IC1

Cards (146)

  • 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.