problem 1a - varla.pptx

8/12/2019 PROBLEM 1A - VARLA.pptx

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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

problem 1a - varla.pptx

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