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Top Notch Patho Flash > Cell Injury > Flashcards

Cell Injury Flashcards

2
Q

<p>Increase in size of cells resulting in increased size of organ.</p>

A

<p>Hypertrophy(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.3</p>

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3
Q

<p class=”large” style=”text-align:center”;>Increase in number of cells.</p>

A

<p class=”large” style=”text-align:center”;>Hyperplasia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.3</p>

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4
Q

<p class=”large” style=”text-align:center”;>Hypertrophy of hyperplasia?Uterus during pregnancy</p>

A

<p class=”large” style=”text-align:center”;>Both Estrogen stimulated SM hyperthrophy and hyperplasia (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.3</p>

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5
Q

<p class=”large” style=”text-align:center”;>Hypertrophy or hyperplasia?Wound healing</p>

A

<p class=”large” style=”text-align:center”;>Hyperplasia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.4</p>

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6
Q

<p class=”large” style=”text-align:center”;>Type of cell death characterized by nuclear dissolution, without complete loss of membrane integrity.</p>

A

<p class=”large” style=”text-align:center”;>Apoptosis(TOPNOTCHRobbins Basic Pathology, 8th ed. p.7</p>

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7
Q

<p class=”large” style=”text-align:center”;>Type of cell death which is energy-dependent, tightly regulated, and associated with normal cellular functions.</p>

A

<p class=”large” style=”text-align:center”;>Apoptosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.7</p>

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8
Q

<p class=”large” style=”text-align:center”;>Type of cell death which results from a pathologic cell injury. </p>

A

<p class=”large” style=”text-align:center”;>Necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.9</p>

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9
Q

<p class=”large” style=”text-align:center”;>Type of cell death associated with inflammation.</p>

A

<p class=”large” style=”text-align:center”;>Necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10</p>

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10
Q

<p class=”large” style=”text-align:center”;>It is the irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis.</p>

A

<p class=”large” style=”text-align:center”;>Pyknosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10</p>

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11
Q

<p class=”large” style=”text-align:center”;>It is the destructive fragmentation of the nucleus of a dying cell. </p>

A

<p class=”large” style=”text-align:center”;>Karyorrhexis (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10</p>

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12
Q

<p class=”large” style=”text-align:center”;>It is the complete dissolution of the chromatin of a dying cell. </p>

A

<p class=”large” style=”text-align:center”;>Karyolysis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10</p>

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13
Q

<p class=”large” style=”text-align:center”;>This is the first manifestation of almost all forms of injury to cells.</p>

A

<p class=”large” style=”text-align:center”;>Cellular swelling(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.8</p>

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14
Q

<p class=”large” style=”text-align:center”;>Small clear vacuoles within the cytoplasm, representing pinched-off segments of the endoplasmic reticulum.</p>

A

<p class=”large” style=”text-align:center”;>Hydropic change or Vacuolar degeneration (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.23</p>

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15
Q

<p class=”large” style=”text-align:center”;>Appearance of lipid vacuoles in the cytoplasm.</p>

A

<p class=”large” style=”text-align:center”;>Fatty Change(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.23</p>

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16
Q

<p class=”large” style=”text-align:center”;>Surface blebs, increased eosinophilia of the cytoplasm, cellular swelling.</p>

A

<p class=”large” style=”text-align:center”;>Reversible/ Early Ischemic Injury(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18</p>

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17
Q

<p class=”large” style=”text-align:center”;>Cell injury with loss of nuclei, cellular fragmentation and leakage of cellular contents.</p>

A

<p class=”large” style=”text-align:center”;>Irreversible/ Necrotic cellular injury(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18</p>

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18
Q

<p class=”large” style=”text-align:center”;>These are chemical species with a single unpaired electron in the outer orbital.</p>

A

<p class=”large” style=”text-align:center”;>Free radicals(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18</p>

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19
Q

<p class=”large” style=”text-align:center”;>Most common cause of cell injury in clinical medicine.</p>

A

<p class=”large” style=”text-align:center”;>Ischemia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18</p>

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20
Q

<p class=”large” style=”text-align:center”;>Composed of membrane-bound vesicles of cytosol and organelles seen in programmed-cell death.</p>

A

<p class=”large” style=”text-align:center”;>Apoptotic Bodies(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.19</p>

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21
Q

<p class=”large” style=”text-align:center”;>Restoration of blood flow to ischemic but otherwise viable tissue paradoxically results in exacerbated and accelerated injury.</p>

A

<p class=”large” style=”text-align:center”;>Ischemia-Reperfusion Injury(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.18</p>

22
Q

<p class=”large” style=”text-align:center”;>Pathway of apoptosis trigerred by loss of survival signals, DNA damage and accumulation of misfolded proteins. Inhibited by Anti-apoptotic members of the Bcl family.</p>

A

<p class=”large” style=”text-align:center”;>Mitochondrial / Intrinsic Pathway(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.22</p>

23
Q

<p class=”large” style=”text-align:center”;>Pathway of apoptosis responsible for elimination of self-reactive lymphocytes and damage by cytotoxic T lymphocytes. Initiated by TNF receptors.</p>

A

<p class=”large” style=”text-align:center”;>Death Receptor / Extrinsic Pathway(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.22</p>

24
Q

<p class=”large” style=”text-align:center”;>Refers to any abnormal accumulation of triglycerides within parenchymal cells. Most often seen in the liver but can also occur in the heart, sk m., and kidneys.</p>

A

<p class=”large” style=”text-align:center”;>Fatty Change(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.23</p>

25
Q

<p>Other name for macrophages in contact with lipid debris of necrotic cells or abnormal forms of lipoproteins. Filled with minute, membrane-bound vacuoles of lipid, imparting a foamy appearance to their cytoplasm.</p>

A

<p>Foam cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.24</p>

26
Q

<p class=”large” style=”text-align:center”;>Presence of cholesterol-filled macrophages in subepithelial connective tissue of skin or tendons.</p>

A

<p class=”large” style=”text-align:center”;>Xanthomas(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.24</p>

27
Q

<p class=”large” style=”text-align:center”;>Hypertrophy or hyperplasia?Cardiomegaly due to hypertension</p>

A

<p class=”large” style=”text-align:center”;>Hypertrophy Due to increased workload(TOPNOTCH)</p>

28
Q

<p class=”large” style=”text-align:center”;>Most common exogenous pigment?</p>

A

<p class=”large” style=”text-align:center”;>Carbon(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26</p>

29
Q

<p class=”large” style=”text-align:center”;>”Wear and Tear pigment”?</p>

A

<p class=”large” style=”text-align:center”;>Lipofuschin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26</p>

30
Q

<p class=”large” style=”text-align:center”;>Pigment produced by tyrosinase-catalyzed oxidation of tyrosine to dihydroxyphenylalanine.</p>

A

<p class=”large” style=”text-align:center”;>Melanin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26</p>

31
Q

<p class=”large” style=”text-align:center”;>Hemoglobin-derived granular pigment that is golden-yellow to brown in color. Accumulates in excess of iron.</p>

A

<p class=”large” style=”text-align:center”;>Hemosiderin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26</p>

32
Q

<p class=”large” style=”text-align:center”;>Histochemical reaction used to identify hemosiderin.</p>

A

<p class=”large” style=”text-align:center”;>Prussian blue test(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26</p>

33
Q

<p class=”large” style=”text-align:center”;>Abnormal calcium deposition occuring in the absence of calcium metabolic derangements.</p>

A

<p class=”large” style=”text-align:center”;>Dystrophic calcification.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26</p>

34
Q

<p class=”large” style=”text-align:center”;>Calcium deposition in normal tissues occuring in the presence of hypercalcemia.</p>

A

<p class=”large” style=”text-align:center”;>Metastatic calcification (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26</p>

35
Q

<p class=”large” style=”text-align:center”;>Grossly seen as fine white granules or clumps, often felt as gritty deposits. Histologically, intra/extracellular basophilic deposits.</p>

A

<p class=”large” style=”text-align:center”;>Calcium salts(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.27</p>

36
Q

<p class=”large” style=”text-align:center”;>A result of a progressive decline in the proliferative capacity and lifespan of cells.</p>

A

<p class=”large” style=”text-align:center”;>Cellular aging(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.29</p>

37
Q

<p class=”large” style=”text-align:center”;>Appears as round or oval masses with intensely eosinophilic cytoplasm, nuclei with various stages of chromatin condensation and aggregation, karyorrhexis.</p>

A

<p class=”large” style=”text-align:center”;>Apoptotic cell(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.20</p>

38
Q

<p class=”large” style=”text-align:center”;>Membrane bound vesicles of cytosol and organelles quickly extruded and phagocytosed without eliciting inflammatory response.</p>

A

<p class=”large” style=”text-align:center”;>Apoptotic bodies(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.20</p>

39
Q

<p class=”large” style=”text-align:center”;>Clear vacuoles within parenchymal cells, displacing the nucleus to the cell periphery.</p>

A

<p class=”large” style=”text-align:center”;>Fatty change (TOPNOTCHRobbins Basic Pathology, 8th ed. p.24</p>

40
Q

<p class=”large” style=”text-align:center”;>Focal, intracellular fat deposits creating alternating bands of yellowed myocardium with alternating bands of darker red-brown uninvolved heart or “tigered effect”.</p>

A

<p class=”large” style=”text-align:center”;>Fatty change of the heart(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.24</p>

41
Q

<p class=”large” style=”text-align:center”;>Rounded, eosinophilic accumulation of newly synthesized immunoglobulins in the rough ER of plasma cells.</p>

A

<p class=”large” style=”text-align:center”;>Russel bodies(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.25</p>

42
Q

<p class=”large” style=”text-align:center”;>Eosinophilic cytoplasmic inclusion in liver cells composed of aggregated intermediate filaments which resist degradation. Seen in patients woth alcoholic liver disease.</p>

A

<p class=”large” style=”text-align:center”;>Mallory body / “alcoholic hyalin”(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.25</p>

43
Q

<p class=”large” style=”text-align:center”;>Aggregated protein inclusions that contain microtubule-associated proteins and neurofilaments, reflecting disrupted neuronal cytoskeleton.</p>

A

<p class=”large” style=”text-align:center”;>Neurofibrillary tangles in Alzheimer’s disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26</p>

44
Q

<p class=”large” style=”text-align:center”;>An insoluble brownish-yellow granular intracellular material that accumulates as a function of age and atrophy. Appears as perinuclear electron-dense granules on electron microscopy.</p>

A

<p class=”large” style=”text-align:center”;>Lipofuschin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.26</p>

45
Q

<p class=”large” style=”text-align:center”;>A form of tissue necrosis in which the component cells are dead but the basic tissue architecture is preserved. The affected tissues take on a firm texture.</p>

A

<p class=”large” style=”text-align:center”;>Coagulative necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10</p>

46
Q

<p>Refers to focal areas of fat destruction, typically resulting from release of activated pancreatic lipases into the substance of the pancreas and the peritoneal cavity. The foci of necrosis contain shadowy outlines of necrotic fat cells with basophilic calcium deposits, surrounded by an inflammatory reaction.</p>

A

<p>Fat necrosis (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.11</p>

47
Q

<p>A special form of necrosis usually seen in immune reactions involving blood vessels. Deposits of immune complexes, together with fibrin that has leaked out of vessels, result in a bright pink and amorphous appearance in H&amp;E stains, called "fibrinoid" (fibrin-like) by pathologists. </p>

A

<p>Fibrinoid necrosis (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.11</p>

48
Q

<p class=”large” style=”text-align:center”;>Seen in focal bacterial or, occasionally, fungal infections, because microbes stimulate the accumulation of inflammatory cells and the enzymes of leukocytes digest the tissue.</p>

A

<p class=”large” style=”text-align:center”;>Liquefactive necrosis (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10</p>

49
Q

<p class=”large” style=”text-align:center”;>This term is usually applied to a limb, generally the lower leg, that has lost its blood supply and has undergone coagulative necrosis involving multiple tissue layers. </p>

A

<p class=”large” style=”text-align:center”;>Gangrenous necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.10</p>

Top Notch Patho Flash (1 decks)

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