Problem 2 GIT

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 STOMACH
• The stomach is a J-shaped, pouchlike organ, about
25-30 centimeters long, which hangs inferior to the
diaphragm in the upper left portion of the abdominal
cavity
• The stomach is divided into 4 parts
1. Cardia : surrounds the gastroesophageal
sphincter
2. Fundus : is the rounded portion above and to the
left of the cardia
 3. The body : below the fundus is the large central
portion of the stomach
4. Pylorus or Antrum : is the narrow inferior region
that connects with the duodenum of the small
intestine via pyloric sphincter
• When there is no food in the stomach, the mucosa
lies in large folds called rugae, which are visible
with the unaided eye
• The wider and more superior part of pyloric region,
the pyloric antrum narrows to form the pyloric canal,
which terminates at the pylorus
• The pylorus is continuous with the duodenum
through the pyloric valve or sphincter, which
controls stomach emptying
• The convex lateral surface of the stomach is its
greater curvature and its concave medial surface is
the lesser curvature
• Extending from these curvatures are two
mesenteries, called omenta  help tether the
stomach to other digestive organs and the body wall
• The lesser omentum runs from the liver to the lesser
curvature of the stomach, where it becomes
continuous with the visceral peritoneum covering
the stomach
• The greater omentum drapes inferiorly from the
greater curvature of the stomach to cover the coils
of the small intestine
• Then runs dorsally and superiorly, wrapping the
spleen and the transverse portion of the large
intestine before blending with the mesocolon
• The greater omentum is riddled with fat deposits
that give it the appearance of a lacy apron
• Also contain large collections of lymph nodes
Stomach
ESOPHAGUS-GASTER JUNCTION
 Gaster
• Cardiac
• Corpus
• Fundus
A. Tunica mucosa
1. Columnar surface
epithelium
2. Gastric foveolae
3. T.propria + fundus
glands
4. Elastic membran
5. T. M. Mucosae
B. Tunica Submucosa
 Gaster
• Pyloric
A. Tunica Mucosa
1. Columnar surface
epithelium
2. Gastric foveolae
(wide and deep)
3. T.propria + pyloric
glands
4. Elastic membran
5. T. M. Mucosae
B. Tunica Submucosa
C. Tunica Muscularis
 STOMACH
• Specialized for accumulation of food
• Capable of considerable expansion (can hold 2-3L)
• Gastric juice converts food into semiliquid called
chyme
• 4 Parts
• Cardia
• Fundus
• Body
• Pylorus
 STOMACH
• Three main functions :
• Store ingested food until it can be emptied into
small intestine
• Secretes hydrochloric acid (HCl) and enzymes that
begin protein digestion
• Mixing movements convert pulverized food to
chyme
 STOMACH
• Gastric mucosa has numerous openings called
gastric pits
• 3 functionally different cell types compose glands
• Mucous cells
• Chief cells
• Parietal cells
 GASTRIC MOTILITY
• Four aspects
• Filling
• Involves receptive relaxation
• Enhances stomach’s ability to accommodate the extra volume of
food with little rise in stomach pressure
• Triggered by act of eating
• Mediated by vagus nerve
• Storage
• Takes place in body of stomach
• Mixing
• Takes place in antrum of stomach
• Emptying
• Largely controlled by factors in duodenum
Chapter 16 The Digestive System
Human Physiology by Lauralee Sherwood
©2007 Brooks/Cole-Thomson Learning
Sherwood L. Introduction to human physiology. 8th ed. United
States: Brooks/Cole-Cengage Learning; 2013.
Sherwood L. Introduction to human physiology. 8th ed. United
States: Brooks/Cole-Cengage Learning; 2013.
BIOCHEMESTRY
 GASTRIC SECRETION
• Gastric mucosal cells secrete gastric juice
• HCl and pepsinogen initiate protein digestion
• Intrinsic factor required for absorption of vitamin B 12
• Mucus protects gastric mucosa from HCl

• Cell Types of Gastric Mucosa

• Parietal cells → HCl and Intrinsic Factor
• Chief cells → Pepsinogen
• G cells → Gastrin into the circulation
• Mucous neck cells → Mucus, HCO 3-
Sherwood L. Introduction to human physiology. 8th ed. United
States: Brooks/Cole-Cengage Learning; 2013.
 HCl SECRETION
• Functions of HCl
• Activates pepsinogen to active enzyme pepsin
and provides acid medium for optimal pepsin
activity
• Aids in breakdown of connective tissue and
muscle fibers in foods
• Denatures protein
• Along with salivary lysozyme, kills most of the
microorganisms ingested with food
Sherwood L. Introduction to human physiology. 5th ed. United
States: Brooks/Cole-Thomson Learning; 2007.
 HCl SECRETION
• Parietal cells secrete HCl which converts inactive
pepsinogen to pepsin

1.Within cell, CO2 combines with H2O to form H+ and HCO3-

2.H+ secreted into lumen of stomach via H+-K+ ATPase
(proton pump)
• Cl- follows H+ into the lumen by diffusing through Cl-
channels
3.HCO3- absorbed into blood via a Cl--HCO3- exchanger
• Eventually HCO3- secreted back into GI tract by
pancreas
Sherwood L. Introduction to human physiology. 8th ed. United
States: Brooks/Cole-Cengage Learning; 2013.
 PHASES OF GASTRIC SECRETION
• Cephalic phase
• Refers to increased secretion of HCl and pepsinogen that
occurs in response to stimuli acting in the head before food
reaches stomach
• Gastric phase
• Begins when food actually reaches the stomach
• Presence of protein increases gastric secretions
• Intestinal phase
• Inhibitory phase
• Helps shut off flow of gastric juices as chyme begins to
empty into small intestine
Chapter 16 The Digestive System
Human Physiology by Lauralee Sherwood
©2007 Brooks/Cole-Thomson Learning
 REGULATION OF HCl SECRETION
• ACh
• Released from vagus nerve
• Binds to receptors on parietal cells
• Produces H+ secretion by parietal cells
• Histamine
• Released from mastlike cells in gastric mucosa
• Binds to H2 receptors on parietal cells
• Produces H+ secretion by parietal cells
• Gastrin
• Released into circulation by G cells of stomach antrum
• Binds to receptors on parietal cells
• Stimulates H+ secretion
GASTRIC MUCOSAL BARRIER
• Enables stomach to contain acid without injuring
itself

Chapter 16 The Digestive System

Human Physiology by Lauralee Sherwood
©2007 Brooks/Cole-Thomson Learning
 ALARM SYMPTOMS
• Age older than 55 with new-onset dyspepsia
• Unintended weight loss
• Persistent/continuous vomiting
• Progressive dysphagia
• Odynophagia
• Unexplained anemia or iron deficiency
• Jaundice
 ALARM SYMPTOMS
• Palpable abdominal mass or
lymphadenopathy
• Hematemesis, melena, hematochezia
(chronic GI bleeding)
• Anorexia
• Family history of upper GI cancer
• Previous gastric surgery
• Suspicious barium meal
 VOMITING (EMESIS)
• Forceful expulsion of gastric contents through the
mouth
• Not accomplished by reverse peristalsis
• The force for expulsion comes from :
• The diaphragm
• The abdominal muscles
• Coordinated by vomiting center in the medulla of
brain stem
 VOMITING (EMESIS)
1. Deep inspiration, closure of glottis
2. Contracting diaphragm + abdominal muscles → the
intra-abdominal pressure ↑
3. Flaccid stomach is squeezed
4. Gastric contents forced upward through relaxed
sphincters till mouth
 CAUSES OF VOMITING (EMESIS)
• Tactile (touch) stimulation of the back of the throat
• Irritation or distention of stomach and duodenum
• Elevated intracranial pressure (e.g. cerebral
hemorrhage)
• Rotation or acceleration of the head → dizziness
• Chemical agents (drugs, noxious substances)
• Psychogenic (emotional factors)
 EFFECTS OF VOMITING (EMESIS)
• Reduction in plasma volume → dehydration,
circulatory problems
• Loss of acid → metabolic alkalosis
DYSPEPSIA
 DYSPEPSIA
• Syndrome that consists of intermittent epigastric
pain or discomfort, nausea, bloating, vomiting, early
satiation and flatus
• The symptoms characteristically develops after
eating
 DYSEPSIA ETIOLOGY
• Food or drug intolerance
• Functional dyspepsia
• Luminal GI tract dysfunction
• Helicobacter pylori infection
• Pancreas disease (pancreas carcinoma and
pancreatitis)
• Other conditions (DM, thyroid disease, CKD,
myocardial ischemia, malignancy, gastric volvulus or
paraesophageal hernia, pregnancy)
Harmon RC, Peura DA. Evaluation and management of dyspepsia.
Ther Adv Gastroenterol. 2010;3(2):87-98.
DIFFERENTIAL DIAGNOSIS OF DYSPEPSIA
COMPLAINTS

Vojvodic M, Young A, editors. Toronto notes 2014. Toronto: Toronto

Notes for Medical Students Inc.; 2014.
 FUNCTIONAL DYSPEPSIA
• Symptoms thought to originate in gastroduodenal
origin
• Absence of any organic, systemic or metabolic
disease

Tack J, Talley NJ, Camilleri M, Holtmann G, Hu P, Malagelada J, et al.

Functional gastroduodenal disorders. Gastroenterology.
2006;130:1466-79.
 THREE GROUPS OF FUNCTIONAL
DYSPEPSIA
• Ulcer-like type → epigastric pain and nocturnal pain
symptoms are the more dominant symptoms
• Dismotility-like type → bloating, nausea, vomiting,
fullness and early satiety are the more dominant
symptoms
• Non-specific dyspepsia → no dominant complaints
FUNCTIONAL DYSPEPSIA DIAGNOSTIC
CRITERIA (ROME III)

Rome III Diagnostic Criteria for Functional Gastrointestinal Disorders

 DIAGNOSIS FOR HELICOBACTER
PYLORI INFECTION
• Serology
• Cheap, acceptable for asymptomatic or pediatric
patients
• Look for IgG antibody to H. pylori
• ELISA, Westernblot, complement fixation,
immunofluorescent
• Urea Breath Test (UBT)
• Golden standard
• The patients swallow urea that contain carbon isotopes
• (+) → there is urease activity from the bacteria that
produce carbon dioxide and ammonia → the carbon
dioxide detected from patient’s exhalation by mass
spectrometer
 DIAGNOSIS FOR HELICOBACTER
PYLORI INFECTION
• Invasive examination → gastric mucosal biopsy
• Biopsy urease test (BUT)
• Endoscopy
 REGIMENS FOR HELICOBACTER
PYLORI THERAPY
• Triple therapy :
• PPI + Amoxicillin + Clarithromycin
• PPI + Metronidazole + Clarithromycin
• PPI + Metronidazole + Tetracycline
Regiments given in 7 – 14 days
• Quadruple therapy :
• Colloidal bismuth subcitrate + PPI + Amoxicillin + Clarithromycin
• Colloidal bismuth subcitrate + PPI + Metronidazole +
Clarithromycin
• Colloidal bismuth subcitrate + H2 RA + Metronidazole +
Tetracycline
 REGIMENS FOR HELICOBACTER
PYLORI THERAPY
Dosage :
• Proton pump inhibitor :
• Omeprazole 2 x 20 mg
• Lansoprazole 2 x 30 mg
• Rabeprazole 2 x 10 mg
• Esomeprazole 2 x 20 mg
• Amoxicillin 2 x 1 g/day
• Clarithromycin 2 x 500 mg/day
• Metronidazole 3 x 500 mg/day
• Tetracycline 4 x 250 mg/day
• Colloidal bismuth subcitrate 4 x 120 mg/day
• Ranitidine 3x150 mg
 MEDICAL NUTRITION THERAPY FOR
DYSPEPSIA PATIENTS
• Reduction of dietary fat intake
• Use of smaller meals
• Diets with low calories
• Achieve a healthy weight
• Limiting alcohol intake
• Mild exercise
• Behavioral management and emotional support
 MEDICAL NUTRITION THERAPY FOR
PEPTIC ULCER PATIENTS
• Limit the consumption of alcohol, spices and
caffeine-containing foods or beverages
• Food combinations to inhibit the growth of
Helicobacter pylori
• Increase the consumption of omega-3 and omega-6
fatty acids → may have immune and cytoprotective
effect
• Nutritionally complete diet + adequate dietary fiber
• Behavioral management : avoid tobacco products
PYLORIC STENOSIS
 DEFINITION
• A narrowing of the pylorus, the opening from the
stomach into the small intestine
 ETIOLOGY
• The cause of the thickening is unknown, although
genetic factors may play a role. Children of parents
who had pyloric stenosis are more likely to have this
condition
• Pyloric stenosis occurs more often in boys than in
girls, and is rare in children older than 6 months. The
condition is usually diagnosed by the time a child is
6 months old
 EPIDEMIOLOGY
• Pyloric stenosis is one of the most common
conditions requiring surgery in infants
• It is more common in boys than girls and usually
affects children who are born at full term
• It rarely occurs in premature infants
 SIGN AND SYMPTOMS
• Vomiting is the first symptom in most children
• Vomiting may occur after every feeding or only
after some feedings
• Vomiting usually starts around 3 weeks of age, but
may start any time between 1 week and 5 months
of age
• Vomiting is forceful (projectile vomiting)
• The infant is hungry after vomiting and wants to
feed again
• Other symptoms generally appear several weeks
after birth
• Abdominal pain
• Belching
• Constant hunger
• Dehydration (gets worse with the severity of the
vomiting)
• Failure to gain weight or weight loss
• Wave-like motion of the abdomen shortly after
feeding and just before vomiting occurs
 DIFFERENTIAL DIAGNOSIS
• Enteritis
• Neonatal intestinal obstruction
• Intracranial birth injury
• Overfeeding
 CLINICAL ASSESSMENT
• The condition is usually diagnosed before the baby is 6
months old
• A physical exam may reveal signs of dehydration. The infant
may have a swollen belly. The doctor may detect the
abnormal pylorus, which feels like an olive-shaped mass,
when touching the stomach area
• An ultrasound of the abdomen may be the first imaging test
performed
• Other tests that may be done include:
• Barium x-ray  reveals a swollen stomach and narrowed
pylorus
• Blood chemistry panel  often reveals an electrolyte
imbalance
 TREATMENT
• Treatment for pyloric stenosis involves surgery to
split the overdeveloped muscles
• Balloon dilation does not work as well as surgery,
but may be considered for infants when the risk of
general anesthesia is high
 COMPLICATIONS
• Failure for the baby to gain weight
 PROGNOSIS
• Surgery usually provides complete relief of
symptoms. The infant can usually tolerate small,
frequent feedings several hours after surgery
HIATAL HERNIA
 DEFINITION
• A condition in which a portion of the stomach
protrudes upward into the chest through an opening
in the diaphragm (the sheet of muscle used in
breathing that separates the chest from the
abdomen)
• Stomach content is coming out of the stomach into
the esophagus for an extended period of time
• Hiatal hernia is usually associated with
gastroesophageal reflux in infants
• Regurgitation of gastric acid from the stomach into
the esophagus can result from this condition
 ETIOLOGY
• The cause is unknown but may be the result of a
weakening of the supporting tissue
• Obesity and smoking may be risk factors in adults
• Children often have this condition present at birth
(congenital)
 CLASSIFICATION
• Type I
• Sliding hiatal hernia comprising at least 95% of
the overall total
• Gastroesophageal junction and gastric cardia slide
upward as a result of weakening of the
phrenoesophageal ligament attaching the
gastroesophageal junction to the diaphragm at
the hiatus
• Type II, III, IV
• Paraesophageal hernia
• The herniation into the mediastinum includes a visceral
structure other than the gastric cardia
• Type II : the gastric fundus also herniates with the
distinction being that in type II, the gastroesophageal
junction remains fixed at the hiatus
• Type III : mixed sliding/paraesophageal hernia
• Type IV : viscera other than the stomach herniate into
the mediastinum, most commonly the colon
 SIGN AND SYMPTOMS
• Swallowing difficulty 
• Aspiration pneumonia
• Apnea
• Asthma
• Hoarseness
• Gastric or esophageal dysmotility may also
contribute to symptoms
• Chest pain 
• Belching
 CLINICAL ASSESSMENT
• Barium swallow X-ray
• EGD (esophagogastroduodenoscopy)
• External esophageal pH monitoring
• Gastric emptying scan
 TREATMENT
• The goals of treatment are to relieve symptoms and prevent
complications
• Medical therapy is aimed at reducing regurgitation of
stomach contents into the esophagus (gastroesophageal
reflux)
• Medications that neutralize stomach acidity, or that
strengthen the lower esophageal sphincter, may be
prescribed
• Medications that improve esophagus and gastric motility
may be used
• Failure to control the symptoms by general or medical
measures, or the onset of complications, may require
surgical repair of the hernia
 COMPLICATIONS
• Slow bleeding and iron deficiency anemia
(esophagitis)
• Pulmonary (lung) aspiration
• Stricture of the esophagus
 PROGNOSIS
• Most symptoms are alleviated with treatment
TRACHEOESOPHAGEAL
FISTULA
 DEFINITION
• An abnormal connection in one or more places
between the esophagus (the tube that leads from
the throat to the stomach) and the trachea (the tube
that leads from the throat to the windpipe and
lungs)
• When a baby with a TE fistula swallows, the liquid
can pass through the abnormal connection between
the esophagus and the trachea. When this happens,
liquid gets into the baby's lungs. This can cause
pneumonia and other problems
 EPIDEMIOLOGY
• About one in 4,000 babies in the United States is
born with these problems
• A common congenital anomaly with an incidence of
1 case in 2000-4000 live births
 PATHOPHYSIOLOGY
• As a fetus is growing and developing in its mother's
uterus before birth, different organ systems are
developing and maturing
• The trachea and the esophagus begin developing as one
single tube
• At about four to eight weeks after conception, a wall
forms between the fetus' esophagus and trachea to
separate them into two distinct tubes
• If this wall does not form properly, TE fistula and/or
esophageal atresia can occur
 SIGNS AND SYMPTOMS
• Frothy white bubbles in the mouth
• Coughing or choking when feeding
• Vomiting
• Blue color of the skin, especially when the baby is
feeding
• Difficulty breathing
• Very round, full abdomen
 CLINICAL ASSESSMENT
• Along with a physical examination and medical
history, imaging studies are usually done to evaluate
whether a baby has TE fistula and/or esophageal
atresia
• X-rays are taken to look at the chest and abdomen
 GASTROESOPHAGEAL REFLUX DISEASE
(GERD)
• Condition which the stomach contents (solid or
liquid) leak backwards from the stomach into the
esophagus (the tube from the mouth to the
stomach)

Vojvodic M, Young A, editors. Toronto notes 2014. Toronto: Toronto

Notes for Medical Students Inc.; 2014.
 ETIOLOGY OF GERD
• Inappropriate transient relaxations of lower
esophageal sphincter (LES) → most common
• Low basal LES tone (especially in scleroderma)
• Contributing factors : delayed esophageal clearance,
delayed gastric emptying, increased intra-abdominal
pressure
• Acid hypersecretion (rare): Zollinger-Ellison
syndrome or gastrinoma (gastrin-secreting tumour)

Vojvodic M, Young A, editors. Toronto notes 2014. Toronto: Toronto

Notes for Medical Students Inc.; 2014.
SIGN AND SYMPTOMS OF GERD

Vojvodic M, Young A, editors. Toronto notes 2014. Toronto: Toronto

Notes for Medical Students Inc.; 2014.
 DIAGNOSIS OF GERD
• Based on symptom history and relief following a trial
of pharmacotherapy (proton pump inhibitor (PPI):
symptom relief 80% sensitive for reflux)
• Gastroscopy; indications :
• Heartburn accompanied by red-flags (bleeding,
weight loss, etc.)
• Persistent reflux symptoms or previous severe
corrosive esophagitis after trial therapy
• History of esophageal stricture with persistent
dysphagia Vojvodic M, Young A, editors. Toronto notes 2014. Toronto: Toronto
Notes for Medical Students Inc.; 2014.
 DIAGNOSIS OF GERD
• Esophageal manometry (study of esophageal
motility) → to diagnose abnormal peristalsis and/or
decreased LES tone, but cannot detect presence of
reflux; indicated before surgical fundoplication
(wrapping of gastric fundus around the lower end of
the esophagus)
• 24 hours pH monitoring: most accurate test, but
rarely required or performed. Most useful if PPIs do
not improve symptoms
Vojvodic M, Young A, editors. Toronto notes 2014. Toronto: Toronto
Notes for Medical Students Inc.; 2014.
 MANAGEMENT OF GERD
• PPIs → the most effective therapy and usually need
to be continued as maintenance therapy
• Antacids (Mg(OH)2, Al(OH)3, alginate)
• H2-blockers or PPIs can be used for NERD
• Diet helps symptoms, not the disease; avoid alcohol,
coffee, spices, tomatoes and citrus juices
• Lifestyle changes are weight loss (if obese) and
elevating the head of bed (if nocturnal symptoms)

Vojvodic M, Young A, editors. Toronto notes 2014. Toronto: Toronto

Notes for Medical Students Inc.; 2014.
 COMPLICATIONS OF GERD
• Esophageal stricture disease → can lead to
dysphagia (solids)
• Ulcer
• Bleeding
• Barrett’s esophagus and esophageal
adenocarcinoma

Vojvodic M, Young A, editors. Toronto notes 2014. Toronto: Toronto

Notes for Medical Students Inc.; 2014.
MEDICAL NUTRITION THERAPY FOR GERD
PATIENTS
• Avoid large, high-fat meals prior to going to bed →
delay gastric emptying, prolong acid secretion
• Lifestyle modification :
• Change in dietary practices
• Weight loss (if overweight)
• Smoking cessation
• Elevation of the head of the bed
• Avoid alcohol, wine
MEDICAL NUTRITION THERAPY FOR GERD
PATIENTS
• Limiting or avoiding aggravating foods or
beverages :
• Caffeine (chocolate, coffee, tea)
• Onions
• Peppermint (may lower LES pressure)
• Spices
• Citrus food
• Carbonated beverages
 NUTRITION CARE GUIDELINES FOR REDUCING
GASTROESOPHAGEAL REFLUX AND ESOPHAGITIS

• Avoid large, high-fat meals

• Avoid eating at least 3 to 4 hours before lying down
• Avoid smoking
• Avoid alcoholic beverages
• Avoid caffeine-containing food

Krenitsky JS, Decher N. Medical nutrition therapy for upper gastrointestinal tract disorders.
In Mahan LK, Stump SE, Raymond JL, editors. Krause’s food and nutrition care process
(chapter 28). 13th ed. St Louis: Saunders; 2012: p. 592-608.
 NUTRITION CARE GUIDELINES FOR REDUCING
GASTROESOPHAGEAL REFLUX AND ESOPHAGITIS

• Stay upright and avoid vigorous activity soon after

eating
• Avoid tight-fitting clothing, especially after a meal
• Consume a healthy, nutritionally complete diet with
adequate fiber
• Avoid acidic and highly spiced foods when
inflammation exists
• Lose weight if overweight

Krenitsky JS, Decher N. Medical nutrition therapy for upper gastrointestinal tract disorders.
In Mahan LK, Stump SE, Raymond JL, editors. Krause’s food and nutrition care process
(chapter 28). 13th ed. St Louis: Saunders; 2012: p. 592-608.
 Peptic Ulcers
• Peptic ulcers : open sores that develop on the inside
lining of esophagus, stomach and the upper portion of
small intestine.
• Peptic ulcers occur when acid in the digestive tract
eats away at the inner surface of the esophagus,
stomach or small intestine.
• Peptic ulcers include:
– Gastric ulcers that occur on the inside of the
stomach.
– Esophageal ulcers.
– Duodenal ulcers that occur on the inside of the
upper portion of your small intestine (duodenum).
 Peptic Ulcers
• Sign and symptoms :
– Burning pain / abdominal pain (the pain may : worsen
when stomach is empty, flare at night, often be
temporarily relieved by eating certain foods).
– The vomiting of blood.
– Dark blood in stools or stools that are black or tarry.
– Nausea or vomiting.
– Unexplained weight loss.
– Appetite changes.
 Peptic Ulcers
• Causes :
– A bacterium. H.pylori commonly live in the mucous layer that covers
and protects tissues that line the stomach and small intestine. Often it
cause no problem, but it can cause inflammation of the stomach's
inner layer, producing an ulcer. It may be transmitted by close contact
(kissing). Also through food and water.
– Regular use of certain pain relievers. Certain pain medications can
irritate or inflame the lining of stomach and small intestine. These
medications include aspirin, ibuprofen, naproxen, ketoprofen and
others.
– Other medications. Other prescription medications that can also lead to
ulcers include medications used to treat osteoporosis called
bisphosphonates and potassium supplements.
• Risk factor:
– Smoke.
– Drink alcohol. Alcohol can irritate and erode the mucous lining of
stomach, and it increases the amount of stomach acid that's
produced.
 Peptic Ulcers
• Test and diagnosis :
– Test fot H. Pylori (using blood, breath, stool).
– Endoscopy.
– X-ray (barium swallowing).
• Treatment for peptic ulcers depends on the cause,
including :
– Antibiotic medications to kill H. pylori.
– Medications that block acid production and promote
healing. (omeprazole, lansoprazole, etc).
– Medications to reduce acid production (ranitidine,
famotidine, cimetidine, etc).
– Antacids that neutralize stomach acid (antacid).
– Medications that protect the lining of your stomach
and small intestine.
 Peptic Ulcers
• Complication :
– Internal bleeding (leads to anemia or sometime need
blood transfusion). Severe blood loss may cause black
or bloody vomit or black or bloody stools.
– Infection. Peptic ulcers can eat a hole through the wall
of stomach or small intestine, increase risk of
peritonitis.
– Scar tissue. Scar tissue can block passage of food
through the digestive tract, causing to become full
easily, to vomit and to lose weight.
• Prevention and health education :
– Choose a healthy diet.
– Consider switching pain relievers.
– Control stress.
– Don't smoke.
– Limit or avoid alcohol.
 Gastritis
• Gastritis is an inflammation, irritation, or erosion of
the lining of the stomach. It can occur suddenly
(acute) or gradually (chronic).
• Gastritis can be caused by irritation due to excessive
alcohol use, chronic vomiting, stress, or the use of
certain medications such as aspirin or other anti-
inflammatory drugs. It may also be caused by :
– Helicobacter pylori (H. pylori). Without treatment
the infection can lead to ulcers.
– Pernicious anemia (lacks of vitamin B12).
– Bile reflux : a backflow of bile into the stomach from
the bile tract (that connects to the liver and
gallbladder).
– Infections caused by bacteria and viruses.
 Gastritis
• Signs and symptoms :
– Gnawing or burning ache or pain (indigestion) in
upper abdomen that may become either worse or
better with eating
– Nausea
– Vomiting, can be blood or coffee ground-like
material
– A feeling of fullness in your upper abdomen after
eating
– Abdominal bloating
– Abdominal pain
– Hiccups
– Loss of appetite
– Black, tarry stools
 Gastritis
• Diagnosis :
– Endoscopy and X-ray.
– Blood test and tes for H.pylori.
– FOB (fecal occult blood test).
• Risk factor :
– Bacterial infection.
– Regular use of pain relievers.
– Older age.
– Excessive alcohol use.
– Stress.
– Autoimmune disorders.
– HIV, chron’s disease, pasasite infection.
 Gastritis
• Complication :
– Stomach ulcers and stomach bleeding.
– Increase risk of stomach cancer.
• Treatment :
– Taking antacids and other drugs to reduce stomach
acid.
– Avoiding hot and spicy foods.
– Antibiotics for gastritis caused by H. pylori infection
plus an acid blocking drug (used for heartburn).
– If caused by pernicious anemia, B12 vitamin shots.
– Eliminating irritating foods from diet such as lactose
from dairy or gluten from wheat.
– Medications that block acid production and promote
healing.