Gosh, Mrs.

Doubtfireyou
look pale
Created by:
Group 1
Tutor : dr. Krisnha Lestadi

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: Melissa Santoso
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Marwin Tjandra

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Toni Periyanto
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Problem
While you were watching Harry Potter and The Goblet of Fire in
TV at the emergency department you worked for as a doctor,
suddenly came a woman, who looks pale, held by her husband. At
the doorway, shes vomiting blood with a coffee ground appearance.
Its known that the patient is Mrs. Doubtfire, a 55-years old
woman. Tonight, at home, she had a sudden episode of
hematemesis. 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 woke up nauseated and has 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 NSAIDs.

Learning Objective
To learn and know about :

Anathomy of gastrointestinal system

Physiology of gastrointestinal system
Mechanism of vomit
Differential between UGIB and LGIB
Diseases of UGIB

Dyspepsia

Dyspepsia
Ascertaining the location of the pain
(upper or lower, localized or diffuse),
its character (sharp, burning,
cramping), and its relationship to
meals will often provide clues into the
most important diagnostic
considerations.

Gastrointestinal Bleeding
Hematemesis is the vomiting of blood,
which may be obviously red or have an
appearance similar to coffee grounds.
Occasionally hemoptysis or vomiting of
swallowed blood from epistaxis can be
confused with hematemesis
Melena is the passage of black, tarry
stools.
Hematochezia is the passage of fresh
blood per anus, usually in or with stools.

Bleeding diagnosed
X-rays or other imaging tests (abdominalCTscan,
abdominalMRI)
Endoscopy
Capsule endoscopy
Other procedures
Angiography
is a technique that uses dye to highlight blood
vessels allows the dye to leak out of the blood
vessel, which identifies the site of bleeding.
Radionuclide scanning
is a non-invasive screening technique used for
locating sites of acute bleeding, especially in the
lower GI tract.

Abdominal/bowel sound
Abdominal sounds (bowel sounds) are
made by the movement of the intestines as
they push food through.
Bowel sounds can echo throughout the
abdomen much like the sounds heard from
water-pipes.
The majority of bowel sounds are harmless
and simply indicate that the
gastrointestinal tract is working.
A doctor can evaluate abdominal sounds by
listening to the abdomen with a
stethoscope.

Abdominal/bowel sound
Reduced (hypoactive) bowel sounds include a
reduction in the loudness, tone, or regularity of
the sounds. They indicate a slowing of
intestinal activity.
Hypoactive bowel sounds are normal during sleep,
for a short time after the use of certain
medications and after abdominal surgery.
Decreased or absent bowel sounds often indicate
constipation.
Hyperactive bowel sounds reflect an increase
in intestinal activity. This can sometimes occur
with diarrhea and after eating.

Vomiting
Vomiting is abnormal emptying of stomach and
upper part of intestine via esophagus through
mouth.
Causes:
1. Irritation in GIT
2. Mechanical stimulation of pharynx
3. Pregnancy
4. Alcohol
5. Stimulation of labyrinth of ear eg sea sickeness,
mountain sickeness
6. Acute GI infection
7. Metabolic disorders
8.Increase Intracranial Pressure

Emesis mechanism

Emesis mechanism

Anatomy and Physiology

Physiology - Digestive
System
The functions of the digestive system are:
Ingestion - eating food
Digestion - breakdown of the food
Absorption - extraction of nutrients
from the food
Defecation - removal of waste products
The digestive system is a group of organs
that breakdown the chemical components
of food, with digestive juices, into
micromolecul nutrients which can be
absorbed to generate energy for the body

The bucal cavity (mouth) and

salivary glands

Food enters the mouth and is chewed by the

teeth, turned over and mixed with saliva by
the tongue.
Mouth: the salivary glands. Saliva produced
by these glands contains an enzyme that
begins to digest the starch from food into
smaller molecules. ptyalin enzyme

The Stomach
It is the widest part of the alimentary canal
and acts as a reservoir for the food where it
may remain for between 2 and 6 hours.
Here the food is churned over and mixed
with various hormones, enzymes including
pepsinogen which begins the digestion of
protein, hydrochloric acid, and other
chemicals
The stomach has an average capacity of 1
liter, varies in shape, and is capable of
considerable distension.
At regular intervals a circular muscle at the
lower end of the stomach, the pylorus opens
allowing small amounts of food, now known
as chyme to enter the small intestine.

Duodenum

Small Intestine
The small intestine measures about 7m in an
average adult and consists of the duodenum,
jejunum, and ileum.
Both the bile and pancreatic ducts open into
the duodenum together.
The small intestine, because of its structure,
provides a vast lining through which further
absorption takes place.

The Large Intestine

The large intestine averages about 1.5m
long and comprises the caecum, appendix,
colon, and rectum.
Here most of the water and electrolytes is
absorbed, much of which was not ingested,
but secreted by digestive glands further up
the digestive tract.
The colon is divided into the ascending,
transverse and descending colons, before
reaching the anal canal where the
indigestible foods are expelled from the
body.

Chase

Table 282-1. Overview of Approach to Patients with Common Gastrointestinal Disorders

Possible Physical
Signs

Site of Disorder

Common Symptoms

Potential Procedures or
Laboratory Studies

Esophagus

Dysphagia
Odynophagia
Heartburn,chestpain
Hematemesis/melena

Stomach

Nauseaandvomiting
Epigastricpain
Hematemesis/melena

Distention
Tenderness
Succussionsplash
Mass

Gastroscopy
UpperGIx-rayseries
Nasogastricaspiration
Gastricemptying

Duodenum

EpigastricPain
Nausea/vomiting
Hematemesis

Tenderness
Alteredbowelsounds
Distention
Mass

Duodenoscopy
Smallbowelfollow-through,
enteroclysis
Kidney-ureter-bladderx-rayseries
D-Xyloseabsorptiontests

Jejunum

Pain
Diarrhea

Alteredbowelsounds
Distention
Mass

CT
Stoolcultures,stoolexaminationfor
ovaandparasites
Smallbowelbiopsy

Esophagoscopy
Bariumswallow
Manometry
Bernsteintest

SmallIntestine

Gastrointestinal Bleeding

Esophagitis

Esophagitis
Reflux esophagitis
Often found in conjunction with sliding hiatal hernia.
Etiology:
AGENTS (alcohol, chocolate, fatty foods, cigarette,
drugs)
Certain conditions (pregnancy, estrogen therapy,
etc)
Gastric fluid (acid, pepsin) harmful for
esophageal mucosa
Phatogenesis
Agents that decrease the pressure of the lower
esophageal sphincter frequent & long transient
reflux inflamation necrosis mucosesubmucose

Esophagitis
Reflux esophagitis
Clinical manifestations
Dysphagia
Heartburn
Hematemesis
Regurgitation of a sour brash
Melena
Complication: Barrett esophagus

Esophagitis
Barrett esophagus
Is a result of chronic gastroesophageal reflux
The distal squamous mucosa is replaced by
metaplastic columnar epithelium response of
prolonged injury
Phatogenesis: still unclear
- Inflamation & ulceration ++ ingrowth of
pluripotent stem cell differentiated into a
columnar epithelium ---- more resistant to acid
peptic injury.
Clinical features:
- Secondary complications of local ulcerations with
bleeding and stricture --- adenocarcinoma

Varices Esophageal

Causes
Causes of portal hypertension usually are
classified as prehepatic, intrahepatic, and
posthepatic.
1. Prehepatic
Splenic vein thrombosis
Portal vein thrombosis
Extrinsic compression of the portal vein
2. Posthepatic
Budd-Chiari syndrome
Thrombosis of the inferior vena cava
Constrictive pericarditis
Venoocclusive disease of the liver

Causes
3. Intrahepatic
Congenital hepatic fibrosis
Idiopathic portal hypertension
Sclerosing cholangitis
Schistosomiasis
Primary biliary cirrhosis
Alcoholic cirrhosis
Hepatitis B virusrelated and hepatitis C
virusrelated cirrhosis
Alpha-1 antitrypsin deficiency
Chronic active hepatitis

PATHOPHYSIOLOGY
Obstruction of the portal venous system
at any level leads to increased portal
pressure.
An elevated portal venous pressure (>10
mm Hg) distends the veins proximal to the
site of the block and increases capillary
pressure in organs drained by the
obstructed veins.
The anastomoses connecting the portal
and systemic circulation may enlarge to
allow blood to bypass the obstruction and
pass directly into the systemic circulation.

PATHOPHYSIOLOGY
Studies have demonstrated the role of endothelin1 (ET-1) and nitric oxide (NO) in the pathogenesis
of portal hypertension and esophageal varices.
ET-1 is a powerful vasoconstrictor synthesized by
sinusoidal endothelial cells that has been
implicated in the increased hepatic vascular
resistance of cirrhosis and in the development of
liver fibrosis.
NO is a vasodilator substance that is synthesized
by sinusoidal endothelial cells.
In the cirrhotic liver, the production of NO is
decreased, and endothelial nitric oxide synthase
(eNOS) activity and nitrite production by sinusoidal
endothelial cells are reduced.

Gastritis

What is Gastritis?
An inflammation, irritation or erosion of the
stomach lining. Can be of acute or a
chronic complaint.
Acute gastritis often due to chemical injury
(alcohol/drugs)
Chronic gastritis: H. Pylori infection,
chemical, autoimmune.

Etiology
Bile reflux Drugs
NSAIDs, such as aspirin, ibuprofen, and naproxen
Cocaine
Iron
Colchicine, when at toxic levels, as in patients
with failing renal or hepatic function
Kayexalate
Chemotherapeutic agents, such as mitomycin C,
5-fluoro-2-deoxyuridine, and floxuridine
Potent alcoholic beverages, such as whisky, vodka,
and gin
Bacterial infections
H pylori (most frequent)
H heilmanii (rare)
Streptococci (rare)

Etiology
Fungal infections
Candidiasis
Histoplasmosis
Phycomycosis
Parasitic infection (eg, anisakidosis)
Acute stress (shock)
Radiation
Allergy and food poisoning
Spicy food
Smoking
Viral infections (eg, CMV)

Acute Gastritis
Acute gastritis can be broken down into 2
categories:
erosive (eg, superficial erosions, deep
erosions, hemorrhagic erosions)
nonerosive (generally caused by
Helicobacter pylori).

Erosive Gastritis
Acute erosive gastritis can result from
the exposure to a variety of agents or
factors. This is referred to as reactive
gastritis.
These agents/factors include
nonsteroidal anti-inflammatory
medications (NSAIDs), alcohol,
cocaine, stress, radiation, bile reflux,
and ischemia.
This results from oral or systemic
administration of these agents either
in therapeutic doses or in
supratherapeutic doses.

Chronic Gastritis

Autoimmune
Bacterial (H. Pylori)
Chemical (NSAIDs)
Chronic noninfectious granulomatous
gastritis
Lymphocytic gastritis
Eosinophilic gastritis
Ischemic gastritis
Radiation gastritis

PEPTIC ULCER DISEASE

Definition
Peptic ulcers are defects in the gastric or
duodenal mucosa that extend through the
muscularis mucosa
Peptic ulcer disease (PUD) is one of the most
common diseases affecting the
gastrointestinal (GI) tract.
It causes inflammatory injuries in the gastric
or duodenal mucosa, with extension beyond
the submucosa into the muscularis mucosa.

Epidemiology
The incidence of DUs declined steadily
from 1960 to 1980 and has remained
stable since then.
Gastric Ulcers GUs tend to occur later
in life than duodenal lesions, with a
peak incidence reported in the sixth
decade.
More than half of GUs occur in males

Etiology

H. pylori infection
Predominant cause
NSAIDs
Cigarette smoking
Genetic predisposition
blood group O
Psychological stress

The majority of GUs can be attributed to either

H. pylori or NSAID-induced mucosal damage.
The majority of DUs can be attributed to H.
pylori

Campylobacter pyloridis
It is S-shaped (~0.5 3 um in size)
and contains multiple sheathed
flagella.
Its ability to colonize the gastric
mucosa and produce mucosal injury.
a gram-negative microaerophilic
This rate of colonization increases with
age, with about 50% of individuals age
50 being infected.

Figure 1: Helicobacter pylori invading epithelial

cells.

Campylobacter pyloridis
Transmission of H. pylori occurs from
person to person, following an oraloral or fecal-oral route.

PATHOPHYSIOLOGY H. pylori

PATHOPHYSIOLOGY
NSAIDs

PATHOPHYSIOLOGY
NSAIDs

CLINICAL FEATURES
Epigastric pain can be present in both DU and GU.
Pain pattern in DU occurs 90 min to 3 h after a
meal and is frequently relieved by antacids or
food.
Pain that awakes the patient from sleep (between
midnight and 3 A.M.) is the most discriminating
symptom, with two-thirds of DU patients
describing this complaint.
GU discomfort may actually be precipitated by
food.
Nausea and weight loss occur more commonly in
GU patients.
Hematemesis

CLINICAL FEATURES
Other symptoms are :

losing weight
not feeling like eating
having pain while eating
feeling sick to your stomach
vomiting

Related Complications
Gastrointestinal Bleeding
Perforation
Gastric Outlet Obstruction

Treatment

GASTRIC ADENOCARCINOMA

Epidemiology
Gastric cancer incidence has decreased
worldwide but remains high in Japan, China,
Chile, and Ireland.
The risk of gastric cancer is greater among
lower socioeconomic classes.

Etiology

PATHOPHYSIOLOGY
Gastric carcinomas spread by direct
extension through the gastric wall to the
perigastric tissues, occasionally adhering to
adjacent organs such as the pancreas,
colon, or liver.
The disease also spreads via lymphatics or
by seeding of peritoneal surfaces.
The liver is the most common site for
hematogenous spread of tumor.

Clinical Features

upper abdominal discomfort

Anorexia
slight nausea and vomiting
Weight loss
Dysphagia (caused by lesions of the
cardia)
iron-deficiency anemia
occult blood in the stool

TREATMENT
Gastrectomy
subtotal gastrectomy is the treatment
of choice for patients with distal
carcinomas, total or near-total
gastrectomies are required for more
proximal tumors.
chemotherapy combined with
radiation therapy has been shown to
reduce the recurrence rate and
prolong survival

Conclusion
Mrs. Doubtfire probably having UGIB
disease based on the symptoms that
she had
The diseases of UGIB are:

Varices Esophagus
Gastritis
Peptic Ulcers (DU and GU)
Adenocarsinoma Gaster

Suggestion
Mrs. Doubtfire needs to have an
endoscopy to make sure what illness
that she has
Take a meal in a small portion, but
frequently
Give education to patients and other
people

Summary
1.
2.
3.
4.
5.
6.
7.

Contran, Kumar, Collins. Robbins Pathologic Basis of

Disease. 6th edition. Saunders company
Rubin, Ravael. Rubins Phatology clinicopathologic
foundation of Medicine. 5th edition. Philadelphia
Buku Ajar Ilmu Penyakit Dalam, edisi 3, jil. 1, Balai Penerbit
FKUI: Jakarta, 2001.
Litien,scott C. Mayo Clinic Family Heath Book. 5th edition.
2009. Jakarta : Gramedia.
http://digestive.niddk.nih.gov/ddiseases/pubs/cvs/index.ht
m
http://www.nlm.nih.gov/medlineplus/ency/article/003118.h
tm
http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=
1411788&blobtype=pdf