Gastroentrology & Hepatology day

2. Gastroentrology & Hepatology day Today we are going to learn about : Jaundice ,Investigations and Management Chronic Liver diseases Cirrhosis Hepatic encephalopathy Esophageal diseases & Peptic Ulcer

3. Jaundice Approach,investigation & management Yasir M Khayyat MBcHB,FRCPC,FACP Assistant Professor of Medicine

4. Jaundice : defination • Yellow discoloration of the tissues caused by retention of bilirubin. • Detected when serum bilirubin exceed 3 mg/100 ml.

5. History : • Age • Onset • Pregnant females • Noticed: by the Patient/Relative • Progression • Associated Symptoms: fever, weight loss,viralprodrome • Past medical history: Hem-Liver • Past surgical history: including post operative phase • Previous Drugs/Illict drugs • Previous GI Imaging or Lab works to compare • Family history ( such as hemolytisdisorders,wilson’sdisease,Gilbert’sdisease,alpha 1 antitrypsin defeciency )

6. Physical examination: • General appearance : Wasted/Weak • Vital Signs • Hands : Yellow, Clubbing, vasculitic lesions,SBE • Face : Malnutrition,Icterus,Fetor hepaticus • Trunk : signs of CLD • Abdomen : Ascites,signs of CLD,Splenomegaly,masses • LL : LL edema

8. Causes of Jaundice = Differential diagnosis of Jaundice • Prehepaic • Hepatic • Post hepatic • Isolated Disorders of Bilirubin Metabolism • Liver Disease • Obstruction of the Bile Ducts

9. Isolated Disorders of Bilirubin MetabolismCongugatedhyperbilirubinemiaUncongugatedhyperbilirubinemiaLiver DiseaseAcute hepatocellular dysfunction Chronic hepatocellular dysfunction Hepatic disorders with prominent cholestasis Jaundice in pregnancy Jaundice in the postoperative periodObstruction of the Bile DuctsCholedocholithiasis Diseases of the bile ducts Extrinsic compression of the bile ducts

10. Most Common causes of Jaundice • Hemolysis • Viral hepatitis • Alcoholic liver disease • Drugs • Bile duct stones • Pancreatic carcinoma • Liver metastasis

12. Jaundice Work up • CBC : hemolysis ( Hb , Bilirubin ,LDH • LFT : AlK P, GGT • Hepatitis Virus serology : HBV ( HBsAg , HBeAg ) – HCV (HCV Ab ) – HAV ( IgM,IgG ) • PBC ( AMA , IgM ) , PSC ( MRCP , ERCP ) • Imaging Modalities : Abd US , MRI , MRCP

13. Chronic liver disease Cirrhosishepatic Encephalopathy Dr . Yasir M Khayyat MBcHB,FRCPC,FACP,ABIM Assistant professor of Medicine Faculty of Medicine Umm AlQura University

14. Chronic Liver disease …? • Does this means there is acute liver disease ? Yes ,but its ” acute liver insult “ • Viral • Metabolic • Alcohol • Autoimmune • Vascular • Toxins • Drugs • Inherited disorders سمعوني ايش هي ؟

15. Chronic Inflammation Or Chronic Hepatitis Healing with Fibrosis Or Liver Cirrhosis Acute Liver insult Resolution without Clinical or histological consequences Development of Portal hypertension And Development of stigmata of Chronic Liver disease End Stage liver disease HCC death Compensated State Compensated Cirrhosis Decompensated State Or Decompensated Cirrhosis

16. Natural history of Cirrhosis • 50 % over 10 years Decompensated Cirrhosis Which is …… Compensated Cirrhosis Variceal hemorrhage Ascites 50 % die in 2 years Hepatic Encephalopathy

17. Cirrhosis • Development of fibrosis as a consequence of inflammatory reaction at the hepatocytes and the portal triangle

19. Clinical features Symptoms Complications: Portal hypertension • Hepatic encephalopathy • GI bleeding • Ascites • Lower limbs edema Incidental abnormality of LFT

20. Varices develop in 50-60 % of cirrhotics • Annual rate of development 2-5 % • 30% of them develop UGIB • Risk of rebleeding (2nd bleeding ) 60-70% over 24 months • Death in cirrhotics 1/5 – 1/3 ,due to variceal bleeding

21. Gynecomastiadue to • hypersestogenemiastate • Also spironolactone use Flapping tremor due to False neurotransmitters Causing imbalance at the cerebellar function

22. Caput medusa • due to portal • hypertension with collateral • formation between paraumbilical veins that arise from the umbilical portion of the left portal vein that connect to the epigastric and and internalmammry veins through the round ligament

24. How the liver disease patient present to you

25. Differential Diagnosis of Ascites

26. Causes of Chronic Liver diseases

27. Causes of chronic liver disease

30. Laboratory markers for HBV infection and its interpretation

33. Diagnosis of HCV infection

34. Hemochromatosis • Genetic abnormality ( Autosomal recessive ) leading to iron overload and deposition in organs. • C/F : dark bronze colored skin,Heart : cardiomyopathy,arrythmia , Pancreas : DM, Pancraetitis, Adrenal : Adrenocorticalinsuffiency,Endocrine: impotence,hypopitutirism,hypogonadism. • Diagnosis : serum iron,Ferritin.% saturation,Liver biopsy • Treatment : Chelation ( desferoxamine), phlebotomy

35. Wilson’s Disease • Genetic abnormality in Cu transport within the hepatocytes ( Autosomal recessive ) • C/F : psychiatric : △ social relations, labile emotions, mood disorders,depression,worsening handwriting, • Neuro : dysarthria,dysphagia,drooling,tremors,gaitimbalance,dystonia,rigidity. • Acute liver failure • Acute hemolytic anemia • Diagnosis : serum Cu, 24 h urine Cu collection,serumceruloplasmin

37. Wilson’s Disease • Treatment : Chelating agents ( penicillamine,trientine ,Zinc ) • Manage acute liver failure

38. Autoimmune Hepatitis • Autoimmune inflammation of the hepatocytes • Could be associated with other autoimmune diseases • Presentation : Hepatitis ( Flu like illness ) Diagnosis : • Serum : IgG ( ≥ 1.5 times ) , smooth m Ab + , anti- LKM ≥ 1:80 • Histology : interface hepatitis, portal plasma infiltration. Treatment : Steroids, Azathioprine,

39. Primary biliary cirrhosis • Fatigue • Pruritus (itchy skin) • Jaundice . • Xanthelasmata (focal collections of cholesterol in the skin) Diagnosis : AlkP, GGT, + ANA , + Mitochondrial Ab , + Ig M

40. Primary biliary cirrhosis Treatment : • UDCA : Ursodeocholic acid, 13-15 mg/kg • Pruritus : Cholestryramine ,Rifampin,Naloxone • Liver transplant

41. Hepatic Encephalopathy a reversible decrease in neurologic function caused by liver disease

43. Pathophysiology • Ammonia Hypothesis • γ-Aminobutyric Acid (GABA) Hypothesis

46. Esophageal Diseases

47. Approach to difficulty/painfull swallowing • Onset : sudden ,progressive • Progression : intermittent ( functional ) ,progressive ( mechanical ). • Pain: painful ( odynophagia ) likely esophagitis, ( painless )  pure dysphagia. • Associated symptoms : weight loss( duration ) ,whether the patient is eating well ,regurgitation of the food contents ,choking ( fistula between the esophagus and the trachea) • Any previous : investigations/treatment

48. Approach to difficulty/painfull swallowing Physical examination : • Vital signs, Cachexia appearance, Lymph nodes ,Jaundice ( liver metastasis) • Abdominal exam : masses, tenderness Investigations : • CBC : anemia ( malignancy ,blood loss ) • Electrolytes : low Cl if vomiting, • Barium Swallow /meal : • Manometry : for esophageal motility disorders • Upper endoscopy

49. The esophagus acts as a conduit for the transport of food from the oral cavity to the stomach. • To carry out this task safely and effectively, the esophagus is an 18- to 26-cm hollow muscular tube with an inner skinlike lining of stratified squamous epithelium . • Between swallows, the esophagus is collapsed, but the lumen distends up to 2 cm anteroposteriorly and 3 cm laterally to accommodate a swallowed bolus

50. The smooth muscle portion of the esophageal wall is innervated by both parasympathetic and sympathetic nerves; • parasympathetic nerves regulate peristalsis through vagus nerve . • The cell bodies of the motor neurons of vagus nerves originate in the medulla. • Those located within the nucleus ambiguus control skeletal muscle, and those of the dorsal motor nucleus control smooth muscle. • The former medullary vagal efferent nerves terminate directly on the motor end plate of the skeletal muscle of the upper esophagus, whereas the latter vagal preganglionic efferent nerves to the smooth muscle of the distal esophagus terminate on neurons within Auerbach's (myenteric) plexus, located between the circular and longitudinal muscle layers .