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49 Cards in this Set
- Front
- Back
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what is adaptation
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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 |
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what is the difference between pathologic and physiological atrophy
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phys=removal of thyroglossal duct
path=lack of use, aging,nutrition |
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what are some of the causes of cell injury
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-hypoxia
-infection -immunologic reactions -genetic causes |
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what is reversible injury
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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 |
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what is the irreversible injury
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necrosis
apoptosis |
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what is necrosis
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-irreversible cell death
-death of material |
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what is apoptosis
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normal cell death
-intracellular programmed -membranes persist |
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what is the difference b/t apop and necrosis
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necrosis has membranes disrupted but apoptosis does not
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what are the differnt types of necrosis
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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 |
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what is the only exception to liquefactive necrosis as in death can occur w.out infection
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CNS
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what are the normal function of apoptosis
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normal= embryogenesis, hormone dependent tumor death
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what are the pathologic factors of apoptosis
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seen following duct obstruction, viral infection, effect of CTL
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what are some sub cellular response regarding apoptosis
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-lysosomal enz
-hypertrophy of SER -change in mitochondria -cytoskeltal change in chediak higashi -inetercellular accumultations |
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what is problem with chediak higashi
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it is problem with the formation of phagolysosome
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what are different types of calcification
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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 |
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what is inflammation
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respons to cell injury
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what is acute inflammation
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-short duration
-sudden onset -edema -neutrophills |
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what are the cardinal signs of inflammation
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-rubor=redness
-calor=heat -tumor=swelling -dolor=pain and -functio lasae |
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what is the difference between signs and symptoms
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sign=measurable, like Bp, fever
symptom=not measurable, what the patient tells us |
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what are some of the vascular mechanisms of inflammation
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-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 - |
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what roles do the chemical mediators play in inflammation
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-short loved
-double edged -tissue/specied sp |
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what are some of the chemical mediators
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-histmaine=mast cells
-serotonin=mast cells -arachiodonic acid=makes -prostaglandins= cause fever -leukotrienes= -platelet activating factor -cytokines -nox -plasma enz |
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what are/roles of plasma enzmes
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-complement systems=mainly C3a and C5a
-kinin=mainly bradykinin involved in heart tissue and vascular permeability -clotting=mainly hagman factor, interacts w/kinin pathway |
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what is chemotaxis
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2 types
1)exogenous=bacteria, 2)endogenous=imp is C3a, and C5a complement compnent, LT(LTB4), and chemokines (IL-8) |
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is there such thing as negative chemotaxis
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no
it is always poistive |
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what are the components of phagocytosis
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-opsonization= on the surfact
-engulfment= covering -degradation |
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what are some of the morphologic patterns of inflammation
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-purulent= pus
-urticaria= hives -cellulits=inflamamtion bt the cells -fibrinous=pours out of the serum and it organizes -fibrinoid=intense red but not fibrous |
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what are some of the outcomes of acute inflammation
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-resolution
-chronic inflamation=grnuloma -abcess=localized infectionm keeps inflammatory material from leaking out -fibrosis |
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what are some of the causes of chronic inflammation
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chronic inflammation=comes after acute due to continued stimulus or poor resolution, interfernce with healing
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how is chronic iflammation caused if their was no acute inflammation
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that would be due to
-intracellular pathogens -large extracellular pathogen like parasites -continued exposure to the inflammatory agent -autoimmune disease |
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what are some of the cells involved with chronic inflammation
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-esosinophills
-lymphocytes -plasma cells -mononuclear cells, including giant epithelioid cells |
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what are some of the factors that are involved in inflammation
(LOOK AT NOTES PG 14) HANDOUT 6 |
IL-4,
-IFN-gamma -MIF -MAf |
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what happens to the number of nuclei in casceous granuloma
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increases all over the cell
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what are some of the examples of caseous granuloma
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-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 |
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what is the difference and similarities between sarcoidosis and TB
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both are very similar in how they present but steroid is good for sarcoidosis treatment but it is bad for TB
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what are some of the non granuloma chronic inflammation
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-hashimoto thyroiditis
-viral hepatitis -chronic polynephritis |
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what happens with hashimoto's thyroiditis
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loss of thyroid function
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whats the first thing that musy happen before inflammation can take place
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tissue injury must take place
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how does tissue injury effect the process of inflammation
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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
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what are the chronic inflammatory lynmphocytes
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-mac
-lymphocytes -plasma cells |
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what are acute inflammatory mediators
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PMN
platelets |
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what does proliferative potential refer to
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repair
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what type of prolifertor potentials are there?
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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) |
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how do cells grow
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they grow via ligand binding, signal transduction, transcriptional factors,and eyclins
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what are some of the growth factors
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epidermal growth factors, vegf, fgf, cytokines, vegf
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what is the extracellular matirx of the cells made of
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it is made off collagen,adhesive glycoproteins, fibronectin, integrin, laminin and proteoglycans
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what are some of the factors involved with wound healing
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-blood clot
-granulation of tissue=scabs -migration of epithelia cells -scar -remodeling |
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what are some of the comlications with wound healig
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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 |
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what are some of the things that influence wound healing
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-nutrition
-gluccocorticoids -infections -foreign body -vascular alteration |
