acute inflammation Flashcards
what is acute inflammation?
- “The immediate and early response to injury, designed to deliver leukocytes to the site of injury.”
- Inflammation is not a disease, but is often a manifestation of disease
- Inflammation can be beneficial but can also cause harm
what are the 2 types if inflammation?
acute = initial & often transient series of tissue reactions to injury
chronic = subsequent & often prolonged tissue response following initial response
nomenclature note:
a) what is it when words end with “itis”?
b) what is it when words end with “osis”?
a) inflammation of
b) disease or condition
what are causes of acute inflammation?
- Microbial infections →e.g. bacteria & viruses
- Hypersensitivity reactions →Excessive immune response →tissue damage
- Physical agents →Trauma, radiation or heat injury
- Chemicals →Corrosives, acids or bacterial toxins
- Tissue necrosis →Secondary to ischaemia (dead tissue releases peptides which stimulate)
what parts of microbial infection stimulate inflammation?
- bacterial exotoxins & endotoxins
- viral intra-cellular multiplication (leads to cell death & debris stimulate inflammation)
- organisms causing hypersensitivity
what are cardinal signs of acute inflammation?
- redness (rubor) = due to dilation of vessels
- heat (calor) = due to increase blood flow
- swelling (tumor) = due to accumulation of fluids (also increase of inflammatory cells migrating to area)
- pain (dolar) = due to physical distortion of tissue & due to release of some chemical mediators
- loss of function
what are stages of inflammation?
- release of chemical mediators
- vasodilation
- increased vascular permeability
- fluid accumulation
- cellular recruitment
- phagocytosis
what are 2 major components of acute inflammation?
vascular changes (permeability & vasodilation) & cellular events (formation of cellular extrude)
what are the vascular changes in acute inflammation?
increased vascular permeability & changes in vascular calibre
vasodilation - lasts from 15 mins to several hours
increased vascular permability = increased net flow of fluid out of vessels - called exudation
what do neutrophil polymorphs do in acute inflammation?
they accumulate - they usually flow in middle of vessels:
margination - they marginate towards endothelial cells = loss of intravascular fluid & slowing
adhesion - also called pavementing - they stick to vascular endothelium
emigration - pass between endothelial cells & through basal lamina & into adventitia
what is process of adhesion of neutrophils?
ligands on neutrophil surface engage with P-selectin on endothelial cells and PAF (platelet activating factor) dock with corresponding receptor on neutrophil & promote expression of other molecules which overall results in firm adhesion
what are P-selectin & PAF?
they’re factors on endothelial cells that help adhesion of neutrophils
- the release of histamine & thromin (in original inflammatory stimulus) causes up regulation of P-selectin & PAF
(PAF = platelet activating factor)
what are chemical mediators released by cell in acute inflammation?
- histamine
- lysosomal compounds
- leukotrines
- prostaglandins
- seratonin
how does seritonin affect blood vessels?
vasoconstrictor = released by platelets
what are prostaglandins?
- derived from arachadonic acid
- Some cause increased vascular permeability
- Some cause platelet aggregation
- Released by lots of cell types
what are leukotrienes?
vasoactive properties - often made in neutrophils from arachidonic acid(a fatty acid in cell membrane)
(it’s a chemical mediator)
-some types attract immune cells to site of infection
what are lysosomal compounds?
- Lots of different functions, such as vascular permeability
- Some can stimulate histamine release from mast cells
- Released by neutrophils
= lysosomes are membrane-bound organelles containing a variety of enzymes that have different functions
what is histamine?
- released by mast cells - Released mainly by mast cells
- cause vascular dilation & permeability
what are chemokines?
family of chemicals which attract more white blood cells to site of inflammation (they’re cytokines and help direct for chemotaxis)
what are the 4 enzyme cascades in plasma? (part of cellular part of acute inflammation)
- coagulation system (converts fibrinogen -> fibrin)
- kinins (activated by coagulation factor - bradykinin = important peptide in mediating vasodilation)
- fibrinolytic system
- complement system
what are the benefits of inflammation?
- dilution of toxins (mitigate effect of toxins on tissues)
- entry of antibodies (stimulates immune response, facilitates immune cells)
- transport of drugs
- fibrin formation
- delivery of nutrient & oxygen
what are the harmful effects of inflammation?
- digestion of normal tissue (innapropriate overactive immune response)
- swelling (necessary by-product, if in neck you can get airway obstruction, anywhere in body it can end up with dangerous comprimise)
- innappropriate inflammatory response
why are neutrophils good?
they can move = by contracting cytoplasmic microtubules = calcium ion dependant mechanism, chemotaxis in response to inflammatory chemicals
they can stick to opsonised microorganisms
they can phagocytose
they can kill them, once gobbled up - with variety of intra-cellular methods to produce microbicidal agents
