Dyspepsia refers to pain or discomfort centered in the upper abdomen. It is a common symptom with various potential causes. The document discusses the definitions, epidemiology, evaluation, and management approaches for different types of dyspepsia including functional dyspepsia and its subtypes of epigastric pain syndrome and postprandial distress syndrome. Testing and treatment are targeted based on alarm features and potential underlying causes, with a focus on lifestyle changes, antisecretory drugs, H. pylori treatment, prokinetics, and other pharmacological and psychological interventions.

2. DYSPEPSIA
Greek word means “difficult digestion.”
Symptoms located in upper abdomen

7. AGE DISTRIBUTION IN KAUVERY
0
2
4
6
8
10
12
14
16
18
20
<21 YRS 21-30 YRS 31-40 YRS 41-50 YRS 51-60 YRS >61 YRS
MALE
FEMALE

8. 0
20
40
60
80
AT KAUVERY

9. 38%
22%
11%
12%
9%
8%
KAUVERY
EPS
PDS
EPS+PDS
EPS+GERD
PDS+GERD
EPS+PDS+GERD

10. HISTORY & EXAM
ALARM
 Chronicity of the symptoms
 Nature
 Frequency
 Relationship to meals
 Influence of specific dietary factors
 Systemic disorders
 Family and personal history
 Medications
 Blood loss
 Anemia
 Dysphagia
 LOW
 Persistent vomiting
 Abdominal mass

11. TESTING
 After the age of 45
 Complete blood count
 Serum electrolytes
 Calcium
 Liver biochemical tests
 Thyroid function
 Serum amylase
 Celiac disease Antibodies
 Stool for ova, parasites
,Giardia antigen
 Pregnancy test

12. Endoscopy
 Erosive esophagitis
 Barrett’s esophagus
 Esophageal cancer
 Peptic ulcer-Gastric/Duodenal
 Mechanical obstruction(GOO)
Duodenitis or gastritis- Minor findings

13. DRUGS

14. LUMINAL CAUSES

15. SYSTEMIC DISEASES

16.  No evidence of structural disease on endoscopy or
imaging or basic evaluation.

17. Functional Dyspepsia
 1. Epigastric pain
 2. Epigastric burning
 3. Early satiation
 4. Bothersome postprandial fullness
1 or more

18. Epigastric Pain Syndrome
 1. Pain or burning - epigastrium -moderate severity, 1/week
 2. Intermittent
 3. Not generalized or localized to other abdominal or chest
regions
 4. Not relieved by defecation or passage of flatus
 5. Not fulfilling criteria for gallbladder or sphincter of Oddi
disorders
all the above.
 Supportive Criteria
1. Pain may be of a burning quality but without a retrosternal
component
2. Pain is commonly induced or relieved by ingestion of a
meal but may occur while fasting
3. Postprandial distress syndrome may coexist

19. Postprandial Distress Syndrome
 1. Bothersome postprandial fullness, after ordinary sized
meals, at least several times/week
 2. Early satiation that prevents finishing regular meal, at least
several times/week
Supportive Criteria:
1. Upper abdominal bloating or nausea or belching
2. Epigastric pain syndrome may coexist

21. PATHOPHYSIOLOGY
 Hypersensitivity to gastric distention
 Delayed gastric emptying
 Impaired gastric accommodation to a meal
 Altered duodenal sensitivity to lipids or acid
 Abnormal intestinal motility
 Central nervous system dysfunction

23. GASTRIC EMPTYING
 Distal stomach-grinding and sieving until particles are small
enough to pass through pylorus
 Delayed gastric emptying ranges from 20% to 50%
 Solid gastric emptying- 30-40%
 Postprandial fullness, nausea and vomiting

26. IMPAIRED GASTRIC ACCOMMODATION
 Impaired in 40%
 Proximal stomach-reservoir during and after ingestion
of a meal.
 Relaxation- vagally mediated
 Rise in intragastric pressure
 Meal-induced satiation
 Activation of tension-sensitive mechanoreceptors

29. Hypersensitivity to Gastric Distension
 To isobaric gastric distention
 Tension-sensitive mechanoreceptors
 Altered visceral afferent nerves and the central
nervous system

30. Altered Duodenal Sensitivity to Lipids or Acid
 Gastric distention- cholecystokinin
 Duodenal hypersensitivity to acid
 Increased postprandial duodenal acid exposure-
impaired clearancE of acid

31. OTHERS
 Rapid gastric emptying
 Phasic fundic contractions
 Lack of suppression of phasic contractility of the proximal
stomach
 Duodenal retrograde contractions
 Genetic predisposition-G-protein beta polypeptide 3
 Hp Infection
 Postinfection Functional Dyspepsia-acute Salmonella
gastroenteritis
 Anxiety, depressive,somatoform disorders, physical or sexual
abuse

32. DIABETIC GASTROPARESIS
 Loss of ICCs
 Reduced receptive relaxation and accommodation
 Antral hypomotility.
 Isolated pyloric contractions-Pylorospasm.
 Gastric dysrhythmias-abnormal intragastric distribution of
food.
 Antral dilation
 Impaired action of prokinetic drugs.
 Modifies upper GI sensations
 Gastric smooth muscle dysfunction

33. General measures
 Lifestyle and dietary measures
 Eat smaller, more frequent meals
 Avoiding meals with a high fat
 Avoid spicy foods- capsaicin
 Avoid- coffee
 Cessation of smoking and consumption of alcohol
 Avoidance of aspirin and other NSAIDs
 Treat- coexisting anxiety disorder or depression

34. APPROACHES
 (1) Prompt diagnostic endoscopy followed by targeted
medical therapy
 (2) Noninvasive testing for Hp infection, followed by
treatment based on the result (“test-and-treat”
strategy)
 (3) Empirical anti-secretory drug therapy
Not Recommended= empirical therapy with a
prokinetic agent

35. Prompt Endoscopy and Directed Treatment
 Family history of gastric cancer
 High rate of gastric cancer country
 Had a partial gastrectomy
 Peptic ulcer, erosive esophagitis, or malignancy
 Reassures-patients and physicians
 Diagnosis of Hp infection- eradication therapy
 Functional dyspepsia and GERD recurs after
discontinuing PPI

36. Test and Treat for Hp Infection
 Hp- associated with peptic ulcers & gastric cancer
 Young patients- noninvasive testing
 Eliminates chronic gastritis
 The test and- treat strategy= Hp infection rate is high

37. Empirical Antisecretory Drug Therapy
 Beneficial in 1/3rd of functional dyspepsia
 Response usually within 2 weeks of therapy
 Economically- equally or more cost-effective than test
& treat strategy

38. Acid-Suppressive Drugs
 Both therapeutic and diagnostic value
 H2RAs & PPI are effective
 Half-dose=full-dose=double-dose PPI therapy
 Hp status did not affect the response
 Most effective for GERD also.
 Less effective- epigastric pain & dysmotility

39. Eradication of Hp Infection
 Induce sustained remission of dyspepsia
 Low number of responder
 Delayed symptomatic benefit
 Protects against- peptic ulcer, gastric cancer
 Short duration and low cost of treatment.

40. Prokinetic Agents
 Dopamine receptor agonists-upper GI motility
 5-hydroxytryptamine 4 (5-HT4) receptor agonism
 Motilin receptor agonist ABT-229
 Mixed 5-HT4 receptor agonist and 5-HT3 receptor
antagonist mosapride
 5-HT4 receptor agonist tegaserod
 Dopamine D2 antagonist/acetylcholinesterase inhibitor
itopride

41. Antidepressants
 Functional GI disorders not initially responding
 Anxiolytics and antidepressants-TCA
 The effect- independent of the presence of depression,
decrease visceral sensitivity
 SSRI- increased gastric accommodation

42. OTHERS
 M1 and M2 muscarinic receptor antagonist & inhibits
cholinesterase- Acotiamide
 Bismuth salts
 Simethicone
 5-HT1A, 5-HT3, 5-HT4- agonists-enhance gastric
accommodation
 Neurokinin receptor antagonists and peripherally kappa
opioid receptor agonists-Visceral hypersensitivity
 Alleviating postprandial fullness, early satiation and upper
abdominal bloating.

43. Psychological Interventions
 Group support with relaxation training
 Cognitive therapy
 Psychotherapy
 Hypnotherapy

44. EPS
2 WEEKS
PPI
RESOLUTIO
N
STOP
RECURRENCE
OGD OBSERV
E
OGD
H.pylori
ANTIBIOTICS
GASTROPARESIS/
SPASM
INSULIN/SILDENAFIL/ACOTIAMIDE/
PROKINETICS
ULCER
6-12 WEEKS
PPI
Y N
Y N Y N

45. PDS
2 WEEKS PPI±PROKINETICS
RESPONSE
OBSERVE OGD
OBSTRUCTION
SURGERY/DILATATION PROKINETICS
RESPONSE
PYLOROSPASM
INSULIN/SILDENAFIL/
DILATATION/BOTOX
GASTROPARESIS
DM/SUR/ISCH/OBST
Y N
Y N
YN