Hemoroidy – Patofizjologia i mechanizm

Hemoroidy
Patofizjologia i mechanizm

Hemoroidy są anatomicznymi strukturami kanału analnego, których patologia wynika z dezintegracji tkanek podporowych poduszek analnych, prowadzącej do ich przemieszczenia i powiększenia. Kluczową rolę w patogenezie odgrywa teoria ślizgania poduszek analnych, gdzie osłabienie tkanki łącznej kotwiczącej oraz degeneracja mięśnia podśluzówkowego skutkują obniżeniem i wypadaniem poduszek. Współistnieje dysregulacja napięcia naczyniowego z nadmierną produkcją syntazy tlenku azotu, hiperperfuzją splotu hemoroidalnego (zwiększona średnica i przepływ krwi w gałęziach tętnicy odbytniczej górnej), a także nadekspresją metaloproteaz macierzy (MMP-9) i zaburzeniem stosunku kolagenu typu I/III, co prowadzi do degradacji włókien elastycznych i osłabienia struktury tkanki łącznej. Dodatkowo obserwuje się neowaskularyzację oraz nasilony stan zapalny z udziałem cytokin prozapalnych (np. TNF-α), co sprzyja obrzękowi, bólowi i podrażnieniu. Podwyższone spoczynkowe ciśnienie w odbycie i wzmożone napięcie zwieracza wewnętrznego utrudniają odpływ żylny, nasilając zastój krwi i objawy kliniczne.

Patofizjologia hemoroidów

Teoria ślizgania poduszek analnych
Zmiany patologiczne w tkance hemoroidalnej
Dysregulacja napięcia naczyniowego i zmiany naczyniowe
Rola metaloproteaz macierzy i neowaskularyzacji
Zmiany w składzie kolagenu
Zmiany fizjologiczne w kanale analnym

Mechanizmy powstawania objawów

Hemoroidy wewnętrzne
Hemoroidy zewnętrzne

Czynniki wpływające na rozwój hemoroidów
Patofizjologia molekularna hemoroidów
Rola flawonoidów w mechanizmie choroby
Podsumowanie mechanizmów patofizjologicznych

Kolejne rozdziały

Patofizjologia hemoroidów

Hemoroidy (guzki krwawnicze) są normalnymi strukturami anatomicznymi człowieka, obecnymi w kanale analnym od urodzenia, składającymi się z poduszek naczyniowych zawierających sploty tętniczo-żylne, tkankę łączną i mięśnie gładkie. Patologia hemoroidalna rozwija się, gdy dochodzi do nieprawidłowego powiększenia i przemieszczenia tych struktur, co prowadzi do objawów klinicznych¹². Mimo wielu lat badań, dokładna patofizjologia rozwoju choroby hemoroidalnej nadal nie jest w pełni wyjaśniona, a mechanizmy prowadzące do powstania objawowych hemoroidów są złożone i wieloczynnikowe³.

Teoria ślizgania poduszek analnych

Najbardziej akceptowaną obecnie teorią patogenezy hemoroidów jest teoria ślizgania się poduszek analnych (ang. sliding anal cushion theory). Według tej teorii hemoroidy rozwijają się, gdy dochodzi do dezintegracji lub degeneracji tkanek podporowych poduszek analnych⁴⁵. W normalnych warunkach poduszki analne są utrzymywane w miejscu przez system tkanki łącznej kotwiczącej, który przymocowuje je do zwieracza wewnętrznego i warstwy podłużnej. Wraz z wiekiem, system kotwiczący i podporowy tkanki łącznej ulega osłabieniu i degeneracji⁶⁷.

Gdy dochodzi do osłabienia tych struktur, poduszki analne nie tylko uwypuklają się, ale też zsuwają się w dół światła kanału odbytniczego. Proces ten zwykle staje się zauważalny w trzeciej dekadzie życia, z indywidualnymi różnicami⁸. Wraz z utratą podparcia żyły ulegają rozszerzeniu. Obniżona, luźna wyściółka staje się bardziej wrażliwa na ucisk podczas parcia i uraz spowodowany przechodzącym kałem. Może to prowadzić do zastoju krwi w żyłach, tworzenia się skrzeplin, obrzęku lub erozji wyściółki, co skutkuje krwawieniem. W ten sposób hemoroidy stają się objawowe⁹.

Zmiany patologiczne w tkance hemoroidalnej

Poduszki analne pacjentów z hemoroidami wykazują istotne zmiany patologiczne, które obejmują¹⁰¹¹:

Nieprawidłowe rozszerzenie i zniekształcenie kanałów naczyniowych
Degenerację włókien kolagenowych i tkanek sprężystych
Zniekształcenie i przerwanie mięśnia podśluzówkowego odbytu
Nasiloną reakcję zapalną obejmującą ścianę naczyniową i otaczającą tkankę łączną
Owrzodzenie błony śluzowej, niedokrwienie i zakrzepicę¹²

Chroniczny wzrost ciśnienia wewnątrzbrzusznego, w połączeniu z brakiem zastawek w żyłach odbytniczych, może ograniczać drenaż żylny z zatok podczas defekacji, co prowadzi do nieprawidłowego rozszerzenia połączeń tętniczkowo-żylnych splotu hemoroidalnego wewnętrznego¹³. Końcowym rezultatem jest utrzymywanie się wypadniętych poduszek analnych poza odbyt po defekacji¹⁴.

Połączenie przekrwienia zatok, uduszenia i przewlekłego procesu zapalnego w obrębie guzka ostatecznie prowadzi do zastoju krwi w zatokach. Zakrzepica może z czasem prowadzić do niedokrwienia, owrzodzenia i martwicy powierzchni guzka¹⁵.

Dysregulacja napięcia naczyniowego i zmiany naczyniowe

Na podstawie histologicznych obserwacji nieprawidłowego rozszerzenia i zniekształcenia żył w hemoroidach uważa się, że dysregulacja napięcia naczyniowego może odgrywać rolę w rozwoju hemoroidów¹⁶¹⁷. W hemoroidach zaobserwowano znaczący wzrost syntazy tlenku azotu – enzymu, który syntezuje tlenek azotu z L-argininy¹⁸¹⁹. Te nieprawidłowe zmiany utrzymywały się nawet po chirurgicznym usunięciu hemoroidów, co potwierdza związek między hiperwaskularyzacją a rozwojem hemoroidów²⁰.

Aigner i wsp. zidentyfikowali strukturę podobną do zwieracza, utworzoną przez pogrubioną tunica media zawierającą 5-15 warstw komórek mięśni gładkich, między splotem naczyniowym w przestrzeni podśluzówkowej strefy przejściowej odbytu w normalnych preparatach odbytnicy²¹. Badacze zaproponowali, że jeśli ten mechanizm zostanie zaburzony, hiperperfuzja splotu tętniczo-żylnego doprowadzi do powstawania hemoroidów²².

Aigner i wsp. stwierdzili również, że końcowe gałęzie tętnicy odbytniczej górnej zaopatrujące poduszkę analną u pacjentów z hemoroidami miały znacznie większą średnicę, większy przepływ krwi, wyższą prędkość szczytową i prędkość przyspieszenia w porównaniu do zdrowych ochotników²³. Sugeruje to, że hiperwaskularyzacja odbytnicy przyczynia się do rozwoju hemoroidów, a nie jest jego konsekwencją²⁴.

Rola metaloproteaz macierzy i neowaskularyzacji

Badano szereg enzymów i mediatorów biorących udział w degradacji tkanek podporowych w poduszkach analnych²⁵²⁶. Jednym z najważniejszych jest metaloproteaza macierzy (MMP), proteaza zależna od cynku, która może rozkładać białka pozakomórkowe, takie jak kolagen, fibronektyna i elastyna²⁷. Zaobserwowano nadekspresję MMP-9 w hemoroidach, co wiązało się z rozpadem włókien elastycznych²⁸.

Ponadto, niedawno zaobserwowano zwiększoną gęstość mikronaczyń w tkance hemoroidalnej, co sugeruje, że neowaskularyzacja może być kolejnym ważnym zjawiskiem w chorobie hemoroidalnej²⁹³⁰³¹.

Zmiany w składzie kolagenu

Opublikowane w ostatnich latach badania dotyczące etiopatogenezy choroby hemoroidalnej sięgają poziomu molekularnego. Wskazują na obniżony stosunek kolagenu typu I/III u pacjentów z chorobą hemoroidalną w porównaniu do pacjentów bez tej choroby, co sprzyja zmniejszeniu sprężystości tkanki splotów hemoroidalnych³². Te nieprawidłowości w składzie kolagenu mogą przyczyniać się do patogenezy hemoroidów³³.

Zmiany fizjologiczne w kanale analnym

U pacjentów z hemoroidami zaobserwowano szereg zmian fizjologicznych w kanale analnym. Spoczynkowe ciśnienie w odbycie było znacznie wyższe u pacjentów z wypadającymi lub niewypadającymi hemoroidami niż u zdrowych osób³⁴. Zwiększone napięcie zwieracza wewnętrznego odbytu powoduje, że kał naciska na hemoroidy w kierunku mięśni, zmniejszając odpływ żylny i nasilając objawy³⁵.

Mechanizmy powstawania objawów

Hemoroidy wewnętrzne

Hemoroidy wewnętrzne nie mogą powodować bólu skórnego, ponieważ znajdują się powyżej linii grzebieniastej i nie są unerwione przez nerwy skórne. Mogą jednak krwawić, wypadać i, w wyniku osadzenia się substancji drażniącej na wrażliwej skórze okolicy odbytu, powodować świąd i podrażnienie okolicy odbytu³⁶.

Hemoroidy wewnętrzne mogą wywoływać ból okolicy odbytu przez wypadanie i powodowanie skurczu kompleksu zwieraczy wokół hemoroidów³⁷. Najczęściej powodują bezbolesne krwawienie podczas wypróżnień. Nabłonek pokrywający zostaje uszkodzony przez twardy stolec, a leżące pod nim żyły krwawią. Przy skurczu kompleksu zwieraczy, który podnosi ciśnienie, żyły hemoroidalne wewnętrzne mogą tryskać krwią³⁸.

Nadmierne powiększenie i przekrwienie wewnętrznych poduszek hemoroidalnych prowadzi do rozciągnięcia mięśni podporowych i ostatecznie do wypadania tkanki odbytnicy przez kanał odbytu. Powiększona błona śluzowa odbytu jest łatwo urazowa, co prowadzi do krwawienia z odbytnicy, które jest typowo jasnoczerwone ze względu na wysoką zawartość tlenu we krwi w obrębie zespoleń tętniczo-żylnych³⁹.

Wypadanie prowadzi do brudzenia i wydzielania śluzu (wywołującego świąd) oraz predysponuje do uwięźnięcia i uduszenia⁴⁰.

Hemoroidy zewnętrzne

Hemoroidy zewnętrzne powodują objawy na dwa sposoby. Po pierwsze, może wystąpić ostra zakrzepica leżącej u podstawy zewnętrznej żyły hemoroidalnej. Ostra zakrzepica jest zwykle związana z konkretnym zdarzeniem, takim jak wysiłek fizyczny, parcie przy zaparciu, epizod biegunki lub zmiana diety. Są to ostre, bolesne zdarzenia⁴¹.

Czynniki wpływające na rozwój hemoroidów

Etiopatogeneza choroby hemoroidalnej jest wieloczynnikowa i nie jest do końca poznana. Do głównych czynników przyczyniających się do rozwoju objawowych hemoroidów zalicza się⁴²⁴³:

Dieta uboga w błonnik
Przewlekłe zaparcia i przedłużone parcie podczas defekacji
Spędzanie nadmiernego czasu na toalecie
Biegunka
Ciąża
Siedzący tryb życia
Predyspozycje genetyczne
Zwiększone ciśnienie wewnątrzbrzuszne z różnych przyczyn (np. chroniczny kaszel, podnoszenie ciężarów)
Zaburzenia odpływu żylnego spowodowane przez ciążę lub masy miedniczne
Zaleganie stolca w bańce odbytnicy⁴⁴

Większość autorów zgadza się, że dieta uboga w błonnik powoduje powstawanie stolca o małej objętości, co prowadzi do parcia podczas defekacji. To zwiększone ciśnienie powoduje przekrwienie hemoroidów, prawdopodobnie poprzez zakłócanie odpływu żylnego⁴⁵.

Gdy pacjent starzeje się i występuje stała obecność jednego lub więcej z wyżej wymienionych czynników, integralność „poduszek” hemoroidalnych pogarsza się, a tkanka hemoroidalna zaczyna uwypuklać się i obniżać do kanału odbytu. Ponadto, gdy poduszka uwypukla się do kanału, jest narażona na potencjalny uraz i podrażnienie przez przechodzący stolec⁴⁶.

Patofizjologia molekularna hemoroidów

Na poziomie molekularnym w patogenezie hemoroidów istotną rolę odgrywają⁴⁷:

Cytokiny prozapalne, takie jak TNF-α, które nasilają stan zapalny w tkance hemoroidalnej
Transformujący czynnik wzrostu (TGF-β), który odgrywa rolę w procesach naprawczych i remodelingu tkanki
Metaloproteazy macierzy (MMP), zwłaszcza MMP-9, które biorą udział w degradacji macierzy pozakomórkowej i mogą przyczyniać się do osłabienia tkanki podporowej
Stosunek kolagenu typu I/III, którego zaburzenie może prowadzić do zmniejszonej elastyczności tkanki hemoroidalnej

Niedawne badania wykazały, że komórki macierzyste mezenchymalne (MSCs) mogą odgrywać rolę terapeutyczną w chorobie hemoroidalnej poprzez hamowanie stanu zapalnego, co powoduje znaczną redukcję obrzęku tkanki w grupach leczonych. MSCs promują gojenie ran poprzez szybkie zakończenie fazy zapalnej, co udowodniono przez zwiększoną ekspresję TGF-β. Przeciwzapalne działanie MSCs jest mediowane przez uwalnianie czynników troficznych i przeciwzapalnych, które wchodzą w interakcje z komórkami immunologicznymi i hamują odpowiedzi zapalne⁴⁸.

Rola flawonoidów w mechanizmie choroby

Diosmina, należąca do grupy flawonoidów, wykazuje wieloaspektowy mechanizm działania, który obejmuje poprawę napięcia żylnego, zwiększenie drenażu limfatycznego, ochronę mikrokrążenia łożyska naczyniowego, hamowanie reakcji zapalnych i zmniejszenie przepuszczalności naczyń włosowatych⁴⁹.

Diosmina wywiera swój efekt fleboktoniczny poprzez przedłużenie działania naczynioskurczowego noradrenaliny na ścianę żylną, zwiększa napięcie żylne, a tym samym zmniejsza rozszerzalność i zastój. Te wieloaspektowe działania diosminy prawdopodobnie zbiegają się, aby zapewnić maksymalne korzyści osobom z hemoroidami⁵⁰.

Flebotoniki to heterogenna klasa leków składająca się z ekstraktów roślinnych (tj. flawonoidów) i związków syntetycznych (tj. dobesilanu wapnia), które mogą być stosowane w leczeniu zarówno ostrej, jak i przewlekłej choroby hemoroidalnej. Chociaż ich mechanizm działania nie został ustalony, flebotoniki są związane ze wzmacnianiem ścian naczyń krwionośnych, zwiększaniem napięcia żylnego, zwiększaniem drenażu limfatycznego i normalizacją przepuszczalności naczyń włosowatych⁵¹.

Teoria patogenetyczna	Główne mechanizmy	Zmiany patologiczne
Teoria ślizgania poduszek analnych	Dezintegracja tkanek podporowych poduszek analnych	Obniżenie poduszek analnych, wypadanie
Dysregulacja napięcia naczyniowego	Zwiększona produkcja tlenku azotu, zaburzenie równowagi między czynnikami naczynioskurczowymi i naczyniorozszerzającymi	Rozszerzenie naczyń, przekrwienie
Hiperperfuzja splotu hemoroidalnego	Większa średnica i przepływ krwi w końcowych gałęziach tętnicy odbytniczej górnej	Powiększenie poduszek naczyniowych, wzmożony przepływ krwi
Zmiany w macierzy pozakomórkowej	Nadekspresja metaloproteaz macierzy (MMP-9), zaburzony stosunek kolagenu typu I/III	Degradacja włókien elastycznych, zmniejszona spoistość tkanki łącznej
Neowaskularyzacja	Zwiększona gęstość mikronaczyń	Formowanie nowych naczyń krwionośnych w tkance hemoroidalnej
Zwiększone ciśnienie w kanale analnym	Podwyższone spoczynkowe ciśnienie w odbycie, wzmożone napięcie zwieracza wewnętrznego	Utrudniony odpływ żylny, zastój krwi
Reakcja zapalna	Nasilona ekspresja cytokin prozapalnych (np. TNF-α)	Obrzęk tkanki, ból, podrażnienie

Podsumowanie mechanizmów patofizjologicznych

Patofizjologia hemoroidów jest złożona i wieloczynnikowa, obejmująca mechanizmy takie jak⁵²⁵³:

Osłabienie integralności tkanki łącznej kotwiczącej poduszki hemoroidalne
Dysregulacja napięcia naczyniowego i hiperperfuzja splotu hemoroidalnego
Zmiany w składzie macierzy pozakomórkowej (zaburzony stosunek kolagenu I/III, nadekspresja MMP)
Neowaskularyzacja i zwiększona gęstość mikronaczyń
Reakcja zapalna w ścianie naczynia i otaczającej tkance łącznej
Zwiększone napięcie zwieracza wewnętrznego odbytu
Nieprawidłowe rozszerzenie połączeń tętniczo-żylnych w poduszkach analnych
Czynniki środowiskowe i genetyczne zwiększające ciśnienie wewnątrzbrzuszne i wpływające na odpływ żylny

Zrozumienie tych mechanizmów jest kluczowe dla opracowania skutecznych strategii leczenia, które mogą być ukierunkowane na konkretne aspekty patofizjologii hemoroidów. Najbardziej obiecujące wydają się podejścia terapeutyczne, które łączą różne mechanizmy działania, takie jak flebotoniki (wpływające na napięcie naczyń i przepuszczalność), preparaty przeciwzapalne (zmniejszające obrzęk i ból) oraz metody usprawniające przepływ krwi i wzmacniające tkankę łączną⁵⁴⁵⁵.

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Materiały źródłowe

#1 Hemorrhoids: From basic pathophysiology to clinical management
https://www.wjgnet.com/1007-9327/full/v18/i17/2009.htm
Hemorrhoids are defined as the symptomatic enlargement and distal displacement of the normal anal cushions. […] The abnormal dilatation and distortion of the vascular channel, together with destructive changes in the supporting connective tissue within the anal cushion, is a paramount finding of hemorrhoids. […] It appears that the dysregulation of the vascular tone and vascular hyperplasia might play an important role in hemorrhoidal development, and could be a potential target for medical treatment. […] The exact pathophysiology of hemorrhoidal development is poorly understood. […] Today, the theory of sliding anal canal lining is widely accepted. […] Hemorrhoids develop when the supporting tissues of the anal cushions disintegrate or deteriorate. […] The anal cushions of patients with hemorrhoids show significant pathological changes.
#2 Natural Products with Potential Effects on Hemorrhoids: A Review
https://www.mdpi.com/1420-3049/29/11/2673
Hemorrhoid disease represents a complex ailment for which the pathogenic mechanisms remain unclear. The etiology of hemorrhoids is typically multifactorial. Predominant contributing factors include human physiological structure, dietary habits, lack of physical exercise, and defecatory behaviors. These factors collectively increase intra-abdominal pressure during bowel movements, adversely affecting blood flow in the anal and rectal vessels, which may lead to swelling, bleeding, and the development of hemorrhoids. Additionally, inflammatory responses, dysbiosis of the intestinal microbiota, and perianal infectious abscesses can also indirectly contribute to the onset of hemorrhoids. Lastly, certain specific conditions such as sexual activity, pregnancy, and genetic factors may also be associated with the development of hemorrhoids.
#3 Pathophysiology of internal hemorrhoids
https://pmc.ncbi.nlm.nih.gov/articles/PMC6479658/
Hemorrhoidal disease is a fairly common and debilitating clinical entity. […] Despite numerous efforts, the true etiopathogenesis of hemorrhoidal disease still remains elusive. […] The pathophysiology of internal hemorrhoids is still not fully understood. Many functional, histopathological and anatomical findings have been accumulated during the last decades, but the relation between them remains obscure. […] Four theories have been developed regarding the pathophysiology of hemorrhoids. First, the varicose vein theory has been shown to be faulty, as it is now globally accepted that hemorrhoids are not varicosities. […] The globally accepted theory is that of the sliding anal canal, or cushion theory, which postulates the abnormal slippage of cushions through the anal canal as the major pathophysiological event.
#4 Hemorrhoids: From basic pathophysiology to clinical management
https://pmc.ncbi.nlm.nih.gov/articles/PMC3342598/
This review discusses the pathophysiology, epidemiology, risk factors, classification, clinical evaluation, and current non-operative and operative treatment of hemorrhoids. […] The abnormal dilatation and distortion of the vascular channel, together with destructive changes in the supporting connective tissue within the anal cushion, is a paramount finding of hemorrhoids. […] It appears that the dysregulation of the vascular tone and vascular hyperplasia might play an important role in hemorrhoidal development, and could be a potential target for medical treatment. […] The exact pathophysiology of hemorrhoidal development is poorly understood. […] Today, the theory of sliding anal canal lining is widely accepted. […] Hemorrhoids develop when the supporting tissues of the anal cushions disintegrate or deteriorate.
#5 Pathophysiology of internal hemorrhoids
https://pmc.ncbi.nlm.nih.gov/articles/PMC6479658/
Hemorrhoidal disease is a fairly common and debilitating clinical entity. […] Despite numerous efforts, the true etiopathogenesis of hemorrhoidal disease still remains elusive. […] The pathophysiology of internal hemorrhoids is still not fully understood. Many functional, histopathological and anatomical findings have been accumulated during the last decades, but the relation between them remains obscure. […] Four theories have been developed regarding the pathophysiology of hemorrhoids. First, the varicose vein theory has been shown to be faulty, as it is now globally accepted that hemorrhoids are not varicosities. […] The globally accepted theory is that of the sliding anal canal, or cushion theory, which postulates the abnormal slippage of cushions through the anal canal as the major pathophysiological event.
#6
https://journals.lww.com/dcrjournal/abstract/1984/27070/the_pathogenesis_of_hemorrhoids.2.aspx
The structure of the anal canal was examined in histology slides. Hemorrhoids are normal features of the human anatomy. They are pads that bulge into the lumen. Hemorrhoids have three parts: 1) the lining, which can be mucosa or anoderm; 2) the stroma with blood vessels, smooth muscle, and supporting connective tissue; and 3) the anchoring connective tissue system, which secures the hemorrhoids to the internal sphincter and the conjoined longitudinal coat. The anchoring and supporting connective tissue system deteriorates with aging. The hemorrhoids not only bulge, but descend into the lumen. This becomes observable in the third decade of life, with individual differences. The veins become distended as they lose their support. The descended loose lining becomes more sensitive to pressure from straining and to trauma from the stool. There can be a stasis in the veins, with clot formations and swelling or erosions of the lining, with bleeding. The hemorrhoids become symptomatic.
#7 (PDF) The pathogenesis of Hemorrhoids
https://www.academia.edu/72972362/The_pathogenesis_of_Hemorrhoids
The structure of the anal canal was examined in histology slides. Hemorrhoids are normal features of the human anatomy. They are pads that bulge into the lumen. Hemorrhoids have three parts: 1) the lining, which can be mucosa or anoderm; 2) the stroma with blood vessels, smooth muscle, and supporting connective tissue; and 3) the anchoring connective tissue system, which secures the hemorrhoids to the internal sphincter and the conjoined longitudinal coat. The anchoring and supporting connective tissue system deteriorates with aging. The hemorrhoids not only bulge, but descend into the lumen. This becomes observable in the third decade of life, with individual differences. The veins become distended as they lose their support. The descended loose lining becomes more sensitive to pressure from straining and to trauma from the stool. There can be a stasis in the veins, with clot formations and swelling, or erosions of the lining, with bleeding. The hemorrhoids become symptomatic.
#8
https://link.springer.com/article/10.1007/BF02555533
Hemorrhoids are normal features of the human anatomy. They are pads that bulge into the lumen. Hemorrhoids have three parts: 1) the lining, which can be mucosa or anoderm; 2) the stroma with blood vessels, smooth muscle, and supporting connective tissue; and 3) the anchoring connective tissue system, which secures the hemorrhoids to the internal sphincter and the conjoined longitudinal coat. The anchoring and supporting connective tissue system deteriorates with aging. The hemorrhoids not only bulge, but descend into the lumen. This becomes observable in the third decade of life, with individual differences. The veins become distended as they lose their support. The descended loose lining becomes more sensitive to pressure from straining and to trauma from the stool. There can be a stasis in the veins, with clot formations and swelling or erosions of the lining, with bleeding. The hemorrhoids become symptomatic.
#9
https://journals.lww.com/dcrjournal/abstract/1984/27070/the_pathogenesis_of_hemorrhoids.2.aspx
The structure of the anal canal was examined in histology slides. Hemorrhoids are normal features of the human anatomy. They are pads that bulge into the lumen. Hemorrhoids have three parts: 1) the lining, which can be mucosa or anoderm; 2) the stroma with blood vessels, smooth muscle, and supporting connective tissue; and 3) the anchoring connective tissue system, which secures the hemorrhoids to the internal sphincter and the conjoined longitudinal coat. The anchoring and supporting connective tissue system deteriorates with aging. The hemorrhoids not only bulge, but descend into the lumen. This becomes observable in the third decade of life, with individual differences. The veins become distended as they lose their support. The descended loose lining becomes more sensitive to pressure from straining and to trauma from the stool. There can be a stasis in the veins, with clot formations and swelling or erosions of the lining, with bleeding. The hemorrhoids become symptomatic.
#10 Hemorrhoids: From basic pathophysiology to clinical management
https://pmc.ncbi.nlm.nih.gov/articles/PMC3342598/
The anal cushions of patients with hemorrhoids show significant pathological changes. […] In addition to the above findings, a severe inflammatory reaction involving the vascular wall and surrounding connective tissue has been demonstrated in hemorrhoidal specimens, with associated mucosal ulceration, ischemia and thrombosis. […] Several enzymes or mediators involving the degradation of supporting tissues in the anal cushions have been studied. […] Recently, increased microvascular density was found in hemorrhoidal tissue, suggesting that neovascularization might be another important phenomenon of hemorrhoidal disease. […] Based on the histological findings of abnormal venous dilatation and distortion in hemorrhoids, dysregulation of the vascular tone might play a role in hemorrhoidal development.
#11 Hemorrhoids: From basic pathophysiology to clinical management
https://www.wjgnet.com/1007-9327/full/v18/i17/2009.htm
Hemorrhoids are defined as the symptomatic enlargement and distal displacement of the normal anal cushions. […] The abnormal dilatation and distortion of the vascular channel, together with destructive changes in the supporting connective tissue within the anal cushion, is a paramount finding of hemorrhoids. […] It appears that the dysregulation of the vascular tone and vascular hyperplasia might play an important role in hemorrhoidal development, and could be a potential target for medical treatment. […] The exact pathophysiology of hemorrhoidal development is poorly understood. […] Today, the theory of sliding anal canal lining is widely accepted. […] Hemorrhoids develop when the supporting tissues of the anal cushions disintegrate or deteriorate. […] The anal cushions of patients with hemorrhoids show significant pathological changes.
#12 Hemorrhoids: From basic pathophysiology to clinical management
https://www.wjgnet.com/1007-9327/full/v18/i17/2009.htm
A severe inflammatory reaction involving the vascular wall and surrounding connective tissue has been demonstrated in hemorrhoidal specimens, with associated mucosal ulceration, ischemia and thrombosis. […] Several enzymes or mediators involving the degradation of supporting tissues in the anal cushions have been studied. […] MMP-9 was found to be over-expressed in hemorrhoids, in association with the breakdown of elastic fibers. […] Recently, increased microvascular density was found in hemorrhoidal tissue, suggesting that neovascularization might be another important phenomenon of hemorrhoidal disease. […] Aigner et al found that the terminal branches of the superior rectal artery supplying the anal cushion in patients with hemorrhoids had a significantly larger diameter, greater blood flow, higher peak velocity and acceleration velocity, compared to those of healthy volunteers. […] Based on the histological findings of abnormal venous dilatation and distortion in hemorrhoids, dysregulation of the vascular tone might play a role in hemorrhoidal development.
#13 Pathophysiology of internal hemorrhoids
https://pmc.ncbi.nlm.nih.gov/articles/PMC6479658/
A chronic rise in intraabdominal pressure, in combination with the absence of valves within rectal veins, can limit venous drainage from sinusoids during defecation, resulting in abnormal dilatation of the arteriolar-venular anastomoses of the internal hemorrhoidal plexus. […] The final result is the persistence of the prolapsed anal cushions outside the anus after defecation. […] The sliding down process of anal cushions is the most crucial pathophysiologic feature of the disease. […] The combination of sinusoidal congestion, strangulation and chronic inflammatory process inside the nodule results ultimately in blood stagnation inside sinusoids. […] Thrombosis may eventually lead to ischemia, ulceration and necrosis of the surface of the nodule.
#14 Pathophysiology of internal hemorrhoids
https://pmc.ncbi.nlm.nih.gov/articles/PMC6479658/
A chronic rise in intraabdominal pressure, in combination with the absence of valves within rectal veins, can limit venous drainage from sinusoids during defecation, resulting in abnormal dilatation of the arteriolar-venular anastomoses of the internal hemorrhoidal plexus. […] The final result is the persistence of the prolapsed anal cushions outside the anus after defecation. […] The sliding down process of anal cushions is the most crucial pathophysiologic feature of the disease. […] The combination of sinusoidal congestion, strangulation and chronic inflammatory process inside the nodule results ultimately in blood stagnation inside sinusoids. […] Thrombosis may eventually lead to ischemia, ulceration and necrosis of the surface of the nodule.
#15 Pathophysiology of internal hemorrhoids
https://pmc.ncbi.nlm.nih.gov/articles/PMC6479658/
A chronic rise in intraabdominal pressure, in combination with the absence of valves within rectal veins, can limit venous drainage from sinusoids during defecation, resulting in abnormal dilatation of the arteriolar-venular anastomoses of the internal hemorrhoidal plexus. […] The final result is the persistence of the prolapsed anal cushions outside the anus after defecation. […] The sliding down process of anal cushions is the most crucial pathophysiologic feature of the disease. […] The combination of sinusoidal congestion, strangulation and chronic inflammatory process inside the nodule results ultimately in blood stagnation inside sinusoids. […] Thrombosis may eventually lead to ischemia, ulceration and necrosis of the surface of the nodule.
#16 Hemorrhoids: From basic pathophysiology to clinical management
https://pmc.ncbi.nlm.nih.gov/articles/PMC3342598/
The anal cushions of patients with hemorrhoids show significant pathological changes. […] In addition to the above findings, a severe inflammatory reaction involving the vascular wall and surrounding connective tissue has been demonstrated in hemorrhoidal specimens, with associated mucosal ulceration, ischemia and thrombosis. […] Several enzymes or mediators involving the degradation of supporting tissues in the anal cushions have been studied. […] Recently, increased microvascular density was found in hemorrhoidal tissue, suggesting that neovascularization might be another important phenomenon of hemorrhoidal disease. […] Based on the histological findings of abnormal venous dilatation and distortion in hemorrhoids, dysregulation of the vascular tone might play a role in hemorrhoidal development.
#17 Hemorrhoids: From basic pathophysiology to clinical management
https://www.wjgnet.com/1007-9327/full/v18/i17/2009.htm
A severe inflammatory reaction involving the vascular wall and surrounding connective tissue has been demonstrated in hemorrhoidal specimens, with associated mucosal ulceration, ischemia and thrombosis. […] Several enzymes or mediators involving the degradation of supporting tissues in the anal cushions have been studied. […] MMP-9 was found to be over-expressed in hemorrhoids, in association with the breakdown of elastic fibers. […] Recently, increased microvascular density was found in hemorrhoidal tissue, suggesting that neovascularization might be another important phenomenon of hemorrhoidal disease. […] Aigner et al found that the terminal branches of the superior rectal artery supplying the anal cushion in patients with hemorrhoids had a significantly larger diameter, greater blood flow, higher peak velocity and acceleration velocity, compared to those of healthy volunteers. […] Based on the histological findings of abnormal venous dilatation and distortion in hemorrhoids, dysregulation of the vascular tone might play a role in hemorrhoidal development.
#18 Hemorrhoids: From basic pathophysiology to clinical management
https://pmc.ncbi.nlm.nih.gov/articles/PMC3342598/
In hemorrhoids, nitric oxide synthase, an enzyme which synthesizes nitric oxide from L-arginine, was reported to increase significantly. […] These abnormal findings still remained after surgical removal of the hemorrhoids, confirming the association between hypervascularization and the development of hemorrhoids. […] Aigner et al identified a sphincter-like structure, formed by a thickened tunica media containing 5-15 layers of smooth muscle cells, between the vascular plexus within the subepithelial space of the anal transitional zone in normal anorectal specimens. […] Aigner et al then proposed that, if this mechanism is impaired, hyperperfusion of the arteriovenous plexus will lead to the formation of hemorrhoids.
#19 Basic Pathophysiology of Hemorrhoids and Their Clinical Management
https://www.ijpsjournal.com/article/Basic+Pathophysiology+of+Hemorrhoids+and+Their+Clinical+Management
Nitric oxide synthase, an enzyme that produces nitric oxide from L-arginine, has been shown to dramatically rise in haemorrhoids. […] Haemorrhoid patients have been found to exhibit a number of physiological alterations in the anal conduit. […] While there was no discernible alteration in the internal sphincter’s consistency, […] resting anal pressure was significantly higher in patients with prolapsing or non-prolapsing haemorrhoids than in healthy people.
#20 Hemorrhoids: From basic pathophysiology to clinical management
https://pmc.ncbi.nlm.nih.gov/articles/PMC3342598/
In hemorrhoids, nitric oxide synthase, an enzyme which synthesizes nitric oxide from L-arginine, was reported to increase significantly. […] These abnormal findings still remained after surgical removal of the hemorrhoids, confirming the association between hypervascularization and the development of hemorrhoids. […] Aigner et al identified a sphincter-like structure, formed by a thickened tunica media containing 5-15 layers of smooth muscle cells, between the vascular plexus within the subepithelial space of the anal transitional zone in normal anorectal specimens. […] Aigner et al then proposed that, if this mechanism is impaired, hyperperfusion of the arteriovenous plexus will lead to the formation of hemorrhoids.
#21 Hemorrhoids: From basic pathophysiology to clinical management
https://pmc.ncbi.nlm.nih.gov/articles/PMC3342598/
In hemorrhoids, nitric oxide synthase, an enzyme which synthesizes nitric oxide from L-arginine, was reported to increase significantly. […] These abnormal findings still remained after surgical removal of the hemorrhoids, confirming the association between hypervascularization and the development of hemorrhoids. […] Aigner et al identified a sphincter-like structure, formed by a thickened tunica media containing 5-15 layers of smooth muscle cells, between the vascular plexus within the subepithelial space of the anal transitional zone in normal anorectal specimens. […] Aigner et al then proposed that, if this mechanism is impaired, hyperperfusion of the arteriovenous plexus will lead to the formation of hemorrhoids.
#22 Hemorrhoids: From basic pathophysiology to clinical management
https://pmc.ncbi.nlm.nih.gov/articles/PMC3342598/
In hemorrhoids, nitric oxide synthase, an enzyme which synthesizes nitric oxide from L-arginine, was reported to increase significantly. […] These abnormal findings still remained after surgical removal of the hemorrhoids, confirming the association between hypervascularization and the development of hemorrhoids. […] Aigner et al identified a sphincter-like structure, formed by a thickened tunica media containing 5-15 layers of smooth muscle cells, between the vascular plexus within the subepithelial space of the anal transitional zone in normal anorectal specimens. […] Aigner et al then proposed that, if this mechanism is impaired, hyperperfusion of the arteriovenous plexus will lead to the formation of hemorrhoids.
#23 Hemorrhoids: From basic pathophysiology to clinical management
https://www.wjgnet.com/1007-9327/full/v18/i17/2009.htm
A severe inflammatory reaction involving the vascular wall and surrounding connective tissue has been demonstrated in hemorrhoidal specimens, with associated mucosal ulceration, ischemia and thrombosis. […] Several enzymes or mediators involving the degradation of supporting tissues in the anal cushions have been studied. […] MMP-9 was found to be over-expressed in hemorrhoids, in association with the breakdown of elastic fibers. […] Recently, increased microvascular density was found in hemorrhoidal tissue, suggesting that neovascularization might be another important phenomenon of hemorrhoidal disease. […] Aigner et al found that the terminal branches of the superior rectal artery supplying the anal cushion in patients with hemorrhoids had a significantly larger diameter, greater blood flow, higher peak velocity and acceleration velocity, compared to those of healthy volunteers. […] Based on the histological findings of abnormal venous dilatation and distortion in hemorrhoids, dysregulation of the vascular tone might play a role in hemorrhoidal development.
#24 (PDF) The pathogenesis of Hemorrhoids
https://www.academia.edu/72972362/The_pathogenesis_of_Hemorrhoids
The abnormal dilatation and distortion of the vascular channel, together with destructive changes in the supporting connective tissue within the anal cushion, is a paramount finding of hemorrhoids. It appears that the dysregulation of the vascular tone and vascular hyperplasia might play an important role in hemorrhoidal development, and could be a potential target for medical treatment. […] The pathophysiology is most likely multifactorial and complex, manifested by muscle weakness, intrarectal prolapse, changes in vascular pressure and flow in blood vessels, malformations, sphincter damage and failure, venostasis, inflammatory reactions, endothelin and collagen abnormalities, matrix metalloproteinases activity, etc. […] Our findings demonstrate that increased caliber and arterial blood flow of the terminal branches of the SRA are correlated with the appearance of hemorrhoids. We suggest that the hypervascularization of the anorectum contributes to the growth of hemorrhoids rather than being a consequence of hemorrhoids. […] More and more evidence guides us towards the hypothesis that reduced connective tissue stability is associated with a higher incidence of hemorrhoids.
#25 Hemorrhoids: From basic pathophysiology to clinical management
https://pmc.ncbi.nlm.nih.gov/articles/PMC3342598/
The anal cushions of patients with hemorrhoids show significant pathological changes. […] In addition to the above findings, a severe inflammatory reaction involving the vascular wall and surrounding connective tissue has been demonstrated in hemorrhoidal specimens, with associated mucosal ulceration, ischemia and thrombosis. […] Several enzymes or mediators involving the degradation of supporting tissues in the anal cushions have been studied. […] Recently, increased microvascular density was found in hemorrhoidal tissue, suggesting that neovascularization might be another important phenomenon of hemorrhoidal disease. […] Based on the histological findings of abnormal venous dilatation and distortion in hemorrhoids, dysregulation of the vascular tone might play a role in hemorrhoidal development.
#26 Hemorrhoids: From basic pathophysiology to clinical management
https://www.wjgnet.com/1007-9327/full/v18/i17/2009.htm
A severe inflammatory reaction involving the vascular wall and surrounding connective tissue has been demonstrated in hemorrhoidal specimens, with associated mucosal ulceration, ischemia and thrombosis. […] Several enzymes or mediators involving the degradation of supporting tissues in the anal cushions have been studied. […] MMP-9 was found to be over-expressed in hemorrhoids, in association with the breakdown of elastic fibers. […] Recently, increased microvascular density was found in hemorrhoidal tissue, suggesting that neovascularization might be another important phenomenon of hemorrhoidal disease. […] Aigner et al found that the terminal branches of the superior rectal artery supplying the anal cushion in patients with hemorrhoids had a significantly larger diameter, greater blood flow, higher peak velocity and acceleration velocity, compared to those of healthy volunteers. […] Based on the histological findings of abnormal venous dilatation and distortion in hemorrhoids, dysregulation of the vascular tone might play a role in hemorrhoidal development.
#27 Basic Pathophysiology of Hemorrhoids and Their Clinical Management
https://www.ijpsjournal.com/article/Basic+Pathophysiology+of+Hemorrhoids+and+Their+Clinical+Management
One of the most powerful of these is matrix metalloproteinase (MMP), a zinc-dependent proteinase that can break down extracellular proteins like collagen, fibronectin, and elastin. […] The breakdown of elastic filaments was linked to the overexpression of MMP-9 in haemorrhoids. […] Increased microvascular viscosity has recently been observed in haemorrhoidal towels, indicating that neovascularisation may be another significant haemorrhoidal problem cause. […] Dysregulation of the vascular tone may contribute to the development of haemorrhoids, based on the histological observations of aberrant venous dilatation and deformation in haemorrhoids. […] Unbalanced endothelium-derived relaxation […] Numerous vascular disorders are caused by endothelium-derived vasoconstricting factors (such to endothelin and reactive oxygen revolutionaries) and factors (similar to prostacyclin, nitric oxide, and endothelium-derived hyperpolarising factor).
#28 Hemorrhoids: From basic pathophysiology to clinical management
https://www.wjgnet.com/1007-9327/full/v18/i17/2009.htm
A severe inflammatory reaction involving the vascular wall and surrounding connective tissue has been demonstrated in hemorrhoidal specimens, with associated mucosal ulceration, ischemia and thrombosis. […] Several enzymes or mediators involving the degradation of supporting tissues in the anal cushions have been studied. […] MMP-9 was found to be over-expressed in hemorrhoids, in association with the breakdown of elastic fibers. […] Recently, increased microvascular density was found in hemorrhoidal tissue, suggesting that neovascularization might be another important phenomenon of hemorrhoidal disease. […] Aigner et al found that the terminal branches of the superior rectal artery supplying the anal cushion in patients with hemorrhoids had a significantly larger diameter, greater blood flow, higher peak velocity and acceleration velocity, compared to those of healthy volunteers. […] Based on the histological findings of abnormal venous dilatation and distortion in hemorrhoids, dysregulation of the vascular tone might play a role in hemorrhoidal development.
#29 Hemorrhoids: From basic pathophysiology to clinical management
https://pmc.ncbi.nlm.nih.gov/articles/PMC3342598/
The anal cushions of patients with hemorrhoids show significant pathological changes. […] In addition to the above findings, a severe inflammatory reaction involving the vascular wall and surrounding connective tissue has been demonstrated in hemorrhoidal specimens, with associated mucosal ulceration, ischemia and thrombosis. […] Several enzymes or mediators involving the degradation of supporting tissues in the anal cushions have been studied. […] Recently, increased microvascular density was found in hemorrhoidal tissue, suggesting that neovascularization might be another important phenomenon of hemorrhoidal disease. […] Based on the histological findings of abnormal venous dilatation and distortion in hemorrhoids, dysregulation of the vascular tone might play a role in hemorrhoidal development.
#30 Hemorrhoids: From basic pathophysiology to clinical management
https://www.wjgnet.com/1007-9327/full/v18/i17/2009.htm
A severe inflammatory reaction involving the vascular wall and surrounding connective tissue has been demonstrated in hemorrhoidal specimens, with associated mucosal ulceration, ischemia and thrombosis. […] Several enzymes or mediators involving the degradation of supporting tissues in the anal cushions have been studied. […] MMP-9 was found to be over-expressed in hemorrhoids, in association with the breakdown of elastic fibers. […] Recently, increased microvascular density was found in hemorrhoidal tissue, suggesting that neovascularization might be another important phenomenon of hemorrhoidal disease. […] Aigner et al found that the terminal branches of the superior rectal artery supplying the anal cushion in patients with hemorrhoids had a significantly larger diameter, greater blood flow, higher peak velocity and acceleration velocity, compared to those of healthy volunteers. […] Based on the histological findings of abnormal venous dilatation and distortion in hemorrhoids, dysregulation of the vascular tone might play a role in hemorrhoidal development.
#31 Basic Pathophysiology of Hemorrhoids and Their Clinical Management
https://www.ijpsjournal.com/article/Basic+Pathophysiology+of+Hemorrhoids+and+Their+Clinical+Management
One of the most powerful of these is matrix metalloproteinase (MMP), a zinc-dependent proteinase that can break down extracellular proteins like collagen, fibronectin, and elastin. […] The breakdown of elastic filaments was linked to the overexpression of MMP-9 in haemorrhoids. […] Increased microvascular viscosity has recently been observed in haemorrhoidal towels, indicating that neovascularisation may be another significant haemorrhoidal problem cause. […] Dysregulation of the vascular tone may contribute to the development of haemorrhoids, based on the histological observations of aberrant venous dilatation and deformation in haemorrhoids. […] Unbalanced endothelium-derived relaxation […] Numerous vascular disorders are caused by endothelium-derived vasoconstricting factors (such to endothelin and reactive oxygen revolutionaries) and factors (similar to prostacyclin, nitric oxide, and endothelium-derived hyperpolarising factor).
#32 Haemorrhoids – current view on aetiology, pathogenesis and methods of treatment. A review of literature • Nowa Medycyna 2/2016 • Czytelnia Medyczna BORGIS
https://www.czytelniamedyczna.pl/5629,haemorrhoids-current-view-on-aetiology-pathogenesis-and-methods-of-treatment-a.html
Haemorrhoids current view on aetiology, pathogenesis and methods of treatment. A review of literature […] Etiopatogeneza choroby hemoroidalnej jest wieloczynnikowa i nie jest do koca poznana. Opublikowane w ostatnich latach badania dotyczce tego tematu sigaj do zmian na poziomie molekularnym i wrd nieprawidowoci wymieniaj m.in. obniony stosunek kolagenw typu I/III, w porwnaniu z pacjentami bez choroby hemoroidalnej, co sprzyja zmniejszeniu sprystoci tkanki splotw hemoroidalnych. […] The etiopathogenesis of haemorrhoids is multifactorial and not fully understood. Recent publications on this topic reach a molecular level, pointing to a decreased ratio between collagen type I/III in comparison to patients without the disease, which promotes a decrease in haemorrhoid tissue elasticity. […] The studies published over the recent years concerning the etiopathogenesis of haemorrhoidal disease have reached as deep as the molecular level. The disorders that have been discussed have included a decrease in type I/III collagen ratio in patients with haemorrhoidal disease as compared to patients without the disease, facilitating reduced tissue elasticity in the haemorrhoidal plexus.
#33 Anatomy, Physiology, and Pathophysiology of Hemorrhoids | SpringerLink
https://link.springer.com/10.1007/978-3-319-53357-5_2
The understanding of anatomy, physiology, and pathophysiology of hemorrhoids is fundamental to selecting an appropriate treatment of hemorrhoids, improving treatment outcomes, developing novel methods for managing hemorrhoids, and preventing recurrent diseases. […] This chapter deals with some essential knowledge and current views of applied anatomy, anorectal physiology, and pathophysiology of hemorrhoids which includes four main concepts of hemorrhoid formation: sliding anal cushions (loss of fixation network), vascular abnormality (dysregulation of vascular tone, high arterial blood flow, venous hypertension of anorectal vascular plexus, vascular hyperplasia, and neovascularization), rectal redundancy, and an increased pressure on anorectal vascular plexus. […] Abnormalities in collagen composition may contribute to the pathogenesis of hemorrhoids: morphometric analysis. […] Matrix metalloproteinases in pathogenesis of hemorrhoidal disease.
#34 Basic Pathophysiology of Hemorrhoids and Their Clinical Management
https://www.ijpsjournal.com/article/Basic+Pathophysiology+of+Hemorrhoids+and+Their+Clinical+Management
Nitric oxide synthase, an enzyme that produces nitric oxide from L-arginine, has been shown to dramatically rise in haemorrhoids. […] Haemorrhoid patients have been found to exhibit a number of physiological alterations in the anal conduit. […] While there was no discernible alteration in the internal sphincter’s consistency, […] resting anal pressure was significantly higher in patients with prolapsing or non-prolapsing haemorrhoids than in healthy people.
#35 Hemorrhoids pathophysiology – wikidoc
https://www.wikidoc.org/index.php/Hemorrhoids_pathophysiology
Hemorrhoids develop due to a combination of genetic predisposition (weak rectal veins) and certain diet and defecation habits. […] Internal hemorrhoids are located above the dentate line and they occur due to dilatation of the superior hemorrhoidal plexus. […] The first step in the pathogenesis of either type of hemorrhoids is weakening of the surrounding connective tissue and vein wall. All the risk factors (old age, pregnancy, portal hypertension, etc) lead to aggravating this weakness or add more pressure from within the vein. […] Increased tone of the internal anal sphincter causing the feces to press the hemorrhoid against the muscle and thus decreasing venous return and aggravating the symptoms. […] The arteriovenous anastomosis may play a role in the development of hemorrhoids. This is supported by the fact that some hemorrhoids improve after ligating the connecting arteries. […] The redundant bulging mucosa is easily injured causing bleeding. The blood is usually bright red reflecting high oxygen content due to the proximity of AV anastomosis.
#36 Hemorrhoids: Background, Anatomy, Etiology and Pathophysiology
https://emedicine.medscape.com/article/775407-overview
Most authors agree that low-fiber diets cause small-caliber stools, which result in straining during defecation. This increased pressure causes engorgement of the hemorrhoids, possibly by interfering with venous return. […] Internal hemorrhoids cannot cause cutaneous pain, because they are above the dentate line and are not innervated by cutaneous nerves. However, they can bleed, prolapse, and, as a result of the deposition of an irritant onto the sensitive perianal skin, cause perianal itching and irritation. Internal hemorrhoids can produce perianal pain by prolapsing and causing spasm of the sphincter complex around the hemorrhoids. […] Internal hemorrhoids most commonly cause painless bleeding with bowel movements. The covering epithelium is damaged by the hard bowel movement, and the underlying veins bleed. With spasm of the sphincter complex elevating pressure, the internal hemorrhoidal veins can spurt.
#37 Hemorrhoids: Background, Anatomy, Etiology and Pathophysiology
https://emedicine.medscape.com/article/775407-overview
Most authors agree that low-fiber diets cause small-caliber stools, which result in straining during defecation. This increased pressure causes engorgement of the hemorrhoids, possibly by interfering with venous return. […] Internal hemorrhoids cannot cause cutaneous pain, because they are above the dentate line and are not innervated by cutaneous nerves. However, they can bleed, prolapse, and, as a result of the deposition of an irritant onto the sensitive perianal skin, cause perianal itching and irritation. Internal hemorrhoids can produce perianal pain by prolapsing and causing spasm of the sphincter complex around the hemorrhoids. […] Internal hemorrhoids most commonly cause painless bleeding with bowel movements. The covering epithelium is damaged by the hard bowel movement, and the underlying veins bleed. With spasm of the sphincter complex elevating pressure, the internal hemorrhoidal veins can spurt.
#38 Hemorrhoids: Background, Anatomy, Etiology and Pathophysiology
https://emedicine.medscape.com/article/775407-overview
Most authors agree that low-fiber diets cause small-caliber stools, which result in straining during defecation. This increased pressure causes engorgement of the hemorrhoids, possibly by interfering with venous return. […] Internal hemorrhoids cannot cause cutaneous pain, because they are above the dentate line and are not innervated by cutaneous nerves. However, they can bleed, prolapse, and, as a result of the deposition of an irritant onto the sensitive perianal skin, cause perianal itching and irritation. Internal hemorrhoids can produce perianal pain by prolapsing and causing spasm of the sphincter complex around the hemorrhoids. […] Internal hemorrhoids most commonly cause painless bleeding with bowel movements. The covering epithelium is damaged by the hard bowel movement, and the underlying veins bleed. With spasm of the sphincter complex elevating pressure, the internal hemorrhoidal veins can spurt.
#39 Hemorrhoids: Background, Anatomy, Etiology and Pathophysiology
https://emedicine.medscape.com/article/775407-overview
Hemorrhoids are swollen blood vessels in the lower rectum. They are among the most common causes of anal pathology, and subsequently are blamed for virtually any anorectal complaint by patients and medical professionals alike. […] Hemorrhoids generally cause symptoms when they become enlarged, inflamed, thrombosed, or prolapsed. […] Most symptoms arise from enlarged internal hemorrhoids. Abnormal swelling of the anal cushions causes dilatation and engorgement of the arteriovenous plexuses. This leads to stretching of the suspensory muscles and eventual prolapse of rectal tissue through the anal canal. The engorged anal mucosa is easily traumatized, leading to rectal bleeding that is typically bright red due to high blood oxygen content within the arteriovenous anastomoses. Prolapse leads to soiling and mucus discharge (triggering pruritus) and predisposes to incarceration and strangulation.
#40 Hemorrhoids: Background, Anatomy, Etiology and Pathophysiology
https://emedicine.medscape.com/article/775407-overview
Hemorrhoids are swollen blood vessels in the lower rectum. They are among the most common causes of anal pathology, and subsequently are blamed for virtually any anorectal complaint by patients and medical professionals alike. […] Hemorrhoids generally cause symptoms when they become enlarged, inflamed, thrombosed, or prolapsed. […] Most symptoms arise from enlarged internal hemorrhoids. Abnormal swelling of the anal cushions causes dilatation and engorgement of the arteriovenous plexuses. This leads to stretching of the suspensory muscles and eventual prolapse of rectal tissue through the anal canal. The engorged anal mucosa is easily traumatized, leading to rectal bleeding that is typically bright red due to high blood oxygen content within the arteriovenous anastomoses. Prolapse leads to soiling and mucus discharge (triggering pruritus) and predisposes to incarceration and strangulation.
#41 Hemorrhoids: Background, Anatomy, Etiology and Pathophysiology
https://emedicine.medscape.com/article/775407-overview
External hemorrhoids cause symptoms in two ways. First, acute thrombosis of the underlying external hemorrhoidal vein can occur. Acute thrombosis is usually related to a specific event, such as physical exertion, straining with constipation, a bout of diarrhea, or a change in diet. These are acute, painful events.
#42 Recent advances in the management of hemorrhoids
https://www.wjgnet.com/2219-2832/full/v4/i3/55.htm
Hemorrhoids are considered one of the most common anorectal diseases with a prevalence of 4.4% up to 36.4% of the general population, and a peak incidence between 45 and 65 years. […] The pathogenesis of hemorrhoids is not completely clear. Aigner et al concluded that there is an association between hypervascularization and the incidence of hemorrhoidal disease as they reported that the terminal branches of the superior hemorrhoidal artery in patients with hemorrhoidal disease had a significantly larger diameter and greater blood flow, as well as higher peak velocity and acceleration velocity, when compared to those of healthy controls. […] However, the sliding anal canal lining theory, which is the most accepted theory, stated that hemorrhoidal disease develops upon disintegration of the supporting tissues of anal cushions leading to their downward displacement. A number of possible contributing factors leading to migration of the hemorrhoidal cushions have been suggested, including lack of dietary fiber, prolonged straining, spending excess time on the commode, constipation, diarrhea, pregnancy, sedentary lifestyle, and a family history.
#43 Natural Products with Potential Effects on Hemorrhoids: A Review
https://www.mdpi.com/1420-3049/29/11/2673
Hemorrhoid disease represents a complex ailment for which the pathogenic mechanisms remain unclear. The etiology of hemorrhoids is typically multifactorial. Predominant contributing factors include human physiological structure, dietary habits, lack of physical exercise, and defecatory behaviors. These factors collectively increase intra-abdominal pressure during bowel movements, adversely affecting blood flow in the anal and rectal vessels, which may lead to swelling, bleeding, and the development of hemorrhoids. Additionally, inflammatory responses, dysbiosis of the intestinal microbiota, and perianal infectious abscesses can also indirectly contribute to the onset of hemorrhoids. Lastly, certain specific conditions such as sexual activity, pregnancy, and genetic factors may also be associated with the development of hemorrhoids.
#44 Management of hemorrhoids – Walter Bushnell Healthcare Foundation
https://wbhf.walterbushnell.com/publications/bush-beats/item/7-management-of-hemorrhoids
The pathophysiology of hemorrhoidal development, cause of enlargement and symptoms is debatable; various theories and etiologies have been proposed (Table 3). […] Studies implicate intrinsic weakness of the blood vessel wall, heredity, increased intra-abdominal pressure from many causes, including prolonged forceful Valsalva during defecation or resistance training, obstruction of venous outflow secondary to pregnancy or pelvic masses, and constipated stool in the rectal ampulla are possible contributing factors. […] It appears that the dysregulation of the vascular tone and vascular hyperplasia might play an important role in hemorrhoidal development, and could be a potential target for medical treatment. […] The abnormal dilatation and distortion of the vascular channel, together with destructive changes in the supporting connective tissue within the anal cushion, is a paramount finding of hemorrhoids.
#45 Hemorrhoids: Background, Anatomy, Etiology and Pathophysiology
https://emedicine.medscape.com/article/775407-overview
Most authors agree that low-fiber diets cause small-caliber stools, which result in straining during defecation. This increased pressure causes engorgement of the hemorrhoids, possibly by interfering with venous return. […] Internal hemorrhoids cannot cause cutaneous pain, because they are above the dentate line and are not innervated by cutaneous nerves. However, they can bleed, prolapse, and, as a result of the deposition of an irritant onto the sensitive perianal skin, cause perianal itching and irritation. Internal hemorrhoids can produce perianal pain by prolapsing and causing spasm of the sphincter complex around the hemorrhoids. […] Internal hemorrhoids most commonly cause painless bleeding with bowel movements. The covering epithelium is damaged by the hard bowel movement, and the underlying veins bleed. With spasm of the sphincter complex elevating pressure, the internal hemorrhoidal veins can spurt.
#46 Management of hemorrhoids – Walter Bushnell Healthcare Foundation
https://wbhf.walterbushnell.com/publications/bush-beats/item/7-management-of-hemorrhoids
As a patient ages and has continual presence of one or more of the above mentioned factors, the integrity of the hemorrhoid „cushions” deteriorates, and the hemorrhoid tissue begins to bulge and descend into the anal canal. Further, when the cushion bulges into the canal, it is exposed to potential trauma and irritation from the passage of the stool.
#47
https://www.archivesofmedicalscience.com/Synergistic-therapeutic-approach-for-hemorrhoids-integrating-mesenchymal-stem-cells,183465,0,2.html
Mesenchymal stem cells (MSCs) have promising regenerative properties in tissue repair and anti-inflammatory responses. This study aimed to investigate the effects of MSCs and their combination with micronized purified flavonoid fraction (MPFF) in a croton oil-induced hemorrhoids model on tissue edema, inflammation, and underlying molecular mechanisms. Treatment with MSCs alone or in combination with MPFF significantly reduced tissue edema, inflammation, TNF- expression, and MMP-9 activity. Additionally, MSCs increased TGF- expression, and collagen type I/III ratio, and accelerated wound healing by resolving inflammation. These findings suggest that MSCs play a crucial role in modulating TNF-, TGF-, collagen remodeling, and MMP-9 activity, highlighting their promising role in hemorrhoid treatment and wound healing processes.
#48
https://www.archivesofmedicalscience.com/Synergistic-therapeutic-approach-for-hemorrhoids-integrating-mesenchymal-stem-cells,183465,0,2.html
The pathological changes in anal cushions in hemorrhoidal disease result from inflammation, characterized by hemorrhoidal plexus dilation in the rectoanal area with associated connective tissue damage. […] This study revealed that MSCs were effective in suppressing inflammation, demonstrated by a significant reduction in tissue edema in the treatment group (T1 and T2) compared to the hemorrhoid group (C-1 and C-2). This demonstrates the anti-inflammatory effects of MSCs by reducing interstitial edema during inflammation. […] MSCs promoted wound healing by promptly terminating the inflammatory phase, as evidenced by increased expression of TGF- in the treatment group (T1 and T2) compared to the hemorrhoid group (C-1 and C-2). This finding demonstrated the role of MSCs in initiating proliferation by inducing TGF- expression. […] The anti-inflammatory effects of MSCs are mediated by the release of trophic and anti-inflammatory factors, which interact with immune cells and inhibit inflammatory responses.
#49 The Role of Diosmin in Hemorrhoids Management – Walter Bushnell Healthcare Foundation
https://wbhf.walterbushnell.com/publications/bush-beats/item/387-the-role-of-diosmin-in-hemorrhoids-management
Diosmin exhibits a multifaceted mechanism of action, which includes improvement of venous tone, increased lymphatic drainage, protection of capillary bed microcirculation, inhibition of inflammatory reactions, and reduced capillary permeability. Diosmin exerts its phlebotonic effect by prolonging the vasoconstrictor effect of norepinephrine on vein wall, enhances venous tone, and thus reduces distensibility and stasis. […] Overall, these multifaceted actions of diosmin possibly converge to provide maximal benefit to individuals with hemorrhoids.
#50 The Role of Diosmin in Hemorrhoids Management – Walter Bushnell Healthcare Foundation
https://wbhf.walterbushnell.com/publications/bush-beats/item/387-the-role-of-diosmin-in-hemorrhoids-management
Diosmin exhibits a multifaceted mechanism of action, which includes improvement of venous tone, increased lymphatic drainage, protection of capillary bed microcirculation, inhibition of inflammatory reactions, and reduced capillary permeability. Diosmin exerts its phlebotonic effect by prolonging the vasoconstrictor effect of norepinephrine on vein wall, enhances venous tone, and thus reduces distensibility and stasis. […] Overall, these multifaceted actions of diosmin possibly converge to provide maximal benefit to individuals with hemorrhoids.
#51 Management of Hemorrhoids (2024) | ASCRS Toolkit – FREE Resources
https://www.ascrsu.com/ascrs/view/ASCRS-Toolkit/2851101/all/Management_of_Hemorrhoids__2024_
Medical therapy for hemorrhoids includes a variety of topical agents comprising creams, ointments, foams, and suppositories. The majority of these are available over the counter, although some require a prescription. There are limited data to guide the use of these medications, including hydrocortisone, phenylephrine, pramoxine, and witch hazel. A small prospective observational study of 88 pregnant patients demonstrated that combined hydrocortisone acetate 1% and pramoxine hydrochloride 1% foam provided effective symptom control for hemorrhoid-related pain, pruritus, and swelling in late pregnancy even after correcting for a potential placebo effect. Of note, this compound was found to be safe in late pregnancy without any adverse fetal effects. […] Phlebotonics are a heterogenous class of drugs consisting of plant extracts (ie, flavonoids) and synthetic compounds (ie, calcium dobesilate), which can be used to treat both acute and chronic hemorrhoidal disease. Although their mechanism of action has not been established, phlebotonics are associated with strengthening blood vessel walls, increasing venous tone, increasing lymphatic drainage, and normalizing capillary permeability.
#52 (PDF) The pathogenesis of Hemorrhoids
https://www.academia.edu/72972362/The_pathogenesis_of_Hemorrhoids
The abnormal dilatation and distortion of the vascular channel, together with destructive changes in the supporting connective tissue within the anal cushion, is a paramount finding of hemorrhoids. It appears that the dysregulation of the vascular tone and vascular hyperplasia might play an important role in hemorrhoidal development, and could be a potential target for medical treatment. […] The pathophysiology is most likely multifactorial and complex, manifested by muscle weakness, intrarectal prolapse, changes in vascular pressure and flow in blood vessels, malformations, sphincter damage and failure, venostasis, inflammatory reactions, endothelin and collagen abnormalities, matrix metalloproteinases activity, etc. […] Our findings demonstrate that increased caliber and arterial blood flow of the terminal branches of the SRA are correlated with the appearance of hemorrhoids. We suggest that the hypervascularization of the anorectum contributes to the growth of hemorrhoids rather than being a consequence of hemorrhoids. […] More and more evidence guides us towards the hypothesis that reduced connective tissue stability is associated with a higher incidence of hemorrhoids.
#53 Hemorrhoids | Concise Medical Knowledge
https://www.lecturio.com/concepts/hemorrhoids/
Hemorrhoids become symptomatic when enlarged, inflamed, thrombosed, or prolapsed. Hemorrhoidal veins are located in the submucosal layer in the lower rectum. Arise from a plexus or cushion of dilated arteriovenous channels and connective tissue. May be external or internally located based on position in relation to dentate line. […] Unclear pathogenesis; possible theories include: deterioration of connective tissue anchoring hemorrhoids, hypertrophy or increased internal anal sphincter tone, abnormal arteriovenous distention within hemorrhoidal cushions, and abnormal dilation of internal hemorrhoidal venous plexus.
#54 Natural Products with Potential Effects on Hemorrhoids: A Review
https://www.mdpi.com/1420-3049/29/11/2673
The main mechanisms of natural productsâ effects on hemorrhoids may be associated with promoting the coagulation process, suppressing inflammatory responses, inhibiting the growth of perianal pathogenic bacteria, and promoting the healing of tissue injuries. The mechanisms of anti-inflammatory natural products primarily involve regulating inflammatory signaling pathways, acting on inflammation receptors, and controlling the biosynthesis of inflammatory mediators (pro-inflammatory and anti-inflammatory factors). […] Natural products can achieve hemostatic effects through promoting the first and second phases of aggregation platelets, promoting the processes of the intrinsic and extrinsic coagulation pathways, and inhibiting the fibrinolytic system. Additionally, promoting the contraction of vascular smooth muscle to decrease blood flow, thereby reducing the time required for coagulation at sites of vascular damage, is also a possible way.
#55 The Role of Diosmin in Hemorrhoids Management – Walter Bushnell Healthcare Foundation
https://wbhf.walterbushnell.com/publications/bush-beats/item/387-the-role-of-diosmin-in-hemorrhoids-management
Diosmin exhibits a multifaceted mechanism of action, which includes improvement of venous tone, increased lymphatic drainage, protection of capillary bed microcirculation, inhibition of inflammatory reactions, and reduced capillary permeability. Diosmin exerts its phlebotonic effect by prolonging the vasoconstrictor effect of norepinephrine on vein wall, enhances venous tone, and thus reduces distensibility and stasis. […] Overall, these multifaceted actions of diosmin possibly converge to provide maximal benefit to individuals with hemorrhoids.