Chapter 9 Diseases of Digestive System
OBSERVATION METHODS OF SPECIMEN
Digestive system includes digestive tract and digestive gland. Digestive tract
consists of esophagus, stomach, small intestine and large intestine. In the process of
observation, one should confirm what tissue or organ it is, and then observe its figure;
observe mucosa, muscular layer and serous membrane from inner to outer. Student
should pay attention to color, thickness of mucosa; whether mucosa suffered edema,
hemorrhage, necrosis, ulcer and pesudomembrane; one should also observe color
and luster of serous membrane; whether it suffered exudation, thickening or
conglutination with other organs. If lesion is found, student should observe the
position, size, shape, color and change of neighbor muscular wall of lesion. We also
should observe number, size, hardness, cutting surface and color of lymph node. To
tissue section, one should observe whether degeneration, necrosis, congestion,
hemorrhage, exudation and proliferation in each layer of digestive tract mainly.
Normal liver is brown red color with smooth surface; average volume is
25cm×12cm×9cm, average weight is 1200-1500g. One should observe the color,
volume of the liver; whether exudation, thickening or conglutination exist; surface of
liver is smooth or nodular. If nodes exist, student should observe number, size, color
and distribution of nodes. We also should observe the structure, change of color of
cutting surface; whether congestion, hemorrhage, necrosis, capsule or nodes exist. If
nodes are found, we should observe size, distribution, color, texture, margin and
secondary lesions of nodes.
Liver tissue is composed of hepatic lobule, there is central vein in the center of
lobule, hepatocytes arrange radially surrounding central vein. There is hepatic sinus
between hepatocyte plates. Portal space exists among lobules. There are interlobular
bile duct, interlobular artery, interlobular vein, lymphatic vessel and nerve fiber in
portal space. The portal tracts are circumscribed by a boundary of liver cells, known
as the “limiting plate”. We should notice whether normal lobule structure exist,
whether arrangement of hepatocyte plates disorder; whether limiting plate is in order;
whether hepatocytes suffered degeneration, necrosis, proliferation or carcinomatous
change; whether cholestasis or inflammatory exudation exist; whether portal space
and bile duct dilate or proliferate; whether vessels undergo any change; whether
connective tissue proliferate; whether capsule undergo thickening or inflammatory
exudation.
AIMS
1. To grasp the pathological characteristics, complication and clinicopathological
relationship of peptic ulcer.
2. To grasp the basic pathological characteristics of viral hepatitis and
characteristics of each type hepatitis.
3. To grasp the pathological characteristics and clinicopathological relationship of
cirrhosis of liver.
4. To be familiar with pathological characteristics of chronic gastritis and its
influence on body.
5. To be familiar with the pathological characteristics and clinicopathological
relationship of appendicitis.
6. To be familiar with the pathological characteristics and results of different types
of esophageal carcinoma, gastric carcinoma, colon carcinoma and primary
hepatic carcinoma.
7.
To be familiar the gross difference between gastric ulcer and ulcerative type gastric cancer.
CONTENTS
Esophagus
Gross specimen
Tissue section
Carcinoma of the esophagus
Squamous cell carcinoma of the
esophagus
Stomach
Chronic atrophic gastritis
Chronic atrophic gastritis
Chronic hypertrophic gastritis
Chronic hypertrophic gastritis
Chronic gastric ulcer
Chronic gastric ulcer
Duodenal ulcer
Tubular gastric carcinoma
Early stage gastric carcinoma
Signet-ring cell carcinoma
Advanced gastric carcinoma
Intestinal tract
Acute phlegmonous appendicitis
Acute phlegmonous appendicitis
Villous adenoma in rectum
Villous adenoma in rectum
Adenomatous polyposis
Adenocarcinoma of colon
Carcinoma of colon
Liver
Acute severe hepatitis
Acute severe hepatitis
Subacute severe hepatitis
Subacute severe hepatitis
Portal cirrhosis
Acute common hepatitis
Postnecrotic cirrhosis
Chronic common hepatitis
Biliary cirrhosis
Portal Cirrhosis
Primary hepatocellular carcinoma
Postnecrotic cirrhosis
Billiary cirrhosis
Hepatocellular carcinoma
Gallbladder
Chronic cholecystitis
Chronic cholecystitis
Pancreas
Carcinoma of pancreas
Carcinoma of pancreas
KEY POINTS OF SPECIMEN OBSERVATION
1. Carcinoma of esophagus
Basic pathologic changes
(1) Gross morphology
The tumor usually locates in the middle and lower parts of the esophagus;
◆
◆
The gross patterns are ulcerative type, fungating type, medullary type and
contractive type;
◆
There are hemorrhage, necrosis and formation of ulcer on surface of tumor
with poor-defined margin and a uneven base.
(2) Histopathology
◆
Squamous cell carcinoma is the most common; adenocarcinoma and
undifferentiated carcinoma are rare.
Specimen observation
Case abstract: Male, 56 years old. Swallowing obstructing sensation was for 2
years，progressive dysphagia was for about half a year. Patient can’t take food,
suffered severe thinness and cachexia and then was dead.
Gross specimen: (Fig. 9-01 a, b) (a) Gross view of an ulcerated carcinoma of
esophagus, showing irregular shape, protruded margin and uneven base with
hemorrhage and necrosis. (b) A cauliflower carcinoma of the esophagus protrudes
into the lumen, with poorly defined margin and uneven base. The surface of the
tumor is hemorrhage and necrosis.
Tissue section: (Fig. 9-02) Highly differentiated squamous cell carcinoma, tumor
cells arranged as irregular nests. There are keratin pearls in the center of some
nests.
2. Disease of stomach
(ⅰ) Chronic atrophic gastritis
Basic pathologic change
(1) Gross morphology
◆ Lesion mainly distributes in gastric antrum and gastric body focally or
diffusively.
◆
The mucosa of the stomach becomes thinned or flattened and shows grey color,
revealing more readily the submucosal vasculature. Rugal folds are flattened
or disppear.
(2) Histopathology
◆
Mucosa glands become lessen, and persisting glands atrophy and disappear.
◆
Mucosa may become partially replaced by metaplastic columnar absorptive
cells and goblet cells of intestinal morphology.
◆
Inflammation of the lamina propria involves lymphocytes and plasma cells.
Specimen observation
Case abstract: Male, 62 years old. Patient suffered upper abdominal pains for more
than 30 years, progressive thinness and anemia for 10 years. Patients died of
pneumonia accompanying infective shock.
Gross specimen: (fig 9-03) Note the color, rugal folds, submucosal vessel, location
and area of lesion of gastric mucosa.
Tissue section: (fig 9-04a,b) Note degree of mucosa atrophy, infiltration of
inflammatory cells and intestinal metaplasia.
(ⅱ) Chronic hypertrophic gastritis
Basic pathologic change
(1) Gross morphology
◆
Mucosa of gastric fundus and body are thick; rugal folds, hypertrophy, widen,
like “gyrus”.
(2) Histopathology
◆Gland
of mucosa proliferate, hypertrophy, elongate and pseudopyloric gland
metaplasia.
Specimen observation
Gross specimen: (fig 9-05) Note the change of rugal folds and thickness of mucosa.
Tissue section: (fig 9-06a,b) Note thickness of mucosa, and the component of
proliferation and whether it undergoes metaplasia.
(ⅲ) Peptic ulcer
Basic pathologic changes
(1) Gross morphology
◆
Favorite locations: the lesser curvature of antrum of stomach or duodenal
ampulla;
◆
Round to oval; diameter is less than 2.5cm;
◆
Sharply punched-out defect with relatively straight wall;
◆
The depth of ulcers varies from superficial involving only the mucosa and
muscularis mucosa, to deeply excavated ulcers having their bases on the
muscularis propria, even the entire wall is penetrated. The base of the ulcer is
smooth and clean;
◆
Surrounding mucosa folds radiate from the crater in spokelike.
(2) Histopathology
◆
◆
Ulcer forms on mucosa and reach muscularis propria;
In active ulcers with ongoing necrosis four zones are demonstrable:
inflammatory exudation layer, necrosis layer, active granulation tissue and scar
layer from superficial to deep layer;
◆
Thick wall vessels and traumatic neurofibroma can be seen in scar tissue;
◆
Chronic inflammation and intestinal metaplasia can be seen in mucosa tissue
surrounding ulcer.
Specimen observation
(1)Gastric peptic ulcer
Case abstract: Male, 38 years old. He suffered upper abdominal pains
accompanying sour regurgitation and belching for 18 years, which aggravated after
eating. He suffered black stool and haematemesis twice. It’s showed that there was a
protruding niche at the lesser curve of gastric antrum by barium meal x-ray test. The
patient received gastric greater resection.
Gross specimen: (Fig. 9-07) The ulcer is located in the antrum of stomach, oval
shaped; the diameter is less than 2cm, with a sharply punched-out appearance, and
the margins are not elevated. The ulcer is deep into the muscularis propria. The ulcer
base shows clean and smooth, the surrounding mucosa radiate from the center.
Question: What complications could be happened?
Tissue section: (Fig. 9-08a,b) Note the structural characteristics of base of ulcer；
Note the change of mucosa surrounding ulcer.
The mucosa of ulcer lose its normal structure, there are four layers from the
surface to the deep layer.
1) Exudative layer: the zone of a nonspecific inflammatory infiltrate and fibrin,
with neutrophils predominating.
2)
Necrotic layer: a thin layer of necrotic fibrinoid debris.
3)
Granulation tissue layer. In the deeper layer, there is active granulation
tissue composed of new blood vessels, fibroblasts and inflammatory cells.
4)
The granulation rests on a more solid fibrous or collagenous scar. Vessel
walls within the scarred area are typically thickened. Inflammatory infiltrate
and adhesion of muscularis mucosae and muscularis are present in the
surrounding mucosa.
(2) Duodenal ulcer
Gross specimen: (Fig. 9-09) to observe and describe by yourself.
(ⅳ) Gastric Carcinoma:
(1) Early gastric carcinoma
Basic pathologic changes
1) Gross morphology
◆
Lesion is confined to mucosa and submucosa.
◆
There are three types mainly: protruded type, superficial type and excavated
type.
2) Histopathology
◆
Tubular type adenocarcinoma is common.
◆
Carcinoma is only localized in mucosa and submucosa.
Specimen observation
Gross specimen: (Fig. 9-10a,b) Note location, scope, shape and classification of
lesion.
(a) Type I. There are two gray polypoid masses with 1cm in diameter at the left
lower corner of gastric antrum. There are several gray ridgy focuses between two
masses. (b) Type IIc. There are irregular superficial depression at the gastric
mucosa of the lesser curve besides gastric antrum，which is slightly lower than
surrounding mucosa.
(2) Advanced gastric carcinoma
Basic pathologic changes
1) Gross morphology
◆
Favorite location: the less curve of gastric antrum;
◆Three
macroscopic growth patterns: ulcerative type: crater-like, protruding
margin, uneven base, diameter>2.5cm; polypoid type: a tumor mass protrude
into lumen; infiltrative type: a rigid, thickened leather bottle like stomach―
“Linitis plastica”.
2) Histopathology
◆
Adenocarcinoma is common;
◆
The neoplasm has extended below the submucosa into the muscular wall or has
spread more widely.
Specimen observation
Case abstract: Male，52 years old. He felt upper abdominal pains for 8 years.
Abdominal pains aggravated accompanying thinness for 1 year. Barium meal test
shows: There was a crescent niche at the lesser curve side of gastric antrum, which is
located out of gastric profile. The patient received gastric greater resection.
Gross specimen: (Fig. 9-11a,b, c) (a) The huge ulcerative tumor is located in the
antrum of the stomach, 6cm in diameter. The cancerous crater is large, irregular,
shadow, and with a shaggy base covered by necrotic material, and surrounding
mucosa is thick and heaped-up. (b, c) Observe pathological characteristics and
classification of the specimen.
Tissue section: (Fig. 9-12a,b) Note and analyze histological types and infiltrative
depth.
3. Disease of the intestine
(ⅰ) Acute phlegmonous appendicitis
Basic pathologic changes
(1) Gross morphology
◆
The inflammed appendix is swollen;
◆
Serosa is congested and covered with purulent exudates;
◆
On the cutting surface, the lumen of the appendix is strictured, and filled with
pus; the wall thickens.
(2) Histopathology
◆
Pus fill the lumen consisting of living and degenerate neutrophil polymorphs
together with liquefied tissue debris;
◆
Numerous neutrophils infiltrate throughout the mucosa to muscularis propria
and serosa, vessels undergo congestion and edema;
◆
Partial mucosa shed and necrosis;
◆
Part of serosa and peripheral adipose tissue are covered with purulent exudates
leading to periappendicitis.
Specimen observation
Gross specimen: (fig 9-13) Note pathological characteristics and analyze its
sequel. （see also Chapter 5, Inflammation）
Tissue section: (fig 9-14a,b) To observe and describe by yourself.（see also
Chapter 5, Inflammation）
(ⅱ) Intestinal adenoma
Basic pathologic changes
(1) Gross morphology
◆
It mainly involves colon, single or multiple;
◆
It shows villus or polyp form and protruding into the lumen.
(2) Histopathology
◆Villous
◆
adenoma shows papillary or ramified arrangement;
Polypoid adenoma shows tubular arrangement.
Specimen observation
1) Villous adenoma of rectum
Gross specimen: (Fig. 9-15) The villous adenoma is sessile, with a villus like
protuberance and unclear margin. It shows red color because of local congestion.
Tissue section: (Fig. 9-16) It consists of elongated villi in a papillary growth
pattern, the villi are again lined by columnar epithelium showing dysplasia.
Fibrovascular cord is localized in the middle of papilla.
2) Adenomatous polyposis of colon
Gross morphology: (Fig. 9-17) The colonic mucosa is studded with numerous
polypoid adenomas, almost no normal mucosa can be found.
(ⅲ) Carcinoma of colon
Basic pathologic changes
(1) Gross morphology
◆Favorite
location is rectum, and then is sigmoid colon.
◆Macroscopically
there are four types: protrude type, ulcerative type,
infiltrative type and colloid type.
(2) Histopathology
Adenocarcinoma is common, showing varying degrees of mucin production
◆
and differentiation;
◆Cancer
tissues involve all layers.
Specimen observation
Gross specimen: (Fig. 9-18) Note: which part this segment of intestine is belonged
to? What is its pathological characteristics and classification?
The circumferential tumor protrudes into the lumen, having an ulcerated
central portion and heaped-up edges producing local constriction of the lumen.
4. Disease of the liver
(ⅰ) Viral hepatitis
(1) Acute common hepatitis
Basic pathologic changes
1) Gross morphology
◆
Liver enlarges slightly with tender texture; liver of jaundice patient shows green
yellow color.
2) Histopathology
◆
Comprehensive degeneration of liver cells (cytoplasm loose and balloon
degeneration);
◆
Scattered spotty necrosis or focal necrosis, and/or apoptosis of liver cells;
◆
Few inflammatory cells infiltrate into lobular necrosis focuses and portal space.
Specimen observation
Case abstract：Male，23 years old. He suffered distending pain in upper abdominal,
hypodynamia, inappetence and aversion to greasy food for 1 week. Physical
examination：hepatomegaly, tenderness, ALT level increasing，HBs Ag (+), HBe Ab
(+).
Tissue section: (Fig. 9-19a, b, c, d) Note: scope of the lesion; characteristics and
distribution of hepatocellular degeneration and necrosis; the types of inflammatory
cells and infiltration position, accompanying cholestasis or not; whether it undergoes
proliferative lesion.
Microscopic view shows diffusive degeneration of hepatocytes. Most of them
take the form of diffuse swelling, with light-stained cytoplasm, called hydropic
degeneration. In severe cases, the cytoplasm looks empty and contains only scattered
wisps of plasmic remnants, called ballooning degeneration. Another pattern is, some
hepatocytes shrink and stain more eosinophilic, round intensely eosinophilic
Councilman body (acidophilic body) may be seen with loss of nuclei.
Spotty necrosis of hepatocytes appears within hepatic lobule infiltrated by
inflammartory cells. Portal tract and focal necrosis have inflammatory cells
infiltration. Regenerated hepatocytes are large and have dark stained nuclear, or even
binucleate hepatocytes appear.
Question: What clinical manifestations do patient show?
(2) Chronic mild hepatitis
Basic pathologic changes
1) Gross morphology
◆Liver
enlarges with smooth surface.
2) Histopathology
◆
Degeneration and necrosis of hepatocytes cells are slight;
◆
Piecemeal necrosis can be seen in some portal space;
◆
Inflammatory cells infiltrate into portal space and lobules;
◆
Fibrosis develops around portal space with intact lobular structure.
Note: Ground glass liver cells can be seen in the cases of chronic type B
hepatitis.
Specimen observation
Tissue section: (Fig. 9-20) Hepatocytes at portal area and limiting plate are necrosis
with mild fibrosis and lymphocytes infiltration (mild piecemeal necrosis).
Note: What’s the difference in degree of degeneration, necrosis and its
characteristics compared with acute common hepatitis? Pay special attention to the
portal area. What is the basis of this specimen diagnosed as chronic mild hepatitis?
(3) Chronic moderate hepatitis
Basic pathologic changes
1) Gross morphology
Liver enlarges with smooth surface.
◆
2) Histopathology
◆
Apparent degeneration and necrosis of hepatocytes;
◆
Bridging necrosis and moderate piecemeal necrosis of hepatocytes;
◆
Inflammatory cells infiltrate into portal space and lobules apparently;
◆
Fibrous tissues surrounding portal space proliferate and form fibrous septa in
lobules accompanying normal or mussy lobular structure. No sclerosis of liver
is seen.
Specimen observation
Tissue section: (Fig. 9-21) Hepatocytes between the central vein and portal area are
necrosis, in which irregular fibrous strips are formed, accompanying with mild
proliferation of fibrous tissue and infiltration of lymphocytes, it is mild bridging
necrosis.
①To observe the grade of severity of the liver cell damage and inflammation.
②To observe the stage of fibrosis and architectural disturbance.
③Main differences compared with mild chronic hepatitis
(4) Chronic severe hepatitis
Basic pathologic changes
1) Gross morphology
◆Liver
enlarges with granular surface and stiff texture.
2) Histopathology
◆
Severe and extensive degeneration and necrosis of hepotocytes.
◆
Severe piecemeal necrosis and extensive bridging necrosis spanning adjacent
lobules in a portal to portal, portal to central, or central to central fashion.
◆
Lobular structure is mussy or pseudolobules form.
◆
Fibrous septa form between peripheral and central necrotic zone.
Specimen observation
Case abstract: Male，34 years old. He suffered acute viral hepatitis 5 years ago and
relieved after treatment. He suffered hypodynamia, pain of hepatic region and
aversion to greasy food ， which relived after rest and treatment. Symptoms
aggravated recently, physical examination: hepatomegaly and stiffness, ALT level
incresing，HBsAg(+).
Tissue section: (Fig. 9-22) There were comprehensive strip necrosis between
adjacent central veins or between central vein and portal area. Note:① the integrity
of lobular structure; ② the characteristics, degree and scope of hepatocyte necrosis;
③ whether it suffers hyperplasia; What’s hyperplasia?
(5) Acute severe hepatitis
Basic pathologic changes
1) Gross morphology
◆
Liver shrink with lightweight, soft texture and a wrinkled capsule.
◆
Cutting surface is yellow or brown red color.
2) Histopathology
◆
◆
Liver cells undergoes severe and extensive necrosis.
Hepatic sinus dilate, congest and hemorrhage; kupffer cell proliferate and
hyperplasia and engulf.
◆
Regeneration of remaining hepatocytes cannot be seen.
◆
Inflammatory cells predominantly lymphocyte and macrophage infiltrate into
portal space and lobules.
Specimen observation
Case abstract：Male，28 years old. He suffered pain of hepatic region, hypodynamia
and jaundice for 5 days，abdominal distention, subcutaneous hemorrhage and trance
for 2 days, ALT increase apparent. He died of haematemesis, hematochezia and
coma.
Gross specimen: (Fig. 9-23) To observe the change of live size, capsule and color
（see also chapter 5 Inflammation ）
Tissue section: (Fig. 9-24a,b) （see also chapter 5 Inflammation）
①Which kind of lesion is apparent?
②Is lesion diffusive or local distribution?
③What secondary changes are patients shown?
Question: To explain clinical manifestations with pathological changes of the liver.
(6) Subacute severe hepatitis
Basic pathologic changes
1) Gross morphology
◆
Liver shrinks with crumpled capsule.
◆
Surface and cut surface of liver is green yellow color.
◆
Nodes in different size can be seen in cases with long disease history.
2) Histopathology
◆
Massive and severe hepatocytes necrosis.
◆
Nodular regeneration of hepatocytes.
◆
Lobular structure is destroyed.
◆Small
bile ducts proliferate accompanying formation of biliary embolus.
Specimen observation
Case abstract: Female，36 years old. He was diagnosed as acute common hepatitis
15 days ago and aggravated. ALT increased apparently. She suffered subcutaneous
hemorrhage, haematemesis, hematochezia, and abdominal distention and died of
aggravated jaundice and coma.
Gross specimen: (Fig. 9-25) Hepatic capsule is crimple，plane of section is yellow
green. Earthy yellow necrosis zone and gray island regeneration nodes can be seen.
Note: ①What’s abnormality of volume, shape and color?
② What’s difference compared with acute severe hepatitis?
Tissue section: (Fig. 9-26a,b)
① Lobular structure is destroyed.
② There is massive necrosis of hepatocytes, which is severe in central part of
lobule.
③ Inflammatory cells infiltrate interlobular and extra lobules
④ Irregular nodes of regenerated hepatocytes can be seen.
(ⅱ) Cirrhosis of the liver
Basic pathologic changes
(1) Gross morphology
◆
Liver shrinks apparently accompanying lightweight and hard consistency.
◆
The liver shows coarse nodular or granular surface.
◆
On cutting surface, nodes in different size are separated by gray fibrous septa.
(2) Histopathology
◆
The basic change is the formation of pseudolobules. Also, bridging fibrous
septa and disruption of the architecture of the entire live are characteristics.
◆
Pseudolobules are characterized by an irregular arrangement of hepatic cells;
by loss of normal distribution of central vein and portal tracts.
◆
The fibrous septa contain fine or dense collagen fibers accompanying small
bile duct hyperplasia, formation of pseudobiliary ducts and lymphocytes
infiltration.
Specimen observation
Case abstract：Male，41 years old. He suffered chronic viral hepatitis for 12 years
and suffered thinness, hypodynamia, abdominal distention recently. B hypersonic
test showed there were 200ml ascites，liver wane and strong echo group in different
size. CT showed there were severe nodes in different size in liver, with high CT
value, which is suspected to be cancer. AFP increased slightly.
1) Portal cirrhosis
Gross specimen: (Fig. 9-27) The liver is misshapen, stiffen, and shrink. The cut
surface reveals regular nodules, with similar diameter 0.5 to 1cm, and thin
connective tissue septa.
Tissue section: (Fig. 9-298a,b) It is characterized by pseudolobule formation, losing
the normal lobular architecture. Fibrous septa divide hepatic lobules into several
round, oval cell groups in different size, which is pseudolobule. Hepatocytes in
pseudolobules arrange turbulently, with absent or deviated central vein. There are
hydrophic or fatty degeneration or focal necrosis or regeneration of hepatocytes.
Regenerated hepathocytes, are large sized, with deep-stained nucleus or even
binucleate. Proliferated small bile ducts can be seen in fibrous tissue accompanying
with infiltration of lymphocytes.
2) Postnecrotic cirrhosis
Gross specimen: (Fig. 9-29) Note difference compared with portal cirrhosis
Tissue section: (Fig. 9-30) Note the histological difference compared with portal
cirrhosis; to analyze their clinical differences
3) Biliary cirrhosis
Gross specimen: (Fig. 9-31) The liver is enlarged, green yellow color, with smooth
or granular surface. On cut surface nodes are usually unobvious.
Tissue section: (Fig. 9-32) Bile pigments deposit in hepatocytes accompanying
feather-like degeneration and necrosis, and accompanying bile stasis and bile
embolus formation in cholangioles. Bile ducts dilate; bile ductules and fibrous tissue
proliferate. Destruction of lobular structure is mild.
(ⅲ) Primary carcinoma of the liver
Basic pathologic changes
(1) Gross morphology
◆
Liver enlarges apparently.
◆
There are many grey nodes in different size in liver, without capsule. It may
appear grossly as huge massive type, multiple nodular type and diffuse
infiltrated type.
(2) Histopathology
◆
Hepatocellular carcinoma is most common. Tumor cells are polygonal and
arranges in cords or nests accompanying dilated blood sinusoid or capillary.
◆
Cholangiocarcioma is rare, which shows adenocarcinoma manifestation.
Specimen observation
Gross specimen: (Fig. 9-33a, b, c) Note: ① main pathological characteristics; ②
the changes other part.
(a) Size of liver increase apparently, there is a large soft node with 15 cm in
diameter on the liver surface. Hemorrhage and necrosis can be seen on its surface.
(b、c) please describe by yourself.
Tissue section: (Fig. 9-34) Note:
① Morphology and arrangement of cancer cells;
② The difference to other kinds of carcinoma;
③ Changes of liver tissue in non-cancer region.
5.Chronic cholecystitis (Cholelithiasis)
Specimen observation
Gross specimen: (Fig. 9-35) The gall bladder enlarges with a thick flattened wall
and some black stones in the lumen.
Tissue section: (Fig. 9-36a,b) (a) The mucosa epithelium is mild hyperplasia, and
the wall thicken with lymphocytes infiltrate. The Rokitansky-Aschoff sinuses are
more prominent in muscularis. (b) There are large amounts of lipid filled foam cells
in the lamina propria.
6.Carcinoma of the pancreas
Specimen observation
Gross specimen: (Fig. 9-37) A cross section through the head of the pancreas and
adjacent common bile duct shows an ill-defined tumorous mass in the pancreatic
substance and the green discoloration of the duct resulting from total obstruction of
the bile flow.
Tissue section: (Fig. 9-38) Poorly formed glands are present in densely fibrotic
stroma within the pancreatic substance; and there are some inflammatory cells.
CASES DISCUSSION
Autopsy case 1
Case abstract. Male, 36-year old, was hospitalized because of the abdominal pain
after eating some seafood. Patient suddenly felt pain on the upper abdomen and
peri-umbilicus 4 hours before he came to see the doctor, accompanying nausea and
vomiting mixed the food and coffee substance, also with watery diarrhea but no
purulent and bloody in the stool.
Past history.
The patient suffered a chronic duodenal ulcer and received an
appendectomy.
Physical examination. T:36.8C, P:98/min, R: 18/min, BP:100/70 mmHg.
Abdomen is flat. Abdominal respiration exits without visible intestinal pattern and
peristaltic waves; with upper abdomen and peri-umbilicus tenderness; without
rebound tenderness. No shifting dullness. No muscle guarding. Liver and kidney are
impalpable. Bowel sound exists, 6-7/min.
Treatment process. After hospitalization, the patient had watery stools twice, more
than 200 ml each time. Antibiotics and transfusion therapy didn’t take effects.
During the treatment, upper abdomen pain aggravated suddenly and extended to
entire abdomen; shifting dullness was positive. BP is 70/50mmHg; heart rate is
120/min. There is some yellow fluid in the peritoneal cavity. Abdominal X-ray
shows subdiaphragm gas. During the operation preparation, the patient’s heart
beating and breath suddenly stopped, and was dead.
Autopsy findings. There are about 1250 ml yellow-green turbid fluids in peritoneal
cavity. Diaphragm is located in the 4th and 5th intercostals space. Lower margin of
liver is 2.5 cm below the processus xiphoideus. There are some purulent exudates on
the great epiploon and the serosa of the bowel that conglutinated. Part of the bowel
appears red in color. The great epiploon is conglutinated under the right operation
scar. There is a round, 0.8 cm in diameter perforation in the front wall of the stomach,
with very sharp margin (Fig. 9-39). The pancreas slightly conglutinate with the
duodenum.
Histological features. There are abundant acute inflammatory cells, necrotic debris,
granulation tissues, proliferative connective tissues, and fibrous scar and jaundice
deposition at the site of gastric perforation (Fig. 9-40). There are also plenty of fibrin
and neutrophils exudates on the duodenal serosa and epiploon(Fig. 9-41).
Discussion:
1.
What is the main cause of death and mechanism?
2.
Please explain the progression of the disease.
Autopsy Case 2
Case abstract. 51 year-old male patient, he was hospitalized a month ago because of
discontinuous abdominal pain.
Physical examination.T:36.2C, P: 80/min, R: 20/min, BP: 120/80 mmHg
Patients suffered slight upper right abdominal tenderness. Ultrasound showed
enlargement of general bile duct, pancreatitis and a cystic-solid mass above the
pancreas. Anti-symptom therapy didn’t take effects. And ultrasound cued to some
fluid accumulating in pelvic cavity. Exudates examination shows WBC 1/2 HPF,
amylase: 40000U/L. After receiving the exploratory laparotom, the patient died of
the multi-organ failure (MOF). Death diagnosis: acute severe pancreatitis, infective
shock, and multi-organ failure.
Autopsy findings. Both side plural cavities are filled with straw yellow exudates,
about 300ml in left side and 250ml in right side. There is also about 100 ml bloody
fluid in peritoneal cavity. Opening the duodenum, pressing the gallbladder, no bile
gets out. There is a brown solid mass (0.8 cm) in the duodenal papilla. There are
several yellow-white calcification foci on the great epiploon and the mesentery.
Pancreas, 1132 cm, sticks to the surrounding tissue. There is a cyst (3.53.0cm)
formed in the pancreas filled with brown materials (Fig. 9-42), and several dilated
cavities on the cutting surface. Stomach is filled with brown fluid. There is another
large cyst among stomach, duodenum and pancreas, full of gray necrotic substance
(Fig. 9-43).
Microscopic findings. Partial normal structure of pancreas loses, with foci of
liquefactive necrosis and calcification encircled with fibrous tissues (Fig. 9-44). The
bile duct undergoes cystiform dilation accompanying with inflammatory exudates
and secretions inside (Fig. 9-45). The brown material on the duodenal papilla is
composed of inflammatory fibrinous exudates, bile, blood clot and necrotic debris.
The cyst, which is located among stomach, duodenum and pancreas, is liquefactive
necrotic tissue encircled with fibrous tissue. There are also fatty necrosis and oily
cyst formation on the great epiploon, with scatter lymphocytes infiltration, vessels
congestion (Fig. 9-46).
Discussion.
1. What is the main pathological diagnosis and diagnostic gist?
2. Please analyze the relationship among these pathological changes.
3. To describe the cause to death and mechanism.
PRACTICE REPORT
1. Drawing
(1) Microscopic four-layer structure on the base of ulcer;
(2) Microscopic changes of portal cirrohsis.
2. Describe
(1) Histological characteristics of chronic atrophic gastritis;
(2) Difference between portal and postnecrotic cirrhosis.
QUESTIONS FOR REVIEW
1．Please give some examples of the diseases that can cause peptic hemorrhage
and compare the pathological and clinical characteristics of these diseases.
2．What diseases can cause the ulcer formation in the intestine? Compare the
pathological and clinical characteristics of these diseases.
3．What diseases can cause acute abdomen? Compare the pathological and
clinical characteristics of these diseases.
4．What diseases can form a mass in the liver? How to distinguish these
diseases?
5．Please write down the pathologic progressive process from the viral hepatitis,
cirrhosis to primary hepatocellular carcinoma.
6．How to distinguish the node of the well-differentiated hepatocellular
carcinoma from that of the liver cirrhosis?
(Tianjin Medical University Xu Dongbo, Zhang Mingfang)