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Questions and Answers
What is the ultimate result of cell injury?
What is the ultimate result of cell injury?
- Inflammation
- Cell adaptation
- Cell swelling
- Cell death (correct)
Which of the following is a characteristic of necrosis?
Which of the following is a characteristic of necrosis?
- Physiologic process
- Occurs after ischemia (correct)
- Internally controlled suicide program
- Elimination of unwanted cells during embryogenesis
Apoptosis is primarily involved in:
Apoptosis is primarily involved in:
- Inflammatory response after tissue damage
- Uncontrolled cell proliferation
- Cell death due to external injury
- Eliminating unwanted cells during development (correct)
Which of the following can lead to hypoxia?
Which of the following can lead to hypoxia?
Which of these is NOT a physical agent that can cause cell injury?
Which of these is NOT a physical agent that can cause cell injury?
Arsenic, cyanide, and mercuric salts are examples of:
Arsenic, cyanide, and mercuric salts are examples of:
Which infectious agent can cause cell injury?
Which infectious agent can cause cell injury?
Which of the following is NOT a cause of cell injury?
Which of the following is NOT a cause of cell injury?
What is the primary mechanism by which ATP depletion leads to cell swelling?
What is the primary mechanism by which ATP depletion leads to cell swelling?
What is the result of glycolysis during ischemia?
What is the result of glycolysis during ischemia?
Failure of the $Ca^{2+}$ pump leads to:
Failure of the $Ca^{2+}$ pump leads to:
Detachment of ribosomes from the RER leads to:
Detachment of ribosomes from the RER leads to:
Misfolded proteins in cells deprived of oxygen or glucose, trigger:
Misfolded proteins in cells deprived of oxygen or glucose, trigger:
Which of the following can damage mitochondria?
Which of the following can damage mitochondria?
What is the consequence of mitochondrial permeability transition?
What is the consequence of mitochondrial permeability transition?
Leakage of cytochrome c into the cytosol is associated with:
Leakage of cytochrome c into the cytosol is associated with:
Increased cytosolic calcium concentration activates which of the following enzymes?
Increased cytosolic calcium concentration activates which of the following enzymes?
Which enzyme, activated by increased $Ca^{2+}$, causes membrane damage?
Which enzyme, activated by increased $Ca^{2+}$, causes membrane damage?
What is the role of endonucleases in cell injury?
What is the role of endonucleases in cell injury?
Reactive oxygen species are produced as a byproduct of:
Reactive oxygen species are produced as a byproduct of:
Oxidative stress is a result of:
Oxidative stress is a result of:
Which of the following scenarios does NOT typically involve free radical-mediated damage?
Which of the following scenarios does NOT typically involve free radical-mediated damage?
Free radicals are chemical species that have:
Free radicals are chemical species that have:
Absorption of radiant energy like ultraviolet light can initiate:
Absorption of radiant energy like ultraviolet light can initiate:
During normal respiration, toxic intermediates produced include:
During normal respiration, toxic intermediates produced include:
Nitric oxide (NO) can act as:
Nitric oxide (NO) can act as:
Lipid peroxidation of membranes results in:
Lipid peroxidation of membranes results in:
Which of the following is NOT a mechanism cells use to remove free radicals?
Which of the following is NOT a mechanism cells use to remove free radicals?
Which vitamin acts as an antioxidant to minimize cell injury?
Which vitamin acts as an antioxidant to minimize cell injury?
Catalase breaks down:
Catalase breaks down:
In ischemic cells, membrane damage is a result of ATP depletion and:
In ischemic cells, membrane damage is a result of ATP depletion and:
Membrane damage can be caused directly by bacterial toxins and:
Membrane damage can be caused directly by bacterial toxins and:
Which of the following is a biochemical mechanism contributing to membrane damage?
Which of the following is a biochemical mechanism contributing to membrane damage?
The point of 'no return' in cell injury refers to the stage when:
The point of 'no return' in cell injury refers to the stage when:
Which of the following best describes the role of the glycolytic pathway in cell injury?
Which of the following best describes the role of the glycolytic pathway in cell injury?
A researcher observes that a cell undergoing injury shows increased levels of ATPases, phospholipases, proteases, and endonucleases activity. Which of the following is the MOST likely cause?
A researcher observes that a cell undergoing injury shows increased levels of ATPases, phospholipases, proteases, and endonucleases activity. Which of the following is the MOST likely cause?
A scientist discovers a new drug that effectively inhibits the mitochondrial permeability transition. What potential effect might this drug have on cell injury?
A scientist discovers a new drug that effectively inhibits the mitochondrial permeability transition. What potential effect might this drug have on cell injury?
A cell is exposed to a toxin that directly impairs its ability to regulate intracellular calcium levels. Which of the following downstream effects is MOST likely to exacerbate cell injury?
A cell is exposed to a toxin that directly impairs its ability to regulate intracellular calcium levels. Which of the following downstream effects is MOST likely to exacerbate cell injury?
In a scenario involving ischemia-reperfusion injury, which of the following mechanisms MOST directly contributes to the increased production of reactive oxygen species (ROS) upon reperfusion?
In a scenario involving ischemia-reperfusion injury, which of the following mechanisms MOST directly contributes to the increased production of reactive oxygen species (ROS) upon reperfusion?
A researcher is investigating a novel antioxidant compound. To determine its efficacy in preventing free radical-mediated cell injury, which of the following experimental approaches would be MOST appropriate?
A researcher is investigating a novel antioxidant compound. To determine its efficacy in preventing free radical-mediated cell injury, which of the following experimental approaches would be MOST appropriate?
Flashcards
Cell Injury
Cell Injury
A variety of stress a cell encounters due to internal and external environmental changes, leading to disruption of cellular components.
Cell Death
Cell Death
The ultimate result of cell injury, characterized by two main patterns: necrosis and apoptosis.
Necrosis
Necrosis
A type of cell death that occurs after ischemia or chemical injury; it is always pathologic.
Apoptosis
Apoptosis
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Hypoxia
Hypoxia
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Physical Agents of Cell Injury
Physical Agents of Cell Injury
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Chemical Agents of Cell Injury
Chemical Agents of Cell Injury
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Infectious Agents of Cell Injury
Infectious Agents of Cell Injury
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Immunologic Reactions (Cell Injury)
Immunologic Reactions (Cell Injury)
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Genetic Derangements (Cell Injury)
Genetic Derangements (Cell Injury)
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Depletion of ATP
Depletion of ATP
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ATP Production Pathways
ATP Production Pathways
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Effect of ATP Depletion: Sodium Pump Failure
Effect of ATP Depletion: Sodium Pump Failure
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Effect of ATP Depletion: Anaerobic Metabolism
Effect of ATP Depletion: Anaerobic Metabolism
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Other Effects of ATP Depletion
Other Effects of ATP Depletion
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Mitochondrial Damage
Mitochondrial Damage
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Causes of Mitochondrial Damage
Causes of Mitochondrial Damage
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Influx of Intracellular Calcium
Influx of Intracellular Calcium
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Calcium-Activated Enzymes
Calcium-Activated Enzymes
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Accumulation of Oxygen-Derived Free Radicals
Accumulation of Oxygen-Derived Free Radicals
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Antioxidants
Antioxidants
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Cellular Antioxidant Enzymes
Cellular Antioxidant Enzymes
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Defects in Membrane Permeability: Causes
Defects in Membrane Permeability: Causes
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Biochemical Mechanisms of Membrane Damage
Biochemical Mechanisms of Membrane Damage
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Study Notes
- Cell injury arises from cellular stress due to internal and external environmental changes, disrupting cellular components
- It underlies all pathological processes and is reversible up to a point, beyond which it leads to irreversible damage and cell death
Patterns of Cell Death
- Necrosis occurs post-ischemia and chemical injury, and is always pathologic
- Apoptosis is internally programmed cell suicide, eliminating unwanted cells during embryogenesis, physiological processes, and certain pathological conditions
Causes of Cell Injury
- Oxygen Deprivation (Hypoxia): Common cause of cell injury/death, due to cardiorespiratory failure or loss of blood's oxygen-carrying capacity (anemia, carbon monoxide poisoning); severity dictates adaptation, injury, or death
- Physical Agents: Mechanical trauma, burns, deep cold, pressure changes, radiation, electric shock
- Chemical Agents and Drugs: Oxygen (high concentrations), arsenic, cyanide, mercuric salts, pollutants, insecticides, herbicides, industrial hazards, alcohol, narcotics, and therapeutic drugs
- Infectious Agents: Bacteria, fungi, viruses, and parasites
- Immunologic Reactions
- Genetic Derangements
- Nutritional Imbalances
Mechanism of Cell Injury
-
Depletion of ATP: Linked to hypoxic and toxic injury, ATP is crucial for cellular processes
- Production: Oxidative phosphorylation and glycolysis (anaerobic, using glucose from fluids or glycogen)
- Effects of depleted ATP:
- Reduced sodium pump activity: Accumulation of intracellular sodium, potassium efflux, cell swelling, and ER dilation
- Reduced oxygen supply: Oxidative phosphorylation stops, cells rely on glycolysis which leads to glycogen depletion; lactic acid builds up, lowering intracellular pH and decreasing enzyme activity
- Ca2+ pump failure: Ca2+ influx damages cellular components
- Ribosome detachment: Reduced protein synthesis and necrosis
- Protein Misfolding: Unfolded protein response leads to cell injury/death
-
Mitochondrial Damage: Target of hypoxia and toxins, resulting from:
- Increases in cytosolic Ca2+
- Oxidative stress
- Phospholipid breakdown
- Lipid breakdown products
-
Mitochondrial Permeability Transition: Formation of a high-conductance channel which is reversible initially but becomes irreversible, causing cell death; associated with cytochrome c leakage into the cytosol
-
Influx of Intracellular Calcium & Loss of Calcium Homeostasis: Ischemia increases cytosolic calcium, activating:
- ATPases which hasten ATP depletion
- Phospholipases which cause membrane damage
- Proteases that break down membranes and cytoskeletal proteins
- Endonucleases which cause DNA and chromatin fragmentation
-
Accumulation of Oxygen-Derived Free Radicals (Oxidative Stress): Imbalance between free radical generation and scavenging causes cell injury
- Reactive oxygen species (ROS) damage lipids, proteins, and nucleic acids
- Free radical-mediated damage seen in chemical/radiation injury, ischemia-reperfusion, cellular aging, and phagocytosis
-
Free Radicals: Unpaired electron species initiated by:
- Radiant energy absorption (UV light, x-rays)
- Enzymatic metabolism of chemicals/drugs
- Redox reactions during metabolism produce superoxide anion (O2-), hydrogen peroxide (H2O2), and hydroxyl ions (OH)
- Transition metals (iron, copper)
- Nitric Oxide (NO) acts as a free radical
-
Effects of reactive species include:
- Lipid peroxidation of membranes which leads to extensive damage
- Oxidative modification of proteins which results in fragmentation
- DNA lesions implicated in aging and malignancy
-
Cells combat free radicals with mechanisms like:
- Antioxidants (vitamins E, A, ascorbic acid)
- Enzymes that break down hydrogen peroxide and superoxide anion include Catalase, Superoxide dismutases, and Glutathione peroxidase
-
Defects in Membrane Permeability: May result from ATP depletion and calcium-modulated phospholipase activation in ischemic cells or direct damage by toxins/proteins
-
Biochemical mechanisms contributing to membrane damage:
- Mitochondrial dysfunction
- Cytoskeletal abnormalities
- Reactive oxygen species
- Lipid breakdown products
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Description
Cell injury arises from cellular stress due to internal and external environmental changes which disrupts cellular components. Necrosis occurs post-ischemia and chemical injury, and is always pathologic. Apoptosis is internally programmed cell suicide.
