Peptic Ulcer Disease + Carcinoma Stomach.

UthamalingamMurali 95 views 79 slides Mar 19, 2025
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About This Presentation

This topic is very important for MBBS Students in applying it in both the theoretical as well as clinical knowledge. It covers most of the facts about 2 common diseases which the students have to face in... It covers widely about the latest strategy used in the treatment of Ca. Stomach...


Slide Content

Prof. U.Murali.
Peptic Ulcer
&
Ca. Stomach

Peptic Ulcer
Prof. U.Murali.

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Learning Objectives
•Introduction
•Definition
•Aetiopathogenesis
•Types
•Clinical presentation
•Investigations
•D/D | Complications
•Treatment

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•PUD is one of the most common gastro-
enterologic disease affecting the UGIT.
•Each year approx. 300,000 to 500,000 new
cases of PUD occur.
•Three to four million people are self-
medicating for symptoms of PUD.
•Most peptic ulcers are caused by H.pylori or
NSAID’s and mirror changes occurs in these
factors.
•DU are more common than gastric ulcers,
but the symptoms are indistinguishable.
Introduction

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•The term ‘peptic ulcer’ describes a condition
in which there is a discontinuity in the entire
thickness of the gastric (or) duodenal mucosa
that persists because of acid & pepsin in the
gastric juice.
•Peptic ulcers are defects in the gastric (or)
duodenal mucosa that extend through the
muscularis mucosa into the deeper layers.
•A refractory peptic ulcer is defined as an
endoscopically proven ulcer greater than 5
mm in diameter that does not heal after 12
weeks of treatment with a proton-pump
inhibitor.
Definition

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Etiology
•Impairment of protective
mechanisms by the damaging
factors.
•H. pylori infection – > 70%.
•Chronic NSAID’s / Alcohol.
•Smoking / Stress / Chronic
Steroids or Drugs – 3 “S”.
•Hypercalcemia (↑gastric
secretion).
•Improper diet intake.
•Genetic factors.

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Pathogenesis

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Types
•Acute Ulcers – It is
confined to mucosa &
submucosa.
•Chronic Ulcers – It
penetrates the muscularis
layer of stomach.
•Curling’s Ulcers – These
are acute ulcers which
develop after major burns.
•Cushing’s Ulcers – These
are acute ulcers which
develop after cerebral
trauma.

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Features Gastric UlcerDuodenal Ulcer
Incidence Less common –
15%
More common –
80%
Age Usually 50 & olderBetween – 30-60
M:F Ratio Almost equal 2-3:1
Blood group No differentiationMost often type
‘O’
Common LocationLC & Antrum Ant. wall of 1
st

part
Asso. i H.pylori 65% 85-100%
Acid secretionNormal /
Decreased
Increased
Malignancy Chances - < 10%Very rare
Features Gastric Ulcer Duodenal Ulcer
Course -
Periodicity
Less common More common
Weight Loss – due to reduced
intake
Gain – as pt feels
better with eating
Pain (site) Felt over the left of
midline
Felt over the right of
midline
Vomiting Common Uncommon
Epigastric pain –
Time of onset
Occurs ½-1 hr after a
meal. ↑by ingestion of
food
Occurs 3 hrs after a
meal mainly at
night. ↓ after
ingestion of food
Gastric symptomsSatiety, indigestion,
heartburn, gas trouble
or belching
Bloating feeling
Hemorrhage Hematemesis Melena
Perforation Very rare More likely
Clinical Features – Symptoms

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•Serology – Detects IgG antibodies to H.pylori –
ELISA test.
•Urea breath test – ‘Gold-standard’ {Pt drinks a
carbon-enriched urea sol. – Excreted CO₂ is then
measured}
•Rapid urease test – Cod liver oil test / CLO test|
> 90% sensitivity & > 98% specificity.
•Biopsy & Culture – More expensive.
Investigations – Tests for H.Pylori
•Non-Invasive
•Invasive

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Investigations – UGI - Scopy

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Investigations – Barium Study

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Differential Diagnosis

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Complications - Types
Acute
•Perforation
•Bleeding
Chronic
•Stenosis - GOO
•Deformities
•Malignancy
•Penetration
•Residual
abscess

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G U / D U – Chronic Complications
Tea-pot
deformity
•Shortening – LC –
Fibrosis
•FO –PS
•Partial G + B 1
anastomosis
Penetration
•Ant – Liver
•Post -Pancreas
Malignancy
•Incidence –
5 - 10%
•GC & LC
Residual
Abscess
•Subacute /
Chronic
Perforation –
Sealed off –
R A

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Treatment – G M
•General Measures
•Avoid spicy food
•Avoid smoking & alcohol.
•Avoid drugs – NSAIDs,
Steroids.
•Encourage small frequent
meals.
•Adequate mental & physical
rest.
•Coffee / Tea – Moderate
consumption.

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Treatment - Medical

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Treatment - Medical

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Treatment - Surgical

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Treatment - Surgical

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Treatment - Surgical

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Treatment - Surgical

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Complications – Gastric Surgery

P U – Complications
&
Treatment
Prof. U.Murali.

Perforated Peptic Ulcer
•It is the terminology used for
perforation of duodenal ulcer (or)
gastric ulcer (or) stomal ulcer.
Otherwise all clinical features and
management are similar.
•Perforation is common in
duodenal ulcer (75% of perforated
peptic ulcers).
•Mortality is more in gastric ulcer
perforation and perforation in
elderly.

Perforated Duodenal Ulcer [PDU]
•It is common in males between 35-45
years of age group, but can occur in
any age group.
Anterior ulcer perforates, commonly –
•In 80% of cases, there is a history of
chronic DU.
•In 20% cases, it is silent perforation.
•Perforation may be precipitated by
steroids, analgesics (NSAIDs), alcohol
(or) antimalarials.

Perforated Duodenal Ulcer
Chemical Peritonitis
(Peritonism)
•Contents leak – peritoneal
cavity – acid – chemical
peritonitis – irritation
•Severe pain / vomiting /
guarding / rigidity
•Lasts for 2-4 hrs
Reaction/Illusion
•Peritoneum – secretes –
fluid – neutralize contents
•Pain reduces –illusion
•Signs become worse
•Lasts for about 6 hrs
Bacterial Peritonitis
•No acid barrier – Easy
bacterial invasion – G-ve
•Patient –Toxic
•F 0 –Shock sets in
•Starts after 10 –12 hrs
Stages of Perforation

P D U – Clinical Features
•Sudden severe pain
abdomen
•Fever / vomiting
•Distension –
abdomen
•Tenderness /
Guarding / Rigidity
•Obliteration –liver
dullness
•Signs -dehydration
•Absent –BS
•Hippocratic facies
•F O –Shock
•Oliguria
•Septicaemia
•MODS
Initial Stages Terminal Stages

Perforated Duodenal Ulcer
Investigations
•CBP / Electrolytes
•Sr. amylase
•Plain X-ray chest i
abd(or) Left lateral
decubitus
•U/S –abdomen
•CT –scan abdomen
–confirms &
accurate
D / D
•Appendicitis
•Pancreatitis
•Cholecystitis
•Rup.AAA
•Mesenteric
ischemia

P D U – Treatment
•Admission
•Analgesia
•I V -Fluids
•Antibiotics
•N P O
•RT –Aspiration
•Monitor I/O -chart
Preliminary

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PDU - Treatment

Perforated Gastric Ulcer
•Commonly ulcer in the lesser curve near the
antrum perforates. Mostly they are prepyloric
in position.
•Malignancy should always be suspected and
so biopsy from the edge is a must.
•Primary closure with an edge biopsy is
commonly used.
•Distal gastrectomy including ulcer area is
better option if patient’s general condition is
favourable.
•Posterior GU perforation is often difficult to
diagnose both clinically and radiologically.

Bleeding Peptic ulcer
•It is bleeding either from duodenal ulcer,
(or) gastric ulcer (or) stomal ulcer.
•Mortality in bleeding peptic ulcer - is high
(20-30%). Elderly age, associated
systemic diseases increase the mortality.
•NSAID’s and H. pylori infection,
coagulopathy and anticoagulant drugs
are common precipitating factors.
•Need of more than 5 units of blood
transfusion during hospital stay is called
as massive haemorrhage.

Bleeding Peptic Ulcer
•Hb% / PCV
•Blood grouping
•Platelet count
•UGI –scopy

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Upper GIB - Score

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Bleeding D & GU Treatment

Pyloric Stenosis / G O O
•The term ‘pyloric stenosis’ is normally a
misnomer. The stenosis is seldom at the
pylorus.
•Commonly, when the condition is due to
underlying PUD, the stenosis is found in
the first part of the duodenum, the most
common site for a peptic ulcer.
•In recent years, the most common cause
of G O O has been gastric cancer.
•Chronic DU after many years undergoes
scarring and cicatrisation causing total
obstruction of the pylorus.

Pyloric Stenosis / G O O
•Persistent pain in epigastric region with feeling
of fullness. Confused status…
•Vomiting— foul smelling and contains partially
digested (or) undigested food - Dehydration.
•Loss of periodicity. Loss of appetite and weight.
•Distended abdomen – Mostly upper abdomen.
•Visible gastric peristalsis (VGP)—may be elicited
by asking the patient to drink a cup of water.
•Positive succussion splash which is done with 4
hours empty stomach.
•Auscultopercussion test shows dilated stomach.

Pyloric Stenosis / G O O
Metabolic Effects
•Na/K/Mg/Cl – Drop
•Hypo-chloraemic
alkalosis
•Hypocalcaemia –
“Gastric tetany”
•Kidney secretes –
excess HCO3 + H2 ion
•Acidic urine
•Paradoxical aciduria
Investigations
•Electrolyte study
•Barium meal
study
•UGI –scopy

Pyloric Stenosis / G O O
•Correction of dehydration and electrolytes by
IVF— normal saline, calcium, potassium,
magnesium.
•Stomach wash to clean the stomach contents
(using normal saline) is given.
Surgery
•HSV with gastrojejunostomy can be done.
•T V + GJ of Mayo - (posterior, vertical/oblique,
short loop, retrocolic, isoperistalsis) is done—
ideal, commonly advocated procedure.
•Vagotomy, antrectomy (acid secreting area) is
the other option.
•Endoscopic balloon dilatation - benefits only
temporarily with high recurrence rate.

G U - Hourglass contracture
•Due to cicatricial contraction of saddle-shaped
ulcer at LC. The stomach is divided into 2
chambers – admits barely a pencil.
•Females > males.
Clinical features:
– Loss of periodicity.
– Persistent pain.
– Vomiting.
– Loss of appetite and weight.
•Barium meal / UGI – scopy
•Partial gastrectomy with removal of 2
nd
pouch –
Billroth I anastomosis – treatment of choice.

Ca. Stomach
Prof. U.Murali.

Learning Objectives
▪List the types of tumours of Stomach.
▪Introduction.
▪Aetiology & pathological types.
▪Clinical Features.
▪Staging & Investigations.
▪Treatment.

Tumours of Stomach
Benign
•Gastric Polyps
•Leiomyoma/ GIST
•Lipoma
Malignant
•Carcinoma
•Lymphoma
•Sarcoma

Carcinoma Stomach
▪Gastric cancer is one of the most common causes of
cancer death in the world.
▪Marked variations in its incidence worldwide. Highest
incidence in Eastern Asia – (Japan, Korea, China).
▪More common in males 2:1.
▪It is a curable disease, provided detected & treated
early. So, early diagnosis is the key to success.
▪Ca. of the distalstomach and body of the stomach is
most common in old & low socioeconomic groups,
whereas the increase in proximal gastric cancer seems
to affect principally young & higher socioeconomic
groups.
▪Proximal gastric cancer does not seem to be associated
with H. pylori infection, in contrast with carcinoma of
the body and distal stomach.

Carcinoma Stomach - Etiology
▪Genetic / Familial – related – 10%.
▪Smoking / Alcohol / Obesity / B. Group - A.
▪H-pylori infection – EB – Virus - High risk.
▪Patients with pernicious anaemia & gastric
atrophy (chronic gastritis) are at increased risk.
▪Diet - Excessive salt intake, deficiency of
antioxidants and exposure to N-nitroso
compounds are also related.
▪Gastric polyps as well as duodeno-gastric reflux
& reflux gastritis are related to the increased
risk of malignancy.

Carcinoma Stomach
Pre - cancerous
•Chronic atrophic
gastritis
•Pernicious anaemia
•Intestinal metaplasia
•Polyps > 2 cm
•Benign gastric ulcer
•Previous gastric surgery
•Menetrier’sdisease
•Agammaglobulinaemia
Common Sites
•Pre & Pyloric – 65%
•Body –25%
•Fundus& OG jn–10%

Ca. Stomach – Pathology
Lauren’s
•Intestinal type
•Diffuse type
Japanese’s
Early
Borrmann’s
Advanced
W H O
•Adenocarcinoma
•Adenosquamous
Ca.
•S C C
•Undifferentiated
Ca.
CLASSIFICATIONS

Ca. Stomach – Spread
Direct
•Horizontal
•Vertical
Lymphatic
•Permeation &
embolization
•Retrograde
spread
Blood
•Liver
•Lungs
•Bones
Trans-peritoneal
•Ascites
•Krukenberg’s
•Sister Mary Joseph
•Rectal deposits

Ca. Stomach – Clinical Features
▪Asymptomatic:
In EGC (or) in cancer of body of
stomach.
▪Non-specific symptoms:
Indigestion / Vague epigastric
discomfort / early satiety / bloating
sensation.
▪Specific symptoms:
Site – Vomiting – GOO / dysphagia /
mass per abdomen / anaemia /
haematemesis / loss of appetite &
weight.
▪Metastatic symptoms:
Ascites / Liver, lung & bone sec. /
Troisier’s sign / Trousseau sign / Sister
Mary Joseph nodule / Irish node /
Rectal deposits.

Ca. Stomach – Investigations
▪Basic tests.
▪LFT & RFT.
▪Barium meal study.
▪UGI – scopy with biopsy.
▪U/S / CT scan – abdomen.
▪FNAC – Lymph node.
▪Tumour markers–CA 72-4.

Ca. Stomach – Treatment
▪Early growth – Pylorus / Distal Ca.:
Lower radical gastrectomy / Sub-total
gastrecomy - removal of tumour [5 cm margin
clearance] + nodal clearance & Billroth II
anastomosis.
▪Growth – OG junction / Upper part:
Upper radical gastrectomy - removal of tumour
+ nodal clearance + both omentum, +/- removal
of spleen & later oesophago-gastric
anastomosis.
▪Growth – Body:
Total radical gastrectomy + Roux–en-Y - OJA.
▪Endoscopic mucosal resection [EMR]:
Tumour < 2cm, well-differentiated without
nodal disease is ideal for EMR.

Ca. Stomach – Treatment
▪Advanced Growth:
Neoadjuvant CT + Gastrectomy.
▪PO – RT + CT: has become standard
adjuvant treatment.
ECF – Epirubicin / Cisplatin / 5-fluorouracil
FLOT – 5FU/Leucovorin/Oxaliplatin/docetaxel
▪D1 or D2 gastrectomy – Present
concept:
D1 – clearance of peri-gastric nodes.
D2 – clearance of nodes along major vessels.
[depending on level of lymph nodes cleared]
▪D2 gastrectomy + chemoradiation is ideal
present concept therapy in Ca. stomach.
▪At least 15 lymph nodes should be removed.

Ca. Stomach – Palliative Procedures
▪Palliative partial / total gastrectomy is the best
palliation.
▪Anterior gastrojejunostomy is one of the
palliative procedures used in case of inoperable
carcinoma stomach. It is anterior, antecolic GJ.
▪Devine’s exclusion procedure wherein instead
of removal of tumour, it is excluded with
Billroth II anastomosis.
▪M-B tube/Celestin tube insertion for proximal
stomach growths.
▪Endoscopic stenting / dilatation – can be tried.
▪Laser re-canalisation.
▪Palliative chemotherapy—ECF / FLOT regime|
Trastuzumab (Herceptin) for advanced growths.

References

To Summarize
▪Definition & Types –
Peptic ulcer.
▪Aetio-pathogenesis.
▪Clinical Features.
▪D/D & Complications.
▪Investigations – Various.
▪Treatment – M & S.
▪Types & Etiology – Ca.
Stomach.
▪Precancerous Lesions.
▪Classifications.
▪Clinical Features.
▪Staging & Modes of spread.
▪Investigations / Treatment.
“ P U D ” “Ca. Stomach”

Question Time
▪List the types of PUD & Gastric ulcer.
▪Outline the etio-pathogenesis of PUD.
▪Write 5 differences between gastric & duodenal ulcer.
▪Mention 5 complications of Gastric surgery.
▪Classify carcinoma stomach.
▪Enumerate 5 pre-cancerous lesions of Ca. stomach.
▪List 4 eponymous clinical signs of advanced gastric cancer.
▪Identify the palliative treatment methods of Ca. stomach.

Type – III Gastric ulcer is located at –
▪a) Lesser curvature.
▪b) Body of stomach.
▪c) Pre-pyloric region.
▪d) Gastro-esophageal junction.

All of the following are predisposing factors
for Carcinoma stomach, except –
▪a) Chronic gastric atrophy.
▪b) Hyperplastic polyp.
▪c) Pernicious anemia.
▪d) Intestine mataplasia.

Which of the following vessel is most commonly
involved in hemorrhage from duodenal ulcer? –
▪a) Superior pancreatico-duodenal artery.
▪b) Gastro-duodenal artery.
▪c) Superior mesenteric artery.
▪d) Inferior pancreatico-duodenal artery.

Surgery of choice for Chronic duodenal ulcer is –
▪a) Vagotomy + antrectomy.
▪b) Total gastrectomy.
▪c) Truncal vagotomy + pyloroplasty.
▪d) Highly selective vagotomy.

All of the following drugs are used in the
management of peptic ulcer, except –
▪a) Alginic acid.
▪b) Sucralfate.
▪c) Misoprostol.
▪d) Ipratropium.

A 60 years old male diagnosed to have Carcinoma
stomach. CT scan of abdomen showed a mass
measuring 4 x 4 cm in the antrum with involvement of
celiac nodes and right gastric nodes. Management of
choice is –
▪a) Total gastrectomy.
▪b) Subtotal gastrectomy.
▪c) Palliative surgery.
▪d) Radiotherapy + Chemotherapy.


Thank You

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