Cell Injury Flashcards

1
Q

Is cell injury reversible

A

initially it is reversible;
then becomes irreversible.
if injury is severe from onset, cell undergoes apoptosis

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2
Q

2 ways cell death occurs

A

apoptosis

necrosis

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3
Q

causes of cell injury (8)

A
  1. oxygen deprivation
  2. nutritional imbalances
  3. infectious agents
  4. immune response
  5. genetic defects
  6. chemical agents
  7. physical agents
  8. AGING
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4
Q

hypoxia

A

deficiency of oxygen

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5
Q

ischaemia

A

inadequate blood flow to tissues . leads to hypoxia.

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6
Q

ischaemia - causes

A
  1. narrowing of blood vessel
  2. blockage of bv
  3. decresed blood pressure
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7
Q

effects of ischaemia

A

oxygen deficiency
glucose deficiency
nutrient deficiency

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8
Q

causes of hypoxia (4)

A
  1. lung disease
  2. ischaemia
  3. low O2 concn (high altitudes)
  4. reduced oxygen carrying capacity of blood (anaemia/ CO poisoning)
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9
Q

when are gross morphological changes visible in a cell

A

long after cell has died

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10
Q

sequence of events in cell death?

A
  1. decreasing cell function
  2. cell death ensues
  3. ultrastructural changes
  4. light microscopic changes
  5. gross morphological changes
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11
Q

morphological changes of reversibly injured cell detectable by light microscope

A
  1. swelling
  2. vacuolar degeneration OR hydropic change (accumulation of water intracellularly)
  3. fatty change
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12
Q

morphological changes of reversibly injured cell detectable by electron microscope (ultrastructurally)

A
  1. nuclear: clumping of CHROMATIN
  2. dilation of ER
  3. swelling of mitochondria & appearance of phospholipid-rich densities & calcification
  4. PM blebbing;
  5. loosening of intercellular attachments
  6. distortion of microvilli/blunting
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13
Q

define the fatty change in reversible injury

A

abnormal build up of triglycerides within parenchymal cells

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14
Q

causes for fatty change

A
  1. alcohol / toxins
  2. protein malnutrition
  3. diabetes
  4. obesity.
  5. hypoxia
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15
Q

cells affected by fatty change

A
those dependent on fat metabolism:
-myocardial cells
-hepatocytes
skeletal muscle
kidney and others
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16
Q

what’s different about necrotic, H&E stained cells

A

they have increased eosinophilia (redness) due to loss of RNA and less proteins (denatured proteins)

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17
Q

what can ultimately happen to necrotic cells

A

become calcified (dystrophic calcification)

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18
Q

ultrastructural changes in cell necrosis

A
  1. discontinuities in membrane of organelles and plasma membrane
  2. dilation of mitochondria
  3. disruption of lysosomes
  4. nuclear dissolution
  5. intracytoplasmic myelin figures
19
Q

nuclear changes in necrotic cells

A

dissolution of basophilic chromatin (KARYOLYSIS)
PYKNOSIS - nuclear shrinkage +increased basophilia
KARYorrHEXIS - fragmentation pyknotic nucleus

20
Q

why all these nuclear changes

A

due to breakdown of DNA and chromatin

21
Q

types of tissue necrosis (patterns) (6)

A
  1. fibrinoid necrosis
  2. fat necrosis
  3. coagulative necrosis
  4. liquefactive necrosis
  5. gangrenous necrosis
  6. caseous necrosis
22
Q

coagulative necrosis facts

A

basic tissue architecture preserved;

but firm texture

23
Q

infarction

A

term can be used to describe necrosis of all organs/tissues EXCEPT brain

24
Q

liquefactive necrosis

A

digestion of dead cells = transformation into liquid viscous mass
typical of bacterial infections (pus) = abscesses

25
Q

gangrenous necrosis

A

caused by acute ischaemia
may/not have infection present too
coagulative&often superimposed liquefactive necrosis

26
Q

caseous necrosis

A

cheese-like, friable white appearance. encountered mainly w TB

27
Q

with which necrosis pattern is granuloma often seen

A

caseous necrosis

28
Q

granuloma?

A

gathering of cell debris and fragmented cells bordered by inflammatory cells

29
Q

fat necrosis

A

saponification of fat - whitish/chalky material produced.

30
Q

examples of fat necrosis

A

breast - following trauma

acute pancreatitis

31
Q

fibrinoid necrosis

A

deposition of fibrin in the walls of blood vessels

32
Q

how to detect tissue necrosis

A

detect biochemical markers (enzymes and other proteins) in blood and urine

33
Q

biochemical markers of tissue necrosis?

A

substances released from necrotic cells

34
Q

Apoptosis

A

programmed cell death

activation of internal self-destruction programme

35
Q

is apoptosis only pathological?

A

it’s necessary for normal function also

36
Q

when apoptosis

A

injury beyond repair

37
Q

morphology of apoptosis

A
  • cell membrane stays intact

- fragmentation into apoptotic bodies

38
Q

fate of apoptotic bodies

A

phagocytosed by macrophages and neighbouring cells

39
Q

pro of apoptosis

A

minimal disruption to neighbouring cells

40
Q

compare cell size in APOPTOSIS v NECROSIS

A

A - reduced (shrinkage)

N - swelling

41
Q

compare nucleus

A

A - fragmentation

N - Pyknosis –> karyorrhexis –> Karyolysis (?)

42
Q

compare PM

A

A - intact

N- disrupted

43
Q

compare Adjacent inflammation

A

A - no

N - frequent

44
Q

compare Physiologic or pathologic

A

A - can be either

N - always PATHOLOGIC