PROBLEM 1
ALMIRA NABILA VALMAI
405130193
LO
LO 1
ANATOMY OF DIGESTIVE
SYSTEM
Pipi
Dens
Dens
Vaskularisasi Dens
Palatum &
Lidah
Otot Penggerak
Lidah
Otot
Penggerak
Lidah
Otot
Penggerak
Lidah
Vaskularisasi &
Persarafan Lidah
Kelenjar
Lidah
LO 2
PHYSIOLOGY OF
DIGESTIVE SYSTEM
Mouth
Entry to the digestive tract is through
the mouth or oral cavity. The opening
is formed by the muscular lips.
The palate , which forms the arched
roof of the oral cavity, separates the
mouth from the nasal passages.
The tongue, which forms the floor of
the oral cavity, is composed of
voluntarily controlled skeletal muscle.
LO 3
HISTOLOGY OF DIGESTIVE SYSTEM
DIGESTIVE SYSTEM
Two groups of organs compose the
digestive system:
Gastrointenstinal (GI) tract or alimentary
canal mouth, most of pharynx,
esophagus, stomach, small intestine,
and large intestine
Accessory digestive organs teeth,
tongue, salivary glands, liver,
gallbladder, and pancreas
diFiore Atlas of Histology, 247
Histologic organization:
Mucosa:
Epithelium, lamina propria, muscularis mucosa
Submucosa:
connective tissue, vessels, and Meissners plexuses,
some times mucous glands
Muscularis externa: 2-3 layers of smooth muscle (plus
skeletal muscle in esophagus), myenteric (Auerbach)
plexus in between muscle layers
Serosa and adventitia: Outermost layer of loose
connective tissue and blood vessels. Call serosa if
covered my mesothelium; adventitia otherwise
mucosa
submuco
muscula
serosa
ORAL CAVITY
Inner surface of the lips, cheeks, soft
palate, surface of tongue, and floor of the
mouth
Nonkeratinized stratified squamous epithelium
Lamina propria
Submucosa
THE LIP
THE TONGUE
TONGUE PAPILLAE
fungiform
filliform
foliate
circumvall
ate
TASTE BUD
TEETH
ESOPHAGUS
Mucosa: non-keratinizing stratified
squamous
Submucosa: contains mucous glands
Increased mucous glands at lower esophagus
(GE junction) to protect esophagus from
gastric juices
Esophagus
Squamous
mucosa
Submuco
sa
Musculari
s Externa
Mucosa
Adventitia /
Serosa
Muscularis
mucosa
Lower esophagus
Upper esophagus
LO 4
BIOCHEMISTRY
Mouth
DIGESTION & ABSORPTION OF CARBOHYDRATES
Amylases Catalyze the Hydrolysis of Starch
The hydrolysis of starch by salivary and pancreatic amylases
catalyze random hydrolysis of (14) glycoside bonds, yielding
dextrins, then a mixture of glucose, maltose, and isomaltose (from
the branch points in amylopectin).
Disaccharidases Are Brush Border Enzymes
The disaccharidasesmaltase, sucrase-isomaltase (a
bifunctional enzyme catalyzing hydrolysis of sucrose and
isomaltose), lactase, and trehalaseare located on the brush
border of the intestinal mucosal cells where the resultant
monosaccharides and others arising from the diet are absorbed. In
most people, apart from those of northern European genetic origin,
lactase is gradually lost through adolescence, leading to lactose
intolerance. Lactose remains in the intestinal lumen, where it is a
substrate for bacterial fermentation to lactate, resulting in
discomfort and diarrhea.
LO 5
MOUTH INFECTION
Sumber: http://www.cdc.gov/ncbddd/birthdefects/cleftlip.h
Etiology:
- Changes in theirgenes
- A combination of genes and other
factors, such as things the mother
comes in contact with in her
environment, or what the mother
eats or drinks, or certain medications
she uses during pregnancy.
Sumber: http://www.cdc.gov/ncbddd/birthdefects/cleftlip.h
Sumber: http://www.cdc.gov/ncbddd/birthdefects/cleftlip.h
b. Micrognathia &
macrognathia
1. Micrognathia a severely deficient jaw, most
commonly affects the mandible.
Types:
- Apparent micrognathia: this is not due to abnormality
of small jaw, in terms of size but rather due to an
abnormal positioning or abnormal relation of one jaw
to another, which produces illusion of micrognathia
- True micrognathia: it is due to small jaw. It is again
classified as:
a. Congenital
b. Acquired
Etiology
Congenital:
- Congenital abnormalities: in
many instances, it is associated
with other congenital
abnormalities, particularly
congenital heart disease and
Pierre Robin syndrome (cleft
palate, micrognathia and
glossoptosis)
- Forceps delivery trauma: the use
of forceps on either side of the
head. If the joint, in this area,
called the temporomandibular
joint, is badly bruised, the
mandible does not develop
Acquired:
Ankylosis
Mouth breathing
Agenesis of condyle
Posterior positioning
Management:
- Orthognathic surgery: recommended
treatment modality for micrognathia.
This surgery is followed by
orthodontic appliance to correct
malocclusion
Clinical features:
- prognathism: mandibular protrusion or proganthism is common
occurrence, which is due to disparity in the size of maxilla to
mandible and posterior positioning of maxilla in relation to the
cranium
- Mandible: mandible is measurably larger than normal. Increased
mandibular body length
- Gummy smile: in certain patients with congenital abnormalities,
there may be elongation of maxilla. There is much show when
the patient smiles, so that there is so-called gummy smile.
This is due to the upper jaw being too long
- Ramus: large ramus which forms less step angle with body of
mandible
- Chin: there is prominent chin button
Sumber: Textbook of Oral Medicine 3th edition, 2014
Management:
- Osteotomy: resection of portion of
mandible to decrease the length,
followed by orthodentic treatment
3. Leukoplakia
Leukoplakia patches on the tongue, in the mouth, or on the inside of
the cheek.
Etiology:
Rough teeth
Rough places on dentures, fillings, and crowns
Smoking or other tobacco use (smoker's keratosis), especially pipes
Holding chewing tobacco or snuff in the mouth for a long period of time
Drinking a lot of alcohol
The disorder is most common in elderly persons.
A type of leukoplakia of the mouth called hairy leukoplakia is caused by
the Epstein-Barr virus. It is seen mostly in persons withHIV/AIDS. It may
be one of the first signs of HIV infection. Hairy leukoplakia can also
appear in other people whose immune system is not working well, such
as after a bone marrow transplant.
Sumber: https://www.nlm.nih.gov/medlineplus/ency/article/001046.h
Symptoms:
- Patches in the mouth usually develop on the tongue
(sides of the tongue with hairy leukoplakia)and on the
insides of the cheeks.
- Leukoplakia patches appear:
Usually white or gray
Uneven in shape
Fuzzy (hairy leukoplakia)
Slightly raised with a hard surface
Unable to be scraped off
Painful when the mouth patches come into contact with
acidic or spicy food
Sumber: https://www.nlm.nih.gov/medlineplus/ency/article/001046.h
Sumber: https://www.nlm.nih.gov/medlineplus/ency/article/001046.h
Prognosis
- Leukoplakia is usually harmless.Patches inthe mouthoften clear up
in a few weeks or months after the source of irritation is removed.
- Insome cases, the patches may be an early sign of cancer.
Sumber: https://www.nlm.nih.gov/medlineplus/ency/article/001046.h
Mouth Ulcers
Definition
Etiology
Sign &
Symptoms
Mouth Ulcers
Complication
Prevention
Oral Candidiasis
Definition A condition in which candida albicans accumulates
on the lining of your mouth. (*)
Symptom -Creamy white lesions on your tounge, inner cheeks,
s
and sometimes on The roof of your mouth, gums,
and tonsils
- A cottage cheese-like appearance
- Redness or soreness
- Slight bleeding
- Cracking and redness at the corner of your mouth
- A cottony feeling in your mouth
- Loss of taste (**)
-Some health conditions HIV/AIDS, cancer, DM,
Risk
Factors
vaginal yeast
Infections
- Undergoing chemotherapy or radiation treatment
for cancer
- Wearing dentures
Diagnosis
Glossitis
Definition
Etiology
Sign &
Symptoms
Treatmen
ts
Angina Ludwig
Ludwigs angina
Ludwig's angina is an infection of the floor of the
mouth under the tongue. It is due to bacteria.
Causes
Ludwig's angina is a type of skin infection that
occurs on the floor of the mouth, under the tongue.
It often develops after an infection of the roots of
the teeth (such as tooth abscess) or a mouth injury.
This condition is uncommon in children.
Symptoms
The infected area swells quickly. This may block the airway or
prevent you from swallowing saliva.
Symptoms include:
-Breathing difficulty
-Confusion or other mental changes
-Fever
-Neck pain
-Neck swelling
-Redness of the neck
-Weakness, fatigue, excess tiredness
Other symptoms that may occur with this disease:
-Difficulty swallowing
-Drooling
-Earache
-Speech that is unusual and sounds like the person has a "hot
potato" in the mouth
Treatment
If the swelling blocks the airway. A breathing tube through your
mouth or nose and into the lungs to restore breathing. need to
have surgery called a tracheostomy that creates an opening
through the neck into the windpipe.
Antibiotics are given to fight the infection. Antibiotics taken by
mouth may be continued until tests show that the bacteria
have gone away.
Dental treatment may be needed for tooth infections that
cause Ludwig's angina.
Surgery may be needed to drain fluids that are causing the
swelling.
Prognosis
Ludwig's angina can be life
threatening. However, it can be cured
with getting treatment to keep the
airways open and taking antibiotic
medicine.
Prevention
Visit the dentist for regular checkups.
Treat symptoms of mouth or tooth
infection right away.
Parotitis
Parotitis is the name given to
inflammation and infection of the
largest of the salivary glands known
as the parotid glands. Inflammation
results in swelling of the tissues that
surround the salivary glands,
redness, and soreness.
etiologi
Infection
Drugs
Radiation
and various diseases
The signs and symptoms of parotitis : can
vary among individuals. Some people with
parotitis may not realize they have a disease,
while others may have severe swelling and
pain.
prevention
practicing good oral hygiene, drinking plenty of
fluids, washing your hands, and receiving the
MMR vaccine to prevent mumps.
Seek immediate medical care for serious
symptoms such as a high fever and difficulty
breathing or swallowing.
Seek prompt medical care if you are being
treated for parotitis but mild symptoms recur or
are persistent.
Treatment
Treatment may involve:
Fillings
Crowns
Root canals
Prognosis
Complications
Discomfort or pain
Fractured tooth
Inability to bite down on tooth
Tooth abscess
Tooth sensitivity
prevention
Oral hygiene is necessary to prevent
cavities. This consists of regular
professional cleaning (every 6
months), brushing at least twice a
day, and flossing at least daily.
Achalasia
Definition
a primary motor disorder of the esophagus characterized by insufficient lower esophageal
sphincter relaxation and loss of esophageal peristalsis
Classification
Divided into 2 parts:
primary achalasia -> neurotropic virus (nukleus dorsalis vagus,ganglia misentrikus)
secondary achalasia-> chagas diseases,interluminary tumor
Common symptoms
Difficulty in swallowing(dysphagia), chest pain and regirgitation of food and liquids
Complication
Lung problems,weight loss,(> the risk of cancer)
Diagnose
X-ray(chest xray: mediastinum hipertrophy ), endoscopy, esophageal manometry(LES
increases,abnormality of sphingtr relaxation,no peristaltic)
Farmacology treatments
Oral
medications:
nitrat
(isosorbid
dinitrat),calcium
channel
blockers(nifedipin&verapamil),tingtur beladona,atrofin sulfat -> (<LES pressure) & (>emptying
esophagus).
LES dilatation-> businasi hurst,esofagomiotomi distal,injection of muscle relaxing-> botulinum
toxin directly to the esophagus
Non-farmaco treatments
Drinking liquid foods, drinking more water with meals and drinking carbonated beverages
DD : adenokarsinoma gaster to esophagus,karsinoma paru&pankreas,sarkoma sel retikulum
Atresia
Definition
Absence of a normal opening, or failure of structure to be tubular, it can affect many structures in the
body
Causes
congenital defect
Symptomps
Bluish coloration to the skin (cyanosis) with attempted feedings, coughing, gagging, choking with
attempted feeding, drooling, poor feeding
Diagnose
USG on the pregnant mom: show too much amniotic fluid or other blockage of digestive tract, after birth
when feeding is attempted and the infant cough,chokes,turns blue, Xray: shows an air filled pouch and
air in the stomach&intestine
Treatment
Surgery to repair esophagus, before the surgery, the baby is not fed by mouth
Complication
Feeding problems, reflux, Narrowing of the esophagus due to scarring from surgery
Esophagitis Corrosive
Corrosive Esophagitis is an inflammation of the
esophagus caused by injury fuel because the
chemicals that are corrosive, such as strong
acids, strong bases and organic substances.
Ingested chemicals that can be toxic or corrosive.
Chemicals corrosive will cause damage to the
canal path,
whereas chemical substances that are toxic only
cause symptoms of poisoning when it has been
absorbed by the blood.
Etiology Esophagitis
Corrosive
Corrosive esophagitis most often caused by
swallowing cleaning agent household, usually by
children. The most damaging substances are sodium
hydroxide, or which cause lysis of tissue and often
penetrate the esophageal wall. Duct cleaning fluids
can damage the esophagus or creating lesions.
Type and the amount of chemicals ingested
determines the severity and location damage. These
chemicals may damage limited to the mucosa,
submucosa, even the entire lining of the esophagus.
Symptoms worsened by alcohol use, smoking,
poor lifestyle and obesity.
Pathophysiology Esophagitis
Corrosive
Strong bases
Ingestion strong base causes tissue necrosis melt
(liquefactum necrosis), a process that involves
the saponification of fats and dissolving protein.
Emulsification cell death and destruction caused
by the structure cell membrane.
Hydroxyl ions (OH-) derived from reacting with
alkaline substances collagen tissue that causes
swelling and shortening tissue (contractures),
thrombosis in capillaries, and heat production
by network
Strong acids
Tissue damage due to strong acids are
ingested necrosis
clot (coagulation necrosis), a process of
protein denaturation superficial which will
lead to clot, crusts or scabs that can protect
underlying tissues from damage.
Stomach is the organ most
often affected in the case of swallowing
strong acid, in 20% of cases the small
intestine also can be exposed
latent phase
Lasts for 2-6 weeks, at this phase of the patient's
complaints is reduced, the temperature Weight,
patients feel has been cured, it can swallow
properly, but the actual process is still running by
forming scar tissue(cicatricial)
Chronic Phase
After 1-3 years will occur again because of
dysphagia have formed a network scarring,
resulting in esophageal stricture. Other symptoms
that can arise is
fistula, hipomotilitas gastrointestinal tract, and
increased risk of gastrointestinal cancer
physical examination
Influx corrosive substances through the
mouth can be seen with bad breath or vomit.
The presence of vaginal discharge burns in
the mucosa of the mouth or on the lips and
gray chin showed caustic or corrosive
materials due to both strong acidsand a
strong base.
Severe corrosive damage due to alkali (base)
of the esophagus is more powerful heavier
than due to strong acids, the greatest
damage when PH> 12, but concentration
also depends on the material
supporting investigation
Examination of radiological
Photos thorac and abdomen
b. CT-Scan
Laboratory tests
Complete blood count, electrolytes, liver
function, blood urea and creatinine for see
signs of systemic poisoning
Examination of the amount of urine and
urinalysis to help keep fluid balance.
therapy
Management aims to prevent corrosive
esophagitis stricture formation. Divided
corrosive esophagitis therapy in the acute
phase and phase chronic. In the acute
phase, carried out general maintenance
and special treatment in the form of
medical therapy and esofagoskopi.
Chronic phase there has been a stricture,
sondilatation with the help esofagoskop.
Complications
shock, coma, laryngeal edema, aspiration
pneumonia, esophageal perforation,
mediastinitis, and death.
Causes
Symptoms
People with chronic liver disease and esophageal
varices may have no symptoms.
If there is only a small amount of bleeding, the only
symptom may be dark or black streaks in the stools.
If larger amounts of bleeding occur, symptoms may
include:
Black, tarry stools
Bloody stools
Light-headedness
Paleness
Symptoms of chronic liver disease
Vomiting blood
Treatment
To treat acute bleeding:
The health care provider may inject the varices directly with a
clotting medicine, or place a rubber band around the bleeding
veins. This procedure is done using a small lighted tube called
an endoscope.
A medication that tightens blood vessels (vasoconstriction)
may be used. Examples include octreotide or vasopressin.
Rarely, a tube may be inserted through the nose into the
stomach and inflated with air. This produces pressure against
the bleeding veins (balloon tamponade).
Once the bleeding is stopped, varices can be treated with
medicines and medical procedures to prevent future bleeding
including:
Drugs called beta blockers, such as propranolol and nadolol
that reduce the risk of bleeding.
Prognosis
Bleeding often comes
back with or without
treatment. Bleeding
esophageal varices are
a serious complication
of liver disease and
have a poor outcome.
Placement of a shunt
can result in a decrease
of blood supply to the
brain, leading to mental
status changes or
encephalopathy.
Possible Complications
Encephalopathy
(sometimes called
hepatic
encephalopathy)
esophageal stricture
after surgery or
endoscopic therapy
Hypovolemic shock
Infection (pneumonia,
bloodstream infection,
peritonitis)
Return of bleeding after
treatment
Gastroesophageal reflux
Definition
Gastroesophageal reflux disease (GERD) is a condition in which the stomach contents leak
backwards from the stomach into the esophagus. This can irritate the esophagus and cause
heartburn and other symptoms.
Causes
Stomach contents back into the esophagus. Reflux may cause symptomps, harsh stomach
acids can also damage the lining of the esophagus
Risk Factors
Alcoholic, obesity, preganancy, sclerodema, smoking
Can also be caused by certain medicines, such as : antiholigernics,beta-blockers for high blood
pressure,dopamine active for parkinsons dss, progestin for abnorm menstrual, sedative for
insomnia/anxiety, tricyclic antidepressant.
Symptoms
Feeling that food is stuck the breastbone, heartburn/burning pain in the chest, nausea after
eating (symptomps may get worse when you lie down and eat,may be worse at night)
Diagnoses
Upper endoscopy, esophageal monometry
Farmaco treatment
Antacid, Proton pump inhibitors (PPIs)& H2 blockers: decrease the amount of acid, endoscopy
Non farmaco treatment
Maintaining a healthy body weight
Compications
Asthma, cancer, bronchospasm, chronic cough/hoarseness, dental problems, ulcer in the
esophagus, stricture