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5 Written questions

5 Matching questions

  1. Hypertrophy
  2. Dysplasia
  3. Cellular Accumulations - Protein
  4. Cellular Accumulations - Glycogen
  5. Drowning
  1. a mutations 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. b
    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
  3. c an 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
  4. d seen in genetic disorders called 'glycogen storage disease' and in disorders of glucose and glycogen metabolism; results in excessive vacuolation of cytoplasm (like water); most common cuase is diabetes mellitus; when not storing glucose or glycogen correctly, breakdown in energy of cell
  5. e 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

5 Multiple choice questions

  1. 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)

  2. 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. 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
  4. 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)

  5. 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

5 True/False questions

  1. Cellular Injury Induced by Ischemia - Irreversible
    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)


  2. 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


  3. Cellular Accumulations(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)


  4. Gangrenous Necrosis
    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. Fat Necrosis
    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.