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5 Written questions

4 Matching questions

  1. Strangulation
  2. Gangrenous Necrosis
  3. Cellular Injury
  4. Cellular Accumulations - Glycogen
  1. a
    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
  2. b caused by compression and closure of blood vessels and air passages resulting from external pressure on neck; causes cerbral hypoxia or anoxia secondary to alteration or cessation of blood flow to and from brain; hanging (inverted V on neck), ligature (horizontal mark on neck), manual strangulation (hands on neck)
  3. c 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
  4. d

5 Multiple choice questions

  1. 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

  2. 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
  3. 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)
  4. the 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

  5. 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

5 True/False questions

  1. Gas Gangrenerefers 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.


  2. Hyperplasiaan increase in the number of cells resulting from an increased rate of cellular division; as a response to injury, occurs when ijury has been severe and prolonged enough to have caused cell death; cells still relatively uniform, almost normal looking, just more of them; hormonal and pathologic


  3. 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


  4. 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)


  5. 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)