Professional Documents
Culture Documents
Dr Alex Mogere
Consultant Physician
Cancer of the oesophagus:
incidence and aetiology
Cont. incidence and aetiology
• Almost all esophageal cancers are either squamous cell carcinomas or
adenocarcinomas;
• The 2 histologic subtypes have a similar clinical presentation but
different causative factors.
• SCC is the more common cell type, having an incidence that rises
strikingly in association with geographic location
• It occurs frequently within a region extending from the southern
shore of the Caspian Sea to northern China , encompassing parts of
Iran, central Asia, Afghanistan, Siberia, and Mongolia
Cont. incidence and aetiology
• Gene associations are not yet defined
• High-incidence “pockets” of the disease are also present in such
disparate locations as Finland, Iceland, Curaçao, southeastern Africa,
and northwestern France.
• In North America and western Europe, the disease is more common in
blacks than whites and in males than females
• It appears most often after age 50 and seems to be associated with a
lower socioeconomic status
Adenocarcinomas
• Adenocarcinomas arise within dysplastic columnar epithelium in the
distal esophagus.
• These adenocarcinomas behave clinically like gastric
adenocarcinomas, although they are not associated with Helicobacter
pylori infections.
• Approximately 15% of esophageal adenocarcinomas overexpress the
HER2/neu gene.
Clinical presentation
• About 5% of esophageal cancers occur in the upper third of the
esophagus (cervical esophagus),
• 20% in the middle third,
• 75% in the lower third
• SCC and adenoCas cannot be distinguished radiographically or
endoscopically.
• Progressive dysphagia
• Wt loss of short duration
Clinical presentation
• Dysphagia initially occurs with solid foods and gradually progresses to
include semisolids and liquids.
• Dysphagia does not occur until >60% of the esophageal circumference
is infiltrated with cancer.
• The disease most commonly spreads to adjacent and supraclavicular
lymph nodes, liver, lungs, pleura, and bone.
• Tracheoesophageal fistulas may develop, primarily in patients with
upper and mid-esophageal tumors
• As with other SCCs, hyperCa 2+ may occur in the absence of osseous
mets, probably from PTH-rP secreted by tumor cells
DX SCC
• Esophagoscopy
• endoscopic inspection of the larynx, trachea, and bronchi should also
be carried out-to check spread
• A thorough examination of the fundus of the stomach (by retroflexing
the endoscope) is imperative as well
• CT scan chest and abdomen
• Endoscopic u/s
• PET scan for distant mets
Tx esophageal Ca
• The prognosis for patients with esophageal carcinoma is poor.
• Approximately 10% of patients survive 5 years after the diagnosis
• Surgical resection of all gross tumor (i.e., total resection) is feasible in
only 45% of cases, with residual tumor cells frequently present at the
resection margins.
• Experienced thoracic surgeons are now favoring minimally invasive
transthoracic esophagectomies
• About 20% of pts who survive a total surgical resection live for 5 years
Tx esophageal Ca
• 15–25% of patients given single-agent treatment ,show significant
tumor size reduction
• While there is a greater response of 30–60% of patients treated with
drug combinations that include cisplatin
• For tumors that overexpress the HER2/neu gene, the addition of the
monoclonal ab trastuzumab (Herceptin) is beneficial, esp in pts with
gastroesophageal lesions.
• Combination chemotx and radiation tx as the initial therapeutic
approach, either alone or followed by an attempt at operative
resection
Cont tx esophageal Ca
• The use of preoperative chemotherapy and radiation therapy
followed by esophageal resection appears to prolong survival
compared with surgery alone
• Approaches to palliation include repeated endoscopic dilatation, the
surgical placement of a gastrostomy or jejunostomy for hydration and
feeding, endoscopic placement of an expansive metal stent to bypass
the tumor, and radiation therapy.
Tumors of the stomach
Aetiological factors for Gastric Ca
Ct. aetiology Gastric Ca
• The long-term ingestion of high concs of nitrates found in dried,
smoked, and salted foods appears to be associated with a higher risk
• The nitrates are thought to be converted to carcinogenic nitrites by
bacteria
Incidence & epidemiology
• The disease is the 2nd most frequent cause of worldwide cancer-
related death.
• Although the incidence of gastric Ca has decreased w/wide, it
remains high in Japan, China, Chile, and Ireland.
• The risk of gastric Ca is greater among lower socioeconomic classes
• Migrants from high- to low-incidence nations maintain their
susceptibility to gastric Ca, whereas the risk for their offspring
approximates that of the new homeland
Pathology
• 85 % are adenocarcinomas,
• 15% due to lymphomas, gastrointestinal stromal tumors (GISTs), and
leiomyosarcomas
• Gastric adenoCa- can be diffuse type or intestinal type
• The diffuse carcinomas occur more often in younger patients, develop
throughout the stomach , result in a loss of distensibility of the gastric wall
(so-called linitis plastica, or “leather bottle” appearance), and carry a poorer
prognosis.
• Intestinal-type lesions are frequently ulcerative, more commonly appear in
the antrum and lesser curvature of the stomach, and are often preceded by
a prolonged precancerous process, often initiated by H. pylori infection.
Cont. pathology
• The intestinal type tends to predominate in the high-risk geographic
regions
• In US, ∼30% of gastric Cas originate in the distal stomach, ∼20% in
the mid portion, and ∼40% originate in the proximal third of the
stomach. The remaining 10% involve the entire stomach.
Cont. clinical presentation
• Gastric Cas, when superficial and surgically curable, usually produce
no symptoms.
• Unusual clinical features include migratory thrombophlebitis, MAHA,
diffuse seborrheic keratoses (Leser-Trélat sign), and acanthosis
nigricans.
• The liver is the most common site for hematogenous spread of tumor
Clinical presentation ;in advanced stage
• Anemia(bleeding from tumor)
• Asthenia(septic absorption from the tumor)
• Anorexia
• Recent onset early satiety, dyspepsia, epigastric discomfort
• Specific symptoms depending on site of tumor
• Gastric outlet obstruction symptoms-if in pyloric rgn
• Dysphagia,hematemesis if in proximal rgn
• Mass per abdomen if in the body of the stomach
• Jaundice, ascites –in mets
Clinical signs
• Pallor-anemia
• Cachexia
• Epigastric mass, liver secondaries
• Virchows nodes
• Sister mary joseph node(metastatic nodules to periumbilical region)
• Krukenberg’s tumor(ovarian mets)
• Blumer shelf secondaries(peritoneal cul-de-sac)
• Irish node
Morphological features
• Polypoid
• Ulcerative
• Superficial spreading
• Infiltrative(linitis plastic,leather bottle stomach)
Staging for Gastric Ca
Japanese’s classification for early gastric Ca
Spread of gastric Ca
INVXs
• FBC
• LFT, RFT
• Stool examination for occult blood
• Cxr
• Tumor markers- CA 19-9, CEA,
• CA 72-4
• UGI endoscopy(of choice)-high diagnostic accuracy ,if upto 7 samples
taken(98%)
• Ct scan/US/mri- check wall thickness, mets
• Laparascopy- detection of peritoneal mets
Endoscopy
Endoscopy findings
• Ulcer- 25%
• Polypoid mass- 25%
• Superficial spreading-10%
• Infiltrative – difficult to detect
• Accuracy – 50-95 %,depending on gross appearance,location and
number of biopsies
ULCER ON ENDOSCOPY
Benign Malignant
• Round to oval punched out lesion • Irregular outline with necrotic or
with straight walls and flat hemorrhagic base
smooth base • Irregular and raised margins
• smooth margins with normal
• Anywhere
surrounding mucosa
• Mostly on lesser curvature(most
• Any size
<2cm) • Prominent and irregular rugal
• Normal adjoining rugal folds usu folds that don’t usu extend to
extending to the base margins the margins
MANAGEMENT
• SURGERY
• CHEMOTHERAPY
• RADIOTHERAPY
Supportive care
• Correct anemia
• IVF, electrolytes
• Nutritional support-parenteral/enteral