Diseases of gb & biliary tree final

1. GALL - BLADDER
&
BILIARY
DISEASES
Dr. Wondwossen M.

2. Introduction
Cholelithiasis
GB-Stone Complications
Obstructive Jaundice
GB ca & Cholangiocarcinoma

3. GallBladder
 Pear-shaped sac
 Average capacity 30-50ml / 300ml
 Fundus, Body, Infundibulum &
Neck
 Columnar epithelium

4.  Cystic artery / Triangle of
Calot
 Venous drainage to liver
 Vagus & celiac plexus
 Function
Storage
Concentration of bile
Mucus / H+ secretion

5. Bile Ducts
• Intra & Extra-hepatic
• Extra hepatic bile ducts
 Rt. & Lt. hepatic ducts
 Common hepatic duct
 Cystic duct
 Common bile duct
• CBD enters 2nd portion of the
duodenum through sphincter of
Oddi

6. PHYSIOLOGY
 Liver 500 - 1000 ml of bile/day
 Neurogenic & chemical stimuli
 Bile Composition
 Water
 Electrolytes
 Bile acids
 Proteins
 Cholesterol & pigments

7.  Digestion & Absorption of fats
 80% of the conjugated bile acids are
absorbed in the terminal ileum
Eventually, about 95% of the bile acid pool
is reabsorbed-(enterohepatic circulation)
 5% is excreted in the stool

8. DIAGNOSTIC STUDIES
• WBC
– Leukocytosis
• LFT
– Bilirubin (T/D)
– AST/ALT
– ALP
• Ultrasound
 Initial investigation choice
 It is noninvasive, no radiation
 Stones ,Cholecystitis, biliary obstruction, mass

9. • HIDA scan
• Acute cholecystitis
• Biliary obstruction
• Biliary leaks
• CT-scan
• Inferior to ultrasound in diagnosing gallstones
• Best to Dx & staging of
– GB ca
– Extrahepatic biliary system
– Pancreatic malignancy
• MRCP
• ERCP
• PTC

10. CHOLELITHIASIS
 Etiology
1. Bile super-saturation
 Solutes > Solvent
 Female, Obesity, Hemolysis, Ileal resection
2. Infection
 E.coli, proteus, anerobes
 “a gall stone is a tomb stone erected in the memory
of organisms within it.”
3. Bile Stasis
 Pregnancy, Vagotomy, Prolonged fasting ,TPN,
Obstruction, Intrahepatic GB

11. Types of Stones
1. Cholesterol stones
 Account for 10% of gall stones
 Occurs in patients with increased cholesterol
levels
 Usually single , almost always formed in the
GB
 Females , obesity
2. Mixed stones
 Constitute 80% of gallstones
 Usually multiple

12. 3. Pigment Stones
 Cholesterol content < 20%
 Dark because of the presence of calcium bilirubinate
 Can be Black or Brown
 Black stones
 Formed by supersaturation of calcium bilirubinate
 most often secondary to hemolytic disorders such as hereditary
spherocytosis,sickle cell disease, cirrhosis.
 Like cholesterol stones, they almost always form in the GB.
 Brown stones
 May form either in the GB / Bile ducts
 usually secondary to bacterial infection caused by bile stasis(
parasites or strictures)

14. Effect of stone in the GB
1- Asymptomatic Cholelithiasis
2- Symptomatic Cholelithiasis
3- Complications
• In the Gallbladder
• Acute Cholecystitis
• Chronic Cholecystitis
• GB empyema ,gangrene, perforation, mucocele
• Gallbladder Ca.
• In the Bile Ducts/pancreas
• Choledocolithiasis
• Obstructive jaundice
• Cholangitis
• Acute pancreatitis
• In the Intestine
• Gall stone ileus

15. Asymptomatic Cholelithiasis
Incidental finding of stone in the GB (silent
stones)
• Porcelain GB
• Diabetic patients
• Stone size > 3cm
• Polyps >1cm
Indication
for
cholecystectomy

16. Symptomatic Cholelithiasis
The common presenters are 5 Fs
• Female / Fertile / Fatty / Forties / Flatulent
Due to transient stone blockage of the cystic duct
Severe RUQ pain & typically after a fatty meal, ass.
With Dyspeptic symptoms
Dx - Sx + Ultrasound
Rx - Cholecystectomy (Laparascopic / Open)

17. Complications
 Acute Calculus Cholecystitis
 Obstruction of the cystic duct is the initiating event leading to
 Distention , inflammation, & edema of the GB wall
 Dx
 begins as an attack of biliary colic, but in contrast to biliary
colic, the pain does not subside; it is unremitting & may persist
for several day
 Fever, anorexia, nausea, & vomiting
 RUQ tenderness & +ve Murphy’s sign

18.  Leukocytosis
 Ultrasound , HIDA scan
 Rx - IV fluids, Abc, Analgesic / Interval
cholecystectomy
 Other complications like empyema, gangrene &
perforation mandates an immediate surgery

19. Acalculous Cholecystitis
• Acute inflammation of the GB without gallstones
• The cause is unknown, but GB distention with bile stasis & ischemia has
been implicated as causative factors
• Typically develops in critically ill patients in the intensive care unit.
• Patients at risk
• Parenteral nutrition
• Extensive burns
• Sepsis,
• Major operations
• Multiple trauma
• Diabetics
• The symptoms are similar to acute calculous cholecystitis
• Ultrasonography

20. Choledocholithiasis
• Stone in the common Bile Duct (CBD)
• Primary Vs Secondary stones
 Primary Stones
 stones that form in the bile ducts
 are usually of the brown pigment type.
 are associated with biliary stasis & infection
 Secondary Stones
 are formed within the GB & migrate to the CBD
 are usually cholesterol stones
 Fates can be
 Silent stones
 Symptomatic (biliary colic)
 Obstructive jaundice
 Cholangitis

21. Carcinoma of the Gallbladder
• Rare malignancy
• Occurs predominantly in the elderly
• It is an aggressive tumor, with poor prognosis
• The overall reported 5-year survival rate is about 5%
• Three times more common in females than males
• Peak incidence is in the seventh decade of life

22. • Etiology
• Cholelithiasis is the most important risk factor-----
chronic inflammation
• 95% of patients with GB ca have gallstones
• Larger stones (>3 cm) are associated with a 10-fold
increased risk of cancer.
• The risk of developing cancer of the GB ca is higher in
patients with symptomatic than asymptomatic
gallstones.
• Polyps > 1cm
• Calcified “porcelain” GB  >20% incidence of GB ca
• Choledochal cysts
• Sclerosing cholangitis

23. • 90% of GB tumors are adenocarcinoma
• When diagnosed, about
– 25% of GB cancers are localized to the GB wall,
– 35% have regional nodal involvement and/or extension into liver,
– 40% have distant metastasis
• RUQ pain, Jaundice, weight loss, anorexia, ascites, abdominal mass
• Ultrasound, CT scan
• Cholecystectomy
• Extended cholecystectomy
• Most patients with GB cancer have unresectable disease at the time of
diagnosis.

24. Obstructive Jaundice
• Anatomy of Biliary tree
• Bilirubin Metabolism
• Causes of obstructive jaundice
• Clinical features of obstructive jaundice
• Work-up of a patient

26. Bilirubin Metabolism
1- Source of bilirubin
 Bilirubin comes from RBCs
 Normally, 1% of RBC retire every day, to be replaced by fresh
RBCs
 HAEMOGLOBIN SPLITS INTO HAEM & GLOBIN
 GLOBIN & CELL WALL PROTEIN ENTER THE AMINO ACID
POOL
 HAEM SPLITS INTO IRON & BILIRUBIN
 IRON STORED AS FERRITIN FOR REUSE
 BILIRUBIN ENTERS THE LIVER

27. 2- Journey through the liver (Conjugation)
• BILIRUBIN COMBINE WITH GLUCOURINC
ACID TO FORM THE CONJUGATED
[DIRECT] BILIRUBIN
– Bilirubin taken up Liver
– Conjugated to form water soluble
conjugate
– Conjugated Bilirubin secreted into
bile ducts

28. 3- In the INTESTINE
 Conjugated Bilirubin pass by the bile ducts into the
intestine.
 Bacterial degradation, mainly in the colon, converts it to
urobilinogen
 Some urobilinogen is reabsorbed and goes via the portal
system to the liver
 Urobilinogen is water soluble that is filtered off by the
kidney & is excreted in the urine which gives the yellow
colour to the urine
 The urobilinogen that is not reabsorbed from the
intestine is excreted in the faeces, which is responsible
for the colour of the faeces.

29. Composition of Bile
• Bile is produced in the Liver
• Composed of
– Water
– Cholesterol
– Bile salts & acids
– Phospholipids
– Bilirubin (pigment)
• Helps in fat & Vitamin absorption

30. What is Jaundice??
• Jaundice is not a disease but rather a sign that can occur in
many different diseases.
• Jaundice is the yellowish staining of the skin & sclera that is
caused by high levels of bilirubin in blood.
• Normal Serum Bilirubin (SB) is 0.3 to 1.0 mg/dl
• Clinically obvious when > 2.5mg/dl
• The color of the skin & sclera vary depending on the level of
bilirubin.
• When the bilirubin level is mildly elevated, they are yellowish.
When the bilirubin level is high, they tend to be brown/green

31. Types of Jaundice

32. Jaundice occurs when there is
1) Excessive breakdown of RBCs resulting in too
much bilirubin being produced for the liver to
remove from the blood - hemolytic jaundice /
PREHEPATIC JAUNDICE
2) A defect in the liver that prevents bilirubin from
being removed from the blood, defect in
conjugation , due to toxic damage/infection of
the liver – hepatocellular HEPATIC JAUNDICE
3) Blockage of the bile ducts that decreases the
flow of bile & bilirubin from the liver into the
intestines - Obstructive jaundice or
POSTHEPATIC JAUNDICE

33. OBSTRUCTIVE / SURGICAL JAUNDICE
• It is due to intra / extra hepatic obstruction of bile
ducts
• Causes include
• Intra-luminal
–Stones
–Parasites
–Polyps
• Intra-mural
–Benign & Malignant strictures
• Extra-mural
– Pancreatic head mass
– Periampullary tumor
– Lymph nodes

34. 1. Congenital: Biliary Artesia, choledochal cyst
2. Inflammatory: Ascending cholangitis, sclerosing
cholangitis
3. Obstructive: CBD stones, biliary stricture, parasitic
infestation
4. Neoplastic: Carcinoma of head/periampullary
region of pancreas, cholangiocarcinomas
5. Extrinsic compression of CBD by lymph nodes /
tumors.

35. Clinical approach
• History
• Jaundice (duration, intermittent Vs progressive)
• Painful Vs Painless
• Dark urine, pale stool, itching, steathorea, bleeding
• RUQ pain, fat intolerance, dyspepsia
• Hx of previous biliary surgery / cholangitis
• Associated weight loss, anorexia, night sweat, cough, fever
• Hx of drug, alcohol, blood transfusion

36. Physical Exam
• Acutely / Chronically sick looking
• Jaundice (sclera, skin)
• Pallor
• Scratch marks
• Easy bruising
• Stigmata of liver disease
• Palpable gall bladder (Courvoisier's law)

37. • CHARCOT`S TRIAD
• Jaundice, Fever & RUQ pain
• REYNODS PENTAD
• Charcot’s triad + shock & altered mentation
• VIRCHOW`S NODE
• ASCITES

39. Investigations
• CBC
• Urine Analysis
• Liver function test
• Bilirubin (total, direct & indirect)
• Alkaline phosphatase (ALP)
• ALT, AST
• Coagulation profile (PT,PTT,INR)
• Abdominal Ultrasound
• CT- scan
• ERCP
• MRCP

40. Bile Duct Carcinoma(Cholangiocarcinoma)
• May occur anywhere along the biliary tree
• About 2/3rd are located at the hepatic duct
bifurcation
• Many patients have advanced disease at the time of
diagnosis
• Male-to-female ratio is 1.3:1
• Average age of presentation is between 50 & 70
years

41. • Risk factors associated with
cholangiocarcinoma
– Primary sclerosing cholangitis
– Choledochal cysts
– Ulcerative colitis
– Biliary-enteric anastomosis,
– Biliary tract infections with Clonorchis
• 95% of bile duct cancers are
Adenocarcinomas
• Usual presentation is obstructive jaundice
• CA19-9, CT scan, MRCP
• Surgery

42. Thanks