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Anatomy

Histologi GIT• In the oesophagus, the mucosa is

formed by a stratified squamous epithelium (non-keratinised)

• Oesophageal glands are located in the submucosa. These submucosal glands produce a mucous secretion, which lubricates the epithelium and aids the passage of food. The mucous glands in the part of the oesophagus closest to the stomach protect the oesophageal mucosa from acidic reflux from the stomach.

• The adventitia consists only of a layer of loose connective tissue. Only the lowest part of the oesophagus (approx. the lowest 2 cm) enters the peritoneal cavity.

Histologi

• Chief cells (or zymogenic cells)– They produce

pepsinogen, which is a precursor of the proteolytic enzyme pepsin.

• Parietal cells (or oxyntic cells)– Parietal cells secrete the

hydrochloric acid of the gastric juice

Histology of Ileum

VOMITING

Complication

• Metabolic disorder• Nutritional disorder• Mallory Weiss tear• Esophagitis• Aspiration • Shock

SYNDROME OF DYSPEPSIA

• persistent or recurrent upper abdominal pain or discomfort characterized by postprandial fullness, early satiety, nausea, and bloating.

SYNDROME OF DYSPEPSIA

• Epidemiology: Each year 10-20% of US population seeks medical attention. NUD 2-3 x peptic ulcer disease.

• Etiology & Pathogenesis: Imbalance of the aggravating factors and defensive factors. The aggravating factor increased and the defensive factors decrease will cause functional and organic /ulcer dyspepsia.

AGGRAVATING FACTORS OF SYNDROME DYSPEPSIA:

• Gastric acid • Pepsin• Helicobacter pylori infection• Gastric motor activity: 25-50% patients exhibit postprandial antral

hypomotility or delayed gastric emptying• Psychological factors: anxiety and depression• Diet: foods: spicy/hot, sour, vinnegar, drinks: coffee, smoking/tobacco, alcohol • Drugs: non-steroidal anti-inflammatory drugs(nsaid), traditional pain killer

drugs, steroids, antibiotics(erythromycin, ampicillin), iron, potassium, digoxin, theophylline.

• Metabolic diseases: diabetes mellitus, hypothoroidism• Hypopotassemia.• Free radicals

DEFENSIVE FACTORS OF SYNDROME DYSPEPSIA:

• Prostaglandin• Mucus• Mucosal blood flow• Surfactant• Bicarbonat• Heat shock protein• Epitel/preepithelial factors• etc

CLINICAL FEATURES IN SYNDROME DYSPEPSIA

• Non Ulcer Disease: – Ulcer like: dominant epigastric pain, relieved by

antacids or food– Dysmotility like: epigastric discomfort aggravated by

food or associated with early satiety, fullness, nausea, retching, vomiting, or bloating.

– Nonspecific: symptoms does not fit the other categories

– Reflux like: heartburn and regurgitation• Ulcer: the same with NUD

PHYSICAL EXAMINATION IN SYNDROME DYSPEPSIA

• not specific• epigastric tenderness some times• abdominal mass if advanced gastric carcinoma

GERD

• Gastroesophageal reflux disease (GERD) is a condition in which food or liquid travels backwards from the stomach to the esophagus (the tube from the mouth to the stomach).

• This action can irritate the esophagus, causing heartburn and other symptoms.

• Gastroesophageal reflux is a common condition that often occurs without symptoms after meals.

Epidemiology

• Infant reflux becomes evident: 1st few mo of life, peaks at ~ 4 mo, resolves in most by 12 mo and nearly all by 24 mo

• Common: America & Europe; relatively low incidence in Asia – Africa

• GERD likely has genetic predispositions– Family clustering of GERD symptoms, endoscopic

esophagitis, hiatal hernia, Barrett’s esophagus, & adenocarcinoma has been identified

Etiology • Lifestyle - Use of alcohol or cigarettes, obesity, poor posture

(slouching) • Medications - Calcium channel blockers, theophylline,

nitrates, antihistamines • Diet - Fatty and fried foods, chocolate, garlic and onions,

drinks with caffeine, acid foods such as citrus fruits and tomatoes, spicy foods, mint flavorings

• Eating habits - Eating large meals, eating soon before bedtime

• Other medical conditions - Hiatal hernia, pregnancy, diabetes, rapid weight gain

Pathophysiology• Transient LES Relaxation (TLESR): primary mechanism

allowing reflux to occur• TLESR = independent of swallowing, reducing LES pressure

to 0-2mmHg, last >10sec; appear by 26wk gestation• Gastric distention (postprandially, or due to abnormal

gastric emptying, or air swallowing) main stimulus• GERD is caused whether by increased frequency of TLESR or

greater incidence of reflux during TLESR is still debated• Risk factors: positions, factors that influencing gastric

pressure-volume dynamics (eg: increased movement, straining, obesity, large volume or hyperosmolar meals, increased respiratory effort [cough, wheeze])

GERD – Clinical Manifestations• Infantile reflux

– More often w/ regurgitation (especially postprandially), signs of esophagitis (irritability, arching, choking, gagging, feeding aversion), & resulting failure to thrive

– Symptoms resolve spontaneously in the majority by 12-24 mo– May manifest as obs apnea, or as stridor (in which reflux complicates

primary airway disease*)• Older children

– May have regurgitation preschool years; complaints of abd & chest pain later childhood & adolescence

– Occasional children present w/ neck contortions (arching, turning of head) Sandifer Syndrome

– Airway manifestations in older children frequently related to asthma, otolaryngologic disease (eg: laryngitis, sinusitis)

GERD – Clinical Manifestations

• Otitis media, sinusitis, lymphoid hyperplasia, hoarseness, vocal cord nodules, & laryngeal edema have all been associated w/ GERD

• Other symptoms:– Belching, Cough or wheezing, Difficulty

swallowing, Heartburn, Hoarseness, Nausea and vomiting, Regurgitation of food, Sore Throat, Vomiting Blood

Diognostic for Infant

GERD – Treatment

• 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

Treatment – Lifestyle 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 sudden infant death syndrome, thus, recommended positions are:– Prone when infant is awake, supine positioning during

sleep• Older children & Adult benefits from head elevation,

less GER in LLD than in RLD

Treatment – Pharmacotherapy

Step up & Step down Therapy

Approach to acid reducing therapy:• Step up:

– Begin: H2RA at standard dosage, following with a PPI at standard dosage and then a PPI at higher dosage if necessary to achieve improvement

• Step down– Begin: PPI at higher dosage to achieve improvement,

following with a PPI at standard dosage and then an H2RA to maintain improvement

• Adults step down > cost effective & recommended, but there are no published studies in children

Drugs demonstrated to be effective in gastroesophageal reflux disease(North American Society of Pediatric Gastroenterology and Nutrition)

Treatment – Surgery • Surgery, usually fundoplication:

– Effective th for intractable GERD particularly those with refractory esophagitis or strictures and those at risk for significant morbidity from chronic pulmonary disease.

– It may be combined with a gastrostomy for feeding or venting– Long term studies suggest fundoplication frequently become

incompentent in children & adults (due uses of PPI for long term pharmacotherapy)

– Some of the risks of fundoplication include a wrap that is "too tight" (producing dysphagia or gas-bloat) or "too loose“ (and thus incompetent)

– Tight (360, Nissen), loose (< 360, Thal) wrap

Complications

Complications• Barrett’s esophagus (a change in the lining of the

esophagus that can increase the risk of cancer)• Bronchospasm (irritation and resulting spasm of

airways due to acid)• Chronic pulmonary disease• Esophageal ulcer• Hoarseness• Inflammation of the esophagus• Stricture (a narrowing of the esophagus due to

scarring from the inflammation)

Hold the baby upright for a time after feeding to help prevent spitting up.

Propping a baby up after feeding helps keep fluid from traveling up from the stomach.

The Acid Reflux Wedge Pillow For BabyPosisition of feeding

30 degree

Prevention

Prognosis

• The majority of people respond to nonsurgical measures, with lifestyle changes and medications.

• However, many patients need to continue to take drugs to control their symptoms.

Gastritis

• Definition: inflammation of the gastric mucosa• Acute Gastritis• Chronic Gastritis

Acute GastritisAcute gastritis is a term covering a broad spectrum of entities that induce inflammatory changes in the gastric mucosa. Acute gastritis can be broken down into 2 categories:•erosive (e.g, superficial erosions, deep erosions, hemorrhagic erosions)•non-erosive (generally caused by Helicobacter pylori)Symptoms include nausea, vomiting, loss of appetite, belching, and bloating. Occasionally, acute abdominal pain can be a presenting symptom.

• One or more of the following influences are thought to be operative in these varied settings:– Disruption of the adherent mucous layer– Stimulation of acid secretion with hydrogen ion back

diffusion into the superficial epithelium– Decreased production of bicarbonate buffer by superficial

epithelial cells– Reduced mucosal blood flow– Direct damage to the epithelium

Risk Factors• Acute gastritis is frequently associated with:– Heavy use NSAID, particularly aspirin– Excessive alcohol consumption– Heavy smoking– Treatment with cancer chemotherapeutic drugs– Systemic infections (eg. Salmonellosis)– Severe stress (eg. Trauma, burns, surgery)– Ischemia and shock– Suicide attempts with acids and alkali– Mechanical trauma (eg. Nasogastric intubation)– Reflux of bilious material after distal gastrectomy

Sign and Symptoms

• Acute gastritis may be entirely asymptomatic• Epigastric pain• Nausea • Vomiting• Hematemesis• Melena• Potentially fatal blood loss

• 25% of persons who take daily aspirin for rheumatoid arthritis develop acute gastritis at some time in their course, many with occult or overt bleeding

• The risk of gastric bleeding from NSAID induced gastritis is dose related, thus increasing the likelihood of this complication in persons requiring longterm use of such drugs

Chronic Gastritis• Definition: the presence of chronic inflammatory

changes in the mucosa leading eventually to mucosal atrophy and epithelial metaplasia

• Most individuals with the infection also have the associated gastritis but are asymptomatic

• Epidemiology: american adults older than age 50 show prevalence rates approaching 50%. In areas where the infection is endemic, it seems to be acquired in childhood and persists for decades

Pathophisiology

• Most important etiologic association is chronic infection by the bacillus H. pylori

• Gastritis develops as a result of the combined influence of bacterial enzymes and toxins and release of noxious chemicals by the recruited neutrophils

• Characterized by mononuclear cell infiltration in the lamina propia with intestinal metaplasia and frequently proliferation of lymphoid tissue

• After initial exposure to H. pylori, gastritis may develop in 2 patterns:– An antral-type with high acid production and

higher risk for the development of duodenal ulcer– A pangastritis with multifocal mucosal atrophy,

with low acid secretion and increased risk for adenocarcinoma

Sign and Symptoms

• Usually causes few or no symptoms• Upper abdominal discomfort• Nausea• Vomiting

• Most important is the relationship of chronic gastritis to the development of peptic ulcer and gastric carcinoma

• Most individuals with a peptic ulcers, whether duodenal or gastric, have H. pylori infection

Duodenal Ulcer

• A duodenal ulcer is a raw area in the lining in the upper part of the small intestine (duodenum), where it connects to the stomach.

Etiology• Infection with Helicobacter pylori• More than a quarter of people in the UK become infected with H. pylori at

some stage in their life. Once you are infected, unless treated, the infection usually stays for the rest of your life. In many people it causes no problems and a number of these bacteria just live harmlessly in the lining of the stomach and duodenum. However, in some people this bacterium causes an inflammation in the lining of the stomach or duodenum. This causes the defence mucus barrier to be disrupted (and in some cases the amount of acid to be increased) which allows the acid to cause inflammation and ulcers.

• Anti-inflammatory drugs - including aspirin• However, these drugs sometimes affect the mucus barrier of the

duodenum and allow acid to cause an ulcer. About 1 in 20 duodenal ulcers are caused by anti-inflammatory drugs.

• Other causes and factors• Other causes are rare. For example, the Zollinger-Ellison syndrome. In this

rare condition, much more acid than usual is made by the stomach. Other factors such as smoking, stress, and drinking heavily may possibly increase the risk of having a duodenal ulcer. However, these are not usually the underlying cause of a duodenal ulcers.

Symptoms

• Pain in the upper abdomen just below the sternum (breastbone) is the common symptom. It usually comes and goes. It may occur most before meals, or when you are hungry. It may be eased if you eat food, or take antacid tablets. The pain may wake you from sleep.

• Other symptoms which may occur include: bloating, retching, and feeling sick. You may feel particularly 'full' after a meal. Sometimes food makes the pain worse.

Test • Endoscopy is the test that can confirm a duodenal ulcer. In

this test a doctor or nurse looks inside your stomach and duodenum by passing a thin, flexible telescope down your oesophagus. They can see any inflammation or ulcers.

• A test to detect the H. pylori bacterium is usually done if you have a duodenal ulcer. If H. pylori is found then it is likely to be the cause of the ulcer. Briefly, it can be detected in a sample of faeces, or in a 'breath test', or from a blood test, or from a biopsy sample taken during an endoscopy.

Treatment • Acid suppressing medication• A 4-8 week course of a drug that greatly reduces the amount of acid that

your stomach makes is usually advised. The most commonly used drug is a proton pump inhibitor (PPI). These are a class (group) of drugs that work on the cells that line the stomach, reducing the production of acid. They include: esomeprazole, lansoprazole, omeprazole, pantoprazole and rabeprazole, and come in various brand names. Sometimes a drug from another class of drugs called H2 blockers is used. H2 blockers work in a different way on the cells that line the stomach, reducing the production of acid. They include: cimetidine, famotidine, nizatidine and ranitidine, and come in various brand names. As the amount of acid is greatly reduced, the ulcer usually heals. However, this is not the end of the story ...

• If your ulcer was caused by H. pylori• Nearly all duodenal ulcers are caused by infection with H. pylori. Therefore,

a main part of the treatment is to clear this infection. If this infection is not cleared, the ulcer is likely to return once you stop taking acid-suppressing medication. Two antibiotics are needed. In addition, you need to take an acid-suppressing drug to reduce the acid in the stomach. This is needed to allow the antibiotics to work well. You need to take this 'combination therapy' (sometimes called 'triple therapy') for a week.

• After treatment, a test to check that H. Pylori has gone may be advised. If it is done it needs to be done at least four weeks after the course of combination therapy has finished. In most cases, the test is 'negative' meaning that the infection has gone. If it has not gone, then a repeat course of combination therapy with a different set of antibiotics may be advised. Some doctors say that for people with a duodenal ulcer, this 'confirmation' test is not necessary if symptoms have gone. The fact that symptoms have gone usually indicates that the ulcer and the cause (H. pylori) have gone. But, some doctors say it is needed to play safe. Your own doctor will advise if you should have it. (Note: a test to confirm that H pylori has gone is usually always recommended if you have a stomach ulcer.)

• If your ulcer was caused by an anti-inflammatory drug• If possible, you should stop the anti-inflammatory drug. This allows the ulcer to heal. You will

also normally be prescribed an acid-suppressing drug for several weeks (as mentioned above). This stops the stomach from making acid and allows the ulcer to heal.

• Surgery• In the past, surgery was commonly needed to treat a duodenal ulcer. This

was before it was discovered that H. pylori was the cause of most duodenal ulcers, and before modern acid-suppressing drugs became available. Surgery is now usually only needed if a complication of a duodenal ulcer develops such as severe bleeding or a perforation.

Complications

• Bleeding ulcer. This can range from a 'trickle' to a life-threatening bleed.

• Perforation. This is where the ulcer goes right through ('perforates') the wall of the duodenum. Food and acid in the duodenum then leak into the abdominal cavity. This usually causes severe pain and is a medical emergency.

Peptic Ulcer

Definition• A peptic ulcer is erosion in the lining of the stomach or the first

part of the small intestine, an area called the duodenum.

• PU includes Duodenal ulcer. (commonest) Gastric ulcer.

Common causes of PU• Infection with H.pylori.

• NSAID and the usual suspects (Alcohol ,smoking, stress)

• Imbalance between the aggressive and protective mechanisms.

• Acid hypersecretion due to increase number of parital cells or as seen in (Zollinger-Ellison syndrome).

Clinical Features (PU)

• Small ulcers may not cause any symptoms. Large ulcers can cause serious bleeding.

• Abdominal pain is a common symptom but it doesn't always occur. • M > F ,20-50 yrs.• Epigastric pain during fasting (hunger pain), relieved by food and

Antacids.• Back pain if ulcer is penetrating posteriorly.• Hematemesis from ulcer penetrating GD artery posteriorly.• Can lead to peritonitis if ulcer occurs anteriorly.

• Other possible symptoms include:* Belching* Bloody or dark tarry stools* Chest pain* Fatigue* Heartburn* Indigestion* Nausea* Vomiting, possibly bloody* Weight loss

Exams and Tests• To diagnose an ulcer, your doctor will order one of the following

tests:* Esophagogastroduodenoscopy (EGD) * Upper GI is a series of x-rays taken after you drink a thick substance called barium.

• Your doctor may also order these tests:* Hemoglobin blood test to check for anemia* Stool guaiac to test for blood in your stool

Treatment• Treatment involves a combination of medications to kill the H. pylori

bacteria (if present), reduce acid levels, and protect the GI tract. This strategy allows your ulcer to heal and reduces the chance it will come back.

• Medications may include one or more of the following:* Acid blockers (such as cimetidine, ranitidine, or famotidine)* Antibiotics to kill H. pylori* Bismuth to help protect the lining and kill the bacteria* Medications that protect the tissue lining (such as sucralfate)* Proton pump inhibitors such as omeprazole (Prilosec), lansoprazole (Prevacid), or esomeprazole (Nexium)

• If you have an ulcer without an H. pylori infection, your doctor will likely prescribe a proton pump inhibitor for 8 weeks. You may also be prescribed this type of medicine if you must continue taking aspirin or NSAIDs for other health conditions.

Possible 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

Prevention• Lifestyle changes may help prevent peptic ulcers:• Tips include:

* Avoid aspirin, ibuprofen, naproxen, and other NSAIDs. Try acetaminophen instead. If you must take such medicines, talk to your doctor first.* Don't smoke or chew tobacco.* Limit alcohol to no more than two drinks per day.

Gastric Ulcer

Type I Type IISame as PUM>F 3:1 , 50+ yrs.

Epigastric pain induced by eating.Weight loss.Nausea and vomiting.Anaemia from chronic blood loss.

Drug 1 Drug 2 Drug 3 Drug 4PPI Clarithomycin

eAmoxcycyline

PPI Clarithomycine

Metronidazole

PPI Tetracycline Metronidazole Subsalicylate / SubcitralDrugs Example

Antacide Mylanta, maalox, tums, gaviscon

Antagonist H2 Receptor Cimetidine, ranitidine, famotidine, nizatidinie

PPI Omeprazole, lansoprazole, rabeprazole, pantoprazole, esomeprazole

Protective Mucous Sucralfate drug

sucralfate

Prostaglandin Analog misoprostolBismuth Drugs Bismuth, subsalicylate

(BSS)