CPC Case Presentation Script
Slide 1: Title Slide
Good [morning/afternoon], everyone. We are Group 2A. Today, we will be present-
ing a Clinicopathologic Conference case that highlights the diagnostic challenges in a
patient with chronic gastrointestinal and systemic symptoms. The case ultimately
revealed an uncommon but critical diagnosis that emphasizes the need for thorough
clinical reasoning.
Slide 2: General Data
Our patient is a 39-year-old Caucasian male, a graduate student and former mer-
chant marine, residing in New York City. He was admitted on April 22, 1993. He has
been married for eight years.
Slide 3: Chief Complaint
His chief complaints were abdominal bloating, diarrhea, and peripheral edema.
These symptoms had been troubling him intermittently over a span of several
months.
Slide 4: History of Present Illness – Onset
Six months prior to admission, the patient and his wife developed illness like
malaise, nausea, vomiting and low grade fever. They both improved over several
days. However, only the patient began experiencing recurrent monthly episodes of
abdominal distension, audible bowel sounds with visible peristalsis, and loose stools
—up to 10 times per day. These resolved spontaneously within days without spe-
cific treatment.
Slide 5: Initial Diagnosis and Treatment
He was initially diagnosed with Irritable Bowel Syndrome and treated with Chlor-
diazepoxide and Amitriptyline, which led to some improvement, but the episodes
continued.
Slide 6: Between Episodes
Between episodes, the patient felt generally well, maintained a normal appetite and
bowel pattern. Despite this, he had an unexplained weight loss of 30 pounds over 8–
10 months, which was a significant red flag.
Slide 7–9: Past Medical History
Notable past events include:
- 1983: Bloody diarrhea after eating raw seafood in the Caribbean.
Patient evaluated with endoscopy, barium enema, sigmoidoscopy which all seems
to be normal and patient diagnosed with infectious diarrhea and treated with antibi-
otics.
He visited a local physician who noticed peripheral edema, hypokalemia, and hy-
poalbuminemia, with imaging showing small bowel obstruction. This led to hospital
admission for further workup.
- 1983: Received a blood transfusion in NYC—important considering transfusion-re-
lated Hepatitis C risk.
- 1987–1990:Patient had 3 episodes of prolonged febrile illness and was presumed
to be malaria
On peripheral blood smear no organisms were seen
He was treated with chloroquine
- 1990: Right inguinal herniorrhaphy.
Slide 10–11: Social and Travel History
Socially, he was married for 8 years with history of homosexual contact or multiple
sexual partner.
no IV drug use or alcohol.
Travel history: Between 1975 and 1985, the patient extensively traveled to several
regions His destinations included:
West Africa,Pakistan,Saudi Arabia,Europe, and The Caribbean(1983)
Slide 12–15: Physical Examination
On examination:
- the patient appeared Thin appearance with no apparent distress, and normal vital
signs
“On physical examination, the head and neck
There was no thyromegaly, There was no cervical or supraclavicular lym-
phadenopathy
Thoracic examination was also unremarkable:Lung fields were clear and cardio-
vascular was without abnormality
The patient presented with normal nervous system examination with no skin rash
- his Abdomen was distended, tympanitic with visible peristalsis and high-pitched
'tinkling' bowel sounds
- No organomegaly or occult blood
- Extremities showed 3+ pitting edema and mottled skin
- Other systems were normal
Slide 16: Lab Findings
Lab findings revealed:
The patient’s hemoglobin is 14.4 g/dL and hematocrit is 40.2%, both within normal
limits. The white blood cell count is 7,200/mm³, also normal, with a differential
showing mild neutrophilia at 77% and low lymphocytes at 14%. Platelet count is el-
evated at 378,000/mm³.
---- slide change ----
Sodium is slightly low at 133 mEq/L, potassium is normal at 4.4 mEq/L, chloride
is normal at 100 mEq/L, and bicarbonate is mildly elevated at 33 mEq/L. BUN is
17 mg/dL and creatinine is 1.0 mg/dL—both normal. Calcium is low at 8.0 mg/dL,
phosphorus is normal at 3.3 mg/dL. Albumin is significantly low at 2.1 g/dL, and
total protein is also low at 4.6 g/dL. Cholesterol is markedly low at 57 mg/dL.
----slide change ---
AST is mildly elevated at 59 U/L, alkaline phosphatase is slightly high towards
upper limit of normal range at 137 U/L, and bilirubin is normal at 0.7 mg/dL.
---- slide change ---
Iron is 68 µg/dL, with a low TIBC of 80 µg/dL and high transferrin saturation at
85%, while ferritin is within normal range. Vitamin B12 levels are also normal.
These results suggest possible chronic illness, liver issues, or malnutrition
Slide 17: Differential Diagnosis
We considered a broad differential including:
- Malabsorption syndromes
- Infections: Tropical sprue, Whipple’s, Giardiasis
- Celiac disease
- Strongyloides hyperinfection
- Crohn’s disease
- Small Bowel Lymphoma
Each was systematically evaluated based on history, labs, and imaging.
Slide 18–23: Rule In / Rule Out
Whipple’s Disease: Fits many symptoms but lacked CNS signs, arthralgia, and typical
imaging findings.
Crohn’s Disease: Ruled out due to absence of pain, normal ESR, and normal colon
imaging.
Tropical Sprue: Considered due to endemic exposure and GI symptoms but lacked
B12 deficiency or antibiotic response.
Celiac Disease: No gluten sensitivity, villous atrophy, or iron deficiency.
Strongyloides Hyperinfection: Suspected due to exposure and symptoms, but ruled
out due to absent eosinophilia, rash, or respiratory signs.
Slide 24: Pertinent Positives
Key findings that pointed us toward the final diagnosis:
- Chronic intermittent diarrhea, bloating, and visible peristalsis
- Hypoalbuminemia and peripheral edema
- History of blood transfusion with possible Hepatitis C exposure
- Mild liver dysfunction and segmental narrowing of small bowel on imaging
Slide 25: Final Impression
Based on the cumulative evidence, our final diagnosis is:
Small Bowel Lymphoma secondary to Chronic Hepatitis C infection.
The chronic antigenic stimulation from HCV may have predisposed him to lymphoid
neoplasia.
Slide 26: Pathophysiology
Initial infection with Hepatitis C virus, potentially acquired through a blood trans-
fusion, can lead to persistent viremia.(next slide)
This chronic viral presence acts as a persistent antigen stimulus, which may re-
sult in genetic modifications and subsequently, B-cell transformation, leading to
the formation of extranodal lymphoma. Additionally, chronic Hepatitis C can
cause hepatic dysfunction, characterized by protein production abnormalities and
fluctuating aminotransferase levels.(next slide )
The extranodal lymphoma can directly contribute to small bowel obstruction
through mucosal destruction, leading to luminal narrowing and thickening of the
intestinal wall. This partial obstruction then causes bowel distension proximal to
the blockage, (slide change)
which in turn can lead to decreased absorption of nutrients and fluids, abdominal
bloating, and further mucosal damage within the bowel. (Slide change)
Decreased absorption leads to gas and fluid accumulation which is responsible
for visible peristalsis and tinkling sensation that will further progress to forced
propulsion of unabsorbed food which would result in diarrhea (slide change)
The decreased absorption can promote bacterial overgrowth, causing deconjuga-
tion of bile salts and fat malabsorption, manifesting as steatorrhea.(slide change )
Furthermore, mucosal damage can lead to tumor infiltration of lymphatics, result-
ing in lymphatic obstruction and loss of plasma protein into the intestinal lumen.
This process causes hypoalbuminemia and an imbalance in oncotic pressure, ul-
timately contributing to edema.
Slide 27–30: Supporting Journals
Multiple studies have described the link between HCV infection and the develop-
ment of lymphomas. It’s rare, but well documented in literature. Small bowel lym-
phomas often present with vague GI symptoms and are frequently diagnosed late
due to nonspecific features.
Slide 31: Thank You
Thank you all for your attention. This case reminds us that nonspecific gastrointesti-
nal symptoms can mask serious underlying pathology, and highlights the impor-
tance of a holistic, thorough diagnostic approach.
Slide 32: Closing Note
Take care of yourself—and your patients. Diagnoses like this may be rare, but they
are critical not to miss.