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5 Written Questions

5 Matching Questions

  1. Suffocation
  2. Asphyxial Injuries
  3. Fat Necrosis
  4. Celular Death
  5. Common Themes in Cell Injury and Cell Death
  1. a 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)
  2. b
    is cellular dissolution caused by power enzymes, called LIPASES, that occur in BREAST, PANCREAS, and, other ABDOMINAL ORGANS; Lipases break down triglycerides, releaseing free fatty acids that then combine with calcium, magnesium and sodium ions, creating SOAPS (saponification); Necrotic tissue appears opaque and chalk-white.
  3. c ATP deletion, Reactive Oxygen Species, Ca++ entry, Mitochondrial damage, Membrane damage, Protein misfolding/DNA damage - Table 3-2
  4. d 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
  5. e 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 Multiple Choice Questions


  1. occurs in LUNGS; usually results from TB PULMONARY INFECTION, especially by Myobacterium tuberculosis; Combination of COAGULATIVE AND LIQUEFACTIVE necroses; The dead cells disintegrate, bt debris is not completely digested by hydrolases; Tissues resemble clumped cheese in that they are soft and granular; A granulomatous inflammatory wall encloses areas of caseous necrosis; Tb starts to kill lung tissue (liquefactive) and macrophages come in and stop it and coagulate the tissue - why you see tubricles in lungs

  2. very common w/any hypoxia, even as momentary as leg falling asleep; can be reversed; 1) injury, 2) ATP production decreases, 3) sodium and water move into cell, Potassium moves out of cell, 4) Osmotic pressure increases 5) more water moves into cell, 6) cisternae of endoplasmic reticulum distend, rupture, and form vacuoles, 7) extensive vacuolation, 8) hydropic degeneration
  3. "dropping off" is an important distinct type of cell death taht differs from necrosis in several ways; is an active process of cellular self-destruction called programmed cell death and is implicated in both normal and pathologic tissue changes; Cells need to die; otherwise, endless proliferation would lead to gigantic bodies; occurs in 1) severe cell injury, 2) accumulation of misfoled proteins, 3) infections, 4) obstruction in tissue ducts; When cell injury exceeds repair mechanisms, the cell triggers apoptosis

  4. 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

  5. a reversible, structural, or functional response both to normal or physiologic conditions and to adverse or pathologic conditions; Atrophy, Hypertrophy, Hyperplasia, Dysplasia, Metaplasia

5 True/False Questions

  1. Atrophyan increase in the size of cells and consequently in size of affected organ; heart and kidneys are very prone; associated with increased accumulation of protein in the cellular components (PM, ER, mitochondrea) and NOT with an increase in cellular fluid; can be physiologic or pathologic; is REVERSIBLE

          

  2. Coagulative Necrosis
    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.

          

  3. Necrosisthe sum of cellular changes after local cell death and the process of cellular self-digestion, knon as autodigestion (autolysis); Damage to the plasma membrane and cell structures; 6 Major Types of Necrosis are Coagulative necrosis, Liquefactive Necrosis, Caseous Necrosis, Fat Necrosis and Gangrenous Necrosis

          

  4. Cellular Injury Induced by Ischemia - Reversible
    membrane damage, 2a) loss of phospholipids, alterations of cytoskeleton, activtation of inflammation (complement, cytokines, and leukocytes), increase free radicals, lipid breakdown; 3a) release of enzymes (CPK, LDH) (end), 3b) increase CA influx; 2b) increase swelling of lysosomes, 3) increased release of lysosomal enzymes (hydrolases), 4) cellular digestion (autodigestion)

          

  5. Wet Gangrene
    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)

          

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