Chapter 4 Flashcards
causes of cell injury
- hypoxia
- physical, thermal, chemical
- microorganisms
- inflammation/immune reactions
- nutritional imbalance
- genetic defects
- trauma
- aging
most common cell injury?
hypoxia, due to ischemia (insufficient blood supply)
loss of oxygen leads to decrease in..
ATP, failure of Na/K pump, sodium moves into cell, water follows and cell swells/potentially dies
glycolysis without oxygen = ?
lactate (lactic acid), more acidic, alters cell proteins
steatosis
increase in lipid/fat, deposited between or into cells
hydropic changes
cell swelling
- loss of ATP
- failure of pump
- sodium remains in cells
- water moves into cells
atrophy
without size, shrinkage, decrease in cell size due to physiological (aging) or pathological (decreased blood supply, nutrition, lack of neural/hormone support)
hypertrophy
increase in cell size
hypertrophy is due to..
- hormonal stimulation
- increased functional demand
hypertrophy results in..
- increased protein synthesis within cell
- decreased protein breakdown
hyperplasia
increase in cell number
hyperplasia due to..
- hormonal stimulation
- increased functional demand
- chronic stress
hyperplasia results in..
increased cell division if the cell can divide
metaplasia
replacement of one cell type with another
metaplasia is most common in..
epithelium
- reversible if stressed removed
- smokers
dysplasia
change in cell, abnormal cell division
- premalignant -> precancerous
- often not reversible
apoptosis
DNA degrades, cell shrinks, programmed cell death
- removes cells that are “warn out”
- removes unwanted tissue
- physiological or pathological
necrosis
pathologic cell death, explosion, leads to inflammation of other cells because of contents leaked
- damage nearby cells
- inflammation results
different types of necrosis
- coagulation necrosis (observed with infarcts)
- liquefaction necrosis
- caseous necrosis - cheese, observed with tuberculosis
- gangrenous necrosis (gangrene)
infarcts
lack of blood flow/oxygen leads to cell death
inflammation
cell response to injury
function of inflammation
- limit extent of injury
- remove necrotic debris
- prepare for healing process
types of inflammation
- acute: short, resolve
- chronic: issue, months/years (obesity)
vascular sequence in acute inflammation
- blood vessels vasodilate
- increase blood flow to injured area
- increased vascular permeability (WBC and plasma leave)
- mast cells release histamine
exudate
fluid that leaks out of blood vessels
inflammation hallmarks
- swelling (increased leakiness)
- redness (more blood flow)
- warmth (more blood flow)
mediators of inflammation
- prostaglandins: increase vasodilation
- leukotrienes
inhibitor of mediators
NSAID - nonsteroidal antiinflammatory drug
cellular phase sequence of events in acute inflammation
- leukocytes move from blood to injury site
- neutrophils mediate inflammation
puss
dead neutrophils
phagocytosis
cell eating
cellular phase steps
- margination
- emigration/diapedesis - squeeze through blood vessel
- chemotaxis - bacteria releases chemical for neutrophil to follow
chemical mediators of inflammation
cytokines: messenger between WBC
chronic inflammation
weeks to years, may result from acute inflammation that persists or non-acute cause present at low level for a long time
characteristics of chronic inflammation
- edema and hyperemia less pronounced
- few or no neutrophils present
- fibrosis (scar tissue)
clinical appearance or acute and chronic inflammation
- abscess: collection of puss in the center
- cellulitis: inflammation of dermis, deep skin infection
- ulcer: type of lesion, cut in the membrane of the cell, stomach
regeneration
nearly complete restoration
fibrous connective tissue repair
scarring, does not restore original function
type of repair depends on type of cells forming tissue
continuously dividing vs. non dividing
would healing stages
- inflammation
- proliferative
- remodeling
proliferation
- create new
- collagen (laid by fibroblasts) and extra cellular matrix (in between connective tissue)
- granulation tissue (epithelial cells migrate to site, “soft scab”, vascularized, made up of macrophages and fibroblasts)
remodeling
- maturation of scar (turns white)
- laying new collagen
- can continue for year +
- loss of blood vessels (not needed when collagen arrives)
repair hindering
- continuation of inflammation (poor immune system)
- advancing age (bed sores)
- poor nutrition (lack of vitamin C for collagen, vitamin A for epithelial cells, protein to make collagen and WBC)
- diabetes (cardiovascular and circulation and WBC lack)
- steroid therapy (decreased immune system and inflammation so healing takes longer)
