Cell Injury 1 Flashcards
pathology
the nature, cause and development of diseases
study of pathology requires
tissue/biopsy to see cellular changes
homeostasis
maintenance of constant cellular environment. Volume regulation is critical, 25% of energy is needed to regulate. Plasma membrane is critical.
cellular adaptations
attempt to reach new steady state. can cause injury if unable to adapt.
reversible changes (5)
hypertrophy, hyperplasia, atrophy, metaplasia, dysplasia
hypertrophy
increase in cell size/max function. cells unable to replicate. Caused by increased demand or growth hormone. increased gene expression, survival
hyperplasia
increase in cell number/tissue. cells able to proliferate. does increase tissue size.
atrophy
reduction in cell size, ultimately reduction in tissue/organ size. Longterm, decreased number of cells. “disuse, denervation, ischemia”
metaplasia
cell type replacement, response to repeat stress. can become malignant.
dysplasia
disordered cell growth/maturation. Can improve if stimulus is removed.
what reversible changes often occur together, and what can they both be?
hyperplasia and hypertrophy, pathological or physiologic
example of hypertrophy
hypertension/myocyte or muscle cell from exercise, myometrial smooth muscle during pregnancy, cardiac mycoses
example of hyperplasia
prostatic hyperplasia, endometrial glands
examples of atrophy
muscle tissues, decreased blood supply, aging, hormone changes
examples of metaplasia
barettes esophagus, smoking squamous cell epithelium in smoking
example of dysplasia
cervical dysplasia
ischemic vs hypoxic injury
hypoxic- decreased o2 level, ischemia- decreased o2 level and decreased substrate levels (low oxygen IN THE BLOOD)
reversible cell injury- volume
temporary loss of control, swelling, leakage of small molecules, influx of h20/ions
reversible cell injury- energy
alterations in metabolism, decreased aerobic
reversible cell injury- morphology
ER dilation, condensed mitochondria, plasma blebbing
irreversible cell injury- volume
permanent loss of permeability, large molecule leakage
irreversible cell injury- morphology
cytoplasmic staining, pyknosis, karyolysis, karyohexis, mitochondria gets granules, swells and ruptures
irreversible cell injury- energy
uncoupled phosphoralative oxidation. increased glycogen, decreased PH, mitochondria issues
mechanisms of injury (5)
aerobic respiration, mitochondria, systolic calcium levels, ROS, cell membrane, protein synthesis, genetic apparatus integrity
ischemia/re perfusion paradox
some cells die after reestablished blood flow> new processes, new free radicals, calcium availability, leukocytes cause damage
autophagy
self devouring of certain cellular contents, controlled by ATG genes.
all diseases can be traced to
changes in normal cells
causes of cell injury
oxygen deprivation, physical agent, infection, immunologic reactions, genetic derangement, nutritional imbalance
domino effect
compromising one intracellular system leads to damage in the others
what comes first, biochemical or morphological changes?
biochemical!
aerobic respiration and cell injury
low ATP/ glyclytic depletion leads to loss of energy, can’t maintain volume regulation
mitochondria damage and cell injury
MPTP pore stays open, city c leaks, triggers apoptosis
calcium homeostasis and cell injury
enzyme activation can lead to protease activation and cell damage
oxygen derived free radicals and cell injury
imbalance of generation vs scavanging> tissue and cell damage
pyknosis
nucleus shrivels
karyolysis
punctured nucleus> halo
karyorrhexis
nucleus fragmented
autophagy process
phagopore> autophagosome, fuse with lysosome. Degrade and reuse cellular materials
