Liver Disease
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Liver Disease Liver Disease Presentation Transcript

    • Pascale Gehy-Andre PA-C
    Diseases of the Liver & Biliary System
  • Liver regeneration
    • If individual hepatocytes are destroyed but the architecture of the lobule is not destroyed, the remaining hepatocytes will totally regenerate the liver parenchyma.
    • If whole lobules are destroyed, the remaining lobules will expand. They will function normally, though bile may not be drained quite so well.
    • Of course, if scar tissue alters the flow of blood through the liver (i.e., cirrhosis has occurred), regeneration will only produce less-than-fully-perfused nodules of liver cells.
      • (This will disappoint well-read problem drinkers who understood that their hepatocytes had unlimited capacity to regenerate....)
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  • NORMAL CT SCAN
  • Liver blood supply
    • Blood enters the liver from the hepatic artery and the portal vein and leaves the liver from the hepatic vein .
    • The blood from the artery carries oxygen while the portal vein carries nutrients from the intestine.
  • Functional anatomy
    • The portal vein is formed by the junction of the splenic & superior mesenteric veins.
    • Within the liver, the hepatic artery & portal vein come together with the bile ducts & lymphatics.
    • The branches of all of these vessels extend into the liver into the central lobular vein
  • Functional anatomy
    • The acinus make up the primary functional unit of the portal tract which contains branches of the hepatic artery, bile ducts, branches of the portal vein.
    • Hepatocytes (liver cells) are in the ascini. They contain glycogen. Each cell abuts the sinusoids.
    • The bile canaliculi run between the liver cells forming a network which end up in the bile ducts.
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  • Hepatic Ducts
    • Inside the two lobes is a network of tubes, also called the biliary tree that carries bile from the liver to the intestine.
    • Bile is a substance that helps carry away wastes and is needed for the breakdown and absorption of dietary fats.
    • Each tube is called a duct. Smaller ducts connect to larger ducts. The larger ducts join to form the hepatic duct .
    • This duct network allows bile to drain out of the liver.
  • Gallbladder
    • Concentrate & conduct the 1-1.5L of bile produced by the liver to the intestine
    • Fasting diversion of bile into the gall bladder for storage & concentration
    • Food intake  releases CCK to relax sphincter of Oddi for delivery of bile into the intestine
    • Bile acids & detergents  cholesterol & phospholipids to the intestine.
    • Also solubilizes dietary fat & promotes its digestion & absorption
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  • What Does the Liver Do?
    • The liver has multiple functions:
    • Making bile to help digest foods
      • Bile acid synthesis & secretion
    • Stopping cuts from bleeding (coagulation)
      • Responsible for the synthesis of prothrombin, factor VII, IX, and X from vitamin K absorption .
    • Killing germs, helping keep the body healthy
    • Filtering toxic chemicals from the body
      • Remove waste products of nutrient breakdown
        • Biotransformation, detoxification & excretion of various endogenous & exogenous compounds
  • Role of Liver (cont)
    • Helps with disposing of bilirubin
      • excretes bilirubin into the small bowel so that bowel bacteria can change it into the safe green colored biliverdin.
      • Break down the major nutrients in foods (protein, fats and carbohydrates)
    • Helping to build muscles/ proteins
        • Plasma protein synthesis
        • Lipid & lipoprotein synthesis
    • Glucose homeostasis
  • Role of the liver (cont)
    • Albumin is synthesized exclusively in the liver
        • albumin is essential for carrying molecules (and drugs), and for keeping fluid in the blood vessels.
        • Hypoalbuminemia causes fluid shift into tissue and patient will show signs of edema.
        • albumin decreases in malabsorption & tumor necrosis, or any form of chronic liver disease.
  • Role of the liver (cont)
    • Storing energy
      • Store vitamins A, D, E and K, & B12
  • Liver Physiology
    • Bilirubin is the primary waste product of heme metabolism -degradation of hemoglobin (RBC’s).
    • Unconjugated bilirubin is transported in the plasma bound to albumin .
    • The liver is the major site of metabolism of bilirubin & ammonia
  • Hepatic Physiology (cont.)
    • The metabolism of carbohydrate in the liver is regulated by insulin, glycogen, catecholamines, corticosteroids, & thyroxine
    • Most drugs are metabolized by the liver, microsomal enzymes such as cytochrome p450 system and rendered water soluble
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  • Disorders
    • Liver Function
    • Hepatic Test
    • Jaundice
    • Biliary Tract Disease
      • Cholelithiasis-Choledocholithiasis
      • Cholecystitis-Cholangitis
      • Biliary tract obstruction
    • Hepatic Disease
      • Hepatitis Acute & Chronic A/B/C/D/E, ETOH/drug
      • Cirrhosis
      • Hepatic Failure
    • Neoplasm (later section)
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  • History
    • FHx: Hx of jaundice or liver disease.
    • Social Hx-Recent travel. Exposure to alcohol, Exposure to individuals or animals with liver or parasitic disease. Exposure to alcohol. Multiple sex partners. IV drug use. Exposure to alcohol.
  • Physical exam
    • General:
      • fever & weight loss
    • Cutaneous:
      • spider angiomas, telangiectasias, palmar erythema, jaundice, xanthomas & xanthelasma
    • Endocrine:
      • gynecomastia, testicular atrophy, hypoglycemia
    • G.I.:
      • RUQ pain, abdominal swelling/ascites, heptosplenomegaly, G.I. Bleed
    • Hematological:
      • pale skin/mucous membranes, ecchymoses
    • Neuro:
      • Ataxia, somnolence, confusion, asterixis & obtundation
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  • Tests of liver function
    • Serum albumin (or prealbumin levels):
      • multipurpose serum protein synthesized in the liver.
      • It is decreased when disease is prolonged enough to deplete the blood levels.
      • Albumin is the protein of the highest concentration in plasma.
      • Albumin transports many small molecules in the blood (for example, bilirubin, calcium, progesterone, and drugs).
      • It is also of prime importance in maintaining the oncotic pressure of the blood (that is, keeping the fluid from leaking out into the tissues).
      • This is because, unlike small molecules such as sodium and chloride, the concentration of albumin in the blood is much greater than it is in the extracellular fluid.
      • Because albumin is synthesized by the liver, decreased serum albumin may result from liver disease.
      • It can also result from kidney disease, which allows albumin to escape into the urine.
      • Decreased albumin may also be explained by malnutrition or a low protein diet. 
      • The normal range is 3.4 to 5.4 g/dL.
  • Tests of Liver Function
      • Prothrombin time (PT)-
        • Prolongation of the PT is one of the most sensitive prognosticators of severe liver disease .
        • Tests capacity for protein synthesis
        • It measures the function of the livers clotting ability of factors I (fibrinogen), II (prothrombin), V, VII, and X.
        • When any of these factors is deficient, the PT is prolonged.
          • Coumadin or vitamin K deficiency impair the function
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  • PT (prothrombin time) & INR (international normalized ratio)
    • The normal PT range is 11 to 15 seconds
      • ("normal" varies somewhat in different labs).
    • The normal value for the INR is 1.0
    • Also used for oral anticoagulant monitoring following venous thromboembolism, myocardial infarction, atrial fibrillation or rheumatic heart disease
    • For a person on full anticoagulant therapy, the PT should be 2 to 3 times the laboratory "control" value. INR 2.0-3.0
    • For oral anticoagulant monitoring for those with mechanical heart valves: INR 2.5-3.5
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  • LFT’s/Transaminases
    • Transaminases Aspartate- AST (SGOT) & Alanine- ALT (SGPT) :
      • AST (SGOT)
        • is normally found in a diversity of tissues including liver, heart, muscle, kidney, and brain. It is released into serum when any one of these tissues is damaged.
          • For example, its level in serum rises with heart attacks and with muscle disorders.
        • It is therefore not a highly specific indicator of liver injury.
      • ALT (SGPT)
        • is, by contrast, normally found largely in the liver.
        • This is not to say that it is exclusively located in liver but that is where it is most concentrated.
        • It is released into the bloodstream as the result of liver injury.
        • It therefore serves as a fairly specific indicator of liver
  • AST/ALT
      • status.released into the circulation following hepatocyte injury or death.
    • The ratio of AST:ALT can be helpful
      • AST:ALT > 2:1 suggesting alcoholic liver disease
      • AST:ALT < 1:1 suggesting viral hepatitis.
      • They are sensitive, but non-specific for liver damage.
      • Need isoenzymes
      • The normal range of values for AST (SGOT) is from 5 to 40 units per liter of serum (the liquid part of the blood).
      • The normal range of values for ALT (SGPT) is from 7 to 56 units per liter of serum.
        • Normal range can vary according to a number of factors, including age and gender.
  • AST/ALT
    • The highest levels of AST and ALT are found with disorders that cause the death of numerous liver cells (extensive hepatic necrosis ).
      • Although, the precise levels of these enzymes do not correlate well with the extent of liver damage or the prognosis
    • This occurs in such conditions as acute viral hepatitis A or B, pronounced liver damage inflicted by toxins as from an overdose of acetaminophen (Tylenol), and prolonged collapse of the circulatory system (shock) when the liver is deprived of fresh blood bringing oxygen and nutrients
  • Serum Alkaline Phosphatase- (Alk Phos)
    • Derived from liver, intestines, bones & placenta.
    • Released causing high levels during
      • liver damage, particularly necrosis,
      • cholestasis/ bile duct obstruction,
      • neoplastic,
      • infiltrative & granulomatous liver disease.
    • Need isoenzymes
  • Alk Phos
  • Alk Phos
  • Alk Phos
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  • LFT’s/ Diagnostic Tests
    • Liver biopsy- U/S or CT guided.
      • Valuable in the histological differential, diagnosis & treatment of diffuse or localized parenchymal disease.
      • Generally safe.
      • Must check coagulation values and platelets before procedure secondary to risk of severe hemorrhage.
  • Tests for biliary obstruction/cholestasis &/or hepatocellular damage
    • Serum bilirubin- Balance between bilirubin production and its conjugation & excretion into bile by the liver.
    • Elevated level is not specific for any etiology of liver disease
      • Direct bilirubin (already conjugated by the liver): elevated in intra- or extra hepatic obstruction.
      • Indirect bilirubin (Unconjugated , insoluble): elevated when hemolysis releases it from red blood cells (RBC’s) or in rare genetic deficiencies in conjugating enzymes.
  • Approach to Jaundice
    • Jaundice - yellow/green appearance to the skin & eyes (Icterus) produced by increased serum bilirubin.
    • Usually given in a direct/total relationship
    • Normal Bilirubin ranges 0.5 to 1.0 mg/dl.
    • Levels >3.0 mg/dl to be clinically jaundiced.
      • Newborn period is the exception
  • Bilirubin Metabolism
    • Red cells (Heme) break down forming biliverdin (bile pigment).
    • This is unconjugated (indirect bilirubin).
    • It is transported by albumin & is not soluble.
      • (No Bilirubin in the urine).
    • (i.e., Binding Bilirubin (&quot; indirect&quot;, unconjugated ) to plasma albumin.)
    • The bile pigment is converted to conjugated (Direct bilirubin) by the Kupffer cells of the liver.
    • In the liver, the bilirubin is conjugated
      • with UDPglucuronate, making it water-soluble Bilirubin diglucuronide,
    • i.e. (&quot;direct&quot; conjugated bilirubin).   
    • This is soluble & only shows up in blood & urine with obstruction in the system.
  • Bilirubin conjugation
    • In the terminal ileum the bilirubin is converted to stercobilinogen & urobilinogen by natural bacteria.
    • Conjugated bilirubin is excreted into the bile and passed into the intestine where it is further metabolised: urobilinogen ->urobilin-> stercobilin , which colors the feces brown .
    • Some is reabsorbed and returned to the liver.
    • Some urobilinogen is found in the urine.
    • If excretion of conjugated bilirubin is hindered, it is excreted by the kidney.
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  • Bilirubin Metabolism
    • Pre-hepatic jaundice
      • Hemolytic disease
    • Post hepatic jaundice
      • Hepatitis
      • Drug induced hepatitis
      • Cirrhosis
    • Notes:
      • Obstruction of biliary system prevents production of urobiligen & stercobilinogen
        • Stool is light and urine is dark showing bilirubin
  • Hyperbilirubinemia
    • Diseases that elevate blood levels of bilirubin fall into one of these four categories of disorder:
      • 1. Increased bilirubin production
      • 2. Decreased bilirubin uptake by the liver
      • 3. Impaired conjugation in the liver
      • 4. Decreased excretion of bilirubin into the bile (cholestasis)
    • The first 3 types listed are unconjugated (indirect)= normal stool and urine color.
    • The 4 th (decreased excretion/ cholestasis) shows increased conjugated bilirubin (direct) with dark urine and light stool color.
  • Unconjugated (Indirect) hyperbilirubinemia
    • Due to overproduction, decreased hepatic uptake or decreased conjugation of bilirubin
      • 1. Overproduction 2 0 hemolysis (autoimmune), ineffective erythropoiesis (megablastic anemia), increase RBC fragility/turnover (2,3 DPG deficiency)
      • 2. Impaired hepatic uptake : Gilbert’s syndrome & certain drugs such as rifampin, anesthetics & radiographic dyes
  • Unconjugated (Indirect) hyperbilirubinemia
    • 3. Impaired conjugation : Hepatocellular disease, drug inhibition such as chloramphenicol, anabolic steroids, genetic disorders such as Gilbert’s syndrome or Crigler- Najjar syndrome (decreased UDP-glucuronyl transferases).
  • Unconjugated (Indirect) hyperbilirubinemia
    • The most common cause of jaundice is neonatal jaundice
      • They do not have a significant quantity of glucouronyl transferase (the enzyme used for conjugation), due to enzyme immaturity, but kicks in within a few weeks.
    • Bilirubin is very toxic to the neonatal brain ( kernicterus ), UV light is used to isomerize the bilirubin, which prevents it from crossing the blood-brain barrier.
      • Common causes of neonatal jaundice Rh disease/ABO incompatibility is hemolytic and also impaired hepatic intake.
      • Kernicterus: is a type of brain damage that causes athetoid cerebral palsy and hearing loss. It also causes problems with vision and teeth and sometimes can cause mental retardation.
  • Conjugated (Direct) hyperbilirubinemia
    • 4. Due to Altered biliary drainage, impaired hepatic excretion of bile, or extra hepatic obstructions :
      • A. Altered biliary drainage of bile (TPN, cholestasis, drugs), hepatocellular disease, cirrhosis.
        • May occur in setting of cholestasis with impaired formation or excretion of all components of bile or hepatocellular injury independent of cholestasis.
        • May indirectly cause increase in unconjugated also if severe enough
        • **You will have change in color of stool and urine**
  • Conjugated (Direct) hyperbilirubinemia
      • B. Impaired hepatic excretion : intrahepatic cholestasis- Dubin-Johnson syndrome & all disorders in the transport of conjugated bile from the hepatocytes to intrahepatic bile ducts.
        • Drug-induced cholestasis-phenothiazines, OCP’s & methyltestosterone.
      • C. Extra hepatic : Gallstones, pancreatic/biliary obstructive tumors, strictures & biliary atresia
    • ** Dark brown or green urine implies conjugated hyperbilirubinemia
  • Causes of Conjugated (Direct) hyperbilirubinemia
    • Cholestatic jaundice- -Increased alk phos to 3-4 times normal.
      • Hypercholesterolemia, pruritus, malabsorption of fat & fat-soluble vitamins.
      • Minimal or marked evidence of liver cell damage.
    • Determine mechanism involved:
    • Hx : pale stools & pruritus--> cholestasis.
      • & nausea--> gallstones = biliary obstruction.
      • Inquire about drugs & alcohol use, risks for viral hepatitis & pre-existing liver disease.
    • Laboratory :
      • biliary obstruction : <5-10 fold increase in transaminases & >2-3x normal alk phos .
      • Hepatocellular disease : >10-15 fold increase in transaminases & < 2-3x normal alk phos.
    Diagnosis of conjugated hyperbilirubinemia
  • Disorders of the Biliary System
    • Sepsis -
      • mainly gram-negative organisms.
      • Mildly elevated serum alk phos
    • Post-op jaundice- - 1-10 days post-op.
      • 15% incidence following heart/ 1% elective abdominal surgery.
      • Increased alk phos & minimally elevated levels of transaminases.
      • Secondary to anesthesia side effects
    • Hepatocellular disease (hepatitis, cirrhosis ) –
      • elevated transaminases, prolonged PT, hypoalbuminemia & clinical features of hepatic dysfunction.
    • Extrahepatic biliary obstruction–
      • obstruction of extra hepatic bile ducts--gallstones, neoplasias, bile duct strictures, chronic pancreatitis.
      • Clay-colored stools .
  • Special diagnostic procedures in cholestatic jaundice
    • Extra hepatic obstruction : CT or U/S to determine stone or bile duct dilation.
    • Bile duct dilation : endoscopic retrograde cholangiography (ERCP) for management & treatment.
    • Liver biopsy : for determining cause of intrahepatic cholestasis.
  • Hyperbilirubin Mneumonic
    • &quot; HOT L iver&quot;: H emolysis O bstruction T umor L iver disease
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  • Hepatitis
    • The word &quot;hepatitis&quot; means inflammation of the liver.
    • It can be caused by a number of agents, including bacteria, drugs, toxins and excess alcohol , but of serious concern is hepatitis that results when any one of several hepatitis viruses infect the liver.
  • Hepatitis Causes
    • 1. Virus
      • A. Hepatitis A (HAV)
      • B. Hepatitis B (HBV)
      • C. Hepatitis C (HCV)
      • D. Hepatitis D (HDV)
      • E. Hepatitis E (HEV)
      • F. Cytomegalic (CMV)
      • G. Epstein-Barr (EBV)
    • 2. Toxins
    • 3. Alcohol
    • 4. Other diseases
    • a. Wilson’s disease
    • b. Leukemia
    • c. Lymphoma
    **Hepatitis E & A are fecal-oral (f E c A l –oral) **While Hep B,C,D are blood borne (parenteral) “ C oming in the B ack D oor”
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  • Acute Hepatitis
    • Hepatitis can be defined as a constellation of signs & symptoms resulting from inflammation & hepatic cell necrosis
    • In a previously asymptomatic individual the term “ acute ” is applied
    • Virus is the most common cause of hepatitis .
      • Only occasionally can bacterial infections like syphilis or TB be considered
    • Most cases of acute hepatitis are sub-clinical & usually undiagnosed
  • Acute Hepatitis
    • The different types of hepatitis cannot be distinguished clinically & their distinction depends upon serological testing
    • Histologically they are all the same:
    • Classically the histological appearance of acute hepatitis is liver damage & necrosis in the centrilobular area
    • Mild edema occurs in the portal tracts with some degree of cholestasis causing jaundice, depending on the degree of obstruction
  • Acute Hepatitis
    • The hepatic cells undergo degeneration with some scarring
    • Most cases only have minimal damage & go on to complete recovery
    • Some cases progress to liver failure and death
  • Symptoms of Hepatitis
    • Malaise
    • Nausea
    • Anorexia
    • Fatigue
    • Vomiting
    • Diarrhea
    • Low grade fever
    • Rash
    • Arthralgias
  • Clinical findings of Hepatitis
    • Tenderness of the liver
    • Hepatomegally on occasion
    • Dark urine
    • Jaundice
  • Laboratory Tests (LFT’s)
    • Bilirubin elevated
    • SGPT (ALT) (very specific for liver)
    • SGOT ( AST) (not as specific)
    • Alkaline phosphatase (alk phos)
      • Nonspecific- represents obstruction of liver
        • Can be elevated in bone ds. or child growth
    • PT,PTT (elevated c ~55% liver destruction)
    • Hypoglycemia
    • Serum markers for viral hepatitis
        • Anti-HAV (IgM-IgG) HBsAg
        • HBeAg Anti-HBc (IgM-IgG)
        • Anti-HBe Anti-HBs
        • Anti-HCV Anti-HDV
    • Monospot, Heterophile
    • (also do Urinalysis)
  • Complications of Hepatitis
    • 1. Massive hepatic necrosis (1%)
      • Usually in B,C,D,E
    • 2. Chronic Hepatitis
    • 3. Cholestatic Hepatitis Syndrome
      • Pruritis
      • Dark urine
      • Light stools
      • Hyperbilirubinemia
      • Alk phos elevation
  • Don’t complain about the seating arrangements
  • Mononucleosis Epstein-Barr Virus (EBV)
    • Age: 15-25 yo “ Kissing Disease”
    • Symptoms:
      • Fever Hepatosplenomegally
      • Malaise** Lymphadenopathy*
      • Loss of appetite Sore throat**
      • Nausea/Vomiting Rash (maculopapular)
      • Fatigue Abd pain
      • Jaundice Headache**
      • **Most common symptoms
  • Mononucleosis (EBV)
    • Maculopapular rash:
    • NEVER GIVE AMPICILLIN FOR SORE THROAT TO MONO PATIENT  causes rash
  • Mononucleosis (EBV)
    • Key Signs:
      • Fever
      • Exudative Pharyngitis
      • Lymphadenopathy
      • Splenomegaly
  • Mononucleosis Epstein-Barr virus
    • Labs
      • 1. CBC
        • shows a relative lymphocytosis
          • Atypical lymphocytes
        • Reduction in platelet count
      • 2. Mono spot test Heterophile
      • 3. EBV specific serology
        • IgM specific IgG confirms prior illness
      • 4. Transaminase elevated slightly (AST/ALT)
  • Mononucleosis (EBV)
    • Complications-
      • Bacterial pharyngitis
      • Upper airway obstruction
      • Bells palsy
      • Ruptured spleen
  • Mononucleosis (EBV)
    • Treatment-
      • Supportive therapy
      • Tylenol for fever and malaise
      • Antibiotic if bacterial pharyngitis is present
        • Avoid ampicillin (RASH)
      • Steroids for severe pharyngitis & fever
        • 40-60 mg of prednisone/day
      • Activities reduced- no contact sports for 6 weeks
  • Cytomegalic Virus
    • Similar to EBV in many ways
    • No pharyngitis or respiratory symptoms
    • Atypical lymphocytes
    • Abnormal liver function studies
    • Diagnosis made by CMV titers
    • Transmitted in same manner as mono
    • more common in transplant and AIDS patients.
    • **If mono test neg  due CMV titer
  • Hepatitis A
    • Approximately 25% of all cases of hepatitis
    • Less morbidity & mortality
    • Contact by fecAl-oral route
    • Incubation period 2-6 weeks (shortest)
    • Symptoms: (more severe sx than mono)
      • Malaise Abd pain
      • Fever Jaundice
      • Hepatosplenomegally(25%) Diarrhea
      • Anorexia
    • ** h/o eating clams, out of country travel, etc.
  • Hepatitis A (cont)
    • Duration: 4 weeks
    • Complications: rare (no chronic type)
    • Lab:
      • SGOT  , SGPT  , Bilirubin  ,
      • HAV IgM, HAV IgG
    • Treatment:
      • Good nutrition
      • No alcohol
  • Hepatitis A (cont)
    • Prophylaxis:
      • Administration of Gamaglobulin
        • effective in prevention (prior to exposure)
      • Post exposure: is recommended for household & sexual contacts within two weeks, plus Hepatitis A vaccine
      • Travelers: recommended in normal dose for 2 mo stay, and triple dose for 4-6 mo stay
      • Hepatitis A vaccine given 15 days prior to travel, followed by 6 mo later
  • Hepatitis B
    • Incubation: 1-6 months
    • Symptoms: same as Hep A, but even more severe
    • Contact: Parenteral inoculation, sexual (blood or mucus membrane)
  • Hepatitis B
    • Course:
      • 90% recover
      • 10% develop chronic hepatitis (with HBsAg carrier state)
      • A small amount go onto chronic progressive hepatitis which goes on to cirrhosis
      • 1% develop a fulminate course
    • Lab tests:
      • SGPT (ALT) & SGOT (AST) rise with symptoms
      • Bilirubin & alk phos
      • PT, PTT
      • **(all these labs are higher than in HAV)
  • Hepatitis B (Lab continued)
    • Serological tests :
      • HBcAg : disappears soon after the peak of ALT
      • HBeAg : Positive in acute HBV
      • HBsAg : positive in acute & chronic
      • Anti-HBs : + in late acute HBV and immunized (protective)
      • HBeAb : appears when antigen decreased
      • HBcAb :
        • IgM marker for acute infection.
        • IgG chronic HBV & carrier
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  • Serologic Markers:
    • HBsAg: First virologic marker detectable in serum in acute HBV infection ;
    • precedes elevations of liver enzymes and clinical symptoms.
    • Usually detectable 4 weeks after infection and typically disappears at 6 months after active infection.
    • Persistence of HBsAg beyond 6 months implies chronic HBV infection .
  • Serologic Markers:
    • Anti-HBs : Appears shortly after HBsAg disappears from serum and persists indefinitely in patients who have recovered from acute infection .
    • Anti-HBs is felt to be the protective antibody against HBV infection; thus, vaccine consists of nonglycosylated HbsAg particles that are safe and highly immunogenic, thereby inducing active immunity.
  • Serologic Markers: (cont)
    • HBcAg : Not detectable in serum
  • Serologic Markers: (cont)
    • Anti-HBc :
      • IgM
        • appears at 1 to 2 weeks after the appearance of HBsAg ;
        • its detection in serum is indicative of acute HBV infection .
        • It is the only marker of acute HBV during the window period between the disappearance of HBsAg and the appearance of anti-HBs in serum .
        • IgM predominates for the first 6 months following acute infection but may persist up to 2 years.
      • IgG
        • predominates after 6 months and generally persists indefinitely in patients who have recovered from HBV infection.
        • Present in virtually all patients who have ever been exposed to HBV
    • HBeAg:
      • Considered to be a marker of active virus replication and infectivity ;
      • also correlates with detection of HBV DNA in serum.
      • Usually appears with or after the appearance of HBsAg in serum and disappears shortly after peak elevations in serum aminotransferase activity in acute infection.
      • In chronic infection, HBeAg may persist for years prior to seroconversion to anti-HBe ;
      • its presence is indicative of the replicative stage of HBV infection, which represents a time of maximal infectivity and liver injury.
      • Likelihood of perinatal transmission correlates with presence of HBeAg: ~90% of HBeAg-positive mothers transmit HBV to their offspring but only 10-15% of anti-HBe positive mothers do so.
      • In a small subset of patients with acute HBV infection, HBeAg is not detected because of a viral mutation; in such patients, HBV DNA levels are elevated, representing the replicative stage of the virus.
  • Serologic Markers: (cont)
    • Anti-HBe:
      • Appears after seroconversion of HBeAg to anti-HBe.
      • Its presence in chronic HBV infection signals the onset of the nonreplicative phase , where HBV DNA becomes undetectable in serum and liver injury tends to subside.
      • Generally exists in serum indefinitely unless seroconversion back to HBeAg occurs.
  • Serologic Markers: (cont)
    • HBV DNA:
      • Probably the most reliable indicator of active viral replication .
      • Can be detected by hybridization methods or PCR.
      • Recovery from acute HBV infection is accompanied by the disappearance of HBV DNA from serum ; however, very low levels may remain detectable by PCR.
      • Persistence of HBV DNA implies chronic infection .
      • Useful in predicting response to interferon therapy ;
        • high pretreatment HBV DNA levels > 200 pg/ml by hybridization assay are predictive of poor response to interferon.
        • Also, clearance of HBV DNA is used as an endpoint in assessing response to treatment.
  • Immunization for HBV (with HBsAg) - - - + - Low-level HBsAg carrier or remote past infection +/- - IgG - - Recovery from HBV infection +/- - IgG + - Acute HBV infection (anti-HBc window) +/- +/- IgM - - Heterotypic anti-HBs with HBsAg; usually indicates chronic HBV carrier state +/- +/- + + + Late-acute or chronic HBV infection, low infectivity + - IgG - + Chronic HBV, high infectivity - + IgG - + Acute HBV, high infectivity - + IgM - + Interpretation Anti-HBe HBeAg Anti-HBc Anti-HBs HbsAg
  • Screening
    • Screening for acute viral hepatitis:
      • anti-HAV IgM
      • HBsAg
      • anti-HBc IgM
      • anti-HCV
    • Screening for chronic viral hepatitis:
      • HBsAg
      • anti-HCV
      • if + HBsAg then check HBeAg
      • +/- HBV DNA.
    • Chronic hepatitis B is characterized by the persistent presence of HBV DNA and usually HBeAg in the serum;
    • remissions are characterized by the disappearance of HBV DNA and HBeAg from serum despite the persistence of HBsAg.
  • Hepatitis B
    • Treatment:
      • After exposure:
        • give hepatitis B immunoglobulin (IG) +
        • active immunization with HBV vaccine (Combivax) in any patient who is:
          • Stuck by a needle
          • Within 14 days of sexual exposure
          • An infant born to a mother HBsAg positive
      • Preventative to:
        • Health care workers
        • Homosexual men
        • Household & sexual contacts of HBsAg carriers
  • Hepatitis B
    • Follow up:
      • Recheck in 3 months if tests are normal
      • A liver biopsy if patient appears to have chronic hepatitis
      • Keep in mind patients with chronic hepatitis B can develop hepatocellular carcinoma
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  • Hepatitis C
    • (Blood) Parenteral
      • Associated with transfusion in 85% of the time
      • inoculation from drug abuse
    • 50-70% go onto chronic hepatitis which can lead to cirrhosis of the liver 20% of the time
    • Incubation is 5-10 weeks
    • Anti-HCV (antibody to the C virus) is 70% accurate
    • Hepatitis C account for 80-90% of the Non A, Non B hepatitis
  • Hepatitis C
    • New serologic test for Hep C
      • Anti-HCV if present indicates the presence of viremia (80%)
      • + HCV plus  ALT (SGPT) is confirmatory
      • A second generation recombinant immunoblot assay (RIBA) is used for confirmation.
      • Polymerase chain reaction (PCR) is used in equivocal cases, but is not + for at least 6-8 weeks (this is a test to specifically find the HCV RNA virus)
  • Hepatitis C
    • Treatment:
      • The patient is given alpha interferon for the chronic infection 3 x’s/ wk for 6 months
      • What is interferon:
        • 30% of circulating lymphocytes are B cells & 70% are T cells
          • B cells produce immunoglobulins that produce antibodies
          • T cells produce cytokines (hormone like proteins) that bind to the target cells. There are many kinds, one of which is interferon which limit viral replication.
  • Hepatitis C treatment (cont)
    • The latest treatment is 6-12 mo of combination therapy using a-2b interferon plus ribavirin
    • The cure rate varies around 40% with no HCV detectable 6 mo after cessation of treatment
    • Do not use if the patient is depressed or on alcohol (must be off ETOH x 6 mo)
  • Hepatitis C
    • Recommendations:
      • Treatment is worth considering on selective basis on some patients with mild liver disease
      • Patients with geno type 2 or 3; treatment is stopped at 6 mo. Cure rate 50-70% to 90%
      • Patients with geno type 1 is less responsive with overall cure rate of 27%
    • Toxicity:
      • Ribavirin can cause hemolytic anemia
      • Interferon causes depression
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  • Hepatitis D
    • Requires HBV for its replication
    • Incubation 4-6 weeks
    • Can accelerate chronic hepatitis B to cirrhosis
    • Anti-HDV become positive in 12-15 weeks
    • Hepatitis B vaccine is preventative
    • Treatment poor. Interferon can be tried
    • **Must have B to get D**
  • Hepatitis E
    • Found mostly in India, Asia, Mexico, Africa
    • Usually water borne (fEcal- oral)
    • Incubation 2-9 weeks
    • All cases in US have been imported by immigrants
    • HEV antibodies found in blood
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  • Alcoholic Hepatitis
    • An acute or chronic illness involving the liver with necrosis, inflammation & scarring
    • 95% develop a fatty liver which is a reversible process
    • Encephalopathy & death 20%
    • 30% go on to cirrhosis within 6 mo
    • 50% of those abstaining for 6 mo recover completely
  • Alcoholic Hepatitis Symptoms
    • Most patients are symptomatic. The most common complaints are:
      • Anorexia, nausea, vomiting
      • Abdominal pain (RUQ)
      • Fever (due to infection or inflammation of liver)
      • Weight loss due to anorexia
      • Jaundice is usually mild
      • Diarrhea which is due to portal hypertension
  • Alcoholic Hepatitis Physical Findings
    • Jaundice
    • Spider angiomas
    • Palmar erythema
    • Clubbing of fingers
    • Gynecomastia
    • Hepatomegaly
    • Splenomegaly
    • Pruritis
    • Ascites
    • Edema
    • Caput medusa
    • Testicle atrophy
    • Dark urine, light stool
  • Alcoholic Hepatitis Damage to liver causes
    • Hepatic insufficiency: which is responsible for the following:
      • Coma
      • Jaundice
      • Ascites
      • Anemia
      • Hemorrhagic tendency
      • Ankle edema
    • Hyperestrinism: which is responsible for:
      • Spider nevi
      • Alopecia
      • Gynecomastia
      • Palmar erythema
      • Testicle atrophy
  • Alcoholic Hepatitis Damage to the Portal System
    • Portal Hypertension: causes the following:
      • Esophageal varices
      • Splenomegaly
      • Caput medusa
      • Ascites
    • Hypersplenism: causes the following:
      • Anemia
      • Leukopenia
      • Thrombocytopenia
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  • Alcoholic Hepatitis Diagnostic Studies
    • A. Laboratory Test:
      • The SGOT (AST) 2-10x’s normal
      • SGPT (ALT) is less elevated
      • Bilirubin mild to moderate
      • Alk phos is usually 2-3x’s normal
      • Globulins elevated with reverse A/G ratio
      • Prothrombin time elevated (poor prognosis)
      • Leukocytosis
      • Blood NH3 (Ammonia) level
  • Alcoholic Hepatitis Diagnostic Studies
    • B. Ultrasound
    • C. Liver Biopsy
      • To be done early, but not to be done if PT/PTT are elevated
      • Microscopic exam confirms the diagnosis
      • Findings of biopsy
        • Hepatocellular necrosis
        • Inflammatory exudates
        • Fibrosis
        • Fatty infiltration
        • Cholestasis
        • Hemosiderosis (iron accumulation in the lungs)
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  • Acute Hepatitis Course
    • 1. Mortality of 10-15%
    • 2. Worsening of symptoms in early recovery program
    • 3. Complication:
      • Varices gastritis
      • Peptic ulcer coagulopathy
      • Kidney infection lung infection
      • Peritonitis
    • 4. Seizures with withdrawal
      • Use of benzodiazepines are helpful
      • Can also cause encephalopathy
  • Acute hepatitis course (cont.)
    • 5. Hepato-renal syndrome
      • Development of Acute Renal Failure
      • Renal functions are excluded
      • There is an intense intra-renal vasoconstriction and distribution of blood flow, causing oliguria
  • Acute hepatitis Therapy
    • A. Supportive therapy with bed rest
      • Stop the BOOZE
    • B. Diet
      • Multiple vitamins: folic acid & thiamine
        • Magnesium, calcium, phosphate, & glucose are carefully monitored
      • 2500 calories at least.
        • Low protein if encephalopathy is present.
        • Vegetable protein & milk are acceptable.
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  • Acute Hepatitis Therapy (cont)
    • C. Benzodiazepines if
      • Alcohol withdrawal
        • Seizures- delerium tremons
        • Encephalopathy may occur
    • D. Steroids:
      • Used with encephalopathy
      • Minimal value in less severely ill patients
  • Acute Hepatitis Nutritional Complications:
    • Wernicke Encephalopathy
        • Ophthalmoplegia
        • Ataxia
        • Nystagmus
    • Korsakoff Syndrome
        • Loss of new memory
        • Disorientation to time & place
        • Confabulation
      • **Treatment: large doses of thiamine Hcl
  • Drug Related Hepatitis
    • 1. Pathology:
      • hepatocellular necrosis similar to virus (cholestatic reaction)
    • 2. Diagnosis:
      • usually established by history of drug use
    • 3. Lab:
      • similar to viral disease
    • 4. Cholestatic reaction:
      • impairment of bile secretion by hepatocytes (BC pills)
    • 5. Hepatocellular reaction:
      • very similar to viral hepatitis ( acetominophen, isoniazid, methyldopa)
  • Drug Related Hepatitis
    • 6. Symptoms:
      • Arthralgias
      • Fever
      • Rash
      • Eosinophilia
    • Treatment:
      • Removal of offending agent
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    • Chronic Hepatitis
  • Chronic Hepatitis
    • Refers to inflammation, necrosis & fibrosis for at least 6 months.
    • Varying from benign process to death.
    • Groups:
      • Viral
      • Autoimmune
      • Alcoholic
      • Primary biliary cirrhosis
      • Drug induced liver disease
      • Wilson’s disease
      • Anti-trypsin deficiency
      • Hemochromatosis
      • Sclerosing cholangitis
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  • Chronic Hepatitis
    • Forms:
      • A. Chronic Active Hepatitis :
        • Refers to the form of CH were the liver test & histology are compatible with active & progressive inflammation & necrosis
      • B. Chronic Persistent Hepatitis :
        • Refers to the mild & histological non progressive CH where the inflammation is confirmed only to the portal tracts. The enzymes are normal or only moderately elevated.
  • Chronic Hepatitis Autoimmune Hepatitis
    • Mainly a disease of young women
    • Most have hypergamaglobulinemia & ANA positive
    • Patients have multisystem disease which include:
      • Arthritis kidney involvement
      • Colitis heart
      • Thyroiditis portal hypertension
      • Pulmonary fibrosis
  • Chronic Hepatitis Autoimmune Hepatitis
    • Diagnosis:
      • Consider any young female with elevated liver function studies without course with hepatitis for greater than 6 months
      • Positive ANA
      • Elevated GG =means chronic
      • Liver biopsy showing chronic inflammation
    • Treatment:
      • Steroids
        • Decrease in symptoms
      • Prognosis: is good. About 50% live more than 15 years from the time of diagnosis
  • Other causes of Chronic Hepatitis
    • Inherited Chronic Liver Disorders
      • A. Wilson’s disease
      • B. Hemachromatosis
      • C. Alpha 1-antitrypsin deficiency
      • D. Reye syndrome
  • Wilson’s Disease
    • Pathogenesis:
      • a rare treatable genetic disorder of copper metabolism.
      • There is an abnormal accumulation of copper in the hepatocytes.
      • This is a metabolic disorder affecting basal ganglia, eyes, & kidney.
      • The defect is in the ceruloplasm which carries the copper.
      • The serum ceruloplasm & copper are both low (copper low b/c it can’t be carried)
  • Wilson’s disease (cont)
    • Diagnosis:
      • Made by seeing neurological, psychiatric, hepatitis, cirrhosis in a young person .
      • Liver disease with the Kayser-Fleischer ring in the eyes in the young is characteristic
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  • Haemochromatosis
    • Pathogenisis : A group of disorders with excessive absorption of iron.
    • The iron is layed down in liver, heart, pancrease, kidney, & skin (bronze diabetes)
      • Primary cause unknown
      • Secondary- Iron overload :
        • anemias
        • cirrhosis
        • Dietary
      • Diagnosis :
        • Lethargy, weakness in men 40-60 yo
        • Skin hyperpigmentation
        • Diabetes 30-60% of pt’s
        • arthopathy
  • Alpha 1-Antitrypsin Deficiency
    • In children associated liver disease
    • In teenagers & adults, a progressive liver disease with pulmonary manifestations
    • Pathogenesis: Alpha 1-trypsin is a potent protease inhibitor found in the serum, body fluids, & tissues
    • It is synthesized by the liver to protect from tissue injury resulting from protease like trypsin
  • Reye’s Syndrome
    • An illness seen in the pediatric age group associated with the flu
    • Symptoms: Nausea, vomiting, hyperactivity, confusion, seizures, & coma, Increasing drowsiness, Belly Pains
    • On liver biopsy there are fatty infiltration
    • Chemistry: elevated liver enzymes, NH3
    • ***NEVER give Aspirin to children with varicella infection (chicken pox), or during flu sx.***
  • REYE'S SYNDROME
    • only happens in kids less than 15 years old.
    • The cause is unknown, but it is strongly associated with Aspirin use during flu's.
    • The liver becomes inflamed and destroyed for unknown reasons.
    • It is important because Reye's syndrome kills about half of kids who get it.
    • NEVER give aspirin containing medications to your kids under 15 years old for fever control.
    • Use Acetaminophen/ Ibuprofen instead.
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  • Hepatic (Liver) Failure
    • May result from:
      • A. Slow deterioration as part of a chronic progress
      • B. Rapid worsening after repeated injuries
      • C. catastrophic event such as massive necrosis
    • Causes :
      • 1. Functional liver failure without overt necrosis
        • Reye’s syndrome, tetracycline toxicity
      • 2. Chronic liver disease
        • Chronic active hepatitis
        • Cirrhosis
      • 3. Fulminate failure : refers to acute severe impairment of liver function with encephalopathy & coma in patients who have had liver disease for less than 8 weeks
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  • Hepatic Failure (cont)
    • Clinical features:
      • Jaundice
      • Hypoalbuminemia
      • Hyperestrogenism which causes
        • Testicular atrophy
        • Gynecomastia
        • Palmar erythema
        • Spider angiomas
      • Hepatorenal Syndrome
      • Fetor odor
      • Coagulopathy
  • Liver failure (chronic): signs found on the arms Mneumonic
    • CLAPS : C lubbing L eukonychia A sterixis P almar erythema S cratch marks
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  • Hepatic Failure (cont)
    • Hepatic encephalopathy :
      • A metabolic disorder of the CNS system & neuromuscular system with slight changes in the brain (edema)
      • Clinical Features :
        • Confusion
        • Flapping tremor (asterixis)
        • Drowsiness
        • Coma  death
      • Caused by elevated levels of NH3 (ammonia)
  • Hepatic encephalopathy: precipitating factors Mneumonic
    • HEPATICS : H emorrhage in GIT/ H yperkalemia E xcess protein in diet P aracentesis A cidosis/ A nemia T rauma I nfection C olon surgery S edatives
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  • Hepatic failure (cont) Hepatic Encephalopathy
    • Treatment:
      • Remove precipitating causes (drugs/ETOH)
      • Decrease enteric toxins (BUN-NH3)
      • Gut enema
      • Low protein diet
      • Neomycin 1-2 gms Q 2 hrs PO
      • Lactulose 50 ml orally Q 2hrs until diarrhea ensues. Then reduce dosage until there are two stools per day
      • Transplantation:
        • Any young patient with progressive disease
        • Metabolic disease: wilson’s, alpha antitrypsin def.
  • Cirrhosis
    • Etiology: triad
      • 1. necrosis
      • 2. regenerating nodules
      • 3. fibrosis
    • Categories:
      • Major
        • Alcoholic (#1 cause in western world)
        • Post necrotic
      • Minor
        • Wilson’s disease
        • Haemochromatosis
        • Biliary
        • Chronic hepatic congestion
          • Budd-Chiari syndrome
            • uncommon condition induced by thrombotic or nonthrombotic obstruction to hepatic venous outflow
          • Cardiac
            • Right sided heart failure
            • Tricuspid insufficiency
  • Causes of hepatic cirrhosis Mneumonic
    • HEPATIC : H emochromatosis (primary) E nzyme deficiency (alpha-1-anti-trypsin) P ost hepatic (infection + drug induced) A lcoholic T yrosinosis I ndian childhood (galactosemia) C ardiac/ C holestatic (biliary)/ C ancer/ C opper (Wilson's)
  • Cirrhosis: differential: common and rarer · Mneumonic
    • Common causes are ABC : A lcohol B (Hepatitis) C (Hepatitis)
    • · Rarer are also ABC : A utoimmune B iliary cirrhosis C opper (Wilson's)
  • Cirrhosis
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  • Cirrhosis (cont)
    • Biliary Cirrhosis:
      • One of the more common causes of nonalcoholic liver disease
      • Pathology is destruction of the intrahepatic bile ducts
      • 90% are found in middle age females
      • Most common symptoms are fatigue & pruritis
      • Antimitochondrial antibodies (90%)
        • Order after all hepatitis profile excluded
  • Cirrhosis (cont)
    • Complications of cirrhosis:
      • Spontaneous bacterial peritonitis (SBP) which occurs in 10% of alcoholic cirrhosis (E. coli)
      • Ascites :
        • Refers to the accumulation of excessive volumes of fluid within the peritoneal cavity
        • Always a poor prognostic sign
        • Ultrasound & CT scans are best method of detection of small amounts of fluid. Flat plate has ground glass look.
  • Cirrhosis (cont)
    • Ascites (cont)
      • Diagnosis of ascites:
        • Bulging flanks
        • Umbilical hernia
        • Shifting dullness
        • Scrotal edema
        • Right sided pleural effusion
      • Paracentesis:
        • 50cc of fluid removed, look at color
        • CBC, WBC, protein, LDH, glucose, amylase, albumin
        • Gram stain, AFB, fungus cultures, cytology
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  • Ascites (cont)
    • Pathophysiology:
      • Alteration of hepatic blood flow causing portal hypertension.
      • Reduction in liver function:
        • Reduction in synthesis of albumin & coagulation proteins
        • Reduction in detoxification of bilirubin, ammonia, & drugs
  • Ascites
  • Ascites (cont)
    • Complications of ascites:
      • Dyspnea vomiting
      • Decreased cardiac output hydrothorax
      • Anorexia scrotal edema
      • Reflux esophagitis
    • Treatment:
      • Improve hepatic function
      • Restrict sodium & fluid intake
      • Aldactone which inhibits aldosterone
      • Paracentesis (removal of fluid with addition of IV albumin)
      • Shunts
      • Abstain from alcohol
      • Diuretics
        • Aldactone
        • Lasix
  • Ascites treatment (cont)
    • Treatment (cont):
      • Supportive
        • Nutrition high calories, low protein with encephalopathy
        • Minerals & vitamins
        • Sodium restriction
        • Copper restriction if wilson’s disease
      • Neomycin & Lactulose if NH3 elevated
      • Liver Transplants
  • Portal Hypertension
    • Classification:
      • Portal vein (prehepatic)
      • Intrahepatic (sinusoids)
      • Hepatic (posthepatic) (Budd Chiari- usually due to tumor)
    • Findings:
      • Ascites
      • Varices
        • Gastric, esophageal, hemorrhoids
        • Caput medusa
      • Encephalopathy
      • Splenomegaly which causes:
        • Sequestration & destruction of RBC’s
        • Neutropenia
        • thrombocytopenia
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  • Portal Hypertension (cont)
    • Diagnosis:
      • Barium swallow for varices of esophagus
      • Angiography
      • Endoscopy
    • Treatment:
      • Transfusion of platelets
      • Vasopressin decrease splanchnic blood flow
      • Balloon tamponade
      • Endoscopic sclerotherapy
      • Portal shunts
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  • Liver Review
    • Signs of liver disease & causes
      • Jaundice - diminished bilirubin secretion
      • Fetor hepaticus- sulfur compounds produced by intestinal bacteria, not cleared by liver
      • Spider angiomas, palmar erythema, & gynecomastia- elevated estrogen levels
      • Ecchymoses - decreased synthesis of clotting factors
      • Xanthomas - elevated cholesterol levels
  • Liver Review
    • Hypoglycemia - decreased glycogen stores
    • Hypersplenism - portal hypertension
    • Encephalopathy, asterixis- portosystemic shunt, NH3
    • Hepatorenal syndrome (rapid decline of GFR)- renal failure of unknown pathogenesis, kidneys are normal (may be transplanted), assoc c ascites, almost always fatal
  • Liver review
    • Liver cell damage= AST, ALT
    • Bile duct obstruction= alk phos
    • Cholestasis= bilirubin
    • Hep A: IgG antibodies= previous exposure
        • IgM antibodies= recent infection
    • Hep B: HBsAg-acute or chronic inf. ( used for blood bank screening
            • HBeAg- high degree of infectivity
            • Anti-HBc- earliest indicator of acute infection
            • Anti-HBe- resolution of acute infection
            • Anti-HBs- indicates immunity (post infection or vaccine)
  • Liver Jeopardy Facts
    • The liver is the largest internal organ
    • The liver has a right lobe and a left lobe.
    • The liver holds about 13 percent of the body's blood supply at any given moment.
    • The liver is visible on plain abdominal film
    • Ultrasound exam of the liver shows size and consistency
    • The liver has the ability to regenerate