Necrosis And Apoptosis Flashcards

1
Q

MECHANISMS OF CELL INJURY?

A

1.Depletion of ATP
2.Damage to Mitochondria
3.Defects in Membrane Permeability
4.Damage to DNA and Proteins
5.Influx of Calcium: Increased Ca2+ in turn activates a number of enzymes which
cause damage eg: ATPases, phospholipases, proteases &
endonucleases .
6. Free radical injury: Accumulation of oxygen-derived free radicals (oxidative stress):

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2
Q
  1. Free radical injury: Accumulation of oxygen-derived free radicals (oxidative stress They are produced via: ?
A

Normal metabolism/ respiration. ii. Ionizing radiation injury e.g. UV light, x-rays result in production of
free radicals. iii. Chemical toxicity: enzymatic metabolism of exogenous chemicals
or drugs. iv. Oxygen therapy and reperfusion injury v. Immune response or inflammation (neutrophil oxidative burst)

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3
Q

Earliest changes associated with cell injury are reversible. They are: ?

A

Swelling & vacuolization of cytoplasm called hydropic/ vacuolar
degeneration. 2. Mild mitochondrial swelling. the rough endoplasmic reticulum and
plasma membrane damage. 3. Defect in protein synthesis. 4. Mild eosinophilia of cytoplasm (due to decrease in cytoplasmic RNA)

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4
Q

type of cell death, in which there is enzymatic

digestion and denaturation of intracellular protein in the dying cell.

A

Necrosis

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5
Q

NECROSIS properties

A

cell death, in which there is enzymatic
digestion and denaturation of intracellular protein in the dying cell. • Necrotic cells are unable to maintain membrane integrity, and
their contents often leak out, It is usually associated with
inflammation in the surrounding tissue. • The enzymes responsible for digestion of the cell are derived either
from the lysosomes of the dying cells themselves or from the
lysosomes of leukocytes that are recruited as part of the
inflammatory reaction to the dead cells. • It involves the death of a group of cells in one area.

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6
Q

Necrosis Nuclear changes ?

A
1.karyolysis : fading of
chromatin basophilia.
   2. pyknosis: characterized
by nuclear shrinkage and
increased basophilia.
   3. karyorrhexis: the nucleus
undergoes fragmentation.
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7
Q

There are 6 types/pattern

of necrosis ?

A
   coagulative necrosis
   liquefactive necrosis
   caseous necrosis
   fat necrosis
   fibrinoid necrosis
 Gangrenous necrosis
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8
Q

Coagulative necrosis properties ?

A
  1. blood flow to an organ is affected
    leading to ischemic/hypoxic death of cells in that organ
  2. . It is seen in all organs except the brain.
  3. A localized area of coagulative necrosis is called an infarct.
  4. Gross: The affected organ looks pale and firm/solid.
  5. preservation of the general tissue architecture
  6. initially the basic ghost outline of the affected/coagulated cell remains preserved for a few day
  7. the nucleus is lost. The cell cytoplasm is eosinophilic.
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9
Q

preservation of the general tissue architecture and initially the basic ghost outline of the affected/coagulated cell remains preserved for a few days but the nucleus is lost. The cell cytoplasm is eosinophilic.

Necrosis ?

A

Coagulative necrosis

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10
Q

Liquefactive necrosis properties ?

A
  1. Seen in focal bacterial or, fungal infections
  2. enzymes of leukocytes digest (“liquefy”) the tissue.
  3. hypoxic death of cells within the central
    nervous system often induces liquefactive necrosis .
  4. liquefaction completely digests
    the dead cells, resulting in transformation of the tissue into a
    liquid viscous mass.
  5. process was initiated by acute inflammation, the material is frequently creamy yellow and is called pus
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11
Q

Caseous necrosis properties?

A
  1. Tuberculosis infection
  2. friable yellow-
    white appearance
  3. Tissue architecture is completely
    obliterated and cellular outlines
    cannot be detected.
  4. necrosis often enclosed within a
    distinctive inflammatory border;
    this appearance is characteristic
    and known as a granuloma .
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12
Q

Tuberculosis of the lung, with a large Occur in foci of tuberculous
area of ????? containing infection.
yellow-white (cheesy) debris.

A

Caseous necrosis

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13
Q

Fat necrosis ?

A
  1. acute pancreatitis in which the injured pancreatic cells
    release the lipase enzyme into the fat in the abdominal cavity and cause
    enzymatic digestion of fat cells. • The released lipase breaks down the fat cells into glycerol and free fatty acids.
    The produced fatty acids combine with calcium circulating in the blood to
    produce calcium soaps which looks like chalky white spots in the necrotic fat.
    This process is called as fat saponification.
  2. outlines of necrotic/dead fat cells can be seen, with basophilic calcium
    deposits, surrounded by an inflammatory reaction.
  3. breast fat and other fatty areas due to
    traumatic injury.
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14
Q

saponification in the mesentery. The areas of white chalky deposits represent calcium soap formation at sites of lipid breakdown.

Eg ?

A

Foci of fat necrosis

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15
Q

Fibrinoid necrosis properties?

A
  1. Seen in immune reactions
    involving blood vessels .
  2. Complexes of antigens and
    antibodies are deposited in the
    walls of arteries.
  3. result in a bright pink and
    amorphous appearance in
    H&E stains, called “fibrinoid”
    (fibrin-like)
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16
Q
Deposits of these “immune
complexes,” together with fibrin
that has leaked out of vessels,
result in a bright pink and
amorphous appearance in
H&E stains, called “fibrinoid”
(fibrin-like)
A

Fibrinoid necrosis

17
Q

usually applied to a limb, generally the lower leg, that has
lost its blood supply and has undergone necrosis (typically
coagulative necrosis).

A

Gangrenous necrosis

18
Q

wet gangrene ??

A

When bacterial infection is superimposed there is more
liquefactive necrosis because of the actions of degradative
enzymes in the bacteria and the attracted leukocytes

19
Q

• Dry gangrene?

A

ischemic coagulative necrosis of tissue without

superadded infection .

20
Q

is ischemic coagulative necrosis of tissue without
superadded infection .
• The affected part is dry, shrunken and dark reddish-black .

??

A

Dry gangrene

21
Q

Programmed cell death.

A

Apoptosis

22
Q

Apoptosis properties?

A

Is a pathway of cell death that is induced by a tightly regulated
suicide program in which cells destined to die activate enzymes
capable of degrading the cells’ own nuclear DNA and nuclear and
cytoplasmic proteins. • The plasma membrane of the apoptotic cell remains intact. The cells rapidly shrink and fragment into apoptotic bodies.

23
Q

Two distinct pathways
involved on caspase
activation ?

A
  1. Mitochondrial
    pathway.
    1. Death receptor
      pathway.
24
Q

Physiological cause of apoptosis ?

A
  1. during embryogenesis,
    including implantation,
    organogenesis
  2. hormone-
    dependent tissues upon
    hormone deprivation in
  • endometrial cell breakdown
    during the menstrual cycle,
  • regression of the lactating
    breast after weaning
25
Q

Pathological cause of apoptosis?

A

Damaged DNA: Elimination of the cell may be a better alternative than risking mutations.
Infection: • Viral infections, in which loss of infected cells is
largely due to apoptotic death