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9 Cards in this Set

  • Front
  • Back
What is acute inflammation?
Response of *vascularised* tissue to injury.
What does acute inflammation result in?
Build-up of fluid, plasma proteins, and leukocytes
What are the 5 cardinal signs of acute inflammation?
Rubor (redness)
Calor (increased heat)
Tumour (swelling)
Dolor (pain)
Loss of function
What are 4 major classes of inflammatory mediators?
Give 2 examples of each
Vasoactive amines
(histamine, serotonin)

Arachidonic Acid Derivatives
(Prostaglandins, leukotrienes)

Plasma Protease Systems
(complement, kinins)

Cytokines
(Tumour necrosis factor, Interleukin 1)
List 6 inflammatory stimuli, and give examples
Infection
(bacterial, viral, parasitic)
or microbial toxins

Trauma
(blunt or penetrating)

Physical
(e.g. Temperature, irradiation)
or chemical agents

Tissue necrosis
(from any cause)

Foreign bodies
(splinters, dirt, sutures [surgical wire])

Immune reactions
(hypersensitivity)
List 2 mechanisms that lead from stimuli up to vasodilation of arterioles (vascular smooth muscles relax)
Mast cells degranulate -> release Histamine, Prostaglandins, and Serotonin

Endothelial cells -> release Nitric Oxide

-> Vasodilation
How do rubor and calor (heat) occur?
Arteriole vasodilation
-> Increased vessel diameter and flow
-> R & C
How does pain occur in inflammation?

3 things.
Chemical factors activate noiceptive fibres

Pressure/swelling

Pain mediators: Prostaglandins and kinins
How does tumour occur in inflammation?

2 paths
Increased vessel diameter and flow (arterioles)
-> Increased hydrostatic pressure = transudate (low protein)

Chemical mediators
(Vascoactive amins, C3a, Bradykinin, LTC4, LTD4, LTE4, etc.)
-> Increased vessel permeability (venules)
-> Leakage of plasma proteins, decreased *plasma oncotic pressure* (keeps fluid in circulatory system) = exudate (high protein)

-> fluid into interstitial space
-> tumour