BileLyndon Woytuck, BSc, MBBS student

What is bile?

Bile is a fluid made by liver cells (hepatocytes), secreted into the biliary tract and stored in the gallbladder.

Bile aids in digestion by breaking down fats into fatty acids, which can be absorbed by the digestive tract for further use by the body.

Bile is mainly composed of cholesterol, bile acids (or bile salts), and bilirubin (a breakdown product of red blood cells). Bile also contains water, potassium and sodium salts, copper and trace metals

A note on the Anatomy

The common hepatic duct then merges with the cystic duct from the gallbladder to form the common bile duct.

The common bile duct joins with the duodenum at the Ampulla of Vater.

About half of the bile produced by the liver is first stored in the gallbladder before emptying into the duodenum through the sphincter of Oddi.

The gallbladder is a pear-shaped organ attached beneath the liver. When food enters the duodenum, the gallbladder contracts and

releases stored bile into the intestinal lumen to aid digestion.

Bile secreted from hepatocytes is collected by a system of ducts flowing within the liver and eventually draining into the left and right hepatic ducts.

The hepatic ducts drain into the common hepatic duct.

Naturally, the physiology

The biliary system drains waste products from the liver into the duodenum,

And aids in digestion via CCK controlled release of bile Bile is a greenish-yellow fluid and serves two primary

functions: Excretion of waste Fat digestion

Bile acids emulsify and absorb fats with vitamins A, D, E, K Stercobilin is excreted from the body in faeces, and is

what gives faeces its dark brown color. Urobilin is carried through the blood plasma and excreted

in urine, giving urine a yellow (sometimes brown) colour

For the image shown, answer the following questions:1. Identify the labeled structures (A-G).2. What is the name of the sphincter that controls the

structure labeled (L)?3. What life-threatening complication can develop as a

result of a gallstone becoming lodged within the structure labeled (L)?

4. BONUS: Which hormone stimulates the release of bile from the gallbladder?

Answer:1. (A) Right hepatic duct, (B) left hepatic duct, (C) cystic duct, (D) common

hepatic duct, (E) common bile duct, (F) accessory pancreatic duct, and (G) pancreatic duct.

2. The sphincter responsible for controlling the major duodenal papilla (ampulla of Vater) (L) is the sphincter of Oddi.

3. Gallstone-induced pancreatitis can result from a gallstone that becomes lodged within the major duodenal papilla (ampulla of Vater) (L).

4. Cholecystokinin (CCK), which is produced by I cells of the duodenum and jejunum, stimulates the gallbladder to contract and release bile.

Explain how disruption of bilirubin metabolism and excretion can cause jaundice Jaundice is caused by an accumulation of bile pigments

(biliverdin, bilirubin) in the body. This is usually first visible in mucus membranes (sclerae), then followed by the skin.

Haemolytic increased haemoglobin breakdown produces more bilirubin, which

overloads the conjugation. Increase in unconjugated form. Other LFTs usually normal, with reduced haptoglobin, reticulocytosis and abnormal red cells on film. Anaemia may occur.

Hepatocellular failure of conjugation resulting in increased bilirubin. Increased ALT

(marker of hepatocellular damage). Damage to hepatocytes may cause leakage of bilirubin into plasma and conjugated bilirubin may be found in the urine.

Obstructive biliary obstruction results in conjugated bilirubin to pass from the

liver to plasma. Very high levels may cause the patient to turn green and turn the urine dark. Less stercobilin and faeces turn pale. Elevated ALP due to cholestasis.

Carotenaemia or quinacrine ingestion can result in yellow or green skin colour precipitated by eating large amounts of green and yellow vegetables, corn or tomatoes. In absence of yellow mucous membranes and sclerae, with normal urine color, and accentuated yellow-brown pigment on palms, soles, and nasolabial folds. Quinacrine used for treatment of giardiasis may colour skin yellow, but with normal urine. Serum bilirubin levels are normal.

Describe the pathogenesis of conjugated and unconjugated hyperbilirubinaemia and list conditions associated with each Conjugated:

Obstructive – cholestasis, cholangitis Hepatocellular – infection, hepatocellular carcinoma, cirrhosis Physiologic jaundice of the newborn Breast milk jaundice Dubin-Johnson's / Rotor's: impairment of hepatocyte bilirubin secretion

Unconjugated: Haemolytic – haemolytic disease of the newborn (Rh), Wilson’s,

autoimmune hepatitis, alcoholic, drug induced Ineffective erythropoiesis Gilbert's: hepatocyte bilirubin uptake alteration Crigler-Najjar's: glucuronyl transferase deficiency

Lab report of liver function tests of a patient with jaundice showed predominantly conjugated hyperbilirubinaemia. Which of the following conditions is most likely to be responsible for conjugated hyperbilirubinaemia?

A. Acute haemolytic crisis in sickle cell diseaseB. Gilbert syndromeC. Haemolysis due to rhesus incompatibilityD. Obstructive jaundice due to carcinoma of common

bile ductE. Physiological jaundice of the newborn

Lab report of liver function tests of a patient with jaundice showed predominantly conjugated hyperbilirubinaemia. Which of the following conditions is most likely to be responsible for conjugated hyperbilirubinaemia?

A. Acute haemolytic crisis in sickle cell diseaseB. Gilbert syndromeC. Haemolysis due to rhesus incompatibilityD. Obstructive jaundice due to carcinoma of

common bile ductE. Physiological jaundice of the newborn

Describe the symptoms and signs in a patient presenting with jaundice

Yellow colouring of the skin and eyes (usually beginning on the face and moving down the body)

Direct and indirect bilirubin levels. These reflect whether the bilirubin is bound with other substances by the liver so that it can be excreted (direct), or is circulating in the blood circulation (indirect). Either measurement may be high.

Red blood cell counts. Haemolytic jaundice may present with anaemia or reticulocytosis.

Explain how features of the history and examination can be used to distinguish between haemolytic, hepatocellular or cholestatic jaundice Onset

Few days, one week – hepatitis: viral, bacterial, drug or toxin Weeks – subacute hepatitis, extrahepatic obstruction Fluctuating intensity – cholelithiasis, ampullary cancer, drug hepatitis Past history – chronic hepatitis, cirrhosis, benign recurrent intrahepatic

cholestasis, genetic non-haemolytic hyperbilirubinaemia Age

>40 pancreatic carcinoma, cholelithiasis <25 Hepatitis A

Constitutional symptoms – anorexia, nausea, emesis, weight loss within 2 weeks prior: hepatitis or cholelithiasis Continuously >2 weeks: malignant biliary obstruction, chronic hepatitis,

toxin (alcohol) Recurrent brief episodes over months/years and RUQ pain: cholelithiasis

Features of History and Exam:Symptoms

Abdominal pain Dull ache RUQ: acute hepatitis Acute abdomen (fever, jaundice and leucocytosis): alcoholic

hepatitis RUQ episodically with radiation to right scapula or girdle

distribution: cholelithiasis Epigastric or RUQ with radiation to back: pancreatic head carcinoma

Fever Acute hepatitis or with chills, biliary obstruction (stones or stricture

>> malignancy) Pruritis

Biliary tract obstruction, occasionally viral hepatitis Recent onset: large ducts – neoplasm, or canaliculi – intrahepatic

(drug) Long standing, middle-aged woman: primary biliary cirrhosis

Features of History and Examination:Portals of entry

Drug and toxin exposures Pain relievers, tranquilizers, oestrogens, chemicals, alcohol

Hepatic infection (viral, etc.) Patients, transfusions, needles, narcotics, raw shellfish, travel

(entamoeba), sexual, animals or stagnant water (leptospirosis), immunocompromise, infectious mono, sepsis

Surgery (<3 weeks) Increased bilirubin load: transfusion haemolysis, haematoma

resorption and G6PDd, drug reactions, malarial transfusion Impaired hepatic function: halogenated anaesthesia, drugs,

sepsis, hepatic ischaemia Obstruction: surgical injury, biliary calculus, cholecystitis

Previous biliary surgery (<2 years): biliary stricture

Features of History and Examination: Historical insights Systemic conditions:

Inflammatory bowel disease primary sclerosing cholangitis, cholangiocarcinoma, chronic hepatitis, cirrhosis,

hepatic amyloid. Resection – cholelithiasis Cirrhosis

Cystic fibrosis, haemochromatosis, Wilson’s, alpha-1 antitrypsin def., galactosaemia, hereditary fructose intolerance, tyrosinaemia

Systemic lupus erythematosus Hypoxic injury – hepatitis

Family history of jaundice or hepatic disease Genetically transmitted non-haemolytic hyperbilirubinaemias: Crigler-Najjar,

Gilbert’s, Dubin-Johnson, Rotor’s Benign recurrent intrahepatic cholestasis, Wilson’s disease,

haemochromatosis, alpha-1 antitrypsin def, hereditary spherocytosis

Features of History and Examination:Physical Inspection

Hepatocellular diseased patient appears more acutely ill than obstructive disease

Greenish jaundice – prolonged obstruction Orange-yellow jaundice – hepatocellular Mental derangements – hepatocellular >> obstruction Spider telangiectasias: chronic hepatocellular Scratch marks: pruritis Decreased axillary/pubic hair, gynaecoid changes: cirrhosis Dupuytren’s contracture: chronic liver disease Xanthelasma, tuberous xanthomas: long standing biliary

obstruction with hyperlipidaemia, primary biliary cirrhosis

Features of History and Examination:Physical Auscultation, Palpation Hepatic bruits

malignancy, hepatitis, haemangioma Hepatic friction rub

malignancy, inflammatory (Glisson’s capsule) Standing up may aid here

Very large liver congested or fatty cirrhosis, neoplasm or amyloid

Rapidly shrinking liver acute liver failure – viral or toxin

Hard or nodular fibrotic or malignant infiltration

Features of History and Examination:Palpation, Percussion

Unusual tenderness acute hepatitis, abscess or rapid enlargement (vascular

congestion or fatty changes) Splenomegaly

w/out hepatomegaly: primary haemolytic or portal vein occlusion

Portal hypertension, viral hepatitis w/ hepatomegaly: malignancy (haematologic) or storage

disease Ascites

cirrhosis with portal hypertension or malignancy >> massive or subacute hepatic necrosis or hepatic vein obstruction

A 52 year old man, who was previously well, presented with a 3 week history of increasing jaundice associated with pale stools, dark urine and itching. There was no associated pain or fever. He was not on any medication. Blood tests confirmed a cholestatic pattern of hyperbilirubinaemia with markedly raised alkaline phosphatase, moderate elevation of transaminases and normal serum albumin. Regarding the planning of his further investigation, which is true

A. Absence of pain excludes gallstone obstruction of the common bile duct (CBD)

B. Absence of bile duct dilatation on ultrasound scan makes it safe to immediately proceed to liver biopsy

C. Magnetic resonance cholangio-pancreatography (MRCP) is inferior to endoscopic retrograde cholangio-pancreatography (ERCP) in the investigation of extrahepatic cholestasis where ultrasonography fails to show the cause

D. The role of ERCP is primarily to undertake therapeutic measures, which might avoid surgical intervention

E. A prolonged prothrombin time due to extra-hepatic cholestasis requires a 5 day course of intravenous vitamin K (5mg) to correct

A 52 year old man, who was previously well, presented with a 3 week history of increasing jaundice associated with pale stools, dark urine and itching. There was no associated pain or fever. He was not on any medication. Blood tests confirmed a cholestatic pattern of hyperbilirubinaemia with markedly raised alkaline phosphatase, moderate elevation of transaminases and normal serum albumin. Regarding the planning of his further investigation, which is true

A. Absence of pain excludes gallstone obstruction of the common bile duct (CBD)

B. Absence of bile duct dilatation on ultrasound scan makes it safe to immediately proceed to liver biopsy

C. Magnetic resonance cholangio-pancreatography (MRCP) is inferior to endoscopic retrograde cholangio-pancreatography (ERCP) in the investigation of extrahepatic cholestasis where ultrasonography fails to show the cause

D. The role of ERCP is primarily to undertake therapeutic measures, which might avoid surgical intervention

E. A prolonged prothrombin time due to extra-hepatic cholestasis requires a 5 day course of intravenous vitamin K (5mg) to correct

Correct answer – D (www.medicinecpd.co.uk) Explanation: Absence of pain does not exclude the passage of gallstones obstructing the CBD; even the appearance of bile duct dilatation may not be obvious on USG if the obstruction is intermittent. In this situation MRCP should be undertaken and the more invasive ERCP reserved for the therapeutic procedures such as stenting, sphincterotomy or stone extraction. With a 3 week history of cholestatic jaundice malabsorption of vitamin K is likely to have led to prothrombin time (INR) prolongation and it would be highly dangerous to undertake liver biopsy without first correcting it. The INR should return to normal within 6 hours of a single intravenous dose of vitamin K (5mg).

Give a differential diagnosis for a patient presenting with jaundice

Benign recurrent intrahepatic cholestasis

Cholangitis – primary sclerosing

Cholangiocarcinoma Cholecystitis Cholelithiasis Chronic pancreatitis Cirrhosis Common bile duct stricture Extrahepatic malignancy Genetic non-haemolytic

hyperbilirubinaemia (Gilbert’s

or Dubin-Johnson syndrome) Haemolysis HELLP syndrome (hemolysis,

elevated liver tests, and thrombocytopenia)

Hepatitis: viral, bacterial, drug or toxin

Hepatocellular carcinoma Hyperbilirubinemia of the

newborn Neonate – breast milk

jaundice, physiologic jaundice, haemolytic disease

Primary biliary cirrhosis

Take a structured history from a patient with jaundice to determine aetiology

Amy

Joan

Dice

•Presents to ED•Recent onset upper abdominal discomfort•Chills•Yellow sclerae

Wha

t should you

ask?

•Focused HoPC•Medications – liver damage•Alcohol or IVDU•Surgery – biliary, cancer•Transfusions•Pregnancy•Occupation

Sy

mpto

ms?

•Character •Sequence•Relievers or conceivers•Associated signs/Sx•Urine/stool•PMHx, FHx

Explain the relevance of changes in colour and bilirubin and urobilinogen content of stools and urine in the assessment of jaundice Dark urine, with green foam upon shaking is

caused by bile pigment excludes hemolysis or a hepatic uptake or

conjugating defect of bilirubin metabolism acting alone

Brown stool: haemolysis, mild to moderate hepatocellular

Clay coloured stool: moderate to severe hepatocellular, obstructive

Blood in clay-coloured stool: carcinoma of the pancreas or ampulla of Vater.

A 40 year old woman, who is jaundiced, presents to you with reports of laboratory tests that reveal conjugated hyperbilirubinaemia. Urine bilirubin levels are significantly above normal while urine urobilinogen levels are significantly below normal. Which of the following is most likely cause of her jaundice?

A. Blockage of the common bile ductB. Deficiency of glucuronyltransferaseC. Gilbert syndromeD. Haemolytic anaemiaE. Primary shunt hyperbilirubinaemia

A 40 year old woman, who is jaundiced, presents to you with reports of laboratory tests that reveal conjugated hyperbilirubinaemia. Urine bilirubin levels are significantly above normal while urine urobilinogen levels are significantly below normal. Which of the following is most likely cause of her jaundice?

A. Blockage of the common bile ductB. Deficiency of glucuronyltransferaseC. Gilbert syndromeD. Haemolytic anaemiaE. Primary shunt hyperbilirubinaemia

Outline the mechanisms whereby drugs may cause jaundice and give examples of drugs which have each effect Hepatitis/Hepatotoxicity

Acetaminophen, NSAIDs, Amiodarone, Anabolic steroids, Birth control pills, Chlorpromazine, Erythromycin, Halothan, Methyldopa, Isoniazid, Methotrexate, Statins, Sulfa drugs, Amoxicillin-clavulanate, Anti-epileptics

Cholestasis Cyclosporine, bosentan, glibenclamide, troglitrazone, rifampicin

Normally, the liver metabolises certain pharma Susceptible individuals may be poor metabolisers Hepatocellular uptake and biotransformation results in more water soluble

metabolites from lipid soluble drugs Phase I reactions involve the oxidation, hydroxylation and other reactions mediated

by the cytochrome P-450 (CYP) system, particularly CYP3A4. Activity of the cytochrome P-450 system varies greatly among individuals.

Phase II reactions involve esterification reactions that form conjugates with sulfate, glucuronic acid, amino acids or glutathione molecules - enhances detoxification of the compounds.

Can also lead to the production of toxic intermediates Drug induced cholestasis may happen with high drug concentrations, genetic alterations of

enzyme or transporter expression, and/or lower concentrations of anti-oxidants, such as glutathione. Can be caused by direct toxic effects of drugs or their metabolites on liver cells or through by immune mediation

Describe how you would investigate a patient with jaundice Phlebotomy

1) Complete blood cell count and blood smear1) Haemolysis, reticulocytosis, leukocytosis and neutrophilia, eosinophilia

2) In newborns, blood type and testing for Rh incompatibility (Coomb's)

3) Urinalysis: bilirubin, protein4) Conjugated and unconjugated (direct and indirect) bilirubin5) Associated liver function tests (ALP, SGPT and SGOT)6) Prothrombin and prothrombin precursor, prothrombin time –

prognostic7) Albumin – chronicity8) Hepatitis A, B, C serology9) Antibody titres – ANA, delta agent, Epstein-Barr, herpes,

cytomegalovirus (leptospirosis, syphilis, entamoeba)10)Specific markers: ceruloplasmin, transferrin sat, HFE, alpha

fetoprotein, protease inhibitors

Describe how you would investigate a patient with jaundice

Imaging Chest X-Ray, Abdomen Abdominal sonography CT Percutaneous transhepatic cholangiography (PTC) Endoscopic retrograde cholangiopancreatography

(ERCP) Hepatobiliary scintigraphy (HBS) MRI: metastasis

Biopsy

Describe the hepatic origins of ALP, AST and GGT and explain how changes in these may indicate the origin of the jaundice

Alkaline phosphatase ALP = removes phophates – dephosphorylation cholestasis, hepatocellular enzyme induction, canalicular injury, bone growth or

disease, placenta Acute lithic biliary obstruction may have aminotransferase levels >500 U/L and

normal or mildly elevated ALP Aminotransferases

AST = amino group catalysis – amino acid metabolism hepatocellular injury, acute biliary obstruction, coeliac disease, skeletal

muscle (AST) Progression and resolution of hepatocellular injury AST:ALT >2:1 may indicate alcoholic liver disease

Gamma-glutamyl transpeptidase GGT catalyses glutathione to an acceptor – detox and glutamate cycle cholestasis, medications, ethanol, hyperthyroidism, myotonic dystrophy

Jaundice is yellowing of the skin, sclerae and other tissues caused by excess circulating bilirubin. Jaundice is likely to be due to:

A. Common bile duct obstruction if the serum aminotransferases are elevated and alkaline phosphatase is low

B. Haemolytic disease if plasma albumin is low and globulin high

C. Haemolytic disease if prothrombin time is prolongedD. Hepatic disease if plasma albumin is low and serum

aminotransferase elevations >500 unitsE. Hepatic disease if plasma acid phosphatase level is

raised

Jaundice is yellowing of the skin, sclerae and other tissues caused by excess circulating bilirubin. Jaundice is likely to be due to:

A. Common bile duct obstruction if the serum aminotransferases are elevated and alkaline phosphatase is low

B. Haemolytic disease if plasma albumin is low and globulin high

C. Haemolytic disease if prothrombin time is prolongedD. Hepatic disease if plasma albumin is low and

serum aminotransferase elevations >500 units

E. Hepatic disease if plasma acid phosphatase level is raised

Give a differential diagnosis for extrahepatic biliary obstruction

Cancer Cholangiocarcinoma pancreatic carcinoma

Iatrogenic surgical injury, stricture, biliary leak

Cholelithiasis Cholecystitis Cholangitis

Describe the investigation of a patient with extrahepatic biliary obstruction, including endoscopic, radiological and surgical techniques available for treatment/palliation of the underlying condition Cholelithiasis

Extract lodged stones from the common bile duct tree by performing a procedure called ERCP (endoscopic retrograde cholangiopancreatography).

Strictures surgical or by interventional endoscopy or radiology with possible further

operations to remove stone source Bile duct cancer

Diagnosed by radiology, furthered by ERCP or PTC and EUS Resection of the cancer and pathologic exam

Pancreatic cancer Diagnosed by radiology, multidisciplinary treatment Resection and biliary tree reconstruction

Cholecystitis; Cholangitis Cure infection, then cure the underlying cause

Among the following, which is the investigation of choice for evaluation of ONLY the common bile duct?

A. CECT abdomen (computed tomography)B. MRCP (magnetic resonance cholangio-

pancreatography)C. HIDA (hepatobiliary) scanD. Ultrasonography

Among the following, which is the investigation of choice for evaluation of common bile duct?

A. CECT abdomenB. MRCP (magnetic resonance cholangio-

pancreatography)C. HIDA (hepatobiliary) scanD. Ultrasonography

Describe the symptoms of biliary colic

Pain 1-5 hours of constant severe or dull pain in the epigastrium or RUQ Peritoneal irritation localises to RUQ May radiate to scapula or back Patients move around to seek pain relief Pain onset hours after meal, often at night, wakes patient

Nausea Vomiting Pleuritic pain Fever

Give a differential diagnosis for right upper quadrant pain

Cholecystitis, cholelithiasis, cholangitis, hepatitis, carcinoma of liver, pancreas or biliary tract

Abdominal aneurysm Diverticular disease Gastroenteritis Inflammatory bowel Mesenteric ischaemia Myocardial infarction Pancreatitis

Pleural effusion, right lower lobe pneumonia or tumour

Pregnancy: Eclampsia, Urinary tract infection

Renal calculi Right colon cancer Small bowel obstruction Fractured rib(s) Spinal root compression

Describe the pathogenesis of gallstone formation (cholelithiasis)

Bile is composed mainly of water, bile salts, lecithin (phospholipid) and cholesterol (5%)

Most bile flows into the gallbladder through the cystic duct, while a small amount drains directly to duodenum

Water is removed from bile in the gallbladder (2-5cups/day) 70% of stones are formed of cholesterol 30% are pigmented (black or brown) Cholesterol is solubilised in micelles In imbalance between cholesterol and bile salts

cholesterol and calcium bilirubinate sludge cholesterol crystal precipitation

Predisposing factors: high cholesterol, low gallbladder emptying and absorption, high bilirubin

List the risk factors for developing gallstones 4 F’s

Fair Fat Female Fertile

Oral contraceptives or oestrogen replacement Pregnancy

incidence 5.1% second trimester, 7.9% third, 10.2% 4-6weeks postpartum

Older age

Describe investigations that can be used to confirm the diagnosis of gallstones

Ultrasound – 98% sensitive and specific Hepatobiliary scintigraphy (HBS) if unclear US

Adjunctive plain radiography, CT, ERCP

US findings for cholecystitis include Gallstones or sludge Gallbladder wall thickening (>2-4 mm) Gallbladder distention (diameter > 4 cm, length

>10 cm) Pericholecystic fluid from perforation or exudate Air in the gallbladder wall (indicating gangrenous

cholecystitis) Ultrasonographic Murphy sign (86-92% sensitive,

35% specific) - pain when the probe is pushed directly on the gallbladder (not related to breathing)

The ultrasound shows gallstones within the gallbladder without evidence of Cholecystitis.

Regarding the diagnosis of cholelithiasis, which of the following is true?

A. Offer liver function tests and ultrasound to people with suspected gallstone disease, and to people with abdominal or gastrointestinal symptoms that have been unresponsive to previous management.

B. Consider endoscopic retrograde cholangio-pancreatography (ERCP) if ultrasound has not detected common bile duct stones but the: bile duct is dilated and/or liver function test results are abnormal.

C. Consider T2 weighted computed tomography (CT) abdomen with enteric contrast if MRCP does not allow a diagnosis to be made.

D. Do not refer a person for further investigations if faecal impaction or duodenal atresia is suspected.

Regarding the diagnosis of cholelithiasis, which of the following is true?

A. Offer liver function tests and ultrasound to people with suspected gallstone disease, and to people with abdominal or gastrointestinal symptoms that have been unresponsive to previous management.

B. Consider endoscopic retrograde cholangio-pancreatography (ERCP) if ultrasound has not detected common bile duct stones but the: bile duct is dilated and/or liver function test results are abnormal.

C. Consider T2 weighted computed tomography (CT) abdomen with enteric contrast if MRCP does not allow a diagnosis to be made.

D. Do not refer a person for further investigations if the cause is suspected to be faecal impaction or duodenal atresia.

The truth from NICE!1. Offer liver function tests and ultrasound to people

with suspected gallstone disease, and to people with abdominal or gastrointestinal symptoms that have been unresponsive to previous management.

2. Consider MRCP if ultrasound has not detected common bile duct stones but the: bile duct is dilated and/or liver function test results are abnormal.

3. Consider endoscopic ultrasound (EUS) if MRCP does not allow a diagnosis to be made.

4. Refer people for further investigations if conditions other than gallstone disease are suspected.

Describe the potential complications of gallstones Cholecystitis Gallbladder gangrene in cholecystitis (diabetics, elderly or

immunocompromised) In cholecystitis and/or biliary colic may be cholangitis, sepsis,

pancreatitis, hepatitis, and choledocholithiasis Gallbladder perforation occurs in 10% of cholecystitis Abscess formation Free perforation, bile and inflammatory release intra-

peritoneally peritonitis Gallbladder enteric fistula if perforation occurs next to a hollow

organ. Most commonly duodenum. Gallstones may pass through the fistula into small bowel, and if

they >2.5cm can obstruct the ileocecal valve, causing gallstone ileus. Mortality ~20%

Discuss the management of a patient with gallstones, including the indications for cholecystectomy Expectant management (watch and wait)

Asymptomatic patients, 5mm < stones < 3cm Age for future surgery likelihood

30% at 30, 20% at 50, 15% at 70 Symptomatic antibiotics and NSAIDs (or stronger) Nonsurgical lithic removal

Lithotripsy <2cm, few Medication: ursodiol, chenodiol <1.5cm (or contact MTBE)

ERCP removal (endoscopic sphincterotomy) Surgical cholecystectomy

Laparoscopic or open No gallstone protection from lowering cholesterol

A 25 year old Hispanic woman, who is 4 months post-partum has pain in the right upper quadrant/ Her laboratory values are as follows: leukocyte count 9.0x103/mm3; total serum bilirubin 0.9mg/dL; serum alkaline phosphatase 100U/L; serum amylase 300 U/L. Which of the following statements regarding her condition is INCORRECT?

A. If she undergoes a laparoscopic cholecystectomy, there is an approximately 5% chance that conversion to an open cholecystectomy will be necesasary

B. If she undergoes laparoscopic cholecystectomy, she will have a 1.0% to 1.5% chance of having a surgically attributable injury to the common bile duct

C. She is likely to have gallstones, which are common in Hispanic women and frequently discovered during or following pregnancy

D. She most likely has experienced biliary colic and has passed a gallstone that resulted in mild pancreatitis, rather than having biliary obstruction at this time

E. Unless she has cholecystitis, cholelithiasis with symptomatic biliary colic is unlikely

A 25 year old Hispanic woman, who is 4 months post-partum has pain in the right upper quadrant/ Her laboratory values are as follows: leukocyte count 9.0x103/mm3; total serum bilirubin 0.9mg/dL; serum alkaline phosphatase 100U/L; serum amylase 300 U/L. Which of the following statements regarding her condition is INCORRECT?

A. If she undergoes a laparoscopic cholecystectomy, there is an approximately 5% chance that conversion to an open cholecystectomy will be necesasary

B. If she undergoes laparoscopic cholecystectomy, she will have a 1.0% to 1.5% chance of having a surgically attributable injury to the common bile duct

C. She is likely to have gallstones, which are common in Hispanic women and frequently discovered during or following pregnancy

D. She most likely has experienced biliary colic and has passed a gallstone that resulted in mild pancreatitis, rather than having biliary obstruction at this time

E. Unless she has cholecystitis, cholelithiasis with symptomatic biliary colic is unlikely

E. Unless she has cholecystitis, cholelithiasis with symptomatic biliary colic is unlikely. Symptomatic and asymptomatic cholelithiasis commonly occur in the absence of cholecystitis, an infection of the gallbladder. Cholecystitis can develop from bacteria alone or as a consequence of cystic duct obstruction by a stone. Hispanic women have a high prevalence of biliary disease, including cholelithiasis, which often occurs during and after pregnancy. The laparoscopic approach has become the standard technique for cholecystectomy. The frequency of common bile duct injury is reported to range from 1.0% to 1.5%, or approximately twice that of the open procedure. The reported need to convert to an open cholecystectomy is 5%; to proceed safely, the surgeon should not hesitate to convert to an open technique. The patient is unlikely to have a bile duct obstruction, given her normal serum bilirubin and alkaline phosphatase levels. The elevated serum amylase level suggests that she has experienced biliary colic while passing a stone that resulted in mild pancreatitis.

Explain to a patient the function of the gallbladder, how, if at all, its removal may affect them and what steps they can take to minimise such effects The gallbladder is a pear-shaped organ that rests

beneath the right side of the liver. Its main purpose is to collect and concentrate a

digestive liquid (bile) produced by the liver. Bile is released from the gallbladder after eating, aiding digestion. Bile moves through bile ducts into the gut.

Removal of the gallbladder is not associated with any impairment of digestion in most people, but may cause loose stools.

Gallbladder removal is a major operation with postoperative pain, nausea and vomiting up to 2 days.

Recovery is within 7 days, with follow up in 2-3 weeks.

Explain to a patient the function of the gallbladder, how, if at all, its removal may affect them and what steps they can take to minimise such effects Cholecystectomy can relieve the pain and discomfort of

gallstones Cholecystectomy is the only way to prevent gallstones Contact surgeon if:

Persistent pain, worsening pain Fever >38.3C Continuous vomiting Swelling, redness, bleeding or foul smelling site No vowel movements 2-3 days post-op

Increasing fibre intake should minimise digestive issues Balancing to a healthy weight may help

Discuss the advantages and disadvantages of laparoscopic surgery

5-7 inch incision versus 4 small openings in the abdomen

Patients usually have minimal post-operative pain Patients usually experience faster recovery than

open gallbladder surgery patients Most go home same and quicker return to normal

Severe COPD or CHF may not tolerate CO2 pneumoperitoneum

Gallbladder cancer is only operable by open Common bile duct injury (0.24%)

Regarding laparoscopic cholecystectomy, which of the following is correct?

A. Primarily done for cholecystitis in third trimester of pregnancy

B. Associated with higher rate of bile duct injury than open cholecystectomy

C. Contraindicated in acute cholecystitisD. Safer than open cholecystectomy in patients with

cardiorespiratory disease

Regarding laparoscopic cholecystectomy, which of the following is correct?

A. Primarily done for cholecystitis in third trimester of pregnancy

B. Associated with higher rate of bile duct injury than open cholecystectomy

C. Contraindicated in acute cholecystitisD. Safer than open cholecystectomy in patients with

cardiorespiratory disease

References

MedLine Plus. Updated by: Laura J. Martin, MD, MPH, ABIM Board Certified in Internal Medicine and Hospice and Palliative Medicine, Atlanta, GA. Also reviewed by David Zieve, MD, MHA, Isla Ogilvie, PhD, and the A.D.A.M. Editorial team. Accessed Aug 14 2015. Available from: http://www.nlm.nih.gov/medlineplus/ency/article/002237.htm

John Hopkins Medicine Health Library. Biliary System: Anatomy and Functions Available from: http://www.hopkinsmedicine.org/healthlibrary/conditions/liver_biliary_and_pancreatic_disorders/biliary_system_anatomy_and_functions_85,P00659/

Available from: http://www.clinbiochem.info/studentlft5.html Iron storage. Available from: http://library.med.utah.edu/NetBiochem/hi11b.htm Hyperbilirubinemia and Jaundice. University of Rochester Medical Center Health

Encyclopedia. Available from: https://www.urmc.rochester.edu/encyclopedia/content.aspx?ContentTypeID=90&ContentID=P02375

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When performing biliary drainage and stenting as a palliative treatment for malignant obstructive jaundice. Which kind of equipment is preferable?

A. Plastic retrievable endoprosthesesB. Self-expanding metallic stentsC. Balloon-expanding metallic stentsD. Covered self-expanding stents

When performing biliary drainage and stenting as a palliative treatment for malignant obstructive jaundice. Which kind of equipment is preferable?

A. Plastic retrievable endoprosthesesB. Self-expanding metallic stentsC. Balloon-expanding metallic stentsD. Covered self-expanding stents