IC1

• Pathologenesis is the study of the structural and functional changes in cells, tissues, and organs that underlie disease.
• A successful cell needs energy, compartmentalization of organelles, control mechanisms, quality control systems, and repair processes to maintain homeostasis.
• Hypertrophy is an increase in size due to an abnormal stimulus, such as a dedicated workout.
• Cell death can be reversible or irreversible, and can be caused by physical, chemical, biological, genetic, or environmental factors.
• Atrophy is a decrease in size due to loss of required stimulus, resulting in smaller cells with smaller nuclei.
• Cells can be injured in several ways: physical, chemical, biological, genetic, and environmental.
• Hyperplasia is an increase in size due to physiological response to hormonal changes, resulting in small spindle-shaped smooth muscle cells and large plump cells.
• The cellular response to injurious stimuli depends on the type of injury, its duration, and its severity.
• Metaplasia is the replacement of one differentiated cell type by another cell type, often seen in the bronchus of cigarette smokers.
• Dysplasia is characterized by loss of orderly arrangement, large, distorted cells with large dark nuclei and are haphazardly arranged.
• Injury can be reversible or irreversible, and mild injury or stress causes reversible cell change, while severe injury or stress causes cell death.
• Homeostasis is the steady state where cells actively control the composition of their environment and intracellular milieu within a narrow range of physiological parameters.
• Cellular adaptation is the process by which cells can undergo adaptation to achieve a new steady state that would be compatible with their viability in the new environment.
• Cell injury, or cell damage, is a variety of changes of stress that a cell suffers from internal or external changes.
• Cell injury can be reversible or irreversible.
• Cell death occurs when the severity of the injury exceeds the cell’s ability to repair itself, this is referred to as “irreversible injury”.
• Adaptive responses enable the cells to cope with an increased workload.
• Some stresses are bad and the cells are damaged, some are so badly damaged that they die.
• Pathological conditions that trigger apoptosis include DNA damage, removal of cells with extensive improperly folded proteins, during infections, and the elimination of aberrant cells.
• The high-point in apoptosis is the activation of caspases (proteases) that break down the cell into fragments.
• Necrosis is always pathological
• Pigments in the liver tissue can be endogenous melanin, bilirubin, lipofuscin, or haemosiderin.
• Proteins can accumulate as misfolded or abnormal proteins in neurons of patients with Alzheimer disease or as aggregates of abnormal protein in some forms of Amyloidosis.
• Lipofuscin is a "wear and tear pigment" found in long-lived neurons, cardiac myocytes, and hepatocytes.
• Environmental particles such as carbon deposits from cigarette smoking and color pigments from tatooing can contribute to intracellular accumulations.
• Initiators of apoptosis can include binding of specific ligands, cell damage pathway, DNA damage/p53-p73 pathway, and cell membrane damage pathway.
• Although reversible, longstanding steatosis of the liver can progress to cirrhosis and liver failure.
• Apoptosis is the physiological and programmed elimination of unwanted cells, while necrosis is always pathological.
• Melanin is a pigment that can cause freckles in light-skinned children following sun exposure.
• Bilirubin is a pigment that deposits in tissues, resulting in the yellow discoloration of jaundice.
• Intracellular accumulations can lead to irreversible injury, often referred to as a "point of no return".
• Hemosiderin is an aggregate of denatured ferritin/iron complex where there is local or systemic excess of iron.
• Cholesterol and cholesterol esters can accumulate in smooth muscle cells and macrophages of arteries, leading to atherosclerosis and xanthomas.
• Apoptosis features include cell size reduction, chromatin condensation, cytoplasmic blebs and apoptotic bodies, and phagocytosis by macrophages.
• Fibroblasts from newborn can divide more times than fibroblasts from elderly.
• Possible mechanisms of aging include interference with replication, telomere shortening, accumulated damage, genetic and environmental insult, and DNA repair defects.
• Inflammation is the transition/overlap between injury and repair, and is the defense against microbial insult.
• Injurious agents can be physical, chemical, or biological, and can cause cell injury or cell death.
• Most infections can be eradicated with appropriate antibiotics, but non-infective inflammation can only be treated symptomatically with anti-inflammatory or immunosuppressive medications.
• Telomerase and Senescence are related to aging.