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Parietal cells
These are in the bodacid-secreting portion) of the stomach

and line the gastric crypts,They

are responsible for the production of hydrogen ions to form

hydrochloric acid.

Chief cells
proximally in the gastric crypts and produce

pepsinogen. Two forms of pepsinogen are described: pepsinogen

I and pepsinogen II.

Endocrine cells
In the gastric antrum, the mucosa contains 

G cells

,

which produce 

gastrin

. Throughout the body of the stomach,

enterochromaffin-like (ECL) cells 

are abundant and produce

Histamine

,

somatostatin-producing D

cells 

throughout the stomach, and 

somatostatin

has a negative

regulatory role


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Flexible endoscopy
Contrast radiology
Ultrasonography
CT scanning and magnetic resonance imaging
CT/positron emission tomography
Laparoscopy
Gastric emptying studies
Angiography


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13C and 14C Urea breath test
HISTOLOGICALLY Giemsa or the Ethin–Starey silver 

stains,
Serological test

Breath tests or faecal antigen tests are recommended for the 

pretreatment      diagnosis of H. pylori infection in the 

community
It causes chronic gastritis,peptic ulcer and gastric cancer

eradication therapy is recommended for patients with duodenal 

ulcer                      disease, but not for patients with nonulcer

dyspepsia or in asymptomatic patients who are infected

H. pylori is now classed by the World Health Organisation as a 

class 1 carcinogen


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The spiral bacterium 

H. pylori 

is critical in the development of type 

B gastritis, peptic ulceration and gastric cancer

Infection appears to be acquired mainly in childhood and the 

infection rate is inversely associated with socioeconomic 

status

Eradication, 

recommended specifically in patients with peptic 

ulcer disease, can be achieved in up to 90 per cent of patients 

with a combination of a proton pump inhibitor and 

antibiotics, and reinfection is uncommon (<0.5 percent)

Erosive gastritis 

is usually related to the use of NSAIDs

Type A gastritis 

is an autoimmune process and is associated

with the development of pernicious anaemia and gastric

cancer


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Autoimmune
Circulating antibodies to the parietal cell
hypochlorhydria and ultimately achlorhydria
pernicious anaemia
Production of high levels of gastrin from the antral G 

cells
Patients with type A gastritis are predisposed to the 
development of gastric cancer


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Affect antrum

Association of this type of gastritis with H. pylori
Patients with
pangastritis seem to be most prone to the development 
of gastric cancer.


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This is caused by enterogastric reflux and is 

particularly common after gastric surgery
have had a cholecystectomy. Bile chelating or 

prokinetic agents may be useful in treatment
Operation for the condition should be reserved 
for the most severe cases..


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The NSAID-induced gastric lesion is associated with 

inhibition of the cyclo-oxygenase type 1 (COX-1) 

receptor enzyme, hence reducing the production of 

cytoprotective prostaglandins in the stomach.
The use of specific COX-2 inhibitors reduces the 
incidence of these side effects.


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common sequel of serious illness(follows 

cardiopulmonary bypass) or injury and is
characterised by a reduction in the blood supply 

to superficial mucosa of the stomach.
the routine use of H2-antagonists with or without 

barrier agents, such as sucralfate, in patients 

who are on intensive care unit.


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Unusual condition
gross hypertrophy of the gastric mucosal folds, mucus 

production and hypochlorhydria.
Hypoproteinemia & anemia
Premalignant condition
Over expression of TGF-ᾳ
Treatment : gastrecomy


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Rare type

infiltration of the gastric mucosa by T cells and is 

probably associated with H. pylori infection.
resembles pattern seen in coeliac disease or 

lymphocytic colitis..
Eosinophilic gastritis: allergy
Granulomatous gastritis: Crohns disease and TB
Acquired immunodeficiency syndrome (AIDS) gastritis
Phlegmonous gastritis: bacterial


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Common

sites for peptic ulcers are the first part of the 

duodenum and the lesser curve of the stomach.

They

also occur on the stoma following gastric surgery, 

the oesophagus and even in a Meckel’s diverticulum

infection

with H. pylori and the consumption of NSAIDs 

are the most important factors in the development of 

peptic ulceration

Cigarette

smoking predisposes to peptic ulceration and 

increases the relapse rate after treatment, with either 

gastric antisecretory agents or, in the past, elective 

Surgery


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the peak incidence is now in a much older age 

group

More common in men,


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Most

occur in the first part of the duodenum 

chronic

ulcer penetrates the mucosa and into the muscle coat, 

leading to fibrosis. 

The fibrosis 

causes deformities such as pyloric stenosis

‘kissing ulcers’.

Anterior ulcer 

tend to perforate ,

Posterior ulcer 

tend to 

bleed 

malignancy

in this region is so uncommon that under 

normal circumstances surgeons can be confident that 
they are dealing with benign disease


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Destruction

of the muscular coat is observed and the 

base of the ulcer is covered with granulation tissue,

THE

arteries in this region showing the typical changes 

of endarteritis Obliterans


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As with duodenal ulceration, H. pylori and NSAIDs are 

the important aetiological factors.

Gastric ulceration is also associated with smoking 

gastric ulceration is substantially less common than 
duodenal ulceration

The sex incidence is equal and the population with 

gastric ulcers tends to be older.

It is more prevalent in low socioeconomic groups


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Gastric ulcers tend to be larger

Fibrosis rarely seen hourglass contraction of the

stomach.

Large chronic ulcers may erode posteriorly into the

pancreas and, on other occasions, into major vessels 

such as the splenic artery

. Chronic gastric ulcers are much more common on the 
lesser curve (especially at the incisura angularis)


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Giant ulcers are those that are more than 3 cm in 

diameter. 
These ulcers have an increased association with cancer: 

30% of those larger than 3 cm harbor malignant 

disease. 
Earlier surgical intervention is generally warranted 

given this association.

Endoscopy with multiple biopsies (at least four with 

jumbo forceps and eight with regular) to include 

both the ulcer base and edge usually provide 

sufficient tissue for diagnosis to guide therapy, with 

treatment of nonmalignant ulcers adhering to 

guidelines as outlined previously, depending on the 

location.


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It is fundamental that any gastric ulcer should be 

regarded as being malignant,

Multiple biopsies should always be taken, perhaps as 

many as ten well-targeted biopsies

It is important 

that further biopsies are taken while the 

ulcer is healing and when healed.

At operation

, even experienced surgeons may have 

difficulty distinguishing between the gastric cancer 

and a benign ulcer


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Pain
Periodicity
Vomiting : fibrosis
Alteration in weight
Bleeding: 
microcytic anaemia

is not uncommon


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Peptic ulcer and H. pylori 

then eradication Rx

NSAIDS  and stomal ulcer

Patients with 

Zollinger–Ellison syndrome 

should be 

treated in the long term with proton pump inhibitors 

unless the tumour can be adequately managed by 
surgery.


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Agent

Length of treatment

PPI (omeprazole 20 mg OR lansoprazole
30 mg)
+ Amoxicillin 1000 mg
+ Clarithromycin 500 mg

Orally, twice daily for 14 days

PPI (omeprazole 20 mg OR lansoprazole
30 mg)
+ Metronidazole 500 mg
+ Clarithromycin 500 mg

Orally, twice daily for 14 days

Alternative regimen:
Bismuth subsalicylate 525 mg qid
+ Metronidazole 500 mg tid
+ Tetracycline 500 mg qid
+ PPI (omeprazole 20 mg OR lansoprazole
30 mg daily)

Orally, given as indicated for 14 days


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persistent H. pylori
Infection
poor compliance
ingestion of NSAIDs
Zollinger–Ellison syndrome


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Billroth II gastrectomy:Two-thirds 

of the stomach 

removed, the duodenal stump is closed and the stomach 

.

anastomosed to the jejunum

Gastrojujenostomy

Truncal vagotomy with drainage(HM)

Highly Selective vagotomy with drainage

Truncal vagotomy with antrectomy


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Billroth I 

gastrectomy


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Most

peptic ulcers are caused by H. pylori or NSAIDs

Duodenal ulcers 

are more common than gastric ulcers, but 

the symptoms are indistinguishable

Gastric ulcers 

may become malignant and an ulcerated 

gastric cancer may mimic a benign ulcer

Gastric

antisecretory agents and H. pylori eradication 

therapy are the mainstay 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

The

treatment of the perforated peptic ulcer is primarily 

surgical, although some patients may be managed
conservatively


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1.

Recurrent ulceration

2.

Small stomach syndrome

3.

Bile vomitting

4.

Early and late dumping

5.

Postvagotomy diarrhea

6.

Malignant transformation

7.

Nutritional consequences(B12,iron,bone)

8.

Gall stones


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The small bowel is filled with foodstuffs from the 

stomach, which have a high osmotic load, and this 

leads to the sequestration of fluid from circulation 

into the gastrointestinal tract..

The principal treatment is 

dietary manipulation

. Small, 

dry meals are best, and avoiding fluids with a high 

carbohydrate content..

Surgery: 

Roux en Y reconstruction


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This is reactive 

hypoglycaemia

. The carbohydrate load 

in the small bowel causes a rise in the plasma 

glucose, which, in turn  causes insulin levels to rise, 

causing a secondary hypoglycaemia

The treatment is essentially the same as for early 

dumping. 

Octreotide

is very effective in dealing with this problem


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late

Early 

5%

5-10%

incidence

Second hour after 

meal

immediately

Relation to meal

same

30-40 min

Duration of attack

food

Lying down

relief

exercise

More food

Aggrevated by

CHO

CHO

Precipitating factor

Tremor faintness 

and prostration

Fullness,sweating, 

tacchycardia and 

sometimes diarrhea

Major symptom


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Epidemiology 

Previously

, most patients were middle aged, with a 

ratio of 2:1 of male:female.

With time, there has been a steady increase in the age 

of the patients suffering this complication and an 

increase in the numbers of females, such that 
perforations now occur most commonly in 

elderly 

female 

patients. 

NSAIDs appear to be responsible for most of these
perforations.


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sudden onset 

severe generalised abdominal pain

Initially, the patient may be 

shocked

with a tachycardia 

but a pyrexia is not usually observed until some 

hours after the event.

Boardlike rigidity 

and the patient is disinclined to move 

because of the pain. The abdomen does not move 

with respiration.

The perforation may be 

self-limiting

??how


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Erect plain 

chest radiograph 

will reveal free gas under 

the diaphragm in an excess of 50 per cent of cases..

CT

imaging is more accurate

serum amylase: WHY?


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The treatment is principally surgical

.

systemic antibiotics resuscitation and analgesia

Laparotomy

is performed, usually through an upper midline incision 

,thorough peritoneal toilet to

remove all of the fluid and food debris

If the perforation is in the duodenum it can usually be closed by 

several well-placed

sutures, closing the ulcer in a transverse direction as with a 

pyloroplasty.

It is common to place an omental patch over the perforation .

Gastric ulcers shouldbe excised and closed, so that malignancy can be 

Excluded

Massive duodenal 

or gastric perforation such that simple closure is 

impossible; in these patients a Billroth II gastrectomy or subtotal 

gastrectomy with Roux-en-Y reconstruction

s

tomach 

is kept empty postoperatively by nasogastric suction,

and that gastric antisecretory agents are commenced to promote

healing of the residual ulcer.


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• delay in diagnosis (>24 hours)

• medical comorbidities

• shock

• increasing age (>75).

Patients who have suffered one perforation may suffer 
another one


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The 

two

common causes of gastric outlet obstruction 

are:

1-

gastric cancer

2-pyloric stenosis secondary to peptic 

ulceration.


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pain

may become unremitting and in other cases it may 

largely disappear

The 

vomitus

is characteristically unpleasant in nature 

and is totally lacking in bile.

It is possible to recognise foodstuff taken several days 

previously

losing weight

, and appears unwell and 

dehydrated

.

succussion splash 

may be audible on shaking the 

patient’s abdomen.


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vomiting

of hydrochloric acid results in 

hypochloraemic

alkalosis

Initially, the 

sodium

and 

potassium

may be relatively normal

Dehydration Progresses lead to renal dysfunction
Initially, the 

urine

has 

a low chloride 

and 

high bicarbonate 

content
This 

bicarbonate

is excreted along with 

sodium

, and so with time 

the patient becomes progressively 

hyponatraemic

and more 

profoundly dehydrated
Because of the 

dehydration

, a phase 

of sodium retention 

follows 

and potassium and hydrogen are excreted

The urine becoming paradoxically acidic and 

hypokalaemia

Alkalosis leads to a lowering in the circulating ionised calcium,
and tetany can occur


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The patien should be rehydrated with intravenous isotonic 

saline with potassium supplementation

Replacing the sodium chloride and water allows the kidney to 

correct the acid–base abnormality

gastric antisecretory agent given intravenously

a wide-bore gastric Tube

endoscopy and contrast radiology

Biopsy of the area around the pylorus is essential to exclude 

malignancy

Dilatation, stent ,drainage procedure and surgery for CA


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Adult pyloric stenosis

Pyloric mucosal diaphragm


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Risak of CA
Biopsy is essential
Types:

Metaplastic

: most common associated with H.P and 

regress after eradication therapy

Inflammatory

polyps: common

Fundic gland polyps

: associated with PPI use and FAP

Adenomatous

polyp: pre malignant,10% of polyps

Gastric carcinoids arising from the ECL cells are seen in 

patients with pernicious anaemia and usually appear 
as small polyps


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major cause of cancer mortality Worldwide

prognosis tends to be poor, with cure rates little better 

than 5–10 per cent

Early diagnosis is the key to success

The only treatment modality able to cure the disease is 

resectional surgery


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In the UK, it is approximately 15/100 000 per Year

USA 10/100 000 per year

70/100 000 per Year in Japan

men are more affected by the disease than women
Increase the proximal stomach, particularly the 

oesophagogastric junction
Proximal gastric cancer does not seem to be associated with 

H. pylori infection,

Proximal CA : high SE
Distal CA : Low SE


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H. pylori
gastric atrophy ,intestinal metaplasia ,Pernicious Anaemia

gastric polyps

Billroth II, gastroenterostomy or pyloroplasty, duodenogastric reflux 

and reflux gastritis

Cigarette smoking and dust ingestion

DIETS: spirit , salt intake,

Obesity: proximal CA

Genetic factors:

Mutation APC gene(Tumor supressor gene) or b-catenin, E cadherin

hereditary non-polyposis colorectal(HNPCC) (Lynch syndrome)

Inactivation of p53


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Dyspepsia
In advanced cancer, early satiety, bloating, distension

Vomiting
iron deficiency anaemia

Obstruction leads to dysphagia, epigastric Fullness
Gastric outlet obstruction

Thrombophlebitis (Trousseau’s sign) and deep venous
thrombosis.


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Upper oesophagus:2%
Mid oesophagus:6%

Lower oesophagus:22%
GE:18%
Cardia :17%

Body:15% 
Antrum :13% 
Pylorus:7%

60%


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Intestinal : polyp or ulcer

Diffuse : without mass but more 
involvement(worse Px)


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early gasric CA: 
Mucosa and submucosa with or without LN 

involvement

T1 & any N
CURABLE 
5yrs survival rate 90%


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involves the muscularis

Bormann classification from I to IV

III & IV are incurable


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T1 :Tumour involves lamina propria, submucosa
T2 :Tumour invades muscularis propria
T3 :Tumour involves subserosa
T4a: Tumour perforates serosa
T4b :Tumour invades adjacent organs

N0: No lymph nodes
N1 :Metastasis in 1–2 regional nodes
N2 :Metastasis in 3–6 regional nodes
N3a: Metastasis in 7–15 regional nodes
N3b :Metastasis in more than 15 regional nodes

M0 :No distant metastasis
M1 : Distant metastasis (this includes peritoneum and distant
lymph nodes)

Lymph node involvement can occur in stage I
No distant metastasis before stage IV disease


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Direct spread pancreas, colon and liver

Lymphatic spread  (Troisier’s sign).

Blood-borne metastases liver,lung and bone

Transperitoneal spread:Krukenberg’s tumours and 

Sister Joseph’s nodule


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For tumours distally placed in the stomach

This will lead to enterogastric reflux So Roux loop 
will solve the problem


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Leakage

of the oesophagojejunostomy

fistula

from the wound or drain site

perform

a water-soluble contrast swallow at 5–7 days 

after the operation to determine whether the 

anastomosis is intact

leakage

from the duodenal stump

Paraduodenal

collections can be drained radiologically

Biliary

peritonitis requires a laparotomy and peritoneal 

toilet

secondary

haemorrhage from the exposed or divided 

blood vessels


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obstruction

bleeding

,


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Radiotherapy is contraversal

Chemotherapy by :epirubacin, cis-platinum and 

infusional 5-FU or an oral analogue such as 
capecitabine


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Gastric cancer is one of the most common causes of cancer death 

in the world

The outlook is generally poor, owing to the advanced stage of 

the tumour at presentation

Better results are obtained in Japan, which has a high population 

incidence, screening programmes and a high quality surgical 

treatment

The aetiology of gastric cancer is multifactorial, but H. pylori is 

an important factor for distal but not proximal gastric cancer

Early gastric cancer is associated with very high cure rates

Gastric cancer can be classified into intestinal and diffuse types, 

the latter having a worse prognosis


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In the West, proximal gastric cancer is now more 

common than distal cancer and is usually of the 

diffuse type

Spread may be by lymphatics, blood, transcoelomic or 

direct, but distant metastases are uncommon in the 

absence of lymph node involvement

The treatment of curable cases is by radical surgery 

and removal of the second tier of nodes (around the 

principal arterial trunks) may be advantageous

Gastric cancer is chemosensitive and chemotherapy 

improves survival in patients having surgery for the 

condition and in advanced disease


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50 per cent will be found in the Stomach

tumours of mesenchymal origin and are observed equally 

in males and females

mutation in the tyrosine kinase c-kit oncogene.

sensitive to the tyrosine kinase antagonist imatinib, an 80 

per cent objective response rate

size and mitotic figures index are the best predictors of 

metastasis.


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GIST comprise 1–3 per cent of all gastrointestinal neoplasia.

The only ways that many stromal tumours are recognised

are either that the mucosa overlying the tumour ulcerates  leading to bleeding, 

or that they are noticed incidentally

at endoscopy.

Targeted biopsy by endoscopic ultrasound is more helpful

Tumours over 5 cm in diameter should be considered to have metastatic 

potential.

surgery is the primary mode of treatment

lymphadenectomy is not required

The prognosis of advanced metastatic GIST has been dramatically improved 

with imatinib chemotherapy but resection of metastases, especially from 

the liver, still has an important role


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It is first important to distinguish primary gastric 

lymphoma from involvement of the stomach in a 

generalised lymphomatous process

incidence of lymphoma increasing
accounts for approximately 5 per cent of all gastric 

Neoplasms

Common in 6

th

decade

pain, weight loss and bleeding
Acute presentations(

POUB

)

obstruction, are not common


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B cell derived

the tumour arising from the mucosa-associated lymphoid 

tissue (MALT)

Diffuse mucosal thickening, which may ulcerate

Diagnosis is made as a result of the endoscopic biopsy

CT scans of the chest 

abdomen and bone marrow aspirate are required, full

blood count

early gastric lymphomas may regress and disappear when 

the Helicobacter infection is treated.

Treatment: surgery although some prefer chemoRx??


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Benign : villous adenoma(FAP), periampullary area and 

premalignant
Doudenal adenocarcinoma: uncommon, ass. With FAP
most common site for adenocarcinoma arising in the 

small bowel.
anaemia due to ulceration of the tumour or obstruction 

as the polypoid neoplasm begins to obstruct the 

duodenum.
obstructive jaundice
70 per cent of the patients have resectable disease

The five-year survival rate is in the region of 20 per 

cent
Curative surgical treatment(Whiplle procedure)


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Found in doudenum and head of pancreas
It is a cause of persistent peptic ulceration
sporadic or associated with the autosomal dominantly 

inherited multiple endocrine neoplasia (MEN) type I
PASSARO triangle
Dx: 
Fasting serum gastrin
In case of moderate hypergastrinemia, a secretin

stimulation test can help in the diagnosis
Localization by somatostatin scintigraphy(octeriotide

scan)
Rx : PPI and surgery


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Doudenal causes

Pancreatic causes

Superior mesentric artery syndrome

Metastasis from colorectal and gastric CA


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Rotation of the stomach usually occurs around the axis 

and between its two fixed points: cardia& pylorus
horizontal (organoaxial)common
vertical (mesenteroaxial) direction
Associated with a large diaphragmatic defect
(paraoesophageal herniation)
The condition is commonly chronic,
the patient presenting with difficulty in eating
Ischemia when acutely presented
contrast radiograph is superior to endoscopy in Dx


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Diphragmatic defect repair with mesh

Seperation of stomach from tansverse colon

Anterior gastopexy




رفعت المحاضرة من قبل: Ahmed 95
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