Problem 1B

Felix Halim
405110204
Group 13
ANATOMY
MOUTH
 Esophagus
The largest part of thorax
Pars thoracalis (behind trachea)
Pars abdominalis : enter to the gastric cardia ventriculi
transition ostium cardiacum/ cardiac orificium/ junctio
gastroesophagei
It has LES and its function for preventing reflux
The closing of spincter is controlled by vagal and amplified by gastrin
, and decreased by secretin response, cholecystokinin, glucacon
Vascularitation:
a. gastrica sinistra
Branch of a. phrenica inferior
V. azygos
V. gastrica sinistra
nerves : N. vagus (parasimpatis), N. splanchnici (simpatis)
HISTOLOGY
 Lips
Zone of lips

Cutanea Intermediate Oral mucuos

non- non-
keratinsed
keratinised keratinised
stratified
stratified stratified
squamuosa
squamous squamous
epithelium
epithelium epithelium
Lingua
Lingua is a skeletal muscular organ
which is used to manipulate and to
taste foods. Lingua usually contains
types of papilae which is :
1. Filiform papilae
2. Fungiform papilae
3. Foliate papilae
4. Circumvalatte papilae
 The greatest number of papilae and spread all
over 2/3 anterior of tongue
Taste bud ( - )
Secondary papilae ( + )
Sharp pointed
Squamous cell keratinized epithel
 Spread among filiform
papilae
Squamous cell w/wto
keratinized epithel
Mushroom like shaped
Taste bud ( + ), small
Secondary papilae ( + )
 Not well developed in
human
Located in dorsolateral
of tongue
Taste bud + and huge
Ebner glands at the
bottom of cryptus

Foliate papilae
 Are the largest (up to 1/8 in diameter) papillae
Many taste buds are located on their sides.
Shaped like fungiform papilae
Secondary papilae +
Circular sulcus (cryptus)
Cells of taste buds:

sensory cells
has microvilli
supporting (or
sustentacular)
cells
basal cells
 Teeth
Blood vessels - carry nutrients to the tooth.
Bone - alveolar bone forms the tooth socket
and provides it with support.
Cementum - the layer of hard bone-like tissue
covering the root of the tooth.
Cemento-enamel junction - the line where the
enamel and cementum meet.
Dentin - the hard yellow tissue underlying the
enamel and cementum, making up the main
bulk of the tooth.
Enamel - the hard, white outer layer of the
tooth.
Gingiva - the gum tissue surrounding the
tooth.
Ligament - the connective tissue that
surrounds the tooth and connects it to bone.
Nerves - relay signals such as pain to and from
your brain.
Pulp - located in the center of the tooth, it
contains the arteries, veins and nerves.
Root canal - canal in the root of the tooth
where the nerves and blood vessels travel
through.
Esophagus
 Longitudinal section of esophagus
shows mucosa consisting of
nonkeratinized stratified squamous
epithelium (SS), lamina propria (LP),
and smooth muscles of the
muscularis mucosae (MM). Beneath
the mucosa is the submucosa
containing esophageal mucous
glands (GL) which empty via ducts
(D) onto the luminal surface. X40.
PHYSIOLOGY
 Physiology
There are four basic digestive
processes:
Motility
Secretion
Digestion
Absorption
 Motility
MOTILITY The term motility refers to
the muscular contractions that mix and
move forward the contents of the
digestive tract.
maintains a constant low level of
contraction known as tone
2 basic types of phasic digestive motility
are:
propulsive movements
mixing movements
 Propulsive movements propel or
push the contents forward through
the digestive tract
Mixing movements serve a twofold
function.
First, by mixing food with the digestive juices,
these movements promote digestion of the
food
Second, they facilitate absorption by exposing
all parts of the intestinal contents to the
absorbing surfaces of the digestive tract
 Secretion
Exocrine glands
On appropriate neural or hormonal
stimulation, the secretions are
released into the digestive tract
lumen.
Normally, the digestive secretions
are reabsorbed in one form or
another back into the blood after
their participation in digestion.
 Digestion
Humans consume three different
biochemical categories of energy-rich
foodstuffs: carbohydrates, proteins,
and fats.
The term digestion refers to the
biochemical breakdown of the
structurally complex foodstuffs of the
diet into smaller, absorbable units by
the enzymes produced within the
digestive system as follows:
 The simplest carbohydrates are the simple
sugars or monosaccharides (one-sugar
molecules), such as glucose, fructose, and
galactose
Most ingested carbohydrate is in the form of
polysaccharides (many-sugar molecules)
meat contain glycogen
Cellulose, another dietary polysaccharide,
found in plants, (represents the indigestible
fiber or bulk of our diets.)
 proteins consist of various
combinations of amino acids held
together by peptide bonds
digestion, proteins are degraded
primarily into their constituent amino
acids as well as a few small
polypeptides
 Most dietary fats are in the form of
triglycerides, which are neutral
fats, each consisting of a glycerol
with three fatty acid molecules
attached (tri means three)
Triglycerides monoglycerides
+ free fatty acids
 Absorption
Through the process of absorption,
the small absorbable units that result
from digestion, along with water,
vitamins, and electrolytes, are
transferred from the digestive tract
lumen into the blood or lymph
Accessory digestive organs
The accessory digestive organs
include the salivarynglands, the
exocrine pancreas, and the biliary
system, which is composed of the
liver and gallbladder.
 Four factors are involved in
regulating digestive system function
1. Autonomous smooth muscle function
2. Intrinsic nerve plexuses
3. Extrinsic nerves
4. Gastrointestinal hormones
 Autonomous Smooth Muscle
Function
The prominent type of self-induced electrical
activity in digestive smooth muscle is slow-
wave potentials alternatively referred to as
the digestive tracts basic electrical rhythm
(BER).
Interstitial cells of Cajal are the pacemaker
cells that instigate cyclic slow-wave activity
These pacemaker cells lie at the boundary
between the longitudinal and circular smooth
muscle layers.
 At threshold, voltagegated Ca2 channels are
activated resulting in Ca2 influx into the smooth
muscle cell. The resultant Ca2 entry has two
effects:
1. It is responsible for the rising phase of an action
potential, with the falling phase being brought about
as usual by K efflux
2. it triggers a contractile response
The greater the number of action potentials, the
higher the cytosolic Ca2 concentration, the
greater the cross-bridge activity, and the
stronger the contraction.
 Intrinsic Nerve Plexus
intrinsic nerve plexuses are the
two major networks of nerve fibers
the submucosal plexus and the
myenteric plexus
Some of the output neurons are
excitatory (acetylcholine), and some
are inhibitory (nitric oxide,
vasoactive intestinal peptide)
 Extrinsic Nerve
extrinsic nerves are the nerve fibers
from both branches of the autonomic
nervous system that originate outside
the digestive tract and innervate the
various digestive organs
Th e sympathetic system, which
dominates in fight-or-flight situations,
tends to inhibit or slow down digestive
tract contraction and secretion
 the autonomic nerves, especially the
vagus nerve, can be discretely
activated to modify only digestive
activity
To coordinate activity between
different regions of the digestive
system.
 Gastrointestinal Hormones
gastrointestinal hormones are
carried through the blood to other
areas of the digestive tract, where
they exert either excitatory or
inhibitory influences on smooth
muscle and exocrine gland cells
 Physiology
Swallowing
Preparatory phase (food bolus suitable for
swallowing is prepared) transfer phase (bolus is
pushed into the pharynx by contraction of the
tongue) bolus then activates oropharyngeal
sensory receptors deglutition reflex (to propel
food through the pharynx and the esophagus and
to prevent its entry into the airway) larynx
moves forward and the upper esophageal sphincter
(UES) opens contraction of the superior
pharyngeal constrictor against the contracted soft
palate peristaltic contraction The lower
esophageal sphincter (LES) opens as the food
enters the esophagus stomach.
 Primary peristalsis Peristaltic
contraction in response to a swallow
It involves inhibition followed by
sequential contraction of muscles
along the entire swallowing passage.
The inhibition that precedes the
peristaltic contraction is called
deglutitive inhibition
distention of the esophagus from
residual food activates secondary
peristalsis.
BIOCHEMISTRY
Biochemistry
DISORDERS
Indigestion/ dyspepsia
 Definition
Indigestion is a general term that
describes discomfort in your upper
abdomen.
Indigestion isnt a disease, but rather a
collection of symptoms.
ETIOLOGY
Disorders or diseases in the lumen of the
digestive tract
Drugs
Diseases of the liver, pancreatic, biliary
system
Systemic diseases
 Symptoms
Early fullness during a meal
Uncomfortable fullness after a meal
Pain in the upper abdomen. You feel a mild to
severe pain in the area between the bottom of
your breastbone (sternum) and your navel
Burning in the upper abdomen. You feel an
uncomfortable heat or burning sensation between
the bottom of the breastbone and navel
Less frequent symptoms :
Nausea. You feel like you are about to vomit
Bloating. Your stomach feels swollen, tight and
uncomfortable
diagnose
Full blood count and erythrocyte
sedimentation rate
The x-ray tests include:
The upper gastrointestinal series
The small bowel series
The barium enema
CT scan
The endoscopic tests include:
EGD
Colonoscopy
Treatment

Antacids

Anticholinergics

Prokinetik

Sitoprotektif

Histamine H2 Antagonist
 Nausea and Vomiting
Nausea is the subjective feeling of a need
to vomit.
Vomiting (emesis) is the oral expulsion of
gastrointestinal contens resulting from
contractions of gut and
thoracoabdominal wall musculature.
Vomiting is contrasted with regurgitation.
 Mechanism of Nausea and
Vomiting
Vomit
Expulsion with persistent of stomach contents out
from mouth,commonly its consider cause by
abnormal gastric motility.
Vomit doesnt appear by reverse peristaltic.
The most important force that press gastric contents
such as diaphragm contraction(priory inspiration
muscle) and abdominal muscle (active extrinsic
muscle)
Nausea is the sensation of having an urge to
vomit.
 Vomit is start with:
Inhale and glottis closingcontraction of
diaphragm descend to press gastric and
abdominal muscles contraction press
abdomen cavityintraabdomen
pressure () and abdomen contents pushed
to the top gastric pushed from top and
under gastric contents push to in
oesophagus and out from mouth.
 Glottis closingvomit didnt enter to
resporatory tract.
Uvula was liftedclose a nasal
cavity.
Vomit a yellow appearancetheres
a gall that enter to duodenum from
hepar and gall bladder.
 Usually,vomit was started by many
common sign:
Expulsion of saliva >>>
Sweating
Heartbeats velocity ()
Nausea
Etiology of vomit
Tactil stimulation on larynxs backside.
Iritation on stomach or duodenum
Intracranial pressure ()ex/ intercerebrum
bleeding
Rotation or head accelerationdizzy ex/
carsick/seasick/airsick
Intensive pain from another organ
Chemicalex emetic drugs
Pshycis vomit (by emotion factor)
 Vomit >>>body will get liquid and
acid expulsion that was reabsorption
on normal condition.
Plasma volume decreasedwill get
dehidration and circulation problems
Acid is outmetabolic alcalosis.
Management
Identification and elimination of
the underlying cause if possible
Control of the symptoms if it is
not possible to eliminate the
underlying cause
Correction of electrolyte, fluid or
nutritional deficiencies
Diagnostic
Blood tests
Urinalysis
X-rays of the abdomen
Treatment
Give intravenous fluids.
If dehydration is severe
Antivomiting drugs (anti-emetics)
may be helpful but they should
be used only when the potential
benefits outweigh the risks.
ESOPHAGITIS
 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 of the esophagus is called
esophagitis.
 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 a 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 develop after years of
gastroesophageal reflux. Rarely, Barrett's esophagus
may lead to cancer of the esophagus.
GERD
 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
empty properly.
Barium swallow indicating hiatal hernia.
 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 the

gastroesophageal junction
When gastric pressure is increased
 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 intra-
abdominal 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).