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Questions and Answers
What is the initial consequence of hypoxia on cellular respiration?
What is the initial consequence of hypoxia on cellular respiration?
Which of the following best describes a mechanism of irreversible injury?
Which of the following best describes a mechanism of irreversible injury?
What happens to the cytoskeleton during continued hypoxia?
What happens to the cytoskeleton during continued hypoxia?
What metabolic consequence follows a reduction in intracellular ATP?
What metabolic consequence follows a reduction in intracellular ATP?
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Which enzyme is stimulated due to decreased ATP and AMP levels?
Which enzyme is stimulated due to decreased ATP and AMP levels?
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What are the consequences of calcium influx during ischemia?
What are the consequences of calcium influx during ischemia?
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What is a characteristic effect of reperfusion injury?
What is a characteristic effect of reperfusion injury?
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Which of the following is NOT a feature of reversible injury?
Which of the following is NOT a feature of reversible injury?
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Which of the following is a mechanism by which free radicals can cause cellular injury?
Which of the following is a mechanism by which free radicals can cause cellular injury?
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What is a primary consequence of oxygen free radicals reacting with deoxyribonucleic acid (DNA)?
What is a primary consequence of oxygen free radicals reacting with deoxyribonucleic acid (DNA)?
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Which of the following free radicals is generated during normal physiological oxidative phosphorylation?
Which of the following free radicals is generated during normal physiological oxidative phosphorylation?
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What effect does the conversion of carbon tetrachloride (CCl4) into CCl3 have on liver cells?
What effect does the conversion of carbon tetrachloride (CCl4) into CCl3 have on liver cells?
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Which intracellular enzyme is specifically mentioned as responsible for generating superoxide radicals?
Which intracellular enzyme is specifically mentioned as responsible for generating superoxide radicals?
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What is one of the features of reversible cell injury observable under a light microscope?
What is one of the features of reversible cell injury observable under a light microscope?
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In which of the following scenarios are free radicals NOT generally implicated?
In which of the following scenarios are free radicals NOT generally implicated?
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Which metal is mentioned for its role in the formation of free radicals through electron donation?
Which metal is mentioned for its role in the formation of free radicals through electron donation?
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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 of the following is a potential cause of fatty change?
Which of the following is a potential cause of fatty change?
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What histological feature indicates the presence of fatty change under the light microscope?
What histological feature indicates the presence of fatty change under the light microscope?
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What are foamy cells indicative of in the context of lipid accumulation?
What are foamy cells indicative of in the context of lipid accumulation?
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What condition may lead to the appearance of xanthomas?
What condition may lead to the appearance of xanthomas?
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Which pigment is derived from hemoglobin and typically accumulates when there is excess iron?
Which pigment is derived from hemoglobin and typically accumulates when there is excess iron?
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What type of pathological process involves the abnormal accumulation of calcium salts?
What type of pathological process involves the abnormal accumulation of calcium salts?
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Which of the following is less commonly associated with cellular accumulation?
Which of the following is less commonly associated with cellular accumulation?
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What is the primary cause of cytoplasmic eosinophilia during cellular injury?
What is the primary cause of cytoplasmic eosinophilia during cellular injury?
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Which type of necrosis is characterized by preservation of structural outlines for days after cell death?
Which type of necrosis is characterized by preservation of structural outlines for days after cell death?
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What is the consequence of karyolysis in necrotic cells?
What is the consequence of karyolysis in necrotic cells?
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Which of the following processes can result in liquefactive necrosis?
Which of the following processes can result in liquefactive necrosis?
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What distinguishes gangrenous necrosis from other types of necrosis?
What distinguishes gangrenous necrosis from other types of necrosis?
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What is the typical ultrastructural change seen in mitochondrial damage during cellular injury?
What is the typical ultrastructural change seen in mitochondrial damage during cellular injury?
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Which type of necrosis is commonly associated with tuberculous infections?
Which type of necrosis is commonly associated with tuberculous infections?
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What morphological changes occur in the endoplasmic reticulum during cellular injury?
What morphological changes occur in the endoplasmic reticulum during cellular injury?
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What characterizes dystrophic calcification?
What characterizes dystrophic calcification?
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Which of the following conditions is NOT a cause of hypercalcemia?
Which of the following conditions is NOT a cause of hypercalcemia?
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What is a primary consequence of nephrocalcinosis?
What is a primary consequence of nephrocalcinosis?
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Which statement about atrophy is correct?
Which statement about atrophy is correct?
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Which of the following defines hypertrophy?
Which of the following defines hypertrophy?
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In pathological adaptations, what is the intended effect on cells?
In pathological adaptations, what is the intended effect on cells?
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Which of the following features is associated with metastatic calcification?
Which of the following features is associated with metastatic calcification?
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What is typically the result of physiologic cellular adaptations?
What is typically the result of physiologic cellular adaptations?
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What is the result of the initial effect of hypoxia on the cellular environment?
What is the result of the initial effect of hypoxia on the cellular environment?
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What happens to the cytoplasmic pH as a result of anaerobic glycolysis due to decreased ATP levels?
What happens to the cytoplasmic pH as a result of anaerobic glycolysis due to decreased ATP levels?
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Which of the following is a characteristic of irreversible cell injury?
Which of the following is a characteristic of irreversible cell injury?
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What is a consequence of free radical generation following reperfusion injury?
What is a consequence of free radical generation following reperfusion injury?
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Which cellular component is affected by toxic oxygen radicals released after reperfusion?
Which cellular component is affected by toxic oxygen radicals released after reperfusion?
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How does ATP depletion influence intracellular ion concentrations during ischemia?
How does ATP depletion influence intracellular ion concentrations during ischemia?
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What cellular alteration occurs as a consequence of prolonged hypoxia and ATP depletion?
What cellular alteration occurs as a consequence of prolonged hypoxia and ATP depletion?
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Which is NOT a feature associated with the mechanisms of irreversible injury?
Which is NOT a feature associated with the mechanisms of irreversible injury?
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What is the primary cause of fat necrosis following acute pancreatitis?
What is the primary cause of fat necrosis following acute pancreatitis?
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Which of the following best describes the process of apoptosis?
Which of the following best describes the process of apoptosis?
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What feature is NOT typically associated with apoptosis as observed on H&E stained sections?
What feature is NOT typically associated with apoptosis as observed on H&E stained sections?
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What initiates the process of apoptosis?
What initiates the process of apoptosis?
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Intracellular accumulations can lead to damage. Which situation does NOT describe a typical case of such accumulation?
Intracellular accumulations can lead to damage. Which situation does NOT describe a typical case of such accumulation?
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Which intracellular accumulation category describes the liver's fatty change?
Which intracellular accumulation category describes the liver's fatty change?
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What is a characteristic change that occurs during apoptosis?
What is a characteristic change that occurs during apoptosis?
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Which of the following stimuli is NOT associated with the activation of apoptosis?
Which of the following stimuli is NOT associated with the activation of apoptosis?
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What is one of the main cell components that oxygen free radicals react with?
What is one of the main cell components that oxygen free radicals react with?
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What result occurs following the conversion of carbon tetrachloride (CCl4) into the free radical CCl3 in liver cells?
What result occurs following the conversion of carbon tetrachloride (CCl4) into the free radical CCl3 in liver cells?
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Which process is primarily responsible for generating superoxide radicals within cells?
Which process is primarily responsible for generating superoxide radicals within cells?
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Which of the following statements correctly describes a mechanism of chemical injury?
Which of the following statements correctly describes a mechanism of chemical injury?
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In the context of free radicals, which of the following species is generated during normal physiological conditions?
In the context of free radicals, which of the following species is generated during normal physiological conditions?
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What role do xanthine oxidase enzymes play concerning free radicals?
What role do xanthine oxidase enzymes play concerning free radicals?
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What is the primary consequence of lipid peroxidation when free radicals react with plasma membranes?
What is the primary consequence of lipid peroxidation when free radicals react with plasma membranes?
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Which scenario correctly describes a phenomenon caused by the influence of free radicals on cellular aging?
Which scenario correctly describes a phenomenon caused by the influence of free radicals on cellular aging?
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What primarily causes fatty change in cells?
What primarily causes fatty change in cells?
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What histological feature is first observed in fatty change under a light microscope?
What histological feature is first observed in fatty change under a light microscope?
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Which of the following conditions is known to lead to the development of xanthomas?
Which of the following conditions is known to lead to the development of xanthomas?
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What is the primary role of macrophages in the context of cholesterol deposition?
What is the primary role of macrophages in the context of cholesterol deposition?
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What distinguishes dystrophic calcification from metastatic calcification?
What distinguishes dystrophic calcification from metastatic calcification?
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What type of pigment accumulation is characterized by golden brown granules and is derived from hemoglobin?
What type of pigment accumulation is characterized by golden brown granules and is derived from hemoglobin?
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Which of the following is NOT a known cause of hypercalcemia?
Which of the following is NOT a known cause of hypercalcemia?
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Which of the following is a consequence of severe fatty change in cells?
Which of the following is a consequence of severe fatty change in cells?
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What type of pathological condition involves the abnormal accumulation of calcium salts in tissues?
What type of pathological condition involves the abnormal accumulation of calcium salts in tissues?
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What is one effect of atrophy on cells?
What is one effect of atrophy on cells?
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What impact does anoxia have on fatty acid metabolism?
What impact does anoxia have on fatty acid metabolism?
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In which type of cellular adaptation do cells increase in size due to increased synthesis of proteins?
In which type of cellular adaptation do cells increase in size due to increased synthesis of proteins?
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Which condition is associated with the formation of bone in tissues where it normally would not occur?
Which condition is associated with the formation of bone in tissues where it normally would not occur?
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What typically happens to organ function during extensive nephrocalcinosis?
What typically happens to organ function during extensive nephrocalcinosis?
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What drives the formation of physiological adaptations in cells?
What drives the formation of physiological adaptations in cells?
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Which of the following best describes the appearance of dystrophic calcification under a microscope?
Which of the following best describes the appearance of dystrophic calcification under a microscope?
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Study Notes
Ischemic and Hypoxic Injury
- Ischemia or toxins promote calcium influx from the extracellular space and release of mitochondrial calcium.
- This activates enzymes such as phospholipases, proteases, ATPases, and endonucleases.
- Oxygen free radicals play a significant role in cell death.
### Reversible Injury
- Hypoxia affects aerobic respiration, leading to reduced intracellular ATP.
- Decreased ATP results in extracellular calcium influx, sodium pump reduction, and sodium accumulation within the cell.
- Potassium diffuses out of the cell, causing water gain and acute cellular swelling.
- This is accompanied by accumulation of metabolites like inorganic phosphates, lactic acid, and purine nucleotides.
- Decreased ATP and AMP stimulate phosphofructokinase and increase anaerobic glycolysis.
- Glycogen depletion, lactic acid accumulation, and reduced pH lead to cytoplasmic eosinophilia under a microscope.
- Ribosome detachment from RER reduces protein synthesis.
- Persistent hypoxia causes cytoskeleton disappearance, loss of microvilli, and formation of cell surface blebs.
### Irreversible Injury
- Characterized by severe mitochondrial vacuolization, calcium particle accumulation, extensive plasma membrane damage, and lysosome swelling.
- Reperfusion of oxygen leads to calcium-mediated injury.
- Continued protein, coenzyme, and RNA loss from hyperpermeable membranes.
- Lysosomal enzymes leak into the cytoplasm, degrading cellular components.
- Dead cells may be replaced by myelin figures.
Mechanisms of Irreversible Injury
- Progressive loss of membrane phospholipids.
- Cytoskeletal abnormalities due to protease activation and increased calcium.
- Toxic oxygen radicals generated during reperfusion by neutrophils.
- Lipid breakdown products with detergent effects.
Free Radical Mediation of Cell Injury
- Free radicals are unstable molecules with unpaired electrons, readily reacting with organic and inorganic chemicals.
- Free radicals can be generated within the cell through:
- Absorption of radiant energy
- Redox reactions during normal physiological processes
- Enzymatic catabolism of oxygenous chemicals
### Chemical Injury
- Two main mechanisms of chemical injury:
- Combining with critical molecular components or cellular organelles
- Conversion to reactive toxic metabolites through P-450 oxidases in the SER.
### Patterns of Acute Cell Injury
Reversible Cell Injury
-
Light microscopic changes:
- Cell swelling, seen as small clear vacuoles in the cytoplasm.
- Cytoplasmic eosinophilia, due to acidosis and loss of ribosomes.
- Fatty change, seen in hypoxic and chemical injury in liver and myocardial cells.
-
Ultrastructural changes (EM):
- Plasma membrane blebbing, microvilli distortion, and loosened intercellular attachments.
- Mitochondrial swelling and appearance of phospholipid-rich amorphous densities.
- Dilatation of endoplasmic reticulum, ribosome detachment, and polysome dissociation.
- Nuclear alterations, including disaggregation of granular elements.
#### Necrosis
- A sequence of morphological changes following cell death in living tissue.
- Characterized by enzymatic digestion of the cell and protein denaturation.
- Cytoplasmic changes: Eosinophilia, glassy appearance, glycogen loss, cytoplasmic vacuolation, and calcification.
-
Nuclear changes:
- Karyolysis: DNA digestion leading to nuclear dissolution.
- Pyknosis: Nuclear shrinkage and increased basophilia.
- Karyorrhexis: Fragmentation of the pyknotic nucleus.
Types of Necrosis
-
Coagulative necrosis:
- Preservation of structural outlines of the coagulated cell or tissue.
- Injury and acidosis denature enzymes, blocking cellular hydrolysis.
- Characteristic of hypoxic death in all tissues except the brain.
-
Liquefactive necrosis:
- Caused by bacterial or fungal infection with white cell accumulation.
- Also occurs in hypoxic cell death in the CNS.
-
Gangrenous necrosis:
- Ishcemic coagulative necrosis with superimposed infection and liquifactive necrosis.
-
Caseous necrosis:
- Seen in tuberculous infection with a cheesy, white appearance.
Fatty Change (Steatosis)
- Abnormal accumulation of triglycerides within parenchymal cells.
- Most often seen in the liver, but can also occur in the heart, skeletal muscle, kidney, and other organs.
- Caused by toxins, diabetes mellitus, protein malnutrition, obesity, and anoxia.
- Excess triglyceride accumulation can result from defects in any step from fatty acid entry to lipoprotein synthesis.
- Mild fatty change may not affect cellular function, but severe changes can impair function.
### Cholesterol and Cholesterol Esters
- Macrophages in contact with lipid debris of necrotic cells may become filled with lipid, appearing as foamy cells.
- In atherosclerosis, smooth muscle cells and macrophages are filled with cholesterol and cholesterol ester vacuoles.
- Xanthomas are accumulations of fat within macrophages of subcutaneous connective tissues.
### Proteins
- Less commonly seen, but can accumulate in proximal convoluted tubules in glomerular diseases with proteinuria.
### Glycogen
- Seen in cases of abnormal glucose or glycogen metabolism, appearing as vacuoles under a microscope.
### Pigments
- Colored substances, either exogenous or endogenous.
- Melanin accumulates in basal cells of the epidermis (freckles) or dermal macrophages.
- Hemosiderin is a hemoglobin-derived granular pigment, accumulating in tissues with excess iron.
### Pathological Calcification
- Abnormal accumulation of calcium salts with smaller amounts of iron, magnesium, and other minerals.
-
Dystrophic calcification: Deposition in dead or dying tissues, despite normal serum calcium levels.
- Encountered in areas of necrosis, atheromas, advanced atherosclerosis, and aortic valves.
- Appears as intracellular or extracellular basophilic deposits.
-
Metastatic calcification: Occurs in normal tissues due to hypercalcemia.
- Causes of hypercalcemia include endocrine dysfunction, tumors associated with increased bone catabolism, ingested exogenous substances, sarcoidosis, and advanced renal failure.
- Metastatic calcification can occur in kidneys, lungs, and gastric mucosa.
### Cellular Adaptations of Growth and Differentiation
- Physiological adaptations are responses to normal stimulations by hormones or endogenous chemicals.
- Pathological adaptations allow cells to modulate their environment and escape injury.
### Atrophy
- Shrinkage in cell size by loss of cell substance, affecting the entire organ.
- Atrophic cells have diminished function but are not dead.
- Causes:
- Decreased workload
- Loss of innervation
- Diminished blood supply
- Inadequate nutrition
- Loss of endocrine stimulation
- Aging.
### Hypertrophy
- Increase in cell size due to increased synthesis of structural proteins and organelles.
- Results in an increase in the size of the organ.
Ischemia and Hypoxia
- Ischemia and toxins cause calcium influx from the extracellular space and release of mitochondrial calcium.
- This activates enzymes like phospholipases, proteases, ATPases, and endonucleases.
- Oxygen free radicals are key mediators of cell death.
Reversible Injury
- Hypoxia affects aerobic respiration, decreasing ATP production.
- This leads to:
- Extracellular calcium influx
- Reduced sodium pump activity
- Sodium accumulation
- Potassium diffusion
- Water gain (cellular swelling)
- Other metabolites accumulate: inorganic phosphates, lactic acid, and purine nucleotides.
- Decreased ATP and AMP stimulate phosphofructokinase, increasing anaerobic glycolysis.
- Glycogen depletion occurs, leading to lactic acid and inorganic phosphate accumulation, and reduced pH.
- Ribosome detachment from RER reduces protein synthesis.
- If hypoxia persists, the cytoskeleton disappears, affecting microvilli and forming cell surface blebs.
Irreversible Injury
- Severe mitochondrial vacuolization with calcium accumulation
- Extensive plasma membrane damage
- Lysosome swelling
- Reperfusion injury mediated by calcium
- Loss of proteins, coenzymes, and RNA from damaged membranes
- Lysosomal enzymes leak into the cytoplasm, degrading cellular components.
- Dead cells may form myelin figures (whorled masses of phospholipids).
Mechanisms of Irreversible Injury
- Progressive loss of membrane phospholipids
- Cytoskeletal abnormalities: Protease activation and increased calcium can detach the cell membrane.
- Toxic oxygen radicals: Generated after reperfusion, released by neutrophils.
- Lipid breakdown products: Have detergent effects.
Free Radical Mediation of Cell Injury
- Free radicals are unstable chemical species with unpaired electrons. They react with organic and inorganic chemicals.
- Free radical generation can occur within the cell through:
- Radiant energy absorption (e.g., water hydrolysis into OH. and H.)
- Redox reactions (e.g., generation of superoxide radicals, hydrogen peroxide, and hydroxyl radicals during oxygen reduction)
- Enzymatic catabolism of oxygenous chemicals (e.g., CCl4 conversion to CCl3.)
- Free radicals react with:
- Lipid peroxidation of plasma membranes
- DNA (react with thymine)
- Cross-linking of proteins
Chemical Injury
- Two main mechanisms:
- Direct combination with critical molecular components or organelles (e.g., mercury binding to sulfhydryl groups)
- Conversion to reactive toxic metabolites by enzymes like P-450 oxidases (e.g., CCl4 conversion to CCl3.)
Patterns of Acute Cell Injury
Reversible Cell Injury (Light Microscopic Changes)
- Cell swelling (hydropic changes or vacuolar degeneration)
- Fatty change (accumulation of triglycerides)
- Microscopically, it is composed of structureless amorphous granular debris within granulomatous inflammation.
Fat Necrosis
- Focal fat destruction following acute pancreatitis
- Release of activated pancreatic enzymes hydrolyzes triglyceride esters in fat cells.
Apoptosis
- Programmed cell death, seen in physiological and pathological conditions.
- It usually involves single cells or clusters of cells.
- Apoptotic cells appear round with intensely eosinophilic cytoplasm.
- Nuclear chromatin condenses and aggregates.
- Karyorrhexis occurs through endonuclease activation.
- Cells shrink, form cytoplasmic buds, and fragment into apoptotic bodies.
- No inflammatory response.
Apoptosis Initiators:
- Withdrawal of growth factors or hormones
- Engagement of specific death receptors (e.g., FAS, TNF)
- Injury by radiation, toxins, and free radicals
- Intrinsic protease activation (e.g., in embryogenesis)
Apoptosis Mechanism
- Activation of intracellular proteases (e.g., calpain I, interleukin 1β converting enzyme)
- Endonuclease activation
- Cytoskeleton catabolism
- Formation of apoptotic bodies recognized by phagocytic cells
Intracellular Accumulations
- Abnormal substances accumulate in normal cells, either transiently or permanently.
- Accumulations can be harmful or injurious.
- Can be found in the cytoplasm or nucleus.
- Synthesized by the affected cell or produced elsewhere.
Categories of Intracellular Accumulation
- Normal endogenous substance produced at normal or increased rates with inadequate metabolism (e.g., fatty change in the liver)
- Normal or abnormal endogenous substance that cannot be metabolized due to genetic enzymatic defects (e.g., storage diseases)
- Abnormal exogenous substance that cannot be metabolized or transported (e.g., deposition of foreign substances)
Fatty Change (Steatosis)
- Abnormal accumulation of triglycerides within parenchymal cells.
- Most frequently seen in the liver.
- Reversible.
- Can occur in the heart, skeletal muscle, kidney, and other organs.
- Causes: toxins, diabetes mellitus, protein malnutrition, obesity, and anoxia.
- Excess triglyceride accumulation can arise from defects in any step of fatty acid entry or lipoprotein synthesis.
- Hepatotoxins (e.g., alcohol) impair mitochondrial and SER function.
- CCl4 and protein malnutrition decrease apoprotein synthesis.
- Anoxia inhibits fatty acid oxidation.
- Starvation increases fatty acid mobilization.
Cholesterol and Cholesterol Esters
- Macrophages engulfing lipid debris from necrotic cells can become filled with lipids (foamy cells).
- Smooth muscle cells and macrophages accumulate cholesterol and cholesterol esters in atherosclerosis.
- Xanthomas are lipid accumulations in macrophages within subcutaneous connective tissues.
Proteins
- Less common accumulations.
- Example: Proteinuria in glomerular diseases leading to protein accumulation in proximal convoluted tubules.
Glycogen
- Seen in cases of abnormal glucose or glycogen metabolism.
- Appear as vacuoles under the light microscope.
Pigments
- Colored substances, either endogenous or exogenous.
- Melanin accumulates in basal cells of the epidermis (e.g., freckles) and dermal macrophages.
- Hemosiderin: Iron-containing, granular, golden-brown pigment derived from hemoglobin, accumulating in tissues during iron overload.
Pathologic Calcification
- Abnormal accumulation of calcium salts, often with smaller amounts of iron, magnesium, and other minerals.
Dystrophic Calcification
- Deposition of calcium salts in dead or dying tissues.
- Occurs despite normal serum calcium levels.
- No calcium metabolic derangement associated.
- Seen in areas of necrosis, atheromas of advanced atherosclerosis, intimal injuries of large arteries, aging, and aortic valves.
- Appears as intracellular or extracellular basophilic deposits.
- Can lead to heterotopic bone formation.
Metastatic Calcification
- Deposition of calcium salts in normal tissues due to hypercalcemia.
- Causes of hypercalcemia include:
- Primary endocrine dysfunction (e.g., hyperparathyroidism)
- Tumors with increased bone catabolism (e.g., multiple myeloma, metastatic cancer, leukemia)
- Ingested exogenous substances (e.g., vitamin D intoxication, milk alkali syndrome)
- Sarcoidosis
- Advanced renal failure
- Deposits occur primarily in interstitial tissues, kidneys, lungs, and gastric mucosa.
- May not significantly impair organ function, but extensive nephrocalcinosis can impair kidney function.
Cellular Adaptations of Growth and Differentiation
- Physiologic adaptations are responses to normal stimulation by hormones or endogenous chemicals (e.g., breast growth and lactation).
- Pathological adaptations share similar underlying mechanisms.
- They allow cells to modulate their environment and avoid injury.
Atrophy
- Decrease in cell size due to loss of cell substance.
- Can affect an entire organ.
- Atrophic cells have diminished function but are not dead.
- Apoptotic death can be induced by the same signals that cause atrophy.
Causes of Atrophy
- Decreased workload
- Loss of innervation
- Diminished blood supply
- Inadequate nutrition
- Loss of endocrine stimulation
- Aging
Mechanism of Atrophy
- Cells shrink to a size that allows for survival with reduced resources.
- Decreased synthesis and increased catabolism of cellular components.
Hypertrophy
- Increase in cell size due to increased synthesis of structural proteins and organelles.
- Leads to an increase in organ size.
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Description
This quiz explores the mechanisms of ischemic and hypoxic injuries at the cellular level. It discusses the impact of reduced ATP, calcium influx, and the role of free radicals in cell death. Gain insights into reversible injuries and their biochemical consequences.
