pathology of inflammation Flashcards
Symptoms of inflammation: tumor
inflammatory tissue swelling
Symptoms of inflammation: rubor
inflammatory hyperemic erythema
Symptoms of inflammation: calor
inflammatory heat in the tissue
Symptoms of inflammation: dolor
pain in the inflamed area
Symptoms of inflammation: Functio laesa
functional impairment of the inflamed organ or tissue
Local inflammation
is limited to a circumscribed area
Generalized infection
the pathogen spreads diffusely throughout the entire body
Metastatic inflammation
the transmission of the inflammatory pathogens into other tissues, where the pathogen can trigger a septico-pyemia (septic metastases)
Cells involved in the process of inflammation
- T helper CD4+ cells for humoral immune response
- T cytotoxic CD8+ cells for cellular immune response
- B cells which transform into plasma cells, that produce antibodies
What types of cells have granules containing heparin and histamine?
Mast cells and basophils.
What additional effect do the substances in the granules of mast cells and basophils have aside from increasing permeability?
they cause platelet aggregation
Neutrophils are phagocytic cells, which generate:
lysozyme - unspecific germicide
NO synthase - produces nitrous oxide (a bactericide)
the NADPH oxidase system - uses myeloperoxidase to produce oxygen metabolites, a bactericides
Endothelial cells: pro inflammatory cells that generate:
selectins – cause adhesion of lymphocytes and granulocytes
factor VIII activator – activates the complement and kinin cascade → increases permeability
Thrombocytes: pro-inflammatory cells that generate
inflammation mediators and PDGF
Inflammation Mediators
definition
Chemical substances that trigger certain processes in an inflammatory reaction
inflammation mediators Effects:
vasodilatation, increased vascular permeability and chemotaxis.
Cell-Derived Mediators
- Histamine (produced by mast cells)
- Serotonin (produced by entero-chromaffin cells)
- Neutrophilic proteases (produced by PMN)
Interleukins (IL-1, TNF-α) - Chemokines (produced by macrophages and lymphocytes): link up with CXC-R & CC-R mediated by G-proteins
- Arachidonic acid derivatives (from cell membranes):
Lipo-oxygenase breaks it down into leukotrienes
Cyclo-oxygenase breaks it down into prostaglandins - Platelet activating factor produced by thrombocytes
Plasma-Derived Mediators
- Kinin system (activated by necrosis)
- Complement system (from serum)
- C-reactive protein (from hepatocytes)
Exudative Inflammatory Reaction definition
Response pattern of acute inflammation, characterized by exudation of blood components and emigration of blood cells.
Exudative Inflammatory Reaction - Biologic purpose:
- Increased perfusion due to hyperemia → rapid removal of the noxious agent from the site.
Exudation of blood serum → rapid dilution of the noxious agent. - Elimination of pathogens by phagocytosis → rapid destruction of the noxious agent.
- Rapid containment of the noxious agent.
Exudative Inflammatory Reaction - Pathogenetic elements:
- Changes in microcirculation
- Increases in permeability
- Leukocyte transmigration
Changes in Microcirculation - First phase
A transient arteriolar vasoconstriction lasting a few seconds to a few minutes.
Changes in Microcirculation - second phase
Inflammation mediators lead to vasodilatation of the arterioles, capillaries, and post-capillary venules.
This causes exudation of blood serum that leads to inflammatory tissue swelling with stimulation of the nociceptive nerves (pain nerves)
Result: erythema, swelling, and pain in the inflamed area
Changes in Microcirculation - third phase
It is brought about by vasodilatation of the capillaries and arterioles and is accompanied by vasoconstriction of the venules.
The circulation slows, filtration pressure elevates, and vascular permeability increases in the inflamed area
The area damaged by the noxious agent is sealed off, paving the way for the “strike force” of leukocytes
