inflammation repair Flashcards
what is inflammation
heal wounds and chronic conditions
define inflammation as it pertains to the immune system
the immune systems response to stimulus
when a wound swells up, turns red and hurts
when does inflammation happen?
inflammation happens when the immune system fights against something the may turn out to be harmful
how does the body use inflammation to protect the body?
protective response to cell injury and cell death
facilitates tissue repair
controlled inflammation
uncontrolled inflammation
what are responses from tissue injury that are noticed
chemical agents
cold
heat
trauma
invasion of microbes
cancerous cells
what is the desirable response
when it is controlled and proportional
what is a undesirable response
chronic and harmful
what does reparative mean
induces and supports tissue repair
what is the potential harm when it comes to inflammation?
leads to chronic bowl conditions
arthritis and chronic obstructive bowel disease
how can you distinguish between acute vs chronic
onset duration and type of infiltrating inflammatory cells
what are the major cells involved in acute inflammation
neutrophils basophils eosinophils
mononcytes and macrophages
what are the major cells involved in the chronic inflammation
monocytes
macrophages
lymphocytes
plasma cells
fibroblasts
what is the onset period of acute inflammation
onset (few days)
what is the onset time for chronic inflammation
delayed (up to many months or years)
what are the ourcomes associated with acute inflammatory responses
resolution, absess formation, chronic inflmmation
what are the outcomes for chronic inflammation
tissue destruction
fibrosis
what are the causative agents of acute inflammatory responses
pathogens irritants and damage
what is the causative agent for chronic inflammation
persistent acute inflammation due to non degradable pathogens persisitant foreign bodies or autoimmune reactions
what are the cardinal signs of inflammation
heat
redness
swelling
pain
increasing the chance of loss of function
give a brief recap of the inflammation response
foreign agent will enter the body -> local vasodilation and increased vascular permability ->
accumulation of white blood cells at the blood cells wall ->
white blood cells will exit the blood vessel ->
will be drawn to the injury area
CHEMOTAXIS
what are the symptoms seen with the pathological response of releasing of soluble mediators
heat (calor)
redness (rubor)
swelling (tumor)
pain (dolor)
what are the symptoms noticed with the pathological response of vasodilation
heat. (calor)
readness (rubor)
swelling (tumor)
what are the symptoms noticed with the patological response of increased blood flow
swelling (tumor)
what are the symptoms noticed with the patological response to extravasation of fluid
(increased permeability)
swelling (tumor)
what are the symptoms related to the pathological response of cellular influx (chemotaxis)
swelling (tumor)
what are physiological components of vascularity
vasoconstriction- few seconds of blanching
vasodilation- smooth muscle relaxes called active hyperermia
increased permeability- vascular leakage- edema
what are the physiological components of cellular mean
leukocyte accumulation and infiltration
where would you find active hyperemia?
arterial hyperemia
due to arteriolar dilatation
sympathic stimulation
the affected tissue is redder than normal because of engorgement with oxygnated blood
what are some examples of active hyperemia
at sites of inflammation
in skeletal muscle during exercise
angioneurothic- face redness
what does active hyperemia account for?
redness swelling and warmth
what is main difference between exudate and transudate
cell/ protein rich fluid vs low cell/protein fluid
describe some details about transudate leakage/ permeability
result of high hydrostatic pressure and low osmotic pressure
fluid is clear
low cell/protein fluid
describe some details about exudate leakage/ permeability
result of increased vascular permeability
cloudy
high cell/ protein fluid
what does exudate permeability do?
supplies antibodies and complement protein to affected areas contributes to swelling
causes pain and decreased mobility
if permeability accounts for swelling what might you also notice with the patient
decreased ROM and Function
what are the five known causes of vascular leakiness?
- mediators
- cytokine mediators
- severe injuries
- leukocytes adhering and damaging the endothelium
- certain mediators may increase transcytosis
describe what occurs with the mediators that causes vascular leakiness
hisamines bradykinis and leukotrienes cause a <30 minute response in the form of reversible endothelial cell contraction
this will widen the gaps of venules that is specific to allergic reactions
describe what occurs with the cytokine mediators that causes vascular leakiness
reversible endothelial cell junction retraction
happens 4-6 hours post injury or infection
last up to 24 hours or more
where brusing can be noticed
how will severe injuries cause vascular leakiness
immediate direct endothelial cell damage making them leaky until they are repaired
vascular permeability follows what process
flows vasodilation
vascular permeability causes what type of dysfunction
endothelial cell dysfunction
how does leukocytes that adhere and damage the endothelium cause vascular permeability
through activation and release of toxic oxygen radicals and proteolytic enzymes making the vessel leaky
how does mediators increasing transcytosis cause vascular permeability
intracellular vesicles extend from the luminal surface to basal lamina surface of the endothelial cells
what is meant by degranulation?
a cellular process that releases: neutrophils
basophils
eosinophils
mast cells
cytotoxic cells
natural killer cells
main purpose is to destroy pathogens
innate immune system
what is meant by diapedesis
leukocytes leave the vasculature and enter the interstitium through a sequence
if you know the sequence say it now
what is the sequence followed by diapedesis
margination and rolling
adhesion
chemotaxis
activation
transmigration
after the sequence of diapedesis what can the leukocytes participate in
degranulation
phagocytosis- macrophage
leukocyte/cytokine - protects and repair (controlled)
leukocyte/ cytokine ‘storm’ induced tissue injury (uncontrolled or chronic)
what is special about the cytokine storm
long covid and disproportionallity to the response which creates a chronic disease
cells of the enate immune system
explain the vasoconstriction stage of acute inflammation stage
release of vasoconstrictor substances
constriction of cells- thought to be immediate response to control blood loss BLANCHING
<60 seconds
explain the vasodilation stage of acute inflammation stage
Mechanism of action- cellular release of mediators
relaxation of the blood vessel walls
what relax the blood vessels walls in the vasodilation stage of acute inflammation
histamine, prostacyclin and nitric oxide relax the blood vessel walls
why does the vasodilation stage happen in acute inflammation
increased hydrostatic pressure (pressure inside the cell pushing out) causes a decrease in blood flow rate
leukocytes will marginate among the blood vessel wall
what is the mechanism of action in the increased vascular permeability stage of acute inflammation
increased vascular permeability occurs through release of histamine and leukotrienes
why does increased vascular permeability occur
allows fluid, WBC, and proteins to move the interstitial tissue
this will decrease the osmotic pressure in the blood vessels and increase osmotic pressure in the interstitial space
what is the result of the increased vascular permeability stage of acute inflammation
edema or increased fluid in the interstitial tissue
what are the physiological mechanisms that increase vascular permeability?
endothelial relaxation and contraction
provide a defintion of endothelial relaxation
HBP cause fluid leakage. the fluid leakage is transudate
provide a definition of endothelial contraction
immediate response that is exudate fluid leakage
initiated by the cell mediators: histimine and leukotrines
time: immediate up to 30 minutes
Provide a definition for endothelial cell retraction
Delayed response that is a exudate leakage
Happens in 4 to 6 hours, but is long lasting
what are the physical mechanisms of increased vascular permeability
direct endothelial injury
what is direct endothelial injury
immediate -sustained response
time: IMMEDIATE
give a detailed depiction of what happens during chemotaxis
pathogens charge macrophages that secrete cytotines. The release of cytotines causes the endotheilal cells to secrete adhession molecules. luekocytes are atracted to the presence of cytokines and adhession molecules
give a detailed depiction of what happens during rolling and rolling adhession
luekocytes bind to adhession molicules with moderate affinity
causes leukocytes in the blood ro slow down and begin rolling among the inner surface of blood vessel walls
give a detailed depiction of what happens during firm and tight adhessions
release of chemokine by machrophages to transition modetate affinity to high bonding to endotheilial cells
give a detailed depiction of what happens during transmigration
cytoskeleton reorganization in conjunction with leukocyte pseudopod extensions
leukocytes pass through gaps in endothelial cells
what should you KNOW about diapedesis?
hint: COPS AND ROBBERS
diapedesis is blood vessel escape
how do leukocytes move to injury and infection
through chemotactic gradients
what details can you associate with acute inflammation
- rapid onset
- lasts minutes to days
- exudation of fluid and proteins from vessels
- emigration of WBC
what is the purpose of acute inflammation
quick attack on foreign agents and initiate the repair process
what are the cardinal signs associated with acute inflammation
rubor
heat
edema
pain
tumor
loss of function
whats the cause of acute inflammation
infection
trauma
physical and chemical agents
necrosis
foreign bodies
immune reaction
what are the outcomes of acute inflammation
resolution
abscess
ulcer
chronic inflammation
scar formation
Contributors in scar formation for acute inflammation
neurophils and macrophages
contributors in scar formation for chronic inflammation
lymphocytes, plasma cells, macrophage, fibroblasts
Scar formation on acute inflammation is connected to what
calcification
what are the phases of the inflammatory process
- acute phase
- tissue formation (proliferation)
- remodeling phase
describe the acute phase of inflammatory process
inflammatory response lasts 2-4 days but complete in 2 weeks
describe the tissue formation phase of the inflammatory process
-subacute phase tissue rebuilding, approximately 2-3 weeks
-this does not include chronic inflammation
describe the remodeling phase of the inflammatory process
-adapt to original tissue
-continues for up to 1 year post injury
describe chronic inflammation
- lasts week to years
- involves lymphocytes and macrophages
-tissue repair and tissue injury happen simultaneously
describe active inflammation for chronic inflammation
lymphocyte, macrophage, plasma cell infiltration
what are the three characteristics of chronic inflammation?
- active inflammation
- tissue destruction by inflammatory cells and stimuli
- tissue healing
describe tissue destruction by inflammatory cells and stimuli when it comes to chronic inflammation
lack of complete resolution
describe tissue healing when it comes to chronic inflammation
fibrosis + regeneration
both require angiogenesis
what does angiogenesis mean
new vasculature, critical to wound repair
what does regeneration mean
formation of new tissue
Give a description for what chronic inflammation is
- simultaneously active inflammation- lymphocytes
- tissue destruction - tissue repair
injuries stimulus that the body cannot remove
what are the causes of chronic inflammation
viral micronial infection, prolonged exposure to toxin, autoimmune
UNDESIRABLE MOVEMENT PATTERNS
what are the cells involved in chronic inflammation?
macrophage- produce enzymes and mediators
Lymphocytes- stimulate fibroblasts to produce collagen
scarring
discribe the resolution stage of inflammation
irritating agent is removed
damage is repaired
inflammatory process completed
what are the requirements for the resolution phase of inflammation
-affected tissue is capable of healing
- body capble of removing the irrritating agent
what are the important points in the resolution phase of inflammation
intact epithelium
basement membrane must be intact in order to guide the healing process in laying down new tissue
what happens if the basement membrane is destroyed
new tissue is unorganized and otherwise known as scare tissue
causing tissue repair
what is an abscess?
collection of pus
neutrophils are primary responders
what are the requirements for abscess formation
body is unable to elimminate the irritant
tissue injury rate» tissue repair
where can an abscess occur
in all tissue
what is the potential sequelae for an abscess
pain, fever, rupture, and swelling
what is an ulcer
loss of mucosa, basement membrane and deeper tissue
Erosion that occurs with an ulcer means what excatly
loss of mucosa only
basement membrane is still intact
what are the requirements for a an ulcers formation
body is unable to eliminate the irritant
tissue injury rate» tissue repair
where would you find and ulcer
most often in the GI tract
what is the potential sequelae of an ulcer
pain, hemorrhage, pertonitis
what is a fistula
abnormal connection between two organs
what are the requirements for the formation of a fistula
Full thickness opening of walls of adjacent organs, vessels, ducts due to the inflammatory process
Communication between the two structures
Potential Sequelae
Structure dependent➔ infection, hemorrhage
what is scar formation from chronic inflammation?
disorganized connective tissue»_space; healing and repair
loss of parenchyma cells
what is the requirement for scare tissue
loss of basement membrane= loss of regenerative tissue, loss of resolution
what is the potential sequelae for scare tissue
loss of finction
give a breif review defintion for resoulution
original tissue
give a breif review defintion for tissue repair
tissue healing
regeneration and replacement (fibrosis/scare tissue)
give a breif review defintion for regeneration
restoration of damaged tissue to the original state
give a breif review defintion for replacement
laying down of collegen
whats the process of granulation on a young scar
granulation tissue is highly vascularized connective tissue that is composed of newly formed capilliaries proliferating fibroblasts and residual inflammatory cells.
whats the time frame for granulation tissue
2-5 days post wounding, starts as early as 24 hours.
what type of growth pattern does granulation take
granulation tissue normally fills the base of the wound new tissue. Then fills the wound.
what are the physcial therapy implications for repair
manual therapy, concetric and eccentric stregthening to promote organization
repair =
regeneration + replacement
scare tissue will
decrease functions and increased risk of reinjury
what is the difference between regeneration and repair and healing
regeneration of parenchyma calls complete regeneration of tissue
repair/healing= regeneration combined with scaring and fibrosis
what is the process of complete regeneration
- process of renewal, restoration, and growth of parenchyma cells
- new tissue is the same as the lost or damage tissue- no scare formation
- requires cells that can divide
- requires an intact basement membrane
- requires an intact connective tissue scaffolding
what occurs during partial regeneration or healing/ repair
replacement of damaged or lost tissue with fibrosis tissue
how long does the repair process take
begins in early inflammation within 24 hours to 10 days
what happens in the repair process
fibroblasts and vascular endothelial cells begin to proliferate to form granulated tissue
pink, soft, and granular
give a defintion of angiogenesis
angiogenesis- formation of new blood vessels; granulation tissue lays down a new capillary bed
-new vessels are leaky allowing protein and RBC passage.
what does proliferation of fibroblasts secrete
collagen
How would you describe the makeup of the extracellular matrix
the extra cellular matrix is edematous
granulation tissue - soft infrastructure
explain wound contraction
approximation of wound edges
3 days to 20 days
quickly describe the migration and proliferation of fibroblasts
fibroblasts within granulation tissue produce collagen fibers and contractile proteins to pull edges of damaged tissue together
How do parenchyma cells regenerate
parenchyma cells regenerate to the extent possible
they are capable of cell division
Scar formation take how many days
> 7 days
how long does the reogranization of fibrous tissue take
remodling for weeks to months even years
give a breif overview of the wound healing timeline
- inflammation: dilute or neutralize the injurious agent
- granulation tissue formation : regeneration of damaged connective tissue
- epithelial healing : regeneration of damaged epitheilial tissue
- wound contraction: approximation of wound edges
- scar formation and remodling: provide strength and return tissue to uninjured states
