SURGICAL PATHOLOGY

(1 SEMESTER)|Liver and Gallbladder Pathology|Dr. Bayotas

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OUTLINE
MOST COMMON PATTERNS OF INJURY
I. LIVER
II. PATHOLOGIC FINDINGS
III. MOST COMMON PATTERNS OF INJURY HEPATOCELLULAR COMPARTMENT
IV. CLINICAL SYNDROMES o Portal inflammation
V. CHOLESTASIS • Inflammatory cell predominating
VI. NEONATAL CHOLESTASIS ▪ Chr hepatitis
▪ Autoimmune disorder
VII. LIVER NEOPLASMS
(mononuclear)
VIII. METASTASES TO THE LIVER o Interface activity (periportal hepatitis, piecemeal
IX. ACUTE ALLOGRAFT REJECTION necrosis)
X. CHRONIC REJECTION (DUCTOPENIC • Lymphocytes predominating
REJECTION) • Active means ongoing injury
XI. GALL BLADDER o Lobular inflammation
• Lymphocytes distant from the portal
LIVER tract
Keywords: o Vacuolar degeneration (balloon cell change)
• Needle core biopsy • Hydrophic degeneration
o Biopsy is done to monitor disease o Acidophilic bodies
progression (Hepatitis) • Dyskeratotic (pyknotic nuclei)
o Graft vs Host Disease (Evaluation of o Fibrosis
transplant) • Increase of collagen on the portal tract
o Dx suspicious mass • Bridging fibrosis
o Stain use: Trichomes, Iron stain, Prussian • End process is cirrhosis, the division of
blue liver into individual lobules separated by
thick band of fibrous tissue
LEARNING OBJECTIVES o Steatosis
• Deposits of fats at hepatocytes
• >5%-30 Mild
• Recognize the histomorphologic features of
• 30-60% Moderate
conditions affecting the liver and the biliary
• >60% Severe or
tract.
marked
• Describe the pathogenesis of the disease
▪ Due to Rye’s syndrome
process
o Steatohepatitis
• Correlate the morphologic changes with the
• Steatosis with inflammation
clinical presentation of the disease
o Mallory’s hyaline (Mallory bodies)
• Apply basic concepts learned given a case
• Irregular, whorled-like, pink structure
involving disorder of the liver and biliary tract
• Cytoskeleton collapse
• Enumerate important diagnostic procedures
o Megamitochondria
needed to evaluate conditions involving the liver
• Sized like RBC
and biliary tract.
o Iron accumulation
• Interpret results of basic laboratory tests used
• Use Prussian blue to observe
to evaluate disorders of the liver and biliary

PATHOLOGIC FINDINGS

A. Acute Injury
o Widespread edema
o Acute and chronic inflammation
o Necrosis
B. Subacute or chromic injury
o Mononuclear Inflammatory cells
o Necrosis or degeneration

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 SURGICAL PATHOLOGY
(1 SEMESTER)|Liver and Gallbladder Pathology|Dr. Bayotas
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o Seen mostly in patients with congenital biliary

atresia
CLINICAL SYNDROMES

HEPATIC FAILURE
o Jaundice
BILIARY COMPARTMENT o Hypoalbuminemia
o Cholestasis o Hyperammonemia
• Accumulation of bile o Palmar erythema
o Bile duct proliferation o Spider angioma
• Increase number bile duct profiles that o Hypogonadism and gynecomastia in men
occurs at each portal tract o Coagulopathy
• The normal ratio is average 1:2 per tract o Hepatic encephalopathy
o Bile duct injury o Hepatorenal syndrome
• Defined as presence of lymphocytes, PORTAL HYPETENSION ASSOCIATED WITH
and vacuolar degeneration: dropped out CIRRHOSIS
epithelial cells o Ascites
o Ductopenia o Splenomegaly
• Recurrent bouts of bile duct injury o Esophageal varices
• Loss of bile duct (chronic damage of the o Hemorrhoids
biliary system) o Caput medusae-abdominal skin
• End stage injury CHOLESTASIS
o Jaundice
VASCULAR COMPARTMENT o Pruritus
o Venulitis (endothelitis) • Bile acid deposit in the skin
• Damage of the endothelium of the o Skin xanthomas
portal/central vein by the inflammatory • Accumulation of fat in macrophages in
cells the skin
• Indication of rejection, graft vs host o Increase alkaline phosphatase
disease o Intestinal malabsorption of fat-soluble vitamin
o Extramedullary hematopoiesis CIRRHOSIS
• Generalized indication of bone marrow o Anorexia
disease o Weight loss
▪ Look for the age of the patient o Weakness
• Fetal, infant o Frank debilitation
(Physiologic) o Progressive liver disease
• Adult (Pathologic) o Portal HPN
o Hepatocellular
• Presence of megakaryocytes

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 SURGICAL PATHOLOGY
(1 SEMESTER)|Liver and Gallbladder Pathology|Dr. Bayotas
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CHOLESTASIS NEONATAL CHOLESTASIS

o Bile stagnation due to o Prolonged elevation of conjugated bilirubin in the

• Hepatocellular dysfunction serum
• Intra hepatic biliary obstruction o 1 in 2500 live birth
• Extrahepatic biliary obstruction o Major causes
▪ Amenable to surgery • Biliary atresia
o Other causes: • Neonatal hepatitis
• Pregnancy o Other causes:
• Benign familial recurrent cholestasis • Tumor
• Medication • Toxic or metabolic
▪ Amiodarone • Idiopathic
• Sepsis ▪ Not amenable to surgery
• Rarely malaria falcifarum • Infection
o Symptoms o Clinical features
• Jaundice • Jaundice
• Pruritus • Dark Urine
• Skin xanthomas • Light or alcoholic stools (greyish white)
• Fat soluble vitamin deficiency – ADEK • Hepatomegaly hypoprothrombinemia
▪ Intestinal malabsorptive o Morphologic features:
dysfunction affecting fat • Lobular disarray
analytes ▪ Disorganize lobule
• Giant cell transformation of hepatocyte
(unique feature: pointed by the arrow)
• Hepatocellular and canalicular
cholestasis
• Mononuclear infiltration of portal areas
• Reactive changes in Kupffer cells
• Extramedullary hematopoiesis
(presence of megakaryocytes)

o Bile pigment accumulated within the Kupffer

cells
o Laboratory
• Elevated serum bilirubin
• Elevated serum alkaline phosphatase

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 SURGICAL PATHOLOGY
(1 SEMESTER)|Liver and Gallbladder Pathology|Dr. Bayotas
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• Surrounding liver tissue is normal

LIVER NEOPLASMS
• Central stellate scar with radiating septa

WHO Classification of Primary Liver Mass Lesions

Epithelial Mass Lesion Nonepithelial Mass
Lesion

o Microscopic findings
o Metastatic is more common than primary • Multiple focal nodules without fibrosis
o Benign primary lesion is more common than • Nodular overgrowth of normal appearing
malignant primary lesion hepatocytes
o Metastatic>benign primary lesion> malignant • Large caliber vessels in central stellate
primary lesion scar
▪ Blue area
FOCAL NODULAR HYPERPLASIA (FNH) • Bile ductular proliferation in scar
o Non-neoplastic mass lesion caused by nodular • Absence of bridging fibrosis (differential
overgrowth of hepatocytes in region of altered for cirrhosis)
hepatic blood flow
• Multifocal nodular hyperplasia if it co-
exists with
▪ 20% cases with cavernous
hemangioma
▪ Berry aneurism
▪ Astrocytoma or
▪ Meningioma
o Clinical manifestation
• 80% asymptomatic
• 70-80% solitary
• 80-90 occurs in women of reproductive
age
o Clinical features
• Usually, incidental finding
• Associated with oral contraceptive use
in 50% to 60% of cases
• Rarely associated with abdominal pain,
hepatomegaly, or tenderness
• Associated with extrahepatic vascular
lesions
• Normal alpha-fetoprotein
o Gross findings
• Single subcapsular lesion in in right lobe
• Well-circumscribe lesion
• Average size less than 5cm to 10 cm

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 SURGICAL PATHOLOGY
(1 SEMESTER)|Liver and Gallbladder Pathology|Dr. Bayotas
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LIVER CELL ADENOMA • Microscopic findings

• Arises in normal or nearly normal liver in o Benign heaptocytes without acinar
patients with abnormal hormonal or metabolic architecture or portal tracts
condition o Tumor cells often contain glycogen or
• 95% women, usually child-bearing age history of fat
5+ years of OCP o Thin-walled vascular channels scattered
• Adenoma are encapsulated mass having a throughout tumor
uniform bland-looking hepatocyte with no septal o No biliary epithelium
vein or bile duct, diffuse prominent arteriole
o Cells are pale
▪ Steatosis
▪ Glycogen
o Reticulin
▪ Every cell touches the reticulin
• In 85% regresses with discontinued use
spontaneous
• 2-4% hepatic tumors in children
• Associated with
o Glycogen storage disease type Ia and III
o Fanconi’s anemia Normal portal structures are lacking, and there is no
o Familial Adenomatous Polyposis biliary epithelium. The hepatocytes are bland.
o Familial DM Haphazardly arranged parenchymal vessels are
o Hurler’s disease or Tyrosinemia characteristic
• Associated with anabolic steroids (in men), anti-
estrogens, Klinefelter’s syndrome or other
abnormal secretion of sex steroids HEPATOCELLULAR CARCINOMA
• Gross Findings • Also called Liver Cell Carcinoma
o Yellow tan or red-brown solitary nodule • HEPATOMA
in noncirrhotic liver • 85% of hepatic malignancies (30% in children)
o Most measure 5 to 15 cm • Major cause of cancer death worldwide (20-40%
o May be hemorrhagic in China, Japan, sub-Saharan Africa), although
not in North America
o Primary carcinomas are rare in North
America, but more common in countries
bordering Mediterranean Sea Endemic
for viral hepatitis
• Causes of HCC
o The most common cause of HCC is the
scarring of the liver due to
▪ Alcohol Abuse
▪ Hep B
▪ Hemochromatosis or iron
overload
▪ Autoimmune diseases
▪ Diseases that causes
inflammation of the liver
• Risk Factors/Causes
o HBV-infant carriers have 200x risk
o Cirrhosis
Hepatic adenomas are sharply circumscribed lesions.
o Hep C virus
Intrahepatic hemorrhage is a common in resected
o Genetic variation
specimens
o Thorotrast exposure
o Androgenic steroids
o Tyrosinemia

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 SURGICAL PATHOLOGY
(1 SEMESTER)|Liver and Gallbladder Pathology|Dr. Bayotas
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o Aflatoxins o Death usually within 1 year from

▪ Aspergillus flavus- a potent cachexia
carcinogen in some areas o GI bleed
endemic for HCC is activated by o Liver failure
the hepatocytes, products o Rupture of tumor (10%)
intercalate into DNA to form • Metastases
mutagenic adducts with o Initially within the liver
guanosine o Distant metastases late to
▪ Aflatoxin B1, a metabolite of the ▪ Lungs
fungus ▪ Bone
• Gross ▪ Adrenal gland
o Unifocal, multifocal or diffusely ▪ Porta hepatis lymph nodes
infiltrative soft tumor, paler than normal • Gross
tissue, may be green due to bile o Soft yellow-green or reddish masses of
o Extensive intrahepatic metastases are varying sizes
common o 3 basic patterns
o Snakelike masses of tumor – involve ▪ Multinodular
the: ▪ Solitary
▪ Portal vein (35%-80%) ▪ Massive or diffuse
▪ Hepatic vein (20%) o For symptomatic individuals- most
▪ Inferior vena cava common is large mass surrounded
o Hemorrhage and necrosis by several satellite nodules,
o Occasionally tumor is pedunculated multinodular appearance may be difficult
o Liver usually chronic, often enlarged to distinguish from cirrhosis.
o Among the three diffuse pattern is rare
o Tumor thrombi in veins are common as
is spontaneous rupture of larger masses
• Microscopically
o Patterns
▪ Trabecular (most common) with
4+ cells surrounded by layer of
flattened endothelial cells
▪ Solid (compact)
▪ Pseudo glandular (acinar with
proteinaceous material or bile in
lumina, may be resemble
thyroid follicles)
▪ Pelioid
o May arise in setting of cirrhosis, may be due ▪ Giant cell
to viral hepatitis, chronic alcoholism. ▪ Sarcomatoid
• Laboratory ▪ Clear cell patterns
o Elevated serum AFP o Sinusoidal vessels surrounding tumor
▪ Not a diagnostic marker but a marker to cells is important diagnostic feature
determine the effectivity of the therapy o Scantly stroma, from well differentiated
▪ 70% sensitive to bizarre (often within same tumor)
▪ Reduced sensitivity in Alcohol related o Cells
cirrhosis (65%) ▪ Polygonal with distinct cell
▪ Tumors arising in non-cirrhotic liver membranes
(33%) ▪ Higher N/C ratio
▪ Tumors 2cm or less (25%) ▪ Abundant granular eosinophilic
• 5 Year Survival cytoplasm
o 10% normally to 50% in tumors 5cm or ▪ Round nuclei with coarse
less with resection chromatin and thickened
nuclear membrane
▪ Prominent nucleoli

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 SURGICAL PATHOLOGY
(1 SEMESTER)|Liver and Gallbladder Pathology|Dr. Bayotas
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• Divided into two entities, intrahepatic and the

more common among the two is extrahepatic
• Extrahepatic aka Klatskin tumor [American
internist]: hilar tumor arising at confluence of left
and right hepatic ducts
• Laboratory: Normal AFP, occasional
hypercalcemia
• Poor prognosis
o Death within 6 months; 5-year survival
in resectable cases is 30%
o 50-75% metastasize to regional lymph
▪ Also intranuclear pseudo nodes, lungs, vertebrae, adrenals, brain,
inclusion (pointed by the arrow) elsewhere at autopsy 50% are
▪ Mallory’s hyaline (2-25%) metastatic to perihilar, peripancreatic
▪ Bile (5-33%) and bile canaliculi and paraaortic nodes
▪ Vascular invasion and portal • Poor prognosis factors: Lymphatic or
vein thrombosis are common intrahepatic metastases
▪ Mitotic figures are common • Reduced keratin 903 expression may be
▪ Minimal desmoplasia favorable prognostic factor
▪ Occasionally fibrous variants, • Grossly:
vascular lakes (pelioid pattern), o Solitary, 7-10 cm, multinodular or diffuse
abundant fat, no central veins small nodules <1cm; gray white and
CHOLANGIOCA (INTRAHEPATIC) firm.
• Called BILE DUCT CARCINOMA o Often hepatomegaly and satellite
• 10% of primary liver cancers nodules
• Adenoma arising from intrahepatic bile duct o No peripheral hyperemic zone seen in
epithelial cells metastatic disease
• High prevalence in southeast and eastern Asia, o Rarely cirrhosis
including Korea o Rarely bile stained, although may see
bile in periphery
CHOLANGIOCARCINOMA (INTRAHEPATIC) o May invade portal vein
• 10-20% are associated with • Microscopic
o Chronic bile stasis or cholangitis due to o Moderate to well differentiated adenoca
autosomal dominant polycystic disease with glandular and tubular structures,
o Congenital dilated hepatic ducts mucin production and dense
(Caroli’s disease) desmoplasia
o Congenital hepatic fibrosis o Epithelial cells are anaplastic, cuboidal
• Infection by liver flukes Clonorchis sinensis or to columnar with eosinophilic cytoplasm
Opisthorchis viverrini and round central nuclei, tumor cells are
• Thorotrast, anabolic steroids, intrahepatic heterogenous even within the same
lithiasis (5-10% of these patients) gland nut resemble bile duct cells, not
hepatocytes
• Primary sclerosing cholangitis (7-42% of these
o Spread along hepatic plates, duct walls,
patients)
via nerves (81% perineural), but not
• Choledochal cysts
sinusoidal
• Rarely associated with neoplastic transformation o Stroma may be circumferential around
of von Meyenburg complexes glands
• Not associated with cirrhosis o Associated with neutrophils
• Diagnosis of exclusion (must rule out metastatic o Variable vascular invasion
adenocarcinoma) o No bile production
• Usually age 60+ years; no gender preference; o Positive stain
but mean age 40 years in those with primary ▪ Mucin (almost always)
sclerosing cholangitis or chronic inflammatory ▪ CEA (cytoplasmic and luminal,
bowel disease not canalicular)

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 SURGICAL PATHOLOGY
(1 SEMESTER)|Liver and Gallbladder Pathology|Dr. Bayotas
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▪ CAM 5.2, (Pancytokeratin:) Note the numerous mass lesions that are of variable
AE1- AE3, keratin 903 (74%), size. Some of the larger ones demonstrate central
CK7 (90-96%), CK19 (84%), necrosis. The masses are metastases to the liver. The
CK20 (30-70%, more often obstruction from such mases generally elevates
positive in non-peripheral alkaline phos. but not all bile ducts are obstructed, so
tumors), EMA, amylase, PTH- hyperbilirubinemia is typically not present. Also, the
related peptide, p53 (10-94%) transaminases are usually not greatly elevated.
o Negative Stain: AFP
o Molecular: Kras mutations

• Microscopic
o Sinusoids are dilated
o Cholestasis is seen
o Brown pigment (bile)
o Disorganize as seen on the right side of
the slide
- Has a glandular appearance ACUTE ALLOGRAFT REJECTION
- A liver CA may have both HCC and
cholangiolar differentiation • Hepatic Allograft rejection is an injury to the
- DO NOT MAKE BILE, but the cells do make transplanted liver caused by the
mucin, and they can be almost impossible to IMMUNOLOGIC REACTIONS of the HOST
distinguish from mets Adenoca or biopsy or • Three Types of Rejections
FNA 1. Humoral Rejection (Hyperacute/Antibody
Mediated)
o Rare
METASTASES TO THE LIVER o Common in ABO Incompatible Donor
o C4d Immunostains help for the
• The liver and the lungs most common visceral diagnosis
organs involve in the metastases of cancer, for o Keys to the diagnosis of humoral
instance colon cancer, (primary cancer such as: rejection
breast, lungs, pancreas, melanoma, lymphomas, ▪ Graft dysfunction diagnosed
leukemia) by clinical evaluation and
laboratory tests
▪ Liver biopsy with evidence
of active graft damage
suggests humoral rejection
▪ Any pattern of intense
reactivity for C4d
▪ Circulation of anti-donor
specific antibody
2. Acute Rejection (Cellular)
o Most common form
o Occurs usually at 1st– 3rd weeks after
transplantation (7-10 days)
o CELL MEDIATED IMMUNE REACTION
directed to Bile Duct Epithelium and

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 SURGICAL PATHOLOGY
(1 SEMESTER)|Liver and Gallbladder Pathology|Dr. Bayotas
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Endothelium of Portal and Centrilobular ▪ Ductal injury: ductulitis of lymphocytes

Veins and degeneration of ducts
o Microscopic: Triad of portal infiltration, ▪ Endotheliitis: portal and/or central
bile duct damage, and endotheliosis subendothelial inflammation
(2 features may satisfy the diagnosis)
o Inflammation: Predominantly
Lymphocytes
o The Banff rating system assigns a
numerical weight each criterion or
morphological parameter according to
the severity. The well-known Rejection
Activity Index (RAI) for acute cellular See enlarged copy at the appendix
rejection assigns a score from 1-3 with
maximum of possible score of 9.

See enlarged copy at the appendix See enlarged copy at the appendix

o The higher the grade the more severe CHRONIC REJECTION (DUCTOPENIC REJECTION)
the cellular rejection
o Loss of bile duct
o This is an immunologic injury to the allograft
o Severe or persistent acute rejection that may
lead to IRREVERSIBLE DAMAGE of the bile
ducts, arteries, terminal hepatic veins
o Centrilobular and Portal Tracts may be affected
GALL BLADDER

o Cholelithiasis (Gallstone)
o Cholesterosis
o Acute Cholecystitis
o Chronic Cholecystitis
o Carcinoma of the Gall Bladder
CHOLELITHIASIS
o This is one of the most common GIT diseases
worldwide affecting F>M
Representative C4d staining in crossmatch-negative o Formation and Risk of Gallstones are due to:
patients. Brown pigment (Humoral Rejection) • Body Weight
A. Capillary staining of C4d in the portal area • Childbearing
showing acute rejection • Estrogens
B. Internal lamina of hepatic artery • Other conditions that cholelithiasis are
C. Acute rejection with portal stroma staining ▪ Hemolysis
surrounding blood vessels or bile ducts ▪ Chron’s disease
D. Faint capsular staining in time zone biopsy ▪ Congenital anomaly
o Key to diagnosis of acute cellular rejection o Gallstone (Stones) – formed based on the
▪ Portal inflammation: heterogenous amount of Cholesterol
infiltrate with activated lymphocytes and o Cholesterol (Mixed Type) (>80% Stones: most
eosinophils common) – Cholesterol, Bile Salts, and
Phospholipids

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 SURGICAL PATHOLOGY
(1 SEMESTER)|Liver and Gallbladder Pathology|Dr. Bayotas
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o Pigment (Medical Condition Related due to o Lipitor- antilipemic drug

Hyperbilirubinemia) – Calcium Bilirubinate, • Targets HMGCoAR
phosphate and carbonate o Complications
o Key for the development Stones: • Hydrops
• Cholesterol crystal aggregates and ▪ Gallbladder distended by watery
mucin fluid
• Bile Supersaturation and destabilization • Mucocele
• Gallbladder hypomotility ▪ Distended mucosa
o Other Types of Stones: • 3% of cholecystectomies
1. Brown Stone: Calcium Salts of Bilirubin and • Due to obstruction
Palmitate ▪ Rarely due to cystic fibrosis
2. Calcium Carbonate and Phosphate Stones
3. Brown-Green Stones- Associated with
infections (E. coli and Biliary Flukes)
o Choledocholithiasis – can occur with or without
obstruction but are secondary to Cholelithiasis
o Hydrops – caused by impaction gallstone to
cystic duct
o Obstruction at Common Bile Duct or Ampulla –
can cause severe colicky pain and obstructive
jaundice

• Mirrizi Syndrome – impacted cystic duct stone

causes edema and compression and
obstruction of common hepatic duct
• Internal Biliary Fistulas- 90% occur at the area:
(due to inflammatory Adhesions between
Affected Biliary Tree and Adjacent Organ)

o Duodenum and gallbladder

o Gallbladder and Colon
o Cystic Bile Duct and Duodenum

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 SURGICAL PATHOLOGY
(1 SEMESTER)|Liver and Gallbladder Pathology|Dr. Bayotas
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ACUTE CHOLECYSTITIS o Associated findings

• Gross: • Cholesterol Stones
o Angry red color, large and distended, • Cholesterol Polyps
hemorrhagic external surface
o Foci of gangrene perforation
o Stone is present 95% cases
• Complication
o Chronic perforation into adjacent viscus
(cholecystoenteric fistula)
▪ Air is seen in the biliary tree
• Microscopic

ADENOCARCINOMA OF THE GALLBLADDER

• Most common type accounting 80-90% of cases
• Common among females with the ratio of 3-4:1
• 50% in the age of 50-year-old
• Associated risk factors:
o Cholecystoenteric fistula (intestine is
another site of gallbladder cancer)
o Mucosa, portion of muscularis and serosa
o Porcelain gallbladder
shows hemorrhage
o Adenomyosis
o Mononuclear infiltration (Lymphocytes and
o Garder’s syndrome
Plasma Cells
o Anomalous connection of the common
o Fibrosis
bile duct and pancreatic duct
o Rokitansky-Aschof sinuses – lined by
columnar or cuboidal epithelium and may • Clinical Signs
contain bile stones (benign) o Elevation of alkaline phos
o Nodular polypoid capillary masses some
are not so apparent on gross
examination
• Microscopic is important
• Anatomic Portion
o Fundus (70-80% of CA is located at the
fundus)
o Body (10%)
o Neck (10%)
• Gallstone is the most common predisposition
factor of this cancer
o 2% of patient progress to gallbladder CA
• Molecular Aberration:
o KRAS mutation (60%)
• Sinuses protruded down to the o TP53 mutation (50%) – high grade
muscularis of the gallbladder tumor types
• Feature of chronic cholecystitis and o Loss of histidine (early signs)
fibrosis • Spread and metastasis (all half the patients
CHOLESTEROSIS already have this at the time surgery)
o Accumulation of LIPIDS within the macrophages o Liver invasion is directly (common)
in the lamina propria o Stomach and duodenum invasion
o Gross: linear yellow streaks in the muscosal o Ovarian metastasis with stimulate of
ridges (strawberry bladder) primary ovarian risk

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 SURGICAL PATHOLOGY
(1 SEMESTER)|Liver and Gallbladder Pathology|Dr. Bayotas
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FREEDOM WALL

a. Fungating hemorrhagic mass

b. Nodular

e. Polypoid within the mucosa

f. Thickening and no obvious mass (diffuse type of
gallbladder CA)

REFERENCES

Dr. Bayotas PPT

RECORDINGS

APPENDIX

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(1 SEMESTER)|Liver and Gallbladder Pathology|Dr. Bayotas
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