Dr. Segui Case 1 Draft
Content
Dr. Dr. Segui Segu i Case 1 Patient R.C, 49y/o, Burgos, Pangasinan, Single, RC, 1 st hospital admission at RIMC !to"er #4, #$1% CC& 'pigastri! pain (PI& Di )o masyadong nasundan yung (PI niya. •
9 months P*+ P*+ sa !hart - epigas epigastri tri! ! pain pain a!!o a!!ompa mpanie nied d "y nausea nausea and 0omiti 0omiting ng Pain ain e0e e0ery ry ate aterr mea meal, l, on and and o2 o2 da3 da3 e Sa"i Sa"i naman naman nung nung apat apatid id niya niya yung yung pag0o pag0omit mit niya niya e 3ala 3ala naman naman da3 da3 lumala"as na solids ganun, tinanong )o )ung li5uid, hindi rin da3, e3an )o na )ung ano lumala"as, 6yahaha, "asta eeling nasusu)a da3 yung pasyente. Soug Sought ht !on !onsul sultt sa" sa"ii niya niya sa sa +lam +lamin inos os da3 da377 8* 3as done, done, re0ea re0ealed led (ydrop (ydropi! i! :all"l :all"ladd adder er Pres!r es!rii"ed 3it 3ith med meds mga nasa !hart radiating to th the "a "a!) !rampy in in !ha !hara ra! !ter - "la "la!) tar tarry ry sto stools ;ung med med na asa !hart !hart na na pinres! pinres!ri"e ri"e sa )anya )anya e Bus!opan Bus!opan (yos! (yos!ine6 ine6 ButylBromide-
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May episodes o epigastri! pain pa na nagpa!onsult siya.. pero di )o alam )ung )elan.. 3ala a)o a)o naisulat huhu.. ano )aya isusulat natin.. huhu.. "asta yung sa"i niya na sa Dasul Community (ospital da3. *apos ang d< eh ul!er da3. Den "inigyan siya ng Pantopra=ole unre!alled dose, ta)en on!e a day. Di natin natanong )ung ilang months niyang tina)e. May sina"i pa )asi siya tineta)e na da3 niya yung Pantopra=ole Pantopra=ole pag may nararamdaman n araramdaman siyang sa)it, hindi na lang da3 on!e a day. *apos *apos sa tu3ing sumasa)it da3 da3 hinihilot niya to relie0e relie0e the pain. 'pigastri! pain persisted and 3orsened sa"i sa !hart- (aha 'to yung 4 meds na pina)ita niya sa)in na tineta)e, e3an )o )ung )elan to pinres!ri"e sa)anya. Re"amip e"amipide ide Mu! Mu!ost ostaa- 1$$ 1$$ mg ta" ta" >< a day day ta)en ta)en e0ery e0ery at ater er meal meal mep mepra ra=o =ole le mi mi?n ?n-- #$ #$ mg mg !ap !ap on! on!e e a day day (yos (yos!i !ine ne (yo (yosp span an-- 1$ 1$ mg mg ta" ta" on!e on!e a day day Ceuro Ceuro<im <ime e @yr @yro< o<-- %$$ %$$ mg mg !ap !ap #< #< a day day +M +M and and PM
Past Medi!al (istory& Ay/o polio 6o 0a!!ination 6o pre0ious operations 6o allergies • • • •
amily (istory& Mother hypertension, h< o stro)e ather h< o anemia Patient th among 1$ si"lings (< o DM sa !hart• • • •
Personal and So!ial and 'n0ironmental (istory& (istory& Eo!ational graduate Smo)er& started 1%y/o, > !igarettes a day pero sa !hart !igarettes a day-F dis!ontinued > months agoF !!asional drin)er, di niya ma5uantiyF sa !hart na)alagay G "ottle a day Siya lang da3 na)atira sa "ahay niya e 1 storey house Hater Hater sour!e& deep3ell • •
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RS& 6o pertinent positi0es and negati0es sa"i niya 3ala da3 masa)it eP'& Initial Impression& P8D7 Chroni! Cal!ulous Chole!ystitis7
Gallbladder hydrops Gallbladder hydrops refers to marked dilatation of the gallbladder due due to chronic obstruction of the cystic duct results in accumulation of the sterile non pigmented mucin.
Pathology Chronic obstruction of the cystic duct results in accumulation of the sterile non pigmented mucin in a distended gall bladder which sometimes can reach to the pelvic Causes are including: •
impacted stone
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tumours or polyps
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extrinsic compression by tumour, lymph node, or fibrosis
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Kawasaki syndrome
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parasites: Ascariasi Ascariasis s
Clinical presentation Abdominal pain with with palpable gall bladder without any signs of infection. infection. In an asymptomatic patient, it likely is related to fasting.
Radiographic features •
! cm transverse measurement
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" cm longitudinal measurement
Treatment and prognosis If seen on C# without an explanation, it is followed up with ultrasound if the patient has biliary colic symptoms.
(ydropi! :all"ladder A $%&year&old woman presented presented with a %'&year %'&year history of mild, mild, episodic abdominal abdominal pain in the the right upper (uadrant and a palpable, slowly growing mass in the right side of the abdomen. )he had no history of *aundice, fever, fever, or weight weight loss. #he #he results of laboratory laboratory investigations, investigations, including measurement measurement of liver en+ymes, were unremarkable. indings on abdominal ultrasonography were abnormal, and subse(uent magnetic resonance imaging of the abdomen revealed a markedly distended gallbladder -anel A, axial image, arrow/ anel 0, coronal reconstruction, arrow1, measuring %2 cm by 3 cm, but no evidence of gallstones, extrinsic compression of the biliary tree, or biliary d uct dilatation. A laparoscopic laparoscopic cholecystectomy was performed, and intraoperative aspiration of colorless mucus from the gallbladder led to a diagnosis of hydropic gallbladder. In adults, a hydropic gallbladder is usually a conse(uence of chronic obstruction -resulting from gallstones or tumors1 or narrowing -resulting from a congenital or
fibrotic condition or extrinsic compression1 of the cystic duct. Cholecystectomy is the definitive treatment. #his patient4s symptoms resolved after surgery, and she remained asymptomatic at follow&up % year later.
Discussion:
Hydropic Gallbladder (Mucocele) Right upper quadrant pain has a long list of possible causes to include but not limited to acute and chronic cholecystitis, choledocholithiasis, pancreatitis, peptic ulcer disease, acute hepatitis, liver abscess, liver neoplasm with complication, pneumonia, and heart disease.
Diagnosis: Workup Workup for right upper quadrant general begins b egins with ultrasound to evaluate for gallbladder wall thickening, pericholecystic fluid, gallstones, biliary ductal dilitation and positive Murphy's sign. Remember periportal edema and abdominal ascites can cause gallbladder wall thickening in the absence of gallbladder disease. Hepatobiliary study maybe used to assess for acute or chronic cholecystits however, false positive may also be seen with hydropic gallbladder !mucocele" or gallbladder#liver mass that causes lack of filling of the gallbladder. $he diagnosis of a mucocele should be considered in the following% •
Minimal acute inflammatory signs
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&arge, palpable, minimally tender gallbladder on clinical eamination.
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&aboratory test results are normal or within the upper limit of normal
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(lain radiograph of the abdomen shows a soft)tissue*density, globular globular shadow in the subhepatic region
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+ltrasonography of the R+ shows evidence of minimal wall thickening, an impacted stone in the neck, or infundibulum of an enlarged e nlarged gallbladder and clear content
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-ntraoperatively, -ntraoperatively, the aspirate from the gallbladder is clear and watery or mucoid !white bile"
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Resected gallbladder on opening shows a white wall, clear and watery or mucoid content, a stone or stones impacted in the neck or cystic duct, a narrowed cystic duct, or a tumor and#or polyp causing obstruction of the neck of the gallbladder. M/-0-1.
Pathogenesis: 2econdary to long)standing obstruction to gallbladder's outflow resulting in overdistention of gallblader. 3allbladder 3allbladder contents usually sterile, but if infected forms emypyema of gallbladder. &ongstanding case causes thinning of wall however, recurrent cholecystitis may thicken the wall. (otential causes% impacted stone in gallbladder neck or cystic duct, spontaneously resolved acute cholecystitis, polyps or malignancy of the gallbladder, etrinsic compression of neck or cystic duct by lymph nodes or inflammation#fibrosis or malignancy in ad4acent organs, prolonged $(1 or ceftriaone therapy, congenital congenital narrowing of cystic duct, parasites !ascaris"
Signs and symptoms: Right upper quadrant or epigastric pain#discomfort, nausea and vomiting. -f pain#tenderness 5 6 hours favor acute cholecystitis. 7ever and chills suggest infected bile and possible empyema of gallbladder (alpable mildly tender mass in the right upper quadrant.
Treatment: 2urgery however, may be contraindications in some medical conditions. 1o absolute contraindication eists. 0hemical ablation of the gallbladder mucosa might be an alternative in patients who are medically unfit, elderly, or critically ill. 0ombination of ethanol, sodium tetradecyl sulfate, and mucosal efoliant has been successfully tried in rats.
Hepatobiliary (IDA) Scan or holescintigraphy holescintigraphy Indications •
$o diagnose diagnose suspected acute cholecystitis
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$o investigate possible biliary obstruction
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$o detect biliary leak
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$o differentiate differentiate biliary atresia from neonatal hepatitis
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$o diagnose biliary dyskinesia
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$o confirm the presence of a choledochal cyst
Radionuclide diagnosist imaging study that evaluates hepatocellular function and patency of the biliary system. system. -t follows the production production and flow of bile from liver and through biliary system into the small intestine.
(rocedure% (atient should have fasted for minimum of 8 but preferrably 9 hours. -f patient has fasted for longer than 89 hours or is on $(1 the patient may be pretreated with sincalide !this empties the gallbladder so it can fill with radiopharmaceutical". :ttention should be paid to recent medications such as opoids !best to do procedure 9 hours after last dose". $c);;m $c);;m labeled /-2-/: or <R-/: is then administered -= with doses ranging from >.?)? m0i in adults !higher doses may be required in hyperbilirubinemia @)>A m0i". -nfants and children may be given A.A?)A.8 m0i#kg with minimum of A.9)A.? m0i. &arge field of view, &ow energy all)purpose or high)resolution collimater. collimater. -maging !frontal view" begins at in4ection and serially for 6A minues or until activity noted in gallbladder and small bowel. :dditional :dditional right lateral, left or right anterior oblique views may also be obtained to clarify anatomy. anatomy.
7indings% -n setting of suspected acute cholecystitis, if gallbladder not seen within 6A minutes Morphine augmentation or delayed 9 hour images may be obtained to visualiBe the gallbladder. -f gallbladder activity noted after augmentation or delay then diagnosis of chronic cholecystitis is suggested. -7 no activity noted in gallbladder after delay or augmentation acute cholecystitis suggested but differential also includes other causes of bile obstruction to the gallbladder.
Gallstone Disease Chronic calculous cholecystitis
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3allstone disease is a disease of hepato)biliary system, caused by cholesterol and#or bilirubin metabolic metabolic disorder, and characteriBed by formation of stones in the gallbladder and#or the biliary tract !>". 3allstones are categoriBed as cholesterol, mied, black pigment, or brown pigment stones !8". 0holesterol gallstones are the main type of gallstones and contain cholesterol as the ma4or chemical constituent. Mied cholesterol gallstones are composed of more than ?AC cholesterol !8". 0holesterol and mied gallstones are formed from biliary sludge, which stays for a long time in the gallbladder lumen. <iliary sludge consists of calcium bilirubinate granules, cholesterol monohydrate crystals, and biliary polymeriBed glycoprotein mucin !8)D". $he dynamics of the transformation of biliary sludge into cholesterol stones has been shown as follows% diffused biliary sludge E surface biliary sludge E precipitating biliary sludge E a cholesterol gallstone without acoustic shadow E a cholesterol gallstone with acoustic shadow !;". $he time of formation of cholesterol stones depends on the intensity of the precipitation processes of cholesterol monohydrate crystals in biliary sludge, and equals @ to @6 months !8". $ransformation proportion varies from ? to ?AC depending on the cause !8". <lack pigment stones are composed of either pure calcium bilirubinate or polymer) like complees consisting of calcium, cooper, and large amounts a mounts of mucin glycoproteins. <rown pigment stones are composed of calcium salts of uncon4ugated bilirubin, with varying amounts of cholesterol and protein. $hese stones are usually associated with infection !8". $he natural history of gallstones is typically defined in two separate groups of patients% those with symptomatic gallstones gallstones and those who are asymptomatic. asymptomatic. $he vast ma4orities of gallstones are asymptomatic and remain asymptomatic !8". :s a rule, gallstone disease is asymptomatic, which is called FsilentG stones. $he rate of development of biliary pain is approimately 8C per year for ? years and then decreases over time. $he incidence of complications in patients with asymptomatic stones is low, and prophylactic removal of the gallbladder for this condition is not necessary !8". (atients who had an episode of uncomplicated biliary pain in the year,
@DC per year had recurrent r ecurrent biliary pain !8". :n incidence of recurrent biliary pain as high as ?AC per year in those with symptomatic gallstones. @AC of patients with one episode of biliary pain will not have a recurrent episode !8". $he estimated risk of developing biliary complications is estimated to be >C to 8C per year and is thought to remain relatively constant over time !8". -f biliary pain occurs in the right upper abdomen and the gallbladder wall inflames, gallstone disease transforms into chronic calculous cholecystitis. 0hronic 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 !>, @". $he motoric motoric dysfunction of the gallbladder gallbladder can be caused by increased increased basal common bile duct duct resistance, muscle hypertrophy, hypertrophy, and chronic inflammation inflammation in the gallbladder wall. <iliary colic is the most common presenting symptom of cholelithiasis. :pproimately :pproimately ?C of patients with symptomatic gallstone disease seek medical attention because of episodic abdominal pain !8". $he syndrome of biliary colic is caused caused by intermittent obstruction obstruction of cystic duct by gallstones !8". 0holecystectomy should be offered to patients only after significant biliary symptoms develop.
Diagnostic criteria of the chronic calculous cholecystitis
1. Re!urre Re!urrent nt episodes o "iliary "iliary pain in the the right upper upper a"domen, sometimes in epigastrium, oten 3ith irradiation to the right s!apular region. Biliary pains may "e in the right hypo!hondrium, re5uently or o!!asionally, o di2erent intensity and duration, related to inta)e o atty meals 1-. In addition, a "iliary pain may o!!ur 3ith one or more o the ollo3ing symptoms& a. regular regular or periodi!al periodi!al eeling o "itter "itter taste ". nausea, nausea, somet sometimes imes 0omit 0omiting ing !. regular regular or periodi!al periodi!al a"domina a"dominall "loating "loating and "or"orygmus "or"orygmus
d. unsta"le stool stool 3ith !onstipation !onstipation or diarrhe diarrhea a pre0ailing pre0ailing #. Impair Impaired ed gall"ladd gall"ladder er emptying. emptying. >. +!!ording +!!ording to ultrasound ultrasound e<amination, e<amination, thi!)en thi!)ening ing o the gall"ladder 3all up to >4 mm and presen!e o gallstones in the gall"ladder lumen.
Causes of the gallbladder evacuation dysfunction, dysfunction, biliary pain and chronic inammation in the gallbladder wall
1. Pathology o the smooth smooth mus!le !ells and and epithelial epithelial !ells in the gall"ladder 3all high degree o C@# e<pression in the smooth mus!le !ells and epithelial !ells o the gall"ladder 3all-. #. (yperse!retion (yperse!retion o gly!oprotein gly!oprotein "iliary "iliary mu!in mu!in into gall"ladde gall"ladderr lumen and in!rease o !on!entration o gly!oprotein "iliary mu!in in the gall"ladder "ile o0er the point o polymeri=ation L#.$ mg/ml- high degree o C@# e<pression in the epithelial !ells o the gall"ladder mu!osa-. >. Contra!tile dys!oordin dys!oordination ation o the gall"ladder gall"ladder and !ysti! du!t high degree o C@# e<pression in the smooth mus!le !ells o the gall"ladder and !ysti! du!t-. 4. In!reased In!reased "asal !ysti! du!t resistan!e resistan!e high degree degree o C@ C@# e<pression e<pression in the smooth mus!le !ells o the !ysti! du!t-. %. In!reased In!reased "asal !ommon !ommon "ile du!t du!t resistan!e resistan!e high degree degree o C@# e<pression in the smooth mus!le !ells o the sphin!ter o ddi-.
Mechanism of development of pathologic disorders High degree of 0IJ)8 epression in the smooth muscle cells of the gallbladder wall causes the decrease of the evacuation function of gallbladder and FactiveG passage of hepatic bile into the gallbladder !fig. ! fig. 8". 8".
Surplus C@# e<pression in the epithelial !ells o the gall"ladder mu!osa ma)es or de!rease o the a"sorption un!tion o the gall"ladder de!rease o 3ater and "iliary !holesterol a"sorptionand passi0eN passage o the hepati! "ile into the gall"ladder ?g. #K-. #K -. +lso, gallstones 0olume in the gall"ladder lumen may "e the !ause o de!reased a!ti0eN and passi0eN passage o the hepati! "ile into the gall"ladder rom %$O to %O-. $his is accompanied by decrease in concentration of total bile acids in the gallbladder bile and increase of concentration concentration of biliary cholesterol in phospholipid vesicles, vesicles, and causes disturbance in colloidal stability of gallbladder bile and precipitation of the cholesterol monohydrate crystals from unstable multilamellar aggregated phospholipid vesicles vesicles and calcium bilirubinate bilirubinate granules, i.e. formation formation of FlithogenicG gallbladder bile !fig. !fig. 8D". 8D". :lso, increased 0IJ)8 epression in the epithelial cells of the gallbladder mucosa activates the hypersecretion of glycoprotein mucin into the gallbladder lumen and gallbladder bile. $he increase of the concentration of the glycoprotein biliary mucin in the gallbladder bile over 8.A mg#ml causes its polymeriBation and formation of sites of the ecessive viscosity and it is accompanied by rise of gallbladder bile viscosity. (recipitation of cholesterol monohydrate crystals and calcium bilirubinate granules in the sites of the ecessive viscosity of polymeriBed glycoprotein biliary mucin causes the formation of biliary sludge, the increase in its echogenicity and its revelation during ultrasound eamination. $he decrease in FactiveG and FpassiveG passage p assage of the hepatic bile into the gallbladder causes increase of passage of hepatic bile into duodenum and gallbladder)independent enterohepatic circulation of bile acids, biliary cholesterol and biliary bilirubin ! fig. 8;". 8; ". $he increase in the gallbladder)independent enterohepatic circulation of bile acids causes increase of concentration of bile acids in the hepatocytes and the decrease in the accumulation function and ecretion function of the liver !i.e. for mation of chronic FblandG intrahepatic cholestasis" !fig. ! fig. 8;". 8;".
$he increase of the gallbladder)independent enterohepatic circulation of biliary cholesterol causes increase of absorption of the biliary cholesterol in the small intestine, the biliary cholesterol entering hepatocytes and hypersecretion biliary cholesterol into hepatic bile !fig. ! fig. @A". @A". $hese two factors contribute to the formation of the FlithogenicG hepatic bile !fig. ! fig. @>". @>". $he decrease in the gallbladder)dependent output of biliary cholesterol and in the concentration of total bile acids in the gallbladder bile cause the formation of the FlithogenicG gallbladder bile and the precipitation of cholesterol monohydrate crystals in the gallbladder lumen among patients with chronic calculous cholecystitis ! fig. @8". @8". &ong)term storage of gallstones and chronic aseptic inflammation in the infundibulum mucosa of the gallbladder may cause the acute gallbladder obstruction of infundibulum and transformation of the chronic calculous cholecystitis into acute calculous cholecystitis, which need urgent surgical treatment.
Pathogenetic treatment of patients with chronic calculous cholecystitis :ccordingly, :ccordingly, treatment of chronic calculous cholecystitis !with biliary b iliary pain" aiming for prophylactics of the acute calculous cholecystitis, duodeno)gastral reflu, antral atrophic !bile)acid)dependent" gastritis and chronic biliary pancreatitis includes%
1. Cele!o<i" Cele!o<i" 1$$ mg, # times times a day ater ater meal or % days, ater ater 3hi!h #. 8rsodeo<y!holi! 8rsodeo<y!holi! a!id %$ mg, on!e a day day in the e0ening- or or > month. 0elecoib is a selective inhibitor of 0IJ)8. -nhibiting 0IJ)8 activity in the smooth muscle cells of the gallbladder wall and cystic duct it brings relief of the biliary pain within @)? days, restoration of the evacuation function of the gallbladder and the gallbladder)dependent gallbladder)dependent output of biliary cholesterol, FactiveG and FpassiveG passage of the hepatic bile into the gallbladder, and decrease in the gallbladder)independent gallbladder)independent enterohepatic circulation of bile acids, biliary cholesterol and biliary bilirubin.
0elecoib, a selective inhibitor of 0IJ)8, inhibiting 0IJ)8 activity in the epithelial cells of the gallbladder mucosa causes inhibition of the glycoprotein mucin hypersecretion into the gallbladder lumen, concentration of glycoprotein biliary mucin in gallbladder bile and viscosity of gallbladder bile, which prevents formation of biliary sludge. &ow 0IJ)8 activity in the epithelial cells of the gallbladder mucosa helps restoring the absorption function of the gallbladder !absorption of water and biliary cholesterol from phospholipid vesicles", which results in increase of concentration of total bile acids and decrease of concentration of biliary cholesterol in the gallbladder bile. :lso, :lso, low 0IJ)8 activity in the epithelial and smooth muscle cells of the gallbladder infundibulum helps lowering the risk of development of acute calculous cholecystitis. +rsodeoycholic acid, is a hydrophilic hepatoprotective bile acid. -t helps in dissolving the cholesterol monohydrate crystals in the gallbladder, decrease of lithogenicity of gallbladder and hepatic bile, disappearance of the chronic FblandG intrahepatic cholestasis !i.e. results in the restoration of the accumulation and ecretion functions of liver" and in some patients helps in dissolving cholesterol gallstones. 0elecoib and +rsodeoycholic acid, blocking main pathogenetic mechanisms of gallstones formation, help in slowing down the growth of cholesterol gallstones and lower the risk of acute calculous cholecystitis. -n some patients the chronic calculous cholecystitis can transfer into the gallstone disease !without biliary pain" or the FsilentG gallstones group. 0elecoib is a selective inhibitor of 0IJ)8. -nhibiting 0IJ)8 activity in the smooth muscle cells of the biliary tract and the sphincter of Iddi it brings relief of the biliary pain within @)? days, restoration of the passage of the the hepatic bile into the the duodenum. 0elecoib is a selective inhibitor of 0IJ)8, inhibiting 0IJ)8 activity in the epithelial cells of the biliary tract mucosa causes decrease in secretion of glycoprotein mucin into the biliary tract lumen, concentration of the glycoprotein biliary mucin in the hepatic bile and viscosity of hepatic bile, which prevents formation of biliary sludge and gallstones in the common hepatic duct and common bile duct. &ow 0IJ)8 activity in the epithelial cells and the smooth muscle cells of the biliary tract helps in lowering the risk of choledocholithiasis development.
+rsodeoycholic acid !+/0:" is a hydrophilic hepatoprotective bile acid. -t helps in dissolving the cholesterol monohydrate crystals in the biliary tract, decrease in lithogenicity of hepatic bile, disappearance of the chronic FblandG intrahepatic cholestasis !i.e. results in the restoration of the accumulation and ecretion functions of liver", and in some patients helps in dissolving the biliary sludge in the biliary tract. +rsodeoycholic acid !+/0:" is a hydrophilic hepatoprotective bile acid, decreasing aggressive properties of bile, prevents development of chronic atrophic antral gastritis !duodenogastric reflu and bile reflu gastritis" and duodeno)gastroesophageal reflu !incompetence of Iddi's sphincter", chronic biliary pancreatitis !biliopancreatic reflu" or chronic spastic aseptic pancreatitis !pancreatic type --- of sphincter of Iddi dysfunction". 0elecoib and +rsodeoycholic acid !+/0:", pathogenetically blocking main mechanisms of gallstone formation, help in prophylactics of gallstone formation in the biliary tract, and lower the the risk of development of choledocholithiasis choledocholithiasis and and chronic biliary pancreatitis !>)66". !>)66". !stimated e""ecti#eness is $%&' emission period is *+,- months'
Attention... Attention ... In"ormation "or patients:
<efore using this scheme of treatment please check the contraindications !below" and side effects of using pharmacological preparations of 0elecoib and +rsodeoycholic acid, and obtain your doctorKs permission. ontraindications "or eleco/ib: •
allergi! rea!tions nettlerash, "ron!hial spasm- to a!etylsali!yli! a!id or other 6S+IDs in anamnesis-F
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>rd trimester o pregnan!yF
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high sensiti0ity to sulphonamidesF
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high sensiti0ity to any !omponent o the preparation.
ontraindications "or 0rsodeo/ycholic acid: •
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high sensiti0ity to the preparationF a!ute inammatory diseases o the gall"ladder and the "ile du!tsF
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ul!erati0e !olitisF
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CroneQs disease.
This web page does not bear any legal responsibility for the use of the proposed treatment schemes without consulting your doctor.
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9 months P*+ P*+ sa !hart - epigas epigastri tri! ! pain pain a!!o a!!ompa mpanie nied d "y nausea nausea and 0omiti 0omiting ng Pain ain e0e e0ery ry ate aterr mea meal, l, on and and o2 o2 da3 da3 e Sa"i Sa"i naman naman nung nung apat apatid id niya niya yung yung pag0o pag0omit mit niya niya e 3ala 3ala naman naman da3 da3 lumala"as na solids ganun, tinanong )o )ung li5uid, hindi rin da3, e3an )o na )ung ano lumala"as, 6yahaha, "asta eeling nasusu)a da3 yung pasyente. Soug Sought ht !on !onsul sultt sa" sa"ii niya niya sa sa +lam +lamin inos os da3 da377 8* 3as done, done, re0ea re0ealed led (ydrop (ydropi! i! :all"l :all"ladd adder er Pres!r es!rii"ed 3it 3ith med meds mga nasa !hart radiating to th the "a "a!) !rampy in in !ha !hara ra! !ter - "la "la!) tar tarry ry sto stools ;ung med med na asa !hart !hart na na pinres! pinres!ri"e ri"e sa )anya )anya e Bus!opan Bus!opan (yos! (yos!ine6 ine6 ButylBromide-
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May episodes o epigastri! pain pa na nagpa!onsult siya.. pero di )o alam )ung )elan.. 3ala a)o a)o naisulat huhu.. ano )aya isusulat natin.. huhu.. "asta yung sa"i niya na sa Dasul Community (ospital da3. *apos ang d< eh ul!er da3. Den "inigyan siya ng Pantopra=ole unre!alled dose, ta)en on!e a day. Di natin natanong )ung ilang months niyang tina)e. May sina"i pa )asi siya tineta)e na da3 niya yung Pantopra=ole Pantopra=ole pag may nararamdaman n araramdaman siyang sa)it, hindi na lang da3 on!e a day. *apos *apos sa tu3ing sumasa)it da3 da3 hinihilot niya to relie0e relie0e the pain. 'pigastri! pain persisted and 3orsened sa"i sa !hart- (aha 'to yung 4 meds na pina)ita niya sa)in na tineta)e, e3an )o )ung )elan to pinres!ri"e sa)anya. Re"amip e"amipide ide Mu! Mu!ost ostaa- 1$$ 1$$ mg ta" ta" >< a day day ta)en ta)en e0ery e0ery at ater er meal meal mep mepra ra=o =ole le mi mi?n ?n-- #$ #$ mg mg !ap !ap on! on!e e a day day (yos (yos!i !ine ne (yo (yosp span an-- 1$ 1$ mg mg ta" ta" on!e on!e a day day Ceuro Ceuro<im <ime e @yr @yro< o<-- %$$ %$$ mg mg !ap !ap #< #< a day day +M +M and and PM
Past Medi!al (istory& Ay/o polio 6o 0a!!ination 6o pre0ious operations 6o allergies • • • •
amily (istory& Mother hypertension, h< o stro)e ather h< o anemia Patient th among 1$ si"lings (< o DM sa !hart• • • •
Personal and So!ial and 'n0ironmental (istory& (istory& Eo!ational graduate Smo)er& started 1%y/o, > !igarettes a day pero sa !hart !igarettes a day-F dis!ontinued > months agoF !!asional drin)er, di niya ma5uantiyF sa !hart na)alagay G "ottle a day Siya lang da3 na)atira sa "ahay niya e 1 storey house Hater Hater sour!e& deep3ell • •
• • • •
RS& 6o pertinent positi0es and negati0es sa"i niya 3ala da3 masa)it eP'& Initial Impression& P8D7 Chroni! Cal!ulous Chole!ystitis7
Gallbladder hydrops Gallbladder hydrops refers to marked dilatation of the gallbladder due due to chronic obstruction of the cystic duct results in accumulation of the sterile non pigmented mucin.
Pathology Chronic obstruction of the cystic duct results in accumulation of the sterile non pigmented mucin in a distended gall bladder which sometimes can reach to the pelvic Causes are including: •
impacted stone
•
tumours or polyps
•
extrinsic compression by tumour, lymph node, or fibrosis
•
Kawasaki syndrome
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parasites: Ascariasi Ascariasis s
Clinical presentation Abdominal pain with with palpable gall bladder without any signs of infection. infection. In an asymptomatic patient, it likely is related to fasting.
Radiographic features •
! cm transverse measurement
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" cm longitudinal measurement
Treatment and prognosis If seen on C# without an explanation, it is followed up with ultrasound if the patient has biliary colic symptoms.
(ydropi! :all"ladder A $%&year&old woman presented presented with a %'&year %'&year history of mild, mild, episodic abdominal abdominal pain in the the right upper (uadrant and a palpable, slowly growing mass in the right side of the abdomen. )he had no history of *aundice, fever, fever, or weight weight loss. #he #he results of laboratory laboratory investigations, investigations, including measurement measurement of liver en+ymes, were unremarkable. indings on abdominal ultrasonography were abnormal, and subse(uent magnetic resonance imaging of the abdomen revealed a markedly distended gallbladder -anel A, axial image, arrow/ anel 0, coronal reconstruction, arrow1, measuring %2 cm by 3 cm, but no evidence of gallstones, extrinsic compression of the biliary tree, or biliary d uct dilatation. A laparoscopic laparoscopic cholecystectomy was performed, and intraoperative aspiration of colorless mucus from the gallbladder led to a diagnosis of hydropic gallbladder. In adults, a hydropic gallbladder is usually a conse(uence of chronic obstruction -resulting from gallstones or tumors1 or narrowing -resulting from a congenital or
fibrotic condition or extrinsic compression1 of the cystic duct. Cholecystectomy is the definitive treatment. #his patient4s symptoms resolved after surgery, and she remained asymptomatic at follow&up % year later.
Discussion:
Hydropic Gallbladder (Mucocele) Right upper quadrant pain has a long list of possible causes to include but not limited to acute and chronic cholecystitis, choledocholithiasis, pancreatitis, peptic ulcer disease, acute hepatitis, liver abscess, liver neoplasm with complication, pneumonia, and heart disease.
Diagnosis: Workup Workup for right upper quadrant general begins b egins with ultrasound to evaluate for gallbladder wall thickening, pericholecystic fluid, gallstones, biliary ductal dilitation and positive Murphy's sign. Remember periportal edema and abdominal ascites can cause gallbladder wall thickening in the absence of gallbladder disease. Hepatobiliary study maybe used to assess for acute or chronic cholecystits however, false positive may also be seen with hydropic gallbladder !mucocele" or gallbladder#liver mass that causes lack of filling of the gallbladder. $he diagnosis of a mucocele should be considered in the following% •
Minimal acute inflammatory signs
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&arge, palpable, minimally tender gallbladder on clinical eamination.
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&aboratory test results are normal or within the upper limit of normal
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(lain radiograph of the abdomen shows a soft)tissue*density, globular globular shadow in the subhepatic region
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+ltrasonography of the R+ shows evidence of minimal wall thickening, an impacted stone in the neck, or infundibulum of an enlarged e nlarged gallbladder and clear content
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-ntraoperatively, -ntraoperatively, the aspirate from the gallbladder is clear and watery or mucoid !white bile"
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Resected gallbladder on opening shows a white wall, clear and watery or mucoid content, a stone or stones impacted in the neck or cystic duct, a narrowed cystic duct, or a tumor and#or polyp causing obstruction of the neck of the gallbladder. M/-0-1.
Pathogenesis: 2econdary to long)standing obstruction to gallbladder's outflow resulting in overdistention of gallblader. 3allbladder 3allbladder contents usually sterile, but if infected forms emypyema of gallbladder. &ongstanding case causes thinning of wall however, recurrent cholecystitis may thicken the wall. (otential causes% impacted stone in gallbladder neck or cystic duct, spontaneously resolved acute cholecystitis, polyps or malignancy of the gallbladder, etrinsic compression of neck or cystic duct by lymph nodes or inflammation#fibrosis or malignancy in ad4acent organs, prolonged $(1 or ceftriaone therapy, congenital congenital narrowing of cystic duct, parasites !ascaris"
Signs and symptoms: Right upper quadrant or epigastric pain#discomfort, nausea and vomiting. -f pain#tenderness 5 6 hours favor acute cholecystitis. 7ever and chills suggest infected bile and possible empyema of gallbladder (alpable mildly tender mass in the right upper quadrant.
Treatment: 2urgery however, may be contraindications in some medical conditions. 1o absolute contraindication eists. 0hemical ablation of the gallbladder mucosa might be an alternative in patients who are medically unfit, elderly, or critically ill. 0ombination of ethanol, sodium tetradecyl sulfate, and mucosal efoliant has been successfully tried in rats.
Hepatobiliary (IDA) Scan or holescintigraphy holescintigraphy Indications •
$o diagnose diagnose suspected acute cholecystitis
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$o investigate possible biliary obstruction
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$o detect biliary leak
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$o differentiate differentiate biliary atresia from neonatal hepatitis
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$o diagnose biliary dyskinesia
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$o confirm the presence of a choledochal cyst
Radionuclide diagnosist imaging study that evaluates hepatocellular function and patency of the biliary system. system. -t follows the production production and flow of bile from liver and through biliary system into the small intestine.
(rocedure% (atient should have fasted for minimum of 8 but preferrably 9 hours. -f patient has fasted for longer than 89 hours or is on $(1 the patient may be pretreated with sincalide !this empties the gallbladder so it can fill with radiopharmaceutical". :ttention should be paid to recent medications such as opoids !best to do procedure 9 hours after last dose". $c);;m $c);;m labeled /-2-/: or <R-/: is then administered -= with doses ranging from >.?)? m0i in adults !higher doses may be required in hyperbilirubinemia @)>A m0i". -nfants and children may be given A.A?)A.8 m0i#kg with minimum of A.9)A.? m0i. &arge field of view, &ow energy all)purpose or high)resolution collimater. collimater. -maging !frontal view" begins at in4ection and serially for 6A minues or until activity noted in gallbladder and small bowel. :dditional :dditional right lateral, left or right anterior oblique views may also be obtained to clarify anatomy. anatomy.
7indings% -n setting of suspected acute cholecystitis, if gallbladder not seen within 6A minutes Morphine augmentation or delayed 9 hour images may be obtained to visualiBe the gallbladder. -f gallbladder activity noted after augmentation or delay then diagnosis of chronic cholecystitis is suggested. -7 no activity noted in gallbladder after delay or augmentation acute cholecystitis suggested but differential also includes other causes of bile obstruction to the gallbladder.
Gallstone Disease Chronic calculous cholecystitis
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3allstone disease is a disease of hepato)biliary system, caused by cholesterol and#or bilirubin metabolic metabolic disorder, and characteriBed by formation of stones in the gallbladder and#or the biliary tract !>". 3allstones are categoriBed as cholesterol, mied, black pigment, or brown pigment stones !8". 0holesterol gallstones are the main type of gallstones and contain cholesterol as the ma4or chemical constituent. Mied cholesterol gallstones are composed of more than ?AC cholesterol !8". 0holesterol and mied gallstones are formed from biliary sludge, which stays for a long time in the gallbladder lumen. <iliary sludge consists of calcium bilirubinate granules, cholesterol monohydrate crystals, and biliary polymeriBed glycoprotein mucin !8)D". $he dynamics of the transformation of biliary sludge into cholesterol stones has been shown as follows% diffused biliary sludge E surface biliary sludge E precipitating biliary sludge E a cholesterol gallstone without acoustic shadow E a cholesterol gallstone with acoustic shadow !;". $he time of formation of cholesterol stones depends on the intensity of the precipitation processes of cholesterol monohydrate crystals in biliary sludge, and equals @ to @6 months !8". $ransformation proportion varies from ? to ?AC depending on the cause !8". <lack pigment stones are composed of either pure calcium bilirubinate or polymer) like complees consisting of calcium, cooper, and large amounts a mounts of mucin glycoproteins. <rown pigment stones are composed of calcium salts of uncon4ugated bilirubin, with varying amounts of cholesterol and protein. $hese stones are usually associated with infection !8". $he natural history of gallstones is typically defined in two separate groups of patients% those with symptomatic gallstones gallstones and those who are asymptomatic. asymptomatic. $he vast ma4orities of gallstones are asymptomatic and remain asymptomatic !8". :s a rule, gallstone disease is asymptomatic, which is called FsilentG stones. $he rate of development of biliary pain is approimately 8C per year for ? years and then decreases over time. $he incidence of complications in patients with asymptomatic stones is low, and prophylactic removal of the gallbladder for this condition is not necessary !8". (atients who had an episode of uncomplicated biliary pain in the year,
@DC per year had recurrent r ecurrent biliary pain !8". :n incidence of recurrent biliary pain as high as ?AC per year in those with symptomatic gallstones. @AC of patients with one episode of biliary pain will not have a recurrent episode !8". $he estimated risk of developing biliary complications is estimated to be >C to 8C per year and is thought to remain relatively constant over time !8". -f biliary pain occurs in the right upper abdomen and the gallbladder wall inflames, gallstone disease transforms into chronic calculous cholecystitis. 0hronic 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 !>, @". $he motoric motoric dysfunction of the gallbladder gallbladder can be caused by increased increased basal common bile duct duct resistance, muscle hypertrophy, hypertrophy, and chronic inflammation inflammation in the gallbladder wall. <iliary colic is the most common presenting symptom of cholelithiasis. :pproimately :pproimately ?C of patients with symptomatic gallstone disease seek medical attention because of episodic abdominal pain !8". $he syndrome of biliary colic is caused caused by intermittent obstruction obstruction of cystic duct by gallstones !8". 0holecystectomy should be offered to patients only after significant biliary symptoms develop.
Diagnostic criteria of the chronic calculous cholecystitis
1. Re!urre Re!urrent nt episodes o "iliary "iliary pain in the the right upper upper a"domen, sometimes in epigastrium, oten 3ith irradiation to the right s!apular region. Biliary pains may "e in the right hypo!hondrium, re5uently or o!!asionally, o di2erent intensity and duration, related to inta)e o atty meals 1-. In addition, a "iliary pain may o!!ur 3ith one or more o the ollo3ing symptoms& a. regular regular or periodi!al periodi!al eeling o "itter "itter taste ". nausea, nausea, somet sometimes imes 0omit 0omiting ing !. regular regular or periodi!al periodi!al a"domina a"dominall "loating "loating and "or"orygmus "or"orygmus
d. unsta"le stool stool 3ith !onstipation !onstipation or diarrhe diarrhea a pre0ailing pre0ailing #. Impair Impaired ed gall"ladd gall"ladder er emptying. emptying. >. +!!ording +!!ording to ultrasound ultrasound e<amination, e<amination, thi!)en thi!)ening ing o the gall"ladder 3all up to >4 mm and presen!e o gallstones in the gall"ladder lumen.
Causes of the gallbladder evacuation dysfunction, dysfunction, biliary pain and chronic inammation in the gallbladder wall
1. Pathology o the smooth smooth mus!le !ells and and epithelial epithelial !ells in the gall"ladder 3all high degree o C@# e<pression in the smooth mus!le !ells and epithelial !ells o the gall"ladder 3all-. #. (yperse!retion (yperse!retion o gly!oprotein gly!oprotein "iliary "iliary mu!in mu!in into gall"ladde gall"ladderr lumen and in!rease o !on!entration o gly!oprotein "iliary mu!in in the gall"ladder "ile o0er the point o polymeri=ation L#.$ mg/ml- high degree o C@# e<pression in the epithelial !ells o the gall"ladder mu!osa-. >. Contra!tile dys!oordin dys!oordination ation o the gall"ladder gall"ladder and !ysti! du!t high degree o C@# e<pression in the smooth mus!le !ells o the gall"ladder and !ysti! du!t-. 4. In!reased In!reased "asal !ysti! du!t resistan!e resistan!e high degree degree o C@ C@# e<pression e<pression in the smooth mus!le !ells o the !ysti! du!t-. %. In!reased In!reased "asal !ommon !ommon "ile du!t du!t resistan!e resistan!e high degree degree o C@# e<pression in the smooth mus!le !ells o the sphin!ter o ddi-.
Mechanism of development of pathologic disorders High degree of 0IJ)8 epression in the smooth muscle cells of the gallbladder wall causes the decrease of the evacuation function of gallbladder and FactiveG passage of hepatic bile into the gallbladder !fig. ! fig. 8". 8".
Surplus C@# e<pression in the epithelial !ells o the gall"ladder mu!osa ma)es or de!rease o the a"sorption un!tion o the gall"ladder de!rease o 3ater and "iliary !holesterol a"sorptionand passi0eN passage o the hepati! "ile into the gall"ladder ?g. #K-. #K -. +lso, gallstones 0olume in the gall"ladder lumen may "e the !ause o de!reased a!ti0eN and passi0eN passage o the hepati! "ile into the gall"ladder rom %$O to %O-. $his is accompanied by decrease in concentration of total bile acids in the gallbladder bile and increase of concentration concentration of biliary cholesterol in phospholipid vesicles, vesicles, and causes disturbance in colloidal stability of gallbladder bile and precipitation of the cholesterol monohydrate crystals from unstable multilamellar aggregated phospholipid vesicles vesicles and calcium bilirubinate bilirubinate granules, i.e. formation formation of FlithogenicG gallbladder bile !fig. !fig. 8D". 8D". :lso, increased 0IJ)8 epression in the epithelial cells of the gallbladder mucosa activates the hypersecretion of glycoprotein mucin into the gallbladder lumen and gallbladder bile. $he increase of the concentration of the glycoprotein biliary mucin in the gallbladder bile over 8.A mg#ml causes its polymeriBation and formation of sites of the ecessive viscosity and it is accompanied by rise of gallbladder bile viscosity. (recipitation of cholesterol monohydrate crystals and calcium bilirubinate granules in the sites of the ecessive viscosity of polymeriBed glycoprotein biliary mucin causes the formation of biliary sludge, the increase in its echogenicity and its revelation during ultrasound eamination. $he decrease in FactiveG and FpassiveG passage p assage of the hepatic bile into the gallbladder causes increase of passage of hepatic bile into duodenum and gallbladder)independent enterohepatic circulation of bile acids, biliary cholesterol and biliary bilirubin ! fig. 8;". 8; ". $he increase in the gallbladder)independent enterohepatic circulation of bile acids causes increase of concentration of bile acids in the hepatocytes and the decrease in the accumulation function and ecretion function of the liver !i.e. for mation of chronic FblandG intrahepatic cholestasis" !fig. ! fig. 8;". 8;".
$he increase of the gallbladder)independent enterohepatic circulation of biliary cholesterol causes increase of absorption of the biliary cholesterol in the small intestine, the biliary cholesterol entering hepatocytes and hypersecretion biliary cholesterol into hepatic bile !fig. ! fig. @A". @A". $hese two factors contribute to the formation of the FlithogenicG hepatic bile !fig. ! fig. @>". @>". $he decrease in the gallbladder)dependent output of biliary cholesterol and in the concentration of total bile acids in the gallbladder bile cause the formation of the FlithogenicG gallbladder bile and the precipitation of cholesterol monohydrate crystals in the gallbladder lumen among patients with chronic calculous cholecystitis ! fig. @8". @8". &ong)term storage of gallstones and chronic aseptic inflammation in the infundibulum mucosa of the gallbladder may cause the acute gallbladder obstruction of infundibulum and transformation of the chronic calculous cholecystitis into acute calculous cholecystitis, which need urgent surgical treatment.
Pathogenetic treatment of patients with chronic calculous cholecystitis :ccordingly, :ccordingly, treatment of chronic calculous cholecystitis !with biliary b iliary pain" aiming for prophylactics of the acute calculous cholecystitis, duodeno)gastral reflu, antral atrophic !bile)acid)dependent" gastritis and chronic biliary pancreatitis includes%
1. Cele!o<i" Cele!o<i" 1$$ mg, # times times a day ater ater meal or % days, ater ater 3hi!h #. 8rsodeo<y!holi! 8rsodeo<y!holi! a!id %$ mg, on!e a day day in the e0ening- or or > month. 0elecoib is a selective inhibitor of 0IJ)8. -nhibiting 0IJ)8 activity in the smooth muscle cells of the gallbladder wall and cystic duct it brings relief of the biliary pain within @)? days, restoration of the evacuation function of the gallbladder and the gallbladder)dependent gallbladder)dependent output of biliary cholesterol, FactiveG and FpassiveG passage of the hepatic bile into the gallbladder, and decrease in the gallbladder)independent gallbladder)independent enterohepatic circulation of bile acids, biliary cholesterol and biliary bilirubin.
0elecoib, a selective inhibitor of 0IJ)8, inhibiting 0IJ)8 activity in the epithelial cells of the gallbladder mucosa causes inhibition of the glycoprotein mucin hypersecretion into the gallbladder lumen, concentration of glycoprotein biliary mucin in gallbladder bile and viscosity of gallbladder bile, which prevents formation of biliary sludge. &ow 0IJ)8 activity in the epithelial cells of the gallbladder mucosa helps restoring the absorption function of the gallbladder !absorption of water and biliary cholesterol from phospholipid vesicles", which results in increase of concentration of total bile acids and decrease of concentration of biliary cholesterol in the gallbladder bile. :lso, :lso, low 0IJ)8 activity in the epithelial and smooth muscle cells of the gallbladder infundibulum helps lowering the risk of development of acute calculous cholecystitis. +rsodeoycholic acid, is a hydrophilic hepatoprotective bile acid. -t helps in dissolving the cholesterol monohydrate crystals in the gallbladder, decrease of lithogenicity of gallbladder and hepatic bile, disappearance of the chronic FblandG intrahepatic cholestasis !i.e. results in the restoration of the accumulation and ecretion functions of liver" and in some patients helps in dissolving cholesterol gallstones. 0elecoib and +rsodeoycholic acid, blocking main pathogenetic mechanisms of gallstones formation, help in slowing down the growth of cholesterol gallstones and lower the risk of acute calculous cholecystitis. -n some patients the chronic calculous cholecystitis can transfer into the gallstone disease !without biliary pain" or the FsilentG gallstones group. 0elecoib is a selective inhibitor of 0IJ)8. -nhibiting 0IJ)8 activity in the smooth muscle cells of the biliary tract and the sphincter of Iddi it brings relief of the biliary pain within @)? days, restoration of the passage of the the hepatic bile into the the duodenum. 0elecoib is a selective inhibitor of 0IJ)8, inhibiting 0IJ)8 activity in the epithelial cells of the biliary tract mucosa causes decrease in secretion of glycoprotein mucin into the biliary tract lumen, concentration of the glycoprotein biliary mucin in the hepatic bile and viscosity of hepatic bile, which prevents formation of biliary sludge and gallstones in the common hepatic duct and common bile duct. &ow 0IJ)8 activity in the epithelial cells and the smooth muscle cells of the biliary tract helps in lowering the risk of choledocholithiasis development.
+rsodeoycholic acid !+/0:" is a hydrophilic hepatoprotective bile acid. -t helps in dissolving the cholesterol monohydrate crystals in the biliary tract, decrease in lithogenicity of hepatic bile, disappearance of the chronic FblandG intrahepatic cholestasis !i.e. results in the restoration of the accumulation and ecretion functions of liver", and in some patients helps in dissolving the biliary sludge in the biliary tract. +rsodeoycholic acid !+/0:" is a hydrophilic hepatoprotective bile acid, decreasing aggressive properties of bile, prevents development of chronic atrophic antral gastritis !duodenogastric reflu and bile reflu gastritis" and duodeno)gastroesophageal reflu !incompetence of Iddi's sphincter", chronic biliary pancreatitis !biliopancreatic reflu" or chronic spastic aseptic pancreatitis !pancreatic type --- of sphincter of Iddi dysfunction". 0elecoib and +rsodeoycholic acid !+/0:", pathogenetically blocking main mechanisms of gallstone formation, help in prophylactics of gallstone formation in the biliary tract, and lower the the risk of development of choledocholithiasis choledocholithiasis and and chronic biliary pancreatitis !>)66". !>)66". !stimated e""ecti#eness is $%&' emission period is *+,- months'
Attention... Attention ... In"ormation "or patients:
<efore using this scheme of treatment please check the contraindications !below" and side effects of using pharmacological preparations of 0elecoib and +rsodeoycholic acid, and obtain your doctorKs permission. ontraindications "or eleco/ib: •
allergi! rea!tions nettlerash, "ron!hial spasm- to a!etylsali!yli! a!id or other 6S+IDs in anamnesis-F
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>rd trimester o pregnan!yF
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high sensiti0ity to sulphonamidesF
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high sensiti0ity to any !omponent o the preparation.
ontraindications "or 0rsodeo/ycholic acid: •
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high sensiti0ity to the preparationF a!ute inammatory diseases o the gall"ladder and the "ile du!tsF
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ul!erati0e !olitisF
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CroneQs disease.
This web page does not bear any legal responsibility for the use of the proposed treatment schemes without consulting your doctor.
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