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Flashcards

Cell degeneration and necrosis

Teresa Richards Pathology BSc English 61 cards

Cards in this deck (61)

  1. 1Name the 5 changes in cell growth/adaptationshypertrophy
    hyperplasia
    atrophy
    metaplasia
    neoplasia
  2. 2What are the 2 types of cellular degenerationcellular swelling
    fatty change
  3. 3What is cellular swellingmildest, earliest detectable degenerative change
  4. 4How does cellular swelling appear macroscopicallymay be no visible change
    or
    tissue may be paler than normal and may bulge on sectioning
  5. 5How does cellular swelling appear microscopicallyindividual cells will be swollen with pale cytoplasm or small clear vacuoles due to distension of the ER "hydropic degeneration"
  6. 6What is the electron and light microscopic appearance of cellular swellingexcess fluid accumulates in the ER
    ER swells and eventually fragments, leaving a fluid filled vacuole
  7. 7How does fatty change appear macroscopicallyswollen, pale, friable, greasy texture
  8. 8How does fatty change appear microscopicallyaccumulation of variably sized round vacuoles
    nuclei pushed to the edge of the cell
  9. 9Where is fatty change commonly seenparenchyma of the liver, kidney and heart
  10. 10What is the term for fatty change in the liver and what distribution can occurheptic lipidosis
    diffuse, zonal, focal
  11. 11How can fatty change be identifiedH&E
    Sudan black
    Oil Red O
  12. 12Why are sections frozen prior to stainingfat dissolves in alcohols used in processing of sections to make slides leaving empty vacuoles
  13. 13What are the 5 causes of fatty change within the liver1 - excess delivery of free fatty acids/TG
    2 - impaired metabolism
    3 - impaired synthesis of apoprotein
    4 - impaired production and release of lipoprotein
    5 - decreased oxidation of fatty acids
  14. 14What are the causes of hypoxia associated with fatty changeanaemia
    chronic passive congestion
    ischaemia
    toxins
  15. 15What are the causes of fatty change within the bodystarvation
    overeating
    metabolic disease
    Diabetes
  16. 16How does starvation cause fatty changemobilisation of fat reserves, liver is unable to metabolise all released free fatty acids so they are stored
  17. 17How does overeating cause fatty changeobesity where the dietary intake is greater than the energy expenditure. Fat is stored by the liver before movement to fat stores
  18. 18How does metabolic disease lead to fatty changederanged carbohydrate metabolism - glucose not available for uptake into the tissues.
    Alternative energy sources are used
  19. 19How does Diabetes mellitus lead to fatty changedeficiency of insulin which is required for cellular glucose utilisation.
    Cells can't use glucose so demand for alternative energy leads to fat mobilisation
  20. 20T/F Cellular swelling and fatty change are reversibleTrue
  21. 21What processes occur during necrosis- irreversible cell injury -> cell death
    - loss of membrane integrity
    - evokes an inflammatory reaction
  22. 22What are the 3 main causes of necrosisloss of blood supply - tissue needs blood supply to remain alive
    living agents - bacteria, viruses, fungi, parasites
    non-living agents - chemicals or physical injuries
  23. 23How does loss of blood supply cause necrosishypoxia - reduced blood supply
    ischaemia - loss of blood supply
    infarction - necrosis of a portion of tissue due to an interruption of blood supply to that portion
  24. 24How does tissue ischaemia occur- compression of blood vessel from outside
    - narrowing of vessel lumen due to mural wall thickening
    - blockage of vessel lumen
  25. 25Describe the process of intestinal torsion1 - venous outflow impeded
    2 - organ swells due to congestion
    3 - swelling impedes arterial flow
    4 - arterial flow stops
    5 - tissue undergoes ischaemic necrosis
    6 - intestinal blood barrier compromised
    7 - bacterial toxins absorbed - death or intestine friable, prone to rupture
  26. 26What processes occur following narrowing of the vessel lumenarteriosclerosis - hardening/ thickening of the artery. May occur in hypertension
    atherosclerosis - cholesterol deposits, inducing an inflammatory reaction. Rare in animals
  27. 27What processes occur following blockage of the lumenthrombosis and embolism
  28. 28Name physical agents that can cause necrosisburns, cold, frostbite, x rays, pressure, pinching/crushing of tissue
  29. 29Name chemical agents that can cause necrosisdirectly caustic or corrosive in action or exert their effects when absorbed and metabolised to a more toxic substance
  30. 30What are the gross and histological features of necrotic tissue- colour change in the tissue - dead tissue tends to be paler
    - consistency of the tissue - appearance of the centre of the necrotic lesion will vary depending on the agent responsible/tissue it is acting on
  31. 31What are the 3 types of necrosis - gross description1 - coagulative - remains firm
    2 - liquefactive - becomes liquid
    3 - caseous - a mixture of the two - cottage cheese like.
  32. 32How does coagulative necrosis appear grossly?firm and dry on cut surface
    still resembles in outline the adjacent viable tissue
  33. 33How does coagulative necrosis appear microscopically- tissue architecture is preserved
    - cells may appear larger and their outline may be lost
    - cytoplasm appears larger and their outline may be lost
    - cytoplasm appears structureless and homogenous
    - important nuclear changes
  34. 34What are the causes of coagulative necrosis- bacterial toxins
    - infarction
    - some foci of viral replication e.g. herpesvirus
  35. 35What are the 2 types of liquefactive necrosismalacia - CNS
    abscesses - anywhere in the body
  36. 36What is the cause of cerebrocortical necrosis in ruminantsthiamine (Vit B) deficiency
  37. 37What are abscesses-pyogenic organisms
    - bacteria cause necrosis and attract vast numbers of neutrophils
    - dying neutrophils release proteolytic enzymes which digest necrotic tissue
    - pus = dead and dying neutrophils, dead tissue and organisms
  38. 38What are the 3 features of liquefactive necrosis that appear microscopically- necrotic area
    - pyogenic membrane
    - fibrous tissue capsule
  39. 39What is the necrotic area composed of- varying stages of degeneration and death of neutrophils
    - homogenous structureless mixture of remnants staining faintly bluish
  40. 40What is the pyogenic membrane and what is it composed of- reddish membrane on inner surface of the capsule
    - composed of blood vessels responsible for transporting the vast number of neutrophils to the lesion
  41. 41What is the fibrous tissue capsule- part of the host inflammatory reaction
    - walls off the irritant
  42. 42How does caseous necrosis appear grossly- cheese like necrosis
    - white to grey to yellow in colour
    - varying consistency
    - mixture of coagulative and liquefactive necrosis
  43. 43What are the causes of caseous necrosiscaused by specific organisms e.g. mycobacteria or fungi
  44. 44Mycobacterium tuberculosis is an example of which type of necrosis and which stain confirms its presenceCaseous
    Zhiel-Neelsen
  45. 45How does mycobacterium tuberculosis appear microscopically- complete loss of architecture
    - purplish necrotic material - due to random mixing of nuclear/cytoplasmic components that stain with H&E
    - large proportion of necrotic tissue is composed of macrophages
  46. 46What is dystrophic calcification and which species is it commonly found in- calcium deposits makes the tissue more inert
    - common in cattle and sheep
  47. 47How does dystrophic calcification appear grossly- calcium granules can be palpated
    - knife grates on sectioning
    - chalk white in colour
    - yellow-green tinge due to eosinophils
  48. 48How does dystrophic calcification appear microscopically and what stain is used for identification- dark blue colour
    - shattering of tissue - microtome mark
    - stains black with Von Kossa stain
  49. 49How does fat necrosis appear grossly- area of focal opacity
    - v hard consistency
  50. 50What is the pathogenesis of fat necrosis- adipocytes die
    - fat broken down into fatty acids
    - FA combine with salts e.g. Ca2+, Na+, K+
    - soaps are formed - provokes inflammatory response
    - foci remain indefinitely and calcify
  51. 51Which condition is fat necrosis commonly seen in and whypancreatitis
    lipase release from pancreas
  52. 52What are the 3 types of fat necrosis1 - enzymatic
    2 - traumatic
    3 - diet related
  53. 53What is enzymatic necrosis- release of pancreatic enzymes especially lipase from a damaged pancreas
    - goes into adjacent mesenteric fat
  54. 54What is traumatic necrosis- subcut tissue following trauma
    - especially brisket of recumbent animals due to prolonged pressure
  55. 55What is diet related necrosis- rarely in cats associated with diets lacking antioxidants e.g. vit E
  56. 56What are the nuclear changes in necrosispyknosis
    karyorrhexis
    karyolysis
  57. 57What is pyknosis- normal nuclear structure is replaced by a very dense, hazily staining, smaller angular mass of chromatin
  58. 58What is karyorrhexisnucleus has broken up into several dense pieces
  59. 59What is karyolysisnuclear staining with haemotoxylin becomes faint and ghost outline of nucleus remains
  60. 60What are the cytoplasmic changes that appear in necrosissometimes stains brighter pink
  61. 61What are the mitochondrial changes that appear in necrosisdense bodies

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BSc Pathology Flashcards on Cell degeneration and necrosis, created by Teresa Richards on 04/10/2016.
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Teresa Richards
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