Injury, Inflammation, and Repair Flashcards
what is inflammation?
- a wound that swells up, turns red and hurts
~ generally speaking ~ its the bodies immune system response to a stimulus
- ex. wound or splinter
- happens when immune system is fighting against something that may be harmful
uncontrolled inflammation
is potentially damaging
- regulation is critical
ex. irritable bowl disease -> critical of digestive tract
does inflammation facilitate tissue repair?
yes
controlled inflammation
critical in protecting the body from harmful invaders
inflammation provoked response to tissue injury
- chemical agents
- cold
- heat
- trauma
- invasion of microbes
- cancerous cells
inflammation: reparative
includes and supports tissue repair
when is inflammation potentially harmful?
when it leads to chronic conditions such as arthritis and chronic obstructive bowel disease
inflammation: protective
destroys and contains the injurious agent
inflammation desirable response
controlled and proportional
inflammation undesirable response
chronic and harmful
what distinguishes acute and chronic inflammation?
- onset
- duration
- type of infiltrating inflammatory cells
acute inflammation causative agent
- pathogens
- irritants
- damage
acute inflammation major cells
- neutrophils
- basophils
- eosinophils
- monocytes
- macrophages
acute inflammation onset
immediate
acute inflammation duration
few days
acute inflammation outcomes
- resolution
- abscess formation
- chronic inflammation (if longer than 2 weeks)
chronic inflammation causative agent
- persistent acute inflammation due to non-degradable pathogens
- persistent foreign bodies or autoimmune reactions
chronic inflammation major cells
- monocytes
- macrophages
- lymphocytes
- plasma cells
- fibroblasts
chronic inflammation onset
delayed
chronic inflammation duration
up to many months or years
chronic inflammation outcomes
- tissue destruction
- fibrosis
cardinal signs of acute inflammation
- heat
- swelling
- redness
- pain
- loss of function
inflammation physiology
1) foreign agent enters the body
2) local vasodilation and increased vascular permeability
3) accumulation of WBC in blood vessels
4) WBC exit the blood vessels
5) drawn to an area of foreign agent/injury = chemotaxis
the two components of inflammation physiology
- vascular
- cellular
vascular components of inflammation physiology
- vasoconstriction
- vasodilation
- increased permeability
vasoconstriction
release of vasoconstrictor substances
- few seconds of blanching
- usually happens with blood trauma
vasodilation
smooth muscle relaxes called active hyperemia
- what causes redness
increased permeability
vascular leakage -> edema
- increased seperation of cells
cellular component of inflammation physiology
leukocyte accumulation and infiltration
vasodilation: active hyperemia
- due to arteriolar dilation
- sympathetic stimulation
- affected tissue is redder than normal because of engorgement with oxygen blood
~ accounts for redness, swelling, and warmth
transudate leakage
- low cell/protein
- result of high hydrostatic pressure and low osmotic pressure
- clear fluid
exudate leakage
- cell/protein rich
- result of increased vascular permeability
- cloudy fluid
~ supplies antibodies and complement protein to affected areas to contribute to swelling -> causes pain and decreased mobility
vascular permeability mediators
- histamines
- bradykinins
- leukotrienes
histamines, bradykinins and leukotrienes all cause what response?
and early, brief (30min) immediate response in the from of reversible endothelial cell contraction
cytokine mediators
reversible endothelial cell junction retraction
~ 4-6 hours post injury/infection, lasting 24 hours or more
sever injuries may cause ____ making them ______?
may cause immediate direct endothelial cell damage making them leaky until they are repaired
leukocytes may adhere to and damage the endothelium through?
activation and release of toxic radicals and proteolytic enzymes making the vessel leaky
transcytosis
- brings proteins and molecules across endothelium
- some vesicles may fuse to create temporary channels
vascular permeability mechanisms that cause leakiness
- mediators
- cytokine mediators
- severe injures
- leukocytes that adhere and damage the endothelium
- mediators that increase transcytosis
diapedesis
leukocytes leave the vasculature and enter the interstitium through:
1) margination and rolling
2) adhesion
3) chemotaxis
4) activation
5) transmigration
what are leukocytes free to participate in?
- degranulation
- phagocytosis
- leukocyte/cytokine -> protection and repair (controlled)
- leukocyte/ cytokine -> ; ‘storm’ induced tissue injury (uncontrolled/chronic)
degranulation
cellular process that releases
- neutrophils
- basophils
- eosinophils
- mast cells
- cytotoxic cells
- natural killer cells
~ main purpose is to destroy pathogens (innate immune system)
stages of acute inflammation
1) vasoconstriction (<60)
2) vasodilation
3) increased vascular permeability
4) diapedesis
MOA for vasodilation
1) cellular release of mediators
- histamine
- prostacyclin
- nitric oxide
2) relaxation of blood vessel walls
why does vasodilation occur?
due to increased hydrostatic pressure ( pressure inside the vessel pushing out) that causes a decrease of blood flow rate
MOA for increased vascular permeability
occurs through the release of histamine and leukotrienes (mediators)
why is there an increased vascular permeability
to allow fluid and protein to move to the interstitial tissue
- results in edema or increased fluid in the interstitial tissue
endothelial contraction
- immediate response
- initiated via cell mediators: histamine and leukotrienes
- time: immediate up to 30 min
endothelial cell retraction
- delayed response
- initiated via cell mediators: cytokines
- time: 4-6 hour delayed response (long lasting)
direct endothelial injury
- immediate sustained response
- time: immediate
(physical mechanism) ex. major incision on leg
activation of macrophages by pathogens causes a release of?
cytokines
the release of cytokines from the activation of macrophages causes?
endothelial cells of local blood vessels to secrete adhesion moleculrs
what are leukocytes attracted to during acute stages of inflammation?
the presence of cytokines and adhesion molecules
what happens during rolling and rolling adhesion
- circulating leukocytes bind to adhesion molecules with moderate affinity causing leukocytes to slow done and begin rolling along the inner surface of blood vessel walls
firm and tight adhesion
release of chemokine by macrophages to transition from moderate affinity to high affinity (bonding to endothelial cells)
transmigration
cytoskeleton reorganization in conjunction with leukocyte pseudopod extensions -> leukocytes pass through gaps in endothelial cells
how do blood vessels escape during acute stages of inflammation?
diapedesis
how doe leukocytes migrate during acute inflammation?
chemotactic gradient to injury or infection
acute infalmmation
- rapid onset
- lasts minute to days
- exudation of fluid and protein from vessels
- emigration of WBCs
purpose of acute inflammation
quick attack on foreign agents and initiate the repair process
cardinal sign of acute inflammation
- rubor
- heat
- edema
- pain
- tumor
- loss of function
what causes acute inflammation?
- infection
- trauma
- physical and chemical agents
- necrosis
- foreign bodies
- immune reaction
