Introduction to Clinical Medicine

(ICM)
Diseases of the Gastrointestinal
Tract and Liver
Discussion of Case Studies
Prepared by:
Robert W. Wilhoite M.D.
Edited by
Patrice Thibodeau MD 2017
Presented by:
Teresita Maguire MD
 Case # 1
• This 52 year old man presents with a history of
abdominal cramps and bloody diarrhea. These
symptoms persisted for 10 days following which the
patient felt better. Past history reveals that he has
experienced similar episodes many times over the past
five years.
• His stool specimen is positive for blood but no ova or
parasites are seen. A colonoscopy was performed and
showed diffuse mucosal inflammation and superficial
ulcerations in the rectum and descending colon. A
biopsy was performed and the microscopic sections
that follow are representative of his disease process.
 Problem List
• Abdominal cramps
• Bloody diarrhea
• Multiple previous episodes
• Mucosal inflammation and ulceration of
rectum and descending colon
 Case # 1
• What is your differential diagnosis?
– Inflammatory bowel disease (IBD)
• Ulcerative colitis
• Crohn’s disease
• Infectious enterocolitis
Normal Large intestine
Biopsy of patient’s large intestine
 Case # 1
• What is your interpretation of the
microscopic section of patient bx above?
– Superficial mucosal ulceration
– Crypt abscess formation
 Case # 1
• What is your final diagnosis?
• Ulcerative colitis
 Case # 1
• What are the classic symptoms of
patient’s with ulcerative colitis
– Fever
– Abdominal cramping pain
– Tenesmus
– Low volume bloody diarrhea
 What are some extraintestinal manifestations
or associated conditions of the disease?
– Migratory
polyarthritis
– Sacroiliitis
– Uveitis, optic neuritis
– Aphthous ulcers
– Erythema nodosum
– Sclerosing cholangitis
What are the characteristic gross and microscopic findings
one might expect to see in this disease process?

• Gross:
– Thin wall, mucosal ulceration, edema
– Pseudopolyposis

• Micro:
– Inflammation limited to mucosa and lamina propria
– Superficial ulceration
– No granulomas or skip areas
– Crypt abscess
 This patient may be at risk of developing
other complications. What are they?

• Cellular dysplasia
and adenocarcinoma
• Toxic megacolon
Final diagnosis

Ulcerative colitis
 Case # 2
• This 36 year old woman gives a long history of
diarrhea, flatulence, weight loss and fatigue.
She notes the stool is fairly foul smelling and
embarrassing.
• Over the past year she has lost eighteen pounds
without intentional dieting. She now consults
her physician because of multiple blistering
itchy skin lesions.
Describe the lesion
 Findings in our patient
• Protracted diarrhea
• Flatulence and foul smelling stool
• Weight loss of 18 lbs in one year
• Blistering itchy skin lesions
An endoscopy was performed
A biopsy was taken
A biopsy of the small intestine illustrates a comparison
between normal small intestine (left side) and the
patient (right side)
What do you see?
From the clinical history and biopsy specimen
what is the basic problem? Why the weight
loss and diarrhea?

A malabsorption syndrome
Definition:
A decreased absorption of nutrients
(protein, CHO, fat, electrolytes, water
vitamins and minerals)
What are the “classic” symptoms of a
malabsorption syndrome?

– Diarrhea
– Steatorrhea
– Weight loss
– Abdominal distention
– Weakness
– Muscle wasting
– Growth retardation
A malabsorption syndrome may be the
result of a disturbance in one of the
following:

– Intraluminal digestion – lack of enzymes

– Transepithelial transport
• Reduction in epithelial surface (intestinal
resection, loss of villi)
– Terminal digestion –rapid movement
 Diff Dx of malabsorption?
• Pancreatic insufficiency – Lactase deficiency
• Crohn’s disease – Bacterial overgrowth
• Celiac disease (gluten –antibiotic induced
sensitive enteropathy) – Viral gastroenteritis
• Bile salt deficiency – Neoplasm and
(cirrhosis, cholestasis) lymphatic obstruction
• Whipple’s disease (PAS
macrophages)
 Clinical and Lab findings with
malabsorption
• Steatorrhea – Macrocytic anemia
– Vitamin ADEK • Decreased vitamin B12 or
deficiency (fat soluble folate
vits) – Paresthesias
• Diarrhea (increased fecal • Decreased calcium or
water) magnesium
– Osteoporosis
– Increased stool volume
• Decreased vitamin D and
• Weight loss calcium
– Decreased CHO – Bleeding tendency
absorption • Decreased vitamin K
• Microcytic anemia – Edema
– Low serum iron • Decreased protein
 What other tests would you
order for this patient?
• Endoscopic mucosal biopsy (obtained already)
• CBC –anemia ( indicating ? iron, B12, folate deficiency)
• Iron studies - (FE, TIBC, Ferritin), B12 and Folate levels
• Serum calcium and Vit D levels – impaired absorption
• Total IgA and IgA tTG antibody (tissue transglutaminase)
– screening tests of choice for celiac dz
– 90 % sensitivity and 95% specificity for celiac disease
 Celiac Disease
• 1:2000 in the white population
• About 95% of patients have the HLA-DQ2 allele, which
suggests a genetic basis.
• Begins in childhood with exposure to gluten which contains the
protein gliadin. Gluten is found in wheat, rye, barley, oats.
• Antibodies develop against gluten (gliadin)
• Leads to immunologic destruction of villi of small intestine and
hyperplasia of the crypts
• Associated with increase risk for enteropathy associated T cell
lymphoma, non-Hodgkins lymphoma and adenocarcinoma of
small bowel; Type 1 DM
What is the cause of her blistering skin
lesion?

– Dermatitis herpetiformis
• A cutaneous manifestation of Celiac disease
• Pruritic papulovesicles over the extensor
surfaces of extremities, trunk , scalp and neck
• Seen in 20 % of patients with Celiac disease
• Caused by IGA autoantibodies directed at
dermal keratinocytes.
 Final diagnosis

Celiac disease
Dermatitis herpetiformis
 Case # 3
• This 32 year old woman has had intermittent attacks of
mild fever, diarrhea and abdominal pain. She usually
recovers from these acute episodes with alleviation of
her symptoms for several weeks to months. She also
gives a history of migratory polyarthritis and peculiar
nodular skin lesions.
• She has recently lost her job and has experienced an
exacerbation of these old complaints together with
some right lower quadrant pain. An Upper GI series of
the small intestine was obtained and follows.
• She subsequently underwent a segmental resection of
her small intestine. The gross picture that follows is
representative of her underlying disease process.
 Findings
• Fever
• Diarrhea
• Abdominal pain
• Migratory arthritis
• Skin lesions
• Relapsing/remitting symptoms
 Differential Dx?
– Inflammatory bowel disease
• Crohn’s disease
• Ulcerative colitis
• Infectious enterocolitis (can this explain all the
findings?)
What are the typical gross and microscopic
features one would expect to see in this
disease state?

– Transmural involvement with thickening of

the bowel wall
– Linear ulcerations
– Skip areas of involvement
– Non-caseating granulomas
Ulceration

Granulomas
Non-caseating granulomas with giant cells
 What are some of the complications
associated with Crohn’s disease?
– Abscess
– Obstruction
– Fistulas
– Perianal disease
– Carcinoma
– Hemorrhage
– Malabsorption
Early fistula formation
 Crohn’s disease
• Crohn’s disease can be considered a multi-
system disease.
• What are some of the extra-intestinal
manifestations of this disease?
– Migratory polyarthritis
– Ankylosing spondylitis
– Erythema nodosum
– Oral aphthous ulcers ( common)
– Gall stones- malabsorption of bile salts
Final diagnosis

Crohn’s disease
 Case # 4
• This 51 year old man complains of increasing
abdominal girth. Physical exam reveals mild
jaundice, moderate hepatosplenomegaly and
dilated veins around his umbilicus. There is
also a suggestion of a fluid wave within the
abdomen.
• Initial laboratory findings:
– Total bilirubin=5.4 (H), direct bilirubin=4.2 (H)
– Alkaline phosphatase elevated
– AST= 300 (H), ALT= 158 (H)
– Total protein= 6.4 (L) albumin= 2.2 (L)
– Prothrombin time = 18 seconds (H)
– A liver biopsy was obtained.
 Findings
• Increasing abdominal girth
• Jaundice
• Moderate hepatosplenomegaly
• Dilated periumbilical veins
• Fluid wave
• Labs consistent with liver dysfunction (both cholestatic
and hepatocellular)
 Differential Dx?
• Alcoholic cirrhosis of the liver
• Viral Hepatitis
• Primary biliary cirrhosis
• Primary hemochromatosis
• Wilson’s disease
• Alpha-1-antitrypsin
 Any additional information
needed from patient?
• History of alcohol abuse
• History of prior hepatitis
• History of possible toxic drug exposure
 Interpretation of lab findings
LABS
• Total bilirubin=5.4 (H), direct
bilirubin=4.2 (H)
• Alkaline phosphatase
elevated
• AST= 300 (H), ALT= 148 (H)
• Total protein= 6.4 (L)
albumin= 2.2 (L)
• Prothrombin time = 18
seconds (H)
• The jaundice is due to an
elevation of conjugated
bilirubin
• The alkaline phosphatase is
elevated indicating cholestasis
• AST>ALT suggests an alcohol
related liver disease rather
than viral hepatitis
• Prolonged PT of 18 seconds
suggests hepatic dysfunction
What is your principal
diagnosis?

Cirrhosis
Describe the histologic findings in the biopsy
Normal liver
architecture
 Thought questions
• What are the potential complications of this
disease process (cirrhosis)?
– Portal hypertension
– Splenomegaly
– Ascites
– Esophageal varices (and GI bleeding); hemorrhoids
• What other physical findings might you see in
this patient?
– Hypogonadism, palmar erythema
• (estrogen effect)
What is the major underlying basis for
this patient’s physical findings of caput
medusa and hepatosplenomegaly?

Portal hypertension
Caput medusa
Splenomegaly due to portal hypertension
 Causes of cirrhosis?
• Alcohol
• Chronic hepatitis – B or C
• Biliary disease – PBC
• Cardiac disease
• Autoimmune hepatitis
• Inherited disease
– Hemochromatosis
– Wilson’s disease
– Alpha-1-antitryptsin disease
• Non-alcoholic steatohepatitis
Nonalcoholic Fatty Liver Disease
(NFLD)
• Results from fatty liver changes unrelated
to alcohol intake
• Most common cause of elevated liver
enzymes in adults in USA
• Associated with insulin resistance, obesity,
weight gain and diabetes: progression from
steatosis to cirrhosis may be uncommon,
but obesity and diabetes may increase the
risk of progression
 NAFLD spectrum
• NAFL-nonalcoholic fatty liver
– Hepatic steatosis without evidence of hepatocellular
injury or fibrosis
– Minimal risk of progression to cirrhosis and liver failure
• NASH-nonalcoholic steatohepatitis (NASH)
– Hepatic steatosis with inflammation and hepatocyte injury
with or without fibrosis
– Risk of progression to cirrhosis, liver failure and rarely
liver cancer
• NASH cirrhosis-cirrhosis with current or previous
histological evidence of steatosis or steatohepatitis.
Differential diagnoses for Ascites?

– Cirrhosis of the liver

– Abdominal malignancy – e.g. pancreas, ovary
– Nephrotic syndrome -hypoalbuminemia
– Cardiac failure – congestive heart failure
– Peritoneal tuberculosis
– Peritoneal mesothelioma
How would your treat massive ascites?
Paracentesis

What are the potential consequences of

paracentesis?
– Rupture of a vessel
– Bacterial peritonitis
 Case # 4
Final diagnosis

Cirrhosis of the liver

Portal hypertension
 Case # 5
• This 53 year old Italian male consulted his
physician complaining of increased fatigue and
arthralgia.
• Physical exam revealed the liver to extend 5 cm
below the right mid-costal line. There was also
noted hyperpigmentation of his skin.
• The heart was enlarged with displaced PMI.
• A basal metabolic profile revealed a blood
glucose of 210 and HbA1c of 8.0 (high).
 Findings
• Italian ancestry
• Fatigue
• Arthralgia
• Hyperpigmentation
• Cardiomegaly
• Hepatomegaly
• Diabetes mellitus of recent onset
 Initial Lab findings
• Hemoglobin 14.0
• WBC 8,600
• Total bilirubin 3.0 (H)
• Direct bilirubin 2.8 (H)
• Alkaline phosphatase and cholesterol
levels are markedly elevated.
 From the available information what
are your diagnostic considerations?
• Alcoholic cirrhosis
• Hemochromatosis
• Hepatitis
• Primary sclerosing cholangitis
Is there any significance to his
recently diagnosed diabetes? Does
this help narrow the diagnoses?
What additional tests would you
order?

• Serum iron, ferritin and transferrin saturation

levels
 What is your final diagnosis?

Primary (Hereditary) Hemochromatosis

 What is the underlying
pathogenesis of this condition?
– A genetic defect, most commonly in the
hemochromatosis (HFE) gene, resulting in excessive
absorption of iron from the small intestine.
– Normally there is no major excretory pathway for
iron and thus it accumulates in various organs from
iron overload.
– It is an autosomal recessive disease that results in
the abnormal accumulation of iron within multiple
organs including liver, heart, pancreas, skin, joints.
– Rarely affects Afro-Amer., Asians or other minority
groups
 Tidbits
• Dietary iron is primarily absorbed in the
duodenum as ferrous iron. For it to be
absorbed it must be converted to the ferric
state at which time it is bound to transferrin as
a carrier protein.
• Iron is stored in the body as water soluble
ferritin and water insoluble hemosiderin
 Organs affected
• Liver
– Deposition of iron, may result in cirrhosis
• Pancreas
– Deposition of iron results in the destruction of the
beta cells with a lack of insulin production and the
subsequent development of diabetes
• Skin
– Bronze skin (deposition of both iron and melanin)
• Heart:
– conduction abnormalities, CHF
• Testes
– atrophy
 What are the potential complications
of this disease process?

• Cirrhosis with hepatic coma and portal HTN

• Diabetes
• CHF
• Hepatocellular carcinoma
• Hypogonadism (in both sexesloss of libido,
impotence, amenorrhea, gynecomastia,
testicular atrophy)
 Significant laboratory studies
in hemochromatosis:
• Increased transferrin saturation > 45%
• Ferritin level > 300 ng/L in men and > 200 in
women
– is less sensitive than transferrin saturation
• HFE gene testing looking for the C282Y
polymorphism
 How would you treat this
patient?
• Phlebotomy
• Limit alcohol consumption, Vit C and
Iron supplements
• Stay away from iron rich foods such as:
– Red meat, alcohol, shellfish
 Case # 5
Final diagnosis

Primary hemochromatosis
 Case # 6
• This 32 year old woman developed diarrhea
approximately 10 days ago. One month ago she
took 10 days of amoxicillin for bronchitis. Her
diarrhea has persisted and she is currently
having 6-7 liquid stools per day. She has not
seen any blood in the stool. She denies nausea
or vomiting.
• Physical exam reveals a dehydrated woman
with a temperature of 38.5 degrees and diffuse
abdominal pain.
 Findings
• Persistent diarrhea
• Recent antibiotics
• No gross blood in stool
• Fever
• Diffuse abdominal pain
 Thought questions
• How would you define diarrhea?
– stool with increased water content, volume, or
frequency
• How would you define dysentery
– Bloody diarrhea
• How do you classify the various types of
diarrhea?
– Secretory, osmotic, malabsorptive,
inflammatory/infectious
– Acute versus chronic (<4weeks vs > 4 weeks)
 How would you proceed in
your evaluation of this patient?
– Determine the nature of the stool
• Large volume, watery stools that does not stop with fasting (secretory
 cholera)
• Diarrhea stops with fasting, has associated bloating and gas (osmotic
 carbohydrate malabsorption)
• bulky, greasy, oily, malodorous (malabsorptive/steatorrhea
pancreatic insuf)
• +/- fever, bleeding, weight loss, fecal WBC’s (inflammatoryIBD,
infection)
– History of medications:
• Recent antibiotics use?
• Laxatives?
– Any associated symptoms:
• fever, rash, weight loss, edema
Is this a case of acute or
chronic diarrhea?

Acute
 Acute diarrhea -non inflammatory
• A watery, non-bloody stool associated with
periumbilical cramps, bloating, n/v
• Usually indicative of a small intestinal source
• Viral
• Protozoal
– Giardia, cryptosporidium, cyclospora
• Bacterial
– Preformed enterotoxins
• Staph, Clostridium
– Enterotoxin producing
• Enterotoxigenic E. coli
 Acute diarrhea - inflammatory

– Fever with blood; left lower quadrant pain,

urgency or tenesmus; fecal leukocytes
present
– May be indicative of an invasive organism
• Cytotoxin production:
– Viral - cytomegalovirus
– Protozoal - Entamoeba histolytica
– Bacterial
» E. coli – 157, vibrio, C. difficile
• Mucosal invasion
– Shigella, Salmonella, Campylobacter
 Chronic diarrhea:
– Osmotic diarrhea
• Ingestion or malabsorption of osmotically active substance
• Laxative abuse
– Secretory
• Infections
• Neuroendocrine
• Bile acid
– Inflammatory/Infectious
• Inflammatory bowel disease
• Infectious agents- C. difficile Giardia, entamoeba, cyclospora
• Microscopic colitis
– Malabsorption
• Celiac disease, Whipple’s disease, pancreatic disease
• Bacterial overgrowth
– Motility disorders -IBS
 Patient’s initial lab findings
• No increased fecal fat
– Helps rule out malabsorption, pancreatic insufficiency,
bacterial overgrowth
• Positive occult blood
– Consider inflammatory diarrhea (e.g. UC or infection)
• Fecal leukocytes present
– Implies inflammatory diarrhea
• No ova or parasites
 What additional tests would
you order for the patient?
• CBC, BMP
• Stool culture
• C. difficile testing using rapid antigen test
for toxin A and B
 Anything else?
• May need to consider Colonoscopy but
NOT at first in this patient.
• Colonoscopy will help rule out
• Inflammatory bowel disease
• Villous adenoma
• Pseudomembranous colitis ( C. difficile)
• Flask shaped ulcers – amebiasis
• Melanosis coli
(I would not do this initially. Only if other
testing unrevealing of diagnosis. )
So here is that colonoscopy…you
do not need to order!
Melanosis Coli
 Final diagnosis
Acute inflammatory diarrhea
due to
C. difficile
 Case # 7
• This 38 year old man has experienced persistent
heartburn with occasional retrosternal pain for many
years. The pain usually occurs 30-60 minutes after a
meal and seems to be exacerbated by hot, spicy foods.
At one time, several years ago, it was thought he may
have had an acute MI but cardiac enzymes did not
support that diagnosis.
• More recently his symptoms have become worse
particularly at night. Because of this an
esophagogastroscopic (EGD) examination was
performed. The gross and microscopic pictures are
representative of the findings.
 Findings
• Postprandial persistent heartburn
• Retrosternal pain – worse with spicy food
• Progressive symptoms – worse at night
 Diff Dx?
• Erosive esophagitis
• GERD
• Barrett's esophagitis
• Peptic ulcer
• Angina
 What are the various causes of
esophagitis?
• Herpes, CMV - punched out ulcers
• Candida –gray-white pseudomembrane
• Bacterial – invasion of esophageal wall
• Corrosive substances
• Cytotoxic drugs/radiation – atrophy and fibrosis
• Smoking, alcohol – liquefactive necrosis
• Scleroderma – rubber hose appearance
Normal mucosa Mucosal erythema
and erosion
Describe the gross and
microscopic findings.
Gross: areas of hyperemia and erosion
Micro: metaplastic columnar epithelial cells
with goblet cells (intestinal metaplasia)
What is your primary diagnosis

Gastro-esophageal reflux disease

(GERD) and Barrett's
esophagus
 Case # 7
• 10 % of patients with GERD will develop
Barrett’s esophagus:
– Most important risk factor for esophageal Ca
– >3 cm involvement – 30-40 x risk of Ca
– Patho-physiology of GERD
• Transient relaxation of LES
• Regurgitation of acid and bile
• Cellular metaplasia
 Evaluation of a patient with
long standing GERD.
• Screening endoscopy in patients with persistent GERD
symptoms at age 50
• If diagnosed with low grade Barrett’s esophagus, f/u
endoscopy every 6-12 months
• If diagnosed with high grade Barrett’s
– 20% progress to adenocarcinoma
– Treat with esophagectomy, endoscopic mucosal
resection or photodynamic therapy and do close
endoscopic follow up every 3 months.
• Note that established metaplasia dose not regress with
antisecretory treatment
 Final diagnosis

GERD with Barrett’s

esophagus
 Case # 8
• This 55 year old man complains of pain which tends to
remain well localized to the epigastric area. It is
described as a gnawing, dull, aching hunger-like pain
which is not severe.
• The pain is relieved by eating but returns 3-4 hours
later. Occasionally the pain will waken him at night.
• More recently the pain has become more severe and
constantly associated with some nausea and vomiting.
• There is no history of NSAID ingestion or indulgence in
alcohol.
• Patient complains of dark colored loose stool.
 Findings
• Epigastric pain
• Dull and gnawing in character
• Progressively worse
• No history of NSAID or ETOH use
• Melena
 Differential Diagnosis?
• Peptic ulcer disease
– Gastric versus duodenal
• Gastrointestinal reflux disease
• Acute or chronic gastritis
• H Pylori infection
• Esophageal disease, (esophagitis , rupture –
Boerhaave’s syndrome vs Mallory-Weis tear)
• Biliary tract disease
• Pancreatitis
• Hypersecretory state (i.e. ZE syndrome)
What additional studies would
you order
• Rectal exam (is guaiac positive)
• CBC
– anemic
• Amylase/lipase
– normal  rule out pancreatitis
• Stool antigen for H. pylori
– positive
• Endoscopy with gastric biopsy
– See next slide
What do you see?
 Case # 8
• What is your principal diagnosis?
 Peptic ulcer disease:
– More common in men
– Gastric
• Burning pain with eating, relieved by antacids
– Duodenal
• Decreased pain with meals
• Recurrence of pain 1-3 hours later
• Frequently wakes patient at night
– Just reviewing this in case on your boards,
but not clinically relevant since management
is the same
What is the Zollinger-Ellison
syndrome?
Caused by a gastrin secreting gut neuroendocrine
tumor (gastrinoma)
– Account for 1% of peptic ulcer disease
– Fasting gastrin levels > 150pg/ml.
– Location of gastrinomas (Per Dr. Wilhoite):
• Pancreas 25 %
• Duodenal wall 45%
• Unknown 20%
• 2% are malignant
Acute gastric ulcer
Acute ulcer with penetration to underlying
vessel
H. Pylori – methylene blue
Duodenal ulcer
Perforated duodenal ulcer
 Final diagnosis

Chronic peptic ulcer

due to
H. Pylori infection
 Case # 9
• This 42 year old man, a known i.v. drug abuser,
presents with a history of malaise, fever and jaundice.
Serologic testing reveals the presence of HBsAg and
anti-HBc IgG antibodies. The slide that follows is of a
liver biopsy performed at that time.
• He was lost to follow-up but was seen again two years
later in an ER because of hematemesis and ascites.
Repeat serologic testing revealed the same results. He
was treated and discharged. He was not seen again for
five years at which time he now presents with weight
loss, abdominal pain and rapidly enlarging abdomen.
• Physical exam suggests a fluid wave in the abdomen. A
paracentesis revealed 2500 ml. of bloody fluid.
 Problem List
• Drug abuser
• Fever and jaundice
• Positive HBsAg and anti-HBc IgG
antibodies
• Two years later – ER with hematemesis
and ascites
• Five years later – abdominal pain and
rapidly enlarging abdomen and fluid
wave
Initial liver biopsy
 Thoughts questions
• 1. What do you suggest was the original diagnosis?
– Hepatitis B infection as evidenced by a positive
HBsAg and anti-HBc IgG
• 2. What chain of events do you believe has evolved over
the past seven years?
– He has developed chronic hepatitis with post
necrotic cirrhosis
• 3. What is the significance of the bloody ascitic fluid?
– Frequently associated with the development of
hepatocellular carcinoma or hepatic vein thrombosis
What additional tests would
your order?
– alpha-fetoprotein –rule out hepatocellular Ca
• A helpful but not diagnostic test (positive in 50-75%)
• Elevated levels may also be seen in:
– Yolk sac tumors
– Cirrhosis of the liver
– Massive liver necrosis
– Chronic hepatitis
– Fetal neural tube defects
– Ultra sound of the liver
• May detect small tumors (< 2cm) within the liver
– MRI
Large hepatocellular carcinoma

Note
satellite nodules
Diffuse hepatocellular carcinoma
Hepatocellular carcinoma
 Final diagnosis
Chronic hepatitis B infection

Post necrotic cirrhosis of the liver

Hepatocellular carcinoma
 Case # 10
• This 42 year old man complains of epigastric
pain, nausea, vomiting over the past 24 hours.
He is a known chronic alcoholic with frequent
episodes of binge drinking. Over the past 12
hours his pain has intensified and he describes
a knife-like pain radiating to his back.
• Physical exam reveals tremors, alcohol on his
breath, active bowel sounds, epigastric pain but
no abdominal masses. Some rebound
tenderness is elicited. There are areas of
ecchymosis along the left flank and
periumbilical area.
 Case # 10
• Laboratory findings:
– WBC 14,000 (H)
– Hgb 11 (L)
– Platelets 200,000
– Bilirubin total 1.8 (H)
– AST/ALT elevated
– LDH/ALP elevated
– Calcium 7.0 (L)
 Case # 10
• X-ray findings
– Few dilated loops
of small intestine
with fluid levels
– No pleural
effusion
– No free air
 Findings
• Chronic alcoholic
• Epigastric pain radiating to back
• Areas of ecchymosis along the flank and
umbilicus
• Dilated loops of small intestine with fluid
levels
• No pleural effusion or free air
 What is your differential
diagnosis?

– Acute cholecystitis
– Peptic ulcer disease (? Perforation)
– Acute gastritis
– Acute pancreatitis
– Acute alcoholic hepatitis
– Acute esophagitis
– Acute bowel obstruction
What additional laboratory
tests would you order?
– Serum amylase
– Serum lipase
– CT scan
 Thought questions
• What significance to you attach to:
– Epigastric pain radiating to the back
• Pancreatitis
– Dilated loops of small intestine with fluid
• Paralytic ileus
– No pleural effusion or free air
• No GI perforation
– Areas of ecchymosis along the flank and umbilicus
• Pancreatic necrosis and retroperitoneal bleeding
– Calcium 7.0
• Fatty saponification
What is your primary
diagnosis?

Acute necrotizing pancreatitis

What are the various causes of
acute pancreatitis?
– Alcohol/gall stones - 80 % of cases
– Drugs
– Viral, bacterial infection
– Hypertriglyceridemia
– Vascular ischemia
Fat Necrosis
Fat Necrosis
Chronic Pancreatitis
What are the potential complications
of acute pancreatitis ?
– Pseudocyst
– Abscess
– Shock
– DIC
– ARDS
– ATN (Acute tubular necrosis)
– Tetany
 What is Trousseau’s sign?
– Spontaneous venous thromboses which may recur
resulting in migratory thrombophlebitis
– Associated with visceral malignancy
• Frequently associated with pancreatic carcinoma
• Usually related to the release of mucin from tumors which
results in an activation of the extrinsic pathway of
coagulation.
 Final diagnosis

Acute necrotizing pancreatitis

 Case # 11 Fun case!
• This 21 year old medical student is preparing
for her final exam in pathology. One day
before the exam she notices a slight yellowing of
her sclerae. There is no history of any such
prior occurrence.
• Two days later her scleral icterus clears and she
feels well.
• (She passed the exam!)
 Problem list
21 year old woman
Transient scleral icterus
 Labs
• Total bilirubin 4.2
• Direct bilirubin 0.8
• AST, ALT and AP are all normal
What is the basic problem of
this woman?

Transient hyperbilirubinemia
 Thought questions
• What is your interpretation of the laboratory findings?
– There is an unconjugated hyperbilirubinemia
• What would you consider in the differential diagnosis.
– The various hyperbilirubinemia syndromes:
• Crigler-Najjar – absence of UGT – uncong. bilirubin
• Gilbert’s disease – diminished UGT – uncong.
bilirubin
• Dubin-Johnson syndrome – conj. Bilirubin – black
liver
• Rotor’s syndrome – conj. Bilirubin – no black liver
• What is your final diagnosis?
• Gilbert’s disease
 Thought questions
• What is the underlying mechanism of
this woman’s condition?
– Diminished UGT activity
• What advice would you give her?
• Avoid stress and stay cool!
• No long term complications
Hyperbilirubinemic syndrome
Gilbert’s disease
Thank you