Transcript Salient Features

Group D – Analyst Grp
Vigilia, Patrice
Villaflor, Irene
Villafuerte, Marc
Villar, Cherry
Villasis, Ramon
Vistal, Kristine
Yap, Margaux
Presentation Objectives
1.
Review of the anatomy and physiology of the digestive
tract.
2.
Presentations of GI bleeding, its classifications, and its
sources.
3.
Approach to a patient with Upper GI bleeding.
4. Enumerate the different tools used in the evaluation and
diagnosis of patients presenting with GI bleeding.
The Anatomy GI Tract
 extends from the mouth to the
anus, and comprises several organs
with distinct functions
 separating
the
organs
are
specialized
independently
controlled thickened sphincters
that
assist
in
the
gut
compartmentalization
 gut wall: is organized into well-
defined layers that contribute to
the functional activities in each
region
Harrison’s Principle of Internal Medicine, 17th ed.
Important Point:
 The anatomic cut-off for
upper GI is the Ligament
of Treitz
 It is located in the fourth
portion of the duodenum
(the last 2 inches).
 It
connects the fourth
portion of the duodenum
to the diaphragm near the
splenic flexure of the
colon.
Snell’s Clinical Anatomy, 7th ed.
Functions
of
the
GI
Tract
• Two main functions:
o Assimilation of nutrients
o Elimination of wastes
ORGANS
FUNCTION
Esophagus
Propels the bolus of food to the
stomach
Stomach
Furthers food preparation by
triturating and mixing the bolus with
pepsin and acid.
Small Intestines
Site of major nutrient absorption.
Large Intestines
Prepares the waste materials for
controlled evacuation.
Harrison’s Principle of Internal Medicine, 17th ed.
GI Bleeding Presentation
 Hematemesis - vomitus of red blood or
coffee-grounds material
 Melena – black, tarry, foul-smelling stool
 Hematochezia – passage of bright red or
maroon blood from the rectum
 Occult GI Bleeding – identified through fecal
occult blood test or the presence of iron
deficiency
 Systemic signs of Blood Loss or Anemia –
lightheadedness, syncope, angina, dyspnea
Harrison’s Principle of Internal Medicine, 17th ed.
GI Bleeding Classification
 Acute vs Chronic
 UGI Bleeding vs LGI Bleeding
Acute vs Chronic
 Acute - typically presents with overt blood loss that can
be readily recognized by the patient or treating
physician
 Chronic - long-term GI bleeding may go unnoticed or
may cause fatigue, anemia, black stools, or a positive test
for microscopic blood
Washington manual of medical therapeutics, 32nd edition
emedicinehealth.com
UGI Bleeding vs LGI Bleeding
UGI
Source of bleeding is ABOVE the
ligament of Treitz
• Usually presented as:
– HEMATEMESIS
– MELENA,
indicates that
blood has been present in
the GI tract for at least 14 hrs
– May
also
present
as
HEMATOCHEZIA
if an
upper lesion bleeds briskly
that blood does not remain
in the bowel long enough for
melena to develop.
– May be occult
Harrison’s Principle of Internal Medicine, 17th ed.
LGI
• Source of bleeding is BELOW
the LIGAMENT of TREITZ
• Usually presented as
– HEMATOCHEZIA – passage
of bright red or maroon
blood from the rectum.
– May be occult
Esophagus
Upper GI
Stomach
Duodenum
Sources of GI
Bleeding
Lower GI
The remaining
portion of the
Small Intestines
Colonic Source
Harrison’s Principle of Internal Medicine, 17th ed.
Approach to the patient
 Measurement of the heart rate and blood pressure is
the best way to assess the patient.
 Clinically significant bleeding leads to postural changes
in HR or BP, tachycardia and recumbent hypotension.
Approach to the patient
 Hemoglobin Determination
 Does not fall immediately with acute GIB: this is due to
the proportionate reduction in plasma and red cell
volumes.
 As extravascular fluid enters the vascular space to
restore volume, the hemoglobin falls.
UPPER GI BLEEDING
 History and PE in not usually diagnostic.
 Upper endoscopy is the test of choice and should be
performed urgently in patients with hemodynamic
instability.
Harrison’s Principle of Internal Medicine, 17th ed.
Endoscopy
• procedure is the best method for examining upper GI
•
•
•
•
mucosa
minimally invasive diagnostic medical procedure
used to assess interior surfaces of organs by inserting a
tube into the body
instrument may have a rigid or flexible tube & not only
provide an image for visual inspection and
photography, but also enable taking biopsies &
retrieval of foreign objects
sedatives may be given so as to relieve discomfort
Harrison’s Principle of Internal Medicine, 17th ed.
Endoscopy
• Used to determine the cause of bleeding, pain, nausea
and vomiting, weight loss, altered bowel function and
fever
• Upper endoscopy
– evaluates the esophagus, stomach and duodenum
– initial test performed in patients with suspected ulcer
disease, esophagitis, neoplasm, malabsorption and
Barrett's metaplasia because it directly visualizes
abnormality
Harrison’s Principle of Internal Medicine, 17th ed.
Endoscopy
 Risks of procedure:
 risk of bleeding
 gastrointestinal perforation
Harrison’s Principle of Internal Medicine, 17th ed.
Algorithm for patients with acute upper
gastrointestinal bleeding
Acute Upper GI Bleeding
Ulcer
Esophageal
Varices
Active bleeding
or visible vessel
Adherent Clot
Flat,
pigmented
spot
Clean
base
IV PPI therapy
+ endoscopic
therapy
IV PPI therapy
+/- endoscopic
therapy
No IV PPI or
endoscopic
therapy
No IV PPI or
endoscopic
therapy
ICU for 1 day;
ward for 2 days
Ward for 3 days
Ward for 3 days
Harrison’s Principle of Internal Medicine, 17th ed.
Discharge
Mallory-Weiss
Tear
Ligation (preferred)
or sclerotherapy +
IV octreotide
Active
bleeding
No
active
bleeding
ICU for 1-2 days;
ward for 2-3 days
Endoscopic
therapy
No
endoscopic
therapy
Ward for
1-2 days
Discharg
e
Other tests that may be performed:
 Laboratory Tests (CBC, Serum Electrolyte, Fecal
Occult Blood, BUN/Crea Ratio)
 Radiography (Barium Swallow, CT Scan)
Harrison’s Principle of Internal Medicine, 17th ed.
Summary
 Assess the patient by doing History and PE
 Heart Rate and Blood Pressure
 Do an Endoscopic Exam
 Perform other laboratory and radiographic exams if
necessary
Salient Features
 55 y/o female
 History of vague epigastric discomfort
 hematochezia [2 episodes of melena (2
cupfuls/episode)]
 hematemesis [1 episode of coffee ground
vomiting]
 cold clammy sweats and dizziness
 intake of Diclofenac Na intermittently
 regular medications: clopidogrel
(anticoagulant)
 (+) DM
 overweight [BMI = 26.5]
 10 kg weight loss for the past 6 months
 orthostatic hypotension (BP 120/80 when supine,
100/60 at sitting)
 PR 105/min RR 22/min
 Pale palpebral conjuctiva and anicteric sclera
 no cervical lymphadenopathy
 lung and heart sounds are normal
 apex beat at 6th LICS
 Abdomen with hyperactive bowel sounds, soft
non tender, without palpable mass or
organomegaly
 DRE maroon colored stools
Clinical Impression:
 Acute Upper GI bleeding secondary to PUD (to rule
out Gastric CA)
Peptic Ulcer
Mallory Weiss
Tears
Causes of Upper GI
Bleeding
Esophageal
Varices
Hemorrhagic or
Erosive gastropathy
Gastric CA
Differential Diagnosis
Siy, Jeniffer, So, Roizza, Solang, Jenifer, Soriano,
Whitney, Soto, Ian,
Suelto, Jeremy, Suero, Diane
 Acid peptic disorders - 4 million individuals (new
cases and recurrences) affected per year
 Lifetime prevalence of PUD in the United States
▪
~12% in men and 10% in women
 an estimated 15,000
deaths per year - as a
consequence of complicated PUD
 estimated burden on direct and indirect health care
costs of ~$10 billion per year in the United States
Harrisons principles of internal madicine 17th ed p1838
Duodenal Ulcers
 occur in 6–15% of the Western population
 incidence of DUs declined steadily from 1960 to 1980 and
has remained stable since then.
 death rates, need for surgery, and physician visits have
decreased by >50% over the past 30 years
 Eradication of H. pylori has greatly reduced recurrence
rates.
Harrisons principles of internal madicine 17th ed p1838
Gastric Ulcers
 occur later in life than duodenal lesions (peak
incidence reported in the sixth decade)
 More than half occur in males
 less common than Duodenal Ulcers
 Autopsy studies suggest a similar incidence of
DUs and GUs.
Harrisons principles of internal madicine 17th ed p1838
Helicobacter pylori
 Prevalence : developing parts of the world (80%
of the population by age of 20)
industrialized countries (20 – 50 %)
United States (~30%)
 About 10% of Americans <30 are colonized with the
bacteria
Harrisons principles of internal madicine 17th ed p1838
Helicobacter pylori
 The rate of infection in the United States has fallen by
>50% when compared to 30 years ago.
Harrisons principles of internal madicine 17th ed p1838
Helicobacter pylori
 Risk Factors :
 (1) birth or residence in a developing country
 (2) domestic crowding
 (3) unsanitary living conditions
 (4) unclean food or water
 (5) exposure to gastric contents of an infected
individual.
Harrisons principles of internal madicine 17th ed p1838
History
PE
History
 Abdominal or Epigastric pain
 Described as burning, gnawing, aching sensation or hunger pain
 Important to know the temporal pattern
Duodenal Ulcer
• Occurs 90 mins to 3 h after a meal
• Relieved by antacids or food
• Pain that awakes the patient fr sleeping (bet. midnight & 3 am)
Gastric Ulcer
• Discomfort precipitated by food
• Nausea & weight loss occur here more commonly
NSAID induced mucosal disease
• Can present with complications like bleeding, perforation, and
obstruction without antecedent symptom
History
Penetrating ulcer (pancreas)
• Constant dyspepsia , no longer relieved by food or antacids,
radiates to the back
Perforation
• Sudden onset of severe, generalized abdominal pain
Gastric outlet obstruction
• Pain worsening with meals, nausea & vomiting of
undigested food
Bleeding
• Tarry stools or coffee ground emesis
Physical Examination
Epigastric tenderness is the most frequent finding in
patients with GU or PU
Pain may be found at the right side of the midline.
Tachycardia and orthostasis may be suggestive of
dehydration secondary to vomiting or active
gastrointestinal blood loss.
Physical Examination
Perforation is possible if patients
manifest severely tender broad like
abdomen
Presence of succussion splash
indicated retain fluid in the stomach
suggestive of intestinal obstruction.
Radiographic Procedure (Barium
Study)
 Commonly used as a first test for documenting an
ulcer
 Sensitivity: 80% (single contrast barium meals); 90%
(double contrast)
 Sensitivity is decreased in small ulcers (<0.5cm),
presence of previous scarring, postoperative patients
Benign duodenal ulcer appears as a well demarcated crater, seen at the bulb
Benign gastric ulcer
 Ulcer crater-collection of barium on
dependent surface which usually projects
beyond anticipated wall of stomach in
profile (penetration)
 Hampton’s line-1 mm thin straight line
at neck of ulcer in profile view which
represents the thin rim of undermined
gastric mucosa
 Ulcer collar-smooth, thick, lucent band
at neck of ulcer in profile view
representing thicker rim of edematous
gastric wall
 Ulcer mound-smooth, sharply
delineated tissue mass surrounding a
benign ulcer
 Ring shadow-thin rim of contrast which
represents an ulcer on the non-dependent
surface of an air-contrast study
 Thickened folds radiating directly to the
base of the ulcer en face
Endoscopy
 Provides the most sensitive and the most specific
approach for examining the upper GI
 Permits direct visualization of the mucosa
 Facilitates photographic documentation of mucosal
defect and tissue biopsy to rule out malignancy or H.
pylori
 Helpful in identifying lesions too small to detect by
radiographic examination, for evaluation of atypical
radiographic abnormalities, determine if ulcer is
source of loss of blood
A
B
GOALS in treating PUD
Provide relief of symptoms (pain or dyspepsia)
2. Promote ulcer healing
3. Prevent ulcer recurrence and complications
1.
Drugs used in the Treatment of
PUDDrug Type
Examples
Dose
Acid-suppressing
(Antacids)
H2 receptor antagonists
Proton Pump
inhibitors
Mylanta, Maalox, Tums,
Gaviscon
100-140 meq/L 1-3 h after
meals and hs
Cimetidine
400 mg bid
Ranitidine
300 mg hs
Famotidine
40 mg hs
Nizatidine
300 mg hs
Omeprazole
20 mg/d
Lansoprazole
30 mg/d
Rabeprazole
20 mg/d
Pantoprazole
40 mg/d
Esomeprazole
20 mg/d
Harrison’s Principle of Internal Medicine 17th edition
Mucosal
Protective
Agents
Drug Type
Examples
Dose
Sucralfate
Sucralfate
1 g qid
Prostaglandin
analogue
Misoprostol
200 ug qid
Bismuth-containing
compounds
Bismuth
subsalicylate
(BSS)
See anti-H. pylori
regimen
Harrison’s Principle of Internal Medicine 17th edition
 Acid neutralizing/inhibitory drugs (Antacids)
 MOA: neutralize secreted acids
 Often used by patients for symptomatic relief of dyspepsia
Antacids
Maalox
Side effects
Magnesium
OH
Diarrhea and hypermagnesemia
Aluminum OH
Constipation and phospahte depletion
Calcium carbonate
Milk alkali syndrome – hypercalcemia,
hyperphosphatemia, renal calcinosis  renal
insufficiency (long term use)
Sodium bicarbonate
Systemic alkalosis
 H2 receptor antagonists
 MOA: Competitive inhibitors of the action of histamine
at H2 receptors
 Healing in 80-90% of cases after 4-8 weeks of therapy
 Cimetidine has an anti-androgenic effect due to
cytochrome p450 enzyme inhibition  reversible
gynecomastia and impotence
Harrison’s Principle of Internal Medicine 17th edition
 Proton Pump (H+,K+ ATPase) inhibitors
 MOA: Covalently bind and irreversibly inhibit H+K+ ATPase
 Given before meal, activation in acidic environment
Examples of drugs
Omeprazole
Lanoprazole
Administered as enteric-coated
grabules in a sustained-release capsule
that dissolves in SI at pH 6,
Lanoprazole can be taken in an orally
disintegrating tablet (with or w/out
water)
Pantoprazole
Enteric-coated tablet, Parenteral
Rabeprazole
Enteric-coated tablet
 Cytoprotective agents
Drugs
MOA
Sucralfate
Physicochemical barrier, promote trophic
action by binding to growth factors,
enhance prostaglandin synthesis, stimulate
mucous and HCO3 secretion, enhance
mucosal defense and repair
Colloidal bismuth subcitrate and
bismuth subsalicylate
Prevention of further pepsin/HCl-induced
damage, stimulation of prostaglandin,
HCO3 and mucous secretion
Prostaglandin analogue
Maintain mucosal integrity and repair,
enhance mucous and HCO3 secretion,
stimulate mucosal blood flow, decrease
mucosal cell turnover
Harrison’s Principle of Internal Medicine 17th edition
Regimens recommended for
eradication of H. pylori infection
TRIPLE THERAPY
Dose
Bismuth salicylate
Metronidazole
Tetracycline
2 tablets qid
250 mg qid
500 mg qid
Ranitidine bismuth citrate
Tetracycline
Azithromycin or Metronidazole
400 mg bid
500 mg bid
500 mg bid
Omeprazole (lansoprazole)
Clarithromycin
Metronidazole or Amoxicillin
20 mg (30 mg) bid
250 or 500 mg bid
500 mg bid or 1 g bid
Harrison’s Principle of Internal Medicine 17th edition
Regimens recommended for
eradication of H. pylori infection
QUADRUPLE THERAPY
Dose
Omeprazole (Lansoprazole)
Bismuth subsalicylate
Metronidazole
Tetracycline
20 mg (30 mg) daily
2 tablets bid
250 mg bid
500 mg bid
** combination therapy for 14 days provides greatest efficacy
Harrison’s Principle of Internal Medicine 17th edition
SURGICAL THERAPY
 Surgical intervention in PUD
 1. elective for treatment of medically refractory disease
 2. urgent/emergent for the treatment of ulcer-related
complications ( hemorrhage, perforation and
obstruction)
 Pharmacologic and endoscopic approaches for
treatment of PUD and its complications  decreased
number of operations
NSAID Gastropathy
Pathophysiology
 NSAIDs decrease mucosal defense and repair through
prostaglandin depletion





HCl secretion
Mucin secretion
Bicarbonate secretion
Surface active phospholipid secretion
Epithelial cell proliferation
 Direct toxicity “ion trapping”
 Endothelial effects causing stasis
Harrison’s Principles of Internal Medicine 17th edition
Pathophysiology
Symptoms:
• dyspepsia
• nausea, vomiting
• diarrhea
• gastric and duodenal ulceration
• upper GI bleeding
Harrison’s Principles of Internal Medicine 17th edition
Risk Factors:
•
•
•
•
•
•
•
•
advanced age (>60 y/o)
History of ulcer
Concomitant use of glucocorticoids
Multiple, high-dose NSAIDs
Corticosteroids
Concomitant anticoagulation or coagulopathy
Serious or multisystem disease
Potential risk factors: smoking, alcohol, H. pylori
infection
Harrison’s Principles of Internal Medicine 17th edition
Treatment of
NSAID-related mucosal injury
CLINICAL SETTING
RECOMMENDATION
Active Ulcer
NSAID discontinued
NSAID continues
H2 receptor antagonist / PPI
PPI
Prophylactic Therapy
Misoprostol
PPI
Selective COX-2 Inhibitor
H. Pylori infection
Eradication if active ulcer present or
there is a past history or peptic ulcer
disease
Harrison’s Principles of Internal Medicine 17th edition
Guide to NSAID therapy
NO Cardiovascular
Risk
(no Aspirin)
NO or LOW NSAID GI Risk
NSAID GI Risk
Traditional NSAID
Traditional NSAID / Coxib
plus PPI
Consider non-NSAID therapy
WITH
Cardiovascular Risk
(consider Aspirin)
Traditional NSAID plus PPI if GI
risk warrants gastroprotection
A gastro-protective agent must
be added if a traditional NSAID
is prescribed.
Consider non-NSAID therapy
Consider non-NSAID therapy
Harrison’s Principles of Internal Medicine 17th edition
Group C
Trias - Ventura
Epidemiology
 Incidence and mortality decreased markedly
for the past 75 years, worldwide
 Remains high in Japan, China, Chile & Ireland
 Risk is greater among lower socioeconomic
classes
• Environmental exposure (begins in early life)
 Migrants (high  low) maintain their susceptibility,
while the risk of offspring approximate the homeland
 Dietary carcinogens – most likely factors
Clinical Features of Gastric Carcinoma
 Superficial & surgically curable – no symptoms
 More extensive – insidious upper abdominal discomfort
 Anorexia with slight nausea – very common but is not
the usual presenting complaint
 Weight loss - observed
 Nausea and vomiting – prominent with tumors of the
pylorus
 Dysphagia and early satiety – symptoms caused by
diffuse lesions originating in the cardia
 No early physical signs
 Palpable abdominal mass – long standing growth and
regional extension
 Gastric CA spread by:
 Direct extension through the gastric wall to the
perigastric tissues, adhering to adjacent organs
(pancreas, colon, or liver). Liver is most common site for
hematogenous spread.
 Lymphatics
 Seeding of peritoneal surfaces
• Metastases that occur frequently:
 intraabdominal and supraclavicular nodes
 Krukenberg’s tumor – metastatic nodules to the ovary
 “Sister Mary Joseph node” – periumbilical region
 Peritoneal cul-de-sac (Blumer’s shelf palpable on
rectal/vaginal exam)
 Presence of Iron deficiency anemia in men and
occult blood in stool for both sexes mandates a
search for occult GI tract lesion
 Careful assessment is of particular importance
in patients with atrophic gastritis or pernicious
anemia
 Unusual clinical features:
 Migratory thrombophlebitis
 Microangiopathic hemolytic anemia
 Acanthosis nigricans
Risk Factors
Diet
Environment
• high concentration of nitrates
• smoked, dried, salted food
• lower socioeconomic classes
• bacterially-contaminated food
• exogenous source of nitrateconverting bacteria
Risk Factors
Medical
Conditions
Genetic
•
•
•
•
Menetrier’s disease
pernicious anemia
atrophic gastritis
hx of gastric ulcer
• blood type A
• adenomatous polyps
• mutation in E-cadherin gene
Risk Factors •+decreased
Hypothesis
gastric acidity
Acquired
• H. pylori infection
• prior gastric surgery (antrectomy)
• prolonged exposure to histamine
H2-receptor antagonists
↑ Nitrate-converting Bacteria
Conversion of dietary nitrates to carcinogenic nitrites
Diagnosis




Double-Contrast Radiographic Examination
Gastroscopy
Gastroscopic Biopsy and Brush Cytology
Endoscopic Biopsy
Diagnosis

Double-Contrast Radiographic Examination

Simplest diagnostic procedure

Evaluates patient with epigastric complaints


Helps detect small lesions by improving mucosal
detail
Stomach should be distended every radiographic
examination, decrease distensibility is the only
indication of a diffuse infiltrative carcinoma
Diagnosis

Gastroscopy



Diagnostic method of choice
Involves insertion of a fibre optic camera into the
stomach to visualize it
Not a mandatory if the radiographic features are
typically benign
Diagnosis

Gastroscopic Biopsy and Brush Cytology


Recommended to all patient with gastric ulcer in order to
exclude a malignancy
Endoscopic Biopsy


done with the help of a fiber-optic endoscope which is
inserted into the gastrointestinal tract
Since gastric carcinomas are difficult to distinguish clinically
or radiographically from gastric lymphomas, endoscopic
biopsy should be made as deeply as possible due to the
submucosal location of lymphoid tumors.
TREATMENT
 Complete surgical removal of the tumor + resection of
adjacent lymph nodes
-only chance for cure
 Subtotal gastrectomy
 Treatment of choice for distal tumors
 Total / Near-Total gastrectomy
 Treatment for proximal tumors
• Extended lymph node dissection
• Added risk of complications w/o enhancement of survival
• Reduction of tumor bulk is the best form of palliation
• May enhance benefit from subsequent therapy
TREATMENT
• PROGNOSIS depends on
• Degree of tumor penetration into gastric wall
• Regional lymph node involvement
• Vascular invasion
• Abnormal DNA content (aneuploidy)
 5 year survival probability
 ~20% for distal tumors
 <10% for proximal tumors
 Recurrences for ≥ 8 years post surgery
TREATMENT
 Radiotherapy
 Palliation of pain
 Radiotherapy alone after complete resection does not
prolong survival
 Chemo + Radio therapy
 5FU combined with radiation therapy slightly improved
survival
 5FU may function as a radiosensitizer
TREATMENT
 Cytotoxic Drugs
 Cisplatin + epirubicin or 5FU (infusional) or irinotecan
 Associated with partial responses in 30-50% of cases
 Minimal improvement of survival with adjuvant
chemotherapy alone ff. complete resection
 Perioperative treatment and post-op chemotherapy +
radiotherapy reduces recurrence rate and prolongs
survival
 Thank You!
Analysis
Gastrointestinal Bleeding
 Upper
 Lower
- Refers to bleeding from
esophagus, stomach,
duodenum (above the
Ligament of Treitz)
- Refers to bleeding from
distal small bowel, colon,
rectum, and anal canal
(below the Ligament of
Treitz)
Fauci et al. 2008. Harrison’s Principles of Internal Medicine (17th ed)
Clinical Presentation
 Upper GI Bleeding
 Lower GI Bleeding
- Hematemesis
- Hematochezia
- Melena
- Hematochezia (associated
with hemodynamic
instability and dropping
hemoglobin)
- Hyperactive bowel sounds
- Elevated BUN
Fauci et al. 2008. Harrison’s Principles of Internal Medicine (17th ed)
Mallory Weiss Tears
 Hx: vomiting, retching, coughing preceding
hematemesis especially in alcoholics
 Stops spontaneously (80-90%)
Fauci et al. 2008. Harrison’s Principles of Internal Medicine (17th ed)
Esophageal Varices
 4-31% of causes
 Most often it is a consequence of portal
hypertension
Fauci et al. 2008. Harrison’s Principles of Internal Medicine (17th ed)
Hemorrhagic or Erosive gastropathy
 3-11% (less common)
 mucosal lesions and thus do not cause major
bleeding.
 Risk factors for NSAID-induced gastroduodenal
ulceration: old age,high dose/multiple NSAID use,
concomitant use of anticoagulant (clopidogrel),
serious or multisystem disease (DM, HPN)
Fauci et al. 2008. Harrison’s Principles of Internal Medicine (17th ed)
Gastric CA
 1-4% of causes (rare)
 risk factors present in our patient: old age and
overweight
 Presents with significant weight loss, progressive
epigastric pain and GI bleeding
Fauci et al. 2008. Harrison’s Principles of Internal Medicine (17th ed)
Peptic Ulcer
 35-62% (most common),1/3 of patients w/ active
bleeding
 abdominal or epigastric pain is described as burning,
gnawing, aching sensation or hunger pain
 Risk Factors present in our patient: age, NSAID use ,
anticoagulant use (clopidogrel)
Fauci et al. 2008. Harrison’s Principles of Internal Medicine (17th ed)