Minarcik robbins 2013_ch18-liver
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Transcript of Minarcik robbins 2013_ch18-liver
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Chapter 18Chapter 18LIVERLIVER
&&
BILIARY TRACTBILIARY TRACT
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DUCT
SYSTEM
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N
OFIBROUS
TISSUE
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PORTAL
“TRIAD”
CENTRAL
VEIN
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PATTERNS OF HEPATIC INJURY
• Degeneration:– Balooning, “feathery” degeneration, fat,
pigment (hemosiderin, bile, both intrinsic)
• Inflammation: Viral or Toxic– Regeneration
– Fibrosis
• Neoplasia: 99% metastatic, 1% primary
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BALOONING DEGENERATION
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“FEATHERY” DEGENERATION
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FATTY LIVER
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“MICRO”-VESICULAR STEATOSIS
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“MACRO”-VESICULAR STEATOSIS
Obesity
Diabetes
Toxic
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“Golden” pigment stained with Prussian Blue stain to make it blue. Hemosiderin? Bile? Melanin?
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APOPTOSIS
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APOPTOSIS
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INFLAMMATION•PORTAL TRIADS
(early)
•SINUSOIDS(more severe)
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MILD “TRIADITIS”
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More severe portal infiltrates with sinusoidal infiltrates also.
Understanding the “limiting plate” is important!
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Hepatic Regeneration
• The LIVER is classically cited as the most “REGENERATIVE” of all the organs!
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FIBROSIS• FIBROSIS is the end stage of
MOST chronic liver diseases, and is ONE (of TWO) absolute criteria needed for the diagnosis of cirrhosis.
• What is the other?
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CIRRHOSIS• PORTAL-to-PORTAL (bridging)
FIBROSIS• The “normal” hexagonal
“ARCHITECTURE” is
replaced by NODULES
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CIRRHOSIS• Liver
• Alcoholic
• Biliary (Primary or Secondary)
• Laennec’s (nutritional)
• Advanced (kind of a “redundant” adjective)
• Post-necrotic
• Micronodular
• Macronodularhttp://www.onelook.com/?w=*+cirrhosis&ls=a 50 adjectives
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ALL CIRRHOSIS IS:• IRREVERSIBLE• The end stage of ALL chronic liver disease,
often many years, often several months
• Associated with a HUGE degree of nodular regeneration, and therefore represents a significant “risk” for primary liver neoplasm, i.e.,
“Hepatoma”, aka, Hepatocellular Carcinoma
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BLIND MAN’s LIVER
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Blind Man’s Diagnosis
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N
OFIBROUS
TISSUE
BETWEEN
PORTAL
AREAS
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IRREGULAR NODULES SEPARATED BY PORTAL-to-PORTAL FIBROUS BANDS
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TRICHROME
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CIRRHOSIS, TRICHROME STAIN
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CIRRHOSIS, TRICHROME STAIN
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DEFINITIONS:• CIRRHOSIS is the name of
the disease as demonstrated by the anatomic changes
• LIVER FAILURE is the series and sequence of abnormal pathophysiologic events
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“SPIDER” ANGIOMA, CIRRHOSIS
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Common Clinical/Pathophysiological
Events• Portal Hypertension WHY? WHERE?
• Ascites WHY? (Heart/Renal?)
• Splenomegaly WHY? Hepatomegaly?
• Jaundice WHY? Anemia WHY?
• “Estrogenic” effects WHY?
• Coagulopathies (II, VII, IX, X) WHY?
• Encephalopathy WHY?
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Hepatic Enzymology• Transaminases (AST/ALT), aka (SGOT/SGPT),
and LDH are “hepatic INTRACELLULAR” enzymes, and are primarilly indicative of hepatocyte damage.
• Alkaline Phosphatase (AlkPhos), Gamma-GTP (Gamma-glutamyl transpeptidase), and 5’-Nucleotidase (5’N) are MEMBRANE enzymes and are primarilly indicative of bile stasis/obstruction
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Intracellular = DAMAGEAST/ALT/LDH
Membrane = OBSTRUCTION
AlkPhos/GGTP/5’N
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JAUNDICE
Where else?
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Bilirubin: (0.3-1.2 mg/dl)
UN-conjugated (IN-direct)
Conjugated (direct)
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JAUNDICE• Hemolytic (UN-conjugated)
• Obstructive (Conjugated)
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JAUNDICE• Excessive bilirub. production
• Reduced hepatic uptake
• Impaired conjugation
• Defective Transportation
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Neonatal Jaundice• Neonatal, genetic
–Gilbert Syndrome (5-10%, ↓ glucuronyl-transferase)
–Dubin-Johnson Syndrome (transport problem)
• Neonatal, NON-genetic–MASSIVE differential diagnosis, i.e.,
everything
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CHOLESTASIS• Def: Suppression of bile flow• Associated with membrane
enzyme elevations, “primarily”, ie, AP/GGTP/5’N
• Familial, drugs (steroids and many common
antibiotics), but bottom line is OBSTRUCTION
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Bile “plugs”, Bile “lakes”
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VIRAL HEPATITIS• A, B, C, D, E• They all look similar, ranging from a few
extra portal triad lymphocytes, to “FULMINANT” hepatitis with total collapse of lobules
• Associated with full recovery (usual), chronic progression over years leading to cirrhosis (not rare), risk of hepatoma (uncommon), or death (uncommon)
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VIRAL HEPATITIS• Jaundice, urine dark, stool chalky
• Usual viral “prodrome”
• Upper respiratory infection
• All have multiple antigen (virus) and antibody (serology) serum tests
• “Councilman” bodies on biopsy are very very nice to find. Why?
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Chiefly Portal Inflammation
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FULMINANT HEPATITIS
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“FULMINANT” Acute Viral Hepatitis
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“Councilman” Bodies……Diagnostic? Probably!
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B
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CLESS common than B (one fourth)
LESS dangerous than B in the acute phase
MORE likely to go chronic than B
MORE closely linked with hepatoma than B
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Comple recovery Chronic disease
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NON-Viral hepatitides• Staph aureus (toxic shock)
• Gram-Negatives (cholangitis)
• Parasitic:– Malaria– Schistosomes– Liver flukes (Fasciola hepatica)
• Ameba (abscesses)
• AUTOIMMUNE• ALCOHOLIC HEPATITIS
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DRUGS/TOXINS• Steatosis (ETOH)
• Centrolobular necrosis (TYLENOL)
• Diffuse (massive) necrosis
• Hepatitis
• Fibrosis/Cirrhosis (ETOH)
• Granulomas
• Cholestasis (BCPs, steroids)
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“Metabolic” Liver Disease• Steatosis (i.e., “fat”, fatty change,
fatty “metamorphosis”)• Hemochromatosis (vs. hemosiderosis)
–Hereditary (Primary)
–Iron Overload (Secondary), e.g., hemolysis, increased Fe intake, chronic liver disease
• Wilson Disease (Toxic copper levels)• Alpha-1-antitrypsin (NATURAL protease inhibitor)
• Neonatal Cholestasis
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PAS positive inclusions with alpha-1-antitrypsin deficiency
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INTRAHEPATIC
BILE DUCTS
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Points of Interest•
INTRA-hepatic vs. EXTRA-hepatic
• PRIMARY biliary cirrhosis is a bona-fide AUTOIMMUNE disease of the INTRA-hepatic bile ducts
• SECONDARY biliary cirrhosis is caused by chronic obstruction/inflammation/both of the intrahepatic bile ducts
• CHOLANGITIS, or inflammation of the INTRA-hepatic bile ducts, is associated with chronic bacterial (often gram negative rods) infections, or Crohns/Ulcerative colitis (IBD)
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CIRCULATORY
Disorders
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Points of Interest• Infarcts are rare. WHY? (hint: “lung”)
• Passive congestion with “centrolobular” necrosis, is EXTREMELY COMMON in CHF, and a VERY COMMON cause of cirrhosis, i.e., “cardiac” cirrhosis
• Various semi reliable clinical and anatomic findings are seen with disorders of:– Portal Veins– Hepatic veins/IVC– Hepatic arteries
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MISC.• Hepatic Diseases are seen often with
–Pregnancy• PRE-Eclampsia/Eclampsia (HTN, proteinuria,
edema, coagulopathies, DIC)• Fatty Liver• Cholestasis
–Transplant—Bone Marrow or other Organs
• Drug Toxicities• GVH
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BENIGN LIVER TUMORS*
• …..are, in most cases, really regenerative nodules
• Have been historically linked to BCPs
• Can really be neoplasms of blood vessels also, if they appear like angiomas
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MALIGNANT LIVER TUMORS• 99% are metastatic, i.e., SECONDARY, esp. from
portal drained organs• Just about every malignancy will wind up
eventually in the liver, like the lungs
• PRIMARY liver malignancies, i.e., hepatomas, aka hepatocellular carcinomas, arise in the background of already very serious liver disease chronic hepatitis/cirrhosis, are slow growing, and do NOT metastasize readily
• CHOLANGIOCARCINOMAS are malignancies if the INTRA-hepatic bile ducts and look MUCH more like adenocarcinomas than do hepatomas
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HEPATIC ANGIOMA
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Classical hepatocellular Carcinoma, HCC, also called Hepatoma
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HEPATOMA, or HEPATOCELLULAR
CARCINOMA
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CHOLANGIOCARCINOMA
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EXTRAHEPATICEXTRAHEPATICBILE DUCTSBILE DUCTS
&&GALLBLADDERGALLBLADDER
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MAINCONSIDERATIONS
• Anomalies
• Stones (Clolesterol/Bilirubin)• (Chole[docho]lithiasis)• Inflammation
(Cholecystitis/Cholangitis)• Cysts• Neoplasms
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Anomalies• Congenitally absent
Gallbladder
• Duct Duplications
• Bilobed Gallbladder
• Phrygian Cap
• Hypoplasia/Agenesis
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Phrygian Cap
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CholelithiasisFactors
• Bile supersaturated with cholesterol
• Hypomotility
• Cholesterol “seeds” in bile, i.e., crystals
• Excess mucous in gallbladder
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Cholesterolosis of gallbladder mucosa
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Cholesterolosis of gallbladder mucosa
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Cholecystitis• Acute: fever, leukocytosis, RUQ pain• Chronic: Subclinical or pain• Ultrasound can detect stones well• HIDA (biliary) nuclear study can help
• Go hand in hand with stones in gallbladder or ducts, age, sex, weight
• If surgery is required, most is laparoscopic
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Choledochal Cysts
• Dilatations of the common bile duct usually in children.
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Adenocarcinoma of the gallbladder