This document discusses disorders of the stomach, including anatomy, physiology, dyspepsia, and peptic ulcer disease (PUD). It covers the anatomy and layers of the stomach, as well as its functions like storage, digestion, and secretion. Gastric secretion and the phases of secretion are described. Dyspepsia is defined and its etiology, differential diagnosis, and approaches to evaluation and management are outlined. PUD and its causes like Helicobacter pylori infection and NSAID use are also summarized. Key signs and symptoms of duodenal and gastric ulcers are provided.

1. By Dr. Getasew kassaw
stomach
3/4/2018 GK,MD 1

2. disorders of stomach
• Outline
-anatomy
-physiology
-Dyspepsia
-PUD
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3. ANATOMY
• Parts
• Curvatures
• Layers
• vessels
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4. 3/4/2018 GK,MD 4

5. 3/4/2018 GK,MD 5

6. FUNCTIONS
• storage
• digestion
• secretion
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7. Gastric Secretion
 mucus-secreting cells that line the entire surface of the stomach
 two other important types of tubular glands.
 oxyntic ( gastric glands) cells - HCl ,pepsin ,intrinsic factor
,mucus
 pyloric (chief) cells - mucus for protection of the pyloric mucosa
from the stomach acid & gastrin.
 The oxyntic glands are located on the inside surfaces of the body
and fundus of the stomach, constituting the proximal 80% of the
stomach.
-The pyloric glands are located in the antral portion of the stomach
& the distal 20% of the stomach.
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8. Secretion phases:
Cephalic phase:
» 20 % of secretions
» Vagus nerve.
Gastric phase:
» 70% of gastric acid secretion
» vagovagal reflex, local enteric reflexes, and gastrin.
Intestinal phase:
» 10 % of secretions.
» Distension of the duodenum.
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9. PHYSIOLGY OF GASTRIC ACID
SECRETION
• Hydrochloric acid and pepsinogen are the two
principal gastric secretery products capable of
inducing mucosal injury
• Gastric acid and pepsinogen play a physiologic
role in protein digestion, absorption of iron and
vitamin B12 as well as killing ingested bacteria.
• Acid secretion:- Basal or Stimulated (cephalic,
gastric, and intestinal)
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10. • HCl synthesis
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11. • Parietal cell & Acid regulation
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12. Noxious agents to gastric mucosa:
• Acid
• pepsin
• bile acids
• pancreatic enzymes
• Drugs
• bacteria
• Some foods
• drinking's
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13. • Mucosal protective factors
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14. Dyspepsia
• persistent or recurrent pain or discomfort
centered in the upper abdomen.
• The term discomfort refers to symptoms such
as early satiety, postprandial fullness, bloating,
and nausea.
• Clinically relevant dyspepsia is defined as a
relapsing or chronic condition, present for at
least 12 weeks in the prior year
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15. Dyspepsia
• Dyspepsia is a common symptom with an
extensive differential diagnosis and a
heterogeneous pathophysiology.
• It occurs in 25% of the population each year, but
most affected people do not seek medical care.
• Dyspepsia is responsible for substantial health
care costs and considerable time lost from work
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16. DEFINITION
• Rome III - one or more of the following
symptoms
Postprandial fullness(postprandial distress
syndrome)
Early satiation (meaning inability to finish a
normal sized meal)
Epigastric pain or burning (termed epigastric
pain syndrome)
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17. Dyspepsia
Functional
Dyspepsia
Non-GI
Causes of Symptoms
(cardiac disease,
muscular pain, etc.)
Structural Dyspepsia
(GERD, PUD, pancreatic
disease, gallstones, etc.)
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18. ETIOLOGY
-Approximately 25% of patients with dyspepsia
have an underlying organic cause.
-However, up to 75% of patients have functional
(idiopathic or non ulcer) dyspepsia with no
underlying cause on diagnostic evaluation
-We need to R/O structural disease by
endoscopy to diagnose non ulcer dyspepsia.
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19. Differential diagnosis of upper
abdominal pain
 Diagnosis
 Functional dyspepsia (up to 75 percent)
Dyspepsia caused by structural or biochemical disease
 Peptic ulcer disease
 Gastroesophageal reflux disease (GERD)
 Biliary pain
 Chronic abdominal wall pain
 Gastric or esophageal cancer
 Gastroparesis
 Pancreatitis
 Carbohydrate malabsorption
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20.  Medications (digitalis, iron, theophylline, oral
antibiotics, NSAIDs, corticosteroids,….
 Infiltrative diseases of the stomach (e.g.Crohn's disease
sarcoidosis)
 Metabolic disturbances (hypercalcemia, hyperkalemia)
 Hepatoma
 Ischemic bowel disease
 Systemic disorders (DM,thyroid and parathyroid
disorders, connective tissue disease)
 Intestinal parasites
 Abdominal cancer
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21. Functional dyspepsia
-Functional (idiopathic or non ulcer) dyspepsia is
defined as the presence of one or more of the
following:
 postprandial fullness,
 early satiation,
 epigastric pain or burning, plus
 no evidence of structural disease to explain the
symptoms.
-These criteria should be fulfilled for the last three
months with symptom onset at least six months
before diagnosis.
-A diagnosis of functional dyspepsia can therefore
only be established exclusion of other causes of
dyspepsia
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22. History
PUD-Upper abdominal pain or discomfort is the most
prominent symptom in patients with peptic ulcers.
-Although discomfort from ulcers is usually centered in the
epigastrium, it may occasionally localize to the right or left upper
quadrants.
-While the pain may radiate to the back, back pain as the primary
symptom is atypical of peptic ulcer disease.
-While classic symptoms of duodenal ulcer occur when acid is
secreted in the absence of a food buffer ( 2-5 hours after meals or
on an empty stomach), peptic ulcers can be associated with food-
provoked symptoms.
-Peptic ulcers can also be associated with postprandial belching,
epigastric fullness, early satiation, fatty food intolerance, nausea,
and occasional vomiting.
GERD -The most common symptoms of GERD :retrosternal
burning pain and regurgitation.
-GERD should be suspected when these symptoms accompany
dyspepsia and are the predominant complaints.
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23. History
•A dominant history of heartburn, regurgitation, or
cough is suggestive of GERD.
•NSAID use raises the possibility of NSAID dyspepsia
and peptic ulcer disease.
•Radiation of the pain to the back, a personal or family
history of pancreatitis may be indicative of underlying
chronic pancreatitis.
•Significant weight loss, anorexia, vomiting, dysphagia,
odynophagia, and a family history of gastrointestinal
cancers suggest the presence of an underlying
malignancy.
•The presence of severe episodic epigastric or right
upper quadrant abdominal pain lasting more than an
hour or pain that occurs at any time is suggestive of
symptomatic cholelithiasis
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24. CLINICAL APPROACH
History — Three common patterns of dyspepsia
Ulcer-like or acid dyspepsia (eg, burning,
epigastric hunger pain with food, antiacid, and
antisecretory agent relief)
Dysmotility-like dyspepsia (with predominant
nausea, bloating, and anorexia)
 Unspecified dyspepsia
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25. • Physical examination — The physical
examination is usually normal, except for
epigastric tenderness..
• Routine laboratory tests — Routine blood
counts and blood chemistry determinations
are commonly obtained. They can be
requested selectively depending upon patient
features such as age, symptom duration, and
other factors.
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26. Alarm features…UGI endoscopy & biopsy
Age older than 55 years with new-onset dyspepsia
Family history of upper gastrointestinal cancer
Unintended weight loss
Gastrointestinal bleeding
Progressive dysphagia
Odynophagia
Unexplained iron deficiency anemia
Persistent vomiting
Palpable mass or lymphadenopathy
Jaundice
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27. • Diagnostic strategies
New onset dyspepsia not caused by drugs have
been evaluated
Dyspepsia caused by drugs –stop drug
Noninvasive testing for H. pylori infection
Endoscopy in all patients alarm features & age
>55yrs
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28. dyspepsia
Age <55 & no alarm feature
• H. pylori TEST & treat
• Empiric PPI
Alarm feature or age>55
• UGI endoscopy
• Biopsy
• Treat specific cause.
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29. EVALUATION OF PERSISTENT SYMPTOMS
-some patients continue to have symptoms of
dyspepsia despite the above approach.
-Patients with continued symptoms of dyspepsia fall
into the following categories:
-patients with persistent H. pylori infection,
-patients with an alternate diagnosis, and
-patients with functional dyspepsia.
-Patients with continued symptoms of dyspepsia should be carefully
reassessed, paying specific attention to the
-type of ongoing symptoms
- the degree to which symptoms have improved or worsened
- compliance with medications
- upper endoscopy
- H. pylori with biopsy for histology
- Gastric emptying time
- Abdominal U/S e.t.c should be done.
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30. -Approximately 75 percent of patients have functional (idiopathic or
non ulcer) dyspepsia with no underlying cause on diagnostic
evaluation.
-Functional dyspepsia is classified into
-postprandial distress syndrome and
-epigastric pain syndrome
-The management of functional dyspepsia
.test and treat for H. pylori
.treat if the local prevalence of H. pylori is >10 percent
.PPIs in patients who test negative for H. pylori
.H2 receptor antagonists
.Antidepressants - (try with TCA if no improvement after 8wks
of PPI)
.Psychological therapy
.Dietary modification
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31. PEPTIC ULCER DISEASE
An ulcer is defined as disruption of the
mucosal integrity(>5mm in size) of the
stomach and/or duodenum leading to a local
defect or excavation due to active
inflammation.
Ulcers occur within the stomach and/or
duodenum and are often chronic in nature.
Can be: gastric or duodenal
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32. • PUD
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33. Duodenal Ulcers
• DUs occur most often in the first portion of
the duodenum (>95%), with ~90% located
within 3 cm of the pylorus.
• They are usually 1 cm in diameter but can
occasionally reach 3–6 cm (giant ulcer)
• H. pylori and NSAID-induced injury account for
the majority of DU .
• Associated with increase acid secretion &
decrease bicarbonate secretion
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34. Gastric ulcer
• Tends to occur in late age(median age 60)
• mostly silent & present with complication
• GUs can represent a malignancy and should be
biopsied upon discovery
• Gastric acid output (basal and stimulated) tends
to be normal or decreased in GU patients.
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35. Gastric ulcers
• have been classified based on their location:
 Type I -gastric body and
-low gastric acid production;
 Type II -antrum and
 -gastric acid can vary from low to normal
 Type III
-within 3 cm of the pylorus and are commonly
accompanied by duodenal ulcers and
-normal or high gastric acid production
 Type IV -cardia
-low gastric acid production.
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36. 3/4/2018 GK,MD 36

37. ETIOLOGY
 The two most common causes of PUD are:
– Helicobacter pylori infection ( 70-80%)
– Non-steroidal anti-inflammatory drugs (NSAIDS)
• One half of world’s population has H.pylori (80-90 %
developing world)
• The annual incidence H. pylori infections in
industrialized countries is 0.5% compared with ≥ 3% in
developing countries
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38. H. Pylori infection
• Gastric infection with the bacterium H. pylori
accounts for the majority of PUD
• Is a gram-negative micro aerophilic rod found
most commonly in the deeper portions of the
mucous gel coating the gastric mucosa or
between the mucous layer and the gastric
epithelium.
• higher colonization rates in poor
socioeconomic status.
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39. Other risk factors for H. pylori
infection
-Birth or residency in developing country.
- Domestic crowding
-Unsanitary living condition
-Exposure to infected gastric content
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40. • H .pylori infection
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41. 3/4/2018 GK,MD 41

42. The particular end result of H. pylori infection
-Gastric ulcer
-PUD
-gastric MALT lymphoma
-gastric cancer is determined by a complex
interplay between bacterial and host factors
1.Host factor genetics susceptibility , durations
, location , inflammatory response
2. Bacterial structure , virulence factor & strain.
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43. NSAID-Induced Disease
• NSAIDs represent a group of the most commonly
used medications
• The spectrum of NSAID-induced morbidity ranges
-from nausea and dyspepsia ( 50–60%)
-serious endoscopy-documented peptic ulceration
(15–30% of individuals taking NSAIDs regularly)
-complicated by bleeding /perforation in as many as
1.5% of users per year
• no dose of NSAID is completely safe.
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44. Risk factor to develop PUD
• Established risk factors include
-advanced age
-history of ulcer
-concomitant use of gluco corticoids
-high-dose NSAIDs
-multiple NSAIDs
-concomitant use of anticoagulants
-psychosocial factores
-diets
-serious or multisystem disease
-concomitant H. pylori infection
-cigarette smoking
-alcohol consumption.
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45. NSAIDS
• The effects ; mucosal hemorrhage , erosions , acute
ulcers.
 Inhibits the production of prostaglandins.
1. Decrease mucus & HCO3 production
2. Decrease mucosal blood flow
3. Reduce cell renewal
4. generate oxygen-free radicals that may contribute to
ulceration.
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46. C/M of DU
• Abdominal pain
• Epigastric pain : a burning or gnawing discomfort
can be present in both DU and GU .
• The discomfort : an ill-defined, aching sensation
or as hunger pain. The typical pain pattern in DU
occurs 90 minutes to 3 hours after a meal and is
frequently relieved by antacids or food.
• Pain that awakes the patient from sleep is the
most discriminating symptom, with two-thirds of
DU patients describing this complaint
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47. C/M Of GU
• Can be assymptomatic
• The pain : precipitated by food.
• Nausea and weight loss occur more .
• Endoscopy detects ulcers in <30% of patients
who have dyspepsia
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48. Symptoms that suggest complications
related to PUD include
• Penetrating ulcers classically present with a shift from the
typical vague visceral discomfort to a more localized and
intense pain that radiates to the back and is not relieved by
food or antacids.
• The sudden development of severe, diffuse abdominal pain
may indicate perforation.
• Vomiting is the cardinal feature present in most cases of
pyloric outlet obstruction.
• Hemorrhage may be heralded by nausea, hematemesis,
melena, or dizziness.
• Gastrocolic fistula, a very rare complication, can present
with halitosis, feculent vomiting, postprandial diarrhea,
dyspepsia, and sometimes weight loss
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49. PUD-Related Complications
• Gastrointestinal Bleeding is the most
common complication observed in PUD. It
occurs in ~15% of patients and more often in
individuals >60 years of age( likely due to the
increased use of NSAIDs in this group of age) .
• Up to 20% of patients with ulcer-related
hemorrhage bleed without any preceding
warning signs or symptoms
• Common in anterior part of DU.
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50. Perforation
• The second most common ulcer-related
complication is perforation ( occur in 6–7% of
PUD patients).
• DUs tend to penetrate posteriorly into the
pancreas, leading to pancreatitis, whereas
GUs tend to penetrate into the left hepatic
lobe.
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51. Gastric Outlet Obstruction
• Gastric outlet obstruction is the least common
ulcer-related complication, occurring in 1–2%
of patients.
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52. Gastric carcinoma
Alarm symptom of Gastric ca
• Unintended weight loss
• Bleeding
• Anemia
• Dysphagia
• Odynophagia
• Hematemesis
• A palpable abdominal mass or lymphadenopathy
• Persistent vomiting
• Unexplained iron deficiency anemia
• Family history of upper gastrointestinal cancer
• Previous gastric surgery
• Jaundice
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53. Diagnosis:
1) Diagnosis of ulcer
2) Diagnosis of H. pylori
 Diagnosis of PUD depends mainly on
-endoscopic
-radiographic confirmation
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54. Tests for H. Pylori Infection
1 Invasive (Endoscopy/Biopsy Required)
 Rapid urease
 Histology
Culture
2. Noninvasive
 Serology
 Urea breath test
Stool antigen
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55. Treatment Of Peptic Ulcer Disease
• Although acid secretion is still important in
the pathogenesis of PUD,
• eradication of H. pylori and therapy &
• prevention of NSAID-induced disease is the
mainstay of treatment.
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56. Goals of Treatment
Relieve pain
Prevent
complications Minimize
Recurrence
Bleeding Perforation Obstruction
563/4/2018 GK,MD

57. General approach
• All patients with PUD should receive anti secretory
therapy.
• Patients with PUD should be tested for H. pylori
• Patients with H. pylori should be treated with a goal
of H. pylori eradication.
• Anti secretory therapy is the mainstay of therapy in
uninfected patients.
• It is essential to withdraw potential offending or
contributing agents such as NSAIDs, cigarettes, and
excess alcohol.
• There is no evidence that addressing stressful
psychosocial situations and psychological
comorbidity benefits treatment outcomes
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58. Treatment
• Rapid relief of symptoms
• Healing of ulcer
• Preventing ulcer recurrences
• Reducing ulcer-related complications
• Reduce the morbidity (including the need for
endoscopic therapy or surgery)
• Reduce the mortality
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59. General Strategy
Treat complications aggressively if present
Determine the etiology of ulcer
Discontinue NSAID use if possible
Eradicate H. pylori infection if present or strongly
suspected, even if other risk factors (e.g., NSAID
use) are also present;
Use antisecretory therapy to heal the ulcer if H.
pylori infection is not present
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60. • Smoking cessation should be encouraged
• If DU is diagnosed by endoscopy, Rapid urea
testing of endoscopically obtained gastric biopsy
sample, with or without histologic examination
should establish presence or absence of H. pylori
• If DU is diagnosed by x-ray , then a serologic , UBT,
or fecal antigen test to diagnose H. pylori infection
is recommended before treating the patient for H.
pylori
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61. Drugs Used in the Treatment of PUD
Acid-suppressing drugs
• Anti acids Mylanta, Maalox, Tums, Gaviscon
100–140 meq/L 1 and 3 h after meals.
• H2 receptor antagonists
Cimetidine 400 mg bid Ranitidine 300 mg
Famotidine 40 mg Nizatidine 300 mg
• Proton pump inhibitors Omeprazole 20
mg/d Lansoprazole 30 mg/d Rabeprazole 20
mg/d Pantoprazole 40 mg/d Esomeprazole
20 mg/d
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62. Mucosal protective agents
-Sucralfate 1gm qid
-Prostaglandin analogue Misoprostol 200 g qid
-Bismuth-containing compounds Bismuth
subsalicylate (BSS)
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63. Therapy of H. Pylori
• H. pylori should be eradicated in patients with
documented PUD.
• No single agent is effective in eradicating the
organism.
• Combination therapy for 14 days provides the
greatest efficacy.
• The agents used with the greatest frequency
include amoxicillin, metronidazole, tetracycline,
clarithromycin, and bismuth compounds.
3/4/2018 GK,MD 63

64. TRIPLE THERAPY
• Regimens Recommended for Eradication of H. Pylori
Infection
1. Bismuth subsalicylate 2 tablets qid
Metronidazole 250 mg qid
Tetracycline 500 mg qid 2.
2. Ranitidine bismuth citrate 400 mg bid
Tetracycline500 mg bid
Clarithromycin or metronidazole 500 mg bid
3. Omeprazole (lansoprazole) 20 mg bid (30 mg bid)
Clarithromycin 250 or 500 mg bid
Metronidazole 500 mg bid/ Amoxicillin 1 g bid
3/4/2018 GK,MD 64

65. Therapy of NSAID-Related Gastric or
Duodenal Injury
• Recommendations for Treatment of NSAID-
Related Mucosal Injury
• Active ulcer -NSAID discontinued
-H2 receptor antagonist or
-PPI
• Prophylactic therapy Misoprostol/ PPI
• H. pylori infection Eradication if active ulcer
present or there is a past history of peptic ulcer
disease
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66. Non Healing PUD
1
• Non compliance with medicines
2
• Ulcer turning malignant
3
• False –ve H.pylori – empirically treat for it
4
• Inadvertent NSAID or ulcerogenic drugs
5
• Rare causes – ZE, MALT, Chron’s, MEN 1
663/4/2018 GK,MD

67. REFRACTORY
 Majority (>90%) of GUs and DUs heal with the conventional
Tx.
 A GU that fails to heal after 12 weeks and a DU that does not
heal after 8 weeks of therapy should be considered refractory
Exclude –
 poor compliance and persistent H. pylori infection
NSAID use, either inadvertent or surreptitious
Cigarette smoking
For a GU, malignancy must be meticulously excluded, gastric
acid hyper secretory state such as ZES .
 8 weeks of Rx high dose PPI (>90% improve) . . . SURGERY
 RARE ,,, Crohn's disease, amyloidosis, sarcoidosis, lymphoma,
eosinophilic gastroenteritis, or infection [cytomegalovirus
(CMV), tuberculosis, or syphilis].
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68. ?
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