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What happens if a cell's adaptive capability is exceeded?
What happens if a cell's adaptive capability is exceeded?
Which of the following describes necrosis?
Which of the following describes necrosis?
Which of the following is a cause of cell injury?
Which of the following is a cause of cell injury?
What type of cell death occurs under normal physiological conditions?
What type of cell death occurs under normal physiological conditions?
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Which of the following is not a mechanism of cell injury?
Which of the following is not a mechanism of cell injury?
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Which factor is NOT a cause of cell injury?
Which factor is NOT a cause of cell injury?
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Cell injury response is influenced by which of the following factors?
Cell injury response is influenced by which of the following factors?
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What is a significant implication of diets rich in animal fat?
What is a significant implication of diets rich in animal fat?
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What is the initial effect of hypoxia on cells?
What is the initial effect of hypoxia on cells?
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What is fatty change (steatosis) primarily characterized by?
What is fatty change (steatosis) primarily characterized by?
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What consequence arises from reduced ATP levels in the context of hypoxic injury?
What consequence arises from reduced ATP levels in the context of hypoxic injury?
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Which organ is most commonly affected by fatty change?
Which organ is most commonly affected by fatty change?
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Which of the following is a mediator of cell death in ischemic conditions?
Which of the following is a mediator of cell death in ischemic conditions?
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What can cause excess accumulation of triglycerides?
What can cause excess accumulation of triglycerides?
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What structural cellular change indicates irreversible injury?
What structural cellular change indicates irreversible injury?
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What are foamy cells indicative of?
What are foamy cells indicative of?
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Which enzyme's activation leads to degradation of structural proteins during ischemic injury?
Which enzyme's activation leads to degradation of structural proteins during ischemic injury?
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What may result from severe fatty change?
What may result from severe fatty change?
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Which metabolic byproducts accumulate in cells during hypoxia?
Which metabolic byproducts accumulate in cells during hypoxia?
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What type of pigment results from an excess of iron in tissues?
What type of pigment results from an excess of iron in tissues?
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What is one of the mechanisms of irreversible injury related to cytoskeletal damage?
What is one of the mechanisms of irreversible injury related to cytoskeletal damage?
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What effect do toxic oxygen radicals have following reperfusion in ischemic areas?
What effect do toxic oxygen radicals have following reperfusion in ischemic areas?
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Which condition is most likely associated with the accumulation of xanthomas?
Which condition is most likely associated with the accumulation of xanthomas?
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What is the primary concern of pathological calcification?
What is the primary concern of pathological calcification?
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Which of the following is NOT a characteristic of free radicals?
Which of the following is NOT a characteristic of free radicals?
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What is one of the ways free radicals can be generated within cells?
What is one of the ways free radicals can be generated within cells?
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Which of the following statements regarding chemical injury is true?
Which of the following statements regarding chemical injury is true?
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What role do enzymes like xanthine oxidase play in free radical generation?
What role do enzymes like xanthine oxidase play in free radical generation?
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What type of injury is characterized by small clear vacuoles in the cytoplasm?
What type of injury is characterized by small clear vacuoles in the cytoplasm?
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What happens to the endoplasmic reticulum (ER) when carbon tetrachloride is converted to its toxic metabolite?
What happens to the endoplasmic reticulum (ER) when carbon tetrachloride is converted to its toxic metabolite?
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Which molecule reacts with free radicals to form toxic species like hydrogen peroxide?
Which molecule reacts with free radicals to form toxic species like hydrogen peroxide?
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What is a common consequence of free radical attack on DNA?
What is a common consequence of free radical attack on DNA?
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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 is NOT a condition associated with apoptosis?
Which of the following is NOT a condition associated with apoptosis?
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In what form does apoptosis typically present in H&E stained sections?
In what form does apoptosis typically present in H&E stained sections?
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Which initiator is NOT associated with apoptosis?
Which initiator is NOT associated with apoptosis?
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What constitutes an abnormal substance that can lead to intracellular accumulation?
What constitutes an abnormal substance that can lead to intracellular accumulation?
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Which best describes the nuclear characteristics observed in apoptotic cells?
Which best describes the nuclear characteristics observed in apoptotic cells?
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Which type of intracellular accumulation cannot be metabolized due to genetic defects?
Which type of intracellular accumulation cannot be metabolized due to genetic defects?
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What happens to cells undergoing apoptosis?
What happens to cells undergoing apoptosis?
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Study Notes
Cell Injury
- Cells strive to maintain a stable internal environment.
- When cells encounter stress or harmful stimuli, they adapt to preserve their function.
- If adaptive mechanisms are overwhelmed, cell injury occurs.
- There are two main types of cell death:
- Necrosis: Caused by severe injury, characterized by swelling, protein breakdown, and organelle damage.
- Apoptosis: A programmed cell death that happens in normal and pathological conditions.
Causes of Cell Injury
- Hypoxia: Lack of sufficient oxygen, impedes aerobic respiration. It differs from ischemia, which also causes hypoxic injury.
- Physical Agents: Include trauma, temperature extremes, radiation, electric shock, and sudden pressure changes.
- Chemicals and Drugs: Chemicals can disrupt cell membranes, osmotic balance, or enzyme function.
- Microbiologic Agents: Range from viruses to parasites.
- Immunologic Reactions: The body’s immune system can cause cell injury, as seen in allergic reactions.
- Genetic Defects: Examples include Down syndrome and sickle cell anemia.
- Nutritional Imbalances: Protein-calorie deficiency, vitamin deficiencies, and diets high in animal fat.
Mechanisms of Cell Injury
- Cell Membrane Integrity: Disruption of the cell membrane leads to changes in ionic and osmotic homeostasis.
- Aerobic Respiration: Hypoxia disrupts mitochondrial function and ATP production.
- Protein Synthesis: Cell injury can affect ribosome function and protein production.
- Genetic Apparatus: Damage to DNA can lead to cell dysfunction or death.
Ischemic and Hypoxic Injury
-
Reversible Injury: Initially, lack of oxygen affects aerobic respiration, decreasing ATP production. This leads to:
- Influx of calcium
- Reduced sodium pump activity
- Intracellular sodium accumulation
- Potassium loss
- Water accumulation, causing cell swelling.
- Accumulation of metabolites like lactic acid and inorganic phosphates.
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Irreversible Injury: Continued hypoxia results in:
- Severe mitochondrial damage
- Plasma membrane damage
- Lysosomal swelling
- Release of lysosomal enzymes into the cytoplasm, further damaging the cell.
- Formation of myelin figures (whorled masses of phospholipids).
Mechanisms of Irreversible Injury
- Progressive Loss of Membrane Phospholipids: Detergent effects on the cell membrane.
- Cytoskeletal Abnormalities: Protease activation and increased calcium levels can disrupt the cytoskeleton and cell membrane integrity.
- Toxic Oxygen Radicals: Generated during reperfusion, they can damage cell components.
- Lipid Breakdown Products: Can have detergent effects on the cell membrane.
Free Radical Mediation of Cell Injury
- Free radicals are unstable molecules with unpaired electrons.
- They are implicated in various forms of cell injury, including:
- Chemical injury
- Radiation injury
- Oxygen toxicity
- Cellular aging
- Microbial killing
- Inflammatory damage
- Tumor killing.
- Free radicals can be generated within the cell through:
- Absorption of radiant energy (e.g., hydrolysis of water)
- Redox reactions (normal metabolic processes)
- Enzymatic catabolism of oxygenous chemicals.
- Free radicals can damage:
- Lipid Peroxidation: Damage to cell membranes.
- DNA Damage: Reaction of thymine bases in DNA.
- Protein Cross-Linking: Altering protein structure and function.
Chemical Injury
- Direct Toxic Effects: Chemicals can bind to critical cell components, interrupting function (e.g., mercury binding to sulfhydryl groups).
- Metabolic Conversion: Some chemicals are not toxic themselves but become reactive metabolites, often through P-450 oxidases in the smooth endoplasmic reticulum (SER). Example: Carbon tetrachloride (CCl4).
Patterns of Acute Cell Injury
-
Reversible Cell Injury:
- Cell Swelling: Difficult to see microscopically, but small clear vacuoles may appear in the cytoplasm.
- Fatty Change: Accumulation of triglycerides within cells.
-
Irreversible Cell Injury:
- Necrosis: Marked by cellular swelling, organelle breakdown, and protein denaturation.
- Apoptosis: Programmed cell death, characterized by cell shrinkage, chromatin condensation, and formation of apoptotic bodies.
Apoptosis
- Physiological Roles: Embryonic development, hormonal involution, cell deletion in proliferating populations, deletion of autoreactive T cells.
- Pathological Roles: Cell death in response to DNA damage, viral infections, etc.
- Morphological Features: Cell shrinkage, chromatin condensation, nuclear fragmentation, formation of apoptotic bodies.
- Process: Initiated by various stimuli that activate intracellular proteases (e.g., caspases).
Intracellular Accumulations
- Mechanisms: Excessive production, defective metabolism, or inability to transport.
-
Types:
- Normal Endogenous Substances: Ex: fatty change in the liver.
- Abnormal Endogenous Substances: Genetic defects leading to storage diseases.
- Exogenous Substances: Cell lacks the machinery to metabolize or excrete them.
Fatty Change (Steatosis)
- Definition: Abnormal accumulation of triglycerides within parenchymal cells.
- Common Location: Liver, but can occur in the heart, skeletal muscle, and kidneys.
- Causes: Toxins, diabetes mellitus, protein malnutrition, obesity, anoxia.
- Mechanisms: Defects in any step from fatty acid entry to lipoprotein synthesis.
- Impact: Mild steatosis may have no effect on function; severe steatosis can impair cell function.
Cholesterol and Cholesterol Esters
- Accumulation: Macrophages, smooth muscle cells, can become filled with lipid vacuoles in response to necrotic debris or in atherosclerosis.
- Xanthomas: Accumulation of fat in macrophages of subcutaneous connective tissue, appearing as white nodules.
Proteins
- Accumulation: Less common, but occur in conditions like glomerular disease with proteinuria.
Glycogen
- Accumulation: Seen in cases of abnormal glucose or glycogen metabolism.
- Appearance: Vacuoles under the light microscope.
Pigments
- Exogenous: Pigments from outside the body, e.g., coal dust, tattoo ink.
-
Endogenous: Pigments produced within the body.
- Melanin: Brown pigment produced by melanocytes.
- Hemosiderin: Golden-brown pigment derived from hemoglobin breakdown, indicates iron overload.
Pathological Calcification
- Abnormal Accumulation: Calcium salts, with smaller amounts of iron, magnesium, etc.
-
Types:
- Dystrophic Calcification: Occurs in dead or dying tissues.
- Metastatic Calcification: Occurs in normal tissues due to hypercalcemia.
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Description
Explore the fundamental concepts of cell injury and the mechanisms behind cell death, including necrosis and apoptosis. Learn about the various causes of cell damage, such as hypoxia, physical agents, and immunologic reactions. This quiz aims to deepen your understanding of how cells respond to stress and harmful stimuli.
