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jaundice
Ami
purohit
• Jaundice, or icterus, is a yellowish discoloration
of tissue resulting from the deposition of
bilirubin.
• The presence of scleral icterus indicates a serum
bilirubin level of at least 51 μmol/L (3 mg/dL)
• Yellow discoloration of skin and sclera(icterus)
and body fluid
• It may arise due to
• 1)increase bile pigment load to liver
• 2)defective conjugation
• 3)defective excretion
The differential diagnosis for yellowing
of the skin is limited
• carotenoderma
• quinacrine
• excessive exposure to phenols
• In jaundice the yellow coloration of the skin is
uniformly distributed over the body, whereas in
carotenoderma the pigment is concentrated on the
palms, soles, forehead, and nasolabial folds.
• Carotenoderma can be distinguished from jaundice
by the sparing of the sclerae.
• Quinacrine causes a yellow discoloration of the skin
in 4–37% of patients treated with
Types of jaundice
Pre hepatic Hepatic Post hepatic
Excessive amount of
billirubin is presented to
liver due to excess
hemolysis
Impaired cellular
uptake,defective
conjugation or abnormal
secretion of billirubin by
liver cell
Impaired excretion due
to mechanical
obstruction to bile flow
Eleveted unconjugated
billirubin in serum
Both conjugated and
uncojjugated billirubin
may be increased in
serum
Eleveted conjugated
billirubin in serum
Diagnostic evaluation
• History and physical examination
• Use of medications,herbal medications,recreational
drugs
• Use of alcohol
• Hepatitis risk( travel,possible parental exposure)
• History of abdominal operation,including GB surgery
• HIV status
• Exposure to toxic substances
• Other important points exposure to people with
jaundice; exposure to possibly contaminated foods;
occupational exposure to hepatotoxins; the duration of
jaundice
Associated symtoms
• A history of fever,perticularly when associated
with chills or right upper quadrant pain/or
history of prior billiary surgery-acute cholangitis
• Anorexia,malaise and myalgias-viral hepatitis
• Right upper quadrant pain –extrahepatic biliary
obstruction
• Acholic stool(clay colored stool)-CBD
obstruction from cancer of pancreatic head or
the duodenal ampulla
Physical examination
• Courvoisier sign
• Signs of liver cell failure/portal hypertension-
ascites,splenomegaly,spider angiomata and
gynecomastia
• Hyperpigmentation:in hemochromatosis
• KS ring in wilson disease
• Xanthoma in primary billiary cholangitis
• Temporal and proximal muscle wasting suggests
long-standing disease such as pancreatic cancer
or cirrhosis
• An enlarged left supraclavicular node (Virchow’s
node) or a periumbilical nodule (Sister Mary
Joseph’s nodule) suggests an abdominal
malignancy.
• Severe right-upper-quadrant tenderness with
respiratory arrest on inspiration (Murphy’s sign)
suggests cholecystitis.
• Ascites in the presence of jaundice suggests
either cirrhosis or malignancy with peritoneal
spread.
Initial laboratory test
• Normal alkaline phosphates and
aminotransferases-
• Not likely due to hepatic or biliary tract disease
• hemolysis or inherited disorders of billirubin
metabolism may be responsible
Some normal values
• Total billirubin: 0.2 – 1.30 mg/dl
• Conjugated billirubin: 0.0-0.3 mg/dl
• Uncongugated billirubin: 0.0-1.10
• Alkaline phosphtase: 38-126u/l
• Serum SGPT: 9-52 u/l
• Predominant alkaline phosphatase elevation:
• Biliary obstruction or intrahepatic cholestasis
• Also found in granulomatous liver disease such
as tuberculosis and sarcoidosis this condition
may or may not be associated with jaundice
Pre dominant aminotransferase
elevation
• Jaundice is caused by intrincic hepatocellular
disease
• Alcoholic hepatitis disproportionate elevation of
the AST(SGOT) compared with ALT(SGPT)
• AST elevation is less than eight times of upper
limitation than normal and ALT elevation less
than five times the upper limit of normal
• AST ALT ratio is greater than 2
• Patients with acute viral hepatitis and toxin-
related injury severe enough to produce jaundice
typically have aminotransferase levels >500
U/L, with the ALT greater than or equal to the
AST.
• While ALT and AST values <8 times normal may
be seen in either hepatocellular or cholestatic
liver disease, values 25 times normal or higher
are seen primarily in acute hepatocellular
diseases
Elevated INR
• Elevated INR that corrects with vitamin K
administartion –impaired intestinal absorption
of fat soluble vitamin and compatible with
obstructive jaundice
• Does not correct with vit K suggest moderate to
severe hepatocellular disease with impaired
synthetic function
• A low albumin level suggests a chronic process
such as cirrhosis or cancer. A normal
• albumin level is suggestive of a more acute
process such as viral hepatitis or
choledocholithiasis
Signs and symptoms
• Early features
yellow discolouration ( skin,sclera)
pale/clay coloured stool
dark urine
pruitis
• Late features
-xanthelmas and xanthoma
-malabsorption-
weightloss,steatorrhea,osteomalacia,incresed
bleeding tendency
hepatocellular obstructive Hemolytic
Abdominal pain absent present Present in crisis
pruritus transient marked Abscent
Past history a.Contact with
jaundice patient
b.drugs
a.Pain
b.Weight loss
c,.surgery
a.Of crisis
b.drugs,blood
transfusion
Examination
Tenderl iver May be present absent Absent
spleen May be present absent Present
Gall bladder Not palpable Palpable if due to
neoplasum
Not palpable
pallor absent present Present
hepatocellular obstructive Hemolytic
Urine:
Bilirubin
urobilinogen
Present
Present
Present
Absent
Absent
present
Stool
stercobilinogen present absent Present
Peripheral smear Leucopenia in
infective hepatitis
normal Reticulocytosis
Spherocytosis
LFT
Billirubin
Alkaline
phosphate
SGOT
++
Raised
Markedly raised
++
Markedly raised
raised
+
Normal
normal
General concepts
Treatment depends on underlying cause
May involve removal of offending agent
Adminstration of antibiotic,antiviral,antifungle
or anti parasitic drug
Surgery to correct blockage
Use of chemotherapy,anti inflamatory
Dietary changes
Or combination of above
Activity should be limited
Case study
• 1. 24 year male suffering from malaria was put
on primaquin. He developed malaise,fatigue and
yellow discoloration of sclera and skin
• Pallor present
• Icterus present
• Febrile
• Hepatosplenomegaly +
Lab investigation
• Hb:5%
• Tlc: 13000
• S.billirubin: 6mg%
• Ven den berg test positive
• Urine : hemoglobin +
• Color of urine brown black
• Probable diagnosis ??
Case 2
• 40 year/female presents with intolerance to fatty
foods,pain in right side of abdomen,yellowing of
eyes and passage of clay color stool
• Lab investigation
• Total billirubin:20%
• Direct billirubin:16%
• Alkaline phosphates: 800 U/L
• SGPT: 90 IU/l
• Urine
• Deep yellow
• Biliirubin++
• Urobillinogen absent
• Stool
• Clay colored
• Stercobillinogen-absent
• Probable diagnosis?
Thank you

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Jaundice

  • 2.
  • 3. • Jaundice, or icterus, is a yellowish discoloration of tissue resulting from the deposition of bilirubin. • The presence of scleral icterus indicates a serum bilirubin level of at least 51 μmol/L (3 mg/dL)
  • 4. • Yellow discoloration of skin and sclera(icterus) and body fluid • It may arise due to • 1)increase bile pigment load to liver • 2)defective conjugation • 3)defective excretion
  • 5.
  • 6. The differential diagnosis for yellowing of the skin is limited • carotenoderma • quinacrine • excessive exposure to phenols • In jaundice the yellow coloration of the skin is uniformly distributed over the body, whereas in carotenoderma the pigment is concentrated on the palms, soles, forehead, and nasolabial folds. • Carotenoderma can be distinguished from jaundice by the sparing of the sclerae. • Quinacrine causes a yellow discoloration of the skin in 4–37% of patients treated with
  • 7.
  • 8.
  • 9.
  • 10.
  • 11.
  • 12. Types of jaundice Pre hepatic Hepatic Post hepatic Excessive amount of billirubin is presented to liver due to excess hemolysis Impaired cellular uptake,defective conjugation or abnormal secretion of billirubin by liver cell Impaired excretion due to mechanical obstruction to bile flow Eleveted unconjugated billirubin in serum Both conjugated and uncojjugated billirubin may be increased in serum Eleveted conjugated billirubin in serum
  • 13. Diagnostic evaluation • History and physical examination • Use of medications,herbal medications,recreational drugs • Use of alcohol • Hepatitis risk( travel,possible parental exposure) • History of abdominal operation,including GB surgery • HIV status • Exposure to toxic substances • Other important points exposure to people with jaundice; exposure to possibly contaminated foods; occupational exposure to hepatotoxins; the duration of jaundice
  • 14. Associated symtoms • A history of fever,perticularly when associated with chills or right upper quadrant pain/or history of prior billiary surgery-acute cholangitis • Anorexia,malaise and myalgias-viral hepatitis • Right upper quadrant pain –extrahepatic biliary obstruction • Acholic stool(clay colored stool)-CBD obstruction from cancer of pancreatic head or the duodenal ampulla
  • 15. Physical examination • Courvoisier sign • Signs of liver cell failure/portal hypertension- ascites,splenomegaly,spider angiomata and gynecomastia • Hyperpigmentation:in hemochromatosis • KS ring in wilson disease • Xanthoma in primary billiary cholangitis • Temporal and proximal muscle wasting suggests long-standing disease such as pancreatic cancer or cirrhosis
  • 16. • An enlarged left supraclavicular node (Virchow’s node) or a periumbilical nodule (Sister Mary Joseph’s nodule) suggests an abdominal malignancy. • Severe right-upper-quadrant tenderness with respiratory arrest on inspiration (Murphy’s sign) suggests cholecystitis. • Ascites in the presence of jaundice suggests either cirrhosis or malignancy with peritoneal spread.
  • 17. Initial laboratory test • Normal alkaline phosphates and aminotransferases- • Not likely due to hepatic or biliary tract disease • hemolysis or inherited disorders of billirubin metabolism may be responsible
  • 18. Some normal values • Total billirubin: 0.2 – 1.30 mg/dl • Conjugated billirubin: 0.0-0.3 mg/dl • Uncongugated billirubin: 0.0-1.10 • Alkaline phosphtase: 38-126u/l • Serum SGPT: 9-52 u/l
  • 19. • Predominant alkaline phosphatase elevation: • Biliary obstruction or intrahepatic cholestasis • Also found in granulomatous liver disease such as tuberculosis and sarcoidosis this condition may or may not be associated with jaundice
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  • 22. Pre dominant aminotransferase elevation • Jaundice is caused by intrincic hepatocellular disease • Alcoholic hepatitis disproportionate elevation of the AST(SGOT) compared with ALT(SGPT) • AST elevation is less than eight times of upper limitation than normal and ALT elevation less than five times the upper limit of normal • AST ALT ratio is greater than 2
  • 23. • Patients with acute viral hepatitis and toxin- related injury severe enough to produce jaundice typically have aminotransferase levels >500 U/L, with the ALT greater than or equal to the AST. • While ALT and AST values <8 times normal may be seen in either hepatocellular or cholestatic liver disease, values 25 times normal or higher are seen primarily in acute hepatocellular diseases
  • 24. Elevated INR • Elevated INR that corrects with vitamin K administartion –impaired intestinal absorption of fat soluble vitamin and compatible with obstructive jaundice • Does not correct with vit K suggest moderate to severe hepatocellular disease with impaired synthetic function
  • 25. • A low albumin level suggests a chronic process such as cirrhosis or cancer. A normal • albumin level is suggestive of a more acute process such as viral hepatitis or choledocholithiasis
  • 26. Signs and symptoms • Early features yellow discolouration ( skin,sclera) pale/clay coloured stool dark urine pruitis • Late features -xanthelmas and xanthoma -malabsorption- weightloss,steatorrhea,osteomalacia,incresed bleeding tendency
  • 27. hepatocellular obstructive Hemolytic Abdominal pain absent present Present in crisis pruritus transient marked Abscent Past history a.Contact with jaundice patient b.drugs a.Pain b.Weight loss c,.surgery a.Of crisis b.drugs,blood transfusion Examination Tenderl iver May be present absent Absent spleen May be present absent Present Gall bladder Not palpable Palpable if due to neoplasum Not palpable pallor absent present Present
  • 28. hepatocellular obstructive Hemolytic Urine: Bilirubin urobilinogen Present Present Present Absent Absent present Stool stercobilinogen present absent Present Peripheral smear Leucopenia in infective hepatitis normal Reticulocytosis Spherocytosis LFT Billirubin Alkaline phosphate SGOT ++ Raised Markedly raised ++ Markedly raised raised + Normal normal
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  • 31. General concepts Treatment depends on underlying cause May involve removal of offending agent Adminstration of antibiotic,antiviral,antifungle or anti parasitic drug Surgery to correct blockage Use of chemotherapy,anti inflamatory Dietary changes Or combination of above Activity should be limited
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  • 35. Case study • 1. 24 year male suffering from malaria was put on primaquin. He developed malaise,fatigue and yellow discoloration of sclera and skin • Pallor present • Icterus present • Febrile • Hepatosplenomegaly +
  • 36. Lab investigation • Hb:5% • Tlc: 13000 • S.billirubin: 6mg% • Ven den berg test positive • Urine : hemoglobin + • Color of urine brown black • Probable diagnosis ??
  • 37. Case 2 • 40 year/female presents with intolerance to fatty foods,pain in right side of abdomen,yellowing of eyes and passage of clay color stool • Lab investigation • Total billirubin:20% • Direct billirubin:16% • Alkaline phosphates: 800 U/L • SGPT: 90 IU/l
  • 38. • Urine • Deep yellow • Biliirubin++ • Urobillinogen absent • Stool • Clay colored • Stercobillinogen-absent • Probable diagnosis?