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(Riola) Intestinal Neoplasm, Obesity and Overweight
(Riola) Intestinal Neoplasm, Obesity and Overweight
Neoplasm
Prepared by: Lovely Roan R. Riola
Tumors of the Small Intestine
Epidemiology
Primary neoplasms of the small intestine are very rare,
comprising approximately 4% (range 1.6-6%) of all tumors of
the gastrointestinal tract. Approximately 60% of these tumors
are malignant. Benign neoplasms of the small intestine
comprise 5% of benign tumors of the intestinal tract.
The most frequent malignant tumors are:
•adenocarcinoma
•carcinoid tumor
•leiomyosarcoma
•Lymphoma
•small bowel carcinoid: 30-45% occurs in the appendix, 25-35% in the small
intestine (90% in distal ileum)
•characterized by increased serotonin production
•typically invasive growth and pronounced perifocal fibrotic reaction (
desmoplastic reaction)
•features: muscularis propria thickening, puckering, wall retraction, serosal
invasion, mesenteric metastases (similar echogenicity to the primary tumor, may
calcify)
•MRI
Malignant Tumors:
•MRI
Malignant Tumors:
Adenomatous Polyps
Asymptomatic
Adenomatous polyps, often known as adenomas, are a type of polyps that
can turn into cancer.
Adenomas may form in the mucous membrane of the lining in the
large intestine, making them colon polyps. Another type of adenoma is
gastric polyps, which form in the lining of the stomach.
•Stool test: A doctor may check for blood in a person’s stool. During this
exam, they may also test the DNA in the stool. If certain results arise, the
doctor may then carry out a colonoscopy to investigate further.
Treatment:
If a person has colon polyps, a doctor will usually remove them during a
polypectomy.
Familial adenomatous polyposis
Familial adenomatous polyposis (FAP) is a rare inherited cancer predisposition
syndrome characterized by hundreds to thousands of precancerous colorectal polyps
(adenomatous polyps).
The signs and symptoms of familial adenomatous polyposis (FAP) vary both within
families and between families. Classic FAP is characterized primarily by hundreds to
thousands of noncancerous (benign) polyps (growths) in the colon that begin to appear
at an average age of 16 years. Unless the colon is removed, these polyps will become
malignant (cancerous), leading to early-onset colorectal cancer at an average age of 39
years.
Causes:
Familial adenomatous polyposis is caused by a defect in
the adenomatous polyposis coli (APC) gene. Most people
inherit the genetic abnormality from a parent. But in
about 25 percent of cases, the genetic mutation occurs
spontaneously.
Treatment:
To prevent cancer, Mayo specialists recommend surgery for familial adenomatous
polyposis, usually by your late teens or early 20s. Surgery may not be required for
attenuated FAP.
Surgery doesn't cure FAP. Polyps can continue to form in the remaining or
reconstructed parts of your colon, stomach and small intestine. But with careful
monitoring, these polyps usually can be found and removed during colonoscopy before
becoming cancerous.
Lynch syndrome, also known as hereditary non-polyposis colorectal cancer (HNPCC),
is the most common cause of hereditary colorectal (colon) cancer. As a genetic
disorder, Lynch syndrome occurs when a person inherits an altered or mutated gene.
•stomach pain
•constipation
•fatigue
•bleeding inside the gut
•unintentional weight loss
•reduced ability to absorb nutrients from foods
•glioblastoma, an aggressive type of brain tumor
Diagnostic Test:
Analyzing their DNA, before offering genetic testing, a doctor will usually review the
individual’s personal and family medical history to determine their likelihood of having
Lynch syndrome.
Treatment:
Nutrition
Foods to eat:
•Choose minimally processed, whole foods
•Whole grains (whole wheat, steel cut oats, brown rice, quinoa)
•Vegetables (a colorful variety)
•Whole fruits (not fruit juices)
•Nuts, seeds, beans, and other healthy sources of protein (fish
and poultry)
•Plant oils (olive and other vegetable oils)
Crohn’s Disease
A more extensive distribution of intestinal inflammation has been reported among
African American or Black (AA), Hispanic, and Asian patients with CD than among
White patients. In studies that directly compared disease location among patients from
different racial groups, higher proportions of White patients were found to have
isolated ileal disease compared with AA, Hispanic, or Asian patients with CD.
There are variations among reports of the presence of more complicated disease
phenotypes. Many studies found that AA patients with CD have increased rates of
perianal disease and other complications compared with White patients. However,
other studies found that AA and White patients have similar rates of perianal disease. A
recent systematic review and meta-analysis concluded that AA patients were
significantly more likely to have penetrating disease compared with the 3 other
reported racial or ethnic groups, and more likely to have perianal disease compared
with White patients.
Colitis
In comparisons of disease extent, AA patients were more likely to have proctitis or left-
sided colitis compared with White patients (who were more likely to have extensive
colitis) in multiple studies. However, no racial differences were observed in other
comparisons. A study of Hispanic patients found an increased frequency of extensive
colitis compared with White patients, whereas multiple studies found no significant
difference in disease location. In an evaluation comparing Asian patients and White
patients, Asian patients were less likely to have extensive disease. In summary, a
consistent difference in disease extent between patients of different races or
ethnicities with UC has not been demonstrated.
Reference: