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    Gastro 2006

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    Nyoman Tapayana
    The document discusses various gastrointestinal diseases including dyspepsia, gastritis, and peptic ulcers. It defines dyspepsia as pain or discomfort in the upper abdomen for at least 12 weeks, and differentiates between organic dyspepsia with an identifiable cause and functional dyspepsia without an organic cause. Gastritis is defined as inflammation of the stomach lining and can be acute or chronic. Peptic ulcers are breaches in the mucosa caused by acid and pepsin attack and can occur in the esophagus, stomach, or duodenum.

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    Gastro 2006

    Uploaded by

    Nyoman Tapayana
    64 views66 pages
    The document discusses various gastrointestinal diseases including dyspepsia, gastritis, and peptic ulcers. It defines dyspepsia as pain or discomfort in the upper abdomen for at least 12 weeks, and differentiates between organic dyspepsia with an identifiable cause and functional dyspepsia without an organic cause. Gastritis is defined as inflammation of the stomach lining and can be acute or chronic. Peptic ulcers are breaches in the mucosa caused by acid and pepsin attack and can occur in the esophagus, stomach, or duodenum.

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    The document discusses various gastrointestinal diseases including dyspepsia, gastritis, and peptic ulcers. It defines dyspepsia as pain or discomfort in the upper abdomen for at least 12 weeks, and differentiates between organic dyspepsia with an identifiable cause and functional dyspepsia without an organic cause. Gastritis is defined as inflammation of the stomach lining and can be acute or chronic. Peptic ulcers are breaches in the mucosa caused by acid and pepsin attack and can occur in the esophagus, stomach, or duodenum.

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    64 views66 pages

    Gastro 2006

    Uploaded by

    Nyoman Tapayana
    The document discusses various gastrointestinal diseases including dyspepsia, gastritis, and peptic ulcers. It defines dyspepsia as pain or discomfort in the upper abdomen for at least 12 weeks, and differentiates between organic dyspepsia with an identifiable cause and functional dyspepsia without an organic cause. Gastritis is defined as inflammation of the stomach lining and can be acute or chronic. Peptic ulcers are breaches in the mucosa caused by acid and pepsin attack and can occur in the esophagus, stomach, or duodenum.

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    of 66

    Stomach Diseases

    Suryadarma

    Gastroenterology-hepatology Division,
    Udayana university-Sanglah Hospital
    2006
    Resources
    Sleisenger & Fordtran’s gastrointestinal
    and liver disease, 2002
    Textbook of gastroenterology, Ed.
    Yamada, 2003
    Current diagnosis & treatment in
    gastroenterology, 2003
    Crash course gastroenterology,2004
    Netter’s gastroenterology, 2005
    Gastroenterology and liver disease,
    Ed.Richard G. Long, 2005
    Clinical gastroenterology and liver
    disease,Ed. Wilfred M Weinstein, 2005
    DYSPEPSIA
    Dyspepsia approach

    Definition: (Symptom) : pain or discomfort centered in upper


    abdomen for at least 12 weeks, in previous 12 month, no
    evidence related to defication or stool form ) with addition :
    nausia, vomiting, bloating, early satiety, etc)
    (adopted ROME II Criteria )

    Differensiate : *organic dyspepsia (OD)


    *functional dyspepsia (FD)
    OD : gastritis,gastric ulcer,gastric ca & etc
    FD : ulcer type, dysmotility type, nonspesific type

    * FD/OD With different mechanism


    Nonulcer dyspepsia
    Diagnostic approach :
    Usefull : cereful history and physical Ex.
    endoscopy UGI
    Lab :fool bood count, ESR, BS
    renal,liver function,thyroid.f
    Optional: H.pylori test
    USG Hepatobiliary
    Esophageal pH test
    Uncertain value
    Gastric emptying study
    Fundus relaxation study
    Electrogastrography
    Gastroduodenal manometry
    Water load test
    Pathogenesis of nonulcer dyspepsia

    Disturbed of motor function


    Disturbed of sensory function
    Duodenogastric reflux
    Post infection
    Psychososial factor and Alteration of
    CNS
    Enviromental factor
    Principles management NUD
    Make true diagnosis
    Minimize invasive investigation
    Education (reassurance, reinforce)
    Dietary modification
    Realistic treatment (strategies)
    Symtomatic treatment
    Psychoterapy
    Management strategies

    In patien > 45 y, with alarm symptom :


    Endoscopy immediately
    If young and no alarm sign
    Option 1. Empiric therapy strategies
    Option 2. Test and Treat strategies
    Option 3. Endoscopy strategies
    Option 4. Pharmacological strategies
    first line
    second line
    Option 5. Complementary strategies
    Option 6. Psychological strategies
    Drug for NUD
    Acid inhibition
    Cytoprotection
    Prokinetic
    Fundus relaxing
    Viseral analgesic
    Antispasmodic
    Antinausiant
    Antidepresant
    GASTRITIS
    Gastritis
    Definition : Gastric mucosa inflammation
    (acute or chronic)
    Etiology : multifactorial
    Location : gastritis antral dominant
    pangastritis
    Classification : modified Sydney System
    Gastritis
    Inflammation of the mucosa of the
    stomach
    Acute
    – Often due to dietary intake
    – Can last few hours to few days
    Chronic
    – Usually associated with peptic ulcer disease
    – 95% of patients with pernicious anemia have
    chronic gastritis
    Diagnosis
    – Made by clinical history; Endoscopy
    Acute Gastritis
    Clinical feature :
    *nausea,vomiting,indigestion,
    *gastrointestinal bleeding,
    *asymtomatic

    Diagnosis : History (alcohol,NSAID)


    Acute illnness patient
    Endoscopic: erotion,bleeding

    Patology: inflammatory infiltrat,predominantly neutrophils

    Treatment : antacid and causal


    Chronic gastritis
    Can progression of acute gastritis
    Common etiology H. pylori
    Autoimmun gastritis associated
    autoimmune diseases.

    Clinical feature:
    >> asymtomatic
    similar to acute G (long period)
    pernicious anemia
    Etiopatology
    Etiology:
    H. pylori
    NSAID
    Alcohol
    Reflux of bile

    Patology:
    Lost of parietal and chief cell,
    plasma cell and lymphocyte infiltration,
    chronic atrophic changes.
    Diffuse Corporal Atrophic Gastritis
    Disease Pathogenesis
    Antibodies against gastric fundic region antigens

    Atrophy of fundic glands with antral and intestinal metaplasia

    Decreased acid Decreased intrinsic factor

    Hypo- or a-chlorhydria Decreased B-12 absorption

    B-12 deficiency
    G cell stimulation in antrum

    Hypergastrinemia

    Fundic ECL cell hyperplasia and +/- carcinoids


    Clinical Manifestations
    Anorexia
    Nausea/vomiting
    Epigastric tenderness
    Abnormal full feeling
    Signs of vitamin B12 deficiency
    Natural history of H.pylori infection
    H.pylori infection
    weeks to months

    Chronic superficial gastritis


    (Histological gastritis)
    years

    Peptic Chronic MALT Chronic


    ulcer superficial lymphoma atrophic
    disease gastritis gastritis

    Gastric
    cancer
    H.pylori Cover,T.L.,et al.:ASM News, 61(1),21,1995
    Natural history H pylori infection
    Enviroment
    factors
    Gastric ca

    Gastric ulcer
    Multifocal
    Atrophic
    gastritis lymphoma
    Acute
    gastritis
    CHRONIC ACTIVE GASTRITIS

    Antral
    Predominant Duodenal ulcer
    gastritis

    lymphoma
    Diagnosis
    Endoscopy:
    atropic mucosa,
    erythema, erotion mucosa
    Lab: pernicious anemia
    antiparietal cell antibodies
    Complication :
    Intestinal metaplasia predisposes
    malignancy( adeno ca )
    Treatment :
    underlying cause
    H. pylori eradication
    Vit B12
    Management
    Depends on severity
    Mild
    – Symptoms relieved
    – Monitor for dehydration
    – Monitor for signs of bleeding
    Chronic
    – Lifestyle modification
    PEPTIC ULCER
    Definition:

    Ulceration (breach in mucosa) due to


    acid & pepsin attack.
    Deeper than just mucosa
    Single, punched out, clean base.
    Etiology:
    Helicobacter pylori – most common.
    Hyperacidity - eg. zollinger ellison.
    Drugs - anti-inflammatory (NSAIDs)
    & Corticostroids.
    Cigarette smoking, Alcohol,
    Rapid gastric emptying
    Personality and psychological stress
    Peptic ulcer
    Included :
    Esophageal ulcer
    Gastric ulcer
    Duodenal ulcer
    Definition: breaches of mucosa with
    tissue destruction at list to
    muscularis mucosa
    Pathophysiology
    There is a breakdown in the mucosal layer.
    Increase in acid-pepsin production from
    – Increase in number of cells that produce HCL
    and pepsin
    – Increase in the sensitivity of parietal cells to
    food and other stimuli
    – Excessive vagal stimulation
    Gastric mucosal barrier is impaired
    – Reflux
    – Helicobacter pylori
    Stress/Anxiety
    Pathogenesis of gastric ulceration
    Clinical Manifestations
    Gastric: Duodenal:
    Burning or gassy
    sensation in high More cramplike
    epigastric area discomfort
    Occurs within ½ hr. Occurs on empty
    after eating, food can stomach, food relieves
    worsen symptoms
    symptoms
    Rarely occurs at
    night Often occurs at night
    Vomiting may ease Vomiting uncommon
    discomfort
    May gain weight
    May lose weight
    Pyrosis Pyrosis
    Diagnosis
    Endoscopy is preferred procedure
    Hemoccult stools
    CLO (campylobacter-like organism)
    Helicobacter Pylori IgG Antibody
    PUD - Diagnosis
    Endoscopy
    Barium meal – contrast x-ray
    Biopsy – bacteria & malignancy
    H.Pylori:
    – Endoscopy cytology
    – Biopsy – Special stains
    – Culture - difficult
    – Urease Breath test
    – Stool antigen
    Peptic ulcer
    Location of gastric ulcers
    Type I gastric ulcer

    60% of GU
    Large volume of
    secretion with low
    or normal acid
    secretion
    Type II gastric ulcer

    25% of GU
    Usually acid
    hypersecretor
    DU usually precedes
    GU
    Type III gastric ulcer

    23% of GU
    Prepyloric ulcer
    Typically acid
    hypersecretor
    Type IV gastric ulcer

    Less than 10% of


    GU
    High-lying ulcer
    Complications:

    Bleeding – Chronic-IDA, Acute,


    Massive
    Fibrosis, Stricture obstruction.
    Perforation – Peritonitis.
    Gastric carcinoma.
    Management
    Medications Stress
    – Antacids management
    – Histamine Receptor
    Antagonists
    Smoking cessation
    – Proton pump
    inhibitors
    – Cytoprotective Diet Changes
    Medications
    – Treating H. Pylori
    Surgical
    Intervention
    Surgical Intervention
    Vagotomy w/ pyloroplasty
    Bilroth I – gastroduodenostomy
    – Partial gastrectomy with removal of
    distal 2/3 of stomach & anastamosis to
    duodenum
    Bilroth II – gastrojejunostomy
    – Partial gastrectomy with removal of
    distal 2/3 of stomach & anastamosis to
    jejunum
    Common Complications from
    Peptic Ulcer Surgery
    Dumping Syndrome

    Postprandial hypoglycemia

    Bile reflux gastritis


    DUODENAL ULCER
    Clinical Manifestations
    Gastric: Duodenal:
    Burning or gassy
    sensation in high More cramplike
    epigastric area discomfort
    Occurs within ½ hr. Occurs on empty
    after eating, food can stomach, food relieves
    worsen symptoms
    symptoms
    Rarely occurs at
    night Often occurs at night
    Vomiting may ease Vomiting uncommon
    discomfort
    May gain weight
    May lose weight
    Pyrosis Pyrosis
    Pathogenesis of duodenal ulceration
    Duodenal ulcer
    Zollinger-Ellison syndrome
    Clinical features suspicious ZES
    * post bulbar duodenal ulcer
    * multiple duodenal ulcer
    * PUD associated Chronic diarrhea
    * refractory PUD
    * PUD + nefrolithiasis
    * recurrent PUD without H.pylori,NSAID
    * PUD + hypercalsemia
    Diagnosis ZES
    Clinical features
    Serum gastrin level > 1000pg/mL
    Hyperparathyroidism

    DD/ carsinoid
    insulinoma
    glucagonoma
    somatostatinoma
    VIPoma
    Treatment : PPI

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