Problem 2

Gastrointestinal System Block

Vicka Azwita Inovia
405130157
Kelompok 15
 LO 1
Anatomy, histology and biochemistry of upper
GI track
ANATOMY
Figure 2.30. Abdominal part of esophagus and stomach.
Arterial Supply to Stomach
Veins of stomach, duodenum, and spleen
HISTOLOGY
Esophagus
Gaster
Histology of Cardia
BIOCHEMISTRY
 LO 2
Physiology of digestion
 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, protein, etc
 LO 3
Definition, classification, etiology,
pathophysiology, signs & symptoms, diagnosis
(anamnesis, physical examination, additional
investigation), treatment (pharmacologicaL 
prescription, non-pharmacological), prognosis,
complications, prevention, education of
dyspepsia and esophageal refluks
DYSPEPSIA
 Dyspepsia
• Dyspepsia = indigestion
• Is a mild discomfort in the upper belli or abdomen, it occurs during
or after eating
• It may feel like (symptoms) :
– Pain or discomfort in the upper belli or abdomen (epigastric pain)
– Feeling unusual fullness with very little intake food
– Nausea
– vomiting
– Loss of appetite
– Bloating
– Heatburn
– Belching

• Classification of dyspepsia :
– Organic dyspepsia
– Functional dyspepsia
 Functional dyspepsia
• Is a situation where UGI tract endoscopy did not reveal
a potential cause for dyspepsia (the cause is not clear)
• Sometimes called non ulcer dyspepsia/idiophatic
dyspepsia
• Pathophysiological mecanism underlying FD are :
– Delayed gastric emptying
– Increased gastric acid
– Hypersensitivity to gastric distention
– Altered duodenal sensitivity to lipids or acids
– Infection of Helicobacter pylori
– etc
 FD
• Factors are affected prevalence of FD are :
– Body mass index
– Smokers
– Alchoholic
– Psychological factors
– Diet and environment
– Hormones (CCK & secretin)
 FD
• Divided into 2 subtypes :
– Epigastric pain syndrome
– Postprandial distress syndrome
 Organic dyspepsia
• Is a versus of functional dyspepsia
• Cause :
– Peptic ulcer
– GERD
– Esophageal / gastric cancer
– Pancreatic / billiary disorders
– Intolerance of food or drug
– infection / systemic disease
– Malignancy
• Investigation of dyspepsia :
– Laboratory : for exlude the other causes of organic
dyspepsia (pancreatitis, diabetic mellitus, etc).
FD : usually normal
– Endoscopy (esofagogastro-duodenoscopy) : usually
normal and not specific in FD
– Gastric emptying time : about 30-50% patients
with FD have delayed emptying time of gaster
– Electrogastrografi : delayed emptying time of
gaster
– Hp test
• Treatment for dyspepsia :
It’s important to know the cause of dyspepsia
(organic / functional)
– Functional dyspepsia :
• Non pharmacologic : life style, psycological treatment
• Pharmacologic : empiric therapy (therapy based on the
subtype) for 4 weeks (PPI, prokinetics, citoprotective,
antidepressan, eradication of Hp, antasida, etc)
PEPTIC ULCER
 Peptic ulcers
• Peptic : relating to digestion especially that in
which pepsin in concerned
• Ulcer : disintergation of the surface of the skin
or mucous membrane resulting in an open
sore that heals very slowly
• Peptic ulcer : an erosion of mucous membrane
of the lower esophagus, stomach or
duodenum caused action of gastric juice
• Epidemiology :
– Men > women
– Increased in elderly and lower social economy
– Occurs in all ages
– Gastric ulcer more often affect in 55-70 years old
group
– Duodenal ulcer : 30-55 years old
– More frequently occurs in smokers, NSAID drug user
– Alcohol and stress are still debating
– Gastric ulcer more frequently occurs in Indonesia and
related with NSAID drug
– Incidence of infection and recurence of Hp decreased
caused of eradicated
• Cause of peptic ulcer :
– NSAID drugs
– Infection of HP
– Hypersecretion of gastric acid (Zollinger Ellison
Syndrome)
• Helicobacter pylori
– microaerophile microorganism
– Gram negative
– Spiral shape
– Movement by flagel
– Has an urease enzyme
• Transmission :
– Person to person (oral-oral,fecal-oral)
 Defenses mechanism in
Helicobacter pylori & patophysiology
of peptic ulcer
Ammonia, CO2, Increased of
Helicobacter pylori
Bicarbonat acid PH gaster

Adhesion to epitel
Damage of cells and caused
Adaptation
epitelial cells immune respons
induction

*. Microaerophile
can protect the
microorganism from
oxydative stress of
mucous inflamation
• Signs and symptoms (usually dyspepsia) :
– Epigastric pain
– Nausea
– Vomiting
– Bloating
– Belching
– Fullness, etc

• In severe case, the symptoms can include :

– Dark or black stool (bleeding)
– Vomiting blood
– Weight loss
– Severe pain in the mid to upper abdomen
• Diagnose :
– Anamnese : history of NSAID drug user, smokers, alcoholic, family
history of peptic ulcer

Gastric ulcer Duodenal ulcer

Pain occurs after eating Pain occurs while hungry and
relieve with food or drink
(Hunger pain food relief)
Pain in the left side of midline Pain in the right side of
of the body midline of the body

– Physical exam :
• To find out the complications (such as peritonitis, retention of liquid in
gaster, bleeding)
– Investigation :
• Laboratory
• Barium meal contrast radiograft
• Endoscopy
• Hp test (rapid test urease, urea breath test, fecal antigen testing,
serology test)
• Complications :
– Bleeding
– perforation
– Obstruction

• Treatment :
– Non pharmacologic : bed rest, diet, avoid NSAID
– Pharmacologic : secretoric inhibitor (PPI, H2
receptor antagonist), mucous protective (Bistmuth,
misoptostol, antasida), eradication of Hp (Triple /
quadruple therapy)
GERD
 GERD
• Gastroesophageal reflux disease (GERD) is a condition
in which food or liquid travels backwards from the
stomach to the esophagus (the tube from the mouth to
the stomach).
• 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
• This action can irritate the esophagus, causing
heartburn and other symptoms.
• Gastroesophageal reflux is a common condition that
often occurs without symptoms after meals.
 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)
Gastroesophageal Reflux Disease
(GERD)
 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
 Gastroesophageal Reflux
Pathophysiology
Swallow

The lower esophageal sphincter relaxes or

Decrease the pressure of the LES or
Increased intra-abdominal pressure

Stomach contents and corrosive acid well up

Regurgitation

Damage the lining of the esophagus

 GERD – Treatment
• Lifestyle changes
– dietary modifications (avoid acidic / reflux-
inducing foods (tomatoes, chocolate, mint), &
beverages (juices, carbonated, caffeinated drinks,
alcohol), altered sleep position, weigh reduction,
smoking cessation
• Pharmacotherapy
• Surgical therapies
Treatment – Pharmacotherapy
 Examination
• Bernstein test
• Barium meal test
• Endoscopy
• Ph
• Ppi test
GASTRITIS
 GASTRITIS
• Gastritis is an inflammation, irritation, or
erosion of the lining of the stomach /
gastric mucosa. It can occur suddenly
(acute) or gradually (chronic).

RISK FACTOR OF GASTRITIS

 H. pylori infection
 Regular use of aspirin or other NSAIDs
 Older age
 ETIOLOGY OF GASTRITIS
• Bacterial infection
• Regular use of pain relievers
• Excessive alcohol use
• Stress
• Bile reflux disease
• Your own body attacking cells in your stomach
(autoimmune gastritis)
• Other diseases and conditions
 CLASSIFICATION OF GASTRITIS
• Acute gastritis
– Acute H. pylori infection
– Other acute infectious gastritis
• Chronic atrophic gastritis
– Type A
– Type B
– Indeterminant
• Uncommon forms of gastritis
– Lymphocytic
– Eosinophilic
– Crohn’s disease
– Sarcoidosis
– Isolated granulomatous gastritis
 SYMPTOMS OF GASTRITIS
• Nausea or recurrent upset stomach
• Abdominal bloating
• Abdominal pain
• Vomiting
• Indigestion
• Burning or gnawing feeling in the stomach
between meals or at night
• Vomiting blood or coffee ground-like material
• Black, tarry stools
 Infection of H. PILORY

gastritis TH 1 motility
H.Pylory
infects gaster
urease
protective TH2
Vac A Urea
ammonia
+CO2
Provides a survival needs for bacteria
Causes epithelial injury
 Pathogenesis of Helicobacter pylori infection

• An ability to colonize and adhere to gastric

epithelial cells.
• The possesion of flagella that allows movement
through the luminal mucous layer to site of higher
Ph.
• An ability of adherent strains to supress acid
secretion to improve their survival.
• Secretion of urease that produces ammonia
results in a more alkaline environment.
• Release of vacuolating cytotoxin (VacA) that
promotes bacterial survival and causes epithelial
injury.
• The presence of cytotoxin-assosiated gene (CagA) strains that can escape
normal immune responses and cause inflammation with release of
inflammatory cytokines and reactive oxygen metabolites that damages
mucosal epitelial cells and loss of the protective mucosal barrier.
• Recruitment and activation of neutrophils,macrophages,and mast cells
with release of inflammatory cytokines that promote celllar injury.
• Down-regulation of antral somatostatin leading to increased
gastrin,acid,impaired mucosal bicarbonat production and increased
mucosal exposure to acid and pepsin.
• Activation/inhibition of T-and B- cell immune
responses that may contribute to mucosal
injury.
• Release of cytokines and chemokines that
promote gastric epithelial cell death and cell
proliferation that can result in
atrophy,ulcers,or malignant growth.
 Examination
• Urea breath test
• Serologi
• Biopsy urea test
• Manifestacion:
– Burn feeling (in epigastrium)
– Nausea
– Bitter in the tounge
– Disfagia

Complication:
Esophagitis is classified into the following 4
gradesI,II,III,IV.