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-old-
woman. 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 Carbohydrate digestion No foodstuffs; a few
Amylase begins medicationsfor example,
Mucus nitroglycerin
Lysozyme
None
Mucus None

Gastric Juice Carbohydrate digestion No foodstuff; a few lipid

HCl continues in body of soluble substances, such as
Pepsin stomach; protein digestion alcohol and aspirin
Mucus begins in antrum of stomach
Intrinsic factor
Pancreatic digestive These pancreatic anzymes Not applicable
enzymes accomplish digestion in
Trypsin, chymotrypsin, duodenal lumen
carboxypeptidase
Amilase
Lipase

Pancreatic aqueous
NaHCO3 secretion
SECRETION DIGESTION ABSORPTION

Bile Bile doesnt digest anything, Not applicable

Bile salts but bile salts facilitate fat
Alkaline secretion digestion & absorption in
Bilirubin duodenal lumen
Succus entericus In lumen, under influence of All nutrients, most
Mucus pancreatic enzymes and electrolytes, and water
Salt bile, carbohydrate & protein
(Small intestine enzymes digestion continues and fat
are not secreted but digestion is accomplished;
function within the brush in brush border,
border membrane --- carbohydrate and protein
disaccharidases and digestion completed
aminopeptidases)
None Salt and water, converting
Mucus contents to feces
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 coffee-
grounds 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 Melena Hematochezia
is the vomiting of blood, which is the passage of black, tarry is the passage of fresh
may be obviously red or have an stools blood per anus, usually
appearance similar to coffee in or with stools.
grounds.

Bleeding ulcer in the stomach, hemorroids

first part of the small intestine, or diverticulosis
esophagus Gastritis
Colorectal cancer
Bleeding esophageal varices or Esophageal Varices
enterocolitis
stomach varices Bleeding Ulcers
inflammantory bowel
gastroenteritis NSAIDs disease
esophagitis Mallory-Weiss Tear
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
 Defining Gastrointestinal Bleeding
1. Identify the probable presence of bleeding
1. Hematemesis
2. Melena
3. Hematochezia
4. 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
CMV
HSV
Helicobacter heilmanni
Drug/toxin
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 GASTRIC ULCER
A duodenal ulcer is a Ulceration of the
particular type of peptic GASTRIC MUCOSA due
ulcer (stomach ulcer) that to contact with GASTRIC
afflicts the lining of the JUICE.
duodenum It is often associated with
HELICOBACTER PYLORI
infection or consumption of
nonsteroidal anti-
inflammatory 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 GASTRIC 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)
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
DUODENAL ULCERS
1. Abdominal pain
2. Abdominal pain at night
3. Abdominal pain after meals
4. Pain below the ribs
5. Gastrointestinal bleeding
6. Nausea, vomiting
7. Weight loss
8. Fatigue
9. Heartburn, indigestion,
belching
10. Chest pain
11. Vomiting blood
12. Bloody or dark tarry
stools
GASTRIC ULCERS
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
 Inflammation of the gastric
mucosa caused by any of several conditions,
Gastritis
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 anti-
inflammatory 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.