Hepatobiliary

• Liver dysfunction: hepatic insufficiency

  • liver cells are not working like they should
• Portal hypertension

  • Exaggerated levels of what you see in hepatic insufficiency
• Fluid accumulation: build up of fluid

  • Reduced plasma protein = reduced osmotic pressure
  • More interstitial fluid; only 1mmhg taken by lymphatics and rest drips out of liver and pools in peritoneal cavity
  • Increasing interstitial fluid everywhere
• Result of Fluid accumulation

  • Ascites: build up fluid in peritoneal
  • Pitting edema: accumulation within interstitial space
  • can stick fingers into skin leaving indentations
  • in general, pooling shows up first in ankles (exacerbated by gravity)
• Jaundice

  Elevated bilirubin
• Prehepatic/hemolytic - due to increase RBC destruction

  • reticuloendothelial cell -> phagocytize RBC -> heme -> unconjugated/free bilirubin (transported by albumin)
  • kernicterus = assoc. w/ newborns; mismatch blood type between mom and baby
• hepatic/hepatocellular - liver dysfunction

  • hepatocyte unable to convert unconjugated -> conjugated bilirubin -> increase in free/unconjugated bilirubin
  • combine with glucoronic acid or sulfate = water soluable
  • neonatal jaundice - mom regulates bilirubin but once born take 7-10 days before baby enzymes able to do this
• Choleostatic/post hepatic - don't excrete bilirubin in bile

  • due hepatocyte or obstructed bile duct = Increase conjugated bilirubin
  • if can't dump bilirubin into bile duct -> dumped into blood stream
  • UV light helps break down bilirubin
• Malabsorption - decrease bile salts


  • without bile salts can't make micelle, can't absorb fat
  • fat not absorbed, use own fat = weight loss
  • fat sol vit not absorbed = vit k = can't make clotting factors (2,7,9,10) = clotting disorder
• Clotting disorder

  1. Can't make prothrombin (Factor II)

  2. Makes thrombin
• Hepatic encephalopathy - elevated ammonia

  • aa reanimated -> ammonia, can't convert to urea
  • Increased ammonia = Nervous tissue shutting down = Hepatic coma
  • Asterixus = flapping tremor of extended hand
• Fatty liver


  • Triglycerides accumulate in hepatocytes
  • Make fat but don't have energy to take out garbage = Fatty liver
  • Usually red, but fatty liver = pink
• Altered steroid synthesis - breakdown

  • decreased cholesterol = can't make steroids
  • Men: Testicular atrophy due to low cholesterol = decreased testosterone
  • decreased Steroid breakdown - Gynocomastia
  • Estrogen not broken down -> Increased estrogen = Estrogen feminization = Enlarged breasts
• Hepatorenal syndrome

  Renal failure due to vasoconstriction
• Portal hypertension

  • increased Hydrostatic pressure = Congestion
  • Long term destruction / Chronic illness associated with liver = Scar tissue = increased contracture = increased hydrostatic pressure -> Increased movement of fluid plasma to Interstitial but not coming in = dripping into peritoneal cavity = can turn bacterial
  • Crushing liver / Hepatic portal vein
  • If hard to move forward, starts to back up = splenomegally / Varicies
  • Result: Splenomegally, Varicies, Ascites
  • End Stage of liver failure
• Infectious Liver Disease

  • Hepatitis A, B, C, D, E
  • Can cause acute or chronic
  • Infective agent virus: Lymphocytes accumulate but no exudate
  • Inflammatory event: have fever, Jaundice, nausea, decreased appetite
• hepatitis A

  • acute inflammation, but resolves
  • fatality - 0.1%
  • fecal - oral transmission
  • assoc. with unsanitary conditions
  • day care/schools/crowded conditions - children or people that work with children
• Course of Hep A

  • 2-6 week incubation
  • lifelong immunity
  • vaccine (1992)
  • incidence in US is variable
• Hepatitis B

  • both - acute and chronic
  • transmission - assoc. w body fluid (blood, vaginal secretions, semen, saliva)
  • 90% mother to baby during birth
• Course of Hep B

  • lots of outcomes
  • acute -> resolve or severe or chronic
  • chronic -> non-progressive or progressive or carrier
  • incubation: 4-26 weeks
  • serum hepatitis - liver signs
  • HbsAg vaccine - capsule antigen
  • 2 billion infected wordwide
• Hep C

  • chronic
  • transmission blood borne - IV users, multisex partners, surgery post transfusion (90% of cases), needle stick, contact with HCV person
  • employed in med
• Course of Hep C

  • no vaccine
  • acute -> chronic active liver disease
  • cause of 50% of liver transplants
• Hepatitis D (dual)


  • Have to have Hepatitis B + Hepatitis D
  • acute with hep b infection
  • co-infections results -> liver necrosis
  • transmission: blood borne
• Hepatitis E (exotic)


  transmission:

  • waterborne
  • zoonotic disease = transmitted from animals: monkey, cat, dog
• Acute: hep A

  • Lymphocytes infiltrate, hepatocytes swell, fatty changes, cholestasis
• Chronic

  • Losing hepatocytes, fatty changes
  • scarring -> collagen laid down -> contracture -> difficult for blood to flow
  • distorts lobule = liver can't function
  • hepatocytes regenerate but depends if stroma intact
  • contracture -> destroy CT architecture (stroma) -> hepatocytes don't regenerate
• Toxins

  • Substances -> broken down into toxic metabolites in hepatocytes
  • toxic to liver cells because they are broken down there
• carbon tetrachloride (not toxic in this form)

  • liver breaks down -> releases Cl -> toxic/deadly

  amanita toxins (assoc. w death cap mushrooms)

  • takes 8-12 hours after eating before hepatic necrosis
  • 20% mortality - lethal within 24 hours

  acetaminophen (Tylenol) -> NAPQI (toxic)

  • 35% of cases of liver failure assoc with this
  • taken in higher doses than should be

  anabolic steroid (testosterone)

  • if not prescribed by doctor can consume more than should

  alcohol -> acetyl aldehyde (toxic)
• Results of cirrhosis

  Long term inflammation -> Lots of scar tissue

  Alter lobule architecture -> Contracture (shrinking) results in nodules

  • micro nodular <3mm
  • macro nodular > 1cm
• Signs of cirrhosis

  • Liver failure
  • Portal hypertension -> Ascites
• Role of alcohol

  alcohol -> alcohol dehydrogenase (enzyme) -> acetyl aldehyde
• Course of disease

  1. Fatty liver (common sequel) -> enlarges 2-3x (hepatic insufficiency)

  • to 16% of alcoholics develop cirrhosis in 10 years
  • scarring result in shrinking (nodular)
  • 60% die within 6 years of cirrhosis development
• Cholelithiasis

  • Occurs in 15% of adults
  • Due to diet, genetics (high cholesterol), Inflammation of biliary system
  • form gall stones: 80-90% cholesterol but can be calcium bilirubate/calcium carbonate
  • incidence increase with age
• Signs of cholelithiasis

  
  

  asymptomatic - no blockage

  symptomatic - blockage

  • biliary colic - blocked duct
  • elevated blood conjugated bilirubin -> jaundice
  • biliary cirrhosis = scarring
  • abnormal fat digestion
  • gall bladder rupture = peritonitis
• Treatment for cholelithiasis

  Remove gall bladder to get rid of gallstones
• Biopsy

  Looking for normal lobular structure
• Imaging

  Look for obstructions in billary tree
• Blood tests


  • Albumin: low
  • Bilirubin: high
  • Liver specific enzymes (ALT, AST, ALP) - supposed to be in hepatocyte, if in ECF = hepatocytes lysed
  • Clotting time (prothrombin)
• Urine

  Elevated bilirubin - usually exits biliary -> small intestine, forced to get rid of through kidney