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Gastrointestinal Pathology Case Studies Part II. CASE

1. Clinical History:

case slide 4 slide 2 slide 1

lesions slide 4 low power slide 4

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1. Gastrointestinal Pathology Case Studies
Part II

2. CASE 1 Clinical History: • A 31 year old woman

has a 10 year history of intermittent, bloody
diarrhea. Radiographic studies and
sigmoidoscopy revealed a friable, ulcerated
mucosa extending to the splenic flexure (Slide
1.1). The descending with sigmoid colon and
rectum were resected. The gross specimen
shown in Slide 1.2 is from another case with even
more severe disease, in which the ulceration
extends nearly to the ileocecal valve. On closer
inspection (Slide 1.3) the mucosa is completely
eroded away, except for reddish "pseudopolyps".
Microscopic examination shows diffuse mucosal
ulceration, with several ulcers extending to the
muscularis propria. The intervening mucosa
shows misshapen, distorted crypts with
occasional crypt abscesses (Slides 1.4 and 1.5).

3. Slide 1.1These views on endoscopy reveal

the typical friable, erythematous mucosa with
diminished haustral folds.

4. Slide 1.2The gross specimen shown here is

from another case with even more severe
disease, in which the ulceration extends nearly to
the ileocecal valve.

5. Slide 1.3On closer inspection, grossly the

mucosa is completely eroded away, except for
reddish "pseudopolyps". The radiographic view
below is from a barium enema (not typically
performed nowadays when colonoscopy can
define the location of lesions and provide
opportunity for biopsy) that reveals a coarsely
granular mucosal pattern.

7. Slide 1.4Microscopic examination shows

diffuse mucosal ulceration, with several ulcers
extending to the muscularis propria.

8. Slide 1.5At higher power, the intervening

mucosa shows misshapen, distorted crypts
with occasional crypt abscesses.

9. Questions: • What are the major differential

diagnoses? • What is the diagnosis here? • What
is the course of this disease and what kinds of
complications can develop?

10. CASE 1: Ulcerative Colitis • What are the

major differential diagnoses? The history
suggests inflammatory bowel disease. The major
differential diagnoses are ulcerative colitis and
Crohn's disease. Given the chronicity, an
infectious cause is unlikely. • What is the
diagnosis here? The gross appearance of a
continuous mucosal involvment of the colon,
starting from the rectum, along with microscopic
ulceration of the mucosa, is most typical for
ulcerative colitis. • What is the course of this
disease and what kinds of complications can
develop? The typical course is relapsing disease-
-flareups with intervening quiescent periods of
months to years. Slightly more than half of
patients have fairly mild disease that can be well-
managed by medical means. About 1/4 of
patients may develop a fulminant colitis. The
long-term risk is colonic adenocarcinoma, which
may be multifocal.

11. CASE 2 Clinical History: • A 27 year old man has

had recurrent attacks of abdominal pain,
diarrhea, and low-grade fever. He also developed
steatorrhea. Colonoscopy revealed erythema and
erosions of the terminal ileum (Slide 2.1).
Radiographic studies demonstrated an
enteroenteric fistula that bypassed much of the
small intestine, which was the cause of the
malabsorption and steatorrhea (Slide 2.2). He
was taken to surgery where a portion of small
intestine was resected. The gross specimen
shows an area in which the small intestinal serosa
is reddened, the wall is thickened, the lumen
narrowed, and the mucosa ulcerated (Slide 2.3).
The microscopic section shows small intestine
with extensive mucosal ulceration, transmural
chronic inflammation, fibrosis, and granulomas
(Slides 2.4 and 2.5).

12. Slide 2.2On colonoscopy, there were no

lesions of the colon, but the appearance of the
terminal ileum with erythema and erosions is seen
here.

13. Slide 2.2The abdominal CT scan views seen

here demonstrate enteroenteric fistula
formation in a case of Crohn's disease. Loops of
small bowel converge because of adhesions
resulting from the transmural inflammation. The
panel above is without contrast and the panel
below with contrast.

14. Slide 2.3The gross specimen shows an area

in which the small intestinal serosa is reddened,
the wall is thickened, the lumen narrowed, and
the mucosa ulcerated.

15. Slide 2.4Microscopically at low power, the

small intestine has extensive mucosal
ulceration, transmural chronic inflammation,
fibrosis, and granulomas.

16. Slide 2.5Microscopically at high power, the

granulomas are evident. No infectious agents
can be demonstrated in these granulomas.

17. Questions: • What is the diagnosis? • Could the

patient also have colonic involvement? • What is
the course of this disease and what kinds of
complications can develop?

18. CASE 2: Crohn's Disease • What is the

diagnosis? This is Crohn's disease, typified by
discontinuous small bowel disease which
microscopically is transmural and demonstrates
granulomas. • Could the patient also have
colonic involvement? Yes, about half of patients
with small intestinal Crohn's disease will also
have colonic Crohn's disease. • What is the
course of this disease and what kinds of
complications can develop? The course typically
involves intermittent flareups with intervening
asymptomatic periods of weeks to months.
Compications of the inflammation include fibrosis
with stricture leading to obstruction, fistulas to
other loops of bowel or to bladder or skin, and
malabsorption. Extraintestinal manifestations of
Crohn's disease include: erythema nodosum,
ankylosing spondylitis, migratory polyarthritis, and
sacroilitis. There is a slightly increased risk for
small or large bowel carcinoma, but this risk is far
less than that in ulcerative colitis.

19. CASE 3 Clinical History: • Following heart

transplantation for idiopathic dilated
cardiomyopathy, this 40 year old female
developed rejection, as shown on
endomyocardial biopsy. Her immunosuppressive
therapy was increased. She then developed
bacterial and fungal sepsis. She was treated with
antimicrobial therapy, including clindamycin. She
patient then developed diarrhea. A colonoscopy
was performed (Slide 3.1). A colectomy was
performed, and the surface of the colon showed
diffuse reddening with an overlying friable tan-
green exudate (Slide 3.2). The microscopic
section of colon shows surface mucosal erosions
with overlying fibrinopurulent exudate (Slides 3.3
and 3.4).

20. Slide 3.1On colonoscopy can be seen an

extensive tan-green exudate over the mucosa.

21. Slide 3.2The surface of the colon shows

diffuse reddening with an overlying friable tan-
green exudate.

22. Slide 3.3At low power microscopically, the

colon shows surface mucosal erosions with
overlying fibrinopurulent exudate.

23. Slide 3.4At high power microscopically, the

colon shows surface mucosal erosions with
overlying fibrinopurulent exudate.

24. Questions: • What is the diagnosis? • What

laboratory test was done that helped to make the
diagnosis? • What is the pathogenesis of this
lesion?

25. CASE 3: Pseudomembranous Colitis • What

is the diagnosis? This is pseudomembranous
colitis. In some cases the small intestine can also
be involved to produce pseudomembranous
enterocolitis. • What laboratory test was done
that helped to make the diagnosis? An assay for
C. difficile was done and was positive. • What is
the pathogenesis of this lesion? This disease is
produced by mucosal injury from the toxin of
Clostridium difficile. C. difficile is a normal gut
commensal organism that can overgrow with
broad spectrum antibiotic therapy (clindamycin,
lincomycin, ampicillin, etc.) and lead to extensive
mucosal injury. Overgrowth of other organisms
such as Candida and Staphylococcus can
produce similar findings.

26. CASE 4 Clinical History: • A 45 year old man

was found to have a stool positive for occult
during a routine physical examination. A
colonoscopy was performed and a 1.3 cm
diameter polypoid lesion on a short stalk was
found in the descending colon, along with a
smaller 0.5 cm polyp in the sigmoid region (Slide
4.1). Both were resected. The gross photograph
shows another case of a patient with several of
these lesions (Slide 4.2). Another patient with a
different gross appearance is shown in slide 4.3.
The microscopic section demonstrates the polyp
removed at colonoscopy at low power (Slide 4.4)
that consists of closely packed tubular glands
lined by cells with depleted cytoplasmic mucin
and hyperchromatic, stratified nuclei and
occasional mitoses (Slide 4.5).

27. Slide 4.1The colonoscopic views of the

smaller and larger polyps are seen here.

28. Slide 4.2The gross lesion here is from

another case of a patient with several of these
lesions. The barium enema view below
demonstrates a colonic polyp. The head of the
polyp is partially obscured by the pool of barium
contrast in which it rests.

30. Slide 4.3Another patient with a similar

disease but different gross appearance is shown
here.

31. Slide 4.4Seen here microscopically at low

power is one of the polyps.

32. Slide 4.5Seen here microscopically at higher

power, the polyp at the right consists of closely
packed tubular glands lined by cells with
depleted cytoplasmic mucin and hyperchromatic,
stratified nuclei and occasional mitoses.
Compare with the normal colonic mucosa at the
left.

33. Questions: • What is the diagnosis? • This is

thought to be a precursor for what lesion? •
Name a syndrome in which the patient has
hundreds of these polyps (A gross photograph of
such a patient is shown in Slide 4.4). • Name a
syndrome that not only has hundreds of these
polyps, but also has osteomas, desmoids, and
other extracolonic manifestations.

34. CASE 4: Tubular Adenoma • What is the

diagnosis? These are benign tubular adenomas
(adenomatous polyps). • This is thought to be a
precursor for what lesion? This is thought to be a
precursor for adenocarcinoma. Polyps greater
than 2 cm have a greater chance for containing
adenocarcinoma. Over time, more genetic "hits"
occur in the neoplasm to drive transformation to
malignancy. • Name a syndrome in which the
patient has hundreds of these polyps (A gross
photograph of such a patient is shown in Slide
4.4). The syndrome is familial polyposis coli, with
an autosomal dominant inheritance pattern.
Colectomy is performed to prevent development
of adenocarcinomas. • Name a syndrome that
not only has hundreds of these polyps, but also
has osteomas, desmoids, and other extracolonic
manifestations. The syndrome is Gardner
syndrome, also with an autosomal dominant
inheritance pattern, but with variable expression.
These patients are also at risk for development of
gastrointestinal tract adenocarcinomas.

35. CASE 5 Clinical History: • A 44 year old male

emergency medical technician has been feeling
fatigued for months. He just doesn't have the
same level of energy he used to have. He
remembers that he had experienced an episode
of jaundice about 10 years ago, but that resolved
and he had been healthy since. A CBC reveals
that he is not anemic. A chemistry panel reveals
normal serum electroytes, but he has an elevated
alanine aminotransferase of 132 U/L and
aspartate aminotransferase of 113 U/L. He has a
total bilirubin of 1.3 mg/dL with direct bilirubin of
0.8 mg/dL. His total protein is 5.4 g/dL with
albumin of 2.9 g/dL. A liver biopsy is performed.

36. Slide 5.1The gross appearance of another

liver with this process is shown here. What is
abnormal?

37. Slide 5.2The medium power appearance of

the liver is shown here. How has the
architecture been altered?

38. Slide 5.3The medium power appearance of

the liver is seen here. What is happening to the
hepatocytes (arrows)?

39. Slide 5.4The gross appearance of the liver

seen here illustrates a complication of this
disease process.

40. Slide 5.5The gross appearance of the liver

seen here illustrates another complication of this
disease process.

41. Questions: • What is suggested by the clinical

laboratory and biopsy findings? • What is the
differential diagnosis? Further History: • A
hepatitis panel revealed the following: TestResult:
Hepatitis A antibodies, total Positive Hepatitis A,
IgM Negative Hepatitis B surface antigen Positive
Hepatitis B surface antibody Negative Hepatitis B
core antibody Positive Hepatitis C antibody
Negative • How do you explain these additional
laboratory findings? • What complications of this
disease are illustrated by slides 5.5 and 5.6?

42. CASE 5: Hepatitis B Infection with Chronic

Hepatitis • What is suggested by the clinical
laboratory and biopsy findings? Hepatitis. Slide
5.1 shows a typical gross appearance of a liver
with ongoing hepatitis, with necrosis and lobular
 collapse seen as areas of hemorrhage and
irregular furrows and granularity on the cut
surface. Slide 5.2 demonstrates a mononuclear
inflammatory cell infiltrate that extends from portal
areas and disrupts the limiting plate of
hepatocytes which, in Slide 5.3 are seen to be
are undergoing necrosis ("ballooning
degeneration") with a small round Councilman
body. This is the so-called "piecemeal" necrosis
of chronic active hepatitis. • What is the
differential diagnosis? Viral hepatitis is the most
likely diagnosis. Hepatitis A is generally a mild,
self-limited illness. Hepatitis B and C can produce
more chronic disease. The latter two agents are
more commonly parenterally acquired
(transfusion of blood products, penetrating
injuries in the health care setting, injection drug
use, vertical transmission from mother to fetus)
while hepatitis A is more often acquired via fecal-
oral contamination. However, an identifiable risk
may not be found in all cases. • How do you
explain these additional laboratory findings? The
hepatitis A tests suggest that he has IgG
antibodies from a remote, not current infection.
The hepatitis B surface antibody is negative,
though a positive value should be found in a
person who received a hepatitis B vaccination.
With chronic liver disease from hepatitis B, the
surface antigen and core antibody are typically
positive. The histologic findings are consistent
with chronic hepatitis B. If a person with hepatitis
B clears the infection, then hepatitis B surface
antibody appears. • What complications of this
disease are illustrated by slides 5.4 and 5.5? The
complications are those of chronic liver disease.
In about two-thirds of patients, hepatitis B
produces a subclinical disease. About 20%
develop a clinically apparent hepatitis. About 5 to
10% go on to chronic hepatitis with both fibrosis
and inflammation. The fibrosis can proceed to a
macronodular cirrhosis. In this setting, the risk for
hepatocellular carcinoma is increased. The
fibrosis can proceed to a macronodular cirrhosis
(slide 5.5). In this setting, the risk for
hepatocellular carcinoma (slide 5.6) is increased.

43. CASE 6 • Clinical History: • A 63 year old man

sought medical help because of increasing
abdominal girth over many months along with a
recent episode of vomiting blood. Serum
chemistries showed sodium 120, potassium 4.2,
chloride 99, bicarbonate 20, glucose 75, total
protein 6.2, albumin 1.9, total bilirubin 5.0, AST
190, ALT 123, and protime 18 seconds (normal
12). A gross photograph (Slide 6.1) shows how
his liver and spleen would appear. The
microscopic section is also representative of his
liver. It shows a diffusely disorganized architecture
with nodules of hepatocytes with focal
cholestasis and surrounded by fibrous bands
with bile duct proliferation (Slides 6.2 and 6.3). At
high magnification, globular eosinophilic material
is seen in some hepatocytes (Slide 6.4).

44. Slide 6.1This is how his liver and spleen

would appear. The shrunken, nodular
appearance of the liver and the enlarged spleen
are both seen in the abdominal MRI scan below.

46. Slide 6.2There is portal fibrosis and marked

macrovesicular steatosis (fatty change) at low
power.

47. Slide 6.3There are nodules of regenerating

hepatocytes surrounded by dense fibrous
bands seen here microscopically at low power.

48. Slide 6.4At high magnification, globular

eosinophilic material is seen in some
hepatocytes.

49. Questions: • What is the diagnosis? What do

the clear vacuoles in the hepatocytes represent?
What is the clumped eosinophilic material seen in
some of the swollen hepatocytes? • What is the
probable etiology? • Correlate the clinical and
laboratory findings in this patient. • What are
potential complications of this disease?

50. CASE 6: Alcoholic Liver Disease • What is the

diagnosis? What do the clear vacuoles in the
hepatocytes represent? What is the clumped
eosinophilic material seen in some of the swollen
hepatocytes? This is cirrhosis. It can be further
classified as a micronodular cirrhosis on the basis
of the size of the nodules (<5 mm). The vacuoles
are of fat from fatty change. The clumped
eosinophilic material is Mallory's hyaline. • What
is the probable etiology? Given the above
findings, the most probable etiology is
alcoholism. • Correlate the clinical and laboratory
findings in this patient. Patients with cirrhosis can
develop portal hypertension with esophageal
varices, which may explain the hematemesis.
Liver failure from cirrhosis can lead to
hypoalbuminemia, hypoprothrombinemia, and
ascites. • What are potential complications of this
disease? Complications leading to morbidity and
mortality include gastrointestinal hemorrhage,
hepatic coma, infection (pneumonia, peritonitis),
renal failure with hepatorenal syndrome, and
hepatocellular carcinoma.

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