Inflammation I Flashcards
what is inflammation
what are the types
a biological reaction to NOXIOUS STIMULUS such as microbes, burns and trauma
- fundamentally PROTECTIVE, but can be harmful if it leads to tissue injury
Types: acute, chronic
what are the 4 cardinal signs of inflammation
what is the 5th one
- Rubor (Redness)
- Tumor (Swelling)
- Calor (Heat)
- Dolor (Pain)
5th sign: Functio Laesa (Loss of function)
describe acute inflammation
rapid host response to deliver leukocytes and plasma proteins eg such as ANTIBODIES to the sites of infection or tissue injury
what does acute inflammation protect the body from
- infection
- trauma (blunt/penetrating)
- burns/frostbite (thermal/chemical)
- allergic reaction
- tissue necrosis
how quickly does acute inflammation last
what does it consist of
hours to days
consists of: vascular and cellular reaction
what are the 3 major components of acute inflammation
1) VASCULAR DILATION: inc blood flow
2) STRUCTURE CHANGES: in microvasculature to allow plasma proteins and leukocytes to leave circulation
3) EMIGRATION: of leukocytes from microvasculature, their accumulation in the injury site and their activation to eliminate the offending agent
what is the vascular reaction as a result of inflammation
- vessel dilation and INC blood flow
- leakage of plasma fluid and protein
- leukocyte EMIGRATION and accumulation in the site of injury
what is the purpose of VESSEL DILATION
what does VESSEL DILATION result in
what is it induced by
- inc blood flow
- result in HEAT and REDNESS (hyperaemia)
- induced by: HISTAMINE, BRADYKININ, NO
what is the source and function of histamine as a mediator of vascular reactions
source:
mast cells, basophils, platelets
function: arteriole dilatation, inc of venous permeability
what is the source and function of bradykinin as a mediator of vascular reactions
source:
Kinin system
function: vasodilatation, inc vascular permeability, PAIN
what is the source and function of nitric oxide as a mediator of vascular reactions
source:
endothelial cells
function:
vasodilation
increased vascular permeability is a hallmark of what
acute inflammation
what is the purpose of inc vascular permeability
- allows plasma fluid and protein to escape from circulation into extracellular tissue (causes oedema)
what are mechanisms of increasing vascular permeability
- endothelial cell contraction to INC INTRACELLULAR SPACES
- endothelial cell injury and detachment
- INC transport of fluid and protein through the endothelial cells
what is extravasation
movement of leukocytes from VESSEL LUMEN to interstitial lumen to INTERSTITIAL TISSUE
what are the endothelial adhesion molecules used by leukocytes
P-selectin E-selectin CD34 ICAM-1 VCAM-1
describe chemotaxis of leukocytes
a process in which leukocytes EMIGRATE to the site of injury, driven by substances called CHEMOATTRACTANTS
what are the initially phagocytic cells
what do they do
neutrophils, followed by monocytes
- produce inflammatroy mediators that maintain the inflammatory response
what is chemotaxis
process by which leukocytes are attracted by CHEMOTACTIC AGENTS to the site of injury once outside the blood vessel
what are the 2 types of chemoattractants
give examples of each
endogenous and exogenous exogenous: - bacterial products endogenous: - complement components - cytokines - products of lipoxygenase pathway (leukotriene B4)
what do leukocytes use for recognition
LEUKOCYTE RECEPTORS:
- Toll-like receptors (TLRs) for MICROBIAL PRODUCTS
- G-protein coupled receptors for SHORT BACTERIAL PEPTIDES CONT N-FORMYLMETHIONYL RESIDUES
- Opsonin receptors for antibodies, complements, lectins
- Cytokine receptors
what is phagocytosis
removal of offending agents
what are the stages of phagocytosis
1) recognition and attachment
2) engulfment ( engulfed particle fuses with lysosome to form PHAGOLYSOSOME, degranulation)
3) killing (ROS, other lysosomal enzymes)
what are the acute inflammatory cytokines
TNF-alpha
IL-1
IL-6
chemokines
what are the sources of the acute inflammatory cytokines
TNF-alpha: macrophages, mast cells, T-lymphocytes
IL-1: macrophages, endotheilial cells, epithelial cells
IL-6: macrophages,other cells
chemokines: macrophages, endothelial cells, T lymphocytes, mast cells, other cells
what is fibrinous inflammation
characterised by FIBRINOUS EXUDATE which can lead to SCAR FORMATION and LIMITATION OF FUNCTION
what is purulent inflammation
pus filled fluid consisting of NEUTROPHILS and DEAD CELLS
- typically caused by Staph. infections
what is serous inflammation
copious EFFUSION of non-viscous SEROUS FLUID
eg skin blister
what is ulcerative inflammation
NECROTIC loss of tissue from the surface, exposing LOWER layers leading to ulcer formation
what are the possible outcomes of acute inflammation
- complete resolution (injury is limited/short lived or little tissue damage)
- healing by CONNECTIVE TISSUE REPLACEMENT(fibrosis) (if substantial tissue damage, fibroblats grow into area of damage)
- progression to CHRONIC inflammation