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Questions and Answers
Which of the following is NOT a consequence of free radical mediation in cellular injury?
Which of the following is NOT a consequence of free radical mediation in cellular injury?
What is the primary reason for the instability of free radicals?
What is the primary reason for the instability of free radicals?
What initiates the production of superoxide radicals in cells?
What initiates the production of superoxide radicals in cells?
Which type of injury occurs due to the binding of chemicals to critical molecular components?
Which type of injury occurs due to the binding of chemicals to critical molecular components?
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What is the byproduct of the reduction-oxidation reaction of O2 in normal physiological conditions?
What is the byproduct of the reduction-oxidation reaction of O2 in normal physiological conditions?
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Which enzyme is primarily responsible for generating superoxide radicals?
Which enzyme is primarily responsible for generating superoxide radicals?
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Which scenario exemplifies chemical-mediated cell injury due to metabolism of non-toxic substances?
Which scenario exemplifies chemical-mediated cell injury due to metabolism of non-toxic substances?
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What cell change is often first observed in reversible cell injury?
What cell change is often first observed in reversible cell injury?
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What is the primary effect of hypoxia on aerobic respiration?
What is the primary effect of hypoxia on aerobic respiration?
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Which enzyme is NOT activated during cellular injury caused by ischemia or toxin exposure?
Which enzyme is NOT activated during cellular injury caused by ischemia or toxin exposure?
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What is a characteristic of irreversible injury in cells?
What is a characteristic of irreversible injury in cells?
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What indicates a decrease in protein synthesis during cell injury?
What indicates a decrease in protein synthesis during cell injury?
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Which of the following processes can result from prolonged hypoxia?
Which of the following processes can result from prolonged hypoxia?
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What is the primary consequence of ATP depletion in a cell during ischemic injury?
What is the primary consequence of ATP depletion in a cell during ischemic injury?
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What is the consequence of reperfusion injury following ischemia?
What is the consequence of reperfusion injury following ischemia?
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What role do oxygen free radicals play in cell death during ischemic injury?
What role do oxygen free radicals play in cell death during ischemic injury?
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Which of the following statements correctly describes necrosis?
Which of the following statements correctly describes necrosis?
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What is the main difference between hypoxia and ischæmia?
What is the main difference between hypoxia and ischæmia?
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Which factor is NOT a potential cause of cell injury?
Which factor is NOT a potential cause of cell injury?
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Which intracellular system is least likely to be affected by cell injury?
Which intracellular system is least likely to be affected by cell injury?
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What role do ATP-dependent calcium transporters play in cellular health?
What role do ATP-dependent calcium transporters play in cellular health?
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Apoptosis is characterized by which of the following?
Apoptosis is characterized by which of the following?
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Which of the following contributes to the pathogenesis of atherosclerosis?
Which of the following contributes to the pathogenesis of atherosclerosis?
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During cell injury, which of the following is a key factor in determining the consequences of an injurious stimulus?
During cell injury, which of the following is a key factor in determining the consequences of an injurious stimulus?
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What characterizes fat necrosis following acute pancreatitis?
What characterizes fat necrosis following acute pancreatitis?
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Which of the following conditions is related to apoptosis?
Which of the following conditions is related to apoptosis?
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What is a typical feature observed in cells undergoing apoptosis?
What is a typical feature observed in cells undergoing apoptosis?
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What initiates the process of apoptosis?
What initiates the process of apoptosis?
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Intracellular accumulations can result from which of the following scenarios?
Intracellular accumulations can result from which of the following scenarios?
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What type of enzyme activation is a critical step in apoptosis?
What type of enzyme activation is a critical step in apoptosis?
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Which category of intracellular accumulation involves genetic enzymatic defects?
Which category of intracellular accumulation involves genetic enzymatic defects?
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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 dystrophic calcification characterized by?
What is dystrophic calcification characterized by?
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Which of the following is a cause of hypercalcemia?
Which of the following is a cause of hypercalcemia?
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What is the primary difference between dystrophic calcification and metastatic calcification?
What is the primary difference between dystrophic calcification and metastatic calcification?
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What cellular change is described as 'shrinkage in the size of the cell by loss of cell substance'?
What cellular change is described as 'shrinkage in the size of the cell by loss of cell substance'?
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Which of the following results in hypertrophy of cells?
Which of the following results in hypertrophy of cells?
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In which condition might metastatic calcification significantly impair organ function?
In which condition might metastatic calcification significantly impair organ function?
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Which of the following best describes physiological adaptations?
Which of the following best describes physiological adaptations?
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What is a characteristic feature of apoptotic cell death?
What is a characteristic feature of apoptotic cell death?
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Study Notes
Cell Injury
- Cell injury occurs when the cell's adaptive capabilities are exceeded
- There are two main types of cell death:
- Necrosis: Occurs due to noxious conditions, characterized by swelling, protein denaturation, and organellar breakdown
- Apoptosis: Programmed cell death occurring under normal or physiologic conditions
Causes of Cell Injury
- Hypoxia: Reduced oxygen supply to tissues
- Physical agents: Trauma, temperature extremes, radiation, electric shock, atmospheric pressure changes
- Chemicals and drugs: Can alter membrane permeability, osmotic homeostasis, or enzyme integrity
- Microbiologic agents: Viruses, bacteria, parasites
- Immunologic reactions: Immune system can cause cell injury (e.g., anaphylactic reactions)
- Genetic defects: Inherited conditions (e.g., Down's syndrome, sickle cell anemia)
- Nutritional imbalances: Protein-calorie insufficiency, vitamin deficiencies
- Aging: Cellular aging contributes to cell injury
Mechanisms of Cell Injury
- Four intracellular systems are vulnerable to injury:
- Cell membrane integrity
- Aerobic respiration (mitochondrial function)
- Protein synthesis
- Genetic apparatus (DNA)
- Calcium plays a key role in cell injury:
- Excess calcium influx activates enzymes like phospholipases, proteases, ATPases, and endonucleases, leading to cellular damage
- Oxygen free radicals are crucial mediators of cell death
Ischemic and Hypoxic Injury
-
Reversible injury:
- Hypoxia affects aerobic respiration, leading to ATP depletion
- Reduced ATP leads to an influx of calcium, sodium retention, and potassium efflux
- Cell swelling occurs due to water accumulation
- Anaerobic glycolysis increases, depleting glycogen and lowering intracellular pH
- Reduced protein synthesis and cytoskeletal breakdown
-
Irreversible injury:
- Severe mitochondrial damage and calcium accumulation
- Extensive plasma membrane damage
- Lysosomal swelling
- Reperfusion injury (damage after restoration of blood flow)
- Cell lysis and release of lysosomal enzymes into the cytoplasm
Mechanisms of Irreversible Injury
- Progressive loss of membrane phospholipids
- Cytoskeletal abnormalities (detachment of cell membrane)
- Toxic oxygen radicals (generated during reperfusion)
- Lipid breakdown products (detergent effects)
Free Radicals
- Unstable molecules with an unpaired electron
- Implicated in chemical and radiation injury, oxygen toxicity, aging, microbial killing, inflammation, and tumor killing
- Generation within cells:
- Absorption of radiant energy (e.g., hydrolysis of water)
- Redox reactions (normal metabolic processes)
- Enzymatic catabolism of oxygenous chemicals (e.g., CCl4)
- Free radicals react with cell components:
- Lipid peroxidation of plasma membranes
- DNA damage (thymine)
- Protein cross-linking
Chemical Injury
- Two main mechanisms:
- Direct interaction with cellular components (e.g., mercury binding to sulfhydryl groups)
- Conversion to toxic metabolites (e.g., CCl4 converted to CCl3• in the liver)
Patterns of Acute Cell Injury
-
Reversible cell injury (light microscopic changes):
- Cell swelling (hydropic change or vacuolar degeneration)
- Fatty change (accumulation of fat in the cytoplasm)
- Microscopically: Structureless amorphous granular debris within granulomatous inflammation
-
Irreversible cell injury:
- Necrosis (cellular death)
- Features include: nuclear changes (pyknosis, karyorrhexis, karyolysis), cytoplasmic changes (homogenous eosinophilia, cell fragmentation)
Fat Necrosis
- Focal areas of fat destruction, often associated with acute pancreatitis
- Release of activated pancreatic enzymes hydrolyzes triglycerides in fat cells
Apoptosis
- Programmed cell death, essential for:
- Embryonic development
- Hormonal involution (e.g., menstrual cycle)
- Cell deletion in proliferating populations (e.g., intestinal crypt epithelium)
- Elimination of autoreactive T cells (in the thymus)
- Apoptosis results in:
- Single cell or cluster death, appearing as round masses with eosinophilic cytoplasm
- Nuclear chromatin condensation
- Cell shrinkage, budding, and fragmentation into apoptotic bodies
- Minimal inflammatory response
- Initiation of apoptosis:
- Withdrawal of growth factors or hormones
- Engagement of specific receptors (e.g., FAS, TNF)
- Injury by radiation, toxins, or free radicals
- Intrinsic protease activation (e.g., embryogenesis)
- Activation of intracellular proteases (calpain I, ICE) leads to endonuclease activation, cytoskeletal breakdown, and formation of apoptotic bodies
Intracellular Accumulations
- Abnormal substances accumulate in cells, either transiently or permanently
- May be harmful or injurious, located in the cytoplasm or nucleus
- Categories:
- Normal endogenous substance produced at a normal or increased rate with inadequate metabolism (e.g., fatty liver)
- Normal or abnormal endogenous substance that can't be metabolized due to enzymatic defects (storage diseases)
- Deposition in dead or dying tissues (dystrophic calcification)
Dystrophic Calcification
- Deposition occurs in dead or dying tissues
- Occurs despite normal serum calcium levels
- Example: Atheromas in advanced atherosclerosis, areas of intimal injuries in large arteries
- Appears as basophilic deposits, sometimes with heterotopic bone formation
Metastatic Calcification
- Occurs in normal tissues when hypercalcemia exists
- Causes of hypercalcemia:
- Primary endocrine dysfunction (hyperparathyroidism)
- Bone catabolism (multiple myeloma, metastatic cancer, leukemia)
- Vitamin D intoxication
- Sarcoidosis
- Advanced renal failure
- Metastatic calcification is found in interstitial tissues, kidneys, lungs, gastric mucosa
Cellular Adaptations of Growth and Differentiation
- Physiologic adaptations: Responses to normal stimuli by hormones or endogenous chemicals (e.g., breast growth)
- Pathological adaptations: Cell responses to modulate their environment and avoid injury
Atrophy
- Shrinkage in cell size due to loss of cell substance
- Causes:
- Decreased workload
- Loss of innervation
- Diminished blood supply
- Inadequate nutrition
- Loss of endocrine stimulation
- Aging
- Decreased synthesis and increased catabolism contribute to atrophy
Hypertrophy
- Increase in cell size due to increased synthesis of structural proteins and organelles
- Associated with an increase in organ size.
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Description
This quiz explores the concept of cell injury, including the distinction between necrosis and apoptosis. Learn about the various causes of cell injury such as hypoxia, chemical factors, and immunologic reactions. Test your knowledge on how these factors affect cellular health and function.
