HEPATOLOGY by sateesh1234



Normal liver span 6-12cm in the midclavicular line

Normal liver functions:

    -   Synthetic (clotting factors, protein, chol. Etc)
    -   Metabolic( steroids, drugs detoxification etc)
    -   Excretory(bile)

Evaluation of liver disease:

Liver functionality:

    -   PT
    -   Bilirubin
    -   Albumin
    -   Cholesterol

Structural integrity and cellular intactness:

    -   Transaminases ( progressive decrease means either RECOVERY from liver injury or that only a
        few hepatocytes are functional)
    -   GGT
    -   ALP

ALT is more specific for liver disease

Acute pancreatitis:

Risk factors: GET SMASHED

       Hypertriglyceridemia > 1000mg/dl is a RF. During attack levels can become as high as 3000-
        5000mg/dl. Hyper lipidemia type I and V are associated with pancreatitis.
       Even when there is a blockade of secretion, synthesis continues hence causing leakage of
        digestive enzymes from the acinar cells interstitial space systemic circulation.
       Serum amylase rises within 6-12hrs of symptom onset and remains elevated for 3-5days
        (most common test ordered in the Dx of AP)

If etiology is gallstones, once pt is stable perform lap chole otherwise recurrent pancreatitis attacks will

Evaluation of etiology do abd USG ( to look for gall stones in all pts experiencing the 1st attack.

Abdominal CT Most valuable imaging technique. Used in those who fail to respond to conservative
Mx. To ideantify areas of infection or necrosis

Mild pain control(meperidine or fentanyl favored over morphine), IV fluids, NPO (most pts recover in
5-7 days)

Moderate to severe Aggressive fluid resuscitation, Pain control (meperidine or fentanyl favored over
morphine), and ANTIBIOTICS


      -   Exudative left sided pleural effusion (high amylase conc.)
      -   Abd. Compartment syndrome
      -   Intraabdominal hemorrhage
      -   Shock
      -   Diabetes
      -   Pseudocyst
      -   Abd. pseudoaneurysm
      -   Hypovolemic shock is an early Cx and results from I/V vol loss d/t local and systemic vascular
          endothelial injury by pancreatic enzymes increases vascular permeability and transudation of
          plasma. Systemic vasodilation may also contribute.

Acute necrotizing pancreatitis:


      -   Enteral feeding
      -   Decontamination of gut with non-absorbable antibiotics
      -   Prophylactic systemic antibiotics

Recurrent pancreatitis:

When no obvious cause is identified do ERCP, it will help to :

Diagnose pancreatic divisum, choledochal cysts and CBD stones

Aspiration bile from GB to look for biliary crystals and microlithiasis

Pancreatic CA: (4th leading cause of CA death)


      -   Male
      -   >50
      -   Black
      -   Cigarette  most consistent RF (risk increased 2-3times)
      -   Chronic pancreatitis
      -   Long standing DM
      -   Obesity
      -   Familial pancreatitis
      -   Pancreatic CA in a close relative

Alcohol, gallstones, coffee are NOT risk factors for pan. CA

Tumor location:

      -   Body and tail wt loss and abdominal pain
      -   Head wt loss, steatorrhea, jaundice
      -   Abd mass or ascites present only in 20% pts.
      -   Palpable gall bladder in pts. with jaundice (courvoisier’s sign)
      -   Left supraclavicular lymphadenopathy(virchow’s node) in metastatic disease
      -   Migratory thrombophlebitis can occur chronic DIC and atypical venous thrombosis


Labs Increases bilirubin, ALP and mild anemia

Ist test in jaundiced Abd. USG

      -   Abdominal CT (very specific)  detects bile and pancreatic duct dilation, mass lesions in
          pancreas, extrahepatic spread (e.g. mets or ascites)
      -   ERCP(invasive) done when USG and CT are non-Dx
      -   PTC done in pts in whom ERCP can’t be done and have previously identified biliary tract
          dilation. Can be therapeutic:
           Drainage of infected bile ( cholangitis)
           Extraction of stones in the biliary tract
           Dil. Of benign strictures
           Stent placement across malignant strictures

Evaluation of chemotherapy response of the pancreatic CA CA 19-9

Colon CA:

Most common site of mets liver

Non-alcoholic steatohepatitis: (NASH)

Hepatic fibrosis develops in 40% while cirrhosis in 10-15%

Risk factors:

      -   Obesity (40% obese have some form of steatosis)
      -   DM
      -   Hypertriglyceridemia
      -   Medications amiodarone, corticosteroids, HAART, diltiazem, tamoxifen)
      -   Endocrinopathies ( cushing syndrome)
      -   TPN


 IR leads to increased fat accumulation in the hepatocytes by incresig the rate of lipolysis and elevating
the circulating insulin levels  this intrahepatic fatty acid oxidation leads to and increase oxidative
stress  local increase in the proinflamm cytokines TNF alfa inflamm, fibrosis and ultimately cirrhosis


         Mostly asymptomatic, Presents with hepatomegaly


      -   Percutaneous liver biopsy macrovesicular fat deposition with displacement of nucleus to the
      -   Mildly elevated ALT, AST, ALP


      -   Treat underlying co morbid condition
      -   Ursodeoxycholic acid maybe of some help in decreasing tranaminase levels and improving

Alcoholic liver disease:

      -   Alcoholic steatosis(fatty liver)
      -   Alcoholic hepatitis (mallory bodies, neut. Infiltration, perivent. Inflamm, liver cell necrosis)
      -   Alcoholic fibrosis/cirrhosis

All are reversible if alcohol intake is stopped except late stages of fibrosis and cirrhosis

Acute alcoholic hepatitis:

      -   Acute onset RUQ pain and fever
      -   AST/ALT > 2 (sec. to deficiency of vit B6 which is a cofactor for ALT enzymatic activity)
      -   AST and ALT are almost always < 500IU/L (if higher transaminases, suspect concurrent hepatic
          injury sec. to viral hepatitis, ischemic hepatiis or acetaminophen usage)


      -   Abstinence from alcohol
      -   Nutritional support
      -   Corticosteroids (e.g. methylprednisolone)
Hepatitis A:

Tx supportive (recovery in 3-6wks) , contacts should given immune globulin.


Paracentesis is both Dx and Tx

Postcholecystectomy pain:


      -    Sphincter of oddi dysfunction (SOD): may have normal USG and ERCP findings
      -    CBD stone(Dx with USG and ERCP)
      -    Functional pain(Dx of exclusion, when everything comes out normal)

Dx USG, ERCP (for CBD stone Dx), Sphincter of oddi manometry(for SOD Dx)

USG: If biliary tree dilated do ERCP to confirm and Tx (CBD stone: stone removal, SOD:

If LFTs normal and biliary tree not dilated then it is functional pain (Analgesics and reassurance)



      -    Biliary enteric fistula (presence of air in the biliary tree)
      -    Pancreatitis
      -    Biliary peritonitis(acute abdomen, free fluid under diaphragm)
      -    Sepsis
      -    Hge
      -    S/E from contrast, sedative or antichol.


Dx Abd USG

Tx If symptomatic : Lap chole (asymptomatic gall stones should not be treated)


      -    ursodeoxycholic acid , biles salt that decreases chol. Content of the bile by reducing the hepatic
           secretion and intestinal reabsorption of chol. (gall stones recur in 50%, med is expensive and
           therapy may need to be done for months)
      -    Extracorporeal shock-wave lithotripsy (in high-risk pts with symptomatic small gall stones in
           whom surgery can’t be done)
All pts with CLD should be immunized against Hep A and B unless already immune.


Eso. Varices can be asymptomatic hence all pts. should undergo screening for varices via ENDOSCOPY.
And start prophylaxis with beta blockers which will reduce the risk of bleeding.

Hypothalamic-pit. Dysfunction can occur in pts. with cirrhosis (pt. had hypothyroidism)

Fulminant hepatic failure:

      -   Hepatic enceph that develops within 8 weeks of onset of AHF (if liver failure without hep enceph
          occurs in 8 wks acute hepatic failure, if liver failure + hep enceph occurs b/w 8 weeks and 6
          months subfulminant hepatic failure)
      -   Coagulopathy is always present
      -   0.1-0.5% pts with hep B develop it.

Usually in those with:

      -   Heavy acetaminophen use(accounts for 40% cases) has the most favorable prognosis.
          Mortality 50% (fasting or concurrent alcohol abuse increase chance of developing)
      -   Heavy alcohol use
      -   Heavy methamphetamine use
      -   Co infection with B and D

Adverse prognostic factors in cases of acetaminophen toxicity:

      -   Acidosis (pH < 7.3)
      -   INR >6.5
      -   Azotemia (creatinine > or = 3.4mg/dl)
      -   Blood lactate level > 3.5mmol/L


      -   Grossly elevated AST (often >10,000)


      -   Tx is focused on correcting coagulation, electrolyte and acide base disturbances, renal failure,
          hypoglycemia and encephalopathy
      -   Mannitol  If cerebral edema
      -   Orthoptic liver transplant (can be used emergently)

C/I to transplant:

      -   Irreversible cardiopulm. Disease
      -   Recent (<5yrs) or incurable malignancy external to liver
      -   Active alcohol and drug abuse

Hepatitis B:

IgM anti-HBc most specific marker for Dx acute hep B b/c it is also present in the window period and
is present from early disease to cure

Mother with HBsAg +, HBeAg -  20% neonate risk of infection

Mother with HBsAg +, HBeAg +  95% neonate risk of infection

Hepatitis C:

      -   Vertical transmission 2-5%
      -   Mother CAN breastfeed infact it is recommended (even though HCV RNA foun din milk but still
          almost no rate of transmission)
      -   Mother with hep C has to get vaccines against hep A and B (these vaccines are safe in
      -   Chronic hep C presents with waxing and waning transaminases but few symptoms. Pts may
          present with arthralgias or myalgias.


      -   PCR RNA (gold standard) appear in serum within days-wks after exposure
      -   Anti-HCV  appear in serum about 8 wks or so later but some pts. may not be positive for
          several months or may never test +


      -   Combination therapy with interferon and ribavarin Elevated ALT, detectable HCV RNA and
          chronic hepatitis atleast of moderate grade
      -   Monotherapy with interferon Mild grade of chronic hep C

Hepatitis E:

      -   FHF occurs in 0.5-3% cases
      -   15-25% chance of FHF in pregnant woman
      -   Significantly vertically transmitted


      -   PCR HEV RNA in serum or feces
      -   IgM-anti HEV

Amebic liver abscess: (entameba histolytica)

      -   Suspect in someone traveled recently to an endemic area
       -   Prim infection is in the colon leading to bloody diarrhea. Ameba may be transported to the liver
           via portal circulation causing abscess


       -   MOST pts are asymptomatic
       -   Dysentery
       -   RUQ pain
       -   Single cyst in the liver usually on the right side
       -   Abcess on the superior liver surface can cause a pleuritic type pain and radiation to the shoulder


       -    Liver imaging (USG, CT or MRI) , supplemented with leukocytosis >10,000 or an elevated ALP
       -   Serology is helpful esp when there are no extraintestinal findings on imaging
       -   stool exam for trophozites usually not helpful < 20% identified.
       -    Aspirate from the abscess is usually STERILE and is like anchovy paste but you usually don’t
           aspirate b/c of associated risk factors


Tissue agents:

       -   Metro (cure in 90% pts in 7-10 days)
       -   Tinidazole

Luminal agents:

       -   Paromomycin
       -   Iodoquinol
       -   Diloxanide furoate
Pyogenic liver abcess:

Causes: Secondary to :

       -   Surgery
       -   GI infection
       -   Acute appendicitis

Condition of pt is more severe than the amebic liver abscess.

Hydatid disease: (echinococcus granulosus) close contact with dogs and sheeps


       -   Mostly asymptomatic
       -   May cause compression of surrounding structures and hence symptoms like nausea , vomiting,
           RUQ pain, hepatomegaly
       -   Unilocular cystic lesions in liver, lung, muscle or bones.
       -   Look for travel or immigration

Dx CT scan : eggshell calcifications of a hepatic cyst
Diagnosis usually made with imaging studies plus SEROLOGY


      -   Surgical resection under the cover of albendazole.

Simple liver systs:

      -   Congenital
      -   Mostly asymptomatic
      -   When symptomatic dull RUQ pain, abd bloating or early satiety
      -   Pathophysiology fluid secretion by the epithelial lining

Autoimmune hepatitis:

May cause large increases in the AST and ALT associated with hyperbilirubinemia


      -   Anti smooth muscle antibodies
      -   ANA maybe present

Liver malignancy:

      -   Solitary liver mass more likely to be metastatic than primary
      -   Pt had presented with abd pain, wt loss and liver mass, so we had to do colonoscopy as the
          next step in Mx as the colon CA was supposedly the cause of the metastasis.

Most common primaries metastasizing to liver:

      -   Lung
      -   Breast
      -   Skin
      -   GI (most common)

Hemochromatosis: 30% deaths are d/t hepatocellular CA

Reliable screening tests:

      -   Percent saturation of transferring > or = to 45%
      -   Serum ferritin level > 1000microg/L

Asymptomatic elevation of transaminases:

      -   Take a thorough Hx to rule out MC causes of hepatitis risk factors alcohol/drug use, travel
          outside, bld transfusions, high risk sexual practices
      -   Repeat LFTs in 6 months  if still elevated they are chronic
      -   Now test for hep B and C, hemochromatosis, fatty liver.  if these are unremarkable
      -   Now search for muscle disorders polymyositis, seizures, heavy exercise and thyroid disorders
      -   Uncommon causes Occult celiac disease and adrenal insufficiency

Acute cholecystitis:

Gall stone impactionstasis causes bacterial overgrowth tissue behind duct obstruction gets
inflamed ischemic changes gangrene and perforation generalized peritonitis or a well-
circumscribed abscess are more common outcomes also cholangitis and chronic cholecystitis may occur.

Bile peritonitis can occur  severe abd. Pain and rigidity. USG shows free fluid under diaphragm


      -   Supportive (NPO, IV antibiotics, alimentation , analegesics)
      -   Elective lap chole (but do it emergently if perforation or gangrene)


Risk factors:

      -   Chronic hep B and C
      -   Hemochromatosis
      -   Alfa 1 antitrypsin def.
      -   Aflatoxin exposure
      -   Tyrosinemia

sudden and sustained elevation of ALP and marked elevation of AFP (>500ng/ml)

Abrupt appearance of ascites which maybe bld tinged showing that tumor is bleeding or has caused
thrombosis of portal or hepatic veins.


      -   Helical CT and MRI with contrast
      -   Liver biopsy is diagnostic

Hepatic angiosarcoma:

      -   Rare malignant neoplasm
      -   Vascular spaces that are lined with malignant cells
      -   More common in older men exposed to vinyl chloride, thorium dioxide and arsenic.

Hepatic adenoma:


      -   OCPs
      -   Anabolic steroids
      -   Glycogen storage disease
      -   Pregnancy
      -   DM

First presentation maybe  pt. collapses suddenly d/t rupture of adenoma and intraabdominal bleed.



      -   LFTs usually normal but elevated on occasion
      -   Increased ALP and GGT most commonly in those with intratumor bleed OR multiple adenomas
      -   AFP normal unless malignant transformation occurs

Imaging studies:

      -   USG or CT
      -   Don’t do biopsy risk of bleeding
      -   M/S large adenoma cells with lipid and glycogen


      -   All symptomatic adenomas can be resected
      -   Non symptomatic initially Mx conservatively ( discontinue OCPs and careful observation with
          repeated imaging and serial AFP measurements)

Focal nodular hyperplasia:

      -   Very common benign tumor
      -   Not of vascular origin
      -   Arises as hyperplastic response to hyperperfusion by anomalous arteries that are present in the
          center of the nodule.
      -   Biopsy sinusoids and kupffer cells which are not seen with hep adenoma

Dx of cholecystitis and SOD  HIDA scan is very sensitive

Histology difference b/w alcoholic and viral hepatitis:

Alcoholic balloon degeneration with polymorphic cellular infiltrates. Accumulation of fat, protein and
water within hepatocytes cause cellular swelling necrosis.

Viral panlobular mononuclear infiltration with hepatic cell necrosis. Kupffer cells phagocytose
hepatocellular debris and confluent hepatic cell necrosis connects adjacent lobules (bridging necrosis)

Vanishing bile duct syndrome:

      -   Rare disease involving progressive destruction of the intrahepatic bile ducts.
   -      Histological hallmark ductopenia


   -      PBC  most common cause
   -      Liver transplant
   -      Hodgkin’s disease
   -      Graft-versus-host disease
   -      Sarcoidosis
   -      CMV
   -      HIV
   -      Medication toxicity

Drug-induced liver disease:

Classification according to mechanism of action:

   1-     Direct toxins: These are dose-dependent and have short latent periods
   -      CCl 4
   -      Acetaminophen
   -      Tetracycline
   -      Amanita phalloides mushroom
   2-     Idiosyncratic reactions:
   -      INH
   -      Chlorpromazine
   -      Halothane
   -      Antiretrovirals


   -      Hepatic manifestations
   -      Extrahepatic manifestations hypersensitivity like ( rash, arthralgias, fever,
          leukocytosis,eosinophilia) EXCEPT ISONIAZID

Classification according to morphology:

   1-     Cholestasis:
   -      Chlorpromazine
   -      Anabolic steroids
   -      Nitrofurantoin
   -      Erythromycin
   2-     Steatosis: Fatty liver
   -      Valproate
   -      Antiretrovirals
   -      Tetracycline
    3-     Hepatitis:
    -      Halothane
    -      INH
    -      Phenytoin
    -      Alpha methyl dopa
    4-     Fulminant hepatic failure:
    -      CCl4
    -      Acetaminophen
    5-     Granulomatous:
    -      Phenylbutazone
    -      Allopurinol

Halothane toxicity:

Type I:

    -      Aminotransferase elevation
    -      Mild or no symptoms

Type II:

    -      Severe or fulminant hepatic failure

Evaluation of liver damage in:

Acute hepatitis:

    -      LFTs
    -      Viral serology

Chronic hepatitis: (that persists for at least 6 months)

    -      Liver biopsy is the best means of determining the current hepatic function

Ischemic hepatitis:

    -      Uncommon b/c of dual blood supply of liver
    -      When it does occur such as in a pt. of liver transplantation nausea, vomiting, hepatomegaly
       Porcelain gallbladder: 11-33% will develop gallbladder CA

       -   Cx of chronic cholecystitis either from gallstones or as a component of the natural progression if
           chronic inflammation.


       -   Mostly asymptomatic
       -   May present with RUQ pain or
       -   Firm, non tender mass in the RUQ

Dx X-ray (rim of Ca deposits that outline the GB)

Tx cholecystectomy for ALL pts.

       Emphysematous cholecystitis: Form of acute cholecystitis

       -   Mostly male 50-70yrs

Predisposing factors:
       -   Vascular compromise (obstruction or stenosis of cystic artery)
       -   Immunosuppression ( e.g. DM)
       -   Gall stones
       -   Infection with gas forming bacteria


       -   RUQ pain
       -   Nausea, vomiting
       -   Low grade fever
       -   Crepitus in the abdominal wall adjacent to GB


       -   Abd. X-ray air fluid level in GB
       -   USG curvilinear gas shadowing in GB
       -   CT done when other imaging modalities are unclear


       -   Mild to mod. Unconjugated bilirubinemia
       -   Small increase in AST and ALT


       -   Immediate fluid and electrolyte resuscitation
       -   Early cholecystectomy
       -   Antibiotics (parenteral)  amino/quinolones with clinda/metro OR ampi/sublactum OR

Shock liver:

Pt. presented with septic shock developed AST, ALT elevation one day later most consistent with
ischemic hepatic injury or shock liver. There is a rapid elevation of transaminases with modest elevation
in total bilirubin and ALP.( hep A or B massive increase in AST and ALT, with HYPERbilirubinemia)

In pts who survive the underlying cause of their hypotension (e.g. septic shock, Heart failure etc). liver
enzymes return back to normal within 1-2 wks.

-Iron overload can cause chronic hepatic injury with low-grade elevations in the AST and ALT. 4
transfusions are unlikely to cause it.

Common indications for TIPS:

       -   Refractory cirrhotic hydrothorax
       -   Refractory ascites (defined as diuretic resistant or diuretic refractory ascites)
       -   Recurrent variceal bleed not controlled by other minimal invasive means
      -   Pts waiting for liver transplant and needing portocaval shunts

Refractory pleural effusion pleurodesis

A1AT deficiency:

Dx: Serum A1AT levels followed by genetic testing (testing is indicated in all pts with premature onset of
chronic bronchitis, emphysema, dyspnea as well as nonsmokers suffering from COPD.


      -   Purified human A1AT for those with severe deficiencies.
      -   Liver transplant in those with hepatic failure
      -   Lung transplant in those with severe pul. Impairment.

Primary sclerosing cholangitis:


      -   ALP and bilirubin elevated
      -   Transaminases usually < 300IU/L
      -    Hypergammaglobulinemia
      -   Increased IgM
      -   Atypical p-ANCA
      -   Hypoalbuminemia in those with IBD


      -   CHOLANGIOGRAPHY is diagnostic (ERCP)


      -   Ursodeoxycholic acid
      -   Endoscopic therapy for dilation and stenting of dominant strictures
      -   OR liver transplant (otherwise mean survival is only 12 yrs)

Dubin-Johnson syndrome:


      -   Conjugated hyperbilirubinemia with a direct bili fraction of at least 50%
      -   Rest, normal liver function profile
      -   Urinary coproporphyrin I  unusually high levels

Tx NO tx

Acute ascending cholangitis:

       -   Charcot’s triad fever, RUQ pain, severe jaundice
       -   Reynold’s pentad confusion and hypotension + charcot’s triad (occurs in suppurative

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