Path 1: Cell injury
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36 terms
Terms | Definitions |
|---|---|
 Four aspects of a disease process | Etiology (cause), pathogenesis (mechanism), morphology (appearance), functional consequences (clinical significance) |
| Mechanisms by which a cell achieves homeostasis (protect cell integrity) | cell membrane, phagocytosis, excretion of exogenous chemicals, host defense mechanisms, systems of repair |
| Mechanisms of cell injury (pathogenesis) | Most vulnerable -> maintenance of integrity of cell membrane, aerobic respiration (with ATP production), synthesis of structural proteins and enzymes, preservation of the genetic apparatus -> most susceptible cells are the most metabolically active |
| Causes of cell injury (etiology) | physical, metabolic, chemical, immunologic, genetic, biologic (microbes) |
| Cell injury (outcomes) | temporary alteration of cell function followed by complete recovery by normal homeostatic mechanisms OR structural damage causes permanent impairment of function OR DNA damage with mutation and its consequences |
| Point of no return leading to cell death | permanent mitochondrial damage or rupture of large cell membrane blebs |
| SER | target of indirectly toxic substances -> suffer metabolic activation by target cell -> ex. CCl4 converted to CCl3 free radical |
| Lysosomes | when this is damaged, cell degeneration occurs -> may produce: increased or incomplete autophagy, hereditary absence of an enzyme in primary lysosomes, failure of degradation of phagocytosed material, liberation and activation of lysosomal enzymes -> usually due to drugs and antibiotics, may be hereditary |
| Mitochondria | target that affects oxidative phosphorylation (hypoxia and hypoglycemia) -> results in energy deficiency (low ATP) |
| Four main mechanisms of cell injury | hypoxia (may be involved in all 4), injury by free radicals (including activated oxygen), chemical injury, viral injury |
| Ischemic injury | interruption of blood flow |
| Reversible ischemic injury | impaired aerobic respiration (mitochondria) -> decreased ATP (energy) -> anaerobic glycolysis -> glycogen depletion -> accumulation of lactic acid (intracellular acidosis) with associated nuclear chromatin clumping; ATP is needed for cell membrane integrity and active sodium transport -> can't get Na+ out and causes cell swelling, dilation of ER -> ribosomes fall off of RER (degranulation), blebs begin to form, myelin figures from plasma and organelle membranes are seen within or outside the cell (disassociation of lipoproteins) -> mitochondria swell -> ALL CHANGES REVERT TO NORMAL IF OXYGEN IS RESTORED |
| Irreversible ischemic injury | severe vacuolization of mitochondria, damage of plasma membranes, cell swelling of lysosomes and massive Ca2+ influx into cell -> marked intracellular acidosis, ruptured lysosomal membrane -> cell digestion and cell death; INABILITY OF MITOCHONDRIA TO RECOVER FROM INJURY AFTER REOXYGENATION |
| Marked influx of Ca2+ | denatures proteins and causes cell coagulation |
| Injury by free radicals | activated oxygen radicals are most common (aging, chemical, X-rays, infections, inflammation, tumor necrosis) -> combine with substances in cell membranes (lipid peroxidation) and nucleic acids (mutations), and promote cross-linking of proteins with increased degradation -> chronic injury by free radicals (and aging) is lipofucsin (pigment accumulates in the cell) |
| Chemical injury | either directly affects specific organelle or cell component OR (most commonly) indirectly through metabolic activation (reactive toxic metabolites) -> ex. |
| CCl4 poisoning (becomes CCl3) | a type of chemical injury which causes lipid accumulation within the cytoplasm (can't synthesize lipoproteins for TGs to leave the hepatic cell) -> causes characteristic fatty liver of this poison |
| Virus induced injury | can have cytopathic, cytolyitic (cell killing) or oncogenic effect (tumor production -> can also affect cells by interfering with cellular skeleton (ciliated cells of respiratory epithelium) or producing fusion of cells (giant cells) and by producing including bodies in nuclei or cytoplasm (viral aggregates) -> due to rapid replication within affected cells -> also induces immunologic host response |
| Cytolytic effect | this type of viral injury is often cell specific through receptors and causes cell death |
| Cell injury in microscope | cell swelling, bleb formation, myelin figures, swelling of mitochondria, accumulation of dense material in mitochondria (Ca2+, lipoprotein complexes), dilatation of ER, increase in lysosomes (autophagia) |
| Apoptosis | selective removal of individual cells -> usual physiological processes -> cell shrink, fragmentation of nucleus and cell (karyorrhexis) -> apoptotic bodies are released and phagocytosed -> residual (acidophilic) body -> NO INFLAMMATION |
| Necrosis | pathological cell death -> cell swelling (hydropic change, cloudy swelling and feathery degeneration) and rupture (karyolysis -> loss of nuclear staining -> cell fading) -> cells are typically found in contiguous sheets and often associated with striking acute inflammatory reaction |
| Coagulative necrosis | ischemic, coagulation of cells -> proteins are denatured and the cell becomes histologically an opaque, acidophilic mass, nucleus disappears -> cells usually removed by phagocytosis and enzymatic destruction by inflammatory cells |
| Liquefaction necrosis | hydrolytic enzymes cause protein denaturation in brain tissues and in some bacterial infections (ex. cerebral infarct, bronchopneumonia |
| Fat necrosis | occurs in adipose tissue as a result of the release of lipases from dead cells (ex. acute pancreatitis) -> lipases break down TGs and generate free FAs -> react with Ca2+ and make soaps (chalky-cheese nodules in the fat surrounding the pancreas or in the abdominal cavity) -> dead fat cells, inflammatory cells and phagocytes filled with fat |
| Caseous necrosis | characteristic of tuberculosis -> combination of Coagulative and liquefactive necrosis -> macroscopically have cheesy-milk appearance, eosinophilic |
| Gangrenous necrosis | not a distinct type of cell death but is a common clinical term that refers to combination of ischemic coagulative necrosis (typically a limb) with a superimposed infection (wet gangrene) |
| Intracellular accumulations | normal cell components, abnormal substance, pigments, lipids (fatty change -> reversible), protein (Ig = Russell bodies), glycogen (seen in diabetics, storage disorders), mucopolysaccharides (mixture of fats and carbohydrates) -> can have no effect, transient effect or lethal effect |
| Atrophy | decreased size and function of cell -> caused by decreased workload/blood supply, loss of innervation, interruption of trophic signal, aging -> if persists cells may die |
| Hypertrophy | increase in size of cell -> caused by increased functional demand (myocardial, muscle) or physiologic (hormone) hypertrophy (ex. sex organs at puberty) |
| Hyperplasia | increase in number of cells in an organ or tissue) -> caused by increased functional demand (increased RBC's in high altitude), hormonal stimulation (endometrium in early phase of menstrual cycle) or persistent cell injury (skin in calluses) |
| Metaplasia | conversion of one differentiated cell type to another -> not precancerous -> conversion of bronchial ciliated columnar epithelium to squamous epithelium in smokers -> protective mechanism but has loss of function (also seen in Barrett's esophagus) |
| Dysplasia | premalignant condition -> alteration of size, shape and organization of the cellular components of a tissue -> irregularity and hyperchromatism (dark) of nuclei, disordered arrangement of cell -> due to persistent injury (ex. in bronchial epithelium or cervical epithelium) |
| Cellular aging (senescence) | progressive deterioration of the cell functions with age -> irregularly lobed nuclei, vacuolated mitochondria -> free radical damage through life -> accumulation of lipofucsin granules (non-toxic) |
| REVERSIBLE cell damage | Dilatation of organelles and general cell swelling, ribosome disaggregation, blebbing; |
| IRREVERSIBLE cell damage | membrane ruptures, dispersal of organelles, mitochondrial damage, breakdown of lysosomes, activation of inflammatory response |
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