Cell Injury Flashcards

1
Q

Define: Reversible Cell Injury

A

Can return to normal when the injurious stimuli are removed

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2
Q

What are some examples of reversible cell injury?

A
  • Cellular Swelling

- Fatty Changes

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3
Q

Define Irreversible Cell Injury

A

Cell injury that is past the point of no return. This will result in cell death.

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4
Q

What are examples of irreversible cell injury?

A
  • Necrosis

- Apoptosis

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5
Q

Cell Swelling is also known as…

A

Hydropic Degeneration OR Hydropic Change

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6
Q

CNS Cell Swelling is referred to as..

A

Cytotoxic Edema

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7
Q

Epidermis Cell Swelling is referred to as…

A

Ballooning Degeneration

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8
Q

—- Cardiomyocytes, renal tubual epithelium, hepatocytes
- Endothelium — 
- CNS neurons, oligodenrocytes, astrocytes
All the above are cells that are…

A

VERY vulnerable to hypoxic/cell swelling

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9
Q

Cell swelling is characterized by an increase in ___________ & ___________

A

Cell size & Volume

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10
Q

If a cell has an overload of intracellular water…

A

The cell can’t maintain homestasis

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11
Q

The etiology of cellular swelling is defined as: any agent capable of disrupting cell homeostasis. T or F?

A

TRUE

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12
Q

What are the 2 main etiologies of cellular swelling?

A
  • Hypoxia

- Toxic Agents

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13
Q

Describe the gross appearance of cellular swelling:

A
  • Swollen organ, rounded edges
  • Pallor
  • Edges bulge when they are cut
  • Heavier than normal
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14
Q

What are the 4 characteristics we will see with cellular swelling at the histological/microscopic level?

A
  • Diluted cytoplasm
  • Enlarged cells (pale cytoplasm)
  • NUCLEUS IN NORMAL POSITION
  • Water does not stain, will have clear vacuoles
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15
Q

Define: Infarct

A

Area that is deprived of blood—- cells die there

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16
Q

Mild swelling (cells are pale & granular) is also known as…

A

“Cloudy Swelling”

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17
Q

As the cells become more swollen, vacuoles appear in the cytoplasm: This is termed ___________.

A

Hydropic Degeneration

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18
Q

Sever form, where the cells enlarge and eventually rupture: _____________

A

“Ballooning Degeneration”

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19
Q

When do we see “Ballooning Degeneration”?

A

It’s seen in some viral diseases (ex- Swinepox). It forms vesicles

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20
Q

What is the difference between hydropic degeneration of a cell and hypertrophy of a cell?

A

Hydropic change = Cell SWELLING

Hypertrophy = cell ENLARGEMENT

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21
Q

What are 3 cells where fatty changes occur?

A
  • HEPATOCYTES
  • Cardiomyocytes
  • Renal Tubular Epithelium
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22
Q

When fatty change occurs in Hepatocytes (fat metabolism), what happens?

A

There will be a decrease in protein synthesis, wihc results in a decrease in lipid transport

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23
Q

Cell damage characterized by intracytoplasmic vacuolation of fat can precede or accompany cell swelling. T or F?

A

TRUE

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24
Q

Define: Lipidosis

A

Impaired metabolism of fatty acids that results in accumulation of triglycerides in cytoplasm of parenchymal cells

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25
What organs does lipidosis occur in?
- LIVER! - Heart Muscle - Skeletal Muscle - Kidney
26
Hepatic Lipidosis >
Accumulation of triglycerides and other lipid metabolites (neutral fats and cholesterol) within parenchymal cells
27
What species/breed do we see this commonly in?
Shetland ponies / Minis
28
When we see fat on histology, what color will it be?
It will be clear. b/c fat will be washed off w/ the alcohol step of gram staining
29
What is the only way triglycerides can be transported out of the liver?
By lipoproteins. BUT in order to make a lipoprotein, you need to a apoprotein and triglyceride. If there is impaired synthesis of apoprotein...then you cannot make a lipoprotein... and therefore cannot transport the triglyceride out of the liver.
30
There are 3 different conditions associated with Fatty Liver. They are...
- Physiological - Nutritional - Endocrine Disease
31
_________: late pregnancy, lactation, or dietary excess of fats
PHYSIOLOGICAL
32
__________: obesity, protein malnutrition, STARVATION*
NUTRITIONAL
33
__________: diabetes mellitus & feline fatty liver syndrome
ENDOCRINE DISEASE
34
Fatty change gross appearance of liver:
- Diffuse yellow - Enhanced reticular pattern if specific zones of hepatocytes are affected - edges are rounded & budge on cut section - tissue is soft & friable - cuts easily - GREASY - LIVER SECTIONS MAY FLOAT IN FORMALIN
35
What is Niemann Pick Disease?
Phospholipids sphingomyelin, its a lysosomal storage disease
36
Histologically, you can tell a slide is fat compared to edema because the nucleus will be where?
It will be pushed to the side! Peripheral nuclear displacement!!!
37
The prognosis of fatty change initially is...
Reversible, but can lead to hepatocytes death---- which is irreversible.
38
Irreversible Cell Injury is associated with:
- Severe swelling of mitochondria - Damage to plasma membrane (giving rise to myelin figures) - Swelling of lysosomes
39
Cell Death:
MAINLY NECROSIS | -apoptosis also contributes
40
Necrosis is also called:
- Oncosis | - Oncotic Necrosis
41
Necrosis occurs following cell death in the ________ animal.
LIVING ANIMAL.
42
Cell death after irreversible cell injury by:
- Hypoxia - Ischemia - Direct cell membrane injury
43
Is necrosis a physiological event?
NO!!!!
44
Necrosis process=
Dewatering of proteins and enzymatic digestion of the cell
45
Necrosis outcome:
INFLAMMATION
46
Will apoptosis be accompanied by inflammation?
NO!! NEVER!!
47
Necrotic change timelines:
Ultrastructure-
48
Cell that has nuclear fading / undergoing dissolution: ________
Karyolysis (chromatolysis)
49
Cell that is undergoing nuclear shrinkage/small shrunken nucleus: _______
Pyknosis
50
Cell that is undergoing nuclear fragmentation/ruptured nucleus:__________
Karyorrhexis
51
Dnatured proteins on histology will look more pink (eosinophilic) T or F?
TRUE
52
Cells will look LESS basophilic (blue) when there has been a loss of _____.
RNA
53
Glassy appearance is due to a loss of ________.
Glycogen
54
"Moth eaten look" and vacuolation is due to enzymes digesting the cytoplasm. T or F?
TRUE
55
Calcification will not be seen. T or F?
FALSE! Calcification CAN be seen
56
Gross appearance of a fatty liver:
Pale, soft, friable, and zones of inflammation.
57
What is the one type of necrosis that is NOT seen grossly?
Firbrinoid Necrosis
58
Define COAGULATIVE NECROSIS:
Architecture of the tissue is preserved
59
Coagulative necrosis is always ACUTE. T or F?
TRUE!
60
Common causes:
ISCHEMIA / HYPOXIC INJURY ****except in the brain
61
Infarct=
Localized area of coagulative necrosis
62
_____: usually are in a wedge/triangular shape
Coagulative Necrosis
63
Nutritional Myopathy/White Muscle Disease is caused by:
Vit. E / Selenium Deficiency
64
Liquefactive Necrosis is typical in what location?
CNS
65
Dead cells are digested and transform into a liquid viscous mass
Liquefactive necrosis
66
Occurs in tissues with high neutrophils recruitment, high enzymatic release, or high lipid content.
Liquefactive necrosis
67
Necrotic Material =
PUS aha dead WBC
68
An example of liquefactive necrosis:
abscess
69
Polioencephalomacia
Softening of the GREY matter of the brain
70
_________: Associated with sulfur/ sulfate toxicity and Thiaminase production
Polioencephalomacia
71
Leukoencephalomalacia
Softening of the WHITE matter in the brain
72
________: Ingestion of Fusarium moniliforma (moldy corn!)
Leukoencephalomalacia
73
Leukomyelitis:
inflammation of the white matter in the spinal cord
74
________: Sarcocyst neurona in horses
Leukomyelitis
75
Polioencephalomalacia in Sheep
- Thiamine deficiency - Increased thiaminase activity - High level of sulfur/ water - Lead toxicity - Thiaminase containing plant= BRACKEN FERN
76
What are the 2 different kinds of abscesses?
- Septic > infection **MOST COMMON | - Sterile > nonliving irritants (drugs/injection)
77
What is the most common pus forming bacteria?
Pyogenic bacteria / Staphylococcus aureus
78
Caseous Necrosis
think cottage cheese! - Friable white area - Chronic - Not easily digestible by macrophages--- that's why there is so much inflammation
79
Causes of caseous necrosis: COWS> SHEEP>
COWS> Mycobacterium | SHEEP> Corynebacterium
80
Gangrenous Necrosis
Begins as coagulative necrosis > due to ischemia | Usually applies to distal extremities
81
_______ GANGRENE- No bacterial infection —-Mummification of tissue
DRY
82
_______GANGRENE- bacterial superinfection - Tissue looks wet and liquefactive
WET
83
Fat Necrosis
Pancreatic necrosis of fat - Release of lipasesà “cooks” fat in surrounding area - Fatty acids + Ca+ = calcium soaps (saponification)
84
Jersey and Guernsey cattle are predisposed what kind of fat necrosis?
Necrosis of abdominal fat
85
*Dystocia > induces fat necrosis in birth canal *SQ in inter-muscular fat (sternum of recumbent cattle) What kind of fat necrosis is this?
Traumatic necrosis of fat
86
Apoptosis
Programmed cell death
87
Can be physiological OR pathological. And there is NO INFLAMMATION.
Apoptosis
88
Initiators = Caspases
Initiatorsà Caspases 9 & 8
89
Executioners = caspase
caspases 3 &6
90
Intrinsic pathway
mitochondrial pathway
91
Extrinsic pathway
Death receptor initiated pathway
92
- Major mechanism of apoptosis | - Increased permeability of mitochondria> cytochrome C released = initiates apoptosis
Intrinsic Pathway of Apoptosis
93
Cytochrome-C:
Essential for life, it's released into cytoplasm of cell and initiates suicide of apoptosis
94
PRO- Apoptotic enzymes...
Bim, Bid, Bad, Bak, Bax
95
ANTI- Apoptotic enzymes...
Bcl-2, Bcl-x, Mcl-1
96
What protein from the anti-apoptotic enzyme family is the main regulator of apoptosis?
Bcl-2
97
- Initiated by death receptors of the TNF receptor family | - FADD activates caspase 8 activating the execution phase of apoptosis
Extrinsic Pathway
98
What are the best known types of TNF receptors used in the extrinsic pathway of apoptosis?
TNFR-1 & Fas (CD95)
99
FADD activates caspase __ , that will activate the execution phase of apoptosis
8
100
Thrombospodin is a...
Marker of apoptotic cells
101
Disorders of defective apoptosis are...
- Mutations on p53 - Lymphocytes that react against self antigens - failure to eliminate dead cells
102
Disorders of increased apoptosis...
- Neurodegenerative disease - Ischemic injury - Death of virus infected cells
103
If we have too little apoptosis=
Neoplastic and Auto-immune disorders will arise