Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

classifications of reverisble cell injurt?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

degrees of water accumaltion in a cell ad their name

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

mild accumaltion of water is called?

A

cloudy swelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

moderate accumulation of water in a cell is called?

A

vacuolar degeneration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

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

A

hydropic degeneration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what organs are affected during disturbed water metabolism?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

pathogenesis of cloudy swelling?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

pathogenesis of hydropic degenration

A

inc cell membrane permeability thus influx of water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

organs affected from steatosis?

A

liver,kidney heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

gross pic of fatty change in the organs?

A

inc size of organ
pale yellow color
soft

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is signet ring cell?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is lipomatosis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

mention the changes associated with mucopolysaccharide metabolism

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

cell size of cell during nEcrosis?

A

Enlarges

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

cell size during apoptosis

A

Shrinked

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

cell membrane during necrosis and apoptosis?

A

necrosis: disruoted
apoptosis: intact

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

necrosis or apoptosis is present with adjacent inflamamtion?

A

Necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
gross pic of necrosis?
pale tissue with peripheral hyperaemia
25
which is due to pathologic reasons only... necrosis or apoptosis?
necrosis
26
types of necrosis?
1. Coagulative necrosis 2. Liquefactive necrosis 3. Caseous necrosis 4. Fat necrosis 5. Fibrinoid necrosis 6. Gangrenous necrosis
27
where does coagulative necrosis occur?
in hypoxic cell death (anywhere except for the brain)
28
which type of necrosis the cell architecture is still intact?
coagulative necrosis
29
caseous necrosis
TB
30
gross description of tb/caseous necrosis
yellow-white, friable , necrotic tissue
31
microscopic description of caseous necrosis
-no cellular outline -necrotic area is surrounded by specific inflammatory reaction
32
whats fat necrosis?
A focal area of fat destruction
33
mechanism of fat necrosis
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
GANGRENE def
Massive necrosis followed by putrefaction
35
causes of gangrene?
A. Arterial occlusion. examples: Thrombosis Embolism Strangulation Vascular compression B.Venous occlusion C.Bacterial infection “infective gangrene”/putrefaction.. example: Saprophytes “bacteria”
36
causitive agent of putrefaction and how?
SAPROPHYTES act on dead tissues Dead tissues hydrogen sulphide Hydrogen sulphide + Iron “from HB” → Iron sulphide “black”
37
What is the cause of the black coloration of the gangrenous tissue?
Saprophytes “bacteria” → act on dead tissues Dead tissues hydrogen sulphide Hydrogen sulphide + Iron “from HB” → Iron sulphide “black”
38
senile gangrene is a type of dry gangrine which can occur in limbs especially feet... why is that?
most distant from heart”
39
senile gangrene is a type of dry gangrine which can occur with old age.... why?
atheroscelrosis
40
why dry gangrenes are dry?
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
tight shoes can lead to what?
its a slight trauma that can cause dry gangrene
42
whats line of demarcation
its a line that can be seen by naked eyes that between gangrenous and healthy tissue A red zone of acute inflammation
43
whats line of separation?
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
why is the stump is conical??
Because gangrene spreads higher up in skin & SC tissue (less arterial blood supply) than muscle and bones.
45
how is moist gangrene 7slt?
Sudden occlusion of artery and vein so No evaporation of fluid → rapid putrefaction→ toxemia
46
site of moist gangrene?
-internal organs (intestine) -extremities in severe crush wounds.
47
what characterizes moist gangrene?
Poor line of demarcation * Absent line of separation * Rapid spread of gangren
48
what is diabetic foot?
wet gangrene affecting the foot of the diabetic folks
49
why diabetic gangrene occur?
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
whats bed pressure sore?
wet gangrene :Bed ridden→ thrombosis of vessels → tissue necrosis → ulcers over bony prominences (vertebrae sites)
51
why in the intestinal gangrene (wet gangrene) the Gangrene extends very rapidly
Because intestine is rich in tissue fluids& saprophytes
52
examples on infective gangrene?
-Lung gangrene on top of lung abscess -Cancrum oris cheeks of debilitated children “bacteria: Treponema vincenti” Severe toxemia
53
whats cancrum oris / noma?
necrotizing ulcerative Stomatitis.
54
involved bacteria in gas gangrene?
clostridia family
55
involved bacteria in cancrum oris (infective gangrene)?
treponema vincenti
56
bacteria involoved in putrefaction in wet gangrene?
saprophytes
57
Predisposing factors of gas gangrene om ree7a zeft?) co2 and H2S
ompound fractures, penetrating injury and agricultural acciden
58
just read ana already t3bt
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
gross description of gas gangrene?
area is swollen, oedematous with a foul smelling discharge
60
microscopic description of gas gangrene?
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
OSPE: mention the causes of necrosis
loss of blood supply trauma toxins physical and chemical agent
62
pathopgenesis of diabetic gangrene?
-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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions