inflammation Flashcards
what is inflammation?
Inflammation is the reaction of a tissue and its microcirculation to a noxious stimulus, e.g. microbes, injury or stress.
characteristics of inflammation?
- production of inflammation mediators.
2. moving out of leukocytes to the extravascular tissues.
five signs of inflammation.
- Rubor (redness)
- Calor (heat)
- Tumor (swelling)
- Dolor (pain)
- Functio laesa (loss of function).
components of microvasculature.
- arterial capillaries.
- venous capillaries
- arteriole
- venule
purpose of inflammation.
- Elimination of pathogenic insults
2. Removal of injured tissue component.
CAUSES AND OUTCOMES OF INFLAMMATION.
trigger physiological pathological
purpose consequences
- infection -to eliminate - Autoimmunity
- tissue injury -repairing -tumor growth
- tissue stress -adaptation -change in
homestatic
set point.
stages of inflammation.
- Initiation
- Amplification
- Termination
classes of inflammation mediators according to their origin.
- Plasma derived mediators: derived mediators are derived majorly from complement, kinin or clotting system.
- Cell-derived mediators: are derived from platelets, neutrophils, monocytes, macrophages and mast cells.
Plasma derived mediators.
- C3b and C3bi are opsonins; C5a- a potent chemotactic factor for neutrophils, monocytes..
- Bradykinin- increases vascular permeability, contraction of smooth muscle & dilation of blood vessels.
- Factor Xa and fibrinopeptide- increase vascular permeability and leucocyte exudation.
- Thrombin- leucocyte adhesion and fibroblast proliferation.
Cell-derived mediators.
- Histamine: mast cells, basophils, and platelets; acts via H2 receptor.
- Serotonin: Platelets and enterochromaffin cells. Also in mast cells of rodents.
- Platelet-activating factor (PAF): mast cells, basophils, neutrophils, monocytes, macrophages, endothelial cells, platelets, etc.
- Arachidonic acid metabolites
what are the inducers and functions of histamine mediator?
inducers: 1. Physical injury: cold, heat, and trauma.
2. Cytokines: IL-1, IL-8.
3. substance p.
function: 1. Dilation of the arterioles, increased vascular permeability of the venules.
inducers and function of serotonin mediator.
inducer: 1. The release of serotonin is stimulated when platelets aggregate after contact with collagen.
function: 1. serotonin causes dilation of arterioles and increased vascular permeability of the venules.
Action of Platelet activating factor (PAF).
Actions: Increased vascular permeability, leucocyte adhesion, platelet activation, leucocyte chemotaxis, stimulation and release of other mediators.
TYPES OF INFLAMMATION.
- Acute inflammation: is of relatively short duration.
2. Chronic inflammation: is of long duration.
characteristics of acute inflammations.
- Exudation of fluid and plasma protein
2. Emigration of leucocytes, predominantly neutrophils.
characteristics of chronic inflammation.
Presence of lymphocytes, plasma cells and macrophages.
Vascular proliferation, fibrosis and necrosis.
EVENTS IN ACUTE INFLAMMATION.
- Changes in the vascular calibre, leading to an increase in blood flow.
- Structural changes in the microvasculature, allowing extravasation of plasma protein and leucocytes.
- Emigration of leucocytes from the microcirculation and their accumulation in the focus of injury.
The first two constitute the vascular event in inflammation, while the last is part of the cellular event in inflammation.
VASCULAR CHANGES IN INFLAMMATION.
- Transient vasoconstriction of arterioles, occurring at the site of injury, mediated by both neurogenic and chemical mediator systems. It usually resolves within seconds or minutes.
- Vasodilation of the precapillary arterioles, which increase blood flow to the tissue, a condition known as hyperaemia.
- Increase in vascular permeability, resulting in leakage of fluid from intravascular compartment into extravascular space, which is later cleared within minutes to hours through lymphatics.
CELLULAR EVENTS IN INFLAMMATION.
- Cell recruitment
2. Phagocytosis
Cell recruitment
Cell recruitment involves the accumulation of leucocytes, especially polymorphs at the site of injury. The steps involved are:
- Margination of cells along the vascular wall.
- Adherence of the leucocytes to the endothelium.
- Transmigration across the endothelium.
- Chemotaxis- a unidirectional movement towards soluble chemotactic agents.
Phagocytosis
Phagocytosis simply means the ingestion and elimination of foreign material or debri of injured cells. The effector cells are known as phagocytes (polymorphs, monocytes and tissue macrophages).
It involves 3 distinct but inter-related steps:
- Recognition and attachment
- Internalization (engulfment)
- Digestion/killing/degranulation
OUTCOMES OF ACUTE INFLAMMATION.
- Complete resolution (mild injury)
- Absess formation (pyogenic organism infection, staphylococcus aureus)
- Healing by connective tissue replacement –fibrosis (large/severe injury)
- Progression to chronic inflammation.
Features OF CHRONIC INFLAMMATION.
- Infiltration with mononuclear cells, e.g. macrophages, lymphocytes and plasm cells.
- Tissue destruction
- Proliferation of small blood vessels (angiogenesis)
- Fibrosis.
DEFECTS IN LEUCOCYTE FUNCTION.
- Leucocyte adhesion deficiency type 1
–This is due to deficiency of β-integrin - Leucocyte adhesion deficiency type 2
–In this type, sialyl lewis s is absent - Defect in phagocytosis: Chediac Higashi syndrome
–The defect is caused by a mutation in the lysosomal trafficking regulator
protein that leads to decreased phagocytosis and predisposition to recurrent bacterial infection. - Defect in microbicidal activity –inherited defect in the gene encoding several components of NADPH oxidase.
