‫ Jaundice

4th year medical student _ Tabuk University

1. Presented by : Elaf Ibrahim Afrah hamroon Norah Abdurrahman Badria saad Reem eid Supervised by : Dr.abdullah alatawi

2. Jaundice is yellow discoloration of the sclera , skin , and mucus membrane resulting from an increased bilirubin concentration in the blood ( more than 3mg/dl ) Jaundice

3. anatomy

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5. Causes of jaundice Category Pre-hepatic: Hepatic: Post-Hepatic : Definition increased bilirubin load for the liver cell ( haemolytic jaundice ) defects in conjugation ( hepatocellular, neonatal jaundice) Disturbance of excretion. ( Obstructive jaundice )

6. Types of jaundice Hemolytic jaundice Hepatocellular jaundice Obstructive jaundice Neonatal jaundice

7. The increased breakdown of red cells leads to an increase in production of bilirubin . Etiology Haemolytic jaundice Intraerythrocyte Extra erythricyte Hemolytic anemia 1- spherocytosis 2- G6PD- deficiency 3- Thalasemia 4- Vit-B12 & Folate deficiency Malaria Autoimmune Physical trauma ( burn , prosthetic heart valve ) Drugs : ( dapsone )

8. 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 Haemolytic jaundice

9. 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

10. 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

11. 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 Hepatocellular jaundice

12. 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

13. 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

14. Urine : bilirubinurea Stoole : Abscent bile pigment Ultrasound : Dilated bile duct Obstructive jaundice

15. 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 Obstructive jaundice

16. US

17. ERCP

18. Conjugated Unconjugated Dubin -Johnson syndrome Gilberts syndrome Due to Partial deficiency of glucorunyle transeferase Rotor syndrome Crigel-najjar syndrome Type1 : Abscent glucorunyle transeferase Type2 : Partial deficiency of glucorunyle transeferase Congenital hyperbilrubinemia

19. ■ 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

20. ■ 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

21. 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 ) Differential diagnosis of jaundice

22. -History -Physical exam -Labs (LFTs)–ALT, AST, bilirubin, ALK-P, albumin, PT -imaging: US, ERCP, CT Evaluation of jaundice

23. 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

24. 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 Neonatal jaundice

25. Case scenario

26. 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.

27. 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.

28. 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.

29. 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.