Professional Documents
Culture Documents
02
November 06, 2017
GASTROINTESTINAL DISORDERS IN CHILDREN PART II
Dra. Ruby Ann Punongbayan
Department of Pediatrics
TOPIC OUTLINE
I. Peptic Ulcer Disease
a. Role of Helicobacter pylori
b. Clinical Manifestations
c. Diagnosis
d. Treatment
II. Stress Ulcer Disease
III. Gastroenteritis
a. General Etiology
b. Risk Factors
c. Complications
d. General Approach to Diarrhea
e. Common Causative Organisms with Corresponding
Presentations and Treatment
Figure 1. Peptic Ulcer Disease
- Five Major Groups of E.coli
- Management
- Diagnosis of E.coli Ulcers are deep lesions that breach the integrity of the epithelium
and penetrate through the muscularis mucosa with exposure of
- Indications for PCR and DNA Probes
submucosa
- Treatment
f. Clinical Syndromes Erosions are superficial lesions that stop short of the muscularis
IV. Chronic Diarrhea propria
a. Evaluation of Chronic Diarrhea Both lesions occur in the presence of gastric inflammation or
b. Treatment gastritis
V. Diseases of the Pancreas
a. Acute Pancreatitis
- Pathogenesis
- Clinical Manifestations
- Diagnosis
- Treatment
- Prognosis
VI. Diseases of the Liver
a. Manifestations of Liver Disease
- Viral Hepatitis
- Hepatitis B Antigens and Antibodies
Clinical Manifestations
Figure 4. Difference of DU and GU
Classic symptom of epigastric pain alleviated by ingestion of food is
present only in a minority of children
Treatment
Majority of children present with poorly localized pain
After 6 years old, clinical features may be similar to those of adults With H. pylori who have ulcers, MALT lymphoma, atrophic gastritis
o Dull or aching pain with intestinal metaplasia; cost-benefit ratio of eradicating H.
o GI blood loss Pylori
o Exacerbations and remissions PPI + Clarithromycin + Amoxicillin or
<33% of patients presenting with typical ulcer pain experience PPI + Clarithromycin + Metronidazole
prompt relief after intake of antacids Taken for 4 to 6 weeks
Diagnosis
Method of Choice
Esophagogastroduodenoscopy
Direct Visualization
Gold standard for diagnosis is
histologic demonstration or
isolation
To test for:
• Undocumented duodenal
or gastric ulcer
• MALT lymphoma
(anrtalmicronodules
representing lymphoid
follicles)
Taken from
Biopsy
• Antrum
• Body
• Transition zone
CHRONIC DIARRHEA
Increased total daily stool output with increased stool water content
Diarrhea that lasts more than 2 weeks
Results from altered intestinal water and electrolyte transport
GI tract of an infant handles 285 ml/kg/day of fluid (intake plus
intestinal secretion) with a stool output of 5 – 10 g/kg/day
Stool output in infants & children contains approximately per liter
(20-25 meq of na, 50-70 meq of k, 20-25 meq of cl)
Mechanisms responsible for the absorptive capacity are caused by
the function of several transport proteins located at the brush
border membrane of the small and large intestine
Acute Pancreatitis
Most common pancreatic disorder in children
Most common causes: CULLEN’S SIGN GREY TURNER SIGN
o Blunt abdominal injury
o Mumps and other viral illnesses (Measles, VIRAL)
o Multisystem disease
o Congenital abnormalities
o Biliary microlithiasis
o Drugs and toxins
Pathogenesis
Theory: Following an insult, lysosomal hydrolase co-localizes with
pancreatic proenzymes within the acinar cell pancreatitis with
continued synthesis of enzymes occur proenzymes are activated
by cathepsin leading to autodigestion, further activation and release DIAGNOSIS
of active proteases lecithin is activated by phospholipase A2 AMYLASE LIPASE
into the toxic lysolecithin (which attack the pancreatic cells) Serum levels elevated for up to 4 More specific in acute
days inflammatory pancreatic disease
Rises by 4-8 hours
Peaks at 24-48 hours
Remains elevated 8-14 days
longer than serum amylase
Ag/Ab Features
Anti-HBcAg • Most valuable single serologic marker foracute
HBV infection because it is present asearly as HBsAg
and continues to be presentlater in the course of the
disease whenHBsAg has disappeared
HBcAg • Inner portion of the virion that encodes viralDNA
HBeAg • Serves as a marker of active viral replication
• Identification of infected individuals at
increased risk of transmitting HBV
HBsAg First serologic marker to appear and its rise
coincides with onset of symptoms; detectionof
acutely or chronically infected people;antigen used in
hepatitis B vaccine
Anti-HBs • Identification of people who have
resolvedinfections with HBV; determination of
immunity after immunization
Anti-HBe • Identification of infected people with lower
risk of transmitting HBV
Anti-HBc Identification of people acute, resolved or
chronic HBV infection
IgM Anti-HBc Identification of people acute or recent HBV
infections (including HBsAg-negative people
during the “window” phase of infection)