INtestinal Path 3: Polyps Flashcards
Types of Colorectal Polyps
Non-neoplastic
- Hamartomatous polyps
- Inflammatory Polyps
- Hyperplastic Polyps
Neoplastic
- Sessile serrated Adenoma
- Adenoma
- Polyposis Syndromes when numerous polyps are present
Hamartomatous Polyps
Haphazard arrangement of normal stromal and epithelial elements.
Occur mainly as a component of a polyposis syndrome but can occur as a sporadic hamartomatous polyp
It is important to recognize these polyps because of associated intestinal and extraintestinal malignancies.
- Peutz-Jegher syndrome
- Juvenile polyposis
Peutz-Jegher syndrome
- Autosomal dominant syndrome presents at a median age of 11 years
Multiple GI hamartomatous * polyps and * mucocutaneous hyperpigmentation.
Polyps of * Peutz-Jegher syndrome most common in the small intestine
Peutz-Jegher syndrome is associated with a markedly increased risk of malignancies
(40% life time risk: colon, pancreas, breast, lung, urinary, gynecologic).
Polyps- SMOOTH MUSCLE
Juvenile (Retention) Polyp
Majority of juvenile polyps occur in children younger than 5 years of age
Juvenile polyps have essentially * no malignant potential when solitary (70% of patients)
Juvenile polyposis syndrome can be associated with * dysplasia
** Autosomal dominant
30% to 50% of patients with juvenile polyposis syndrome develop colonic adenocarcinoma by age 45.
Juvenile polyp.
- what we see
surface erosion and cystically dilated crypts.
Inflammatory Polyp
Inflammatory polyps are found in the regenerative and healing phases of inflammation
- Severe colitis, including chronic inflammatory bowel disease, amebic colitis,ischemic colitis, or bacterial dysentery, can give rise to inflammatory polyps.
- Solitary rectal ulcer syndrome associated polyp
Solitary or multiple ulcerated or polypoid lesions 4-10 cm from anal margin
Hyperplastic Polyp
Colonic hyperplastic polyps are benign epithelial proliferations that are typically discovered in the sixth and seventh decades of life.
Hyperplastic polyps are the most common type of polyps in the colon. 50% of 50+ year olds
Endoscopically, hyperplastic polyps are small, sessile, smooth bumps or nodules
Sessile Serrated Adenoma
Histologically resemble hyperplastic polyp
Most commonly found in right colon
High rate of DNA methylation and BRAF mutations
Patients with multiple serrated polyps (serrated polyposis syndrome) have an increased risk of adenocarcinoma
Conventional Adenoma
Adenomas are common lesions that are almost always asymptomatic
Clinical importance of adenomas related to their well-established * premalignant nature.
50% of the population >50 yo in Western countries such as the United States have adenomas
Adenomas > 2 cm have increased risk of malignancy (adenocarcinoma)
National Polyp Study 1990
Conventional Adenoma treatment
The appropriate treatment for all colorectal adenomas is complete removal
- Colonoscopy has virtually replaced all other modalities (sigmoidoscopy, fecal occult blood testing, barium enema) as the optimal screening tool
Persons over 50
need to start colorectal screening
Colonoscopy
If adenomas
present –>
Screen more frequently
Tubular Adenoma- what we might see
Pedunculated adenoma (endoscopic view). velvety surface.
a hemorrhagic surface (which is why they may first be detected with stool occult blood screening) and a long narrow stalk.
The size of a polyp–above 2 cm–makes the possibility of malignancy more likely.
Adenomatous Histology
. The neoplastic glands are more irregular with darker (hyperchromatic) and more crowded nuclei.
Malignancy Risk of Adenoma
Polyp Size
Between 1-2 cm 5% risk of cancer
> 2 cm 10-20% risk of cancer
* > 4 cm 40% risk of cancer
Histologic Architecture * (Villous>Tubular)
Severity of Epithelial Dysplasia (Severe>Moderate>Mild)
High grade dysplasia does not increase risk of carcinoma elsewhere in the colon
Small and Large Bowel Risk Factors for Malignancy
Family history is particularly important in assessing colorectal cancer risk especially in patients younger than 50 years
Adenoma
- Familial adenomatous polyposis (germline)
- Lynch syndrome (germline) (HNPCC)
Hamartoma polyposis syndromes
Crohn’s disease
Celiac disease
Ulcerative colitis
Familial Adenomatous Polyposis
Autosomal dominant disorder that accounts for 1% to 2% of all CRC
Characterized by the presence of * hundreds to thousands of adenomas in the colorectal mucosa by 20 to 30 years
Result of an inherited defect in one allele of the* APCtumor suppressor gene
Lynch Syndrome
Hereditary Nonpolyposis Colorectal Cancer (HNPCC)
3% of CRC can be linked to Lynch syndrome
- Life time risk approximately 80%
Early onset CRC (mean age 44 years)
Secondary to * germline mutations in DNA mismatch repair genes
Associated with * other cancers including the endometrium, ovaries, pancreas and stomach
Molecular Changes in the Adenoma Carcinoma Sequence
The classic adenoma-carcinoma sequence, accounts for up to 80% of sporadic colon adenocarcinoma and typically includes mutation ofAPCearly in the neoplastic process
Colorectal Adenocarcinoma
Males more than females
5-year survival rate 55% to 60%
Begin as * intramucosal epithelial lesions, usually arising in adenomatous polyps or glands
Average age at diagnosis in seventh decade of life (5th decade for HNPCC (Lynch))
Surgical resection most effective treatment for early stage (T1 and T2)
- Metastases are common
survival related to early dx; deeper extent is bad.
classic lesion of colon adenocarcinoma
apple core lesion
colorectal carcinoma- serosa involvement
very bad prognosis
differentiation of carcinoma
Well-differentiated carcinoma. The neoplasm forms uniform gland structures, and the nuclei are localized to the basal half of the neoplastic cells.
Moderately differentiated carcinoma.
The neoplasm is composed of complex glandular structures, with loss of polarity of the nuclei. Most colorectal carcinomas are moderately differentiated.
Poorly differentiated carcinoma. The carcinoma shows minimal to no gland formation.
colorectal carcinoma- Pathologic features that can adversely influence prognosis
include lymph node invasionand vascular invasion
liver metastases commonly associated with
colorectal carcinomas (due to portal drainage system)
Tumors of Small Intestines
Small intestine tumors are * uncommon in comparison with those occurring elsewhere in the GI tract
Benign
- Hyperplastic polyp
- Hamartoma
- Adenoma
malignant Tumors of Small Intestines
Adenocarcinoma
Carcinoid
Lymphoma
Gastrointestinal Stromal Tumors (benign and malignant)
Metastases (50% of small intestine tumors)
kinds of tumors of small intestines
Half of all benign small intestine tumors are found only incidentally
Most small intestine adenocarcinoma / adenoma occur at the ampulla of Vater in the duodenum
Small intestine neuroendocrine tumors (carcinoid tumors) are now the most common malignancy
Most small intestine lymphomas are B-cell derived
Small Intestine adenomas
Small intestine Adenoma less than 0.05% of all intestinal adenomas
> 50% of small intestine adenocarcinoma in duodenum
Celiac disease has 80 fold increased risk for small intestine adenocarcinoma
Metastatic tumors are more common than primary neoplasms of small intestine
Carcinoid Tumor (Neuroendocrine Tumor)
Arise from enterochromaffin cells (Kulchitsky Cells)
Of 67,843 patients with SB malignancies
- 37% Carcinoid
- 37% Adenocarcinoma
- 26% Stromal tumors or lymphoma
Ileum and appendix are the most common sites
Often are identified by symptoms caused by the hormones they secrete
most important prognostic factor for gastrointestinal carcinoid tumors is
location:
Carcinoid tumors arising in esophagus and stomach, rarely metastasize and are generally cured by resection.
Carcinoid tumors arising in the jejunum and ileum are often * multiple and tend to be aggressive
Carcinoid tumors arising in the appendix and rectum are typically discovered incidentally.
- Most carcinoid tumors should be considered at least low grade malignancies
Carcinoid Syndrome
Classical carcinoid syndrome (under 10% of patients) consists of the clinical symptoms of:
Severe episodic skin flushing
Diarrhea, abdominal cramping
Asthma, bronchoconstriction
Rapid heart rate and tricuspid valve insufficiency
Generally requires tumors to * secrete hormones into a non-portal venous circulation and therefore is strongly associated with metastatic disease.
Serotonin, 5-hydroxytryptophan, kallikrein, histamine, prostaglandins
(tumors are typically yellow)
Robbins Key Concepts: Benign and malignant proliferative lesions of the colon
Intestinal polyps can be classified as non-neoplastic or neoplastic. The non-neoplastic polyps can be further defined as hyperplastic, inflammatory, or hamartomatous.
Hyperplastic polyps are benign epithelial proliferations most commonly found in the left colon and rectum. They have no malignant potential, and must be distinguished from sessile serrated adenomas.
Inflammatory polyps form as a result of chronic cycles of injury and healing.
Hamartomatous polyps occur sporadically or as a part of genetic diseases. The latter include juvenile polyposis and Peutz-Jeghers Syndrome, which are associated with increased risk of malignancy.
Benign epithelial neoplastic polyps of the intestines are termed adenomas. The hallmark of these lesions, which are the precursors of colonic adenocarcinomas, is cytologic dysplasia.
In contrast to traditional adenomas, sessile serrated adenomas lack cytologic dysplasia and share morphologic features with hyperplastic polyps.
Key Concepts - FAP and HNPCC
Familial adenomatous polyposis (FAP) and hereditary non-polyposis colorectal cancer (HNPCC) are the most common forms of familial colon cancer.
FAP is caused by APC mutations. Patients typically have more than 100 adenomas and develop colon cancer before 30 years of age.
HNPCC is caused by mutations in DNA mismatch repair enzymes. HNPCC patients have far fewer polyps and develop cancer at older ages than FAP patients but younger ages than those with sporadic colon cancer.
FAP and HNPCC typify distinct pathways of neoplastic transformation and progression that also contribute to the majority of sporadic colon cancers.
Nearly all colonic cancers are adenocarcinomas. The two most important prognostic factors are depth of invasion and the presence or absence of lymph node metastases.
Anal Canal Malignant tumors
Upper third more commonly adenocarcinoma
Lower third Squamous cell carcinoma
- HPV associated
- * Cloacogenic carcinoma
Squamous cell carcinoma with basaloid growth pattern
Melanoma
Vermiform Appendix
arises from cecum
no known specific function
6-7 cm. in adult
lymphoid rich
Acute Appendicits
Disease of industrialized countries
Mainly a disease of adolescents and young adults
Males slightly more than females
Life time risk for acute appendicitis is 7%
Classical clinical findings
- initial peri-umbilical pain, localizing to right lower quadrant ** (McBurney sign)
- nausea and/or vomiting
- abdominal tenderness, rebound
- mild fever
- leucocytosis (15,000 – 20,000/cu.mm)
false positives of acute appendicitis
False positive acceptable rate was once 20-25%
Routine use of preoperative computed tomography (CT)has decreased false positive rate to ~3%
Tumors of the Appendix
- Carcinoid most common, usually incidental finding
Typical bowel Adenomas and Adenocarcinomas, uncommon
Mucinous cystadenoma (mucocele)
Pseudomyxoma peritonei
Key Concepts- hemorrhoids, appendix
Hemorrhoids are collateral vessels that develop secondary to persistently elevated venous pressure within the hemorrhoidal plexus. They also occur in portal hypertension.
Acute appendicitis is most common in children and adolescents. It is thought to be initiated by increased intraluminal pressure and compromised venous outflow
The most common tumor of the appendix is the benign carcinoid.
Peritoneal dissemination of mucinous tumors can cause pseudomyxoma peritonei.
Peritonitis Most often caused by:
Leakage of bile or pancreatic enzymes (sterile/suppurative/hemorrhagic)
Foreign material (talc) especially post-op (granulomatous)
Endometriosis (sterile)
Ruptured dermoid cysts (granulomatous)
Perforation of abdominal viscera (Suppurative)
PERITONEAL CAVITY Tumors
Mesothelioma is most common primary malignancy almost always associated with asbestos exposure
Direct spread or metastatic seeding
- Ovary
- Colon
- Pancreas
- Appendix
- Leiomyosarcoma
- Liposarcoma
