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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
- Neoplasia: 99% metastatic, 1% primary
Hepatic Regeneration
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.
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)