01 Cellular Responses to Stress and Toxic Insults UU (To Page 102)

They provide a nidus for the deposition of calcium salts and other minerals.

Dystrophic calcification.

The study of disease, focusing on structural, biochemical, and functional changes in cells, tissues, and organs.

Fatty change.

The process by which cells adjust to changes in their environment to maintain function.

For days or weeks.

The biochemical and molecular mechanisms of disease development.

Irreversible injury and cell death.

A round or oval mass of intensely eosinophilic cytoplasm with fragments of dense nuclear chromatin.

The basophilia of the chromatin fades and there is a loss of DNA due to enzymatic degradation by endonucleases.

A longer duration of injury increases the likelihood of irreversible injury and cell death.

Growth factor deprivation.

It triggers apoptosis.

BCL2, BCL-XL, and MCL1.

The pyknotic nucleus undergoes fragmentation.

The type, state, and adaptability of the injured cell.

It induces cleavage of DNA.

They are rapidly devoured by phagocytes before leaking contents, preventing inflammation.

No, it is caspase-independent programmed cell death.

They disappear due to enzymatic digestion and phagocytosis by leukocytes.

Cellular swelling.

The intrinsic (mitochondrial) pathway.

Apoptosis is triggered.

Caspases-8 and -10.

Phagocytosis of fragments.

The nature of the injury, its duration, and its severity.

Hypoxic injury, various forms of toxic or metabolic injury.

Molecular, microbiologic, immunologic, and morphologic techniques.

By examining tissue samples under a microscope to identify abnormalities.

Infectious, nutritional, chemical, and physical factors.

Plasma membrane alterations, mitochondrial changes, dilation of the ER, and nuclear alterations.

Calcium soap (saponification).

Generalized swelling of the cell and organelles, blebbing of the plasma membrane, detachment of ribosomes from the ER, and clumping of nuclear chromatin.

The two initiating pathways converge.

Cells may exhibit potentially reversible damage.

They degrade the cell's own nuclear DNA and nuclear and cytoplasmic proteins.

A firm texture due to denaturation of structural proteins and enzymes.

The signs and symptoms of diseases.

A special form of necrosis occurring in immune reactions involving blood vessels.

It cross-links TNFR1, triggering downstream events.

They act on many cellular components, including cleaving an inhibitor of a cytoplasmic DNase.

It remains intact but its structure is altered, making it a target for phagocytes.

Areas of white chalky deposits representing foci of fat necrosis.

The structural alterations in the cells and organs.

Induction of apoptosis.

Neurodegenerative diseases, ischemic injury (myocardial infarction and stroke), and death of virus-infected cells.

FasL binding to Fas.

Activation of multiple executioner caspases.

Caspase-9.

Formation of apoptotic bodies.

Genetic and acquired.

A minimally invasive procedure to obtain a sample of tissue or fluid.

A normal phenomenon to eliminate no longer needed cells and maintain a steady number of various cell populations.

BCL2 and BCL-XL.

By phagocytosis and digestion by lysosomal enzymes.

Foci of tuberculous infection.

A bright pink and amorphous appearance.

It arises from the effects of various external triggers on a genetically susceptible individual.

Cysteine proteases that cleave proteins after aspartic residues.

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

Fragments formed from the breakdown of apoptotic cells, making them edible for phagocytes.

Through fine needle aspiration, exfoliative cytology, or other sampling methods.

It flips from the inner leaflet to the outer layer of the membrane.

They maintain the integrity of mitochondrial membranes and prevent leakage of mitochondrial proteins.

Aspiration materials and exfoliative cytology (smear).

Karyolysis, Pyknosis, and Karyorrhexis.

A physiological event that removes unwanted, aged, or potentially harmful cells.

Adaptation, injury, and death.

During development and throughout adulthood.

Pyknosis.

Survival of abnormal cells, potentially resulting in cancer due to mutations in TP53 and defective DNA repair.

Survive and continue to function by establishing new but altered steady states.

It serves to remove unwanted and potentially harmful cells.

Destruction of cells during implantation, organogenesis, developmental involution, and metamorphosis.

BIM and other pro-apoptotic members of the BCL2 family.

Microbial products.

Pathology acts as a bridge between the basic sciences and clinical medicine.

It helps in diagnosing and treating diseases related to cell injury and death.

It cleaves a precursor form of IL-1 and releases its biologically active form.

The cell is no longer able to adapt.

It helps in diagnosing diseases and determining treatment options.

There is a time lag; changes may be seen in minutes to hours with histochemical techniques, and longer (hours to days) with light microscopy.

A sequence of events including exceeded adaptive responses, exposure to injurious agents or stress, and deprivation of essential nutrients.

Prof. Dr. Aptullah HAHOLU.

It binds to Fas on the same or neighboring lymphocytes to induce apoptosis.

Incapable of maintaining ionic and fluid homeostasis due to failure of energy-dependent ion pumps in the plasma membrane.

They are interconnected and their combined activation delivers a fatal blow to the cells.

Etiology; the cause of the disease.

Autoimmune diseases in humans and mice.

Elimination of damaged cells beyond repair.

Foreign antigens on the surface of infected host cells.

It does not elicit inflammation, making it more difficult to detect histologically.

A test used to screen for cervical cancer by examining cells from the cervix.

In the outer mitochondrial membranes, cytosol, and ER membranes.

It provides the basis for clinical care and therapy.

Biopsy specimens and surgical resections.

Cheese-like appearance.

Denaturation of intracellular proteins and enzymatic digestion of the lethally injured cell.

Apoptosis is caused by mutations and misfolded proteins.

Decreased generation of ATP, loss of cell membrane integrity, defects in protein synthesis, cytoskeletal damage, and DNA damage.

Friable white appearance.

There is no membrane integrity; contents often leak out, causing inflammation in the surrounding tissue.

The alterations and underlying mechanisms in organ-specific diseases.

It may progress through a reversible stage and culminate in cell death.

They become rapidly nonfunctional, although they may still be viable.

A pathway of cell death induced by a tightly regulated suicide program.

A type of tissue necrosis where the architecture of dead tissues is preserved for some days.

The process of maintaining a steady state within the cell.

A sample of cells used for diagnostic purposes.

Fragments that apoptotic cells break up into.

The study of tissue changes caused by disease.

Complexes of antigens and antibodies in the walls of arteries.

A form of programmed cell death accompanied by the release of fever-inducing cytokine IL-1.

It totally disappears within a day or two.

Nutritional and hormonal status, metabolic needs, and vulnerability.

Cytotoxic T lymphocytes.

It refers to 'falling off.'

Molecular or biochemical level changes.

Loss of immature lymphocytes in the bone marrow and thymus.

Increased permeability of the mitochondrial outer membrane.

Yes, it is a highly regulated and programmed process.

A narrow range of function and structure, including its state of metabolism, differentiation, and specialization.

Cross-linking of TNFR1 by TNF.

It helps prevent autoimmune diseases.

Plasma membrane disruption, cell death, and inflammation.

Reversible functional and structural responses to changes in physiologic states and some pathologic stimuli.

Inherited mutations and disease-associated gene variants or polymorphisms.

Failure to eliminate potentially harmful cells, leading to autoimmune disorders.

Perforin.

Cell death.

Ischemia caused by obstruction in a vessel.

It promotes the entry of granzymes into target cells.

Cellular swelling.

Hematoxylin and eosin (H&E) stains.

Tissues or organs removed during surgery for diagnostic or treatment purposes.

Induction of anti-apoptotic proteins such as BCL2 by survival signals.

In focal bacterial or fungal infections.

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

A flexible connective tissue found in various parts of the body.

By directly inducing the effector phase of apoptosis.

DNA damage.

Cellular injury or death.

Hepatocytes and myocardial cells.

A branch of pathology that studies and diagnoses diseases at the cellular level.

A type of tissue that covers body surfaces and lines cavities.

They keep the mitochondrial outer membrane impermeable and prevent leakage of cytochrome c and other death-inducing proteins into the cytosol.

Blebbing, blunting, and loss of microvilli.

A regulated mechanism of cell death.

A type of connective tissue that provides structural support.

BAX and BAK.

Swelling and the appearance of small amorphous densities.

To eliminate unwanted and irreparably damaged cells.

They provide critical information for diagnosis, treatment planning, and understanding disease progression.

Excessive intracellular levels of iron or reactive oxygen species.

Dilation of the ER and detachment of polysomes; intracytoplasmic myelin figures may be present.

A programmed cell death process that occurs in a regulated manner.

They undergo apoptosis.

Radiation or chemotherapeutic agents.

A balance between pro-apoptotic and anti-apoptotic proteins.

Caspases.

Pulmonary pathology.

The end result of progressive cell injury and a crucial event in the evolution of disease in any tissue or organ.

4 to 12 hours later.

By producing proteins that bind specifically to apoptotic cells.

Rupture of lysosomal and plasma membranes.

Large, whorled phospholipid masses from damaged cell membranes.

Gastrointestinal system pathology.

Macroscopic (Gross) examination.

Mutant huntingtin impairs autophagy.

Cellular damage that can be repaired.

Identical lesions may have distinct molecular mechanisms; different courses, therapeutic responses, and prognosis.

Many pathogens, like mycobacteria and Shigella spp., are degraded by autophagy.

Engagement of death receptors by ligands on adjacent cells.

Involution occurs, leading to cell breakdown, such as endometrial cell breakdown during the menstrual cycle.

For histopathological examination using Hematoxylin-Eosin staining.

The Intrinsic (Mitochondrial) Pathway.

An infarct.

Striated muscle cells in the leg are more resilient compared to striated muscle cells in the heart.

Damage to cell membranes, loss of ion homeostasis, and lysosomal enzymes digesting the cell.

Defective apoptosis leads to the survival of lymphocytes that can react against self antigens.

To prevent reactions against one’s own tissues.

Mitochondrial outer membrane permeability.

The liberation of enzymes.

Caspase-11.

IRE1 forms oligomers and is activated by phosphorylation.

Small clear vacuoles in the cytoplasm, which are distended and pinched-off segments of the ER.

The nucleus may break up, producing two or more fragments.

Necrosis takes more time than reversible damage.

It disrupts fluidity, lipid-protein interactions, ion and nutrient transport, and signaling pathways.

Through gross examination and microscopy.

Dysregulation of autophagy is involved in neurodegenerative disorders.

Proteins and DNA.

Loss of ATP, swelling of the cell and organelles, generation of ROS, release of lysosomal enzymes, and ultimately rupture of the plasma membrane.

Cytoplasm and tightly packed organelles, with or without nuclear fragments.

More than 20 members.

The mitochondrial pathway of apoptosis is induced, leading to cell death.

When repair mechanisms cannot cope with the injury, such as from radiation, cytotoxic anticancer drugs, and hypoxia.

They can be phagocytosed by other cells or degraded into fatty acids.

Diseases of the skin.

Excessive accumulation in the endoplasmic reticulum (ER) leads to ER stress and apoptotic cell death.

On T cells.

Diseases of the nervous system.

Mutations that lead to neoplastic transformation.

Hypoxia is oxygen deprivation that reduces aerobic oxidative respiration.

Irreversible damage leading to the loss of cell function.

The functional consequences of the changes caused by the disease.

An 'accidental' and unregulated form of cell death characterized by damage to cell membranes and loss of ion homeostasis.

The examination of cells to identify abnormalities and diseases.

The common reactions of cells and tissues to injurious stimuli.

A variety of cellular caspases.

It is difficult to appreciate with the light microscope but may be more apparent at the organ level.

The cell is smaller in size, and the cytoplasm is dense.

Sensors in the ER membrane, such as the kinase IRE1.

Pallor, increased turgor, and increase in weight of the organ.

Cancer, infections, and inflammatory diseases.

To support, bind together, and protect tissues and organs.

A distinctive inflammatory border.

The end results of genetic, biochemical, and structural changes in cells and tissues.

A more glassy homogeneous appearance.

They are fixed, sectioned, and stained for microscopic examination.

BAD, BIM, BID, Puma, and Noxa.

As liquefactive necrosis.

An increase in the number of cells.

It accumulates in cells and arrests the cell cycle at the G1 phase.

Specimen reception and registration.

Accelerated neurodegeneration occurs due to impaired autophagy.

Numerous receptors on phagocytes and ligands on apoptotic cells that facilitate binding and engulfment.

Leakage of cytochrome c and other proteins, leading to caspase activation and apoptosis.

It is a highly regulated process driven by a series of genetic pathways.

It does not denote a specific pattern of necrosis.

The mitochondrial pathway and the death receptor pathway.

Programmed necrosis.

No, it is uncontrolled and accidental.

Inositol requiring enzyme-1.

Loss of nuclei, fragmentation of cells, and leakage of contents.

Discontinuities in membranes, dilation of mitochondria, and aggregates of denatured protein.

Deposition of calcium at sites of cell death.

By degrading structural components of the nuclear matrix.

It is the digestion of dead cells and the transformation of tissue into a liquid viscous mass.

In the mesentery.

Incisional biopsy.

Inactive forms of enzymes that undergo cleavage to become active.

In all organs except the brain.

The cell can repair the derangements and return to normalcy.

Structureless collection of fragmented or lysed cells and amorphous granular debris.

The initiation phase and the execution phase.

They recruit phagocytes to the site of cell death.

Unchecked membrane lipid peroxidation.

Hematoxylin-Eosin staining.

It may take hours to develop.

The BCL2 family of proteins.

Severe mitochondrial damage with depletion of ATP.

TP53.

The apoptotic cell shows extensive surface blebbing and fragments into membrane-bound apoptotic bodies.

They analyze the specimens to provide diagnoses and inform treatment decisions.

It protects the cell from the harmful consequences of misfolded proteins.

Increased eosinophilic staining.

Adaptation, injury, and death.

It is a normal and essential process.

Molecular or structural alterations in cells.

Pro-apoptotic, anti-apoptotic, and those with BCL2 homology (BH) domains.

An adaptive cellular response triggered by nutrient deprivation.

Plasma membranes are thought to remain intact until the last stages of apoptosis.

Deprivation of glucose and oxygen, and stress such as heat.

Molecular analysis and next generation sequencing.

It increases susceptibility to tuberculosis.

Reversible cell injury can restore normal function, while cell death is irreversible.

It acts as a critical 'life or death' switch.

Severe injury, lack of blood flow, or toxins.

A death-inducing signaling complex (DISC) from adaptor proteins.

Induces leukocyte recruitment and fever.

They influence the responses of different individuals to various injurious agents.

Ischemia, exposure to toxins, various infections, and trauma.

It results in the least possible host reaction.

Cardiovascular system pathology.

They form a channel in the outer mitochondrial membrane, allowing leakage of cytochrome c.

Pus.

An increase in the size of cells and functional activity.

An adhesive glycoprotein that coats some apoptotic bodies, recognized by phagocytes.

Formation of a granuloma.

Apoptosis involves rapid removal of cellular debris without leakage of cellular contents and no inflammatory reaction.

It usually does not cause inflammation and is a clean process.

Diseases related to blood and bone marrow.

Ischemia (reduced blood flow), infection, and toxins.

It eliminates cells that are injured beyond repair without eliciting a host reaction, limiting collateral tissue damage.

They are very important in the study of disease.

The cell cannot recover and dies.

They are rapidly ingested by phagocytes and degraded by lysosomal enzymes.

Alzheimer's, Huntington's, Parkinson's diseases, and type 2 diabetes.

Loss of mitochondrial cristae and ruptured outer mitochondrial membrane.

The sequence of cellular, biochemical, and molecular events from the initial cause to the manifestation of the disease.

The cell can recover to its original state without any harmful consequences.

Cancer, neurodegenerative diseases, and stroke.

A type of cell injury that can be repaired if the stressor is removed.

It now includes molecular biologic and proteomic approaches for analyzing disease states.

It provides foundational knowledge about disease processes.

Reversible injury, irreversible injury, and cell death.

Receptor associated kinase 1 and 3 (RIP1 and RIP3).

Cellular signals, such as DNA damage or developmental cues.

Activation of caspases leading to apoptosis.

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

Endoplasmic reticulum stress.

Engagement of plasma membrane death receptors on various cells.

In a matter of minutes.

Loss of survival signals, DNA damage, and other insults.

A form of cell death characterized by nuclear dissolution and fragmentation of the cell without complete loss of membrane integrity.

Swelling of cells, loss of plasma membrane integrity, and release of inflammatory mediators.

An adaptive unfolded protein response.

A form of cell death that shares aspects of both necrosis and apoptosis.

The mitochondrial pathway and the death receptor pathway.

4 to 12 hours after the onset of ischemia.

BAX and BAK.

They may be characteristic of a disease or diagnostic of an etiologic process.

An overview of the fundamental concepts in pathology.

Genetic mutations, aging, or unknown environmental factors.

By reducing iron levels.

They appear healthy and intact.

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

It refers to the situation where irreparably damaged cells die due to excessive misfolded proteins.

Surface blebs, increased eosinophilia of cytoplasm, and swelling of occasional cells.

The generation of calcium soaps.

They regulate mitochondrial permeability and influence the balance between pro-apoptotic and anti-apoptotic proteins.

The defective gene, the gene product, the biochemical events, and the morphologic events.

They are liquefied by pancreatic enzymes.

It may be induced by the virus itself or by the host immune response, such as in adenovirus, HIV infections, or viral hepatitis.

Autophagy is implicated in the pathology of inflammatory bowel diseases.

A limb, generally the lower leg, that has lost its blood supply.

To enhance the visibility of tissue structures.

Necroptosis, Pyroptosis, and Ferroptosis.

It undergoes necrosis involving multiple tissue planes.

Traumatic fat necrosis.

Through injurious reactions to endogenous self antigens, such as in autoimmune diseases.

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

Enzymes from the lysosomes of dying cells and from leukocytes.

Death-inducing molecules such as cytochrome c.

Mitochondria, cell membranes, protein synthesis machinery, and DNA.

Structural alterations in cells or tissues.

Dysregulation of autophagy can contribute to cancer development.

They die due to deprivation of survival signals, such as growth factors.

For histopathological examination.

Clinical manifestations (symptoms and signs) of disease.

The cell activates caspases and induces apoptosis, a process known as ER stress.

Loss of plasma membrane permeability, resembling necrosis.

A decrease in the size and metabolic activity of cells.

Mitochondrial (intrinsic) pathway and Death receptor (extrinsic) pathway.

Genetically programmed signal transduction events that culminate in cell death.

Fas ligand (FasL).

Leakage of pro-apoptotic proteins from the mitochondrial membrane into the cytoplasm.

They fail to undergo p53-mediated apoptosis and may survive with damaged DNA.

Necroptosis, Pyroptosis, and Ferroptosis.

The irreversible loss of cellular function and structure.

In degenerative diseases of the central nervous system and other organs.

The clinical course and outcome.

Processes that lead to cellular damage and dysfunction.

Ligation of the receptor TNFR1 by its ligand.

Reduced blood flow, inadequate oxygenation due to cardiorespiratory failure, decreased oxygen-carrying capacity (anemia, carbon monoxide poisoning), and severe blood loss.

Characteristic morphologic and functional changes.

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

Cellular function can return to normal after the removal of the stressor.

BAX and BAK.

Reporting.

Abnormal deposition of calcium salts in tissues.

Build-up of substances within cells due to metabolic disturbances.

Through mechanisms such as hypertrophy, hyperplasia, atrophy, and metaplasia.

The gradual decline in cellular function and viability over time.

They sense damage and are activated in response to stress.

Chromatin condenses and aggregates peripherally under the nuclear membrane into dense masses.

Cancer, inflammatory diseases, and other pathological conditions.

Early stages or mild forms of injury, including reduced oxidative phosphorylation and cellular swelling.

Disaggregation of granular and fibrillar elements.

It allows for early detection and treatment of diseases at the cellular level.

They accumulate and trigger the unfolded protein response.

They antagonize the anti-apoptotic proteins.

Hydropic change or vacuolar degeneration.

The cytoplasm becomes vacuolated.

The study of disease and its effects on the body.

They act as sensors of cellular stress and damage, regulating the balance between anti-apoptotic and pro-apoptotic proteins.

A method of obtaining cell samples via smear for cytopathology.

As early as 2 hours after necrosis.

Cell swelling, rupture, and inflammation.

To determine the nature of disease.

A change in the phenotype of cells.

Oxygen deprivation, physical agents, chemical agents and drugs, infectious agents, immunologic reactions, genetic abnormalities, and nutritional imbalances.

To collect tissue for further analysis.

They appear as a result of functional abnormalities.

A type of cell injury that can recover and restore normal function.

Formaldehyde, water, alcohol, xylene, paraffin.

To eliminate self-reactive lymphocytes.

The formation of cysts and fibrosis in the lungs, pancreas, and other organs.

They split the triglyceride esters.

Reversible injury can be repaired, while necrosis is irreversible.

Grossly visible chalky-white areas, known as fat saponification.

In both physiologic and pathologic conditions, such as during mammalian bone growth plate formation and in diseases like steatohepatitis and Parkinson's disease.

Foci of shadowy outlines of necrotic fat cells with basophilic calcium deposits and surrounding inflammatory reaction.

The abnormal deposition of calcium salts in tissues.

The loss of cytoplasmic RNA and denatured cytoplasmic proteins.

Persistent or excessive injury, leading to a 'point of no return.'

Adaptation, reversible injury, irreversible injury, and cell death.

TNF receptor family.

It often causes inflammation and damage to surrounding tissues.

Nervous tissue.

Changes in ion concentrations and water influx.

They contain a cytoplasmic domain involved in protein-protein interactions called the death domain.

It can lead to certain B cell lymphomas due to chromosomal translocations.

To facilitate movement of the body and its parts.

Alterations in intracellular organelles like mitochondria and the cytoskeleton.

A regulated form of necrosis that is also considered a type of programmed cell death.

Type 1 TNF receptor (TNFR1) and Fas (CD95).

It may progress to irreversibility.

Apoptosis.

Necrosis and Apoptosis.

Natural antibodies and complement system proteins, notably C1q.

Necrosis and apoptosis.

Adaptation, injury, and death.

Release of activated pancreatic lipases during acute pancreatitis.

Metabolic derangements in cells leading to accumulations of proteins, lipids, and carbohydrates.

A process where cells degrade and recycle components.

The unfolded protein response.

To cut thin sections of tissue for examination.

Virus-infected and tumor cells.

To develop new therapeutic approaches.

The distal death effector machinery, including caspases.

Coagulative necrosis.

Overview of cellular responses to stress and noxious stimuli.

It can occur in tumors and during cellular rejection of transplants.

The gradual decline in cellular function and viability over time.

To eliminate the initial cause of cell injury and initiate healing.

Cells adapt, become injured, or die in response to stress and toxic insults.

To understand how cells react to harmful stimuli and stress.

It shows increased eosinophilia.

Necrosis and Apoptosis.

They can cause inflammation and damage to tissues.

Microscopic examination.

It can lead to deficiencies or excesses that disrupt normal cellular functions.

Viruses, rickettsiae, bacteria, fungi, and parasites.

Apoptosis or necrosis.

Includes mitochondrial damage, membrane damage, damage to DNA, oxidative stress, disturbance in calcium homeostasis, and endoplasmic reticulum stress.

Accumulation of oxygen-derived free radicals.

The process of gradual deterioration of cellular function over time.

Damaged DNA and misfolded proteins induce ER stress.

Autophagy.

By cannibalizing itself and recycling the digested contents.

A multimeric structure called the apoptosome.

Inflammatory cells.

It leads to the leakage of substances from mitochondria that activate caspases.

Various factors that lead to cellular damage and dysfunction.

Relationships between clinical findings and pathological changes.

The process by which cells adjust to changes in their environment.

Changes in cell size, number, or type in response to stimuli.

The exposure of cells or tissues to an injurious agent.

Build-up of substances within cells due to various factors.

Reversible cell injury and cell death.

The gradual decline in cellular function and viability over time.

Abnormal deposition of calcium salts in tissues.

Protein-calorie deficiencies, specific vitamin deficiencies, self-imposed deficiencies (anorexia nervosa), and nutritional excesses (cholesterol leading to atherosclerosis, obesity with diabetes and cancer).

Chaperone-mediated autophagy, microautophagy, and macroautophagy.

Coagulative necrosis.

Oxygen deprivation, toxic substances, and genetic factors.

They induce apoptosis specific for viral proteins.

Hypoxia, chemical exposure, and infectious agents.

Specific examples of cell injury and death in clinical settings.

Severe damage that results in cell death.

Bacterial infection, leading to more liquefactive necrosis.

An extra chromosome, single base pair substitutions, deficiency of functional proteins, and accumulation of damaged DNA or misfolded proteins.

Understanding how cells adapt, become injured, or die under stress.

Build-up of substances within cells due to various stresses.

Caspase-9 (the initiator caspase).

They show preserved cellular outlines with loss of nuclei.

After duct obstruction in parenchymal organs such as the pancreas, parotid gland, and kidney.

Simple chemicals (glucose, salt, oxygen), poisons (arsenic, cyanide, mercuric salts), environmental pollutants, insecticides, herbicides, recreational drugs, and therapeutic drugs.

A process by which cells degrade and recycle components.

Build-up of substances within cells that can lead to injury.

It helps in diagnosing and treating various diseases.

The ability of cells to adjust to stressors.

BAX and BAK.

APAF-1 (apoptosis-activating factor-1).

A cascade of caspase activation by cleaving other pro-caspases.

Changes in cell size, number, or type in response to stress.

The abnormal deposition of calcium salts in tissues.

The gradual decline in cellular function and viability over time.

Abnormal deposition of calcium salts in tissues.

A process in which a cell eats its own contents.

Inward invagination of lysosomal membrane for delivery.

Proteins from the inner mitochondrial membrane, including cytochrome c.

Adaptation, injury, and death.

Atgs.

A surgical procedure where a portion of a lesion is removed for diagnostic purposes.

Changes in cell structure or function in response to stress.

Gangrenous necrosis with superimposed bacterial infection causing liquefactive necrosis.

Disturbance in calcium homeostasis can lead to cell injury.

Growth factors and other survival signals.

Selected examples of cell injury and death.

Abnormal deposition of calcium salts in tissues.

Aging and exercise.

It indicates coagulative necrosis in the kidney.

Direct translocation across the lysosomal membrane by chaperone proteins.

The gradual deterioration of cellular function over time.

Formation of an isolation membrane from the ER, elongation of the vesicle, maturation of the autophagosome, and fusion with lysosomes.

A technique that uses a circular blade to remove a small core of tissue for examination.

Normal kidney cells and necrotic cells showing preserved outlines but loss of nuclei.

The execution phase of apoptosis.

The study of diseases and their effects on the body.