Presented by :
Elaf Ibrahim
Afrah hamroon
Norah Abdurrahman
Badria saad
Reem eid
Supervised by :
Dr.abdullah alatawi
Jaundice
Jaundice is yellow discoloration of the
sclera , skin , and mucus membrane
resulting from an increased bilirubin
concentration in the blood
( more than 3mg/dl )
`
Causes of jaundice
Category Definition
Pre-hepatic: increased bilirubin load for the liver cell
( haemolytic jaundice )
Hepatic: defects in conjugation
( hepatocellular, neonatal jaundice)
Post-Hepatic: Disturbance of excretion.
( Obstructive jaundice )
Types of jaundice
Hemolytic jaundice
Hepatocellular jaundice
Obstructive jaundice
Neonatal jaundice
Haemolytic
jaundice
The increased breakdown of red cells
leads to an increase in production of
bilirubin.
Etiology
Extraerythricyte Intraerythrocyte
Malaria Hemolytic anemia
Autoimmune 1- spherocytosis
Physical trauma ( burn , 2- G6PD- deficiency
prosthetic heart valve ) 3- Thalasemia
Drugs : ( dapsone ) 4- Vit-B12 & Folate
deficiency
Haemolytic
jaundice
Clinical Feature :
Mild Jaundice * why ????
Pallor * Why ??
Splenomegaly
LFT :
increased plasma unconjugated bilirubin ( less than 6mg/dl )
Liver enzyme & Albumen are normal
Urine :
no bilirubinurea * why ??
Increase urinary urobilinogen
Serum :
Low RBCs _ High Reticulocyte _ Low Haptoglobulin
Hepatocellular
jaundice
Liver cell damage leads to an increase in production of
bilirubin
Etiology :
Hepatitis ( Viral _ Autoimmune _ Alcoholic )
Cirrhosis due to any cause
Recurrent idiopathic cholestasis
Pregnancy
Drugs : contraceptive _ anabolic steroids
Leptospirosis
Physiological Neonatal jaundice
Hepatocellular
jaundice
Liver cell damage can cause increased levels of
unconjugated bilirubin in blood due to decreased
conjugation.
The bilirubin that is conjugated is not efficiently
secreted into the bile, but instead diffuses (“leaks”)
into the blood.
So , in hepatocellular jaundice all conjugated &
unconjugated bilirubin will be increased
Hepatocellular
jaundice
Clinical feature :
Jaundice
Fever * why ?
Hepatomegaly
Splenomegaly
Dark urine & normal stool
LFT :
High ALT & AST
Serum :
Conjugated & unconjugated hyperbilrubinemia
Viral markers
prolonged PT * Chronic liver disease *
Decrease Albumin* Chronic liver disease *
Urine :
bilirubinurea
Obstructive
jaundice
It results from obstruction of common bile duct
Etiology :
1)- Common duct stone
2)- Carcinoma in :
head of pancreas
Ampulla
Bile duct ( cholangiocarcinoma )
3)- Traumatic biliary sricture
4)- Cystic fibrosis
Obstructive
jaundice
Clinical features :
Jaundice : intermittent > stone … progressive >> Carcinoma
Dark urine & clay colored * pale * stool
Pruritus
Palpable gallbladder * carcinoma *
Charcot triad ?!
LFT :
increase liver enzymes
Increase Alkaline phosphatase + GGT * role of GGT ?!
Serum :
Conjugated hyperbilrubinemia
Obstructive
jaundice
Urine :
bilirubinurea
Stoole :
Abscent bile pigment
Ultrasound :
Dilated bile duct
Obstructive
jaundice
Late Features :
In prologed obstructive jaundice secondary
malabsorbtion develop due to deficiency of bile salt
Presenting with :
Weight loss
Vit K deficiency ( Bleeding )
Vit D deficiency ( bone pain )
Steatorrhoea
Congenital
hyperbilrubinemia
Unconjugated Conjugated
Gilberts syndrome Dubin-Johnson syndrome
Due to Partial deficiency of
glucorunyle transeferase
Crigel-najjar syndrome Rotor syndrome
Type1 : Abscent glucorunyle
transeferase
Type2 : Partial deficiency of
glucorunyle transeferase
Differential diagnosis of
jaundice
■ Country of origin. The incidence of hepatitis B virus
(HBV) infection is increased in many parts of the world.
■ Duration of illness. A history of jaundice with prolonged
weight loss in an older patient suggests malignancy. A
short history, particularly with a prodromal illness of
malaise, suggests a hepatitis.
■ Recent outbreak of jaundice. An outbreak in the
community suggests hepatitis A virus (HAV).
■ Recent consumption of shellfish. This suggests HAV
infection.
■ Intravenous drug use, or recent injections or tattoos.
These all increase the chance of HBV and hepatitis C
virus (HCV) infection.
Differential diagnosis of
jaundice
■ Blood transfusion or infusion of pooled blood
products Increased risk of HBV and HCV.
■ Alcohol consumption. A history of drinking habits
should be taken
■ Drugs taken
Differential diagnosis of
jaundice
Hepatomegaly.
A smooth tender liver is seen in hepatitis,
but a Knobbly irregular liver suggests metastases.
Shrinking Liver suggests chronic liver disease
Splenomegaly.
This indicates portal hypertension in patients when
signs of chronic liver disease are present
( clubbing _ palmar erythema _ spider nevi _ascites _
Gynecomastia _ pitting edema )
Evaluation of jaundice
-History
-Physical exam
-Labs (LFTs)–ALT, AST,
bilirubin, ALK-P,
albumin, PT
-imaging: US, ERCP, CT
Neonatal jaundice
Newborn infants, particularly
if premature, often accumulate bilirubin,
because the activity of hepatic bilirubin glucuronyl-
transferase is low at birth (it reaches adult levels in
about 4 weeks).
Elevated bilirubin, in excess of the binding capacity
of albumin, can diffuse into the basal ganglia and
cause toxic encephalopathy (kernicterus).
Neonatal jaundice
Treatment:
Newborns with significantly elevated bilirubin levels are
treated with blue fluorescent light.
This light converts bilirubin
to more polar and, so,
water - soluble isomers.
These photoisomers can be
excreted into the bile without
conjugation with glucuronic acid
An 80-year-old African American female with a past medical history
(PMH) of osteoarthritis (OA) is admitted to the hospital with a chief
complaint (CC) of jaundice for 2 months. The patient did not notice
the jaundice or felt any differently but her physician was worried
and she was admitted to a different hospital 2 months ago. The liver
ultrasound (U/S) showed gallstones and she had a laparoscopic
cholecystectomy 2 months ago. After surgery, the jaundice
decreased slightly but then returned.
The reason for her admission to the hospital is the persistent
jaundice. She has no other complaints but itching for 2-3 days.
No abdominal pain, no nausea, vomiting, diarrhea or constipation
(N/V/D/C). She also noticed that her urine has been tea-colored for
the last month. She lost 30 lbs for 1 year despite her good appetite.
Past medical history (PMH):
Osteoarthritis (OA), esophagogastroduodenoscopy (EGD) and
colonoscopy 4 months ago were both reported as normal.
Past surgical history (PSH):
Cholecystectomy 2 months ago, appendectomy and explorative
laparotomy for intestinal obstruction years ago.
Medications:
Celebrex (celecoxib), Arthrotec (diclofenac and misoprostol),
aspirin (ASA).
Family medical history (FMH):
Hypertension (HTN).
Social history (SH):
She quit drinking and smoking 40 years ago.
Physical examination:
Vital signs:
TMP: 36.5
P:86
RR:16
BP:155/66 mmHg.
Normal body weight.
visible skin and scleral icterus.
No stigmata of chronic liver disease.
Abdomen: Soft, not distended, 4 "keyhole" scars from the
laparoscopic cholecystectomy, old laparotomy scar.
The CT of the abdomen showed
nondilated bile ducts and nothing
more in terms of helping us to sort
out the reason for the jaundice.
