Dr. Segui Case 1 Draft

8/17/2019 Dr. Segui Case 1 Draft

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Dr. SeguiCase 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*+ sa !hart-- epigastri! pain a!!ompanied "y nausea and 0omiting

Pain e0ery a ter meal, on and o2 da3 eSa"i naman nung apatid niya yung pag0omit niya e 3ala naman da3lumala"as na solids ganun, tinanong )o )ung li5uid, hindi rin da3, e3an )ona )ung ano lumala"as, 6yahaha, "asta eeling nasusu)a da3 yungpasyente.Sought !onsult sa"i niya sa +laminos da37-8* 3as done, re0ealed (ydropi! :all"ladderPres!ri"ed 3ith meds

mga nasa !hartradiating to the "a!)!rampy in !hara!ter

- "la!) tarry stools;ung med na asa !hart na pinres!ri"e sa )anya e Bus!opan (yos!ine 6Butyl Bromide-

• May episodes o epigastri! pain pa na nagpa!onsult siya.. pero di )o alam)ung )elan.. 3ala a)o naisulat huhu.. ano )aya isusulat natin.. huhu.. "astayung sa"i niya na sa Dasul Community (ospital da3. *apos ang d< eh ul!erda3. Den "inigyan siya ng Pantopra=ole unre!alled dose, ta)en on!e a day. Dinatin natanong )ung ilang months niyang tina)e. May sina"i pa )asi siyatineta)e na da3 niya yung Pantopra=ole pag may nararamdaman siyangsa)it, hindi na lang da3 on!e a day.

• *apos sa tu3ing sumasa)it da3 hinihilot niya to 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"amipide Mu!osta- 1$$ mg ta" >< a day ta)en e0ery a ter meal

mepra=ole mi?n- #$ mg !ap on!e a day(yos!ine (yospan- 1$ mg ta" on!e a dayCe uro


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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&• 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 ma5uanti yF sa !hart na)alagay G "ottle a day• Siya lang da3 na)atira sa "ahay niya e• 1 storey house• Hater sour!e& deep 3ell

R S&6o pertinent positi0es and negati0es

sa"i niya 3ala da3 masa)it e-

P'&

Initial Impression&P8D7Chroni! Cal!ulous Chole!ystitis7


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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 limitedto acute and chronic cholecystitis, choledocholithiasis, pancreatitis, peptic ulcerdisease, acute hepatitis, liver abscess, liver neoplasm with complication, pneumonia,and heart disease.

Diagnosis:

Workup for right upper quadrant general begins with ultrasound to evaluate forgallbladder wall thickening, pericholecystic fluid, gallstones, biliary ductal dilitationand positive Murphy's sign. Remember periportal edema and abdominal ascites cancause 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" orgallbladder#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

• &arge, palpable, minimally tender gallbladder on clinical e amination.

• &aboratory test results are normal or within the upper limit of normal

• (lain radiograph of the abdomen shows a soft)tissue*density, globular shadowin the subhepatic region

•

+ltrasonography of the R+ shows evidence of minimal wall thickening, animpacted stone in the neck, or infundibulum of an enlarged gallbladder andclear content

• -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 ormucoid content, a stone or stones impacted in the neck or cystic duct, anarrowed cystic duct, or a tumor and#or polyp causing obstruction of the neckof the gallbladder. M /-0-1 .

Pathogenesis:

2econdary to long)standing obstruction to gallbladder's outflow resulting inoverdistention of gallblader. 3allbladder contents usually sterile, but if infected formsemypyema 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, spontaneouslyresolved acute cholecystitis, polyps or malignancy of the gallbladder, e trinsic

compression of neck or cystic duct by lymph nodes or inflammation#fibrosis ormalignancy in ad4acent organs, prolonged $(1 or ceftria one therapy, congenitalnarrowing 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 absolutecontraindication e ists.

0hemical ablation of the gallbladder mucosa might be an alternative in patients whoare medically unfit, elderly, or critically ill. 0ombination of ethanol, sodium tetradecylsulfate, and mucosal e foliant has been successfully tried in rats.


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Hepatobiliary (IDA) Scan orholescintigraphy Indications

• $o diagnose suspected acute cholecystitis

• $o investigate possible biliary obstruction

• $o detect biliary leak

• $o differentiate biliary atresia from neonatal hepatitis

• $o diagnose biliary dyskinesia

• $o confirm the presence of a choledochal cyst

Radionuclide diagnosist imaging study that evaluates hepatocellular function and patency of the biliary system. -t follows the production and flow of bile from liver andthrough biliary system into the small intestine.

(rocedure%

(atient should have fasted for minimum of 8 but preferrably 9 hours. -f patient hasfasted for longer than 89 hours or is on $(1 the patient may be pretreated withsincalide !this empties the gallbladder so it can fill with radiopharmaceutical".

:ttention should be paid to recent medications such as opoids !best to do procedure 9hours after last dose".

$c);;m labeled /-2-/: or .?)? 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.

-maging !frontal view" begins at in4ection and serially for 6A minues or until activitynoted in gallbladder and small bowel. :dditional right lateral, left or right anterioroblique views may also be obtained to clarify anatomy.


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7indings%

-n setting of suspected acute cholecystitis, if gallbladder not seen within 6A minutesMorphine 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 oraugmentation acute cholecystitis suggested but differential also includes other causesof bile obstruction to the gallbladder.


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G a l l s t o n e D i s e a s eC h r o n i c c a l c u l o u s c h o l e c y s t i t i s

See more at&http&//333.drturumin.!om/en/CaChole!ystitis en.htmlJsthash.Kr8ee%H+.dpu

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3allstone disease is a disease of hepato)biliary system, caused by cholesterol and#or bilirubin metabolic disorder, and characteriBed by formation of stones in thegallbladder and#or the biliary tract !>".

3allstones are categoriBed as cholesterol, mi ed, black pigment, or brown pigmentstones !8". 0holesterol gallstones are the main type of gallstones and containcholesterol as the ma4or chemical constituent. Mi ed cholesterol gallstones arecomposed of more than ?AC cholesterol !8". 0holesterol and mi ed gallstones areformed from biliary sludge, which stays for a long time in the gallbladder lumen.


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@DC per year had recurrent biliary pain !8". :n incidence of recurrent biliary pain ashigh as ?AC per year in those with symptomatic gallstones. @AC of patients with oneepisode of biliary pain will not have a recurrent episode !8". $he estimated risk ofdeveloping 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 thegallbladder 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 dysfunction of the gallbladder can be caused by increased

basal common bile duct resistance, muscle hypertrophy, and chronic inflammation inthe gallbladder wall.


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d. unsta"le stool 3ith !onstipation or diarrhea pre0ailing

#. Impaired gall"ladder emptying.

>. +!!ording to ultrasound e. Contra!tile dys!oordination o the gall"ladder and !ysti! du!thigh degree o C @ # e


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Surplus C @ # e


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$he increase of the gallbladder)independent enterohepatic circulation of biliarycholesterol causes increase of absorption of the biliary cholesterol in the smallintestine, the biliary cholesterol entering hepatocytes and hypersecretion biliarycholesterol into hepatic bile ! fig. @A".

$hese two factors contribute to the formation of the FlithogenicG hepatic bile ! fig. @>".

$he decrease in the gallbladder)dependent output of biliary cholesterol and in theconcentration of total bile acids in the gallbladder bile cause the formation of theFlithogenicG gallbladder bile and the precipitation of cholesterol monohydrate crystalsin the gallbladder lumen among patients with chronic calculous cholecystitis ! fig. @8".

&ong)term storage of gallstones and chronic aseptic inflammation in the infundibulum

mucosa of the gallbladder may cause the acute gallbladder obstruction ofinfundibulum and transformation of the chronic calculous cholecystitis into acutecalculous cholecystitis, which need urgent surgical treatment.

Pathogenetic treatment of patients with chronic calculouscholecystitis:ccordingly, treatment of chronic calculous cholecystitis !with biliary pain" aiming

for prophylactics of the acute calculous cholecystitis, duodeno)gastral reflu , antralatrophic !bile)acid)dependent" gastritis and chronic biliary pancreatitis includes%

1. Cele!o


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0eleco ib, a selective inhibitor of 0IJ)8, inhibiting 0IJ)8 activity in the epithelialcells of the gallbladder mucosa causes inhibition of the glycoprotein mucinhypersecretion into the gallbladder lumen, concentration of glycoprotein biliary mucinin 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 restoringthe absorption function of the gallbladder !absorption of water and biliary cholesterolfrom phospholipid vesicles", which results in increase of concentration of total bileacids and decrease of concentration of biliary cholesterol in the gallbladder bile. :lso,low 0IJ)8 activity in the epithelial and smooth muscle cells of the gallbladderinfundibulum helps lowering the risk of development of acute calculous cholecystitis.

+rsodeo ycholic acid, is a hydrophilic hepatoprotective bile acid. -t helps indissolving the cholesterol monohydrate crystals in the gallbladder, decrease oflithogenicity of gallbladder and hepatic bile, disappearance of the chronic FblandGintrahepatic cholestasis !i.e. results in the restoration of the accumulation ande cretion functions of liver" and in some patients helps in dissolving cholesterolgallstones.

0eleco ib and +rsodeo ycholic acid, blocking main pathogenetic mechanisms ofgallstones formation, help in slowing down the growth of cholesterol gallstones and

lower the risk of acute calculous cholecystitis. -n some patients the chronic calculouscholecystitis can transfer into the gallstone disease !without biliary pain" or theFsilentG gallstones group.

0eleco ib is a selective inhibitor of 0IJ)8. -nhibiting 0IJ)8 activity in the smoothmuscle 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 hepatic bile into the duodenum.

0eleco ib 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 glycoproteinmucin into the biliary tract lumen, concentration of the glycoprotein biliary mucin inthe hepatic bile and viscosity of hepatic bile, which prevents formation of biliarysludge and gallstones in the common hepatic duct and common bile duct. &ow 0IJ)8activity in the epithelial cells and the smooth muscle cells of the biliary tract helps inlowering the risk of choledocholithiasis development.


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+rsodeo ycholic acid !+/0:" is a hydrophilic hepatoprotective bile acid. -t helps indissolving the cholesterol monohydrate crystals in the biliary tract, decrease inlithogenicity of hepatic bile, disappearance of the chronic FblandG intrahepaticcholestasis !i.e. results in the restoration of the accumulation and e cretion functions

of liver", and in some patients helps in dissolving the biliary sludge in the biliary tract.

+rsodeo ycholic acid !+/0:" is a hydrophilic hepatoprotective bile acid, decreasingaggressive 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 !biliopancreaticreflu " or chronic spastic aseptic pancreatitis !pancreatic type --- of sphincter of Iddidysfunction".

0eleco ib and +rsodeo ycholic acid !+/0:", pathogenetically blocking mainmechanisms of gallstone formation, help in prophylactics of gallstone formation in the

biliary tract, and lower the risk of development of choledocholithiasis and chronic biliary pancreatitis !>)66".

!stimated e""ecti#eness is $%&'emission period is *+,- months'

Attention... In"ormation "or patients:


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ontraindications "or 0rsodeo/ycholic acid:

• high sensiti0ity to the preparationF

• a!ute in ammatory diseases o the gall"ladder and the "iledu!tsF

• ul!erati0e !olitisF

• CroneQs disease.

This web page does not bear any legal responsibility for the use of the proposedtreatment schemes without consulting your doctor.

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Dr. Segui Case 1 Draft