Group D – Analyst Grp Vigilia, Patrice Villaflor, Irene Villafuerte, Marc Villar, Cherry Villasis, Ramon Vistal, Kristine Yap, Margaux

Group D – Analyst Grp

Vigilia, PatriceVillaflor, Irene

Villafuerte, Marc Villar, Cherry

Villasis, RamonVistal, KristineYap, Margaux

Presentation Objectives1. 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.

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

The Anatomy GI Tract

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 PresentationHematemesis - vomitus of red blood or

coffee-grounds materialMelena – black, tarry, foul-smelling stoolHematochezia – passage of bright red

or maroon blood from the rectumOccult 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


GI Bleeding ClassificationAcute 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 BleedingUGISource 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

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



Approach to the patientMeasurement 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 patientHemoglobin 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 BLEEDINGHistory and PE in not usually diagnostic.Upper endoscopy is the test of choice and

should be performed urgently in patients with hemodynamic instability.


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


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


EndoscopyRisks of procedure:

risk of bleedinggastrointestinal perforation


Algorithm for patients with acute upper gastrointestinal bleeding

IV PPI therapy + endoscopic

therapy

ICU for 1-2 days; ward for 2-3 days

Endoscopic therapy

No endoscopic

therapy

Ward for 1-2 days Discharg

eICU for 1 day;

ward for 2 days

IV PPI therapy +/- endoscopic

therapy

No IV PPI or endoscopic

therapy

No IV PPI or endoscopic

therapy

Ward for 3 days Ward for 3 days Discharge

Active bleeding or visible

vessel

Ligation (preferred) or sclerotherapy +

IV octreotide

Clean base

Adherent Clot Flat, pigmented

spot

Active bleeding

No active

bleeding

Acute Upper GI Bleeding

Ulcer Esophageal Varices

Mallory-Weiss Tear


Other tests that may be performed:

Laboratory Tests (CBC, Serum Electrolyte, Fecal Occult Blood, BUN/Crea Ratio)

Radiography (Barium Swallow, CT Scan)


SummaryAssess 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)

Causes of Upper GI Bleeding

Peptic Ulcer

Mallory Weiss Tears

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.


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.



Helicobacter pylori

The rate of infection in the United States has fallen by >50% when compared to 30 years ago.


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.


HistoryPE

HistoryAbdominal or Epigastric pain

Described as burning, gnawing, aching sensation or hunger pain

Important to know the temporal pattern

History

Physical Examination

Physical Examination

Radiographic Procedure (Barium Study)Commonly used as a first test for

documenting an ulcerSensitivity: 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

1. Provide relief of symptoms (pain or dyspepsia)

2. Promote ulcer healing3. Prevent ulcer recurrence and complications

Drugs used in the Treatment of PUDDrug Type Examples Dose

Acid-suppressing (Antacids)

Mylanta, Maalox, Tums, Gaviscon

100-140 meq/L 1-3 h after meals and hs

H2 receptor antagonists

Cimetidine 400 mg bid

Ranitidine 300 mg hs

Famotidine 40 mg hs

Nizatidine 300 mg hs

Proton Pump inhibitors

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

Drug Type Examples Dose

Mucosal Protecti

ve Agents

Sucralfate Sucralfate 1 g qid

Prostaglandin analogue

Misoprostol 200 ug qid

Bismuth-containing compounds

Bismuth subsalicylate

(BSS)

See anti-H. pylori regimen


Acid neutralizing/inhibitory drugs (Antacids)MOA: neutralize secreted acidsOften used by patients for symptomatic relief of

dyspepsia

Antacids Side effects

MaaloxMagnesium

OHDiarrhea 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 antagonistsMOA: Competitive inhibitors of the action of

histamine at H2 receptorsHealing in 80-90% of cases after 4-8 weeks of

therapyCimetidine has an anti-androgenic effect due to

cytochrome p450 enzyme inhibition reversible gynecomastia and impotence


Proton Pump (H+,K+ ATPase) inhibitorsMOA: Covalently bind and irreversibly inhibit H+K+

ATPaseGiven before meal, activation in acidic environment

Examples of drugs

Omeprazole 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)

Lanoprazole

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

Regimens recommended for eradication of H. pylori infection

TRIPLE THERAPY Dose

Bismuth salicylateMetronidazoleTetracycline

2 tablets qid250 mg qid500 mg qid

Ranitidine bismuth citrateTetracycline

Azithromycin or Metronidazole

400 mg bid500 mg bid500 mg bid

Omeprazole (lansoprazole)Clarithromycin

Metronidazole or Amoxicillin

20 mg (30 mg) bid250 or 500 mg bid

500 mg bid or 1 g bid


Regimens recommended for eradication of H. pylori infection

QUADRUPLE THERAPY Dose

Omeprazole (Lansoprazole)Bismuth subsalicylate

MetronidazoleTetracycline

20 mg (30 mg) daily2 tablets bid250 mg bid500 mg bid


** combination therapy for 14 days provides greatest efficacy

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

PathophysiologyNSAIDs 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


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


Treatment of NSAID-related mucosal injury

CLINICAL SETTING RECOMMENDATION

Active Ulcer

NSAID discontinued NSAID continues

H2 receptor antagonist / PPIPPI

Prophylactic Therapy MisoprostolPPISelective COX-2 Inhibitor

H. Pylori infection Eradication if active ulcer present or there is a past history or peptic ulcer disease


NO or LOW NSAID GI Risk

NSAID GI Risk

NO Cardiovascular Risk (no Aspirin)

Traditional NSAID Traditional NSAID / Coxibplus PPI

Consider non-NSAID therapy

WITHCardiovascular 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.



Group CTrias - Ventura

EpidemiologyIncidence and mortality decreased markedly

for the past 75 years, worldwideRemains high in Japan, China, Chile &

IrelandRisk 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 CarcinomaSuperficial & surgically curable – no symptomsMore extensive – insidious upper abdominal

discomfortAnorexia with slight nausea – very common but

is not the usual presenting complaintWeight loss - observedNausea and vomiting – prominent with tumors of

the pylorusDysphagia and early satiety – symptoms caused

by diffuse lesions originating in the cardiaNo early physical signsPalpable 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.

LymphaticsSeeding of peritoneal surfaces

• Metastases that occur frequently: intraabdominal and supraclavicular nodes Krukenberg’s tumor – metastatic nodules to the ovary“Sister Mary Joseph node” – periumbilical regionPeritoneal 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 anemiaAcanthosis nigricans

Risk Factors

Risk Factors

Risk Factors + Hypothesis

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.

TREATMENTComplete surgical removal of the tumor +

resection of adjacent lymph nodes-only chance for cure

Subtotal gastrectomyTreatment of choice for distal tumors

Total / Near-Total gastrectomyTreatment 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

TREATMENTRadiotherapy

Palliation of pain Radiotherapy alone after complete resection

does not prolong survivalChemo + Radio therapy

5FU combined with radiation therapy slightly improved survival

5FU may function as a radiosensitizer

TREATMENTCytotoxic 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 BleedingUpper

- Refers to bleeding from esophagus, stomach, duodenum (above the Ligament of Treitz)

Lower

- 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 PresentationUpper GI Bleeding- Hematemesis- Melena- Hematochezia

(associated with hemodynamic instability and dropping hemoglobin)

- Hyperactive bowel sounds

- Elevated BUN

Lower GI Bleeding- Hematochezia


Mallory Weiss Tears

Hx: vomiting, retching, coughing preceding hematemesis especially in alcoholics

Stops spontaneously (80-90%)


Esophageal Varices

4-31% of causes Most often it is a consequence of portal

hypertension


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)


Gastric CA1-4% of causes (rare) risk factors present in our patient: old age

and overweightPresents with significant weight loss,

progressive epigastric pain and GI bleeding


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)


Documents

Group D – Analyst Grp Vigilia, Patrice Villaflor, Irene Villafuerte, Marc Villar, Cherry Villasis, Ramon Vistal, Kristine Yap, Margaux