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BY: VARLA S. G (405090215)
PROBLEM 1A
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ANATOMY OF DIGESTIVE
TRACT
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EmbryologyPart Range in
adult
Gives rise to Arterial
supply
Foregut The pharynx,
to the upper
duodenum
Pharynx, esophagus, stomach, upper
duodenum, respiratory tract (including
the lungs), liver, gallbladder, and
pancreas
Branches of
the celiac
artery
Midgut Lower
duodenum, to
the first half of
the transverse
colon
Lower duodenum, jejunum, ileum,
cecum, appendix, ascending colon,
and first half of the transverse colon
Branches of
the superior
mesenteric
artery
Hindgut Second half of
the transverse
colon, to the
upper part of
the anal canal
Remaining half of the transverse
colon, descending colon, rectum, and
upper part of the anal canal
Branches of
the inferior
mesenteric
artery
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PHYSIOLOGY OF DIGESTIVE
TRACT
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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
Th b l i ( h) d li
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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.ptyalinenzyme
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The Stomach
It is the widest part of the alimentary canaland acts as a reservoir for the food where itmay remain for between 2 and 6 hours.
Here the food is churned over and mixed with
various hormones, enzymes includingpepsinogenwhich begins the digestion ofprotein, hydrochloric acid, and otherchemicals
The stomach has an average capacity of 1
liter, varies in shape, and is capable ofconsiderable distension.
At regular intervals a circular muscle at thelower end of the stomach, the pylorus opens
allowing small amounts of food, now knownas chymeto enter the small intestine.
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Duodenum
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Small Intestine
The small intestine measures about 7m in anaverage adult and consists of the duodenum,
jejunum, and ileum. Both the bile and pancreaticducts open into
the duodenum together. The small intestine, because of its structure,
provides a vast lining through which furtherabsorptiontakes place.
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The Large Intestine
The large intestine averages about 1.5m longand 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 thedigestive tract.
The colon is divided into the ascending,transverse and descending colons, before
reaching the anal canal where the indigestiblefoods are expelled from the body.
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Picture : process of swallowing
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PEPTIC ULCER
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DEFINITION
Peptic ulcers are open sores that develop on theinside lining of stomach and the upper portion of
small intestine.
The most common symptom of a peptic ulcer is
abdominal pain
Peptic ulcers that occur on the inside of the
stomach are called gastric ulcers.
Peptic ulcers that affect the inside of the upperportion of small intestine (duodenum) are called
duodenal ulcers.
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Gross pathology of a gastric ulcer.
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EPIDEMIOLOGY
United States statistics In the United States, PUD affects approximately 4.5
million people annually. Only about 10% of young
persons have H pylori infection; the proportion of
people with the infection increases steadily withage.
Overall, the incidence of duodenal ulcers has been
decreasing over the past 3-4 decades.
The prevalence of PUD has shifted frompredominance in males to similar occurrences in
males and females
International statistics
The frequency of PUD in other countries is variable
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ETIOLOGY
Normally, the lining of the stomach and smallintestines are protected against the irritating acids
produced in stomach. If this protective lining
stops working correctly, and the lining breaks
down, it results in inflammation (gastritis) or anulcer.
Most ulcers occur in the first layer of the inner
lining. A hole that goes all the way through the
stomach or duodenum is called a perforation. Aperforation is a medical emergency.
The most common cause of such damage is
infection of the stomach by bacteria
called Helicobacter pylori(H.pylori). Most people
ADDITIONAL ETIOLOGIC
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ADDITIONAL ETIOLOGIC
FACTORS
Hepatic cirrhosis Chronic obstructive pulmonary
disease
Allergic gastritis and eosinophilicgastritis
Cytomegalovirus infection
Graft versus host disease Uremic gastropathy
Henoch-Schnlein gastritis
Corrosive gastropathy
Celiac disease
Bile gastropathy
Autoimmune disease
Crohn disease
Other granulomatous gastritides(eg, sarcoidosis, histiocytosisX,tuberculosis)
Phlegmonous gastritis and
emphysematous gastritis
Other infections, includingEpstein-Barr virus,HIV, Helicobacterheilmannii,herpessimplex, influenza, syphilis, Candidaalbicans,histoplasmosis, mucormycosis, and anisakiasis
Chemotherapeutic agents, suchas 5-fluorouracil (5-FU),methotrexate (MTX), andcyclophosphamide
Local radiation resulting inmucosal damage, which may lead
to the development of duodenalulcers
Use of crack cocaine, whichcauses localized vasoconstriction,resulting in reduced blood flowand possibly leading to mucosaldamage
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PATOPHYSIOLOGY
Peptic ulcers are defects in the gastric or duodenalmucosa that extend through the muscularis mucosa.
The epithelial cells of the stomach and duodenumsecrete mucus in response to irritation of the epitheliallining and as a result of cholinergic stimulation.
The superficial portion of the gastric and duodenalmucosa exists in the form of a gel layer, which isimpermeable to acid and pepsin.
Other gastric and duodenal cells secrete bicarbonate,
which aids in buffering acid that lies near the mucosa. Prostaglandins of the E type (PGE) have an important
protective role, because PGE increases theproduction of both bicarbonate and the mucous layer.
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Under normal conditions, a physiologic balance
exists between gastric acid secretion and
gastroduodenal mucosal defense.
Mucosal injury and, thus, peptic ulcer occur when
the balance between the aggressive factors andthe defensive mechanisms is disrupted.
Aggressive factors, such as NSAIDs, H
pyloriinfection, alcohol, bile salts, acid, and
pepsin, can alter the mucosal defense by allowingback diffusion of hydrogen ions and subsequent
epithelial cell injury.
The defensive mechanisms include tight
intercellular junctions, mucus, mucosal blood flow,
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When H pyloricolonizes the gastric mucosa,inflammation usually results.
In patients infected with H pylori,high levels of
gastrin and pepsinogen and reduced levels of
somatostatin have been measured.
In infected patients, exposure of the duodenum to
acid is increased.
Virulence factors produced by H pylori,including
urease, catalase, vacuolating cytotoxin, and
lipopolysaccharide, are well described.
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RISK FACTORS
Drinking too much alcohol Regular use of aspirin, ibuprofen, naproxen, or other
nonsteroidal anti-inflammatory drugs (NSAIDs).Taking aspirin or NSAIDs once in awhile is safe formost people.
Smoking cigarettes or chewing tobacco Being very ill, such as being on a breathing machine
Radiation treatments
A rare condition called Zollinger-Ellisonsyndrome causes stomach and duodenal ulcers.
Persons with this disease have a tumor in thepancreas that releases high levels of a hormone,which causes an increase in stomach acid.
Many people believe that stress causes ulcers. It isnot clear if this is true, at least for everyday stress at
home.
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SYMPTOMS
Small ulcers may not cause any symptoms. Some ulcerscan cause serious bleeding.
Abdominal pain is a common symptom but it doesn'talways occur. The pain can differ a lot from person toperson.
Feeling of fullness -- unable to drink as much fluid Hunger and an empty feeling in the stomach, often 1 - 3 hours
after a meal
Mild nausea (vomiting may relieve symptom)
Pain or discomfort in the upper abdomen
Upper abdominal pain that wakes you up at night Other possible symptoms include:
Bloody or dark tarry stools
Chest pain
Fatigue
Vomiting, possibly bloody
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PHYSICAL EXAMINATION In uncomplicated PUD, the clinical findings are few and
nonspecific and include the following:
Epigastric tenderness (usually mild) Guaiac-positive stool resulting from occult blood loss Melena resulting from acute or subacute gastrointestinal
bleeding Succussion splash resulting from partial or complete gastric
outlet obstruction
Patients with perforated PUD usually present with asudden onset of severe, sharp abdominal pain.
Most patients describe generalized pain; a few presentwith severe epigastric pain. As even slight movement cantremendously worsen their pain, these patients assume afetal position.
Abdominal examination usually discloses generalizedtenderness, rebound tenderness, guarding, and rigidity.
However, the degree of peritoneal findings is stronglyinfluenced by a number of factors, including the size ofperforation, amount of bacterial and gastric contents
contaminating the abdominal cavity, time betweenerforation and resentation and s ontaneous sealin of
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SIGNS AND TESTS
Esophagogastroduodenoscopy (EGD) is aspecial test performed by a gastroenterologist in
which a thin tube with a camera on the end is
inserted through your mouth into the GI tract to
see your stomach and small intestine. During anEGD, the doctor may take a biopsy from the wall
of your stomach to test for H. pylori.
Upper GI is a series of x-rays taken after you
drink a thick substance called barium.
Other tests:
Hemoglobin blood test to check for anemia
Stool guaiac to test for blood in your stool
A i h
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Angiography Angiography may be necessary in patients with a massive GI
bleed in whom endoscopy cannot be performed. An ongoingbleeding rate of 0.5 mL/min or more is needed for theangiography to be able to accurately identify the bleeding source.
Angiography can depict the source of the bleeding and can helpprovide needed therapy in the form of a direct injection ofvasoconstrictive agents.
Serum Gastrin Level A fasting serum gastrin level should be obtained in certain cases
to screen for Zollinger-Ellison syndrome. Such cases include the
following: Patients with multiple ulcers
Ulcers occurring distal to the duodenal bulb
Strong family history of PUD
Peptic ulcer associated with diarrhea, steatorrhea, or weight loss
Peptic ulcer not associated with H pyloriinfection or NSAID use
Peptic ulcer associated with hypercalcemia or renal stones
Ulcer refractory to medical therapy Ulcer recurring after surgery
Secretin Stimulation Test A secretin stimulation test may be required if the diagnosis of
Zollinger-Ellison syndrome cannot be made on the basis of theserum gastrin level alone. This test can distinguish Zollinger-
Ellison syndrome from other conditions with a high serum gastrinlevel, such as use of antisecretory therapy with a proton pump
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Gastric ulcer with punched-out ulcer base with whitish
fibrinoid exudates
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Gastric ulcer (lesser curvature) with punched-out ulcer base with whitishexudate
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Gastric cancer. Note the irregular heaped up overhanging
margins
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Gastric cancer with ulcerated
m
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Duodenal ulcer in a 35-year-old woman who presented with tarry stools and a hemoglobin
level of 75 g/L.
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Duodenal ulcer in a 65-year-old man with osteoarthritis who presented
with hematemesis and melena stools. The patient took naproxen on a
daily basis.
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DIFFERENTIAL DIAGNOSE
Nonulcer dyspepsia (NUD) or functional dyspepsia Functional dyspepsia is a diagnosis of exclusion made in patients
with chronic persistent epigastric pain in whom a thoroughevaluation shows no organic disease. Patients may primarilyhave epigastric pain, which is referred to as ulcerlike dyspepsia,or they may have symptoms of postprandial bloating, which isreferred to as motility-like dyspepsia.
Crohn disease Crohn ulceration can involve any part of the GI tract from the
buccal mucosa to the rectum. Isolated Crohn ulceration of thestomach is rare, although it may cause duodenal or ilealulcerations.
Zollinger-Ellison syndrome Zollinger-Ellison syndrome (ZES) is a rare disorder that can
cause gastric or duodenal ulcers (usually multiple) fromexcessive acid secretion. Consider ZES if a patient has severepeptic ulceration, kidney stones, watery diarrhea, ormalabsorption. ZES can also be associated with multipleendocrine neoplasia type I, which occurs earlier than isolatedZES. Patients with ZES usually have fasting serum gastrin levels
of more than 200 pg/mL and basal gastric acid hypersecretion of
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DifferentialsAcute Coronary SyndromeAneurysm, Abdominal Cholangitis Cholecystitis
Cholecystitis and Biliary Colic in Emergency Medicine Cholelithiasis Diverticular Disease Esophageal Perforation, Rupture and Tears Esophagitis
Gastritis, Acute Gastritis, Chronic Gastroenteritis Gastroesophageal Reflux Disease Inflammatory Bowel Disease
Viral Hepatitis
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TREATMENT
Treatment involves a combination of medications tokill the H. pyloribacteria (if present), and reduce acidlevels in the stomach. This strategy allows your ulcerto heal and reduces the chance it will come back.
A peptic ulcer with an H. pyloriinfection, the standard
treatment uses different combinations of the followingmedications for 5 - 14 days:
Two different antibiotics to kill H. pylori, suchas clarithromycin (Biaxin), amoxicillin, tetracycline, ormetronidazole (Flagyl)
Proton pump inhibitors such as omeprazole(Prilosec), lansoprazole (Prevacid), or esomeprazole(Nexium)
Bismuth (the main ingredient in Pepto-Bismol) may beadded to help kill the bacteria
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An ulcer without an H. pyloriinfection, or one thatis caused by taking aspirin or NSAIDsprotonpump inhibitor for 8 weeks.
Other medications that may be used for ulcer
symptoms or disease are: Misoprostol, a drug that may help prevent ulcers in
people who take NSAIDs on a regular basis
Medications that protect the tissue lining (suchas sucralfate)
If a peptic ulcer bleeds a lot, an EGD may beneeded to stop the bleeding. Surgery may beneeded if bleeding cannot be stopped with anEGD, or if the ulcer has caused a perforation.
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Alternative triple-therapy regimens The alternative triple therapies, also administered for 14 days,
are as follows: Omeprazole (Prilosec): 20 mg PO bid or Lansoprazole (Prevacid): 30
mg PO bid or Rabeprazole (Aciphex): 20 mg PO bid or Esomeprazole(Nexium): 40 mg PO qd PlusClarithromycin (Biaxin): 500 mg PO bidand Metronidazole (Flagyl): 500 mg PO bid
Quadriple therapy Quadriple therapies for H pyloriinfection are generally
reserved for patients in whom the standard course oftreatment has failed.
Quadriple treatment includes the following drugs, administeredfor 14 days: PPI, standard dose, or ranitidine 150 mg, PO bid
Bismuth 525 mg PO qid Metronidazole 500 mg PO qid Tetracycline 500 mg PO qid
Consider maintenance therapy with half of the standard dosesof H2-receptor antagonists at bedtime in patients with
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ULCERS THAT FAIL TO HEAL
Peptic ulcers that don't heal with treatment are calledrefractory ulcers. There are many reasons why an ulcermay fail to heal. These reasons may include: Not taking medications according to directions.
The fact that some types of H. pylori are resistant toantibiotics.
Regular use of tobacco. Regular use of pain relievers that increase the risk of ulcers.
Less often, refractory ulcers may be a result of: Extreme overproduction of stomach acid, such as occurs in
Zollinger-Ellison syndrome An infection other than H. pylori Stomach cancer Other diseases that may cause ulcer-like sores in the stomach
and small intestine, such as Crohn's disease
Treatment for refractory ulcers generally involveseliminating factors that may interfere with healing, along
with using different antibiotics.
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PATIENT EDUCATION
Patients should be warned of known or potentiallyinjurious drugs and agents. Some examples are asfollows: NSAIDs
Aspirin
Alcohol Tobacco
Caffeine (eg, coffee, tea, colas)
Obesity has been shown to have an association with
peptic ulcer disease (PUD), and patients should becounseled regarding benefits of weight loss.
Stress reduction counseling might be helpful inindividual cases but is not needed routinely.
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Lifestyle and home remedies
Choose a healthy diet.Choose a healthy diet fullof fruits, vegetables and whole grains.
Consider switching pain relievers.
Control stress.Stress may worsen the signs and
symptoms of a peptic ulcer. Don't smoke.stomach acid .
Limit or avoid alcohol.Excessive use of alcohol
can irritate and erode the mucous lining in stomach
and intestines, causing inflammation and bleeding.
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PROGNOSIS
When the underlying cause is addressed, theprognosis is excellent.
Most patients are treated successfully with eradicationof H pyloriinfection, avoidance of NSAIDs, and theappropriate use of antisecretory therapy.
Eradication of H pyloriinfection changes the naturalhistory of the disease, with a decrease in the ulcerrecurrence rate from 60-90% to approximately 10-20%.
With regard to NSAID-related ulcers, the incidence ofperforation is approximately 0.3% per patient year,and the incidence of obstruction is approximately0.1% per patient year.
Combining both duodenal ulcers and gastric ulcers,
the rate of any complication in all age groups
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The mortality rate for PUD, which has decreasedmodestly in the last few decades, is
approximately 1 death per 100,000 cases.
If one considers all patients with duodenal ulcers,
the mortality rate due to ulcer hemorrhage isapproximately 5%.
However, evidence from meta-analyses and other
studies has shown a decreased mortality rate
from bleeding peptic ulcers when intravenousPPIs are used after successful endoscopic
therapy
Emergency operations for peptic ulcer perforation
carr a mortalit risk of 6-30%.
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Factors associated with higher mortality in thissetting include the following: Shock at the time of admission
Renal insufficiency
Delaying the initiation of surgery for more than 12hours after presentation
Concurrent medical illness (eg, cardiovasculardisease, diabetes mellitus
Age older than 70 years
Cirrhosis Immunocompromised state
Location of ulcer (mortality associated withperforated gastric ulcer is twice that associated with
perforated duodenal ulcer.)
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COMPLICATIONS
Bleeding inside the body (internal bleeding) Gastric outlet obstruction
Inflammation of the tissue that lines the wall of
the abdomen (peritonitis)
Perforation of the stomach and intestines
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PREVENTION
Avoid aspirin, ibuprofen, naproxen, and otherNSAIDs. Try acetaminophen instead.
The following lifestyle changes may help prevent
peptic ulcers:
Do not smoke or chew tobacco. Limit alcohol to no more than two drinks per day.
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GASTRITIS
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Chronic Gastritis
Atrophic Gastritis Erosive Gastritis
Variliform Gastritis
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GASTRITIS
Gastritis is an inflammation, irritation, or erosionof the lining of the stomach / gastric mucosa. It
can occur suddenly (acute) or gradually (chronic).
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RISK FACTOR OF GASTRITIS
H. pylori infection Regular use of aspirin or other NSAIDs
Older age
Etiology
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gyThe most common are:
Alcohol
Erosion (loss) of the protective layer of the stomach lining Infection of the stomach with Helicobacter pyloribacteria
Medications such as aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs)
Smoking
Less common causes are:
Autoimmune disorders (such as pernicious anemia)
Backflow of bile into the stomach (bile reflux)
Eating or drinking caustic or corrosive substances (such as
poisons)
Excess gastric acid secretion (such as from stress)
Viral infection, especially in people with a weak immunesystem
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SYMPTOMS OF GASTRITIS
Nausea or recurrent upset stomachAbdominal bloating
Abdominal pain
Vomiting Indigestion
Burning or gnawing feeling in the stomachbetween meals or at night
Vomiting blood or coffee ground-likematerial
Black, tarry stools
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Diagnosis
Upper endoscopy
Blood tests
Fecal occult blood test (stool test
Treatment
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Treatment
Mediacation
1.H2-blockers :cimetidine (Tagamet), famotidine (Pepcid),nizatidine (Axid), ranitidine (Zantac).
2.Proton pump inhibitors (PPIs) :
lansoprazole (Prevacid),omeprazole (Prilosec, Losec).3.Coating agents:
Sucralfate (Carafate), Misoprostol (Cytotec)
4.Antacids5.Antibiotic6.Antiemetic
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Complications
MalignancyHemorrhage
Perforation
Obstruction
Prognosis
The prognosis is excellent. Most patients are curedwhen the cause has been identified and treated
appropriately.
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GERD
a condition in which the liquid content of thestomach 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 ofpatients.
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Epidemiology
It rares in Asia-Africa but common seen ineurope countries
There is no epidemiology data in Indonesia,but we can see 22,8 % esophagitis case in
RSCM from all gastrointestinal disease
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Etiology
Lifestyle - Use of alcohol or cigarettes, obesity,poor posture (slouching)
Medications - Calcium channel blockers,theophylline, nitrates, antihistamines
Diet - Fatty and fried foods, chocolate, garlicand onions, drinks with caffeine, acid foodssuch as citrus fruits and tomatoes, spicy foods,mint flavorings
Eating habits - Eating large meals, eating soonbefore bedtime
Other medical conditions - Hiatal hernia,pregnancy, diabetes, rapid weight gain
Autosomal dominant (13q )
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etiology
hormonal
Anatomic
and physiology
environmental
genetic
neurogenic
diet
smoking
Nervous X
Disorder of gastrin secretiong
Gastric emptying
Esophageal clearance
Anti reflux barrier
TLERS
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Risk Factors
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Dietary Habits
Eating large portions.
Eating certain foods,
including onions, chocolate,
peppermint, high-fat or spicy
foods, citrus fruits, garlic,
and tomatoes or tomato-
based products.
Drinking certain beverages,
including citrus juices,
alcohol, caffeinated drinks,and carbonated drinks.
Eating before bedtime
Lifestyle Habits
Being overweight
Smoking Wearing tight-fitting clothing or
belts
Lying down or bending over,
especially after eating
Stress
Medical Causes
Pregnancy
Bulging of part of the stomach into
the chest cavity, also called hiatal
hernia.
GERD.
Taking certain medications,
especially some antibiotics and
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PATHOPYSIOLOGY
Esophagus and gaster are separated by ahigh pressure zone as the result of LowerEsophageal Sfingter contaraction.
Normally this pressure is defended, except
when swallowing, bleching and vomiting. Reflux occurs when the gradient of
pressure between the LES and thestomach is lost or under 3mmHg/contraction of the LES is decrease.
The pathogenesis of reflux depend on thebalance of defensive and ofensive factors.
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PATHOPHYSIOLOGY
DEVENSIVE FACTORS1. Esophagus barrier
tonus of LES
2. Esophageal clearence
depend on gravitation,peristaltic, saliva andbicarbonate excretion
3. Epithelial resistence
Cell membrane
Differentiation of epithelial
tissue Intracellular junction which is
bordering the diffusion of H+to esophageal tissue
OFENSIVE FACTORS
1. Gastric Secretion
2. Power of M. Sfingter
Pylorus3. Delayed gatric emptying
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echanisme Reflux in Normal Tonus of LES
Transient Lower Esophageal SfingterRelaxation
Spontanious LES relaxation ( 5s) withoutearly swalowing process -> reflux stomatch
content
Mechanisme is idiophatic, possibility :
- Delayed gastric emptying
- Gastric dilatation
- Gastric obstruction
- Neuroreflex disorder
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Pathophyisiology
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Extraesophageal Manifestations of
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GERD:Pulmonary
AsthmaAspiration
pneumonia
Chronic bronchitis
Pulmonary fibrosis
Other
Chest painDental erosion
ENT
Hoarseness
Laryngitis
Pharyngitis
Chronic coughGlobus sensation
Dysphonia
Sinusitis
Subglottic stenosisLaryngeal cancer
Barium Swallow
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Useful first diagnostic test for patients
with dysphagia Stricture (location, length) Mass (location, length) Birds beak Hiatal hernia (size, type)
Limitations Detailed mucosal exam for erosive
esophagitis, Barretts esophagus
Most useful for detecting pept icstr ic tures
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SPECTRUM OF ENDOSCOPIC FINDINGS
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WITH GERD
Normal esophagus Grade 3 esophagitis
Grade 4 esophagitis Barretts esophagus
Ambulatory 24 hr. pH Monitoring
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y p g
Physiologic study
Quantify reflux in
proximal/distal
esophagus
% time pH < 4
DeMeester score
Symptom
correlation
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GERD T
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GERDTreatment
Lifestyle changes Infant: alterations in formula compositions
(thickening formula), sleep positioning
Adolescents: 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
T t t Lif t l Ch
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TreatmentLifestyle Changes
Position therapy: Less GER in prone than in supine. Similar
reflux in left, right, & supine positions Prone is superior to semi supine positioning in
infant seat
However, supine has < risk of suddeninfant death syndrome, thus,recommended positions are: Prone when infant is awake, supine positioning
during sleep Older children & Adultbenefits from
head elevation, less GER in LLD than inRLD
T t t Ph th
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TreatmentPharmacotherapy
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Drugs demonstrated to be effective in gastroesophageal reflux disease
(North American Society of Pediatric Gastroenterology and Nutrition)
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Th
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Therapy
Stage 1 Heartburn < 2-3x/week Lifestyle changes, diet,position, weight-losing.
Antacid, receptor H2
antagonis
Stage 2 Heartburn with esofagitis,
>2-3x/week
PPI (omeprazole,
esomeprazole,
rabeprazole,
lansoprazole)
Stage 3 chronic, continue signs andsymptoms, relaps,
esophagus complication
PPI (omeprazole,esomeprazole,
rabeprazole,
lansoprazole)
T t t
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TreatmentTreatment
Life stylemodification
Elevation of the upper body at night generally is recommended for all patientswith GERD
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 refluxthey 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
Antagonist
The first medication developed for more effective and convenient treatment of
acid-related diseases, including GERD, was a histamine antagonist, specifically
cimetidine(Tagamet)
Histamine is an important chemical because it stimulates acid production by the
stomach
Four different H2 antagonists are available by prescription, including cimetidine
(Tagamet), ranitidine(Zantac), nizatidine(Axid), and famotidine, (Pepcid)
Treatment
Protein Pump The second type of drug developed specifically for acid-related diseases,
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Protein Pump
Inhibitor
The second type of drug developed specifically for acid related diseases,
such as GERD, was a proton pump inhibitor (PPI), 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 timeFive 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 gastrointestinaltract, 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 foamingagent.
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 fundoplicationand is called reflux
surgery or anti-reflux surgery
Endoscopy It is not clear how effective they are, especially long-term. Because theeffectiveness and the full extent of potential complications of endoscopic
techniques are not clear, it is felt generally that endoscopic treatmentshould onl be done as art of ex erimental trials.
Esophageal
Esophageal mucosal
resistance: Alginic
acid Sucralfate
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http://www.gerd.com/intro/noframe/grossovw.htm
sophageal
clearance:
Cisapride
acid, Sucralfate
Gastric emptying:
Metoclopramide
Cisapride
LES pressure:MetoclopramideCi
sapride
Gastric acid:Antacids
H2RAs PPIs
Breastfeeding
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Breastfeeding is definitely best for a baby with reflux
because it is more hypoallergenic than formula and is
digested twice as fast as formula.
Feeding Time
Smaller more frequent meals through out the day work much
better than larger, less frequent meals.
Avoid feeding baby right before bedtime
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Prognosis
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Prognosis
The majority of people respond to nonsurgicalmeasures, with lifestyle changes and
medications.
However, many patients need to continue to take
drugs to control their symptoms.
Prevention
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Prevention Maintain a healthy body weight.
Avoid large meals and eating within 3 hours ofbedtime.
Limit fatty or greasy foods, chocolate, caffeine, andother irritating foods.
Avoid alcohol. Stop smoking.
Avoid working out, bending, or stooping on a fullstomach
Prevention
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DD
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DD
Bowel Obstruction: Blockage in the bowel of the digestive tract.
Cyclic vomiting syndrome: A rare disorder involving repeated cyclic episodes
of vomiting which occur for no obvious reason. Pyloric stenosis:
Narrowed opening between stomach and intestines
Hiatus Hernia Which causes LES doesnt work as it supposed tobe
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REFERENCES
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REFERENCES
http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001255/
http://emedicine.medscape.com/article/181753-
differential