Here are brief summaries of the requested liver conditions: - Primary Biliary Cirrhosis (PBC) and Primary Sclerosing Cholangitis (PSC): - PBC affects small bile ducts, PSC affects large bile ducts - PBC more common in females, PSC more common in males - PBC associated with autoimmune diseases, PSC associated with IBD - Wilson's disease involves copper accumulation in liver due to ceruloplasmin defect - Alpha-1 antitrypsin deficiency results in decreased protease inhibition and liver damage - Hemochromatosis involves iron overload due to HFE gene mutation - Hemosiderosis is iron overload from other causes like

1. Never offer the devil (desire) a ride,
He always want to be in the driving seat…!
-- BK

2. CPC 4.2.3 – 2013 – ―yellow eyes‖
• Fatigue / Anorexia..?
• Nausea, Vomiting..?
• Haematemesis… ?
• Itching..?
• Fever..?
• Abdominal distension slow..?
• Bleeding / Bruising..?
• 10 stubbies/day /more..?
• Many Tattoos..?
• BMI – if low / High..?
2
Mr. T.D. 50 year old, presents to his GP. ‗My stomach appears big
and my wife has noticed a yellow tinge in my eyes‘.
CASE STUDY 1
Abd distension, fatigue, yellow discoloration of eyes for 1 week
Presenting Symptoms:
• Liver failure…
• Liver failure…
• Portal Hypertension
• Obstructive jaundice.
• Hepatitis.
• Cirrhosis.
• Vit-K deficiency.
• Alcoholic hepatitis.
• Viral Hepatitis (B/C)
• Anorexia / Obesity –
steatosis.
• Differential Diagnosis:
• Hepatitis: Alcoholic/Infective/Malignant/Drug/Toxins
• Acute / Chronic? Primary/Secondary?
• ―HBV / HCV, CMV, Lepto, Dengue, Melioidosis.

3. Case2: Mr.GG, 48y, fatigue & yellow…
• Abdominal distension, fatigue, yellow
sclera – 6 weeks.
• Hardware business, Alcohol 40units / wk.
• Travel: Thailand, had tattoo / surgery /
transfusion.. *
• PE: abdomen nil sig. mild RUQ
tenderness. No organomegaly.
• Differential: Acute hepatitis.
– CMV, Lepto, Hep A,B,C..
– Hepatitis - Alcohol
– Chronic hepatitis.
– Drugs, toxins,
3
AST = 1320 U/l
ALT = 1780 U/l
Alk. Phos. = 133 U/l
GGT = 192 U/l
Hep B Serology
Hep B sAg +ive
Hep B sAb <10
Hep B cAb IgM +ive
Hep B e Ag +ive
Hep B eAb –ive

4. 4
CPC 4.2.2 - 2010
• George, 62 year old farmer from Tully, presents
to his GP with fatigue. His wife has asked him to
consult you as his eyes look a bit yellow'.
• Fatigue: Progressing 2wk. Unable to get out.
• nausea : no
• vomiting/haematemesis : no
• Anorexia, wt loss: yes thinks lost a bit of weight.
• bowel habit : constipated, stool pale, no blood.
• 2 x episodes fatigue last 2 years preceded by 2
weeks of fever. Lab: ―liver not working so well'.
then felt better and has not been to see GP since.
• Banana farmer from Greece - 26 years ago.

5. 5
Laboratory Investigations:
• FBC: Hb 13.8 g/dl, PCV 45%; WBC 7000/mm3, 70%
N, 25% L; Platelets 200,000/mm3
• Blood film: Normocytic, normochromic cells
• Bilirubin: Total serum Bilirubin = 98 μmol/l, (Direct 67)
• Liver enzymes:
• Aspartate amino transferase (AST) = 182 U/l
• Alanine amino transferase (ALT) = 55 U/l
• Alkaline Phosphatase = 190 U/I
• Serum Protein: Total protein = 59 g/l, Albumin = 20 g/l,
• Hepatitis B Surface Antigen (HbsAg): Positive
Hep B sAg +ive
Hep B sAb <10
Hep B cAb IgM +ive
Hep B e Ag +ive
Hep B eAb –ive

6. 6
Differential Diagnosis:
• Viral fever -?
– Yellow fever, Relapsing fever, Dengue, Ebola,
– Leptospirosis (common in Tully) - ?
• Hepatitis – Acute / Chronic - ?
• Chronic Hepatitis B – why chronic?
• History & presentation in Hep. A & C ?
• Other causes of Jaundice?
• Alcoholic liver disease ?
• Toxins, chemical, Reyes syndrome?
• Hemolytic / Anemia - ?
• Malignancy - ?

7. 7
CPC23: HBS – Hepatitis & Cirrhosis
• Pathology Major CLI:
– Acute & Chronic Liver injury.
– Pathophysiology of Jaundice, Clinical & Pathological types.
– Alcoholic Liver disease – Pathophysiology, types & complications.
– Hepatitis – Causes, types, Pathology (Alcohol, viral, Drug)
– Pathology of cirrhosis – Types, morphology & Clinical.
• Pathology Minor CLI:
– Primary Biliary cirrhosis & Primary Sclerosing Cholangitis.
– Wilson's disease, α1-Antitrypsin (AAT) deficiency.
– Hemosiderosis, Hemochromatosis, Wilson‘s disease.
– Liver tumours – adenoma, hyperplasia & cancer.
– Cysts: Amoebic liver abscess & Hydatid disease of liver.
– Congenital: Gilberts sy, Childhood cirrhosis
– Dengue, Ebola virus, Reye‘s sy,
– Liver blood supply disorders: Budd-Chiari Sy.

8. "When you speak, speak the truth;
perform when you promise;
discharge your trust... Withhold your
hands from striking, and from taking
that which is unlawful and bad..."
-- From Wings of Fire, book by Dr. APJ Abdul Kalam, Foremer President of India.

9. 9
Pathology of
Common Liver Disorders
Dr. Venkatesh M. Shashidhar.
Assoc.Prof & Head of Pathology

10. 10
• 1.5 kg, wedge shape
• 4
lobes, Right, left, (Caudate,
Quadrate)
• Double blood supply
• Hepatic arteries
• Portal – Venous blood
Normal

11. Normal Liver - Infant
Much larger, both lobes big, palpable below costal margin

12. 12
CT Upper abdomen - Normal
Liver
Stomach
Spleen

13. 13
Normal Liver – Microscopy
Acinus – showing zones 1, 2 & 3.
Portal Triad
Central Vein

14. 14
Structure of Liver Lobule
Portal Triad: Art, Vein, BD
GIT Venous bl.
Heart
IVC
Liver failure in
Cirrhosis…?

15. 15
Acinus Lobule
Functional Anatomic
Zone 1 – Toxin damage. Zone 3 – Ischemic damage
Toxins Ischemia
Toxins
Ischemia

16. 16
Liver Function Tests: Interpretation
• Synthesis / Function.
– Total protein & albumin low, PT prolonged why? (vit K..)
• Hepatocyte Injury.
– ALT, AST, LDH - high. – why?
– Alk Phos – moderately increased. – why?
• Bile Duct Damage:
– Alk Phos – increased – why?
• Other:
– GGT – increased with alcohol use. – why?
– Viral serology -
– Auto-Antibody panel.
GGT ↑ Alcohol (centrilobular)
IgG ↑ Autoimmune hepatitis
IgM ↑ Primary biliary cirrhosis
IgA ↑ Alcoholic cirrhosis
AFP +ve Hep. Cell. Carcinoma
Anti-
mitochondrial
antibody
+ve Primary biliary cirrhosis
Anti-smooth
muscle, & ANA
+ve Autoimmune hepatitis

17. 17
• Overproduction
(Hemolytic - Unconjugated)
• Impaired uptake
(Hepatitis - mixed)
• Block in metabolism
(Congenital)
• Impaired transport.
(Hepatitis, toxins)
• Intrahepatic Obst.
(Hepatitis)
• Extrahepatic Obst.
(Obstructive - Congugated)
Jaundice Types:

18. 18
Jaundice Clinical Types:
Stool Urine Ser. chem. Diagnosis
Dark Normal Un.Conj / ID Hemolysis.
Pale Dark Conj./D + ALP Cholestasis
Pale Dark ID+D ALT/AST Hepatitis.
Variable Variable Variable Cong. Syndr.

19. A wise man watches his faults more
closely than his virtues; others
reverse the order.
--Napoleon Hill

20. 20
Pathology of Viral Hepatitis
Dr. Venkatesh M. Shashidhar.
Assoc.Prof & Head of Pathology

21. 21
Viral Hepatitis: Introduction
• Viral Hepatitis:
– Specific – Heptitis B, C, D (serum), A, E
– Non-Specific - Many viruses CMV, EBV, etc.
– Acute, Chronic (CPH, CAH), Fulminant.
• Specific viral hepatitis important cause of
morbidity & mortality.
• Horizontal transmission – Blood.. Sex.
• Vertical transmission – Mother to fetus.
• Hepatitis  Cirrhosis  Hepatic Ca. (not in A/E)

22. 22
Hepatitis A
• 'faecal-oral' spread, Travel / exposure.
• Relatively short incubation period (2-6wk)
• Epidemics common, may be sporadic.
• Direct cytopathic virus (immune in B & C)
• No carrier state – prolonged immunity.
• Usually mild illness, full recovery usual.
• Rarely – severe or fulminant.
• IgM Ab is diagnostic. (no IgG tests).

23. 23
Viral Hepatitis A: Serology

24. 24
History Hep B Virus:
• In 1965 - Dr. Blumberg who was
studying haemophilia, found an
antibody in two patients which reacted
against an antigen from an Australian
Aborigine. Later the antigen was found
in patients with serum type hepatitis and
was initially designated "Australia
Antigen". Later proved to be hepatitis B
virus surface antigen (HBsAg). Dr.
Blumberg was awarded the Nobel Prize
in 1976.

25. 25
Hepatitis B
• Spread by blood, Sex & birth (serum hepatitis..)
• Relatively long incubation period (4-26wk)
• liver damage by antiviral immune reaction
• Carrier & Chronic state exist.
• Relatively serious infection – chronic
• Complications: cirrhosis, carcinoma.
• Diagnosis: Viral serology (HBs, HBc & HBe)
IgM anti-HAV
antibody
Acute Hepatitis A
HBsAg Hepatitis B or
carrier – exp./inf.
HBeAg Active hepatitis B
infection
Anti-HCV antibody Hepatitis C virus
exposure
HCV RNA Active hepatitis C
infection

26. 26
Viral Hepatitis B: Serology
Sequence of serologic markers for hepatitis B viral hepatitis demonstrating (A)
acute infection with resolution and (B) progression to chronic infection.

27. 27
Pathogenesis of Hepatitis A & B:

28. 28
Pathogenesis:
• Ingestion / inoculation
• Replication - Viremia
• Liver – major site replication.
• Cellular immune response.
• Apoptosis, necrosis of hepatocytes.
• Inflammation - Hepatitis
• Bridging Hepatocyte necrosis (Central vein,
portal triad)
• Fibrosis – patchy/bridging
• Cirrhosis – extensive fibrosis with loss of
archetecture & regenerating nodules.
• Liver Failure, Coma, Carcinoma..

29. 29
Pattern of Liver Damage
• Zonal – Toxin/Hypoxia
• Bridging – Viral & severe
• Interface – CAH, Immune
• Apoptotic – Acute Viral

30. 30
Clinical Viral Hepatitis: (A,B,C, D & E)
• Carrier state / Asymptomatic phase
• Hepatic dysfunction:
• Acute hepatitis – fever, icterus.
• Chronic Hepatitis – non specific.
– Chronic Persistent Hepatitis (CPH)
– Chronic Active Hepatitis (CAH)
• Fulminant hepatitis – massive necrosis
• Cirrhosis – total fibrosis.
• Hepatocellular Carcinoma

31. 31
Viral Hepatitis: Microbiology
Virus Hep-A Hep-B Hep-C Hep-E
agent ssRNA dsDNA ssRNA ssRNA
Incubation 2-6 wk 4-26 wk 2-6 wk 4-6 wk
Transm. Faeco-oral Parenteral Parenteral Faeco-oral
Carrier None 5-10% Rare/None None
Chronic
Cirrhosis
None
None
4-10%
1-3%
80%
50%
None
None
Other Young Mild /
fulminant,
travel.
Long incubat.
~ 120d
Steatosis
Severe.
Severe in
Pregnant

32. 32
Acute viral Hepatitis: Swelling & Apoptotic cells.
• Diffuse Inflammation.
• Necrosis & Apoptosis.
• Liver enzymes raised.

33. 33
Liver Biopsy – CPH:
Inflammation
• Portal Inflammation.
• No Necrosis
• Liver enzymes normal

34. 34
Chronic Active Hepatitis(CAH):
• Portal & Diffuse Inflammation.
• Necrosis & Apoptosis.
• Liver enzymes abnormal.

35. 35
Viral – Steatosis - Alcoholic
Microvesicular (viral) Macrovesicular (alcoholic)

36. 36
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.

37. 37
Fulminant Hepatitis:

38. 38
Clinical Spectrum of HBV inf:

39. Failure is a blessing when it pushes
one out of a cushioned seat of self-
satisfaction and forces him to do
something useful.
--Napoleon Hill

40. Laboratory Diagnosis
Viral Hepatitis

41. 41
Viral Hepatitis C: Serology

42. Hepatitis B – Lab result interpret

43. 43
Learn from the mistakes
of others. You can't live
long enough to make
them all yourself…!
61% of 5th year students exceeded ‘sensible’ limits
Drugs and alcohol were taken mainly for pleasure and were
perceived as a normal part of life for many students…
Capability of advising patients…?
http://www.lycaeum.org/research/researchpdfs/1996_webb_1.pdf

44. "The past, the present and the
future are really one: they are
today!"
-Harriet Beecher Stowe
The past has gone and future you cannot see. The present, when you can do something, that is the Gift
(Present) with which you can make your future & past memorable.
- Sai Baba

45. 45
Other Hepatitis

46. Drug Induced Zonal Hepatitis:
46
• Autopsy specimen in a case of
acetaminophen (paracetamol /
NSAID) overdose.
• Prominent hemorrhagic necrosis
of the centrilobular zones of all
liver lobules.
• greater activity of drug-
metabolizing enzymes in the
central zones.
• Other agents that produce such
injury are carbon tetrachloride,
toxins of the mushroom Amanita
phalloides.
• Patients either die in acute
hepatic failure or recover without
sequelae.

47. Autoimmune Hepatitis:
47
• Clinical & pathology similar
to Chronic hepatitis.
• Female predominance
(70%)
• Elevated serum IgG
• High titers of
autoantibodies.
• Autoimmune diseases.

48. Reye Syndrome:
48
• Acute disease of children
• Following a febrile
illness, commonly
influenza or varicella
infection with use of
aspirin.
• Microvesicular
steatosis, hepatic
failure, and
encephalopathy.
• Cerebral edema and fat
accumulation in the brain.
• Pathogenesis remains
unknown (Aspirin..)
Fat stain (oil-red o)

49. Toxemia of Pregnancy:
49
• Abnormal LFT in 3-5% of preg.
• Acute Fatty Liver of Pregnancy
• Intrahepatic Cholestasis of Preg.
• Hypertension, proteinuria, edema
and coagulation abnormalities
(pre-eclampsia) with convulsions
& coma (eclampsia).
• HELLP syndrome
(hemolysis, elevated liver enz. &
low plt).
• Patchy hemorrhages over
capsule, DIC
• Fibrin thrombi in portal vessels.
• Hepatocellular necrosis.

50. Self Study: brief
• Primary Biliary cirrhosis & Primary Sclerosing Cholangitis
(differences, Male, female, associated conditions etc).
• Wilson's disease & α1-Antitrypsin (AAT) deficiency.
• Hemosiderosis, Hemochromatosis – differences.
• Liver tumours – adenoma, hyperplasia & cancer.
• Cysts: Congenital, Amoebic & Hydatid.
• Congenital: Gilberts sy, Childhood cirrhosis
• Hepatitis in Dengue & Leptospirosis
• Reye‘s syndrome.
• Budd-Chiari Syndrome.
50

51. 51
Pathology of Cirrhosis

52. 52
Normal
Cirrhosis 
Cirrhosis
End stage of many
diffuse liver damages.
Resulting in scaring &
regenerating nodules
(liver failure due to
loss of archetecture)
Nodular
Shrunken

53. 53
Clinical Features - Pathogenesis
• Hypoalbuminemia/edema
• Hyperammonemia/CNS coma.
• Hypoglycemia
• Palmar erythema
• Spider angiomas
• Hypogonadism
• Gynecomastia
• Weight loss
• Muscle wasting
• Ascites
• Splenomegaly
• Esophageal varices
• Hemorrhoids
• Caput medusae-abdominal skin
• Coagulopathy
• Hepatic encephalopathy
• Hepatorenal syndrome
• Decreased Albumin synthesis
• Hepatorenal syndrome
• Glycogen metabolism.
• Excess Oestrogens
• Excess Oestrogens
• Excess Oestrogens
• Excess Oestrogens
• Decreased metabolism.
• Decreased metabolism
• Portal Hypertension
• Portal Hypertension
• Portal Hypertension
• Portal Hypertension
• Portal Hypertension
• Coag factory synthesis.
• Detoxification.
• ? Renal ischemia

54. 54
MRI Cirrhosis
Nodular
Shrunken

55. 55
Liver Biopsy – Cirrhosis
Reg. nodule
Fibrous septa

56. 56
Liver Biopsy – Cirrhosis
Reg. nodule
Fibrous septa

57. 57
Liver Needle Biopsy – Cirrhosis:
(Blue collagen stain)
Reg. nodule
Fibrous septa

58. 58
Etiology of Cirrhosis
• Alcoholic liver disease 60-70%
• Viral hepatitis 10%
• Biliary disease 5-10%
• Primary hemochromatosis 5%
• Cryptogenic cirrhosis 10-15%
• Wilson‘s, 1AT def rare

59. 59
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.

60. 60
Cirrhosis – Portal hypertension
• Cirrhosis-
obstruction
• Portal
hypertension
• Splenomegaly
• transudation -
Ascites

61. 61
Clinical
Features
Hepatic encephalopathy

62. 62
Gynaecomastia in Cirrhosis
??
?
?

63. 63
Palmar erythema & Spider nevi
? Pathogenesis

64. Primary Biliary Cirrhosis
• Autoimmune.
• Females 6:1.
• Pruritis, jaundice,
hepatosplenomegaly (initial).
• Intrahepatic Bile duct inflammation
• Cholestasis (bile stained liver)
64

65. Neonatal cholestasis / Cirrhosis
• Infections;
– CMV, Syphilis, Septicemia.
• Extrahepatic biliary atresia.
• Drugs & Toxins
– Nutrition, drugs.
• α1-Antitrypsin deficiency
– Protease inhibitor (inflam).
– Mild hepatitis  cirrhosis.
• Cystic fibrosis.
• Idiopathic
– Indian child hood cirrhosis.
65

66. 66
Normal / Cirrhosis Liver

67. 67
Hepatocellular Carcinoma
Normal - Carcinoma

68. 68
Hepatic Adenoma: rare
adenoma
adenoma

69. 69
Nutmeg Liver:
• Chronic Passive
Congestion – Heart failure.
• Central zone (Zone-3) –
congestion and necrosis.
• Hemorrhage – RBCs in
zone-3 - Mottled
appearance (nutmeg).
• Symptoms similar to
chronic
hepatitis, Ascites, distende
d abdomen, ankle
edema, Hepatic
encephalopathy, confusion.

70. 70
Liver Metastasis:
• Multiple
• Clear
demarcation
• Hemorrhage /
Central necrosis
(+/-)
• Microscopy
depends on type.

71. 71
Learn from the mistakes
of others. You can't live
long enough to make
them all yourself…!
61% of 5th year students exceeded ‘sensible’ limits
Drugs and alcohol were taken mainly for pleasure and were
perceived as a normal part of life for many students…
Capability of advising patients…?
http://www.lycaeum.org/research/researchpdfs/1996_webb_1.pdf

72. Alcoholic
Liver Disease

73. 73
Incidence is increasing…!

74. 74
Chronic Alcoholism:
• Clinical Features:

75. 75
Alcoholic Liver Injury:
• Ethyl alcohol : Common cause of
acute/Chronic liver disease
• Alcoholic Liver disease - Patterns
– Fatty change,
– Acute hepatitis (Mallory Hyalin)
– Chronic hepatitis with Portal fibrosis
– Chronic Liver failure
– Cirrhosis
• All reversible except cirrhosis stage.

76. 76
Alcoholic Liver Injury: Pathogenesis
• Acetaldehyde – metabolite – hepatotoxic
• Diversion of metabolism to alcohol
• Fat storage – fatty change. Cell swelling..
• Rupture Fat necrosis  severe
inflammation  fibrosis.
• Alcohol stimulates collagen synthesis
• Inflammation, Portal bridging fibrosis
• Micronodular cirrhosis.

77. 77
Alcoholic Liver Injury: Pathogenesis
• Diversion of fat metabolism
to alcohol – fat storage.
• Acetaldehyde – hepatotoxic
– denatures Proteins
• Increased peripheral release
of fatty acids.
• Alcohol stimulates collagen
synthesis
• Mutant ALDH2 gene with
low activity enzyme is
observed in Caucasians but
is found in some 40% of
Orientals (autosomal
dominant).
Acetaldehyde

78. 78
Alcoholic Liver Damage
Ito Cells

79. 79
High Risk
Intermediate
Low Risk
Safe drinking…

80. 80
Risk of Alcohol injury
1 Unit = 10ml = 8gm

81. 81
Alcohol Toxicity:
Liver Fatty change Toxicity
Acute hepatitis
Alcoholic cirrhosis
Nervous system Wernicke syndrome Thiamine deficiency
Korsakoff syndrome Toxicity and thiamine deficiency
Cerebellar degeneration Nutritional deficiency
Peripheral neuropathy Thiamine deficiency
Cardiovascular system Cardiomyopathy Toxicity
Hypertension Vasopressor
Gastrointestinal tract Gastritis Toxicity
Pancreatitis Toxicity
Skeletal muscle Rhabdomyolysis Toxicity
Reproductive system Testicular atrophy ?
Spontaneous abortion ?
Fetal alcohol syndrome Growth retardation Toxicity
Mental retardation, Birth
defects.

82. 82
Alcoholic Liver Damage

83. Alcoholic Hepatitis:
83
• Centrilobular necrosis. Ballooned degenerating hepatocytes (BC) Mallory bodies
(MB) Many Neutrophils, few lymphocytes & Macrophages.
• The central vein(or terminal hepatic venule (THV), is encased in connective
tissue (C) (central sclerosis). Fat-laden hepatocytes (F) are evident in the lobule.
The portal tract displays moderate chronic inflammation.

84. 84
Alcoholic Hepatits - Mallory's hyalin

85. 85
Alcoholic hepatitis & Mallory Hyalin:

86. 86
Alcoholic Fatty Liver

87. 87
Alcoholic Fatty Liver

88. 88
Alcoholic Fatty Liver

89. Diffuse fatty liver - un-enhanced CT.
Hamer O W et al. Radiographics 2006;26:1637-1653
©2006 by Radiological Society of North America
Normal

90. 90
Alcoholic Fatty Liver - CT

91. 91
Alcoholic Fatty Liver - CT

92. 92
Alcoholic Fatty liver:

93. 93
Alcoholic Fatty Liver - collagen stain

94. 94
Alcoholic Cirrhosis:

95. 95
Alcoholic Fatty Liver - collagen stain

96. 96
Alcoholic Liver Injury: Complications
• Pancreatitis – Acute or Chronic. Due to
ischemic damage to pancreas.
• Alcoholic hepatitis – similar to viral hepatitis.
• Fulminant hepatitis
• Alcoholic Cirrhosis – Micronodular.
Alcohol & Medical students
http://www.m-c-a.org.uk/about_us/about_mca

97. Miscellaneous Conditions
97

98. Primary Biliary Cirrhosis
• Autoimmune, Chronic, progressive
• Destruction of intrahepatic bile ducts, portal
inflammation & scarring – cholestasis.
• Leading to cirrhosis and liver failure.
• Females common (6:1)
• Insidious onset of Pruritis & cholestatic jaundice.
• Markedly high ALP, +ve antimitochondrial Ab.
• Histopathology: Portal inflammation, bile
stasis, bile plugs & lakes, Later stages cirrhosis
– Firm fibrotic, nodular, greenish, Shrunken.

99. Macronodular Cirrhosis - PBC

100. PBC – Microscopy:

101. Cholestasis: Bile ―plugs‖, Bile ―lakes‖
Bile Plugs
Bile Lakes

102. Biliary Atresia in a 3m child.
Dark bile stained liver tissue, cirrhosis & death before 2 years of age.

103. 103
Hepatosplenic schistosomiasis:
• Schistosoma Mansoni /
haematobium
• Granulomas in the liver.
• Fibrotic reaction around egg
• Pipe stem Portal Fibrosis
• Cirrhosis, spleenomegaly,
ascitis.

104. 104
Hepatosplenic schistosomiasis:
• Schistosoma Mansoni /
haematobium
• Granulomas in the liver.
• Fibrotic reaction around egg
• Pipe stem Portal Fibrosis
• Cirrhosis, spleenomegaly,
ascitis.

105. "It's not the will to win, but the will
to prepare to win that makes the
difference."
- - Bear Bryant 1913-1983, Football Coach

106. 106
CPC-2.2– Major Pathology CLI:
• Pathology of Acute & Chronic Liver injury.
• Hepatitis – Causes, Types, Pathophysiology, Gross &
Microscopic Pathology. Complications.
• Common types: Viral (Specific & Non specific), Alcoholic
& Drug induced.
• Pathophysiology of Jaundice, Clinical & Pathological
types.
• Pathology of cirrhosis – Classification, morphology &
Complications.
• Pathology of Alcoholic Liver disease – Pathophysiology,
types & complications.

107. 107
CPC-2.2– Minor Pathology CLI:
• Hemosiderosis & Hemochromatosis.
• Pathogenesis of Hepatic coma, Liver failure.
• Primary Biliary cirrhosis.
• Hepatocellular carcinoma.
• Liver cysts & tumours – adenoma, hyperplasia & cancer.
• Amoebic liver abscess & Hydatid disease of liver.
• Congenital liver disorders – enzyme disorders.

108. 108
Clinical Case Study

109. 109
Case # 2 - ? Diagnosis
• 60yr Male, 8 month slowly developing weakness,
mild icterus.
• PE: Mild Abdominal tenderness, No
organomegaly. Mild Scleral icterus.
• Labs: ALT: 52 (N= 8-33 U/L)
• AST: 58 (N= 4-36 U/L)
• Alk Phos: 150 (N= 20-130 u/L)
• Bilirubin 3.9 (N= 0.1-1.2 mg/dL) (direct 1.8)
• T Protein 4.8 (N= 6.0-7.8 g/dL)
• Albumin 2.5 (N= 3.2-4.5 g/dl)
• PT = 16 sec (N= 11-14.7 sec )
• Differential diagnosis?
• What further investigations?

110. 110
Diagnosis pathway:
• Jaundice?
– Mild increase, Mixed (combined)
• Synthesis?
– Total protein, albumin – Low & PT abnormal.
• Obstruction & Bilirubin Clearance ?
– Alk Phos is up a bit – but not high – some obstruction.
• Hepatocyte Direct Injury:
– ALT & AST are up a bit, but not dramatically.
• Discussion:
– Chronic Mild compromise - chronic Active
hepatitis. (In CPH LFT will be normal)
ALT: 52
AST: 58
Alk Phos: 150
Bilirubin 3.9 (direct 1.8)

111. 111
• 28y Male, 3 weeks after visiting east
Timor, presents with malaise, fatigue, loss
of appetite. Mild icterus. AST & ALT mild
elevation. Total bil 3.9mg/dl (Direct 2.8).
Which of the following would be positive?

112. 112
Alcohol Metabolism:

113. 113
Chronic Hepatitis:
• Passive CPH
• Limited Periportal
inflammation.
• Mild Periportal fibrosis
• No hepatocyte
Necrosis.
• LFT normal or mild
change.
• Late cirrhosis
• Active CAH
• Extensive
Inflammation
• More fibrosis.
• Necrosis of
hepatocytes.
• LFT abnormal.
• Early cirrhosis & other
complication.

114. “Nearly all men can stand adversity,
but if you want to test a man's
character, give him power!”
— Abraham Lincoln