Name

NIM

Occupation

Adelia Melanti

405070017

Member

Adrian Hartanto L

405070039

Member

Eeng Sapta Hadi

405070078

Member

Nina Amelia Gunawan

405070092

Member

Dian Natalia

405070097

Secretary

Anthony Kane B

405070098

Scriber

Devi Regina

405070099

Member

Agnes Santoso

405070100

Member

Clement Drew

405070104

Member

Risma Kamilah

405070121

Member

Christiani

405070161

Leader

Tutor: dr Susilodinata

Group 6

Gosh, Mrs. Doubtfire you look pale

While you were watching Harry Potter and The Goblet of
Fire in television at the emergency departement you worked for
as a doctor, suddenly came a woman, who looks pale, hels by her
husband. At the doorway, shes vomiting blood with a coffee
ground appearance.
It is known that the patients is Mrs. Doubtfire, a 55-year-oldwoman. Tonight, at home she had a sudden episode of
haematemesis. She also feels dizzy. She describes abdominal
discomfort in the epigastric area that started 3 days prior to
presentation. But actually, she has felt that symptom comes and
goes for about the past 6 months. Usually, it can be relieved either
by eating food, or by taking the over-the counter antacid.
Yesterday, she had 2 bowel movements that were dark, sticky,
and foul-smelling. She woked up nauseated and his since twice
vomited a small amount of bright red blood.
On physical exam, you find an alert patient. Her blood
pressure is 90/60 mmHg, and her pulse is 110 beats/minute. Her
abdomen is flat with hypoactive bowel sounds. She denies using
aspirin or NSAID.

SECRETION

DIGESTION

ABSORPTION

Saliva
Amylase
Mucus
Lysozyme

Carbohydrate digestion
begins

No foodstuffs; a few
medicationsfor example,
nitroglycerin
None

Mucus

None

Gastric Juice
HCl
Pepsin
Mucus
Intrinsic factor

Carbohydrate digestion
No foodstuff; a few lipid
continues in body of
soluble substances, such as
stomach; protein digestion
alcohol and aspirin
begins in antrum of stomach

Pancreatic digestive
enzymes
Trypsin, chymotrypsin,
carboxypeptidase
Amilase
Lipase

These pancreatic anzymes

accomplish digestion in
duodenal lumen

Pancreatic aqueous
NaHCO3 secretion

Not applicable

SECRETION

DIGESTION

Bile
Bile salts
Alkaline secretion
Bilirubin

Bile doesnt digest anything, Not applicable

but bile salts facilitate fat
digestion & absorption in
duodenal lumen

Succus entericus
Mucus
Salt
(Small intestine enzymes
are not secreted but
function within the brush
border membrane --disaccharidases and
aminopeptidases)

In lumen, under influence of

pancreatic enzymes and
bile, carbohydrate & protein
digestion continues and fat
digestion is accomplished;
in brush border,
carbohydrate and protein
digestion completed

All nutrients, most

electrolytes, and water

None

Salt and water, converting

contents to feces

Mucus

ABSORPTION

Nausea
Discomfort characterized by a loss of
appetite and the sensation of impending
vomiting, Its causes include local irritation
of the GI tract, a systemic disease brain
disease or injury, overexcretion, oe the
effect of medication or drug overdosage

Gastrointestinal Bleeding
May present in five ways :
Hematemesis : vomitus of red blood or coffeegrounds material blood
Melena : black, tarry, foul smelly stoul
Hematoschezia : passage bright red or maroon from
rectum
Occult GI bleeding : may be identified in the absence
of overt bleeding by fecal occult blood test or the
presence of iron deficiency.
Symptoms of bood loss or anemia : syncope, angina
or dypsnea

Hematemesis
is the vomiting of blood, which
may be obviously red or have an
appearance similar to coffee
grounds.
Bleeding ulcer in the stomach,
first part of the small intestine, or
esophagus
Bleeding esophageal varices or
stomach varices
gastroenteritis
esophagitis
Gastritis
Irritation or erosion of the lining
of the esophagus or stomach
Swallowing blood (for example,
swallowed after a nosebleed)
Tumors of the stomach or
esophagus

Melena
is the passage of black, tarry
stools

Gastritis
Esophageal Varices
Bleeding Ulcers
NSAIDs
Mallory-Weiss Tear

Hematochezia
is the passage of fresh
blood per anus, usually
in or with stools.

hemorroids
diverticulosis
Colorectal cancer
enterocolitis
inflammantory bowel
disease

Defining Gastrointestinal Bleeding

1. Identify the probable presence of bleeding
1.
2.
3.
4.

Hematemesis
Melena
Hematochezia
Hypovolemia

2. Estimate the amount and rapidity of bleeding

1. Frequency and volume of stools or emesis
2. Symptoms of hypovolemia
3. Hematemesis

3. Ask about site and potensial causes

1. Upper gastrointestinal
1. Melena and/or hematemesis
2. Symptoms of peptic ulcer, varices, gastritis,
esophagitis, Mallory-Weiss tears, and
malignancy

2. Lower intestinal
1. Hematochezia
2. Symptoms of arteriovenous malformations,
diverticulosis, cancer, hemorrhoids, inflammatory
bowel disease, ischemic colitis

4. Determine the presence of diseases or

situations having poorer prognosis
1. Congestive heart failure or prior myocardial
infarction
2. Chronic obstructive lung disease
3. Cirrhosis
4. Renal failure
5. Advanced malignancy
6. Age over 60 years
7. Clotting disorder

ESOPHAGITIS
is a general term for any
inflammation, irritation, or swelling of
the esophagus.

Risk Factor
Excessive vomiting
Medications such as aspirin, ibuprofen,
potassium, alendronate, tetracycline, and
doxycycline
Vitamin C supplements
Surgery or radiation to the chest (for
example, treatment for lung cancer)

Etiology
Esophagitis is frequently caused by the backflow of
acid-containing fluid from the stomach to the
esophagus, a condition called gastroesophageal
reflux.
An autoimmune disorder called eosinophilic
esophagitis also causes this condition.
Persons with weakened immune systems due to HIV
and certain medications (such as corticosteroids)
may develop infections that lead to esophagitis.
Esophageal infection may be due to fungi, yeast
(especially Candida infections), or viruses such as
herpes or cytomegalovirus.

Pathophysiology
Reflux esophagitis develops when gastric contents are
passively regurgitated into the esophagus. Reflux
happens commonly and does not cause major harm
because natural peristalsis of the esophagus clears the
refluxate back to the stomach.
In others, where acid reflux from the stomach is
persistent, the result is damage to the esophagus
causing symptoms and macroscopic changes.
Gastric acid, pepsin, and bile irritate the squamous
epithelium, leading to inflammation, erosion, and
ulceration of the esophageal mucosa.

Symptoms

Difficulty swallowing
Painful swallowing
Heartburn (acid reflux)
Oral lesions (herpes)

Examination
Endoscopy
Upper GI x-ray with barium
Biopsy

Treatment
Treatment depends on the specific cause.
Reflux disease may require medications to
reduce acid. Infections will require
antibiotics.

Complication
severe discomfort
swallowing difficulty to the extent of causing
malnutrition or dehydration
eventual scarring of the esophagus. This
scarring may lead to a stricture of the
esophagus, and food or medications may
not be able to pass through to the
stomach.

Differential Diagnoses
Acute Coronary Syndrome
Cholecystitis and Biliary Colic
Esophageal Perforation, Rupture and
Tears
Foreign Bodies, Gastrointestinal
Gastritis and Peptic Ulcer Disease
Myocardial Infarction

Barrets Esophagus
Barrets Esophagus is one of the disease
that happens because of recurrent exposure
from gastric HCl.
Normally, the epithel that forms the
esophagus mucosae is the non keratinized
stratified squamous type, but in barrets
disease, the HCl which keep on injuring the
epithel, the mucosae undergoes metaplasia.

The mucosae now changes into columnar

with cell goblets epithelium, which is the
defense mechanism from recurrent
exposure to HCl.
For this reason, the patient with Barrets
Esophagus, have a more higher probability
to have adenocarcinoma, up to 40 times fold

Esophageal Varices
Is an abnormally enlarged
veins in the lower part of your esophagus.

Etiology
liver disease (portal hypertension)

Pathophysiology
The portal vein carries blood from the intestine to the
liver.
Increased pressure causes the veins to balloon outward.
The vessels may break open (rupture). Any cause of
chronic liver disease can cause bleeding varices.
Normally, blood from your intestine, spleen and pancreas
enters your liver through a large blood vessel called the
portal vein. But if scar tissue blocks circulation through
your liver, the blood backs up, leading to increased
pressure within the portal vein (portal hypertension). This
forces blood into smaller veins in your esophagus,
stomach and occasionally your rectum. The excess
blood causes these fragile, thin-walled veins to balloon
outward and sometimes to rupture and bleed. Once
varices develop, they continue to grow larger.

Esophageal Varices
2 complementary strategic guide therapy
of bleeding varices :
local treatment of the bleeding vessel :
endoscopy sclerotherapy, endoscopic band
ligand, and baloon tamponade with a
Sengstaken-Blackmore tube,
and treatment of the underlying portal
hypertension (pharmacology therapy)

Symptoms
Vomiting blood
Black, tarry or bloody stools
Decreased urination from unusually low
blood pressure
Excessive thirst
Lightheadedness
Shock, in severe cases

Mallory Weizz Syndrome

A laceration of the lining of the
gastroesophageal junction or just
above it - often caused by severe
vomiting,hiatal hernia and coughing

Risk Factor
Male : female = 2-4:1.
Age = 40 50 years old, but the age
range is quite wide.

Pathophysiology

A Mallory-Weiss tear (MWT) likely occurs as a result of a large,

rapidly occurring, and transient transmural pressure gradient across
the region of the gastroesophageal junction. Acute distension of the
nondistensible lower esophagus can also produce a linear tear in
this region.
With a rapid rise in intragastric pressure due to precipitating factors,
such as retching or vomiting, the transmural pressure gradient
increases dramatically across the hiatal hernia, which abuts a low
intrathoracic pressure zone. If the shearing forces are high enough,
a longitudinal laceration eventually occurs. Within the hernia, the
tear is more likely to involve the lesser curvature of the gastric
cardia, which is relatively immobile compared to the remainder of
the stomach.
Another potential mechanism for MWTs is the violent prolapse or
intussusception of the upper stomach into the esophagus, as can be
witnessed during forceful retching at endoscopy.

Symptoms

Esophageal bleeding
Vomiting
Severe retching
Vomiting blood (bright red)
Melena
Pallor
Tachycardia
Hiccups

Examination
Fiber-optic endoscopy
(esophagogastroduodenoscopy confirms
Mallory-Weiss syndrome by identifying
esophageal tears. Recent tears appear as
erythematous longitudinal cracks in the
mucosa; older tears appear as raised
white streaks surrounded by erythema.

Treatment
proton pump inhibitors or histamine-2
receptor antagonists to help decrease acidity
blood transfusions if blood loss is great
endoscopy with electrocoagulation or heater
probe for hemostasis
transcatheter embolization or thrombus
formation with an autologous blood clot or
other hemostatic material (such as a
shredded adsorbable gelatin sponge)
surgery to suture each esophageal laceration.

Complication
Gastrointestinal bleeding
Peritonitis
Abdominal pain

Differential Diagnosis
Boerhaave Syndrome
Esophagitis
Gastric Ulcers

PEPTIC ULCER DISEASE

 Ulcers :
defined as a break in the mucosal surface >5
mm in size, with depth to the submucosa

Peptic ulcer disease (PUD) refers to:

a discrete mucosal defect in the portions of
the gastrointestinal tract (gastric or duodenal)
exposed to acid and pepsin secretion

Predisposing Factors
Ulcers are more common in :
Smokers
amount of hydrochloric acid in the stomach
the bicarbonate content of pancreatic secretions
degree of acid neutralization

NSAIDs users.

Diet and alcohol dont appear to contribute to

the development of peptic ulcer disease.
Its unclear whether emotional stress is a
contributing factor.

Etiology of PUD
Normal
Increased Attack
Hyperacidity

Weak defense
Helicobacter pylori*

Etiology
3 major causes of peptic ulcer disease:
1. infection with Helicobacter pylori,
2. use of nonsteroidal anti-inflammatory drugs
(NSAIDs), and
3. pathologic hypersecretory states such as
Zollinger-Ellison syndrome.

Causes of Ulcers not Caused by

H.pylori and NSAID

Infection

Drug/toxin

CMV
HSV
Helicobacter heilmanni
Biphosphonates
Chemotherapy
Clopidogrel
Crack cocaine
Glucocorticoids (when combined with NSAID)
Mycophenolate mofetil
Potassium chloride

Miscellaneous

Basophilia in myeloproliferative disease

Duodenal obstruction (e.g. annular pancreas)
Infiltrating disease
Ischemia
Radiation therapy
Sarcoidosis
Crohns disease
Idiopathic Hypersecretory state

Peptic Ulcer Morphology:

Microscopy: 4 zones.

Superficial necrotic layer.

Inflammatory cells zone.
Granulation tissue zone
Collagenous scar layer.

PUD - Diagnosis

Endoscopy
Barium meal contrast x-ray
Biopsy bacteria & malignancy
H.Pylori:
Endoscopy cytology
Biopsy Special stains
Culture - difficult
Urease Breath test.

Complications:
Bleeding Chronic-IDA, Acute, Massive
Fibrosis, Stricture obstruction pyloric
stenosis.
Perforation Peritonitis- emergency.
Gastric carcinoma. (not duodenal ca)

2 Types
DUODENAL ULCER
A duodenal ulcer is a
particular type of peptic
ulcer (stomach ulcer) that
afflicts the lining of the
duodenum

GASTRIC ULCER
Ulceration of the
GASTRIC MUCOSA due
to contact with GASTRIC
JUICE.
It is often associated with
HELICOBACTER PYLORI
infection or consumption of
nonsteroidal antiinflammatory drugs
(NSAIDS).

Epidemiology
Sex :
Male-to-female ratio is approximately 2:1

Age :
Duodenal ulcers usually occur in those aged
25-75 years.
Gastric ulcer prevalence peaks in those aged
55-65 years.

ETIOLOGY
DUODENAL ULCER
Excess stomach acid
Helicobacter pylori
bacteria
See underlying conditions
of peptic ulcers
The most common cause
of such damage is
infection of the stomach
with a bacterium called
Helicobacter pylori
(H.pylori)

GASTRIC ULCER

Non-cancerous (benign) gastric

ulcers are caused by an imbalance
between stomach acid, an enzyme
called pepsin, and the natural
defenses of the stomach's lining.
This imbalance leads to
inflammation, which can be made
worse by aspirin and nonsteroidal
anti-inflammatory medications
(NSAIDs) such as ibuprofen
Leiomyoma, gastric
Gastric polyp (hyperplastic)
Helicobacter pylori
Stomach cancer
Gastric polypoid adenoma
Drug interactions causing Gastric
Ulcer

Pathology
Duodenal ulcers :
Occur in the first portion of duodenum (>95%)
Located within 3 cm of the pylorus
Ussualy 1 cm in diameter but can occasionaly 3-6
cm (giant ulcers)
Ulcers sharply demarcated, with dept at time reaching
the muscularis propia
The base of the ulcer often consist of a zone of
eosinophilic necrosis with surounding fibrosis
Malignant DUS rare extremely

Phatology
Gastric ulcers :
GUs can represent a malignancy
Benign GUs are most often found distal to the junction
between the and the acid secretory mucosa (quite rare
in the gastric fundus)
Associated with H.pylori are also associated with
antral gastritis.
In contras, NSAID-related GUs are not accompanied
by chronic active gastritis but may instead have
evidence of a chemical-gastropathy, typified by
foveolar hyperplasia, edema of lamina propia and
ephitel regeneration in the absence of H.pylori.
Extension of smooth muscle fibers into upper portion
of mucosa may also occur

Pathophysiology
Duodenal ulcers :
H.pylori and NSAID induced injury account of the
majority of DUs
Many acid secretory abnormalities have been
describes in DU patient.
Of these, average basal and nokturnal gastric acid
secretion appears to be increased in DU patient as
compared as control;however, the level of overlap
between DU patient and control subject is substantial
Bicarbonate secretion is significantly decreasedin the
duodenal bulb of patient with an active DU as
compare to control subject. H.pylori infection may
also play role in this process.

Pathophysiology
Gastric ulcers :
Gastric acid output (basal and stimulated) tends to be
normal or decreased in GU patient
When GUs develop in the presence minimal acid
levels, impairment of mucosal defense factors may be
present
Abnormalities in resting anf stimulated pyloric
sphincter increase duodenal gastric reflux have been
implicated some GU patients
Delayed gastric emptying of solids has been
described in GU patients but has not been reported
consistely.

SYMPTOMs
GASTRIC ULCERS

DUODENAL ULCERS
1. Abdominal pain
2. Abdominal pain at night

3.
4.
5.
6.
7.
8.
9.

Abdominal pain after meals

Pain below the ribs
Gastrointestinal bleeding
Nausea, vomiting
Weight loss
Fatigue
Heartburn, indigestion,
belching
10. Chest pain
11. Vomiting blood
12. Bloody or dark tarry
stools

1.

Recurrent abdominal pain - dull and

burning type pain usually located in
epigastric area (area between belly
button and rib cage)
2. Abdominal pain when eating
3. Vomiting blood
4. Nausea, Anorexia, Black stools
5. Fatigue, Breathlessness
6. Abdominal pain
7. Lack of sleep
8. May be relieved by antacids or milk
9. Worsened on eating
10. Abdominal indigestion
11. Blood in stools or black, tarry stools
12. Unintentional weight loss

Complications
DUODENAL ULCER
Bleeding internally
Perforation of the intestine
and peritonitis
Bowel obstruction
Pancreatitis, acute
Gastrointestinal perforation
Hypovolaemic shock
Abdominal pain
Gastroduodenal ulcers

GASTRIC ULCER
Chronic blood loss, iron
deficiency anaemia
Bleeding from the ulcer
Perforation (hole) in the
stomach
Blockage in the stomach
that prevents movement
of stomach contents
Malignancy

Differential Diagnosis
NUD (Non Ulcer Dyspepsia) also known
as functional dyspepsia or essential
dyspepsia
Proximal gastrointestinal tumors
Gastroesophageal reflux
Vascular disease
Pacreaticobiliary disease
Gastroduodenal Crohn disease

Gastritis
Inflammation of the gastric
mucosa caused by any of several conditions, including
infection (Helicobacter pylori), drugs (NSAIDs, alcohol),
stress, and autoimmune phenomena (atrophic gastritis).

Etiology
The most common are:
Alcohol
Erosion (loss) of the protective layer of the stomach lining
Infection of the stomach with Helicobacter pylori bacteria
Medications such as aspirin or other nonsteroidal antiinflammatory drugs (NSAIDs)
Smoking
Less common causes are:
Autoimmune disorders (such as pernicious anemia)
Backflow of bile into the stomach (bile reflux)
Eating or drinking caustic or corrosive substances (such as
poisons)
Excess gastric acid secretion (such as from stress)
Viral infection, especially in people with a weak immune system

Symptoms

Nausea or recurrent upset stomach

Abdominal bloating
Abdominal pain
Vomiting
Indigestion
Burning or gnawing feeling in the stomach between meals or
at night
Hiccups
Loss of appetite
Vomiting blood or coffee ground-like material
Black, tarry stools

Diagnosis
Upper endoscopy
Blood tests
Fecal occult blood test (stool test

Treatment
Mediacation
1.H2-blockers :
cimetidine (Tagamet), famotidine (Pepcid),niza
tidine (Axid), ranitidine (Zantac).
2.Proton pump inhibitors (PPIs) :
lansoprazole (Prevacid),omeprazole (Prilosec,
Losec).
3.Coating agents:
Sucralfate (Carafate), Misoprostol (Cytotec)
4.Antacids
5.Antibiotic
6.Antiemetic

 Prevention
Avoid substances that trigger gastritis symptoms:
1. Cigarette smoking
2. Coffee and other beverages that contains caffein (cola,
tea)
3. Alcohol
4. Aspirin (use coated aspirin if you must take aspirin)
5. NSAIDs such as ibuprofen (Motrin, Advil) or naproxen
(Naprosyn)

Differential Diagnosis

Acute Coronary Syndrome

Gastroenteritis
Aneurysm, Abdominal
Hepatitis
Cholangitis
Inflammatory Bowel Disease
Cholecystitis and Biliary Colic
Mesenteric Ischemia
Cholelithiasis
Myocardial Infarction
Diverticular Disease
Pancreatitis
Esophageal Perforation, Rupture and Tears
Pulmonary Embolism
Esophagitis
Renal Calculi

 Complications
Malignancy
Hemorrhage
Perforation
Obstruction
Prognosis
The prognosis is excellent. Most patients
are cured when the cause has been
identified and treated appropriately.

Conclusion
Based on the signs and symptoms
Mrs.Doubtfire, shows upper
gastrointestinal bleeding.
She probably experiencing peptic ulcer
disease.
To make a firm diagnosis, the patient have
to take further examination.

Suggestion
Mrs.Doubtfire has to avoid eating sour and
spicy food, drinking beverages that
contains caffein and alcohol.

References
Price, Sylvia A., Wilson, Lorraine M. Patofisiologi
vol 1. Ed 6. Jakarta : EGC, 2006.
Fauci, Braunwald, Kasper, dkk. Harrisons
Principles of Internal Medicine vol II. Ed
17.United Stated : mcGraw-Hills, 2008.
Sherwood, Lauralee. Physiology from Cells to
Systems. Ed 6. United Stated : Thomson Higher
Education, 2007.
Reid Robin, Roberts Fiona. Pathology Illustrated
6th ed. London: Elsevier, 2005.