Upper abdominal

Liver

Author: Mikael Häggström

Comprehensiveness

On this resource, the following formatting is used for comprehensiveness:

• Minimal depth
• (Moderate depth)
• ((Comprehensive))

Tissue sampling

• Autopsy
• Liver biopsy

Fixation

Generally 10% neutral buffered formalin. Non–formalin-fixed tissue may be needed for tests such as microbiological analysis or copper quantification studies.

Gross processing in autopsy

• ((Measure the distance from the liver edge to the right costal margin.))
• Inspect the color and texture of the surfaces, including external and cut surfaces. Potential pathologies:

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  Diffuse areas of pallor in cirrhosis, see Cirrhosis

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  Pale macronodules of cirrhosis, see Cirrhosis

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  Nutmeg texture of congestive hepatopathy

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  Liver metastases

• Look for any focal change in the liver volume, mainly any tumor. If found: Further information: Liver tumor
• Determine liver weight. The standard reference range for men is 970–1,860 g (2.14–4.10 lb) and for women 600–1,770 g (1.32–3.90 lb).
• Make consecutive liver slices, such as in the sagittal or coronal plane.

Gross report in autopsy

• ((Distance from the liver edge to the right costal margin.))
• Weight. If abnormally low or high, preferably include the reference range.
• Color and texture of cut surfaces
• Any focal change

Example:

Minimal	More comprehensive	Normal ranges
The liver weighs ___g.	The liver is << of normal size / {{enlarged}}, at ___g.	[[Men: 970-1860 g. Women 600-1770g..]]

The liver surface is <<smooth ((and glistening)) {{/deformed by small and large nodules}}((, and is <<light tan / dark brown>> in color)). << Normal/ {{/ firm}} consistency. Cut surface is normal / << (shows normal homogeneous brown parenchyma) / {{Yellowish color, indicating steatosis}} / {{dark nutmeg similar paths, indicating congestion}}. (No focal changes.)((The liver edge is _cm below the right costal margin.))

Microscopic evaluation

Pathologies can be topographically classified by liver zones. P: portal tract. V: central vein.

A general screening includes (with further information in sections below):

• Looking at the referral/requisition form (and looking at the medical records) for particular conditions to look for or evaluate. (Perform a severity grading of previously known liver diseases.)

• Commonly, this includes to quantify any cirrhosis, at least if the patient had alcohol abuse.
• Steatosis is also common.

• Signs of acute liver failure.
• Signs of malignancy. If a tumor is found: Further information: Liver tumor
• Signs of congestive hepatopathy (indicating heart failure).
• Signs of inflammation at least around the portal triads.

Cirrhosis

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  Steatohepatitis with mild fibrosis (van Gieson's stain).

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  Histopathology of steatohepatitis with moderate fibrosis (van Gieson's stain).

Further information: Cirrhosis

Steatosis

At least classify steatosis by severity:

Steatosis grading: a: none. b: mild. c: moderate. d: severe.

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  Note the presence of microvesicular steatosis, as it is usually more harmful. It shows foamy hepatocytes (two annotated by arrows), as opposed to the more common macrovesicular steatosis (insert).

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  Note any particular pattern of the steatosis, mainly centrilobular (pictured) or periportal.

Signs of acute liver failure

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  Lobular disarray and associated lymphocytic inflammation, acidophil acidophil body formation (arrow) and bilirubinostasis, suggesting acute hepatitis.

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  Shock liver, showing its hallmark pathologic finding centrilobular necrosis but viable periportal hepatocytes. The necrotic hepatocytes are seen as slightly more eosinophilic (red) and discohesive.

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  Massive hepatic necrosis: Liver cell dropout, residual hepatocytes and intact portal tract pattern.

Congestive hepatopathy

Histopathology of congestive hepatopathy, with sinusoidal dilation in zone 3. As the severity of the lesion increases, the sinusoids around the central vein become distended with extravasated red cells and there is adjacent hepatocyte plate atrophy.

• Acute hepatic congestion shows dilated sinusoidal capillaries predominantly in zone 3 of the hepatic acinus.
• Typical findings of chronic hepatic congestion are atrophy of hepatocytes in zone 3, perisinusoidal edema, thrombosis and hemorrhage. Chronic congestion typically displays perivenous and perisinusoidal fibrosis, with fibrous septa that bridge central hepatic veins. In contrast, other causes of distortion and cirrhosis typically have fibrous septa predominantly between portal triads. However, nonalcoholic steatohepatitis also may show perisinusoidal fibrosis in early stages; in later stages, the fibrosis tends to be in the portal triad. Cirrhosis develops in the final stages of congestive hepatopathy. Regenerating hepatocytes tend to grow in a sleevelike pattern along portal tracts, resulting in a nodular liver with preserved portal triads and obliterated or fibrosed hepatic veins, a pattern called "reverse lobulation". This pattern can also be seen in venous obstruction due to Budd-Chiari syndrome.

Hemosiderin

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  Look for Kupffer cells with significant hemosiderin deposition (shown next to a hepatocyte with lipofuscin pigment.

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  Iron stain can highlight the hemosiderin (blue stain) in unclear cases.

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  Hepatocyte lipofuscin alone is of no real pathologic importance and does not warrant a mention in the report.

Report

• Presence of any liver disease

• (Quantification of its severity.)

• ((Even absence of hepatitis, malignancy, congestive hepatopathy and/or steatosis.))

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Liver tumor

Author: Mikael Häggström

Tissue sampling

• Liver biopsy
• Autopsy: Further information: Autopsy

Gross examination

Note the following:

• Whether the tumor is sell demarcated from surrounding tissue
• Whether there is visible infiltration or invasion into surrounding tissue
• Any necrosis or bleeding

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  Hepatocellular carcinoma

Microscopic evaluation

A bile duct hamartoma is also very common. This image shows typical features:
- Small to medium sized, irregularly shaped bile ducts lined by bland cuboidal epithelium (may also be flattened).
- Prominent intervening collagenous stroma.
- Bile ducts containing eosinophilic debris (may also contain inspissated bile)

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  Liver tumor types by relative incidence in adults in the United States.

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  Hepatocellular carcinoma, typically resembling hepatocytes, with abundant granular eosinophilic cytoplasm.

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  Hepatocellular adenoma (inflammatory type pictured) may have minor atypia.

Further information: Evaluation of suspected malignancies

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Adrenals

Author: Mikael Häggström

Comprehensiveness

On this resource, the following formatting is used for comprehensiveness:

• Minimal depth
• (Moderate depth)
• ((Comprehensive))

Main targets

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  Adrenal tumors

Autopsy

Autopsy processing

In autopsy:

• Make a couple of cuts through the adrenal glands, such as transversal ones, and look mainly for adrenal tumors.
• ((Remove the adrenals, trim them from excessive adherent fat, and weight them. Their combined weight in an adult human ranges from 7 to 10 grams.))

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  Adrenal cortical necrosis. Hemorrhage, fibrin thrombi and short postmortem interval indicate ante-mortem necrosis, otherwise it can be regarded as a postmortem change.

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  Adrenal venous congestion in circulatory failure.

Autopsy report

Normal status can be described as either:

• Adrenal glands are normal bilaterally.
• (Adrenal glands are ordinarily configured and with no definable focal changes on cut surfaces.)
• ((The adrenals are normal in size, shape and consistency, with a weight of __ grams on the right and __ grams on the left. The cortices are orange with <normal / increased / decreased thickness>. The medullae are <grey / autolyzed>.))

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Adrenal tumors

Incidences and prognoses of adrenal tumors.

Adenoma versus carcinoma

The most common adrenal tumors are adrenocortical adenomas and carcinomas. These are most commonly distinguished by the Weiss system, as follows:

Characteristic	Score
High nuclear grade (enlarged, oval to lobated, with coarsely granular to hyperchromatic chromatin and easily discernible, prominent nucleoli)	1
More mitoses than 5/50 high power fields	1
Atypical mitoses	1
Eosinophilic cytoplasm in >75% of tumor cells	1
Diffuse architecture of >33% of tumor	1
Necrosis	1
Venous invasion	1
Sinusoidal invasion (no smooth muscle in wall)	1
Capsular invasion	1

Total score indicates:

• 0-2: Adrenocortical adenoma
• 3: Undetermined
• 4-9: Adrenocortical carcinoma

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  Gross pathology of adrenocortical adenoma.

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  Zona fasciculata versus adrenocortical adenoma. An adrenocortical adenoma typically has mild changes in comparison, including larger cells with larger and more pleomorphic nuclei with more coarse chromatin. H&E stain.

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  Adrenocortical adenoma with focal high grade nuclear atypia.

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  Adrenocortical adenoma with focal necrosis

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  Gross pathology of adrenocortical carcinoma. They are generally large, with a tan-yellow cut surface, and often have areas of hemorrhage and necrosis.

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  Histopathology of adrenocortical carcinoma, with marked mitotic activity.

Other adrenal tumors

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  Pheochromocytoma, with typical features shown.

Reporting

For cancers, generally include a synoptic report, such as per College of American Pathologists (CAP) protocols at cap.org/protocols-and-guidelines.

Kidney with tumor

{{Renal tumor - entire article}

Urinary tract stone

Author: Mikael Häggström
When sent to the pathology department, these are generally sent for stone analysis to determine the chemical composition.

Gross processing

Abide by local practices for what container to use and where to leave stone specimens. Generally submit the entire specimen, or as much as you can conveniently fit in the container.

Example report:

The specimen is received dry and consists of __ irregular fragment(s) of {{tan}} calculus measuring up to __ cm in maximum dimension. The entire specimen is submitted for spectrographic analysis.

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Pancreas

Author: Mikael Häggström

Comprehensiveness

On this resource, the following formatting is used for comprehensiveness:

• Minimal depth
• (Moderate depth)
• ((Comprehensive))

Upper limits of pancreas weight

Patient age	Men	Women
<20 years	115g	80g
21-30 years	115g	125g
31-40 years	155g	140g
41-50 years	155g	110g
51-60 years	175g	125g
>60 years	160g	110g
Overall	160g	120g

In autopsy

Inspect the pancreas regarding color and consistency. ((Separate it and measure its dimensions.))

Cut it in consecutive short axis slices. Note the appearance of the parenchyma (and the size of the duct).

Microscopic examination

Look for pancreatic intraepithelial neoplasia and pancreatic tumors.

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  Pancreatic lipomatosis is a common finding. This case shows moderate to severe lipomatosis, with mainly interlobular but also scattered intralobular fatty infiltration. Reporting is optional in at least mild to moderate cases.

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  Stages of pancreatic intraepithelial neoplasia.

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Pancreatic tumors

Microscopic evaluation

If a biopsy has been processed both for histology and cytology, make sure that their results are not contradictory.

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  Stages of pancreatic intraepithelial neoplasia.

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  Relative incidences of various pancreatic neoplasm.

Cancer type	Relative incidence	Microscopy findings	Micrograph
Pancreatic ductal adenocarcinoma (PDAC)	90%	Glands and desmoplasia
Pancreatic acinar cell carcinoma (ACC)	1% to 2%	Granular appearance
Solid pseudopapillary tumor		Discohesive tumor nests surrounded by thin fibrous bands.	Low and high magnification
Adenosquamous carcinoma	1% to 4%	epithelial cells.
Pancreatic neuroendocrine tumor	5%	Multiple nests of tumor cells	Gastrinoma
Pre-cancer below for comparison:
Precancer: Intraductal papillary mucinous neoplasm (IPMN)	3%	Mucinous epithelial cells. Growth within the pancreatic ducts.

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  Types of intraductal papillary mucinous neoplasm (IPMN)

Staging

Stage pancreatic cancers as follows:

Tumor (T)	Criteria
TX	The primary tumor cannot be evaluated.
T0	No evidence of cancer was found in the pancreas.
Tis	Carcinoma in situ. This includes: High-grade pancreatic intraepithelial neoplasia (PanIn-3) Intraductal papillary mucinous neoplasm with high-grade dysplasia Intraductal tubulopapillary neoplasm with high-grade dysplasia Mucinous cystic neoplasm with high-grade dysplasia.
T1	The tumor is in the pancreas only, and is ≤2 cm in greatest dimension
- T1a	Tumor ≤0.5 cm in greatest dimension
- T1b	Tumor >0.5 cm and <1 cm in greatest dimension
- T1c	Tumor 1–2 cm in greatest dimension
T2	The tumor is in the pancreas only, and it is >2 cm and ≤4 cm in greatest dimension
T3	Tumor >4 cm in greatest dimension
T4	Tumor involves celiac axis, superior mesenteric artery, and/or common hepatic artery, regardless of size

Node (N)	Criteria
NX	The regional lymph nodes cannot be evaluated.
N0	Cancer was not found in the regional lymph nodes.
N1	Metastasis in 1 to 3 regional lymph nodes.
N2	Metastasis in 4 or more regional lymph nodes.

Metastasis (M)	Criteria
M0	No distant metastasis
M1	Distant metastasis, including distant lymph nodes. Pancreatic cancer most commonly spreads to the liver, the peritoneum, and the lungs.

Pancreatic ductal adenocarcinoma

Microscopic evaluation on biopsies

Histopathology of pancreatic ductal adenocarcinoma

The main findings are glands formations with atypical epithelial cells and desmoplasia. If histology, clinical history and radiology are consistent, then no further immunohistochemistry or other molecular workup is needed for the diagnosis.

Make sure to also evaluate any concurrent aspiration and/or bile duct brushing.

Further information: Pancreatic tumor

Grading

Grade as follows:

• Well differentiated: > 95% tumor composed of glands
• Moderately differentiated: 50 - 95% glands
• Poorly differentiated: < 50% glands

Reporting

Example report:

A. Pancreas, core biopsy: Pancreatic ductal adenocarcinoma, moderately differentiated. Comment: Note is made of concurrent aspiration cytology (DN-12-1234), which is positive for adenocarcinoma.