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Presented by:

Amer AlQaisi
Faisal AlEnezi

:Supervised by
Prof. Kamal Gharaibeh


of gallbladder
2.Anatomy of biliary tree
3.Physiology of biliary system
4.Bilirubin metabolism cycle.
5.Congenital abnormalities
7.Complications of gallstones
8.Clinical presentation & Management
9.Choledocolithiasis & cholangitis

Anatomy of Gallbladder
• Gallbladder is a pear-shaped sac lying
on the undersurface of the live which is
7.5-12 cm long and it has a capacity
of 30-50 ml.
• It is divided to :
- Fundus
- Body
- Neck
 The Hartmann's pouch : is a dilatation
in the gallbladder just before the
origin of cystic duct .

.the inferior surface of the liver  Posteriorly : the transverse colon(proximal) .1st and 2nd part of duodenum  The fundus is usually projects inferiorly (at the level of the 9 th costal cartilage in the midclavicular line) and the neck directed upward backward. Relation:  Anteriorly : the anterior abdominal wall and .

.cystic vein which drain directly into the portal vein. a branch from the right hepatic artery .  The lymph drainage: . and the right phrenic nerve conveys sensory information. the vagus nerve supplies parasympathetic innervation.into the cystic lymph node of Lund which situated near the neck of the gallbladder. The celiac plexus supplies sympathetic innervation. .by the cystic artery .  Nerve supply: supplied by 3 types of innervation. Blood supply: .

ANATOMY OF BILIARY TREE  The ducts of biliary tree are :  The common hepatic duct : it is about 4 cm (result from the union of.duct  The common bile duct : it is about 8 -10 cm that is result from theunion of the common hepatic duct with .Rt.& Lt hepatic duct)  Cystic duct : it is about 3. somewhat S shapedwhich connect the neck of the gallbladder with the common hepatic .the cystic duct .8 cm.

they open into a small ampulla in the duodenal wall ( ampulla of vater ). and together.• The common bile duct descends behind the duodenum and pancreas and usually joined by pancreatic duct. called Duct of Luschka . There are a small ducts that drain bile directly into the . gallbladder from the liver.

the common hepatic duct. and the cystic artery • .• Cystohepatic triangle an anatomic space bordered by the common hepatic duct medially. the cystic duct laterally and the inferior edge of the liver superiorly. Calot's Triangle : cystic duct.

the resistance to flow through the sphincter of Oddi is reduced. . resistance to flow through the sphincter is high. and bile excreted by the liver is diverted to the gall bladder. These motor responses of the biliary tract are in part effected by the hormone CCK. During fasting. and the bile enters the duodenum.PHYSIOLOGY  Gallbladder is under control of Cholecystokinin (CCK ) and its functions are :  Contraction of the gallbladder  Relaxation of the Sphincter of Oddi  Slowing gastric emptying  increase pancreatic enzyme secretion The gall bladder is a reservoir for bile. After feeding. the gall bladder contracts.

PHYSIOLOGY The second main function of the gall bladder is concentration of bile by active absorption of water. . cholesterol and calcium. a mucocele develops on account of this function of the mucosa of the gall bladder. The third function of the gall bladder is the secretion of mucus – approximately 20 ml is produced per day. with a corresponding increase in the proportion of bile salts. bile pigments. With total obstruction of the cystic duct in a healthy gall bladder. sodium chloride and bicarbonate by the mucous membrane of the gall bladder. The hepatic bile that enters the gall bladder becomes concentrated 5–10 times.

Bile Components of bile: Water 95% electrolytes bile salts (like cholic acid & chenodeoxycholic acid ) phospholipids ( like licithin) bilirubin (conjugated) fatty acids  The function of bile is to emulsify fat. .

 Absence of bile causing malabsorption of fat and fat soluble vitamins ( A . . resection of terminal ileum will decrease bile salts that will cause GB stones formation. K )  95% of bile salts are reabsorbed in the terminal ileum . D . So. E . pass back via the portal venous drainage to the liver and once again secreted in the bile (EHC).

cytochromes (to 25% 20) Hemoglobin (to 80% 70) Heme Heme oxygenase Biliverdin Biliverdin reductase Bilirubin albumin indirect unconjugated pre-hepatic .BILIRUBIN PRODUCTION Heme proteins myoglobin.

BILIRUBIN PROCESSING albumin-Bilirubin albumin ligandin hepatocyte ligandin-Bilirubin UDP-Glucuronyl transferase ER Bilirubin diglucuronide bile (gall bladder) direct conjugated post-hepatic .

BILIRUBIN EXCRETION Bilirubin diglucuronide glucuronate 2 liver 90% Bacterial enzyme Bilirubin Bacterial enzyme intestines Urobilinogen <-------kidneys 10% 20% Bacterial enzymes 80% Stercobilinogen Stercobilin Urobilin urine feces .

the gall bladder is absent.CONGENITAL ABNORMALITIES Absence of the gall bladder Occasionally. which makes it liable to undergo torsion of GB to occur with consequent gangrene & rupture . The Phrygian cap present of septum that incompletely divides the GB. Failure to visualise the gall bladder is not necessarily a pathological problem. (SINGLE OR MULTIPLE) Floating gall bladder The organ may hang on a mesentery.

One may be intrahepatic Absence of the cystic duct This is usually a pathological.Double gall bladder Rarely. the gall bladder is duplicated. the GB open directly ino the side of common bile duct A long cystic duct travelling alongside the common hepatic duct to open near the duodenal orifice ( occur in 10% of cases ) .


CHOLEDOCHAL CYST :  Presence of cystic dilation in the biliary tree (most commonly in CBD) Classification according to the site of the cyst or dilatation       Type I: Most common variety (80-90%) involving saccular or fusiform dilatation of a portion or entire common bile duct (CBD) with normal  intrahepatic duct. . Type II: Isolated diverticulum protruding from the CBD. Type III or Choledochocele: Arise from dilatation of duodenal portion of CBD or where pancreatic duct meets. Type IVb: Multiple dilatations involving only the extrahepatic bile ducts. Type V: Cystic dilatation of intra hepatic biliary ducts. Type IVa: Characterized by multiple dilatations of the intrahepatic and extrahepatic biliary tree.


idiopathic. absent vena cava and a preduodenal portal vein. The aetiology is unclear. situs inversus. in about 20% of cases. -Associated anomalies include. The inflammatory destruction of the bile ducts has been classified into three main types : • type I: atresia restricted to the common bile duct. cardiac lesions. .BILLIARY ATRESIA  . • type III: atresia of the right and left hepatic ducts. • type II: atresia of the common hepatic duct. fibroobliterative disease of the extrahepatic biliary tree that presents with biliary obstruction exclusively in the neonatal period. polysplenia.The extrahepatic bile ducts are progressively destroyed by an inflammatory process.Biliary atresia (BA) is a progressive. . which starts around the time of birth.


Liver transplantation is the main choice of treatment . .COMPLICATIONS : -Ascending cholangitis Intrahepatic changes can occur and eventually result in biliary cirrhosis and portal hypertension. death from the consequences of liver failure occurs before the age of 3 years. Untreated.

(the most common biliary pathology) affect more than 15% of adult in USA . Asymptomatic (most common) >80 % Symptomatic (complicated) 10-20% : pain. pruritus. 10% of gallstones are radio-opaque . fever……etc. . jaundice.GALLSTONES      Cholelithiasis means stones in the gallbladder.

2. forty (>40) . Pigmented ( Black . Cholesterol 20 %.”  less common : -Oral Contraceptives. Brown ) 5 %. Mixed 75 %  . 3. fat .Rapid weight loss. fertile.Risk factors : The big 5 : “five Fs : female 3:1 . -Family history -Ileal diseases or resection Types of GB stones : 1. -Hyperlipidemia -Gallbladder stasis.fair. .

unstable unilamelar phospholipid vesicles are formed. greasy.  Pathogenesis: → When bile is supersaturated with cholesterol. Characteristics : Yellowish . (Cholesterol > 80%) → This leads to formation of cholesterol crystals. CHOLESTEROL STONES . firm Single or multiple Most are radiolucent. Ovoid .

 Associated with the presence of foreign bodies within the bile ducts such as stents. Contain bilirubin and calicium  Two types : Black and Brown. sickle cell anemia). PIGMENTED STONES . Contains less than 30% cholesterol.  Black  stones : Accompanies hemolysis (hereditary spherocytosis .  Brown Stones :  Form in bile duct and related to bile stasis and infected bile. or parasites .

small. friable.or extrahepatic ducts. numerous. radiolucent . single or few. soft & greasy.  Black: in sterile GB bile . 50-75% are radio-opaque  Brown: in infected intra.• Characteristic :  Anywhere in the biliary tree.

MIXED STONES  Is the most common 75% cut surface is laminated with alternate dark &light zones of pigment & cholesterol respectively .


 In gallbladder : .Perforation .Biliary Colic .08%) . .Acute cholecystitis.Chronic cholecystitis .Empyema.Carcinoma (0. . .Mucocele.

Obstructive jaundice .Gallstone ileus (intestinal obstruction)  .Ascending cholangitis .In the Bile Ducts: .Acute pancreatitis  In the intestine .

Transient obstruction of the GB by a stone in Hartmann’s pouch or cystic duct . So  not a true colic Caused by: .BILIARY COLIC  It is a misnomer because the pain increases in intensity then reaches a plateau then decreases but never disappears . which leads to spasm in the wall of GB .

O: suddenly after fatty meals C: gripping pain. T: Less than 6 hours. flatulence.  .Presentation: pain: S:Right upper quadrant. dull. R: referred to the tip of the right shoulder and radiate to the back A: Associated with . dyspepsia . if more then it is acute cholecystitis.Nausea. vomiting.

ACUTE CHOLECYSTITIS   1-acute calculous cholecystitis – 95% 2-acute Acalculous cholecysitis – 5% .

.ACUTE CALCULOUS CHOLECYSTITIS  Definition: Inflammation of the gallbladder that develops over hours.  Not everyone who has gallstones will go on to develop cholecystitis . This form of gallbladder disease usually subsides within 1 to 7 days with a conservative plan of treatment . usually resulting from a cystic duct obstruction by a gallstone.

A stone obstructing the gallbladder neck (Hartmann’s pouch) or anywhere in cystic duct.Stasis and Concentrated bile .• inflammation of the mucosa by the congested bile salt. 3 2 1 Pathophysiology . This will lead to edema and distention in the wall causing increased intraluminal pressure and compromises blood flow to mucosa. with superimposed bacterial infection • . • .

• Unrelieved obstruction .Decrease blood flow with infection lead to gangrene that cause softness of GB wall 5 4 .Gangrene may cause perforation (causing abscess and chemical peritonitis ) • . without infection and continuous mucus secretion >> Mucocele 6 • Unrelieved obstruction with infection and pus formation >> Empyema • .




Presentation in younger patients.CLINICAL PRESENTATION (ACUTE CHOLECYSTITIS) Age : Typically 30-60 year old. may be due to congenital hemolytic anemia(sickle-cell disease often form pigment stones. Gender : Females are more commonly affected . which may precipitate an attack of acute cholecystitis).

. vomiting and fever T: continuous .Analysis of Pain: S: RUQ O: sudden onset C: sharp R: radiates to the back (close to the inferior angle of right scapula) A: associated with nausea . Duration of pain usually >6 hours E: aggravated by movements and breathing S: severe *The patient May have previous history of flatulent dyspepsia or biliary colic .

PHYSICAL EXAMINATION  General Examination : _ Patient appears ill _ shallow breathing _ Tachycardia +ve.stone passed to the CBD “obstuctive jaundice” 2.Mirrizi syndrome : occur when the cystic duct is densely adhered to the CBD . Pyrexia +ve ** few patients with AC have jaundice by two mechanisms : 1. . the stone in the cystic duct cause compression of the CBD .

PHYSICAL EXAMINATION  Abdominal Examination : RHC mass and tenderness. Murphy's sign : Cessation of breath at deep inspiration during the deep palpation at the tip of 9th rib Bowel sounds are normally present except in biliary peritonitis(GB has infarcted/ruptured ) rare complication . guarding/rigidity Zackary-cope's sign : RHC fullness Boas Sign : hyperaesthesia (increased or altered sensitivity) below the right scapula.

What are the differences in the clinical presentation between biliary colic and Acute cholecystitis ??? Biliary colic : pain duration < 6 hrs Afebrile patient vomiting once or twice mild tenderness Acute cholecystitis : pain duration > 6 hrs febrile patient repeated vomiting severe tenderness .

INVESTIGATION 5. X-ray (not useful.reveals leukocytosis KFT LFT – bilirubin (to detect bile duct obstuction) Amylase and lipase level ( for acute pancreatitis) US abdomen ( THE GOLD STANDARD) 6.only10-15% of stones are visible) MRCP ERCP 1. 4. 3. Full blood count . 2. 8. HIDA scan ( if US is not diagnostic) 7. 9. .

What are the ultrasonic features of ??Acute Cholecystitis 1) Distended gall bladder 2) Fluid surrounding the gall bladder 3) Gall bladder wall thickening (>3mm) 4) Dilated cystic duct 5) Stones in the gall bladder .

 MRCP : magnetic resonance cholangiopancreatography  ERCP : endoscopic retrograde cholangiopancreatography  Both are used for diagnosis .  ERCP used also for therapy of CBD stones . .


. HIDA scan : reveal non-opacification of the gallbladder from obstruction of the cystic duct.


sepsis  It occurs because of : 1) Dehydration 2) GB stasis 3) Vascular compromise 4) Bacterial contamination ( mostly Gram –ve: E-coli . usually seen in seriously ill patients after : major surgeries. Klebsiella . trauma. Enterobacter ) . burns.ACUTE ACALCULOUS CHOLECYSTITIS  Inflammation of the gallbladder in the absence of gall stone .

 Supersaturation of bile predisposes to chronic inflammation & stone formation.CHRONIC CHOLECYSTITIS  Chronic inflammation of the gall bladder because of recurrent attacks of acute cholecystitis or biliary colic ending in thickening and fibrosis of its wall. .  Stones are almost always present.  Bacteria are isolated in 1/3 of the cases.

Heartburn . and last for 30 to 90 mins)) (most common complaint). ((begins 15 to 30 mins after a meal.PRESENTATION -Upper abdominal pain after eating. .flatulent dyspepsia(post-prandial belching) .

PHYSICAL EXAMINATION     Signs of jaundice Abdomen looks normal RHC mass and tenderness Percussion and auscultation should be normal .

Perforated peptic ulcer 2. Acute pyelonephritis 5.: DDX OF RUQ PAIN Common: 1. High appendicitis 3. Right lower lobe pneumonia 6. MI(inferior) . Acute pancreatitis Uncommon: 4.

*Sometimes we do Cholecystostomy in case of empyema .to evaluate whether there's any local complications 8) Plan for cholecystectomy ( open or laparoscopic ) A) Early (within 72 hours). B) Late ( after 2-3 months).MANAGEMENT  Conservative management : ( >90% of cases will respond) 1) Nil by mouth [NPO] 2) Gain IV access. and lastly regular diet 7) US . then followed by fat-free diet. give IV fluids 3) Administration of antibiotics 4)Administration of analgesics 5) Monitoring of vital signs 6) If symptoms subsided. initially oral fluid intake is allowed.

not well defined anatomy uncontrolled bleeding bile duct injury . 2.CHOLECYSTECTOMY Usually we do it by laparoscopy. but in the following cases we do it by Laparotomy : 1. 3.

** the patient complains of persistent abdominal pain.POST – OPERATIVE COMPICATIONS 1. or features of hypovolemic shock 2. obstructive jaundice .bile leak 4-bile duct stricture **the most dangerous complication . secondary biliary cirrhosis and hepatic failure. 5-post cholecystectomy syndrome . leads to : cholangitis .hemorrhage **usually the source is from cystic artery.wound infection 3.

. myxoma . lipoma . fibroma . adenomyoma . carcinoid .NEOPLASMS   Benign tumors of the GB: papilloma . Malignant tumors of the GB : 80 % of the tumors are adenocarcinoma 90 % of pts have cholelithiasis Porcelain GB Carry a risk of 50 % of malignancy (calcification of GB due to excessive stones).


Stones present within the biliary tree.CHOLEDOCOLITHIASIS .Stones may be: 1) derived from gallbladder 2) primary ductal & intrahepatic stone formation . .

  .Symptoms due to: 1) cholangitis (Charcot’s triad). Dark urine . biliary obstruction (Obstructive Jaundice .itching) 2) pancreatitis 3) Liver abscess 4) chronic liver disease with secondary biliary cirrhosis 5) acute cholecystitis . Pale stool .Asymptomatic in 10% .

ERCP are the diagnostic modalities Liver function test are consistent with obstructive jaundice Surgical TT : Cholecystectomy . . T tube placement & operative cholangiogram . choledocotomy . CBD exploration .CHOLEDOCHOLITHIASIS CAN BE PRIMARY OR SECONDARY    u/s .

sclerosing cholangitis. Neoplasm 4. CBD stones.op stricture. relief of the obstruction . 5. Treatment : NPO . IV antibiotics . billiary contrast studies . 2.CHOLANGITIS : INFECTION OF THE BILLIARY TREE . . post. 3.Etiology : 1.

2.chronic parasitic infection of the bile duct. cystic duct .Gall stones.  The tumor may be located in : distal CBD .Sclerosing cholangitis. common hepatic duct . 3. left or right hepatic duct (most common site)  Treatment by : Whipple procedure. .CHOLANGIOCARCINOMA  Malignant tumors of the bile duct may be associated with : 1.