Ходоодны хавдрын талаар оюутан байхад хийж байсан ppt

1. АУС-ийн 402-р хэсгийн оюутан
Х.Балдандорж
Улаанбаатар хот 2019 он
Ходоодны хавдар

2. Agenda
• Ходоодны морфологи
• Хавдрын ангилал
• Ходоодны хавдрын ангилал
• Ходоодны хоргүй хавдар
• Ходоодны хортой хавдар
• Төрөл
• Adenocarcinoma
– Intestinal type
– Архаг архаг ходоодны үрэвсэл
• Шалтгаан, эмгэг жам(adenocarcinoma)
• Үүсгэгч
– Diffuse type
– Эмнэлзүйн илрэл
– Оношилгоо
– эмчилгээ
• Эмнэлзүйн илрэл
• Оношилгоо
• Урьдчилан сэргийлэлт
• Эмчилгээ
• Ном зүй

3. • Анатом
• Гистологи бүтэц ?
Ходоодны морфологи

4. Ходоодны морфологи

31. • Гистологийн бүтэц ?
• Ходоодны өөрийн бие даасан
мэдрэлжүүлэлтийн талаар дурдна уу

32. Гистологийн бүтэцийн хувьд

57. Хавдрын ангилал
• Nomenclature
– A. Benign tumors
– B. Malignant tumors (cancer)

58. 1. Тодорхойлолт
• A. Benign tumors
Unregulated proliferation
of cells that does not
invade or spread to other
sites
• B. Malignant tumors
(cancer)
Unregulated proliferation
of cells that invade and
are able to spread to
other sites

59. 2. Suffix
A. Benign tumors
• “-oma” generally indicates a
benign tumor.
 seminomas (testicular
cancer),
 lymphoma (malignancy of
lymph nodes),
 glioma (malignancy of glial
cells in the brain),
 mesothelioma (malignancy
of pleural serosa),
 neuroblastoma (malignancy
of neuroblasts).
B.Carcinomas
a. Derive from epithelial
tissue
b. Sites for squamous cell
carcinoma
c. Sites for adenocarcinoma
• Sarcomas
a. Derive from connective
tissue

60. 3. Unusual tumors that are usually
benign
• A. Benign tumors
• a. Mixed tumors
• b. Teratomas
B.Carcinomas

61. 4. Ялгаран хөгжил
A. Benign tumors
• Definition—usually well
differentiated (resemble
parent tissue)
B.Carcinomas
a. Well-differentiated or
low grade cancer
b. Poorly differentiated,
high grade, or
anaplastic
c. Intermediate grade

62. 5. Эсийн эрхтэнцэр
A. Benign tumors B.Carcinomas
• a. Fewer mitochondria
• b. Less prominent rough
endoplasmic reticulum
(RER)
• c. Loss of cell-to-cell
adhesion molecules
(cadherins

63. 6. Бөөмийн онцлог
A. Benign tumors B.Carcinomas
• a. Nucleus is larger, has
irregular borders, and has
more chromatin
(hyperchromatic)
• b. Nucleolus is larger and
has irregular borders
• c. Mitoses have normal
and atypical mitotic
spindles

64. 7. Ургалтын онцлог
A. Benign tumors
• Benign tumors usually
have a slow growth
rate.
B.Carcinomas
• Malignant tumors have
a variable growth rate.
• Growth rate correlates
with degree of
differentiation of the
malignant tumor.

65. 8. Эсийн гарал
• Benign and most malignant tumors derive
from a single precursor cell.

66. 9.Telomerase activity in benign and
malignant tumors

67. • A. Benign tumors
normal telomerase
activity.
• B.Carcinomas
upregulation of
telomerase activity, which
prevents the naturally
programmed shortening
of telomere complexes
with cell replication;
hence the cell no longer
undergoes apoptosis.
9.Telomerase activity in benign and
malignant tumors

68. 11.Upregulation of decay accelerating
factor (DAF) by malignant cells

69. 12. Local invasion and metastasis
• Do not invade
• Usually enclosed by a
fibrous tissue capsule
a. Invade tissue
• Second most important
criterion for malignancy
b. Some tissues resist
invasion.
• Examples—mature cartilage,
elastic tissue of arteries
c. All malignant tumors require
O2 and nutrients to survive
and do so by stimulating
angiogenesis within the tumor
and its metastatic sites

70. Malignant tumor
1.Судасжилтын механизм

71. Malignant tumor
1. Angiogenesis, or new blood vessel formation
-endothelial precursor cells (EPCs) ясны чөмөгнөөс
ирнэ
-(preexisting capillaries)
2. (TNF)=(TNF)
3. Chemotactic factors
4. angiostatin, endostatin буурна
5. EPCs улам судасжилт (Хавдрын бай эмчилгээ !!!)

72. • 2. Clonal proliferation of cells that develops
the capacity to invade and metastasize.
• Бүх хавдрын эс invade хийж чадахгүй!!!!

73. • 3. lose their cell-to-cell adhesion
• molecules (cadherins)

74. 4. cell
• receptors to attach to laminin
• release metalloproteinases (collagenases,
stromelysins, gelatinases)
• degrade the interstitial connective tissue.
• Tissue inhibitors of metalloproteinases
neutralize these tumor-produced enzymes
and limit the degree of invasion.

75. 5. extracellular matrix (ECM) and to break it
down.
ECM задрана

76. 6. Өөрсдийн хөдөлгөөнийг хангах цитокин
ялгаруулна.

77. • 7. called intravasation гэдэг процесоор
микроциркуляц руу ордог.

78. • 8. хавдрын эсийн эмболи (covered by fibrin)
Дархлаанаас зайлсхийх механизм гэж юу вэ?

79. • 9. target organ дээрээ очоод саяны 1-6 ийн
хооронд дурдсан механизмаар дахин өсч
олшрон үсэрхийлэл үүсгэнэ.
• Batson paravertebral plexus рүү очвол
тэндээс өвөрмөц цитокин хемокин ялгарч
тэр зүг рүү үсэрхийлэл өгнө.
• target organ-с ялгарсан хемокиноор нь тэнд
нь очиж үсэрхийлнэ

80. • BCC хортой хавдар мөртлөөнө үсэрхийлэл
өгдөггүй

81. Pathways of dissemination
a. Lymphatic spread of cancer
b. Hematogenous spread of cancer

82. Ходоодны хавдар
GASTRIC NEOPLASM

83. GASTRIC NEOPLASM
Epithelial
Mesenchymal
1.Primary
Adenocarcinoma
Gastrointestinal stromal tumors
‘GIST’
Lymphoma
2. Secondary:
invasion from adjacent tumors.
Benign Malignant

84. Ходоодны хоргүй хавдар
Leiomyoma
a. Stomach is most common site
b. May ulcerate or bleed

85. •Ходоодны хортой
хавдар

86. GASTRIC NEOPLASM
Epithelial
Mesenchymal
1.Primary
1. Adenocarcinoma
2. Gastrointestinal stromal
tumors ‘GIST’
3. Lymphoma
4. Primary gastric malignant
lymphoma
2. Secondary:
invasion from adjacent tumors.
Benign Malignant

88. Gastrointestinal Stromal Tumor
‘GIST’
Previously leiomyoma & leomyosarcoma.
<1 %
Rarly cause bleeding or obstruction.
The origion: Intestinal Cells of Cajal ‘ICC;s’
autonomic nervous system.
The distinction bw benign & malignant is
unclear. In general terms, the larger the
tumor & greater mitotic activity, the more
likely to metastases.
The stomach is the most common site of
GIST.

89. Usually are discovered incidentally on
endoscopy or barium meal
The endoscopic biopsies may be
uninformative bcz the overlying mucosa is
usually normal
Small tumorswedge resection
Larger onesgastrectomy

91. Gastric Lymphoma
Most common primary GI Lymphoma .
It’s increasing in frequency.
Presentation:
Similar to gastric carcinoma.
May reveal peripheral adenopathy,
abdominal mass or spleenomegaly.

92. Diagnosis:
1.EGD 2.contrast GI x-ray.
3.CT guided fine needle biopsy.
Treatment :
1. surgery: total or subtotal gastrectomy with
spleenectomy or palliative resection.
2.Adjunct radiotherapy: may improve 5 year
survival
3.Adjunct Chemotherapy: may prevent
recurrance.

93. •Primary gastric
malignant lymphoma

94. Primary gastric malignant lymphoma
• a. Stomach is the most common site for
extranodal malignant lymphoma.
• b. Low-grade B-cell lymphoma
– (1) Related to H. pylori
– (2) MALToma (derives from mucosa-associated
lymphoid tissue)
• c. High-grade B- or T-cell lymphomas
• d. 50% cure rate if H. pylori treated

96. Phatophysiology
• H.pylori
• Chronic gastritis

97. H.pylori
• (1) Most common cause is H. pylori
– • Gram-negative, curved rod
• (2) Present in 30% to 50% of the population in
the United States
• (3) Prevalence increases with age
• (4) Transmitted by fecal-oral (organism passed in
stools and can live in water)/
– oral-oral route
– • Common in areas of poor sanitation

98. Pathophysiology
• a. Involves the antrum and pylorus
• (1) Gram-negative, curved rod
• (2) Produces urease, proteases, cytotoxins
– (a) Urease converts amino groups in proteins to
ammonia
– (b) Secretion products produce chronic gastritis and
PUD.
• (3) Colonizes mucus layer lining
• (a) Attaches to blood group O receptors on
mucosal cells

99. Microscopic findings
• (1) Chronic inflammatory infiltrate in the
lamina propria
• (2) Intestinal metaplasia (similar to picture for
Barrett esophagus)
• • Precursor lesion for adenocarcinoma

100. Tests to identify H. pylori are highly
sensitive and specific.
• (1) Urea breath test
– (a) Documents active infection
– (b) Sensitivity and specificity >90%
• (2) Stool antigen test (excellent screen; cheaper than
urea breath test)
– (a) Positive when there is active infection
– (b) Negative when infection has been eradicated
– (c) Sensitivity and specificity >90%
• (3) Tests to detect urease in a gastric biopsy
– • Considered to be the gold standard test albeit an invasive
test
• (4) Serologic tests have been discontinued.

101. Хүндрэлээр нь
Other disease associations with H. pylori
• (1) Duodenal and gastric ulcers (see later)
• (2) Gastric adenocarcinoma (see later)
• (3) Low-grade B-cell mucosa-associated
lymphoid tissue lymphoma

104. Chronic atrophic gastritis
1. Type A chronic atrophic gastritis
2. Type B chronic atrophic gastritis

105. Type A chronic atrophic gastritis
• a. Involves the body and fundus
• b. Most often due to pernicious anemia (PA;
refer to Chapter 12)
• c. Complications
– (1) Achlorhydria with hypergastrinemia (loss of
negative feedback)
– (2) Macrocytic anemia due to vitamin B12
deficiency
– (3) Increased risk for gastric adenocarcinoma

106. Type B chronic atrophic gastritis
• a. Involves the antrum and pylorus
• b. Epidemiology
– (1) Most common cause is H. pylori
• • Gram-negative, curved rod
– (2) Present in 30% to 50% of the population in the
United States
– (3) Prevalence increases with age
– (4) Transmitted by fecal-oral (organism passed in
stools and can live in water)/
• oral-oral route
• • Common in areas of poor sanitation

107. 3. Ménétrier disease (hypertrophic
gastropathy)
• a. Giant rugal folds
– (1) Due to hyperplasia of mucus-secreting cells
– (2) Causes hypoproteinemia (protein-losing
enteropathy)
• b. Atrophy of parietal cells (achlorhydria)
• • Increased risk for adenocarcinoma

108. Adenocarcinoma

110. Gastric Carcinoma
55 year old Japanese male who is living in Japan
& working in industry.
DEFINITION Malignant lesion of the stomach.
Epidemiology & Risk Factors
Can occur at any age
But Peak incidece
Is 50-70 years old.
It is more aggressive
In younger ages.
Japan has the world
highest Rate of
gastric cancer.
Studies have confirmed
that incidence decline in
Japanese immigrant to
America.
dust ingestion
from a variety
of industrial
processes
may be a risk.
Twise more common
In male than in female
Incidence of Gastric Carcinoma:
Japan 70 in100,000/year
Europe 40 in 100,000/year
UK 15 in 100,000/year
USA 10 in 100,000/year
It is decreasing worldwide.

111. Epidemiology
• 1) Decreasing incidence in United States
• (2) Increasing incidence in mongolia& japan
(smoked foods)
• (3) Increased incidence in blood group A
people

112. Adenocarcinoma-ийн төрлүүд
• Intestinal type of gastric adenocarcinoma
• Diffuse type of gastric adenocarcinoma

113. Intestinal type of gastric
adenocarcinoma
• (1) Most common gastric carcinoma
• (2) Risk factors
– (a) Intestinal metaplasia due to H. pylori (type B; most
important)
– (b) Nitrosamines
– (c) Smoked foods (Japan)
– (d) Diets lacking fruits/vegetables
– (e) Type A chronic atrophic gastritis (PA)
– (f) Ménétrier disease
• (3) Polypoid or ulcerated (Fig. 18-15A)
• (4) Locations
– (a) Lesser curvature of pylorus and antrum (50%–60% of cases)
– (b) Cardia (25% of cases), body and fundus

115. Diffuse type of gastric adenocarcinoma
• (1) Incidence has remained unchanged.
• (2) Not associated with H. pylori
• (3) Diffuse infiltration of malignant cells in the
stomach wall
– (a) It is sometimes called linitis plastica.
– (b) Stomach does not have peristalsis.
– (c) Signet ring cells infiltrate the stomach wall (see Fig.
18-15C).
– (d) It produces Krukenberg tumors of the ovaries.
• • Signet ring cells spread hematogenously to both
ovaries.

116. Gastric Carcinoma:
Risk Factors
Predisposing :
1. Pernicious anemia
& atrophic gastritis
(achlorhydra)
2. Previous gastric
resection
3. Chronic peptic ulcer
(give rise to 1%)
4. Smoking.
5. Alcohol.
Environmental:
1.H.pylori infection
Sero(+)patients
have 6-9 folds risk
2.low
socioeconomic
Status
3. Nationality
(JAPAN)
4. Diet (prevention)
Genetic:
1.Blood group A
2.HNPCC:
Heriditory non-
polyposis colon
cancer.

117. Clinical Presentation
Most patients present with advanced stage..
why?
They are often asymptomatic in early stages.
Common clinical Presentation:
The patient complained of loss of appetite that was
followed by weight loss of 10Kg in 4 weeks.
He had notice
epigastric discomfort & postprandial fullness.
He presented to the ER complaining of vomiting of
large quantities of undigested food & epigastric
distension.
Dyspepsia
epigastric pain
Bloating
early satiety
nausea & vomiting*
dysphagia*
anorexia
weight loss
upper GI bleeding
(hematemesis, melena,
iron deficiency anemia)

118. signs
-Anemia.
-Wt.loss ( cachexia)
-Epigastric mass,Hepatomegaly,Ascitis
-Jaundice.
-Blumers shelf
-Virchows node
-Sister mary joseph node
-Krukenberg tumor
-Irish node

119. Clinical findings
• (1) Cachexia and weight loss (most common; 60% of
cases)
• (2) Epigastric pain (50% of cases)
• (3) Vomiting, often with melena (20% of cases)
• (4) Metastasis to left supraclavicular node (Virchow
node)
• (5) Paraneoplastic skin lesions (refer to Chapter 9)
– (a) Acanthosis nigricans (see Fig. 25-7B)
– (b) Multiple outcroppings of seborrheic keratoses (Leser-
Trélat sign; see Fig. 25-7A)
• (6) Metastasis to umbilicus (Sister Mary Joseph nodule)

120. Common metastatic sites
• Liver, lung, ovaries

121. Pathology
DIO Classification
Lauren Classification:
1. Intestinal Gastric ca.
It arises in areas of intestinal metaplasia to form
polypoid tumors or ulcers.
2. Diffuse Gastric ca.
It infiltrates deeply in the stomach without forming
obvious mass lesions but spreads widely in the gastric
wall “Linitis Plastica”
& it has much more worse prognosis
3. Mixed Morphology.

122. Morphology
• Polypoid
• Ulcerative
• Superficial spreading
• Linitis plastica

123. Gastric cancer can be devided into:
 Early:
 Limited to mucosa & submucosa with or without
LN (T1, any N)
 >> curable with 5 years survival rate in 90%.
 Advanced:
 It involves the Muscularis.
 It has 4 types( Bormann’s classification). Type III
& IV are incurable.

124. Primary tumor (T)
• See the list below:
• TX - Primary tumor cannot be assessed
• T0 - No evidence of primary tumor
• Tis - Carcinoma in situ, intraepithelial tumor without invasion of lamina
propria
• T1 - Tumor invades lamina propria, muscularis mucosae, or submucosa
• T1a - Tumor invades lamina propria or muscularis mucosae
• T1b - Tumor invades submucosa
• T2 - Tumor invades muscularis propria
• T3 - Tumor penetrates subserosal connective tissue without invasion of
visceral peritoneum or adjacent structures
• T4 - Tumor invades serosa (visceral peritoneum) or adjacent structures
• T4a - Tumor invades serosa (visceral peritoneum)
• T4b - Tumor invades adjacent structures/organs

125. Regional lymph nodes (N)
• NX - Regional lymph node(s) cannot be assessed
• N0 - No regional lymph node metastases
• N1 - Metastases in 1-2 regional lymph nodes
• N2 - Metastases in 3-6 regional lymph nodes
• N3 - Metastases in 7 or more regional lymph
nodes
• N3a - Metastases in 7-15 regional lymph nodes
• N3b - Metastases in 16 or more regional lymph
nodes

126. Distant metastasis
• See the list below:
• M0 - No distant metastasis
• M1 - Distant metastasi

127. Clinical Staging-TNM ангилал
• Stage 0 - Tis, N0, M0
• Stage I - T1-2, N0, M0
• Stage IIA - T1-2, N1-3, M0
• Stage IIB - T3, N0, M0 or T4a, N0, M0
• Stage III - T3, N0, M0 or; T4a, N1-3, M0
• Stage IVA - T4b, any N, M0
• Stage IVB - Any T, any N, M1

128. Survival rates
• See the list below:
• Stage IA - 94%
• Stage IB - 88%
• Stage IIA - 82%
• Stage IIB - 68%
• Stage IIIA - 54%
• Stage IIIB - 36%
• Stage IIIC - 18%
• Stage IV - 5%

129. T1 lamina propria & submucosa
T2 muscularis & subserosa
T3 serosa
T4 Adjacent organs
N0 no lymph node
N1 Epigastric node
N2 main arterial trunk
M0 No distal metastasis
M1 distal metastasis
Staging of gastric cancer
Spread of Gastric Cancer
Direct Spread
Blood-borne
metastasis
Lymphatic spread
Transperitoneal
spread
Tumor penetrates the
muscularis, serosa &
Adjacent organs
(Pancreas,colon &liver)
What is important here is
Virchow’s node
(Trosier’s sign)
Usually with extensive
Disease where liver 1st
Involved then lung &
Bone
This is common
Anywhere in peritoneal cavity
(Ascitis)
Krukenberg tumor (ovaries)
Sister Joseph nodule
(umbilicus)

130. Complications
 Peritoneal and pleural effusion
 Obstruction of gastric outlet or small bowel
 Bleeding
 Intrahepatc jaundice by hepatomegaly

131. Differential Diagnosis
1.Gastric ulcer
2.Other gastric neoplasms
3.Gastritis
4.Gastric Polyp
5.Crohns disease.
From history,
Cancer is not relieved by antacids
Not periodic
Not releived by eating or vomiting.

132. Screening MODALITIES
• Upper endoscopy
• Contrast radiography
• Other tests
– CBC

133. INVESTIGATIONS
Full blood count –IDA-
LFT,RFT
Amylase & lipase.
Serum tumor markers (CA 72-
4,CEA,CA19-9) not specific
Stool examination for occult blood
CXR ,Bone scan.

134. Specific:
UGI endoscopy with biopsy
Double contrast study
CT, MRI & US
Laparoscopry

135. EGD esophagogastroduodenoscopy
Diagnostic accuracy is 98%
if upto 7 biopsies is taken.
Double Contrast barium upper GI x-ray
Diagnostic accuracy 90%
WHY?
Diagnostic study of Choice
1.Early superficial gastric mucosal lesion
can be missed.
2. can’t differentiate b/w benign ulcer &
Ulcerating adenocarcinoma.

136. X-ray showing Gastric ulcer
With symmetrical radiating
Mucosal folds.
By histology, no evidence of
Malignancies was observed.
X-ray showing Extensive
carcinoma involving
the cardia & Fundus
Pyloric stenosis

137. CT,MRI & US:
Laparoscopy:
Help in assessment of wall thickness,
metastases (peritoneum ,liver & LNs)
Detection of peritoneal
metastases

139. THE GOLD STANDARD
 It allows taking biopsies
 Safe (in experienced hands)
UGI ENDOSCOPY

141. UGI ENDOSCOPY,contd.
 You may see an ulcer (25%), polypoid
mass (25%), superficial spreading
(10%),or infiltrative (linnitis plastica)-
difficult to be detected-
 Accuracy 50-95% it depends on gross
appearance,size,location & no. of
biopsies

142. IF YOU SEE ULCER ASK UR
SELF…BENIGN OR MALIGNANT?
MALIGNANT
BENIGN
Irregular outline with
necrotic or hemorrhagic
base
Round to oval punched out
lesion with straight walls &
flat smooth base
Irregular & raised margins
Smooth margins with
normal surrounding
mucosa
Anywhere
Mostly on lesser curvature
Any size
Majority<2cm
Prominent & edematous
rugal folds that usually do
not extend to the margins
Normal adjoining rugal
folds that extend to the
margins of the base

143. Management
• Surgery
• Chemotherapy
NO PROVEN BENEFIT
• Radiotherapy

144. Treatment
Initial treatment:
1.Improve nutrition if
needed by parentral or
enteral feeding.
2.Correct fluid
&electrolyte
& anemia if they are
present.
Preoperative Care
Preoperative Staging is
important because we
don’t want to subject the
patient to radical surgery
that can’t help him.

145. PRE-OPERATIVE CARE
 Careful preoperative staging
 Screen for any nutritional deficiencies &
consider nutritional support
 Symptomatic control
 Blood transfusion in symptomatic anemia
 Hydration
 Prophylactic antibiotics
 ABO & crossmatch
 Ask about current medications & allergies
 Cessation of smoking

146. BASIC SURGICAL PRINCIPLES
3 TYPES: TOTAL,SUBTOTAL,PALLIATIVE
 ANTRAL DISEASESUBTOTAL GASTRECTOMY
 MIDBODY & PROXIMAL TOTAL GASTRECTOMY

147. TOTAL (RADICAL) GASTRECTOMY
o Remove the stomach +distal part of
esophagus+ proximal part of dudenum +
greater & lesser omenta + LNs
o Oesophagojejunostomy with roux-en-y .

149. SUBTOTAL GASTRECTOMY
Similar to total one except that the
PROXIMAL PART of the stomach is
preserved
Followed by reconstruction & creating
anastomosis
( by gastrojejunostomy,billroth II )

150. PALLIATIVE SURGERY
• For pts with advanced (inoperable) disease &
suffering significant symptoms e.g.
obstruction, bleeding.
• Palliative gastrectomy not necessarily to be
radical, remove resectable masses &
reconstruct
(anastomosis/intubation/stenting/
recanalisation)

151. POSTOPERATIVE ORDERS
• Admit to PACU
• Detailed nutritional advise (small
frequent meals)

152. Post-Operative Complications
1.Leakage from duodenal
stump.
2.Secondary hemorrhage.
3.Nutritional deficiency in
long term.

153. 2.Chemotherapy:
Responds well, but there is no effect on servival.
Marsden Regimen
Epirubicin, cisplatin &5-flurouracil (3 wks)
6 cycles
Response rate : 40% .
3. Radiotherapy:
Postperative-radiotherpy: may decrease the
recurrence.

154. • Хэрхэн урьдчилан сэргийлэх вэ?

155. Preventive measures
By diet
Convincing:
vegetable & fruits.
Probable:
Vit.C &E
Possible
Carotenoids,whole grean cereals and green tea.
Smoking cessation
Cessation of alcohol intake
Early diagnosis remains the Key
Problem

156. PROGNOSTIC FEATURES
2 important factors influencing survival in resectable
gastric cancer:
 depth of cancer invasion
 presence or absence of regional LN involvement
• 5yrs survival rate:
10% in USA
50% in Japan