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5 Written questions

5 Matching questions

  1. Gangrenous Necrosis
  2. Caseous Necrosis
  3. Fat Necrosis
  4. Chemical Asphyxiants
  5. Hypoxia
  1. a lack 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)
  2. b either 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
  3. c
    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
  4. d
    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
  5. e
    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.

5 Multiple choice questions

  1. an alteration of oxygen delivery to tissues resulting from inhalation of fluid, usually water; major mechanism of injury is hypoxemia (low blood O2 levels); can have dry-lung drowning that causes laryngospasms instead of actual water

  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. reversible replacement of one mature cell type by another, sometimes less differentiated, cell type; develops from a reprogramming of stem cells that exist on most epithelia or of undifferentiated mesenchymal cells present in connective tissue; Normal process (such as uterus); uniform to each other and relatively organized; is REVERSIBLE
  4. reduced blood supply; often caused by gradual narrowing of arteries (artiosclerosis) and complete blockage by blood clots (thrombosis); progressive hypoxia caused by gradual arterial obstruction is better tlerated than acute anoxia (total lack of oxygen)
  5. abnormal intercellular accumulation of carbohydrates and lipids; priamarily found in spleen, liver, and CNS; can cause "fatty liver": as lipids fill cells, vacuolation pushes the nucleus and other organelles aside; liver's outward appearance is yellow and greasy; Alcohol abuse most common cause

5 True/False questions

  1. Cellular Accumulations - Glycogenmutations 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)

          

  2. 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)

          

  3. Dry Gangreneusually result of COAGULATIVE necrosis; SKIN becomes very dry and shrinks resulting in wrinkles, and its color changes to dark brown or black;

          

  4. Celular Deathclassified 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. Cellular Injury Induced by Ischemia - Irreversible
    1) obstruction or cessation of blood flow; 2) Ischemia, 3a) decrease mitochondrial oxygenation, 4a) severe vaculization of mitochondria (end); 4b) decrease ATP; 5a) decrease Na+ pump, 6) increase intracellular Na, xcellular K,intracellular Ca, 7) increase H2O, 8) increase acute cellular swelling, 5b) 5+6+7 is dilation of endoplasmic reticulum, 6) detatchment of ribosomes, 7) decrease protein synthesis, 8) lipid deposition, 5b) increase glycolysis, 6) decrease glycogen, 7) increase lactate, 8) decrease pH, 9a) nuclear chromatin clumping, 9b) increase swelling of lysosomes