Colon Cancer

Profile

• CL • 54/M • from Batangas • Chief complaint of rectal bleeding

History of Present Illness

• 2 years PTA– patient noted dark/blackish stools. There were no

associated symptoms at the time.• 1 year PTA– patient started having abdominal pain at the

hypogastric area, described as squeezing in quality, intermittent, pain scale 4/10, accompanied by blood-tinged stools. No consult done.

History of Present Illness

• 2 months PTA– persistence of hypogastric pain VAS now 7/10.

Patient consulted at PGH OPD. Colonoscopy and biopsy were subsequently done A> Colon CA, Adenocarcinoma St. I. Patient was then scheduled for elective admission.

Review of Systems

• (-) wt loss• (+) good appetite• (+) difficulty in

defecation• (+) melena

• (+) hematochezia• (+) good urine output• (-) diarrhea• (+) constipation

Past Medical History

• (+) Hypertensive suspect– LBP 100/80 HBP 150/100 UBP 140/100, currently

no medications• (+) Benign prostatic hyperplasia, 2005, treated

medically• (-) BA/DM/PTB• (-) known allergies• (-) previous hospitalizations/surgeries

Family Medical History

• (+) Colon Cancer- sibling• (+) CVD-mother• (-) DM/ PTB/ HPN/ BA

Personal Social History

• (+) Smoker, 72 pack years• (+) regular alcoholic beverage drinker, almost

everyday, stopped when he was confined• Used to work as a farmer but stopped due to

current illness.

Physical ExamGeneral Survey alert, coherent, ambulatory, not in cardiorespiratory distressVital Signs BP 140/100 HR 70 RR 20 Temp 36.5

HEENT: anicteric sclerae, pink conjunctivae, (-) CLAD, (-) NVE, ANM, TPCChest/Lungs: equal chest expansion, clear breath sounds, (-) crackles/wheezesCVS: adynamic precordium, distinct S1 and S2, normal rate, regular

rhythm, (-) murmurs, (-) heaves/thrills

Abdomen: Abdomen soft, (+) tenderness on deep palpation at the hypogastric area, non-distended (-)palpable masses, (-)Psoas, (-) obturator, (-) Rovsing’s

DRE (+) External hemorrhoids (1 o’clock & 9 o’clock position) good sphincter tone, (+) anal wink, smooth rectal mucosa, empty rectal vault (-)masses (+)pararectal tenderness, (-)blood per examining finger

Skin/Extremities: full and equal pulses, pink nail beds, good CRT, (-) clubbing, cyanosis, edema

Laboratory

CBC• Hgb 146• Hct 0.446• WBC 6.40• Plt 155• Monocytes 0.075• Eosinophils 0.035• Basophils 0.003• Neutrophils 0.512• Lymphocytes 0.375

Laboratory

• AST 32• ALT 35• TB 8.9• DB 2.0• IB 6.9

• (01-13-12) Tumor marker: CEA 1.85 (N: 0-5)

Laboratory

• CXR– No significant chest findings

• Colonoscopy report– Scope inserted up to cecum, noted circumferential fungating

mass 45cm FAV, obstructing 60% of the lumen• Abdominal CT

– Irregular thickening of the anterior wall of the rectum– Distal Ileal wall thickening, consider tumor focus– Cardiomegaly– Renal cortical cysts, bilateral, Bosniak I– Compression deformity, L2 vertebra

Laboratory

• Histopathologic Report – Adenocarcinoma, well-differentiated

Assessment

• Adenocarcinoma, descending colon St. 1 (T2 N0 M0)

Clinical Presentation

• Rectal bleeding• Abdominal pain• Change in bowel habits• Intestinal obstruction or perforation• Weight loss

Right LeftBleeding Bowel ObstructionDiarrhea

Clinical Presentation

• Iron deficiency anemia– weakness, fatigue, dyspnea, or palpitations

• Advanced cancer can cause cancer cachexia, involuntary weight loss, anorexia, muscle weakness

Laboratory anomalies

• Blood Tests– Anemia– Hypoalbuminemia

• Alkaline Phosphatase – elevated if with liver metastasis

• CEA– Not useful for screening, moderately sensitive– For prognosis and baseline for comparison post-op

Pathophysiology

• Arises from mucosal colonic polyps– Hyperplastic• Increased number of glandular cells with decreased

cytoplasmic mucus• Lack nuclear hyperchromatism, stratification, or atypia

– Adenomatous• Hyperchromatic, enlarged, cigar -shaped, and crowded

together in a palisade pattern

• Almost all colon cancers arise from adenomas

Pathophysiology

• Familial Adenomatous Polyposis (FAP)– Mutation of APC gene on chromosome 5q – Autosomal dominant

• Hereditary Nonpolyposis Colon Cancer (HNCC)– Mutation of mismatch repair genes hMSH2

Risk FactorsParameters Mechanism

Old age Acquired colonocyte mutations accumulate with age

Living in United States and other highly industrialized nations, possibly excluding Japan

Dietary and environmentalcarcinogens

Physical inactivity? Physical activity may stimulate immunosurveillance, and stimulate intestinal peristalsis to decrease mucosal contact with fecal carcinogens

Smoking cigarettes Carcinogens present in tobacco

Alcohol May promote cell proliferation and inhibit DNA repair

FAP Develops hundreds of adenomatous colonic polyps. Inevitably develops colon cancerbecause of small but significant risk of malignant transformation in each adenoma

Risk FactorsParameters Mechanism

Gardner’s syndrome Variant of FAP

HNPCC (Lynch syndrome) Mutant mismatch repair gene leads to accumulation of genetic mutations, including mutations of tumor suppressor genes

Peutz-Jeghers syndrome Syndromic hamartomatous polyps may occasionally transform to adenomas

Juvenile polyposis Syndromic juvenile polyps can transform to adenomas and then cancers over time

Hyperplastic polyposis Genetic mutation in hyperplastic polyposis may predispose to cancer

Inflammatory Bowel Diease Dysplasia and genetic mutations associated with mucosal injury and repair

Screening of Average Risk Patients

• Fecal Occult Blood test– low cost, simple, non-invasive, safe– low specificity

• Barium Enema• Flexible sigmoidoscopy– every 3 to 5 years has been recommended in

conjunction with annual FOBT for screening• Colonoscopy– recommended for patients more than 50 years old at

average risk for colon cancer or colonic polyps

Stage Primary Tumor (T) Regional Lymph Node (N)

Remote Metastasis (M)

Stage 0 Carcinoma in situ (Tis) N0 M0

Stage I Tumor may invade submucosa (T1) or muscularis propria (T2)

N0 M0

Stage II Tumor invades muscularis (T3) or adjacent organs or structures (T4)

N0 M0

Stage IIA T3 N0 M0Stage IIB T4a N0 M0

Stage IIC T4b N0 M0Stage IIIA T1-4 N1-2 M0Stage IIIB T1-4 N1-2 M0Stage IIIC T3-4 N1-2 M0Stage IVA T1-4 N1-3 M1aStage IVB T1-4 N1-3 M1b

Surgical Management

• Surgery is the only curative modality for localized colon cancer (stage I-III)

• Removal of the primary tumor with adequate margins including areas of lymphatic drainage

• Right hemicolectomy– cecum and right colon– ileocolic, right colic, and right branch of the

middle colic vessels are divided and removed

Surgical Management

• Extended right hemicolectomy– proximal or middle transverse colon– ileocolic, right colic, and middle colic vessels are

divided and the specimen is removed with its mesentery.

• Left hemicolectomy– splenic flexure and left colon– left branch of the middle colic vessels, the inferior

mesenteric vein, and the left colic vessels along with their mesenteries are included with the specimen

Surgical Management

• Sigmoid colectomy– sigmoid colon lesions– inferior mesenteric artery is divided at its origin,

and dissection proceeds toward the pelvis until adequate margins are obtained

Adjuvant Chemotheraphy

• Standard therapy for patients with stage III and some patients with stage II colon cancer

Prevention of Colon Cancer

• Dietary modification– Fiber decreases exposure to carcinogens

• Chemoprevention with aspirin and other NSAIDs– Reduce cellular proliferation, slow cell cycle

progression, induce apoptosis– Inhibit COX whichis required for PGE synthesis

• Colonic polypectomy• Endomusosectomy