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141 Cards in this Set

  • Front
  • Back
3 cell reactions to stress
adapt, reversible or irreversible injury (cell death)
6 causes atrophy
decreased workload, hormonal or nervous stim, nutrition, blood supply, or aging.
hypertrophy causes
physiologic or pathologic - response to hormone, workload, or limited adaptive response: L.ventricle hypertrophy.
02 deprivation
loss of blood flow
tissue injury time in ischemia vs. hypoxia
ischemia injures more quickly, compromises avail. of metabolic substrates
causes of cell injury
O2 deprivation, physical agents, chemical, infectious agents, genetic disorders, nutritional imbalance
change of a differentiated cell type to another
metaplasia - response to persistent (chronic) injury
2 common chronic injury cell type changes
smoker:ciliated epithelium - stratified squamous. Cervix - glandular to squamous epithelium
4 systems in cell vulnerable to injury
membrane pump, genetic apparatus, aerobic respiration, structural-enzymatic proteins
4 mediators - cell death
02 and 02 free radicals, intracellular Ca+, ATP depletion, membrane permeability defects
most common cause of cell injury and the tissue result
hypoxic ischemia - coagulative necrosis
2 energy mechs affected in cell injury
aerobic respiration (oxydative phosphorylation), glycolysis (anaerobic respiration)
result when each energy mech. injured
aerobic - ATP production lost. glycolysis - depletion of glucogen, byproducts and acidity
byproducts - glycolysis
lactic acid, reduces intercellular pH
mechanisms of injury - ischemia
ATP depletion, Na+-K+ pump stops working,Potassium leaks, sodium stays, cell swells. ribosomes detach, protein synthesis slows, lipid accumulates, nuclear chromatin clumps
3 factors IRREVERSIBLE cell injury
massive amounts Ca+, mitochondria covered, ATP production lost. Cell membrane leaks, lysosomes leak. Enzymes digest cell components.
2 diffs - reversible vs. irreversible injury
CELL MEMBRANE DAMAGE - most important (integrity) Can’t reverse mitochondrial damage (no energy)
4 mechanisms free radical injury
peroxidation of membrane lipids, DNA breaks, X-linking of proteins destroys function, damage to mitochondria.
6 free radical injuries
reperfusion/hypoxia, aging, radiation, 02 toxicity, chemical injury, INFLAMMATION
2 mechanisms chemical injury
direct (chemotherapy), toxic reactive metabolite reaction (in liver)
2 morpological signs REVERSIBLE cell injury
SWELLING, fatty change
imp. cause of liver damage
hepatotoxin - ALCOHOL - causes incr. fatty synthesis
inflammatory cause of free radicals
produced to kill bacteria
5 types necrosis
COAGULATIVE, liquefactive, caseous, gangrenous, fat/enzymatic
necrosis type determinants
cell type and cause of death
2 methods necrotic cell removal
denaturation, enzymatic digestion
3 changes to nucleus in cell death
shrinkage, fracturing, disappearance
indicator of nucleus shrinkage - cell death
increased staining
nuclear shrinkage
nuclear fragmentation
nuclear disappearance
many cytoplasmic proteins denature - result?
cytoplasmic eosinophilia (incr. staining)
coagulative necrosis histology
well demarcated - determined by blood supp.
dead cell structure - coag. nec.
eosinophilic ‘tombstone’ architecture there, nucleus not
liquefactive necrosis cause
enzymatic digestion cell architecture/lysosomes, enzymes released
usual cell death cause - liquefactive necrosis
markers of infarct in brain
cyst, tissue debris, fluid, inflamm. cells, bacteria
necrosis - comb. liquefactive/coagulative
caseous. granular, eosinophilic debris
disease assoc. w. caseous necrosis
normally seen in caseous necrosis
granulomatous inflammatory border with giant cells, epitheloid histiocytes
adipose necrosis
fatty enzymatic necrosis in adipose tissue - assoc. w/calcification
location/cause fatty necrosis
peripancratic (sometimes mesenteric) acinar cell damage, lipases released, calcification --calc.soaps
liquefactive or coag. necrosis of limbs called
gangrene - wet or dry (eg diabetes)
apoptosis result
nuclear disintegration, DNA cleavage
2 conditions assoc. w apoptosis
viral infections, radiation injury
fast necrosis dev. in organs with?
high met. rate (int. mucosa), cytolytic enzymes(pancreas), vital organs - high O2 (brain, heart, lungs)
hypertrophy seen in cells which
can’t divide
hyperplasia occurs where
cells capable of mitosis
physiologic hyperplasia 2 types, examples
compensatory (liver regen) hormonal (breast/uterus - pregnancy)
reversible change of one differientiated cell type to another
metaplasia results from
common response to chronic injury/inflammation/irrit.
physiologic adaptation feature
cells tissues modify to new demands
pathologic causes of apoptosis
viral infection, radiation injury
physiologic causes of apoptosis
embryogenesis, hormonal (breast), proliferating populations (lymph)
inflammation is
reaction of living tissue to injury
inflammation can result in
tissue damage
inflammation mediators
chemicals derived from host
inflammatory changes occur where
terminal vascular bed, blood, conn. tissue
main cells involved in inflammation
monocytes, neutrophils, macrophages
purpose of inflammation
eliminate injurious agent and initiate repair, restoring continuity if not function
clinical symptoms of inflammation
rubor, calor, dolor, tumor, loss of function - redness, heat, pain, swelling, loss of funct.
characteristics acute inflam.
short duration, fluid exudate, plasma proteins (edema), neutrophile and leukocytes to tissue, then macrophages.
2 poss. outcomes acute inflammation
resolution or complications (progress to chronic)
chronic inflam. char.
long duration, lymphocytes, plasma cells, macrophages, vascularization, fibroblasts.
tissue type assoc. w chronic inflam
granulation and connective
scarring problem/consequence
diminishes tissue function, can lead to organ dysfunction (and death)
limiting factor of inflammation
only at site of injury
2 ways injurious agent isolated in inflammation
encapsulation (fibrous capsule) intercellular storage(engulfment - phagocytosis and storage.)
1st vascular chgs in inflammation
momentary vasoconstriction (reflex) followed by vasodilation - incr. blood flow, then congestion - filled w/ blood.
vasodilation and congestion cause
redness, heat.
following vascular chgs
blood tissue barrier chgs - widen endothelial gaps - histamine reaction - edema
swelling of inflammation bc of
capillary leakage - blood plasma and leukocytes to tissue
inflammatory exudate
cellular debris, plasma proteins, fluid
cellular events of inflamm
margination, pavementing w/in vessel wall, emigration from vessel to interstitium, chemotaxis-site, phagocytosis
inflamm cell types
Neutrophils first 24 hrs, then monocytes 24-48 hrs
exudate specific gravity
5 host derived main mediators inflammation
vasoactive amines, plasma proteases, cytokines, adhesion molecules, arachiodonic acid metabolites
2 vasoactive amines
histamine, seratonin
purpose, origin vasoactive amines
vascular chgs inflammation
what produces vasoactive amines
mast cells, platelets
3 systems of plasma proteases
kinin, clotting, complement systems
kinin sys assoc. w?
cytokine, peptide source
cytokine purposes
inflammatory mediators (IL1, TNF), activate polymorphs, macrophages to incr. killing, incr. vasc. permeability
ICAM1 def
cytokine - initiated production by endothelium
ICAM1 purpose
facilitates inflam cell binding to vessel endothelium
AA metabolites are?
arachiodonic acid - degraded phospholipids of cell membranes
AA’s cause?
inflammation - vasodilation, chemotaxis, increase vasc. permeability
2 anti-inflam drugs
aspirin, steroids
non steroid anti inflammatory
aspirin function
blocks prostaglandin synthesis
prostaglandin function
pathogenesis of pain and fever - hyperalgesic
steroid function
blocks prostaglandin, leukotrines
chemotactic, activate neutrophil aggregation and adhesion
chronic inflam cells
MNL, lymphocytes, plasma cells
main processes, chronic inflam
healing and repair and tissue destruction cycle
define granuloma
form of chronic inflam w/ lots of histiocytes, giant cells, LANGHANS cells
granuloma forms bc
bacterial or fungal infection, foreign materials
2 results of tissue dmg
regeneration if same tissue type, or scar repair
purulent exudate
PUS proteins, neutrophils, cell debris: liquefactive nec
walled off localized pus collection
acute vs chronic characteristics
fluid protein exudate and neutrophils versus tissue dest. and repair, lymphocytes, macrophages and chemical mediators for vaso/cellular response
4 vascular events of acute inflam
transitory reflex vasoconstriction - vasodilation - incr. bl.flow - capillary permiability incr.-fluid to interstitium= swelling, stasis, incr. blood viscousity, leukocytes enter
problem w phagocytosis in inflam
lysosomal enzymes to extracellular sp - cell/tiss. dmg
4 outcomes acute inflam
resolution, scarring, abscess, progress - chronic
results of AI resolution
little injury or destruction, normal function
scarring in nonregen tissue result
loss of function (deadly in cases: heart, brain)
3 examples persistent infections causing chronic inflam
tuberculosis, syphilis, fungi
4 causes of chronic inflam
persistent infection, delayed hypersensitivity react., toxic agent exposure (inorganic metals), autoimmune disease
2 autoimmune disorders assoc w chronic nflamm
rheumatoid arthritis, thyroiditis
chronic inflammation: granuloma histology
activated macrophages, large squamous cell epitheloid appearance
3 morphologies inflammation
serous(watery, few proteins), fibrinous, purulent(neutrophils, necrosis, edema, pyogenic orgs).
pyogenic organism example
abscess characteristics
fibroblastic surround (early repair) w/ pus, pyogenic organisms, central necrosis
eroded necrotic epithelium
ulcer - assoc. w acute and chronic inflam
3 systemic effects inflam
fever, elevated WBC count, neutrophylia, lymphocytosis
exudate with fibrin
exudate with RBCs
exudate - yellow/green
clear exudate
serous (plasma) - edema
cause of pain assoc. w inflamm
pressure on nerves, and chem. mediators
inflammation is
response of VASCULARIZED tissue to injury
inflammation designed to
bring plasma proteins to site of injury in fastest poss.time
main chgs in inflammation
blood flow changes, formation of fluid and cellular exudates
3 functions fluid exudate
bring plasma proteins, dilute toxins, loosen conn. tissue to allow diffus-migration of cells to injury site
cell type assoc w/ parasitic infection
polymorphonuclear leukocytes: NEUTROPHILS
chemical attractants at injury site
host factors - plasma proteins, and infectious agents
protein expressed on infectious agent
OPSONIN - labels agent for phagocytic destruction
possible outcomes acute inflammation
resolution, abscess, tissue dest., systemic involvement, progression to chronic
3 conditions lysosomal enzymes released inadvert. during inflamm.
during phagocytosis, trying to digest on flat surface (frustrated phagocytosis), cytotoxic release
result of lysosome enzyme release
tissue destruction
result of tissue dest
catastrophic if in heart, valves, major vessels
flat surf. destruction of what by neutrophils
AgAb complexes
system: removes AgAb complexes in spleen, liver, bone marrow
reticulo-endothelial system
autoimmune disease def
antibodies against self
if AbAg complexes in body for too long?
acute inflamm response, neutrophils - injury site
frustrated phagocytosis in kidney, joints, heart
glomerularnephritis, arthritis, carditis
tissue destruction from cytotoxic release
cytotoxic release
neutrophils phagocytose particles harmful to them, burst, releasing enzymes, destroy tissue.