Cell Injury Flashcards
exam 1
structural and functional barrier separating the cell’s internal milieu from the external environment
Plasma membrane
compartmentalize the internal environment
intracellular membrane
one of the most important factors in the maintenance of homeostasis; 25% energy expenditure used for this
volume regulation
stress leads to
adaptation
increase in the cell size and functional capacity
hypertrophy
hypertrophy can co-exist with
hyperplasia
hypertrophy leads to an increase in
gene expressions, synthesis of structural components and cell survival and decrease in degradation
tissue with cells in hypertrophy are
not capable of replication
increased workload, hypertension, cardiomyocyte, hypertrophy
pathologic hypertrophy
increased workload, pumping iron, skeletal muscle cell and hypertrophy
physiologic hypertrophy
increase in cell number leading to increase in tissue/organ mass
hyperplasia
tisssue with cells in hyperplasia are
capable of replication
Hyperplasia leads to a proliferation
of differentiated cells and stem cells
rapid growth through cell division in endometrial glands and stroma during the proliferative phase of the mestrual cycle
physiologic hyperplasia
benign prostatic hyperplasia
pathologic hyperplasia
uterus during pregnancy
both hyperplasia and hypertrophy
a reduction in the size of an organ or tissue due to a decrease in cell size
atrophy
atrophy leads to decrease and diminished
workload, metabolic activity and protein synthesis
atrophy leads to an increase in
protein degradation and autophagy
often as an adaptive response in which one adult cell type that is sensitive to a particular stress is replaced by a more resistant adult cell type
metaplasia
metaplasia results because of a reprogramming of
stem cells and undifferentiated mesenchymal cells in the connective tissue
persistent stressful condition may predispose to
malignant transformation
reversible change with the replacement of one differentiated cell type by another
metaplasia
Barrett’s esophagus
metaplasia
disordered growth and maturation of the cellular component a tissue
dysplasia
dysplasia results from a response to due a
persistence of injurious influence
dysplasia results from a _________ _________ in a proliferating cell population
sequential mutation
morphological expression of the disturbance in growth regulation
architectural anarchy
shares many cytological features with cancer but usually regress upon removal of stimulus
dysplasia
example of dysplasia
cervical dysplasia
normal cell with injurious stimulus leads to
cell injury
cell injury that is mild and transient
reversible injury
cell injury that is severe and progressive
irreversible injury
two fates of irreversible injury
- necrosis
2. apoptosis
type, duration, severity of injury
responses
type, state, adaptability of the injured cell
consequence
oxidative pathway and glycolytic pathway can lead to
ATP production and depletion
MPTP and Leakage of cytochrome C
irreversible mitochondrial damage
cell injury occurs as a continuum without sharply define steps
progression of cell injury
decrease oxygen level
hypoxia
decreased oxygen and substrates
ischemia
Progression of ischemic cell injury:
Onset–> reversible—> irreversible—->
reperfusion injury
temporary loss of volume and energy regulation
reversible cell injury
reversible cell injury: ATP \_\_\_\_ ADP\_\_\_\_\_ aerobic pathway \_\_\_\_ anaerobic pathway\_\_\_\_\_ Glycogen stores\_\_\_\_ catabolites \_\_\_\_\_ intracellular pH\_\_\_\_ protein synthesis \_\_\_\_\_
ATP decreases ADP increases aerobic pathway decreases anaerobic pathway increases Glycogen stores decreases catabolites accumulate intracellular pH decreases protein synthesis decreases
vacuolar degeneration where cells stain lighter due to dilution of contents with the influx of water
hydropic change associated with reversible cell injury
irreversible cell injury leads to a _______ of selective permeability and leakage of ______ molecules out of the cell
irreversible cell injury leads to a permanent loss of selective permeability and leakage of large molecules out of the cell
appearance of certain large molecules in the serum is a sure sign that
irreversible cell injury has taken place
nuclear changes is a clear indication of
cell death
example of a reversible to irreversible cell injury
myocardial infarction
what appears to be a critical factor in the point of no return
ATP depletion
ischemia paradox
some cells die after re-establishment of blood flow
degradation of a cell’s own contents, self-eating
autophagy
the process is controlled by a number of autphagy-related genes (ATG) and is a selective process mediated by specific
cargo-receptor proteins
a primary driver of the accumulation of cell damage and aging
failure of autophagy
acid phosphatase (AcP)
Prostate and bone
creatine kinase (CK)
cardiac muscle and striated muscle
Asparate transaminase (AST)
liver and cardiac muscle
MM isoform
striated muscle
lipase
pancreas
amylase
pancreas, ovary, salivary glands
alkaline phosphatase (ALP)
liver, bone, intestine, kidney and placenta
MB isoform
cardiac muscle
alanine transaminase
ALT
lactate dehydrogenase
LDH
CCL4, lipid peroxidation, membrane damage fatty change and necrosis in liver
free radical induced cell injury
what occurs when there is a change in membrane permeability?
leakage of small molecules
in protein metabolism, when it is disrupted and the polysomes dissociates into monosomes what happens
there is a reduction of protein synthesis
is there a time lag behind biochemical changes?
yes
cellular swelling
hydropic
temporal relationship
morphological only becomes apparent until after the biochemical systems
rush of calcium into the mitochondria
irreversible cell injury
reversible change:
changes in volume regulation
influx of sodium leads to swelling of the cell
reversible change:
changes in energy
increase in glycolysis and decrease in pH
reversible change:
effects in protein metabolism
reduction in protein synthesis
reversible change:
morphology
tima lag behind biochemical changes
reversible injury:
light microscopy
cellular swelling- hydropic
reversible injury:
electron microscopy
blebbing of the plasma membrane, blunting of microvilli, loosening of intracellular attachment
irreversible:
changes in volume regulation
permanent membrane damage
irreversible:
alteration in energy metabolsim
influx of calcium
irreversible:
other changes
- unfolded protein response
irreversible:
light microscopy
loss of differential staining and nuclear changes
irreversible:
electron microscopy
calcium crystals