Term
|
Definition
| Oxygen deprivation, chemical agents, infection agents, immunological reactions, genetic defects, nutritional imbalance, trauma, extreme temperature. |
|
|
Term
| Consequences of cell membrane injury |
|
Definition
| Ionic concentration gradients, osmotic gradient. |
|
|
Term
| Consequences of ATP generation apparatus |
|
Definition
| ATP essential for cellular function |
|
|
Term
| Consequences of injury to protein synthesis |
|
Definition
| Enzymes and cytoskeletal proteins malfunction |
|
|
Term
| Consequences of Genetic apparatus injury |
|
Definition
| synthesis of mRNA to produce proteins |
|
|
Term
|
Definition
| caused by reduced blood flow, resulting in a decrease in O2 delivery to tissues. Artherosclerosis, thrombus |
|
|
Term
| Potential causes of ischemia |
|
Definition
|
|
Term
|
Definition
| deficiency or absence of O2. blood flow may be adequate. caused by: obstruction in lung, inadequate movement of O2 from lung to blood(pneumonia), inadequate O2 transport(Anemia, CO poisoning), inability to use O2 at tissue level(mitochondria). |
|
|
Term
| Consequences of Hypoxia/ Anoxia |
|
Definition
| increased reliznce on glycolysis, decreased ATP synthesis, lower pH. intracellular accumulation of ions and fluids. --> swelling of cell and organelles. |
|
|
Term
| Cause of inadequate movement of o2 from lung to blood |
|
Definition
|
|
Term
| Cause of inadequate transport of O2 |
|
Definition
| Anemia(low hemoglobin levels), CO poisoning. |
|
|
Term
|
Definition
| chemical species w/ a single unpaired electron in an outer orbital. |
|
|
Term
| T/F. Small amounts of ROS can be produced in normal cell respiration |
|
Definition
|
|
Term
|
Definition
| Oxidative degradation of lipids. Causes oxiation of lipids, producing lipid radical. Lose permeability, become rigid, reactive, and nonfunctional |
|
|
Term
|
Definition
| ROS reacts with thymine of nuclear or mitochondrial DNA, causing a break of DNA strand. Causes cell death or malignant transformation of cell. |
|
|
Term
|
Definition
| ROS promotes protein cross-linking, leads to increased rate of enzyme degradation & loss of enzymatic activity. |
|
|
Term
| Enzymes in Antioxidant System |
|
Definition
| Superoxide Dismutase, Glutathione peroxidase, Catalase. also: Vit E, A,C & B-carotene can block ROS formatino or scavenge them. |
|
|
Term
| Mercuric chloride poisoning |
|
Definition
| binds to sulfhydryl groups of various cell membranes directly. |
|
|
Term
|
Definition
| chemicals are converted to biologically toxic metabolites: Carbon tetrachloride (CCl4) converted to toxic free radical Ccl3- in the liver causing membrane phospholipid peroxidation. |
|
|
Term
|
Definition
| Metabolites of this compound are toxic to the liver after taking overdose. |
|
|
Term
| T/F. Exercise-induced muscle hypertrophy is a pathological adaptive change. |
|
Definition
|
|
Term
| T/F. Atrophy implies that cells are dead. |
|
Definition
| False. Atrophy is chrinkage in size secondary to loss of cell substances resulting in smaller organs. |
|
|
Term
|
Definition
| increase in cell size. increased size of organ skeletal muscle with resistance training & uterus during pregnancy. |
|
|
Term
|
Definition
| driven by hormonal changes. proliferation of glandular epithelium of female breast at puberty & during pregnancy. |
|
|
Term
|
Definition
| driven by tissue loss or damage. Resectinof liver tissue: hyperplasia of remaining liver stimulated. proliferation of fonective tissues in injured site. |
|
|
Term
|
Definition
| excess hormonal or growth factor stimulation. excessive proliferation associated with cancer development. |
|
|
Term
|
Definition
| one adulat cell type is replaced by another adult cell type. ex.) columnar epithelium replaced by stratified squamous cells in the upper airways in smokers. --> llose mucous secretion & ciliary clearance. |
|
|
Term
| Subcellular response to injury |
|
Definition
| lysosomal catabolism, induction of SER, mitochondrial adaptation, heat shock protein, abnormal accumulation of substrates. |
|
|
Term
|
Definition
| digestion of ingested materials from external environment through endocytosis. phagocytes, neutrophils, macrophages. |
|
|
Term
|
Definition
| digestion of intracellular organelles. removal of damaged or senescent organelles during cellular remodeling process. common in cells undergoing atrophy induced by nutrient or hormnoal deprivation. |
|
|
Term
| Induction hypertrophy of Smooth ER |
|
Definition
| Liver SER does detoxification of many drugs and chemical agents. Repeated use of barbiturates induce synthesis of mor enzymes and more SER for effective metabolizing drugs. |
|
|
Term
| Mitochondrial alterations |
|
Definition
| Increase in mitochondria number & size in skeletal muscles after endurance training. Decrease in number in muscle atrophy. Giants in liver w/ nutritional deficiency and alcoholic liver disease. |
|
|
Term
|
Definition
| chaperones, protein folding, disaggregation of protein-protein complex, transport of proteins. Induced in MI & neuronal ischemic injury. |
|
|
Term
|
Definition
| Abnormal accumulations of TG in parenchymal cells, often in liver. |
|
|
Term
|
Definition
| Alcohol, toxins, protein malnutrition, obesity. Defects in any step from Free Fatty Acids entry to exit of lipoproteins. |
|
|
Term
| What disease is Steatosis associated with? |
|
Definition
|
|
Term
| Characteristics of Cell death |
|
Definition
| ATP depletion, loss of cell's ability to control borders, loss of volume regulation, increased permeability to extracellular materials, appearances of intracellular enzymes in the systemic circulation: CPK, troponins, alkaline phosphatase. |
|
|
Term
|
Definition
| refers to a sequence of morphological changes that follow cell death inliving tissues. |
|
|
Term
| What are the causes of Necrosis appearance? |
|
Definition
| enzymatic digestion of dead cell by hydrolytic enzymes, denaturation of cellular proteins, 4-12 hours after an irreversible injury. |
|
|
Term
|
Definition
| typically seen in hypoxic environments, preservatino of basic cell structural outline, MI is a good example. |
|
|
Term
|
Definition
| characteristic of bacterial or fungal infections, cell destruction + pus formation, necrosis of brain after hypoxic death shows this pattern |
|
|
Term
|
Definition
| white gross appearance of central necrotic area, common form of necrosis w/ tuberculous infection in the lungs, tissue architecture is completely obliterated. |
|
|
Term
|
Definition
| describes focal area of fat destruction by lipases. Typically occurs after pancreatic injury. |
|
|
Term
| Proper formation of the toes and fingers of a fetus requires what cellular process? |
|
Definition
|
|
Term
| What cell is responsible for inducing apoptosis in virus-infected cels? |
|
Definition
|
|
Term
| What can result from embryonic DNA damage? |
|
Definition
| Birth defects, or to become cancerous. |
|
|
Term
| This protein is the cells response to DNA damage and is a potent inducer of apoptosis |
|
Definition
|
|
Term
| What are some triggers that initiate apoptosis? |
|
Definition
| lack of growth, tumor necrosis factor-a that binds to TNF receptor, FAs ligand, release of granzymes, radiation & free radicals, intrinsic programmed event. |
|
|
Term
| Death receptor adaptor pathway |
|
Definition
| FasL with Fas, recruits FADD, recruits procaspase 8, procaspase 8 is activated by cleavage into smaller subunits, producing caspase 8, activates caspase 3. |
|
|
Term
|
Definition
| Bcl-2 on membrane, activates Bax which punches holes in outer mitochondrial membrane, cytochrome C to leak out, binds Apaf-1, apoptosomes, bind to caspase-9, activates caspase 3 |
|
|
Term
| Granzyme-mediated apoptosis |
|
Definition
| granzyme B activates procaspase 3 to partially active caspase 3, released cytochrome c fully acitivates caspase 3, Caspase 3-mediated cell death. |
|
|
Term
|
Definition
| enzymes that cleave proteins. |
|
|
