Chapter 2 Cell injury,2024-25

Oxygen deficiency.

They may have diminished function, but they are not dead.

A process where one type of epithelium is replaced by another, often in response to chronic irritation.

Hypoxia and ischemia.

It indicates brown atrophy when present in large amounts.

It slows down aging and prolongs life.

Squamous metaplasia of the respiratory epithelium.

The reliance of rapidly proliferating normal cells and cancer cells on aerobic glycolysis to produce energy.

Acute pancreatitis.

Peritoneal fat cells, including stored triglycerides.

They exacerbate aging, especially those associated with prolonged inflammation.

Cardiac enlargement due to hypertension or aortic valve disease.

Pathologic apoptosis occurs as a response to cellular damage or lack of growth factors, while physiologic apoptosis is a normal process.

Accumulation of DNA damage and mutations.

Mutations.

In the epidermis.

It stimulates the synthesis of several proteins that help the cell survive.

Lysosomes of dying cells or leukocytes recruited during inflammation.

Yes, both can occur together and result in an enlarged organ.

There are no new cells, just bigger cells containing increased amounts of structural proteins and organelles.

Yes, with lifestyle changes and treatment of underlying conditions.

A rapid and uncontrollable form of cell death caused by severe disturbances such as loss of oxygen and nutrient supply or toxins.

Foci of necrosis contain shadowy outlines of necrotic fat cells.

Frequently creamy yellow and is called pus.

An autophagolysosome.

Deposition of calcium salts in normal tissues, usually secondary to hypercalcemia.

Irreversible injury and death of the affected cells.

Damage to proteins and DNA.

Carbon, lipofuscin, melanin, and hemosiderin.

It increases.

It contributes to the aging of individuals.

Amyloidosis.

When there is a local or systemic excess of iron.

An endogenous, brown-black pigment synthesized by melanocytes.

Fatty liver.

Age.

By creating a deficiency of an essential protein or by inducing apoptosis.

Triglycerides, cholesterol, and cholesteryl esters.

Lower rates of cell growth, metabolism, reduced errors in DNA replication, better DNA repair, and improved protein homeostasis.

Hypertrophy, Hyperplasia, Atrophy, Metaplasia.

Several mechanisms are involved.

A progressive decline in the life span and functional capacity of cells.

Responses of cells to normal stimulation by hormones or endogenous chemical mediators.

Brownish-yellow.

Accumulation of fat in liver cells.

Occurs when cells have a limited capacity to divide.

Vascular endothelial growth factor (VEGF).

Mutations or DNA rearrangements, such as translocations.

Air pollutants, insecticides, carbon monoxide (CO), asbestos, cigarette smoke, ethanol, and drugs.

Inability to restore mitochondrial function.

Organelles that contain digestive enzymes, derived from dying cells.

Cellular enzymes catalyze biochemical reactions within cells, facilitating metabolic processes.

Chemical species with a single unpaired electron in an outer orbital.

Within certain limits, yes; cells can return to a stable baseline.

Nephrotic syndrome.

Reduced size of an organ or tissue caused by a reduction in the size and number of cells.

Responses to stress that allow cells to modulate their structure and function to escape injury.

A condition characterized by more extensive accumulations of iron.

Metaplasia.

Grossly visible chalky white areas (fat saponification).

Hypertrophy is an increase in cell size, while hyperplasia is characterized by an increase in cell number due to proliferation.

Liquefactive necrosis.

A pathway of cell death where cells activate enzymes to degrade their own nuclear DNA and proteins.

Cellular abnormalities induced by ROS (free radicals).

The accumulation of inflammatory cells and enzymes from leukocytes that digest the tissue.

They become shrunken and form cytoplasmic fragments.

Increased Reactive Oxygen Species (ROS) production.

Neutrophils, macrophages, lymphocytes, and other leukocytes.

Necrosis of any type, aging or damaged heart valves, indicating past cell injury.

Air pollutants.

It is phagocytosed by alveolar macrophages.

Increased secretion of parathyroid hormone, destruction of bone, vitamin D-related disorders, renal failure.

Myelin figures.

A type of protein accumulation found in the liver.

Excessive hormonal or growth factor stimulation.

It can cause direct damage and disrupt cellular function.

It is an important cause of aortic stenosis in elderly persons.

Responses that include various mechanisms associated with clinical examples.

A bright pink, amorphous appearance.

Apoptosis that occurs in many normal situations to eliminate cells that are no longer needed.

By altering signaling pathways.

Metaplastic transformation of normal stratified squamous epithelium to gastric or intestinal-type columnar epithelium.

In a variety of tissues, particularly the heart, liver, and brain.

There is a loss of normal proteins and accumulation of misfolded proteins.

No, it is not injurious to the cell.

Mucus secretion and ciliary clearance of particulate matter.

Chromatin condensation, aggregation, and ultimately karyorrhexis.

Diminished ability to respond to damage.

Loss of glycogen particles.

Pigments synthesized within the body, such as lipofuscin, melanin, and certain derivatives of hemoglobin.

It becomes vacuolated and appears 'motheaten' due to enzyme digestion of organelles.

Cytosolic proteins that sense nutrient deprivation.

Biochemical pathways that control the balance of death and survival signals.

Yes, substances like glucose, salt, water, and oxygen can be toxic.

It causes detachment of ribosomes from the rough ER, reducing protein synthesis.

Proliferation of glandular epithelium, such as in the female breast at puberty and during pregnancy.

Nutritional imbalances.

A combination of decreased protein synthesis and increased protein degradation in cells.

It increases due to the influx and activation of leukocytes.

In autoimmune diseases and allergies.

Through lymphatic channels to the regional tracheobronchial lymph nodes.

Meter-long tapeworms.

They can undergo adaptation, achieving a new steady state.

Enzyme activity is crucial for maintaining metabolic pathways and overall cellular function.

Failure of energy-dependent ion pumps in the plasma membrane.

The complement system.

As basophilic deposits.

They may predispose to malignant transformation.

Wear-and-tear pigment.

Hemosiderosis.

Stratified squamous epithelial cells.

An increase in the size of cells resulting in an increase in the size of the organ.

The massive enlargement of the uterus during pregnancy due to estrogen stimulation.

An area of caseous necrosis enclosed within a distinctive inflammatory border.

Liver inflammation, fibrosis, or cirrhosis.

Intracellular sodium accumulates and potassium effluxes, causing cell swelling and dilation of the ER.

Cell injury develops.

The abnormal deposition of calcium salts in tissues.

Lipofuscin, melanin, or certain derivatives of hemoglobin.

By phagocytes.

Left ventricular hypertrophy in hypertension.

An inflammatory reaction.

Hypoxic death of cells.

They digest the cellular components within the autophagolysosome.

A firm texture.

It can hydrolyze water into hydroxyl (•OH) and hydrogen (H•) free radicals.

Yes, the same injurious agent may trigger multiple and overlapping biochemical pathways.

They are denatured.

The clearance of apoptotic bodies by phagocytes.

When the tissue contains cell populations capable of replication.

Changes in the environment.

The process in which a starved cell eats its own components to survive.

Alcohol abuse and diabetes associated with obesity.

When blood flow is restored to ischemic but viable tissues.

Brown atrophy.

By the Prussian blue histochemical reaction.

Fine white granules.

Cancer, Alzheimer disease, and ischemic heart disease.

They may become overloaded with lipids such as triglycerides, cholesterol, and cholesteryl esters.

Atherosclerosis.

Deprivation of growth factors or damage to the cell's DNA or proteins beyond repair.

It is associated with neurodegenerative disorders, including Alzheimer's disease.

Insulin-like growth factor receptor signaling.

Immune reactions can result in cell injury.

A hemoglobin-derived granular pigment that is yellow to brown.

Hormone-induced enlargement of the breast and uterus during pregnancy.

Focal areas of fat destruction typically resulting from activated pancreatic enzymes.

A collection of cellular debris with an amorphous granular pink appearance in H&E-stained tissue.

The reduced capacity of cells to divide due to progressive shortening of telomeres.

Because glycolysis generates metabolites needed for cell growth and division, such as proteins, lipids, and nucleic acids.

In caseous necrosis, the tissue architecture is completely obliterated and cellular outlines cannot be discerned.

Rapidly proliferating normal cells and cancer cells.

Lysosomal digestion of the cell’s own components.

To eliminate unnecessary cells.

Autoimmune reactions against one’s own tissues.

Allergic reactions against environmental substances.

As a function of age or atrophy.

Accumulation of substrates in lysosomes.

Alcohol consumption, obesity, diabetes, and certain medications.

Hypertrophy that occurs in response to normal physiological demands, such as skeletal muscles in athletes or uterine muscles during pregnancy.

A type of necrosis seen in focal bacterial or fungal infections.

Distended cisternae of the endoplasmic reticulum (ER).

Peroxidation of membrane lipids.

Cellular swelling.

They break off, giving the appearance that is responsible for the name 'apoptosis'.

In apoptosis, the plasma membrane remains intact.

The response of cells to various types of stress and noxious stimuli.

Carbon, with coal dust as an example.

Necrosis happens accidentally due to severe injury that cannot be repaired, leading to the failure of cellular constituents.

A term commonly used in clinical practice, though not a distinctive pattern of cell death.

Viruses.

A reversible change in which one adult cell type is replaced by another adult cell type.

By undergoing adaptations such as hypertrophy, hyperplasia, atrophy, or metaplasia.

Aging decreases the capacity to correct misfolding.

Chemically reactive molecules containing oxygen that can lead to cellular damage.

Intracellular accumulations of proteins in neurons.

Exposure to radiation, chemotherapeutic agents, intracellular generation of ROS, and mutations.

A programmed and controlled process of cell death that occurs naturally in the body.

Calcium salts.

Inability to maintain ionic and fluid homeostasis.

Troponin.

50 to 75 kg.

They activate additional caspases that degrade the cells' proteins and nucleus.

It serves as a survival mechanism during nutrient deprivation.

Increased eosinophilia due to denatured proteins and loss of RNA.

Cell injury by damaging multiple components.

Fatty change in the liver.

Hypertrophy that occurs due to abnormal conditions, such as left ventricular hypertrophy in hypertension.

Neoplastic transformation.

They can cause cell injury in susceptible patients or if used excessively.

They typically affect different cellular organelles and biochemical pathways.

Failure of the sodium pump.

Loss of DNA and chromatin structural integrity.

Injured cells and infiltrating leukocytes.

Caspase.

Injurious stimuli such as toxins, hypoxia, and physical damage.

It leads to an influx of Ca2+, causing damaging effects on numerous cellular components.

In the liver, but also in the heart, skeletal muscle, kidney, and other organs.

Cells show various stages of chromatin condensation and shrunken appearance.

To assess damage to tissues.

It attaches to cellular proteins and targets them for degradation in proteasomes.

Rickettsiae, bacteria, fungi, and protozoans.

Hypertrophy, Hyperplasia, Atrophy, Metaplasia.

Damage to plasma and lysosomal membranes, resulting in leakage of cellular contents.

It blackens them.

It converts superoxide into hydrogen peroxide (H2O2).

Reactive oxygen species (ROS) and other factors.

Enzymes like superoxide dismutase and catalase convert ROS into less harmful substances.

An adaptive response in cells capable of replication.

Acts as a screen against harmful ultraviolet radiation.

Stress exacerbates the aging process.

It leads to depletion of ATP.

It means 'cheese-like,' describing the friable yellow-white appearance of the necrotic area.

It stimulates glucose uptake and glycolysis while dampening mitochondrial oxidative phosphorylation.

The death of cells and of the organism.

A new steady state.

They activate compensatory mechanisms induced by HIF-1.

Severe damage that is beyond salvage, often due to loss of oxygen, nutrient supply, or the actions of toxins.

Enzymes increase the rate of reactions by lowering the activation energy required.

Because they readily react with nucleic acids, proteins, and lipids.

They may persist for some time or be digested by enzymes and disappear.

Various factors that have roles in cell injury along with their mechanisms.

Their function and morphology can return to normal.

A special form of necrosis visible by light microscopy, usually in immune reactions.

Potassium is lost from the cell (outflux).

Protein-calorie insufficiency.

In the walls of arteries.

To eliminate cells without eliciting an inflammatory reaction.

Marked dilation with large amorphous intramitochondrial densities.

Infections can lead to the synthesis of large amounts of microbial proteins.

Inherently unstable molecules that decay spontaneously.

Yes, it may occur concurrently with hypertrophy and often in response to the same stimuli.

The pyknotic nucleus undergoes fragmentation.

It can lead to increased generation of free radicals.

A type of cell damage that leads to cell death and cannot be reversed.

The fading of basophilia of the chromatin due to digestion of DNA.

The type of cell, its metabolic state, adaptability, and genetic makeup.

Surface molecules that trigger apoptosis in many cells.

A distinctive inflammatory border.

It is a marker of past free radical injury.

They pass a 'point of no return' and undergo cell death.

Deposits of calcium salts in normal tissues.

Estrogen stimulation.

Normal.

They are completely digested, transforming the tissue into a liquid viscous mass.

Loss of structure and functions of the plasma and intracellular membranes.

Lactic acid accumulates, leading to decreased intracellular pH and reduced activity of many cellular enzymes.

Basophilic calcium deposits.

It primarily impairs energy-dependent cellular functions, leading to necrosis.

Homeostasis.

In focal bacterial or fungal infections.

On the inner leaflet of the plasma membrane.

Hypercalcemia.

The mitochondrial pathway (intrinsic) and the death receptor pathway (extrinsic).

An increase in the size of an organ due to increased numbers of component cells.

Calcification can develop in aging or damaged heart valves, compromising valve motion.

The type of injury, its duration, and severity.

Toxins, protein malnutrition, diabetes mellitus, obesity, or anoxia.

Coagulative necrosis involving multiple tissue layers.

Eosinophilic, anucleate cells.

Reversible cell injury.

The diverse ways in which infectious pathogens cause injury.

They are highly reactive molecules that can damage cellular components.

Decreased workload, such as immobilization of a limb to permit healing of a fracture.

It serves to eliminate unwanted cells.

ATP depletion and failure of energy-dependent metabolic pathways.

Transaminases.

Cells with damaged DNA survive.

Deposits of calcium salts in dead and degenerated tissues.

It provides better survival in the harsh environment of habitual cigarette smoke.

Pigments that come from outside the body, such as carbon.

Both deprive oxygen.

The inflammatory reaction elicited by pathogens, necrotic cells, and dysregulated immune responses.

Skeletal muscles in athletes.

They adjust their function.

Apoptotic cells produce 'eat-me' signals.

Compression of capillaries.

An abnormal accumulation of triglycerides within parenchymal cells.

No, it may be histologically undetectable.

Growth of residual tissue after removal or loss of part of an organ, such as the liver.

Inflammation.

Changes that occur during apoptosis and necrosis.

It flips to the outer leaflet of the plasma membrane.

Abnormal stimuli such as chronic irritation and inflammation.

They are either phagocytosed by other cells or further degraded into fatty acids.

They recognize phosphatidylserine on apoptotic cells and lead to their phagocytosis.

Creatine kinase.

When a cell’s DNA or proteins are damaged beyond repair or when deprived of necessary survival signals.

Coagulative necrosis is modified by the liquefactive action of bacteria and attracted leukocytes, resulting in wet gangrene.

They neutralize ROS, preventing cellular damage.

Apoptosis can occur in healthy tissues, while necrosis typically occurs in pathological conditions.

p53 arrests the cell cycle at the G1 phase to allow for DNA repair.

No, it arises from reprogramming of stem cells rather than a phenotypic change of already differentiated cells.

Direct-acting toxins and latent toxins.

The characteristic cellular fragmentation of apoptosis.

Accumulation of carbon pigment.

An endogenous pigment.

By allowing the cell to eat its own contents and recycle them for nutrients and energy.

Friable yellow-white.

A type of hyperplasia that occurs in response to normal physiological stimuli.

It results in a deficiency of essential nutrients and a buildup of toxic metabolites.

Steatosis.

'Falling off', similar to the loss of leaves from a tree.

Fatty change, cholesterol and cholesteryl esters, proteins, glycogen, and pigments.

Products that destroy microbes but may also damage host tissues.

Irreversible cell injury.

They leak through the damaged cell membrane.

It remains fairly constant and tightly regulated.

Nutrient deficiency and disuse.

Vacuolation.

It can disrupt cellular function and lead to cell injury.

Nuclear shrinkage and increased basophilia; DNA condenses into a dark shrunken mass.

A cell type sensitive to a particular stress is replaced by another cell type better able to withstand the adverse environment.

A programmed form of cell death that occurs in a regulated manner, allowing for the removal of damaged or unnecessary cells.

Number, size, phenotype, metabolic activity, and functions.

Reprogramming of stem cells to differentiate along a new pathway.

It helps explain the pathogenesis of related diseases.

1. Cell size: Necrosis involves swelling, while apoptosis involves shrinkage. 2. Membrane integrity: Necrosis shows loss of membrane integrity, apoptosis maintains it. 3. Nuclear changes: Necrosis has random nuclear fragmentation, apoptosis has chromatin condensation. 4. Inflammatory response: Necrosis triggers inflammation, apoptosis does not. 5. Cell death mechanism: Necrosis is passive, apoptosis is active.

A form of cell injury that results in the premature death of cells in living tissue.

Severe hypoxia, toxins, infections, and physical trauma.

A process that leads to alterations in replicative and repair abilities of individual cells and tissues.

Cells are swollen, and the cytoplasm is pale, granular, vacuolated, or clear.

Reduced blood supply.

A process of 'self-eating' where intracellular organelles and portions of cytosol are degraded.

An enlarged organ.

Hydropic change or vacuolar degeneration.

Hypercalcemia.

They cause crosslinking and other changes, leading to degradation or loss of enzymatic activity.

Deposition of calcium salts in dead tissues with normal serum levels of calcium.

They are quickly shed and phagocytosed without eliciting an inflammatory response.

The cell is divided into small pieces called apoptotic bodies.

Absorption of radiant energy, such as ultraviolet (UV) light and x-rays.

Reversible changes in the number, size, phenotype, metabolic activity, and functions of cells in response to environmental changes.

DNA damage.

The buildup of substances within cells that can lead to cellular dysfunction.

A type of cell damage that leads to cell death and cannot be reversed.

It can lead to cellular dysfunction and disease.

They produce products that cause additional tissue injury.

Death.

Failure of energy generation in the form of ATP due to reduced oxygen supply or mitochondrial damage.

Mitochondrial respiration, inflammation, and exposure to environmental toxins.

Metabolic disorders and certain diseases.

Through intracellular sentinel proteins that transmit signals leading to p53 accumulation.

Apoptosis plays a crucial role in maintaining tissue homeostasis and eliminating damaged cells.

They may ultimately become calcified.

Glucose.

It can disrupt electrical activity and cause thermal damage.

Myocardial and cerebral ischemia.

It results in a lack of stimulation to the affected muscles or tissues.

A programmed cell death process that is a normal part of growth and development.

Foci of tuberculous infection.

Colored substances that can be either exogenous or endogenous.

They are recruited as part of the inflammatory reaction to provide digestive enzymes.

Functional and biochemical abnormalities of essential cellular components.

The increase in smooth muscle cells in the uterus during pregnancy.

Pallor, increased turgor, and an increase in organ weight.

It allows cells to adapt to stress and maintain function despite adverse conditions.

They may fail to fold properly, triggering the unfolded protein response.

Intracellular accumulations of proteins.

Gene mutations that lead to the production of proteins that cannot fold properly.

The membrane is altered and becomes highly 'edible' for phagocytes.

It is one of the most crucial events in the evolution of disease in any tissue or organ.

The lower leg that has lost its blood supply.

Cells and intracellular organelles become swollen due to water intake.

Diverse causes.

A form of cell death characterized by the uncontrolled breakdown of cell structures, often due to injury or disease.

Increased cell injury that occurs when blood flow is restored to ischemic but viable tissues.

Reactive Oxygen Species.

Pathogenesis and diseases.

Increased demand for secretory proteins, such as insulin, can lead to misfolding in insulin-resistant states.

Deposited immune complexes and fibrin that has leaked out of vessels.

Necrosis involves cell injury due to factors like ischemia, hypoxia, and chemical injury.

By phagocytosis.

Cellular contents including enzymes.

The transformation of tissue into a liquid viscous mass.

Swelling of the endoplasmic reticulum (ER).

There is an influx of Na and H2O.

Factors include temperature, pH, substrate concentration, and the presence of inhibitors or activators.

They are often converted into other types of free radicals, propagating the chain of damage.

Trauma, extremes of temperature, radiation, electric shock, and sudden changes in atmospheric pressure.

They can cause injury at therapeutic doses in susceptible individuals or excessive use.

Enzyme inhibition is the process by which a molecule decreases the activity of an enzyme.

Apoptotic cell death does not elicit an inflammatory reaction.

Lipids.

Anthracosis.

They can lead to cellular damage or death.

Disturbance of the Na/K pump leads to cellular dysfunction.

Anaerobic glycolysis.

Autophagy, resulting in more autophagic vacuoles.

Fatty liver.

A condition resulting from bacterial infection superimposed on coagulative necrosis.

Inflammation.

It occurs when blood supply returns to tissue after a period of ischemia, causing further damage.

They control the proper folding of newly synthesized proteins.

By causing cumulative damage to cellular structures over time.

Reversible injury.

Necrosis is uncontrolled and often results from injury, while apoptosis is a regulated and orderly process.

Necrosis.

They may block the formation of free radicals or scavenge them after they have formed.

Cells that have served their useful purpose.

A type of necrosis characterized by the deposition of fibrin-like protein in the tissue, often seen in immune-mediated vascular damage.

Cell shrinkage, chromatin condensation, and formation of apoptotic bodies.

An imbalance between free radicals and antioxidants in the body, leading to cell damage.

They can disrupt cellular functions and lead to cell damage or death.

Nuclear fragmentation and formation of apoptotic bodies.

Discontinuities in plasma and organelle membranes.

No, they are reversible changes.

Their enzymatic metabolism can increase free radical production, such as with carbon tetrachloride.

Oxygen deprivation.

Hyperplasia due to disturbed balance between estrogen and progesterone, often causing abnormal menstrual bleeding.

Cell injury.

Free radicals are produced by leukocytes during the inflammatory response.

Disruption of lysosomes occurs.

They are recruited to the site and digest dead cells using lysosomal enzymes.

Irreversible injury and necrosis.

It may significantly contribute to tissue damage, especially after myocardial and cerebral ischemia.

A type of tissue necrosis where the architecture of the tissue remains intact but the cells are dead.

From circulation or hydrolysis of intracellular glycogen.

It is often the culmination of reversible cell injury that cannot be corrected.

It mediates interaction with other proteins involved in cell death.

It is usually triggered by external factors such as toxins, infections, or trauma.

Necrosis that occurs in adipose tissue, often due to trauma or pancreatitis.

Cellular stress, DNA damage, or signals from other cells.

Clumping of chromatin.

They shift the balance in favor of pro-apoptotic Bak and Bax.

Swelling of the smooth ER and dissociation of ribosomes from the RER.

Duct obstruction.

It is required for oxidative phosphorylation and the generation of ATP.

Glycogen storage diseases.

It can cause DNA damage and disrupt cellular processes.

Hyperplasia can be physiologic or pathologic.

Diets rich in animal fat.

Immunologically mediated diseases, such as polyarteritis nodosa.

Atherosclerosis.

1 to 2 days.

By combining with a critical molecular component.

Regression of the lactating breast after weaning.

Hypertrophy, hyperplasia, atrophy, and metaplasia.

A form of irreversible cell injury leading to cell death characterized by cell swelling and inflammation.

Cell swelling, rupture of cell membranes, and inflammation.

Cell swelling, rupture of the cell membrane, and inflammation.

It is a condition where the ER cannot properly fold proteins, leading to cellular dysfunction.

Cytochrome c and other mitochondrial proteins escape into the cytosol.

Cardiac hypertrophy due to high blood pressure.

Squamous metaplasia in the respiratory tract due to smoking.

Certain viral infections, such as papillomaviruses, which cause skin warts.

It markedly increases the risk for type 2 diabetes mellitus.

An uncontrolled form of cell death that results from injury or disease, leading to inflammation.

Collections of phospholipids derived from damaged cellular membranes.

Cell death by apoptosis.

They can cause oxidative stress, leading to cell injury and death.

p53 triggers apoptosis, primarily through the mitochondrial pathway.

Oxidative stress, which can cause cell injury and death.

A programmed and controlled process of cell death that occurs as a normal part of growth and development.

A type of necrosis that involves the death of tissue due to loss of blood supply, often associated with bacterial infection.

Necrosis is uncontrolled and often harmful, while apoptosis is a regulated and beneficial process.

Type I TNF receptor and Fas (CD95).

It is converted to a toxic free radical.

Potentially harmful self-reactive lymphocytes.

The mitochondrial (intrinsic) pathway.

Lack of essential nutrients can impair cellular function and repair.

Cell swelling, nuclear changes, and cytoplasmic granularity.

A programmed cell death process that eliminates damaged or unnecessary cells.

It is preserved for several days despite the loss of details.

A form of cell death where cellular membranes fall apart, and enzymes leak out to digest the cell.

Necrosis is uncontrolled and often results from acute injury, while apoptosis is a controlled process that is part of normal cellular regulation.

It typically does not cause inflammation and is generally beneficial to surrounding tissues.

Cellular swelling.

A condition where cells are damaged due to various stressors or harmful agents.

A form of regulated cell death that shows features of both necrosis and apoptosis.

Diminished blood supply can lead to reduced oxygen and nutrients, causing atrophy.

Blebbing, blunting, or distortion of microvilli.

Reversible injury allows cells to recover, while irreversible injury leads to cell death.

A condition where there is a deficiency of oxygen in the tissues.

They maintain the integrity of mitochondrial membranes by holding pro-apoptotic members Bax and Bak.

Atrophy that occurs as a result of aging.

Fas molecules are crosslinked by FasL and bind adaptor proteins via the death domain.

Caspase-8.

A condition where the endoplasmic reticulum cannot properly fold proteins, leading to cell dysfunction.

It plays a crucial role in tissue homeostasis and the elimination of damaged cells.

A form of necrosis where the underlying tissue architecture is preserved for at least several days, although details are lost.

Deprivation of glucose and oxygen can contribute to the accumulation of misfolded proteins.

Alkaline phosphatase.

A form of cell death characterized by the uncontrolled breakdown of cell structures, often due to injury or disease.

Embryogenesis itself is a cause of physiologic apoptosis.

It catalyzes the decomposition of hydrogen peroxide (H2O2) into oxygen (O2) and water (H2O).

They are ubiquitinated and targeted for proteolysis.

20 to 30 minutes.

Autophagy is a cellular process that degrades and recycles cellular components, helping to maintain cellular homeostasis.

Reactive metabolites.

An increase in the size of cells, leading to an increase in the size of the organ.

Substances that can trigger an immune response, potentially leading to cell injury.

ER membranes of hepatocytes.

Decline in the synthesis of enzymes and plasma proteins.

Viral infected cells.

Mitochondrial swelling, endoplasmic reticulum dilation, and membrane blebbing.

They catalyze the breakdown of hydrogen peroxide (H2O2) into water (H2O).

Causes include developmental signals, DNA damage, oxidative stress, and cellular stress.

It often leads to inflammation and can damage surrounding tissues.

The liver and striated muscle.

DNA, proteins, and lipids.

Endometrial cell breakdown occurs.

Mitochondrial swelling and presence of phospholipid-rich amorphous densities.

Physiologic atrophy of the endometrium after menopause.

A programmed form of cell death that occurs in a controlled manner without causing inflammation.

Programmed cell death that occurs in a controlled manner.

Cell swelling, fatty change, and chromatin clumping.

Downstream caspases.

Alterations to the DNA structure that can lead to mutations and cell death.

A condition where there is a deficiency of oxygen in the tissues.

2 to 3 hours.

Hypoxia, toxins, infections, and physical trauma.

Vitamins E, A, C, and β-carotene.

Toxins can damage cellular structures and disrupt metabolic processes.

Severe hypoxia, toxins, infections, and physical trauma.

Cell shrinkage, chromatin condensation, and formation of apoptotic bodies.

A form of cell death resulting from acute cellular injury.

A decrease in the size of cells, leading to a reduction in the size of the organ.

The reversible replacement of one differentiated cell type with another.

Caspase-9.

By causing tissue damage through the release of inflammatory mediators.

They can cause physical stress and damage to cellular structures.

ATP reduction leads to impaired cellular functions and energy-dependent processes.

A reduction in blood flow to tissues, leading to a lack of oxygen and nutrients.

Tissues with greater glycolytic capacity, like the liver and striated muscle.

Bcl-2 family proteins.

Infectious agents can invade cells and cause damage or death.

A reduction in blood flow to a tissue, leading to a shortage of oxygen and nutrients.

Deprivation of growth factors, exposure to DNA-damaging agents, or accumulation of misfolded proteins.

Factors such as trauma, temperature extremes, and radiation.

By disrupting cellular functions and structures, leading to cell death.

By invading cells and disrupting normal cellular processes.

It helps in cellular maintenance and response to stress, preventing cell death.

Cellular lipids, proteins, and nucleic acids.

It is responsible for apoptosis in most physiologic and pathologic situations.

A form of necrosis characterized by the cheese-like appearance of tissue, often associated with tuberculosis.

They neutralize ROS and protect cells from oxidative damage.

Necrosis and apoptosis.

Chemical injury can occur through direct toxicity, reactive metabolites, or disruption of cellular processes.

Cell swelling, rupture, and inflammation.

Myelin figures.

Necrosis, apoptosis, and loss of membrane integrity.

The death receptor (extrinsic) pathway.

The tumor necrosis factor (TNF) receptor family.

It can be triggered by internal signals (like DNA damage) or external signals (like cytokines).

Reversible cell injury and irreversible cell injury.

Infection, toxins, and lack of blood flow.

Increases the production of chaperones and decreases protein translation.

On activated T lymphocytes.

It occurs when blood supply returns to the tissue after a period of ischemia, causing inflammation and oxidative damage.

Cell shrinkage, chromatin condensation, and formation of apoptotic bodies.

They can indicate underlying disease processes and help in diagnosis and treatment.

Genetic mutations can disrupt normal cellular processes and lead to dysfunction.

Apoptosis involves a series of biochemical events leading to cell shrinkage, chromatin condensation, and DNA fragmentation, often mediated by caspases.

Mercuric chloride poisoning.

A protective cellular response to the accumulation of unfolded or misfolded proteins.

Free radicals are formed through various processes, including metabolic reactions and exposure to toxins.

An increase in the number of cells in an organ or tissue.

A cellular process that degrades and recycles cellular components, often in response to stress.

It leads to a lack of oxygen, impairing cellular metabolism.

Aging can lead to decreased cellular function and increased susceptibility to injury.

Benign prostatic hyperplasia.

Infarcts (areas of ischemic necrosis) in all solid organs except the brain.

Accumulation of ROS over time is linked to aging and age-related diseases.

Free radicals cause oxidative stress, leading to cellular injury and death.

It deprives cells of essential nutrients needed for maintenance and growth.

The brain.

Detachment of ribosomes.

A large amount of misfolded protein accumulation.

Severe DNA damage from radiation or cytotoxic anticancer drugs.

Misfolded proteins.

Accumulation of lipids in hepatocytes and other cells.

Muscle atrophy due to disuse.