Colon Cancer - A Case Presentation
•Download as PPTX, PDF•
18 likes•9,948 views
A Case of Colon Adenocarcinoma
Recommended
More Related Content
What's hot
What's hot (20)
Similar to Colon Cancer - A Case Presentation
Similar to Colon Cancer - A Case Presentation (20)
Recently uploaded
Recently uploaded (20)
Colon Cancer - A Case Presentation
- 1. A case of 75 year old male with a history constipation and abdominal bloatedness PGI Mark Lester Dalanon 1
- 2. General Objective • To present a case of 75 year old male with a history constipation and abdominal bloatedness 2
- 3. Specific Objectives 1. Present a through medical history and physical examination of the index case 2. To present the diagnostic work up and management done to the index case 3. To discuss the pathophysiology and risk factors for developing colon cancer 4. To discuss the treatment guidelines and follow up for patients with colon cancer 3
- 4. General Data • N.E • 75 years old • Male • Retired policeman • Admitted for the 2nd time at CHH • Chief Complaint: Constipation and Abdominal Distention 4
- 5. History of Present Illness 10 Days PTA • Patient reported onset of no passage of stool • Patient was able to pass out flatus 5 Days PTA • Constipation persisted • Noted absence of flatus • Onset of abdominal bloatedness • Occasional abdominal cramps noted 5
- 6. History of Present Illness cont. 2 Days PTA • Condition persisted • Noted abdomen to be distended • Self medicated with Lactulose Syrup 30ml TID providing no relief • Noted decrease in appetite and food intake • Persistence opted for consult at this institution and was subsequently admitted 6
- 7. Pertinent Negatives • No reported weight loss • No fever • No hematochezia • No vomiting 7
- 8. Past Medical History • Hypertensive x 20 years Losartan (Lifezar) 50mg/tab, 1 tab OD • Type 2 Diabetes Mellitus x 15 years Sitagliptin + Metformin (Janumet) 50mg/500mg, 1 tab BID • 03/04/17 - CHH - CAP MR • No previous surgeries done 8
- 9. Family History • Hypertension (Both Parents) • Diabetes Mellitus (Maternal) • Colon Cancer (Paternal Side) 9
- 10. Personal & Social History • Smoker (65 pack years) • Occasional alcoholic beverages drink • Denied illicit drug use • Diet: meat, processed foods, and rice • Had 3 sexual partners 10
- 11. Physical Examination • General Survey: Awake, Alert, Responsive, Not in respiratory distress • Skin: senile turgor, no rash no lesion • HEENT: pink palpebral conjunctivae, anicteric Sclerae, no nasoaural discharge, no alar flaring, pink and dry lips and mucosa, no tonsilopharyngeal congestion • Neck: supple, trachea at midline, no neck vein, non enlarged thyroid gland, no lymphadenopathy • C/L: equal chest expansion, clear breath sounds, no intercostal • CVS: adynamic precordium, distinct heart sounds, PMI at 5th ICS MCL, no heaves, no thrills BP: 110/60 mmHg Wt : 90 kgs Temp: 36.5 C Ht: 160 cm PR: 65bpm BMI: 35.15 kg/m2 (Class II Obesity) RR: 20 cpm 11
- 13. Physical Examination cont. •Cerebral: Alert, Oriented to time place and person •Cranial Nerves I - Able to identify coffee and orange scent II and III - Pupils 3mm OU reactive to light, direct and consensual in each eye III, IV and VI - EOM full range by finger following test, no diplopia V - Muscles of mastication is strong, facial sensation intact, (+) corneal reflex VII - No facial asymmetry, intact taste sensation VIII - Can hear spoken voice at 2 feet IX and X - (+) gag reflex, uvula at midline on rest and when instructed to say “ahh”, voice was well modulated XI - Able to turn neck and shrug shoulders against resistance XII - Tongue midline on rest and on protrusion 13
- 14. Physical Examination cont. • Cerebellar: (-) ataxia, (-) dysmetria, (-)dysdiadochokinesia • Sensory: intact sensation to pain, light touch, vibration, temperature and position sense on upper and lower extremities • Motor: good muscle tone, 5/5 muscle strength on all extremities 14
- 15. • Reflexes - Intact reflexes on all extremities, (-) babinski sign Physical Examination cont. 15
- 17. Primary Impression Acute Intestinal Obstruction probably secondary to Colonic Mass 17
- 18. 18
- 19. Source: American Association of Family Physician, 201419
- 21. Sigmoid Volvulus More Likely Less Likely • Constipation • Cannot be ruled out at this time • Abdominal distention • Tenderness • Abdominal cramping • Patient’s age 22
- 22. Ileus More Likely Less Likely • Constipation • Cannot be ruled out at this time • Abdominal distention • Hypoactive bowel sounds • Diabetes 23
- 23. Diverticular Disease More Likely Less Likely • Constipation • No noted hematochezia • Abdominal distention • Tenderness (LLQ, RLQ, RUQ) • Abdominal cramping • Patient’s age 24
- 24. Work Up 25
- 25. Complete Blood Count WBC 12.57 RBC 4.8 HGB 11.9 HCT 45 PLT 279 NEUTRO 88.5 MCV 87 MCH 30 MCHC 35 RDW 15 PDW 10 MPV 10.2 26
- 26. Blood Chemistry HbA1C (New Method) 4.8% HbA1C (Old Method) 6.5% Urea Nitrogen 30.4 mg/dL Creatinine 1.5 mg/dL Serum Sodium 137 mmol/L Serum Potassium 3.7 mmol/L Chloride 105 mmol/L 27
- 27. Tumor Marker Carcinoembryonic Antigen (CEA) 8.94 ng/ml 28
- 28. CT Whole Abdomen • Dilated Colon and Terminal Ileum • No Colonic Mass Lesion Seen at present study • Dilated Cecum measuring 11.2cm • Findings compatible with Pseudo-Obstruction 30
- 29. Colonoscopy • Obstructing mass about 35cm from the anal verge 31
- 30. Surgical Procedure • Exploratory Laparotomy • Sigmoidectomy • Hartmann’s procedure 32
- 31. Biopsy Result • Sigmoid Mass 33x25x24 mm with attached pericolic fat • Tumor invades through the muscularis propia through the pericolic tissue • Negative tumor on the proximal and distal margins • Negative for metastasis; 4 regional lymph nodes 34
- 32. Final Diagnosis Colonic Adenocarcinoma, Well differentiated Stage IIA (T3,N0,M0) 35
- 33. 36
- 34. Discussion 37
- 35. Epidemiology • 1.2 million new cases of colorectal adenocarcinoma • 600,000 associated deaths • Second only to lung cancer as a cause of cancer death • 10% of all cancer deaths 38
- 36. • Source: Philippine Cancer Society, 2015 39
- 38. Risk Factors 41
- 39. Pathogenesis • Genetic Defects - Mutations may cause activation of oncogenes (K-ras) and/or inactivation of tumor suppressor genes (APC, deleted in colorectal carcinoma) 42
- 40. Pathogenesis Genetic Pathways 1. Loss of heterozygosity pathway 2. The Microsatellite Instability Pathway 3. CpG Island Methylation Pathway 43
- 41. Screening 44
- 42. Screening 45
- 43. Screening 46
- 44. Staging, Prognostic Factors, and Patterns of Spread 47
- 45. Treatment • Total resection of tumor is the optimal treatment when a malignant lesion is detected in the large bowel • 5-FU remains the backbone of treatment • FOLFIRI regimen • FOLFOX regimen • Monoclonal antibodies (Cetuximab, Bevacizumab & Panitumumab) 48
- 46. FOLFIRI regimen • Irinotecan, 180 mg/m2 as a 90-min infusion on day 1 • leucovorin (LV), 400 mg/m2 as a 2-h infusion during irinotecan administration • Immediately followed by 5-FU bolus, 400 mg/m2 • 46-h continuous infusion of 2.4–3 g/m2 every 2 weeks 49
- 47. FOLFOX regimen • 2-h infusion of LV (400 mg/m2 per day) • Followed by a 5-FU bolus (400 mg/m2 per day) and 22-h infusion (1200 mg/m2) every 2 weeks • Together with oxaliplatin, 85 mg/m2 as a 2-h infusion on day 1 50
- 48. Stage Specific Therapy Stage 0 (Tis, N0, M0) • Pedunculated polyps and many sessile polyps may be completely removed endoscopically • Followed with frequent colonoscopy to ensure that the polyp has not recurred Stage I: The Malignant Polyp (T1, N0, M0) • Treatment is based on based on the risk of local recurrence and the risk of lymph node metastasis • Segmental colectomy 51
- 49. Stage Specific Therapy Stages I and II: Localized Colon Carcinoma (T1-3, N0, M0) • Surgical Resection • Adjuvant chemotherapy does not improve survival • Adjuvant chemotherapy has been suggested for selected patients with stage II disease (young patients, tumors with “high-risk” histologic findings) Stage III: Lymph Node Metastasis (Tany, N1, M0) • Surgical Resection • 5-Fluorouracil–based regimens (with leucovorin) and oxaliplatin (FOLFOX) reduce recurrences 52
- 50. Stage Specific Therapy Stage IV: Distant Metastasis (Tany, Nany, M1) • Survival is extremely limited • Focus of treatment is palliation • Most common site of metastasis is the liver followed by the lungs • Approximately 15% will have metastases limited to the liver; 20% are potentially resectable 53
- 52. Prevention • Aspirin and other NSAIDs • Oral folic acid supplements and oral calcium • Vitamin D as a form of chemoprevention is under study • Antioxidant vitamins such as ascorbic acid, tocopherols, and β-carotene are ineffective • Estrogen replacement therapy 56
- 53. Resources • McQuaid K (2012). Approaches to the patient with gastrointestinal disease. In L Goldman, A Shafer, eds., Goldman's Cecil Medicine, 24th ed., pp. 828-844. Philadelphia: Elsevier Saunders • Kasper, D Hauser, S.,Jameson, J., Fauci, A., Longo, D. & Loscalzo, J. (2015). Harrison’s Principles of Internal Medicine. 19th ed. New York: McGraw Hill Education. • Kumar, V., Abbas, A., Fausto, N., & Aster, J. (2010). Robbins and Contran Pathologic Basis of Disease. 8th ed. Philadelphia, PA: Elsevier, Inc. • F. Charles Brunicardi, (2015). Schwartz’s Principles of Surgery. 10th ed. New York: McGraw-Hill Education. • Philippine Cancer Society. (www.philcancer.org.ph) • American Association of Family Physician (www.aafp.org) 57
Editor's Notes
- Hi
- Lactulose is a type of sugar. It is broken down in the large intestine into mild acids that draw water into the colon, which helps soften the stools
- The location and degree of tenderness may provide additional or convincing evidence of such disorders as prostatitis, pelvic inflammatory disease, tubo-ovarian abscesses, ovarian cysts, ectopic pregnancy, and inflammatory bowel disease. Rectal tenderness in suspected appendicitis has been touted as an important diagnostic clue, but the weight of evidence suggests that this finding is of little help
- The patient presented with a 10 day history of constipation accompanied by abdominal bloatedness On physical exam the patient was noted to have tenderness on the RUQ and RLQ aswell as in LLQ The cardinal signs of obstruction are colicky abdominal pain, abdominal distention, emesis, and obstipation
- Algorithm for evaluation and treatment of patients with suspected small bowel obstruction Initial decompression can be performed by placement of a nasogastric (NG) tube for suctioning GI contents and preventing aspiration
- Anything that prevents forward progress of intestinal contents sets into motion this sequence of events, leading to worsening distension, vomiting, and systemic dysfunction. Not only do the resulting dehydration and electrolyte imbalances create significant complications, bacterial proliferation within the static intestinal contents and compromised mucosal integrity set the stage for bacterial translocation across the intestinal wall, with consequent bacteremia and sepsis Intestinal peristalsis slows as the intestine or stomach proximal to the point of obstruction dilates and fills with gastrointestinal secretions and swallowed air Intraluminal air may also accumulate from fermentation, local carbon dioxide production, and altered gaseous diffusion Intraluminal dilation also increases intraluminal pressure. When luminal pressure exceeds venous pressure, venous and lymphatic drainage is impeded. Edema ensues, and the bowel wall proximal to the site of blockage may become hypoxemic Ultimately, arterial blood supply may become so compromised that full-thickness ischemia, necrosis, and perforation result The cecum may progressively dilate such that ischemic necrosis results in cecal perforation This risk is generally greatest when the cecal diameter exceeds 12 cm, as informed by Laplace’s law
- Elevated BUN ⁃ Increased blood urea nitrogen (BUN) may be due to: 1. Prerenal causes (cardiac decompensation, water depletion due to decreased intake and excessive loss, increased protein catabolism, and high protein diet) 2. Renal causes (acute glomerulonephritis, chronic nephritis, polycystic kidney disease, nephrosclerosis, and tubular necrosis) 3. Postrenal causes (eg, all types of obstruction of the urinary tract, such as stones, enlarged prostate gland, tumors) The ratio of BUN to creatinine is usually between 10:1 and 20:1 An increased ratio may be due to a condition that causes a decrease in the flow of blood to the kidneys, such as congestive heart failure or dehydration. It may also be seen with increased protein, from gastrointestinal bleeding, or increased protein in the diet The ratio may be decreased with liver disease (due to decrease in the formation of urea) and malnutrition
- Intraoperatively the obstructing sigmoid mass was noted measuring 33x25x24 Cecum upto the ascending colon was noted to be severely dilated
- Intraoperatively the obstructing sigmoid mass was noted measuring 33x25x24 Cecum upto the ascending colon was noted to be severely dilated
- Approximately 1.2 million new cases of colorectal adenocarcinoma, and 600,000 associated deaths, occur each year worldwide Thus, colorectal adenoma is responsible for nearly 10% of all cancer deaths Cancer of the large bowel is second only to lung cancer as a cause of cancer death
- One hypothesis is that the ingestion of animal fats found in red meats and processed meat leads to an increased proportion of anaerobes in the gut microflora, resulting in the conversion of normal bile acids into carcinogens Obese persons develop insulin resistance with increased circulating levels of insulin, leading to higher circulating concentrations of insulin-like growth factor type I (IGF-I). This growth factor appears to stimulate proliferation of the intestinal mucosa 25% of patients with colorectal cancer have a family history of the disease Polyposis coli (familial polyposis of the colon) is a rare condition characterized by the appearance of thousands of adenomatous polyps throughout the large bowel; autosomal dominant; deletion in the long arm of chromosome 5 (including the APC gene) in both neoplastic (somatic mutation) and normal (germline mutation) cells; loss of this genetic material (i.e., allelic loss) results in the absence of tumor-suppressor genes whose protein products would normally inhibit neoplastic growth If polyposis is not treated surgically, colorectal cancer will develop in almost all patients before age 40 MYH-associated polyposis (MAP) is a rare autosomal recessive syndrome caused by a biallelic mutation in the MUT4H gene; annual to biennial colonoscopic surveillance is generally recommended starting at age 25–30 MUTYH (mutY DNA glycosylase, earlier mutY Homolog (E. coli)) is a human gene that encodes a DNA glycosylase, MUTYH glycosylase, and it is involved in oxidative DNA damage repai
- 5-FU acts in several ways, but principally as a thymidylate synthase (TS) inhibitor. Interrupting the action of this enzyme blocks synthesis of the pyrimidine thymidine, which is a nucleoside required for DNA replication. Thymidylate synthase methylates deoxyuridine monophosphate (dUMP) to form thymidine monophosphate (dTMP). Administration of 5-FU causes a scarcity in dTMP, so rapidly dividing cancerous cells undergo cell death via thymineless death Agents targeting either the vascular endothelial growth factor (VEGF) receptor or the epidermal growth factor receptor (EGFR). Currently available agents in these groups are the anti-VEGF antibody bevacizumab and the anti-EGFR antibodies cetuximab and panitumumab; interference of vital signaling pathways targeted by the antibody and immune cytotoxicity selectively directed against tumor cells by tumor-bound antibody through the Fc portion of the antibody, such as antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity
- Low Dose Aspirin of 81mg OD