Editing Pathophysiology (section)

==Examples==

===Parkinson's disease===

The [[pathophysiology of Parkinson's disease]] is [[apoptosis|death]] of [[dopamine|dopaminergic]] [[neuron]]s as a result of changes in biological activity in the brain with respect to [[Parkinson's disease]] (PD). There are several proposed mechanisms for [[neuron]]al [[apoptosis|death]] in PD; however, not all of them are well understood. Five proposed major mechanisms for neuronal death in Parkinson's Disease include protein aggregation in [[Lewy Body|Lewy bodies]], disruption of [[autophagy]], changes in cell metabolism or [[mitochondria]]l function, [[neuroinflammation]], and [[blood–brain barrier]] (BBB) breakdown resulting in vascular leakiness.<ref>{{cite journal | author = Tansey M. G., Goldberg M. S. | year = 2010 | title = Neuroinflammation in Parkinson's disease: Its role in neuronal death and implications for therapeutic intervention | journal = Neurobiology of Disease | volume = 37 | issue = 3| pages = 510–518 | doi = 10.1016/j.nbd.2009.11.004 | pmc = 2823829 | pmid=19913097}}</ref>

===Heart failure===

The [[pathophysiology of heart failure]] is a reduction in the efficiency of the heart muscle, through damage or overloading. As such, it can be caused by a wide number of conditions, including myocardial infarction (in which the heart muscle is [[ischemia|starved of oxygen]] and dies), 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 increases in workload will produce changes to the heart itself.

===Multiple sclerosis===

The [[pathophysiology of multiple sclerosis]] is that of an [[inflammatory demyelinating diseases of the CNS|inflammatory demyelinating disease of the CNS]] in which activated immune cells invade the central nervous system and cause inflammation, neurodegeneration and tissue damage. The underlying condition that produces this behaviour is currently unknown. Current research in neuropathology, neuroimmunology, neurobiology, and neuroimaging, together with clinical neurology provide support for the notion that MS is not a single disease but rather a spectrum<ref>{{Cite journal |doi= 10.1097/WCO.0000000000000324 |pmid= 27070218 |title= Shifting paradigms in multiple sclerosis |journal= Current Opinion in Neurology |volume= 29 |issue= 3 |pages= 354–361 |year= 2016 |last1= Golan |first1= Daniel |last2= Staun-Ram |first2= Elsebeth |last3= Miller |first3= Ariel|s2cid= 20562972 }}</ref>

===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 hypertension|essential]] (also known as primary or [[idiopathy|idiopathic]]) or [[secondary hypertension|secondary]]. About 90–95% of hypertension is essential hypertension.<ref name="pmid10645931">{{cite journal |vauthors=Carretero OA, Oparil S |title=Essential hypertension. Part I: definition and etiology |journal=[[Circulation (journal)|Circulation]] |volume=101 |issue=3 |pages=329–35 |date=January 2000 |pmid=10645931 |doi=10.1161/01.CIR.101.3.329|doi-access=free }}</ref><ref name="pmid14597461">{{cite journal |vauthors=Oparil S, Zaman MA, Calhoun DA |title=Pathogenesis of hypertension |journal=[[Ann. Intern. Med.]] |volume=139 |issue=9 |pages=761–76 |date=November 2003 |pmid=14597461 |doi=10.7326/0003-4819-139-9-200311040-00011|s2cid=32785528 }}</ref><ref name="isbn0-7216-0240-1">{{cite book |author1=Hall, John E. |author2=Guyton, Arthur C. |title=Textbook of medical physiology |url=https://archive.org/details/textbookmedicalp00acgu |url-access=limited |publisher=Elsevier Saunders |location=St. Louis, Mo |year=2006 |page=[https://archive.org/details/textbookmedicalp00acgu/page/n262 228] |isbn=0-7216-0240-1 }}</ref><ref name="urlHypertension: eMedicine Nephrology">{{cite web |url=http://emedicine.medscape.com/article/241381-overview |title=Hypertension: eMedicine Nephrology |access-date=2009-06-05 }}</ref>

===HIV/AIDS===

The [[pathophysiology of HIV/AIDS]] involves, upon acquisition of the virus, that the virus replicates inside and kills [[T helper cells]], which are required for almost all [[adaptive immune system|adaptive immune responses]]. There is an initial period of [[influenza-like illness]], 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,<ref>{{cite journal | pmid = 26962940 | doi=10.1016/j.chom.2016.02.012 | pmc=4835240 | volume=19 | title=Dissecting How CD4 T Cells Are Lost During HIV Infection | journal=Cell Host Microbe | pages=280–91 | last1 = Doitsh | first1 = G | last2 = Greene | first2 = WC | year=2016| issue=3 }}</ref> a condition characterized by deficiency in [[cell-mediated immunity]] and the resulting increased susceptibility to [[opportunistic infections]] and certain forms of [[cancer]].

===Spider bites===

The [[pathophysiology of spider bites]] is due to the effect of its [[venom]]. A spider envenomation occurs whenever a spider injects [[venom]] into the skin. Not all spider bites inject venom – a dry bite, and the amount of venom injected can vary based on the type of spider and the circumstances of the encounter. The mechanical injury from a spider bite is not a serious concern for humans.

===Obesity===

The [[pathophysiology of obesity]] involves many possible pathophysiological mechanisms involved in its development and maintenance.<ref name="flier">{{cite journal | author = Flier JS | title = Obesity wars: Molecular progress confronts an expanding epidemic | journal = Cell | volume = 116 | issue = 2 | pages = 337–50 | year = 2004 | pmid = 14744442 | doi = 10.1016/S0092-8674(03)01081-X | type = Review | doi-access = free }}</ref><ref name="murri">{{cite journal
 |last1=Rodriguez-Muñoz
 |first1=A.
 |last2=Motahari-Rad
 |first2=H.
 |last3=Martin-Chaves
 |first3=L.
 |last4=Benitez-Porres
 |first4=J.
 |last5=Rodriguez-Capitan
 |first5=J.
 |last6=Gonzalez-Jimenez
 |first6=A.
 |last7=Insenser
 |first7=M.
 |last8=Tinahones
 |first8=F.J.
 |last9=Murri
 |first9=M.
 |title=A Systematic Review of Proteomics in Obesity: Unpacking the Molecular Puzzle
 |journal=Current Obesity Reports
 |date=2024
 |volume=13
 |issue=3
 |pages=403–438
 |pmid = 38703299
 |doi=10.1007/s13679-024-00561-4
 |doi-access=free
 |pmc=11306592
 }}</ref>

This field of research had been almost unapproached until the [[leptin]] gene was discovered in 1994 by J. M. Friedman's laboratory.<ref>{{cite journal|last1=Zhang|first1=Y|last2=Proenca|first2=R|last3=Maffei|first3=M|last4=Barone|first4=M|last5=Leopold|first5=L|last6=Friedman|first6=JM|title=Positional cloning of the mouse obese gene and its human homologue.|journal=Nature|date=Dec 1, 1994|volume=372|issue=6505|pages=425–32|doi=10.1038/372425a0|pmid=7984236|bibcode=1994Natur.372..425Z|s2cid=4359725|type=Research Support}}</ref> These investigators postulated that leptin was a satiety factor. In the ob/ob mouse, mutations in the [[leptin]] gene resulted in the obese phenotype opening the possibility of leptin therapy for human obesity. However, soon thereafter [[Jose F. Caro|J. F. Caro's]] laboratory could not detect any mutations in the leptin gene in humans with obesity. On the contrary [[Leptin]] expression was increased proposing the possibility of Leptin-resistance in human obesity.<ref>{{cite journal|last1=Considine|first1=RV|last2=Considine|first2=EL|last3=Williams|first3=CJ|last4=Nyce|first4=MR|last5=Magosin|first5=SA|last6=Bauer|first6=TL|last7=Rosato|first7=EL|last8=Colberg|first8=J|last9=Caro|first9=JF <!--exactly 9 authors--> |title=Evidence against either a premature stop codon or the absence of obese gene mRNA in human obesity.|journal=The Journal of Clinical Investigation|date=Jun 1995|volume=95|issue=6|pages=2986–8|pmid=7769141|doi=10.1172/jci118007|pmc=295988|type=Research Support}}</ref>