
what are the results of acute inflammation?
- complete resolution ( minor injury)
- tissue destruction and extensive injury
- Progression to chronic inflammation
chronic inflammation is distinguihed by the presents of which cells?
- mononuclear cells: lymphocytes
- macrophages,and plasma cells
what wbc come first in actue inlfmammation? then which cells?
wht kind of cells predominate with viral infections?
where do classically activated macrophages aka come from? how do they kill ?
- intergeron gamma INF γ r microbial products
- kill with ROS and NOS in acute
- secrete IL1 2 and 23 in conhronic inflammation
what is the alternatively activated macrohpahage aka
- made form IL 13 and $ or t cell possibly
- imporatnt in tissue repair anf fibrosis \indces IL 10
what does the t-lympocyte TH1 produce
IFN Y via classical
what does the t-lympocyte TH2 produce
IL 4 ,5 and 13 which activate eosinophls and are via the alternative macrphage pathway
what does the t-lympocyte TH17 produce
IL17 and other cotkines that induce neutrophiles and monocytes
what is a granulomatous inflammation
- chronic inflammation to contain offending agent
- Macrophages process ad present antigen to the helper t cells
- this results in IL-2 being made which in turn activate Th1 and then INF gamma
- when iINFy is activated this cause macrophages to change to epithelioid histeocytes and gaint cells.
what is a granulmoa
aggregation of macrophages transformed into epithelial like cell surrounded by a rim of mononuclear wbcs like lymphocyte and plasma cells
Increased permeability lead to ...
what is the difference btw exudate and transudate
transudate is a low protein, cellular content and SG and result only from oncotic and hydrostatic pressure
what is Bradykinin
- kinin is a vasoactive peptide
- prekallekrein is converted to kalikrein by factor XIIs. ad kallerin cleaves HMW kininogen to brady kinin
what does bradykinin function?
pain short lived
What are the step of the cellular repsonse to inflammation
margination , rolling ( selectins), adhesion ( intergrins like ICAM-1), transmigration ( dipedisis; chemokine stimulat adherent neutro[[hils to migrated to injury site; endothelial cell retract. chemotaxis ( polymerization of actin and myosin via chemotatic agaent hat bing gr protein> 2nd messenger> phopholipas A2> increas in cytoplasmic Ca2+ )