Benign Prostatic Hyperplasia and Colorectal Cancer - Case Study Example

Case Benign Prostatic Hyperplasia Structure of the Pro Gland A pro is a compound tubuloalveolar exocrine gland of the reproductive system of the male, and its main function is for storage and secretion of seminal fluid (Wikipedia, 2008). A human prostate is slightly larger than a walnut. This is anatomically located below the urinary bladder, surrounding the urethra. The prostatic urethra is the part of the urethra situated within the prostate. The human prostate can be divided either by zone or by lobe classification, respectively. The zone classification is oftentimes used in pathology, and the lobe classification is used in the anatomy. For zone classification, the prostate can be divided into four, namely: (a) Peripheral zone, (b) Central zone, (c) Transition zone, and (d) Stroma. Please refer to the table below for the description of each classification, and to the diagrams for the anatomic parts. Zones Description Peripheral zone Constitutes about 70-80% of the normal prostatic volume, and it is from this portion that more that 70% of prostatic cancer originates. Central zone Constitutes about 25% of prostatic volume, and is responsible for more than 25% of prostatic cancer Transition zone Constitutes about 5% of prostatic volume, and is rarely associated with prostatic cancers. Instead, it is from this zone that benign prostatic hypertrophy (BPH) often takes place. Stroma Composes of muscle and fibrous tissue, and is devoid of glandular component. Lobes Description Anterior This part is roughly equated to the transitional zone. Posterior This part is roughly equated to the peripheral zone. Lateral Covers almost all zones. Median This part is roughly equated to the central zone. Physiological Hyperplasia and Pathological Hyperplasia Poore (2007) stated that BPH is "probably a normal part of the aging process of men” and is caused by hormonal imbalance and cell growth factors. Genetics is also known to play a significant role in the disease process. Men, age older than 50, have greater risk of developing BPH. According to Schwartz, et al., (1994), at the age of 30, the normal adult prostate would plateau at a weight of approximately 20 grams. This weight would remain stable until men would reach the age of 50. At the fifth decade of the life of men, hyperplastic growth of the prostate begins, and they have 50% chance of development prostate enlargement. At the age of eighty, almost 90% of men are observed to have histologic evidence of benign prostatic hypertrophy (BPH). At this age, the weight of an average prostate would increase to about 35 grams. Hence, the probability of the developing symptoms is proportional to the probability of histologic hyperplasia. In a clinical setting, the progression of BPH is variable. About 1/3 of the patients who developed BPH will have improvement of symptoms over time, an equal number of patients will have no worsening of symptoms, and the remainder will experience progression of symptoms. According to Schwartz, et al., (1994), “the molecular pathogenesis of BPH is uncertain. It is clear that the process requires aging and testicular androgens.” It was noted that the major androgen in the circulation is the Testosterone (T), which is produced by the testicular Leydig cells. Testosterone diffuses into the prostate cells, and most of it is converted to dihydrotestosterone (DHT), much potent androgen, by the enzyme 5 alpha-reductase. Moreover, both the T and DHT bind to the androgen receptor thereby stimulating the androgen - dependent cell growth, and inhibit the “programmed cell death” seen on the withdrawal of androgen. Even though BPH is not caused by androgen, it is clear that DHT plays a central role in the disease pathogenesis. The 63 - year old patient, who is presented in this case, developed benign prostatic hypertrophy due to a normal physiologic aging process. However, pathologic condition arose secondary to the symptoms presented by the patient, namely: urinary frequency, intermittency, incomplete emptying sensation, and concomitant urinary tract infection. Moreover, as the patient’s age increased, progressive prostatic gland enlargement may pose significant urethral obstruction and would interfere with the normal urinary flow. As mentioned in the earlier part of this section, BPH arise in men over 60 years of age, since it is during the 5th decade of men’s life that hyperplastic growth of the prostate begins, and during this time, men have 50% chance of development prostate enlargement. How BPH Account for the Symptoms of the Patient It is in the periurethral transition zone of the prostate where BPH would first develop. The gland of periurethral zone, proximal to the origin of the transition zone duct, would also undergo hyperplastic growth. In this zonal compartment, the stroma and the epithelial nodules develop leading to the overall size increase of the gland. The peripheral zone, the most common site for prostatic carcinoma development, is compressed between the transition zone and the gland capsule as the prostate enlarges. A human prostate has a prostatic capsule, which plays an important role in prostatism development. Prostatic capsule presumably transmit the expansion of the tissue to the urethra, which leads to urethral resistance increase. Prostatic growth of the aging men is a variable process, and the extensive periurethral zone development may lead to a middle lobe with resulting ball-valve type of obstruction. The tone of the prostatic urethra is influenced by the degree of adrenergic stimulation to the gland because of high density of alpha 1-adrenergic receptors on the surface of the smooth muscle within the prostatic capsule, stroma, and the bladder neck. As a result, this contributes in a dynamic way to outflow obstruction. The development of compensatory muscular hypertrophy is the bladder’s primary response to the enlarging prostate. In order to maintain flow in the face of outflow resistance, the intravesical flow increases. However, due to imperfect adaptation, bladder hypertrophy would lead to urinary frequency and urgency. The bladder wall would become fibrotic, loses compliance, and fails to completely empty the bladder in advanced cases. Post voiding residual time development is common and does not invariably lead to urinary retention and hydronephrosis. BPH is known to be the most common prostate gland disorder, and can have significant impact on the quality of life of the aging male. The disease produces urinary symptoms in the majority of men who are affected with the disease, and the presence of an irritating symptoms or the development of more serious abnormality often leads to therapeutic intervention (Schwartz 1994). Schwartz (1994) added that a mixture of symptoms called prostatism is seen with clinically significant BPH. The following are the symptoms of BPH: urinary frequency and urgency, decreased force of the urinary stream, hesitation of flow initiation, intermittency, incomplete emptying sensation, and nocturia. The patient presented in this study was diagnosed with BPH base from the following evidence: 63 years old male with 6 - month history of difficulty to void, increased urinary frequency, feeling of incomplete emptying sensation, and intermittency. Moreover, the patient also presented with a past medical history of urinary tract infection. This can be explained when BPH causes urinary retention which in turn weakens the muscles of the bladder, thereby, increasing the risk of urinary tract infection and kidney stone development (Lab Tests Online, 2008). This explains why the patient developed to have two episodes of UTI in the past year with concurrent prescription of Ampicillin Prostatic Specific Antigen (PSA) Poore (2007) stated that PSA is the test used to measure the prostatic specific antigen blood level. PSA is released by the prostate gland into the blood. In a normal, healthy man, PSA level in the blood is low. However, as the prostate enlarges with age (in cases of BPH), the amount of blood PSA would normally increase as well. In some cases, PSA will increase during injury, digital rectal examination, sexual activity (ejaculation), prostatitis (inflammation of the prostate gland), and cancer of the prostate. It was further noted that PSA test does not single out well between patients with symptomatic BPH and those with prostate cancer. This is particularly true with pathologically localized and curable cancers. A significant overlap in PSA values between BPH and cancer patients was reported (National Library of Medicine, 2007). Serum PSA level is a valuable test in patients between 50-70 years of age. About 25-30% of men suffering from BPH will have elevated PSA. Outline the approach to assessing urinary outlet obstruction and explain how this might be valuable in the management of BPH. In a patient with BPH, proper extraction of patient’s history and extensive physical examination is the gold standard to have an accurate diagnosis and effective BPH management. Digital rectal examination (DRE) should be a part of the physical examination. DRE should be performed to estimate the size of the prostate, and to detect asymmetry, indurations, and modularity that may lead one to suspect presence of malignancy. Urinalysis must be performed to exclude urinary tract infection and hematuria. The presence of infection may mimic BPH symptoms, or might be an outflow obstruction complication. Furthermore, serum creatinine measurement is important in renal function evaluation. Mild degrees of renal insufficiency should be evaluated by renal sonogram. In rare cases, patients with minimal prostatism may develop obstructive uropathy. PSA should also be determined with BPH patients to rule out prostatic cancer. Other diagnostic examinations are as follows: (a) Uroflow - calculates the urine flow velocity. Maximal urinary flow rate of less than 15 mL/sec is suggestive of an obstruction. (b) Measurement of post void residual (PVR) by catheterization or ultrasound - helps in the assessment of bladder flow response to obstruction. (c) Pressure flow urodynamics - the most sensitive and specific test to confirm the presence of bladder outlet obstruction. This test is done in patients who are at risk in acquiring neurogenic bladder disease as well as to those patients whose diagnosis for BPH remained uncertain after noninvasive tests. (d) Endoscopic evaluation of the lower urinary tract by custourethroscopy - distinguish easily urethral stricture disease from BPH. This also provides information regarding prostatic configuration. This test should be considered prior to invasive or surgical procedures. (e) Renal imaging by excretory urography or by ultrasound - this test is indicated in BPH evaluation in men having concomitant UTI, hematuria, renal insufficiency, history of urolithiasis, and prior urinary tract surgery. Case 2: Colorectal Cancer Why this patient presented with the features illustrated? RM, a 65 - year old, Afro-Caribbean male presented with dyspnoea on exertion, and angina for approximately 3-4 weeks. Past medical history is significant for hypertension, stable angina, and colonic polyps removed 8 years prior by colonoscopy. A smooth and enlarged prostate and a strongly haemoccult-positive stool in the vault were noted during rectal examination. Laboratory findings revealed decreased haemoglobin, haematocrit, and mean cell volume. Liver function tests were within reference range. The ECG revealed mild left ventricular hypertrophy and the chest X-ray was normal. Further investigations were performed, including oesophagogastroduodenoscopy, to evaluate the upper GI tract and colonoscopy to evaluate for a possible colorectal source of bleeding. An abdominoperineal resection was performed and the patient was left with permanent colostomy. In this case, the patient presented with features referable to colorectal carcinoma. The presence of colonic polyps which were removed through colonoscopy eight years prior makes one to suspect likelihood of the patient developing colorectal carcinoma. It was reported that a one-half inch polyp takes 5-10 years or more to turn into cancer (Mansell, 1996). Like any other patient with colorectal cancer, RM presented with symptoms suggestive of colorectal carcinoma such as a strongly haemoccult-positive stool in the vault and iron deficiency anemia. From the laboratory tests, he was found to have decreased haemoglobin, haematocrit, and mean cell volume which are the features of anaemia. The patient was presenting symptoms of colonic lesions of chronic blood loss, with resulting symptoms of angina pectoris. In addition, the advancing age of the patient (65-year old), the history of colonic polyps, high fat diet, and obesity are entailed in colorectal cancer development. Detailed explanation of underlying pathophysiology: Adenomatous polyp gives rise to colorectal carcinoma in nearly all cases. It is estimated that among Americans aged 50 years or older who harbour 40% of adenomatous polyps, 2% of these adenomas will eventually progress into cancer. According to Burke (2003), the colorectal carcinoma develops from a series of molecular and histopathologic changes caused by complex interaction between environmental factors and genetic susceptibleness. These molecular changes are: (a) Multiple, acquired genetic alterations within colonocyte oncogenes, which promotes malignant transformation; and (b) tumor suppressor genes, which causes loss of cellular proliferation inhibition. Mutation in the genes responsible for DNA mismatched base pair (i.e. mismatch repair genes) repair is found to be a newly discovered pathway for carcinogenesis. Cancers in hereditary nonpolyposis colorectal cancer (HNPCC) and approximately 15% of sporadic colorectal cancers are caused by mismatch-repair-gene inactivation. The following are the environmental cofactors implicated in the colorectal carcinoma development. These are: (a) advanced age, (b) high red-meat diet, (c) high fat diet, (d) smoking, (e) alcohol consumption, and (f) and obesity. However, about 70% of newly diagnosed colorectal cancers arise in patients without known risk factors, and only about 30% of colorectal cancer patient have risk factors identified. The following are the risk factors for colorectal carcinoma: (a) adenomas or colorectal cancer history, (b) first-degree relative age < 60 yrs with adenoma or colorectal cancer, or two first-degree relatives of any age with colorectal cancer, (c) inherited colorectal cancer syndromes such as hereditary nonpolyposis colorectal cancer and familiar adenomatous polyposis, and (d) Ulcerative and Crohn’s colitis, respectively. Accordingly, patients with colorectal carcinoma risk are those who possess one of the following dominantly inherited colorectal cancer syndromes: (1) Familial adenomatous polyposis (FAP) caused by tumor suppressor gene APC mutation on the long arm of chromosome 5. APC germline mutation can be detected in about 80% of patient with FAP. Generally, during the second decade of life, APC mutation would result to hundreds to thousands colonic adenoma development. By the age of 40, if prophylactic colectomy is not performed, colonic cancer develops in all FAP patients. (2) Hereditary nonpolyposis colorectal cancer (HNPCC) is caused by alterations of the genes in one of the mismatch repair genes. As a result, adequate repair of DNA is prevented with resultant accumulation of daughter cell mutations leading to carcinogenesis. In about 60% of patients with HNPCC, germ line mutations have been identified in one of six genes. In about 50 of age, colorectal carcinoma would occur in up to 80% of those affected, and is usually right-sided. The following are oftentimes associated with increased risk of colorectal carcinoma: (a) chronic inflammatory colitides, (b) ulcerative colitis, and (c) Crohns disease. The level of risk is distinguished by proximal extent of colonic involvement and the duration of the disease. Pancolitis poses the highest risk, and patients with proctitis pose a negligible risk. The risk of having cancer is increased yearly by 1-2% after a decade of disease. Account for the results obtained in terms of the Development of the Pathology Several factors gathered from the history of the patient as well as from the examinations obtained were of important value in the development of pathology of colorectal carcinoma presented by the patient. The patient was having colonic polyps 8 years prior. Although resection was done through colonoscopy, recurrence is highly expected in patients with colonic polyps, and in nearly all cases, these polyps will give rise to colorectal carcinoma whenever they are left untreated. In addition, several environment cofactors contributed to colorectal carcinoma of this patient, namely: advanced age, high fat diet, and obesity. Staging System of Colorectal Carcinoma The American College of Surgeons’ Commission of Cancer recommended the TNM (tumor-node-metastasis) staging system adoption (Schwartz, et al., 1994). Primary Tumor (T) TX Primary tumor cannot be assessed T0 No evidence of primary tumor Tis Carcinoma in situ T1 Tumor invades sub mucosa T2 Tumor invades muscularis propia T3 Tumor invades through the muscularis propia to the subserosa or into nonperitonealized pericolic or perirectal tissues T4 Tumor perforates the visceral peritoneum or invades directly other organs or structures. Regional Lymph Nodes (N) NX Regional lymph nodes cannot be assessed N0 No regional lymph node metastasis N1 Metastasis in 1 to 3 pericolic or perirectal lymph nodes N2 Metastasis in 4 or more pericolic or perirectal lymph nodes N3 Metastasis in any lymph nodes along the course of a named vascular trunk Distant Metastasis (M) MX Presence of distant metastasis cannot be assessed M0 No distant metastasis M1 Distant metastasis Stage of TNM system: Stage 0 Tis N0 M0 Stage I T1 T2 N0 N0 M0 M0 Stage II T3 T4 N0 N0 M0 M0 Stage III Any T Any T N1 N2, N3 M0 M0 Stage IV Any T Any N M1 More detailed pathologic information is provided by the TNM system and this can easily be converted to Dukes’ system which is simpler staging system. Stage I, II, III, and IV is equivalent to Dukes’ stage A, B, C, and D, respectively. What is the likely prognosis for this patient? Would he require any additional treatment and how would his condition be monitored? From the history of the patient, it was indicated that an abdominoperineal resection was performed and the patient was left with permanent colostomy. Abdominoperineal resection is a “surgical operation to treat usually malignant disease of the rectum or anal canal, and it involves removal of the anus, the rectum and part of the sigmoid colon along with their draining lymph nodes, through incisions made in the abdomen and perineum” (Wikipedia, 2008). Schwartz, et al., (1994) noted that in the absence of obvious metastatic disease, determination of precise colorectal cancer can be determined only after surgical resection and histopathologic analysis. The patient had exhibited unremarkable physical examination except for an enlarge prostate and the presence of strongly haemoccult-positive stool in the vault as well as features of anemia during the laboratory investigation. Liver function test and chest x-ray are all normal. Mild left ventricular hypertrophy noted in the ECG might be the result of the long term effect of hypertension presented in the past medical history of the patient. In the absence of histopathologic results, and from the history, physical examination, and laboratory results of the patient, this patient will likely have a good prognosis. This patient presents with features of having early stage of colorectal carcinoma, and was treated with primary surgical procedure, abdominoperineal resection. The surgical procedure alone would serve as the therapy in the early stage of the disease; however, most surgeons are aggressive in treating colorectal cancer. In so doing, radiation and chemotherapy are added to surgery. According to Schwartz (1994) physical examination, sigmoidoscopy, colonoscopy, liver function tests, carcinoembronic antigen assay, chest radiography, barium enema, liver scan, CT and MRI should be included during the follow - up evaluation of the patient. References Burke, C. (2003). Colon Cancer. Retrieved January 21, 2008 from the database of Cleveland Clinic. Mansell, D. (2006). Colon Polyps and Colon Cancer. Retrieved January 20, 2008 from http://personalweb.sunset.net/mansell/polyp.htm Poore, R. (2007). Illness and Condition. Retrieved from the database of Mount Auburn Hospital. Schwartz, S., and Shires, G., et al. (1994). Principles of Surgery: Neoplastic Disease (6th ed.). USA: McGraw - Hill, Inc. Schwartz, S., and Shires, G., et al. (1994). Principles of Surgery: Benign Prostatic Hypertrophy (6th ed.). USA: McGraw - Hill, Inc. (2007). Highlights of Patient Management. Retrieved January 21, 2008 from http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=hstat6.section.33374 (2007). Overview: Colon and Rectum Cancer. Retrieved January 21, 2008 from the database of American Cancer Society. (2008). Abdominoperineal Resection. Retrieved January 20, 2008 from http://en.wikipedia.org/wiki/Abdominoperineal_resection (2008). Benign Prostatic Hyperplasia. Retrieved January 21, 2008 from http://www.labtestsonline.org/understanding/conditions/bph.html (2008). Esophagogastroduodenoscopy. Retrieved January 20, 2008 from http://en.wikipedia.org/wiki/Esophagogastroduodenoscopy Read More