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PATHOLOGY > Cellular Injury and Adaptation > Flashcards

Cellular Injury and Adaptation Flashcards

1
Q

Homeostasis

A

balance of physiologic and biochemical functions within the body

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2
Q

Alteration of homeostasis results in

A

stress to cell, cellular injury or adaptive changes to survive altered environment

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3
Q

Reversible injury

A

injury is corrected prior to destruction of cellular repair mechanisms; severity of injury does not exceed the cells ability to repair itself

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4
Q

Irreversible injury

A

repair mechanisms are destroyed (removal from altered environment will be insufficient) cell cannot repair itself –> DEATH; injury exceeds the cell’s ability for self-repair, resulting in cell death

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5
Q

Cellular Injury

A

Hypoxia, Physical agents, chemicals, infectious agents, immune reactions, genetic derangements, nutritional imbalance

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6
Q

Hypoxia

A

Decreased supply of O2 to cell or inability to use O2

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7
Q

Anoxia

A

Complete absence of O2

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8
Q

Causes of Hypoxia

A

Ischemia (decreased BF), decreased oxygenation of blood, decreased O2 carrying capacity, inability to utilize O2

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9
Q

Examples of Physical injury to cell

A

mechanical trauma, temperature extremes, atmospheric pressure variation, radiation, electrical injury

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10
Q

Examples of Chemical Injury to cell

A

Simple agents (electrolytes, glucose), Poisons, Pollutants, Insecticides, herbicides, industrial products, drugs (therapeutic or recreational), alcohol

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11
Q

Infectious Causes of cell injury

A

bacteria, rickettsia, fungi, virus, parasite

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12
Q

Immune Response Causes of cell injury

A

Hypersensitivity reaction

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13
Q

4 Key Signs of REVERSIBLE cell injury

A

Decreased aerobic respiration, cellular edema, ribosome detachment from RER, ultrastructural morphological changes

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14
Q

Reversible Injury - Decreased Aerobic Respiration Results in

A

Decreased ATP production, increased AMP and anaerobic glycolysis, Increased lactate (decreased pH), decreased cellular glycogen, clumping of nuclear chromatin, decreased protein synthesis

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15
Q

Examples of nutritional variations that cause cellular injury

A

deficits, excess, malabsorption, altered use

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16
Q

Sites that are altered in cellular injury

A

cell membrane integrity, aerobic respiration, enzyme/protein synthesis, genetic apparatus

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17
Q

What causes cellular edema in reversible cell injury?

A

Suppression of Na+ pump with increased [Na+] retention; increased intracellular Na+

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18
Q

Ultrastructural Morphological Changes in reversible cellular injury

A

Phospholipid membrane alteration, loss of microvilli, myelin figure formation, mitochondrial swelling, RER swelling

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19
Q

Key Signs of IRREVERSIBLE cellular injury

A

ATP Depletion, Cell Membrane Damage

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20
Q

Cell Membrane Damage as a result of irreversible damage

A

Phospholipid Depletion, Cytoskeletal breakdown, toxic ROS, Lipid breakdown products, amino acid loss

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21
Q

Structural changes in IRREVERSIBLE cell injury include

A

vacuolization of mitochondria, PM damage, Lysosomal swelling, Loss of proteins, enzymes, and RNA

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22
Q

What characterizes cell injure as irreversible?

A

ATP depletion, cellular edema -> PM tears and damage, mitochondrial dysfunction (high [Ca2+] intracellularly), Membrane phospholipid depletion, cytoskeleton changes, ROS, lipid breakdown products, and amino acid loss

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23
Q

Irreversible Cellular Damage - What is the determining/most important factor?

A

Cellular Membrane Dysfunction

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24
Q

Irreversible Cellular Damage - What results from mitochondrial dysfunction?

A

ATP depletion -> increased cytosolic [Ca2+] -> mitochondrial phospholipase activation -> phospholipid breakdown + accumulation of FFA -> altered permeability of PM

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25
Q

Myelin figures are characteristic of

A

reversible injury

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26
Q

cellular edema is characteristic of

A

reversible injury

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27
Q

Irreversible Cellular Damage - What causes membrane phospholipid depletion?

A

increase [Ca2+] intracellular activation of phospholipase AND ATP-dependent maintenance and production of phospholipids

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28
Q

Irreversible Cellular Damage - What causes cytoskeletal abnormalities?

A

Hypoxia AND activation of proteases by high intracellular levels of [Ca2+]

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29
Q

Irreversible Cellular Damage - What causes Toxic oxygen radical production?

A

sudden repercussion of hypoxic tissue

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30
Q

Irreversible Cellular Damage - What produces Toxic oxygen radicals?

A

segmented neutrophils

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31
Q

Reperfusion Injury

A

sudden reperfusion of ischemic tissue causes toxic oxygen radical production by segmented neutrophils

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32
Q

Irreversible Cellular Damage - What produces lipid breakdown products?

A

phospholipase breakdown of pospholipids, high [FFA]

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33
Q

Irreversible Cellular Damage - What amino acid is protective?

A

GLYCINE

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34
Q

GLYCINE’s protective feature

A

allows ATP depleted cells to resist high Ca2+ levels

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35
Q

decreased aerobic respiration is a characteristic of

A

reversible injury

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36
Q

increased intracellular pH is a characteristic of

A

reversible injury

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37
Q

Increased intracellular AMP is a characteristic of

A

reversible injury

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38
Q

Decreased glycogen stores v

A

reversible injury

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39
Q

clumping of nuclear chromatin is a characteristic of

A

reversible injury due to decreased pH

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40
Q

Ribosome detachment from RER is a characteristic of

A

reversible injury

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41
Q

decreased function of sodium pump is a characteristic of

A

reversible injury

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42
Q

Increased intracellular sodium is a characteristic of

A

reversible injury

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43
Q

decreased protein synthesis is a characteristic of

A

reversible injury

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44
Q

swelling of mitochondria is a characteristic of

A

reversible injury

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45
Q

loss of microvilli is a characteristic of

A

reversible injury

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46
Q

accumulation of lactate metabolites and phosphate is a characteristic of

A

reversible injury

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47
Q

blebs is a characteristic of

A

reversible edema; due to structural alterations in phospholipid membranes

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48
Q

myelin figures is a characteristic of

A

reversible injury

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49
Q

ATP depletion reversible injury

A

irreversible injury; suppression of ATP-dependent repair mechanisms

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50
Q

vacuolization of mitochondria is a characteristic of

A

irreversible injury

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51
Q

lysosomal swelling is a characteristic of

A

irreversible injury

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52
Q

loss proteins/enzymes and RNA is a characteristic of

A

irreversible injury

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53
Q

PM tearing/damage is a characteristic of

A

irreversible injury

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54
Q

Increased cytosolic [Ca2+] is a characteristic of

A

irreversible injury

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55
Q

Increased [Ca2+] causes

A

activation of mitochondrial phospholipase and lysosomal proteases, ATPases, endonucleases

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56
Q

Phospholipase

A

mitochondrial ([Ca2+] activated) breaks down phospholipids of PM

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57
Q

Accumulation of FFA’s is a characteristic of

A

irreversible injury

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58
Q

Permeability changes in PM is a characteristic of

A

irreversible injury

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59
Q

Membrane phospholipid depletion is a characteristic of

A

irreversible injury

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60
Q

Damage to intermediate cytoskeletal filaments is a characteristic of

A

irreversible injury; hypoxia induced

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61
Q

Separation of PM and cytoskeleton is a characteristic of

A

irreversible injury

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62
Q

Proteases

A

lysosomal proteases released and activated by high intracellular [Ca2+]

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63
Q

Toxic oxygen radicals is a characteristic of

A

irreversible injury

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64
Q

reperfusion injury is a characteristic of

A

irreversible injury

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65
Q

accumulation of lipid breakdown products is a characteristic of

A

irreversible injury

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66
Q

loss of glycine and other amino acids is a characteristic of

A

irreversible injury

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67
Q

Glycine

A

allows ATP depleted cells to resist high Ca2+ levels

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68
Q

Reason for decreased protein synthesis in cellular injury?

A

detachment of ribosomes from RER

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69
Q

Reason for nuclear clumping in cellular injury?

A

increased anaerobic glycolysis and decreased pH

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70
Q

Intracellular release of lysosomal enzymes is a characteristic of

A

irreversible injury

71
Q

What is a free radical?

A

Activated oxygen or carbon species that cause cell damage (ROS, COS)

72
Q

Unstable free radicals react with?

A

inorganic and organic chemicals in membrane lipids and nucleic acids

73
Q

What generates free radicals?

A

autocatalytic reactions within the cell, O2 therapy, radiation, oxidative injury, reperfusion, chemicals, inflammation, microbes, gases, aging

74
Q

Free radicals can result in

A

lipid peroxidation, oxidative protein modification, DNA damage

75
Q

Examples of Free radicals

A

Hydrogen Peroxide (H2O2), Superoxide (O2-), Hydroxyl ions (-OH)

76
Q

Superoxide dismutase

A

converts superoxide (O2-) to hydrogen peroxide (H2O2)

77
Q

Radiation creates free radicals by

A

radiolysing H2O into hydroxyl ions (-OH)

78
Q

Aging and free radicals

A

continuous free radical production, decreased anti-oxidant production, decreased anti-oxidant activity

79
Q

Agents that are protective against free radicals

A

Antioxidants: Vitamin E, Glutathione, D-Penicillamine, serum proteins, flavonoids

80
Q

Catalase enzyme converts

A

H2O2 –> H2O and O2

81
Q

Glutathione peroxidase

A

H2O2 –> H20

82
Q

Free radical production increases with

A

AGE

83
Q

Direct acting chemicals induce chemical injury by

A

DIRECTLY combining with critical components of cellular organelle

84
Q

By-products of glycolysis

A

H2O2 and O2-

85
Q

Toxic metabolites of chemicals induce chemical injury by

A

metabolism of drugs create toxic active metabolites that can either directly bind critical components of cellular organelle or induce freed radical formation

86
Q

Lipid peroxidation in the liver due to drug metabolites free radical production result in

A

lipid peroxidation causing damage to RER and PM -> ribosome detachment and decreased protein synthesis (Fatty liver) OR -> PM damage and increased permeability, cell swelling, influx of Ca, necrosis

87
Q

Viral infections cause cell injury by

A

causing cytolysis or cytopathic changes (degenerative changes)

88
Q

How does a virus directly damage the cell?

A

viral replication interferes with cellular mechanisms

89
Q

How does a virus inadvertently cause cell damage?

A

induces immunologic response: viral tropism (supporting growth of virus) result in phagocytosis, endocytosis or direct fusion of host cell

90
Q

Viral infections may cause host cell

A

lysis, cytoskeletal alterations, syncytial/giant cell formation, or inclusion formation

91
Q

Physiologic and biochemical mechanisms resulting in cellular injury may cause

A

morphological alterations in the cell

92
Q

Ultrastructural morphological changes include

A

PM alterations: swelling, blood formation, microvilli destruction, myelin figures;
Mitochondria: swelling, densities and granule formation
ER: swelling
Lysosome: swelling, rupture

93
Q

What morphological changes may be seen with the LIGHT microscope?

A

Reversible Injuries: Cellular swelling and intracellular accumulations
Irreversible Injuries: cell death

94
Q

Cell Death morphologic changes result from

A

Progressive degradation: enzyme digestion of cellular components and denaturation of proteins

95
Q

Autolysis

A

cellular digestion and denaturation cause by enzymes produced by necrotic cell

96
Q

Heterolysis

A

cellular digestion and denaturation cause by enzymes produced by cells other than the one affected

97
Q

General morphologic appearance of necrotic cell cytoplasm under the microscope?

A

eosinophilic (pink with H&E), glassy (loss of glycogen), and vacuolated

98
Q

General morphologic appearance of necrotic cell nucleus under the microscope?

A

clumped chromatin, pyknosis (shrunken nucleus), karyolysis (degraded nucleus), karyorrhexis (breakup of nucleus)

99
Q

Pyknosis

A

shrunken nucleus (as seen with necrotic cells)

100
Q

Karyolysis

A

degraded nucleus (as seen with necrotic cells)

101
Q

Karyorrhexis

A

breakup of nucleus (as seen with necrotic cells)

102
Q

Apoptosis

A

type of necrosis of an individual cell death by fragmentation and phagocytosis of fragments

103
Q

Coagulation Necrosis

A

Lose of nucleus due to denaturation of nuclear proteins and lysosomal enzymes (thus preventing proteolysis); cell shape maintained, eosinophila prominent

104
Q

Organs typically with coagulation necrosis

A

heart, kidney, and skeletal muscle

105
Q

Liquefeaction Necrosis

A

affected cell is completely digested by hydrolytic enzymes, resulting in a soft, circumscribed lesion consisting of pus

106
Q

Liquefeaction Necrosis hydrolytic enzymes are produced by

A

autolysis (self) or heterolysis (others)

107
Q

Liquefeaction Necrosis occurs primarily in the

A

brain, abdominal viscera and tissues infected with bacteria

108
Q

Liquefeaction Necrosis may result in _________ formation

A

abscess

109
Q

coagulation necrosis may progress to

A

Liquefeaction Necrosis

110
Q

Fat Necrosis

A

lipases cause saponification of fat -> resultant chalky white consistency

111
Q

Fat necrosis may result in ______

A

calcification

112
Q

Fat necrosis primarily occurs in

A

pancreas (after lipase and amylase release) and trauma to adipose tissue

113
Q

Caseation Necrosis is a combination of

A

coagulation and liquefaction necrosis

114
Q

Caseation Necrosis leads to ____ formation

A

granuloma

115
Q

Caseation Necrosis is characterized by

A

soft, granular, “cheesy” proteinacious material, surrounded by multinucleate giant cells, lymphocytes, and macrophages

116
Q

Caseation Necrosis primarily occurs in

A

any tissue infected with Mycobacterium tuberculosis and certain fungal infections

117
Q

Gangrenous Necrosis occurs primarily in

A

ISCHEMIC necrotic tissues, subsequently infected by anaerobic bacteria (Clostridium)

118
Q

Dry Gangrene

A

ISCHEMIA + necrosis and drying of the tissue -> black, mummified appearance

119
Q

Dry gangrene is typically caused by

A

arterial occlusion

120
Q

Dry gangrene microscopically shows ___________ necrosis

A

COAGULATION

121
Q

Wet gangrene is characterized by

A

soft, green-black, foul smelling purulent consistency

122
Q

Wet gangrene microscopically shows ___________ necrosis

A

Liquefaction following the release of autolytic, heterlytic, and bacterial enzymes

123
Q

Wet gangrene is typically caused by

A

arterial occlusion or traumatic injury

124
Q

Intracellular accumulations include

A

normal substances, abnormal substances, pigments; accumulation within the cell

125
Q

Intracellular accumulations may be:

A

harmful or harmless, within the cytoplasm or nucleus, produced by cell or elsewhere

126
Q

Types of intracellular accumulations

A

lipid, protein, glycogen, complex lipids, complex carbohydrates, pigments

127
Q

Lipid intracellular accumulations are characterized by

A

fatty change (fatty degeneration/infiltration)

128
Q

Lipid intracellular accumulations occur in

A

liver, heart, kidney, or skeletal muscle

129
Q

Lipid intracellular accumulations may be composed of

A

triglycerides, cholesterol, or both

130
Q

Protein intracellular accumulations may occur

A

in any tissue as HYALINE or plasma cells as RUSSELL BODIES

131
Q

Russell bodies

A

protein accumulation in plasma cells

132
Q

Protein intracellular accumulations often occur in

A

kidney, liver, or joints

133
Q

Glycogen intracellular accumulations

A

Common in diabetics (many tissues) and in glycogen storage diseases (specific or many tissues)

134
Q

Fatty liver

A

Fat accumulation in hepatocytes due to metabolic abnormality

135
Q

Lysosomal storage disease

A

accumulation in cells due to lack of enzyme

136
Q

Pigment intracellular accumulation

A

Normal or abnormal, produced endogenously or exogenously (uptake of indigestible material)

137
Q

Exogenous pigment accumulation include:

A

carbon (tattoo, anthracosis)

138
Q

Endogenous pigment accumulation include:

A

melanin, lipofuscin, hemosiderin, bilirubin and carotene

139
Q

Subcellular Alterations

A

changes occurring in the cell at the level of organelle

140
Q

Lysosome mechanism

A

vesicle from RER - Golgi - cytoplasm as primary lysosome fuses with phagosome to become secondary lysosome; hydrolytic enzymes digest phagosome particles

141
Q

Heterophagocytosis

A

type of phagocytosis of a compound outside the cell begin brought into the cell

142
Q

Heterophagocytosis is carried out by

A

neutrophils and macrophages

143
Q

Autophagocytosis

A

type of phagocytosis where lysosomes phagocytose damaged organelle originate ding within the same cell

144
Q

SER subcellular alterations due to injury

A

SR is broken down after PM damage

145
Q

Mitochondrial subcellular alterations due to injury

A

mitchondrial permeability transition pore -> loss of mitochondrial membrane potential -> loss of OXphos and ATP

146
Q

Lipofuscin pigment granules

A

finely granular yellow-brown pigment granules composed of lipid-containing residues of lysosomal digestion (aging process)

147
Q

What causes mitchondrial permeability transition pore formation?

A

increased Ca2+, free radicals, toxins, hypoxia

148
Q

Cytoskeleton/Cell membrane sub cellular alteration due to injury are characterized by

A

changes in the filaments and microtubules

149
Q

Damage to cytoskeletal filaments and MT’s result in

A

altered cellular structure, impaired phagocytosis, impaired mitosis, impaired sperm motility

150
Q

Mallory Bodies

A

characteristic cytoskeletal change (twisted rope appearance) indicative of alcoholic liver disease

151
Q

Neurofibrillary tangles

A

characteristic cytoskeletal change - aggregates of hyperphosphorylated tau protein that are a primary marker of Alzheimer’s Disease

152
Q

Atrophy - cellular adaptation

A

decreased cell size due to loss of cell substance

153
Q

Atrophy may be caused by

A

decreased workload (disuse), loss of innervation, decreased blood supply, inadequate nutrition, loss of endocrine stimulation, aging, pressure

154
Q

Hypertrophy

A

increase in cell size; increased demands of cell or increased stimulation by hormones

155
Q

Physiologic hypertrophy

A

uterine and breast enlargement during pregnancy

156
Q

Pathologic hypertrophy

A

cardiac hypertrophy in HTN or valvular incompetence

157
Q

Hyperplasia

A

increase in cell number (with hypertrophy depending on stimulus)

158
Q

Hyperplasia cannot occur in

A

nerve, skeletal, or cardiac muscle

159
Q

Physiologic Hyperplasia

A

Hormonal: epithelium of breast during puberty
Compensatory: to account for damaged tissue

160
Q

Pathologic Hyperplasia

A

Abnormal hormonal stimulation (endometrium, breast, adrenal)

161
Q

Metaplasia

A

Reversible change in cell type as a result of stress, divergent differentiation

162
Q

Metaplasia may lead to

A

pre-malignant (dysplastic) changes

163
Q

Dysplasia

A

Deranged development due to stimulation to proliferate with atypical cytological alterations

164
Q

Dysplasia may be

A

precursor to cancer

165
Q

Calcification

A

Calcium salt + other ions precipitate and deposit in tissues

166
Q

Dystrophic calcification

A

deposition of calcium as a sequelae to necrosis or tissue injury and inflammation; intra- or extracellular

167
Q

Examples of Dystrophic calcification

A

arteriosclerosis, fat necrosis

168
Q

Metastatic Calcification

A

Systemic hypercalcemia -> deposition of calcium in viable tissue

169
Q

What condition is known for systemic increased levels of Ca?

A

Hyperparathyroidism -> systemic metastatic calcification deposition

170
Q

Hyaline

A

translucent, albuminoid protein which is the product of amyloid degeneration

171
Q

Intracellular hyaline deposition may occur

A

in plasma cells + viral infection, hepatocytes + chronic alcohol abuse

172
Q

Extracellular hyaline deposition may occur

A

arterial walls and in scar tissue following chronic inflammatory processes

173
Q

Desmoplasia

A

associated with malignant neoplasms, which can evoke a fibrosis response by invading healthy tissue.

174
Q

Fibrosis

A

formation of excess fibrous connective tissue in an organ or tissue in a reparative or reactive process

PATHOLOGY (18 decks)

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