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49 Cards in this Set

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what is adaptation
atrophy=lack of size, its reversibles, it is due to lack of nutrition among other things
hypertrophy=increase in size
hyperplasia=increse in # of cells
what is the difference between pathologic and physiological atrophy
phys=removal of thyroglossal duct
path=lack of use, aging,nutrition
what are some of the causes of cell injury
-hypoxia
-infection
-immunologic reactions
-genetic causes
what is reversible injury
is only possible in cells that don't die form the injury
-hydropic change= formation of channels that increase influx of H2o
-fatthy change= revesible, usually seen with alcohol
-hyaline degenration=look pink called mallory bodies
-inclusions and deposits=lipofusin
what is the irreversible injury
necrosis
apoptosis
what is necrosis
-irreversible cell death
-death of material
what is apoptosis
normal cell death
-intracellular programmed
-membranes persist
what is the difference b/t apop and necrosis
necrosis has membranes disrupted but apoptosis does not
what are the differnt types of necrosis
4 types
-coagulative =stopped blood flow, membrane stays in the beginning but hen goes away
-liquefactive=due to infection, only exception is CNS, membrane disrupted quickly
-caseous=mainly seen with TB, histoplasmosis, looks like cheese, bacteria
-fibrinoid= intense red color and fiber like but not exactly fibrous
what is the only exception to liquefactive necrosis as in death can occur w.out infection
CNS
what are the normal function of apoptosis
normal= embryogenesis, hormone dependent tumor death
what are the pathologic factors of apoptosis
seen following duct obstruction, viral infection, effect of CTL
what are some sub cellular response regarding apoptosis
-lysosomal enz
-hypertrophy of SER
-change in mitochondria
-cytoskeltal change in chediak higashi
-inetercellular accumultations
what is problem with chediak higashi
it is problem with the formation of phagolysosome
what are different types of calcification
2 types
-dystrophic= necrosis, normal serum ca
-metastatic= increased Ca levels, normal tissue, hypercalcemia mainly die to proliferative parathyroid gland, another example is sarcidosis= macrophages casue inhibtiion of vitmain D metabolism w/c leads to increase levels of calcium in the body
what is inflammation
respons to cell injury
what is acute inflammation
-short duration
-sudden onset
-edema
-neutrophills
what are the cardinal signs of inflammation
-rubor=redness
-calor=heat
-tumor=swelling
-dolor=pain and
-functio lasae
what is the difference between signs and symptoms
sign=measurable, like Bp, fever
symptom=not measurable, what the patient tells us
what are some of the vascular mechanisms of inflammation
-endothelial gaps=most common, the cells are pulled apart and material flows through
-cytoskeletal reorganization
-transcytosis
-immediate sustained
-delayed prolonged= injury happen but the effects show up a few hours later, i.e. sun burn
-leukocyte endothelial injury= seen in burn victims and mainly in the venules
-
what roles do the chemical mediators play in inflammation
-short loved
-double edged
-tissue/specied sp
what are some of the chemical mediators
-histmaine=mast cells
-serotonin=mast cells
-arachiodonic acid=makes
-prostaglandins= cause fever
-leukotrienes=
-platelet activating factor
-cytokines
-nox
-plasma enz
what are/roles of plasma enzmes
-complement systems=mainly C3a and C5a
-kinin=mainly bradykinin involved in heart tissue and vascular permeability
-clotting=mainly hagman factor, interacts w/kinin pathway
what is chemotaxis
2 types
1)exogenous=bacteria,
2)endogenous=imp is C3a, and C5a
complement compnent, LT(LTB4), and chemokines (IL-8)
is there such thing as negative chemotaxis
no
it is always poistive
what are the components of phagocytosis
-opsonization= on the surfact
-engulfment= covering
-degradation
what are some of the morphologic patterns of inflammation
-purulent= pus
-urticaria= hives
-cellulits=inflamamtion bt the cells
-fibrinous=pours out of the serum and it organizes
-fibrinoid=intense red but not fibrous
what are some of the outcomes of acute inflammation
-resolution
-chronic inflamation=grnuloma
-abcess=localized infectionm keeps inflammatory material from leaking out
-fibrosis
what are some of the causes of chronic inflammation
chronic inflammation=comes after acute due to continued stimulus or poor resolution, interfernce with healing
how is chronic iflammation caused if their was no acute inflammation
that would be due to
-intracellular pathogens
-large extracellular pathogen like parasites
-continued exposure to the inflammatory agent
-autoimmune disease
what are some of the cells involved with chronic inflammation
-esosinophills
-lymphocytes
-plasma cells
-mononuclear cells, including giant epithelioid cells
what are some of the factors that are involved in inflammation
(LOOK AT NOTES PG 14) HANDOUT 6
IL-4,
-IFN-gamma
-MIF
-MAf
what happens to the number of nuclei in casceous granuloma
increases all over the cell
what are some of the examples of caseous granuloma
-sarcoidosis=macophages cause malabsorption of vit d
-temporal arterits=granuloma in vessels, old ppl
-crohn's disease=small bowel granuloma
-foreign bosies= splinter in the finger
what is the difference and similarities between sarcoidosis and TB
both are very similar in how they present but steroid is good for sarcoidosis treatment but it is bad for TB
what are some of the non granuloma chronic inflammation
-hashimoto thyroiditis
-viral hepatitis
-chronic polynephritis
what happens with hashimoto's thyroiditis
loss of thyroid function
whats the first thing that musy happen before inflammation can take place
tissue injury must take place
how does tissue injury effect the process of inflammation
it + the inflammatory mediators that can either lead to secretion of vasoactiveamines w/c will increase the cell permeability and eventually cause edema or it can + chemotactic factors w/c will recruit inflammatory cells that cause chronic or acute inflammatory response
what are the chronic inflammatory lynmphocytes
-mac
-lymphocytes
-plasma cells
what are acute inflammatory mediators
PMN
platelets
what does proliferative potential refer to
repair
what type of prolifertor potentials are there?
there are 3
1)labile=some cells divide all the time, for example stratified squamous surfaces of the skin, oral cavity, vagina, and cervix
2)stble= quiescent cells, these cells do not re generate but they do have the ability to divide rapidly so they can generate tissue that way, examplw would be parenchymal cells of the liver or mesenchymal cells like muscles and fibroblasts
3)pemranent= these cells have left the cell cycle and cannot be replaced, i.e. neurons
3)
how do cells grow
they grow via ligand binding, signal transduction, transcriptional factors,and eyclins
what are some of the growth factors
epidermal growth factors, vegf, fgf, cytokines, vegf
what is the extracellular matirx of the cells made of
it is made off collagen,adhesive glycoproteins, fibronectin, integrin, laminin and proteoglycans
what are some of the factors involved with wound healing
-blood clot
-granulation of tissue=scabs
-migration of epithelia cells
-scar
-remodeling
what are some of the comlications with wound healig
keloid growth= this is growth that grows beyond the boundaries of the original wound
pyogenic granuloma=it's very flesh/vascular growth normally seen in mucose
contrations=scar tissue
what are some of the things that influence wound healing
-nutrition
-gluccocorticoids
-infections
-foreign body
-vascular alteration