Cell Injury, Death, and Adaptations Flashcards
Cell and Tissue Adaptations
Hyperplasia
Hypertrophy
Atrophy
Metaplasia
Adaptations are instigated by…
Growth factors, hormones, or cytokines
general examples of cell adaptation response
interacting with receptors at cell surfaces, inducing signaling pathways inside the cell, modify transcription of structural and functional proteins, cause division
hypertrophy
increase in the size of cells leading to increase in size of tissue or organ due to increased synthesis of cellular components
difference between hyperplasia and hypertrophy
hypertrophy in contrast With hyperplasia does not require a cell population to be capable of cell division but it can occur in fully mature- non dividing cells
Hyperplasia
this is an increase in number of cells and increases volume of the organ or tissue
it is ONLY in cell population capable of division
It can be physiologic or pathologic
hypertrophy of hepatocytes is what type
physiologic hypertrophy
hypertrophy of hepatocytes
due to increased endoplasmic reticulum in response to the functional demand for metabolism of ingested drugs such as phenobarbital
muscel hypertrophy is what type
physiologic hypertrophy
muscle hypertrophy
induced by ‘pumping iron’
increased size of individual skeletal muscle fibers is due to increased numbers of actin and myosin fibers and cellular organelles necessary to support increased function, most importantly mitochondria
myostatin
molecule related to TGF-beta family of growth factors- inhibiot of muscle growth
born without it- you have hypertrophy of muscle at a young age without any muscle training
stimulus for muscle hypertrophy
mechanical stretch that cell membrane transducers convert to the appropriate protein transcription signals
pathologic hypertrophy
happens in response to abnormally increased peripheral vascular resistance - like hypertension and signal transduction pathways lead to increased synthesis of functional proteins and growth factors and agents that affect peripheral vessel tone and caliber (maybe even kidney function)
cardiac muscle hypertrophy is an example of what type of hypertrophy
pathiologic hypertrophy
hyperplasia
increase in number of cells and increase in the volume of the organ or tissue
CAN ONLY BE INITIATED WHERE THERE IS A CELL POPULATION CAPABLE OF DIVISION AND PROLIFERATION. can be pathogenic or physiologic
lactating breast is an example of..
physiologic hyperplasia
lactating breast
physiologic hyperplasia- with increase in cell number and size of the breasts lobules in lactation due to stimulation from estrogen and the pituitary hormone prolactin - hormonal hyperplasia
post-hepactomy regeneration
type of physiologic hyperplasia
restoration of the volume of the liver following partial hepactomy for injury or organ donation (compensatory hypertrophy) the stimulus for this regeneration is growth factor production by the residual hepatocytes
follicular hyperplasia of lymph nodes
type of patholigic hyperplasia
could happen in neck in response to an oral infection or dental abscess
exposure to the antigens of the infectious agent leads to B-cell proliferation in the follicles of the regional lymph node
benign prostatic hyperplasia
pathologic hyperplasia
common disorder in men over 50- when testosterone metabolite (DHT) induces nodular enlargement of the gland
impinges on prostatic urethra and causes urinary distention
squamous hyperplasia
pathologic hyperplasia
response to chronic irritation, like ill-fitting denture
area of mucosa may become thickened to compensate for repeated loss of surface epithelial cells
molecular mediator is the TGF-alpha
when does proliferation end in both hyperplasia and hypertrophy
when the stimulus that induced it is removed
if failure to do this it could become neoplastic (autonomous)
T/F hyperplasia can often occur with hypertrophy
T - uterus and breasts in pregnancy and lactation is both hyperplasia and hypertrophic
atrophy
shrinkage of a tissue due to loss of cell size or number
it can be pathologic or physiologic
what drives atrophy?
imbalance between protein synthesis and protein degradation
pathway responsible for accelerating proteolysis in atrophy?
ubiquitin-proteasome pathway
ubiquitin-proteasome pathway
targeted proteins are conjugated with ubiquitin which chaperones the protein into a cytoplasmic organelle called proteasome where it is degraded
autophagic vacuoles and what process is called
atrophic cells that exhibit numerous lysosomes that contain fragments of cell components such as mitochondria or endoplasmic reticulum - process is called autophagy
residual bodies
atrophic cells accumulation of chrunken lysosomes that contain lipofuschin, which is the residue of hydrolytic enzyme digestion
brown atrophy and example
from residual bodies - confer brown color on atrophic organs
on heart of patient with dying illness or cachecia (chronic illness and wasting of body)
atrophy of disuse
something being in a cast - not using is so muscle being immobilized or OSTEOPOROSIS IN ASTRONAUTS that is induced by prolonged weightlessness during space flight
denervation atrophy
interruption of the peripheral nerve supply to muscle due to trauma or disease that results in rapid atrophy and loss of denervated muscle fibers
causes of cell injury and necrosis
oxygen deprivation physical agents chemical agents and drugs infectious agents immunological reactions genetic derangement's nutritional imbalances
most common epithelial metaplasia?
conversion of columnar to a squamous phenotype due to chronic irritation
prime example is smoking - metaplasia of the lower respiratory tract
barrett’s esophagus
more susceptible squamous mucosa in lower esophagus by a more acid -resistant gastric or intestinal columnar mucosa in response to persistant acid reflux from the stomach
adenocarcinoma
caused from barretts esophagus - squamous to columnar and this is a malignant tumor formed from glandular structures in epithelium
reversible injury
cellular swelling
fatty change
cellular swelling
a type of reversible injury
alterations in the plasma membrane energy-dependent ion pump
the cell cytoplasm and endoplasmic reticulum is distended (by water) but cell membranes are in tact
considered a hydrophic change
hydrophic change associated with?
cellular swelling
fatty change
a type of reversible injury
hypoxic or toxic environments - mainly in the liver
associated with obesity, diabetes, and alcoholism
excessive stress in the fat metabolism system
TRIGLYCERIDE ACCUMULATION IN SMALL AND LARGE VACUOLES IN HEPATOCYTES
mallory body
hyaline - associated with the fatty deposits and change within the liver
karyolysis
fading due to compelte absence of the nucleus in necrosis
karyorrhexis
nuclear fragmentation of cells that are necrotic
myelin bodies
whorled aggregations and distruptions/ fragmentations of cell membranes in necrotic cells - at the ultrastructural level and looking at a light microscope will give you indication as to what could have been the nectrotic factor
coagulative necrosis
likely due to a ischemic injury or myocardial infarct
ghost outlines of cells are preserved due to calcium infusion and early denaturation of structural proteins and enzymes - like lysosomal enzymes
CYTOPLASM WITH INCREASED EOSINOPHILIA DUE TO LOSS OF RNA AND FIBRILS AND CROSS STRIATIONS CANNOT BE APPRECIATED
example - gangrenous necrosis - ischemic necrosis
gangrenous necrosis
ischemic necrosis - black discoloration
liquefactive necrosis
no ghost outlines because the dead cells have been hydrolyzed by lysosomal enzymes that were ruptured
viscous liquid and later a cavity
typically due to a bacteria infection and also infarct in the CNS
caseous necrosis
aka ‘cheesy necrosis’
describes the gross appearance of necrosis seen in tuberculosis
fat necrosis
faintly outlined necrotic cells produced by action of enzymes in pancreas and tissues, MAINLY FAT.
release of FA–> early formation of chalky calcium deposits (soaps)
calcium deposits likely to form in multiple types of necrosis
the two apoptosis pathways
extrinsic- use of cell membrane receptor (death receptor initiated)
intrinsic - use of the mitochondrial pathway
apoptosis is accomplished through activation of what enzymes?
caspases
caspases
initial mechanism of apoptosis*
denature cytoplasmic proteins and fragments of the cytoskeleton of both cytoplasm and nucleus
ACTIVATE DNAases - systematically digest DNA into smaller fragments of uniform size
extrinsic apoptosis uses
ligand and receptor interactions
TNF-1 and FAS –> trigger the adapter proteins –> FADD–>pro caspase -8 –> caspase cascade initiated
intrinsic apoptosis uses
removal of growth hormones and factors –> mitochondrial anti apoptopic BCL-x and BCL -2 –> BAX and BAC –> cytochrome c–> increase membrane permeability –> bind to apf-1–> caspase -9 and caspase cascade
caspase 9
intrinisic apoptosis mechanism
caspase 8
activated in the extrinsic apoptosis mechanism
causes of apoptosis
either adaptive or physiologic
pathologic
