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Liver and Pancreas.

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Presentation on theme: "Liver and Pancreas."— Presentation transcript:

1 Liver and Pancreas








9 AST/ALT > 300 < 300 AST/ALT ratio
ABNORMAL LIVER TESTS > 300 Viral, toxin-induced, ischemia, meds < 300 EtOH Hepatitis, cholestasis AST/ALT ratio > 2 = EtOH < 1 = Viral or obstructive



12 Alcoholic Hepatitis Jaundice, fever, ascites, HE, AST/ALT > 2 with AST/ALT < Increased WBC PATH: Steatosis, Fibrosis,Mallory bodies Treatment: If MDF > 32 start prednisone 40 mg X 4 wks After 7 days on steroids if no improvement and Lillie score >.45 Stop Steroids. If steroids are C/I add pentoxifiline to prevent HRS

13 DILI Acetaminophen Antibiotics: Bactrim, Augmentin, E-cin Phenytoin
Valproic acid Immunomodulators INH

14 Viral Hepatitis: Transmission
Fecal-Oral: Hepatitis A and E Sexual: Hepatitis B and D; also C (to a lesser extent) Note: Hepatitis D requires coexisting Hep. B infection

15 Viral Hepatitis: Clinical
Symptoms include fatigue, anorexia nausea and vomiting Lab shows elevated AST/ALT and bili May resolve, turn fulminant, or become chronic

16 Hepatitis A Fecal-oral transmission Symptoms: Adult > children
Transplacental transmission occurs No carrier states, rarely fulminant Can have cholestasis for up to 6 mos Vaccine: Patients with liver dz/risks/ travelers Acute infection: + IgM anti-HAV, Vaccination: + IgG anti-HAV IG prophylactic for Hep A HAV Vaccination 2 doses 6-12 months apart.

17 Hepatitis B Incubation 1-6 months
Transmitted sexually, parenterally, mucous membrane exposure Can present with serum sickness (fever, arthritis, urticaria, angioedema) Associated with polyarteritis nodosa (PAN)

18 Extra intestinal Manifestations of Hep B
Polyarteritis Nodosa Arthritis Glomerulonephritis Urticaria Mixed Cryoglobulinemia Polyneuropathy

19 Celiac arteriogram in PAN
Radiology. 1999;212: , Case 13: Polyarteritis Nodosa-Systemic Necrotizing Vasculitis with Involvement of Hepatic and Superior Mesenteric Arteries1 , Klaus D. Hagspiel, MD, J. Fritz Angle, MD, David J. Spinosa, MD and Alan H. Matsumoto, MD

20 Hepatitis B Serology

21 HBV Scenarios + - HBsAg anti-HBs anti-HBc IgM IgG HBeAg DX
Acute infection Carrier Vaccinated Exposed Immune Acute Window Exposed Ab lost

22 HepB vaccine/prophylaxis
95% of immunocompetent pts develop antibody (anti-HBs) Only 50% of HD pts develop antibody May be given to pregnant pts 3 doses at 1, 2 and 6 months HBIG Alone: sexual contacts of carriers and household members of acute Hep B HBIG + vaccine (exposed is HBsAg negative) blood exposure to pt w/acute Hep B newborns of Hep B mothers HBIG reduces chance of developing chronic infection


24 Interferon: less resistance, more potent, shorter duration
Interferon: less resistance, more potent, shorter duration. Not indicated in decompensated Hep B Hbe Ag + Antiviral to be continued 6 months after the seroconversion Hbe Ag - Antiviral to be continued > 1 year or until HBS Ag seroconverts.

25 Treatment of CHB HBeAg + HBV DNA > 20000, ALT > 2 x ULN
Observe for 6 months and treat if no spontaneous conversion. Consider Liver Bx Rx: Peg IFN o Entecavir, tenofovir, telbivudine Continue Rx for 6 months after seroconversion

26 Treatment of CHB HbeAG – HBV DNA > 20000 , ALT > 2 x ULN RX
Continue till HBsAG loss


28 Hepatitis C Most common liver disease in the US
IVDU, cocaine use, prisons, blood products prior to 1990, tattoo Genotype 1 most common in the US 85 % of Hep C infected become chronic 25% cirrhosis post years of infection 5 %/yr risk to develop HCC in those with cirrhosis 5% sexual transmission over yrs <5% trans placental transmission. HIV co-infection increases transmission rate.

29 Serological Tests Third generation anti-HCV+ >95% sensitive
If high pre-test probability and anti-HCV negative can do PCR testing (more often in renal failure or transplant) Genotype testing required for treatment candidates only

30 Extrahepatic Manifestations
Glomerulonephritis/MPGN Cryoglobulins Porphyria cutanea tarda (PCT) Thrombocytopenia Autoantibody ITP Neuropathy Thyroiditis Sjogren’s Syndrome Inflammatory arthritis



33 Recommended regimen for treatment-naive patients with HCV genotype 1 who are eligible to receive IFN. Daily sofosbuvir RBV plus weekly PEG for 12 weeks is recommended for IFN-eligible persons with HCV genotype 1 infection, regardless of subtype. Recommended regimen for treatment-naive patients with HCV genotype 1 who are not eligible to receive IFN. Daily sofosbuvir RBV for 12 weeks is recommended for IFN-ineligible patients with HCV genotype 1 infection, regardless of subtype.

34 Recommended regimen for treatment-naive patients with HCV genotype 2, regardless of eligibility for IFN therapy: Daily sofosbuvir RBV for 12 weeks is recommended for treatment-naive patients with HCV genotype 2 infection. Recommended regimen for treatment-naive patients with HCV genotype 3, regardless of eligibility for IFN therapy: Daily sofosbuvir RBV for 24 weeks is recommended for treatment-naive patients with HCV genotype 3 infection.

35 Hepatitis D Requires coexistent B Usually found in IVDA
Coinfection: does not worsen acute Hep B or  risk for chronic state Superinfection: frequently severe/fulminant Dx: Anti-HDV IgM

36 Hepatitis E Monsoon flooding Fecal-oral route No chronic forms
Fulminant hepatitis in 3rd trimester of pregnancy

37 A 30 y/o female presents with c/o fatigue,arthralgias,weight loss, amenorrhea. PE reveals Icterus and HSM. No h/o alcohol or drug abuse. No FH of Liver disease.Labs: T.Bili 6mg/dl, AST 300 U/L,ALT350 U/L, ALP 100 U/ml, Albumin 2.9 g/dl. Iron studies are normal. Hepatitis profile and HIV is negative. Which of the following are correct: 1. ANA and ASMA are likely to be positive 2. Liver Biopsy should be done to confirm Dx 3. She will likely respond to steroid therapy 4. All of the above are correct.

38 Autoimmune Hepatitis AIH: Asymptomatic mild disease to Fulminant
Liver failure. Fatigue, Jaundice, Maliase Type I:ANA +, ASMA +, Increased IG,SLA/LP Ab Common in USA Type II: LKM1 Common in Europe, poor prognosis, Rx failures RX: Steroids Immunomodulators.


40 Primary Biliary Cirrhosis
Usually middle aged women Pruritis, fatigue Increased alk phos The clue: elevated Antimitochondrial Antibodies (AMA) Anticentromere antibodies Associated with sicca syndrome and scleroderma Treat with ursodiol

41 Primary Sclerosing Cholangitis
An autoimmune fibrosis of large bile ducts Clinical: RUQ pain, fatigue, weight loss 70% of cases associated with ulcerative colitis Increased risk of cholangiocarcinoma Diagnose with ERCP Beading of the bile ducts on ERCP/MRCP 10-15% get bile duct carcinoma

42 NAFLD NAFLD: Steatosis NASH: Steatohepatitis Characteristics:
Metabolic Syndrome Elevated AST/ALT Liver Biopsy Dx of exclusion: RX: RF Modification Antioxidants Oral hypoglycemics


44 Other liver tests ABNORMAL LIVER TESTS Autoimmune hepatitis (ANA, ASMA, Anti-liver/kidney microsomal, anti-SLA) PBC (AMA) PSC (p-ANCA 70%) Hemochromatosis Iron Saturation >45% Wilsons Disease (low ceruloplasmin, incresed serum and urine Cu) Alfa 1 antitrypsin def

45 Hemochromatosis Most common genetic disease in Caucasians
Iron deposits in liver, heart, pancreas, pituitary, Joints Bronze pigmentation, new onset DM,arthritis,hypogonadism. Can lead to cirrhosis and HCC Iron Sat > 45% Increased Ferritin Abnormal Lft’s HFE gene mutation C282Y and H63D RX: Phlebotomy Goal ferritin < 50

46 Wilson’s Disease Rare Autosomal Recessive d/o 1:30000
Increased cooper uptake and decreased biliary excretion. May present as fulminant liver failure Neuropsychiatry symptoms Increased AST/ALT Low ALP Low Cerruloplasmin Increased urinary copper excretion KF rings on slit lamp


48 Liver Diseases in Pregnancy
1st Trimester 2nd Trimester 3rd Trimester Acute viral hepatitis A-E Hyperemesis GV Gallstones Herpes Hepatitis ICP AFLP Pre-eclampsia HELLP


50 Portal HTN Increased portal blood flow:
Increased cardiac index Splanchnic vasodilation Hypervolemia Increased resistance to portal blood flow: Fixed resistance from fibrosis Dynamic resistance RX: NSBB Octreotide Diuretics TIPS

51 Portal HTN Most common cause is cirrhosis Manifestations:
Hepatic Encephalopathy Gastro-esophageal Varices Ascites

52 Approach to the Patient with Ascites

53 Workup ASCITES Need to know if ascites is CHF, cirrhosis or malignancy (exudate) Serum-ascites albumin gradient > 1.1 = transudate (Portal HTN) If ascites protein > 2.5, then CHF If ascites protein < 2.5, then cirrhosis <1.1 = ascites is NOT from portal hypertension “Higher SAAG = higher pressure”

54 Workup Tap all new ascites
Tap all ascites in cirrhotics with clinical change Labs < 250 cells/μl 1 neutrophil/250 RBC 2 lymphocyte/750 RBC Innoculate cultures at the bedside Gram stain If TB is suspected, you need a peritonal bx

55 Treatment 2g Na restriction/day No benefit in restricting fluids
ASCITES 2g Na restriction/day No benefit in restricting fluids Spironolactone 100mg/day + Lasix 40mg/day Large volume paracentesis TIPS for paracentesis-resistant ascites

56 SBP Translocation of bacteria across they bowel wall into susceptible ascites. Subclinical Fever, Abd pain,encepahlopathy DX: PMN > 250 GN organisms E.coli most common Treat SBP with 3rd generation cephalosporin IV for 5 day and then PO Abx Pplx with oral quinolones after SBP IV Albumin to prevent HRS.


58 Hepatic Encephalopathy
Ppting Factors: GI bleed, SBP, Sepsis, sedatives, constipation, electrolyte abnormalities, acute liver injury, HCC, surgery. RX: Recognize and Correcting ppting factors Correct electrolytes. Lactulose Rifaximin.

59 Hepatorenal syndrome (HRS)
HRS Type I: Rapid decline in renal function HRS Type II: Chronic usually due to refractory ascites. DDX: ATN, Pre-renal DX: Sr Creatinine > 1.5 No improvement after holding diuretics and volume expansion with IV Albumin Absence of shock, hypotension,proteinuria,nephrotoxics Low urine sodium.

60 HRS Rx: Avoiding and holding all nephrotoxics. Hold diuretics
IV Albumin Midodrine and octreotide OLT is the definitive treatment

61 Fulminant Hepatic Failure
Jaundice and hepatic encephalopathy in the absence of chronic liver disease. Acetaminophen is the most common cause in US ( worsened by alcohol, malnutrition and fasting state) Acute viral hepatitis is the most common cause world wide. Other meds: INH, NSAIDS, herbal meds Other causes: AIH, BCS, AFLP, HELLP, Amanita Phalloids

62 Fulminant Hepatic Failure
Complications: Hypoglycemia, Cerebral edema,coagulopathy,infection RX; Supportive care in ICU Early recognition and transfer to the transplant center. NAC for acetaminophen toxicity Acyclovir for HSV hepatitis. Pen G for mushroom toxicity Antiviral for acute hepatitis B

63 Liver Biochemistry Pattern
Disease AP TBili Historical Features Diagnostic Evaluation Primary biliary cirrhosis ↑↑ More common in women, fatigue, pruritus Antimitochondrial antibodies present in 95%, liver biopsy Primary sclerosing cholangitis More common in men, history of inflammatory bowel disease Cholangiography Large bile duct obstruction Pain and fever Drug-induced cholestasis History of drug/medication use within 3 months, often of a drug previously associated with liver injury Improvement with cessation Infiltrative liver disease CT, MRI, liver biopsy

64 Ischemic hepatitis Disease ALT AST History DX Viral hepatitis A ↑↑↑ ↑↑
Liver Enzyme Pattern Disease ALT AST History DX Viral hepatitis A ↑↑↑ ↑↑ Fecal oral exposure (IgM anti-HAV) Viral hepatitis B Blood/body fluid exposure (IgM anti-HBc) and + (HBsAg) Viral hepatitis C Recent intravenous drug use (HCV RNA); variable presence of (anti-HCV) Alcoholic hepatitis Heavy alcohol use, either binge or chr AST:ALT >2, AST usually <500 Drug-induced hepatitis ↑↑↑↑ H/of drug/med use within 3 mo Absence of other liver disease Fatty liver, nonalcohol Late pregnancy, amiodarone History of medication use, absence of other liver disease Ischemic hepatitis Severe hypotension rapid improvement with resolution of hypotension Acute liver failure Ingestion of an associated agent; rapid progression Signs of impaired hepatic synthetic function Alcoholic hepatitis: Absence of other diagnostic markers of liver disease; improvement with cessation of alcohol use Hep C variable presence of (anti-HCV) within the first 3 months after exposure

65 Liver Enzyme Pattern Disease ALT AST Historical Features Diagnostic Findings Viral hepatitis B ↑↑ Fecal oral exposure, endemic area HBsAg; may have hepatitis B DNA (HBV DNA) Viral hepatitis C IVDA, blood tx prior to 1992, Vert Tx , parenteral expos Anti-HCV, HCV RNA Fatty liver, nonalcohol Presence of metabolic syndrome (obesity, insulin resistance, hypertriglycer) Absence of other liver dz imaging shows fat Alcoholic liver disease Remote history of heavy alcohol use Absence of other liver disease Autoimmune hepatitis More common in women Positive , ANA and anti–SMA Hemochromatosis Arthritis, diabetes, family history Ferritin (>1000) and iron sat (>55%), HFE gene mutations Wilson disease Young, movement disorders, psychiatric disease, KF rings Hemolysis, low ALP, low ceruloplasmin α1-Antitrypsin deficiency Lung disease Low serum A1AT, liver biopsy





70 History Pearls Pruritus/Cholestasis Undercooked food, oysters, daycare
ABNORMAL LIVER TESTS History Pearls Pruritus/Cholestasis PBC, PSC Undercooked food, oysters, daycare Hep A ICU, hypotension, Rt. Sided heart failure Hepatic congestion Chronic pancreatitis Stenosis of CBD

71 History Pearls Neurological/Psych findings Metabolic syndrome
ABNORMAL LIVER TESTS Neurological/Psych findings Wilson’s disease Metabolic syndrome Fatty liver Hyperpigmentation Hemochromatosis or PBC Kayser-Fleischer rings and sunflower cataracts

72 History Pearls Splenomegaly Pulsatile liver Hepatic bruits
ABNORMAL LIVER TESTS Splenomegaly Portal HTN or infiltrative process Pulsatile liver Tricuspid insufficieny Hepatic bruits HCC

73 Acute Pancreatitis Alcohol Biliary Tract Disease Trauma Post ERCP
Hyperlipidemia Pancreatic Malignancy

74 Causes of Acute Pancreatitis
Obstructive Gallstones (45%) Pancreas divisum Malignancy Choledochocele Parasites (Ascaris lumbricoides) Toxins/Drugs Alcohol (35%) Azathioprine Sulfa drugs Aminosalicylates Metronidazole Pentamidine Didanosine Metabolic Hyperlipidemia Hypercalcemia Infectious Viral (Cytomegalovirus, Epstein-Barr virus) Parasites (Toxoplasma, Cryptosporidium) Vascular Ischemia Vasculitis

75 Poor Prognostic Indicators In Pancreatitis
SBP < 90 , HR > 130 PO2 < 60 mmHg Urine out put < 50ml/hr or BUN/Cr Elevation GI Bleeding Pancreatic necrosis HCT > 44 CRP > 150 Apache score > 8 Ranson score > 3

76 Complications of Pancreatitis
Sepsis; Necrosis, infected pseudocyst,Abscess Early: Shock, ARDS, GIB, DIC, Uremia,hypocalcemia Splenic infarction & rupture, Pl Effusion. Late: Phlegmon, Pseudocyst, abscess Ascites, Pleural Effusion Splenic Vein thrombosis– GV--GIB

77 Ranson Criteria Admission During 48 hrs Age > 55 WBC > 15K
Glucose > 200 AST > 250 LDH > 350 PO2 < 60 mmHg Drop in HCT > 10 % BUN increases > 5mg/dl Calcium < 8 mg/dl Fluid sequestration

78 Pearls Acute Pancreatitis is a clinical and lab Dx and not imaging
Alcohol and Gall Stones most important causes Prophylactic Abx (Imipenum) in necrotising pancreatitis Early enteral Feeding is preferred.

79 Pancreatic Adenocarcinoma
Risk Factors: Age, Smoking, Chronic pancreatitis,Hereditary pancreatitis, Obesity, Fatty diet Manifestation: Pain radiating to back, Wt Loss, jaundice, Painless jaundice due obstruction of CBD by pancreatic head mass Diagnosis: CT-Scan pancreas protocol, EUS, MRI, ERCP Non-tender palpabale GB (Courvoisier sign) Trousseau syndrome of migrating thrombophelibitis.


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