Card Set Information
Covers cell injury, cell death and cell adaptations
List 5 biochemical themes in cell injury
ATP depletion, generation of ROS, loss of Ca homeostasis, altered plasma membrane permeability, mitochondrial damage
Hypoxia causes what type of morphogenic change? Why?
Hypoxia impairs oxidative phosph. leading to decreased ATP. Lack of ATP causes a disruption in homeostasis and a net gain of solute causing the cell to swell.
Isoosmotic gain of water has what effect on organelles?
mitochondrial swelling, dilation of the ER causing decreased protein synthesis and increased lipid deposition
How does hypoxia effect cellular metabolism?
decreased ox. phosph. and increased glycolysis. increased glycolysis decreases intracellular pH leading to chromatin clumping
what effect does hypoglycemia produce on cells?
lack of ATP production bc no substrate to use for energy (loss of homeostasis)
list 3 types of ROS
), Hydrogen peroxide, hydroxyl radicals
how is superoxide inactivated?
superoxide is inactivated by superoxide dismutase to form hydrogen peroxide
how is hydrogen peroxide metabolized?
detoxified by glutathione peroxidase and catalase
how are hydroxl radicals generated?
by hydrolysis of water by ionizing radiation or by transitional metals Fe or Cu
how do ROS damage cells?
lipid peroxidation, protein cross-linking, thymidine and guanine single strand DNA breaks
what intracellular antioxidant systems exist?
Superoxide dismutase (O
), catalase (H
), glutathione peroxidase (H
what extracellular antioxidant systems exist?
vitamins A, C, E
what type of cell injury occurs by increased cytoplasmic Ca?
high Ca levels will activate various degradative enzymes
list 4 degradative enzymes activated by high Ca levels
phospholipases, proteases, endonucleases, ATPase
list 3 outcomes of cellular injury
reversible cell injury, adaptation, cell death
what is the single biochemical event influencing cell death
there is no single biochemical event that equates with cell death
what morphologic changes occur during necrosis?
cell swelling, protein denaturation, organelle breakdown, inflammation, nuclei changes (karyolysis, pyknosis, karyorrhexis, or total loss)
Describe Coagulative Necrosis
most common form of necrosis, cytoplasmic proteins are coagulated, nucleus is lost
Describe Liquefactive necrosis
has lots of pus (purulence) and the tissue is totally digested by release of lysosomal enzymes during acute inflammatory response
describe caseous necrosis
associated with M. tuberculosis infection. loss of tissue architecture and amorphous pink granular material
describe fat necrosis
dead adipocytes give a "soap bubble" histological appearance, common in breast trauma or pancreatitis
describe 4 morphologic features of apoptosis
cell shrinkage, chromatin condensation/fragmentation, apoptotic bodies formation, phagocytosis without inflammatory response
what are 5 ways a cell can be signaled to start apoptosis
intrinsic, Fas Ligand-receptor binding, removal of trophic signals, ROS/radiation/toxins, cytotoxic T cells
what is the function of the Bcl-2 gene family?
regulation of permeability of the mitochondrial membrane
how do the Bcl-2 and Bcl-x genes affect apoptosis?
how do the bax and bak genes affect apoptosis?
what effect does cytochrome-c have?
it is released from outer mt membrane and disrupts inhibitory function of Bcl-2, in other words it stimulates apoptosis
what effect do caspases have on the cell? what substrates does it have?
apoptosis, substrates include cytoskeletal and nuclear matrix proteins, DNase and transcription proteins
what are the differences between apoptosis and necrosis in terms of stimuli?
apoptosis: physiologic and pathologic; necrosis: hypoxia and toxins
what are the differences between apoptosis and necrosis in terms of cellular morphology
apoptosis: single cells, shrinkage; necrosis: multiple cells, swelling
what are the differences between apoptosis and necrosis in terms of ATP
apoptosis: ATP dependent; necrosis: ATP independent
list 4 cellular adaptations
cell size (atrophy vs hypertrophy), cell number (hyperplasia), cell differentiation (metaplasia), intracellular accumulations
what are two etiologies of hypertrophy?
response to trophic signals, response to increased functional demand
list 2 examples of abnormal hormone stimulation
anabolic steroids: hypertrophy; overproduction of TSH due to iodine deficiency and induces thyroid follicle hypertrophy (goiter)
define barrett's esophagitis and explain what type of cellular adaptation it displays
normal stratified squamous epithelium of esophagus replaced due to prolonged exposure to gastric reflux---metaplasia
list 4 mechanisms of intracellular accumulations
abnormal metabolism, lack of an enzyme, abnormal protein folding/transport, ingestion of indigestibile material
fatty liver; abnormal accumulation of triglycerides within parenchymal cells of the liver, heart, kidney and skeletal muscle
list 6 etiologies of steatosis
obesity, diabetes, alcohol, anorexia, toxins, protein malnutrition
xanthoma is a result from what?
atheromas of atherosclerosis in vessels are caused by what?
cholesterol accumulation in macrophages
list 3 results from abnormal protein accumulation
a1-anti-trypsin deficiency (impaired folding), mallory bodies (impaired secretion), neurofibrillary tangles in Alzheimer's (accumulation of microtubule-associated proteins)
what is Lipofuscin
endogenous brown-yellow pigment, lipoprotein complex due to ROS peroxidation of membranes
what is hemosiderin
yellow-brown pigment due to aggregates of ferritin micelles from excess iron. can lead to hemosiderosis
genetic disease associated with cell death due to uncompensated hemosiderin accumulation
what is bilirubin
end product of heme metabolism that accumulates in hepatocytes and bile ducts due to hemolysis, obstructed bile flow and/or hepatocellular disease