1 / 70

Gastroentrology & Hepatology day

Gastroentrology & Hepatology day. Today we are going to learn about : Jaundice ,Investigations and Management Chronic Liver diseases Cirrhosis Hepatic encephalopathy Esophageal diseases & Peptic Ulcer. Jaundice Approach, investigation & management. Yasir M Khayyat MBcHB,FRCPC,FACP

sevita
Download Presentation

Gastroentrology & Hepatology day

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


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

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

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

  4. 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 )

  5. 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

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

  7. 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

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

  9. 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

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

  11. 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 ؟

  12. 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

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

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

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

  16. 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

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

  18. 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

  19. How the liver disease patient present to you

  20. Differential Diagnosis of Ascites

  21. Causes of Chronic Liver diseases

  22. Causes of chronic liver disease

  23. Laboratory markers for HBV infection and its interpretation

  24. Diagnosis of HCV infection

  25. 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

  26. 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

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

  28. 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,

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

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

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

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

  33. Esophageal Diseases

  34. 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

  35. 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

  36. 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

  37. 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 .

More Related