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Questions and Answers
Which best describes the ultimate outcome of irreversible cell injury?
Which best describes the ultimate outcome of irreversible cell injury?
- The cell undergoes apoptosis. (correct)
- The cell undergoes hypertrophy.
- The cell maintains normal function.
- The cell adapts through hyperplasia.
What type of adaptation occurs when a cell experiences a decrease in workload?
What type of adaptation occurs when a cell experiences a decrease in workload?
- Hypertrophy
- Atrophy (correct)
- Hyperplasia
- Metaplasia
What event occurs upon irreversible mitochondrial permeability transition?
What event occurs upon irreversible mitochondrial permeability transition?
- Fatal damage to the cell (correct)
- Restoration of calcium homeostasis
- Increased ATP production
- Cellular recovery becomes possible
Which statement about cell injury is accurate?
Which statement about cell injury is accurate?
Which of the following enzymes is NOT activated by increased cytosolic calcium during ischemia?
Which of the following enzymes is NOT activated by increased cytosolic calcium during ischemia?
Which adaptation involves a change in the type of cell present in a tissue?
Which adaptation involves a change in the type of cell present in a tissue?
What is the primary consequence of mitochondrial damage related to Cytochrome C?
What is the primary consequence of mitochondrial damage related to Cytochrome C?
Which of the following statements about organ damage due to cellular adaptations is true?
Which of the following statements about organ damage due to cellular adaptations is true?
Which of the following processes is mainly affected by the action of phospholipases during ischemia?
Which of the following processes is mainly affected by the action of phospholipases during ischemia?
Which option describes a reversible stage of mitochondrial permeability transition?
Which option describes a reversible stage of mitochondrial permeability transition?
What is a direct consequence of reduced ATP synthesis in cells?
What is a direct consequence of reduced ATP synthesis in cells?
What role does calcium play when the calcium pump fails due to ATP depletion?
What role does calcium play when the calcium pump fails due to ATP depletion?
Why does cell swelling occur in response to ATP depletion?
Why does cell swelling occur in response to ATP depletion?
What happens to ribosomes and protein synthesis when ATP is depleted?
What happens to ribosomes and protein synthesis when ATP is depleted?
Which pathway primarily generates ATP under aerobic conditions?
Which pathway primarily generates ATP under aerobic conditions?
What is the main consequence of increased cytosolic calcium levels in relation to mitochondrial health?
What is the main consequence of increased cytosolic calcium levels in relation to mitochondrial health?
How does oxygen deprivation affect cellular functions?
How does oxygen deprivation affect cellular functions?
Which process directly results from ribosome detachment from the rough endoplasmic reticulum (RER)?
Which process directly results from ribosome detachment from the rough endoplasmic reticulum (RER)?
Which factor is NOT associated with causing mitochondrial damage?
Which factor is NOT associated with causing mitochondrial damage?
What is a likely outcome if the Na/K pump activity is reduced in a cell?
What is a likely outcome if the Na/K pump activity is reduced in a cell?
What is likely to happen when there is an imbalance between radical-generating and radical-scavenging systems?
What is likely to happen when there is an imbalance between radical-generating and radical-scavenging systems?
Which of the following is NOT a source of free radical generation within cells?
Which of the following is NOT a source of free radical generation within cells?
What effect does lipid peroxidation primarily have on cells?
What effect does lipid peroxidation primarily have on cells?
Which of the following free radicals is produced during normal mitochondrial respiration?
Which of the following free radicals is produced during normal mitochondrial respiration?
What type of injury is most directly associated with reactive oxygen species?
What type of injury is most directly associated with reactive oxygen species?
What is the earliest change associated with cell injury?
What is the earliest change associated with cell injury?
Which of the following phenomena signifies irreversible cell injury?
Which of the following phenomena signifies irreversible cell injury?
Which event would suggest that a cell has crossed the threshold into irreversible injury?
Which event would suggest that a cell has crossed the threshold into irreversible injury?
What type of damage is associated with irreversible injury to lysosomes?
What type of damage is associated with irreversible injury to lysosomes?
Which of the following is NOT a hallmark of irreversible cell injury?
Which of the following is NOT a hallmark of irreversible cell injury?
Which of the following enzymes is specifically known for breaking down hydrogen peroxide in cells?
Which of the following enzymes is specifically known for breaking down hydrogen peroxide in cells?
What primary role do antioxidants play in cellular mechanisms?
What primary role do antioxidants play in cellular mechanisms?
Which of the following is NOT a mechanism leading to membrane damage in ischemic cells?
Which of the following is NOT a mechanism leading to membrane damage in ischemic cells?
Which of the following correctly describes the effect of reactive oxygen species on cellular components?
Which of the following correctly describes the effect of reactive oxygen species on cellular components?
What cellular consequence can result from defects in membrane permeability?
What cellular consequence can result from defects in membrane permeability?
What is the most common target for toxic injury?
What is the most common target for toxic injury?
Which of the following substances can produce toxic injury to liver cells?
Which of the following substances can produce toxic injury to liver cells?
What mechanism can lead to chemical injury in cells?
What mechanism can lead to chemical injury in cells?
Which toxic agent is associated with the blockage of mitochondrial function?
Which toxic agent is associated with the blockage of mitochondrial function?
Reactive oxygen species (ROS) can be generated from which of the following?
Reactive oxygen species (ROS) can be generated from which of the following?
What is a primary characteristic of necrotic cells regarding their cytoplasmic appearance?
What is a primary characteristic of necrotic cells regarding their cytoplasmic appearance?
Which type of necrosis is characterized primarily by preserved cell outlines due to protein denaturation?
Which type of necrosis is characterized primarily by preserved cell outlines due to protein denaturation?
Which of the following nuclear changes represents fragmentation of the nucleus in necrotic cells?
Which of the following nuclear changes represents fragmentation of the nucleus in necrotic cells?
What type of debris is identified in necrotic cells through electron microscopy?
What type of debris is identified in necrotic cells through electron microscopy?
What is a defining feature of intracytoplasmic myelin figures in necrotic cells?
What is a defining feature of intracytoplasmic myelin figures in necrotic cells?
What specific type of liver injury is associated with acetaminophen?
What specific type of liver injury is associated with acetaminophen?
Which process is responsible for the degradation of cells during necrosis?
Which process is responsible for the degradation of cells during necrosis?
Which chemical is known to have a potential effect of fatty liver and hepatitis?
Which chemical is known to have a potential effect of fatty liver and hepatitis?
In the context of necrosis, which of the following statements is true?
In the context of necrosis, which of the following statements is true?
Which enzyme source is NOT involved in the digestion of necrotic cells?
Which enzyme source is NOT involved in the digestion of necrotic cells?
What type of injury is commonly associated with the use of oral contraceptives?
What type of injury is commonly associated with the use of oral contraceptives?
Which of the following drugs has unspecified effects listed in the context of chemical injuries?
Which of the following drugs has unspecified effects listed in the context of chemical injuries?
What mechanism contributes to the formation of toxic metabolites from certain chemicals like acetaminophen?
What mechanism contributes to the formation of toxic metabolites from certain chemicals like acetaminophen?
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Study Notes
Physiological Adaptations and Cell Injury
- Steady State: Cells maintain a balance called homeostasis.
- Adaptations: Cells adjust to persistent stimuli through changes like hypertrophy (growth), hyperplasia (replication), atrophy (shrinkage), and metaplasia (change in cell type).
- Cell Injury: Occurs when the stimulus exceeds adaptation capacity, causing reversible (non-lethal) or irreversible (lethal) damage.
- Irreversible Injury (Cell Death): Leads to apoptosis (programmed cell death) or necrosis (uncontrolled cell death).
Mechanism of Cell Injury
- ATP Depletion: Decrease in ATP synthesis, crucial for cellular functions, triggers various detrimental effects.
- Hypoxia: Reduced oxygen supply leads to reduced ATP production and reliance on glycolysis, producing lactic acid and lowering pH.
- Sodium Pump Failure: Reduced ATP leads to sodium accumulation and potassium loss, causing cell swelling.
- Calcium Pump Failure: Results in calcium influx, activating enzymes that damage cellular components.
- Ribosome Detachment: Decreases protein synthesis, leading to irreversible damage.
- Mitochondrial Damage: Mitochondria are crucial for ATP production and can be damaged by various factors.
- Increased Cytosolic Calcium: Elevated levels damage mitochondria.
- Oxidative Stress: Free radicals produced during metabolism damage mitochondria.
- Phospholipid Breakdown: Directly damages mitochondrial structure.
- Lipid Breakdown Products: Damaged lipids contribute to mitochondrial damage.
- Influx of Calcium & Calcium Homeostasis Loss: Ischemia causes calcium influx, activating enzymes that damage cells.
- ATPases: Hasten ATP depletion.
- Phospholipases: Cause membrane damage.
- Proteases: Break down proteins.
- Endonucleases: Damage DNA.
- Free Radicals: Reactive oxygen species (ROS) damage lipids, proteins, and nucleic acids.
- Cells have defense mechanisms to combat ROS, but an imbalance can lead to oxidative stress and injury.
- Antioxidants (vitamins E, A, C) and enzymes (catalase, superoxide dismutases) neutralize free radicals.
- Membrane Permeability: Damage to cell membranes can be caused by ATP depletion, calcium-modulated phospholipases, bacterial toxins, and viral proteins.
- Mitochondrial dysfunction, cytoskeletal abnormalities, ROS, and lipid breakdown products contribute to membrane damage.
Reversible & Irreversible Cell Injury
- Reversible Injury: Early changes can be reversed if the stimulus is removed (e.g., decreased ATP, membrane damage, decreased protein synthesis).
- Irreversible Injury: Persistent or excessive injury leads to irreversible changes, characterized by:
- Severe mitochondrial damage
- Extensive plasma membrane damage
- Swelling of lysosomes
- Amorphous densities in mitochondria
Chemical Injury
- Toxic Agents: Numerous chemicals cause reversible or irreversible injury, affecting various organs, particularly the liver.
- Examples: carbon tetrachloride, trichloroethylene, alcohol, various drugs, and certain foods.
- Chemicals produce injury through direct interaction with cellular components or by creating toxic metabolites.
- Toxic metabolites can act as free radicals, disrupt cellular processes, or generate ROS.
- Examples of Chemical Injury:
- Acetaminophen (Tylenol): Can cause liver necrosis and potential hepatic failure.
- Halothane, Isoniazid: Can lead to fatty liver, hepatitis, and cirrhosis.
- Alcohol: Can cause hepatocellular cholestasis (bile flow disruption) and hepatic adenomas (liver tumors).
- Oral contraceptives: Can cause hepatic veno-occlusive disease (blockage of blood vessels in the liver).
- Azathioprine, anti-neoplastic agents: Effects not specified in the text.
- Antibiotics (amphotericin B, etc.): Effects not specified in the text.
- Metals (mercury, cadmium, bismuth, etc.): Can cause acute renal failure.
- Solvents (ethylene glycol, etc.): Effects not specified in the text.
- Jodinated contrast agents: Effects not specified in the text.
- Anti-neoplastic agents (cisplatin, etc.): Effects not specified in the text.
Necrosis
- Necrosis: Morphological changes that occur after cell death, resulting from enzyme degradation.
- Occurs in the context of irreversible injury.
- Triggers inflammation in surrounding tissues.
- Involves protein denaturation and cell digestion by enzymes from:
- Autolysis: From lysosomes of the dead cells.
- Heterolysis: From lysosomes of immune cells.
Morphology of Necrosis
- Eosinophilia: Increased eosin staining due to protein denaturation and loss of glycogen.
- Cytoplasmic Changes: Vacuoles (gaps) appear within the cytoplasm (moth-eaten appearance). Calcification may occur later.
- Nuclear Changes: DNA breakdown produces three patterns:
- Karyolysis: Basophilia (dark staining) fades.
- Pyknosis: Nucleus shrinks and becomes more darkly stained.
- Karyorrhexis: Nucleus fragments.
Electron Microscopy Findings
- Plasma Membrane Discontinuities: Breaks in the cell membrane.
- Mitochondrial Dilation/Amorphous Densities: Mitochondria become enlarged and contain dense structures.
- Intracytoplasmic Myelin Figures: Characteristic features of necrotic cytoplasm.
- Amorphous Osmiophilic Debris: Darkly stained debris.
Types of Necrosis
- Coagulative Necrosis: Protein denaturation is predominant, retaining the cell outline for a period of time.
- Liquefactive Necrosis: Characteristic of bacterial or fungal infections, where cells are digested and liquefied.
- Caseous Necrosis: Associated with tuberculosis, where dead cells appear as a cheesy, crumbly substance.
- Fat Necrosis: Areas of fat destruction, often caused by pancreatitis, where fat cells release fatty acids which interact with calcium to produce chalky white deposits.
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