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Problem 2 GI - VICKA AZWITA
Problem 2 GI - VICKA AZWITA
– 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
• 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
– 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
Regurgitation
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
Complication:
Esophagitis is classified into the following 4
gradesI,II,III,IV.