UNP-MEDICINE 2021 INTERNAL

MEDICINE
DISORDERS OF THE GASTROINTESTINAL SYSTEM
LECTURER: Ailyn Agdeppa, MD

February 28,
2020
HEAD NOTES
 TITLE/EMPHASIZED
 AUDIO
 NOTES/RECALLS/ADD-ONS

VOMITINGVOMITING
 Also known as forceful expulsion of gastric contents out of the mouth usually associated with nausea
 A highly-coordinated process, has its center in the medulla which receives inputs from the cerebral cortex, the vestibular
system via the vestibular nuclei, the blood through the chemoreceptive trigger zone, and the GI periphery by way of the vagal
nuclei.

VOMITING SYNDROMES
Regurgitation Cyclic Vomiting Syndrome
 Rumination Superior Mesenteric Artery Syndrome
Bulimia

(FOR THE EXAM FAMILIARIZE/MEMORIZE THE TABLES)

Table 38-1: DIFFERENTIAL DIAGNOSES OF VOMITING IN THE PEDIATRIC GROUPS

NEONATES INFANTS CHILDREN ADOLESCENTS

Congenital Gastroenteritis, GER/GERD, Gastroenteritis, Systemic Gastroenteritis, Systemic infection,

Obstructive Overfeeding, Milk allergy, infection, GERD, Food Gastritis, Peptic ulcer, Food intolerance,
Malformations Respiratory infection, intolerance, Medications, Appendicitis, Hepatitis, Biliary colic,
(atresia, webs of Systemic infection, Otitis Media, Gastritis, Peptic ulcer, Caustic Pancreatitis Caustic ingestion, Increased
esophagus /intestine) Acquired or Milder obstructive ingestion, Hepatitis, Achalasia, ICP, Migraine, Cyclic vomiting,
Systemic infection lesion (pyloric stenosis, Constipation, Increased ICP, Psychogenic vomiting
Hirschsprung disease malrotation, volvulus, Otitis media, Psychogenic Pregnancy, Otitis Media
Inborn error of metabolism intussusception vomiting, Cyclic vomiting,
Inborn errors of metabolism Endocrine metabolic disorders
IEM can be seen only to neonates and infants
ABDOMINAL PAIN

Occurs from 1 to 3 neural pathways: 
Establish whether the pain is:
-Visceral -Emergent or non- emergent
-Somatic pain -Acute or chronic
-Referred pain -Organic or functional
Good history and PE can rule in/rule out for the acute abdomen. When in
doubt, refer to surgery.
Table 38-2: COMMONLY ENCOUNTERED CAUSES OF EMERGENT ABDOMINAL PAIN IN CHILDREN

GASTROINTESTINAL CAUSES NON-GASTROINTESTINAL CAUSES

Appendicitis, Intussusception- telescoping, Pyelonephritis- - flank tenderness, Renal calculi,
Malrotation with volvulus, Strangulated hernia, Uteropelvic junction obstruction, Psoas abscess,
Cholelithiasis, Cholecystitis, Pancreatitis, Rupture of ovarian cysts,
Henoch – Schonlein Purpura- decreased platelet count Tubo-ovarian abscess,
Ectopic pregnancy

Table 38-3: ORGANIC CAUSES OF ABDOMINAL PAIN IN CHILDREN BASED ON THE REGIONAL LOCATION
RIGHT UPPER QUADRANT EPIGASTRIUM LEFT UPPER QUADRANT

Gastritis, PUD, Cholecystitis, Cholangitis, Hepatobiliary Disorders, Gastritis, PUD, Esophagitis,

Cholelithiasis- Murphy’s sign, GERD, Esophagitis Gastritis, Pneumonia, Splenic infarction,
Pneumonia- right lower lobe, Peritonitis PUD,Pancreatitis Hemorrhage, trauma

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PERIUMBILICAL AREA
Gastroenteritis, Intussusception - telescoping, Intestinal Parasitism, Lactose intolerance, Appendicitis, Peritonitis
RLQ HYPOGASTRIUM LLQ

Appendicitis- may start from epigastium to Cystitis, bladder anomalies, Sigmoid Pyelonephritis, renal calculi, Ureteropelvic junction
RLQ, Mesenteric adenitis, Merckel’s volvulus, PID obstruction, Ovarian torsion, cyst, abscess, PID
diverticulitis, Pyelonephritis, renal calculi,
Uteropelvic junction obstruction Ovarian torsion,
Cyst, abscess Pelvic inflammatory disease (PID)

Table 38-4: SOME ALARM SIGNS AND SYMPTOMS IN THE EVALUATION OF ABDOMINAL PAIN

ALARM SYMPTOMS ALARM SIGNS

Pain that awakens the child from sleep GI blood loss, Abdominal tenderness,
Persistent pain, Dysphagia, Persistent vomiting, Presence of mass or organomegaly
Unexplained fever, Chronic severe diarrhea Tenderness over the costovertebral angle or spine,
Involuntary weight loss and/or deceleration of linear Perianal abnormalities
growth, Delayed puberty, Family history of PUD/ IBD Arthritis

 Can be due to fluid, air or solid mass

 Air or fluid- can be generalized or localized
 Proposed theories in the formation of ascites in cirrhosis
- UNDERFILL THEORY
- OVERFILL THEORY
- PERIPHERAL ARTERIAL VASODILATION THEORY

CAUSES OF ABDOMINAL MASSES IN CHILDREN BASED ON REGIONAL LOCATION

RUQ EPIGASTRIUM LUQ

Hepatomegaly, hepatitis, hepatic tumor, Gastric volvulus, gastric bezoar, Splenomegaly, splenic tumors
Cholecystitis, Hydrops of the gall bladder, gastric tumor, Pancreatic
Choledochal cyst, cyst/pseudocyst
Pyloric stenosis, duodenal atresia, intestinal
R-MID PERIUMBILICAL AREA L-MID

Wilm’s tumor, Hydronephrosis, polycystic kidney Mesenteric cyst, omental cyst, Wilms tumor, hydronephrosis, polycystic kidney disease,
disease, renal vein thrombosis, ectopic kidney, Midgut volvulus, intestinal renal vein thrombosis, ectopic kidney
Neuroblastoma, pheochromocytoma, adrenal duplication, Fecal masses Neuroblastoma, pheochromocytoma, adrenal
hemorrhage, adrenal tumor Lymphangioma, GI tuberculosis hemorrhage, adrenal tumor

RLQ HYPOGASTRIUM LLQ

Intussusception, intestinal abscesses, inguinal Distended/obstructed bladder, Fecal masses Sigmoid volvulus, intestinal abscess,
hernia, duplication cyst, GI tuberculosis, Fecal masses, Pregnancy, inguinal hernia, Lymphoma, Ovarian cyst/torsion/tumors,
Lymphoma Fecal masses, Ovarian hydrocolpos, hydrometrocolpos undescended testis, Ectopic pregnancy
cyst/torsion/tumors, undescended testis, Ectopic
pregnancy

DISORDERS OF THE ESOPHAGUS, STOMACH AND DUODENUM

GER/ GERD Acid peptic disease
Reflux Esophagitis Hypertrophic pyloric stenosis
Caustic injuries Malrotation and other duodenal obstruction

Esophageal atresia and thracheoesophageal fistula Functional abdominal pain

Cyclic vomiting syndrome Necrotizing enterocolitis
Hirschsprung disease

GASTROESOPHAGEAL REFLUX AND GASTROESOPHAGEAL REFLUX DISEASE

 GER refers to the passage of gastric contents into the esophagus with or without regurgitation
▪ GERD denotes troublesome symptoms and/or complications caused by persistent reflux of gastric contents
▪ Reflux is considered physiologic if it is brief, effortless, and non-projectile, occurring several times during the day that lasts less than 3
minutes and is seen in normal infants, children, adolescents and adults
▪ Pathologic reflux, on the other hand, is described as frequent and persistent episodes of reflux which are bothersome.

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GASTROESOPHAGEAL REFLUX 1. PROTON PUMP INHIBITORS (PPIS) AND HISTAMINE-3

 The primary mechanism of GER in most circumstances is transient RECEPTOR ANTAGONISTS (H2RAS) – for gastric antisecretion
relaxation of the lower esophageal sphincter (LES) unaccompanied by TABLE 38-10: RECOMMENDED DOSAGE FOR ACID
swallowing, which allows gastric contents to flow into the esophagus.
Main stimulus SUPPRESSANTS IN PEDIATRIC GERD
DRUG DAILY DOSE FREQUENCY
 LES relaxation is gastric distention usually in a postprandial
setting, delayed gastric emptying, or even air swallowing
Other factors Omeprazole 1 mg/kg/day OD
 LES relaxation includes increased physical movement, straining,
obesity, coughing and wheezing Esomeprazole 1-11 yrs old: 10 mg(<20 OD
 Minority of cases, reflux episodes occur due to failure of the LES kg)
pressure to increase in response to a sudden increase in intra- 20mg (>20 kg)
abdominal pressure or when the resting pressure of the LES is 12-17 yrs old: 20-40 mg
chronically decreased
Lansoprazole <30 kg: 15 mg OD
GASTROESOPHAGEAL REFLUX DISEASE >30 kg: 30 mg
 The pathogenesis of GERD is a consequence of alterations in protective
mechanisms which permit physiologic GER to develop into a pathologic Ranitidine 5-10 mg/kg BID/TID
event (or GERD)
Factors:
Famotidine 1 mg/kg BID
 Insufficient esophageal clearance
 Deficient buffering of acidic refluxed material
 Aberration in the repair of damaged epithelium
 Delated gastric emptying 2. ANTACIDS
 Decrease in the GIT neural protective reflexes  Buffering of gastric contents with the use of antacids (e.g.
aluminum hydroxide and magnesium hydroxide) has been the
Clinical manifestations: traditional approach used in the treatment of GERD
While GER characteristically presents as regurgitation, clinical  When taken on demand can provide rapid but transient relief of
manifestations of GERD vary with age, with infants being most reflux symptoms
difficult to evaluate  Long term is not recommended as side effects in the form of
Symptoms description are unreliable for children under 9 years of osteopenia, microcytic anemia, rickets, neurotoxicity, among
age others, have been reported.
Excessive regurgitation, feeding refusal, unexplained crying or 3. MUCOSAL SURFACE PROTECTION
fussiness, and discomfort with spitting up are among the reported  Mucosal surface protective agents in the form of sucralfate (a
compound containing sucrose, sulfate, and aluminum) act by
symptoms of GERD in infants creating a gel that attaches to the erosive mucosa, promoting
relief of symptoms and healing of esophagitis
 Safety and efficacy in infants and children is not yet established
Toddlers and Children upto 8 y/o 4. PROKINETIC AGENTS (METOCLOPRAMIDE,
- Feeding refusal DOMPERIDONE, ERYTHROMYCIN, CISAPRIDE, BACLOFEN)
- Regurgitation  act by increasing the LES Pressure, promoting gastric emptying,
- Abdominal pain enhancing esophageal/intestinal peristalsis
- Choking  metoclopramide, an antidopaminergic agent with
- Gagging cholinomimetic and mixed serotonergic effects, has been
- Coughing  observed to cause lethargy, irritability, extrapyramidal symptoms,
- Weight loss or poor weight gain may also be a presenting gynecomastia and galactorrhea in infants and children
manifestation especially in young children  domperidone, also an antidopaminergic agent, while not
known to cross the blood-brain barrier, has been linked
Older Children (9-17 years) occasionally with extrapyramidal reactions. Cardiac
-Characteristically exhibit the “typical reflux syndrome” (heartburn arrhythmias in
with or without regurgitation)
- Heartburn is defined as a burning sensation in the retrosternal area REFLUX ESOPHAGITIS
- Other symptoms:  The underlying transient LES relaxation brings about reflux and
Vomiting exposes the distal end of the esophagus to prolonged mucosal
contact with gastric and duodenal fluids, such as gastric acid,
Coughing pepsin trypsin, and bile
Epigastric pain  The resultant esophageal inflammation provokes a reduction in
Management esophageal peristalsis, which triggers a vicious cycle of further
esophageal exposure and esophagitis
Positioning  The ensuing esophagitis produces further reduction in LES pressure
 Prone positioning with SDS precautions (less than 1 y/o) and aggravates the existing incompetent LES.
 As right lateral decubitus position promotes gastric emptying, a  Diagnosis is often based on clinical grounds
change to the lateral position may be adopted to infants with  No single test exists at present to establish the diagnosis
 GERD is assumed when investigations reveal excessive reflux and
GERD esophagitis in the absence of other possible diagnoses

Medications  Barium Contrast Radiography (Esophagram or Upper GI

 Pharmacologic therapies primarily consist of acid suppression
through gastric antisecretion, acid buffering, mucosal surface
protection, and prokinetic therapy
series) -useful to detect/ rule out anatomic abnormalities (pyloric
stenosis, malrotation, hiatal hernia, esophageal stricture)
 Esophageal pH monitoring is a tool used to measure the
frequency and duration of acid reflux episodes
o Offers the advantage of determining the temporal association
of acid reflux and symptoms and assessing the effectiveness of
esophageal clearance mechanisms

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o Using the conventional transnasal placement or the newer
device of clipping wireless sensors into the esophageal mucosa
on endoscopy, 1 or more pH electrodes are connected to the
distal end of esophagus. A drop in intraesophageal pH to less
than 4.0 is considered a significant acid reflux episode
 Multiple intraluminal impedance (MII) is used to determine
the movement of solids, fluids and gas in the esophagus. It
measures the changes in electrical impedance or resistance
between different electrodes placed along the esophagus. A
significant finding is detected when the impedance of a liquid bolus
appearing first in the distal esophagus is sequentially noted in the
proximal esophagus
 Nuclear scintigraphy involves the instillation of 99Technetium-
Labelled food or milk into the stomach and subsequent scanning of
the stomach, esophagus and lungs
 Esophagogastroduodenoscopy (EGD) (most commonly
used) allows for direct inspection of the esophageal mucosa. It can
demonstrate the presence and severity of complications related to
GERD such as esophagitis. Strictures and Barrett’s esophagus
o More invasive and requiring sedation in younger patients limits
its use in the diagnosis of GERD
o EGD is only recommended when symptoms do not abate after
2-4 weeks of appropriate treatment or when symptoms recur
after discontinuation of treatment can also be used for
biopsy
 The primary goals in the treatment of GER/GERD compromise the
following:
o Relief of symptoms
o Promotion of normal growth’
o Healing of inflammation caused by refluxed gastric contents
o Prevention of complications associated with chronic reflux
 Parental education, guidance & support may be sufficient to manage
healthy, thriving infants with physiologic GER
 Other infants may require treatment options consisting of lifestyle
changes, pharmacologic therapies and surgery
 Lifestyle changes include feeding and dietary modifications and
positional therapy. For infants and small children,feeding practices
need to be checked as large feeding volumes have been
demonstrated to promote reflux, likely by increasing the frequency of
transient LES relaxation, care should be observed that a reduction in
volume should not compromise energy intake. Increasing the caloric
density of the feeds may be resorted to when feeding volume or
frequency is significantly reduced.
 Mode of thickening of feeds (e.g., 1 tbsp rice cereal per ounce of
milk), while it has not reduced the frequency of reflux episodes, has
been demonstrated to decrease the frequency of overt regurgitation
and the height of reflux in the esophagus
 Termination of breastfeeding is therefore not necessary. For non-
breastfed infants, extensively hypoallergenic formula may be tried
for 4 weeks. Caution should be taken as the use of soy protein and
the allergenicity of thickening agents have not been evaluated in the
treatment of GERD
 In children and adolescents, avoidance of chocolate, caffeine, alcohol
and spicy foods along with weight reduction and elimination of
exposure to smoke are recommended
CAUSTIC INJURIES
 National Poison Management and Control Center if the Philippine
General Hospital in collaboration with the Department of Health
reports an increasing trend in the number of patients younger than
18 years with caustic substance ingestion.
 The most common alkali that is accidentally ingested by Filipino
children is household bleach. It contains sodium hydrochlorite at a
concentration of 3%-6% with pH ranging from 8-10. Accidental
ingestion of a small amount of household bleach produces minimal
injury to the gastrointestinal tract
 Alkali- liquefaction necrosis
 Drain cleaners such as liquid sosa are powerful corrosive agents
and cause serious damage
 Extent of injury depends on the:
o pH (<2 and >12 are highly corrosive)
▪ strong alkali- liquefaction necrosis
▪ strong acid- coagulation necrosis
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✓ The ingestion of a strong alkali results in liquefaction necrosis which
is associated with deep penetration of bowel mucosa and may result in
perforation. Injury typically involves the esophagus but gastric injury
may also occur. Absorption of caustic alkali may result in thrombosis of
blood vessels, which further impedes blood flow to already damage
tissues
COMMON HOUSEHOLD CORROSIVE PRODUCTS AND THEIR
CONTENTS AVAILABLE IN THE PHILIPPINE MARKET
CAUSTIC AGENT COMMERCIAL PRODUCTS
Sodium Hydrochlorite Domex Household Bleach
Greenex All-purpose Cleaner
Zonrox Household Bleach
Sodium Hydroxide Gleam Liquid Sosa
Zim Liquid Sosa
Alkyl dimethyl ammonium Lysol Disinfectant Concentrate
chloride Mr. Muscle Power All-purpose cleaner
Pine Sol Disinfectant Cleaner
Hydrochloric acid Apollo Muriatic Acid (29% maximum
HCl acid)
Cl Muratic Acid (29% maximum HCl
acid)
Duck Power Toilet Bowl cleaner
Gleam Muriatic Acid (15% HCl acid)
Lysol Toilet Bowl Cleaner
Mr. Muscle Power Toilet bowl cleaner
Hydrochloric acid and Mighty Toilet Bowl Cleaner
phosphoric acid
Volume o Form
1) Granular form – higher rate of injury and adherence in
narrowed areas
2) Solid form – adheres to the mouth and pharynx greatest
damage in this area hence sparing the esophagus
3) Liquid form – rapid transit from mouth to pharynx
greatest damage on the esophagus and stomach
4) Concentration of the substances
5) Nature of ingestion (accidental or intentional)
✓ The most common presenting symptoms following caustic ingestion
are dysphagia, drooling, feeding refusal, retrosternal pain, abdominal
pain and vomiting. Rarely, a patient may present with gastric perforation
 In the acute phase, plain chest radiograph may reveal air in the
mediastinum, suggesting esophageal perforation.
 Likewise, free air under the diaphragm may indicate gastric
perforation. Both necessitate immediate surgical intervention.
 In the initial stage, gastric lavage and induced emesis are
contraindicated because of re-exposure of the esophageal mucosa
to the corrosive agent and the risk of perforation
 NGT should be inserted without visual inspection
 Perforation when severe ulceration is present. These tubes may be
beneficial in patients with severe circumferential burns as the
presence of a stent can keep the esophagus patent when the
development off strictures is anticipated as in alkali ingestion.
 Expectant therapy is advised for patients with a questionable
history of ingestion who do not present with any signs or
symptoms. Endoscopy may be withheld in these patients and intake
of liquids followed by a regular diet is allowed. If dysphagia
subsequently occurs between 2-8 weeks following ingestion, barium
swallow is done to rule out the presence of esophageal stricture
 In esophageal injuries due to alkali, prolonged and continuing
damage to the esophageal wall may be present such that
perforation may occur several days after ingestion. Pharyngeal and
oral burns may also cause aspiration due to impaired swallowing
reflexes
 If the upper GI tract is affected with significant mucosal but non-
transmural injuries, a jejunostomy tube may be inserted so that
enteral nutrition may be commenced while awaiting healing of the
gastric burns
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CYCLIC VOMITING SYNDROME provided with the use of ketorolac or narcotics such as morphine
 Cyclic vomiting syndrome (CVS) is a disorder characterized by or fentanyl. Symptomatic treatment for epigastric pain (like PPI
cycles of nausea and vomiting lasting for several hours or
days with intervening periods of wellness or H2Ras), diarrhea (such as antidiarrheals) and hypertension
 Defined by symptom-based criteria and the absence of significant (like captopril) may be administered.
laboratory, radiologic and endoscopic findings Complications
 Each episode can have a predictable clinical course  Complications in patients with CVS relate to the nature of the
 They type, onset of symptoms, severity and duration of symptoms condition; namely, dehydration and electrolyte imbalance due to
the vomiting and poor intake; esophagitis due to the exposure of
are almost identical with each other the esophagus to the acid/bile during the vomiting and acid
 It can be so severe to alter the lifestyle of affected individuals exposure leading to esophageal irritation; and bleeding, which
 Most patients outgrow the condition may lead to Mallory Weiss Tears
 Exact mechanism remains to be fully illlucidated Prevention
 Known trigger factors: infection, stress, excitement, anxiety,  Avoidance of known triggers may be helpful in preventing
allergies, hot weather, motion sickness, exhaustion, menstruation episodes of CVS. Lifestyle modifications like getting adequate
 Dietary triggers: chocolate, cheese sleep, downplaying excitement or anxiety, avoidance of trigger
 CVS has been linked to migraine HA, mostly with family history of foods, and eating meals at regular times may be helpful and
migraine practical.
 Other proposed mechanisms include ACID PEPTIC DISEASE
o Episodic dysautonomia  The cluster of conditions such as gastritis, duodenitis, and peptic
o Mitochondrial DNA mutations that cause deficits in cellular ulcer disease in childhood is the result of an imbalance between
mucosal defensive and aggressive factors
energy production and heightened hypothalamic stress  Aggressive factors in the form of acid and pepsin or decrease in
response that activates the emetic response host defenses such as bicarbonate, mucus, mucosal blood flow,
 The syndrome can affect any age group but is more commonly seen and cell turnover contribute to the development of disease.
among school-aged children, with a predilection for girls rather than
boys. the frequency of episodic attacks in a patient ranges from 1-  Most primary peptic ulcers in children are duodenal in nature and
70 per year but averages 12 in a year occur between the ages of 8-17 (mean age of 11.5 years)
 Secondary ulcer disease occurs at all ages, more often gastric in
Clinical Manifestation location
 Cycle begins on the same time, same duration of vomiting
 Male: female 1.5:1
 Severity reaches its peak on the 1st few hours the diminishes but  No sex difference in infants and young children
nausea remains until end of episode
 Episodes tend to end abruptly and are marked by fast recovery
to wellness, provided that the patient has not experienced any  Gastritis – a histologic diagnosis (inflammation of the gastric
major complication mucosa)
 Accompanying symptoms include pallor; weakness; increased  Peptic ulcers – discontinuities of the gastric or duodenal mucosa
salivation; abdominal pain; intolerance to noise, light and/or with penetration to the muscularis mucosae and exposure to the
odors; headache; loose stools; fever; increased heart rate; submucosa
 H. pylori infection – main cause of peptic ulcers in pediatric age
hypertension; skin blotching; and leukocytosis
 NSAID use – also a significant cause of ulcer
Diagnosis  No evidence on dietary factors
 There are no laboratory examinations that are helpful in  Familial clustering may be due to H. pylori infection
diagnosing CVS. Its diagnosis is made by exclusion of other  Cigarette smoking predisposes to ulcer formation by inhibiting
diseases or disorders that give rise to recurrent vomiting prostaglandin synthesis, hence comprising mucosal integrity
 In 2006, the Rome III criteria for Functional Gastrointestinal
Disorders for neonates, toddlers and children and adolescents CAUSES OF ACID PEPTIC DISEASE IN CHILDREN
defined CVS as the presence of 2 or more periods of intense
nausea and unremitting vomiting or retching lasting for hours to
days, with a return to the usual state of health which may
continue for weeks to months
Management
 Prophylactic measures include lifestyle changes such as
avoidance of excessive excitement, energy-depleted states
 (e.g. fasting, illness), sleep deprivation, triggering foods (like
cheese and chocolates), and motion sickness.
 However, if the episodes become more frequent, are severe to
warrant hospitalization and school absences, or fail to respond to
abortive therapy, preventive pharmacotherapy is recommended
 Pizotifen; B-Blockers like propranolol; and tricyclic
antidepressants such as amitriptyline. Other agents like
anticonvulsants (eg. Phenobarbital, valproic acid) and
supplementation like L-carnitine and coenzyme Q10 have also
been investigated
 During acute attacks, supportive and abortive strategies have to
be instituted. Supportive care includes the provision of a less
stimulating environment (i.e. dark and quiet); replacement of
fluids and electrolytes and energy; use of antiemetic with or
without sedation to lessen nausea and vomiting; and provision of
analgesia.
 Pharmacotherapy in this phase is based on expert opinion due to
lack of well-designed trials. To abort emesis, ondansetron has
been recommended.
 To sedate patients, medications such as diphenhydramine,
lorazepam and chlorpromazine have been utilized. Analgesia is

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CAUSES OF ACID PEPTIC DISEASE IN CHILDREN
MECHAINISM ETIOLOGY
Unknown
Infectious agents Primary Gastritis
Helicobacter pylori
Cytomegalovirus
Herpes simplex
Influenza A
Treponema pallidum
Candida albicans
Drugs Aspirin
NSAIDs
Valproic Acid
Dexamethasone
Chemotheraphy
Alcohol
Physical agents Corrosives
Bile acid gastropathy
Exercise induced
Radiation gastropathy
Stress Critical condition/ multiple trauma
Neurosurgery
Hepatic insufficiency/ cirrhosis
Immunologc/ allergic factors Eosinophilic gastritis/ allergic
gastritis
Graft versus host disease

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Henoch-schonlein gastritis
Celiac disease
Granulomatous inflammation Foreign body reaction
Sarcoidosis
Hisitocytosis X
Tuberculosis
Crohn disease
Hyoersecretory states Zollinger- Ellison syndrome
G-cell hyperplasia/ hyperfunction
Cystic fibrosis
Hyperthyroidism
Short bowel syndrome
Renal failure

 Infants and young children: vomiting, hematemesis or melena
 Older children and adolescents: combination of abdominal pain,
vomiting and nocturnal awakening; temporal relationship meals
occur in only 50% of cases
 GI bleeding may occur
 25% may have subclinical presentation
 Others: anorexia, early satiety, recurrent vomiting and anemia
 Epigastric tenderness alone does not always correlate with PUD.
However, when epigastric pain is accompanied by hematemesis,
melena and weight stagnation, the combination of findings is
significantly associated with ulcers or erosions
Diagnosis
 Mainstay of diagnosis: detailed history and PE along with some
diagnostics
 UGIS with contrast: define gross mucosal changes in the stomach
 Plain abdominal XRay: can detect subdiaphragmatic free air in
cases of perforated PUD
 The definitive diagnosis is made via upper gastrointestinal
endoscopy. It provides direct visualization of the lesion and
biopsies may be taken for histologic examination
 Under sedation or general anesthesia and preferably while off acid
suppression for at least 2 weeks
 H. pylori-related gastritis or ulcer, the gold standard for diagnosis is
the histologic demonstration or isolation by bacteriologic culture of
the organism
o Repeat endoscopy with culture and sensitivity testing,
including alternate antibiotics if not previously performed
o Fluorescence in situ hybridization (FISH) on previous paraffin-
embedded biopsies if clarithromycin susceptibility testing was
not done before
o Modification of treatment through the addition of another
antibiotic (quinolones) or bismuth, or increase in the dose
and/or duration of treatment
HYPERTROPHIC PYLORIC STENOSIS
 a well-described cause of gastric outlet obstruction.
 non-bilious projectile vomiting in 2-4 weeks old, so if bilious na
sya after na sya ng 2nd part of the duodenum kasi dun
lumalabas yung bile
 common among the white race 2-4; 1,000
 rare in Filipinos and other Asians
 usually before the 2nd month of life, with prominent postprandial
vomiting in an otherwise healthy infant
 non-bilious to coffee-ground with the baby becoming emaciated and
dehydrated despite a voracious appetite
 in a quiet infant, palpable olive-shaped mass at epigastric or RUQ
area
 gastric peristaltic waves may be visible

Treatment
Goal of therapy
 Relief of symptoms
- Acid suppression (PPIs, H2 receptor Antagonists)
 Enhancement of ulcer healing in the affected mucosa
- Buffering therapy
- Mucosal protectives – sucralfate
 Prevention of recurrence
 Treatment specific to the underlying cause of mucosal injury
 NSAID related disorders – D/C NSAIDs
 H. pylori-related – antibiotics
 The first line treatment of H. pylori gastritis consists of any of the
following combinations: X-RAY Result
PPI (1 mg/kg/day up to 20 mg twice daily) +
Amoxicillin (50 mg/kg/day up to 1 g twice daily) Diagnosis
+ Imidazole (20 mg/kg/day up to 500 mg twice  palpation of the hypertrophied pylorus
daily)  UGIS: shows the enlarged stomach with delayed gastric emptying
PPI + Amoxicillin + Clarithromycin (15 mg/kg/day up to 500 time and an elongated narrow pyloric channel referred to as the
mg twice daily) string sign.
Bismuth salts + Amoxicillin + Imidazole For 7 to 17 days  Ultrasonography, which has become the gold standard in
diagnosing HPS, demonstrates the pylorus that is generally
 Sequential therapy may be employed consisting of a PPI + >3.5mm in thickness and >15mm long. While this is the ideal
amoxicillin for 5 days. Followed by 5 days of triple drug (PPI + imaging modality due to non-exposure to radiation, it is largely
clarithromycin + metronidazole) operator-dependent.
 Successful eradication may be monitored using stool antigen
detection test since the absence of signs and symptoms following
treatment does not necessarily imply adequacy of treatment. Treatment
Endoscopic follow-up is not necessary  Rehydration and correct electrolyte abnormalities prior to surgery.
 In cases of treatment failure, one of the following option is  The surgical procedure is the Ramstedt-fredet pyloromyotomy,
recommended: which essentially entails an incision of the full thickness of the
pyloric muscle while keeping the mucosa intact.
 Feeding may be started 6-12 hours after surgery in most patients.
The postoperative course is usually uneventful and the patients are
discharged 3-4 days after surgery

MALROTATION AND OTHER DUODENAL OBSTRUCTION

 yung mga congenital abnormalities magmamanifest na sila
newborn up to 1 month

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 whe you start feeding, makikita mo na ang problem.
 Failure to complete the normal sequence of events known as
malrotation. Several underlying mechanisms bring about intestinal
obstruction.
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 Due to the narrowed mesentery, the entire small bowel may twist
around the superior mesenteric artery, leading to volvulus
formation and intestinal gangrene.
 This is the most dreaded complication of malrotation. Ladd’s bands
or attachments of the colon to the retroperitoneum may also cause
extrinsic luminal compression.
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Suspected in neonates with bilious vomiting.
Diagnosis
Treatment
 XRAY: may be normal or paucity of bowel gas, double-bubble
sign indicated complete obstruction and possible duodenal
atresia.
Treatment
Surgery
 4 or more stool motions per day or 2 or less stool motion per week;
 An explanation of the condition, confirmation and reassurance may
S-Stomach
D- Duodenum
ex. patient came in, distended abdomen, vomited fecal
material, no bowel sounds kahit normal yung x-ray…
investigate kasi alamo mo na baka may malrotation!
FUNCTIONAL ABDOMINAL PAIN
 rule out possible reasons.
 Abdominal pain with no visible or detectable abnormality after
thorough physical examination and appropriate tests have been
performed.
 Conventionally referred to as recurrent abdominal pain (RAP)
suggesting its persistent and intractable nature, the condition can
cause distress to patients and their parents, significantly impairing
their quality of life
 Based on the Rome III Criteria for Childhood Functional
Gastrointestinal Disorders, there are 5 abdominal pain- related
functional gastrointestinal disorders (FGID:
o Functional dyspepsia
o Irritable bowel syndrome
o Abdominal migraine
o Childhood functional abdominal pain
o Childhood functional abdominal pain syndrome (FAPS)
 There are 4 mechanism proposed to explain the development of
visceral hypersensitivity following early life pain or stress:
1. Sensitization of central (spinal) neurons
2. Sensitization of primary sensory neurons
3. Impaired stress response (HPA axis)
4. Altered descending inhibitory control
 These can lead to enhanced neurotransmission, increased neuronal
spontaneous activity and decrease firing threshold.
 Atleast once/week for 2 months pero dapat normal ang
findings.
 Based on the Rome III Criteria, abdominal pain-related FGID,
except for abdominal migraine, present with a set of clinical
manifestations, which should be observed at least once per week
for at least 2 months before the diagnosis is made:
FUNCTIONAL
DYSPEPSIA Patient must experience all of the
following:
1. Persistent or recurrent pain or discomfort centered in the upper
abdomen (above the umbilicus).
2. Pain not relived by defecation or associated with a change in stool
frequency or stool form.
3. No evidence of an inflammatory, anatomic, metabolic or neoplastic
process that explains the subject’s symptoms.
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“Smooth seas do not make skilful sailors”
Avoidance of food such as fatty or spicy foods r drugs like NSAIDs is
recommended. For pain predominant symptoms, anti-secretory agents
like H2 blockers or PPIs may be given while for those with discomfort,
prokinetic agents like domperidone or erythromycin may be considered.
These treatment strategies have not been validated in well-controlled
clinical trials.
IRRITABLE BOWEL
SYNDROME All of the following must present:
1. Abdominal discomfort associated with 2 or more of the following at
least 25% of the of the time: improvement with defecation, onset
associated with a change in frequency of stool, or onset associated
with change in the form or appearance of stool.
2. No evidence of an inflammatory, anatomic, metabolic or neoplastic
process.
lumpy/ hard or loose/watery stools, with straining, urgency or feeling of
incomplete evacuation; passage of mucus; and bloating or feeling of
abdominal distention.
already be therapeutic. The use of peppermint oil has not been
absolutely proven to be helpful in children
CHILDHOOD FUNCTIONAL ABDOMINAL
PAIN The following features must be present:
 Episodic or continuous abdominal pain
 Insufficient criteria for other FGID
 No evidence of an inflammatory, anatomic, metabolic or neoplastic
process that explains the subject’s symptoms
 the symptoms must be present at least 25% of the time with 1 or
more of the following:
 some loss of daily functioning
 additional somatic symptoms like headache, limb pain or
difficulty in sleeping
 for both childhood FAP and FAPS, reassurance and explanation of
the possible mechanisms behind the conditions may be helpful.
Amitriptyline, an antidepressant, does not appear to provide any
benefit.
ABDOMINAL MIGRAINE
The following must be present 2 or more times in the last 12 months
before the diagnosis can be made based on the Rome III criteria:
 paroxysmal episodes of intense, acute periumbilical pain lasting for
an hour or more
 intervening periods of usual health lasting weeks to months
 pain interfering with normal activities
 pain associated with 2 or more of the following:
o anorexia
o nauseas o
vomiting o
headache
o photophobia
o pallor
 No evidence of an inflammatory, anatomic, metabolic or neoplastic
process that explains the subject’s symptoms
Treatment
Avoiding potential food-related triggers (such as those with caffeine,
nitrates and amines) and emotional stress, fasting, travel, flickering or
glaring lights may work. Prophylaxis using pizotifen, propranolol,
cyproheptadine, or sumatripan may be used but experience with these
agents is based on very limited data.
NECROTIZING ENTEROCOLITIS
 Feared complication in NICU
 Affect all infants, however 90% of cases, higher risk are PT (<35
weeks) and low BW (<1,000 grams)
 The exact cause of NEC is unknown, but it is widely
accepted that combination of impaired mucosal barrier,
pathogenic bacteria and feeding with milk formula are
inciting fac
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 PT gut have
o Impaired cellular and humoral immunity
o Decreased gastric acid secretion
o Immature villi
 Hypoxia, hypotension may contribute to mucosal injury and ischemia
o Milk formula feeds, apart from being hyperosmolar, also
lack the beneficial components of breast milk such as
trophic hormones, vitamins and immune mediators
Clinical manifestations
 NEC is suspected in a preterm neonate who develops feeding
intolerance manifested as vomiting or increased gastric residual in
those who are fed by tube/ the abdomen becomes distended, and
the neonate may have decreased stool frequency.
 Fecal occult blood becomes positive, indicating mucosal sloughing.
With the progression of ischemia and sepsis, the abdomen becomes
increasingly distended, and gross blood may be seen in stools

-MODIFIED BELL STAGING FOR NEC

CLINICAL RADIOLOGI
STAGE FINDINGS C PHYSICAL
FINDINGS FINDINGS

I ileus Increased gastric

(Suspect) residuals,
positive fecal
Apnea, bradycardia, occult blood, mild
temperature abdominal
instability distention Treatment
II-A Apnea, bradycardia, Ileus, dilated Gross fecal occult  The modified bell staging (table 38-27) is useful in determining the
(Definite) temperature bowel loops, blood, management of a patient with NEC
instabilit  Patient who is suspected to have NEC is placed on NPO with gastric suction,
y focal abdominal and broad-spectrum antibiotics are initiated
pneumatosis distention  The common dilemma is the decision regarding the precise time for
surgical intervention in a very sick neonate, i.e. when bowel gangrene
II-B Thrombocytop Generalized, Abdominal wall or perforation is present, and not any time before that.
enia, mild penumatosis, edema,  Paracentesis is advocated in patients who present with ascites to
metabolic portal vein gas, tenderness, determine if bowel compromise has ensued. There is always a risk of
acidosis ascites palpable bowel causing bowel injury and bleeding, particularly in those who are
thrombocytopenic
III-A Mixed acidosis, Prominent Worsening wall  Laparotomy is indicated when pneumoperitoneum or bowel gangrene is
suspected
(advance oliguria, bowel loops, edema,
d) hypotension, increased erythema,  If an infant is deemed too unstable for a laparotomy, peritoneal drainage may
be performed at bedside.
coagulopathy ascites, no free induration

III-B Pneumoperiton
eum
Shock, disorientation Intestinal
of vital signs and perforation
laboratory values

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