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5 Written questions

5 Matching questions

  1. Celular Death
  2. Atrophy
  3. Liquefactive Necrosis
  4. Gas Gangrene
  5. Dysplasia
  1. a
    commonly results from ischemic injury to neurons and glial cells in BRAIN; dead brain tissue is readily affected because brain cells are rich in digestive HYDROLITIC ENZYMES and lipids and the brain contains little connective tissue; Cells are digested by their own HYDROLASES so the tissue becomes soft, liquefies and segregates from healthy dtissue, forming cytsts; Can be caused by BACTERIAL INFECTION, especially Staphylococci, Streptococci, and Escherichia coli.
  2. b
    a decrease or shrinkage in cellular size; if atrophy happens in sufficient number of an organ's cells, the entire organ shrinks; can be physiological like thymus, pathological (disease process), or disuse; is REVERSIBLE
  3. c
    abnormal changes in the size, shape and organization of mature cells; no considered true adaptive process but is related to hyperplaia and is often called atypical hyperplasia; often encountered in epithelial tissue of the cervix and respiratory tract; can, but not always, turn to cancer; often reversible
  4. d classified as necrosis and apoptosis; Necrosis characterized by rapid loss of plasma membrane structure, organelle swelling, mitochondrial dysfunction and lack of typical features of apoptosis; Apoptosis is known as regulated or programmed cell process characterized by the "dropping off' of cellular fragments called apoptotic bodies
  5. e refers to a special type of gangrene cause by INFECTION of injured tissue by one of many species of Clostridium; these anaerobic bacteria produce HYDROLYTIC ENYMES and TOXINS that detroy connective tissue and cellular membranes and cause bubbles of gas to from in muscle cells; this can be fatal if enzymes lyse the membrane of RBCs, dstorying thier O2 carrying capasity; Death is caused by shock.

5 Multiple choice questions

  1. developes when NEUTROPHILS invade the site, causing LIQUEFACTIVE necrosis; usually occurs in INTERNAL ORGANS, causing site to beome cold, swollen and black; foul odor is present, and if systemic symptoms become severe, death can ensue; Thrombisis/embolism (blockage of blood), strangulated hernia (no adequate O2 or blood), valvulus (twist of intestine), intussusception (intestine falling into self)
  2. oxygen failing to reach the blood, can result from lack of O2 in environment (entrapment in enclosed space or filling enviro w/suffocating gas), or blockage of external airways (compression of chest, choking)
  3. cuased by failure of cells to receive or use oxygen; deprivation of oxygen may be partial (hypoxia) or total (anoxia); grouped into 4 gneral categories; suffication, strangulation, chemical, and drowning
  4. (infiltration); intracellular accoumulation of abnormal amounts of various substances and the resultant metabolic disturbances; results not only from sublethal, sustained injury by cells but also result from normal (but inefficient) cell function; Normal cellular substances ( excess water, proteins, lipids, carbohydrates) or abnormal substance (endogenous - product of abnormalmetabolism or synthesis, exogenous - infectious agents or minerals)

  5. refers to death of tissue from SEVERE HYPOXIC INJURY, commonly occuring beause of arteriosclerosis, or blockage of major arteries, particularly those in LOWER EXTREMITIES; With hypoxia and subsequent bacterial invasion the sittues uncergo necrosis; can be DRY, WET, or GAS

5 True/False questions

  1. Apoptosis vs Necrosis
    Necrosis is caused by exogenous injury whereby cells are swollen and have nuclear changes in ruptured cell membrane; Apoptosis is single cell death. It is genetically programmed (suicide genes) and depends on energy. Apoptotic bodies contain part of nucleus and cytoplasmic organelles, which are ultimately engulfed by macrophages or adjacent cells; Cell membrane stays intact but has 'lubbing'; happenes throughout life and is very benificial component


  2. Common Themes in Cell Injury and Cell DeathATP deletion, Reactive Oxygen Species, Ca++ entry, Mitochondrial damage, Membrane damage, Protein misfolding/DNA damage - Table 3-2


  3. Ischemialack of sufficient oxygen; the single most common cause of cellular injury; can result from reduced amount of oxygen in air, loss of hemoglobin or decreased efficacy of hemoglobin, decreased production of RBCs, diseases of repiratory or cardovascular systems, and poisoning of the oxidative enzymes w/in cell; can induce inflammation and inflamed lesions can become hypoxic; most common form is ischemia (reduced blood supply)


  4. Chemical Asphyxiantseither prevent the delivery of oxygen to the tissues or block its utilization; doesn't allow hemaglobin to attach to oxygen or doesn't allow O2 to pass alveoli; Carbon Monoxide is the most common; Cyanide acts as an asphyxiant by combining w/ferric iron atom in cytochrome oxidase, blocking the intracellular use of oxygen, has same cherry fred appearance as a carbon monoxide intoxication; Hydrogen Sulfide (sewer gas) that may have brown-tinged blood in addition to nonspecific signs of asphyxiation


  5. Cellular Accumulations - Watermutations in protien can slow protein folding so cell is filled with unfolded proteins, which might not be in the proper format to be used; also, metabolites (used to digest some proteins) are released from lysosomes can damage cellular organells and excessive amounts of protien in cytoplsm push against cellular organells, disrupting organelle function and intracellular communication; accumulates primarily in epithelial cells of renal confoluted tubule and antibody-forming plamsam cells (B-lymphocytes)


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