The document discusses the anatomy, histology, functions and common pathologies of the liver. Key points include: - The liver has four lobes and receives dual blood supply from the hepatic artery and portal vein. It performs many metabolic and synthetic functions. - Common liver diseases include viral hepatitis, alcoholic liver disease and cirrhosis. Cirrhosis results from chronic liver injury and scarring that disrupts the liver architecture. - Primary liver cancers like hepatocellular carcinoma often arise in the setting of chronic liver disease and cirrhosis. Treatment options are limited but may include transplantation or resection in early stages.

1. SMS 2044

2. Normal Liver

3. The Liver
The right upper quadrant of the abdomen is
dominated by the liver and its companion
biliary tree and gallbladder.
Residing at the crossroads between the
digestive tract and the rest of the body, the
liver has the enormous task of maintaining the
body's metabolic homeostasis.

4. Autopsy
 1.5 kg, wedge shape
 4 lobes, Right, left,
Caudate, Quadrate.
 Double blood supply
 Hepatic arteries
 Portal – Venous blood
 Acini / Portal triad.
 Lobules – central. V

5. Normal Liver - Infant

6.  Sheets of connective tissue divide the liver into
thousands of small units called lobules.
 The lobule is the structural unit of the liver, with
portal triads at the vertices and a central vein in
the middle.
 The parenchymal cells of the liver are
Hepatocytes
 Hepatocytes make contact with blood in
sinusoids

7. •N
•O
•FIBROUS
•TISSUE
•Normal Liver - Microscopy

8. Hepatocytes are exceptionally active in synthesis
of protein and lipids for export

10. Liver Functions:
Metabolism – Carbohydrate, Fat & Protein
Secretory – bile, Bile acids, salts & pigments
Excretory – Bilirubin, drugs, toxins
Synthesis – Albumin, coagulation factors
Storage – Vitamins, carbohydrates etc.
Detoxification – toxins, ammonia, etc.

11. Hepatitis:
Hepatitis: Inflammation of Liver
Viral, Alcohol, immune, Drugs & Toxins
Biliary obstruction – gall stones.
 Specific – Heptitis A, B, C, D, E, & other

12. Transmission
Hepatitis A and E are typically caused by
ingestion of contaminated food or water.
 Hepatitis B, C and D usually occur as a result
of parenteral contact with infected body fluids.
Like contaminated blood or blood products,
semen, invasive medical procedures using
contaminated equipment, drug abuse
Hepatitis B transmission from mother to baby
at birth.

15. Pattern of Viral Hepatitis:
Carrier state / Asymptomatic phase
Acute hepatitis
Chronic Hepatitis
 Chronic Persistent Hepatitis (CPH)
 Chronic Active Hepatitis (CAH)
Fulminant hepatitis
Cirrhosis
Hepatocellular Carcinoma

16. Acute Hepatitis:
Swelling and Apoptosis
Piecemeal or Bridging, panacinar necrosis
Inflammation – lymphocytes, Macrophages
Ground glass hepatocytes – HBV
Mild fatty change – HCV
Portal inflammation and Cholestasis

17.  Foreign bodies, organisms, and a variety of drugs may incite
a granulomatous reaction.

18. Acute viral Hepatitis:

19. Acute viral Hepatitis C:

21. Acute viral Hepatitis:

22. Acute viral Hepatitis:

23. Signs and Symptoms
 Abdominal pain
 Joint and muscle pain
 Change in bowel function
 Nausea, vomiting, anorexia
 Lethargy, malaise
 Fever (Hepatitis A)
 Irritability

24. More Signs and Symptoms
oJaundice
oclay colored stools
odark urine
oPruritis/urticaria
oSkin abrasions
oRash

25. Fulminant Hepatitis:
 Hepatic failure with in 2-3 weeks.
 Reactivation of chronic or acute hepatitis
 Massive necrosis, shrinkage, wrinkled
 Collapsed reticulin network
 Only portal tracts visible
 Little or massive inflammation – time
 More than a week – regenerative activity
 Complete recovery – or - cirrhosis.

26. Chronic Hepatitis:
Persistent & Active types. CPH/CAH
Lymphoid aggregates
Periportal fibrosis
Necrosis with fibrosis – bridging fibrosis.
Cirrhosis – regenerating nodules.

27. Hepatocyte necrosis is distributed
immediately around the central vein
(centrilobular necrosis).
Destruction of entire lobules (submassive
necrosis) or most of the liver parenchyma
(massive necrosis) is usually accompanied
by hepatic failure.

28. Liver Biopsy

29. B

30. C
LESS 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

31. Jaundice
Yellow discoloration of sclera, skin, mucous
membranes due to deposition of bile pigment
Clinically detected with serum bilirubin 2-
2.5mcg/dL or ↑ (2 times nl)

32. Common Causes of Jaundice
Pre Hepatic (Acholuric) - Hemolytic
Unconjugated/Indirect Bil, pale urine
Hepatic – Viral, alcohol, toxins, drugs
Liver damage - unconjugated
Swelling, canalicular obstruction - Conjugated
Post Hepatic (Obstructive) – Stone, tumor
Conjugated/Direct Bil, High colored urine,

33. Normal bilirubin production
(0.2 to 0.3 g/day) is derived
primarily from the breakdown
of erythrocytes.
Extrahepatic bilirubin is
bound to serum albumin and
delivered to the liver.
Bilirubin Metabolism And
Elimination.

34. (1) excessive production of bilirubin, (2) reduced hepatic
uptake,
 (3) impaired conjugation, (4) decreased hepatocellular
excretion, and
(5) impaired bile flow (both intrahepatic and
extrahepatic).
The first three mechanisms produce unconjugated
hyperbilirubinemia, and the latter two produce predominantly
conjugated hyperbilirubinemia.

36. PATHOPHYSIOLOGY OF
JAUNDICE
 This un-conjugated bilirubin may
accumulate systemically and deposit in
tissues, giving rise to the yellow
discoloration of jaundice.
 This is particularly evident in the
yellowing of the sclerae (icterus).
 Un-conjugated bilirubin is tightly
complexed to serum albumin and is
virtually insoluble in water at
physiologic pH.

37.  This form cannot be excreted in
the urine even when blood levels
are high.
 In contrast, conjugated bilirubin
is water soluble, nontoxic, and
only loosely bound to albumin.

39. •“FEATHERY” DEGENERATION

40. Jaundice is an almost invariable finding.
 Impaired hepatic synthesis and secretion of albumin leads
to hypoalbuminemia, which predisposes to peripheral edema.
 Hyperammonemia is attributable to defective hepatic urea
cycle function.
Fetor hepaticus is a characteristic body odor variously
described as "musty" or "sweet and sour" and occurs
occasionally.
Clinical Features

41.  A coagulopathy develops, attributable to impaired hepatic
synthesis of blood clotting factors II, VII, IX, and X.
 The resultant bleeding tendency may lead to massive
gastrointestinal hemorrhage as well as petechial bleeding
elsewhere.
 Hepatic encephalopathy
 Hepatic encephalopathy is a feared complication of acute
and chronic liver failure

42. Cirrhosis
Cirrhosis is a pathologically defined entity that is
associated with a spectrum of characteristic clininical
manifestation
1.Irreversible chronic injury of the hepatic
parenchyma
2.Extensive fibrosis
3.Formation of regenerative nodules

43. Cirrhosis

44. Cirrhosis
Fibrosis
Regenerating Nodule

45. Etiology of Cirrhosis
Alcoholic liver disease 60-70%
Viral hepatitis 10%
Biliary disease 5-10%
Primary hemochromatosis 5%
Cryptogenic cirrhosis 10-15%
Wilson’s, α1AT def rare

46. Cirrhosis: Pathophysiology
 Primary event is injury to hepatocellular elements
 Initiates inflammatory response with cytokine
release->toxic substances
 Destruction of hepatocytes, bile duct cells,
vascular endothelial cells
 Repair thru cellular proliferation and regeneration
 Formation of fibrous scar

47. Cirrhosis: Pathophysiology
 The normal liver contains interstitial collagens (types I, III,
and IV) in portal tracts and around central veins, with
occasional bundles in the parenchyma.
 Primary cell responsible for fibrosis is stellate cell
 Become activated in response to injury and lead to ↑ed
expression of fibril-forming collagen
 Above process is influenced by Kupffer cells which activate
stellate cells by eliciting production of cytokines
 Sinusoidal fenestrations are obliterated because of ↑ed
collagen and EC matrix synthesis

48. Cirrhosis: Pathophysiology
 Portal vein-to-hepatic vein and hepatic artery-to-
portal vein vascular shunts also develop.
 Prevents normal flow of nutrients to hepatocytes
and increases vascular resistance
 Initially, fibrosis may be reversible if inciting events
are removed
 With sustained injury, process of fibrosis becomes
irreversible and leads to cirrhosis

49. Pathogenesis
Hepatocyte injury leading to necrosis.
 Alcohol, virus, drugs, toxins, genetic etc..
Chronic inflammation - (hepatitis).
Bridging fibrosis.
Regeneration of remaining hepatocytes
Proliferate as round nodules.
Loss of vascular arrangement results in
regenerating hepatocytes ineffective.

50. Cirrhosis Features:
Liver Failure
Portal obstruction, Portal systemic shunts…
Portal hypertension, Splenomegaly
Jaundice, Coagulopathy, hypoproteinemia,
toxemia, Encephalopathy,

51. Clinical Features
Hepatocellular failure.
 Malnutrition, low albumin & clotting factors,
bleeding.
 Hepatic encephalopathy.
Portal hypertension.
 Ascites, Porta systemic shunts, varices,
splenomegaly.

53. Ascitis in Cirrhosis

54. Micronodular cirrhosis:

55. Micronodular cirrhosis

56. Macronodular Cirrhosis

57. Liver Biopsy – Cirrhosis:

58. Nutmeg Liver-Cardiac Sclerosis

59. Cirrhosis
Clinical
Features

60. Complications:
Congestive splenomegaly.
Portal hypertension and esophageal
varices
Hepatocellular failure.
Hepatic encephalitis / hepatic coma.
Hepatic encephalopathy
Hepatocellular carcinoma.

61. Evaluation of the Cirrhotic
 Physical Exam
 Jaundice
 Ascites
 Caput medusae
 Asterixis
 Spider angiomas
 Palmer erythema
 Testicular atrophy
 Gynecomastia
 +/- Palpable spleen
(portal HTN)
 Lab tests
 Anemia
 Thrombocytopenia
 Coagulopathy
 Hypoalbuminemia
 Hepatitis serologies
 α-fetoprotein

62. Prevention Teaching
What would you teach?
• Adequate sanitation and hygiene
• Wash hands before eating and after
using the toilet
• Drink only purified or bottled water
• No sharing of eating utensils,
needles, toothbrushes, razors, etc.
• Choose your tattoo or piercing
person carefully. Inspect the facility

63. ClassificationClassification
HemangiomaHemangioma
Focal nodularFocal nodular
hyperplasiahyperplasia
AdenomaAdenoma
Liver cystsLiver cysts
Primary liver cancersPrimary liver cancers
Hepatocellular carcinomaHepatocellular carcinoma
Fibrolamellar carcinomaFibrolamellar carcinoma
HepatoblastomaHepatoblastoma
Benign Malignant
 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

65.  Primary Carcinoma of
the Liver
 Most arise from hepatocytes
and are termed Hepatocellular
Carcinoma (HCC).


66. Hepatocellular Carcinoma

68.  Pathogenesis
 Several factors relevant to the pathogenesis of HCC.
 Three major etiologic associations have been established:
infection with HBV, chronic liver disease.
 Many factors, including age, sex, chemicals, viruses,
hormones, alcohol, and nutrition, interact in the
development of HCC.
 The development of cirrhosis appears to be an important,
but not requisite, contributor to the emergence of HCC.

69. Treatment
 Liver transplatation
 Surgical resection (best prognosis for
long-term survival, but possible in only
10-15% of cases)
 Radiotherapy