Term
|
Definition
maintenence of the normal physiologic steady state including: 1) normal metabolic fluxes 2) normal variation in living cells 3) in a stress FREE state |
|
|
Term
|
Definition
what happens if a cell cannot adapt to stress? |
|
|
Term
irr-severe and progressive rev-mild, transient |
|
Definition
what is the difference between the precedent of irreversible injury and reversible injury? |
|
|
Term
1) apoptosis 2) necrosis (both result in cell death) |
|
Definition
what are the 2 results of irreversible injury to a cell? |
|
|
Term
|
Definition
reversible functional and structural responsses to more severe physiologic stresses and some pathologic stimuli, during which new but altered steady states are achieved allowing the cell to survive and continue to function |
|
|
Term
1) hypertrophy/hyperplasia 2) atrophy 3) metaplasia 4) intracellular accumulations |
|
Definition
What are the 4 cellular adaptations to stress? |
|
|
Term
|
Definition
increase in the size of a cell(or organ) often due to increased functional requirement, the end result of increased production of cellular proteins(can be physiologic or pathologic) |
|
|
Term
|
Definition
increase in the number of cells in an organ or tissue that takes place if the cell population is capable of dividing |
|
|
Term
1) hormones/growth factors 2) compensatory(increased functional demand-body builder) 3) pathologic/atypical (virus) |
|
Definition
what can stimulate hyperplasia? |
|
|
Term
the uterus during pregnancy |
|
Definition
give an example of hormone induced hypertrophy |
|
|
Term
|
Definition
myocytes hypertrophy ________ly in response to increased load |
|
|
Term
smooth ER in hepatocytes increases to increase cytochrom p450 oxidases to help metabolize the drug
*can affect other drug metabolism, so can be a prob in multi-drug pts |
|
Definition
organelles can hypertrophy, what hypertrophies with barbituate intake? |
|
|
Term
prostatic hyperplasia in response on androgens -> weak stream, urinary retention, bladder infxn |
|
Definition
give an example of pathologic hyperplasia in a male |
|
|
Term
|
Definition
decrease in the size(and function) of a cell or organ |
|
|
Term
1)reduced functional demand(disuse) 2)inadequate supply of O2(hypoxia) 3)inadequate nutrition(protein-calorie deficiency aka marasmus) 4)interruption of trophic signals(denervation) 5) persistent cell injury(radiation) 6) physiologic(ex: notochord, thyroglossal duct) 7)pressure 8) loss of endocrine stimulation |
|
Definition
what are the causes of atrophy? |
|
|
Term
the most metabolically active part: the coretex |
|
Definition
what part of the kidney atrophies primarily when the renal artery is atherosclerotic? |
|
|
Term
|
Definition
conversion of one cell type to another, often due to repetitive injury |
|
|
Term
replacement of glandular epithelium by squamous epithelium |
|
Definition
most common type of metaplasia |
|
|
Term
metaplasia->dysplasia OR neoplasia (meta comes first) |
|
Definition
put these in order: neoplasia, dysplasia, metaplasia |
|
|
Term
|
Definition
is metaplasia reversible? |
|
|
Term
esophageal-stomach GEJ(squam->columnar larynx-trachea(columnar-> squam) stones in ducts vitamin A deficiency-retinoic acid(squamous metaplasia in resp.) |
|
Definition
list some common sites for metaplasia |
|
|
Term
Reprogramming of: A) stem cells existing in normal tissues B) undifferentiated mesenchymal cells present in CT |
|
Definition
list the mechanisms for metaplasia |
|
|
Term
|
Definition
what is the most common epithelial metaplasia? |
|
|
Term
transformation of esophageal squamous epithelium to intestinal-like columnar cells due to refluxed gastric acid
-get goblet cells etc, and HIGH risk of cancer esp adeno(glandular) carcinomas |
|
Definition
What is Barret esophagus? |
|
|
Term
formation of cartilage, bone, or adipose tissue(mesenchymal tissues) in tissues that do not normally contain these elements
ex: myositis ossificans-bone formation in muscle can occur after intramusc. hemhorrage |
|
Definition
|
|
Term
REVERSIBLE: 1) decreased cell function IRREVERSIBLE: 2) biochemical alterations->cell death 3) ultrastructural changes 4) light microscopic changes 5) gross morphologic changes |
|
Definition
list the order of events that occur with prolonged cell injury |
|
|
Term
1) generalized swelling of cell & organelles 2) blebbing of plasma membrane 3) ribosome detachment from ER 4) clumping of nuc. chromatin 5) lipid vacuoles in cytoplasm |
|
Definition
list the morphologic changes in REVERSIBLE cell injury: |
|
|
Term
the PM is disrupted and the cell starts leaking contents |
|
Definition
In terms of morphologic changes resulting from cell injury, how do you know when a cell is screwed? |
|
|
Term
1) cellular swelling aka "hydropic change" or vaculolar degeneration 2) fatty change |
|
Definition
list changes that can be seen under the light microscope due to cell injury |
|
|
Term
|
Definition
|
|
Term
1) inability to reverse mito dysfxn(opening of mito permeability transition pore) 2) profound disturbance of PM + influx of Ca++ ions 3) rupture of cytoplasmic lysosomes 4) rupture of PM |
|
Definition
what do you see when there is irreversible injury secondary to ischemia? (not too important apparently) |
|
|
Term
|
Definition
which is ALWAYS pathologic: necrosis or apoptosis? |
|
|
Term
ATP1) many effects MITO2) leakage of pro-apoptotic proteins CA++3) increased mito permeability & activation of many cellular enzymes ROS4) damage to lipids, proteins, DNA PM 5) loss of cellular components LysoM5) enzymatic digestion of cell components 6) activation of pro-apoptotic proteins |
|
Definition
how does the cell respond to each of the following: 1) decreased ATP 2) mito damage 3) entry of Ca++ 4) increased ROS 5) membrane damage 6) protein misfolding & DNA damage |
|
|
Term
Mitochondria involvement (necrosis cant make ATP, apoptosis cytochrome C) |
|
Definition
apoptosis and necrosis have different pathways of cell response, but what do they have in common? |
|
|
Term
|
Definition
Irreversible cell injury causes ______ |
|
|
Term
|
Definition
cell death due to an injury |
|
|
Term
1)coagulative 2)liquefactive 3)fat 4)caseous 5) gangrenous (6)the book incluedes fibrinoid necrosis |
|
Definition
list the 5 types of necrosis |
|
|
Term
1) reduced blood flow(ischemia) 2) inadequate oxygenation of blood due to cardio-resp. failure 3) decreased O2 carrying capacity of blood (like anemia or CO poisoning) 4) severe blood loss |
|
Definition
list some causes of O2 deprivation |
|
|
Term
1) cell and organelle swelling and rupture 2) denaturation of cytoplasmic proteins |
|
Definition
list the ultrastructural changes associated with coagulative necrosis |
|
|
Term
|
Definition
in what type of necrosis is the architecture of the dead tissues preserved(at least for a few days)? |
|
|
Term
1)pyknosis 2)hypereosinophilia 3)karyorrhexis 4)karyolysis |
|
Definition
describe the microscopic changes in the cytoplasm and nucleus of cells underoing coagulative necrosis |
|
|
Term
|
Definition
|
|
Term
fragmentation of the nucleus |
|
Definition
|
|
Term
disintigration of the nucleus |
|
Definition
|
|
Term
1) necrosis causes enlarged cells(swelling, while apoptosis causes reduced cell size(shrinkage) 2) in necrosis the nucleus goes from pyknosis->karyorrhexis->karyolysis, in apoptosis the nucleus fragments into nucelosome size fragments 3)in necrosis the PM is disrupted, it is intact in apoptosis, but has altered structure, esp. in lipid orientation 4)n necrosis there is enzymatic digestion of cellular contents and they may leak out of the cell, in apoptosis, the cell is intact so the contents may be released in apoptitic bodies 5) adjacent inflammation is frequent with necrosis, and doesn't happen with apoptosis 6) necrosis is a culmanation of irreversible cell injury and is therefore invariably pathologic, apoptosis is often physiologic and a means of eliminating unwanted cells, may be pathologic after some forms of injury esp. DNA damage |
|
Definition
describe the difference in cell changes between necrosis and apoptosis in terms of 1)cell size 2)nucleus 3)PM 4)cellular contents 5)adjacent inflammation 6)physiologic/pathologic role |
|
|
Term
1) irreversible injury and death 2) loss of the PM's ability to maintain the ion gradient in the cell 3) influx of Ca++ 4) degradation of cellular RNA 5) precipitation of cellular proteins in situ(dead stuff stays in place, not carried off) |
|
Definition
describe the pathogenesis of coagulative necrosis |
|
|
Term
|
Definition
localized area of coagulative necrosis |
|
|
Term
|
Definition
ischemia caused by obstruction of a vessel causes coagulative necrosis in all organs EXCEPT ____ |
|
|
Term
|
Definition
type of necrosis characterized by dissolution of necrotics cells and removal rather than scar formation |
|
|
Term
-usu in an abcess secondary to bacterial, or fungal infection -inflammatory dissolution of tissue -also common with cerebral infarcts |
|
Definition
when does liquefactive necrosis occur? |
|
|
Term
|
Definition
type of necrosis specific to adipose tissue with triglycerides where there are focal areas of adipose destruction |
|
|
Term
with destruction of fat via enzymes(lipase) fatty acids precipitate as calcium salts, leading to chalky white deposits in tisue |
|
Definition
what is the pathogenesis of fat necrosis? |
|
|
Term
it becomes amorphous basillic/purple deposits at the periphery of necrotic adipocytes |
|
Definition
what happens microscopically to tissue that has undergone fat necrosis? |
|
|
Term
acute pancreatitis pt's, pancreatic lipases split trig's in fat cells, and the released FA's combine with Ca++ |
|
Definition
what is a common example of fat necrosis? |
|
|
Term
casseous necrosis(cheese-like) |
|
Definition
a type of necrosis in which the dead tissue persists indefintitely as amorphous, coarsely granular debris
-cells don't retain cellular outline, and do not dissepear by lysis |
|
|
Term
TB, and some fungal infxns |
|
Definition
what disease typically results in caseous necrosis? |
|
|
Term
you have a granuloma with necrosis in the middle and you see **MULTI-NUCLEATE GIANT CELLS** |
|
Definition
how can you ID TB caseous necrosis? |
|
|
Term
coagulative + liquefactive necrosis = gangrenous necrosis |
|
Definition
cell death involving an entire region(rather than an organ) resulting from loss of blood supply combined with infection |
|
|
Term
|
Definition
what does ischemia do to ATP? |
|
|
Term
1)mito damage 2)ca++ influx, lost of ca++ homeostasis 3)accumulation of ROS 4)defective membrane permeability 5)damage to DNA and proteins |
|
Definition
list some mech of cell injury besides depletion of ATP |
|
|
Term
|
Definition
a unique mechanism of cell death which occurs normally during embryogeneis and throughout adulthood: a tightly regulated suicide program, but can also be pathologic when dieseased cells are irreversibly injured |
|
|
Term
|
Definition
apoptosis causes inflammatory cells, T or F |
|
|
Term
1) embryogenesis 2)involution of hormone dep tissue upon hormone withdrawl, ex: menstruation 3)cell loss in proliferating populations(to maintain homeo) ex: epithelial cells in intestinal crypts 4) elimination of self-reactive lymphocytes(t cells) 5) death of inflammatory cells at end of immune response |
|
Definition
list some apoptosis in physiologic situations |
|
|
Term
1) to eliminate cells damaged beyond repair without eliciting a host rxn(damage to surroundings) 2)when DNA is damaged 3)accumulation of misfolded proteins 4)cell death in viral infxn, transplant rejection 5)pathologic atrophy after duct obstruction(like salivary glands) |
|
Definition
list some pathologic causes of apoptosis |
|
|
Term
|
Definition
|
|
Term
extrinsic: PM receptor intrinsic: mitochondrial |
|
Definition
what are the intrinsic and extrinsic initiators of apoptosis? |
|
|
Term
|
Definition
list the apoptosis "death receptors" |
|
|
Term
1)fat - fatty liver(steatosis) 2)glycogen - glycogen storage disesases 3)complex lipids -lysosomal lipid storage disorders 4)iron - iron overload, hemachromatosis 5)lipofuscin - undigested material from autophagy(wear and teat pigment) 6)melanin - epidermal pigmentation 7)exogenous pigments -anthracosis (carbon in lung/lymph nodes) |
|
Definition
list the causes/type of intracellular accumulations and examples |
|
|
Term
rare, and autosomal recessive |
|
Definition
glycogen storage diseases are --- |
|
|
Term
|
Definition
abnormal accumulation of triglycerides within parynchemal cells often seen in liver, but can see in heart, muscle, kidney |
|
|
Term
alcoholic abuse, and non-alcoholic fatty liver disease(assoc. with obesity & diabetes)
in developing = kwashiorkor and severe GI malabsorbtion |
|
Definition
what are the major causes of significant fatty change in the liver in developed nations? in developing? |
|
|
Term
|
Definition
|
|
Term
zone 1: around arteries, most O2 zone 2: in between zone 3: around veins, least O2 |
|
Definition
describe the "zones" in the liver and which is more oxygenated |
|
|
Term
AUTOSOMAL RECESSIVE: type A & B due to bad sphingomyelinase -> poor cholesterol transport, and neuro damage in brain |
|
Definition
what is Niemann-pick disease? |
|
|
Term
glucocerebrosidase deficiency, = AUTOSMAL RECESSIVE, lipid/glycogen builds up in liver, spleen, bone marrow |
|
Definition
what is Gaucher's disease? |
|
|
Term
|
Definition
a genetic disorder, but also caused by too much iron supplements, hemolysis of blood cells(thallasemia/sickle cell), or transfusions where too much iron builds up in the body |
|
|
Term
|
Definition
deposition of calcium salts in injured or necrotic tissues in the setting of NORMAL calcium levels |
|
|
Term
|
Definition
calcification with atherosclerosis of arteries is an example of what kind of calcificaiton? |
|
|
Term
|
Definition
precipitation of mineral salts from solution and crystallization around foci of organic material |
|
|
Term
|
Definition
deposition of calcium in NORMAL tissues in setting of HYPERCALCEMIA |
|
|
Term
1) high PTH due to parathyroid hyperplasia/tumor/ectopic pdxn by malignancy 2) bone destruction 3) vitamin D disorders 4) renal failure(secondary hyperparathyroidism) |
|
Definition
list the 4 primary causes of hyper calcemia |
|
|
Term
1)accumulation of senescent cells(non-dividing) and depletion of stem cells 2) progressive cell injury with accumulation of metabolic and genetic damage 3)oxidative damage from ROS 4)DNA damage |
|
Definition
list the known contributors to cell aging |
|
|
Term
DNA replication in somatic cells |
|
Definition
what results in the gradual shortening of telomeres |
|
|
Term
TTAGGG repeats at chromosomal ends |
|
Definition
|
|
Term
|
Definition
what pigment accumulates with cell aging? |
|
|