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Questions and Answers
What characterizes necrosis as opposed to apoptosis?
What characterizes necrosis as opposed to apoptosis?
Which of the following conditions can cause cell injury through hypoxia?
Which of the following conditions can cause cell injury through hypoxia?
What aspect of cell injury is influenced by the type of cell and its health status?
What aspect of cell injury is influenced by the type of cell and its health status?
Which of the following intracellular systems is NOT vulnerable to injury?
Which of the following intracellular systems is NOT vulnerable to injury?
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What role do calcium transporters play in cellular injury?
What role do calcium transporters play in cellular injury?
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Which of the following is a common cause of cell injury caused by nutritional imbalances?
Which of the following is a common cause of cell injury caused by nutritional imbalances?
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Which physiological response results when a cell encounters pathological stimuli and reaches its adaptive limits?
Which physiological response results when a cell encounters pathological stimuli and reaches its adaptive limits?
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What distinguishes ischemia from hypoxia?
What distinguishes ischemia from hypoxia?
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What is the first effect of hypoxia on cellular respiration?
What is the first effect of hypoxia on cellular respiration?
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Which enzyme stimulates increased rates of anaerobic glycolysis when ATP and AMP levels decrease?
Which enzyme stimulates increased rates of anaerobic glycolysis when ATP and AMP levels decrease?
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What occurs with the accumulation of extracellular calcium during ischemic injury?
What occurs with the accumulation of extracellular calcium during ischemic injury?
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What is NOT a sign of irreversible cellular injury?
What is NOT a sign of irreversible cellular injury?
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What is a consequence of the continued loss of membrane phospholipids during irreversible injury?
What is a consequence of the continued loss of membrane phospholipids during irreversible injury?
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What happens when hypoxia leads to acute cellular swelling?
What happens when hypoxia leads to acute cellular swelling?
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What mediates cell death following the generation of oxygen free radicals?
What mediates cell death following the generation of oxygen free radicals?
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What role do toxic oxygen radicals play during reperfusion injury?
What role do toxic oxygen radicals play during reperfusion injury?
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What is the primary cause of cytoplasmic eosinophilia?
What is the primary cause of cytoplasmic eosinophilia?
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Which type of necrosis is characterized by the preservation of structural outlines of the coagulated cells or tissue?
Which type of necrosis is characterized by the preservation of structural outlines of the coagulated cells or tissue?
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Which cellular change is associated with karyorrhexis?
Which cellular change is associated with karyorrhexis?
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In which type of necrosis is the central necrotic area described as having a cheesy, white gross appearance?
In which type of necrosis is the central necrotic area described as having a cheesy, white gross appearance?
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Which ultrastructural change indicates damage to the mitochondria?
Which ultrastructural change indicates damage to the mitochondria?
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What is the primary mechanism of autolysis during necrosis?
What is the primary mechanism of autolysis during necrosis?
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What process primarily leads to liquefactive necrosis?
What process primarily leads to liquefactive necrosis?
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Which of the following accurately describes gangrenous necrosis?
Which of the following accurately describes gangrenous necrosis?
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What is the consequence of fat necrosis following acute pancreatitis?
What is the consequence of fat necrosis following acute pancreatitis?
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What is a key characteristic of apoptosis observed in stained sections?
What is a key characteristic of apoptosis observed in stained sections?
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Which of the following can initiate apoptosis?
Which of the following can initiate apoptosis?
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What type of intracellular accumulation results from a genetic enzymatic defect?
What type of intracellular accumulation results from a genetic enzymatic defect?
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How does apoptosis differ from necrosis in terms of its cellular response?
How does apoptosis differ from necrosis in terms of its cellular response?
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What is a consequence of intracellular accumulation of harmful substances?
What is a consequence of intracellular accumulation of harmful substances?
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Which process is NOT associated with apoptosis?
Which process is NOT associated with apoptosis?
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Which of these describes an abnormal endogenous substance accumulation?
Which of these describes an abnormal endogenous substance accumulation?
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What is dystrophic calcification characterized by?
What is dystrophic calcification characterized by?
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In which condition might metastatic calcification occur?
In which condition might metastatic calcification occur?
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Which option does NOT typically cause hypercalcemia?
Which option does NOT typically cause hypercalcemia?
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What happens to cells during atrophy?
What happens to cells during atrophy?
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What is a common cause of atrophy?
What is a common cause of atrophy?
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How does hypertrophy primarily occur?
How does hypertrophy primarily occur?
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Which of the following is NOT a characteristic of dystrophic calcification?
Which of the following is NOT a characteristic of dystrophic calcification?
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Where is metastatic calcification most likely to occur?
Where is metastatic calcification most likely to occur?
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What is the most common organ affected by fatty change (steatosis)?
What is the most common organ affected by fatty change (steatosis)?
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Which type of accumulation results in xanthomas?
Which type of accumulation results in xanthomas?
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What common cause of fatty change could impair the liver's ability to synthesize apoproteins?
What common cause of fatty change could impair the liver's ability to synthesize apoproteins?
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Under the light microscope, how does fatty change present in parenchymal cells?
Under the light microscope, how does fatty change present in parenchymal cells?
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What is pathologic calcification characterized by?
What is pathologic calcification characterized by?
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What leads to the formation of foamy cells in atherosclerosis?
What leads to the formation of foamy cells in atherosclerosis?
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What pigment accumulates in the epidermis to cause freckles?
What pigment accumulates in the epidermis to cause freckles?
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Which of the following conditions is most likely to result in an abnormal accumulation of glycogen?
Which of the following conditions is most likely to result in an abnormal accumulation of glycogen?
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What is the primary process responsible for the disaggregation of granular elements in necrotic cells?
What is the primary process responsible for the disaggregation of granular elements in necrotic cells?
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Which type of necrosis is primarily associated with anoxic cell death in all tissues except the brain?
Which type of necrosis is primarily associated with anoxic cell death in all tissues except the brain?
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What histological feature is specifically associated with karyolysis during necrosis?
What histological feature is specifically associated with karyolysis during necrosis?
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What change occurs in the mitochondria as a result of cellular injury?
What change occurs in the mitochondria as a result of cellular injury?
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Which of the following best describes gangrenous necrosis?
Which of the following best describes gangrenous necrosis?
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In which type of necrosis would you expect to see a 'cheesy' gross appearance of the necrotic area?
In which type of necrosis would you expect to see a 'cheesy' gross appearance of the necrotic area?
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What type of cellular change is associated with cytoplasmic eosinophilia during necrosis?
What type of cellular change is associated with cytoplasmic eosinophilia during necrosis?
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What is a common outcome of liquefactive necrosis?
What is a common outcome of liquefactive necrosis?
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What is the consequence of decreased ATP levels during hypoxia?
What is the consequence of decreased ATP levels during hypoxia?
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Which enzyme is stimulated due to decreased levels of ATP and AMP in hypoxic conditions?
Which enzyme is stimulated due to decreased levels of ATP and AMP in hypoxic conditions?
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What is an early irreversible change observed in cells after persistent hypoxia?
What is an early irreversible change observed in cells after persistent hypoxia?
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What role do oxygen free radicals play in cell injury?
What role do oxygen free radicals play in cell injury?
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Which of the following is NOT associated with irreversible injury?
Which of the following is NOT associated with irreversible injury?
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What happens to ribosomes during early stages of hypoxic injury?
What happens to ribosomes during early stages of hypoxic injury?
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What characterizes the formation of myelin figures in dead cells?
What characterizes the formation of myelin figures in dead cells?
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Which cellular component is damaged by toxic oxygen radicals during reperfusion injury?
Which cellular component is damaged by toxic oxygen radicals during reperfusion injury?
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What does fat necrosis specifically describe?
What does fat necrosis specifically describe?
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Which of the following best describes the appearance of apoptotic cells under H&E staining?
Which of the following best describes the appearance of apoptotic cells under H&E staining?
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What is the primary initiator of apoptosis?
What is the primary initiator of apoptosis?
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Which type of intracellular accumulation is characterized by an inadequate metabolism rate of a normal substance?
Which type of intracellular accumulation is characterized by an inadequate metabolism rate of a normal substance?
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What event primarily occurs during the process of apoptosis?
What event primarily occurs during the process of apoptosis?
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Which of the following is NOT a form of stimuli that can initiate apoptosis?
Which of the following is NOT a form of stimuli that can initiate apoptosis?
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How is apoptosis generally characterized in terms of inflammation?
How is apoptosis generally characterized in terms of inflammation?
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Which process contributes to the formation of apoptotic bodies during apoptosis?
Which process contributes to the formation of apoptotic bodies during apoptosis?
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What underlying condition may lead to hypercalcemia due to increased parathyroid hormone levels?
What underlying condition may lead to hypercalcemia due to increased parathyroid hormone levels?
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In which scenario would dystrophic calcification most likely occur?
In which scenario would dystrophic calcification most likely occur?
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What is the primary difference between atrophy and hypertrophy?
What is the primary difference between atrophy and hypertrophy?
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Which of the following describes a common result of cellular hypertrophy?
Which of the following describes a common result of cellular hypertrophy?
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What may induce both apoptosis and atrophy in cells?
What may induce both apoptosis and atrophy in cells?
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What condition is most likely to cause metastatic calcification?
What condition is most likely to cause metastatic calcification?
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How are intracellular and extracellular calcifications generally characterized?
How are intracellular and extracellular calcifications generally characterized?
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What is the primary regulatory factor of cellular adaptations in response to stress?
What is the primary regulatory factor of cellular adaptations in response to stress?
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Study Notes
### Necrosis vs. Apoptosis
- Necrosis: Characterized by cell swelling, membrane rupture, and inflammation, uncontrolled cell demise.
- Apoptosis: Programmed cell death, characterized by cell shrinkage, nuclear fragmentation, and formation of apoptotic bodies, without inflammation.
Hypoxia and Cell Injury
- Hypoxia: (low oxygen) can cause cell injury by affecting various cellular processes like ATP production, and causing membrane damage
- Conditions causing hypoxia: Cardiac arrest, severe anemia, respiratory failure, severe blood loss, and circulatory shock.
Factors Influencing Cell Injury
- Type of cell and its health status: Influences the severity and nature of cell injury due to differences in metabolic rates, enzyme levels, and reserve capacity.
Intracellular Systems Vulnerable to Injury
- Vulnerable: Cell membranes, mitochondria, DNA, and ribosomes.
- Not vulnerable: Cellular nuclei (nucleus can have damage but is not the initial target)
Calcium Transporters in Cellular Injury
- Calcium Transporters: Regulate intracellular calcium levels, playing a crucial role in cell survival and death.
- Role: Dysfunction during injury leads to increased intracellular calcium, causing activation of enzymes which damage cellular components.
Nutritional Imbalances and Cell Injury
- Common Cause: Prolonged malnutrition, vitamin deficiency, and alcohol abuse, can lead to nutritional deficiencies and oxidative stress.
Adaptive Limits and Cell Injury
- Adaptive Limits: When a cell encounters pathological stimuli exceeding its adaptive capacity, triggers cell injury or death.
- Result: Adaptive mechanisms like hypertrophy, hyperplasia, and atrophy can be overwhelmed leading to cell injury.
### Ischemia vs. Hypoxia
- Ischemia: Reduced blood flow to tissues, meaning reduced oxygen and nutrients, and accumulation of metabolic waste products
- Hypoxia: Low oxygen tension in tissues.
Hypoxia and Cellular Respiration
- First effect: Decreased ATP production, impacting energy-dependent cellular functions.
Enzyme Activation in Hypoxia
- Enzyme: Phosphofructokinase, which stimulates increased rates of anaerobic glycolysis. This helps compensate for decreased ATP production, but leads to lactic acid build-up.
Extracellular Calcium Accumulation
- Ischemic Injury: Accumulation of extracellular calcium in the injured tissue, contributes to cell death by triggering the release of harmful enzymes (e.g., phospholipases).
Irreversible Cellular Injury
- Sign: Cellular swelling, nuclear fragmentation, and mitochondrial damage, are signs of irreversible injury.
- Not a sign: Initially decreased ATP, an early sign of reversible injury.
### Membrane Phospholipid Loss
- Consequence: Loss of membrane integrity, leading to leakage of intracellular contents, further contributing to cell death.
Hypoxia and Cellular Swelling
- Hypoxia: Leads to acute cellular swelling due to impaired ion pumps, causing a buildup of intracellular fluid.
### Oxygen Free Radicals and Cell Death
- Mediation: Oxygen free radicals (ROS) contribute to cell death by causing oxidative damage to lipids, proteins, and DNA.
Toxic Oxygen Radicals in Reperfusion Injury
- Role: Toxic oxygen radicals are generated during reperfusion injury, further exacerbating tissue damage due to oxidative stress.
Cytoplasmic Eosinophilia
- Cause: Increased eosinophilia (pink staining) of the cytoplasm in necrotic cells is due to the loss of cytoplasmic RNA and increased binding of eosin stain to denatured proteins.
Coagulative Necrosis
- Characteristic: Preservation of the structural outlines of the coagulated cells or tissues.
- Example: Most commonly seen in tissues with abundant protein, like the heart, kidney, and liver.
Karyorrhexis
- Association: Karyorrhexis (nuclear fragmentation) is associated with chromatin clumping and nuclear fragmentation, signifying irreversible cell damage.
Caseous Necrosis
- Description: Central necrotic area with a cheesy, white gross appearance.
- Example: Tuberculosis infection.
### Mitochondrial Damage
- Ultrastructural change: Mitochondrial swelling, rupture, and formation of vacuoles.
Autolysis in Necrosis
- Mechanism: Autolysis is a process of self-digestion, where lysosomal enzymes released from dying cells break down the cellular components leading to necrosis.
### Liquefactive Necrosis
- Process: Process where dead cells get dissolved and liquefied by enzymatic activity.
- Example: Occurs in the brain due to the abundance of lysosomes, and also in abscesses (where the contents are liquefied).
### Gangrenous Necrosis
- Description: A form of necrosis caused by ischemia, typically affecting extremities.
- Types: Dry gangrene occurs in the presence of good blood supply, whereas wet gangrene occurs with poor blood supply.
- Characteristics: Dry gangrene is characterized by shrunken tissues with dark brown discoloration, while wet gangrene is characterized by swollen tissues with a foul odor.
### Fat Necrosis
- Consequence: Fat necrosis following acute pancreatitis is characterized by pancreatic lipase-mediated breakdown of triglycerides, leading to saponification (formation of soap-like substances).
### Apoptosis in Stained Sections
- Characteristic: Cell shrinkage, nuclear fragmentation, and formation of apoptotic bodies which appear as small, round, membrane-bounded fragments
### Initiators of Apoptosis
- Initiators: These triggers include, DNA damage, cellular stress, withdrawal of growth factors, and activation of death receptors.
### Intracellular Accumulation Due to Genetic Defect
- Result: Lysosomal storage disease due to inherited genetic defects affecting lysosomal enzymes, leading to accumulation of undigested substances.
### Apoptosis vs. Necrosis
- Apoptosis: Programmed cell death that is energy dependent, involves activation of specific caspases, and does not cause inflammation.
- Necrosis: Uncontrolled cell death associated with cell injury caused by external factors like trauma, toxins, or ischemia, causing inflammation.
### Consequence of Harmful Substance Accumulation
- Consequence: Cellular toxicity, dysfunction, and even cell death depending on the nature and amount of the substance.
### Process Not Associated with Apoptosis
- Process: Inflammation. Apoptosis is a silent process with no inflammation associated with it.
### Abnormal Endogenous Substance Accumulation
- Example: Accumulation of glycogen in various tissues like the liver and muscle in patients with glycogen storage diseases.
- Cause: Due to a defect in enzymes involved in glycogen metabolism.
### Dystrophic Calcification
- Characterized: Localized deposition of calcium salts, primarily in areas of previous tissue injury or necrosis where there is damaged tissue and tissue degradation.
### Metastatic Calcification
- Condition: Hypercalcemia (high levels of calcium in the blood)
- Description: Abnormal calcium deposition in normal tissues, often seen in tissues with high phosphate levels, such as the kidneys, lungs, and blood vessels.
### Hypercalcemia
- Causes: Primary hyperparathyroidism, malignancy, excessive intake of vitamin D, and immobilization.
- Not a cause: Renal failure is associated with hypocalcemia, not hypercalcemia.
Atrophy in Cells
- Cellular change: Decrease in cell size due to a reduction in organelles.
### Common Cause of Atrophy
- Cause: Decreased workload, malnutrition, diminished blood supply, and hormonal stimulation.
### Mechanism of Hypertrophy
- Primarily occurs: Due to increased production of cellular proteins and organelles, leading to larger cell sizes and a greater functional capacity.
### Characteristics of Dystrophic Calcification
- Characteristic: It is not associated with hypercalcemia.
- Location: It occurs in dying or dead tissues, where the tissues undergo necrosis and calcification.
### Metastatic Calcification Location
- Most likely location: Kidney, lungs, and blood vessels, due to their high phosphate levels and ability to excrete calcium.
### Fatty Change
- Most common organ: The liver, due to its central role in lipid metabolism.
### Xanthomas
- Result: Lipid accumulation in macrophages, forming characteristic tumor-like deposits in the skin.
### Impaired Liver Function and Fatty Change
- Impairment: Fatty change can be caused by impairment in the synthesis of apoproteins, crucial components for the transport of lipids, leading to their accumulation in the liver.
### Fatty Change Histology
- Parenchymal cells: Fatty change is evident under a light microscope, appearing as small vacuoles or large globules in the cytoplasm of parenchymal cells.
### Pathologic Calcification
- Characterized: Abnormal calcification, either dystrophic (in dead or injured tissues) or metastatic (in normal tissues with high blood calcium levels).
### Formation of Foamy Cells
- Process: Accumulation of cholesterol and cholesterol esters within macrophages, giving them a foamy appearance, contributing to atherosclerosis plaque formation.
### Freckles and Pigment Accumulation
- Pigment: Melanin, accumulating in the epidermis, leads to freckles, which are focal areas of increased melanin pigmentation.
### Abnormal Glycogen Accumulation
- Condition: Glycogen storage diseases, genetic disorders affecting enzymes involved in glycogen metabolism, leading to excessive glycogen accumulation in various tissues.
### Disaggregation of Granular Elements
- Primary process: Cell injury, causing the disintegration of cellular components.
### Anoxic Cell Death
- Necrosis type: Coagulative necrosis, occurring in most tissues except the brain.
### Karyolysis
- Histological feature: Nuclear fading, a characteristic of karyolysis, where genetic material is degraded by DNAases.
### Mitochondrial Damage
- Change: Cellular injury, especially hypoxia, causes swelling, rupture, and the formation of vacuoles, which disrupt the functions of mitochondria.
### Gangrenous Necrosis Description
- Description: A form of necrosis resulting from ischemia, particularly affecting extremities, affecting tissue due to lack of blood flow.
### Caseous Necrosis Appearance
- Appearance: Cheesy, white gross appearance of the necrotic area, commonly seen in tissues affected by tuberculosis.
### Cytoplasmic Eosinophilia in Necrosis
- Association: The accumulation of eosinophilic (pink-staining) proteins due to loss of cytoplasmic RNA and protein denaturation.
### Liquefactive Necrosis Consequence
- Consequence: Liquefied debris and pus formation, often seen in the brain, bacterial infections, and abscesses.
### Decreased ATP Levels in Hypoxia
- Consequence: Leads to impaired cellular functions, including membrane ion pumps, causing cell swelling and eventual cell death.
### Enzyme Stimulation in Hypoxic Conditions
- Enzyme: Phosphofructokinase, stimulated due to decreased ATP and AMP levels, increases anaerobic glycolysis to compensate for reduced ATP production.
### Early Irreversible Change
- Change: Irreversible cell damage, characterized by extensive mitochondrial swelling, disruption of cell membranes, and cell death.
### Role of Oxygen Free Radicals
- Role: They contribute to damaging cell membranes, proteins, and DNA, leading to cell injury.
### Irreversible Injury
- Not associated: Decreased ATP levels, an early sign of reversible cell injury.
### Ribosomes in Hypoxic Injury
- Change: Detach from the endoplasmic reticulum, impairing protein synthesis, contributing to cell malfunction.
### Myelin Figures
- Formation: Derived from degraded cell membranes during cell injury.
- Appearance: Layered, concentric, whorled structures, often visible under microscopy.
### Cell Component Damaged by Toxic Oxygen Radicals
- Component: Cell membranes, particularly the phospholipid bilayer, are vulnerable to oxidative stress caused by toxic oxygen radicals.
### Fat Necrosis Description
- Description: Refers to the destruction of adipose tissue, typically occurring in the pancreas, caused by the release of pancreatic lipase, which breaks down fat into fatty acids and glycerol.
### Apoptotic Cells Under Microscopy
- Appearance: Apoptotic cells shrink and display nuclear fragmentation, forming small, round, membrane-bound bodies, known as apoptotic bodies.
### Primary Initiator of Apoptosis
- Initiator: The activation of caspases, a family of cysteine proteases, plays a crucial role in triggering the cascade of events leading to apoptosis.
### Intracellular Accumulation Due to Inadequate Metabolism
- Type: Lysosomal storage diseases, a group of genetic disorders resulting from deficient enzymes involved in the breakdown of various molecules.
- Example: Accumulation of glycogen in glycogen storage diseases or accumulation of lipids in lipid storage diseases.
### Event During Apoptosis
- Event: Nuclear fragmentation, involving the breakdown of DNA by endonucleases.
### Stimuli that can Initiate Apoptosis
- Stimuli: Growth factor deprivation, DNA damage, exposure to cytotoxic T cells, and activation of death receptors.
- Not a Stimuli: Increased intracellular sodium levels is not a typical initiator of apoptosis.
### Apoptosis and Inflammation
- Characteristic: Apoptosis is generally characterized by being anti-inflammatory.
### Apoptotic Bodies Formation
- Process: Cells undergoing apoptosis fragment into small membrane-enclosed bodies, known as apoptotic bodies, containing cellular components.
### Hypercalcemia Cause
- Cause: Increased parathyroid hormone (PTH) levels can lead to hypercalcemia due to increased bone resorption and reduced calcium excretion by the kidneys.
### Dystrophic Calcification Scenario
- Scenario: Damaged or dead tissues, such as areas of necrosis, atherosclerotic plaques, and old hematomas.
### Atrophy vs. Hypertrophy
- Difference: Atrophy is a decrease in cell size, while hypertrophy is an increase in cell size.
### Cellular Hypertrophy Result
- Result: Increased functional capacity of the affected tissue or organ.
### Inducer of Apoptosis and Atrophy
- Inducer: Cellular stress, including inadequate nutrition, prolonged hypoxia, and toxic substances can trigger both apoptosis and atrophy in cells.
### Metastatic Calcification Cause
- Cause: Hypercalcemia, due to high calcium levels in the blood.
### Intracellular and Extracellular Calcifications
- Characterized: Intracellular calcification occurs within the cytoplasm of cells, while extracellular calcification occurs in the extracellular matrix or in tissues.
### Cellular Adaptations to Stress
- Primary regulatory factor: The cellular environment, specifically the presence of growth factors, hormones, and other external stimuli, play a crucial role in regulating cellular adaptations.
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Description
This quiz explores the concepts of cell injury, including the differences between necrosis and apoptosis. It covers various causes of cell injury such as hypoxia, physical agents, chemicals, and genetic defects. Test your understanding of how these factors contribute to cellular changes and ultimately cell death.