13/11 weekend Flashcards
What is Inflammation?
Inflammation is a response of vascularized tissues that delivers leukocytes and molecules of host defense from the circulation to the sites of infection and cell damage in order to eliminate the offending agents.
Or simply: The response of living tissues to injury
Robbins & Cotran Pathologic Basis of Disease, Tenth Edition
Basic sequence of events in an inflammatory reaction?
Histamine = example of vasoactive amine
Causes of inflammation?
Foreign bodies
Tissue necrosis
Infection
Immune reactions (Hypersensitivity)
Hypersensitivity= reactions in which the normally protective immune system, is inappropriately activated and damages the individual’s own tissues. Hence inflammation is inappropriately activated and is a major cause of tissue injury in these diseases.
Hypersensitivity?
Are essentially injurious immune reactions to the individual, elicited by exogenous antigens or endogenous self-antigens.
Involves two stages: sensitization and effector stage.
Type 1 Hypersensitivity?
Immediate, or type I, hypersensitivity is a rapid immunologic reaction occurring in a previously sensitized individual that is triggered by the binding of an antigen to IgE antibody on the surface of mast cells.
IMMEDIATE
E.g. Allergies, anaphylaxis
Type 2 hypersensitivity?
IgG/IgM antibodies that react with antigens present on cell surfaces or in the extracellular matrix cause disease by destroying these cells, triggering inflammation, or interfering with normal functions
e.g.autoimmune diseases; myasthenia gravis, Hemolytic disease of newborn
IMMEDIATE
Type 3 hypersensitivity?
Antigen-antibody (IgG/IgM) complexes [immune complexes] produce tissue damage mainly by eliciting inflammation at the sites of deposition.
IMMEDIATE
Antigens are typically free floating, once immune complex formed they deposit.
E.g. Serum sickness, Arthus reaction
Type 4 hypersensitivity?
Delayed or immediate response?
Cell-mediated hypersensitivity is caused mainly by inflammation resulting from cytokines produced by CD4+ T cells. Other mechanism is CD8+ T Cell–Mediated Cytotoxicity.
DELAYED (after a day)
e.g. TUberculosis skin test, Contact dermatitis
Autoimmune disease?
Immune reactions against self antigens.
(I guess its a type of hypersensitivity disease)
T helper cell another name?
CD4+ T cell = T helper cell
T killer cell another name?
CD8+ T cell = T killer cell
Stages of acute inflammation?
(1) dilation of small vessels leading to an increase in blood flow; (2) increased permeability of the microvasculature enabling plasma proteins and leukocytes to leave the circulation; and (3) emigration of leukocytes from the microcirculation, their accumulation in the focus of injury, and their activation to eliminate the offending agent
VASCULAR PHASE- changes in blood flow. Accumulation of exudate
CELLULAR PHASE- Delivery of neutrophils
In acute inflammation what induces vasodilation
Vasoactive amines= histamine
In acute inflammation what induces increased vessel permeability?
It is elicited by histamine, bradykinin, leukotrienes, and other chemical mediators.
Leads to increased interendothelial spaces.
WIth regards to acute inflammation is the oedema fluid exudate or transudate?
Exudate, as increased vascular permeability leads to protein rich fluid.