Cell Injury Flashcards

(44 cards)

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
gangrenous necrosis
caused by acute ischaemia may/not have infection present too coagulative&often superimposed liquefactive necrosis
26
caseous necrosis
cheese-like, friable white appearance. encountered mainly w TB
27
with which necrosis pattern is granuloma often seen
caseous necrosis
28
granuloma?
gathering of cell debris and fragmented cells bordered by inflammatory cells
29
fat necrosis
saponification of fat - whitish/chalky material produced.
30
examples of fat necrosis
breast - following trauma | acute pancreatitis
31
fibrinoid necrosis
deposition of fibrin in the walls of blood vessels
32
how to detect tissue necrosis
detect biochemical markers (enzymes and other proteins) in blood and urine
33
biochemical markers of tissue necrosis?
substances released from necrotic cells
34
Apoptosis
programmed cell death | activation of internal self-destruction programme
35
is apoptosis only pathological?
it's necessary for normal function also
36
when apoptosis
injury beyond repair
37
morphology of apoptosis
- cell membrane stays intact | - fragmentation into apoptotic bodies
38
fate of apoptotic bodies
phagocytosed by macrophages and neighbouring cells
39
pro of apoptosis
minimal disruption to neighbouring cells
40
compare cell size in APOPTOSIS v NECROSIS
A - reduced (shrinkage) | N - swelling
41
compare nucleus
A - fragmentation | N - Pyknosis --> karyorrhexis --> Karyolysis (?)
42
compare PM
A - intact | N- disrupted
43
compare Adjacent inflammation
A - no | N - frequent
44
compare Physiologic or pathologic
A - can be either | N - always PATHOLOGIC