Thursday, Sept 6th, 2012

PROBLEM 2B (CHILD)
Gastrointestinal System Block

GROUP 13

FACULTY OF MEDICINE TARUMANAGARA

UNIVERSITY
2012
GROUP 13
 Tutor : dr. Chrismerry & dr. Andy
 Leader : I Putu Mana Nitia (405100103)
 Secretary : Renata C. F.Tjieputri (405080137)
 Scriber : Eva Fauziah (405100132)
 Personnels :
 Mieliani (405080191)
 Feny Chandra Dewi (405080208)
 Charlie (405100005)
 Felicia Faustine Fajaray (405100070)
 Adhitia Mahardika (405100124)
 Boe, Obet Agung Sanjaya (405100125)
 Andy Halim (405100193)
 Rahma Marini Sulwana (405100200)
 Khairunnisa Nugrahenni (405100210)
 A 9-year-old girl was admitted to hospital with severe
vomiting 20 times for 12 hours. Vomiting contained
yellow liquid and food, but no bile. There was occasional
streaks of blood. Her mother explained that it had
happened before, occuring once a while every 4-6
weeks during the past 2 years. Her condition between
episodes was quite well, no abdominal pain or bowel
symptoms found.
Physical examination showed she was 5% dehydrated,
abdomen was soft, and no other abnormal features.

 What can you learn from the problem ?

UNFAMILIAR TERMS:
1. Vomiting :the foceful contraction of the stomach that
propels its contens up the esophagus and out
throuh.
2. Streaks of blood :strain of blood
3. Dehydration imbalance :a condition of water and
electrolite
Mind Mapping

Congenital
Infection Toxin GERD Gastroentritis
Defect

Vomiting

Dehydration
LEARNING OBJCECTIVE
1. Vomiting
2. Dyspepsia
3. Peptic Ulcer, Gastritis
4. GERD
5. Dehydration
LO 1. Able to know and explain about
physiology & classification of Vomiting
Vomiting

 Vomiting (emesis) is the oral expulsion

of gastrointestinal contents resulting
from contractions of gut and
thoracoabdominal wall musculature

Harrison’s Pricipale of Internal Medicine 17th Edition

Predisposition factor
 Emesis is early manifestation of some disease, therefore closer
identification its so important, there are :
1. Age and sex
2. Diet
3. Nutrient status of child
4.Vomit contains
5. There is child disease which attack
The Vomiting Reflex
Three phases of emesis:
 Nausea :
 an unpleasant sensation that immediately proceeds
vomiting

 Retching
 follows nausea
 comprises laboured spasmodic respiratory movements
against a closed glottis with contractions of the abdominal
muscles, chest wall and diaphragm without any expulsion
of gastric contents.

 Vomiting
 caused by the powerful sustained contraction of the
abdominal and chest wall musculature.
 This is a reflex activity that is not under voluntary control
Type of Vomiting
1. Projectile (forceful vomiting) : increased
intracranial pressure.
2. Non projectile : Gastroesophageal reflux
3. Emesis : clear, yellow, billious, nonbilious,
bloody, nonbloody.
Diagnostic Rome III
Functional Gastroduodenal Disorders
B3b. Functional Vomiting
Must include all of the following:
 On average one or more episodes of vomiting per week.
 Absence of criteria for an eating disorder, rumination, or
major psychiatric disease according to DSM-IV.
 Absence of self-induced vomiting and chronic cannabinoid
use and absence of abnormalities in the central nervous
system or metabolic diseases to explain the recurrent
vomiting.

 *Criteria fullfield for the last 3 months with symptom

onset at least 6 month prior to diagnosis
Diagnostic Rome III
Functional Gastroduodenal Disorders
B3c. Cyclic Vomiting Syndrome
Must include all of the following.
1. Stereotypical episodes of vomiting regarding onset
(acute) and duration (less than one week).
2. Three or more discrete episodes in the prior year.
3. Absence of nausea and vomiting between episodes.

Supportive criterion
 History or family history of migraine headaches
Diagnostic Rome III
Childhood Functional GI Disorders: Child/Adolescent

H1b. Cyclic Vomiting Syndrome

Must include both of the following:
1. Two or more periods of intense nausea and unremitting
vomiting or retching lasting hours to days.
2. Return to usual state of health lasting weeks to months
Diagnostic
 Blood tests
blood tests may be taken to assess whether the
electrolyte balance in the body has been disturbed
due to dehydration from continued vomiting.
 Urinalysis
Concentrated urine is associated with dehydration
as the kidneys try to hold on to water in the body.
 X-rays of the abdomen
Management
 Identification and elimination of the underlying cause
if possible
 Control of the symptoms if it is not possible to
eliminate the underlying cause ex with Antivomiting
drugs (anti-emetics)
 Correction of electrolyte, fluid or nutritional
deficiencies
Treatment Nausea & Vomiting
Complications
 Aspiration of vomit
The individual may choke and asphyxiate or suffer an aspiration
pneumonia
 Dehydration and electrolyte imbalance
 Hypochloremic metabolic alkalosis (low chloride levels together
with high HCO3 and CO2 and increased blood pH)
 Hypokalemia (potassium depletion)
 A less frequent occurrence results from a vomiting of intestinal
contents, including bile acids and HCO3- which can lead to
metabolic acidosis
 Mallory-Weiss tear
 erosions to the esophagus or small tears in the esophageal mucosa
 Esophagitis
 Dentistry problem
 due to the acidity of the vomit
 Digestive enzymes can also have a negative effect on oral health, by
degrading the tissue of the gums
 Malnutrition
 MALLORY-WEISS SYNDROME
(TEAR)

 The cause: the sudden increase of intragastric

pressure

 Alcohol intoxication

 Treatment: Conservative treatment usually

sufficient, no need of operation
LO 2. Able to know and explain about
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.
SYNDROME OF DYSPEPSIA
 persistent or recurrent upper abdominal pain or
discomfort characterized by postprandial fullness, early
satiety, nausea, and bloating.
SYNDROME OF DYSPEPSIA
 Epidemiology: Each year 10-20% of US population seeks
medical attention. NUD 2-3 x peptic ulcer disease.
 Etiology & Pathogenesis:
Imbalance of the aggravating factors and defensive factors.
The aggravating factor increased and the defensive factors
decrease will cause functional and organic /ulcer
dyspepsia.
AGGRAVATING FACTORS OF SYNDROME
DYSPEPSIA:
 Gastric acid
 Pepsin
 Helicobacter pylori infection
 Gastric motor activity: 25-50% patients exhibit postprandial antral
hypomotility or delayed gastric emptying
 Psychological factors: anxiety and depression
 Diet: foods: spicy/hot, sour, vinnegar, drinks: coffee, smoking/tobacco,
alcohol
 Drugs: non-steroidal anti-inflammatory drugs(nsaid), traditional pain
killer drugs, steroids, antibiotics(erythromycin, ampicillin), iron,
potassium, digoxin, theophylline.
 Metabolic diseases: diabetes mellitus, hypothoroidism
 Hypopotassemia.
 Free radicals
DEFENSIVE FACTORS OF SYNDROME
DYSPEPSIA:
 Prostaglandin
 Mucus
 Mucosal blood flow
 Surfactant
 Bicarbonat
 Heat shock protein
 Epitel/preepithelial factors
 etc
CLINICAL FEATURES IN SYNDROME
DYSPEPSIA
 Non Ulcer Disease:
 Ulcer like: dominant epigastric pain, relieved by antacids or
food
 Dysmotility like: epigastric discomfort aggravated by food or
associated with early satiety, fullness, nausea, retching, vomiting,
or bloating.
 Nonspecific: symptoms does not fit the other categories
 Reflux like: heartburn and regurgitation
 Ulcer: the same with NUD
PHYSICAL EXAMINATION IN SYNDROME
DYSPEPSIA
 not specific
 epigastric tenderness some times
 abdominal mass if advanced gastric carcinoma
LO 3. PEPTIC ULCER, GASTRITIS
Peptic Ulcer
Definition

“disruption in the mucosal layer of the stomach or

duodenum. distinguished from an erosion by its
penetration through the muscularis mucosa or the
muscular coating of the gastric or duodenal wall”
Peptic Ulcer
 Etiology :
Peptic ulcer disease results from the imbalance between
defensive factors that protect the mucosa and offensive
factors that disrupt this important barrier
 Protective Aggressive

-Prostaglandin -Acid-pepsin environ-

-Mucous Gel Layer ment
-Bicarbonate -Mucosal Ischemia
-Mucosal Blood Flow -H. Pylori Infection
-NSAID
-Trauma
Peptic Ulcer

 Physiologi :
1. Mucosal defense system can be envisioned asa a three-level
barrier composed of : preepithelial , epithelial and
subepithelial
2. Preepithelial have mucus-bicarbonate and surface active
phospholipids layer which serve as a physicochemical barrier
3. Epithelial cells provide the next line of defense through
several factors, including mucus production , epithelial cell
ionic balance which maintain intracellular pH and bicarbonate
production.
Peptic Ulcer

 Physiologi :
4. If the pre-epthelial barrier were breached, epithelial cells
bordering a site of injury can migrate to restore the
damaged region (restitution). This process requires blood
flow , alkaline pH and growth hormone factor.
5. In the subepithelial an elaborate of microvascular induced
defense/repair system , providing HCO3 – and supply
adequate oxygen to epithelial cells.
Peptic Ulcer
 Physiology :
6. Prostaglandine play a central role in gastric epithelial
defense/repair which release mucosal bicarbonate and mucus ,
inhibit parietal cell secretion and maintaining mucosal blood
flow and epithelial cell restitution.
Peptic Ulcer
 Pathophysiology :
1. NSAID and Mucosal Ischemia will reduce the amount of
mucous and bicarbonate which trigger imbalance
2. Infection of H.Pylori induce mucosal injury
Peptic Ulcer

• Sign and symptoms :

1. Nausea
2. Vomiting
3. Dyspepsia(belching, bloating, distention, and fatty food
intolerance)
4. Heartburn
5. Chest discomfort
6. Anorexia
7. Hematemesis or melena (upper GI tract bleeding)
Peptic Ulcer
 Test :
1. History and physical examination
2. Esophagogastroduodenoscopy (EGD)
3. Gastric biposy
4. Urease Test
Peptic Ulcer

• Esophagogastroduodenoscopy (EGD)
1. Examination of the lining of the esophagus, stomach, and
upper duodenum with a small camera.
2. Procedure :
a. Patient should be on fasting state for 6 - 12
hours before the EGD procedure
b. Patient will be given a sedative and
analgesic (painkiller)
c. Local anesthetic may be sprayed into your
mouth to surpress cough or gag when
endoscope is inserted
Peptic Ulcer
2. Procedure :
d. A mouth guard will be inserted to protect
your teeth and the endoscope
e. Endoscope will go through your esophagus to
upper duodenum with a small camera to
locate the ulcer or cancer.
 Left  Right :
1.1st degree scar
2.2nd degree scar

Left  Right :
1. 1st degree ulcer
2. 2nd degree
ulcer

Left  Right :
1. 1st degree
healing
2. 2nd degree
healing
 1st Degree Ulcer
(duodenum)

2nd Degree Ulcer

(gaster)
Peptic Ulcer
 Gastric Biopsy :
1. Gastric tissue biopsy is the removal of stomach tissue for
examination
2. Procedure :
a. Patient should be on fasting state for 6 - 12
hours before the biopsy procedure
b. The gastric tissue biopsy sample is removed
during an upper endoscopy
Peptic Ulcer
2. Procedure :
c. Then in laboratory staining examines the tissue for bacteria or
other organism that cause the disease
d. Culture of H.Pylori will be stained by hematoxylin-eosin , gram
staining or The Wartin – Starry Silver for the best result (most
sensitive).
Peptic Ulcer
 Urease Test :
1. Urease test is the test to examine the bacteria H.Pylori by
the level of urease
2. There are 2 types of urease test :
a. Invasive :
Biopsy of the gastric epithelial cell to measure the level of urease
a. Non-invasive (Urea Breath Test) :
Test to measure the level of urea in our breath after taking a
specific species of carbon
Peptic Ulcer
3. Procedure :
a. Invasive : same as gastric biposy
b. Non-invasive :
1. Patient drink an isotopically labeled urea acid which dissolved in
aqua (14C or 13C isotype)
2. Breath collection after 30 – 60 minutes
3. Breath sample are transferred to an empty canister to be
examined.
H. pylori

 To survive in the harsh environment of the acidic

stomach, H. pylori produces urease, an enzyme that
catalyzes the conversion of urea in the gastric juice to
ammonia and bicarbonate
 These products buffer the gastric acid and create a
friendly microenvironment for H. pylori
H. pylori
 In most individuals, H. pylori is acquired early in life (before
5 yr)
 The route of transmission may involve fecal-oral, gastric-
oral (in vomitus), or oral-oral routes
 colonization with H. pylori may predispose to the
development of gastric adenocarcinoma and mucosal
associated lymphoid tissue (MALT) lymphoma, particularly
when the infection is acquired early in life
Pathogenesis
 Ulceration occurs when aggressive factors (e.g., gastric
acid, digestive enzymes, H. pylori bacterial products)
overwhelm the natural barriers that protect the
gastroduodenal lining (bicarbonate-mucus barrier, gastric
epithelial cells, mucosal blood flow, prostaglandins)
 Patients with duodenal ulceration may have increased acid
secretion, whereas patients with gastric ulcers may have
reduced acid output
Clinical Manifestations
 In the 1st mo of life, the two main manifestations are
gastrointestinal hemorrhage and perforation
 Between the neonatal period and 2 yr of age, recurrent
vomiting, slow growth, and gastrointestinal hemorrhage
are the major symptoms
 In preschool-aged children, periumbilical postprandial pain
is often elicited whereas vomiting and hemorrhage remain
common
 After 6 yr of age, the clinical features of ulcer disease are
similar to those in adults
 The pain is often described as dull or aching rather than
sharp or burning
Diagnosis
 Endoscopy is the method of choice to diagnose peptic
ulcer disease in children
 Testing for H. pylori is recommended only when there is a
documented duodenal or gastric ulcer and when there is
MALT lymphoma
Treatment
GASTRITIS
Definition
 Gastritis is a condition in which the stomach lining—
known as the mucosa—is inflamed
Signs and symptoms
 The most common symptoms of gastritis are
stomach upset and pain. Other possible symptoms
include:
 Indigestion (dyspepsia)
 Heartburn
 Abdominal pain
 Hiccups
 Loss of appetite
 Nausea
 Vomiting, possibly of blood or material that looks like
coffee-grounds
 Dark stools
Acute gastritis
 The most common causes of acute gastritis are infectious agent,
usually H. pylori.
 H. pylori imbeds itself in the mucous layer, a protective layer that
coats the gastric mucosa. It protects it self from the acidity of the
stomach through the production of large amounts of urease, an
enzyme that catalyzes the breakdown of urea to the alkaline
ammonia and carbon dioxide. The alkaline ammonia neutralizes the
gastric acid in the immediate vicinity of the bacterium conferring
protection.
 H pylori also has flagella that enable it to move and help it to
penetrate the mucous layer so that it comes into contact with
gastric epithelial cells. It also has several adhesions that help it to
adhere to these cells. It produces inflammation by activating a
number of toxins and enzymes that activate IL-8, which eventually
attracts polymorphs and monocytes that cause acute gastritis.
 Infection with H. pylori normally lead to chronic gastritis
 H pylori is associated with 60% of gastric ulcers and 80% of
duodenal ulcers.
Acute gastritis
 Helicobacter heilmanii is a gram-negative bacteri. The prevalence of
H heilmanii is extremely low (0.25-1.5%). The source of H heilmanii
infection is unclear, but animal contact is thought to be the means
of transmission.
 Tuberculosis is a rare cause of gastritis, but an increasing number
of cases have developed because of patients who are
immunocompromised. Gastritis caused by tuberculosis is
generally associated with pulmonary or disseminated disease.
 Secondary syphilis of the stomach is a rare cause of gastritis.
 Phlegmonous gastritis is an uncommon form of gastritis caused by
numerous bacterial agents, including streptococci, staphylococci,
Proteus species, Clostridium species, and Escherichia coli.
Phlegmonous gastritis usually occurs in individuals who are
debilitated. It is associated with a recent large intake of alcohol, a
concomitant upper respiratory tract infection, and AIDS.
Phlegmonous means a diffuse spreading inflammation of or within
connective tissue.
Acute gastritis
 Fungal infections that cause gastritis include Candida albicans and
histoplasmosis and phycomycosis. The common predisposing
factor is immunosuppression. The usual presenting clinical feature
is bleeding from gastric ulcers or erosions on giant gastric folds.
 Parasitic infections are rare causes of gastritis. Anisakidosis is
caused by a nematode that embeds itself in the gastric mucosa
along the greater curvature. Anisakidosis is acquired by eating
contaminated sushi and other types of contaminated raw fish.
This nematode infection is associated with gastric fold swelling,
erosions, and ulcers.
 Viral infections can cause gastritis. Cytomegalovirus (CMV) is a
common viral cause of gastritis. It is usually encountered in
individuals who are immunocompromised, including those with
cancer, immunosuppression, transplants, and AIDS.
Acute gastritis
 Stress causes decreased blood flow to the mucosa, leading
to ischemia with subsequent destruction of the mucosal
lining.
 Alcohol consumption does not cause chronic gastritis. It
does, however, erode the mucosal lining of the stomach
 NSAIDs inhibit cyclooxygenase-1, or COX-1, an enzyme
responsible for the biosynthesis of eicosanoids in the
stomach, which increases the possibility of peptic ulcers
forming. Also, NSAIDs, such as aspirin, reduce a substance
that protects the stomach called prostaglandin. These
drugs used in a short period of time are not typically
dangerous. However, regular use can lead to gastritis
Chronic gastritis
 Chronic gastritis has been classified according to histologic
characteristics. These include superficial atrophic changes
and gastric atrophy.
 Chronic gastritis is also classified according to the
predominant site of involvement. Type A refers to the body-
predominant form (autoimmune) and type B is the antral-
predominant form (H. pylori–related).
Type A Gastritis
 The less common of the two forms involves primarily the
fundus and body, with antral sparing. Traditionally, this form
of gastritis has been associated with pernicious anemia
 Antibodies to parietal cells have been detected in >90% of
patients with pernicious anemia and in up to 50% of
patients with type A gastritis
 The parietal cell–containing gastric gland is preferentially
targeted in this form of gastritis, and achlorhydria results.
Parietal cells are the source of IF, lack of which will lead to
vitamin B12 deficiency and its sequelae (megaloblastic
anemia, neurologic dysfunction).
Type B Gastritis
 Type B, or antral-predominant, gastritis is the more
common form of chronic gastritis. H. pylori infection is
the cause of this entity
 Multifocal atrophic gastritis, gastric atrophy with
subsequent metaplasia, has been observed in chronic H.
pylori–induced gastritis. This may ultimately lead to
development of gastric adenocarcinoma
Miscellaneous Forms of Gastritis
 Lymphocytic gastritis is characterized histologically by intense
infiltration of the surface epithelium with lymphocytes. The
etiology of this form of chronic gastritis is unknown. It has been
described in patients with celiac sprue, but whether there is a
common factor associating these two entities is unknown. No
specific symptoms suggest lymphocytic. Therapy with
glucocorticoids or sodium cromoglycate has obtained unclear
results.
 Marked eosinophilic infiltration involving any layer of the stomach
(mucosa, muscularis propria, and serosa) is characteristic of
eosinophilic gastritis. Affected individuals will often have circulating
eosinophilia with clinical manifestation of systemic allergy.
Involvement may range from isolated gastric disease to diffuse
eosinophilic gastroenteritis. Patients can present with epigastric
discomfort, nausea, and vomiting. Treatment with glucocorticoids
has been successful.
Risk Factors:
 Infection with H. pylori
 Acquired immunodeficiency syndrome (AIDS)
 Any condition that requires relief from chronic pain
using NSAIDS, such as chronic low back pain,
fibromyalgia, or arthritis
 Alcoholism
 Cigarette smoking
 Older age
Diagnosis
 The most common diagnostic test for gastritis is endoscopy with a
biopsy of the stomach. Endoscope can examine the lining of the
esophagus, stomach, and first portion of the small intestine.
 Upper gastrointestinal (GI) series. The patient swallows barium, a
liquid contrast material that makes the digestive tract visible in an x ray. X-
ray images may show changes in the stomach lining, such as erosions or
ulcers.
 Blood test. The doctor may check for anemia, a condition in which the
blood’s iron-rich substance, hemoglobin, is diminished. Anemia may be a
sign of chronic bleeding in the stomach.
 Stool test. This test checks for the presence of blood in the stool,
another sign of bleeding in the stomach.
 Tests for H. pylori infection. The doctor may test a patient’s breath,
blood, or stool for signs of infection. H. pylori infection can also be
confirmed with biopsies taken from the stomach during endoscopy.
Treatment
 Medicamentosa
 For H. pylori: three medications. "Triple therapy," including a
proton pump inhibitor to reduce acid production and two
antibiotics. Bismuth salicylate (Pepto-Bismol) may be used
instead of the second antibiotic. This drug, available over the
counter, coats and soothes the stomach, protecting it from
the damaging effects of acid.
Drugs Dose
Triple Therapy
1. Bismuth subsalicylate plus 2 tablets qid
Metronidazole plus 250 mg qid
Tetracyclinea 500 mg qid
2. Ranitidine bismuth citrate plus 400 mg bid
Tetracycline plus 500 mg bid
Clarithromycin or metronidazole 500 mg bid
3. Omeprazole (lansoprazole) plus 20 mg bid (30 mg bid)
Clarithromycin plus 250 or 500 mg bid
Metronidazoleb or 500 mg bid
Amoxicillinc 1 g bid
Quadruple Therapy
Omeprazole (lansoprazole) 20 mg (30 mg) daily
Bismuth subsalicylate 2 tablets qid
Metronidazole 250 mg qid
Tetracycline 500 mg qid
Treatment
 For non H. pylori
 Antacids --, they may relieve heartburn or indigestion but will not treat an ulcer. Antacids
may block medications from being absorbed and thereby decrease the medicine's
effectiveness. It is recommended to take antacids at least 1 hour before or 2 hours after
taking medications.Antacids include:
 Aluminum hydroxide (Amphojel,AlternaGEL)
 Magnesium hydroxide (Phillips' Milk of Magnesia)
 Aluminum hydroxide and magnesium hydroxide (Maalox, Mylanta)
 Calcium carbonate (Rolaids,Titralac,Tums)
 Sodium bicarbonate (Alka-Seltzer)
Treatment
 H2 blockers -- reduce gastric acid secretion. They
include:
 Cimetidine (Tagemet)
 Ranitidine (Zantac)
 Nizatidine (Axid)
 Famotidine (Pepcid)
 Proton-pump inhibitors -- decrease gastric acid
production. They include:
 Esomeprazole (Nexium)
 Lansoprazole (Prevacid)
 Omeprazole (Prilosec)
 Pantoprazole (Protonix)
 Rabeprazole (Aciphex)
Treatment
 Non Medicamentosa
 Lifestyle change
The treatment for gastritis that is caused by irritants is to stop using
them.These include:
 Alcohol
 Tobacco
 Acidic beverages such as coffee (both caffeinated and decaffeinated),
carbonated beverages, and fruit juices with citric acid
 NSAIDS, such as aspirin and ibuprofen -- switch to other pain relievers
(like acetaminophen)
 These steps may also help:
 Eat a fiber-rich diet.
 Foods containing flavonoids, like apples, celery, cranberries (including
cranberry juice), onions, garlic, and tea may stop the growth of H. pylori.
 Avoid high-fat foods. In animal studies, high-fat foods increase
inflammation in the stomach lining.
LO 4. Able to know and explain about
GERD
GASTROESOPHAGEAL REFLUX
DISEASE
-Excessive reflux of hydrochloric acid into the
esophagus.

Predisposing Factors:
1. Incompetent LES
2. Pyloric Stenosis
3. Other Esophageal disorder:
Pathophysiology
 Primary barrier to
gastroesophageal reflux is
the lower esophageal
sphincter
 LES normally works in
conjunction with the
diaphragm
 If barrier disrupted, acid
goes from stomach to
esophagus
GASTROESOPHAGEAL REFLUX
DISEASE
Signs and Symptoms:
 Pyrosis
 Dyspepsia
 Regurgitation
 Dysphagia
 Odynophagia
 Heart-attack like symptom
Alarms
 Alarm Signs/Symptoms
 Dysphagia
 Early satiety
 GI bleeding
 Odynophagia
 Vomiting
 Weight loss
 Iron deficiency anemia
GASTROESOPHAGEAL REFLUX
DISEASE
Diagnostics:
 EGD – esophagogastroduodenoscopy
 24 hr pH monitoring
 Esophagoscopy
Esophagogastrodudenoscopy
 Endoscopy (with biopsy if
needed)
 In patients with alarm
signs/symptoms
 Those who fail a medication trial
 Those who require long-term tx
 Lacks sensitivity for identifying
pathologic reflux
 Absence of endoscopic features
does not exclude a GERD
diagnosis
 Allows for detection,
stratification, and management of
esophageal manisfestations or
complications of GERD
pH
 24-hour pH monitoring
 Accepted standard for establishing or excluding presence of
GERD for those patients who do not have mucosal changes
 Trans-nasal catheter or a wireless, capsule shaped device
 Trial of Medications
 H2RA or PPI
 Expect response in 2-4 weeks
 If no response
 Change from H2RA to PPI
 Maximize dose of PPI
Trial of Medications
 If PPI response inadequate despite maximal dosage
 Confirm diagnosis
 EGD
 24 hour pH monitor
 Diagnosis in Pediatric
 by questionnaires (the Infant Gastroesophageal Reflux
Questionnaire, the I-GERQ), which also permit
quantitative scores to be evaluated for their diagnostic
discrimination
 Documentation and quantitation of reflux, when necessary,
can be done by ambulatory long-term (24–48 h)
esophageal pH recording
 Reflux of nonacid contents can be documented by the
use of an impedance test.
 Patient with heartburn

Iniate tx with H2RA or PPI

H2RA taken PPI taken QD

BID
No
Good response
No
Good response Yes Yes
Yes
Maintenance therapy Increase to
Frequent relapses max dose QD
with lowest effective dose
or BID
No
Yes
On demand tx
Symptoms persist Good response
No

Consider EGD if
Confirm diagnosis
risk factors present
EGD, ph monitor
(> 45, white, male
and > 5 yrs of sx)
Treatment
 Goals of therapy
 Symptomatic relief
 Heal esophagitis
 Avoid complications
Better Living
 Lifestyle modifications
 Avoid large meals
 Avoid acidic foods (citrus/tomato), alcohol, caffiene, chocolate, onions, garlic,
peppermint
 Decrease fat intake
 Avoid lying down within 3-4 hours after a meal
 Elevate head of bed 4-8 inches
 Avoid meds that may potentiate GERD (CCB, alpha agonists, theophylline,
nitrates, sedatives, NSAIDS)
 Avoid clothing that is tight around the waist
 Lose weight
 Stop smoking
Treatment
 Antacids
 Over the counter acid suppressants
and antacids appropriate initial
therapy
 Approx 1/3 of patients with
heartburn-related symptoms use at
least twice weekly
 More effective than placebo in
relieving GERD symptoms
Treatment
 Histamine H2-Receptor Antagonists
 More effective than placebo and antacids for relieving
heartburn in patients with GERD
 Faster healing of erosive esophagitis when compared with
placebo
 Can use regularly or on-demand
Treatment
AGENT EQUIVALENT DOSAGE
DOSAGES
Cimetadine 400mg twice daily 400-800mg twice daily
Tagamet

Famotidine 20mg twice daily 20-40mg twice daily

Pepcid

Nizatidine 150mg twice daily 150mg twice daily

Axid

Ranitidine 150mg twice daily 150mg twice daily

zantac
Treatment
 Proton Pump Inhibitors
 Better control of symptoms with PPIs vs H2RAs and
better remission rates
 Faster healing of erosive esophagitis with PPIs vs H2RAs
Treatment
AGENT EQUIVALENT DOSAGE
DOSAGES
Esomeprazole 40mg daily 20-40mg daily
Nexium

Omeprazole 20mg daily 20mg daily

Prilosec

Lansoprazole 30mg daily 15-10md daily

Prevacid

Pantoprazole 40mg daily 40mg daily

Protonix

Rabeprazole 20mg daily 20mg daily

Aciphex
Treatment
 H2RAs vs PPIs
 12 week freedom from symptoms
 48% vs 77%
 12 week healing rate
 52% vs 84%
 Speed of healing
 6%/wk vs 12%/wk
Treatment
 Antireflux surgery
 Failed medical management
 Patient preference
 GERD complications
 Medical complications attributable to a large hiatal hernia
 Atypical symptoms with reflux documented on 24-hour
pH monitoring
Treatment
 Antireflux surgery candidates
 EGD proven esophagitis
 Normal esophageal motility
 Partial response to acid suppression
Complications
 Erosive esophagitis
 Stricture
 Barrett’s esophagus
Complications
 Erosive esophagitis
 Responsible for 40-60% of GERD symptoms
 Severity of symptoms often fail to match severity of
erosive esophagitis
Complications
 Esophageal stricture
 Result of healing of
erosive esophagitis
 May need dilation
Complications

 Barrett’s Esophagus
 Columnar metaplasia of the
esophagus
 Associated with the development
of adenocarcinoma
Complications
 Barrett’s Esophagus
 Acid damages lining of
esophagus and causes
chronic esophagitis
 Damaged area heals in a
metaplastic process and
abnormal columnar cells
replace squamous cells
 This specialized intestinal
metaplasia can progress to
dysplasia and
adenocarcinoma
Complications
 Patient’s who need EGD
 Alarm symptoms
 Poor therapeutic response
 Long symptom duration
 “Once in a lifetime” EGD for patient’s with chronic GERD
becoming accepted practice
 Many patients with Barrett’s are asymptomatic
Complications
 Barrett’s Esophagus
 Manage in same manner as GERD
 EGD every 3 years in patient’s without dysplasia
 In patients with dysplasia annual to shorter interval
surveillance
LO 5. Able to know and explain about
DEHYDRATION
 Dehydration or volume depletion is classified as mild,
moderate or severe based on how much body fluid is
lost. When severe, dehydration is a life-threatening
emergency.
 Volume depletion denotes lessening of the total intravascular
plasma, where as dehydration denotes loss of plasma-free
water disproportionate to the loss of sodium. Potassium and
other electrolytes including buffers líke phosphates need to
be considered. Children, especially those younger than 4 years
old, are more susceptible to volume depletion as a result of
vomiting, diarrhea or increases in insensible water losses.
 Dehydration can be caused by losing too much fluid, not drinking
enough water or fluids, or both. Vomiting and diarrhea are
common causes.
 Dehydration is classified as mild, moderate or severe based on
how much body's fluid is lost. Symtons include:
 Dry or sticky mouth.
 Dizziness.
 Low or no urine output; concentrated urine is dark yellow.
 Not producing tears.
 Sunken eyes.
 Markedly sunken fontanelles (the soft spot on the top of the head in a
baby).
 Lethargic or comatose.
 In addition to the symptoms of actual dehydration, you may also have:
 vomiting and
 diarrhea.
 Drinking fluids is usually sufficient for mild dehydration. It is better to
have frequent, small amounts of fluid (using a teaspoon or syringe for
an infant or child) rather than trying to force large amounts of fluid at
one time. Drinking too much fluid at once can bring on more vomiting.
 Electrolyte solutions or freezer pops are especially effective. These are
available at pharmacies. Sport drinks contain a lot of sugar and can
cause or worsen diarrhea. In infants and children, avoid using water as
the primary replacement fluid.
Causes
 In most cases, volume depletion in children is from fluid losses from vomiting
or diarrhea.
 Vomiting may be caused by any of the following systems or processes:
 CNS (eg, infections, space-occupying lesions)
 GI (eg, gastroenteritis, obstruction, hepatitis, liver failure, appendicitis,
peritonitis, intussusception, volvulus, pyloric stenosis, toxicity [ingestion,
overdose, drug effects])
 Endocrine (eg, diabetic ketoacidosis [DKA], congenital adrenal hypoplasia,
Addisonian crisis)
 Renal (eg, infection, pyelonephritis, renal failure, renal tubular acidosis)
 Psychiatric (eg, psychogenic vomiting) - This is not seen in infants and is rare in
children compared with adults.
 Most cases of stomach viruses (also called viral gastroenteritis) tend to resolve
on their own after a few days.
 Boxers under hot lights sip water, then usually spit it out. They don`t seem to
know that that water could save them from a coma during heat prostration!
 Pathophysiology

 Pediatric dehydration is frequently the result of gastroenteritis, characterized

by vomiting and diarrhea. However, other causes of dehydration may include
poor oral intake due to diseases such as stomatitis, insensible losses due to
fever, or osmotic diuresis from uncontrolled diabetes mellitus.
 Pathophysiology

 Pediatric dehydration is frequently the result of gastroenteritis, characterized

by vomiting and diarrhea. However, other causes of dehydration may include
poor oral intake due to diseases such as stomatitis, insensible losses due to
fever, or osmotic diuresis from uncontrolled diabetes mellitus.

 Volume depletion denotes lessening of the total intravascular plasma,

whereas dehydration denotes loss of plasma-free water disproportionate to
the loss of sodium. The distinction is important because volume depletion can
exist with or without dehydration, and dehydration can exist with or without
volume depletion
 In children with dehydration, the most common underlying problem
actually is volume depletion, not dehydration. Intravascular sodium
levels are within the reference range, indicating that excess free
water is not being lost from plasma. Rather, the entire plasma pool is
contracted with solutes (mostly sodium) and solvents (mostly
water) lost in proportionate quantities. This is volume depletion
without dehydration. The most common cause is excessive extrinsic
loss of fluids.
 Pediatric patients, especially those younger than 4 years, tend to
be more susceptible to volume depletion as a result of vomiting,
diarrhea, or increases in insensible water losses. Significant fluid
losses may occur rapidly. The turnover of fluids and solute in
infants and young children can be as much as 3 times that of
adults.This is because of the following:
 Higher metabolic rates
 Increased body surface area to mass index
 Higher body water contents (Water comprises approximately
70% of body weight in infants, 65% in children, and 60% in
adults.)
Sodium considerations

 Volume depletion can be concurrent with hyponatremia. This

is characterized by plasma volume contraction with free
water excess. An example is a child with diarrhea who has
been given tap water to replete diarrheal losses. Free water
is replenished, but sodium and other solutes are not.
Potassium considerations
 Potassium shifts between intracellular and extracellular fluid
compartments occur more slowly than free water shifts.
Serum potassium level may not reflect intracellular potassium
levels. Although a potassium deficit is present in all patients
with volume depletion, it is not usually clinically significant.
However, failure to correct for a potassium deficit during
volume repletion may result in clinically significant hypokalemia.
Potassium should not be added to replacement fluids until
adequate urine output is obtained.
Acid and base problems
 Clinicians may observe derangements of acid-base balance with
volume depletion. Some degree of metabolic acidosis is common,
especially in infants.

Mechanisms include bicarbonate loss in stool and ketone

production. Hypovolemia causes decreased tissue perfusion and
increased lactic acid production. Decreased renal perfusion causes
decreased glomerular filtration rate, which, in turn, leads to
decreased hydrogen (H+) ion excretion. These factors combine to
produce a metabolic acidosis.
 In most patients, acidosis is mild and easily corrected with volume
restoration (as increased renal perfusion permits excretion of
excess H+ ions in the urine). Administration of glucose-containing
fluids further decreases ketone production.
 Physical
 The following table highlights the physical findings seen with different levels of
pediatric dehydration.

Mild (<3% body Moderate (3-9% body Severe (>9% body

Symptom
weight lost) weight lost) weight lost)
Mental Restless or fatigued, Apathetic, lethargic,
Normal, alert
status irritable unconscious
Tachycardia or
Heart rate Normal Normal to increased
bradycardia
Quality of Weak, thready,
Normal Normal to decreased
pulse impalpable
Tachypnea and
Breathing Normal Normal to increased
hyperpnea

Eyes Normal Slightly sunken Deeply sunken

Fontanelles Normal Slightly sunken Deeply sunken

Tears Normal Normal to decreased Absent

Mucous
Moist Dry Parched
membranes

Skin turgor Instant recoil Recoil <2 seconds Recoil >2 seconds

Capillary refill <2 seconds Prolonged Minimal

Extremities Warm Cool Mottled, cyanotic

Mild (<3% body Moderate (3-9% body Severe (>9% body

Symptom
weight lost) weight lost) weight lost)

Restless or fatigued, Apathetic, lethargic,

Mental status Normal, alert
irritable unconscious

Tachycardia or
Heart rate Normal Normal to increased
bradycardia
Quality of pulse Normal Normal to decreased Weak, thready, impalpable

Breathing Normal Normal to increased Tachypnea and hyperpnea

Eyes Normal Slightly sunken Deeply sunken

Fontanelles Normal Slightly sunken Deeply sunken

Tears Normal Normal to decreased Absent

Mucous membranes Moist Dry Parched

Skin turgor Instant recoil Recoil <2 seconds Recoil >2 seconds

Capillary refill <2 seconds Prolonged Minimal

Extremities Warm Cool Mottled, cyanotic

Conclusion
 We are able to explain about vomiting, GERD, Gastritis,
Peptic Ulcer, causing dehydration and dyspepsia
Suggestion
 Treat the cause of vomiting and rehydration
References
 Fauci. Harrison's Principles of Internal Medicine.
17th Edition. The McGraw-Hill Companies, Inc. 2008.
 Ganong, William. F. Review of Medical Physiology.Twenty-
Second Edition. Lange. 2005.
 Netter FH. Atlas of Human Anatomy. 2nd ed. Canada: Icon
Learning System, 1997.
 Rhoades, Rodney A.; Bell, David R. Medical Physiology:
Principles for Clinical Medicine, 3rd Edition. Lippincott
Williams & Wilkins. 2009.
 Silbernagl/Lang, Color Atlas of Pathophysiology. Thieme.
2000.
 Sudoyo A W, Setiyohadi B, Alwi I, Simadibrata M, Setiadi S,
editor. Buku Ajar Ilmu Penyakit Dalam. Edisi ke-4. Jilid I.
Jakarta: Pusat penerbitan ilmu penyakit dalam FKUI, 2007.