GIT pdf - حسن سالم

Lec 4 GIT Dr.Hassan aljumaily
Oral cancer
CA esophagus
CA stomach &lymphoma
Colonic Polyps ,FAP& CA
colon

Oral cancer

Squamous carcinoma is common . The mortality rate is 50%.

risk factors:

1-Poor diet

2-alcohol excess

3-smoking or tobacco chewing

4-papillomavirus (HPV-16 and HPV-18) -- base of tongue, soft

palate and tonsils.

Oral cancer may present in many ways :

• Solitary ulcer

• Solitary white patch (‘leukoplakia’)

• Solitary red patch

• Fixed lump

• Lip numbness

• Trismus

• Cervical lymphadenopathy.

Rx: Sx. Some patients need radical radiotherapy alone.

Carcinoma of the oesophagus

aetiological factors
•

Smoking

• Alcohol excess
• Chewing betel nuts or tobacco
• Achalasia ,

Barrett

• Coeliac disease
• Post-cricoid web
• Post-caustic stricture
• Tylosis

almost all tumours in the upper oesophagus are
squamous cancers. Adenocarcinomas typically arise
in the lower third of the oesophagus from Barrett’s
oesophagus. 5-year survival =13%.

Clinical features:

- dysphagia.

-In late stages, weight loss

-chest pain or hoarseness suggests mediastinal invasion.

- Fistulation between the oesophagus and the trachea--

coughing after swallowing.

- Physical signs may be absent or , cachexia, cervical LAP

Investigations

-OGD with biopsy.

-A barium swallow

-Thoracic and abdominal CT& PET--for metastatic spread and

local invasion.

- EUS : to determine the depth of penetration of the tumour

into the oesophageal.

These investigations will deﬁne the TNM stage of the disease .

Management

1-Sx

- Overall survival =30% at 5 years, but this

can be improved by neoadjuvant

chemotherapy.

2- squamous carcinomas are

radiosensitive

, radiotherapy alone is

associated with a 5-year survival of only

5%, but

combined chemoradiotherapy

achieve 5-year survival rates of 25–30%.

3- 70% of patients have

extensive

disease

--treatment is palliative

Gastric carcinoma
-fourth leading cause of cancer death.
-

50%

lower in women. In both sexes, it rises

sharply after 50 years of age. The overall
prognosis is poor, with

less than 30%

surviving 5 years,.

Pathophysiology

-Infection with

H. pylori

contribute to gastric

cancer in 60–70% of cases .
-

Diets

rich in salted, smoked foods and the

consumption of nitrites and nitrates may
increase cancer risk. Diets lacking fresh fruit
and vegetables, as well as vitamins C and A,
may also contribute

risk factors

•

H. pylori

• Smoking

• Alcohol

• Dietary associations

• Autoimmune gastritis (pernicious

anaemia)

• Adenomatous gastric polyps

• Previous partial gastrectomy (> 20 yrs)

• Hereditary diffuse gastric cancer
• FAP

cancer risk 2-3 fold in ﬁrst-degree relatives of

patients, and links with blood group A

. Rarely,

gastric cancer may be inherited in an

manner

in association with mutations of the

E-cadherin

(

CDH1

) gene.

-Virtually all tumours are adenocarcinomas.
-Cancers are either ‘intestinal’, arising from areas
of intestinal metaplasia with histological features
of intestinal epithelium, or ‘diffuse’, arising from
normal gastric tissue.
Diffuse submucosal inﬁltration by a scirrhous
cancer (

linitis plastica

) is uncommon.

Napoleon Bonaparte

Clinical features

asymptomatic

but may be discovered during

endoscopy for investigation of dyspepsia.
-2/3 with advanced cancers have

weight loss

and 50% have

ulcer-like pain

Anorexia and nausea

occur in 1/3

early satiety, haematemesis, melaena and

dyspepsia

alone are less common.

Dysphagia

occurs in tumours of the gastric

cardia which obstruct the gastro-oesophageal
junction.
-

Anaemia

from occult bleeding is also

common.

Examination:
- weight loss, anaemia and epigastric mass .
Jaundice or ascites signify metastatic spread.
-
-supraclavicular lymph nodes

(Troisier’s sign

at umbilicus (

Sister Joseph’s nodule

) or

metastasis to ovaries (

Krukenberg tumour

-Paraneoplastic phenomena, such as

acanthosis nigricans,thrombophlebitis
(Trousseau’s sign).

Metastases arise most commonly in the liver,

lungs, peritoneum and bone marrow.

Investigations

OGD

is the investigation of choice

‘alarm features’:
•

Weight loss

• Anaemia
• Vomiting
• Haematemesis and/or melaena
• Dysphagia
• Palpable abdominal mass

2-Barium meal

is a poor alternative .

3-CT

is necessary for staging & resectability.

4-laparoscopy

-detect peritoneal spread.

Management

Surgery

- cure, and this can be achieved in about

90%

patients with early gastric cancer.
-

Proximal tumours

involving the oesophago-gastric

junction also require a distal oesophagectomy.
-

Small, distally sited tumours

can be managed by a

partial gastrectomy with lymphadenectomy .
- complete removal of all macroscopic tumour
combined with lymphadenectomy will achieve a
50–60% 5-year survival.

Recent evidence suggests that perioperative
chemotherapy with epirubicin, cisplatin and ﬂuorouracil
ECF) improves survival rates.

Gastric lymphoma
-less than

% of all gastric malignancies.

60%

of all primary gastrointestinal

lymphomas
-

H. pylori

infection is closely associated with

the development of a lowgrade lymphoma

Invex

: EUS ,OGD=ulcerating mass.

While initial treatment of low-grade lesions
conﬁned to the superﬁcial layers of the gastric
wall consists of

H. pylori

eradication

and close

observation, 25%

contain t(11 : 18)

chromosomal translocations

. In these cases,

additional radiotherapy or chemotherapy is
usually necessary.

Colonic Polyps

Polyps may be neoplastic or non-neoplastic. The latter include

hamartomas, metaplastic (‘hyperplastic’) polyps and

inﬂammatory polyps. These have no malignant potential.

. Colorectal adenomas prevalence rises with age; 50% of

people over 60 years of age have adenomas. They are more

common in the rectum and distal colon .

all forms of colorectal carcinoma develop from adenomatous

polyps. Features associated with a higher risk of malignancy

are :

•

Large size (> 2 cm)

• Multiple polyps

• Villous architecture

• Dysplasia

Adenomas are usually asymptomatic and discovered

incidentally ,Or bleeding and anaemia. ..

Once all polyps have

been removed, surveillance colonoscopy should be

undertaken at 3–5-year intervals, as new polyps develop in

50% of patients.

Familial adenomatous polyposis

- AD disorder

→1% of all colorectal cancers.

germline mutation of the tumour suppressor

APC

gene.

20%

of cases

→ have no family history.

-cancer will develop within

10–15 years

of the

appearance of adenomas and

90% of

patients will

develop colorectal cancer by the age of 50 years.

Despite surveillance, 25% with FAP have cancer by the

time they undergo colectomy.

Other polyps

in the stomach.

Duodenal adenomas

occur

in over 90% and are most common around the ampulla of

Vater.

Malignant transformation to adenocarcinoma

occurs in 10% and is the leading cause of death in those

who have had prophylactic colectomy

sometimes respond to hormonal therapy with

tamoxifen, and the NSAID sulindac may lead to
regression in some, by unknown mechanisms.

members should undergo mutation testing at

13–14 years of age and patients who are found
to have the mutation should be offered
colectomy after school or college education
has been completed. The operation of choice is
total proctocolectomy with ileal pouch–anal
anastomosis

Periodic OGD every 1–3 years to detect
duodenal and periampullary adenomas

Colorectal cancer

common over the age of 50 years.

Pathophysiology

environmental and genetic & dietary factors

other:

Medical conditions

• Colorectal adenoma

• UC or Crohn’s colitis

• Ureterosigmoidostomy

• Acromegaly

• Pelvic radiotherapy

Others

•

Obesity and sedentary lifestyle – may be related to diet

• Smoking

• Alcohol (weak association)

• Cholecystectomy (effect of bile acids in right colon)

• Type 2 DM (hyperinsulinaemia)

• Use of aspirin or NSAIDs and statins associated with

reduced

risk

About 5–10% of colon cancers are

caused by

hereditary non-polyposis

colon cancer

(HNPCC). AD , positive

family history of colon cancer occurring

at a young age.

Most tumors arise from malignant

transformation of a benign

adenomatous polyp

. 65%

→rectosigmoid ,

15%

→caecum or ascending colon.

Clinical features

-In left colon

, fresh rectal bleeding &obstruction.

In right colon

anaemia from occult bleeding or with

altered bowel habit, but obstruction is a late feature.

Colicky lower abdominal pain

is present in 2/3 of

patients and

rectal bleeding occurs in 50%

. Carcinoma of the rectum usually causes early
bleeding, mucus discharge or a feeling of incomplete
emptying.

Between 10 and 20% of patients present

with iron deﬁciency anaemia or weight loss.

On examination, there may be a palpable mass, signs
of anaemia or hepatomegaly from metastases. Low
rectal tumours may be palpable on digital examination

Investigations

Colonoscopy

is sensitive and speciﬁc

than

barium enema

2- Patients in whom colonoscopy is

incomplete and those who are at high

risk of complications

→

CT colonography

This is a sensitive and non-invasive

technique for diagnosing tumours and

polyps of more than 6 mm diameter.

CEA.

Surgery:

1-locally advanced rectal cancer should be
offered neoadjuvant radiotherapy or
chemoradiotherapy to increase the
subsequent chance of a complete surgical
resection

2-Carcinomas within 2 cm of the anal verge
may require abdominoperineal resection and
formation of a colostomy

3-Post-operatively, patients should undergo
colonoscopy after 6–12 months and then at 5
years to search for local recurrence or
development of new lesions, which occur in
6% of cases..

Prevention and screening :

Secondary

prevention aims to detect and remove lesions
at an early or pre-malignant stage.
1• people over the age of 50 years screened by
regular

faecal occult blood (FOB)

testing

reduces colorectal cancer mortality
2•

Colonoscopy

remains the gold standard but

is expensive and carries risks.
3•

Flexible sigmoidoscopy

is an alternative

option and has been shown to reduce overall
colorectal cancer mortality by approximately
35% .