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1. Today we are going to learn about : 1) Jaundice,Investigations and Management 2) Chronic Liver diseases 3) Cirrhosis 4) Hepatic encephalopathy 5) Esophageal.

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Presentation on theme: "1. Today we are going to learn about : 1) Jaundice,Investigations and Management 2) Chronic Liver diseases 3) Cirrhosis 4) Hepatic encephalopathy 5) Esophageal."— Presentation transcript:

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2 Today we are going to learn about : 1) Jaundice,Investigations and Management 2) Chronic Liver diseases 3) Cirrhosis 4) Hepatic encephalopathy 5) Esophageal diseases & Peptic Ulcer 2

3 Yasir M Khayyat MBcHB,FRCPC,FACP Assistant Professor of Medicine 3

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

5 History :  Age  Onset  Pregnant females  Noticed: by the Patient/Relative  Progression  Associated Symptoms: fever, weight loss,viral prodrome  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 hemolytis disorders,wilson’s disease,Gilbert’s disease,alpha 1 antitrypsin defeciency ) 5

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 6

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8  Prehepaic  Hepatic  Post hepatic  Isolated Disorders of Bilirubin Metabolism  Liver Disease  Obstruction of the Bile Ducts 8

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10  Hemolysis  Viral hepatitis  Alcoholic liver disease  Drugs  Bile duct stones  Pancreatic carcinoma  Liver metastasis 10

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12  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 12

13 Dr. Yasir M Khayyat MBcHB,FRCPC,FACP,ABIM Assistant professor of Medicine Faculty of Medicine Umm AlQura University 13

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 ؟ 14

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

16  50 % over 10 years Compensated Cirrhosis Decompensated Cirrhosis Which is …… Ascites 50 % die in 2 years Variceal hemorrhage Hepatic Encephalopathy 16

17  Development of fibrosis as a consequence of inflammatory reaction at the hepatocytes and the portal triangle 17

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19 Symptoms Complications: Portal hypertension  Hepatic encephalopathy  GI bleeding  Ascites  Lower limbs edema Incidental abnormality of LFT 19

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

21   Gynecomastia due to  hypersestogenemia state  Also spironolactone use Flapping tremor due to False neurotransmitters Causing imbalance at the cerebellar function 21

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 internal mammry veins through the round ligament 22

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27 Autoimmune VascularMetabolicViral Autoimmune hepatitis Portal Vein thrombosis Hemochromatosis Alcohol Primary biliary cirrhosis Hepatic Vein thrombosis Wilson’s disease Inherited Primary sclerosing cholangitis Non Alcoholic Fatty Liver Disease α1antitrypsin deficiency Toxins CCl 4 Aflatoxin 27

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30 InterpretationMarker Exposure to Hepatitis B virus. Present in acute or chronic infection HBsAg Immunity acquired via natural infection or immunisation Anti-HBs antibody Marker of infectivity. It correlates with high level of viral replication HBeAg It correlates with low level of viral replication Anti-HBe antibody Infection in previous 6 months Anti-HBc IgM antibody Distant HBV infection or chronic HBV infection Anti-HBc IgG antibody Rapid viral replication Hep B DNA >105 copies /mL 30

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34  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 : Adrenocortical insuffiency,Endocrine: impotence,hypopitutirism,hypogonadism.  Diagnosis : serum iron,Ferritin.% saturation,Liver biopsy  Treatment : Chelation ( desferoxamine), phlebotomy 34

35  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,gait imbalance,dystonia,rigidity.  Acute liver failure  Acute hemolytic anemia  Diagnosis : serum Cu, 24 h urine Cu collection,serum ceruloplasmin 35

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37  Treatment : Chelating agents ( penicillamine,trientine,Zinc )  Manage acute liver failure 37

38  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, 38

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

40 Treatment :  UDCA : Ursodeocholic acid, mg/kg  Pruritus : Cholestryramine,Rifampin,Naloxone  Liver transplant 40

41 a reversible decrease in neurologic function caused by liver disease 41

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43  Ammonia Hypothesis  γ-Aminobutyric Acid (GABA) Hypothesis 43

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47  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 47

48 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 48

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 49

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. 50

51  A second neuronal sensory network, Meissner's plexus, located within the submucosa, is the site of afferent impulses within the esophageal wall.  These are transmitted to the central nervous system through both vagal parasympathetic and thoracic sympathetic nerves.  Sensory signals transmitted via vagal afferent pathways travel to the nucleus tractus solitarius within the central nervous system; from there, nerves pass to the nucleus ambiguus and dorsal motor nucleus of the vagus nerve where their signals may influence motor function. 51

52 Esophageal Rings  The distal esophagus contains two "rings," the A and B (Schatzki) rings, that demarcate anatomically the proximal and distal borders of the esophageal vestibule  The A (muscular) ring is located at the proximal border. It is a broad (4–5 mm) symmetric band of hypertrophied muscle that constricts the tubular esophageal lumen at its junction with the vestibule.  The A (muscular) ring is located at the proximal border.  can be treated by passage of a 50-F mercury-weighted esophageal dilator or by injection of botulinum toxin

53  The B ring, otherwise known as the mucosal or Schatzki ring, is very common and found in 6% to 14% of subjects who undergo a routine upper gastrointestinal series.  Symptomatic rings that are refractory to dilatation have been treated by endoscopic rupture using either electrocautery or four- quadrant biopsies 53

54  Esophageal webs are congenital anomalies characterized by one or more thin horizontal membranes of stratified squamous epithelium within the upper esophagus and midesophagus. Unlike rings, these anomalies rarely encircle the lumen but instead protrude from the anterior wall, extending laterally but not to the posterior wall  An association between cervical esophageal webs, dysphagia, and iron deficiency anemia in adults (particularly women) has been described as the Plummer-Vinson or Paterson-Kelly syndrome  dilatation be limited in patients with solid food dysphagia to a maximum diameter of a 40-F bougie 54

55 Esophageal motility disorders Hyper motility of LES Hypo motility of LES Unspecified Motility Disorders 55

56  Achalasia is the most recognized motor disorder of the esophagus and is the hallmark example of hypermotility mechanisms.  means "failure to relax" and describes a cardinal feature of this disorder:  a poorly relaxing LES. Causes :  Unknown  viral cause  multisystem disorder 56

57  Abnormalities in both muscle and nerve  The severity of dysphagia fluctuates  severe weight loss could occur  Patients may report the use of postural changes, such as raising the arms above the head, straightening the back, or standing at very erect posture, to increase intraesophageal pressure and improve emptying.  Slow, deliberate swallowing during a meal seems to alleviate retrosternal fullness in some patients 57

58 Diagnosis :  Barium swallow : bird peak appearance,  Manometry classic diagnosis Treatment :  Medical : Nifedipine  Endoscopic : Botulinum Toxin injection  Surgery 58

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60  Typical symptoms :  Heartburn,regurgitation,dysphagia,  waterbrash, globus sensation, odynophagia  Atypical symptoms :  Posterior laryngitis,Asthma,cough,  noncardiac chest pain  Diagnosis : classic presentation, Barium swallow,24 h pH monitoring 60

61 Complications  Erosive esophagitis  Peptic stricture  Barret’s metaplasia  Adenocarcinoma ( 0.1 % in 100,ooo ) 61

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65 Epithelial abnormalities  Pre : mucus, HCO3 secretion  Epithelial : Apical cell membrane,tight junctions,rapid restituition  Postepithelial : mucosal blood flow Hypersecretory states : ZES,Systemic mastocytosis, myeloproliferative disorders Helicobacter pylori Non steroidal Anti inflammatory drugs ( NSAID’s) 65

66  Symptoms : abdominal pain, weight loss,anorexia, symptoms of complications  Signs: no finding unless there is perforation/penetration/bleeding  Investigations : CBC : anemia, Low MCV, Radiology : Barium swallow  Endoscopy : diagnostic and therapeutic for complications 66

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69 Sung J (2006) Current management of peptic ulcer bleeding Nat Clin Pract Gastroenterol Hepatol 3: 24–32 doi: /ncpgasthep0388 Figure 1 Clinical algorithm for the management of peptic ulcer bleeding adopted at the Prince of Wales Hospital, Hong Kong 69

70  The End 70


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