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....
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
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
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
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