Docsity
Docsity

Prepare for your exams
Prepare for your exams

Study with the several resources on Docsity


Earn points to download
Earn points to download

Earn points by helping other students or get them with a premium plan


Guidelines and tips
Guidelines and tips

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

Liver and Biliary Tract, Patterns of Hepatic Injury, Portal Triads, Hepatic Regeneration, Chronic Liver Diseases, Diagnosis of Cirrhosis, Hepatocellular Carcinoma, Liver Failure. A lecture from Pathology course to teach you a topic. Key points are given above.

Typology: Slides

2011/2012

Uploaded on 12/21/2012

deepaka
deepaka 🇮🇳

4.9

(20)

82 documents

1 / 33

Toggle sidebar

This page cannot be seen from the preview

Don't miss anything!

bg1
LIVER
&
BILIARY TRACT
Docsity.com
pf3
pf4
pf5
pf8
pf9
pfa
pfd
pfe
pff
pf12
pf13
pf14
pf15
pf16
pf17
pf18
pf19
pf1a
pf1b
pf1c
pf1d
pf1e
pf1f
pf20
pf21

Partial preview of the text

Download Liver and Biliary Tract - Pathology - Lecture Slides and more Slides Pathology in PDF only on Docsity!

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)