inflammatory process Flashcards
cell characteristics
cells tend to preserve their environment to maintain homeostasis (body wants to go back to normal ASAP). Physiologic stress or pathologic stimuli cause cells to undergo adaptation and find a new steady state to preserve viability
physiologic stress
stimulation of cells to do something different so cells begin to change. ex. lifting weights at the gym
pathologic stimuli
rupturing of cells from too much stress ex. bowed tendon
atrophy
decrease in cell size, but cells are still there
hypertrophy
increase in cell size by increasing exercise or use
hyperplasia
increase in cell number. May be caused by pregnancy (in uterus/udder) or cancer (tumor)
metaplasia
change in cell type, may change back to original cell type. ex. cigarette smokers (normal cells in trachea have cilia but smokers do not have ciliated cells because they are more resistant to smoke)
is injury reversible?
injury can be reversible, but with persistent or severe stress (ex. broken leg), injury is irreversible (results in cell death)
Necrosis
loss of blood supply or exposure to toxins, cellular swelling, protein denaturation and tissue dysfunction results
apoptosis
programmed cell death, dead cells are removed with minimal disruption of the surrounding tissue
Causes of Cell Injury
- oxygen deprevation (hypoxia) 2. chemical agents 3. infectious agents 4. genetic defects 5.immunologic reactions 6. nutritional imbalance 7. physical agents 8. aging
ischemia
oxygen deprivation, loss of blood supply in tissue due to impeded arterial flow or reduced venous drainage ex. cut, atheriosclerosis, embolism
inadequate oxygenation
type of oxygen deprevation, ex. pneumonia and emphysema
reduced O2 carrying capacity of blood
ex. anemia, loss of red blood cells
chemical agents
any chemical substance can cause cell injury (even salt and water). ethanol causes liver injury that is reversible at first but chronic ethanol use will lead to irreversible injury (liver exhaustion=cerosis)
infectious agent
ex. virus, bacteria, worms, fungi, protozoan
genetic defects
may result in pathologic changes ex. lethal white
immunologic reactions
anaphylactic shock is classical example of an exaggerated immune response, auto-immune disease which is loss of self-tolerance (lupus, rheumatoid arthritis)
anaphylactic shock
disregulated allergy causing an exaggerated immune response (causes swelling in throat, asphyxiation and death)
nutritional imbalance
malnourishment or obesity
physical agents
trauma (cuts, bruises, concussions ect.), burns, cold (frostbite)
aging
the body becomes exhausted, repeated trauma, imperfect restoration of structure or function, cellular senescence
what does response to injurious stimuli depend on?
type of injury, duration and severity
what do consequences of injury depend on?
adaptability and genetic makeup (ex. cats heal faster than dogs) of the injured cell. ex. skeletal muscle can withstand 2-3 hours of ischemia w/o irreversible injury while the cardiac muscle can only tolerate 20-30 mins and the brain can only tolerate 3-4 mins
inflammation
a protective response intended to eliminate the initial cause of cell injury as well as the necrotic (dead) cells and tissues resulting from the original insult, heals and reconstitutes the site of injury, interwoven with the repair process, helps clear infection and makes would healing possible but may cause harm
acute inflammation
immediate and early response to injury, designed to deliver leukocytes to the site of injury
leukocytes (white blood cells)
clear any invading microbes and begin the process of cleaning necrotic tissue
two components of acute inflammation
vascular changes (vasodilation to increase blood flow) and cellular events (cellular recruitment and activation, leukocytes migrate)
5 classical signs of acute inflammation
heat (area becomes hot to the touch, fever, caused by increased blood flow), redness (caused by increased blood flow), swelling (caused by leaky blood vessels allowing WBCs to enter the area), pain (caused by the inflammatory cells) and loss of function (not same as loss of movement)
Neutrophils
first responders to bacterial and fungal infections, form pus
eosinophils
deal with parasitic infection
basophils
granulate, responsible for allergenic and antigen response, releases histamine
lymphocytes
common in the lymphatic system, B cells make antibodies (cells that have memory)
monocytes
perform phagocytosis
vascular changes
- initial vasoconstriction (seconds) to stop bleeding, platelet aggregation,blood coagulation->clot
- vasodilation (responsible for redness and heat in inflamed area, caused by histamine release), brings in leukocytes
- increase vascular permeability-protein rich fluid in extravascular tissue (we see edema or swelling). blood becomes more viscous and circulation slows down
cellular changes
- leukocytes (neutrophils) will transmigrate through intercellular junctions to the extracellular matrix
- leukocytes will release chemical mediators that keep inflammation going ex. histamine, cytokines, leukotrienes, prostaglandins. these recruit more leukocytes to the area
- phagocytosis: leukocytes will ingest (engulfment) injurous particle. Serves to both kill bacteria/virus and also to clean up dead cells
outcome of acute inflammation
resolution, scarring/fibrosis, chronic inflammation
resolution
when injury is limited or short lived, tissue is capable of replacing any irreversibly dead cell with new perfect and functional cells
scarring/fibrosis
after substantial tissue damage or when injury occurs to the tissue that does not regenerate. in cases of abscess formation (bacteria, neutrophils, dead cells->pus). the only outcome is scarring
chronic inflammation
persistant viral or bacterial infection, may be caused by debris in wound, wound constantly being reopened, compromised immune system. may lead to complete regeneration or fibrosis, use of anti-inflammatory agents are necessary
angiogenesis
the creation of new blood vessels and cells, too many new blood vessels may be created that prevents blood from flowing to the area
Extracellular Matrix (ECM)
critically regulates growth, movement and differentiation of cells, aids in mechanical support, determination of cell orientation, control of growth, organized regeneration of tissues
components of the ECM
collagen (confer tensile strength, adds elasticity to new cells, primarily located in tendons, skin etc.), elastin (recoil and return to baseline structure), glycosaminoglycans and hyaluronan (highly hydrated compressible gels that confer resilience and lubrication)
repair by connective tissue
if severe or persistent tissue injury occurs, the repair occurs by replacement of what should be normally functioning cells with connective tissue. granulation tissue (proud flesh) is formed. horses are prone to exuberant granulation tissue formation which impedes healing of wounds
granulation tissue
angiogenesis, fibroblasts, loose ECM. Pink in color, soft and granular-looking tissue. highly populated with macrophages which clear debris and allow for fibroblast proliferation and ECM production. Becomes fibrotic tissue.
wound healing
very organized event, specialized cells first clean the injured site and progressively built the scaffolding to fill in any resulting defect
first intention wound healing
occurs with minor or precise injury ex. clean, uninfected surgical incision approximated by sutures. cells are regenerated, they maintain normal function and scar is minimal
second intention wound healing
open wound, abscess, ulcerations. Normal architecture is not achieved, extensive ingrowth of granulation tissue, fibrotic scar formation is the result
wound strength
carefully sutured wounds have 70% of normal strength of unwounded tissue. when suture is removed, wound strength is only about 10%, by the end of 3 months wound strength is about 70-80%
