Zapalenie pęcherzyka żółciowego
Patofizjologia i mechanizm

Zapalenie pęcherzyka żółciowego to stan zapalny ściany pęcherzyka, najczęściej wywołany zablokowaniem przewodu pęcherzykowego przez kamienie żółciowe (ponad 90% przypadków). Blokada ta prowadzi do zastoju żółci, wzrostu ciśnienia wewnątrzpęcherzykowego oraz uwolnienia fosfolipazy A, która przekształca lecytynę w lizolecytynę – mediator uszkadzający nabłonek. Proces zapalny obejmuje wszystkie warstwy ściany pęcherzyka, a mechanizm błędnego koła między wydzielaniem płynu a stanem zapalnym prowadzi do obrzęku, niedokrwienia i martwicy. Bezkamicze zapalenie pęcherzyka (ok. 10% przypadków) ma patogenezę wieloczynnikową, z dominującą rolą zastoju żółci i niedokrwienia, często w przebiegu ciężkich chorób, urazów czy żywienia pozajelitowego. Wtórna infekcja bakteryjna, obecna w około 20% przypadków, najczęściej obejmuje bakterie Gram-ujemne, takie jak Escherichia coli i Klebsiella spp., które dzięki czynnikom wirulencji uszkadzają nabłonek pęcherzyka.

Patofizjologia zapalenia pęcherzyka żółciowego

Zapalenie pęcherzyka żółciowego (cholecystitis) to stan zapalny obejmujący ścianę pęcherzyka żółciowego. Mechanizm patofizjologiczny tej choroby jest złożony, a jego podstawą jest najczęściej zablokowanie przewodu pęcherzykowego, prowadzące do rozwoju stanu zapalnego.12 Blokada przewodu pęcherzykowego powoduje zaburzenia w odpływie żółci i gromadzenie się jej w pęcherzyku, co prowadzi do zwiększenia ciśnienia wewnątrz narządu oraz inicjacji procesu zapalnego.34

Patogeneza kamiczego zapalenia pęcherzyka żółciowego

Ponad 90% przypadków ostrego zapalenia pęcherzyka żółciowego jest spowodowanych zablokowaniem przewodu pęcherzykowego przez kamienie żółciowe.56 W wyniku tego procesu dochodzi do zastoju żółci w pęcherzyku oraz wzrostu ciśnienia wewnątrzpęcherzykowego. Nagromadzona, zagęszczona żółć wraz z podwyższonym ciśnieniem inicjują proces zapalny, który uszkadza ścianę pęcherzyka.7

Mechanizm patogenetyczny kamiczego zapalenia pęcherzyka żółciowego przebiega w kilku etapach:8910

  1. Kamień żółciowy zostaje zaklinowany w przewodzie pęcherzykowym, powodując jego niedrożność
  2. Zastój żółci prowadzi do zwiększenia ciśnienia wewnątrzpęcherzykowego
  3. Uwolnienie enzymu fosfolipazy A, który przekształca lecytynę w lizolecytynęmediator zapalny
  4. Uszkodzona błona śluzowa wydziela więcej płynu do światła pęcherzyka żółciowego niż absorbuje
  5. Powstałe rozciągnięcie ściany pęcherzyka uwalnia kolejne mediatory zapalne (np. prostaglandyny)
  6. Postępujące uszkodzenie błony śluzowej i niedokrwienie ściany pęcherzyka żółciowego
  7. Proces zapalny obejmuje wszystkie warstwy ściany pęcherzyka

Istotną rolę w patogenezie odgrywa mechanizm błędnego koła, w którym wydzielanie płynu i stan zapalny wzajemnie się napędzają. Prowadzi to do nasilenia obrzęku ściany pęcherzyka, który upośledza przepływ krwi, powodując niedokrwienie i martwicę.1112 Bez odpowiedniego leczenia, przedłużające się niedokrwienie i stan zapalny pęcherzyka żółciowego mogą prowadzić do zgorzelinowego zapalenia (u około 20% pacjentów) oraz perforacji pęcherzyka (również około 20%).13

Rola kamieni żółciowych w patogenezie

Kamienie żółciowe (cholelithiasis) stanowią główny czynnik etiologiczny zapalenia pęcherzyka żółciowego. Tworzą się one z różnych materiałów, takich jak bilirubinian lub cholesterol.14 Możemy wyróżnić trzy główne typy kamieni żółciowych:15

  • Kamienie cholesterolowe – złożone wyłącznie z cholesterolu, powstające w wyniku nadmiernej produkcji cholesterolu; istnieje uznany związek między złą dietą, otyłością a kamieniami cholesterolowymi
  • Kamienie barwnikowe – złożone z barwników żółciowych, powstające w wyniku nadmiernej produkcji barwników żółciowych; często występują u osób z niedokrwistością hemolityczną
  • Kamienie mieszane – składające się zarówno z cholesterolu, jak i barwników żółciowych

Formowanie się kamieni cholesterolowych obejmuje trzy główne czynniki: przesycenie żółci cholesterolem, czynniki jądrowe i przeciwjądrowe oraz hipomotorykę pęcherzyka żółciowego.16 Najważniejszym czynnikiem jest zwiększone nasycenie cholesterolem w żółci, które przekracza zdolność solubilizacyjną kwasów żółciowych i lecytyny.17 Hipomotoryka pęcherzyka żółciowego (upośledzone napełnianie i opróżnianie) sprzyja tworzeniu się kamieni cholesterolowych, utrzymując przesyconą cholesterolem żółć w stanie statycznym i umożliwiając krystalizację cholesterolu.18

Mechanizmy molekularne procesu zapalnego

Na poziomie molekularnym, zapalenie pęcherzyka żółciowego wiąże się z uwolnieniem różnych mediatorów zapalnych. W przypadku kamiczego zapalenia pęcherzyka żółciowego, uszkodzenie śluzówki powoduje uwolnienie fosfolipazy z lizosomów.19 Enzym ten przekształca lecytynę zawartą w żółci w lizolecytynę, która bezpośrednio uszkadza nabłonek pęcherzyka żółciowego.20

Ponadto, w odpowiedzi na infekcję i niedrożność pęcherzyka żółciowego, rezydujące makrofagi i komórki nabłonkowe wydzielają prozapalne cytokiny, w tym IL-1, IL-6 i TNF-alfa.21 Cytokiny te inicjują miejscową odpowiedź zapalną i rekrutują dodatkowe leukocyty. Chociaż taka odpowiedź jest niezbędna do zwalczania infekcji, nadmierny stan zapalny może uszkodzić tkanki gospodarza.22

W przewlekłym zapaleniu pęcherzyka żółciowego zaproponowano mechanizm obejmujący zwiększoną ekspresję COX-2 w komórkach mięśni gładkich ściany pęcherzyka żółciowego, co prowadzi do zmniejszenia funkcji ewakuacyjnej pęcherzyka i aktywnego przechodzenia żółci wątrobowej do pęcherzyka żółciowego.23 Nadmierna ekspresja COX-2 w komórkach nabłonkowych błony śluzowej pęcherzyka żółciowego powoduje zmniejszenie funkcji absorpcyjnej pęcherzyka (zmniejszenie absorpcji wody i cholesterolu żółciowego) i bierne przechodzenie żółci wątrobowej do pęcherzyka żółciowego.24

Patogeneza bezkamiczego zapalenia pęcherzyka żółciowego

Bezkamicze zapalenie pęcherzyka żółciowego (acalculous cholecystitis) stanowi około 10% wszystkich przypadków ostrego zapalenia pęcherzyka żółciowego.25 Jest to ostre martwiczo-zapalne schorzenie pęcherzyka żółciowego występujące przy braku kamieni żółciowych, o wieloczynnikowej patogenezie, charakteryzujące się wysokimi wskaźnikami chorobowości i śmiertelności.2627

Patogeneza bezkamiczego zapalenia pęcherzyka żółciowego jest wieloczynnikowa i prawdopodobnie wynika z połączenia zastoju żółci i niedokrwienia.2829 Można ją podsumować następująco:3031

  1. Brak żywienia dojelitowego i hipoperfuzja powodują hipotonię i rozszerzenie pęcherzyka żółciowego
    • Rozszerzenie pęcherzyka zwiększa napięcie ściany, dodatkowo upośledzając perfuzję ściany pęcherzyka
    • Zastój żółciowy powoduje koncentrację detergentów żółciowych, które mogą uszkadzać ścianę pęcherzyka
  2. Niedokrwienie i zastój żółci prowadzą do:
    • Miejscowej odpowiedzi zapalnej w ścianie pęcherzyka żółciowego
    • Uszkodzenia nabłonka i ostatecznie martwicy tkanki pęcherzyka żółciowego
    • Możliwej martwicy i perforacji pęcherzyka żółciowego
    • Potencjalnej nadkażenie bakteriami jelitowymi (ropniak pęcherzyka żółciowego)

Czynniki ryzyka bezkamiczego zapalenia pęcherzyka żółciowego obejmują ciężkie choroby, oparzenia, urazy, poważne zabiegi chirurgiczne, cukrzycę oraz stany immunosupresji.32 Główną przyczyną tej choroby uważa się zastój żółci i zwiększoną litogenność żółci.33 Również niedokrwienie ściany pęcherzyka żółciowego, występujące z powodu stanu niskiego przepływu spowodowanego gorączką, odwodnieniem lub niewydolnością serca, może odgrywać rolę w patogenezie bezkamiczego zapalenia pęcherzyka żółciowego.34

Rola infekcji bakteryjnej

Chociaż zapalenie pęcherzyka żółciowego pierwotnie rozpoczyna się jako proces nieinfekcyjny, wtórna infekcja bakteryjna może rozwinąć się w późniejszym etapie choroby.35 Infekcja bakteryjna występuje w około 20% przypadków ostrego zapalenia pęcherzyka żółciowego.3637

Najczęściej izolowanymi patogenami w infekcjach żółciowych są bakterie Gram-ujemne, z dominacją Escherichia coli, Klebsiella spp., Acinetobacter baumannii complex i Enterobacter spp.38 W ustabilizowanym zapaleniu pęcherzyka żółciowego często występuje wtórna infekcja patogenami jelitowymi, w tym Escherichia coli, Enterococcus faecalis, Klebsiella spp., Pseudomonas spp., Proteus spp. oraz Bacteroides fragilis i pokrewnymi szczepami.3940

Kluczowe dla zdolności bakterii, pasożytów i grzybów do ustanowienia infekcji pęcherzyka żółciowego jest ekspresja specyficznych czynników wirulencji, które umożliwiają przyleganie do komórek nabłonkowych wyściełających błonę śluzową pęcherzyka żółciowego.41 Patogeny produkują różne białka powierzchniowe i polisacharydy, które pośredniczą w wiązaniu z nabłonkiem gospodarza, co stanowi niezbędny pierwszy krok w patogenezie.42

Poza zdolnością adhezji, wiele patogenów wytwarza toksyny, które bezpośrednio uszkadzają i zakłócają błony komórkowe nabłonka pęcherzyka żółciowego.43 Te tworzące pory toksyny uwalniane przez patogeny pozwalają na wyciek zawartości komórek, napływ wapnia, utratę potencjału błonowego i ostatecznie śmierć komórek gospodarza.44

Powikłania zapalenia pęcherzyka żółciowego

Nieleczone ostre zapalenie pęcherzyka żółciowego może prowadzić do poważnych powikłań, w tym perforacji pęcherzyka, posocznicy i śmierci.45 Bez względu na przyczynę niedrożności, obrzęk ściany pęcherzyka ostatecznie może spowodować niedokrwienie ściany i prowadzić do zgorzelinowego zapalenia pęcherzyka żółciowego.46

Zgorzelnowe zapalenie pęcherzyka żółciowego może zostać zainfekowane przez organizmy wytwarzające gaz, powodując ostre rozedmowe zapalenie pęcherzyka żółciowego; wszystkie te stany mogą szybko zagrażać życiu, a pęknięcie wiąże się z wysokim wskaźnikiem śmiertelności.47 Rozedmowe zapalenie pęcherzyka żółciowego jest spowodowane inwazją wytwarzających gaz patogenów (klasycznie Clostridium welchii) ściany pęcherzyka żółciowego, wywołując gorączkę, ból w prawym górnym kwadrancie brzucha i wczesne markery posocznicy.48

Inne powikłania wymagające pilnego leczenia chirurgicznego obejmują ropniaka, martwicę lub perforację (ograniczoną lub z rozlanym zapaleniem otrzewnej żółciowym) pęcherzyka żółciowego.49 Dodatkowe powikłania to wodniak pęcherzyka żółciowego, ropień wątroby, przetoka jelitowa żółciowa (przejście dużych kamieni żółciowych do światła jelita może skutkować niedrożnością jelit spowodowaną kamieniem żółciowym) oraz zespół Mirizziego (niedrożność szyi pęcherzyka żółciowego lub przewodu pęcherzykowego przez duży kamień żółciowy powodujący objawy ucisku przewodu żółciowego wspólnego).50

Czynniki ryzyka i mechanizmy predysponujące

Istnieje wiele czynników ryzyka, które mogą predysponować do rozwoju zapalenia pęcherzyka żółciowego. Częstość występowania kamieni żółciowych, głównej przyczyny zapalenia pęcherzyka, różni się w zależności od wieku i płci. Kamienie żółciowe występują u około 10-15% mężczyzn i 20-40% kobiet powyżej 60. roku życia.51

Ogólnie rzecz biorąc, ryzyko wystąpienia kamieni zwiększa się wraz z:52

  • Przebytymi ciążami
  • Hormonalną terapią zastępczą
  • Stosowaniem doustnych środków antykoncepcyjnych
  • Otyłością

Kamienie są również związane z hipertriglicerydemią, chorobą Leśniowskiego-Crohna i hiperalimentacją pozajelitową.53 Czynniki dietetyczne zostały powiązane z patogenezą kamicy żółciowej. Wysokie spożycie tłuszczów nasyconych wiąże się ze zwiększonym ryzykiem tworzenia się kamieni żółciowych.54

Wykazano, że spożywanie rafinowanych cukrów jest związane z wyższą syntezą cholesterolu w wątrobie, wtórną do zwiększonej insuliny w odpowiedzi na wysokie spożycie cukru, podczas gdy niskie spożycie błonnika wiąże się ze zwiększonym ryzykiem tworzenia się kamieni żółciowych z powodu wynikającego z tego zwiększenia wydzielania wtórnych kwasów żółciowych z powodu zmniejszonej perystaltyki okrężnicy.55

Ponadto, dieta niskobłonnikowa i wysokocukrowa może prowadzić do zaparć i późniejszego tworzenia się kryształów w żółci.56 Przedłużenie pasażu jelitowego zostało zaproponowane jako mechanizm zwiększenia proporcji kwasu deoksycholowego w żółci.57 Zwiększenie ilości kwasu deoksycholowego w żółci od dawna wiązano z patogenezą kamieni żółciowych bogatych w cholesterol.58

Odwodnienie podczas lata może dodatkowo zwiększyć ryzyko ostrego zapalenia pęcherzyka żółciowego, powodując zastój żółci z powodu zmniejszonego opróżniania pęcherzyka żółciowego.59 Z drugiej strony, rola cholecystokininy (CCK) w sezonowej zmienności ostrego zapalenia pęcherzyka żółciowego została zaproponowana przez kilku autorów.60 Cholecystokinina jest hormonem obwodowym uwalnianym przez proksymalną część jelita cienkiego w odpowiedzi na tłuszcze i aminokwasy w posiłku, co z kolei stymuluje pęcherzyk żółciowy do skurczu i uwolnienia magazynowanej żółci do jelita.61

Warianty kliniczne zapalenia pęcherzyka żółciowego

Zapalenie pęcherzyka żółciowego może rozwijać się jako proces ostry lub przewlekły.62 Główne warianty kliniczne obejmują:

Ostre zapalenie pęcherzyka żółciowego

Ostre zapalenie pęcherzyka żółciowego dotyczy nagłego stanu zapalnego pęcherzyka żółciowego, który rozwija się w ciągu kilku godzin, zazwyczaj z powodu zablokowania przewodu pęcherzykowego przez kamień żółciowy.63 Pacjenci z ostrym zapaleniem pęcherzyka żółciowego zgłaszają stały ból w prawym górnym kwadrancie brzucha lub nadbrzuszu, związany z objawami zapalenia, takimi jak gorączka lub letarg.64

Przewlekłe zapalenie pęcherzyka żółciowego

Przewlekłe zapalenie pęcherzyka żółciowego to długotrwały stan zapalny pęcherzyka żółciowego, spowodowany mechaniczną lub fizjologiczną dysfunkcją jego opróżniania.65 Zaproponowana etiologia obejmuje nawracające epizody ostrego zapalenia pęcherzyka żółciowego lub przewlekłe podrażnienie przez kamienie żółciowe wywołujące odpowiedź zapalną w ścianie pęcherzyka żółciowego.66

Ponad 90% przypadków przewlekłego zapalenia pęcherzyka żółciowego wiąże się z obecnością kamieni żółciowych.67 Kamienie żółciowe, powodując przerywaną niedrożność przepływu żółci, najczęściej blokując przewód pęcherzykowy, prowadzą do stanu zapalnego i obrzęku ściany pęcherzyka żółciowego.68

Zaproponowano, że litogenna żółć prowadzi do zwiększonego uszkodzenia zależnego od wolnych rodników przez hydrofobowe sole żółciowe. To, w połączeniu ze zmniejszoną ochroną błony śluzowej z powodu niższych poziomów prostaglandyny E2, skutkuje ciągłym stanem zapalnym.69 Gdy receptory cholecystokininy mięśni gładkich są dotknięte, występuje upośledzony skurcz pęcherzyka żółciowego, co prowadzi do zastoju i pogarsza sprzyjające środowisko, w którym litogenna żółć sprzyja stanowi zapalnemu.70

Zapalenie pęcherzyka żółciowego bez kamieni

Bezkamicze zapalenie pęcherzyka żółciowego (ostry alitiaziowy stan zapalny) to ostre martwiczo-zapalne schorzenie pęcherzyka żółciowego występujące przy braku kamieni żółciowych, o wieloczynnikowej patogenezie.71 Może być spowodowane przez czynniki takie jak uraz, całkowite żywienie pozajelitowe, wirusowe (wirus hepatotropowy) lub bakteryjne (głównie gram-ujemne lub beztlenowe) infekcje.72

Warianty ciężkich postaci zapalenia pęcherzyka żółciowego

Szczególne, ciężkie postaci zapalenia pęcherzyka żółciowego obejmują:

Zgorzelinowe zapalenie pęcherzyka żółciowego – ciężka forma ostrego zapalenia pęcherzyka żółciowego związana z upośledzeniem naczyniowym i krwotokiem śródściennym, martwicą i tworzeniem się ropnia śródściennego.73 Jest to zwykle spowodowane zablokowaniem przewodu pęcherzykowego przez kamień, z postępującym rozszerzeniem pęcherzyka żółciowego i ostatecznie niedokrwienną martwicą ściany.74 Częstość występowania waha się od 2% do około 30% w różnych seriach chirurgicznych.75

Rozedmowe zapalenie pęcherzyka żółciowego – rzadkie, zagrażające życiu i szybko postępujące powikłanie ostrego zapalenia pęcherzyka żółciowego.76 Uważa się, że upośledzenie tętnicy pęcherzykowej sprzyja rozprzestrzenianiu się organizmów wytwarzających gaz w środowisku beztlenowym i przenikaniu gazu do ściany pęcherzyka żółciowego.77 Najczęściej izolowanymi organizmami są Clostridium welchii i Escherichia coli.78 To powikłanie występuje z większą częstością u pacjentów z cukrzycą (do 50%) i pacjentów płci męskiej (do 71%).79

Nowe kierunki w rozumieniu patogenezy

Postęp biotechnologii i technik molekularnych dostarczył potężnych nowych narzędzi do poprawy diagnostyki, charakterystyki i leczenia ostrego zapalenia pęcherzyka żółciowego.80 Molekularne metody wykrywania, takie jak PCR, pozwalają na szybką, czułą identyfikację patogenów bakteryjnych, pasożytniczych i grzybiczych w tkankach pęcherzyka żółciowego.81

Techniki terapii genowej wykorzystujące systemy CRISPR/Cas9 lub RNAi mogą selektywnie edytować genomy drobnoustrojów, aby wyłączyć mechanizmy wirulencji.82 Podawanie probiotyków wykazuje obiecujące wyniki jako strategia terapeutyczna dla zapalenia pęcherzyka żółciowego, promując wzrost korzystnych mikroorganizmów, które mogą konkurować z patogenami.83 Szczepy probiotyczne, takie jak Lactobacillus i Bifidobacterium, są wybierane na podstawie ich zdolności do bezpośredniego hamowania patogenów jelitowych, takich jak E. coli i Klebsiella.84

Integracja zaawansowanych biotechnologii ma znaczny potencjał zrewolucjonizowania diagnostyki, leczenia i zarządzania zapaleniem pęcherzyka żółciowego.85

Podsumowanie mechanizmów patogenetycznych

Zapalenie pęcherzyka żółciowego (Zapalenie pęcherzyka żółciowego) to wieloczynnikowy proces chorobowy, którego podstawowym mechanizmem patofizjologicznym jest blokada przewodu pęcherzykowego, najczęściej przez kamienie żółciowe. Prowadzi to do zastoju żółci, wzrostu ciśnienia wewnątrzpęcherzykowego i uruchomienia kaskady zapalnej.8687

W kamiczym zapaleniu pęcherzyka żółciowego, uwolnienie fosfolipazy A przekształca lecytynę w lizolecytynę, która uszkadza błonę śluzową pęcherzyka. Uszkodzenie błony śluzowej prowadzi do wydzielania płynu i uwalniania mediatorów zapalnych, takich jak prostaglandyny, które nasilają stan zapalny.8889

W bezkamiczym zapaleniu pęcherzyka żółciowego, główną rolę odgrywają zastój żółci i niedokrwienie, które mogą być spowodowane przedłużonym postem, hipoperfuzją, stosowaniem leków wazoaktywnych i innymi czynnikami ryzyka związanymi z ciężkimi chorobami.9091

Wtórna infekcja bakteryjna, najczęściej patogenami jelitowymi, może komplikować zarówno kamicze, jak i bezkamicze zapalenie pęcherzyka żółciowego, prowadząc do cięższego przebiegu choroby i potencjalnych powikłań.9293

Zrozumienie złożonych mechanizmów patogenetycznych zapalenia pęcherzyka żółciowego jest kluczowe dla rozwoju skutecznych strategii profilaktycznych, diagnostycznych i terapeutycznych, które mogą pomóc w zmniejszeniu zachorowalności i śmiertelności związanej z tą powszechną chorobą.94

Kolejne rozdziały

Zapraszamy do dalszego czytania naszego leksykonu.

Wybierz kolejny rozdział z menu poniżej, aby otworzyć nową podstronę kompedium wiedzy i uzyskać szczegółowe informację o leku, substancji lub chorobie.

  1. 11.04.2026
  2. www.leksykon.com.pl

Materiały źródłowe

  • #1 Acute Cholecystitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK459171/
    Acute cholecystitis refers to inflammation of the gallbladder. The pathophysiologic mechanism of acute cholecystitis is blockage of the cystic duct. […] The etiology of acute cholecystitis is, by definition, cystic duct blockage, which causes inflammation. […] Occlusion of the cystic duct or malfunction of the mechanics of gallbladder emptying is the pathophysiology of this disease. […] Gallstones form from various materials such as bilirubinate or cholesterol. These materials increase the likelihood of cholecystitis and cholelithiasis in conditions such as sickle cell disease where red blood cells are broken down forming excess bilirubin and forming pigmented stones. […] Regardless of the cause of the blockage, the gallbladder wall edema will eventually cause wall ischemia and become gangrenous. The gangrenous gallbladder can become infected by gas-forming organisms, causing acute emphysematous cholecystitis; all of these conditions can quickly become life-threatening, and rupture has a high rate of mortality. […] Cases of acute untreated cholecystitis could lead to perforation of the gallbladder, sepsis, and death.
  • #2 Cholecystitis – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/cholecystitis/symptoms-causes/syc-20364867
    Cholecystitis (ko-luh-sis-TIE-tis) is swelling and irritation, called inflammation, of the gallbladder. […] Most often, gallstones that block the tube leading out of the gallbladder cause cholecystitis. This results in a bile buildup that can cause inflammation. […] Cholecystitis is when your gallbladder is inflamed. Gallbladder inflammation can be caused by: […] Most often, cholecystitis is the result of hard particles of bile that can form in the gallbladder, called gallstones. Gallstones can block the tube that carries bile when it leaves the gallbladder. The tube is called the cystic duct. Bile builds up in the gallbladder, causing swelling and irritation. […] A tumor may keep bile from draining out of the gallbladder as it should. This causes bile buildup that can lead to cholecystitis. […] Stones or thickened bile and tiny particles called sludge can block the bile duct and lead to cholecystitis. Kinking or scarring of the bile ducts also can cause blockage. […] Very serious illness can damage blood vessels and lessen blood flow to the gallbladder. This can lead to cholecystitis.
  • #3 Cholecystitis – Wikipedia
    https://en.wikipedia.org/wiki/Cholecystitis
    More than 90% of the time acute cholecystitis is caused from blockage of the cystic duct by a gallstone. […] Blockage of the cystic duct by a gallstone causes a buildup of bile in the gallbladder and increased pressure within the gallbladder. Concentrated bile, pressure, and sometimes bacterial infection irritate and damage the gallbladder wall, causing inflammation and swelling of the gallbladder. […] Inflammation and swelling of the gallbladder can reduce normal blood flow to areas of the gallbladder, which can lead to cell death due to inadequate oxygen.
  • #4 Cholecystitis – WikiProjectMed
    http://mdwiki.org/wiki/Cholecystitis
    Blockage of the cystic duct by a gallstone causes a buildup of bile in the gallbladder and increased pressure within the gallbladder. Concentrated bile, pressure, and sometimes bacterial infection irritate and damage the gallbladder wall, causing inflammation and swelling of the gallbladder. Inflammation and swelling of the gallbladder can reduce normal blood flow to areas of the gallbladder, which can lead to cell death due to inadequate oxygen.
  • #5 Acute Cholecystitis: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/171886-overview
    Ninety percent of cases of cholecystitis involve stones in the gallbladder (ie, calculous cholecystitis), with the other 10% of cases representing acalculous cholecystitis. […] Acute calculous cholecystitis is caused by an obstruction of the cystic duct, leading to distention of the gallbladder. As the gallbladder becomes distended, blood flow and lymphatic drainage are compromised, leading to mucosal ischemia and necrosis. […] Although the exact mechanism of acalculous cholecystitis is unclear, several theories exist. Injury may be the result of retained concentrated bile, an extremely noxious substance. In the presence of prolonged fasting, the gallbladder does not receive a cholecystokinin (CCK) stimulus to empty; thus, the concentrated bile remains stagnant in the lumen. […] A study by Cullen et al demonstrated the ability of endotoxins to cause necrosis, hemorrhage, areas of fibrin deposition, and extensive mucosal loss, consistent with an acute ischemic insult. Endotoxins also abolish the contractile response to CCK, leading to gallbladder stasis.
  • #6 Cholecystitis – Wikipedia
    https://en.wikipedia.org/wiki/Cholecystitis
    More than 90% of the time acute cholecystitis is caused from blockage of the cystic duct by a gallstone. […] Blockage of the cystic duct by a gallstone causes a buildup of bile in the gallbladder and increased pressure within the gallbladder. Concentrated bile, pressure, and sometimes bacterial infection irritate and damage the gallbladder wall, causing inflammation and swelling of the gallbladder. […] Inflammation and swelling of the gallbladder can reduce normal blood flow to areas of the gallbladder, which can lead to cell death due to inadequate oxygen.
  • #7 Cholecystitis – Wikipedia
    https://en.wikipedia.org/wiki/Cholecystitis
    More than 90% of the time acute cholecystitis is caused from blockage of the cystic duct by a gallstone. […] Blockage of the cystic duct by a gallstone causes a buildup of bile in the gallbladder and increased pressure within the gallbladder. Concentrated bile, pressure, and sometimes bacterial infection irritate and damage the gallbladder wall, causing inflammation and swelling of the gallbladder. […] Inflammation and swelling of the gallbladder can reduce normal blood flow to areas of the gallbladder, which can lead to cell death due to inadequate oxygen.
  • #8 Acute Cholecystitis: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/171886-overview
    Ninety percent of cases of cholecystitis involve stones in the gallbladder (ie, calculous cholecystitis), with the other 10% of cases representing acalculous cholecystitis. […] Acute calculous cholecystitis is caused by an obstruction of the cystic duct, leading to distention of the gallbladder. As the gallbladder becomes distended, blood flow and lymphatic drainage are compromised, leading to mucosal ischemia and necrosis. […] Although the exact mechanism of acalculous cholecystitis is unclear, several theories exist. Injury may be the result of retained concentrated bile, an extremely noxious substance. In the presence of prolonged fasting, the gallbladder does not receive a cholecystokinin (CCK) stimulus to empty; thus, the concentrated bile remains stagnant in the lumen. […] A study by Cullen et al demonstrated the ability of endotoxins to cause necrosis, hemorrhage, areas of fibrin deposition, and extensive mucosal loss, consistent with an acute ischemic insult. Endotoxins also abolish the contractile response to CCK, leading to gallbladder stasis.
  • #9 Acute Cholecystitis – Hepatic and Biliary Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/hepatic-and-biliary-disorders/gallbladder-and-bile-duct-disorders/acute-cholecystitis
    Acute cholecystitis is inflammation of the gallbladder that develops over hours, usually because a gallstone obstructs the cystic duct. […] When a stone becomes impacted in the cystic duct and persistently obstructs it, acute inflammation results. Bile stasis triggers release of inflammatory enzymes (eg, phospholipase A, which converts lecithin to lysolecithin, which then may mediate inflammation). […] The damaged mucosa secretes more fluid into the gallbladder lumen than it absorbs. The resulting distention further releases inflammatory mediators (eg, prostaglandins), worsening mucosal damage and causing ischemia, all of which perpetuate inflammation. Bacterial infection can supervene. The vicious circle of fluid secretion and inflammation, when unchecked, leads to necrosis and perforation. […] The mechanism probably involves inflammatory mediators released because of ischemia, infection, or bile stasis.
  • #10 acute-cholecystitis | Calgary Guide
    https://calgaryguide.ucalgary.ca/acute-cholecystitis/acute-cholecystitis-2022/
    Acute Cholecystitis: Pathogenesis and clinical findings Gallstone blocks the cystic duct, backing up bile into the gallbladder […] Gallstones causing physical trauma to gallbladder wall […] Inflammatory mediator (i.e. prostaglandin) release by gallbladder and systemic inflammatory response […] Inflammation self-perpetuates […] Irritation of inner gallbladder wall/mucosa […] Gallbladder ischemia […] Local inflammation, loss of gallbladder mucosal integrity […] Bacterial invasion transmural inflammation of gallbladder […] Without treatment, prolonged ischemia and inflammation of the gallbladder […] Gallbladder gangrene (20%) […] Gallbladder perforation (20%).
  • #11 Acute Cholecystitis – Hepatic and Biliary Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/hepatic-and-biliary-disorders/gallbladder-and-bile-duct-disorders/acute-cholecystitis
    Acute cholecystitis is inflammation of the gallbladder that develops over hours, usually because a gallstone obstructs the cystic duct. […] When a stone becomes impacted in the cystic duct and persistently obstructs it, acute inflammation results. Bile stasis triggers release of inflammatory enzymes (eg, phospholipase A, which converts lecithin to lysolecithin, which then may mediate inflammation). […] The damaged mucosa secretes more fluid into the gallbladder lumen than it absorbs. The resulting distention further releases inflammatory mediators (eg, prostaglandins), worsening mucosal damage and causing ischemia, all of which perpetuate inflammation. Bacterial infection can supervene. The vicious circle of fluid secretion and inflammation, when unchecked, leads to necrosis and perforation. […] The mechanism probably involves inflammatory mediators released because of ischemia, infection, or bile stasis.
  • #12 acute-cholecystitis | Calgary Guide
    https://calgaryguide.ucalgary.ca/acute-cholecystitis/acute-cholecystitis-2022/
    Acute Cholecystitis: Pathogenesis and clinical findings Gallstone blocks the cystic duct, backing up bile into the gallbladder […] Gallstones causing physical trauma to gallbladder wall […] Inflammatory mediator (i.e. prostaglandin) release by gallbladder and systemic inflammatory response […] Inflammation self-perpetuates […] Irritation of inner gallbladder wall/mucosa […] Gallbladder ischemia […] Local inflammation, loss of gallbladder mucosal integrity […] Bacterial invasion transmural inflammation of gallbladder […] Without treatment, prolonged ischemia and inflammation of the gallbladder […] Gallbladder gangrene (20%) […] Gallbladder perforation (20%).
  • #13 acute-cholecystitis | Calgary Guide
    https://calgaryguide.ucalgary.ca/acute-cholecystitis/acute-cholecystitis-2022/
    Acute Cholecystitis: Pathogenesis and clinical findings Gallstone blocks the cystic duct, backing up bile into the gallbladder […] Gallstones causing physical trauma to gallbladder wall […] Inflammatory mediator (i.e. prostaglandin) release by gallbladder and systemic inflammatory response […] Inflammation self-perpetuates […] Irritation of inner gallbladder wall/mucosa […] Gallbladder ischemia […] Local inflammation, loss of gallbladder mucosal integrity […] Bacterial invasion transmural inflammation of gallbladder […] Without treatment, prolonged ischemia and inflammation of the gallbladder […] Gallbladder gangrene (20%) […] Gallbladder perforation (20%).
  • #14 Acute Cholecystitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK459171/
    Acute cholecystitis refers to inflammation of the gallbladder. The pathophysiologic mechanism of acute cholecystitis is blockage of the cystic duct. […] The etiology of acute cholecystitis is, by definition, cystic duct blockage, which causes inflammation. […] Occlusion of the cystic duct or malfunction of the mechanics of gallbladder emptying is the pathophysiology of this disease. […] Gallstones form from various materials such as bilirubinate or cholesterol. These materials increase the likelihood of cholecystitis and cholelithiasis in conditions such as sickle cell disease where red blood cells are broken down forming excess bilirubin and forming pigmented stones. […] Regardless of the cause of the blockage, the gallbladder wall edema will eventually cause wall ischemia and become gangrenous. The gangrenous gallbladder can become infected by gas-forming organisms, causing acute emphysematous cholecystitis; all of these conditions can quickly become life-threatening, and rupture has a high rate of mortality. […] Cases of acute untreated cholecystitis could lead to perforation of the gallbladder, sepsis, and death.
  • #15 Biliary Colic and Cholecystitis – TeachMeSurgery
    https://teachmesurgery.com/hpb/gall-bladder/colic-and-cholecystitis/
    Bile is formed from cholesterol, phospholipids, and bile pigments (products of haemoglobin metabolism). It is stored in the gallbladder, before passing into the duodenum upon gallbladder stimulation. […] Gallstones form as a result of supersaturation of the bile. There are three main types of gallstones: Cholesterol stones composed purely of cholesterol, from excess cholesterol production. There is a well recognised link between poor diet, obesity, and cholesterol stones. […] Pigment stones composed purely of bile pigments, from excess bile pigments production. Commonly seen in those with known haemolytic anaemia. […] Mixed stones comprised of both cholesterol and bile pigments. […] Biliary colic occurs when the gallbladder neck becomes impacted by a gallstone. There is no inflammatory response, yet the contraction of the gallbladder against the occluded neck will result in pain.
  • #16 AWA – Explanation
    https://awa.auckland.ac.nz/index.php?p=explanation&textid=1208
    There are three main factors involved in the formation of cholesterol gallstones: cholesterol supersaturation, nucleating and anti-nucleating factors and hypomotility of the gallbladder. […] The most important factor is the increased saturation of cholesterol in the bile. […] When the amount of cholesterol secreted exceeds the amount of bile salts and lecithin that are needed to make cholesterol soluble (due to increased activity of the ATP-dependent transporters on hepatocytes), precipitation and crystallisation of the excess cholesterol can lead to the formation of cholesterol gallstones, as seen in Figure 1 (Henderson Yantiss, 2010). […] The motility of the gallbladder is also involved in the formation of gallstones. […] Gallbladder hypomotility or stasis (impaired filling and emptying of the gallbladder) promotes the formation of cholesterol gallstones, by holding the cholesterol saturated bile static and allowing cholesterol to crystallise (Jessurun Pambuccian, 2009).
  • #17 PATHOLOGY AND PATHOGENESIS OF CHOLECYSTITIS – ppt download
    https://slideplayer.com/slide/16683936/
    Pathogenesis of Cholesterol Stones Cholesterol is rendered soluble in bile by aggregation with water-soluble bile salts and water-insoluble lecithins, both of which act as detergents. When cholesterol concentrations exceed the solubilizing capacity of bile (supersaturation), cholesterol can no longer remain dispersed and nucleates into solid cholesterol monohydrate crystals. Cholesterol gallstone formation involves three simultaneous defects: […] Supersaturation of bile with cholesterol: the result of hepatocellular hypersecretion of cholesterol. Gallbladder hypomotility. It promotes nucleation typically around a calcium salt crystal nidus. Mucus hypersecretion in the gallbladder: This traps the crystals, permitting their aggregation into stones. […] Acute Cholecystitis: Pathogenesis Acute calculous cholecystitis results from chemical irritation and inflammation of the obstructed gallbladder. These events occur in the absence of bacterial infection; only later in the course may bacterial contamination develop.
  • #18 AWA – Explanation
    https://awa.auckland.ac.nz/index.php?p=explanation&textid=1208
    There are three main factors involved in the formation of cholesterol gallstones: cholesterol supersaturation, nucleating and anti-nucleating factors and hypomotility of the gallbladder. […] The most important factor is the increased saturation of cholesterol in the bile. […] When the amount of cholesterol secreted exceeds the amount of bile salts and lecithin that are needed to make cholesterol soluble (due to increased activity of the ATP-dependent transporters on hepatocytes), precipitation and crystallisation of the excess cholesterol can lead to the formation of cholesterol gallstones, as seen in Figure 1 (Henderson Yantiss, 2010). […] The motility of the gallbladder is also involved in the formation of gallstones. […] Gallbladder hypomotility or stasis (impaired filling and emptying of the gallbladder) promotes the formation of cholesterol gallstones, by holding the cholesterol saturated bile static and allowing cholesterol to crystallise (Jessurun Pambuccian, 2009).
  • #19 Acute Cholecystitis | Basicmedical Key
    https://basicmedicalkey.com/acute-cholecystitis/
    Acute Calculous Cholecystitis: Key elements are obstruction of cystic duct by stones and bile supersaturated with cholesterol. Trauma to mucosa releases phospholipase from lysosomes. Phospholipase converts lecithin in bile to lysolecithin, which damages gallbladder epithelium. Secondary bacterial infection with enteric organisms occurs in 20% of cases. Overgrowth by gas-producing organisms leads to emphysematous cholecystitis. […] Acute Acalculous Cholecystitis accounts for 5% of cases. Risk factors include critical illness, burns, trauma, major surgical procedures, diabetes, immunosuppression.
  • #20 Acute Cholecystitis | Basicmedical Key
    https://basicmedicalkey.com/acute-cholecystitis-2/
    Inflammation may be sparse in early disease […] Key elements are obstruction of cystic duct by stones and bile supersaturated with cholesterol […] Trauma to mucosa releases phospholipase from lysosomes […] Phospholipase converts lecithin in bile to lysolecithin, which damages gallbladder epithelium […] Secondary bacterial infection with enteric organisms occurs in 20% of cases […] Overgrowth by gas-producing organisms leads to emphysematous cholecystitis.
  • #21 Precision medicine for personalized cholecystitis care: integrating molecular diagnostics and biotherapeutics | Bulletin of the National Research Centre | Full Text
    https://bnrc.springeropen.com/articles/10.1186/s42269-024-01244-9
    For microorganisms to proliferate and thrive within the nutrient-limited environment of the gallbladder, they must adapt their metabolism to obtain essential nutrients from host cells. […] The secretion of toxins and enzymes is a key virulence strategy used by diverse microbes to establish infection and cause damage to the gallbladder epithelium. […] The host responds to acute cholecystitis through a coordinated innate and adaptive immune response aimed at clearing the infectious pathogens and limiting tissue damage. […] Infection and obstruction of the gallbladder activate resident macrophages and epithelial cells to secrete pro-inflammatory cytokines including IL-1, IL-6, and TNF-alpha. […] These cytokines initiate a localized inflammatory response and recruit additional leukocytes.
  • #22 Precision medicine for personalized cholecystitis care: integrating molecular diagnostics and biotherapeutics | Bulletin of the National Research Centre | Full Text
    https://bnrc.springeropen.com/articles/10.1186/s42269-024-01244-9
    While necessary to clear infection, excessive inflammation can damage host tissues. […] The inflammation and obstruction accompanying acute cholecystitis induces significant effects on the gallbladder anatomy and function. […] The pathogenesis of acute cholecystitis is intimately linked to the development of gallstones, which obstruct bile drainage and initiate gallbladder inflammation. […] The obstruction of bile drainage from the gallbladder that occurs in acute cholecystitis has two major detrimental effects-bile stasis within the gallbladder and jaundice due to the backup of bile constituents. […] The advancement of biotechnology and molecular techniques has provided powerful new tools to enhance the diagnosis, characterization, and treatment of acute cholecystitis. […] Molecular detection methods like PCR allow rapid, sensitive identification of bacterial, parasitic, and fungal pathogens in gallbladder tissues.
  • #23 Chronic calculous cholecystitis
    https://www.drturumin.com/en/CaCholecystitis_en.html
    Chronic calculous cholecystitis is an inflammatory disease which affects the gallbladder wall and causes motoric-tonic dysfunctions of the biliary system, accompanied by presence of gallstones in the gallbladder lumen, and reveals as biliary pain. […] The motoric dysfunction of the gallbladder can be caused by increased basal common bile duct resistance, muscle hypertrophy, and chronic inflammation in the gallbladder wall. […] High degree of COX-2 expression in the smooth muscle cells of the gallbladder wall causes the decrease of the evacuation function of gallbladder and active passage of hepatic bile into the gallbladder. […] Surplus COX-2 expression in the epithelial cells of the gallbladder mucosa makes for decrease of the absorption function of the gallbladder (decrease of water and biliary cholesterol absorption) and passive passage of the hepatic bile into the gallbladder.
  • #24 Chronic calculous cholecystitis
    https://www.drturumin.com/en/CaCholecystitis_en.html
    Chronic calculous cholecystitis is an inflammatory disease which affects the gallbladder wall and causes motoric-tonic dysfunctions of the biliary system, accompanied by presence of gallstones in the gallbladder lumen, and reveals as biliary pain. […] The motoric dysfunction of the gallbladder can be caused by increased basal common bile duct resistance, muscle hypertrophy, and chronic inflammation in the gallbladder wall. […] High degree of COX-2 expression in the smooth muscle cells of the gallbladder wall causes the decrease of the evacuation function of gallbladder and active passage of hepatic bile into the gallbladder. […] Surplus COX-2 expression in the epithelial cells of the gallbladder mucosa makes for decrease of the absorption function of the gallbladder (decrease of water and biliary cholesterol absorption) and passive passage of the hepatic bile into the gallbladder.
  • #25 Acalculous cholecystitis – UpToDate
    https://www.uptodate.com/contents/acalculous-cholecystitis
    Acute acalculous cholecystitis is an acute necroinflammatory disease of the gallbladder with a multifactorial pathogenesis, occurring in the absence of gallstones. It accounts for approximately 10 percent of all cases of acute cholecystitis and is associated with high morbidity and mortality rates. […] The pathogenesis of acalculous cholecystitis is multifactorial and likely results from ischemia and cholestasis. The cystic artery, which supplies blood to the gallbladder, is a terminal artery and susceptible to ischemia. Ischemia and necrosis of the gallbladder wall can occur with hypoperfusion in cases of hypotension, vasoactive drug use, or major surgery and trauma. Cholestasis may be seen in prolonged fasting states, usage of total parental nutrition, and ileus or bowel obstruction. Cholestasis results in increased pressure within the gallbladder and distension, further decreasing perfusion to the gallbladder wall. Pathologically, ischemia and cholestasis result in local inflammatory response in the gallbladder wall, epithelial injury, and eventually necrosis of the gallbladder tissue.
  • #26 Acalculous cholecystitis – EMCrit Project
    https://emcrit.org/ibcc/acalculous-cholecystitis/
    Acalculous cholecystitis is defined as cholecystitis that occurs without a gallstone. […] This typically occurs in critically ill patients due to a combination of factors (e.g. bile stasis and hypoperfusion). […] Pathogenesis may be summarized roughly as follows. In some ways, this may be conceptualized as a paralytic ileus of the gallbladder. […] (1) Lack of enteral nutrition and hypoperfusion create a hypotonic, dilated gallbladder. […] Distension of the gallbladder increases wall tension, further impairing perfusion of the gallbladder wall. […] Biliary stasis causes concentration of biliary detergents, which may damage the gallbladder wall. […] (2) Further complications ensue: […] Necrosis and perforation of the gallbladder may occur. […] Superinfection with enteric bacteria may occur (empyema of the gallbladder). Note that many cases of acalculous cholecystitis occur without bacterial infection.
  • #27 Acalculous Cholecystitis: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/187645-overview
    Acalculous cholecystitis is an inflammatory disease of the gallbladder without evidence of gallstones or cystic duct obstruction; it is a severe illness that is a complication of various other medical or surgical conditions. […] The main cause of this illness is thought to be bile stasis and increased lithogenicity of bile. […] Gallbladder wall ischemia that occurs because of a low-flow state due to fever, dehydration, or heart failure may also play a role in the pathogenesis of acalculous cholecystitis.
  • #28 Acalculous cholecystitis – UpToDate
    https://www.uptodate.com/contents/acalculous-cholecystitis
    Acute acalculous cholecystitis is an acute necroinflammatory disease of the gallbladder with a multifactorial pathogenesis, occurring in the absence of gallstones. It accounts for approximately 10 percent of all cases of acute cholecystitis and is associated with high morbidity and mortality rates. […] The pathogenesis of acalculous cholecystitis is multifactorial and likely results from ischemia and cholestasis. The cystic artery, which supplies blood to the gallbladder, is a terminal artery and susceptible to ischemia. Ischemia and necrosis of the gallbladder wall can occur with hypoperfusion in cases of hypotension, vasoactive drug use, or major surgery and trauma. Cholestasis may be seen in prolonged fasting states, usage of total parental nutrition, and ileus or bowel obstruction. Cholestasis results in increased pressure within the gallbladder and distension, further decreasing perfusion to the gallbladder wall. Pathologically, ischemia and cholestasis result in local inflammatory response in the gallbladder wall, epithelial injury, and eventually necrosis of the gallbladder tissue.
  • #29 Acute Acalculous Cholecystitis in Neurological Patients; Clinical Review, Risk Factors, and Possible Mechanism
    https://www.e-jnic.org/journal/view.php?number=33
    Acute cholecystitis is known to be caused by the pathologic mechanism of inflammation and ischemia in the gallbladder (GB) wall, stagnant pooling of bile juice, and the lithogenicity of bile juice in a complex manner. […] Hypoperfusion and bile stasis are the key pathogenesis of AAC, which could be aggravated by hypotension, dehydration, and the usage of vasoactive drugs. […] Bile stasis is caused by the use of opioids, fasting with total parenteral nutrition (TPN), and mechanical ventilation with positive end-expiratory pressure (PEEP). […] Gallbladder ischemia is pathogenesis of AAC. […] Intraluminal pressure is increased by bile stasis, which results in a decrease in gallbladder perfusion pressure. […] Another mechanism closely related to the pathogenesis of AAC is systemic inflammatory response. […] Systemic inflammatory response can cause cholestasis, gallbladder ischemia, therefore could affect the incidence of AAC in neurological patients.
  • #30 Acalculous cholecystitis – EMCrit Project
    https://emcrit.org/ibcc/acalculous-cholecystitis/
    Acalculous cholecystitis is defined as cholecystitis that occurs without a gallstone. […] This typically occurs in critically ill patients due to a combination of factors (e.g. bile stasis and hypoperfusion). […] Pathogenesis may be summarized roughly as follows. In some ways, this may be conceptualized as a paralytic ileus of the gallbladder. […] (1) Lack of enteral nutrition and hypoperfusion create a hypotonic, dilated gallbladder. […] Distension of the gallbladder increases wall tension, further impairing perfusion of the gallbladder wall. […] Biliary stasis causes concentration of biliary detergents, which may damage the gallbladder wall. […] (2) Further complications ensue: […] Necrosis and perforation of the gallbladder may occur. […] Superinfection with enteric bacteria may occur (empyema of the gallbladder). Note that many cases of acalculous cholecystitis occur without bacterial infection.
  • #31 Acute Acalculous Cholecystitis | Abdominal Key
    https://abdominalkey.com/acute-acalculous-cholecystitis/
    Acute acalculous cholecystitis (ACC) can develop with or without gallstones after surgery and in critically ill or injured patients. […] The pathogenesis of AAC is complex and multifactorial. […] Bile stasis has been implicated in the pathogenesis of AAC in both experimental and clinical studies. […] Bile stasis may alter the chemical composition of bile, which may promote gallbladder mucosal injury. […] Gallbladder ischemia is central to the pathogenesis of AAC. […] It has been hypothesized that the fundamental lesion leading to AAC is failure of the gallbladder microcirculation with cellular hypoxia. […] Vasoactive mediators play a role in the pathogenesis of AAC. […] Although bacterial infection is likely a secondary phenomenon, the host response to gram-negative bacteremia or splanchnic ischemia-reperfusion injury may be of primary importance.
  • #32 Acute Cholecystitis | Basicmedical Key
    https://basicmedicalkey.com/acute-cholecystitis/
    Acute Calculous Cholecystitis: Key elements are obstruction of cystic duct by stones and bile supersaturated with cholesterol. Trauma to mucosa releases phospholipase from lysosomes. Phospholipase converts lecithin in bile to lysolecithin, which damages gallbladder epithelium. Secondary bacterial infection with enteric organisms occurs in 20% of cases. Overgrowth by gas-producing organisms leads to emphysematous cholecystitis. […] Acute Acalculous Cholecystitis accounts for 5% of cases. Risk factors include critical illness, burns, trauma, major surgical procedures, diabetes, immunosuppression.
  • #33 Acalculous Cholecystitis: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/187645-overview
    Acalculous cholecystitis is an inflammatory disease of the gallbladder without evidence of gallstones or cystic duct obstruction; it is a severe illness that is a complication of various other medical or surgical conditions. […] The main cause of this illness is thought to be bile stasis and increased lithogenicity of bile. […] Gallbladder wall ischemia that occurs because of a low-flow state due to fever, dehydration, or heart failure may also play a role in the pathogenesis of acalculous cholecystitis.
  • #34 Acalculous Cholecystitis: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/187645-overview
    Acalculous cholecystitis is an inflammatory disease of the gallbladder without evidence of gallstones or cystic duct obstruction; it is a severe illness that is a complication of various other medical or surgical conditions. […] The main cause of this illness is thought to be bile stasis and increased lithogenicity of bile. […] Gallbladder wall ischemia that occurs because of a low-flow state due to fever, dehydration, or heart failure may also play a role in the pathogenesis of acalculous cholecystitis.
  • #35 Cholecystitis | SpringerLink
    https://link.springer.com/10.1007/978-3-540-35280-8_471
    Cholecystitis is the inflammation of the gallbladder occurring most commonly in cases of obstruction of the cystic duct caused by gallstones. […] The inflammation often initiates without contamination, and infection may develop later; therefore, bacterial proliferation may be a result of cholecystitis and not the precipitating factor. […] Severe disease, alcohol abuse, and rarely, tumors of the gallbladder can also be the cause of cholecystitis. […] Cholecystitis may develop either as an acute or a chronic process.
  • #36 Acute Cholecystitis | Basicmedical Key
    https://basicmedicalkey.com/acute-cholecystitis/
    Acute Calculous Cholecystitis: Key elements are obstruction of cystic duct by stones and bile supersaturated with cholesterol. Trauma to mucosa releases phospholipase from lysosomes. Phospholipase converts lecithin in bile to lysolecithin, which damages gallbladder epithelium. Secondary bacterial infection with enteric organisms occurs in 20% of cases. Overgrowth by gas-producing organisms leads to emphysematous cholecystitis. […] Acute Acalculous Cholecystitis accounts for 5% of cases. Risk factors include critical illness, burns, trauma, major surgical procedures, diabetes, immunosuppression.
  • #37 Acute Cholecystitis | Basicmedical Key
    https://basicmedicalkey.com/acute-cholecystitis-2/
    Inflammation may be sparse in early disease […] Key elements are obstruction of cystic duct by stones and bile supersaturated with cholesterol […] Trauma to mucosa releases phospholipase from lysosomes […] Phospholipase converts lecithin in bile to lysolecithin, which damages gallbladder epithelium […] Secondary bacterial infection with enteric organisms occurs in 20% of cases […] Overgrowth by gas-producing organisms leads to emphysematous cholecystitis.
  • #38 Seasonality of Acute Cholecystitis: A Review of Global Patterns
    https://clinmedjournals.org/articles/ijsrp/international-journal-of-surgery-research-and-practice-ijsrp-9-146.php?jid=ijsrp
    Furthermore, a low fiber and high sugar diets can lead to constipation and subsequent crystal formation in the bile. […] Prolongation of intestinal transit has been proposed as the mechanism for the increase in the proportion of deoxycholic acid in bile. […] Increases in biliary deoxycholic acid have long been implicated in the pathogenesis of cholesterol rich gallstones. […] Dehydration during summer can further augment the risk of acute cholecystitis by causing bile stasis due to decreased gallbladder emptying. […] Bacterial infections are associated with acute cholecystitis due to the release of inflammatory mediators. […] The most frequent pathogens in biliary infection are gram-negative anaerobes, dominated by Escherichia coli, Klebsiella spp., Acinetobacter baumannii complex and Enterobacter spp.
  • #39 Acalculous cholecystitis – UpToDate
    https://www.uptodate.com/contents/acalculous-cholecystitis
    Once acalculous cholecystitis is established, secondary infection with enteric pathogens, including Escherichia coli, Enterococcus faecalis, Klebsiella spp, Pseudomonas spp, Proteus spp, and Bacteroides fragilis and related strains, is common. […] The majority of patients with acalculous cholecystitis have multiple risk factors. In some cases, specific primary infections with non-enteric organisms predispose to acalculous cholecystitis. As an example, acalculous cholecystitis occurring in patients with acquired immunodeficiency syndrome (AIDS) and other immunosuppressed patients may be due to opportunistic infections such as microsporidia, Cryptosporidium, or cytomegalovirus. More often, however, these infections cause a cholangiopathy without cholecystitis. There is also association of acalculous cholecystitis with COVID-19, though it is unclear whether disease results from primary infection of the biliary system or critical illness.
  • #40 Acute cholecystitis pathophysiology – wikidoc
    https://www.wikidoc.org/index.php/Acute_cholecystitis_pathophysiology
    Gallbladder stasis is usually due to the lack of gallbladder stimulation and contractility. This leads to concentration of the bile salts with a build-up of pressure within the organ. An increased intraluminal pressure results in ischemia and necrosis of the gallbladder. The gallbladder stasis also facilitates the proliferation of the bacteria such as Escherichia coli, Klebsiella, Bacteroides, Proteus, Pseudomonas, and Enterococcus faecalis. This can also cause an inflammatory reaction in the gallbladder. […] Lith gene is involved in the pathogenesis of cholecystitis. Mutations in the hepatic cholesterol transporter ABCG8 also predispose an individual to the develop gallstones.
  • #41 Precision medicine for personalized cholecystitis care: integrating molecular diagnostics and biotherapeutics | Bulletin of the National Research Centre | Full Text
    https://bnrc.springeropen.com/articles/10.1186/s42269-024-01244-9
    Specific virulent strains of E. coli contain genes that allow them to adhere to and colonize the gallbladder epithelium. […] Understanding the key bacterial players in infectious cholecystitis guides appropriate antibiotic therapy when medical management is undertaken. […] Critical to the ability of bacteria, parasites, and fungi to establish infection of the gallbladder is their expression of specific virulence factors that enable adhesion to epithelial cells lining the gallbladder mucosa. […] These infectious microbes produce various surface proteins and polysaccharides that mediate binding to the host epithelium, representing an essential first step in pathogenesis. […] In addition to adhesion, many pathogens produce toxins that directly damage and disrupt the epithelial cell membranes of the gallbladder.
  • #42 Precision medicine for personalized cholecystitis care: integrating molecular diagnostics and biotherapeutics | Bulletin of the National Research Centre | Full Text
    https://bnrc.springeropen.com/articles/10.1186/s42269-024-01244-9
    Specific virulent strains of E. coli contain genes that allow them to adhere to and colonize the gallbladder epithelium. […] Understanding the key bacterial players in infectious cholecystitis guides appropriate antibiotic therapy when medical management is undertaken. […] Critical to the ability of bacteria, parasites, and fungi to establish infection of the gallbladder is their expression of specific virulence factors that enable adhesion to epithelial cells lining the gallbladder mucosa. […] These infectious microbes produce various surface proteins and polysaccharides that mediate binding to the host epithelium, representing an essential first step in pathogenesis. […] In addition to adhesion, many pathogens produce toxins that directly damage and disrupt the epithelial cell membranes of the gallbladder.
  • #43 Precision medicine for personalized cholecystitis care: integrating molecular diagnostics and biotherapeutics | Bulletin of the National Research Centre | Full Text
    https://bnrc.springeropen.com/articles/10.1186/s42269-024-01244-9
    The pore-forming toxins liberated by these pathogens allow spillage of cell contents, calcium influx, loss of membrane potential, and ultimately host cell death. […] This direct cytotoxicity coupled with the inflammatory response to the microbial toxins leads to the tissue damage, edema, and necrosis observed in acute cholecystitis. […] Pathogenic microbes involved in acute cholecystitis produce a variety of extracellular enzymes that directly breakdown and destroy host cell structural components and the surrounding extracellular matrix. […] The production of virulence factors by bacteria, parasites, and fungi causing cholecystitis involves coordinated transcription and translation of the genes encoding these pathogenicity proteins. […] Understanding the molecular mechanisms regulating virulence factor expression provides insight into microbial triggers for initiating cholecystitis.
  • #44 Precision medicine for personalized cholecystitis care: integrating molecular diagnostics and biotherapeutics | Bulletin of the National Research Centre | Full Text
    https://bnrc.springeropen.com/articles/10.1186/s42269-024-01244-9
    The pore-forming toxins liberated by these pathogens allow spillage of cell contents, calcium influx, loss of membrane potential, and ultimately host cell death. […] This direct cytotoxicity coupled with the inflammatory response to the microbial toxins leads to the tissue damage, edema, and necrosis observed in acute cholecystitis. […] Pathogenic microbes involved in acute cholecystitis produce a variety of extracellular enzymes that directly breakdown and destroy host cell structural components and the surrounding extracellular matrix. […] The production of virulence factors by bacteria, parasites, and fungi causing cholecystitis involves coordinated transcription and translation of the genes encoding these pathogenicity proteins. […] Understanding the molecular mechanisms regulating virulence factor expression provides insight into microbial triggers for initiating cholecystitis.
  • #45 Acute Cholecystitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK459171/
    Acute cholecystitis refers to inflammation of the gallbladder. The pathophysiologic mechanism of acute cholecystitis is blockage of the cystic duct. […] The etiology of acute cholecystitis is, by definition, cystic duct blockage, which causes inflammation. […] Occlusion of the cystic duct or malfunction of the mechanics of gallbladder emptying is the pathophysiology of this disease. […] Gallstones form from various materials such as bilirubinate or cholesterol. These materials increase the likelihood of cholecystitis and cholelithiasis in conditions such as sickle cell disease where red blood cells are broken down forming excess bilirubin and forming pigmented stones. […] Regardless of the cause of the blockage, the gallbladder wall edema will eventually cause wall ischemia and become gangrenous. The gangrenous gallbladder can become infected by gas-forming organisms, causing acute emphysematous cholecystitis; all of these conditions can quickly become life-threatening, and rupture has a high rate of mortality. […] Cases of acute untreated cholecystitis could lead to perforation of the gallbladder, sepsis, and death.
  • #46 Acute Cholecystitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK459171/
    Acute cholecystitis refers to inflammation of the gallbladder. The pathophysiologic mechanism of acute cholecystitis is blockage of the cystic duct. […] The etiology of acute cholecystitis is, by definition, cystic duct blockage, which causes inflammation. […] Occlusion of the cystic duct or malfunction of the mechanics of gallbladder emptying is the pathophysiology of this disease. […] Gallstones form from various materials such as bilirubinate or cholesterol. These materials increase the likelihood of cholecystitis and cholelithiasis in conditions such as sickle cell disease where red blood cells are broken down forming excess bilirubin and forming pigmented stones. […] Regardless of the cause of the blockage, the gallbladder wall edema will eventually cause wall ischemia and become gangrenous. The gangrenous gallbladder can become infected by gas-forming organisms, causing acute emphysematous cholecystitis; all of these conditions can quickly become life-threatening, and rupture has a high rate of mortality. […] Cases of acute untreated cholecystitis could lead to perforation of the gallbladder, sepsis, and death.
  • #47 Acute Cholecystitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK459171/
    Acute cholecystitis refers to inflammation of the gallbladder. The pathophysiologic mechanism of acute cholecystitis is blockage of the cystic duct. […] The etiology of acute cholecystitis is, by definition, cystic duct blockage, which causes inflammation. […] Occlusion of the cystic duct or malfunction of the mechanics of gallbladder emptying is the pathophysiology of this disease. […] Gallstones form from various materials such as bilirubinate or cholesterol. These materials increase the likelihood of cholecystitis and cholelithiasis in conditions such as sickle cell disease where red blood cells are broken down forming excess bilirubin and forming pigmented stones. […] Regardless of the cause of the blockage, the gallbladder wall edema will eventually cause wall ischemia and become gangrenous. The gangrenous gallbladder can become infected by gas-forming organisms, causing acute emphysematous cholecystitis; all of these conditions can quickly become life-threatening, and rupture has a high rate of mortality. […] Cases of acute untreated cholecystitis could lead to perforation of the gallbladder, sepsis, and death.
  • #48 Cholecystitis: Diagnosis & Surgical Management – EM Board Bombs Podcast
    https://www.emboardbombs.com/study-guide/2019-8-25-the-trolling-stones-cholecystitis-7b3h8/
    Gallstone disease, most commonly manifesting as cholecystitis, is seen in up to 10% of patients who have symptomatic gallstones. […] Acute cholecystitis: obstruction of the cystic duct with subsequent inflammation of the gallbladder. Although it is most commonly due to cholesterol or bilirubin stones obstructing the cystic duct, in 5-10% of cases acalculus cholecystitis is the cause. […] In fact, those with emphysematous cholecystitis are by far the most critical biliary pathology patients that who roll into the ED. Gas-forming organisms (classically, Clostridium welchii) invade the gallbladder wall, causing fever, RUQ pain, and early markers for sepsis. […] If untreated, acute cholecystitis often resolves in 7-10 days. However, complications are frequent and have great potential to be life threatening. This is the driving reason for why we operate on gallbladders.
  • #49 Acute Cholecystitis – Bile Duct and Gallbladder Diseases – Gastroenterology – Diseases – McMaster Textbook of Internal Medicine
    https://empendium.com/mcmtextbook/chapter/B31.II.6.3.
    Acute cholecystitis is an acute inflammation of the gallbladder and one of the major complications of cholelithiasis. It may be caused by impaired bile outflow from the gallbladder (as a result of occlusion of the cystic duct or edema of the cystic duct mucosa). Approximately 10% of cases of cholecystitis occur in persons without gallstones and usually with serious systemic diseases (acalculous cholecystitis). […] Complications that require urgent surgical treatment include empyema, necrosis, or perforation (limited or with diffuse biliary peritonitis) of the gallbladder. Other complications include hygroma of the gallbladder, liver abscess, biliary intestinal fistula (passage of large gallstones to the intestinal lumen may result in gallstone ileus), and Mirizzi syndrome (obstruction of the neck of the gallbladder or the cystic duct by a large gallstone resulting in symptoms of common bile duct compression).
  • #50 Acute Cholecystitis – Bile Duct and Gallbladder Diseases – Gastroenterology – Diseases – McMaster Textbook of Internal Medicine
    https://empendium.com/mcmtextbook/chapter/B31.II.6.3.
    Acute cholecystitis is an acute inflammation of the gallbladder and one of the major complications of cholelithiasis. It may be caused by impaired bile outflow from the gallbladder (as a result of occlusion of the cystic duct or edema of the cystic duct mucosa). Approximately 10% of cases of cholecystitis occur in persons without gallstones and usually with serious systemic diseases (acalculous cholecystitis). […] Complications that require urgent surgical treatment include empyema, necrosis, or perforation (limited or with diffuse biliary peritonitis) of the gallbladder. Other complications include hygroma of the gallbladder, liver abscess, biliary intestinal fistula (passage of large gallstones to the intestinal lumen may result in gallstone ileus), and Mirizzi syndrome (obstruction of the neck of the gallbladder or the cystic duct by a large gallstone resulting in symptoms of common bile duct compression).
  • #51 Cholelithiasis, Cholecystitis, Choledocholithiasis, and Hyperplastic Cholecystoses | Radiology Key
    https://radiologykey.com/cholelithiasis-cholecystitis-choledocholithiasis-and-hyperplastic-cholecystoses/
    The prevalence of gallstones varies with age and gender. Gallstones are present in an estimated 10% to 15% of men and 20% to 40% of women older than 60 years. In general, the risk for stones increases with history of childbearing, estrogen replacement therapy, oral contraceptive use, and obesity. Stones are also associated with hypertriglyceridemia, Crohns disease, and parenteral hyperalimentation. Gallstones are symptomatic in 20% to 30% of patients; biliary pain or colic is the most common symptom. This is most often related to impaction of a stone in the cystic duct. The most common acute complications of gallstones are acute cholecystitis, acute pancreatitis, and ascending cholangitis. Chronic complications include chronic cholecystitis, Mirizzi syndrome, cholecystenteric fistula, and gallstone ileus.
  • #52 Cholelithiasis, Cholecystitis, Choledocholithiasis, and Hyperplastic Cholecystoses | Radiology Key
    https://radiologykey.com/cholelithiasis-cholecystitis-choledocholithiasis-and-hyperplastic-cholecystoses/
    The prevalence of gallstones varies with age and gender. Gallstones are present in an estimated 10% to 15% of men and 20% to 40% of women older than 60 years. In general, the risk for stones increases with history of childbearing, estrogen replacement therapy, oral contraceptive use, and obesity. Stones are also associated with hypertriglyceridemia, Crohns disease, and parenteral hyperalimentation. Gallstones are symptomatic in 20% to 30% of patients; biliary pain or colic is the most common symptom. This is most often related to impaction of a stone in the cystic duct. The most common acute complications of gallstones are acute cholecystitis, acute pancreatitis, and ascending cholangitis. Chronic complications include chronic cholecystitis, Mirizzi syndrome, cholecystenteric fistula, and gallstone ileus.
  • #53 Cholelithiasis, Cholecystitis, Choledocholithiasis, and Hyperplastic Cholecystoses | Radiology Key
    https://radiologykey.com/cholelithiasis-cholecystitis-choledocholithiasis-and-hyperplastic-cholecystoses/
    The prevalence of gallstones varies with age and gender. Gallstones are present in an estimated 10% to 15% of men and 20% to 40% of women older than 60 years. In general, the risk for stones increases with history of childbearing, estrogen replacement therapy, oral contraceptive use, and obesity. Stones are also associated with hypertriglyceridemia, Crohns disease, and parenteral hyperalimentation. Gallstones are symptomatic in 20% to 30% of patients; biliary pain or colic is the most common symptom. This is most often related to impaction of a stone in the cystic duct. The most common acute complications of gallstones are acute cholecystitis, acute pancreatitis, and ascending cholangitis. Chronic complications include chronic cholecystitis, Mirizzi syndrome, cholecystenteric fistula, and gallstone ileus.
  • #54 Seasonality of Acute Cholecystitis: A Review of Global Patterns
    https://clinmedjournals.org/articles/ijsrp/international-journal-of-surgery-research-and-practice-ijsrp-9-146.php?jid=ijsrp
    As with many communicable and noncommunicable diseases the incidence of acute cholecystitis rises and falls in an annual seasonal pattern. […] Although the exact mechanism underlying the fluctuation of cholecystitis in a particular time of the year is still not clear, several researchers have suggested that the behavioural and environmental risk factors such as temperature, humidity, dietary habits, and hydration can trigger gallstone formation and subsequent acute cholecystitis. […] Dietary factors have been implicated in the pathogenesis of cholelithiasis. A high intake of saturated fat has been linked to an increased risk of gallstone formation. […] The ingestion of refined sugars has been shown to be associated with higher cholesterol synthesis in the liver secondary to increased insulin in response to high sugar consumption, whereas low fiber intakes have been associated with an increase in the risk of gallstone formation because of the resultant increase in secondary bile acid secretions due to decreased colonic motility.
  • #55 Seasonality of Acute Cholecystitis: A Review of Global Patterns
    https://clinmedjournals.org/articles/ijsrp/international-journal-of-surgery-research-and-practice-ijsrp-9-146.php?jid=ijsrp
    As with many communicable and noncommunicable diseases the incidence of acute cholecystitis rises and falls in an annual seasonal pattern. […] Although the exact mechanism underlying the fluctuation of cholecystitis in a particular time of the year is still not clear, several researchers have suggested that the behavioural and environmental risk factors such as temperature, humidity, dietary habits, and hydration can trigger gallstone formation and subsequent acute cholecystitis. […] Dietary factors have been implicated in the pathogenesis of cholelithiasis. A high intake of saturated fat has been linked to an increased risk of gallstone formation. […] The ingestion of refined sugars has been shown to be associated with higher cholesterol synthesis in the liver secondary to increased insulin in response to high sugar consumption, whereas low fiber intakes have been associated with an increase in the risk of gallstone formation because of the resultant increase in secondary bile acid secretions due to decreased colonic motility.
  • #56 Seasonality of Acute Cholecystitis: A Review of Global Patterns
    https://clinmedjournals.org/articles/ijsrp/international-journal-of-surgery-research-and-practice-ijsrp-9-146.php?jid=ijsrp
    Furthermore, a low fiber and high sugar diets can lead to constipation and subsequent crystal formation in the bile. […] Prolongation of intestinal transit has been proposed as the mechanism for the increase in the proportion of deoxycholic acid in bile. […] Increases in biliary deoxycholic acid have long been implicated in the pathogenesis of cholesterol rich gallstones. […] Dehydration during summer can further augment the risk of acute cholecystitis by causing bile stasis due to decreased gallbladder emptying. […] Bacterial infections are associated with acute cholecystitis due to the release of inflammatory mediators. […] The most frequent pathogens in biliary infection are gram-negative anaerobes, dominated by Escherichia coli, Klebsiella spp., Acinetobacter baumannii complex and Enterobacter spp.
  • #57 Seasonality of Acute Cholecystitis: A Review of Global Patterns
    https://clinmedjournals.org/articles/ijsrp/international-journal-of-surgery-research-and-practice-ijsrp-9-146.php?jid=ijsrp
    Furthermore, a low fiber and high sugar diets can lead to constipation and subsequent crystal formation in the bile. […] Prolongation of intestinal transit has been proposed as the mechanism for the increase in the proportion of deoxycholic acid in bile. […] Increases in biliary deoxycholic acid have long been implicated in the pathogenesis of cholesterol rich gallstones. […] Dehydration during summer can further augment the risk of acute cholecystitis by causing bile stasis due to decreased gallbladder emptying. […] Bacterial infections are associated with acute cholecystitis due to the release of inflammatory mediators. […] The most frequent pathogens in biliary infection are gram-negative anaerobes, dominated by Escherichia coli, Klebsiella spp., Acinetobacter baumannii complex and Enterobacter spp.
  • #58 Seasonality of Acute Cholecystitis: A Review of Global Patterns
    https://clinmedjournals.org/articles/ijsrp/international-journal-of-surgery-research-and-practice-ijsrp-9-146.php?jid=ijsrp
    Furthermore, a low fiber and high sugar diets can lead to constipation and subsequent crystal formation in the bile. […] Prolongation of intestinal transit has been proposed as the mechanism for the increase in the proportion of deoxycholic acid in bile. […] Increases in biliary deoxycholic acid have long been implicated in the pathogenesis of cholesterol rich gallstones. […] Dehydration during summer can further augment the risk of acute cholecystitis by causing bile stasis due to decreased gallbladder emptying. […] Bacterial infections are associated with acute cholecystitis due to the release of inflammatory mediators. […] The most frequent pathogens in biliary infection are gram-negative anaerobes, dominated by Escherichia coli, Klebsiella spp., Acinetobacter baumannii complex and Enterobacter spp.
  • #59 Seasonality of Acute Cholecystitis: A Review of Global Patterns
    https://clinmedjournals.org/articles/ijsrp/international-journal-of-surgery-research-and-practice-ijsrp-9-146.php?jid=ijsrp
    Furthermore, a low fiber and high sugar diets can lead to constipation and subsequent crystal formation in the bile. […] Prolongation of intestinal transit has been proposed as the mechanism for the increase in the proportion of deoxycholic acid in bile. […] Increases in biliary deoxycholic acid have long been implicated in the pathogenesis of cholesterol rich gallstones. […] Dehydration during summer can further augment the risk of acute cholecystitis by causing bile stasis due to decreased gallbladder emptying. […] Bacterial infections are associated with acute cholecystitis due to the release of inflammatory mediators. […] The most frequent pathogens in biliary infection are gram-negative anaerobes, dominated by Escherichia coli, Klebsiella spp., Acinetobacter baumannii complex and Enterobacter spp.
  • #60 Seasonality of Acute Cholecystitis: A Review of Global Patterns
    https://clinmedjournals.org/articles/ijsrp/international-journal-of-surgery-research-and-practice-ijsrp-9-146.php?jid=ijsrp
    Inflammatory bowel disease (IBD) is commonly associated with increased risk of cholelithiasis, particularly in patients with crohn’s disease (CD), the etiology is not clear. […] On the other hand, the role of cholecystokinin (CCK) in the expression of seasonal variation of acute cholecystitis has been proposed by several authors. […] Cholecystokinin is a peripheral hormone released by the proximal small bowel in response to fatty and amino acids in a meal, this in turn stimulates the gallbladder to contract and release stored bile into the intestine. […] The exact reason why acute cholecystitis cases present in summer more than other seasons is still not clear, several extrinsic factors such as, bacterial infection, constipation, dehydration, alcohol consumption and low fiber diet during summer months could contribute to the higher incidence of acute cholecystitis.
  • #61 Seasonality of Acute Cholecystitis: A Review of Global Patterns
    https://clinmedjournals.org/articles/ijsrp/international-journal-of-surgery-research-and-practice-ijsrp-9-146.php?jid=ijsrp
    Inflammatory bowel disease (IBD) is commonly associated with increased risk of cholelithiasis, particularly in patients with crohn’s disease (CD), the etiology is not clear. […] On the other hand, the role of cholecystokinin (CCK) in the expression of seasonal variation of acute cholecystitis has been proposed by several authors. […] Cholecystokinin is a peripheral hormone released by the proximal small bowel in response to fatty and amino acids in a meal, this in turn stimulates the gallbladder to contract and release stored bile into the intestine. […] The exact reason why acute cholecystitis cases present in summer more than other seasons is still not clear, several extrinsic factors such as, bacterial infection, constipation, dehydration, alcohol consumption and low fiber diet during summer months could contribute to the higher incidence of acute cholecystitis.
  • #62 Cholecystitis | SpringerLink
    https://link.springer.com/10.1007/978-3-540-35280-8_471
    Cholecystitis is the inflammation of the gallbladder occurring most commonly in cases of obstruction of the cystic duct caused by gallstones. […] The inflammation often initiates without contamination, and infection may develop later; therefore, bacterial proliferation may be a result of cholecystitis and not the precipitating factor. […] Severe disease, alcohol abuse, and rarely, tumors of the gallbladder can also be the cause of cholecystitis. […] Cholecystitis may develop either as an acute or a chronic process.
  • #63 Acute Cholecystitis – Hepatic and Biliary Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/hepatic-and-biliary-disorders/gallbladder-and-bile-duct-disorders/acute-cholecystitis
    Acute cholecystitis is inflammation of the gallbladder that develops over hours, usually because a gallstone obstructs the cystic duct. […] When a stone becomes impacted in the cystic duct and persistently obstructs it, acute inflammation results. Bile stasis triggers release of inflammatory enzymes (eg, phospholipase A, which converts lecithin to lysolecithin, which then may mediate inflammation). […] The damaged mucosa secretes more fluid into the gallbladder lumen than it absorbs. The resulting distention further releases inflammatory mediators (eg, prostaglandins), worsening mucosal damage and causing ischemia, all of which perpetuate inflammation. Bacterial infection can supervene. The vicious circle of fluid secretion and inflammation, when unchecked, leads to necrosis and perforation. […] The mechanism probably involves inflammatory mediators released because of ischemia, infection, or bile stasis.
  • #64 Biliary Colic and Cholecystitis – TeachMeSurgery
    https://teachmesurgery.com/hpb/gall-bladder/colic-and-cholecystitis/
    Patients with acute cholecystitis will report a constant pain in the RUQ or epigastrium, associated with signs of inflammation, such as fever or lethargy. […] A stone located in Hartmanns pouch (an out-pouching of the gallbladder wall at the junction with the cystic duct) or in the cystic duct itself can cause compression on the adjacent common hepatic duct. This results in an obstructive jaundice, even without stones being present within the lumen of the common hepatic or common bile ducts. Diagnosis is confirmed by MRCP and management is usually with laparoscopic cholecystectomy. […] Inflammation of the gallbladder (typically if recurrent) can cause a fistula to form between the gallbladder wall and the small bowel, termed a cholecystoduodenal fistula, allowing gallstones to pass directly into the small bowel (typically at the duodenum).
  • #65 Chronic Cholecystitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK470236/
    Chronic cholecystitis is a prolonged, subacute condition caused by the mechanical or functional dysfunction of the emptying of the gallbladder. […] Chronic cholecystitis is a chronic condition caused by ongoing inflammation of the gallbladder resulting in mechanical or physiological dysfunction its emptying. […] The proposed etiology is recurrent episodes of acute cholecystitis or chronic irritation from gallstones invoking an inflammatory response in the gallbladder wall. […] Occlusion of the cystic duct or malfunction of the mechanics of the gallbladder emptying is the basic underlying pathologies of this disease. Over 90% of chronic cholecystitis is associated with the presence of gallstones. Gallstones, by causing intermittent obstruction of the bile flow, most commonly by blocking the cystic duct lead to inflammation and edema in the gall bladder wall.
  • #66 Chronic Cholecystitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK470236/
    Chronic cholecystitis is a prolonged, subacute condition caused by the mechanical or functional dysfunction of the emptying of the gallbladder. […] Chronic cholecystitis is a chronic condition caused by ongoing inflammation of the gallbladder resulting in mechanical or physiological dysfunction its emptying. […] The proposed etiology is recurrent episodes of acute cholecystitis or chronic irritation from gallstones invoking an inflammatory response in the gallbladder wall. […] Occlusion of the cystic duct or malfunction of the mechanics of the gallbladder emptying is the basic underlying pathologies of this disease. Over 90% of chronic cholecystitis is associated with the presence of gallstones. Gallstones, by causing intermittent obstruction of the bile flow, most commonly by blocking the cystic duct lead to inflammation and edema in the gall bladder wall.
  • #67 Chronic Cholecystitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK470236/
    Chronic cholecystitis is a prolonged, subacute condition caused by the mechanical or functional dysfunction of the emptying of the gallbladder. […] Chronic cholecystitis is a chronic condition caused by ongoing inflammation of the gallbladder resulting in mechanical or physiological dysfunction its emptying. […] The proposed etiology is recurrent episodes of acute cholecystitis or chronic irritation from gallstones invoking an inflammatory response in the gallbladder wall. […] Occlusion of the cystic duct or malfunction of the mechanics of the gallbladder emptying is the basic underlying pathologies of this disease. Over 90% of chronic cholecystitis is associated with the presence of gallstones. Gallstones, by causing intermittent obstruction of the bile flow, most commonly by blocking the cystic duct lead to inflammation and edema in the gall bladder wall.
  • #68 Chronic Cholecystitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK470236/
    Chronic cholecystitis is a prolonged, subacute condition caused by the mechanical or functional dysfunction of the emptying of the gallbladder. […] Chronic cholecystitis is a chronic condition caused by ongoing inflammation of the gallbladder resulting in mechanical or physiological dysfunction its emptying. […] The proposed etiology is recurrent episodes of acute cholecystitis or chronic irritation from gallstones invoking an inflammatory response in the gallbladder wall. […] Occlusion of the cystic duct or malfunction of the mechanics of the gallbladder emptying is the basic underlying pathologies of this disease. Over 90% of chronic cholecystitis is associated with the presence of gallstones. Gallstones, by causing intermittent obstruction of the bile flow, most commonly by blocking the cystic duct lead to inflammation and edema in the gall bladder wall.
  • #69 Chronic Cholecystitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK470236/
    It has been proposed that lithogenic bile leads to increased free radical-mediated damage from hydrophobic bile salts. That, in association with reduced mucosal protection due to lower levels of prostaglandin E2 results in a continuous inflammatory state. When the cholecystokinin receptors of the smooth muscle are affected, there is impaired gall bladder contraction that leads to stasis and worsens the permissive environment where lithogenic bile promotes inflammation.
  • #70 Chronic Cholecystitis – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK470236/
    It has been proposed that lithogenic bile leads to increased free radical-mediated damage from hydrophobic bile salts. That, in association with reduced mucosal protection due to lower levels of prostaglandin E2 results in a continuous inflammatory state. When the cholecystokinin receptors of the smooth muscle are affected, there is impaired gall bladder contraction that leads to stasis and worsens the permissive environment where lithogenic bile promotes inflammation.
  • #71 Acalculous Cholecystitis | 5-Minute Clinical Consult
    https://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/1688222/all/Acalculous_Cholecystitis
    Acalculous cholecystitis, also known as acute alithiasic cholecystitis (AAC), is an acute necroinflammatory disease of the gallbladder occurring in the absence of cholelithiasis with a multifactorial pathogenesis. […] The pathogenesis of AAC is multifactorial. Bile stasis and ischemia both likely contribute. Bile stasis can be caused by fasting, obstruction, procedural irritation, and/or ileus. This can lead to bile inspissation that is directly toxic to the gallbladder epithelium. Ischemia may occur as a result of systemic inflammation, iatrogenesis, or shock. Trauma, total parenteral nutrition, viral (hepatotropic virus) or bacterial (mostly gram-negative or anaerobic) infections are also associated with AAC.
  • #72 Acalculous Cholecystitis | 5-Minute Clinical Consult
    https://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/1688222/all/Acalculous_Cholecystitis
    Acalculous cholecystitis, also known as acute alithiasic cholecystitis (AAC), is an acute necroinflammatory disease of the gallbladder occurring in the absence of cholelithiasis with a multifactorial pathogenesis. […] The pathogenesis of AAC is multifactorial. Bile stasis and ischemia both likely contribute. Bile stasis can be caused by fasting, obstruction, procedural irritation, and/or ileus. This can lead to bile inspissation that is directly toxic to the gallbladder epithelium. Ischemia may occur as a result of systemic inflammation, iatrogenesis, or shock. Trauma, total parenteral nutrition, viral (hepatotropic virus) or bacterial (mostly gram-negative or anaerobic) infections are also associated with AAC.
  • #73 Cholelithiasis, Cholecystitis, Choledocholithiasis, and Hyperplastic Cholecystoses | Radiology Key
    https://radiologykey.com/cholelithiasis-cholecystitis-choledocholithiasis-and-hyperplastic-cholecystoses/
    Gangrenous cholecystitis is a severe form of acute cholecystitis associated with vascular compromise and intramural hemorrhage, necrosis, and intramural abscess formation. This is usually caused by a stone impacting the cystic duct, with progressive distention of the gallbladder and ultimately ischemic necrosis of the wall. The incidence ranges from 2% to approximately 30% in various surgical series. The incidence is increased in men, patients of advanced age, and those with cardiovascular disease. Once it is diagnosed, treatment is generally emergency cholecystectomy to avoid life-threatening complications, such as perforation. There is a higher rate of conversion to open cholecystectomy than in uncomplicated acute cholecystitis. […] Emphysematous cholecystitis is a rare life-threatening and rapidly progressive complication of acute cholecystitis. Cystic artery compromise is thought to promote the proliferation of gas-producing organisms in an anaerobic environment and penetration of gas into the gallbladder wall. The organisms most commonly isolated are Clostridium welchii and Escherichia coli. At pathologic examination, gallbladders with emphysematous cholecystitis have a higher incidence of endarteritis obliterans, supporting vascular insufficiency as a causative factor. This complication occurs with higher frequency in patients with diabetes (up to 50%) and male patients (up to 71%). Gallstones may be absent in up to one third of patients, and there is a high risk of gangrene and a perforation rate five times higher than in acute uncomplicated cholecystitis.
  • #74 Cholelithiasis, Cholecystitis, Choledocholithiasis, and Hyperplastic Cholecystoses | Radiology Key
    https://radiologykey.com/cholelithiasis-cholecystitis-choledocholithiasis-and-hyperplastic-cholecystoses/
    Gangrenous cholecystitis is a severe form of acute cholecystitis associated with vascular compromise and intramural hemorrhage, necrosis, and intramural abscess formation. This is usually caused by a stone impacting the cystic duct, with progressive distention of the gallbladder and ultimately ischemic necrosis of the wall. The incidence ranges from 2% to approximately 30% in various surgical series. The incidence is increased in men, patients of advanced age, and those with cardiovascular disease. Once it is diagnosed, treatment is generally emergency cholecystectomy to avoid life-threatening complications, such as perforation. There is a higher rate of conversion to open cholecystectomy than in uncomplicated acute cholecystitis. […] Emphysematous cholecystitis is a rare life-threatening and rapidly progressive complication of acute cholecystitis. Cystic artery compromise is thought to promote the proliferation of gas-producing organisms in an anaerobic environment and penetration of gas into the gallbladder wall. The organisms most commonly isolated are Clostridium welchii and Escherichia coli. At pathologic examination, gallbladders with emphysematous cholecystitis have a higher incidence of endarteritis obliterans, supporting vascular insufficiency as a causative factor. This complication occurs with higher frequency in patients with diabetes (up to 50%) and male patients (up to 71%). Gallstones may be absent in up to one third of patients, and there is a high risk of gangrene and a perforation rate five times higher than in acute uncomplicated cholecystitis.
  • #75 Cholelithiasis, Cholecystitis, Choledocholithiasis, and Hyperplastic Cholecystoses | Radiology Key
    https://radiologykey.com/cholelithiasis-cholecystitis-choledocholithiasis-and-hyperplastic-cholecystoses/
    Gangrenous cholecystitis is a severe form of acute cholecystitis associated with vascular compromise and intramural hemorrhage, necrosis, and intramural abscess formation. This is usually caused by a stone impacting the cystic duct, with progressive distention of the gallbladder and ultimately ischemic necrosis of the wall. The incidence ranges from 2% to approximately 30% in various surgical series. The incidence is increased in men, patients of advanced age, and those with cardiovascular disease. Once it is diagnosed, treatment is generally emergency cholecystectomy to avoid life-threatening complications, such as perforation. There is a higher rate of conversion to open cholecystectomy than in uncomplicated acute cholecystitis. […] Emphysematous cholecystitis is a rare life-threatening and rapidly progressive complication of acute cholecystitis. Cystic artery compromise is thought to promote the proliferation of gas-producing organisms in an anaerobic environment and penetration of gas into the gallbladder wall. The organisms most commonly isolated are Clostridium welchii and Escherichia coli. At pathologic examination, gallbladders with emphysematous cholecystitis have a higher incidence of endarteritis obliterans, supporting vascular insufficiency as a causative factor. This complication occurs with higher frequency in patients with diabetes (up to 50%) and male patients (up to 71%). Gallstones may be absent in up to one third of patients, and there is a high risk of gangrene and a perforation rate five times higher than in acute uncomplicated cholecystitis.
  • #76 Cholelithiasis, Cholecystitis, Choledocholithiasis, and Hyperplastic Cholecystoses | Radiology Key
    https://radiologykey.com/cholelithiasis-cholecystitis-choledocholithiasis-and-hyperplastic-cholecystoses/
    Gangrenous cholecystitis is a severe form of acute cholecystitis associated with vascular compromise and intramural hemorrhage, necrosis, and intramural abscess formation. This is usually caused by a stone impacting the cystic duct, with progressive distention of the gallbladder and ultimately ischemic necrosis of the wall. The incidence ranges from 2% to approximately 30% in various surgical series. The incidence is increased in men, patients of advanced age, and those with cardiovascular disease. Once it is diagnosed, treatment is generally emergency cholecystectomy to avoid life-threatening complications, such as perforation. There is a higher rate of conversion to open cholecystectomy than in uncomplicated acute cholecystitis. […] Emphysematous cholecystitis is a rare life-threatening and rapidly progressive complication of acute cholecystitis. Cystic artery compromise is thought to promote the proliferation of gas-producing organisms in an anaerobic environment and penetration of gas into the gallbladder wall. The organisms most commonly isolated are Clostridium welchii and Escherichia coli. At pathologic examination, gallbladders with emphysematous cholecystitis have a higher incidence of endarteritis obliterans, supporting vascular insufficiency as a causative factor. This complication occurs with higher frequency in patients with diabetes (up to 50%) and male patients (up to 71%). Gallstones may be absent in up to one third of patients, and there is a high risk of gangrene and a perforation rate five times higher than in acute uncomplicated cholecystitis.
  • #77 Cholelithiasis, Cholecystitis, Choledocholithiasis, and Hyperplastic Cholecystoses | Radiology Key
    https://radiologykey.com/cholelithiasis-cholecystitis-choledocholithiasis-and-hyperplastic-cholecystoses/
    Gangrenous cholecystitis is a severe form of acute cholecystitis associated with vascular compromise and intramural hemorrhage, necrosis, and intramural abscess formation. This is usually caused by a stone impacting the cystic duct, with progressive distention of the gallbladder and ultimately ischemic necrosis of the wall. The incidence ranges from 2% to approximately 30% in various surgical series. The incidence is increased in men, patients of advanced age, and those with cardiovascular disease. Once it is diagnosed, treatment is generally emergency cholecystectomy to avoid life-threatening complications, such as perforation. There is a higher rate of conversion to open cholecystectomy than in uncomplicated acute cholecystitis. […] Emphysematous cholecystitis is a rare life-threatening and rapidly progressive complication of acute cholecystitis. Cystic artery compromise is thought to promote the proliferation of gas-producing organisms in an anaerobic environment and penetration of gas into the gallbladder wall. The organisms most commonly isolated are Clostridium welchii and Escherichia coli. At pathologic examination, gallbladders with emphysematous cholecystitis have a higher incidence of endarteritis obliterans, supporting vascular insufficiency as a causative factor. This complication occurs with higher frequency in patients with diabetes (up to 50%) and male patients (up to 71%). Gallstones may be absent in up to one third of patients, and there is a high risk of gangrene and a perforation rate five times higher than in acute uncomplicated cholecystitis.
  • #78 Cholelithiasis, Cholecystitis, Choledocholithiasis, and Hyperplastic Cholecystoses | Radiology Key
    https://radiologykey.com/cholelithiasis-cholecystitis-choledocholithiasis-and-hyperplastic-cholecystoses/
    Gangrenous cholecystitis is a severe form of acute cholecystitis associated with vascular compromise and intramural hemorrhage, necrosis, and intramural abscess formation. This is usually caused by a stone impacting the cystic duct, with progressive distention of the gallbladder and ultimately ischemic necrosis of the wall. The incidence ranges from 2% to approximately 30% in various surgical series. The incidence is increased in men, patients of advanced age, and those with cardiovascular disease. Once it is diagnosed, treatment is generally emergency cholecystectomy to avoid life-threatening complications, such as perforation. There is a higher rate of conversion to open cholecystectomy than in uncomplicated acute cholecystitis. […] Emphysematous cholecystitis is a rare life-threatening and rapidly progressive complication of acute cholecystitis. Cystic artery compromise is thought to promote the proliferation of gas-producing organisms in an anaerobic environment and penetration of gas into the gallbladder wall. The organisms most commonly isolated are Clostridium welchii and Escherichia coli. At pathologic examination, gallbladders with emphysematous cholecystitis have a higher incidence of endarteritis obliterans, supporting vascular insufficiency as a causative factor. This complication occurs with higher frequency in patients with diabetes (up to 50%) and male patients (up to 71%). Gallstones may be absent in up to one third of patients, and there is a high risk of gangrene and a perforation rate five times higher than in acute uncomplicated cholecystitis.
  • #79 Cholelithiasis, Cholecystitis, Choledocholithiasis, and Hyperplastic Cholecystoses | Radiology Key
    https://radiologykey.com/cholelithiasis-cholecystitis-choledocholithiasis-and-hyperplastic-cholecystoses/
    Gangrenous cholecystitis is a severe form of acute cholecystitis associated with vascular compromise and intramural hemorrhage, necrosis, and intramural abscess formation. This is usually caused by a stone impacting the cystic duct, with progressive distention of the gallbladder and ultimately ischemic necrosis of the wall. The incidence ranges from 2% to approximately 30% in various surgical series. The incidence is increased in men, patients of advanced age, and those with cardiovascular disease. Once it is diagnosed, treatment is generally emergency cholecystectomy to avoid life-threatening complications, such as perforation. There is a higher rate of conversion to open cholecystectomy than in uncomplicated acute cholecystitis. […] Emphysematous cholecystitis is a rare life-threatening and rapidly progressive complication of acute cholecystitis. Cystic artery compromise is thought to promote the proliferation of gas-producing organisms in an anaerobic environment and penetration of gas into the gallbladder wall. The organisms most commonly isolated are Clostridium welchii and Escherichia coli. At pathologic examination, gallbladders with emphysematous cholecystitis have a higher incidence of endarteritis obliterans, supporting vascular insufficiency as a causative factor. This complication occurs with higher frequency in patients with diabetes (up to 50%) and male patients (up to 71%). Gallstones may be absent in up to one third of patients, and there is a high risk of gangrene and a perforation rate five times higher than in acute uncomplicated cholecystitis.
  • #80 Precision medicine for personalized cholecystitis care: integrating molecular diagnostics and biotherapeutics | Bulletin of the National Research Centre | Full Text
    https://bnrc.springeropen.com/articles/10.1186/s42269-024-01244-9
    While necessary to clear infection, excessive inflammation can damage host tissues. […] The inflammation and obstruction accompanying acute cholecystitis induces significant effects on the gallbladder anatomy and function. […] The pathogenesis of acute cholecystitis is intimately linked to the development of gallstones, which obstruct bile drainage and initiate gallbladder inflammation. […] The obstruction of bile drainage from the gallbladder that occurs in acute cholecystitis has two major detrimental effects-bile stasis within the gallbladder and jaundice due to the backup of bile constituents. […] The advancement of biotechnology and molecular techniques has provided powerful new tools to enhance the diagnosis, characterization, and treatment of acute cholecystitis. […] Molecular detection methods like PCR allow rapid, sensitive identification of bacterial, parasitic, and fungal pathogens in gallbladder tissues.
  • #81 Precision medicine for personalized cholecystitis care: integrating molecular diagnostics and biotherapeutics | Bulletin of the National Research Centre | Full Text
    https://bnrc.springeropen.com/articles/10.1186/s42269-024-01244-9
    While necessary to clear infection, excessive inflammation can damage host tissues. […] The inflammation and obstruction accompanying acute cholecystitis induces significant effects on the gallbladder anatomy and function. […] The pathogenesis of acute cholecystitis is intimately linked to the development of gallstones, which obstruct bile drainage and initiate gallbladder inflammation. […] The obstruction of bile drainage from the gallbladder that occurs in acute cholecystitis has two major detrimental effects-bile stasis within the gallbladder and jaundice due to the backup of bile constituents. […] The advancement of biotechnology and molecular techniques has provided powerful new tools to enhance the diagnosis, characterization, and treatment of acute cholecystitis. […] Molecular detection methods like PCR allow rapid, sensitive identification of bacterial, parasitic, and fungal pathogens in gallbladder tissues.
  • #82 Precision medicine for personalized cholecystitis care: integrating molecular diagnostics and biotherapeutics | Bulletin of the National Research Centre | Full Text
    https://bnrc.springeropen.com/articles/10.1186/s42269-024-01244-9
    Gene therapy techniques using CRISPR/Cas9 systems or RNAi may selectively edit microbial genomes to disable virulence mechanisms. […] Further advances in biotechnology hold enormous potential for improving cholecystitis prevention, diagnosis, and treatment. […] Probiotic administration shows promise as a therapeutic strategy for cholecystitis by promoting growth of beneficial microbes that can outcompete pathogens. […] Probiotic strains like Lactobacillus and Bifidobacterium are selected based on their ability to directly inhibit gastrointestinal pathogens like E. coli and Klebsiella. […] The antimicrobial arsenal produced by probiotics varies widely by strain. […] The integration of advanced biotechnologies holds significant promise for revolutionizing the diagnosis, treatment, and management of cholecystitis.
  • #83 Precision medicine for personalized cholecystitis care: integrating molecular diagnostics and biotherapeutics | Bulletin of the National Research Centre | Full Text
    https://bnrc.springeropen.com/articles/10.1186/s42269-024-01244-9
    Gene therapy techniques using CRISPR/Cas9 systems or RNAi may selectively edit microbial genomes to disable virulence mechanisms. […] Further advances in biotechnology hold enormous potential for improving cholecystitis prevention, diagnosis, and treatment. […] Probiotic administration shows promise as a therapeutic strategy for cholecystitis by promoting growth of beneficial microbes that can outcompete pathogens. […] Probiotic strains like Lactobacillus and Bifidobacterium are selected based on their ability to directly inhibit gastrointestinal pathogens like E. coli and Klebsiella. […] The antimicrobial arsenal produced by probiotics varies widely by strain. […] The integration of advanced biotechnologies holds significant promise for revolutionizing the diagnosis, treatment, and management of cholecystitis.
  • #84 Precision medicine for personalized cholecystitis care: integrating molecular diagnostics and biotherapeutics | Bulletin of the National Research Centre | Full Text
    https://bnrc.springeropen.com/articles/10.1186/s42269-024-01244-9
    Gene therapy techniques using CRISPR/Cas9 systems or RNAi may selectively edit microbial genomes to disable virulence mechanisms. […] Further advances in biotechnology hold enormous potential for improving cholecystitis prevention, diagnosis, and treatment. […] Probiotic administration shows promise as a therapeutic strategy for cholecystitis by promoting growth of beneficial microbes that can outcompete pathogens. […] Probiotic strains like Lactobacillus and Bifidobacterium are selected based on their ability to directly inhibit gastrointestinal pathogens like E. coli and Klebsiella. […] The antimicrobial arsenal produced by probiotics varies widely by strain. […] The integration of advanced biotechnologies holds significant promise for revolutionizing the diagnosis, treatment, and management of cholecystitis.
  • #85 Precision medicine for personalized cholecystitis care: integrating molecular diagnostics and biotherapeutics | Bulletin of the National Research Centre | Full Text
    https://bnrc.springeropen.com/articles/10.1186/s42269-024-01244-9
    Gene therapy techniques using CRISPR/Cas9 systems or RNAi may selectively edit microbial genomes to disable virulence mechanisms. […] Further advances in biotechnology hold enormous potential for improving cholecystitis prevention, diagnosis, and treatment. […] Probiotic administration shows promise as a therapeutic strategy for cholecystitis by promoting growth of beneficial microbes that can outcompete pathogens. […] Probiotic strains like Lactobacillus and Bifidobacterium are selected based on their ability to directly inhibit gastrointestinal pathogens like E. coli and Klebsiella. […] The antimicrobial arsenal produced by probiotics varies widely by strain. […] The integration of advanced biotechnologies holds significant promise for revolutionizing the diagnosis, treatment, and management of cholecystitis.
  • #86 Cholecystitis – Wikipedia
    https://en.wikipedia.org/wiki/Cholecystitis
    More than 90% of the time acute cholecystitis is caused from blockage of the cystic duct by a gallstone. […] Blockage of the cystic duct by a gallstone causes a buildup of bile in the gallbladder and increased pressure within the gallbladder. Concentrated bile, pressure, and sometimes bacterial infection irritate and damage the gallbladder wall, causing inflammation and swelling of the gallbladder. […] Inflammation and swelling of the gallbladder can reduce normal blood flow to areas of the gallbladder, which can lead to cell death due to inadequate oxygen.
  • #87 Acute Cholecystitis – Hepatic and Biliary Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/hepatic-and-biliary-disorders/gallbladder-and-bile-duct-disorders/acute-cholecystitis
    Acute cholecystitis is inflammation of the gallbladder that develops over hours, usually because a gallstone obstructs the cystic duct. […] When a stone becomes impacted in the cystic duct and persistently obstructs it, acute inflammation results. Bile stasis triggers release of inflammatory enzymes (eg, phospholipase A, which converts lecithin to lysolecithin, which then may mediate inflammation). […] The damaged mucosa secretes more fluid into the gallbladder lumen than it absorbs. The resulting distention further releases inflammatory mediators (eg, prostaglandins), worsening mucosal damage and causing ischemia, all of which perpetuate inflammation. Bacterial infection can supervene. The vicious circle of fluid secretion and inflammation, when unchecked, leads to necrosis and perforation. […] The mechanism probably involves inflammatory mediators released because of ischemia, infection, or bile stasis.
  • #88 Acute Cholecystitis – Hepatic and Biliary Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/hepatic-and-biliary-disorders/gallbladder-and-bile-duct-disorders/acute-cholecystitis
    Acute cholecystitis is inflammation of the gallbladder that develops over hours, usually because a gallstone obstructs the cystic duct. […] When a stone becomes impacted in the cystic duct and persistently obstructs it, acute inflammation results. Bile stasis triggers release of inflammatory enzymes (eg, phospholipase A, which converts lecithin to lysolecithin, which then may mediate inflammation). […] The damaged mucosa secretes more fluid into the gallbladder lumen than it absorbs. The resulting distention further releases inflammatory mediators (eg, prostaglandins), worsening mucosal damage and causing ischemia, all of which perpetuate inflammation. Bacterial infection can supervene. The vicious circle of fluid secretion and inflammation, when unchecked, leads to necrosis and perforation. […] The mechanism probably involves inflammatory mediators released because of ischemia, infection, or bile stasis.
  • #89 PATHOLOGY AND PATHOGENESIS OF CHOLECYSTITIS – ppt download
    https://slideplayer.com/slide/16683936/
    Pathogenesis of Cholesterol Stones Cholesterol is rendered soluble in bile by aggregation with water-soluble bile salts and water-insoluble lecithins, both of which act as detergents. When cholesterol concentrations exceed the solubilizing capacity of bile (supersaturation), cholesterol can no longer remain dispersed and nucleates into solid cholesterol monohydrate crystals. Cholesterol gallstone formation involves three simultaneous defects: […] Supersaturation of bile with cholesterol: the result of hepatocellular hypersecretion of cholesterol. Gallbladder hypomotility. It promotes nucleation typically around a calcium salt crystal nidus. Mucus hypersecretion in the gallbladder: This traps the crystals, permitting their aggregation into stones. […] Acute Cholecystitis: Pathogenesis Acute calculous cholecystitis results from chemical irritation and inflammation of the obstructed gallbladder. These events occur in the absence of bacterial infection; only later in the course may bacterial contamination develop.
  • #90 Acalculous cholecystitis – UpToDate
    https://www.uptodate.com/contents/acalculous-cholecystitis
    Acute acalculous cholecystitis is an acute necroinflammatory disease of the gallbladder with a multifactorial pathogenesis, occurring in the absence of gallstones. It accounts for approximately 10 percent of all cases of acute cholecystitis and is associated with high morbidity and mortality rates. […] The pathogenesis of acalculous cholecystitis is multifactorial and likely results from ischemia and cholestasis. The cystic artery, which supplies blood to the gallbladder, is a terminal artery and susceptible to ischemia. Ischemia and necrosis of the gallbladder wall can occur with hypoperfusion in cases of hypotension, vasoactive drug use, or major surgery and trauma. Cholestasis may be seen in prolonged fasting states, usage of total parental nutrition, and ileus or bowel obstruction. Cholestasis results in increased pressure within the gallbladder and distension, further decreasing perfusion to the gallbladder wall. Pathologically, ischemia and cholestasis result in local inflammatory response in the gallbladder wall, epithelial injury, and eventually necrosis of the gallbladder tissue.
  • #91 Acute Acalculous Cholecystitis | Abdominal Key
    https://abdominalkey.com/acute-acalculous-cholecystitis/
    Acute acalculous cholecystitis (ACC) can develop with or without gallstones after surgery and in critically ill or injured patients. […] The pathogenesis of AAC is complex and multifactorial. […] Bile stasis has been implicated in the pathogenesis of AAC in both experimental and clinical studies. […] Bile stasis may alter the chemical composition of bile, which may promote gallbladder mucosal injury. […] Gallbladder ischemia is central to the pathogenesis of AAC. […] It has been hypothesized that the fundamental lesion leading to AAC is failure of the gallbladder microcirculation with cellular hypoxia. […] Vasoactive mediators play a role in the pathogenesis of AAC. […] Although bacterial infection is likely a secondary phenomenon, the host response to gram-negative bacteremia or splanchnic ischemia-reperfusion injury may be of primary importance.
  • #92 Acute Cholecystitis | Basicmedical Key
    https://basicmedicalkey.com/acute-cholecystitis/
    Acute Calculous Cholecystitis: Key elements are obstruction of cystic duct by stones and bile supersaturated with cholesterol. Trauma to mucosa releases phospholipase from lysosomes. Phospholipase converts lecithin in bile to lysolecithin, which damages gallbladder epithelium. Secondary bacterial infection with enteric organisms occurs in 20% of cases. Overgrowth by gas-producing organisms leads to emphysematous cholecystitis. […] Acute Acalculous Cholecystitis accounts for 5% of cases. Risk factors include critical illness, burns, trauma, major surgical procedures, diabetes, immunosuppression.
  • #93 Acalculous cholecystitis – UpToDate
    https://www.uptodate.com/contents/acalculous-cholecystitis
    Once acalculous cholecystitis is established, secondary infection with enteric pathogens, including Escherichia coli, Enterococcus faecalis, Klebsiella spp, Pseudomonas spp, Proteus spp, and Bacteroides fragilis and related strains, is common. […] The majority of patients with acalculous cholecystitis have multiple risk factors. In some cases, specific primary infections with non-enteric organisms predispose to acalculous cholecystitis. As an example, acalculous cholecystitis occurring in patients with acquired immunodeficiency syndrome (AIDS) and other immunosuppressed patients may be due to opportunistic infections such as microsporidia, Cryptosporidium, or cytomegalovirus. More often, however, these infections cause a cholangiopathy without cholecystitis. There is also association of acalculous cholecystitis with COVID-19, though it is unclear whether disease results from primary infection of the biliary system or critical illness.
  • #94 Precision medicine for personalized cholecystitis care: integrating molecular diagnostics and biotherapeutics | Bulletin of the National Research Centre | Full Text
    https://bnrc.springeropen.com/articles/10.1186/s42269-024-01244-9
    Gene therapy techniques using CRISPR/Cas9 systems or RNAi may selectively edit microbial genomes to disable virulence mechanisms. […] Further advances in biotechnology hold enormous potential for improving cholecystitis prevention, diagnosis, and treatment. […] Probiotic administration shows promise as a therapeutic strategy for cholecystitis by promoting growth of beneficial microbes that can outcompete pathogens. […] Probiotic strains like Lactobacillus and Bifidobacterium are selected based on their ability to directly inhibit gastrointestinal pathogens like E. coli and Klebsiella. […] The antimicrobial arsenal produced by probiotics varies widely by strain. […] The integration of advanced biotechnologies holds significant promise for revolutionizing the diagnosis, treatment, and management of cholecystitis.