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skin as epithelium > cell injury degeneration and death > Flashcards

cell injury degeneration and death Flashcards

1
Q

degeneration is …… while cell death is …..

A

reversible….irreversible

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2
Q

classifications of reverisble cell injurt?

A

changes associated with Disturbed
-water metabolism
-Disturbed fat metabolism
-Disturbed Mucopolysaccharides
iHyaline change

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3
Q

degrees of water accumaltion in a cell ad their name

A

mild → cloudy swelling
moderate → vacuolar degeneration
severe → hydropic degeneration

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4
Q

mild accumaltion of water is called?

A

cloudy swelling

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5
Q

moderate accumulation of water in a cell is called?

A

vacuolar degeneration

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6
Q

whats the name of severe accumulation of water in the cell n

A

hydropic degeneration

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7
Q

what organs are affected during disturbed water metabolism?

A

specialized cells of parenchymatous organs (kidney, liver , heart)

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8
Q

pathogenesis of cloudy swelling?

A

mitochondrial swelling → fragmentation →
low ATP production → failure of Na pump→ retention of Na and
water inside cell

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9
Q

pathogenesis of hydropic degenration

A

inc cell membrane permeability thus influx of water

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10
Q

fatty change=steatosis which is abnormal accumulation of fat inside cells… what are its causes?

A

1.Bacterial toxins (diphtheria)
2.Chemical toxins
3.Malnutrition and chronic alcoholism

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11
Q

organs affected from steatosis?

A

liver,kidney heart

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12
Q

gross pic of fatty change in the organs?

A

inc size of organ
pale yellow color
soft

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13
Q

microscopic shape of organs affected from steatosis/fatty change

A

fat globules distend the cell (1)→ unite to a single large one
pushing the nucleus “signet ring cell”(2

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14
Q

what is signet ring cell?

A

it is the result of fusion of accumulated fat globules then pushing the nucleus

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15
Q

what is lipomatosis?

A

Lipomatosis is Localized accumulation of
fat not necessarily
associated with marked
obesity

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16
Q

diff between obesity and lipomatosis?

A

-Obesity: Excessive accumulation of
fats in normal sites due to
over nourishment along
with sedentary life or to
!disturbance of endocrine
glands.!
-Lipomatosis: Localized accumulation of
fat not necessarily
associated with marked
obesity

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17
Q

mention the changes associated with mucopolysaccharide metabolism

A

-Mucoid degeneration: accumulated mucin
within epithelial cell
-Myxomatous degeneration: accumulated MPS
in connective tissue

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18
Q

what’s hyaline change (degeneration)

A

hyaline material is eosinophilic, homogenous and structureless.
can deposit intra or extra cellular within CT depending on the disease process

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19
Q

whats the diff between necrosis and apoptosis?

A

-Necrosis :Local death of a group of cells inside the living tissue
-Apoptosis: Regulated, programmed cell death

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20
Q

cell size of cell during nEcrosis?

A

Enlarges

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21
Q

cell size during apoptosis

A

Shrinked

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22
Q

what happens to the nucleus in both necrosis and apoptosis?

A

necrosis: Pyknosis=nuclear contestation , karyorrhexis: nuclear fragmentation, karyolysis: dissolution of nucleas <:
apoptosis: nuclear fragmentation

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23
Q

cell membrane during necrosis and apoptosis?

A

necrosis: disruoted
apoptosis: intact

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24
Q

necrosis or apoptosis is present with adjacent inflamamtion?

A

Necrosis

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25
Q

gross pic of necrosis?

A

pale tissue with peripheral hyperaemia

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25
Q

which is due to pathologic reasons only… necrosis or apoptosis?

A

necrosis

26
Q

types of necrosis?

A
  1. Coagulative necrosis
  2. Liquefactive necrosis
  3. Caseous necrosis
  4. Fat necrosis
  5. Fibrinoid necrosis
  6. Gangrenous necrosis
27
Q

where does coagulative necrosis occur?

A

in hypoxic cell death (anywhere except for the brain)

28
Q

which type of necrosis the cell architecture is still intact?

A

coagulative necrosis

29
Q

caseous necrosis

A

TB

30
Q

gross description of tb/caseous necrosis

A

yellow-white, friable , necrotic tissue

31
Q

microscopic description of caseous necrosis

A

-no cellular outline
-necrotic area is surrounded by specific inflammatory reaction

32
Q

whats fat necrosis?

A

A focal area of fat destruction

33
Q

mechanism of fat necrosis

A

In acute pancreatitis: release of pancreatic
enzymes into pancreatic substance
→ liquefy membranes of fat cells
→release of fatty acids→ fatty acids + Ca++
→ chalky- white areas

34
Q

GANGRENE def

A

Massive necrosis followed by putrefaction

35
Q

causes of gangrene?

A

A. Arterial occlusion. examples:
Thrombosis
Embolism
Strangulation
Vascular compression
B.Venous occlusion
C.Bacterial infection “infective gangrene”/putrefaction.. example: Saprophytes “bacteria”

36
Q

causitive agent of putrefaction and how?

A

SAPROPHYTES
act on dead tissues
Dead tissues
hydrogen sulphide
Hydrogen sulphide + Iron “from HB” → Iron sulphide “black”

37
Q

What is the cause of the black coloration of the
gangrenous tissue?

A

Saprophytes “bacteria” → act on dead tissues
Dead tissues
hydrogen sulphide
Hydrogen sulphide + Iron “from HB” → Iron sulphide “black”

38
Q

senile gangrene is a type of dry gangrine
which can occur in limbs especially feet… why is that?

A

most distant from heart”

39
Q

senile gangrene is a type of dry gangrine
which can occur with old age…. why?

A

atheroscelrosis

40
Q

why dry gangrenes are dry?

A

arteries are impeded , veins are patent (مفتوحة عادي) therefore normal drainage of fluids
as well as surface evaporation in limbs leads to poor tissue fluids

41
Q

tight shoes can lead to what?

A

its a slight trauma that can cause dry gangrene

42
Q

whats line of demarcation

A

its a line that can be seen by naked eyes that between gangrenous and healthy tissue
A red zone of acute inflammation

43
Q

whats line of separation?

A

line cant be seen by naked eyes which is about : A groove in the area of inflammation →
deepens → dead part separates from the healthy tissue

44
Q

why is the stump is conical??

A

Because gangrene spreads higher up in
skin & SC tissue (less arterial blood supply) than muscle and
bones.

45
Q

how is moist gangrene 7slt?

A

Sudden occlusion of artery and vein so No evaporation of fluid → rapid putrefaction→ toxemia

46
Q

site of moist gangrene?

A

-internal organs (intestine)
-extremities in severe crush wounds.

47
Q

what characterizes moist gangrene?

A

Poor line of demarcation
* Absent line of separation
* Rapid spread of gangren

48
Q

what is diabetic foot?

A

wet gangrene affecting the foot of the diabetic folks

49
Q

why diabetic gangrene occur?

A

Starts dry in big toes→ rapidly moist due to 2ry infection Severe toxemia
so what happens:
premature atherosclerosis→ elevated tissue sugar level → ↓ immunity
→ sensory loss → slight injuries are not felt

50
Q

whats bed pressure sore?

A

wet gangrene :Bed ridden→ thrombosis of vessels → tissue necrosis → ulcers over
bony prominences (vertebrae sites)

51
Q

why in the intestinal gangrene (wet gangrene) the Gangrene extends very rapidly

A

Because intestine is rich in
tissue fluids& saprophytes

52
Q

examples on infective gangrene?

A

-Lung gangrene on top of lung abscess
-Cancrum oris cheeks of debilitated children “bacteria:
Treponema vincenti” Severe toxemia

53
Q

whats cancrum oris / noma?

A

necrotizing ulcerative
Stomatitis.

54
Q

involved bacteria in gas gangrene?

A

clostridia family

55
Q

involved bacteria in cancrum oris (infective gangrene)?

A

treponema vincenti

56
Q

bacteria involoved in putrefaction in wet gangrene?

A

saprophytes

57
Q

Predisposing factors of gas gangrene om ree7a zeft?) co2 and H2S

A

ompound fractures, penetrating injury and
agricultural acciden

58
Q

just read ana already t3bt

A

Agricultural accidents→ deep wounds contaminated by manure
containing anaerobic spores → vascular damage→ local ischemia →
germination of spores
anareboic spores so it will go to SC

59
Q

gross description of gas gangrene?

A

area is swollen, oedematous with a foul smelling discharge

60
Q

microscopic description of gas gangrene?

A

Connective tissue and muscles are
oedematous and necrotic with gas
formation.
Non- specific inflammatory
reaction
The causative organism may be
seen in the wound (gram stain)

61
Q

OSPE: mention the causes of necrosis

A

loss of blood supply
trauma
toxins
physical and chemical agent

62
Q

pathopgenesis of diabetic gangrene?

A

-diabetes… atherosclerosis…thrombosis
-sensory loss so slight injuries are not felt
- inc sugar level in blood so low immunity
it starts in the big toe bc rapidly moist infective gangrene due to 2ndry infection, therefore the areas are edematous and moist
-severe toxiemia

skin as epithelium (3 decks)

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