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Pathophysiology

Pathophysiology is a branch of study, at the intersection of pathology and physiology, concerning disordered physiological processes that cause, result from, or are otherwise associated with a disease or injury. Pathology is the medical discipline that describes conditions typically observed during a disease state, whereas physiology is the biological discipline that describes processes or mechanisms operating within an organism. Pathology describes the abnormal or undesired condition, whereas pathophysiology seeks to explain the functional changes that are occurring within an individual due to a disease or pathologic state.

Etymology
The term pathophysiology comes from the Ancient Greek πάθος (pathos) and φυσιολογία (phisiologia). ==History==
History
Early Developments The origins of pathophysiology as a distinct field date back to the late 18th century. The first known lectures on the subject were delivered by Professor at the University of Erfurt in 1790, and in 1791, he published the first textbook on pathophysiology, Grundriss der Physiologia pathologica, spanning 770 pages. Hecker also established the first academic journal in the field, Magazin für die pathologische Anatomie und Physiologie, in 1796. The French physician Jean François Fernel had earlier suggested in 1542 that a distinct branch of physiology should study the functions of diseased organisms, an idea further developed by in 1617, who first coined the term "pathologic physiology" in a medical text. In 1876, upon Ferdinand Cohn's report of a tiny spore stage of a bacterial species, the fellow German Robert Koch isolated Davaine's bacterides in pure culture—a pivotal step that would establish bacteriology as a distinct discipline—identified a spore stage, applied Jakob Henle's postulates, and confirmed Davaine's conclusion, a major feat for experimental pathology. Pasteur and colleagues followed up with ecological investigations confirming its role in the natural environment via spores in soil. Also, as to sepsis, Davaine had injected rabbits with a highly diluted, tiny amount of putrid blood, duplicated disease, and used the term ferment of putrefaction, but it was unclear whether this referred as did Pasteur's term ferment to a microorganism or, as it did for many others, to a chemical. In 1878, Koch published Aetiology of Traumatic Infective Diseases—unlike any previous work—in which, in 80 pages, Koch, as noted by a historian, "was able to show, in a manner practically conclusive, that a number of diseases, differing clinically, anatomically, and in aetiology, can be produced experimentally by the injection of putrid materials into animals." Scientific medicine The American physician William Henry Welch trained in German pathology from 1876 to 1878, including under Julius Cohnheim, and opened America's first scientific laboratory—a pathology laboratory—at Bellevue Hospital in New York City in 1878. Welch's course drew enrollment from students at other medical schools, which responded by opening their own pathology laboratories. Hopkins medical school, led by the "Four Horsemen"—Welch, William Osler, Howard A. Kelly, and William Stewart Halsted—opened in 1893 as America's first medical school devoted to teaching German scientific medicine. The laboratory of Rockefeller Institute's Oswald T. Avery, an early pneumococcal expert, was so troubled by the report that they refused to attempt repetition. During Avery's summer vacation, Martin Henry Dawson, a British-Canadian who believed everything from England was correct by default, repeated Griffith's results and achieved transformation in vitro, making it a more precise investigation. At the time of Griffith's report, it was unrecognized that bacteria even had genes. The first genetics, Mendelian genetics, began in 1900, yet inheritance of Mendelian traits was localized to chromosomes by 1903, thus chromosomal genetics. Biochemistry emerged in the same decade. In the 1940s, most scientists viewed the cell as a "sack of chemicals"—a membrane containing only loose molecules in Brownian motion—and the only especial cell structures as chromosomes, which bacteria lack as such. Yet the reality of organelles in cells was controversial amid unclear visualization with conventional light microscopy. At Cold Spring Harbor Laboratory in Long Island, New York, Max Delbrück and Salvador Luria led the Phage Group—hosting Watson—discovering details of cell physiology by tracking changes to bacteria upon infection with their viruses, the process transduction. Lederberg led the opening of a genetics department at Stanford University's medical school, and facilitated greater communication between biologists and medical departments. In the late 1970s, as president of Memorial Sloan–Kettering Cancer Center, Thomas collaborated with Lederberg, soon to become president of Rockefeller University, to redirect the funding focus of the US National Institutes of Health toward basic research into the mechanisms operating during disease processes, which at the time medical scientists were all but wholly ignorant of, as biologists had scarcely taken interest in disease mechanisms. ==Examples==
Examples
Parkinson's disease The pathophysiology of Parkinson's disease (PD) involves the apoptosis, or programmed cell death, of dopaminergic neurons as a consequence of alterations in biological activity within the brain related to the disorder. Several mechanisms have been proposed to explain neuronal apoptosis in PD; however, not all of these mechanisms are fully understood. The five primary mechanisms believed to contribute to neuronal death in PD include protein aggregation within Lewy bodies, disruption of autophagy processes, alterations in cellular metabolism and mitochondrial function, neuroinflammation, and breakdown of the blood-brain barrier, resulting in vascular compromise. Heart failure The pathophysiology of heart failure involves a reduction in the efficiency of the cardiac muscle through damage or overloading. As such, it can be caused by a wide number of conditions, including myocardial infarction (in which ischemia of the heart muscle leads to its death), hypertension (which increases the force of contraction needed to pump blood), and amyloidosis (in which misfolded proteins are deposited in the heart muscle, causing it to stiffen). Over time, these increase the workload of the heart, leading to changes in the heart muscle itself. Multiple sclerosis The pathophysiology of multiple sclerosis (MS) is that of an inflammatory demyelinating disease in which activated immune cells invade the central nervous system and cause neuroinflammation, neurodegeneration, and tissue damage. The underlying precipitators of MS are incompletely defined. Current research in neuropathology, neuroimmunology, neurobiology, neuroimaging, clinical neurology, and psychiatry provides support for the notion that MS is not a single disease but rather a spectrum. Hypertension The pathophysiology of hypertension is that of a chronic disease characterized by elevation of blood pressure. Hypertension can be classified by cause as either essential (also known as primary or idiopathic hypertension) or secondary. About 90–95% of hypertension is essential hypertension. HIV/AIDS The pathophysiology of HIV/AIDS involves the acquisition of HIV and the replication of the virus inside T helper cells, causing lysis. T helper cells are required for almost all adaptive immune system responses. There is typically an initial period of influenza-like illness following acquisition, and then a latent, asymptomatic phase. When the CD4 lymphocyte count falls below 200 cells/ml of blood, the HIV host has progressed to AIDS, a condition characterized by deficiency in cell-mediated immunity and resultant increase in susceptibility to opportunistic infections and some cancers. Spider bites The pathophysiology of spider bites involves the effect of injected venom. A spider envenomation occurs when a spider injects venom into the skin. Not all spider bites deliver venom—a dry bite—and the amount of venom injected can vary depending on the type of spider and the circumstances of the encounter. The mechanical injury from a spider bite is generally not a serious concern for humans. Obesity The pathophysiology of obesity involves many developmental and maintenance processes. Research on obesity, as well as clinical obesity medicine, and had been almost unapproached until the leptin gene was discovered in 1994 in Jeffrey M. Friedman's laboratory. The investigators hypothesized that leptin functions as a satiety factor. In the ob/ob mouse, mutations in the leptin gene led to the obese phenotype, suggesting potential for leptin-based therapies for human obesity. However, shortly after, Jose F. Caro's team failed to find any leptin gene mutations in humans with obesity. Instead, they observed increased leptin expression, indicating potential leptin resistance in human obesity. ==See also==
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