Blok GIT

PEMICU 1
ENY MILYARNI
405110130

Anatomi

HISTOLOGY

Labium Oris
There are 3 areas:
Area Cutanea
Area merah bibir ( area Intermedia )
Area oral mukosa

LINGUA
Papilla linguae:
2/3 bagian anterior
papilla filiformis , papilla
fungiformis, papilla foliata dan
papilla circumvallata
1/3 posterior dorsal free from papilla
lidah . There is Tonsilla linguae

Papilla Fungiformis

PAPILA FOLIATA

Papilla Circumvalata

Taste Buds

General nature of the GI tract wall

Gastrointestinal wall layers from the

inside out:
1. Tunica mucosa
2. Submucosal tunica
3. Muscularis tunica externa
4. Tunica adventitia / serous tunica

ESOPHAGUS

Gastric
The entire surface of the gastric
mucosa, gastric pits or areas
containing foveolae gastrica.
Foveola gastrica the cardia and
fundus is narrower and shallower
than the pylorus
Epithelial layer selapis thorax

Biokimia

Source

Enzim

Activator

Substrat

Function or
katalitik
product

Saliva gland

@-Amilase
Saliva

Cl-

Flour
essence

Hidrolisis bond
1:4 @; produce
dextrin @limit,
maltotriosa, and
maltosa

Lingual gland

Lingual lipase

Trigliserida

Lipid acid plus

1,2 diasilgliserol

Gaster

Pepsin
(pepsinogen)

Gaster lipase

Hcl-

Protein and Decompose

polipeptida peptida chain
which closer
with aromatic
amino acid
Trigliserida
Lipid acid and
gliserol

Source

Enzim

Activator Substrat

Function and katalitik

produce

Enteropep Proein and

tidase
polipeptida

Decompose peptida bond

to karboksil various
amino acid basic (arginin
or lisin)

Kemotripsi
n

Tripsin

Proein and
polipeptida

Decompose peptida chain

to karboksil aromatic acid
amino

Elastase

Tripsin

Elastin other
protein

Decompose karboksil
amino acid alifatik chain

Karboksipe
ptidase A

Tripsin

Proein and
polipeptida

Decompose karboksil
teminal acid amino chain
which aromatic chain or
bifurcate alifatik

Karboksipe
ptidase B

Tripsin

Proein and
polipeptida

Decompose karboksil
terminal acid amino chain
which alkali chain

Pancrea Tripsin
s
(tripsinoge
eksocrin n)
e

Kolipase

Lipid items

To open a part of active

lipase pancreas

Pancreas
Lipase

Trigliserida

Monogiserida and fatty

acid

Lipase

Choesteril
ester

Cholesterol

Ester
Kolesteril
hidrolase

Cholesteril
ester

Cholesterol

Starch

@-amilase saliva

Ribonuklea
se

RNA

Nukleotida

Deoksiribo
nuklease

DNA

Nukleotida

Phosfolipid

Fatty acid and

lisophosfolipid

Panckreas
@-amilase

Fosfolipase
A2

Tripsin

Cl-

Tripsin

Source

Enzim

Activato Substrat
r

Function and katalitik

produce

Small
intest
mucous

Enteropeptida
se

Tripsinoge Tripsin
n

Aminopeptida
se

Polipeptid
a

Decompose to amino chain

acid amino terminal from
peptide

Karboksipepti
dase

Polipeptid
a

Decompose to amino chain

acid amino terminal from
peptide

Endopeptidas
e

Polipeptid
a

Decompose to residue
between middle of peptide

Dipeptidase

Dipeptida

2 amino acid

Maltase

Maltosa,
Glucose
maltotrios
a, @-

Source

Enzim

Small intest
mucous

Laktase

Laktosa

Galaktosa and
glucose

Sukrase*

Sukosa;
maltotriosa and
maltosa

Fruktosa and
glucose

@Dekstrinase*

@-dekstrin,
maltosa,
maltotriosa

Glucose

Threhalase

Trehalosa

Glucose

Nuklease and
other enzims

Nukleat acid

Pentosa,purin
and pirimidin

Various
peptidase

Di,tri, and
tetrapeptida

Amino acid

Cytoplasma
cell mucous

Activato Substrat
r

Function and
katalitik
produce

Organ

Hormon

Sasaran

Fungsi

Stomach

Gastrin

Exocrine
glands and
smooth muscle

Motility control, support

absorption and digestion
process

Duodenum Sekretin,
Digestive tract, Motility control, support
kolesistokinin, pancreas, liver, absorption and digestion
gastric
vesica velea
process
inhibitor,
peptide
Liver

Somatomedin

Bones, Soft
Tissues

Growth trigger

Pancreas;
langerhan
s island

-Insulin (B
cell)

Almost all cell

Supporting absorption, using

and saving nutrients by cell for
maintain nutrient level after
absorption phase
Inhibit digestion and absorption

Almost all cell

-Glukagon
(sel A)
-Somastatine
(sel D)

Digestive
system
Pancreatic cell;

Inhibit all pancreatic hormones

secretion

FISIOLOGI

Mouth and
Esophagus
Mastification
Salivary Glandsaliva (secreted in acinar cells )
Saliva contain: mucins,IgA,lysozyme,lactoferrin,
prolinerich protein.
Enzymes: lingual lipase and salivary amylase
Ph at about 7help neutralize gastric acid and
relieve heartburn when gastric juice is
regurgitated into the esophagus.
Control: neural control.
Nervus: parasymphatic (>fluid; organic <)and
symphatic (>thick; organic <<)

 Swallowing is a reflex respone that is triggered by

afferent impulses in the trigeminal,
glossopharyngeal, and vagus nerves.
The voluntary action of collecting the oral
contents on the tongue and propelling them
backward into the pharynx Involuntary
contraction in the pharyngeal muscles that
pushes the material into the esophagus

Stomach

Parietal cellsHCl and

intrinsic factor
Chief cellspepsinogen
Mucus

 Nervus: parasymphatic the vagi ;

sympathicceliac plexus
Gastric juice: cations, anions,pepsin,
lipase, mucus, intrinsic factor
HClkill many ingested bacteria, provides
the necessary pH for pepsin to start
protein digestion and stimulates the flow
of bile.
Gastric motility and emptying

 Regulation of gastric secretion are

regulated by neural and humoral
mechanism.
Vagalstimulates gastrin secretion by
release of GRP
stimulates acetylcholine to
increase acid and pepsin secretion.

UPPER GIT DISORDERS

ESOPHAGI
TIS

Definition
The esophagus is the muscular tube that carries
food through the chest, from the mouth to the
stomach. Normally you don't feel it except when
you are swallowing. However, if the inside lining
of your esophagus becomes inflamed, you may
experience pain or problems swallowing. This
inflammation
esophagitis.

of

the

esophagus

is

called

Common causes
Acid reflux. By far the most common cause of
esophagitis, acid reflux (also called gastroesophageal
reflux disease or GERD) is a backflow of digestive acid
from the stomach, resulting in a chemical burn of the
esophagus.
Eating disorders. Frequent vomiting can cause acid
burn in the esophagus. Esophagitis sometimes is seen in
people with eating disorders who make themselves
vomit.
Medications. Some common medications also can
cause a chemical burn in the esophagus. Pills that are
most likely to cause esophagitis include:
Tetracycline antibiotics, such as doxycycline
Oral potassium
Aspirin in high doses
Nonsteroidal anti-inflammatory drugs (NSAIDs), such
as ibuprofen (Advil, Motrin)
Osteoporosis medications, such as alendronate
(Fosamax) or risedronate (Actonel)
Iron supplements.

 Chemotherapy and radiation therapy for cancer. Some of

these treatments can injure the esophagus lining, resulting in
esophagitis.
Infections. Infections in the esophagus also can cause esophagitis.
Only a few types of infection are common in the esophagus, and
they usually do not occur if your immune system is normal.
If your immune system is weakened, you may develop esophagitis
from

yeast

(candidal

esophagitis)

or

from

viruses

such

as

cytomegalovirus (CMV) or herpes. Even in someone who already

has a herpes infection, herpes rarely causes esophagitis if the
immune system is normal. Esophagitis from infections is common in
people who have HIV infection, use steroid medicines for a long
time, have had organ transplants, or have been treated with
chemotherapy for cancer.

Symptoms
Pain in the chest (behind the breastbone) or throat that
can be burning, heavy or sharp -- If acid reflux is the cause
of esophagitis, the pain may be worse after meals or when
you lie flat. Pain from esophagitis may be constant or may
come and go.
Swallowing problems including worsening of the chest pain
when you swallow or a feeling of food sticking in your
chest after you swallow
Bleeding, seen as blood in vomit or as darkening of the
stools.

Diagnosis
The diagnosis often is made based on your symptoms. The most

accurate way to check for esophagitis is to look directly at the

inside of the esophagus called an endoscope. The endoscope has
a camera at the end of a flexible, plastic-coated cord. This tube is
long enough to reach through the stomach to the first portion of
the intestine (duodenum), so the procedure is sometimes called
esophagogastroduodenoscopy or EGD. Using the endoscope, the
gastroenterologist can see evidence of injury from esophagitis,
such as areas where the lining of the esophagus has worn away
(called erosions or ulcers), blisters or scarred areas.

Some infections leave a deposit on the esophagus

walls that can be sampled through the endoscope
by using a remote-controlled brush. In some
cases

the

doctor

will

do

biopsy

of

the

esophagus by snipping a small sample of the

inside lining through the end of the endoscope.
This tissue is examined under a microscope.
Since esophagitis is only one of the things that
can cause symptoms of chest pain or swallowing
problems, your doctor may order other tests to
evaluate your heart, lungs or digestive tract.

Prevention
Avoid heavy meals, especially within several
hours of bedtime.
Cut out cigarettes and alcohol.
Avoid large amounts of caffeine, chocolate,
peppermint and high-fat foods.
Control your weight.

Complication
If

untreated,

esophagitis

may

cause

severe

discomfort, swallowing difficulty to the extent of

causing malnutrition or dehydration, and eventual
scarring of the esophagus. This scarring may lead
to a stricture of the esophagus, and food or
medications may not be able to pass through to
the stomach.
A condition called Barrett's esophagus. Barrett's
esophagus

can

gastroesophageal

develop

after

reflux.

Rarely,

years

of

Barrett's

GASTRIT
IS

Acute and Chronic

Acute Gastritis
Is an acute mucosal inflammatory process,
usually of a transient nature. Severe erosive
form of the disease is an important cause of
acute GI bleeding
Pathogenesis:
Associated with: NSAID (aspirin), Excessive alcohol
consumption, Heavy smoking, treatment with cancer
chemotherapeutic drugs, systemic infection, severe
stress

Risk Factors
Infection with H. pylori
Acquired
immunodeficiency
syndrome (AIDS)
Any condition that requires relief
from chronic pain using NSAIDS, such
as
chronic
low
back
pain,
fibromyalgia, or arthritis
Alcoholism
Cigarette smoking
Older age

 Clinical feature:
Epigastric pain with nausea
vomitting
Hematemesis (alcoholics)
Melena

and

Diagnosis

The most common diagnostic test for gastritis is

endoscopy with a biopsy of the stomach. Endoscope
can examine the lining of the esophagus, stomach, and first
portion of the small intestine.
Upper gastrointestinal (GI) series. The patient swallows
barium, a liquid contrast material that makes the digestive
tract visible in an X-ray. X-ray images may show changes in
the stomach lining, such as erosions or ulcers.
Blood test. The doctor may check for anemia, a condition
in which the bloods iron-rich substance, hemoglobin, is
diminished. Anemia may be a sign of chronic bleeding in
the stomach.
Stool test. This test checks for the presence of blood in
the stool, another sign of bleeding in the stomach.
Tests for H. pylori infection. The doctor may test a
patients breath, blood, or stool for signs of infection. H.
pylori infection can also be confirmed with biopsies taken

Chronic Gastritis
Gastritis develop as a result of the
combined
influence
of
bacterial
enzyms and toxin and release of
noxious chemical by the recruited
neutrophils
After initial exposure to h.pylori,
gastritis may develop in 2 patterns:
Antral type
Pangastritis

Autoimun gastritis

 Clinical feature:
Upper abdominal discomfort, nausea,
vomiting
Hypochlorhydria (autoimune)
serum gastrin levels are either normal or
only modestly elevated

Prognosis: most important is the

relationship of chronic gastritis to the
development of peptic ulcer and gastric

H.Pylori

Natural history of H. pylori

infection

Treatment
H2 blockers -- reduce gastric acid secretion. They include:

Cimetidine (Tagemet)

Ranitidine (Zantac)

Nizatidine (Axid)

Famotidine (Pepcid)

Proton-pump

inhibitors

production. They include:

Esomeprazole (Nexium)

Lansoprazole (Prevacid)

Omeprazole (Prilosec)

Pantoprazole (Protonix)

Rabeprazole (Aciphex)

--

decrease

gastric

acid

Treatment (NonMedicamentosa)

Lifestyle change
The treatment for gastritis that is caused by irritants is to
stop using them. These include:
Alcohol
Tobacco
Acidic beverages such as coffee (both caffeinated and
decaffeinated), carbonated beverages, and fruit juices
with citric acid
NSAIDS, such as aspirin and ibuprofen -- switch to
other pain relievers (like acetaminophen)
These steps may also help:
Eat a fiber-rich diet.
Foods containing flavonoids, like apples, celery,
cranberries (including cranberry juice), onions, garlic,
and tea may stop the growth of H. pylori.
Avoid high-fat foods. In animal studies, high-fat foods
increase inflammation in the stomach lining.

PEPTIC
ULCER

Peptic Ulcer
A peptic ulcer is a hole in the gut lining of the
stomach, duodenum, or esophagus.
A peptic ulcer of the stomach is called a gastric
ulcer; of the duodenum, a duodenal ulcer; and of
the esophagus, an esophageal ulcer.
An ulcer occurs when the lining of these organs
is corroded by the acidic digestive juices which
are secreted by the stomach cells.

Peptic Ulcers
Pathogenesis
Two conditions are key for the development of
peptic ulcers:
1.H. pylori infection
2.Mucosal exposure to gastric acid and pepsin
3.Peptic

ulcer

are

created

by

an

imbalance

between the gastroduodenal mucosal defenses

and damaging force that overcome such defenses

Symptoms
Indigestion.
Upper abdominal burning or hunger
pain one to three hours after meals
and in the middle of the night.
Ulcers
often
come
and
go
spontaneously without the individual
ever knowing, unless a serious
complication
(like
bleeding
or
perforation) occurs

Diagnosis
The diagnosis of an ulcer is made by either a

barium upper GI x-ray or an upper endoscopy

(EGD-esophagogastroduodenoscopy)
Biopsies

can

also

be

examined

under

microscope to exclude cancer. While virtually all

duodenal ulcers are benign, gastric ulcers can
occasionally be cancerous. Therefore, biopsies
are often performed on gastric ulcers to exclude
cancer.

Complications
Ulcer bleeding
Ulcer perforation
Gastric obstruction.

Treatment
1. Reduction of risk factors (NSAIDs and
cigarettes)
2. Medications
- Antacids: is neutralize existing acid in the
stomach. Such as mylanta
- H2 blockers are cimetidine (Tagamet),
ranitidine (Zantac), nizatidine (Axid), and
famotidine (Pepcid)
- Proton-pump
inhibitors:
omeprazole,
lansoprazole, pantoprazole, esomeprazole,
and rabeprazole
- Antibiotics

GER
D

Physiology
The lower esophageal sphincter (LES) must have a
normal length and pressure and a normal number of
episodes of transient relaxation (relaxation in the
absence of swallowing).
The gastroesophageal junction must be located in the
abdomen so that the diaphragmatic crura can assist
the action of the LES, thus functioning as an extrinsic
sphincter. The presence of a hiatal hernia disrupts this
synergistic action and can promote reflux (see image
below).

Physiology

Esophageal
clearance must be
able to neutralize
the acid refluxed
through the LES.
(Mechanical
clearance
is
achieved
with
esophageal
peristalsis. Chemical
clearance
is
achieved
with
saliva.)
The stomach must
Barium swallow indicating hiatal hernia.
empty properly.

Definition
Gastroesophageal

reflux

disease,

commonly

referred to as GERD or acid reflux, is a condition

in which the liquid content of the stomach
regurgitates (backs up or refluxes) into the
esophagus. The liquid can inflame and damage
the lining of the esophagus although visible signs
of inflammation occur in a minority of patients

 The regurgitated liquid usually contains acid and

pepsin that are produced by the stomach. The refluxed

liquid also may contain bile that has backed-up into
the stomach from the duodenum.
Acid is believed to be the most injurious component of

the refluxed liquid. Pepsin and bile also may injure the
esophagus,

but

their

role

in

the

production

of

esophageal inflammation and damage is not as clear

as the role of acid.

Risk factor

Obesity
Hiatal hernia
Pregnancy
Smoking
Dry mouth
Asthma
Diabetes
Delayed stomach emptying
Connective tissue disorders, such as scleroderma
Zollinger-Ellison syndrome

 Apart

from

incompetent

barriers,

gastric contents are most likely to

reflux :
When gastric volume is increased
When

gastric

contents

are

near

gastroesophageal junction
When gastric pressure is increased

the

Pathophysiology
However, if this valve relaxes abnormally or
weakens stomach acid can flow back up into
esophagus heartburn acid can irritate the
lining of esophagus inflamed (esophagitis).
can erode the esophagus bleeding or breathing
problems.

Pathophysiology
A

functional

(frequent

transient

LES

relaxation)

or

mechanical (hypotensive LES) problem of the LES is the

most common cause of gastroesophageal reflux disease
(GERD).
Certain foods (eg, coffee, alcohol), medications (eg, calcium

channel blockers, nitrates, beta-blockers), or hormones (eg,

progesterone) can decrease the pressure of the LES.
Obesity is a contributing factor in gastroesophageal reflux

disease (GERD), probably because of the increased intraabdominal pressure.

Complication
Narrowing of the esophagus (esophageal stricture). Damage to
cells in the lower esophagus from acid exposure leads to formation of
scar tissue. The scar tissue narrows the food pathway, causing
difficulty swallowing.
An open sore in the esophagus (esophageal ulcer). Stomach
acid can severely erode tissues in the esophagus, causing an open
sore to form. The esophageal ulcer may bleed, cause pain and make
swallowing difficult.
Precancerous
changes
to
the
esophagus
(Barrett's
esophagus). In Barrett's esophagus, the color and composition of the
tissue lining the lower esophagus change. These changes are
associated with an increased risk of esophageal cancer. The risk of
cancer is low, but your doctor will recommend regular endoscopy
exams to look for early warning signs of esophageal cancer.

Diagnose
An X-ray of upper digestive system.
Sometimes called a barium swallow or upper GI series, this procedure
involves drinking a chalky liquid that coats and fills the hollows of
digestive tract.
Then X-rays are taken of upper digestive tract.
Endoscopy
A test to monitor the amount of acid in esophagus.
Ambulatory acid (pH) probe tests use an acid-measuring device to identify
when, and for how long, stomach acid regurgitates into esophagus.
A test to measure the movement of the esophagus.
Esophageal impedance measures movement and pressure in the
esophagus.

Treatment and drug

Antacids that neutralize stomach acid. Antacids, such as Maalox,

Mylanta, Gelusil, Rolaids and Tums, may provide quick relief. But antacids
alone won't heal an inflamed esophagus damaged by stomach acid.
Overuse of some antacids can cause side effects such as diarrhea or
constipation.

Medications to reduce acid production. Called H2 receptor blockers,

these medications include cimetidine (Tagamet HB), famotidine (Pepcid
AC), nizatidine (Axid AR) or ranitidine (Zantac 75). H 2 receptor blockers
don't act as quickly as antacids, but they provide longer relief. Stronger
versions of these medications are available in prescription form.

Medications that block acid production and heal the esophagus.

Proton pump inhibitors block acid production and allow time for damaged
esophageal tissue to heal. Over-the-counter proton pump inhibitors
include lansoprazole (Prevacid 24 HR) and omeprazole (Prilosec OTC).