Description of different types of git tumors

2. GIT tumors
(1)
By
Ahmed Mohammed Mady
MD, internal medicine
Faculty of medicine- Minia University

3. GIT Tumors (Benign, Premalignant &
Malignant lesions)
Esophageal
Gastric
Small intestinal
Colorectal
Functional. NET

4. ITEMS of 1st lecture
Remember gut layers
Aim
General scheme for malignant lesions
General rules for non-malignant lesions
ESOPHAGUS
STOMACH
GEP-NET

5. ITEMS of 1st lecture
Remember gut layers
Aim
General scheme for malignant lesions
General rules for non-malignant lesions
ESOPHAGUS
STOMACH
GEP-NET

6.  Remember gut layers:
 Mucosa; epithelial coverage,
lamina propria: CT supporting
epithelium, contain mucosal
glands(crypts), lymphoid and plasma cells,
enterochromaffin cells
muscularis mucosa
 Submucosa: larger blood, lymph
vessels, nerves, mucus secreting glands
 Muscularis propria: inner circular, outer
longitudinal
 Adventitia

7.  Remember gut layers:
 Mucosa; epithelial coverage,
lamina propria: CT supporting
epithelium, contain mucosal
glands(crypts), lymphoid and plasma cells,
enterochromaffin cells
muscularis mucosa
 Submucosa: larger blood, lymph
vessels, nerves, mucus secreting glands
 Muscularis propria: inner circular, outer
longitudinal
 Adventitia

9.  Aim:
 To raise the ability of linking GIT
symptoms to GIT tumors, for enhancing
early detection
 To Identify screening programs for GIT
tumors

10.  General Scheme for Malignant
tumors:
 Incidence, prognosis.
 Risk factors (genetic, diet, environmental,
premalignant lesion, other diseases).
 Screening & surveillance
 Clinical presentation ( local obstructing
symptom, bleeding" O;; O" , Functional ,
pain),,,,,,,,,,,( Mets, anorexia , weight
loss).
 Diagnosis: imaging, Endoscopic,
Histopathology, lab " CBC, Iron, Occult
blood, others), Staging.

11.  General rules for benign and
premalignant lesions:
 Terms:
 Polyp: any abnormal growth projecting from
mucus membrane into lumen; inflammatory,
hyperplastic, adenomatous, hamartoma, ……
 They could arise either from: epithelial
(glandular), or subepithelial origin; lamina propria,
or muscularis propria
 Mass: usually solitary and large, never
pedunculated
 Malignant potentiality is related to:
-Pathology: adenoma, hyperplastic, carcinoid,
hamartoma
-Size
-Sporadic or familial

12.  General rules for benign and
premalignant lesions:
 NB. Adenoma means: glandular
epithelial benign tumor with cells
hyperchromatic (dense pigmented) dt
excess mitosis and mucin, with degree of
dysplasia, arranged either in tubular,
villous or tubulovillous manner
 Hyperplastic means: hyperplastic
NORMAL glands, same pigmentation as
surrounding mucosa
 Hamartoma: branching smooth muscle
traversing lamina propria

13.  General rules for benign and
premalignant lesions:
 NB.2. NET: arise from Enterochromaffin
cells-which secrete serotonin &other
peptides- within the lamina propria
 NB.3. GIST: arise from interstitial cells of
kajal within the muscularis propria

14.  ESOPHAGUS
 Intestinal metaplasia (Barret
esophagus)
 Carcinoma

15.  ESOPHAGUS: Barret
esophagus
 A premalignant lesion (intestinal
metaplasia), usually complicate severe
reflux, 10% of GERD patients has BE on
endoscopy.
Associated with 30 -50 fold increase of
adenocarcinoma.
 Clinical presentation: long standing
heart burn.
 Screening: some reported improved
outcomes with screening, but till now NO
routine screening is recommended for

16.  ESOPHAGUS: Barret
esophagus
 Diagnostic investigations:
-Upper endoscopy: salmon pink mucosa at lower
esophagus.
-Biopsy:
confirm metaplasia (mucin secreting goblet cells)
determine if it progressed to dysplasia, as BE pass in
stepwise fashion from no to low to high grade dysplasia
to adenocarcinoma.
 Treatment:
 PPI use is proposed to decrease progression
 Surveillance according grade of dysplasia:
 NO ----- 1year then 3 years
 LOW------ every 6 months
 HIGH------ endoscopic ablation

17. BARRET’s esophagus

18.  ESOPHAGUS: Carcinoma
 Squamous (upper, mid esophageal) ,
Adenocarcinoma (lower, Now increasing
incidence).
When symptomatic, carry poor prognosis. 20% 5-
year survival
 Risk factors:
 For squamous; environmental?; smoking,
alcohol, corrosive, Achalasia, esophageal web-
plummer vinson S.
 For adeno; diseases?; smoking, Barret, GERD,
obesity.
 Clinical presentation:
-Asymptomatic, later symptomatic by:
-Dysphagia to solid then fluid

19.  ESOPHAGUS: Carcinoma
 Diagnostic investigations:
Imaging: barium swallow (filling defect,
irregular narrowing), CT neck and chest
with oral and contrast (staging)
Endoscopy: locate the tumor, biopsy for
histopathological diagnosis, Endoscopic
ultrasound; help for staging
 Treatment:
-Surgical, but 10% mortality
-Radiotherapy, chemotherapy alone or with
surgery
-Palliative stenting.

20. Esophageal carcinoma

21. Stomach
 Polyps & masses
 Gastric adenocarcinoma

22. Stomach (Polyps & masses)
POLYPS: most asymptomatic, Incidental finding
in 2 % of upper endoscopies may bleeding "O, O"
Adenomatous polyp:
-Single, located at antrum, > 1 cm
-When > 2 cm---- 70% malignant transformation.
Fundic gland polyps:
 Multiple, located at fundus, < 1 cm
 When familial----- 40% malignant transformation,
when sporadic—NO risk for malignancy.
Hyperplastic polyp:
*Single or multiple, variable in size.
*3% malignant transformation.

23. Stomach (Polyps & masses)
MASSES: GIST, carcinoid (discussed later, NET,,,,,,,,)
 GIST (Gastro Intestinal Stromal Tumor)
Arise from interstitial cells of kajal within muscularis
propria
Potentially malignant to small cell carcinoma
Clinical presentation: 50- 70 years.
-Dyspepsia (epigastric pain, discomfort related to meals
or early satiety)
-Bleeding (IF ULCERATED); overt = hematemesis,
occult = IDA
Diagnostic investigation:
 Endoscopy, subepithlial mass about 5 cm, EUS : 4 th
layer,
 Histopathology: spindle cell tumor, confirmed by
immunohistochemistry

24. Gastric GIST

25. Stomach: ADENOCARCINOMA
 Represent 90% of gastric cancers, more prevalent at
eastern Asia, men have twofold increased risk
2 types: intestinal type: common, older age;;;;
Diffuse type: younger age, poor prognosis
5-year survival: 25%
 Risk factors:
 Diet: spicy food, less fibers,
 Premalignant lesions: adenoma, fundic gland,
carcinoid
 Diseases: H. pylori, autoimmune gastritis
 Genetic: no specific single gene mutation
 Screening: NO recommended routine screening
 Surveillance:
after adenomatous polypectomy: 1, 3 & 5 years

26. Stomach: ADENOCARCINOMA
 Clinical presentation:
-Early: Dyspepsia (upper abdominal pain or
discomfort after meal, early satiety)
ANY DYSPEPSIA WITH ONSET > 55 YRs IS
ALARMING, other alarming: persistent
vomiting, WT loss, bleeding "O, O"
-Late: vomiting, bleeding, anorexia, wt loss,
metastatic (Virchow), mass
 Diagnostic investigations:
Upper endoscopy, histopathology, CBC ,Iron
st.
CT abdomen with contrast, PET scan for
staging

27. NET. (GEP-NET)
Neoplasms arise from cells of endocrinal
and nervous system.
They Most commonly arise from GUT, the
most common is CARCINOD
May arise from any part of body, pancreas,
lung, adrenal medulla, thyroid
Here, we will discuss Gastro entero
pancreatic NET (GEP-NET).

28. GEP-NET: CARCINOID:
 Although the most common of NET,
 it is a rare tumor arise from any part of
gut commonly appendix, then terminal
ileum, duodenum or stomach
 Arise from enterochromaffin cells within
lamina propria, and secrete serotonin
which metabolized into 5 hydroxy indole
acetic acid (5-HIAA), also may secrete
histamine & ACTH.

29. GEP-NET: CARCINOID:
 Clinical presentation:
*Local effect (obstruction, intussusception,
Gastric; dyspepsia, vomiting)
*The secreted serotonin & histamine will by
metabolized in liver, producing NO effect.
*When liver metastasis occur, unmetabolized
serotonin will reach systemic circulation (IVC),
producing clinically CARCINOID SYNDROME:
Flushing
Bronchospasm
Increased gut motility leading to diarrhea
Right valvular stenosis

30. GEP-NET: CARCINOID:
 Diagnostic investigations:
CT abdomen with contrast; locate lesion, liver
mets.
Upper, lower endoscopy (according clinical
presentation)
Histopathology
Urinary 5-HIAA
 TTT:
Surgical resection
Octreotide for diarrhea
Resection or embolization for hepatic Mets.

31. Pancreatic NET (Islet cell tumors)
-Arise from pancreatic endocrinal tissue,
commonly within pancreas leading to
hormonal hypersecretion.
-Mostly occur sporadic or as apart of MEN
-May arise from any part of GUT, and many of
them are nonfunctioning
They are:
Gastrinoma: the most common , excess
gastrin stimulate acid secretion from parietal
cells
Insulinoma: least to metastasize, secrete
insulin
VIPoma: secrete vasoactive intestinal

32. Pancreatic NET (Islet cell tumors)
 Clinical presentation:
Gastrinoma: excess gastrin, acid. Peptic
ulcers at unusual sites as esophagus, 2nd
part duodenal, diarrhea (Zollinger Ellison
S)
Insulinoma: fasting hypoglycemia
(irritability, confusion, drowsiness)
VIPoma: watery diarrhea, hypokalemia,
hypochlorhydria
Glucagonoma: diabetes, dermatitis

33. Pancreatic NET (Islet cell tumors)
 Diagnostic investigations:
-MRI abdomen
-EUS (gold standard)
-Octreotide scanning, except insulinoma
don’t express somatostatin receptors, 90%
diagnosed by EUS
-Laboratory: Gastrin level, serum VIP,
Insulin, glucagon
 TTT: surgical excision, acid suppression
in gastrinoma, octreotide to control
diarrhea.

34. Thank you