-
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
- leukocytes
- vascular changes
- and chemical mediator like cytokine
-
what immune molecules is involved in ACUTE inflammation
neutrophils
-
what immune molecules is involved in CHRONIC inflammation
monocyte macrophages and lymphocytes
-
How does acute inflammation happen ?
- Stimuli
- vascular changes
- cellular changes
- Phagocytosis
- 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.
It increases.
-
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
- Leukotrienes
-
what is ( are) the principal mediator for chemotaxis, leukocyte recruitment, and activation?
- TNF and IL-1
- Chemokines
- C3a C5a
- Luekotriene B4
-
what is ( are) the principal mediator for fever ?
-
what is ( are) the principal mediator for pain ?
- Substance p
- Protaglandins
- Bradykinins
-
what is ( are) the principal mediator for tissue damage ?
- ROS
- 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?
neutrophils? Monocytes
-
wht kind of cells predominate with viral infections?
Lymphocytes
-
where do classically activated macrophages aka come from? how do they kill ?
- M1
- 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
- M2
- 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 ...
exudate
-
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+ )
|
|
