Pemicu 1 GIT

LO I: Anatomi, Histologi,
Fisiologi, Biokimia Saluran
Pencernaan Atas
Anatomi
Upper Gastrointestinal Tract
The upper GI tract consists of the mouth,
pharynx, esophagus, stomach, and upper
duodenum
The mouth contains the buccal mucosa, which
contains the openings of the salivary glands;
the tongue; and the teeth.
Behind the mouth lies the pharynx, which leads
to a hollow muscular tube, the esophagus.
Peristalsis takes place, which is the contraction
of muscles to propel the food down the
esophagus which extends through the chest
and pierces the diaphragm to reach the
stomach.
 Lower gastrointestinal tract
The lower GI tract comprises the intestines and anus.

Bowel or intestine
Small intestine, which has three parts:
Duodenum
Jejunum
Ileum
Large intestine, which has three parts:
Cecum (the vermiform appendix is attached to the
cecum).
Colon (ascending colon, transverse colon, descending
colon and sigmoid flexure)
Rectum
Anus
Fisiologi
 Physiology - Digestive
System
The functions of the digestive system are:
Ingestion - eating food
Digestion - breakdown of the food
Absorption - extraction of nutrients from the
food
Defecation - removal of waste products
The digestive system is a group of organs
that breakdown the chemical components
of food, with digestive juices, into
micromolecul nutrients which can be
absorbed to generate energy for the body
 The bucal cavity (mouth) and
salivary glands
Food enters the mouth and is chewed
by the teeth, turned over and mixed
with saliva by the tongue.
Mouth: the salivary glands. Saliva
produced by these glands contains an
enzyme that begins to digest the
starch from food into smaller
molecules. ptyalin enzyme
 The Stomach
It is the widest part of the alimentary canal and
acts as a reservoir for the food where it may
remain for between 2 and 6 hours.
Here the food is churned over and mixed with
various hormones, enzymes including pepsinogen
which begins the digestion of protein,
hydrochloric acid, and other chemicals
The stomach has an average capacity of 1 liter,
varies in shape, and is capable of considerable
distension.
At regular intervals a circular muscle at the lower
end of the stomach, the pylorus opens allowing
small amounts of food, now known as chyme to
enter the small intestine.
Duodenum
 Small Intestine
The small intestine measures about 7m in an
average adult and consists of the duodenum,
jejunum, and ileum.
Both the bile and pancreatic ducts open into the
duodenum together.
The small intestine, because of its structure,
provides a vast lining through which further
absorption takes place.
 The Large Intestine
The large intestine averages about 1.5m long and
comprises the caecum, appendix, colon, and
rectum.
Here most of the water and electrolytes is
absorbed, much of which was not ingested, but
secreted by digestive glands further up the
digestive tract.
The colon is divided into the ascending,
transverse and descending colons, before
reaching the anal canal where the indigestible
foods are expelled from the body.
LO
Emesis
 Function
Vomiting, as a basic physiologic
protective mechanism, limits the
possibility of damage from ingested
noxious agents by emptying the
contents of the stomach and portions
of the small intestine.
Nausea and vomiting may represent a
total-body response to drug therapy,
including overdosage, cumulative
effects, toxicity, and side effects.
 Mechanism
Vomiting involves two functionally
distinct medullary centers:
the vomiting center
in the dorsal portion of the reticular formation of
the medulla near the sensory nuclei of the vagus.
the chemoreceptor trigger zone.
in a small area on the floor of the fourth ventricle,
where it is exposed to both blood and
cerebrospinal fluid. It is thought to mediate the
emetic effects of blood-borne drugs and toxins.
responds to numerous chemicals and hormones,
including dopaminergic, a2-adrenergic, and opioid
agonists, and cardiac glycosides, cytotoxins, and
CuSO4.
 Receptors and neurotransmitters involved in
mediating vomiting
Structures Receptors Agonist Antagonist
Area postrema D2 Apomorphine Antidopaminergic
drugs
CTZ L-DOPA
Vestibular nuclei M, H1 Cholinomimetics Scopolamine

N. tractus solitarius Histamine Dramamine

Vomiting center M Cholinomimetics Scopolamine

(e.g., physostigmine)

Vagal sensory 5-HT3 Serotonin Ondansetron

nerveendings
Granisetron
Tropisetron
 Treatment
Anticholinergics
The only anticholinergic to have been shown to have any
antiemetic quality is hyoscine. It may be of use in patients for
whom the main stimulus is vestibular (that is, nausea and vomiting
caused by movement or ear, nose, and throat surgery). Its main
use, however, is now in palliative care where it is used to dry upper
airway secretions and ease breathing at the end of life.

Antihistamines
Several drugs inhibit the action of histamine at the H 1synaptic
pathways, which are predominantly involved in signalling from the
vestibular centre, but only cyclizine is used to treat postoperative
nausea and vomiting. Has few side effects. Common mild side
effects are a consequence of its antimuscarinic actions and include
sedation and dry mouth.

Steroids
Steroids such as dexamethasone may be given preoperatively as
prophylaxis in patients with a high risk of nausea and vomiting.
Steroids act by reducing inflammatory oedema and altering central
and peripheral responsiveness to proemetic compounds such as
anaesthetics and analgesics.They can also be used as a last line
rescue treatment.
 Dopamine antagonists
These pharmaceuticals, for example prochlorperazine, haloperidol, and
metoclopramide, have been used as antiemetics for many years. They
work by inhibiting the activity of dopamine at the D 2receptor in the
chemoreceptor trigger zone, thereby limiting the emetic input to the
medullary vomiting centre.
Certain other antipsychotics, especially haloperidol, are often used in
palliative care to treat nausea and vomiting caused by malignancy. Low
doses of haloperidol, such as 1 mg once a day, are effective and are the
treatment of choice for nausea and vomiting caused by intestinal
obstruction.
Metoclopramide closely resembles the phenothiazines but has a limited
role as an antiemetic for postoperative nausea and vomiting. It is
effective in certain settings, such as emesis associated with hepatic
disease, but has been shown to be ineffective in many trials for the
treatment of postoperative nausea and vomiting and should not be
considered without senior input. Because it also increases gastrointestinal
motility, it should never be considered in patients where bowel
obstruction is possible.

Serotonin antagonists
Ondansetron, granitetron, and tropisetron inhibit the action of serotonin
at the 5-hydroxytryptamine 3 (5-HT3) receptor in the small bowel, vagus
nerve, and chemoreceptor trigger zone. They therefore decrease afferent
visceral and chemoreceptor trigger zone stimulation of the medullary
vomiting centre. These drugs were developed for use with chemotherapy
and have been shown in trials to be the most effective of the currently
available agents for both prevention and treatment of postoperative
nausea and vomiting.
 Diagnostic Tests and Clinical Suspicion for Patients with Nausea and Vomiting
Test
Complete blood count
Electrolytes
Erythrocyte sedimentation rate
Pancreatic/liver enzymes
Pregnancy test
Protein/albumin
Specific toxins
Thyroid-stimulating hormone
Radiographic testing
Supine and upright abdominal radiography
Further testing
Esophagogastroduodenoscopy
Upper gastrointestinal radiography with barium Mucosal lesions and higher-grade obstructions; evaluates for proximal
contrast media
Small bowel follow-through
Enteroclysis
Computed tomography with oral and
intravenous contrast media
Gastric emptying scintigraphy
Cutaneous electrogastrography
Antroduodenal manometry
Abdominal ultrasonography
Magnetic resonance imaging of the brain
Clinical suspicion
Laboratory tests
Leukocytosis in an inflammatory process, microcytic anemia from a
mucosal process
Consequences of nausea and vomiting (e.g., acidosis, alkalosis, azotemia,
hypokalemia)
Inflammatory process
For patients with upper abdominal pain or jaundice
For any female of childbearing age
Chronic organic illness or malnutrition
Ingestion or use of potentially toxic medications
For patients with signs of thyroid toxicity or unexplained nausea and
vomiting
Mechanical obstruction
Mucosal lesions (ulcers), proximal mechanical obstruction
lesions
Mucosal lesions and higher-grade obstructions; evaluates the small bowel
to the terminal ileum
Small mucosal lesions, small bowel obstructions, small bowel cancer
Obstruction, optimal technique to localize other abdominal pathology
Gastroparesis (suggestive)
Gastric dysrhythmias
Primary or diffuse motor disorders
Right upper quadrant pain associated with gallbladder, hepatic, or
pancreatic dysfunction
Intracranial mass or lesion
 Complication
Excessive vomiting can lead to large
losses from the stomach of the water
and salts that normally would be
absorbed in the small intestine. This
can result in severe dehydration,
upset the bodys salt balance, and
produce circulatory problems due to
a decrease in plasma volume.
The loss of acid from vomiting results
in a metabolic alkalosis.
 REGURGITATION
Definition:
effortless movement of stomach contents Into the
esophagus and mouth. It is not associated with
distress, and infants with regurgitation are often
hungry immediately after an episode
Regurgitation is a result of GER
(gastroesophageal reflux) through an
incompetent, or in infants, immature lower
esophageal sphincter
This is often a developmental process and
regurgitation or spitting resolves with maturity
Usually revolves in 80% infants by 6mo, 90% by 12mo
REGURGITATION
Sign & Symptoms:

Weight loss
Halitosis
Indigestion
Chronically raw and chapped
lips
 GERD
Gastroesophageal reflux (GER) is a common,
self-limited process in infants that usually
resolves by six to 12 months of age. The
prevalence of GER peaks between 1 ~ 4 mo of
age
If complications develop or regurgitation persists, GER
is considered pathologic (considered as
gastroesophageal reflux disease, GERD) rather than
merely developmental & deserves further evaluation
& treatment
GERD or acid reflux, is a condition in which the
liquid content of the stomach regurgitates
(backs up or refluxes) into the esophagus
 Classifying GERD
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)
 Pathophysiology
GER occurs when the lower esophageal sphincter (LES) opens
spontaneously, for varying periods of time, or does not close
properly and stomach contents rise up into the esophagus. GER
is also called acid reflux or acid regurgitation, because digestive
juicescalled acidsrise up with the food. The esophagus is the
tube that carries food from the mouth to the stomach. The LES
is a ring of muscle at the bottom of the esophagus that acts like
a valve between the esophagus and stomach.
When acid reflux occurs, food or fluid can be tasted in the back
of the mouth. When refluxed stomach acid touches the lining of
the esophagus it may cause a burning sensation in the chest or
throat called heartburn or acid indigestion. Occasional GER is
common and does not necessarily mean one has GERD.
Persistent reflux that occurs more than twice a week is
considered GERD, and it can eventually lead to more serious
health problems. People of all ages can have GERD.
 Symptoms
GER is common in healthy infants. More than half of all babies
experience reflux in the first 3 months of life, but most stop
spitting up between the ages of 12 to 24 months. Only a
small number of infants have severe symptoms.
An infant with GER may experience :
spitting up
vomiting
coughing
irritability
poor feeding
blood in the stools
In a small number of babies, GER results in symptoms that cause
concern. These symptoms include
poor growth due to an inability to hold down enough food
irritability or refusing to feed due to pain
blood loss from acid burning the esophagus
breathing problems
 Examination
Endoscopy
Biopsies
X-rays
Examination of the throat and larynx
Esophageal acid testing
Acid perfusion test
 Treatment
Treatment
Life style Elevation of the upper body at night generally is recommended for all
patients with GERD
modification
GERD Diet * These foods should be avoided and include:
Chocolate, peppermint, alcohol & caffeinated drinks
* Fatty foods (which should be decreased) and smoking (which should
be stopped) also reduce the pressure in the sphincter and promote
reflux
* Chewing gum stimulates the production of more bicarbonate-
containing saliva and increases the rate of swallowing.

Antacids Antacids neutralize the acid in the stomach so that there is no acid to
reflux
they do so for only a short period of time
The best way to take antacids, therefore, is approximately one hour
after meals or just before the symptoms of reflux begin after a meal.
Since the food from meals slows the emptying from the stomach, an
antacid taken after a meal stays in the stomach longer and is
effective longer

Histamin The first medication developed for more effective and convenient
treatment of acid-related diseases, including GERD, was a histamine
Antagonist antagonist, specifically cimetidine (Tagamet)
Histamine is an important chemical because it stimulates acid
production by the stomach
Treatment
Protein Pump The second type of drug developed specifically for acid-related
diseases, such as GERD, was a proton pump inhibitor (PPI),
Inhibitor specifically, omeprazole (Prilosec)
The advantage of a PPI over an H2 antagonist is that the PPI
shuts off acid production more completely and for a longer period
of time
Five different PPIs are approved for the treatment of GERD,
including omeprazole (Prilosec), lansoprazole (Prevacid),
rabeprazole (Aciphex), pantoprazole (Protonix), and esomeprazole
(Nexium). A fifth PPI product consists of a combination of
omeprazole and sodium bicarbonate (Zegerid). PPIs (except for
Zegarid) are best taken an hour before meals

Pro Motility Drug Pro-motility drugs work by stimulating the muscles of the
gastrointestinal tract, including the esophagus, stomach, small
intestine, and/or colon. One pro-motility drug, metoclopramide
(Reglan)
Pro-motility drugs increase the pressure in the lower esophageal
sphincter and strengthen the contractions (peristalsis) of the
esophagus

Foam Barriers Foam barriers are tablets that are composed of an antacid and a
foaming agent.
There is only one foam barrier, which is a combination of
aluminum hydroxide gel, magnesium trisilicate, and alginate
(Gaviscon).

Surgery The surgical procedure that is done to prevent

reflux is technically known as fundoplication and is
called reflux surgery or anti-reflux surgery