Types of Necrosis Quiz

Cellular Adaptations and Injury - Lecture 1

• Each cell has a specific function dictated by its genetic makeup and associated machinery/metabolic pathways.
• Homeostasis is the concept of equilibrium within the external environment, maintaining a dynamically stable internal environment. Input is orchestrated with output.
• External disturbances (physiological or pathological) lead to changes in cell machinery, enabling adaptation to a new steady state.
• Adaptation responses aim to maintain cell viability and prevent injury.

Cellular Adaptations

• Adaptive responses are triggered by physiological or pathological stimuli.
• These responses aim to prevent cell injury.
• Adaptative responses include atrophy, hypertrophy, hyperplasia, metaplasia, and dysplasia.

Hypertrophy

• Hypertrophy is an increase in the size of cells, leading to an increase in the size of the organ.
• It's caused by increased functional demand or specific hormonal stimulation.
• Hypertrophy can be physiological (e.g., in athletes) or pathological (e.g., left ventricular hypertrophy in systemic hypertension).

Hyperplasia

• Hyperplasia is an increase in the number of cells in an organ or tissue leading to an increase in its size..
• Hyperplasia and hypertrophy are closely related and often occur together.
• Physiological hyperplasia can be driven by hormones or to compensate for tissue loss (e.g., the uterus during pregnancy, or following partial liver resection).
• Pathological hyperplasia can result from excessive hormonal stimulation (e.g., estrogen-induced endometrial hyperplasia) or growth factors (e.g., viral warts).

Atrophy

• Atrophy refers to a decrease in the size of cells, organs or tissue.
• It is an adaptive response.
• Causes of atrophy include: decreased workload (e.g., immobilization), denervation (e.g., in poliomyelitis), ischemia, undernutrition (e.g., starvation), or loss of endocrine stimulation (e.g., post-menopausal endometrial atrophy).

Metaplasia

• Metaplasia refers to the replacement of one mature cell type by another mature cell type.
• It's a reversible adaptive response.
• Examples include:
  • Squamous metaplasia of laryngeal & bronchial respiratory epithelium in heavy smokers.
  • Squamous metaplasia in urothelium of urinary bladder in bilharziasis
  • Columnar metaplasia can affect lower esophageal squamous epithelium in gastro-esophageal reflux disease.

Cellular Adaptations and Injury - Lecture 2

• Cell injury occurs when the limits of adaptive capacity are exceeded or no adaptive response is possible.

• Cell injury is classified as reversible or irreversible.

• Irreversible injury leads to cell death.

• Stages in the cellular response to stress and injurious stimuli include stress or increased demand, reversible responses from adaptation, and injury/inability to adapt leading to necrosis or apoptosis.

• Types of injurious agents include hypoxia / ischemia, physical agents (trauma), chemical agents (poisons), infectious agents, immunological reactions, genetic derangements, nutritional imbalances, and aging.

• Factors influencing severity of injury include type and severity of the injurious agent; duration of exposure; and type of affected cells.

• Examples of cell injury and necrosis include Ischemic injuries and hypoxic injuries

• In ischemia, the delivery of substrates for glycolysis is cut off due to impaired blood supply.

• The consequence of ischemia is typically more rapid and severe compared to hypoxia.

• Examples of cellular responses to hypoxia and ischemia involve: loss/decrease of ATP leading to paralysis in ion pumps; anaerobic glycolysis exhausting glycogen stores and producing lactic acid accumulation; and reduction to protein synthesis.

• Reversible cell injury occurs when injurious agents are mild or short-lived, leading to functional/morphological changes that are reversible.

• Irreversible cell injury occurs when an injury has progressed to severe damage of cellular membranes/nucleus, meaning the cell cannot recover and dies.

• Types of irreversible cell injury, which is cell death, include necrosis and apoptosis.

Necrosis

• Necrosis is a form of cell death characterized by morphological changes in a living tissue or organ.
• It results from a degraded action of enzymes within the irreversibly damaged cells with denaturation of proteins.
• Morphologic changes within necrosis include cytoplasmic changes (increased eosinophilia, loss of cytoplasmic RNA), more homogenous appearance (lost of glycogen particles), and vacuolated cytoplasm (from digested organelles).

Types of necrosis

• Coagulative necrosis: outlines of cells are still visible but structural details are lost (Sudden ischemia in organs leads to denaturation of structural proteins and enzymes, stopping proteolysis).
• Liquefactive necrosis: complete digestion of cells by enzymes (Common in ischemic destruction of brain tissue and bacterial infections like abscesses).
• Fat necrosis: involves adipose tissue and is mediated through lipases, which leads to calcium deposits and chalky white areas. (Common in acute pancreatitis).
• Caseous necrosis: a combination of coagulative and liquefactive necrosis, with a cheesy/yellow-white appearance (Common in tuberculosis).
• Gangrenous necrosis: a combination of coagulative necrosis (ischemia) and liquefactive necrosis (bacterial infection) (Common in lower limbs).

Cellular Adaptations and Injury - Lecture 3

• Subcellular responses to injury include autophagy, which is lysosomal digestion of cellular components as a survival mechanism during nutrient deprivation.

• Autophagy involves the cell "eating its own contents" in order to survive.

• Several pigment accumulations occur, including carbon (coal dust), that can lead to pneumoconiosis.

• Endogenous pigments include melanin and hemosiderin(caused by iron overload).

• Exogenous pigments (caused external exposure) include carbon, tattoos, etc.

• Apoptosis is a regulated cell death mechanism in which cells activate enzymes (caspases) to degrade their own nuclear DNA and other nuclear/cytoplasmic proteins. Apoptotic cells are typically round/oval, with intensely eosinophilic cytoplasm, chromatin condensation, fragmentation. Apoptotic bodies are quickly phagocytosed, avoiding inflammation.

• Several mechanisms cause DNA damage that triggers apoptosis and cellular function decline.

• Accumulation of misfolded proteins can occur due to problems with protein synthesis or folding control within the ER.

• Effects of misfolded proteins are generally adverse, including potential pathways for apoptosis, cellular damage, and neurodegenerative diseases like Parkinson’s.

• Accumulations may happen due to abnormal metabolism, mutations, or an inability to degrade phagocytosed particles.

• Lipid accumulations (fatty change): abnormal accumulation of TG within cells, in the liver (from toxins like alcohol, diabetes mellitus, obesity), or in the heart.

• Protein accumulations: Can be due to a variety of causes, in various tissues and cells, including plasma cells with excessive immunoglobulin accumulation (Russel bodies), neurofibrillary tangles in the brain (in Alzheimer's).

• Glycogen accumulations: in poorly regulated diabetes mellitus in various tissues, or in glycogen storage diseases.

• Pigments (colored substances): Normal constituents (melanin etc.) versus abnormal endogenous (like iron overload) or exogenous (like carbon) accumulations

• Calcification: can involve abnormal calcium deposition in tissues (dystrophic; like in necrosis) and also widespread systemic calcification (e.g., due to hypercalcemia), in various tissues.

Test your knowledge on the different types of necrosis and their characteristics. This quiz covers various forms of necrosis, including caseous, liquefactive, and fat necrosis, along with important terms related to cellular death. Challenge yourself with questions about patterns and descriptive terms associated with necrosis.