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Cellular Pathology, TBP Flashcards

1
Q

4 basic types of cellular adaptations

A

1) Hyperplasia
2) Hypertrophy
3) Atrophy
4) Metaplasia

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2
Q

Increase in number of cells

A

Hyperplasia

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3
Q

Permanent cells (do not undergo hyperplasia) (3)

A

1) Cardiac cells
2) Neurons
3) Skeletal muscle cells

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4
Q

Increase in size of cell

A

Hypertrophy

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5
Q

T/F: Hyperplasia and hypertrophy can be distinguished grossly

A

F

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6
Q

Physiologic vs pathologic, hyperplasia vs hypertrophy: Increase in size of breast during pregnancy

A

Physiologic hyperplasia

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7
Q

Physiologic vs pathologic, hyperplasia vs hypertrophy: Adrenal enlargement due to pituitary adenoma

A

Pathologic hyperplasia

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8
Q

Physiologic vs pathologic, hyperplasia vs hypertrophy: Skeletal muscle enlargement during exercise

A

Physiologic hypertrophy

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9
Q

Physiologic vs pathologic, hyperplasia vs hypertrophy: LVH

A

Pathologic hypertrophy

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10
Q

Physiologic vs pathologic, hyperplasia vs hypertrophy: Increase in thickness of endometrium during menstrual cycle

A

Physiologic hyperplasia

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11
Q

Physiologic vs pathologic, hyperplasia vs hypertrophy: Endometrial proliferation due to prolonged estrogen stimulus

A

Pathologic hyperplasia

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12
Q

Physiologic vs pathologic, hyperplasia vs hypertrophy: Liver growth after partial resection

A

Physiologic hyperplasia

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13
Q

Mechanisms by which hyperplasia and hypertrophy can occur (2)

A

1) Up regulation or down regulation of receptors

2) Induction of new protein synthesis

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14
Q

New proteins induced (3)

A

1) Transcription factors
2) Contractile proteins
3) Embryonic proteins

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15
Q

Decrease in size of cell that has once been of normal size

A

Atrophy

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16
Q

Physiologic vs pathologic atrophy: Decrease in size of uterus after pregnancy

A

Physiologic

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17
Q

Stimuli for pathologic atrophy (7)

A

1) Loss of blood supply
2) Loss of nerve supply
3) Loss of endocrine stimulation
4) Disuse
5) Mechanical compression
6) Decreased workload
7) Aging

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18
Q

Organ that is small in size and was never normal in size

A

Hypoplasia

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19
Q

Eccentric vs concentric cardiac hypertrophy: Pressure overload

A

Concentric

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20
Q

Eccentric vs concentric cardiac hypertrophy: Volume overload

A

Eccentric

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21
Q

Change in epithelium from one type to another

A

Metaplasia

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22
Q

Metaplasia: Barrett esophagus

A

Glandular metaplasia

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23
Q

Metaplasia: Smoker’s lung

A

Squamous metaplasia

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24
Q

Occurs when cells cannot adapt to new environment

A

Cell injury

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25
Q

2 common sources of cellular injury

A

1) Ischemia

2) Hypoxia

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26
Q

Ischemia vs hypoxia: Much more damaging

A

Ischemia

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27
Q

T/F Cellular injury always results in cell death

A

F

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28
Q

4 cellular systems especially vulnerable to cellular injury

A

1) DNA
2) Cell membranes
3) Protein generation
4) ATP production

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29
Q

Mechanisms of cellular injury (4)

A

1) Hypoxia
2) Generation of oxygen-derived free radicals
3) Chemical injury
4) Increased mitochondrial cytosolic calcium

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30
Q

Mechanisms of cellular injury: Decrease in O2 results in decreased

A

ATP production

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31
Q

Mechanisms of cellular injury: ATP is required by (2)

A

1) Na/K ATPase pump

2) Ca pump

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32
Q

Mechanisms of cellular injury: Entry of calcium into cells cause

A

Activation of endonucleases, proteases, phospholipases, and DNAses that damage cells

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33
Q

Mechanisms of cellular injury: Decrease in O2 results in increased

A

Anaerobic respiration resulting in accumulation of lactic acid, decreasing cellular pH

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34
Q

Mechanisms of cellular injury: Decrease in intracellular pH results in

A

Disaggregation of ribosomes from RER

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35
Q

Mechanisms of cellular injury: A molecule with an unpaired electron in the outer orbit

A

Free radical

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36
Q

Mechanisms of cellular injury: Another term for free radical

A

ROS

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37
Q

Mechanisms of cellular injury: Normal physiologic reactions that generate free radicals

A

Redox reactions

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38
Q

Mechanisms of cellular injury: Damage by free radicals (3)

A

1) Lipid peroxidation
2) DNA fragmentation
3) Protein cross-linking

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39
Q

Mechanisms of cellular injury: Methods to prevent formation of ROS (4)

A

1) Catalase
2) Superoxide dismutase
3) Glutathione
4) Vitamin ACE

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40
Q

Mechanisms of cellular injury: Action of catalase

A

Degrades hydrogen peroxide

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41
Q

Mechanisms of cellular injury: Action of superoxide dismutase

A

Converts superoxide to hydrogen peroxide

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42
Q

Mechanisms of cellular injury: Action of glutathione

A

Catalyzes breakdown of hydroxyl radicals

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43
Q

Mechanisms of cellular injury: Toxic metabolite of ethylene glycol (antifreeze)

A

Oxalic acid

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44
Q

Mechanisms of cellular injury: Toxic metabolite that directly inactivates cytochrome oxidase, impairing formation of ATP

A

Cyanide

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45
Q

Mechanisms of cellular injury: Increased mitochondrial cytosolic calcium leads to (3)

A

1) Lipid peroxidation
2) Formation of mitochondrial permeability transition
3) Release of cytochrome c

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46
Q

Mechanisms of cellular injury: Mitchondrial permeability transition

A

Nonselective pore that dissipates proton gradient

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47
Q

Mechanisms of cellular injury: Action of cytochrome c

A

Activates apoptosis

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48
Q

Light microscopic findings of reversible cellular injury

A

1) Cellular swelling

2) Fatty change

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49
Q

Ligt microscopic findings of irreversible cellular injury

A

1) Nuclear karyolysis
2) Nuclear pyknosis
3) Nuclear karyorrhexis

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50
Q

2 most important factors determining irreversible cell damage

A

1) Membrane distrubances

2) Inability to reverse mitochondrial dysfunction

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51
Q

Loss of nuclear basophilia

A

Karyolysis

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52
Q

Shrinkage of nucleus

A

Pyknosis

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53
Q

Electron microscopic findings of reversible injury

A

1) Cellular blebs

2) Small mitochondrial densities

54
Q

Electron microscopic findings of irreversible injury

A

1) Ruptured lysosomes
2) Myelin figures
3) Lysis of ER
4) Large calcium rich mitochondrial densities

55
Q

Myelin figures indicate

A

Phospholipid precipitation

56
Q

2 forms of cell death

A

1) Apoptosis

2) Necrosis

57
Q

Cell death: Occurs in response to damage to DNA

58
Q

Cell death: Occurs in response to injurious stimuli

59
Q

Phases of apoptosis

A

1) Initiation

2) Execution

60
Q

Phases of apoptosis: In which caspases become catalytically active

A

Initiation

61
Q

Phases of apoptosis: In which caspases causes death of cell

62
Q

Mechanisms of apoptosis

A

1) Extracellular

2) Intracellular

63
Q

Mechanisms of apoptosis: Initiation of extracellular pathway

A

Fas ligand binds to Fas receptor of the TNF family (Fas-Fas ligand binding)

64
Q

Mechanisms of apoptosis: Action of Fas receptor

A

Activates FADD

65
Q

Mechanisms of apoptosis: Action of FADD

A

Activates caspases

66
Q

Mechanisms of apoptosis: Initiation of intracellular pathway

A

Release of cytochrome c from mitochondria

67
Q

Mechanisms of apoptosis: Cytochrome c combines with __ to activate caspases

68
Q

Mechanisms of apoptosis: Action of caspases

A

Cleave DNA in a coordinated manner

69
Q

Mechanisms of apoptosis: DNA cleavage in necrosis

A

Uncoordinated

70
Q

Mechanisms of apoptosis: Necrosis vs apoptosis, generates inflammatory response

71
Q

Mechanisms of apoptosis: Expressed by cell fragments in apoptosis that are recognised by macrophages and engulfed without generating an inflammatory reaction

A

Phosphatidyl serine

72
Q

Mechanisms of apoptosis: Microscopic key feature of apoptosis

A

Chromatin condensation and fragmentation

73
Q

Necrosis: 2 main types

A

1) Coagulative

2) Liquefactive

74
Q

Necrosis: Protein denaturation is more prominent than enzymatic breakdown

A

Coagulative

75
Q

Necrosis: Microscopic morphology of coagulative necrosis

A

1) Increased eosinophilia of cytoplasm

2) Decreased basophilia of nucleus

76
Q

Necrosis: Type wherein general cellular architecture is identifiable

A

Coagulative

77
Q

Necrosis: Organs with high fat content

A

Coagulative followed rapidly by liquefactive

78
Q

Necrosis: Enzymatic breakdown is more prominent that protein denaturation in organs that lack a substantial protein-rich matrix or have a high concentration of proteolytic enzymes

A

Liquefactive

79
Q

Necrosis: Microscopic morphology of liquefactive necrosis

A

Sheets of lipid-laden/foamy macrophages

80
Q

Necrosis: Chalky deposits due to combination of fat and calcium

A

Fat necrosis

81
Q

Necrosis: Cheesy-looking due to granulomatous disease process

82
Q

Necrosis: Infection commonly associated with caseous necrosis

A

Tuberculosis

83
Q

Necrosis: T/F Coagulative and liquefactive necrosis are mutually exclusive

84
Q

Necrosis: Morphologic vs functional change, first appreciated

A

Functional

85
Q

Intracellular accumulations: Product of lipid peroxidation and free radical injury that accumulates as the cell ages

A

Lipofuscin

86
Q

Intracellular accumulations: Lipofuscin accumulates in what organelle

87
Q

Lipofuscin: Most common organs of accumulation

A

Heart and liver

88
Q

2 forms of calcium deposition

A

1) Metastatic

2) Dystrophic

89
Q

Calcium deposition, metastatic: Calcium level

90
Q

Calcium deposition, metastatic: Tissue of accumulation

A

Normal or abnormal

91
Q

Calcium deposition, sarcoidosis: Metastatic vs dystrophic

A

Metastatic

92
Q

Calcium deposition, sarcoidosis: Increase serum calcium by

A

Activating vitamin D precursor

93
Q

Calcium deposition, dystrophic: Calcium level

94
Q

Calcium deposition, dystrophic: Tissues affected

95
Q

Calcium deposition: Organs most commonly affected

A

1) Vasculature
2) Kidneys
3) Lungs

96
Q

Protein accumulation: Often involve what type of filaments

A

Intermediate filaments

97
Q

Protein accumulation: Liver

A

Mallory hyaline

98
Q

Protein accumulation: Alzheimer disease

A

Neurofibrillary tangles

99
Q

Iron accumulation: Without resulting side effects

A

Hemosiderosis

100
Q

Iron accumulation: With resulting side effects

A

Hemochromatosis

101
Q

Iron accumulation, hemosiderosis: Found within

A

Macrophages

102
Q

Iron accumulation: Aggregates of ferritin micelles

A

Hemosiderin

103
Q

Iron accumulation: (+) Prussian blue stain

A

Hemosiderosis

104
Q

Iron accumulation, hemochromatosis: Found within

A

Parenchymal cells

105
Q

Iron accumulation, hemochromatosis: Common side effects

A

1) CHF
2) DM
3) Cirrhosis

106
Q

Iron accumulation, hemochromatosis: Hereditary vs acquired

107
Q

Iron accumulation, hemochromatosis: Most common organs affected

A

1) Heart
2) Pancreas
3) Liver
4) Skin

108
Q

Fat accumulation: Most common organs affected

A

1) Liver
2) Kidney
3) Heart
4) Skeletal muscle

109
Q

Fat accumulation: 1 fat vacuole per cell

A

Macrovesicular steatosis

110
Q

Fat accumulation: Many vacuoles per cell

A

Microvesicular steatosis

111
Q

Protein accumulation: Most commonly associated with alcohol use

A

Mallory hyaline in the liver

112
Q

Iron accumulation: Macrophages of the liver

A

Kupffer cells

113
Q

Iron accumulation: In the liver, represents

A

Extravascular hemolysis

114
Q

Cholesterol accumulation: Organs affected

A

1) Blood vessels

2) Sites of hemorrhage

115
Q

Glycogen accumulation: Glycogen storage disorder

A

McArdle syndrome

116
Q

Glycogen accumulation: Most common organs affected

A

1) Liver

2) Skeletal muscle

117
Q

Common exogenous pigment accumulation (2)

A

1) Tattoos

2) Anthracotic pigment

118
Q

Common endogenous pigment accumulation (2)

A

1) Melanin

2) Bilirubin

119
Q

Intracellular accumulations: Gross, brown atrophy

A

Lipofuscin

120
Q

Intracellular accumulations: Microscopic, finely granular, yellow-brown pigment that often surrounds the nucleus

A

Lipofuscin

121
Q

Intracellular accumulations: Gross, hard yellow nodules

122
Q

Intracellular accumulations: Microscopic, chunky, smooth, purple granules

123
Q

Intracellular accumulations: Microscopic, chunky, yellow-brown granules

124
Q

Intracellular accumulations: Microscopic, ropy, eosinophilic condensation within a cleared-out hepatocyte

A

Mallory hyaline

125
Q

Intracellular accumulations: Finely stippled black appearance in interstitial and alveolar macrophages

A

Anthracotic pigment

126
Q

TTAGGG repeats

127
Q

Protects the ends of chromosomes and shorten with cell division

128
Q

Telomere too short is interpreted as

A

Broken DNA

129
Q

Enzyme present in immortal cells (germ and stem cells) allowing cell’s lifespan to continue indefinitely

A

Telomerase

130
Q

Action of telomerase

A

Adds telomeres to the end of the chromosome

131
Q

Syndrome of premature aging

A

Werner syndrome

132
Q

Mutation in Werner syndrome

A

Defective DNA helicase

Pathology (14 decks)

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