Liver and Biliary Tract - Pathology - Lecture Slides, Slides of Pathology

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LIVER

BILIARY TRACT

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

Hepatic Regeneration

• The LIVER is classically

cited as the most

“REGENERATIVE” of all

the organs!

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?

CIRRHOSIS

• Liver
• Alcoholic
• Biliary (Primary or Secondary)
• Laennec’s (nutritional)
• Advanced (kind of a “redundant” adjective)
• Post-necrotic
• Micronodular
• Macronodular

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

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?

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 Docsity.com

JAUNDICE

• Hemolytic (UN-conjugated)
• Obstructive (Conjugated)

JAUNDICE

• Excessive bilirub. production
• Reduced hepatic uptake
• Impaired conjugation
• Defective Transportation

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

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)

NON-Viral hepatitides

• Staph aureus (toxic shock)
• Gram-Negatives (cholangitis)
• Parasitic :
  • Malaria
  • Schistosomes
  • Liver flukes (Fasciola hepatica)
• Ameba (abscesses)
• AUTOIMMUNE
• ALCOHOLIC HEPATITIS

DRUGS/TOXINS

• Steatosis (ETOH)
• Centrolobular necrosis (TYLENOL)
• Diffuse (massive) necrosis
• Hepatitis
• Fibrosis/Cirrhosis (ETOH)
• Granulomas
• Cholestasis (BCPs, steroids)