Patho prac 1: Liver

Reversible hepatic changes

Hepatocyte swelling by fat, water, bile pigment

Irreversible hepatic changes

Apoptosis, Necrosis

Pattern of liver damage: Zonal cause

Toxin / Hypoxia

Pattern of liver damage: Bridging cause

Viral severe

Pattern of liver damage: Interface cause

Immune

Pattern of liver damage: Apoptotic cause

Viral

Apoptosis histological marker in liver

Councilman body

Focal necrosis microscopic appearance (M/E)

Necrotic foci indicated by aggregates of lymphocytes & macrophages

Zonal necrosis: Central zonal location and causes

Affects zone III due to acute viral hepatitis & C.V.C.

Zonal necrosis: Mid-zonal location and cause

Affects zone II due to yellow fever

Zonal necrosis: Peripheral zonal (Piecemeal necrosis) location and cause

Affects zone I due to chronic hepatitis

Diffuse necrosis definition

Complete (Massive) or near complete (Sub-massive) destruction of hepatocytes affecting almost the whole liver

Acute viral hepatitis histological features

Councilman body (Acidophil body), Kupffer cell hyperplasia, Inflammatory infiltrate, Dropout necrosis, Regeneration, Ballooning degeneration

Types of hepatocyte degeneration

Feathery degeneration, Ballooning degeneration

Classic viral hepatitis hepatocyte changes

Councilman bodies, Spotty/Focal necrosis

Acute viral hepatitis gross appearance

Liver gets smaller in size, soft, with wrinkled capsule with yellow patchy foci or large areas

Acute viral hepatitis microscopic appearance (M/E)

Extensive hepatocyte necrosis with few surviving ones with reticulin framework collapse

Chronic hepatitis features (M/E)

Hepatocyte destruction and lymphocytes and focal necrosis

Chronic hepatitis B histological marker

Scattered ground glass hepatocytes

Chronic hepatitis C histological feature

Moderate fatty change

Congenital alpha-1 antitrypsin deficiency histological finding

Presence of PAS +ve globules inside the hepatocytes

Cirrhosis gross features (N/E): Size, Consistency, Surface

1. Size: Enlarged then become reduced (shrunken).

2. Consistency: Firm due to fibrosis.

3. Surface & C/S: Nodular (Macronodular: 3mm to 1cm, may reach up to 6cm, Micronodular: 2 - 3mm, and Mixed.)

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Cirrhosis M/E: Regenerating nodules

Proliferated hepatocytes arranged in thick plates and separated by blood sinusoids. Central vein in abnormal sites (eccentric). Hepatocytes may be small, large, or binucleate.

Cirrhosis M/E: Fibrosis patterns

Perivenular, perisinusoidal, pericellular fibrosis

Cirrhosis M/E: Bile ductular proliferation & inflammation

Bile ductular proliferation occurs in fibrous septa with focal cholestasis and feathery degeneration at margins of regenerating nodules.

Inflammation present contains lymphocyte, macrophage, plasma cell infiltrate in fibrous septa.

Etiological classification categories of cirrhosis

Congenital, Acquired

Congenital cirrhosis examples

Primary idiopathic haemochromatosis, and alpha-1-antitrypsin deficiency

Alcoholic cirrhosis progression & gross features

Progresses slowly over few years.

Gross: Liver at first enlarged (fatty change), then normal size, lastly slightly reduced (1.2 kg or more). Micronodular then macronodular then mixed.

Alcoholic cirrhosis M/E features

1. Hepatocytes: Fatty change that decreases progressively; few show increased intracytoplasmic haemochromatosis.

2. Fibrous septa: Regular margins with regenerating nodules, moderate lymphocytic infiltrate, slight bile ductular proliferation.

Primary Biliary Cirrhosis (PBC) staged progression

Stage 1: Bile duct inflammation & damage (early portal tracts with lymphocytes and plasma cells destroying ducts).

Stage 2: Granulomatous inflammation surrounding damaged ducts (hallmark).

Stage 3: Cholestatic changes (bile ductular proliferation, periportal Mallory's hyaline, increased copper in periportal hepatocytes).

Stage 4: End stage micronodular cirrhosis with subsided inflammation.

Primary Biliary Cirrhosis (PBC) histological hallmark

Granulomatous inflammation surrounding the damaged and inflamed bile ducts

Liver cell adenoma characteristics

Highly vascularized, liable for rupture with internal hemorrhage. Formed of groups of hepatocytes which may produce pseudocanaliculi and bile.

Primary liver carcinoma gross forms and features

Arises in irregular cirrhosis.

Forms:

1. Single large well-defined mass with hemorrhage & necrosis.

2. Multiple small nodules scattered all over liver sparing periphery.

3. Diffuse infiltration. Tissue is yellow-white and may be bile-stained (green).

Hepatocellular carcinoma M/E: Well differentiated

Tumor cells resemble hepatocytes, arranged in trabeculae separated by sinusoids & pseudoglandular structure. Bile may be present.

Hepatocellular carcinoma M/E: Poorly differentiated

Large anaplastic cells, may be bi- or multinucleated giant cells or clear cell type. Stroma is scanty and poorly vascular.

Hepatocellular carcinoma M/E: Fibrolamellar carcinoma

Cords of polygonal cells with acidophilic cytoplasm separated by lamellated fibrous stroma

Secondary liver tumors (Metastases) gross features

Marked hepatomegaly, distorted liver. Surface shows central umbilication (central depression due to necrosis). Green color due to intrahepatic cholestasis. Multiple nodules all over including periphery (rarely 1-2 masses). Color varies by primary (e.g. black in melanoma).