Inflammation and Hypersensitivity Flashcards
The process by which the body attempts to destroy or contain a noxious agent and repair damage
Inflammation
What are the four phases of immune-mediated inflammatory responses?
- ) Stimulation
- ) Release of inflammatory mediators and chemotactic agents
- ) Invasion of tissue
- ) Removal of cell debris and secretion of growth factors
Which can act locally or systemically, and the response of local or distant target organs to them
Inflammatory mediators
Attract immune cells to the area and modify endothelium to allow their adhesion and extravasion
Chemotactic agents
The invasion of tissue is by activated immune cells which defend against infection and can also
Damage tissue
Stimulate cell migration and proliferation, with tissue repair and formation of new blood vessels
Growth factors
In acute local inflammation, inflammatory mediators produce which 4 things?
- ) Heat and redness
- ) Edema
- ) Pain
- ) Loss of function
The heat and redness is from
Dilation of small blood vessels
From endothelial retraction and increase in permeability of post-capillary venules
-causes fluid to leak from blood to tissue
Edema
Cytokines with systemic effects are chiefly produced by
Monocytes
Shape the systemic response of the body to infection, and produce many signs and symptoms by which illness is recognized
TNF-a, IL-1, and IL-6
Overproduction of inflammatory cytokines can produce the
Systemic Inflammatory Response Syndrome [SIRS]
Leads to loss of blood volume, and vasodilation, with decreased blood pressure and tissue perfusion, can lead to organ dysfunction, shock, and death
Increased Vascular Permeability
Severe shock produced by systemic infection is called
Septic shock
Bacterial components such as LPS activate the
Blood clotting cascade
Inflammatory cytokines act on endothelium to promote
Blood clotting
Multiplication of bacteria in the bloodstream [septicemia] can lead to
Disseminated Intravascular Coagulation [DIC]
Exhaustion of clotting factors by DIC can lead to simultaneous
Multiple hemorrhages
In chronic inflammation, persistent reactions to a stimulus that cannot be removed results in formation of a
Granuloma
A lesion with a necrotic core surrounded by macrophages and lymphocytes
Granuloma
On a longer time scale the granuloma becomes surrounded by fibrous tissue, to wall off the lesion. Eventually the wall of the lesion may
Calcify
Immune responses which damage the body
Hypersensitivity reactions
The immune system may over-react to an innocuous antigen [allergy]. The antigen is the
Allergen
A genetically-determined state of abnormal responsiveness is called
Atopy
An atopic person is not allergic until exposure to an allergen generates an
-may require months or years of exposure
Immune response
Classified by the mechanism that causes damage
Hypersensitivity reactions
Immediate hypersensitivity because the early phase happens so rapidly
Type I
Delayed or tuberculin-type hypersensitivity, because a classic stimulus is tuberculin, an extract of cultures of the bacterium which causes TB
Type IV
In responses of types I-III The antigen-specific component is
Immunoglobin
In responses of types I-III The antigen-specific component is immunoglobulin, and hypersensitivity can be transferred to an unsensitized individual with
Serum
Type IV antigen sensitivity is conferred by
-antibodies play no significant role
T cells
There are several subtypes of Type IV reactions: (1) granulomatous reactions, where the major cells are
TH and monocyte macrophages
There are several subtypes of Type IV reactions: (2) cytotoxic reactions, in which the important cells are
TH and CTL
Hypersensitivity reactions are used diagnostically. Small, localized, skin reactions are induced as tests of
Immune system competence, prior exposure, and allergic hypersensitivity
Anaphylactic hypersensitivity based on IgE and mast cells
Type I reactions