Intro to acute inflam Flashcards
Inflammation
A protective response intended to eliminate the initial cause of cell injury as well as necrotic cells and tissues resulting from the original insult
Inflammation is innate or adaptive
Innate
Inflammatory reaction goal
Bring cells and molecules of host defence from the blood stream to the site of infection or damage
Components of inflam
Cells and molecules that can leave the circulation (eg Neutro, lymphocytes, monocytes, platelets, plasma pros, etc)
Tissue resident cells (eg macrophages, mast cells, fibroblasts, ECM pros)
Endo and smooth muscle cells of vessel wall
Cause of normal tissue injury
Inflammatory reaction and subsequent repair processes
Pathology becomes dominant in inflam reaction if the reaction is:
Very strong (severe infection) Prolonged (persistent infection) Innapropriate (autoimmune, allergy)
Cause of acute inflam
Injury of biological,
physical
Chemical
Or immunological cause
Result of inflamm reaction
Damaged tissue flooded by excess fluid (exudate) (similar to plasma) escaping through altered vessel walls which dilutes and nutralises irritant chemicals. Tissue invaded by phagocytes to remove cell debris and infectious agent and immune complexes
5 cardinal signs
Heat Red Pain Swelling Loss of fx
Swelling cause
Exudate accum
Inflam cell migration from vessel to EC space
Loss of fx cause
Pain
Cell and tissue destruction
Effect of vascular disturbance on normal fx
Pain cause
Incr pressure
Release of chemicals from damaged cells - stim nerve endings
Redness cause
Same as heat plus maybe incr metabolic rate of tissue cells
Heat cause
Vasodilation
Incr blood flow
Intra and extra vascular accum of blood
Vascular response
Active hyperaemia with changes in vessel calibre
Vessel wall changes and endo swelling
Thrombosis, pavementing, sludging
Inflammatory oedema or exudation of fluid response
Incr hydrostatic pressure so incr filtration of fluid and electrolytes
Plasma pros escape through gaps in endo wall of cap and venules
Where and how inflam mediators found
Widely distributed in sequestered or inact form through body, act locally at injury site.
Mediator fxs and communication
Many fxs overlap and are linked via interactions to give positive feedback/ synergist effects
Inactivation of mediators (general)
Rapid inact locally to five control to inflam process
What is histamine and where found
Rapid acting vasoactive amine
Granules of mast cells and basophils
(Platelet equivalent = serotonin)
Histamine effects
Dilate small blood vessels
Immediate incr vascular permeability
Smooth m contraction
2 phases of incr vascular permeability
Immediate (histamine and serotonin)
Delayed (PGs, leukotrienes and kinins)
What is a kinin and how are they produced
Biologically active polypeptide produced by kallikrein enzyme actions on kininogen
Example of kinin and fx
Bradykinin
In addition to vascular effects it produces pain via an axon reflex
C2-kinin formation
By plasmin enzyme or classical complement activation
Kallikrein enzyme formation (kinins)
Exist in plasma as inact prekks
Act during blood clotting
What are PGs and LTs
Fatty acids from phospholipids in cell mem synthed by activated cells, not stored for release
PL-Archidonic acid by PLase A2
A acid - PG or thromboxane by cyclo-oxygenase
or - LT by lipoxygenasr
PG/LT effects
Delayed vasodilation Delayed incr vascular permeability Smooth m contraction (LTs) Pain Neutrophil chemotaxis (LTs)
Platelet activating factor effect and synth
Synthed by act mast cells from mem PLs
Cause platelet degran
Complement act and component effect
Act inter-related with kinin and coag cascade (plasmin)
C3 and 5a cause histamine release
Important in aggregate anaphylaxis and other immune lesions
Types of Mediators released by neutrophils and their roles
Azurophilic granules (cont proteolytic and degradative enz key to tissue liquefaction and inflam amplification) Specific granules (cont pros with antibact property that cause mast cell degran
Types of mediators released by platelets
Lysosomal granules (cont proteolytic enz and cationic pros) Dense bodies (cont serotonin)
Peptides synth and effect
Exudate pro digested by proteolytic enzyme
Can cause incr vascular permeability
Microbial product examples
Kinase Hyaluronidase Proteases Leucocidins Haemolysin Vasoactive toxins Can have influence on inflam resp dev
What are and where are they found Cytokines
Protein mediators produced by local cells induced during and insult
Cytokine effect
Para and autocrine to prod more cytokines
Affect all inflam stages
Induce incr vasodilation and permeability and induce proteolytic enz production
What are chemokines and their fx
Proteins
Act as leukocyte attractants
