Peptic ulcer disease. Gastritis. Complications.

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Peptic ulcer disease.Gastritis. Complications.
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• Gastritis is an inflammation of the lining of the
  stomach. There are many possible causes of this
  disorder including an infection, an irritant, an
  autoimmune disorder, or a backup of bile into the
  stomach. Gastritis can occur suddenly (acute
  gastritis) or gradually (chronic gastritis).

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• Causes
• Gastritis can be caused by infection, irritation,
  autoimmune disorders, or backflow of bile into
  the stomach (bile reflux). Gastritis can also be
  caused by a blood disorder called pernicious
  anemia.
• Infections can be any of the following types
• Bacterial (usually Helicobacter pylori)
• Viral
• Parasitic
• Fungal

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• Irritation can be caused by a number of things,
  such as the following
• Long-term medication use (for example, aspirin,
  ibuprofen or other anti-inflammatory drugs
  called NSAIDS)
• Alcohol use
• Cigarette smoking
• Chronic vomiting
• Coffee and acidic beverages
• Excess gastric acid secretion (such as from
  stress)
• Eating or drinking caustic or corrosive
  substances (such as poisons)

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• Risk Factors
• Infection with H. pylori
• Acquired immunodeficiency syndrome (AIDS)
• Any condition that requires relief from
  persistent pain using NSAIDS
• Alcoholism
• Cigarette smoking
• Older age
• Genetic abnormalities

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• CLASSIFICATION OF CHRONIC GASTRITIS
• ADOPTED AT THE 9TH INTERNATIONAL CONGRESS OF
  GASTROENTEROLOGISTS
• ( SYDNEY 1990) , MODIFICATED IN HOUSTON IN 1994
• 1. CHRONIC NONATROPHIC ( CHRONIC HELICOBACTERIC
  GASTRITIS , CHRONIC ANTRIAL , TYPE B) , WHICH
  REPRESENTS ALMOST 70 OF ALL GASTRITS TYPES.
• 2. CHRONIC ATROPHIC GASTRITIS ( AUTOIMMUNE ,
  DIFFUSE GASTRITIS OF STOMACH CORPUS , ASSOCIATED
  WITH PERNICIOUS ANEMIA , ATROPHIC , TYPE A ) ,
  PRESENT IN 15 18 CASES OF CHRONIC
  GASTRITIES CHRONIC MULTIFOCAL GASTRITIS.
• 3. SPECIAL FORMS OF CHRONIC GASTRITIS
• CHEMICAL ( REACTIVE CHRONIC GASTRITIS , WHICH
  OCCURS IN CASE OF BILE REFLUX ( ABOUT 15 )
  , AFTER NSAID THERAPY ( ABOUT 10 )
• GRANULOMATOUS ( IN CASE OF CROHNS DISEASE ,
  SARKOIDOSIS , TUBERCULOSIS )
• EOZINOPHILIC ( IN CASE OF BRONCHIAL ASTHMA ,
  FOOD ALLERGY )
• LYMPHOCYTIC ( WITH MANIFESTED LYMPHOCYTIC
  INFILTRATION OF EPITHELIUM )
• GIGANT HYPERTROPHIC GASTRITIS ( MENETRIERS
  DISEASE )
• RADIATION GASTRITIS

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• Type B (Chronic antral gastritis)
• It principally affects the antrum and is
  associated with the presence of Helicobacter
  pylori on the surface epithelium. If organism is
  not present serological tests show antibodies
  against Helicobacter pylori.
• Pathology
• Presence of inflammatory cells such as
  lymphocytes, plasma cells.
• Gastric atrophy destruction of antral mucus
  glands
• Intestinal metaplasia.
• Proliferation or lymphoid tissue within the
  gastric mucosa.

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• Type A (autoimmune gastritis)
• It is an autoimmune disorder involving the fundic
  glands of stomach that secretes both the
  intrinsic factor and acid. The antibodies destroy
  the parietal cells with loss of acid and
  intrinsic factor.
• Intrinsic factor deficiency leads to pernicious
  anemia because intrinsic factor is required for
  the absorption of vitamin B12.
• Loss of acid secretion leads to achlorhydria.
  Achlorhydria leads to hypergastinemia that may
  lead to carcinoid tumors in about 5 of patients.

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• Signs and Symptoms
• Abdominal pain
• Indigestion (also called dyspepsia)
• Heartburn
• Hiccups
• Loss of appetite
• Nausea
• Vomiting, possibly of blood (called hematemesis)
  or material that looks like coffee-grounds
• Dark stools

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• Diagnosis
• There are several tests that may be done to make
  a diagnosis.
• These include endoscopy of the stomach. This
  allows the doctor to see into stomach and, if
  necessary, take samples (called a biopsy) from
  the lining.

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• normal mucous coat of stomach

• acute gastritis

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• Type B (Chronic antral gastritis)

• Type A (autoimmune gastritis)

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• The laboratory tests may need will depend on the
  specific cause of gastritis.
• A stool test may be used to check for the
  presence of blood, or a biopsy may be taken of
  the tissues of stomach to determine the cause of
  discomfort.
• A breath test may detect H. pylori, or samples
  from stomach may be taken to look for this
  organism.

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• Treatment
• The treatment of gastritis depends on the cause
  of the problem. The cure for gastritis caused by
  ingesting irritating substances is to stop the
  long-term use of these substances, which may
  include
• Alcohol
• Tobacco
• Acidic beverages such as coffee, carbonated
  beverages, and fruit juices with citric acid
• NSAIDS, such as aspirin and ibuprofen switch to
  other pain relievers (like acetominophen)
• Eat a fiber-rich diet
• Avoid high fat .

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• Medications
• Medications are often necessary to relieve
  symptoms, eradicate an infection such as H.
  pylori, and prevent or treat complications from
  gastritis such as an ulcer.
• Helicobactor pylori infestation, a common
  bacterial cause of gastritis and ulcers, is
  typically treated with a combination of drugs.
  The typical combination includes antibiotics, a
  bismuth compound, and a proton pump inhibitor.
  (Proton pump inhibitors reduce stomach acid
  secretion.)

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• In addition to the medications used for
  Helicobacter pylori infection, other medications
  that may be used to relieve symptoms of gastritis
  include those that reduce stomach acid secretion
• Antacids such as calcium carbonate and magnesium
  hydroxide with aluminum salts
• H2 blockers such as ranitidine, cimetidine,
  nizatidine, and famotidine
• Proton pump inhibitors such as omeprazole and
  lansoprazole

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• In case of atrophic gastritis, either stimulating
  or replacement therapy is administered.
  Stimulating therapy includes metabolic drugs,
  replacement therapy includes gastric juice or
  acidin pepsin.

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• Peptic Ulcer
• Peptic ulcer is a general chronic and relapsing
  disease characterized by seasonal exacerbations
  with ulceration of the stomach wall or the
  duodenum.

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• Causes
• When the stomach's natural protections from the
  damaging effects of digestive juices (including
  acid and pepsin an enzyme that helps breakdown
  protein) stop working or the acid production is
  too overwhelming for these protective defenses to
  work properly, person can get an ulcer.
• There are a few different ways this happens.
• Helicobacter pylori (H. pylori), a bacterial
  organism, is responsible for most ulcers. This
  organism weakens the protective coating of the
  stomach and duodenum and allows the damaging
  digestive juices to irritate the sensitive lining
  below.

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• Non-steroidal anti-inflammatory drugs (NSAIDs)
  ongoing use of this class of medications is the
  second most common cause of ulcers.
• These drugs are acidic and they block
  prostaglandins, substances in the stomach that
  help maintain blood flow and protect the area
  from injury.
•  

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• ZollingerEllison syndrome people with this
  uncommon condition have tumors in the pancreas
  and duodenum that produce gastrin, a hormone that
  stimulates gastric acid production.
• Other causes of ulcers are conditions that can
  result in direct damage to the wall of the
  stomach or duodenum such as heavy use of alcohol,
  radiation therapy, burns, and physical injury.

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• Risk Factors
• Genetic factors may predispose to developing an
  ulcer
• Chronic pain, from any cause such as arthritis,
  fibromyalgia, repetitive stress injuries or
  persistent back pain, leading to ongoing use of
  aspirin or NSAIDs
• Alcohol abuse
• Diabetes may increase risk of having H. pylori

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• Living in crowded, unsanitary conditions
  increases the risk of H. pylori infection
• Immune abnormalities may, in theory, make it more
  likely for H. pylori or other factors to cause
  damage to the lining of the stomach or duodenum.
• Lifestyle factors, including chronic stress,
  coffee drinking and smoking.
•  

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• PATHOGENESIS
• An ulcer forms when there is an imbalance between
  aggressive factors (e.g. acid and pepsin) and
  defense factors.
• In peptic ulceration, initial damage to defensive
  mucosal barrier results from Helicobacter pylori
  infection, NSAIDS, smoking and other factors.
  This damage of mucosal barrier facilitates the
  damaging effect of acid and pepsin.
• Ulcers occur only in the presence of acid and
  pepsin they are never found in achlorhydric
  patients (i.e. no acid, no ulcer). Therefore we
  can say that aggressive factors (Helicobacter,
  NSAIDS, smoking) break the defensive mucosal
  barrier and then acid pepsin cause destruction
  and ulceration.

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• Signs and Symptoms
• Abdominal pain
• Heartburn
• Indigestion (dyspepsia)
• Belching
• Nausea
• Vomiting
• Poor appetite
• Weight loss

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• PAIN
• Site Epigastrium
• Character Burning in character
• Radiation
• Pain is localized and patient is able to point it
  with his one finger "pointing sign".
• Time of pain
• Soon after eating within 15-30 minutes in gastric
  ulcer while 2-3 hours after eating in duodenal
  ulcer that frequently awakens the patient at
  night.
• Relation with food
• Patient with gastric ulcer are afraid to eat
  because it causes pain due to release of acid in
  response to food. Patients with duodenal ulcer
  feel pain in empty stomach and get relief after
  taking food which causes partial neutralization
  of acid. Then in response to food there is
  increased acid secretion which causes pain after
  2-3 hours.

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• Aggravating factors
• Smoking
• Excessive intake of coffee and tea
• Alcohol
• Eating precipitates pain in gastric ulcer while
• missing a meal in duodenal ulcer.
• Relieving factors
• Antacids and milk
• Vomiting relieves pain in gastric ulcer
• Intake of food relieves pain in duodenal ulcer
• Periodicity
• Pain comes and goes in a 2-3 month cycle in
  gastric ulcer
• In duodenal ulcer episode occurs with 4-6 month
  cycle, often worse in spring and autumn.
• Relapse occurs more frequently in smokers than in
  non smokers.
• Duration of attack
• A few weeks in gastric ulcer
• A month or two in duodenal ulcer

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• VOMITING
• Vomiting relieves pain of gastric ulcer and some
  patients force themselves to vomit after eating
  to relieve symptoms. It is uncommon in duodenal
  ulcer.
• Other symptoms
• Few patients present with haematemasis, due to
  perforation of the ulcer even in the absence of
  prior history of epigastric pain. Take history of
  melena also.
• Some patients may not have pain. They may
  complain of nausea and retrosternal burning.
• ON CLINICAL EXAMINATION
• Deep tenderness in epigastrium is present in most
  of the cases.

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• COMPLICATIONS
• Hemorrhage
• Perforation
• Penetration
• Pyloric obstruction
•  Malignization

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• Perforation

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• Penetration

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Pyloric obstruction
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• Malignization

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malignant neoplastic transformation
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• Investigation
• One of two tests will be performed to try to
  identify an ulcer
• Upper gastrointestinal (GI) series
• Endoscopy
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• For the upper GI, patient drink a chalky liquid
  called barium and then a series of x-rays may
  reveal an ulcer.

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• The endoscopy, which is more accurate, allows
  both direct visualization of organs for an ulcer
  or other problems and sampling of tissue from the
  walls (called biopsies) of the stomach and small
  intestines to test for H. pylori.

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• Lumen of the duodenum of a healthy human male.
  White spots are reflections of the light source.

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DIAGNOSIS OF H.PYLORI

• Histology
• Rapid urease activity test
• Culture  
• Urea breath test with BC or 14C
• Serological test
• The breath test, which is the least invasive, is
  proving to be at least 95 accurate.

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• Urea breath test

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• Treatment
• The main goals for treating a peptic ulcer
  include eliminating the underlying cause
  (particularly H. pylori infection or use of
  NSAIDs), preventing further damage and
  complications, and reducing the risk of
  recurrence. Medication is almost always needed to
  alleviate symptoms and must be used to eradicate
  H. pylori.

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• Doctors used to recommend eating bland foods with
  milk and only small amounts of food with each
  meal. Dietary and other lifestyle measures that
  should help, however, include
• Eat a diet rich in fiber, especially from fruits
  and vegetables.
• Foods containing flavonoids, like apples, celery,
  cranberries and tea may inhibit the growth of H.
  pylori.
• Quit smoking
• Receive treatment for alcohol abuse.

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• Medications
• "Triple therapy" (including a proton pump
  inhibitor for example, omeprazole to reduce
  acid production and two antibiotics to get rid of
  the organism) is commonly used to treat H.
  pylori-related ulcers. Instead of one of the
  antibiotics, bismuth salicylate may be the third
  medication recommended.

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• Some of the same drugs are used for non-H. pylori
  ulcers as well as for symptoms (like indigestion)
  due to ulcers of any cause
• Antacids, available over the counter, may relieve
  heartburn or indigestion but will not treat an
  ulcer
• H2 blockers, such as cimetidine, ranitidine,
  nizatidine, and famotidine, reduce gastric acid
  secretion.
• Misoprostol can be used preventively if patient
  take a lot of NSAIDs because it helps to protect
  the stomach from the damaging effects of these
  pain killers.
• Proton-pump inhibitors, including lansoprazole,
  omeprazole, pantoprazole, and rabeprazole,
  decrease gastric acid production. This is the
  number one choice of medications for treating
  ulcers.
• Sucralfate makes a coating over the ulcer crater,
  protecting it from further damage.