Dysfunctional uterine bleeding pathophysiology: Difference between revisions
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{{Dysfunctional uterine bleeding}} | {{Dysfunctional uterine bleeding}} | ||
{{CMG}}{{AE}}[[User:AroojNaz|Arooj Naz]] | {{CMG}}; {{AE}}[[User:AroojNaz|Arooj Naz, M.B.B.S]] | ||
==Overview== | ==Overview== | ||
Dysfunctional uterine bleeding is a condition that affects many women worldwide, especially because it has a wide range of underlying causes. Bleeding can be acute or chronic. By understanding the [[pathophysiology]] of the causative conditions, one can understand the cause of [[dysfunctional uterine bleeding]]. These include [[polyps]], [[adenomyosis]], [[leiomyoma]], [[malignancy]] or [[hyperplasia]], [[coagulopathies]], [[ovulatory dysfunction]], [[endometrial]] disorders and [[iatrogenic]] causes. In ovulatory causes, unopposed estrogen and progesterone result in continued thickening and proliferation of the [[endometrium]]. Along with the effects of these hormones, [[hypoxia]], [[Cervicitis|inflammation]] and [[vasoconstriction]] result in shedding and subsequent [[scarring]]. | Dysfunctional uterine bleeding is a condition that affects many women worldwide, especially because it has a wide range of underlying causes. Bleeding can be acute or chronic. By understanding the [[pathophysiology]] of the causative conditions, one can understand the cause of [[dysfunctional uterine bleeding]]. These include [[polyps]], [[adenomyosis]], [[leiomyoma]], [[malignancy]] or [[hyperplasia]], [[coagulopathies]], [[ovulatory dysfunction]], [[endometrial]] disorders and [[iatrogenic]] causes. In ovulatory causes, unopposed [[estrogen]] and [[progesterone]] result in continued thickening and proliferation of the [[endometrium]]. Along with the effects of these hormones, [[hypoxia]], [[Cervicitis|inflammation]] and [[vasoconstriction]] result in shedding and subsequent [[scarring]]. | ||
==Pathophysiology== | ==Pathophysiology== | ||
Dysfunctional uterine bleeding can be classified into acute and chronic causes.<ref name="pmid30422508">{{cite journal| author=| title=StatPearls | journal= | year= 2022 | volume= | issue= | pages= | pmid=30422508 | doi= | pmc= | url= }} </ref> | Dysfunctional uterine bleeding can be classified into acute and chronic causes.<ref name="pmid30422508">{{cite journal| author=| title=StatPearls | journal= | year= 2022 | volume= | issue= | pages= | pmid=30422508 | doi= | pmc= | url= }} </ref> | ||
#Acute Dysfunctional uterine bleeding: Acute bleeding can develop in one of two ways. | #[[Acute]] Dysfunctional uterine bleeding: Acute bleeding can develop in one of two ways. Bleeding can develop acutely on which immediate intervention is required to prevent excessive blood loss, or it can be imposed upon chronic [[uterine bleeding]]. The latter often refers to menstrual irregularities that developed of 6 months or longer. | ||
#Chronic Dysfunctional uterine bleeding | #[[Chronic]] Dysfunctional uterine bleeding | ||
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!Pathophysiology | !Pathophysiology | ||
|- | |- | ||
|'''[[Polyps]]''' | |'''[[Endometrial polyp|Polyps]]''' | ||
|Endometrial polyps are overgrowths of [[endometrial tissue]]. They can vary in size and eventually result in obstruction to the endometrial outflow path<ref name="pmid32491756">{{cite journal| author=| title=StatPearls | journal= | year= 2022 | volume= | issue= | pages= | pmid=32491756 | doi= | pmc= | url= }}</ref> which may lead to unexpected bleeding | |Endometrial polyps are overgrowths of [[endometrial tissue]]. They can vary in size and eventually result in obstruction to the [[endometrial]] outflow path<ref name="pmid32491756">{{cite journal| author=| title=StatPearls | journal= | year= 2022 | volume= | issue= | pages= | pmid=32491756 | doi= | pmc= | url= }}</ref> which may lead to unexpected bleeding | ||
|- | |- | ||
|'''[[Adenomyosis]]''' | |'''[[Adenomyosis]]''' | ||
|Adenomyosis is characterized by the presence of ectopic [[Endometrium|endometrial tissue]] (the inner lining of the [[uterus]]) within the [[Uterus|myometrium]] (the thick, muscular layer of the uterus). Although the pathophysiology is not well understood, the basic [[Fibroblast Growth Factor]] receptor/ligand system has shown to be upregulated. Hormones such as [[estrogen]] and [[progesterone]] as well as [[oxytocin]], [[FSH]], and [[prolactin]] also contribute to the pathogenesis of the disease by causing tissue proliferation | |Adenomyosis is characterized by the presence of ectopic [[Endometrium|endometrial tissue]] (the inner lining of the [[uterus]]) within the [[Uterus|myometrium]] (the thick, muscular layer of the uterus). Although the pathophysiology is not well understood, the basic [[Fibroblast Growth Factor]] receptor/ligand system has shown to be upregulated. Hormones such as [[estrogen]] and [[progesterone]] as well as [[oxytocin]], [[FSH]], and [[prolactin]] also contribute to the pathogenesis of the disease by causing tissue [[proliferation]] | ||
|- | |- | ||
|'''[[Leiomyoma]]''' | |'''[[Leiomyoma]]''' | ||
|Also referred to as fibroids, [[leiomyoma]] are | |Also referred to as [[fibroids]], [[leiomyoma]] are tumours of [[benign]] origin made up primarily of [[smooth muscle]] and [[fibrous connective tissue]]. They can presents as [[serosal]], [[Submucosa|submucosal]], [[subserosal]] or [[pedunculated]] masses. Leiomyoma has been linked to underlying [[genetic mutations]] including [[translocations]] (12;14)(q14-q15;q23–24), [[deletions]] (7)(q22q32) and [[Rearrangement|rearrangements]] involving 6p21, 10q, trisomy 12 | ||
|- | |- | ||
|'''[[Malignancy]] and [[hyperplasia]]''' | |'''[[Malignancy]] and [[hyperplasia]]''' | ||
|Typical [[proliferation]] due to underlying hyperplasia or malignancy of the endometrium is an important cause of dysfunctional endometrial bleeding and warrants further investigations, especially in older women | |Typical [[proliferation]] due to underlying hyperplasia or malignancy of the endometrium is an important cause of dysfunctional endometrial bleeding and warrants further investigations, especially in older women | ||
|- | |- | ||
|'''[[Coagulopathies]]''' | |'''[[Coagulopathies]]''' | ||
|Conditions that lead to defective [[blood clotting]], such as [[Von Willebrand disease]], may contribute to DUB. In vWF deficiency, there is a defect in the [[Platelet plug|platelet plug formation]] that results in a defective platelet adhesion and clot formation. | |Conditions that lead to defective [[blood clotting]], such as [[Von Willebrand disease]], may contribute to DUB. In vWF deficiency, there is a defect in the [[Platelet plug|platelet plug formation]] that results in a defective platelet adhesion and clot formation | ||
|- | |||
|'''Ovulatory''' | |||
|Ovulatory causes are due to unopposed effects of [[estrogen]], which result in continued thickening and proliferation of the [[endometrium]]. When there is an imbalance between estrogen and [[progesterone]] hormone levels, heavy menstrual bleeding, as well as an alteration in bleeding patterns and frequency, are noted. Although drugs are considered an anovulatory cause, those drugs that affect [[dopamine]] levels interfere with the [[Hypothalamic|hypothalamic axis]] and also contribute to DUB. Although not entirely understood, endometrial bleeding may be due to [[hypoxia]], [[Cervicitis|inflammation]] and [[vasoconstriction]] <ref name="pmid118662412">{{cite journal| author=Livingstone M, Fraser IS| title=Mechanisms of abnormal uterine bleeding. | journal=Hum Reprod Update | year= 2002 | volume= 8 | issue= 1 | pages= 60-7 | pmid=11866241 | doi=10.1093/humupd/8.1.60 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11866241 }}</ref> that play a role in shedding and subsequent [[scarring]] <ref name="pmid26803558">{{cite journal| author=Whitaker L, Critchley HO| title=Abnormal uterine bleeding. | journal=Best Pract Res Clin Obstet Gynaecol | year= 2016 | volume= 34 | issue= | pages= 54-65 | pmid=26803558 | doi=10.1016/j.bpobgyn.2015.11.012 | pmc=4970656 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26803558 }}</ref> | |||
|- | |||
|'''[[Endometriosis]]''' | |||
|The [[Sampson theory]] of retrograde [[menstruation]], the coelomic [[metaplasia]] theory, and the [[lymphatic]] and [[vascular]] dissemination theory explain the implantation and invasion of the [[Endometrium|endometrial tissue]] outside the [[uterine cavity]]. [[Immunological|Immunologic]] factors and [[genetic]] factors are also thought to play a role in the pathogenesis of [[endometriosis]] <ref name="Bulun2009">{{cite journal|last1=Bulun|first1=Serdar E.|title=Endometriosis|journal=New England Journal of Medicine|volume=360|issue=3|year=2009|pages=268–279|issn=0028-4793|doi=10.1056/NEJMra0804690}}</ref> | |||
|- | |- | ||
|'''[[Iatrogenic]]''' | |'''[[Iatrogenic]]''' | ||
|Iatrogenic causes refer to inadvertent injuries induced my physicians. Such causes include unopposed and continuous exposure to [[estrogen]] and [[progesterone]] therapy, as is seen with [[contraceptive]] medications, [[Gonadotropin-releasing hormone agonist|GnRH agonists]], and [[Selective estrogen receptor modulator|SERMs]].<ref name="pmid268035582 | |[[Iatrogenic]] causes refer to inadvertent injuries induced by my physicians. Such causes include unopposed and continuous exposure to [[estrogen]] and [[progesterone]] therapy, as is seen with [[contraceptive]] medications, [[Gonadotropin-releasing hormone agonist|GnRH agonists]], and [[Selective estrogen receptor modulator|SERMs]].<ref name="pmid268035582">{{cite journal| author=Whitaker L, Critchley HO| title=Abnormal uterine bleeding. | journal=Best Pract Res Clin Obstet Gynaecol | year= 2016 | volume= 34 | issue= | pages= 54-65 | pmid=26803558 | doi=10.1016/j.bpobgyn.2015.11.012 | pmc=4970656 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26803558 }}</ref> | ||
|} | |} | ||
==Blood supply of Endometrium== | ==Blood supply of Endometrium== | ||
The ovarian artery arises from the aorta and descends into the retroperitoneum alongside the gonadal vein and ureter. Eventually, it anastomoses with the ovarian branch of the uterine artery at the uterus. [[Vasoconstriction]] affects these vessels may contribute to DUB. | The [[ovarian artery]] arises from the [[aorta]] and descends into the [[retroperitoneum]] alongside the [[gonadal vein]] and [[ureter]]. Eventually, it anastomoses with the [[Ovarian branch of uterine artery|ovarian branch]] of the [[uterine artery]] at the [[uterus]]. [[Vasoconstriction]] affects these vessels may contribute to DUB. | ||
[[File:Ovarian Arterial Blood Supply.png|none|thumb|300x300px|Henry Gray (1918) ''Anatomy of the Human Body'']] | [[File:Ovarian Arterial Blood Supply.png|none|thumb|300x300px|Henry Gray (1918) ''Anatomy of the Human Body'']] | ||
==References== | ==References== | ||
Latest revision as of 00:23, 19 March 2022
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Arooj Naz, M.B.B.S
Overview
Dysfunctional uterine bleeding is a condition that affects many women worldwide, especially because it has a wide range of underlying causes. Bleeding can be acute or chronic. By understanding the pathophysiology of the causative conditions, one can understand the cause of dysfunctional uterine bleeding. These include polyps, adenomyosis, leiomyoma, malignancy or hyperplasia, coagulopathies, ovulatory dysfunction, endometrial disorders and iatrogenic causes. In ovulatory causes, unopposed estrogen and progesterone result in continued thickening and proliferation of the endometrium. Along with the effects of these hormones, hypoxia, inflammation and vasoconstriction result in shedding and subsequent scarring.
Pathophysiology
Dysfunctional uterine bleeding can be classified into acute and chronic causes.[1]
- Acute Dysfunctional uterine bleeding: Acute bleeding can develop in one of two ways. Bleeding can develop acutely on which immediate intervention is required to prevent excessive blood loss, or it can be imposed upon chronic uterine bleeding. The latter often refers to menstrual irregularities that developed of 6 months or longer.
- Chronic Dysfunctional uterine bleeding
At the end of the menstrual cycle, progesterone levels fall significantly leading to a breakdown of the functional layer of the endometrium. This leads to the phenomenon known as the menstrual cycle. This cycle can become irregular due to several causes, especially any derangements in the architectural structure of the endometrium. Common underlying causes include polyps, adenomyosis, leiomyoma, malignancy or hyperplasia, coagulopathies, ovulatory dysfunction, endometrial disorders and iatrogenic causes. DUB that is due to underlying ovulatory causes occurs due to defects in local endometrial functions whereas anovulatory is often due to systemic disorders, endocrine or neurological imbalances. By understanding the pathophysiology of these conditions, one can understand the cause of dysfunctional uterine bleeding:[2]
| Condition causing DUB | Pathophysiology |
|---|---|
| Polyps | Endometrial polyps are overgrowths of endometrial tissue. They can vary in size and eventually result in obstruction to the endometrial outflow path[3] which may lead to unexpected bleeding |
| Adenomyosis | Adenomyosis is characterized by the presence of ectopic endometrial tissue (the inner lining of the uterus) within the myometrium (the thick, muscular layer of the uterus). Although the pathophysiology is not well understood, the basic Fibroblast Growth Factor receptor/ligand system has shown to be upregulated. Hormones such as estrogen and progesterone as well as oxytocin, FSH, and prolactin also contribute to the pathogenesis of the disease by causing tissue proliferation |
| Leiomyoma | Also referred to as fibroids, leiomyoma are tumours of benign origin made up primarily of smooth muscle and fibrous connective tissue. They can presents as serosal, submucosal, subserosal or pedunculated masses. Leiomyoma has been linked to underlying genetic mutations including translocations (12;14)(q14-q15;q23–24), deletions (7)(q22q32) and rearrangements involving 6p21, 10q, trisomy 12 |
| Malignancy and hyperplasia | Typical proliferation due to underlying hyperplasia or malignancy of the endometrium is an important cause of dysfunctional endometrial bleeding and warrants further investigations, especially in older women |
| Coagulopathies | Conditions that lead to defective blood clotting, such as Von Willebrand disease, may contribute to DUB. In vWF deficiency, there is a defect in the platelet plug formation that results in a defective platelet adhesion and clot formation |
| Ovulatory | Ovulatory causes are due to unopposed effects of estrogen, which result in continued thickening and proliferation of the endometrium. When there is an imbalance between estrogen and progesterone hormone levels, heavy menstrual bleeding, as well as an alteration in bleeding patterns and frequency, are noted. Although drugs are considered an anovulatory cause, those drugs that affect dopamine levels interfere with the hypothalamic axis and also contribute to DUB. Although not entirely understood, endometrial bleeding may be due to hypoxia, inflammation and vasoconstriction [4] that play a role in shedding and subsequent scarring [5] |
| Endometriosis | The Sampson theory of retrograde menstruation, the coelomic metaplasia theory, and the lymphatic and vascular dissemination theory explain the implantation and invasion of the endometrial tissue outside the uterine cavity. Immunologic factors and genetic factors are also thought to play a role in the pathogenesis of endometriosis [6] |
| Iatrogenic | Iatrogenic causes refer to inadvertent injuries induced by my physicians. Such causes include unopposed and continuous exposure to estrogen and progesterone therapy, as is seen with contraceptive medications, GnRH agonists, and SERMs.[7] |
Blood supply of Endometrium
The ovarian artery arises from the aorta and descends into the retroperitoneum alongside the gonadal vein and ureter. Eventually, it anastomoses with the ovarian branch of the uterine artery at the uterus. Vasoconstriction affects these vessels may contribute to DUB.
References
- ↑ "StatPearls". 2022. PMID 30422508.
- ↑ Munro MG (2001). "Dysfunctional uterine bleeding: advances in diagnosis and treatment". Curr Opin Obstet Gynecol. 13 (5): 475–89. doi:10.1097/00001703-200110000-00006. PMID 11547028.
- ↑ "StatPearls". 2022. PMID 32491756 Check
|pmid=value (help). - ↑ Livingstone M, Fraser IS (2002). "Mechanisms of abnormal uterine bleeding". Hum Reprod Update. 8 (1): 60–7. doi:10.1093/humupd/8.1.60. PMID 11866241.
- ↑ Whitaker L, Critchley HO (2016). "Abnormal uterine bleeding". Best Pract Res Clin Obstet Gynaecol. 34: 54–65. doi:10.1016/j.bpobgyn.2015.11.012. PMC 4970656. PMID 26803558.
- ↑ Bulun, Serdar E. (2009). "Endometriosis". New England Journal of Medicine. 360 (3): 268–279. doi:10.1056/NEJMra0804690. ISSN 0028-4793.
- ↑ Whitaker L, Critchley HO (2016). "Abnormal uterine bleeding". Best Pract Res Clin Obstet Gynaecol. 34: 54–65. doi:10.1016/j.bpobgyn.2015.11.012. PMC 4970656. PMID 26803558.