2. Case Presentation - 1
• Mr Smith is a 26-year-old man with no significant past
medical history who presents with diffuse abdominal pain
that began 12 hours ago and is described as a pressure
sensation, most intensely in the mid-abdomen.
• He has a decreased appetite but no nausea or vomiting.
• His last bowel movement was 2 days ago.
• He denies fevers and chills as well as hematuria, dysuria, and
chest pain.
• The patient has no h/o gallstones, kidney stones, or
abdominal surgeries.
• He takes no medications (no aspirin or NSAIDs) and reports
occasional use of alcohol
3. Case Presentation - 1
• Vitals are stable.
• Patient is afebrile.
• Cardiac and lung examinations are normal.
• Abdominal examination reveals a flat
abdomen with hypoactive bowel sounds.
• There is mild, diffuse tenderness present.
• No guarding or rigidity is present.
• Rectal examination is normal.
• Stool is Hemoccult negative
4. Questions
• What should be included in your DDX?
1. Appendicitis (always to be considered in young
adults)
2. Peptic ulcer disease
3. Pancreatitis (may present with epigastric or mid-
abdominal pain)
4. Early bowel obstruction
5. Case Presentation - 2
• Mr Lantern is a 70-year-old man with a history of
hypertension, type 2 DM, and coronary artery disease
who presents with intermittent, crampy, mid-abdominal
pain that started 2 days ago and is associated with
nausea, vomiting, constipation, and an unintentional
weight loss of 5kg over the past 2 months.
• No fever or chills, hematuria, dysuria, or chest pain is
noted.
• The patient has no history of gallstones, kidney stones,
or abdominal surgeries.
• Medications: lisinopril, aspirin, metoprolol, simvastatin,
and insulin. He reports no alcohol use..
6. Case Presentation - 2
• On physical examination the patient looks moderately
distressed.
• Vitals are significant for orthostasis with the heart rate
increasing by 20 beats/min and blood pressure dropping
by 20 mm Hg when the patient sits up.
• The patient is afebrile.
• Sclera are nonicteric.
• Cardiac and lung examinations are normal except for an
irregularly irregular rhythm.
• Abdominal examination reveals a distended abdomen
with hyperactive bowel sounds.
• Rectal examination is normal.
• Stool is Hemoccult positive.
7. Questions
• What should be included in your DDX?
– Large bowel obstruction (LBO)
– Small bowel obstruction (SBO)
8. Case Presentation- 3
• Mr Donaldson is a 47-year-old male who presents to the
emergency department with a 12-hour history of vomiting
bright red blood.
• He has had 4 episodes of emesis during this time span. He
also complains of nausea, fatigue, and light-headedness. He
had 1 episode of melena shortly before arrival.
• He denies abdominal pain, diarrhea, or fevers.
• He has a history of hypertension and chronic back pain
secondary to a car accident.
• His medications include hydrochlorothiazide, amlodipine,
and ibuprofen.
• He smokes 1 pack per day. He also drinks 6 to 8 beers per
day, with more being consumed on the weekends and
holidays.
• He has drunk this amount of alcohol for 22 years.
9. Case Presentation
• On examination, he appears drowsy, with a blood
pressure of 94/46 mm Hg, heart rate of 122 bpm,
respiratory rate of 24 breaths/min, and oxygen
saturation of 96% on room air.
• He is afebrile. His eyes are slightly icteric.
• His oral mucosa is slightly dry. Chest auscultation
reveals clear lungs and a regular heart rhythm.
• Abdominal examination reveals mild distention and
evidence of hepatomegaly.
• His rectal examination reveals heme-positive stool.
• Laboratory data show hemoglobin 9.8, hematocrit 29,
and platelets 98,000. BUN is 28 and creatinine is 1.2.
INR is 1.6. AST is 102 and ALT is 68.
10. Questions
1. What is the most likely diagnosis?
– This is a 47-year-old male with risk factors for GI
bleeding (alcohol abuse and NSAID usage) who
presents with several episodes of hematemesis.
– His vitals, physical examination, and laboratory
data suggest volume loss and hemodynamic
instability.
– He requires rapid evaluation and treatment,
including volume resuscitation and workup for
the cause of his bleeding.
11. Questions
2. What is the initial goal of evaluation and
patient care?
– The initial goals of his care revolve around
volume resuscitation and hemodynamic stability
with an urgent GI consult.
12. Questions
3. What else is on the differential diagnosis?
• The differential diagnosis includes:
– Peptic ulcer disease,
– Esophagitis
– Gastric varices
– Mallory-Weis tear.
13. Case Presentation - 4
• Mrs Hampton's history suggests biliary colic.
• A RUQ ultrasound reveals multiple small gallstones.
• CBC is normal.
• Serum lipase and liver enzymes were normal.
• Urea breath test for H. pylori was negative.
• After surgical consultation, cholecystectomy was
planned in the next few weeks.
• Unfortunately, Mrs Hampton returned to the emergency
department prior to scheduled surgery with constant
pain in her RUQ associated with fever and chills.
• She looks in acute distress.
• She reports dark urine..
14. Case Presentation - 4
• Vitals are stable except for the presence of
fever at 38.3°C.
• Sclera was anicteric.
• Abdominal examination reveals RUQ
tenderness with positive Murphy sign.
15. Questions
1. What should be included in your DDX?
1. Common bile duct (CBD) obstruction (also known as
choledocholithiasis)
2. Ascending cholangitis
3. Acute cholecystitis
4. Hepatitis
1. Acute Pancreatitis
16. Choledocholithiasis and Ascending
Cholangitis
• The classic presentation is RUQ pain, fever,
and jaundice, also known as Charcot triad.
• This occurs due to CBD obstruction, most
commonly from a gallstone.
• Complications include obstruction, jaundice,
fever, leukocytosis, sepsis, and pancreatitis.
17. Choledocholithiasis and Ascending
Cholangitis
• ERCP is both diagnostic and therapeutic.
• It is the preferred test of choice in patients with a
high pretest probability of CBD stone with
obstruction.
• It allows direct cannulation of CBD and relieves
obstruction via simultaneous stone extraction
and sphincterotomy.
• In patients who are less likely to have a CBD
stone, a less invasive test such as magnetic
resonance cholangiopancreatography (MRCP) or
endoscopic ultrasound (EUS) would be
appropriate as an initial study.
18. Choledocholithiasis and Ascending
Cholangitis
• Treatment includes:
– IV hydration
– IV broad-spectrum antibiotics
– Decompression of the biliary system (via ERCP in
patients with persistent pain, hypotension, altered
mental status, persistent high fever, WBC ≥20,000,
bilirubin >10 mg/dL) and electively in more stable
patients
– And/or cholecystectomy
19. Case Presentation - 5
• A 40-year-old woman presents to the
emergency department with a history of
worsening right upper quadrant pain.
• The pain started after she had pizza for dinner
2 days ago and is described as a sharp,
stabbing sensation under her right ribs.
• She has also felt ill, developed slight nausea,
and had a low-grade fever.
• There has been no vomiting or diarrhea.
20. Case Presentation - 5
• The physical examination reveals an obese
woman with a low-grade fever and tenderness
to palpation of the right upper quadrant of
her abdomen.
• An abdominal ultrasound reveals a 2 cm
gallstone lodged in the cystic duct with
swelling of the gallbladder and thickening of
the gallbladder wall
21. Questions
A. What are the mechanisms involved in gallstone formation?
• Many factors are involved in gallstone formation, but they can be
divided into
– Factors affecting bile composition
– Factors affecting gallbladder motility.
• Factors affecting the lithogenicity of bile include the cholesterol
content; the presence of nucleating factors, prostaglandins, and
estrogen; the rate of bile formation; and the rate of water and
electrolyte absorption.
• Gallbladder motility also plays a major factor.
• Usually, bile does not stay in the gallbladder long enough to form a
gallstone, but it may happen if stasis occurs.
22. Questions
B. What factors in the pathogenesis of gallstones
may be responsible for the fact that it is more
common in premenopausal women?
• In premenopausal women, high levels of serum
estrogens promote gallstone formation in two
ways:
– Estrogens both increase the cholesterol concentration
of bile and
– Decrease gallbladder motility.
• Bile stasis and the elevation of its cholesterol
concentration enable gallstone formation.
23. Questions
C. What local complications can ensue from gallstone disease?
• A gallstone may become lodged in the cystic duct, obstructing
gallbladder emptying.
• This can lead to the inflammation (cholecystitis) and infection of the
static contents (empyema) of the gallbladder.
• If untreated, such inflammation and infection can lead to necrosis
of the gallbladder and sepsis.
• If a gallstone becomes lodged in the common bile duct, it can cause
obstructive jaundice with an elevation in serum bilirubin levels.
• If it lodges farther along the common bile duct and blocks the
pancreatic duct near the sphincter of Oddi, it can cause acute
pancreatitis, perhaps because the digestive enzymes of the
pancreas are trapped in the pancreatic duct and cause
inflammation in the pancreas.
24. Case presentation - 7
• A 74-year-old man with severe osteoarthritis
presents to the emergency department
reporting two episodes of melena (black
stools) without hematochezia (bright red
blood in the stools) or hematemesis (bloody
vomitus).
• He takes 600 mg of ibuprofen three times a
day to control his arthritis pain.
• He denies alcohol use.
25. Case presentation - 7
• On examination, his blood pressure is 150/70
mm Hg, and his resting pulse is 96/min.
• His epigastrium is minimally tender to
palpation.
• Rectal examination reveals black tarry stool in
the vault, grossly positive for occult blood.
• Endoscopy demonstrates a 3 cm gastric ulcer.
• Helicobacter pylori is identified on biopsies of
the ulcer site.
26. Questions
A. What are some of the proposed mechanisms for
acid-peptic disease and specifically gastric ulcer
disease?
• Excessive acid secretion or diminished mucosal
defenses predispose to the development of acid–
peptic disease, specifically gastric ulcer.
• Most gastric ulcers are believed to be related to
impaired mucosal defenses, because the acid and
pepsin secretory capacity of some affected
patients is normal or even below normal.
27. Questions
A. What are some of the proposed mechanisms for acid-
peptic disease and specifically gastric ulcer disease?
• Motility defects have been proposed to contribute to
development of gastric ulcer in at least three ways:
1. By a tendency of duodenal contents to reflux back
through an incompetent pyloric sphincter (bile acids in
the duodenal reflux material act as an irritant and may
be an important contributor to a diminished mucosal
barrier against acid and pepsin);
2. By delayed emptying of gastric contents, including reflux
material, into the duodenum; and
3. By delayed gastric emptying and hence food retention,
resulting in increased gastrin secretion and gastric acid
production
28. Questions
A. What are some of the proposed mechanisms for
acid-peptic disease and specifically gastric ulcer
disease?
• Mucosal ischemia may also play a role in the
development of a gastric ulcer.
• Subsets of gastric ulcer patients with each of
these defects have been identified.
• Thus, the risk factors (NSAID ingestion, smoking,
psychologic stress, H pylori infection) that have
been associated with gastric ulcer probably act by
diminishing one or more mucosal defense
mechanisms.
31. Questions
B. How may this patient’s analgesic use predispose
him to acid-peptic disease?
• Prostaglandins are known to increase mucosal
blood flow, as well as bicarbonate and mucus
secretion, and to stimulate mucosal cell repair
and renewal.
• Thus, their deficiency, resulting from NSAID
ingestion or other insults, may predispose to
gastritis and gastric ulcer, as might diminished
bicarbonate or mucus secretion owing to other
causes.
32. Mechanisms by which nonsteroidal anti-inflammatory drugs may induce
mucosal injury
33. Questions
C. What role does H pylori infection play in the pathogenesis of ulcer
disease? How should this be taken into account when treating this
patient?
• H pylori can cause acid–peptic disease by multiple mechanisms,
including altered signal transduction, resulting in increased
inflammation, increased acid secretion, and diminished mucosal
defenses.
• It may also affect apoptosis in the GI tract.
• Despite the high rate of association of inflammation with H pylori
infection, the important role of other factors is indicated by the fact
that only about 15% of H pylori–infected individuals ever develop a
clinically significant ulcer.
• These other factors (both genetic and environmental, such as
cigarette smoking) must account for the individual variations and are
pathophysiologically important
34. Questions
C. What role does H pylori infection play in the pathogenesis of ulcer
disease? How should this be taken into account when treating this
patient?
• Nevertheless, the role of H pylori is of particular clinical importance
because, of patients who do develop acid–peptic disease, most have
H pylori infection.
• Furthermore, treatment that does not eradicate H pylori is associated
with the rapid recurrence of acid–peptic disease in most patients.
• Recent studies have also associated different strains of H pylori with
different forms and degrees of acid–peptic disease and implicated H
pylori infection in the development of GI tract cancers.
• Cornerstones of therapy for this patient include discontinuing
ibuprofen, initiating proton pump inhibitors to decrease acid
production, and initiating antibiotics to treat the H pylori infection.
35. Outline of the bacterial and host factors important in determining H. pylori–induced
gastrointestinal disease. MALT, mucosal-associated lymphoid tissue.
