LO 1

ANATOMY AND HISTOLOGY GASTER

- DUODENUM
 Gaster = Venticulus = Stomach
• Esophagus – Duodenum
• As shelters of food to be digested become
“chyme”
• Regulate the flow of digested food into the small
intestine
• Capacity: ± 1.5 liters, can be dilated un til 2-3
liters
• The stomach capacity of newborn baby: ± 30 cc
• The most common is J-shaped
 Surface Anatomy of the Stomach
• In the supine position, the stomach commonly
lies in the right and left upper quadrants, or
epigastric, umbilical, and left hypochondriac
and lumbar regions.
 Figure 2.30. Abdominal part of esophagus and stomach.
A. The stomach and the greater and lesser omenta are shown. The left part
of the liver is cut away so that the lesser omentum and the omental foramen
(entrance to omental bursa) can be seen. The extent of the intact liver is
indicated by a dotted line. The stomach is inflated with air.
 Figure 2.30. Abdominal part of esophagus and stomach.
B. The internal surface (mucous membrane) is demonstrated. The longitudinal gastric folds, or
rugae, disappear on distension. Along the lesser curvature, several longitudinal mucosal folds
extend from the esophagus to the pylorus, making up the gastric canal along which ingested
liquids pass. C. The pylorus is the significantly constricted terminal part of the stomach. The pyloric
orifice is the distal opening of the pyloric canal into the duodenum.
The muscle layers of the oesophageal
and gastric walls
Figure 2.19. Principal formations of peritoneum.
Figure 2.19. Principal formations of peritoneum.
Arterial Supply to Stomach
 Rami Esophageales
A. Gastrica
sinistra Cabang ke
lambung
Arteriae gastrica
breves
Cabang-cabang ke
A. Splenica dalam lien
Truncus Arteria Gastro-
Celiacus omentalis sinistra
A.
Pancreaticoduodenalis
A. superior
Gasroduodenalis
A. Gastro-omentalis
A. Hepatica dextra
communis Arteria gastrica dextra
A. Hepatica
A. Hepatica sinistra
propria
A. Hepatica dextra
Veins of stomach, duodenum, and spleen
 Small Intestine
• Consisting of the duodenum, jejunum, and
ileum,
• Primary site for absorption of nutrients from
ingested materials
• extends from the pylorus to the ileocecal
junction where the ileum joins the cecum (the
first part of the large intestine).
 DUODENUM
• The duodenum, the first and shortest (25 cm) part of the
small intestine, is also the widest and most fixed part.
• The duodenum pursues a C-shaped course around the head
of the pancreas.
• The duodenum begins at the pylorus and ends at the
duodenojejunal junction. This junction occurs
approximately at the level of the L2 vertebra, 2-3 cm to the
right of the midline. The junction usually takes the form of
an acute angle, the duodenojejunal flexure.
• Most of the duodenum is fixed by peritoneum to structures
on the posterior abdominal wall and is considered partially
retroperitoneal.
• The duodenum is divisible into
four parts:
a. Superior (first) part: short
(approximately 5 cm) and lies
anterolateral to the body of the
L1 vertebra.
b. Descending (second) part: longer
(7-10 cm) and descends along
the right sides of the L1-L3
vertebrae.
c. Horizontal (third) part: 6-8 cm
long and crosses the L3 vertebra.
d. Ascending (fourth) part: short (5
cm) and begins at the left of the
L3 vertebra and rises superiorly
as far as the superior border of
the L2 vertebra.
 Pars Superior Duodeni
• The first 2 cm of the superior part of the duodenum,
immediately distal to the pylorus, has a mesentery and is
mobile. This free part, called the ampulla (duodenal cap).
• The distal 3 cm of the superior part and the other three
parts of the duodenum have no mesentery and are
immobile because they are retroperitoneal.
• The superior part of the duodenum ascends from the
pylorus and is overlapped by the liver and gallbladder.
• Peritoneum covers its anterior aspect, but it is bare of
peritoneum posteriorly, except for the ampulla.
• The proximal part has the hepatoduodenal ligament (part
of the lesser omentum) attached superiorly and the greater
omentum attached inferiorly.
 Pars Descendens Duodeni
• The descending part of the duodenum runs inferiorly,
curving around the head of the pancreas.
• Initially, it lies to the right of and parallel to the IVC
(inferior vena cava).
• The bile and main pancreatic ducts enter its
posteromedial wall. These ducts usually unite to form
the hepatopancreatic ampulla, which opens on the
summit of an eminence, called the major duodenal
papilla, located posteromedially in the descending
duodenum.
• The descending part of the duodenum is entirely
retroperitoneal.
 Pars Inferior (horizontal) Duodeni
• The inferior or horizontal part of the duodenum runs
transversely to the left, passing over the IVC, aorta, and L3
vertebra.
• It is crossed by the superior mesenteric artery and vein and
the root of the mesentery of the jejunum and ileum.
• Superior to it is the head of the pancreas and its uncinate
process.
• The anterior surface of the horizontal part is covered with
peritoneum, except where it is crossed by the superior
mesenteric vessels and the root of the mesentery.
• Posteriorly it is separated from the vertebral column by the
right psoas major, IVC, aorta, and the right testicular or
ovarian vessels.
 Pars Ascendens Duodeni
• The ascending part of the duodenum runs superiorly to reach the
inferior border of the body of the pancreas.
• Here it curves anteriorly to join the jejunum at the duodenojejunal
junction, supported by the attachment of a suspensory muscle of
the duodenum (ligament of Treitz).
• This muscle is composed of a slip of skeletal muscle from the
diaphragm and a fibromuscular band of smooth muscle from the
third and fourth parts of the duodenum.
• Contraction of this muscle widens the angle of the duodenojejunal
flexure, facilitating movement of the intestinal contents. The
suspensory muscle passes posterior to the pancreas and splenic
vein and anterior to the left renal vein.
Artery of duodenum
Veins of stomach, duodenum, and spleen
JEJUNUM - ILEUM
• Jejunum
– begins at the
duodenojejunal flexure
where the alimentary
tract resumes an
intraperitoneal course
• Ileum
– ends at the ileocecal
junction, the union of
the terminal ileum and
the cecum
 Gaster
• Cardiac
• Corpus
• Fundus:
T. Mucosae
1. Columnar surface epithelium
2. Gastric foveolae
3. T.propria+fundus glands
4. Elastic membran
5. T. M. Mucosae
T. Submucosae
• Pyloric
T. Mucosae
1. Columnar surface epithelium
2. Gastric foveolae (wide and deep)
3. T.propria+pyloric glands
4. Elastic membran
5. T. M. Mucosae
T. Submucosae
T.muscularis
Fundus
Pyloric
 Duodenum
A. T. mucosae
1. Vili
2. Columnar surface epithelium+goblet cell
3. Crypt/of lieberkuhn
4. T.M. Mucosae
B. T. submucosae
C. T.muscularis
Duodenum
 Jejunum
A. T. mucosae
1. Vili
2. Columnar surface epithelium+goblet cell
3. Crypt/of lieberkuhn
4. T.M. Mucosae
B. T. submucosae
5. Kerckring’s folds (T/mucosae+T.submucosae)
C. T.muscularis
 Paneth cells 

Intestinal crypts / (Lieberkuhn) glands/rypts

Jejunum
LO 2

BIOCHEMISTRY OF GASTER -
DUODENUM
LO 3

PHYSIOLOGY GASTER - DUODENUM

 Stomach
• 3 main functions
– Store ingested food until it can be emptied into
the small intestine
– Secretes HCl & enzymes, begin protein digestion
– Stomach’s mixing movement  ingested food
pulverized & mixed with gastric secretions  thick
liquid mixture (chyme)

– Gastric’s motility
• Filling, storage, mixing, emptying
 Gastric filling
• Volume about 50 ml; can expand to 1l during
a meal
• Folds of gastric get smaller & nearly flatten
out as stomach relaxes slightly (receptive
relaxation)  enhance stomach to
accomodate the extra volume of food with
little rise in stomach pressure
– Triggered by the act of eating & mediated by the
vagus nerve
 Gastric storage (body of stomach)
• Interstitial cells of Cajal  generates slow
wave potential (Basic electrical rhythm) 
occurs continuously with or without muscle
contraction  food is stored in the relatively
quite body without being mixed

• Fundus contains only pocket of gas

Gastric mixing (antrum of stomach)
• Strong antral peristaltic  mix food & gastric
juice ( chyme)  propels the chyme
towards pyloric sphincter
• Tonic contraction of pyloric sphincter keeps it
almost closed  bulk of the antral chyme
tumbled back into the antrum  propeled
forward  tumbled back again as the new
peristaltic wave advances
 Gastric emptying
• Gastric factor
– Amount of chyme; stomach distention  strecth
of smooth muscle, intrinsic plexuses, vagus nerve,
gastrin  gastric motility >>
– Degree of fluidity
• Duodenum factor
– Fat, acid, hypertonicity, & distention
Mechanism of H & Cl ions secretion
• Function of HCl:
– Activate pepsiongen 
pepsin
– Aids breakdown of
connective tissue &
muscle fibers, reducing
food into smaller
particles
– Denaturates protein
– Along with lysozyme 
kills microorganism
Pepsinogen, activated  protein digestion

Pepsin’s autocatalytic activity

 Mucus
• Lubricating properties, protects gastric
mucosa
• Protect the stomach wall from self-digestion
because of pepsin
– doesn’t affect pepsin activity in the lumen
• Being alkaline  neutralizing HCl
– Doesn’t interfere with the function of HCl in the
lumen
 Regulatory pathways  parietal & chief cells

• Acetylcholine  short local reflexes & vagal

stimulation  parietal & chief cells, G & ECL cells
• G cells  secrete gastrin
– Main factor for increased HCl secretion by stimulating
ECL cells to release histamine
• Enterochromaffin like cells  paracrine histamine
– Speed up HCl secretion, potentiates ACh & gastrin
• D cells  paracrine somatostatin
– Negative feedback fashion
Control of gastric secretion
 Small Intestine
 The site where most digestion and absorbtion
take place.
 Divided into 3 segments: duodenum, jejunum
and ileum
 Its motility includes:
 Segmentation
 Migrating motility complex
 Segmentation
 Segmentation consists of oscillating, ring-like contraction of the
circular smooth muscle along the small intestine’s length; between
the contracted segments are relaxed areas containing a small bolus
of chyme.
 After a brief period of time, the contracted segments relax, and
ring-like contraction appear in the previously relaxed area.
 The new contraction forces the chyme in a previously relaxed
segment to move in both direction into the now relaxed adjacent
segments, shortly thereafter, the areas of contraction and
relaxation is alternate again.
 In this way, the chyme is chopped, churned and thoroughly mixed
 Functions: mixing the chyme with digestive juices secreted in
small-intestine lumen and exposing the chyme to the absorbtive
surface of the small intestines mucosa
Segmentation
 Migrating Motility Complex
 When most meal has been absorbed,
segmentation cease and are replaced
between meals by the migrating motility
complex.
 This between meal motility consists of weak,
repetitive peristaltic waves that move a short
distance down the intestine before dying out.
 Each contraction will sweep any remnants of
the preceding meal plus mucosal debris and
bacteria forward toward the colon
 Secretions
 Exocrine gland cells of small intestine mucosa
secrete about 1.5 liters of an aqueous salt and
mucus solution called succus entericus.
 Functions: provides protection and
lubrication also provides plenty of H2O to
participate in the digestion of food
 No digestive enzymes are secreted inti the
intestinal juice.
 Digestion
 Digestion within the small intestine lumen is
accomplished by pancreatic enzymes with fat
digestion being enhanced by bile secretion.
 This digestion is completed by special hairlike
projections of luminal surface of small instine
epithelial cell, microvilli
 Absorption
 All products of carbohydrate, protein and fat
digestion, as well as electrolytes, vitamin and
water are absorbed by small intestine
indiscriminately. Only absorption calcium and
iron is adjusted by body needs.
 Most absorption occurs in duodenum and
jejunum, very little in ileum (normally only
B12 and bile salt are absorbed by ileum)
LO 4

DISEASE
peptic ulcer disease
 Definition
• Burning epigastric pain exacerbated by fasting and
improved with meals is a symptom complex
associated with peptic ulcer disease (PUD).
• An ulcer is defined as disruption of the mucosal
integrity of the stomach and/or duodenum leading
to a local defect or excavation due to active
inflammation.
• Ulcers are defined as breaks in the mucosal surface
>5 mm in size, with depth to the submucosa.
• Ulcers occur within the stomach and/or duodenum
and are often chronic in nature
 Epidemiology
Duodenal Ulcers
• DUs are estimated to occur in 6–15% of the Western population.
• The death rates, need for surgery, and physician visits have
decreased by >50% over the past 30 years.
• The reason for the reduction in the frequency of DUs is likely related
to the decreasing frequency of Helicobacter pylori.
• Eradication of H. pylori has greatly reduced these recurrence rates.

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 and are less common than DUs,
perhaps due to the higher likelihood of GUs being silent and
presenting only after a complication develops..
 Etiology
• H. pylori infection
Predominant cause
• NSAIDs
• Cigarette smoking
• Genetic predisposition
• 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 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 oral-oral
or fecal-oral route.
•
 Pathology
Duodenal Ulcers
• DUs occur most often in the first portion of duodenum (>95%), with
~90% located within 3 cm of the pylorus.
• They are usually 1 cm in diameter but can occasionally reach 3–6 cm
(giant ulcer).
• Ulcers are sharply demarcated, with depth at times reaching the
muscularis propria.
• The base of the ulcer often consists of a zone of eosinophilic necrosis
with surrounding fibrosis.

Gastric Ulcers
• In contrast to DUs, GUs can represent a malignancy.
• Benign GUs are most often found distal to the junction between the
antrum and the acid secretory mucosa.
• Benign GUs associated with H. pylori are also associated with antral
gastritis.
 Pathophysiology
Duodenal Ulcers
• H. pylori and NSAID-induced injury account for the majority of DUs.
• Many acid secretory abnormalities have been described in DU
patients.
• Bicarbonate secretion is significantly decreased in the duodenal bulb
of patients with an active DU as compared to control subjects.
• H. pylori infection may also play a role in this process
 Pathophysiology
Gastric Ulcers
• GUs that occur in the prepyloric area or those in the body
associated with a DU or a duodenal scar are similar in
pathogenesis to DUs.
• Gastric acid output (basal and stimulated) tends to be
normal or decreased in GU patients.
• When GUs develop in the presence of minimal acid levels,
impairment of mucosal defense factors may be present.
• Abnormalities in resting and stimulated pyloric sphincter
pressure with a concomitant increase in duodenal gastric
reflux have been implicated in some GU patients.
 Pathophysiology
• H. pylori and Acid Peptic Disorders
• Gastric infection with the bacterium H. pylori
accounts for the majority of PUD.
• This organism also plays a role in the development
of gastric mucosal-associated lymphoid tissue
(MALT) lymphoma and gastric adenocarcinoma
PATHOPHYSIOLOGY NSAIDs
 Clinical Features
• Epigastric pain described as a burning or gnawing
discomfort can be present in both DU and GU
• 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.
• The pain pattern in GU patients may be different from that
in DU patients, where discomfort may actually be
precipitated by food.
• Nausea and weight loss occur more commonly in GU
patients.
• Dyspepsia.
 Physical Examination
• Epigastric tenderness is the most frequent finding in
patients with GU or DU.
• Physical examination is critically important for
discovering evidence of ulcer complication.
• Tachycardia and orthostasis suggest dehydration
secondary to vomiting or active gastrointestinal
blood loss.
• A severely tender, boardlike abdomen suggests a
perforation.
• Presence of a succussion splash indicates retained
fluid in the stomach, suggesting gastric outlet
obstruction.
 Prognosis
• When the underlying cause is addressed, the
prognosis is excellent.
• Decreased mortality rate from bleeding peptic
ulcers when intravenous PPIs are used after
successful endoscopic therapy.
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.
• Bile reflux Drugs
Etiology
– 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
GERD
 Overview
• Gastroesophageal reflux disease (GERD) occurs
when the amount of gastric juice that refluxes into
the esophagus exceeds the normal limit, causing
symptoms with or without associated esophageal
mucosal injury (ie, esophagitis).
 Epidemiology
• Approximately 7-10% of Americans experience symptoms of
GERD on a daily basis.
• No sexual predilection exists: GERD is as common in men as in
women.
• However, the male-to-female incidence ratio for esophagitis is
2:1-3:1.
• The male-to-female incidence ratio for Barrett esophagus is
10:1.
• White males are at a greater risk for Barrett esophagus and
adenocarcinoma than other populations.
• GERD occurs in all age groups. The prevalence of GERD
increases in people older than 40 years.
 Classification
Gastroesophageal Reflux

Physiological Gastroesophageal Gastroesophageal Reflux

Reflux - GER Disease – GERD
(Symptomatic)

Primary GERD: Secondary GERD:

Motility problem External factor causing transient
Affecting lower relaxations of lower Esophageal
Esophageal sphincter sphincter (eg. Food allergy)
 Etiology
• Lifestyle - Use of alcohol or cigarettes, obesity, poor
posture (slouching)
• Medications - Calcium channel blockers, theophylline,
nitrates, antihistamines
• Diet - Fatty and fried foods, chocolate, garlic and
onions, drinks with caffeine, acid foods such as citrus
fruits and tomatoes, spicy foods, mint flavorings
• Eating habits - Eating large meals, eating soon before
bedtime
• Other medical conditions - Hiatal hernia, pregnancy,
diabetes, rapid weight gain
 PATOPHYSIOLOGY

Delated gastric
emptying

Increased frequency
Initial esophageal scar Incompetent LES
of transient LES relaxation
lesion

Increased acidity
Recurrent injury
Loss of secondary peristaltis
following transient LES relaxations
Stricture
Barret's esophagus
Decreased LES tone Pain
Obstruction
perforation
Cancer
GERD  imbalance between defensive factor
of esophagus and offensive factor from reflux
agent

OFFENSIVE FACTORS :
• HCl
• Pepsin

GERD
 Defensive Factors of Esophagus

• 1st Line : Antireflux separator LES tone

– LES tone (↓)  retrograd reflux during the
increase of intra abdominal pressure
– Factors that cause LES tone (↓) :
• Hiatal hernia
• LES lenght
• Drugs
• Hormonal Factor
 Defensive Factors of Esophagus
• 2nd Line :
Acid clearance from esophageal luminal
Associated factors:
• Gravitation
• Peristaltic
• Saliva and bicarbonate excretion
 Defensive Factors of Esophagus
• 3rd Line : Esophageal epithelium barrier
Consist of:
– Cell Membrane
– Intracelular junction
– Esophageal blood flow
– Ability of esophageal cells to transport the
ion
 Offensive Factors of Esophagus
• Initially :
– HCl
– Pepsin

• The lower the pH  esophagus mucosal

damage >>
 ALARM SYMPTOMS :
• Odynophagia
• Unexplained weight loss
• Recurrent vomiting
• Occult or gross GI bleeding
• Jaundice
• Palpable mass or adenopathy
• Family history of GI malignancy
 Pharmacologic Therapy
• Antacids
• H2 receptor antagonists and H2 blocker
therapy
• Proton pump inhibitors
• Prokinetic medications and reflux inhibitors
 Barrett esophagus

– Is a result of chronic gastroesophageal reflux

– The distal squamous mucosa is replaced by metaplastic
columnar epithelium  response of prolonged injury
– Clinical features:
- Secondary complications of local ulcerations with bleeding and
stricture --- adenocarcinoma
 Barrett Esophagus
• Replacement of the
normal stratified
squamous epithelium
with intestinal (goblet
cell) metaplasia
• Complications:
ulceration, stricture,
dysplasia, carcinoma
 Lifestyle Modifications
• Losing weight (if overweight)
• Avoiding alcohol, chocolate, citrus juice, and
tomato-based products (The ACG 2005
guidelines also suggest avoiding peppermint,
coffee, and possibly the onion family as well. )
• Avoiding large meals
• Waiting 3 hours after a meal before lying
down
 Prognosis
• Most patients with GERD do well with
medications, although a relapse after cessation of
medical therapy is common and indicates the
need for long-term maintenance therapy.
• In refractory cases or when complications related
to reflux disease are identified (eg, stricture,
aspiration, airway disease, Barrett esophagus),
surgical treatment (fundoplication) is typically
necessary.
• The prognosis with surgery is considered
excellent.
Hold the baby upright for a time
after feeding to help prevent Propping a baby up after feeding helps
spitting up. keep fluid from traveling up from the
stomach.

PREVENTION

Position of feeding The Acid Reflux Wedge Pillow For

Baby
VOMITTING
 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

 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
 Causes of nausea and vomiting in child
Acute vomiting, usually in the context of diarrhoea
• Gastrointestinal infections
– viral (eg. rotavirus, adenovirus, calicevirus)
– bacterial (eg. campylobacter, shigella, salmonella)
– protozoa (eg. Giardia, cryptosporidia)
• Food poisoning
– staphylococcus toxin
• Nongastrointestinal infection
– urinary tract infection
– meningitis
– septicaemia
• Surgical
– appendicitis
– intussusception
– malrotation with or without volvulus
• Food allergy (following recent introduction of new food in the first 2 years of life)
– cow’s milk protein allergy
– Coeliac disease
 Causes of nausea and vomiting in child
Acute vomiting that presents as vomiting alone
• Pyloric stenosis (in infants)
• Appendicitis
• Raised intracranial pressure
• Meningitis
• Surgical obstruction
• Metabolic disease
 Type of Vomiting
1. Projectile (forceful vomiting) : increased
intracranial pressure.
2. Non projectile : Gastroesophageal reflux
3. Emesis : clear, yellow, billious, nonbilious,
bloody, nonbloody.
http://www.wrongdiagnosis.com/bookimages/8/2763.png
 Diagnostic Rome III
• 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.
 Diagnostic Rome III
• 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
 Management
• Identification and elimination of the
underlying cause if possible
• Control of the symptoms if it is not possible to
eliminate the underlying cause
• Correction of electrolyte, fluid or nutritional
deficiencies
 Complications
Excessive or repeated vomiting can cause dehydration and may lead
to severe disturbances in the electrolyte and acid-base balance in
the body.
• Dehydration – due to loss of water from the GI tract.
• Hypokalaemia – due to loss of the potassium ions in GI secretions
• Hypochloremia – due to loss of chloride ions in the vomitus
• Alkalosis - due to loss of H+ ions in the vomitus
• Aspiration syndrome
• Malnutrition and failure to thrive
• Peptic oesophagitis
• Mallory-Weiss tear
 erosions to the esophagus or small tears in the esophageal
mucosa
 Red Flags
Any child who is vomiting blood or bile or has
severe abdominal pain or abdominal signs needs
immediate investigation in a hospital emergency
room setting.
Otherred flags include:
• projectile vomiting
• abdominal distension, tenderness
• high fever
• persistent tachycardia or hypotension
• neck stiffness and/or photophobia.
 Overview
• Gastroenteritis is an inflammation of the
mucous membrane lining the stomach and
intestine caused by microorganisme.
• Gastroenteritis is a very common pediatric
condition and is second only to respiratory
infections as the most common reason for
unscheduled visits to pediatricians.
Source: Department of State Health Services, Center for Health Statistics, Texas Health Care
Information Collection. Texas Inpatient Hospital Discharge Data, 2002.
 Epidemiology
United States
• Incidence rates for diarrhea are 1-2.5 episodes per child per year, which
annually leads to approximately 38 million cases, 2-3.7 million physician
visits, 320,000 hospitalizations, and 325-425 deaths.
International
• More than 1 billion cases and at least 4 million deaths per year are
attributed to diarrhea worldwide.
Mortality/Morbidity
• Mortality and morbidity from diarrhea relate to the degree of dehydration.
Most deaths in the United States correlate to lower maternal
socioeconomic factors and prematurity.
Age
• Dehydration risk in children relates to age, and infants are most susceptible.
 Causes
• 70-85% of Gastroenteritis in developed countries
are due to viruses.
• Rotavirus accounts for 1/3 of all pediatric
gastroenteritis hospitalizations in U.S.
• Most common bacterial causes: Campylobacter,
Salmonella, Shigella, E. coli, Yersinia, and C. difficile
(iatrogenic)
• Parasitic agents (e.g. Giardia) cause less than 10% of
cases
 Physical
• The criterion standard and most accurate
clinical indicator of the extent of dehydration
is the percentage loss of body weight during
the illness, which represents the child's fluid
deficit.
 Physical
• Thirst
• Listlessness
• Dry mucous membranes
• Sunken fontanelles
• Sunken eyes
• Absence of tears
• Decreased skin turgor
• Decreased capillary filling time
• Tachycardia
• Weak pulse
• Reduced blood pressure
 Diagnoses
• Most cases of children with mild-to-moderate dehydration
require no laboratory tests.
• Electrolyte, BUN, serum creatinine, and glucose levels may
be obtained for severely dehydrated children or those with
atypical or inconsistent histories and physical examination
results.
• Other laboratory tests may be performed to assess
hydration status, including hematocrit and urine specific
gravity tests.
• Stool cultures are usually reserved for cases of children
with bloody diarrhea and those who are severely
dehydrated, chronically ill or immunocompromised, or who
have the appearance of toxemia.
 Differential Diagnoses
• Crohn Disease
• Cystic Fibrosis
• Hemolytic-Uremic Syndrome
• Lactose Intolerance
 Treatment
• Oral rehydration solution (ORS)
• Antibiotic
• Antiviral
• Amebisid
 Prognosis
• Prognosis is excellent because gastroenteritis
is usually self-limited.
• Children usually improve after an intravenous
bolus.
• Patients who receive oral rehydration
solutions (ORSs) gradually improve.
Dyspepsia
 Dyspepsia
• Dyspepsia is a collection of symptoms or
syndrome epigastric burning, gnawing
discomfort, or pain, postprandial fullness,
early satiety (an inability to complete a meal
due to premature fullness), bloating,
eructation (belching), and anorexia
 Epidemiology
• Annual prevalence as define by rome II criteria
in western countries is 25%
• Often the symptoms are of short duration, self
limited and self managed
• 2-5% of general practice consultations are for
dyspepsia
Differential diagnosis of dysphagia
• Peptic ulcer disease
• Gastroesophageal reflux
• Gastric malignancy
• Biliary pain
• Irritable bowel syndrome
• Drug induced dyspepsia
• Functional (non-ulcer) dyspepsia