LOM Cell Death & Cell injury Flashcards
What is the concept of a ‘steady state’ in cell physiology?
The normal cell maintains a “steady state,” which allows it to cope with normal physiological demands. It involves intact genome, metabolic pathways, membranes, and adequate supply of substrates and oxygen.
What are the causes and mechanisms of cellular injury?
: Cellular injury can result from various factors including hypoxia/anoxia, physical agents (trauma, radiation), drugs/chemicals, immunological reactions, infections, congenital defects, and metabolic errors.
Describe reversible and irreversible cell injury.
Reversible cell injury occurs when the stress on cells is mild and can be relieved. Irreversible cell injury results from severe and persistent stress, leading to cell death via necrosis or apoptosis.
What are the causes of fatty change of the liver?
Fatty change of the liver can result from conditions such as alcoholism, protein-calorie malnutrition, starvation, obesity, diabetes mellitus, hepatotoxins, drugs, inborn errors of metabolism, and hypoxia/anoxia.
Define the terms hypertrophy, hyperplasia, metaplasia, atrophy, and fatty change.
Hypertrophy: Increase in size of cells.
Hyperplasia: Increase in number of cells.
Metaplasia: Reversible change where one adult cell type changes to another adult cell type.
Atrophy: Acquired diminution in size of organ or tissue due to decrease in size and number of cells.
Fatty change: Abnormal accumulation of fat (triglycerides) within parenchymal cells.
What is necrosis and how is it recognized?
Necrosis is the death of cells in the living organism due to denaturation of cellular proteins and enzymatic digestion of the cell. It is recognized by cytoplasmic changes including swelling, increased eosinophilia, loss of RNA, and nuclear changes including pyknosis, karyorrhexis, and karyolysis.
Words to Define:
lipoid degeneration
Hyalinisation
Necrosis
Gangrene
Apoptosis
Necroptosis
Pyroptosis
Autophagy
Pyknosis
Karyorrhexis
Karyolysis
Lipoid degeneration: Intracellular accumulations of cholesterol and cholesterol esters in histiocytes.
Hyalinisation: Any alteration within cells or in the extracellular space, resulting in a translucent, homogenous, structureless, glassy pink appearance in routine H&E stain.
Necrosis: Death of cells in the living organism due to denaturation of cellular proteins and enzymatic digestion of the cell.
Gangrene: Necrosis with putrefaction of a number of tissues in a body part in a living organism, i.e., digestion of dead tissue by bacterial action.
Apoptosis: A form of programmed cell death involving protein synthesis and energy-dependent fragmentation of DNA by endogenous endonucleases.
Necroptosis: Cell death that shares aspects of necrosis and apoptosis, morphologically resembling necrosis but mechanistically resembling apoptosis and triggered by genetically programmed signal transduction.
Pyroptosis: Another form of programmed cell death characterized by fever due to IL-1 release.
Autophagy: Cell eats its own contents, seen in aging and exercise, and plays a role in cancer, neurodegenerative disorders, and infectious diseases.
Pyknosis: Small, dense, wrinkled mass of tightly packed chromatin in the nucleus.
Karyorrhexis: Fragmentation of chromatin material.
Karyolysis: Progressive dissolution of the nucleus by DNAases.
What are the morphological changes observed in necrosis?
Morphological changes in necrosis include cytoplasmic swelling, increased eosinophilia, loss of RNA, increased binding of eosin to denatured proteins, loss of glycogen, loss of striations, and nuclear changes such as pyknosis, karyorrhexis, and karyolysis.
What are the primary causes of necrosis?
Primary causes of necrosis include ischemia, toxins, infections, hypersensitivity reactions, chemical poisons, and physical factors like heat, freezing, and irradiation.
Describe the types of necrosis and provide examples of where they occur in the body.
Types of necrosis include coagulative necrosis (e.g., infarct), liquefactive necrosis (e.g., brain infarct), caseous necrosis (e.g., tuberculosis), and fat necrosis (e.g., acute pancreatitis).
What is gangrene, and how is it classified?
Gangrene is necrosis with putrefaction of tissues in a body part due to bacterial action. It is classified as primary (infective) gangrene caused by bacterial infection and secondary (ischaemic) gangrene caused by other factors like vascular diseases, trauma, frostbite, chemicals, and mechanical or vascular issues.
Explain apoptosis and its significance in physiological and pathological contexts.
Apoptosis is programmed cell death involving protein synthesis and energy-dependent fragmentation of DNA. It plays roles in embryogenesis, hormone-dependent involution, cell deletion in proliferating tissues, as well as in pathological conditions such as neoplasia, autoimmune diseases, AIDS, and neurodegenerative disorders.
How do necrosis and apoptosis differ, both morphologically and mechanistically?
Necrosis affects many cells, leading to cellular swelling and disorganized nuclear changes, while apoptosis affects single cells, resulting in shrinkage, chromatin condensation, and the formation of apoptotic bodies. Necrosis is always pathological, while apoptosis can be both physiological and pathological.
Autolysis
Heterolysis
Coagulative necrosis
Liquefactive necrosis
Caseous necrosis
Fat necrosis
Primary gangrene
Secondary gangrene
Apoptosis
Apoptotic bodies
Autolysis: Cellular enzymatic degradation by catalytic enzymes derived from lysosomes of dead cells.
Heterolysis: Catalytic enzymes derived from immigrant leucocytes and other living cells, e.g., macrophages.
Coagulative necrosis: The commonest form of necrosis characterized by ghost outlines, preservation of basic cell shape, loss of the nucleus, acidophilic opaque cytoplasm, and caused by protein denaturation without proteolysis of the cell.
Liquefactive necrosis: Necrosis characterized by liquefaction of tissues due to hydrolytic enzymes, i.e., autolysis or heterolysis, typical of ischaemic destruction of the brain and bacterial infections.
Caseous necrosis: A combination of coagulative and liquefactive necrosis, presenting as fragmented coagulated cells surrounded by a granulomatous reaction, resulting in soft, friable, white-grey debris, resembling cheese, typically seen in tuberculosis.
Fat necrosis: Necrosis caused by enzymatic or traumatic factors, leading to the extracellular liberation of fat, often associated with conditions such as acute pancreatitis.
Primary gangrene: Necrosis due to infection with pathogenic bacteria which kill tissue (exotoxins) and then invade and digest dead tissue.
Secondary gangrene: Necrosis due to another cause such as ischaemia or trauma, followed by digestion of dead tissue by saprophytic bacteria incapable of invading living tissue.
Apoptosis: Programmed cell death involving protein synthesis, energy-dependent fragmentation of DNA by endogenous endonucleases, and individual cell deletion of unwanted or defective cells induced by physiological or pathological stimuli.
Apoptotic bodies: Structures resulting from apoptosis, characterized by nuclear condensation and fragmentation, leading to the orderly formation of apoptotic bodies from single cells.
