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RUSVM Pathology I JB1 > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

Describe the gross appearance of acute cell swelling

A

Swollen organ with rounded edges

Pallor when compared to normal

When cut surface - tissue bulges

Heavy “wet” organ

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2
Q

Histologic effects of Liquefactive Necrosis

A

Loss of cellular detail

Granular cells

Eosinophillic and basophillic debris

Neutrophil nuclei may dominate

No tissue architecture preserved

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3
Q

Niemann Pick Disease

A

Lysosomal Storage disease

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4
Q

Caseous necrosis is typically related to (acute/chronic) disease.

A

Caseous necrosis is typically related to (acute/chronic) disease.

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5
Q

Cellular contents in Necrosis vs Apoptosis

A

Necrosis: Enzymatic digestion; may leak

Apoptosis: Intact; released in apoptotic bodies

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6
Q

T/F: Apoptosis induces inflammation

A

False

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7
Q

Which (Necrosis or Apoptosis) causes inflammation

A

Necrosis

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8
Q

Liquefactive Necrosis occurs in

A

Tissues with high neutrophil recruitment and enzymatic release with digestion of tissue

Tissues with high lipid content

Focal bacterial /fungal infections

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9
Q

MDx

A

Bilateral, symmetrical encephalomalacia

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10
Q

MDx

A

Multifocal caseous pneumonia

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11
Q

Sterile Abscess

A

Process caused by non living irritants such as drugs, likely to turn into firm, solid lumps as they scar

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12
Q

Cell size in Necrosis vs Apoptosis

A

Necrosis - Enlarged

Apoptosis - Reduced

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13
Q

Example of cell injury

A

Acute Cell Swelling

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14
Q

Executioner caspases

A

3 and 6

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15
Q

Abscess

A

Localized collection of pus in a cavity formed by disintegration of tissues surrounded by fibrous connective tissue

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16
Q

Cell death can occur by what two processes

A

Necrosis

Apoptosis

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17
Q

Cytochrome C

A

Essential for life; released into cytoplasm to initiate suicide program of apoptosis

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18
Q

Pyknosis

A

Nuclear shrinkage - DNA condenses into shrunken basophilic mass

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19
Q

MDx

A

Hepatitis, multifocal to coalescing, subacute, severe, necrotizing

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20
Q

Cellular changes due to acute cell swelling

A

Dilution of cytoplasm

Cells enlarged

Increased cytoplasmic eosinophilia

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21
Q

Example of cell injury

A

Acute Cell Swelling

_________________________

Ballooning degeneration resuling in formation of a vesicle

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22
Q

Apoptosis has a physiologic or pathologic role?

A

Often physiologic - may be pathologic after some forms of cell injury

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23
Q

Example of cell injury

A

Liquefactive Necrosis

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24
Q

Changes of necrotic cells in cytoplasm

A

Increased binding of eosin

Loosing basophillia

Glassy homogeneous

Vacuolation and moth eaten appearance

+/- Calcification

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25
Q

Possible mechanisms resulting in lipid accumulation

A

Excessive delivery of FFA from fat stores or diet

Decreased oxidation or use of FFAs

Impaired synthesis of apoprotein

Impaired combination of protein and triglycerides to form lipoproteins

Impaired release of lipoproteins from hepatocytes

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26
Q

Apoptotic Bodies

A

Fragments of apoptotic cells that contain portions of the cytoplasm and nucleus

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27
Q

Intrinisic apoptotic pathway initiated by

A

withdrawal of growth factors or hormones

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28
Q

Cause

A

Vitamin E/ Selenium Deficiency

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29
Q

Etiology

A

Vesicular exanthema of swine virus - Calicivirus

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30
Q

Infarct

A

localized area of coagulative necrosis

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31
Q

Example of cell injury

A

Acute Cell Swelling

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32
Q

Name of Disease

A

Blackhead

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33
Q

Cells that are highly vulnerable to hypoxia and cell swelling

A

Cardiomyocytes

Proximal Renal Tubule Epithelium

Hepatocytes

Endothelium

CNS Neurons, Oligodendrocytes, Astrocytes

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34
Q

Gangrenous Necrosis

A

Not a specific pattern of cell death but begins mostly as coagulative necrosis, usually applied to distal extemities and involves multiple planes of tissue

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35
Q

Dry Gangrene

A

No bacterial superinfection; tissue appears dry

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36
Q

Saponification

A

Free Fatty Acids + Ca → Ca Soaps

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37
Q

Septic Abscess

A

Infection, release of enzymes from WBC and infectious agent

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38
Q

Example of cell injury

A

Fatty Change

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39
Q

Example of cell injury

A

Necrosis

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40
Q

Acute cellular swelling and fatty chage are considered to be (reversible/irreversible) cell injuries.

A

Acute cellular swelling and fatty chage are considered to be (reversible/irreversible) cell injuries.

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41
Q

Disease

A

Caseous lymphadenitis

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42
Q

Dystocia and Recumbent Cattle can cause what type of necrosis

A

Fat necrosis

_____________________

Traumatic Fat Necrosis

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43
Q

Liquefactive necrosis typically occurs in the ____________ system.

A

Liquefactive necrosis typically occurs in the central nervous system.

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44
Q

_________ occurs when there is an abnormality of synthesis, utilization and/or mobilization of fat.

A

Fatty Change occurs when there is an abnormality of synthesis, utilization and/or mobilization of fat.

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45
Q

Etiology

A

Histomonas melegridis

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46
Q

Only form in which triglycerides can be transported out of hepatocytes

A

Lipoproteins

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47
Q

Extrinsic Apoptotic Pathway

A

Death-Receptor Initiated Pathway

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48
Q

Example of cell injury

A

Liquefactive Necrosis

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49
Q

Necrosis of Abdominal fat in cattle is of what cause

A

Unknown cause

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50
Q

Acute Cell Swelling

A

Early, sub-lethal manifestation of cell damage, characterized by increased cell size and volume due to H2O overload

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51
Q

Etiology of Fatty Change

A

Hypoxia

Toxicity

Metabolic Disorder

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52
Q

Acute cell swelling is typically due to

A

Acute cell swelling is typically due to loss of ionic and fluid homeostasis

_____________________

Failure of cell energy production

Cell membrane damage

Injury to enzymes regulating ion channels of membranes

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53
Q

MDx

A

Multifocal hemorrhagic polyomyelitis

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54
Q

Prognosis of acute cellular swelling depends on

A

Prognosis of acute cellular swelling depends on the number of cells affected and importance of cells

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55
Q

Physiologic causes of hepatic lipidosis

A

Pregnancy toxemia

Ketosis

56
Q

Etiology

A

Sarcocystis neurona

57
Q

Three types of fat necrosis

A

Enzymatic Necrosis

Traumatic Necrosis

Necrosis of Abdominal Fat

58
Q

Describe the morphology of apoptosis

A

Cell shrinkage, Increased cytoplasmic density

Chromatin condensation

Formation of cytoplasmic blebs and apoptotic bodies

Phagocytosis

59
Q

Fatty Change

A

Sub-lethal cell damage characterized by intracytoplasmic fatty vacuolation

__________________

May be preceded or accompanied by cell swelling

60
Q

Example of cell injury

A

Wet Gangrene

61
Q

Lipofuscin in a cell is evidence of

A

Lipofuscin in a cell is evidence of previous injury

62
Q

Enzymatic Necrosis

A

Action of activated pancreatic lipases in escaped pancreatic fluid

63
Q

Histologic appearance of fatty change

A

Delineated, lipid filled vacuoles in the cytoplasm

May displace nucleus to the periphery

64
Q

Karyolysis

A

Nuclear fading - chromatin dissolution due to action of DNAases and RNAases

65
Q

Plasma membrane in Necrosis vs Apoptosis

A

Necrosis: Disrupted

Apoptosis: Intacted, altered structure

66
Q

Morphologic necrosis due to 2 concurrent processes

A

Denaturation of proteins

Enzymatic digestion of the cell

67
Q

Pathogenesis of fatty change

A

Impaired metabolism of fatty acids → Accumulation of triglycerides → Formation of intracytoplasmic fat vacuoles

68
Q

DDx

A

Equine Herpes Virus 1

Rabies

West Nile Virus

69
Q

Prognosis of fatty change

A

Initially reversible but can lead to irreversible hepatocyte death

70
Q

Liquefactive Necrosis

A

Dead cells are “digested” - transformed from tissue to liquid viscous mass

71
Q

Ketone Bodies

A

Alternative fuel for cells

Produced in liver by mitochondria

72
Q

Example of cell injury

A

Fatty Change

73
Q

Possible causes of caseous necrosis

A

Mycobacterium

Corynebacterium

Fusobacterium

Fungal infections

74
Q

Example of cell injury

A

Fatty change

75
Q

Etiology

A

Corynebacterium pseudotuberculosis

76
Q

Bcl Family Proteins

A

Pro and Anti- Apoptotic

Control release of cytochrome C

77
Q

Clinical manifestations of lipidosis are most commonly detected as alterations in ________ function because it is most central to lipid metabolism.

A

Clinical manifestations of lipidosis are most commonly detected as alterations in liver function because it is most central to lipid metabolism.

78
Q

Increase in cell size can be due to

A

Cell Swelling

Cell Enlargement

79
Q

Necrosis

A

Cell death after irreversible cell injury by hypoxia, ischemia, and direct cell membrane injury

80
Q

Anti-Apoptotic Proteins

A

Bcl-2 Bcl-X, Mcl -1

81
Q

Example of cell injury

A

Fibrinoid Necrosis

82
Q

Disorders associated with too little apoptosis

A

Cells with p53 mutation

Lymphocytes that react against self-Ag

Failure to eliminate dead cells

83
Q

Fibrinoid necrosis occurs when

A

Fibrinoid necrosis occurs when Ag-Ab complexes are deposited in walls of arteries

84
Q

Disease

A

Polioencephalomalacia

85
Q

Caseous necrosis is associated with poorly degradable _________ of bacterial origin.

A

Caseous necrosis is associated with poorly degradable lipid of bacterial origin.

86
Q

Pro-Apoptotic Proteins

A

Bim, Bid, Bad

Bak, Bax

87
Q

Initiator caspases

88
Q

Example of cell injury

A

Dry gangrene

89
Q

A good prognosis is possible with acute cell swelling if

A

A good prognosis is possible with acute cell swelling if oxygen is restored before the “point of no return”

90
Q

Common cause of coagulative necrosis

A

Ischemia in all solid organs except brain

91
Q

Fibrinoid Necrosis

A

Special form of necrosis usually seen in immune reactions involving blood vessels

92
Q

Intrinisic Apoptotic Pathway

A

Mitochondrial Pathway

93
Q

Leukoencephalomalacia causes

A

Necrosis of white matter of cerebral hemispheres, brain stem and cerebellum

94
Q

Endocrine causes of hepatic lipidosis

A

Diabetes mellitus

Feline Fatty Liver Syndrome

Fat Cow Syndrome

95
Q

Caseous Necrosis

A

Friable white area of necrosis, necrotic debris represents dead WBCs

96
Q

Coagulative Necrosis

A

Architecture of dead tissues is preserved, ultimately the necrotic tissue is removed by phagocytosis or digestion by action of lysosomal enzymes of WBC

97
Q

Apoptosis

A

Pathway of cell death

98
Q

Irreversible cell injury is associated morphologically with

A

Severe swelling of mitochondria

Extensive damage to plasma membrane

Swelling of lysosomes

99
Q

Hisologic effects of caseous necrosis

A

Eosinophilic granular cell debris

Rim of inflammatory cells

Obliterated tissue architecture

Dystrophic calcification in center of lesion

100
Q

Leukoencephalomalacia Pathogenesis

A

Ingestion of Fusarium moniliforme containing Fumonisin B1 Toxin Producing Moldy Corn → Sphingolipid Synthesis Inhibition → Direct Cellular Toxicity → Leukoencephalomalacia

101
Q

Disorders associated with too much apoptosis

A

Neurodegenertive disease

Ischemic injury

Death of virus infected cells

102
Q

Example of cell injury

A

Fat necrosis

103
Q

Example of cell injury

A

Caseous Necrosis

104
Q

Wet Gangrene

A

Bacterial superinfection occured, tissue looks wet and liquefactive by actions of degradative enzymes in the bacteria and the attracted WBC

105
Q

Example of cell injury

A

Coagulative Necrosis

106
Q

The most common and fundamental expression of cell injury is ___________.

A

The most common and fundamental expression of cell injury is acute cell swelling.

107
Q

A frequent outcome of necrosis is ___________.

A

A frequent outcome of necrosis is inflammation.

108
Q

Describe the gross appearance of fatty change

A

Diffuse yellow

Enhanced reticular pattern if specific zones affected

Edges rounded and bulge on section

Tissue soft, friable and cuts easily with greasy texture

May float in fix/water

109
Q

MDx

A

Multifocal necrohemorrhagic myelitis

110
Q

Nutritional causes of hepatic lipidosis

A

Obesity

Protein - Calorie Malnutrition

Starvation

111
Q

2 types of abscesses

A

Septic

Sterile

112
Q

Karyorrhexis

A

Nuclear fragmentation - pyknoic nucli membrane ruptures and nucleus undergoes fragmentation

113
Q

Disease

A

Equine Leukomyelitis

114
Q

Disease

A

Leukoencephalomalacia

115
Q

Disease

A

Tuberculosis

116
Q

Most frequent causes of acute cell swelling

A

Hypoxia

Toxic agents

117
Q

Patterns of tissue necrosis

A

Coagulative necrosis

Liquefactive necrosis

Gangrenous necrosis

Caseous necrosis

Fat necrosis

Fribrinoid necrosis

118
Q

Example of cell injury

A

Coagulative Necrosis

119
Q

Example of cell injury

A

Liquefactive necrosis

120
Q

Polioencephalomalacia can be caused by

A

Thiamine deficiency diet

Increased ruminal thiaminase activity

Administration of thiamine analogs

High levels of sulfur in diet

Lead toxicity

Thiaminase containing plants

121
Q

Lipidosis

A

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

122
Q

Example of cell injury

A

Enzymatic Fat Necrosis

123
Q

Apoptosis can occur during what two types of processes

A

Physiologic

Pathologic

124
Q

Pus

A

Necrotic material, frequently creamy yellow because of the presence of dead WBCs

125
Q

Necrosis has a physiologic or pathologic role?

A

Invariably pathologic - culmination of irreversible cell injury

126
Q

Abscesses result due to

A

Abscesses result due to the body’s defensive reaction to foreign material

127
Q

Nucleus in Necrosis vs Apoptosis

A

Necrosis: Pyknosis → Karyorrhexis → Karyolysis

Apoptosis: Fragmented

128
Q

Describe the gross appearance of necrosis

A

Pale, soft, friable

Sharply demarcated by zone of inflammation

129
Q

Example of cell injury

130
Q

Conversion of acetyl coA from fatty acid oxidation causes

131
Q

Extrinisic apoptotic pathway initiated by

A

Receptor- ligand interactions

____________________

Fas

TNF Receptor

132
Q

Major classes of lipids that can accumulate in cells

A

Triglycerides

Cholesterol/ Cholesterol Esters

Phospholipids

Complexes of Lipids and Carbohydrates

133
Q

Species affected by Leukoencephalomalcia

A

Horse

Chicken

Pig

134
Q

Ultrastructural changes of acute cell swelling

A

Plasma membrane alterations

Mitochondrial changes

Dilation of the ER

Nuclear alterations

135
Q

Disease

A

Nutritional Myopathy

White Muscle Disease

RUSVM Pathology I JB1 (18 decks)

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