DR TOQEER HUSSAIN
RESIDENT PHYSICIAN
SKBZ CMH MZD AJK
APPROACH TO A
PATIENT WITH
JAUNDICE
What is jaundice?
⚫Yellowish discoloration of skin, sclerae and mucus
membranes due to hyperbilirubinemia
⚫Total bilirubin > 1.5 mg/dl
Types of jaundice
Prehepatic /
Hemolytic
jaundice
Hepatic
jaundice
Posthepatic /
Obstructive/
Surgical jaundice
Family history of liver disease
Alcohol and drug history
Sexual history
Transfusion history
Nutrition history
Exposure to
n Environmental toxins,Persons with
jaundice , Drugs
n Outbreaks or epidemics in the community
n
History of biliary or pancreatic disease.
History
 Shaking chills or fevers point toward cholangitis or bacterial
infection
 Abdominal pain may indicate pancreatic disease, especially if it
radiates to the back
 Right upper quadrant ache point toward Viral hepatitis
 Weight loss, anorexia, nausea, and vomiting are not helpful signs
because most patients with hepatobiliary disease or obstruction have
anorexia and some weight
 Pruritus can be associated with both intrahepatic cholestasis as well
as biliary obstruction.
Cont.....
Age:
• Children and young adults ——› congenital,viral
hepatitis
• < 30 years ——› acute parenchymal disease
• > 65 years ——› stones or malignancies
• 30 - 50 years ——› chronic liver disease
•
Cont.....
 Men are more likely to develop
• Cirrhosis secondary to alcohol
• Pancreatic cancer
• Hepatocellular carcinoma,
• Hemochromatosis
 Women are more likely to have
• Primary biliary cirrhosis
• Gallstones
• Chronic active hepatitis
Cont....
 Shrunken, nodular liver may ——› cirrhosis
 Palpable mass ——› abscess or malignancy
 A liver span >15 cm ——› fatty infiltration, congestion
other infiltrative diseases, or malignancy
 Liver tenderness ——› acute disease but is generally not
helpful
Cont....

Physical Examinition
 Spider angioma
 palmar erythema
 distended abdominal
veins
 jaundice
 Ascites
 jaundice...........>
 Ascites.............>
Indicate
cirrhosis
Acute
hepatitis
Cirrhosis
Malignancy
 Splenomegaly................>
 A palpable, distended
gallbladder ——›
malignant biliary
obstruction
 Asterixis.......................>
 Fever...........................>
Cont....
Infections
Infiltrative diseases
Fulminant hepatic
failure End-stage liver
diseas
Billiary colic
Infection
1. Is the elevated bilirubin conjugated or unconjugated?
2. If the hyperbilirubinemia is unconjugated, is it caused by
n increased production
n decreased uptake
n impaired conjugation
3. If the hyperbilirubinemia is conjugated, is the problem
n intrahepatic or
n extrahepatic?
4. Is the process acute or chronic?
Several questions must be
answered initially
Pre Hepatic/Hemolytic
Jaundice
⚫Excess production of
bilirubin due to excess
breakdown of hemoglobin
⚫Indirect bilirubin
(insoluble in water since
unconjugated)
⚫E.g.
 Hemolytic anemia
 Malaria
 Glucose-6-phosphate
dehydrogenase deficiency
Icterus .………………. Ascites
Hepatic Jaundice
⚫Liver’s ability to conjugate or
excrete bilirubin is affected
⚫Increased level of conjugated
and unconjugated bilirubin
⚫E.g.:
 Hepatitis, cirrhosis,
hepatocellular carcinoma,
prolonged use of drugs
metabolized by liver
 Genetic disorders:
 Usually acquired disease
 Intrahepatic or Extrahepatic (obstructive) cause.
 Acute disease usually can be differentiated from chronic disease
by the patient's history, physical examination, and laboratory tests
 clinical evaluation
n xanthelasma,
n spider angioma,
n ascites,
n hepatosplenomegaly.
 Laboratory evidence of chronic disease
n Hypoalbuminemia,
n Thrombocytopenia,
• uncorrectable prolongation of the prothrombin time.
Conjugated Hyperbilirubinemia
Obstructive Jaundice
⚫Bilirubin formation rate is
normal
⚫Conjugation is normal =
direct bilirubin
⚫Obstruction of bile duct so
exit is blocked
⚫Tumor of the head of the
pancreas
⚫Cholecystitis
(gallstones)
 Chronic cholestasis may arise from
n Cirrhosis,
n Primary sclerosing cholangitis,
n Primary biliary cirrhosis,
n Secondary biliary cirrhosis,
n Carcinoma
n Drugs.
 Acute disease.
n New-onset bilirubinuria
n Fever
n Right upper quadrant pain,
n Tenderness,
n Hepatomegaly,
CONT......
⚫ Complete blood count
⚫ Liver function tests
⚫ BT/CT
⚫ PT/INR
⚫ Serum albumin
⚫ ?blood culture
Lab investigations
 ALT in hepatocyctes
n Indicator of hepatocellular injury
n High ALT↑↑↑, ALP ↑ suggests hepatocellular
 ALP liver/ bile duct/ bone
n Raised in cholestasis
n ALP ↑↑, ALT↑ suggests cholestasis
Help from LFTs
 GGT
n Raised in biliary epithelium/ bile duct obstn
n Raised in alcohol and phenytoin
 ALP and GGT raised →cholestasis
 ALP isolated = not hepatobiliary
Cont....
 Causes
n Prehepatic
• Haemolysis
n Gilberts syndrome (most common)
Jaundiced ALT/ALP normal
Enzymes
⚫ Alkaline phosphatase
 Bone and liver
 Specific for obstructive jaundice
 Released from biliary canaliculi in case of bile duct obstruction
⚫ Aspartate aminotransferase (AST/SGOT)
 Reflects damage to hepatic cell
 Less specific
 May be elevated in MI
 Used with ALT to diffrentiate between heart and liver disease
⚫ Alanine aminotransferase (ALT/SGPT)
 Produced withing the cells of the liver
 Most sensitive marker for liver cell damage
Liver function tests
LFT
Ser.Billirubin 0.2-0.8 mg/dl
Indirect 0.1 – 0.3 mg/dl
Direct 0.2 – 0.7 mg/dl
SGOT (AST) 0-35 IU
SGPT (ALT) 0-35 IU
Alk. Phosph. 30-120 IU
Ser. Protein 5.5 – 8.5 G/dl
Alb 3.5 – 5.5 G/dl
Glob 2.0 – 3.0 G/dl
 Colour of urine and stools
n Normal urine + normal stools = pre-hepatic cause
n Dark urine + normal stools = hepatic cause
n Dark urine + pale stools = post-hepatic cause
(obstructive)
Urine - Jaundice
⚫ Ultrasound:
 More sensitive than CT for gallbladder stones
 Equally sensitive for dilated ducts
 Portable, cheap, no radiation, no IV contrast
⚫ CT:
 Better imaging of the pancreas and abdomen
⚫ PTC- percutaneous transhepatic cholangiogram
 Gives a picture of the intra and extrahepatic biliary
tree
Radiological investigations
 Anti-nuclear antibody
 Anti-smooth muscle antibody
 Immunoglobulins
 Anti-mitochondrial antibody
 hepatitis serologies
 a1-antitrypsin
 iron levels
 Ceruloplasmin
• a-fetoprotein
Second-line tests for jaundice
“focused” or “screen”
⚫ MRCP:
 Imaging of biliary tree comparable to ERCP
 Non invasive
⚫ ERCP:
 Therapeutic intervention for stones
 Brushing and biopsy for malignancy
• Invasive, chances of developing pancreatitis post
procedure
cont.....
How to differentiate the types of
jaundice?
⚫Hemolytic:
 Increased unconjugated (indirect) more than direct
(conjugated) bilirubin
 Hemoglobin level low
 Anemia
⚫Hepatic:
 Increased amount of both indirect and direct
 Increase in AST and ALT more than increase in
ALP
⚫Obstructive:
 Increased amount of direct (conjugated)
 Significant increase in ALP more than AST and
ALT
Patient A
⚫42 year old female with history of general
weakness of 4 months. She was found to
have moderate anemia,
jaundice and mild splenomegaly.
⚫Hemolytic Jaundice
Clinical Findings—Hemolytic
Jaundice
⚫Decreased hemoglobin
 Explains weakness
 Has moderate anemia
⚫Splenomegaly
 Increased activity of reticuloendothelial system
 Site of RBC filtration
⚫Liver Function Tests:
 Increased Serum bilirubin
 Increased load to the liver (increased hemolysis) =>
increased hemoglobin metabolism
 Hemolysis
n Glucose-6-phosphate deficiency
n Pyruvate kinase deficiency
n Drugs
 Ineffective erythropoiesis
 Uridine diphosphate glucuronosyltransferase deficiencies
n Gilbert syndrome
n Crigler-najjar syndromes (i and ii)
 Miscellaneous causes
n Drugs
n Hypothyroidism
n Thyrotoxicosis
n Pulmonary infarct
n Fasting
UnConjugated Hyperbilirubinemia
Etiology
 Acetominophen
 Alcohol
 Amiodarone
 Azulfidine
 Carbenicillin
 Clindamycin
 Colchicine
 Cyclophosphamide
 Diltiazem
 Ketoconazole
• Methyldopa
Common Drugs Associated With Hyperbilirubinemia
(hepatocellular cause)
Patient B
⚫30 year old male with history of fever of 2
weeks, nausea and highly colored urine.
He
had palpable, soft tender liver.
⚫Hepatic Jaundice
Clinical Findings—Hepatic
Jaundice
⚫ Highly colored urine
 Increased amount of bilirubin excretion
⚫ Tender hepatomegaly
⚫ Liver function tests
 High serum bilirubin
 AST and ALT highly increased
 Alkaline phosphatase increased moderately
Seen in both
hepatocellular
jaundice and
cholestatic
jaundice
 Congenital causes
Rotor syndrome
n Dubin-Johnson syndrome
n Choledochal cysts
 Familial disorders
n Benign recurrent
intrahepatic cholestasis
n Cholestasis of pregnancy
 Hepatocellular defects
n Alcohol abuse
n Viral infection
 Sepsis
Conjugated Hyperbilirubinemia
Etiology
 Cholestatic
n
Primary biliary
cirrhosis
n
Primary
sclerosing
cholangitis
n
Biliary
obstruction
n
Pancreatic
disease
 Systemic disease
 Infiltrative
disorders
 Postoperative
complications
 Renal disease
 Drugs
Patient C
⚫35 yr old male with complaints of pain abdomen,
jaundice,itching and passing clay colored
stools.
⚫Previously he was diagnosed with gall bladder stones
but has not taken treatment.
⚫Gall bladder is not palpable.
⚫Obstructive jaundice due to CBD stones.
Patient D
⚫60 yr old male patient with progressive jaundice,
itching, loss of weight .
⚫On palpation gall bladder is palpable.
⚫Obstructive jaundice due to malignancy
⯍ Periampulary carcinoma
Clinical findings in obstructive
jaundice
⚫Deep jaundice
⚫Scratch marks on body
⚫High colored urine
⚫Clay colored stools
⚫Other features
 ?pain
 ?weight loss
 ?palpable gall bladder
 ?ascites
1. CHOLEDOCHOLITHIASIS
2. NEOPLASMS- periampullary carcinomas
3. BILIARY ATRESIA
4.CHOLEDOCHAL CYST
5. LYMPHADENOPATHY-PORTA HEPATIS
• TRAUMATIC- POST CHOLECYSECTOMY
Obstructive jaundice - etiology
 Amitriptyline
 Androgenic steroids (B)
 Atenolol
 Augmentin
 Azathioprine
 Bactrim (D)
 Benzodiazeprines
 Captopril
 Carbamazole
 Cyclosporine
 Danazol (B)
 Dapsone
 Disopyramide
 Erythromycin
 Estrogens (B)
 Ethambutol
• Floxuridine
Drugs Associated With Hyperbilirubinemia
cholestatic cause
Curvoisier’s law
⚫―In a case of obstructive jaundice, if the gall
bladder is palpable, it is unlikely to be due to
stones.‖
⚫Explanation :
Treatment
⚫Choledocholithiasis
 Open / laparoscopic CBD exploration with stone extraction
and T tube placement.
 Endoscopic papillotomy and extraction
⚫Periampularry carcinoma
 Curative – whipple’s procedure
 Palliative –
- endoscopic stenting of ampulla
- bypass prcodures for
a. Food e.g. gastrojejunostomy
b. Bile e.g. choledochojejunostomy
Whipple’s operation
⚫3 structures removed
 C-loop of duodenum
 Head and neck of pancreas
 Pylorus of stomach
⚫3 anastomosis are made
 Gastro-jejunostomy
 Choledocho-jejunostomy
 Pancreatico-jejunostomy
THANK YOU

clinical approch to jaundice.pptx........

  • 1.
    DR TOQEER HUSSAIN RESIDENTPHYSICIAN SKBZ CMH MZD AJK APPROACH TO A PATIENT WITH JAUNDICE
  • 2.
    What is jaundice? ⚫Yellowishdiscoloration of skin, sclerae and mucus membranes due to hyperbilirubinemia ⚫Total bilirubin > 1.5 mg/dl
  • 3.
    Types of jaundice Prehepatic/ Hemolytic jaundice Hepatic jaundice Posthepatic / Obstructive/ Surgical jaundice
  • 4.
    Family history ofliver disease Alcohol and drug history Sexual history Transfusion history Nutrition history Exposure to n Environmental toxins,Persons with jaundice , Drugs n Outbreaks or epidemics in the community n History of biliary or pancreatic disease. History
  • 5.
     Shaking chillsor fevers point toward cholangitis or bacterial infection  Abdominal pain may indicate pancreatic disease, especially if it radiates to the back  Right upper quadrant ache point toward Viral hepatitis  Weight loss, anorexia, nausea, and vomiting are not helpful signs because most patients with hepatobiliary disease or obstruction have anorexia and some weight  Pruritus can be associated with both intrahepatic cholestasis as well as biliary obstruction. Cont.....
  • 6.
    Age: • Children andyoung adults ——› congenital,viral hepatitis • < 30 years ——› acute parenchymal disease • > 65 years ——› stones or malignancies • 30 - 50 years ——› chronic liver disease • Cont.....
  • 7.
     Men aremore likely to develop • Cirrhosis secondary to alcohol • Pancreatic cancer • Hepatocellular carcinoma, • Hemochromatosis  Women are more likely to have • Primary biliary cirrhosis • Gallstones • Chronic active hepatitis Cont....
  • 8.
     Shrunken, nodularliver may ——› cirrhosis  Palpable mass ——› abscess or malignancy  A liver span >15 cm ——› fatty infiltration, congestion other infiltrative diseases, or malignancy  Liver tenderness ——› acute disease but is generally not helpful Cont....
  • 9.
     Physical Examinition  Spiderangioma  palmar erythema  distended abdominal veins  jaundice  Ascites  jaundice...........>  Ascites.............> Indicate cirrhosis Acute hepatitis Cirrhosis Malignancy
  • 10.
     Splenomegaly................>  Apalpable, distended gallbladder ——› malignant biliary obstruction  Asterixis.......................>  Fever...........................> Cont.... Infections Infiltrative diseases Fulminant hepatic failure End-stage liver diseas Billiary colic Infection
  • 11.
    1. Is theelevated bilirubin conjugated or unconjugated? 2. If the hyperbilirubinemia is unconjugated, is it caused by n increased production n decreased uptake n impaired conjugation 3. If the hyperbilirubinemia is conjugated, is the problem n intrahepatic or n extrahepatic? 4. Is the process acute or chronic? Several questions must be answered initially
  • 12.
    Pre Hepatic/Hemolytic Jaundice ⚫Excess productionof bilirubin due to excess breakdown of hemoglobin ⚫Indirect bilirubin (insoluble in water since unconjugated) ⚫E.g.  Hemolytic anemia  Malaria  Glucose-6-phosphate dehydrogenase deficiency
  • 13.
  • 14.
    Hepatic Jaundice ⚫Liver’s abilityto conjugate or excrete bilirubin is affected ⚫Increased level of conjugated and unconjugated bilirubin ⚫E.g.:  Hepatitis, cirrhosis, hepatocellular carcinoma, prolonged use of drugs metabolized by liver  Genetic disorders:
  • 15.
     Usually acquireddisease  Intrahepatic or Extrahepatic (obstructive) cause.  Acute disease usually can be differentiated from chronic disease by the patient's history, physical examination, and laboratory tests  clinical evaluation n xanthelasma, n spider angioma, n ascites, n hepatosplenomegaly.  Laboratory evidence of chronic disease n Hypoalbuminemia, n Thrombocytopenia, • uncorrectable prolongation of the prothrombin time. Conjugated Hyperbilirubinemia
  • 16.
    Obstructive Jaundice ⚫Bilirubin formationrate is normal ⚫Conjugation is normal = direct bilirubin ⚫Obstruction of bile duct so exit is blocked ⚫Tumor of the head of the pancreas ⚫Cholecystitis (gallstones)
  • 17.
     Chronic cholestasismay arise from n Cirrhosis, n Primary sclerosing cholangitis, n Primary biliary cirrhosis, n Secondary biliary cirrhosis, n Carcinoma n Drugs.  Acute disease. n New-onset bilirubinuria n Fever n Right upper quadrant pain, n Tenderness, n Hepatomegaly, CONT......
  • 18.
    ⚫ Complete bloodcount ⚫ Liver function tests ⚫ BT/CT ⚫ PT/INR ⚫ Serum albumin ⚫ ?blood culture Lab investigations
  • 19.
     ALT inhepatocyctes n Indicator of hepatocellular injury n High ALT↑↑↑, ALP ↑ suggests hepatocellular  ALP liver/ bile duct/ bone n Raised in cholestasis n ALP ↑↑, ALT↑ suggests cholestasis Help from LFTs
  • 20.
     GGT n Raisedin biliary epithelium/ bile duct obstn n Raised in alcohol and phenytoin  ALP and GGT raised →cholestasis  ALP isolated = not hepatobiliary Cont....
  • 21.
     Causes n Prehepatic •Haemolysis n Gilberts syndrome (most common) Jaundiced ALT/ALP normal
  • 22.
    Enzymes ⚫ Alkaline phosphatase Bone and liver  Specific for obstructive jaundice  Released from biliary canaliculi in case of bile duct obstruction ⚫ Aspartate aminotransferase (AST/SGOT)  Reflects damage to hepatic cell  Less specific  May be elevated in MI  Used with ALT to diffrentiate between heart and liver disease ⚫ Alanine aminotransferase (ALT/SGPT)  Produced withing the cells of the liver  Most sensitive marker for liver cell damage
  • 23.
    Liver function tests LFT Ser.Billirubin0.2-0.8 mg/dl Indirect 0.1 – 0.3 mg/dl Direct 0.2 – 0.7 mg/dl SGOT (AST) 0-35 IU SGPT (ALT) 0-35 IU Alk. Phosph. 30-120 IU Ser. Protein 5.5 – 8.5 G/dl Alb 3.5 – 5.5 G/dl Glob 2.0 – 3.0 G/dl
  • 24.
     Colour ofurine and stools n Normal urine + normal stools = pre-hepatic cause n Dark urine + normal stools = hepatic cause n Dark urine + pale stools = post-hepatic cause (obstructive) Urine - Jaundice
  • 25.
    ⚫ Ultrasound:  Moresensitive than CT for gallbladder stones  Equally sensitive for dilated ducts  Portable, cheap, no radiation, no IV contrast ⚫ CT:  Better imaging of the pancreas and abdomen ⚫ PTC- percutaneous transhepatic cholangiogram  Gives a picture of the intra and extrahepatic biliary tree Radiological investigations
  • 26.
     Anti-nuclear antibody Anti-smooth muscle antibody  Immunoglobulins  Anti-mitochondrial antibody  hepatitis serologies  a1-antitrypsin  iron levels  Ceruloplasmin • a-fetoprotein Second-line tests for jaundice “focused” or “screen”
  • 27.
    ⚫ MRCP:  Imagingof biliary tree comparable to ERCP  Non invasive ⚫ ERCP:  Therapeutic intervention for stones  Brushing and biopsy for malignancy • Invasive, chances of developing pancreatitis post procedure cont.....
  • 28.
    How to differentiatethe types of jaundice? ⚫Hemolytic:  Increased unconjugated (indirect) more than direct (conjugated) bilirubin  Hemoglobin level low  Anemia ⚫Hepatic:  Increased amount of both indirect and direct  Increase in AST and ALT more than increase in ALP ⚫Obstructive:  Increased amount of direct (conjugated)  Significant increase in ALP more than AST and ALT
  • 29.
    Patient A ⚫42 yearold female with history of general weakness of 4 months. She was found to have moderate anemia, jaundice and mild splenomegaly. ⚫Hemolytic Jaundice
  • 30.
    Clinical Findings—Hemolytic Jaundice ⚫Decreased hemoglobin Explains weakness  Has moderate anemia ⚫Splenomegaly  Increased activity of reticuloendothelial system  Site of RBC filtration ⚫Liver Function Tests:  Increased Serum bilirubin  Increased load to the liver (increased hemolysis) => increased hemoglobin metabolism
  • 31.
     Hemolysis n Glucose-6-phosphatedeficiency n Pyruvate kinase deficiency n Drugs  Ineffective erythropoiesis  Uridine diphosphate glucuronosyltransferase deficiencies n Gilbert syndrome n Crigler-najjar syndromes (i and ii)  Miscellaneous causes n Drugs n Hypothyroidism n Thyrotoxicosis n Pulmonary infarct n Fasting UnConjugated Hyperbilirubinemia Etiology
  • 32.
     Acetominophen  Alcohol Amiodarone  Azulfidine  Carbenicillin  Clindamycin  Colchicine  Cyclophosphamide  Diltiazem  Ketoconazole • Methyldopa Common Drugs Associated With Hyperbilirubinemia (hepatocellular cause)
  • 33.
    Patient B ⚫30 yearold male with history of fever of 2 weeks, nausea and highly colored urine. He had palpable, soft tender liver. ⚫Hepatic Jaundice
  • 34.
    Clinical Findings—Hepatic Jaundice ⚫ Highlycolored urine  Increased amount of bilirubin excretion ⚫ Tender hepatomegaly ⚫ Liver function tests  High serum bilirubin  AST and ALT highly increased  Alkaline phosphatase increased moderately Seen in both hepatocellular jaundice and cholestatic jaundice
  • 35.
     Congenital causes Rotorsyndrome n Dubin-Johnson syndrome n Choledochal cysts  Familial disorders n Benign recurrent intrahepatic cholestasis n Cholestasis of pregnancy  Hepatocellular defects n Alcohol abuse n Viral infection  Sepsis Conjugated Hyperbilirubinemia Etiology  Cholestatic n Primary biliary cirrhosis n Primary sclerosing cholangitis n Biliary obstruction n Pancreatic disease  Systemic disease  Infiltrative disorders  Postoperative complications  Renal disease  Drugs
  • 36.
    Patient C ⚫35 yrold male with complaints of pain abdomen, jaundice,itching and passing clay colored stools. ⚫Previously he was diagnosed with gall bladder stones but has not taken treatment. ⚫Gall bladder is not palpable. ⚫Obstructive jaundice due to CBD stones.
  • 37.
    Patient D ⚫60 yrold male patient with progressive jaundice, itching, loss of weight . ⚫On palpation gall bladder is palpable. ⚫Obstructive jaundice due to malignancy ⯍ Periampulary carcinoma
  • 38.
    Clinical findings inobstructive jaundice ⚫Deep jaundice ⚫Scratch marks on body ⚫High colored urine ⚫Clay colored stools ⚫Other features  ?pain  ?weight loss  ?palpable gall bladder  ?ascites
  • 39.
    1. CHOLEDOCHOLITHIASIS 2. NEOPLASMS-periampullary carcinomas 3. BILIARY ATRESIA 4.CHOLEDOCHAL CYST 5. LYMPHADENOPATHY-PORTA HEPATIS • TRAUMATIC- POST CHOLECYSECTOMY Obstructive jaundice - etiology
  • 40.
     Amitriptyline  Androgenicsteroids (B)  Atenolol  Augmentin  Azathioprine  Bactrim (D)  Benzodiazeprines  Captopril  Carbamazole  Cyclosporine  Danazol (B)  Dapsone  Disopyramide  Erythromycin  Estrogens (B)  Ethambutol • Floxuridine Drugs Associated With Hyperbilirubinemia cholestatic cause
  • 41.
    Curvoisier’s law ⚫―In acase of obstructive jaundice, if the gall bladder is palpable, it is unlikely to be due to stones.‖ ⚫Explanation :
  • 42.
    Treatment ⚫Choledocholithiasis  Open /laparoscopic CBD exploration with stone extraction and T tube placement.  Endoscopic papillotomy and extraction ⚫Periampularry carcinoma  Curative – whipple’s procedure  Palliative – - endoscopic stenting of ampulla - bypass prcodures for a. Food e.g. gastrojejunostomy b. Bile e.g. choledochojejunostomy
  • 43.
    Whipple’s operation ⚫3 structuresremoved  C-loop of duodenum  Head and neck of pancreas  Pylorus of stomach ⚫3 anastomosis are made  Gastro-jejunostomy  Choledocho-jejunostomy  Pancreatico-jejunostomy
  • 44.