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5 Written questions

5 Matching questions

  1. Metaplasia
  2. Hydropic Degeneration (any type of hypoxia)
  3. Necrosis
  4. Cellular Accumulations - Water
  5. Liquefactive Necrosis
  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 cellular swelling, most common degenerative change, is caused by shift of extracellular water into cells; usually occurs in spleen, liver, CNS; cisternae of ER become distended, rupture, and then unite to form large vacuoles that isolate water from cytoplasm (called vacuolation); results in oncosis (hydropic degeneration)
  3. c
    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. d
    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
  5. e 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 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. 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. 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. ATP deletion, Reactive Oxygen Species, Ca++ entry, Mitochondrial damage, Membrane damage, Protein misfolding/DNA damage - Table 3-2
  5. 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

5 True/False questions

  1. Fat 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

          

  2. Cellular Accumulations - Proteinmutations 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)

          

  3. Cellular Accumulations - Glycogenseen 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. Cellular Accumulations - Lipids and Carbohydratesabnormal 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. 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

          

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