Pemicu 1 GIT

ALEXANDRA ADELINE
405090036
Learning Objective

1. Describe the anatomy of the upper GI tract

2. Describe the physiology of the upper GI tract
3. Describe the biochemistry of the upper GI tract
4. Describe the mechanism of :
1. Dyspepsia
2. Nausea
3. Heartburn
4. Hematemesis
5. Describe :
1. GER / GERD
2. Gastritis
3. Gastric Cancer
1. Anatomy of upper GI tract
 UPPER GASTROINTESTINAL TRACT:
Esophagus-Gaster-Duodenum-Proximal
Jejunum-Treitz ligament

LOWER GASTROINTESTINAL TRACT:

Treitz ligament-Distal Jejunum-Ileum-Colon-
Anus
EUSOFAGUS
Length 25cm
Pharynx gastric
Transition esophagus into the stomach = os
cardiacum
spinchter, smooth muscle circularis at the
lower end of physiological functions as spinchter
(regulate the entry of food from the esophagus
to prevent stomach + stomach contents reflux
into the esophagus)
sometimes part of the intestine that move can
sneak through a defect in the hiatus into the
thorax cavity hiatal hernia
stomach
Esophagus Duodenum
As digested food to shelters into "chyme
Set jetting into the small intestine digestibility
results
1.5-liter capacity, can be dilated 2-3 Liter
The capacity of the newborn 30 cc
Common is a form J-shaped
Shape up like the letter L upside down ("steer
- horn stomach")
Anatomy of the Stomach

7
Duodenum
Pylorus - flexura duodenojejunal turned
jejenum
long 25 cm
C-shaped surrounding the pancreatic caput
Divided parts: pars superior, pars descenden,
pars horizontalis (inferior), pars ascending
 Pars superior duedeni
5 cm long
Vertebra L 1 is located as high as
Move freely on radiography is shaped like a triangle
with its base at the pylorus called fleeced duodeni
(duodenal cap)

Pars descenden duodeni

8 cm long
There is a bulge called duodeni major papilla (vateri),
and has the musculus sphincter ampullae hepato -
pancreaticae (oddi sphincter) that function set
spending bile and pancreatic fluid
 Pars Inferior (horizontalis) duodeni
8 cm long

Pars ascending duodeni

5 cm long
Turning into a groove with called flexura
duodenojejunal
The final part covered by the peritoneum
 Histology of esophagus
The wall of the esophagus consists of
Mucosa
epithelial cells (non-keratinized stratified columnar
epithelium)
lamina popria
muscularis mucosa (longitudinal smooth muscle)
Submucosa
submucosal plexus (Myentric's)
Muscularis externa/popria
inner circular smooth muscle
Meissner plexus (Auerbach's)

outer longitudinal muscle

Adventitia
 The mucosa has a smooth, glistening , and pink-tan
surface. It has three components;
1. a non-keratinizing stratified squamous epithelial
layer : the epithelial layer has mature squamous
cells overlying basal cells
a small number of specialized cell type, such as
melanocytes, endocrine cells, dendritic cells, and
lymphocytes, are present in the deeper portion of
the epithelial layer
2. The lamina propria is the non-epithelial portion of
the epithelial layer, above the muscularis
mucosae.
.It consists of areolar connective tissue and contain
vascular structures and scattered leukocytes.
.Finger-like extensions of the lamina propria, called
papillae, extend into the epithelial layer.
3. The muscularis mucosa is a delicate layer of
longitudinally oriented smooth-muscle bundles.
 The submucosa consists of loose connective tissue
containing;
blood vessels,
a rich network of lymphatics,
a sprinkling of leukocytes with occasional lymphoid
follicles,
nerve fibers (including the ganglia of Meissner
plexus)
submucosal glands.
As is true throughout the alimentary tract, the
muscularis propria/externa consists of an inner
circular and an outer longitudinal coat of smooth
muscle with an intervening, well-developed myenteric
plexus (Auerbach plexus).
In sharp contrast to the rest of the gastrointestinal
tract, the esophagus is mostly devoid of a serosal coat.
Only small segments of the intra-abdominal esophagus
are covered by serosa
2. Physiology of Upper GI tract
Physiology
3. Biochemistry of upper GI tract
Source Enzim Activator Substrat Function or
katalitik
product
Saliva gland @-Amilase Cl- Flour Hidrolisis bond
Saliva essence 1:4 @; produce
dextrin @limit,
maltotriosa, and
maltosa

Lingual gland Lingual lipase Trigliserida Lipid acid plus

1,2 -
diasilgliserol

Gaster Pepsin Hcl- Protein and Decompose

(pepsinogen) polipeptida peptida chain
which closer
with aromatic
amino acid
Gaster lipase Trigliserida
Lipid acid and
gliserol
Source Enzim Activator Substrat Function and katalitik
produce

Pancrea Tripsin Enteropep Proein and Decompose peptida bond

s (tripsinoge tidase polipeptida to karboksil various
eksocrin n) amino acid basic (arginin
e or lisin)
Kemotripsi Tripsin Proein and Decompose peptida chain
n polipeptida to karboksil aromatic acid
amino
Elastase Tripsin Elastin other Decompose karboksil
protein amino acid alifatik chain

Karboksipe Tripsin Proein and Decompose karboksil

ptidase A polipeptida teminal acid amino chain
which aromatic chain or
bifurcate alifatik

Karboksipe Tripsin Proein and Decompose karboksil

ptidase B polipeptida terminal acid amino chain
which alkali chain
Kolipase Tripsin Lipid items To open a part of active
lipase pancreas

Pancreas Trigliserida Monogiserida and fatty

Lipase acid

Lipase Choesteril Cholesterol

ester
Ester Cholesteril Cholesterol
Kolesteril ester
hidrolase

Panckreas Cl- Starch @-amilase saliva

@-amilase

Ribonuklea RNA Nukleotida

se
Deoksiribo DNA Nukleotida
nuklease

Fosfolipase Tripsin Phosfolipid Fatty acid and

A2 lisophosfolipid
Source Enzim Activato Substrat Function and katalitik
r produce

Small Enteropeptida Tripsinoge Tripsin

intest se n
mucous
Aminopeptida Polipeptid Decompose to amino chain
se a acid amino terminal from
peptide
Karboksipepti Polipeptid Decompose to amino chain
dase a acid amino terminal from
peptide

Endopeptidas Polipeptid Decompose to residue

e a between middle of peptide

Dipeptidase Dipeptida 2 amino acid

Maltase Maltosa, Glucose

maltotrios
a, @-
Source Enzim Activato Substrat Function and
r katalitik
produce
Small intest Laktase Laktosa Galaktosa and
mucous glucose

Sukrase* Sukosa; Fruktosa and

maltotriosa and glucose
maltosa
@- @-dekstrin, Glucose
Dekstrinase* maltosa,
maltotriosa
Threhalase Trehalosa Glucose

Nuklease and Nukleat acid Pentosa,purin

other enzims and pirimidin

Cytoplasma Various Di,tri, and Amino acid

cell mucous peptidase tetrapeptida
Dyspepsia
Definition
impairment of the power or function of
digestion; usually applied to epigastric
discomfort after meals
(Dorlands pocket medical dictionary 28th edition)
Nausea
Definition
an unpleasant sensation vaguely referred to
epigastrium and abdomen, with tendency to
vomit
(Dorlands pocket medical dictionary 28th edition)
Nausea
Mechanism :
1. Begins with stimulus either from visceral
organ , labyrinth or emotion
2. Stimulus trigger nervous system to stop
peristaltic on proximal region of gaster (1/3
proximal corpus and fundus)
3. Pressure on the proximal region of gaster
decrease, while the pressure on the distal
region increase.
Nausea
Mechanism :
4. Pressure gradient of the proximal and distal
region gaster trigger retroperistaltic (reverse
peristaltic)
5. Retroperistaltic occur from from duondenum to
gaster (duodenogaster reflux)
6. Reflux and retroperistaltic makes a person to
have an unpleasant feeling.
Vomiting

Vomiting is coordinated by the brain stem

and is effected by neuro-muscular respons in
the gut , pharynx , and thoracoabdominal wall
Vomiting

Several brain stem nuclei :

1.nucleus tractus
solitarius
2.Dorsal Vagal and
phrenic nuclei Coordinate the
initiation of
3.Medullary Nuclei that
emesis
regulate respiration
4. Nuclei that control
pharyngeal,facial,tounge
 Vomiting

Deep
inspiration &
epiglottis
closed

epiglottis clossed &

Diaphragm uvula: upward
presses stomach preventing content
downward nasal cavity
simultaneousl
y
Inspiratory
thoracic and Stomach content Emesis
Abdominal wall esophagus
muscle mouth
contracted
intraabd &
intrathoracic
Heartburn
Definition
pyrosis; a retrosternal sensation of burning
occurring in waves and rising toward the neck;
it may be accompanied by a reflux of fluid into
the mouth and is often associated with
gastroesophageal reflux
(Dorlands pocket medical dictionary 28th edition)
Heartburn
Mechanism :
1. When food or liquid enters your stomach, the
LES (lower esophageal sphincter) at the end of
your esophagus closes off.
2. If LES fails to close tightly enough, stomach
contents can back up (reflux) into the
esophagus
3. This partially digested material is usually acidic
and can irritate the esophagus, causing
heartburn
Hematemesis
Definition
backward flowing (regurgitation) of blood
through the upper gastrointestinal (GI) tract.
The upper GI tract includes the stomach,
mouth, throat, esophagus (the swallowing
tube), and the first part of the small intestine
HEMATEMESIS
Source o Hematemesis
* Esophagus : Esophagitis, ulcer, Mallory-Weiss
tear,
Esophageal varices
* Stomach : Gastric ulcer, Prepyloric ulcer ,
Pyloric
channel ulcer, Gastric erosions,
Gastritis, Varices , Portal-
hypertensive gastropathy, Gastric
cancer , Polyp ,Dieulafoy lesion
* Duodenum : Ulcer, Duodenitis,
Aortoenteric fistula, Pancreatic
pseudocyst, Postsphincterotomy
Sources of Bleeding in Patients Hospitalized for
Upper GI Bleeding in Years 20002002

Sources of Bleeding Proportion of Patients, %

Ulcers 31-59
Varices 7-20
Mallory-Weiss tears 4-8
Gastroduodenal erosions 2-7
Erosive Esophagitis 1-13
Neoplasm 2-7
Vascular ectasia 0-6
No Source indentified 8-14
http://www.wrongdiagnosis.com/bookimages/10/5248.pn
MELENA
Definition
The passage of dark black, liquid, tarry,
metallic-smelling stools

Melenic stools usually indicate bleeding

proximal to the right side of the colon

It usually indicates that hemorrhage has

remained for at least 14 hour in the GI
tract.

The more proximal the bleeding site, the

more likely melena will occur.
MELENA
Sources of melena
All causes of upper gastrointestinal bleeding
Jejunum and ileum: (Meckel's diverticulum,
angiodysplasia, Chron's disease, tumors,
bowel infarction).
Colon: right sided tumors, angiodysplasia,
inflammatory bowel disease.
Differential Diagnosis
Nausea Heartburn Hematemesis
Peptic Ulcer Peptic Ulcer Peptic Ulcer
Gastritis Gastritis Gastritis
GERD GERD GERD
Esophageal Cancer Esophageal Cancer Esophageal Cancer
Gastric Cancer Gastric Cancer Gastric Cancer
Cirrhosis Hepatis Achalasia Cirrhosis Hepatis
Motion Sickness & Oesophagitis Oesophagitis
Labyrinthitis
Unstable Angina Unstable Angina Ebolla Hemoragic
Fever
Stable Angina Stable Angina Duonedal Cancer
Hernia Hernia
Peptic Ulcer
Definition

disruption in the mucosal layer of the

stomach or duodenum. distinguished from
an erosion by its penetration through the
muscularis mucosa or the muscular
coating of the gastric or duodenal wall
Peptic Ulcer
Etiology :
Peptic ulcer disease results from the
imbalance between defensive factors that
protect the mucosa and offensive factors that
disrupt this important barrier
 Protective Aggressive

- Prostaglandin - Acid-pepsin
- Mucous Gel environ-
Layer ment
- Bicarbonate - Mucosal
- Mucosal Blood Ischemia
Flow - H. Pylori
Infection
- NSAID
- Trauma
Peptic Ulcer

Physiologi :
1. Mucosal defense system can be envisioned asa
a three-level barrier composed of : preepithelial
, epithelial and subepithelial
2. Preepithelial have mucus-bicarbonate and
surface active phospholipids layer which serve
as a physicochemical barrier
3. Epithelial cells provide the next line of defense
through several factors, including mucus
production , epithelial cell ionic balance which
maintain intracellular pH and bicarbonate
production.
Peptic Ulcer

Physiologi :
4. If the pre-epthelial barrier were breached,
epithelial cells bordering a site of injury can
migrate to restore the damaged region
(restitution). This process requires blood flow ,
alkaline pH and growth hormone factor.
5. In the subepithelial an elaborate of
microvascular induced defense/repair system ,
providing HCO3 and supply adequate oxygen
to epithelial cells.
Peptic Ulcer
Physiology :
6. Prostaglandine play a central role in gastric
epithelial defense/repair which release mucosal
bicarbonate and mucus , inhibit parietal cell
secretion and maintaining mucosal blood flow and
epithelial cell restitution.
Peptic Ulcer
Pathophysiology :
1. NSAID and Mucosal Ischemia will reduce the
amount of mucous and bicarbonate which
trigger imbalance
2. Infection of H.Pylori induce mucosal injury
Peptic Ulcer

Sign and symptoms :

1. Nausea
2. Vomiting
3. Dyspepsia(belching, bloating, distention,
andfatty food intolerance)
4. Heartburn
5. Chest discomfort
6. Anorexia
7. Hematemesis or melena (upper GI tract
bleeding)
Peptic Ulcer
Test :
1. History and physical examination
2. Esophagogastroduodenoscopy (EGD)
3. Gastric biposy
4. Urease Test
Peptic Ulcer

Esophagogastroduodenoscopy (EGD)
1. Examination of the lining of the esophagus,
stomach, and upper duodenum with a small camera.
2. Procedure :
a. Patient should be on fasting state for 6
- 12 hours before the EGD procedure
b. Patient will be given a sedative and
analgesic (painkiller)
c. Local anesthetic may be sprayed into
your mouth to surpress cough or gag
when endoscope is inserted
Peptic Ulcer
2. Procedure :
d. A mouth guard will be inserted to
protect your teeth and the
endoscope
e. Endoscope will go through your
esophagus to upper duodenum with
a small camera to locate the ulcer or
cancer.
Left Right :
1.1st degree
scar
2.2nd degree
scar

Left Right :
1. 1st degree
ulcer
2. 2nd degree
ulcer

Left Right :
1. 1st degree
healing
2. 2nd degree
healing
 1st Degree Ulcer
(duodenum)

2nd Degree
Ulcer
(gaster)
Peptic Ulcer
Gastric Biopsy :
1. Gastric tissue biopsy is the removal of stomach
tissue for examination
2. Procedure :
a. Patient should be on fasting state for
6 - 12 hours before the biopsy
procedure
b. The gastric tissue biopsy sample is
removed during an upper endoscopy
Peptic Ulcer
2. Procedure :
c. Then in laboratory staining examines the tissue for
bacteria or other organism that cause the disease
d. Culture of H.Pylori will be stained by hematoxylin-
eosin , gram staining or The Wartin Starry Silver
for the best result (most sensitive).
Peptic Ulcer
Urease Test :
1. Urease test is the test to examine the bacteria
H.Pylori by the level of urease
2. There are 2 types of urease test :
a. Invasive :
Biopsy of the gastric epithelial cell to measure the
level of urease
b. Non-invasive (Urea Breath Test) :
Test to measure the level of urea in our breath after
taking a specific species of carbon
Peptic Ulcer
3. Procedure :
a. Invasive : same as gastric biposy
b. Non-invasive :
1. Patient drink an isotopically labeled urea acid which
dissolved in aqua (14C or 13C isotype)
2. Breath collection after 30 60 minutes
3. Breath sample are transferred to an empty canister
to be examined.
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).
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 Reflux

Gastroesophageal Reflux - Disease GERD
GER (Symptomatic)

Primary GERD: Secondary GERD:

Motility problem External factor causing
Affecting lower transient relaxations of
Esophageal sphincter lower Esophageal sphincter
(eg. Food allergy)
Epidemiology
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
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.
Acute Gastritis
Acute gastritis broad spectrum of
entities that induce inflammatory
changes in the gastric mucosa.

2 categories:
erosive (e.g, superficial erosions, deep
erosions, hemorrhagic erosions)
non-erosive (generally caused by
Helicobacter pylori)
Etiology
Bile reflux Drugs
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)
Sign and Symptoms
Acute gastritis may be entirely asymptomatic
Epigastric pain
Nausea
Vomiting
Hematemesis
Melena
Potentially fatal blood loss
Risk Factors
Acute gastritis is frequently associated
with:
Heavy use NSAID, particularly aspirin
Excessive alcohol consumption
Heavy smoking
Treatment with cancer chemotherapeutic drugs
Systemic infections (eg. Salmonellosis)
Severe stress (eg. Trauma, burns, surgery)
Ischemia and shock
Suicide attempts with acids and alkali
Mechanical trauma (eg. Nasogastric intubation)
Reflux of bilious material after distal
gastrectomy
Chronic Gastritis
Definition: the presence of chronic
inflammatory changes in the mucosa leading
eventually to mucosal atrophy and epithelial
metaplasia
Most individuals with the infection also have
the associated gastritis but are asymptomatic
Etiology

Autoimmune
Bacterial (H. Pylori)
Chemical (NSAIDs)
Chronic noninfectious granulomatous
gastritis
Lymphocytic gastritis
Eosinophilic gastritis
Ischemic gastritis
Radiation gastritis
Pathophisiology
Most important etiologic association is
chronic infection by the bacillus H. pylori
Gastritis develops as a result of the
combined influence of bacterial enzymes
and toxins and release of noxious
chemicals by the recruited neutrophils
Characterized by mononuclear cell
infiltration in the lamina propia with
intestinal metaplasia and frequently
proliferation of lymphoid tissue
Sign and Symptoms
Usually causes few or no symptoms
Upper abdominal discomfort
Nausea
Vomiting