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My Pathology 1 > Cell Injury > Flashcards

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
Q

What organs does lipidosis occur in?

A
  • LIVER!
  • Heart Muscle
  • Skeletal Muscle
  • Kidney
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26
Q

Hepatic Lipidosis >

A

Accumulation of triglycerides and other lipid metabolites (neutral fats and cholesterol) within parenchymal cells

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27
Q

What species/breed do we see this commonly in?

A

Shetland ponies / Minis

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28
Q

When we see fat on histology, what color will it be?

A

It will be clear. b/c fat will be washed off w/ the alcohol step of gram staining

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29
Q

What is the only way triglycerides can be transported out of the liver?

A

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.

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30
Q

There are 3 different conditions associated with Fatty Liver. They are…

A
  • Physiological
  • Nutritional
  • Endocrine Disease
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31
Q

_________: late pregnancy, lactation, or dietary excess of fats

A

PHYSIOLOGICAL

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32
Q

__________: obesity, protein malnutrition, STARVATION*

A

NUTRITIONAL

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33
Q

__________: diabetes mellitus & feline fatty liver syndrome

A

ENDOCRINE DISEASE

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34
Q

Fatty change gross appearance of liver:

A
  • 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
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35
Q

What is Niemann Pick Disease?

A

Phospholipids sphingomyelin, its a lysosomal storage disease

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36
Q

Histologically, you can tell a slide is fat compared to edema because the nucleus will be where?

A

It will be pushed to the side! Peripheral nuclear displacement!!!

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37
Q

The prognosis of fatty change initially is…

A

Reversible, but can lead to hepatocytes death—- which is irreversible.

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38
Q

Irreversible Cell Injury is associated with:

A
  • Severe swelling of mitochondria
  • Damage to plasma membrane (giving rise to myelin figures)
  • Swelling of lysosomes
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39
Q

Cell Death:

A

MAINLY NECROSIS

-apoptosis also contributes

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40
Q

Necrosis is also called:

A
  • Oncosis

- Oncotic Necrosis

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41
Q

Necrosis occurs following cell death in the ________ animal.

A

LIVING ANIMAL.

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42
Q

Cell death after irreversible cell injury by:

A
  • Hypoxia
  • Ischemia
  • Direct cell membrane injury
43
Q

Is necrosis a physiological event?

A

NO!!!!

44
Q

Necrosis process=

A

Dewatering of proteins and enzymatic digestion of the cell

45
Q

Necrosis outcome:

A

INFLAMMATION

46
Q

Will apoptosis be accompanied by inflammation?

A

NO!! NEVER!!

47
Q

Necrotic change timelines:

A

Ultrastructure-

48
Q

Cell that has nuclear fading / undergoing dissolution: ________

A

Karyolysis (chromatolysis)

49
Q

Cell that is undergoing nuclear shrinkage/small shrunken nucleus: _______

A

Pyknosis

50
Q

Cell that is undergoing nuclear fragmentation/ruptured nucleus:__________

A

Karyorrhexis

51
Q

Dnatured proteins on histology will look more pink (eosinophilic) T or F?

A

TRUE

52
Q

Cells will look LESS basophilic (blue) when there has been a loss of _____.

A

RNA

53
Q

Glassy appearance is due to a loss of ________.

A

Glycogen

54
Q

“Moth eaten look” and vacuolation is due to enzymes digesting the cytoplasm. T or F?

A

TRUE

55
Q

Calcification will not be seen. T or F?

A

FALSE! Calcification CAN be seen

56
Q

Gross appearance of a fatty liver:

A

Pale, soft, friable, and zones of inflammation.

57
Q

What is the one type of necrosis that is NOT seen grossly?

A

Firbrinoid Necrosis

58
Q

Define COAGULATIVE NECROSIS:

A

Architecture of the tissue is preserved

59
Q

Coagulative necrosis is always ACUTE. T or F?

A

TRUE!

60
Q

Common causes:

A

ISCHEMIA / HYPOXIC INJURY **except in the brain

61
Q

Infarct=

A

Localized area of coagulative necrosis

62
Q

_____: usually are in a wedge/triangular shape

A

Coagulative Necrosis

63
Q

Nutritional Myopathy/White Muscle Disease is caused by:

A

Vit. E / Selenium Deficiency

64
Q

Liquefactive Necrosis is typical in what location?

A

CNS

65
Q

Dead cells are digested and transform into a liquid viscous mass

A

Liquefactive necrosis

66
Q

Occurs in tissues with high neutrophils recruitment, high enzymatic release, or high lipid content.

A

Liquefactive necrosis

67
Q

Necrotic Material =

A

PUS aha dead WBC

68
Q

An example of liquefactive necrosis:

A

abscess

69
Q

Polioencephalomacia

A

Softening of the GREY matter of the brain

70
Q

_________: Associated with sulfur/ sulfate toxicity and Thiaminase production

A

Polioencephalomacia

71
Q

Leukoencephalomalacia

A

Softening of the WHITE matter in the brain

72
Q

________: Ingestion of Fusarium moniliforma (moldy corn!)

A

Leukoencephalomalacia

73
Q

Leukomyelitis:

A

inflammation of the white matter in the spinal cord

74
Q

________: Sarcocyst neurona in horses

A

Leukomyelitis

75
Q

Polioencephalomalacia in Sheep

A
  • Thiamine deficiency
  • Increased thiaminase activity
  • High level of sulfur/ water
  • Lead toxicity
  • Thiaminase containing plant= BRACKEN FERN
76
Q

What are the 2 different kinds of abscesses?

A
  • Septic > infection **MOST COMMON

- Sterile > nonliving irritants (drugs/injection)

77
Q

What is the most common pus forming bacteria?

A

Pyogenic bacteria / Staphylococcus aureus

78
Q

Caseous Necrosis

A

think cottage cheese!

  • Friable white area
  • Chronic
  • Not easily digestible by macrophages— that’s why there is so much inflammation
79
Q

Causes of caseous necrosis:
COWS>
SHEEP>

A

COWS> Mycobacterium

SHEEP> Corynebacterium

80
Q

Gangrenous Necrosis

A

Begins as coagulative necrosis > due to ischemia

Usually applies to distal extremities

81
Q

_______ GANGRENE- No bacterial infection —-Mummification of tissue

A

DRY

82
Q

_______GANGRENE-
bacterial superinfection
- Tissue looks wet and liquefactive

A

WET

83
Q

Fat Necrosis

A

Pancreatic necrosis of fat

  • Release of lipasesà “cooks” fat in surrounding area
  • Fatty acids + Ca+ = calcium soaps (saponification)
84
Q

Jersey and Guernsey cattle are predisposed what kind of fat necrosis?

A

Necrosis of abdominal fat

85
Q

*Dystocia > induces fat necrosis in birth canal
*SQ in inter-muscular fat (sternum of recumbent cattle)
What kind of fat necrosis is this?

A

Traumatic necrosis of fat

86
Q

Apoptosis

A

Programmed cell death

87
Q

Can be physiological OR pathological. And there is NO INFLAMMATION.

A

Apoptosis

88
Q

Initiators = Caspases

A

Initiatorsà Caspases 9 & 8

89
Q

Executioners = caspase

A

caspases 3 &6

90
Q

Intrinsic pathway

A

mitochondrial pathway

91
Q

Extrinsic pathway

A

Death receptor initiated pathway

92
Q
  • Major mechanism of apoptosis

- Increased permeability of mitochondria> cytochrome C released = initiates apoptosis

A

Intrinsic Pathway of Apoptosis

93
Q

Cytochrome-C:

A

Essential for life, it’s released into cytoplasm of cell and initiates suicide of apoptosis

94
Q

PRO- Apoptotic enzymes…

A

Bim, Bid, Bad, Bak, Bax

95
Q

ANTI- Apoptotic enzymes…

A

Bcl-2, Bcl-x, Mcl-1

96
Q

What protein from the anti-apoptotic enzyme family is the main regulator of apoptosis?

A

Bcl-2

97
Q
  • Initiated by death receptors of the TNF receptor family

- FADD activates caspase 8 activating the execution phase of apoptosis

A

Extrinsic Pathway

98
Q

What are the best known types of TNF receptors used in the extrinsic pathway of apoptosis?

A

TNFR-1 & Fas (CD95)

99
Q

FADD activates caspase __ , that will activate the execution phase of apoptosis

A

8

100
Q

Thrombospodin is a…

A

Marker of apoptotic cells

101
Q

Disorders of defective apoptosis are…

A
  • Mutations on p53
  • Lymphocytes that react against self antigens
  • failure to eliminate dead cells
102
Q

Disorders of increased apoptosis…

A
  • Neurodegenerative disease
  • Ischemic injury
  • Death of virus infected cells
103
Q

If we have too little apoptosis=

A

Neoplastic and Auto-immune disorders will arise

My Pathology 1 (4 decks)

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