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Liver diseasesLiver diseases
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Hepatomegaly
Hepatomegaly
Clinic: measure size of liver
Palpate lower edge of liver
Percuss upper edge of liver
Liver scratch test
- patient supine, auscult over epigastrum, scratch skinon midclavic line below right nipple. Upper and lower level of scratching sound = distance
- 10-12 cm = normal
> 14 cm = hepatomegaly
< 8 cm = cirrhosis
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Diagnoses
Diagnoses
Hepatomegaly
Cirrhosis Reidel¶s lobe (normal variant of prominent
right lobe)
Primary hepatocellular carcinoma
Tricuspid regurgitation
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Splenomegaly
Splenomegaly
Palpate in right lateral decubital position
Percuss spleen during inspiration and
expiration
Diagnoses:
Splenomegaly
Splenectomy
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Ascites
Ascites
Percuss abdomen for shifting dullness
Percuss abdomen for fluid waves
Auscult abdomen while percussing flank
(puddle sign)
Visually inspect venous pattern of skin over
abdomen
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CLASSIFICATION OFCLASSIFICATION OF
JAUNDICEJAUNDICE
Unconjugated
Hyperbilirubinemia
A. Decreased hepatic uptake
B. Overproduction
C. Impaired bilirubinconjugation (decreased
glucuronyl transferase
activity )
Conjugated
Hyperbilirubinemia
A. Impaired hepatocellular
secretion of bilirubin
B. Cholestasis
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A. Overproduction
Intravascular hemolysis: Hemolytic anemias
Extravascular hemolysis: Resorption of blood
from large hemorrhagic infarcts (e.g., pulmonary)
large hematomas, gastrointestinal bleeding
Unconjugated HyperbilirubinemiaUnconjugated Hyperbilirubinemia
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B. Decreased hepatic uptake
Prolonged severe fasting
Sepsis
U nconjugated HyperbilirubinemiaU nconjugated Hyperbilirubinemia
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C . Impaired bilirubin conjugation (decreased
glucuronyl transferase activity)
Gilbert's syndrome
Crigler-Najjar syndrome
Jaundice in newborns
Diffuse advanced hepatocellular disease
(e.g., hepatitis, cirrhosis)
U nconjugated HyperbilirubinemiaU nconjugated Hyperbilirubinemia
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C onjugated HyperbilirubinemiaC onjugated Hyperbilirubinemia
B. Cholestasis
Intrahepatic Drug-induced (e.g., methyltestosterone, estrogens, oral contraceptives)
Recurrent jaundice of pregnancy
Recurrent familial jaundice
Early primary biliary cirrhosis
Viral hepatitis
Alcoholic hepatitis
Extrahepatic Obstruction of major excretory bile ducts: gallstones
Carcinomas of common bile duct, ampulla of Vater, head of pancreas
Inflammatory strictures of bile ducts
Atresia of bile ducts
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Acute liver diseaseAcute liver disease
Acute viral hepatitis
Drug-induced liver disease
Alcoholic liver disease
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Chronic liver diseaseChronic liver diseaseChronic active hepatitis
Cirrhosis of the liver
Liver abcess
Hepatic polichistosis
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Systemic diseases with prominent liver Systemic diseases with prominent liver
involvementinvolvement
Alpha 1-antitripsin deficiensy
Amyloidosis
HemochromatosisSarcoidosis
Wilson`s disease
Liver disease of pregnancy
Acute fatty liver
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Inherited disorders of bilirubinInherited disorders of bilirubin
metabolismmetabolism
Gilbert`s syndrome
Crigler ±Najar syndrome
Rotor syndrome
Dubin-Jonson syndrome
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Acute viral hepatitisAcute viral hepatitis
EtiologyHepatitisA= RNA virus transmitted by fecal- oral route
anicteric in 50% of cases.
Hepatitis B = DNA virus transmitted parenterally
Individuals at high risk: - intravenous drug abusers
- exposure to blood and blood products (eg., patients and health
professionals in dialysis units)
Non-A, non-B hepatitis= more than one virus
transmitted by blood transfusions
Delta agent = small, defective RNA, infectious only in presence of hepatitis
B infection (relies on hepatitis B proteins for replication)
Other viruses: Epstein-Barr virus, cytomegalovirus, herpes simplex virus,
yellow fever, rubella
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C linical features of viral hepatitis include
(1) Malaise, anorexia, fatigue(2) Arthritis and urticaria, common in hepatitis
B (circulating immune complexes)
(3) Influenza-Iike syndrome, common in
hepatitis A
(4) Jaundice (with dark urine or light stools), in
50% of cases
(5) Hepatic enlargement or tenderness
(6) Splenomegaly, in 20% of patients
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Diagnosis of acute viral hepatitis
based on clinical features + laboratory
findings = elevated levels of transaminases,
serum bilirubin, serum alkaline phosphatase
the rise in bilirubin exceeds the increase in
alkaline phosphatase.
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P rimary care level attitude
Intravenous fluids hydration, correction of
electrolyte abnormalities
Provide caloric intake if nausea and vomitingare present
Vitamin K should be given if the protime is
elevated
Address patient to hospital of infectiousdiseases
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Agents of Drug Agents of Drug--Induced Liver Disease Induced Liver Disease
Drugs Causing Drugs Causing Viral Granulomatous Inflammatory Chronic Active
Direct Toxicity Altered Metabolism Hepatitis-Iike Hepatitis Cholestasis Hepatitis
Acetaminophen Androgens Halothane Allopurinol Chlorpromazine Acetaminophen
Aspirin Corticosteroids (?) Isoniazid Hydralazine Chlorpropamide Aspirin
Alcohol Estrogens Oxacillin Phenylbutaz. Erythromycin Isoniazid
Carbon tetrachloride Ethanol Phenytoin Phenytoin Estolate Methyldopa
Heavymetals Intravenous Sulfonamides Quinidine Propylthiouracil Nitrofurantoin
tetracycline
Methotrexate Valproic acid Sulfa drugs Thiazides Oxyphenisatin
Mushroom toxins
(phalloidin and phallin)
Phosphorus
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Alcoholic hepatitisAlcoholic hepatitis
acute syndrome due to heavy alcohol
consumption (ingestion > 100 g alcohol daily for
more than 1 year) 8 oz whiskey, 30 oz wine, eight
12-oz cans beer
decreased vitamin and protein intake
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Clinical features
Fever, jaundice, hepatomegaly, liver tenderness
Ascites, encephalopathy, variceal bleeding
occasionally
Laboratory
Leukocytosis
Elevated GOT elevated serum bilirubin
decreased serum albumin
modest increase in serum alkaline phosphatase
Cholestatic phase
marked elevations of alkaline phosphatase and
direct bilirubin
GPT always < GOT
Alcohol-induced thrombocytopenia (10% of patients)
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Diagnosis liver biopsy: large droplet fatty liver,
polymorphonuclear infiltration, alcoholic hyaline
(Mallory bodies), hepatocyte necrosis, sclerosis
of central veins
Therapysupportive
daily diet of 2500-3000 kcal
supplements B vitamins (especially thiamine)
and folate
absolute abstinence from alcohol is crucialCorticosteroids = controversial therapeutic role
(useful in very severe cases)
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GallstonesGallstones
extremely common, occur in 20% of the population in Western populations composed primarily of
cholesterol
pigment gallstones, composed primarily of
calcium bilirubinate, are found in patients withchronic hemolysis as well as in Oriental population
one-third to one-half of patients with gallstones are
asymptomatic and should be treated expectantlySurgical removal of asymptomatic gallstones is
unnecessary except for diabetic patients in whom the
risk of acute cholecystitis with complications is high
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CholedocholithiasisCholedocholithiasis
gallstone passed into the common bile duct from gallbladder
retained gallstone missed during cholangiography or common
duct exploration.
formed de novo in the common duct (stasis from ductal
obstruction)
Symptoms intermittent colicky pain in right upper quadrant
fever, chills, jaundice
sepsis from ascending cholangitis, closed space infection
Lab elevated serum levels of alkaline phosphatase and
transaminases
Dg
Endoscopic retrograde cholangiopancreatography
Percutaneous transhepatic cholangiography
Ultrasound
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Liver Test Patterns in Hepatobiliary DisordersLiver Test Patterns in Hepatobiliary Disorders
Type of Disorder Bilirubin
Hemolysis/Gilbert's syndrome Normal to 5 mg/dl
85% due to indirect fractions
No bilir ubinuria
Acute hepatocellular necrosis Both fractions may be
(viral and dr ug hepatitis, elevated
hepatotoxins, acute heart Peak usually follows
failure) aminotransferasesBilir ubinuria
Chronic hepatocellular disorders Both fractions may be
elevated
Bilir ubinuria
Alcoholic hepatitis / Both fractions may be
Cirrhosis elevatedBilir ubinuria
Intra- and extra-hepatic Both fractions may be
cholestasis elevated
(obstr uctive jaudice) Bilir ubinuria
Infiltrative diseases (tumor, Usually normal
granulomata); partial bile duct
obstr uction
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Pancreatic carcinomaPancreatic carcinoma
Weight loss, anorexia and chronic persistent pain in
the epigastrium ,radiating to the back
Obstructive jaundice with painless palpable
dilatation of the gallblader (Courvoisier`s sign)
Migratory thrombophebitis (Trousseau syndrome)
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Fatty liver
Fatty liver
Accumulation of lipid in hepatocytes
(macro/microvesicular)
Asymptomatic hepatomegaly discovered on
physical examination
No association with biochemical tests for
liver disease
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CirrhosisCirrhosis Diffuse disorganisation of hepatic structure
by regenerative nodules/fibrotic tissue
General signs:- asymptomatic for years
- weakness, anorexia, weight loss
- malnutrition (fat malabsorbtion, fat-solublevitamin deficiency)
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CirrhosisCirrhosisOccasional presentation:
- Massive upper GI bleeding from esophageal
varices secondary to portal hypertension
- Hepatocellular failure with ascites or portal
± systemic encephalopathy
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CirrhosisCirrhosisLab
Decreased serum albumin impaired
Prolonged prothrombin time liver function
Increased serum gamma globulin
AST/ALT elevated
Alkaline P normal/increased
Bilirubin normal/elevated
Normocytic normochromic anemia hypersplenism
Thrombocytopenia/leukopenia
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CirrhosisCirrhosisInvestigations
US
- Confirm hepatomegaly/splenomegaly
- Enlargement/venous obstruction of portal/splenic veins
- Estimate portal vein flow
Isotopic scintiscan
- irregular pattern of liver uptake, increased uptake in spleen
and bone marrow
Biopsy
- etiology
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CirrhosisCirrhosisComplications
Portal hypertension
Hypersplenism
Esophageal varices
H
ypoxemia (intrapulmonary shunting0Hepatic encephalopathy
Hepatocellular carcinoma
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CirrhosisCirrhosisTreatment
- Supportive
- withdrawal of toxic agents- supplemental vitamins
- nutrition
- treatment of complications
- In-hospital ± interferon-gamma, corticosteroids,azathioprine
- Liver transplant
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Hepatic gran
ulomas
Hepatic gran
ulomas
Infiltrative liver disorder +/- additional hepaticinflammation and fibrosis
Etiology Infectious: bacterial (TB, brucella, tularemia),
fungi (histoplasmosis, blastomycosis), parasitic(schistosomiasis, toxoplasmosis, larva migrans),
viral Sarcoidosis
Collagen disease
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Hepatic gran
ulomas
Hepatic gran
ulomas
Clinic
- evolution subclinical
- FUO (fever of unknown origin)!
- liver fct tests normal, except disproportionate
elevation of alk P
Dg
- liver biopsy ( especially important in FUO)
- cultures, skin tests, x-ray
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Hepatic gran
ulomas
Hepatic gran
ulomas
Treatment
Etiologic
Complete regression of infective or drug
induced granulomas
Do not give antibiotics blindly
Sarcoidosis: corticosteroids
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Neoplasms of the liver Neoplasms of the liver Hepatocellular carcinoma
Metastatic disease ± most common
Symptoms
- weight loss
- abdominal pain
- right upper quadrant mass- unexplained deteriorationof previously stable
patient with cirrhosis
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Neoplasms of the liver Neoplasms of the liver Dg: 3 key elements
Hepatic friction rub or bruit
Painful growing hepatomegaly in pts with
cirrhosis
Elevation of alfa-fetoprotein in serum >
400microg/l