Evaluation and management of patients with Dyspepsia. Dyspeptic symptoms. Causes of dyspepsia Approach to adult with Dyspepsia. Newer advancement about diagnosing dyspepsia causes. GERD and peptic ulcer and many more organic diseases. Functional Dyspepsia and organic dyspepsia

1. Evaluation and Management of
patients with DYSPEPSIA
Under the guidance of –
DR. SHYAM BHUTRA SIR (HOD & Unit Head)
DR. BHAGCHAND KHORWAL SIR (Associate Professor)
DR. DINESH YADAV SIR (Assistant Professor)
BY – DR. GARVIT NANECHA

2. DYSPEPSIA
 Dyspepsia is a chronic or recurrent burning discomfort or pain in the upper abdomen that
may be caused by diverse processes, such as gastroesophageal reflux, peptic ulcer disease
and “non ulcer dyspepsia”, a heterogeneous category that includes disorders of motility,
sensation and somatization.
 Dyspepsia may be subdivided into organic and functional.
 Organic dyspepsia is caused by other diseases. The most common are peptic ulcer,
gastroesophageal reflux disease, esophageal and gastric cancer, biliary and pancreatic
disorders, intolerance to food and drugs, and some systemic and infectious diseases.
 The Rome Criteria IV were enacted in 2016 as the result of research on the intestinal
microenvironment, brain gut interactions, pharmacogenomics, biopsychosocial, sexual and
cultural influences in the development of functional disorders. According to them,
functional disorders of the digestive system are now called Disorders of the gut-brain
interaction (DGBI).

3. Pathophysiology
• Gastric motility disturbance: normally cholecystokinin and GLP-1 reduce gastric
emptying while motilin and ghrelin accelerates gastric emptying.
• Altered immune and mucosal function: chronic duodenal low grade inflammation
is founded with higher levels of TNF-α, IL-1β and IL-10 cytokines and duodenal
eosinophilia.
• Altered gut microbiodata: lower prevalence of bacteria of genus Prevotella is
found in patients of functional dyspepsia as compared to healthy population.
Treatment : probiotic yogurt containing bacteria of strain Lactobacillus gasseri.
• Visceral hypersensitivity.
• Altered central nervous system processing.

5. Causes of dyspepsia
Upper GI disorders
• Peptic ulcer disease
• Acute gastritis
• Gallstones
• Esophageal spasm
• Non-ulcer ( functional ) dyspepsia
• Irritable bowel syndrome
Other GI disorders
• Chronic pancreatitis
• Pancreatic cancer
• Colonic carcinoma
• Hepatic disease (hepatitis, metastases)
Systemic disease
• Renal failure
• Diabetes mellitus
• Hypercalcemia
• Hyperkalemia
Drugs
• NSAIDs
• Corticosteroids
• Iron and potassium supplements
• Digoxin
Others
• Psychological (anxiety, depression) • Alcohol

6. Approach to the adult with dyspepsia
• A history, physical examination, and laboratory evaluation are the first steps in the evaluation
• The goal of the initial evaluation is to identify alarm features for serious disease eg.
gastroesophageal malignancy.
Unintentional weight loss
Dysphagia
Odynophagia
Unexplained iron deficiency anaemia
Persistent vomiting
Palpable mass or lymphadenopathy
Family history of upper gastrointestinal cancer
Alarm features

7. History
• A dominant history of heartburn or regurgitation, is suggestive of gastroesophageal reflux disease
(GERD), recognizing that some patients have overlapping GERD and functional dyspepsia.
• Aspirin and other NSAID use: possibility of NSAID dyspepsia and peptic ulcer disease.
• Radiation of pain to the back or personal or family history of pancreatitis may be indicative of
underlying chronic pancreatitis.
• Significant weight loss, anorexia, anemia, vomiting, dysphagia, odynophagia, and a family
history of gastrointestinal cancers suggest the presence of an underlying gastroesophageal
malignancy.
• The presence of severe episodic epigastric or right upper quadrant abdominal pain, usually in
association with nausea or vomiting, lasting at least 30 minutes is suggestive of symptomatic
cholelithiasis.
• Nausea and vomiting, with or without weight loss, occurring with recurrent or persistent upper
abdominal pain raises the possibility of gastroparesis, especially in patients with risk factors.
However, both the pathophysiology and symptom expression of functional dyspepsia and
gastroparesis are quite similar.

8. Physical examination
• The physical examination in patients with dyspepsia is usually normal, except for epigastric
tenderness. The presence of epigastric tenderness cannot accurately distinguish organic
dyspepsia from functional dyspepsia.
• Abdominal tenderness on palpation should be evaluated for the presence of Carnett's sign
to determine if it is due to pain arising from the abdominal wall rather than due to
inflammation of the underlying viscera.
• The presence of increased local tenderness during muscle tensing (positive Carnett's sign)
suggests the presence of abdominal wall pain. However, if the pain is decreased (negative
Carnett's sign), the origin of pain is not from the abdominal wall and likely from an intra-
abdominal organ, as the tensed abdominal wall muscles protect the viscera.

9. Other informative findings on physical examination
Palpable abdominal mass Hepatoma
Lymphadenopathy Left supraclavicular or periumbilical in
gastric cancer
Jaundice Secondary to liver metastasis
Bruit Celiac artery compression syndrome
Succussion splash Gastric outlet syndrome
Pallor Secondary to anemia
Ascites Peritoneal carcinomatosis
Muscle wasting, loss of subcutaneous
fat, peripheral edema
Underlying malignancy

12. Functional dyspepsia
• Benign common gastrointestinal disorder.
• Diagnosed based on the Rome IV criteria
• Etiology : likely multifactorial; however, the
exact cause is not clearly understood. Several risk
factors have been seen to be associated with the
condition.
• Prevalence
global : 5% to 11%
Asian countries : 5% to 30%
Western : 10% to 40%
• More common in females.

13. Pathophysiology
• Although the exact mechanism is not well understood, the disturbances in gastric physiologic
factors divided into macroscopic and microscopic mechanisms.
• Macroscopic mechanisms include :
Gastroesophageal reflux (GERD)
Delayed gastric emptying, gastric dysrhythmias, and antral hypomotility
Visceral hypersensitivity alterations in the nervous system: Lower the threshold for pain in the
presence of normal gastric compliance and contribute to abnormal processing of afferent input in
the spinal cord or brain as well as dysfunction of mechanoreceptors.
• Microscopic mechanisms include :
Impaired barrier function (altered sensitivity to duodenal acid or lipids impairs mucosal integrity.)
Gastroduodenal inflammation (characterized by altered lymphocytes, including "gut-homing" lymphocytes,
increased eosinophils, and mast cells.)
Altered gut microbiome and Helicobacter pylori infection
• Psychological factors like anxiety and depression can cause increased activation of the amygdala,
and the dysregulation of the HPA axis suggests that there is central processing of visceral stimuli
from sensations in the gastrointestinal tract.

14. • The 3 subtypes are epigastric pain syndrome (EPS), postprandial distress syndrome
(PDS), and overlapping PDS and EPS.
Epigastric pain syndrome (EPS)

15. Post-prandial distress syndrome (PDS)

16. Treatment / Management
• The main aim is symptom control.
• Diet modification and lifestyle changes.
• H pylori eradication is recommended as the first treatment for all patients with functional
dyspepsia. This improves symptoms and decreases the risk of peptic ulcers and gastric cancer
Regimen Drugs and Dosages Dosing duration
Clarithromycin triple •PPI regular dose twice a day
•Clarithromycin 500 mg twice a day
•Amoxicillin 1 gram twice a day or
metronidazole 500 mg thrice a day
14 days
Bismuth quadruple •PPI regular dose twice a day
•Bismuth subcitrate 120 to 300 mg or
420 mg 4 times a day
•Tetracycline 500 mg 4 times a day
•Metronidazole 250 4 times a day to
500 mg 3-4 times a day
10-14 days

17. • H2 receptor antagonists
• Antidepressants (TCA): amitriptyline 10mg / nortriptyline 10mg / desipramine 25mg :
administered for 8 to 12 weeks and then continued for 6 months if patient responds
appropriately.
• Mirtazapine has shown benefits in patients with functional dyspepsia and the associated
weight loss.
• Prokinetic agents : 4 to 8 weeks course is recommended when the above therapies fail.
• Optional therapies :-
 Psychotherapy: Usually reserved for patients with associated stressors and those who fail
to respond to medical therapy.
 Buspirone: 10 mg, 3 times daily for 4 weeks, may help relax the gastric fundus
Educating patients on the benign course of this disorder to establish long-term care and
expectations for treatment is essential. Further evaluation is recommended if red flag
signs such as unintentional weight loss, persistent vomiting, or dysphagia are present.

18. GERD (Gastroesophageal reflux disease)
• Most common benign disorder of esophagus
Pathophysiology :-
• due to incompetence of LES, there is retrograde flow of gastric content to the esophagus
which leads to GERD, reflux esophagitis, ulceration and then healing via fibrosis. There is
formation of stricture.
• In long term, it may lead to columnar metaplasia and intestinal metaplasia with goblet
cells known as barret’s esophagus which increases the risk of Adenocarcinoma.

19. Complications :-
• Ulcerations
• Stricture
• Barret’s esophagus
• Carcinoma esophagus
• Pulmonary diseases, etc.
Clinical features :-
• The most common symptom is retrosternal heartburn.
• Have a long history of heartburn with short history of regurgitation.
• Classic triad is retrosternal heartburn, epigastric pain and regurgitation

20. Diagnosis
24 Hours PH monitoring
• Gold standard for diagnosing and quantifying acid reflux.
• Patient should not be on anti-secretory and antacids for at least 5 days-2weeks before the test.
• A disposable probe is inserted in the distal esophagus allowing remote recorders to collect data for
24-48 hrs. Data regarding how many times the probe is bathed with a PH <4 was collected.
• A Demister’s score is calculated and if >14.72 confirms pathological GERD .
Esophageal motility testing
• Done to evaluate peristaltic contractions, to look for motility disorders and incompetent LES, to
distinguish GERD from achalasia or scleroderma.
• In patients with mildly impaired motility in setting of positive PH testing indicates GERD and
floppy or partial fundoplication should be performed.
• However, in long-standing GERD patients with esophageal dysmotility should be counselled
about post-op dysphagia.
• Patients with severe dysmotility should be considered for further workup or nonsurgical therapy.

21. Video-Esophagogram
• Shows both structure and function of the esophagus.
• It diagnoses abnormalities that would modify symptom treatment like stricture, masses,
hiatal hernia, diverticulum.
• It confirms the reflux and is suggestive of motility disorders or achalasia.
Endoscopy
• To evaluate the shape and course of the esophagus
• To evaluate signs of reflux such as esophagitis or metaplasia
• To rule out masses and strictures as a cause of symptoms
• To perform a biopsy (metaplasia, dysplasia or carcinoma)
Confirmation of pathologic acid reflux should be done by at least two objective tests prior
to anti-reflux surgery

22. Management
Lifestyle modification
• Decrease the duration and severity of the symptoms and
results in greater efficacy of medications
• Encouraging weight loss and smoking cessation.
• Avoid chocolate, coffee, alcohol, peppermint and fatty food.
• Smaller and frequent meals are recommended and patient
should not lie immediately after food.
Medical management
• PPI therapy : maximal with twice daily dose.
• There is better response to surgery if patient responds to PPI
well.

23. Indications for surgical therapy
• Patients with a severe esophageal injury such as a ulcer, strictures or barrett’s esophagus.
• Incomplete resolution of symptoms or relapse while on medical therapy.
• If symptoms persist for a long duration at a young age.
Basic tenets of Anti-reflux surgery
• To preserve natural tissue and linings.
• Identify and preserve both vagus nerves
• Identify the true esophagus-gastric junction for placement of wrap.
• Have a sufficient length of the intra-abdominal esophagus.
• Re-establish the angle of HIS
• Collis gastroplasty is done to increase the artificial length of the esophagus.

24. Laparoscopic Nissen’s fundoplication
• Gold standard anti-reflux surgery for GERD
• Recreation of sphincter around G-E junction by 360 degree wrap of fundus
around distal esophagus

25. Toupet’s fundoplication
• 270 degree posterior / partial fundoplication.
• Additional tacking sutures to fix the stomach
to crura in the abdomen.
Dor’s fundoplication
• 180 – 200 degree anterior / partial
fundoplication.

26. Linx : a series of magnetic beads are placed around the gastric esophagus junction that
stretches with slight pressure in the esophagus and mimics the natural lower esophageal
sphincter.
Roux-en-Y reconstruction : considered
for patients with bile or gastric reflux, morbid
obese and diabetes and esophageal motility.
Collis gastroplasty : esophageal lengthening
procedure , creates a few cm of additional non
esophageal length around which stomach can be
wrapped.

27. Helicobacter Pylori
• H. pylori is involved in the etiology of a number of common gastroduodenal diseases,
such as chronic gastritis, peptic ulceration and gastric cancer
• Has ability to hydrolyse urea : leads to production of ammonia which in further act on
antral G cells and releases gastrin and lead to gastric acid hypersecretion.
• the 13C and 14C breath tests and the CLO test (a commercially available urease test kit) :
detect the presence of organism
Antral mucosa showing
colonization with Helicobacter
pylori (modified Giemsa stain).

28. • Helicobacter infection is amenable to treatment with antibiotics.
• The profound hypochlorhydria produced by PPIs combined with antibiotics is also
effective in eradicating the organism. Commonly used eradication regimes include
one PPI and two antibiotics, such as metronidazole and amoxicillin.
• Eradications in patients with PUD can be achieved upto 90% .
• Reinfection following successful eradication appears rare (<0.5%) but incomplete
eradication is a more important clinical problem.
• H. Pylori is now classified by the World Health Organization as a Class 1 carcinogen

29. PEPTIC ULCER
• Most peptic ulcers are caused by H. pylori or NSAIDs and changes in epidemiology mirror
changes in these principal etiological factors.
• Cigarette smoking predisposes to peptic ulceration and increases the relapse rate after
treatment.
• Common sites for peptic ulcers are the first part of the duodenum and the lesser curve of the
stomach, but they also occur on the stoma following gastric surgery, in the esophagus and even
in a Meckel’s diverticulum, which contains ectopic gastric epithelium. In general, the ulcer
occurs at a junction between different types of epithelia, in the epithelium least resistant to acid
damage.
• Duodenal ulcers are more common than gastric ulcers, but the symptoms are indistinguishable.
Gastric ulcers may be malignant and an ulcerated gastric cancer may mimic a benign ulcer.
• Gastric antisecretory agents and H. pylori eradication therapy are the mainstays of treatment,
and elective surgery is very rarely performed.
• The long-term complications of peptic ulcer surgery may be difficult to treat. The common
complications of peptic ulcers are perforation, bleeding and stenosis.

30. Duodenal ulceration
• Most ulcers occur in the first part of the duodenum. A
chronic ulcer penetrates the mucosa into the muscle
coat, leading to fibrosis. The resulting scarring may
cause a deformity such as pyloric stenosis. When an
ulcer heals, a residual scar can be observed in the
mucosa.
• Sometimes there may be more than one duodenal ulcer.
The situation in which there is both a posterior and an
anterior duodenal ulcer is referred to as ‘kissing
ulcers’. Anterior ulcers tend to perforate while posterior
duodenal ulcers tend to bleed, sometimes by eroding
into the gastroduodenal artery.
• With respect to the giant duodenal ulcer, malignancy in
this region is so uncommon that under normal
circumstances surgeons can be confident that they are
dealing with benign disease
Duodenal ulcer at gastroduodenoscopy

31. Gastric ulcers
• H. pylori and NSAID’s are important etiological factors
and also associated with smoking.
• More prevalent in low socioeconomic groups and is
considerably more common in resource-poor than in
resource-rich countries.
• Tends to be larger than duodenal ulcer and fibrosis may
result in hourglass deformity of the stomach.
• Chronic ulcers may erode posteriorly into the pancreas,
major vessels such as the splenic artery or rarely into other
organs such as the transverse colon. Chronic gastric ulcers
are more common on the lesser curve (especially at the
incisura angularis; than on the greater curve).
Benign incisural gastric ulcer
shown at gastroscopy
• In contrast to chronic duodenal ulcers, gastric ulcers are associated with malignancy.
• All gastric ulcers should be regarded as being malignant, no matter how classical the features of a benign
gastric ulcer. Multiple biopsies should always be taken, perhaps as many as 10 well-targeted biopsies,
before an ulcer can be tentatively accepted as being benign.

32. Clinical features :-
The clinical features of gastric and duodenal ulceration cannot be differentiated on the basis of
symptoms
• Epigastric pain, sometimes radiating to back
• Vomiting : in case of stenosis
• Alteration in weight : weight loss or sometimes weight gain may also occur
• Bleeding : chronic associated with microcytic anemia and acute presents with hematemesis
or malena.
Investigations :-
Gastroduodenoscopy
• In stomach any abnormal lesion should be biopsied.
• CLO test(campylobacter like org.) to detect presence of H. pylori.
• A ‘U’ manoeuvre (endoscopy)should be carried out to inspect the incisura, lesser curve and
gastro-esophageal junction (GOJ), given the increasing incidence of cancer at the GOJ.

33. Treatment of peptic ulceration
Medical management : aim to reduce gastric secretion
• H2 receptor antagonists, PPI, Eradication therapy.
Operations for duodenal ulcer : aim of excluding acid from duodenum.
Operations for gastric ulcer : the ulcer is usually excised so that malignancy can be excluded
• Gastrojejunostomy
• Gastrectomy based procedures : Billroth 1 and Billroth 2/ Polya
• Vagotomy-based procedures
 Truncal vagotomy (cutting the vagal nerves at the lower esophagus)
 Heineke–Mikulicz pyloroplasty
 In highly selective vagotomy (only the parietal cell mass of stomach is denervated.)

34. GASTRIC CANCER
• Multifactorial disease and H. pylori seems to be principally associated with carcinoma of the
body, stomach and distal stomach rather than the proximal stomach.
• Associated with cigarette smoking and dust ingestion from a variety of industrial processes.
Clinical features:-
Unfortunately, early gastric cancer has no specific features to distinguish it from benign
dyspepsia and a high index of suspicion is necessary.
In advanced cancer, early satiety, bloating, distension and vomiting may occur.
The tumor frequently bleeds, resulting in iron defciency anaemia.
Obstruction leads to dysphagia, epigastric fullness or vomiting.
Weight loss can be profound. With pyloric involvement the presentation may be of gastric
outlet obstruction,

35. Treatment
• Neoadjuvant chemo: FLOT (fluorouracil, leucovorin, oxaliplatin, docetaxel)
• Total gastrectomy
• Subtotal gastrectomy
• Along with vitamin B12 supplementation
• Palliative radiotherapy : for painful bony metastasis
• Palliative chemotherapy : using FLOT
SPREAD :-
Local : penetrates the muscularis, serosa and ultimately adjacent organs such as the pancreas,
colon and liver.
Lymphatic spread : supraclavicular nodes (Troisier’s sign)
Blood : liver > lungs , bones
Transperitoneal spread : The ovaries may sometimes be the sole site of transcoelomic spread
(Krukenberg’s tumours). Tumor may spread via the abdominal cavity to the umbilicus
(Sister Joseph’s nodule).

36. Irritable bowel syndrome
• IBS is a functional bowel disorder characterized by abdominal
pain or discomfort, stool irregularities and bloating.
• Diagnostic criteria according to Rome IV Foundation
Recurrent abdominal pain on average at least 1 day/week in the last 3 months, associated
with two or more of three criteria:
(1) related to defecation;
(2) associated with a change in the frequency of stool
(3) associated with a change in the form (appearance) of stool.
These criteria should be full filled for the last 3 months with symptom onset at least 6 months
prior to diagnosis

37. IBS subtypes:-
• All patients have abdominal pain but
subtypes vary according to bowel form at
presentation such as to meet criteria for
• IBS with constipation (IBS-C)
• IBS with diarrhoea (IBS-D)
• mixed-type IBS (IBS-M)
• unsubtyped (IBS-U).

38. Treatments for irritable bowel syndrome.

39. Chronic pancreatitis
• Persistent inflammation along with irreversible fibrosis and atrophy of pancreatic
parenchyma leading to chronic pain, exocrine and endocrine insufficiency.
• Pain is initially precipitated by oral intake, afterwards intensity, frequency and duration of
pain will increase gradually with worsening of disease.
• Along with characterized by triad of DPS (DM, pancreatic calcification, steatorrhea)
• Most common cause is due to heavy alcohol consumption.
• IOC : MRCP
• Gold std. : ERCP (diagnostic and therapeutic)
• Management :-removal of predisposing factors
Medical = palliation of symptoms through (NSAID’s, tramadol, TCA, SSRI, SNRI)
Surgical treatment required in case of intractable pain, biliary or pancreatic duct
formation, pseudocyst formation, inability to rule out malignant conditions.

40. Gall stones
• Only 10% of individuals with gall stones develop clinical evidence of gall stone disease.
• Symptomatic stones within the gall bladder manifest as either biliary pain (biliary colic) or
cholecystitis.
• The term biliary colic is a misnomer because the pain does not rhythmically increase and
decrease in intensity like other forms of colic.
• Pain is usually felt in the epigastrium or right upper quadrant and radiates to the interscapular
region or tip of the right scapula, left upper quadrant.
• The pain is often associated with diaphoresis, nausea, and vomiting.
• It is not exacerbated or reproduced by movement and is not relieved by squatting, belching,
bowel movements, or passage of flatus. The pain typically lasts at least 30 minutes, plateauing
within an hour. The pain then starts to subside, with an entire attack usually lasting less than
six hours.
• Combination of fatty food intolerance, dyspepsia and flatulence.

41. Drug-induced dyspepsia
• NSAIDs and COX-2 selective inhibitors can cause dyspepsia even in the absence
of peptic ulcer disease.
• Other drugs that have been implicated in drug-induced dyspepsia include:-
calcium channel blockers, methylxanthines,
alendronate, acarbose, orlistat,
potassium supplements, iron, vitamin D,
dabigatran, selective serotonin reuptake inhibitors, sildenafil, sulfonylureas,
certain antibiotics, including erythromycin, etc.

42. • Dyspepsia is a disorder characterized by dyspeptic symptoms which are located in
the epigastrium and related to digestion of food in the initial part of the digestive
system.
• In functional dyspepsia, unlike organic dyspepsia, there is no underlying organic
disease that would cause dyspeptic symptoms.
• Immune and mucosal function changes, gastric dysmotility, different composition
of the gastrointestinal microbiota, and altered central nervous system processing
are considered responsible for the onset of the disorder.
• The diagnosis is based on history, clinical presentation, and exclusion of other
organic diseases of the gastrointestinal tract manifested by dyspeptic symptoms.
• Therapy includes eradication of Helicobacter pylori infection, proton pump
inhibitors, prokinetics, neuromodulators.
Summary