Cell/Tissue Injury

  1. The ability of cells to maintain structural and functional stability in the face of a constantly changing microenvironment
  2. A decrease in the size (or number) of individual cells that had previously been of normal size. Resulting tissue is smaller and weighs less than normal.
  3. An increase in the size of individual cells in response to an increased functional demand on cells that are not commonly considered capable of mitotic division. Refers predominantly to cardiac and skeletal muscle cells when they are required to work against increased resistance. May ultimately result in cell failure. This tissue is larger and heavier than normal.
  4. An increase in the number of cells in response to an increased functional demand on cells that are capable of mitotic division. Usually in response to hormonal or growth factor stimulation. The resulting tissue is increased in volume.
  5. A substitution of one form of mature cells for another form of mature cells. In most issues, a new harsher environment induces over time a change to a more protective tissue type (stratified squamous epithelium replacing ciliated columnar epithelium in the lungs of smokers). The normal function of original tissue is lost. Persistance of adverse environment may lead to dysplastic or neoplastic transformation.
  6. An atypical (but still potentially reversible) growth of cells that is usually induced by chronic irritation or chronic stimulation. May result in alteration in the shape and size of the cell and/or nucleus, loss of cell orientation to one another, and abnormal mitoses. Generally regarded as a potential precursor to the development of malignant neoplasia.
  7. The first morphologic change to occur after injuries that interfere with plasma membrane permeability and therefore the regulation of intracellular fluid volume and ionic concentrations. Due to increased water, the cell appears enlarged with a pale cytoplasm but normally positioned nucleus
    Cellular Swelling
  8. An exaggerated state of cellular swelling where segments of swollen distended endoplasmic reticulum appear in the cytoplasm as clear vacuoles that may displace the nucleus to the periphery of the cell.
    Hydropic Change
  9. An absolute increase in lipids within parenchymal cells. Most often seen in the liver but may also involve heart and kidney. Clear lipid vacuoles appear in the cytoplasm, and, as they coalesce or enlarge, the displace the nucleus to the periphery of the cell.
    Steatosis (Fatty Change)
  10. A process in which adipose cells accumulate within stromal connective tissue that lies between parenchymal cells. Most frequently seen in the pancreas and heart. Usually asymptomatic
    Fatty Ingrowth
  11. An increase in intracellular glycogen due to abnormal glucose or glycogen metabolism as in the inherited glycogen storage diseases or in hyperglycemic states. Seen as clear vacuoles in the cytoplasm
    Glycogen Infiltration
  12. Finely granular yellow-brown, "wear and tear" pigment indicating chronic free radical (lipid peroxidation) of cell membranes. Frequently becomes more apparent in the aging of a cell, and tends to present as residual bodies in perinuclear lysosomes. Does not appear to interfere with cell function. May impart a brown discoloration ("brown atrophy")
    Lipofuscin (Lipochrome)
  13. A brown-black pigment that is produced by melanocytes. Certain disorders may be related to either generalized or localized under or overproduction of this pigment type
  14. The ferric iron-apoferritin protein complex involved in normal iron absorption and storage
  15. A granular gold-brown protein derived from the breakdown of hemoglobin. Cells laden with this type of iron are frequently found in reticuloendothelial cells responsible for removing senescent RBCs from the circulation or around areas of hemorrhage or chronic congestion. When present in excessive amounts, usually as a result of chronic hemolysis of RBCs, it may be found in a variety of parenchymal cells such as heart, liver, pancreas, and skin.
  16. A severe metabolic disorder that is an inherited genetic defect in normal iron metabolism. Results in massive deposition of iron in tissues throughout the body (particularly liver, pancreas, skin and heart) leading to cirrhosis, diabetes mellitus, bronze discoloration of the skin, and heart failure.
  17. A green-brown pigment that is a breakdown product of hemoglobin (porphyrin rings). Does not contain iron. The major pigment of bile; can accumulate in fluid and tissue wherever there is a disturbance in uptake, conjugation, or excretion by hepatocytes.
  18. The nucleus responds to irreversible injury by dense chromatin condensation (___?___), fragmentation (___?___) or dissolution (___?___). Although is is irreparable damage to the cell membrane that actually spells death for the cell, these nuclear changes are the definitive morphologic (visible) evidence of irreversible injury and cell death.
    Pyknosis, Karyorrhexis, Karyolysis
  19. The most common pattern of necrosis. Due to inadequate oxygenation of cells. Generally the result of a reduction in blood flow (ischemia) to the cells. Nuclear material is usually lost. Denaturation of structural proteins allows retention of underlying tissue architecture. Denaturation of endogenous degradative enzymes prevents cellular digestion. Dead cells removed by exogenous proteolytic enzymes or pagocytic "scavengers." Tissue replaced by regeneration or, more likely, scar.
    Coagulative Necrosis
  20. Ischemic coagulative necrosis of the skin and subcutaneous tissues of the extremities. This type of necrosis of the toes and feet is a common complication of diabetes mellitus. Affected tissue dessicates and assumes a dark green-black coloration. Demarcation from adjacent viable skin is usually distinct.
    Dry Gangrene
  21. This type of necrosis results from tissue hypoxia secondary to ischemia or venous congestion of tissue which secondarily becomes infected resulting in putrefaction of the necrotic tissue. Tissue is moist, dark, and malodorous. If involved in internal viscera can rapidly lead to death unless there is surgical intervention.
    Wet Gangrene
  22. A variant of wet gangrene caused by Clostridium bacteria which ferment carbohydrates to produce carbon dioxide. Tissue appears much like wet gangrene but is also crepitant to palpation
    Gas Gangrene
  23. Pattern of necrosis resulting when proteolytic digestion of dead cells is not delayed by enzyme denaturation. This is characteristic of tissues injured by bacterial infections which attract large numbers of neutrophils (creating an abscess) and ischemic destruction of brain tissue
    Liquefactive Necrosis
  24. A form of necrosis in which the preservation of the underlying tissue outlines is lost and replaced by a granular, amorphous, acellular substance which on gross examination resembles blue cheese. Encountered principly in infectious diseases involving mycobacteria and fungi. Frequently seen in association with a form of chronic inflammation known as granulomatous inflammation.
    Caseous Necrosis
  25. A type of necrosis produced by lipolytic activity of pancreatic enzymes on fat cells. Usually seen during the course of pancreatitis when pancreatic lipases are released into surrounding fatty tissues and convert triglycerides to free fatty acids which complex with calcium to form calcium soaps. Grossly this produces white chalky deposits in fatty tissue
    Enzymatic Fat Necrosis
  26. A type of necrosis produced by traumatic rupture of fat cells with subsequent phagocytosis of the lipid material by macrophages. Seem most frequently in female breast tissue, and produces a granulomatous "foreign body" inflammation. Histologically does not have enzymatically "digested" appearance.
    Traumatic Fat Necrosis
  27. Type of necrosis characterized by a smudgy, amorphous eosinophilic material usually deposited in or around the walls of small blood vessels. Histologic appears resembles fribrin deposits. Often associated with immune complex formation and represents the deposition of immunoglobulins, fibrinogen, and complement in the vessel walls (frequently accompanied by neutrophilic infiltrate as well--vasculitis).
    Fibrinoid Necrosis
  28. The deposition of calcium in degenerating or necrotic tissue in the face of normal serum calcium levels. Within dying cells, calcium accumulates in the irreparably damaged mitochondria but extracellular calcium deposits also develop utilizing membrane bound vesicles as a nidus for propagation. Histologically, calcium may appear as small concentrically laminated spheres (psammoma bodies) or as variably sized amorphous basophilic deposits
    Dystrophic Calcification
  29. The deposition of calcium in normal tissues of patients with high serum calcium levels. Tissues which have a relatively alkaline pH (cornea, lungs, stomach, blood vessels, etc) are most commonly affected. Histologically, calcium may appear as small concentrically laminated spheres (psammoma bodies) or as variably sized amorphous basophilic deposits
    Metastatic Calcification
  30. Poor oxygen saturation of the blood
  31. Insufficient vascular supply of oxygen. Interferes with delivery of all nutrients to the cell (including glucose).
  32. Oxygen deficiency that interferes with mitochondrial oxidative phosphorylation and the production of ATP. Ischemia and hypoxemia may play a role. Hydropic changes may result. Eventually, an increase in cytoplasmic calcium activates endogenous calcium-dependent phospholipases, proteinases, ATPases, and endonucleases which begin to break down the cell membranes and cytoskeleton, further deplete ATP stores, and produce chromatin fragmentation. Cytoskeletal damage may be manifest by the appearance of "cell blebs" and "myelin figures," which indicate damage to both organelle and plasma membranes
  33. Is hypoxia/anoxia indicative of reversible or irreversible cell injury?
    Reversible, but if continued for long periods may lead to irreversible cell death
  34. Extremely unstable and reactive molecules resulting from the presence of an unpaired electron in outer orbit. May cause lipid peroxidation, and inappropriate disulfide bonding of proteins leading to their deactivation and single-stranded breaks in DNA. Mechanism producing these include ionizing radiation and metabolism of chemicals and drugs. These may become deactivated by spontaneous decay or antioxidants.
    Free Radicals
  35. Results when sufficient outside force is applied to body tissues to disrupt their structure or function. Produces wounds such as abrasions, contusions, lacerations, incisions, avulsions, and puncture wounds
    Mechanical Trauma
  36. Loss of superficial cells as a result of friction or crushing
  37. Disruption of blood vessels produced by blunt force
  38. The tearing of tissue resulting from excessive stretching
  39. Cut produced by a sharp instrument
  40. Tearing away of body parts
  41. Piercing or penetration of tissue caused by a sharp object or instrument
    Puncture Wound
  42. Cells with a low nature turnover rate are most radio_____ while those with a high natural turnover are most radio_____?
    Radioresistant; Radiosensitive
  43. Radiation injury resulting in a development of a pancytopenia within a few weeks of exposure. Bleeding and infection are the major complications
    Hematopoietic Syndrome
  44. Radiation injury leading to destruction of GI epithelium resulting in development of nausea, vomiting, and severe diarrhea within several days of exposure. May lead to severe metabolic disturbances, vascular collapse, sepsis, and death
    GI Syndrome
  45. Radiation syndrome marked by vascular endothelial damage resulting in cerebral edema, convulsions, coma, and death within hours of exposure
    Cerebral Syndrome
  46. Type of hypothermia in which cooling of tissue damages vascular endothelium and increases vascular permeability leading to edema and blister formation (frostbite). Prolonged cooling may also cause extensive ischemic injury due to poor blood perfusion of surrounding tissue. Freezing of tissue interferes with ionic concentrations due to crystallization of intracellular water, denatures proteins, and physically disrupts cell membranes leading to cell death. In frozen tissue, these effects may not appear until the tissue thaws
    Localized Hypothermia
  47. Type of hypothermia in which compensatory mechanisms are overwhelmed, leading to continued dissipation of internal core heat. Leads to a decrease in metabolic activity, mental confusion, lethargy, and coma. Vascular collapse and cardiac arrhythmias are major causes of death
    Systemic Hypothermia
  48. Type of hyperthermia in which the heating of tissue causes vasodilation and increased vascular permeability leading to edema and blister formation. If severe enough, the cells show nuclear swelling with disruption of nuclear membranes and coagulation of intracellular proteins. Complications include shock (loss of circulating blood volume), hemoconcentration, electrolyte imbalance, and infection (responsible for over 50% of deaths)
    Localized Hyperthermia (burns)
  49. This type of hyperthermia results from either increased heat production, decreased heat loss, or alteration of the "set point" of the hypothalamic regulatory centers. Compensatory vasodilation leads to pooling of blood and hypotension. Excessive sweating may lead to severe fluid and electrolyte imbalances which could induce shock
    Systemic Hyperthermia
  50. Can cause cell injury or death either due to interruption of neural transmissions of the cadiac conduction/respiratory control systems or by the generation of heat
  51. Type of injury that occurs when the body completes a circuit between two conductors.
    Electrothermal Injury
  52. Disease resulting from a sudden decrease in pressure (as seen in rapid ascents in scuba diving accidents), which produces free gas bubbles as nitrogen is released from solution in the plasma. These can act as emboli with variable clinical results
    Caisson Disease
  53. Injury resulting from rapid increases in pressure which produce considerable damage do to the variable densities and compressibility of tissues. Lacerations or ruptures (esp of air-filled tissues or organs) may produce significant morbidity
    Blast Injuries
  54. This type of injury includes a wide spectrum of microbial organisms from viruses to higher forms of parasites. These can induce cell injury through direct cytopathic or cytotoxic effects or indirectly through inflammatory/immunologic host defense mechanisms
    Biologic Injury
  55. Type of injury that results from imbalances that interfere with the ability of the body to maintain cell structure and function. Includes disorders such as marasmus, kwashiorkor, vitamin mineral deficiencies, and obesity
    Nutritional Injury
Card Set
Cell/Tissue Injury
Pathology Test Review