problem git 1a-adhelina.ppt
TRANSCRIPT
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GERD
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etiology
Obesity Scleroderma
Smoking
Alcohol, coffee, chocolate, fatty or spicy foods
Certain medications (eg, beta-blockers, NSAIDs, theophylline, nitrates,alendronate, calcium channel blockers)
Mental retardation requiring institutionalization Spinal cord injury
Immunocompromise
Radiation therapy for chest tumors
Pill esophagitis is thought to be secondary to chemical irritation of esophagealmucosa from certain medications (eg, iron, potassium, quinidine, aspirin, steroids,
tetracyclines, NSAIDs), especially when medications are swallowed with too littlefluid
Helicobacter pylorieradication therapy has been inversely related to refluxesophagitis; it is postulated that the ammonia (alkaline) produced by H
pylorireduces the acidity of the stomach and, hence, protects the esophagus fromacid spillage
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Epidemiology
Esophagitis is commonly seen in adults and is uncommon in
childhood.The most common type of esophagitis is that
associated with GERD (ie, reflux
esophagitis). Candidaesophagitis is the most common type of
infectious esophagitis. Esophageal reflux symptoms occur
monthly in 33-44% of the general population; up to 7-10% of
people have daily symptoms.
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patfis
Reflux esophagitis
develops when gastric contents are passivelyregurgitated into the esophagus. Reflux happenscommonly; in most cases, it does not cause major harm,
because natural peristalsis of the esophagus clears therefluxate back to the stomach.
In other cases, where acid reflux from the stomach ispersistent, the result is damage to the esophagus,
causing symptoms and macroscopic changes. Gastricacid, pepsin, and bile irritate the squamous epithelium,leading to inflammation, erosion, and ulceration of theesophageal mucosa.
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Medication-induced esophagitis (pill esophagitis)
Medications associated with pill esophagitis cause injury by local ortopical injury.Antibiotics, potassium chloride, nonsteroidal anti-inflammatory drugs (NSAIDs), quinidine, emperonium bromide, andalendronate (Fosamax) account for 90% of the reported cases. The
following are important pill and patient factors: Chemical nature of drug
Solubility
Contact time with mucosa
Size, shape, and pill coating
Amount of water (ie, too little) taken to swallow pill (eg,alendronate)
Preexisting esophageal pathology (eg, stricture, achalasia)
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Radiation and chemoradiation esophagitis
Radiation therapy over 30 Gy to the mediastinumtypically causes retrosternal burning and painfulswallowing, which is usually mild and limited to theduration of therapy.[6]
A dose of 40 Gy causes mucosal redness and edema.
A dose of 50 Gy causes a higher incidence and severity
of esophageal damage. A dose of 60-70 Gy causes moderate-to-severe
esophagitis with strictures, perforations, and fistulas
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Prognosis
The prognosis is good with rapid diagnosis and
proper treatment. Ultimately, prognosis
depends on the underlying disease process.
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GASTRITIS
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What Is Gastritis?
Gastritis is an inflammation, irritation, or
erosion of the lining of the stomach. It can
occur suddenly (acute) or gradually (chronic)
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Causes Gastritis?
Gastritis can be caused by irritation due to excessive alcohol use,chronic vomiting, stress, or the use of certain medications such asaspirin or other anti-inflammatory drugs. It may also be caused byany of the following:
Helicobacter pylori (H. pylori):A bacteria that lives in the mucous
lining of the stomach. Without treatment the infection can leadto ulcers, and in some people,stomach cancer.
Pernicious anemia:A form of anemia that occurs when thestomach lacks a naturally occurring substance needed to properlyabsorb and digest vitamin B12.
Bile reflux:A backflow of bile into the stomach from the bile tract(that connects to the liver and gallbladder).
Infectionscaused by bacteria and viruses
If gastritis is left untreated, it can lead to a severe loss in blood, orin some cases increase the risk of developing stomach cancer.
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Symptoms of Gastritis?
Symptoms of gastritis vary among individuals, and in many people thereare no symptoms. However, the most common symptoms include:
Nausea or recurrent upset stomach
Abdominal bloating
Abdominal pain Vomiting
Indigestion
Burning or gnawing feeling in the stomach between meals or at night
Hiccups
Loss of appetite Vomiting blood or coffee ground-like material
Black, tarry stools
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Gastritis Diagnosed?
To diagnose gastritis, your doctor will review your personal and familymedical history, perform a thorough physical evaluation, and mayrecommend any of the following tests.
Upper endoscopy.An endoscope, a thin tube containing a tiny camera, isinserted through your mouth and down into your stomach to look at thestomach lining. The doctor will check for inflammation and may perform a
biopsy, a procedure in which a tiny sample of tissue is removed and thensent to a laboratory for analysis.
Blood tests.The doctor may perform various blood tests such as checkingyour red blood cell count to determine whether you have anemia, whichmeans that you do not have enough red blood cells. He or she can alsoscreen for H. pylori infection and pernicious anemia with blood tests.
Fecal occult blood test (stool test).This test checks for the presence ofblood in your stool, a possible sign of gastritis.
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Treatment for Gastritis?
Taking antacids and other drugs to reduce stomach acid,which causes further irritation to inflamed areas.
Avoiding hot and spicy foods.
For gastritis caused by H. pylori infection, your doctor willprescribe a regimen of several antibiotics plus an acidblocking drug (used for heartburn).
If the gastritis is caused by pernicious anemia, B12 vitaminshots will be given.
Once the underlying problem disappears, the gastritisusually does, too. You should talk to your doctor beforestopping any medicine or starting any gastritis treatment onyour own.
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Prognosis for Gastritis
Most cases of gastritis improve quickly once
treatment has begun.
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PEPTIC ULCER DISEASE
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Definition
Peptic ulcers are defects in the gastric or
duodenal mucosa that extend through the
muscularis mucosa
Peptic ulcer disease (PUD) is one of the most
common diseases affecting the gastrointestinal(GI) tract.
It causes inflammatory injuries in the gastric or
duodenal mucosa, with extension beyond the
submucosa into the muscularis mucosa.
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Epidemiology
The incidence of DUs declined steadily
from 1960 to 1980 and has remained
stable since then.
Gastric Ulcers GUs tend to occur later in
life than duodenal lesions, with a peak
incidence reported in the sixth decade.
More than half of GUs occur in males
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Etiology
H. pyloriinfection
NSAIDs
Cigarette smoking
Genetic predisposition
blood group O
Psychological stress
The majority of GUs can be attributed to either
H. pylorior NSAID-induced mucosal damage.
The majority of DUs can be attributed to H.
pylori
Predominant cause
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Campylobacter pyloridis
It is S-shaped (~0.5 3 um in size) and
contains multiple sheathed flagella.
Its ability to colonize the gastric mucosa
and produce mucosal injury.
a gram-negative microaerophilic
This rate of colonization increases with
age, with about 50% of individuals age 50
being infected.
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Figure 1: Helicobacter pyloriinvading epithelial cells.
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Campylobacter pyloridis
Transmission of H. pylorioccurs fromperson to person, following an oral-oral
or fecal-oral route.
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PATHOPHYSIOLOGY H. pylori
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PATHOPHYSIOLOGY NSAIDs
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PATHOPHYSIOLOGY NSAIDs
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CLINICAL FEATURES
Epigastric paincan be present in both DU and GU.
Pain pattern in DU occurs 90 min to 3 h after amealand is frequently relieved by antacids or food.
Pain that awakes the patient from sleep (betweenmidnight and 3 A.M.) is the most discriminating
symptom, with two-thirds of DU patients describingthis complaint.
GU discomfort may actually be precipitated byfood.
Nausea and weight loss occur more commonly inGU patients.
Hematemesis
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Other symptoms are :
losing weight
not feeling like eating
having pain while eating
feeling sick to your stomach
vomiting
CLINICAL FEATURES
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Related Complications
Gastrointestinal Bleeding
Perforation
Gastric Outlet Obstruction
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Treatment
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LO 3 PENDAHARAN SALURAN ATAS
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MELENA
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What is melena
melenaor melaenarefers to the black,
"tarry" feces .The black color is caused by
oxidation of the iron in hemoglobin during its
passage through the ileum and colon.
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Causes
The upper part of the GI tract will usually cause black stoolsdue to:
Abnormal blood vessels (vascular malformation)
A tear in the esophagus from violent vomiting (Mallory-
Weiss tear) Bleeding stomach or duodenal ulcer
Inflammation of the stomach lining (gastritis)
Lack of proper blood flow to the intestines (bowelischemia)
Trauma or foreign body
Widened, overgrown veins (called varices) in the esophagusand stomach
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diagnostic tests
Angiography
Barium studies
Bleeding scan (nuclear medicine)
Blood studies, including a complete blood count ( CBC)and differential, serum chemistries, clotting studies
Colonoscopy
Esophagogastroduodenoscopy or EGD
Stool culture
Tests for the presence of Helicobacter pyloriinfection
X-rays of the abdomen
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HEMATEMESIS
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What is Hematemesis
is the vomiting of blood. The source is
generally the upper gastrointestinal tract.
Patients can easily confuse it
with hemoptysis (coughing up blood),although the latter is more common.
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Causes
Prolonged and vigorous retching (may cause a tear in the small bloodvessels of the throat or the esophagus, producing streaks of blood in thevomit, and is called Mallory-Weiss syndrome).
Irritation or erosion of the lining of the esophagus or stomach
Bleeding ulcer located in the stomach, duodenum, or esophagus
Vomiting of ingested blood after hemorrhage in the oral cavity, nose or
throat Vascular malfunctions of the gastrointestinal tract, such as bleeding
gastrointestinal varices
Tumors of the stomach or esophagus.
radiation poisoning
Viral hemorrhagic fevers Gastroenteritis
Gastritis
Peptic ulcer
Chronic viral hepatitis
Intestinal Schistosomiasis (caused by the parasite schistosoma mansoni)
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