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What is the primary effect of hypoxia on cellular respiration?
What is the primary effect of hypoxia on cellular respiration?
Reversible injury leads to an increase in intracellular sodium and a decrease in intracellular potassium.
Reversible injury leads to an increase in intracellular sodium and a decrease in intracellular potassium.
True
What happens to ribosomes during reversible injury?
What happens to ribosomes during reversible injury?
They detach from the rough endoplasmic reticulum (RER).
The accumulation of _____ and lactic acid during hypoxia results in reduced intracellular pH.
The accumulation of _____ and lactic acid during hypoxia results in reduced intracellular pH.
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Which of the following enzymes is NOT activated in response to calcium influx during ischemia?
Which of the following enzymes is NOT activated in response to calcium influx during ischemia?
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What is the result of prolonged hypoxia on the cytoskeleton?
What is the result of prolonged hypoxia on the cytoskeleton?
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Match the injuries to their characteristics:
Match the injuries to their characteristics:
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The accumulation of calcium particles indicates reversible injury.
The accumulation of calcium particles indicates reversible injury.
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Which type of cell death is characterized by swelling and breakdown of organelles?
Which type of cell death is characterized by swelling and breakdown of organelles?
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Apoptosis can occur under pathological conditions only.
Apoptosis can occur under pathological conditions only.
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What is the primary cause of hypoxic cell injury?
What is the primary cause of hypoxic cell injury?
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________ agents such as trauma, extremes of temperature, and radiation can lead to cell injury.
________ agents such as trauma, extremes of temperature, and radiation can lead to cell injury.
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Match the following causes of cell injury with their descriptions:
Match the following causes of cell injury with their descriptions:
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Which intracellular system is NOT explicitly mentioned as vulnerable to injury?
Which intracellular system is NOT explicitly mentioned as vulnerable to injury?
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Calcium levels in the cytosol are maintained at high levels to support cellular functions.
Calcium levels in the cytosol are maintained at high levels to support cellular functions.
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Name one effect of aging on cells.
Name one effect of aging on cells.
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Which of the following is NOT a condition in which free radicals are implicated?
Which of the following is NOT a condition in which free radicals are implicated?
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Free radicals have a stable configuration due to their unpaired electron.
Free radicals have a stable configuration due to their unpaired electron.
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Identify one mechanism by which chemical injury occurs.
Identify one mechanism by which chemical injury occurs.
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The enzymatic catabolism of oxygenous chemicals can lead to the formation of _____ free radicals.
The enzymatic catabolism of oxygenous chemicals can lead to the formation of _____ free radicals.
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Match the free radical with its effect on cell components:
Match the free radical with its effect on cell components:
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What is one of the enzymatic processes that generate superoxide radicals?
What is one of the enzymatic processes that generate superoxide radicals?
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Hydropic changes indicate irreversible cell injury.
Hydropic changes indicate irreversible cell injury.
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Name one reactive species generated through the reduction-oxidation reactions.
Name one reactive species generated through the reduction-oxidation reactions.
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Which of the following conditions is NOT a cause of fatty change (steatosis)?
Which of the following conditions is NOT a cause of fatty change (steatosis)?
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What term is used to describe the accumulation of fat within macrophages of subcutaneous connective tissues?
What term is used to describe the accumulation of fat within macrophages of subcutaneous connective tissues?
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Fatty change is irreversible and often leads to permanent damage to the liver.
Fatty change is irreversible and often leads to permanent damage to the liver.
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An abnormal accumulation of calcium salts in tissues is referred to as __________.
An abnormal accumulation of calcium salts in tissues is referred to as __________.
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Match the following types of deposits with their characteristics:
Match the following types of deposits with their characteristics:
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What is dystrophic calcification associated with?
What is dystrophic calcification associated with?
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Which of the following cells may be stuffed with lipid due to necrotic cell debris?
Which of the following cells may be stuffed with lipid due to necrotic cell debris?
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Excess fatty acid oxidation is a cause of fatty change in tissues.
Excess fatty acid oxidation is a cause of fatty change in tissues.
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Metastatic calcification can occur in normal tissues during hypocalcemia.
Metastatic calcification can occur in normal tissues during hypocalcemia.
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List one cause of hypercalcemia.
List one cause of hypercalcemia.
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What type of change occurs in the liver during fatty change as seen under a light microscope?
What type of change occurs in the liver during fatty change as seen under a light microscope?
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Dystrophic calcification is often found in ____ areas of necrosis.
Dystrophic calcification is often found in ____ areas of necrosis.
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Match the following terms to their descriptions:
Match the following terms to their descriptions:
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Which of the following is a characteristic of hypertrophy?
Which of the following is a characteristic of hypertrophy?
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Atrophic cells are dead cells.
Atrophic cells are dead cells.
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What is the biochemical change associated with atrophy?
What is the biochemical change associated with atrophy?
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Study Notes
Cell Injury
- Cells maintain a narrow range of physiological activities.
- When adaptation mechanisms are exceeded, cell injury occurs.
- Two main patterns of cell death:
- Necrosis: Cell swelling, protein denaturation, and organellar breakdown.
- Apoptosis: Programmed cell death, occurring under normal or physiological conditions.
Causes of Cell Injury
- Hypoxia: Diminishes aerobic respiration, distinct from ischemia (also causes hypoxic cell injury). Occurs with inadequate oxygenation of the blood.
- Physical agents: Trauma, temperature extremes, radiation, electric shock, atmospheric pressure changes.
- Chemicals and drugs: Alter membrane permeability, osmotic homeostasis, or enzyme integrity.
- Microbiologic agents: Viruses, parasites.
- Immunologic reactions: Immune system attacks can cause cell injury, e.g., anaphylaxis.
- Genetic defects: E.g., Down's syndrome, sickle cell anemia.
- Nutritional imbalances: Protein-calorie deficiency, vitamin deficiencies, diets high in animal fat.
- Aging: Cellular processes gradually decline.
Mechanisms of Cell Injury
- Four vulnerable intracellular systems:
- Cell membrane integrity (ionic and osmotic regulation).
- Aerobic respiration.
- Protein synthesis.
- Genetic apparatus.
- Cytosolic free calcium is maintained at low levels by ATP-dependent transporters.
- Ischemia or toxins increase intracellular calcium, activating enzymes:
- Phospholipases (degrade membranes).
- Proteases (protein breakdown).
- ATPases (ATP depletion).
- Endonucleases (DNA fragmentation).
- Oxygen free radicals are key mediators of cell death.
Ischemic and Hypoxic Injury
-
Reversible Injury:
- Reduced ATP leads to:
- Influx of calcium.
- Sodium pump dysfunction.
- Intracellular sodium accumulation.
- Potassium loss.
- Cell swelling.
- Accumulation of metabolites (inorganic phosphates, lactic acid, purine nucleotides).
- Increased anaerobic glycolysis, glycogen depletion.
- Reduced intracellular pH.
- Reduced protein synthesis.
- Loss of cytoskeletal features.
- Reduced ATP leads to:
-
Irreversible Injury:
- Severe mitochondrial vacuolization and calcium accumulation.
- Extensive plasma membrane damage.
- Lysosomal swelling.
- Calcium-mediated injury during reperfusion.
- Loss of proteins from hyperpermeable membranes.
- Lysosomal enzyme release and intracellular degradation.
- Formation of myelin figures.
Mechanisms of Irreversible Injury:
- Progressive loss of membrane phospholipids.
- Cytoskeletal abnormalities.
- Toxic oxygen radicals from reperfusion.
- Lipid breakdown products.
Free Radical Mediation of Cell Injury
-
Free radicals are unstable molecules with unpaired electrons.
-
Generated by:
- Absorption of radiant energy.
- Redox reactions.
- Enzymatic catabolism of chemicals.
-
React with:
- Plasma membranes (lipid peroxidation).
- DNA.
- Proteins.
Chemical Injury
-
Two Mechanisms:
- Direct combination with a critical molecule or organelle.
- Conversion to toxic metabolites (often by P-450 oxidases in the SER).
-
Example: Carbon tetrachloride (CCl4) is converted to CCl3. in the liver, resulting in membrane peroxidation, ER damage, and fatty liver change.
Patterns of Acute Cell Injury
-
Reversible Cell Injury: Light microscopic changes:
- Cell swelling.
- Abnormal exogenous substance deposits.
-
Fatty Change (Steatosis):
- Accumulation of triglycerides in parenchymal cells.
- Occurs in the liver, heart, muscle, kidney.
- Causes: toxins, diabetes, malnutrition, obesity, anoxia.
- Excess triglycerides may result from defects in fatty acid entry or lipoprotein synthesis.
Cholesterol and Cholesterol Esters
- Macrophages in contact with lipid debris become filled with lipid, forming "foamy cells."
- Atherosclerosis: Smooth muscle cells and macrophages are filled with cholesterol and cholesterol esters.
- Xanthomas: Accumulations of fat within macrophages in subcutaneous tissues, appearing as nodules.
Proteins
- Less common accumulation, e.g., in glomerular diseases with proteinuria.
Glycogen
- Accumulation in cases of glucose or glycogen metabolism disorders, appearing as vacuoles.
Pigments
- Colored substances, exogenous or endogenous.
- Melanin: Accumulates in basal cells of the epidermis or dermal macrophages.
- Hemosiderin: A hemoglobin-derived pigment, golden-brown, accumulates with iron excess.
Pathologic Calcification
- Abnormal calcium salt accumulation.
- Dystrophic calcification: Occurs in dead or dying tissues despite normal calcium levels, evident in atheromas, injured arteries, and aging tissue.
-
Metastatic Calcification: Occurs in normal tissues with hypercalcemia. Causes:
- Endocrine disorders (hyperparathyroidism).
- Bone catabolism (multiple myeloma, cancer).
- Vitamin D intoxication, milk alkali syndrome.
- Sarcoidosis.
- Renal failure.
Cellular Adaptations of Growth and Differentiation
- Physiologic Adaptations: Responses to normal stimuli (hormones, chemicals).
- Pathologic Adaptations: Allow cells to modulate their environment and avoid injury.
Atrophy
- Shrinkage in cell size due to loss of cell substance.
- Causes:
- Reduced workload
- Loss of innervation
- Diminished blood supply
- Inadequate nutrition
- Loss of endocrine stimulation
- Aging
- Cells become smaller to survive with reduced resources.
- Biochemically: Decreased synthesis, increased catabolism.
Hypertrophy
- Increase in cell size due to increased synthesis of structural proteins and organelles.
- Results in an increase in organ size.
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Description
Explore the concepts of cell injury, including mechanisms of necrosis and apoptosis. Understand the various factors that lead to cell injury, such as hypoxia, physical agents, and immunologic reactions. This quiz will enhance your knowledge of cellular physiology and pathology.