Cellular Response to Stress and Toxic Insults Flashcards
Atrophy:
A reduction in the size of an organ or tissue due to a decrease in cell size and number.
Mechanisms of atrophy:
Shrinkage of cells due to increased catabolism of cell organelles, decreased protein synthesis and increased protein degradation in cells.
Brown atrophy:
Undigested lipids are stored as residual bodies (lipofuscin granules) when present in sufficient amount impart brown coloration to the tissue.
Hypertrophy:
An increase in the SIZE of cells.
Hyperplasia:
Increased cell numbers in response to hormones and other growth factors.
- Occurs in tissues whose cells can divide or contain abundant tissue stem cells.
Metaplasia:
Transformation or replacement of one adult cell type to another adult cell type.
Cell injury:
When cells are stressed so severely that they are no longer able to adapt or when cells are exposed to inherently damaging agents or suffer from intrinsic abnormalities.
Karyolysis:
Fading of basophilic chromatin of the nucleus.
Pyknosis:
Nuclear shrinkage and increased basophilia.
Karyorrhexis:
Break-up and fragmentation of the nucleus. Eventually totally disappears over 2-3 days.
Coagulative necrosis:
Preserves basic outline of the coagulated cell due to denaturation of proteins by acidosis, anucleated.
- Usually occurs in conditions of ischemia.
Liquefactive necrosis:
Digestion of tissue by hydrolytic enzymes causing it to be completely liquefied.
- Occurs with abscess and fungi of any organ.
- Ischemic brain infarction.
Enzymatic fat necrosis:
Activated pancreatic enzymes (lipase) during pancreatitis leak out of acinar cells and liquefy the membranes of fat cells in the peritoneum.
Fibrinoid necrosis:
Usually seen in immune reaction involving blood vessels. Complexes of antigens and antibodies are deposited in the walls of arteries.
Caseous necrosis:
Composed of fragmented or lysed cells and amorphous granular debris enclosed within distinctive inflammatory debris; surrounded by granulomatous inflammation.
- No cell outline.
Gangrenous necrosis:
Usually applied to a limb that has lost its blood supply and has undergone coagulative necrosis involving multiple tissue layers.
- Coagulative necrosis superimposed with bacterial infection causing liquefactive necrosis.
Apoptosis:
Cell suicide.
Morphological features of apoptosis (4):
- Cell shrinkage.
- Chromatin condensation.
- Formation of cytoplasmic blebs and apoptotic bodies.
- Phagocytosis of apoptotic cells or cell bodies.
Two pathways of caspases activation:
- Mitochondrial (intrinsic).
2. Death receptor pathways (extrinsic).
Free radicals:
Chemical species with a single unpaired electron in an outer orbital.
Superoxide dismutases:
SOD
- Responsible for the decay of superoxide.
Catalyzes breakdown of H2O2:
Glutathione peroxidases (GSH).
Catalase:
Catalyzes the decomposition of hydrogen peroxide.
Most common cause of acute cell injury underlying human disease:
Ischemia.
Reperfusion injury:
Ischemia - The restoration of blood flow to ischemic but viable tissues results in the death of cells that are not otherwise irreversibly injured.
Dystrophic calcification:
- Normal serum calcium.
- Dead and dying tissues.
Metastatic calcification:
- Elevated serum calcium in blood.
- Calcification in normal tissues.
Fatty changes:
Any abnormal accumulation of triglycerides within parenchymal cells.
- Most often seen in the liver.
Most common cause of fatty change in developed nations:
Alcoholism.
Endogenous pigment:
Lipofuscin
- Wear and tear pigment.
- Insoluble brownish-yellow granular intracellular material that accumulates in a variety of tissues as a function of age or atrophy.
