chapter 4 Flashcards
hypoxia
less oxygen then normal
anoxia
no oxygen
how can cells become injured
hypoxia, anoxia, trauma, radiation, inflammation, immune responses, genetic defects, nutritional imbalance, trauma, aging, dehydration
most common cell injury
hypoxia
hypoxia most often occurs due to?
ischemia
ischemia
insufficient blood supply, not enough blood flow, the blood is carrying the oxygen throughout the body
failure of Na+/K+ pump
maintains the balance between sodium and potassium inside and outside of the cell
- water follows salt
sodium should be pumped out and potassium in
steatosis
accumulation of fat
hydropic changes
cell swelling
- loss of atp
- sodium remains in cell
cell response to injury
not an all or nothing phenomenon
- response to a given stress depends on the type, status and genetic make up of the inured cell
- cells are complex interconnected systems, and single local injuries can result in multiple secondary and tertiary effects
adaptations of cells
altered growth, atrophy, hypertrophy, metaplasia, dysplasia
atrophy
shrinkage, decrease in cell size
physiological atrophy
aging
pathological atrophy
decreased blood supply, decreased nutrtiion, lack of neural or hormone support
hypertrophy
increase in cell size
hypertrophy due to
hormonal stimulation
hypertrophy results in
increased protein synthesis within cell, decrease protein breakdown
hyperplasia
increase in cell number
hyperplasia due to
hormonal stimulation, increased functional demand, chornic stress
hypereplasia results in
increased cell division, if the cell can divide
metaplasia
replacement of one cell type with another
- most common is epithelium
reversible
dysplasia
change in cell resulting in abnormal cell size, shape or organization
apoptosis
programmed cell death - not always an indication of injury - removes cells that are "worn out" - removes unwanted tissue physiological or pathological
necrosis
unregulated death
cells swell and rupture - damage nearby cells and inflammation results
different types of necrosis
coagulation, liqufication, caseousm and gangrenous
inflammation
a nonspecific response to any agent that causes cell injury function - limit extent of injury, remove necrotic debris, prepare for healing process
acute inflammation
good, limits and contains, and repairs itself
chronic inflammation
can be bad, a number of diseases that are associated with chronic inflammation, weeks to years, mediator of chronic disease
acute inflammation - vascular
increase of blood flow to injured area, increase in vascular permeability,
vascular permeability
the blood vessels become more leaky during inflammation, white blood cells are able to enter in through the spaces
exudate
fluid that is accumulating in the interstitial space which causes edema and swelling
mast cells stimulated to
release histamine
acute inflammation - cellular
leukocytes move from blood into tissue at injury site, leukocytes move to injury site and activate, phagocytosis
prostaglandins
promote inflammation, vasodilation, chemotaxis, can be reduced by NSAIDs
steps of cellular phase of acute inflammation
leukocytes enter the injured area
- margination
- emigration/diapedesis
- chemotaxis
- phagocytosis
diapedesis
across, the endothelial cells are leaky, white blood cells enter through the leaks
chemotaxis
moving in the direction of the bacteria
chemical mediators of inflammation
some are released by bacteria at infection site, others are produced by cells at injury site during and in response to inflammatory activation
cytokines
molecules that help the immune system to communicate
cardinal signs of inflammation
redness, swelling, heat, and pain
chronic inflammation may result from
acute inflammation that persists because the cause is not completely eliminated, non-acute cause present at low level for long time
characteristics of chronic inflammation
typically low grade, edema and hyperemia less pronounced, few or no neutrophils present, fibrosis is common
transudate
low protein content
abscess
collection of pus
cellulits
deep skin infection of the dermis
ulcer
lesion in an organ
mineral accumulation during inflammation
calcium
accumulation of insoluble protein
amyloid
amyloid
insoluble deposit that never goes away, organ function decreases
repair
inflammation has to end for this to begin
regenration
nearly complete restoration
scarring
fibrous connective tissue repair
- does not restore original function
- not the same cell type as vefore
stages of regeneration
1) inflammation
2) proliferative
3) remodeling
proliferative
a cell proliferates to make new cells
- epithelialization by regenerating basal cells
granulation - filling in the wound with new capillaries, epithelial cells, filling in the gap temporarily until the correct cells can be formed, red because of new capillaries
remodeling
maturation and reorganization
- reorganization of collagen - so its much more uniform in direction, lose blood vessels, you would want to remove blood vessels because blood vessels aren’t as strong as collagen
factors that may detract from the body’s ability to repair
continuation of inflammation, advancing age, poor nutrition, diabetes, steroid therapy
continuation of inflammation
this is the first step of repair, so it needs to be completed before the body can start to heal
