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.