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Questions and Answers
What primarily characterizes necrosis?
Which factor distinguishes hypoxia from ischemia?
Which intracellular system is NOT identified as vulnerable to injury?
What type of agents includes viruses and tapeworms as examples?
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Which of the following is a consequence of aging on cell injury?
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What role do ATP-dependent calcium transporters play in the cell?
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Which statement about cell injury mechanisms is true?
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Which nutritional factor is implicated in the pathogenesis of atherosclerosis?
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What primarily characterizes cytoplasmic eosinophilia?
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Which type of necrosis is characterized by preservation of structural outlines of the coagulated cells?
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What is the significance of karyolysis in the context of necrosis?
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Which morphological change is NOT associated with necrosis?
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In which type of necrosis does the necrotic tissue usually become liquefied due to bacterial infection?
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What are the nuclear changes seen mainly in apoptosis?
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What denotes gangrenous necrosis in clinical terms?
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Which process does NOT contribute to the morphological appearances of necrosis?
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What is the primary effect of hypoxia on cellular metabolism?
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Which of the following changes is associated with irreversible cellular injury?
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What role do oxygen free radicals play in the process of cell injury?
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What consequence results from ATP depletion during ischemia?
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Which morphological change is indicative of severe irreversible injury?
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What is a consequence of cytoskeleton disruption during irreversible injury?
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Which mechanism is NOT involved in the progression of irreversible injury?
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What happens to ribosomes during early stages of reversible cellular injury?
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What characterizes fat necrosis following acute pancreatitis?
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Which of the following processes is NOT associated with apoptosis?
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Which factor is least likely to initiate apoptosis?
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What is a common characteristic of cells undergoing apoptosis observed under H&E staining?
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Which type of intracellular accumulation is characterized by the production of an endogenous substance at an increased rate but with a decreased metabolic rate?
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What generally occurs when growth factors or hormones are withdrawn from a cell?
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Which of the following is not a mechanism known to activate apoptosis?
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What most accurately describes the resultant effect of apoptosis on cellular morphology?
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What primarily causes fatty change (steatosis) in parenchymal cells?
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Which organ is most commonly associated with fatty change due to its parenchymal cell structure?
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What characteristic of cholesterol accumulation in atherosclerosis contributes to the formation of foamy cells?
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Which process is associated with the accumulation of melanin in the skin?
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In the context of pathological calcification, what mineral is less commonly associated with calcium salt accumulation?
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What type of abnormal deposit is seen in conditions associated with proteinuria?
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What is the primary cause of accumulation of haemosiderin in tissues?
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What type of vacuolization is commonly linked with abnormal glucose or glycogen metabolism?
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Study Notes
Cell Injury
- Cells strive to maintain a stable internal environment
- When cells are exposed to stress or stimuli they can adapt to preserve their viability
- If the cell's adaptive capacity is exceeded, cell injury results
- Two main types of cell death: necrosis and apoptosis
Necrosis
- Occurs due to exposure to harmful conditions
- Characterized by cell swelling, protein denaturation, and organelle breakdown
Apoptosis
- A programmed cell death that occurs under normal or physiological conditions
Causes of Cell Injury
- Hypoxia: Deprives cells of oxygen for aerobic respiration, a distinct condition from ischemia which also leads to hypoxic cell injury
- Physical Agents: Trauma, temperature extremes, radiation, electric shock, and sudden atmospheric pressure changes can all injure cells
- Chemicals and drugs: Alter membrane permeability, osmotic balance, or enzyme cofactor integrity
- Microbiologic Agents: Range from viruses to tapeworms
- Immunologic Reactions: The body's immune system can trigger cell injury, such as in anaphylactic reactions
- Genetic Defects: Examples include Down syndrome and sickle cell anemia
- Nutritional Imbalances: Protein-calorie deficiencies, vitamin deficiencies, and diets rich in animal fat can contribute to cell injury (e.g. atherosclerosis)
- Aging: A natural process that contributes to cell deterioration
Mechanisms of Cell Injury
- Membrane Integrity: Disruptions in membrane integrity lead to changes in cellular ionic and osmotic homeostasis
- Aerobic Respiration: Damage to this process severely impacts cellular energy production
- Protein Synthesis: Disruptions in protein production can lead to functional impairments
- Genetic Apparatus: Damage to DNA or RNA can have detrimental effects on cell function and survival
- Calcium Homeostasis: Increased intracellular calcium levels activate enzymes that damage cells (e.g., phospholipases, proteases, ATPases, endonucleases)
- Reactive Oxygen Species: These unstable molecules contribute significantly to cell death
Ischemic and Hypoxic Injury
- Reversible Injury: Initial effects on aerobic respiration result in reduced ATP, leading to calcium influx, membrane pump dysfunction, and cellular swelling
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Irreversible Injury: Characterized by:
- Severely damaged mitochondria
- Extensive plasma membrane damage
- Swelling of lysosomes
- Reperfusion injury
- Loss of cellular components
- Formation of myelin figures
Mechanisms of Irreversible Injury
- Phospholipid Loss: Progressive loss of membrane phospholipids weakens the cell membrane
- Cytoskeletal Damage: Protease activation and calcium influx can disrupt the structural integrity of the cell
- Toxic Oxygen Radicals: Released during reperfusion, damaging cells further
- Lipid Breakdown Products: Detergent-like effects on cell membranes
Necrosis
- Characterized by morphological changes that follow cell death in living tissue
- Results from enzymatic digestion and protein denaturation
- Cytoplasmic Changes: Eosinophilia, glassy appearance, vacuolation, and calcification
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Nuclear Changes:
- Karyolysis: Nuclear DNA digestion
- Pyknosis: Nuclear shrinkage and increased basophilia, common in apoptosis
- Karyorrhexis: Fragmentation of the pyknotic nucleus
Types of Necrosis
- Coagulative Necrosis: Preservation of the structural outlines of dead cells, most common in myocardial infarction
- Liquefactive Necrosis: Associated with bacterial or fungal infections, characterized by the breakdown of tissue into a liquid mass, also seen in the CNS
- Gangrenous Necrosis: Ischemic coagulative necrosis with superimposed infection, often referred to as "wet gangrene"
- Caseous Necrosis: Associated with tuberculosis, characterized by a cheesy, white appearance microscopically consisting of amorphous granular debris
- Fat Necrosis: Occurs in acute pancreatitis, characterized by the enzymatic destruction of fat cells
Apoptosis
- Programmed cell death that is responsible for cell elimination under normal and pathological conditions
- Key characteristics:
- Single or clustered cells with intensely eosinophilic cytoplasm
- Condensed nuclear chromatin with well-defined masses
- Karyorrhexis caused by endonucleases
- Cell shrinkage, budding, and fragmentation into apoptotic bodies
- No inflammatory response
Initiation of Apoptosis
- Withdrawal of growth factors or hormones: Absence of essential signals can trigger apoptosis
- Engagement of specific receptors: Receptors like FAS and TNF can activate apoptotic pathways
- Injury by radiation, toxins, and free radicals: These agents can damage cells leading to apoptosis
- Intrinsic protease activation: Activation of caspases, particularly in developmental scenarios
Intracellular Accumulations
- Normal cells can accumulate abnormal substances in a variety of circumstances
- Accumulations can be transient or permanent, harmful or injurious, and occur in the cytoplasm or nucleus
- Main categories:
- Normal endogenous substances: Produced at a normal or increased rate with inadequate metabolism, common in fatty liver disease
- Normal or abnormal substances: Unaffected by metabolism due to genetic defects, leading to storage diseases
- Abnormal exogenous substances: The cell lacks the machinery to metabolize or transport these substances
Fatty Change (Steatosis)
- Abnormal accumulation of triglycerides within parenchymal cells
- Most often seen in the liver, but can affect other organs
- Caused by various factors: toxins, diabetes, malnutrition, obesity, anoxia
- Defects at any step of fatty acid entry or lipoprotein synthesis can contribute
Cholesterol and Cholesterol Esters
- Foamy cells: Macrophages that ingest lipid debris, accumulating cholesterol
- Atherosclerosis: Accumulation of cholesterol and cholesterol esters in smooth muscle cells and macrophages
- Xanthomas: Accumulation of fat within macrophages of subcutaneous connective tissues appearing as white nodules
Proteins
- Less common accumulations, often associated with proteinuria in glomerular diseases
Glycogen
- Accumulates in cases of abnormal glucose or glycogen metabolism
- Appears as vacuoles in cells
Pigments
- Colored substances, either exogenous or endogenous
- Melanin: Accumulates in epidermal cells, leading to freckles or dermal macrophage deposits
- Hemosiderin: Iron-containing pigment, golden brown in color, accumulates in local or systemic iron overload
Pathologic Calcification
- Abnormal accumulation of calcium salts, often with smaller amounts of other minerals
- Can occur in various tissues, often associated with tissue damage
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Description
Explore the mechanisms of cell injury, including the processes of necrosis and apoptosis. This quiz covers various causes of cell injury, from hypoxia to exposure to harmful agents, emphasizing the importance of cellular homeostasis. Test your knowledge on how cells adapt to stress and the implications of cellular injury.
