cellular adaptations I and II Flashcards
What are the 3 proliferative capacities of tissues
continuously dividing cells (or labile cells)
stable tissues
permanent tissues
ex of continuously dividing cells/labile cells
hematopoietic cells surface epithelia (upper airway, GI, skin...)
definition of stable tissues
minimal replication usually
proliferate in response to injury
parenchyma of most solid organs like kidney, liver, pancreas
endothelial cells, fibroblasts, smooth muscle
definition of permanent tissues
non-proliferative
ex of permanent tissues
neurons
cardiac muscle cells
define hypertrophy
increase in size of cells, leading to increased organ size
what kinds of cells undergo hypertrophy?
cells that have limited or no capacity to divide
physiologic hypertrophy can occur due to
increased functional demand or hormonal stimuli
ex of physiologic hypertrophy
skeletal muscle hypertrophy in weight lifter
uterus in pregnancy
ex of pathologic hypertrophy
cardiac muscle hypertrophy in HTN
define hyperplasia
increased cell number
in what kind of cells does hyperplasia occur?
those that are able to divide (labile and stable)
ex of physiologic hyperplasia
female breast at puberty, pregnancy
compensatory hyperplasia in liver after partial resection
would healing-connective tissue
pathologic hyperplasia examples
excessive hormones–>endometrial hyperplasia
benign prostatic hyperplasia
skin warts and mucosal lesions associated with viruses (papilloma virus)
what differentiates pathologic hyperplasia from cancer?
pathologic hyperplasia cells respond to normal regulatory mechanisms (it’s just that there is excessive stimulation)
in cancer, abnormal regulation
however, pathologic hyperplasia increases the risk for cancer
enlargement of uterus in pregnancy is ex of
both hyperplasia and hypertrophy
atrophy definition
decrease in size of cell due to loss of cell matter
causes of atrophy include
physiologic and pathologic
ex of physiologic atrophy
endometrium at menopause (loss of hormones)
ex of pathologic atrophy
decreased function (broken arm in cast)
loss of innervation (trauma to nerve)
inadequate nutrition
metaplasia defintion
one adult cell type is replaced by another adult cell type (to better tolerate the stress)
- is an adaptive process to chronic stress (ex. chronic smoking, chronic gastric acid reflux..)
- stem cells differentiate through a new pathway
- may be associated with greater chance of cancer
types of metaplasia
epithelial
mesenchymal
Barrett esophagus is example of
epithelial metaplasia (squamous epithelium turns into glandular epithelium like that in stomach)
causes of cell injury and give examples of each
oxygen deprivation (hypoxia, ischemia) physical agents (trauma, temperature, radiation) chemical agents (chemicals like sodium and glucose, poisons, asbestos) infectious agents immunologic reactions (autoimmune diseases, hypersensitivity) genetic (point mutations, polymorphisms) nutritional imbalance (protein/calories, viatmin and mineral deficiency) aging (lowered ability to repair damage)
Types of cell injury
reversible
irreversible
is swelling of ER and mitochondria, membrane blebs in a cell reversible or irreversible?
reversible
Differences btwn necrosis and apoptosis
cell size: swelling for necrosis, shrinkage for apoptosis
nucleus:
necrosis-pyknosis (condensation of chromatin), karyorrhexis (fragmentation of nucleus), karyolysis (breakdown of nuclear membrane)
apoptosis-fragmentation into nucleosome-size fragments
plasma membrane:
necrosis-disrupted
apoptosis-intact
cellular contents
necrosis-enzymatic digestion and may leak out of cell
apoptosis-intact
adjacent inflammation
necrosis: frequent
apoptosis: none
physiologic or pathologic
necrosis: always pathologic
apoptosis: often physiologic to eliminate unwanted cells but myay be pathologic
reversible cell injury
fatty change-lipid vacuoles in cytoplasm, primarily in cells depending on fat metabolism
cellular swelling-results from failure of membrane pumps to maintain homeostatis so get membrane blebs, vacuoles appear in cells corresponding to distended ER
necrosis morphology
increased eosinohpilia
nuclear shrinkage, fragementation
breakdown of plasma membrane and organelle membranes
coagulative necrosis
due to hypoxic or anoxic injury due to ischemia
persistence of dead cells w/ intact outlines but with loss of cellular details
occurs in all solid organs except brain
liquefactive necrosis
complete digestion of dead cells (tissue is semi-liquid) and no residual tissue architecture preserved
commonly seen with bacterial, fungal infec (WBCs release digestive enzymes, necrotic cells with acute inflammatory cells become pus)
exception: brain infarcts become liquefactive necrosis
caseous necrosis
think TB
resembles cheese (crumbly)
fragmented and coagulated cells, loss of tissue architecture so no cell outlines
usually surrounded by border of inflammatory cells (granuloma)
gangrenous necrosis
not a specific type of necrosis but used for ischemic coagulative necrosis of lower or upper extremity
can be wet or dry gangrene
also used for severe necrosis of other organs
ex of gangrenous necrosis
discoloration of toes in diabetic
gangrenous bowel
fat necrosis
usually seen in pancreas in acute pancreatitis b/c injury to pancreas releases lipase which liquefies fat (fatty acids combine with Ca2+ to make chalky white material)
also in trauma to fatty tissue with release of lipases and triglycerides
ex of fat necrosis
acute pancreatitis
fat necrosis of breast in trauma
fibrinoid necrosis
deposition of immune complexes (antigens and antibodies) in vascular wall
looks like fibrin, pink and fuzzy
occurs in vasculitis syndromes
principal targets within a cell due to injury
mito (depletion of ATP and increased ROS)
calcium homeostatis (intracellular entry of Ca)
cellular membranes (increased permeability, also think lysosome)
DNA and cellular proteins (damage to DNA and protein misfolded)
what results from mitochondrial damage/ATP depletion?
Na pump fxn decreases, get influx of calcium and sodium and water–leads to ER swelling, cellular swelling, loss of microvilli and blebs
increase anaerboic glycolysis leading to decreased pH and clumping of nuclear chromatin
production of ROS
what are the effects of increased intracellular calcium in cell injury?
membrane damage, nuclear damage, decreased ATP
effects of decreased oxygen on cell function?
membrane damage is an example
ischemia vs hypoxia
ischemia is worse because no delivery of substrates for glycolysis and no removal of metabolites by blood flow
specific examples of cell injury
ischemic vs hypoxic injury
reperfusion injury
chemical (toxic) injury-direct toxin or toxic metabolites
death induced by cytotoxic T lymphocytes is an example of what type of cell death
physiologic apoptosis
pathologic apoptosis examples
eliminating cells with DNA damage
cell injury induced by viral infec
accumulation of misfolded proteins
organ atrophy with duct obstruction
morphology of apoptosis
cytoplasmic eosinophilia
chromatin condesation and aggregation, eventually karyorrhexis
cell shrinkage with cytoplasmic blebs and apoptotic bodies
phagocytosis w/o inflammation
how does lipofuscin develop in heart muscle? clinical significance?
results from lipid peroxidation
occurs with aging
especially in heart, liver, brain
how does Lysosomal storage disease occur? significance?
lysosomal dysfxn in breaking down a molecule, so large amts accumulate
anthracosis in lung
carbon from air in lung
accumulation of cytoskeleton abnormalities occurs how?
due to toxins like alcohol or unknown causes
Hemosiderin accumulates how?
occurs locally when there’s been hemorrhage
or systemic deposition with increased iron absorption, in anemias, w/many transfusions, etc.
dystrophic vs metastatic calcification?
dystrophic:
- in damaged or dying tissue
- normal serum calcium
- gross apperance is white gritty deposits
- microscopically looks basophilic
metastatic:
- normal tissues
- hypercalcemia
- commonly in interstitial tissues
cellular aging
dna damage
decreased cellular replication
defective protein homeostasis
