(Medicine) Surgical Removal of A Portion of The Colon.: Hemicolectomy-P1. Anastomoses
(Medicine) Surgical Removal of A Portion of The Colon.: Hemicolectomy-P1. Anastomoses
(Medicine) Surgical Removal of A Portion of The Colon.: Hemicolectomy-P1. Anastomoses
p1. anastomoses
1. A union or joining together of blood vessels or other tubular structures. Anastomosis usually refers to the direct connection between
arteries, veins, venules, and arterioles without any intervening capillaries. If an anastomosis is present when an artery is blocked with
a blood clot, the anastomosis forms a collateral circulation enabling other arteries to take over the blocked artery's work. If no
anastomosis is present. the tissue beyond the clot is likely to die. Endurance training may increase anastomoses of coronary arteries,
reducing the effects of a coronary thrombosis.
2. A surgical union of two tubular structures, usually by sutures or staples.
Right Hemicolectomy
The colon, or large bowel, has three sides: the ascending colon (right side), the transverse colon, and the descending colon (left side).
Colectomy
The primary treatment for colon cancer is surgery. The part of the large bowel with cancer is removed, along with surrounding lymph
nodes. Removal of the colon is called a colectomy. The remaining bowel is then joined together. Joining the bowel is called an
anastomosis. When cancer is found in the ascending colon, the right side is removed. The colon is then joined to the small intestine
Right Hemicolectomy before surgery. The grey area shows the part of the bowel the surgeon will remove.
Right Hemicolectomy after surgery. The large bowel now is attached to the small bowel.
At Cedars-Sinai, the majority of colon and rectal operations are performed using minimally invasive techniques (laparoscopy). The
benefits of minimally invasive surgery include less pain after surgery, faster return of bowel function, quicker healing, less scarring and
fewer days in the hospital to recover. Laparoscopy, however, may not be suitable for all patients. Ask your surgeon if you are an
appropriate candidate for minimally invasive surgery.
Chemotherapy
After the surgeon removes the section of the colon, a pathologist evaluates the cancer under a microscope. If the pathologist sees
evidence that cancer has spread to the lymph nodes, or if the cancer is a type that grows quickly, the oncologist will usually
recommend further treatment with chemotherapy.
Follow-up Care
Bowel movements might be more frequent after a colectomy, but usually become more normal after one year. Your doctor can
recommend a bowel care plan to help normalize bowel movements.
The most common time a cancer recurs is within the first two years following diagnosis and treatment. Follow-up care with the
surgeon, gastroenterologist and oncologist is important. Periodic checkups may include a physical exam, blood tests, colonoscopy, CT
scan or PET scan.
Adenocarcinoma
Definition:
Let's break it down. "Adeno-" is a prefix that means "gland." In general, glands secrete things and are classified as endocrine or
exocrine. Endocrine glands secrete things into the bloodstream, like hormones. Exocrine glands secrete things that go outside of the
body, like mucus and sweat.
The word "carcinoma" means a malignant tumor that starts in epithelial tissue.
Put the two words together and you get "adenocarcinoma," which means a malignant tumor in epithelial tissue, specifically in a gland.
Adenocarcinomas account for about 90-95% of all colorectal cancers. For more detailed information, please read Adenocarcinoma of
the Colon and Rectum
Genetically, colorectal cancer represents a complex disease, and genetic alterations are often associated with progression from
premalignant lesion (adenoma) to invasive adenocarcinoma. Sequence of molecular and genetic events leading to transformation from
adenomatous polyps to overt malignancy has been characterized by Vogelstein and Fearon.4 The early event is a mutation of APC
(adenomatous polyposis gene), which was first discovered in individuals with familial adenomatous polyposis (FAP). The protein
encoded by APC is important in activation of oncogene c-myc and cyclin D1, which drives the progression to malignant phenotype.
Although FAP is a rare hereditary syndrome accounting for only about 1% of cases of colon cancer, APC mutations are very frequent in
sporadic colorectal cancers.
In addition to mutations, epigenetic events such as abnormal DNA methylation can also cause silencing of tumor suppressor genes or
activation of oncogenes, compromising the genetic balance and ultimately leading to malignant transformation.
Other important genes in colon carcinogenesis include KRAS oncogene , chromosome 18 loss of heterozygosity (LOH) leading to
inactivation of SMAD4 (DPC4), and DCC (deleted in colon cancer) tumor suppression genes. Chromosome arm 17p deletion and
mutations affecting p53 tumor suppressor gene confer resistance to programmed cell death (apoptosis) and are thought to be late
events in colon carcinogenesis.
A subset of colorectal cancers is characterized with deficient DNA mismatch repair. This phenotype has been linked to mutations of
genes such as MSH2, MLH1, and PMS2. These mutations result in so-called high frequency microsatellite instability (H-MSI), which can
be detected with an immunocytochemistry assay. H-MSI is a hallmark of hereditary nonpolyposis colon cancer syndrome (HNPCC,
Lynch syndrome), which accounts for about 6% of all colon cancers. H-MSI is also found in about 20% of sporadic colon cancers.
International
In 2003, the World Health Organization estimated that approximately 940,000 individuals were be diagnosed with colorectal cancer
worldwide and 492,000 died from it that year.
Mortality/Morbidity
Colorectal cancer is a major health burden worldwide. The incidence and mortality from colon cancer has been on a slow decline over
the past 20 years in the United States; however, colon cancer remained the third most common cause of cancer-related mortality in
2008. A multitude of risk factors have been linked to colorectal cancer, including heredity, environmental exposures, and inflammatory
syndromes affecting gastrointestinal tract.
Race
Recent trends in the United States suggest a disproportionally higher incidence and death from colon cancer in African Americans than
in whites. Hispanic persons have the lowest incidence and mortality from colorectal cancer.
Sex
The incidence of colorectal cancer is about equal for males and females.
Age
Age is a well-known risk factor for colorectal cancer, as it is for many other solid tumors. The timeline for progression from early
premalignant lesion to malignant cancer ranges from 10-20 years. The incidence of colorectal cancer peaks at about age 65 years.
History
Due to increased emphasis on screening practices, colon cancer is now often detected during screening procedures. Other common
clinical presentations include iron-deficiency anemia, rectal bleeding, abdominal pain, change in bowel habits, and intestinal obstruction
or perforation. Right-sided lesions are more likely to bleed and cause diarrhea, while left-sided tumors are usually detected later and
could present with bowel obstruction.
Physical
Physical findings could be very nonspecific (fatigue, weight loss) or absent early in the disease course. In more advanced cases,
abdominal tenderness, macroscopic rectal bleeding, palpable abdominal mass, hepatomegaly, and ascites could be present on physical
examination.
Causes
Colorectal cancer is a multifactorial disease process, with etiology transcending genetic factors, environmental exposures (including
diet), and inflammatory conditions of digestive tract.
Though much about colorectal cancer genetics remains unknown, current research indicates that genetic factors have the greatest
correlation to colorectal cancer. Hereditary mutation of the APC gene is the cause of familial adenomatous polyposis (FAP), where
affected individuals carry an almost 100% risk of developing colon cancer by age 40 years.
3. Multivitamins 1 cap OD
Classification: Vitamins
Trade name: Theravim, Thera Multi
Indications: Treatment and prevention of vitamin deficiencies.
Action: Prevention of deficiency or replacement in patients whose nutritional status is questionable.
Contraindications: Hypersensitivity to preservative, colorants or additives, including tartrazine, saccharin, and aspartame.
Side effects/ Adverse Reactions: Allergic reactions to preservatives, additives, or colorants.
Nursing Considerations:
1. Assess patient for signs of nutrition deficiency prior to and throughout therapy.
2. Instruct to notify side effects of medications to physician.
3. Encourage to comply on medications.
4. Encourage patient to comply with physicians’ recommendations. Explain that the best source of vitamins is a well balanced diet with
foods from the 4 basic
food groups.
5. Advise parents not to refer to chewable multivitamins for children as candy.
Colorectal cancer is a disease in which normal cells in the lining of the colon or rectum begin to change, start to grow uncontrollably,
and no longer die. These changes usually take years to develop; however, in some cases of hereditary disease, changes can occur
within months to years. Both genetic and environmental factors can cause the changes. Initially, the cell growth appears as a benign
(noncancerous) polyp that can, over time, become a cancerous tumor. If not treated or removed, a polyp can become a potentially life-
threatening cancer. Recognizing and removing precancerous polyps before they become cancer can prevent colorectal cancer.
Predisposing Factors:
1. Age above 40 years old
2. Diet
o Low in Fiber
o High in fat, protein and refined carbohydrates
o Obesity
o History of chronic constipation
o History of IBD, familial polyposis or colon polyps
o Family history of colon cancer