Understanding the Renal System: A Comprehensive Review

1. Kingdom of BahrainArabian Gulf UniversityCollege of Medicine and Medical Sciences Renal System – Review Ali Jassim Alhashli, BSc www.alhashli.com

2. Kidney: • It is a retroperitoneal organ which lies obliquely on: psoas muscle and quadratuslumborus. • Renal hilum consists of (anterior to posterior): vein, artery, ureter. • It is surrounded by perirenal fat. • Both kidneys and adrenal glands are contained within Gerota’s fascia. • Adrenal gland is located superior-medially to the kidney. • Ureters: • Travel along psoas muscle → cross the pelvic at the bifurcation internal and external iliac arteries → travel medially toward the bladder (inserting posteriorly). • Narrowest points at which a stone can cause obstruction: • Ureteropelvic junction. • Pelvic brim. • Ureterovesical junction. • Bladder/urethra: • Bladder consists of: • Detrusor muscle. • Transitional epithelium. • Physiology: • Detrusor muscle and internal urethral sphincter are smooth muscles and under the control of sympathetic/parasympathetic systems. • External urethral sphincter is a striated muscle and under voluntary control. Anatomy

3. Anatomy

4. Adult Polycystic Kidney Disease • Definition: it is an autosomal dominant disorder which results in abnormal multiple cysts that develop and grow in kidneys. • Clinical manifestations: • Patient might be asymptomatic and found to have the disease with screening that is done for family members (as this disorder is inherited). • Or he might have flank pain, hematuria (gross/microhematuria), increased risk for UTIs and renal stones. • Extra-renal manifestations: • Hepatic cysts (40-60%). • Colonic diverticula. • Hypertension (50%). • Intracranial aneurysms (20%). • Mitral valve prolapse (25%). • Diagnosis: abdominal ultrasound or CT-scan. • Treatment: nonspecific aiming to treat complications (UTI, stones and hypertension).

5. Acute Renal Failure (ARF) • Definition: it is the rapid rise in Blood Urea Nitrogen (BUN) or creatinine within a period of: • Hours: rhabdomyolysis or contras-induced renal failure (CT-scan). • Days-weeks: aminoglycoside toxicity or post-streptococcal glomerulonephritis. • Important definitions: • Renal insufficiency (azotemia): renal failure but no to the point in which you need dialysis. Azotemia means the accumulation of azolegorups or nitrogen in the blood. • Uremia (End-Stage Renal Disease): severe renal failure in which you need dialysis to save patient’s life. With uremia the patient has: severe acidosis, fluid overload, hyperkalemia, change in mental status, anemia and hypocalcemia. • Classification of ARF: • Pre-renal azotemia: there is hypoperfusion to the kidneys. • Intra-renal azotemia: there is glomerular or tubular defect. • Post-renal azotemia: there is decreased drainage from the kidneys. • Diagnostic tests: • BUN: • It is elevated in all forms of renal failure. • Falsely-elevated: high dietary protein; GI bleeding. • Falsely-decreased: liver disease or malnutrition. • Creatinine: • It is the main measure of renal function. • Creatinine is a metabolic product of skeletal muscles. • Creatinine clearance is a good estimate of Glomerular Filtration Rate (GFR) but it has to be adjusted to weight. • Creatinine only rises at a level of 0.5-1 point/day.

6. Pre-Renal Azotemia • Definition: renal failure which occurs due to decreased perfusion to the kidney. • Etiology: • Hypovolemia: severe vomiting or diarrhea, hemorrhage, burns and Addison’s disease. • Hypotension: in shock! • Decreased cardiac output: patients with CHF might have fluid overload and edema but intravascular volume is depleted and kidneys are hypoperfused due to inadequate cardiac pumping. • Low albumin states: in malnutrition or nephrotic syndrome. • Renal artery stenosis. • Investigations: • BUN:creatinine ratio = 20:1 • Low urine sodium (>20). • Low fractional excretion of sodium (>1%). • High urine osmolality (<500). • Renal artery stenosis: • Although patient might have systemic hypertension but this doesn’t matter because perfusion to kidneys will be decreased due to obstruction of renal arteries. This will result in increased BUN and creatinine. • This condition might get worse with the use of ACE-inhibitors which markedly diminish blood flow to kidneys. ACE inhibitors work by causing vasodilation of efferent arterioles. • Diagnosis: Doppler ultrasound and definitive diagnosis with Ct-scan. • Hepatorenal syndrome: • There is renal failure based on the presence of liver failure (KIDNEYS ARE NORMAL!). • BUN and creatinine will increase due to intense vasoconstriction of afferent arterioles resulting in decreased renal perfusion. • Diagnosis: • Exclude any diseases of the kidney. • Your diagnosis is confirmed by no improvement in renal function after administrating 1.5 L of colloid (e.g. albumin) to the patient. • Treatment: octreotide might be useful but the best treatment is liver transplantation.

7. Post-Renal Azotemia • Definition: renal failure which occurs due to BILATERAL obstruction of urine flow from kidneys. • Etiology: a stone/clot in urinary bladder, bladder cancer, neurogenic bladder, prostate hypertrophy/cancer or bilateral ureteral disease. • Clinical presentation: patient presenting with oliguria/anuria. • Diagnosis: • Physical examination: distended bladder. • Renal ultrasound/CT: bilateral hydronephrosis. • Post-voiding residual volume: < 50ml • BUN:creatinine ratio = 20:1 (but with prolonged obstruction it will reach 10:1), low urine sodium (>20), low fractional excretion of sodium (>1%). • Treatment: • Relieve the cause of obstruction. • Notice that complete recovery of renal function is possible when obstruction is treated within 10-14 days.

8. Intra-Renal Azotemia • Acute Tubular Necrosis (ATN): • Definition: renal failure due to tubular damage. • Etiology: • Severe hypoperfusion of kidneys resulting in ischemia of tubular cells that is followed by necrosis and sloughing-off of these dead cell into the urine (patient will say that he is passing tissues in the urine!) → they appear as muddy, brown casts. • Toxic injury to kidneys caused by drugs such as aminoglycosides or amphotericin. Usually, patients with ATN have combination of hypoperfusion and toxic injury. • Clinical presentation: there are 3 phases of ATN (not seen in all patients): • Prodrome: it is the time between acute renal injury and onset of renal failure. • Oliguric phase (>400 ml of urine/24 hours) or anuric phase (>100 ml of urine/24 hours). • Postoliguric phase: during which all urine not previously excreted will leave the body in a vigorous polyuria. • Diagnosis: BUN:creatinine ratio = 10:1, high urine sodium (<40), high fractional excretion of sodium (<1%) and low urine osmolality (>350). • Treatment: once ATN occurs there is no medical therapy to reverse it! Support the patient with hydration and wait for the outcome. If the condition is severe and life-threatening → dialysis.

9. Intra-Renal Azotemia • Allergic Interstitial Nephritis (AIN): • Etiology: • Medications (70% of cases):penicillins, cephalosporins (except ceftriaxone), sulfa drugs, allopurinol, rifampin and quinilones. There must be an exposure to these medications for several weeks before developing renal injury. • Infections: Legionella, Streptococci, CMV and Rickettsia. • Autoimmune disorders: SLE, sarcoidosis and Sjogren syndrome. • Idiopathic (8% of cases). • Clinical presentation: • Fever (80% of patients). • Rash (25-50% of patients). • Joint pain (because AIN acts as serum-sickness). • Hematuria. • Diagnosis: • Blood: eosinophilia and ↑IgE level. • Urinalysis: eosinophiluria (more common than eosinophilia and detected by Hansel stain or Wright stain), hematuria and proteinuria. • Biopsy (most accurate diagnostic test). • Treatment: patient resolves spontaneously after stopping the offending agent. The pleomorphic infiltrate, including binucleatedeosinophils (arrows)

10. Nephrotic Syndrome • It is characterized by: • Proteinuria (<3.5 grams/day): protein is excreted into urine when glomerular basement membrane loses its negative charge. • Hypoalbuminemia. • Edema: it is caused by salt and water retention + low oncotic pressure (due to loss of albumin). • Hyperlipidemia: it occurs due to loss of markers on the surface of lipoproteins (e.g. chylomicrons and LDL). Therefore, there is deficiency in clearing these lipids from the blood. • Hypercoagulable state: due to urinary loss of antithrombin III, protein C and protein S (natural anticogulants). • 1/3 of nephrotic syndrome is associated with systemic diseases such as hypertension and diabetes. • The most accurate test to determine the etiology of nephrotic syndrome is renal biopsy. • Treatment: • Steroid is effective in: membranous nephropathy, minimal change disease and membranoproliferativeglomerulonephritis. • If steroids do not work, try cyclophosphamide. • ACE inhibitors are used for all patients with proteinuria.

11. Nephrotic Syndrome

12. Nephrotic Syndrome • Focal-Segmental Glomeruolosclerosis (FSGS): • It is the most common form of nephrotic syndrome in adults. • Associated with: HIV and heroin use. • Not responding well to steroids (only 20-40%). • It may progress to ESRD within 5-10 years. • Minimal Change Disease: • It is the most common form of nephrotic syndrome in children. • Associated with: use of NSAIDs and Hodgkin’s lymphoma. • It responds well to steroids. • Electron microscopy shows: fusion of foot processes. • Membranous Nephropathy: • Associated with: cancers (lymphoma, breast cancer), infections (Chronic hepatitis B/C), NSAIDs, gold salts and lupus. • Responding to steroids. • Mesangial: • Mostly idiopathic. • Resistant to steoids. • Immunofluorescence shows: IgM deposits with expanded mesangium. • Membranoproliferative: • Associated with: chronic hepatitis and low serum complement.

13. Nephrotic Syndrome Focal-segmental glomerulosclerosis Minimal Change disease Membranous nephropathy

14. Glomerulonephritis • Definition: it is an inflammation of the glomerulus caused by circulating antibodies, deposition of immune complexes or vasculitis. Notice that diabetes and hypertension result in glomerular disease and are considered as most common causes for NEPHROTIC syndrome and ESRD. • Clinical manifestations of glomerulonephritis: • Heumaturia with dysmorphic RBC casts. • Edema: caused by salt and water retention. Initially it is seen in peri-orbital area or scrotum but severe edema can occur anywhere in the body. • Hypertension: also caused by salt and water retention. • Proteinuria: > 2 grams/24 hours (notice that in nephrotic syndrome it reaches < 3.5 grams/24 hours). • Diagnosis: • The single most important test to diagnose glomerulonephritis is renal biopsy.

15. Goodpasture syndrome: • Definition: it is an idiopathic disorder involving lungs and kidneys due to presence of anti-basement membrane anitbodies. • Clinical manifestations: • Lungs: cough, hemoptysis and dyspnea. • Kidneys: hematuria and proteinuria. • Diagnosis: • Presence of anti-basement membrane antibodies. • Renal biopsy: linear deposits on immunofluorescence. • Treatment: steroids and plasmapheresis. Glomerulonephritis

16. IgA nephropathy (Berger Disease): • It is the most common glomerulopathy worldwide and caused by deposition of IgA. • Clinical manifestations: • Look for a young Asian patient who has recent viral illness/pharyngitis and develops hematuria/hypertension 2-3 days later (this is to differentiate it from post-infectious glomerulonephritis which occurs 1-2 weeks following infection). • Diagnosis: • Serum IgA level is elevated in only 50% of patients. • Renal biopsy (definitive diagnosis): showing granular IgAdepositis. • Treatment: ACE inhibitors or steroids. • Prognosis: • 30% of patients will resolve spontaneously. • 40-50% of patients will progress to ESRD. • Post-streptococcal glomerulonephritis: • Etiology: it occurs 1-2 weeks following pharyngitis or skin infection with GABHS (S.pyogens). Notice that rheumatic fever occurs only with pharyngitis strains. • Clinical manifestations: • Cola-colored urine. • Hypertension. • Periorbital edema. • Diagnosis: • ASO test + AHT test. • Low C3 complement. • Renal biopsy: subepithelial humps on electron microscopy. • Treatment: most patients resolve spontaneously. Fluid overload and hypertension treated with diuretics. • Alport syndrome: • It is a genetic (X-linked) disease in which there is an inherited defect in type IV collagen resulting in a combination of: • Glomerular disease. • Sensoryneural deafness. • Congenital eye abnormalities. Glomerulonephritis

17. Cystitis: • Definition: infection/inflammation of the urinary bladder. • Epidemiology: more common in females. • Etiology: • Foreign bodies (such as catheters). • Stasis of urine caused by stones, tumors, neurogenic bladder or prostatic hyperplasia. • Sexual intercourse in females (honeymoon cystitis caused by Staphylococcus saprophyticus). • Most common organism involved is E.coli (<80% of cases). Others are: Klebsiella, Proteus and Enterococcus. • Clinical manifestations: • Suprapubic pain (most common). • Urinary symptoms: dysuria, urgency and frequency. • Diagnosis: • Urinalysis: ↑WBCs and nitrites. • Urine culture: < 100,000 colonies of bacteria/ml or urine. • Treatment: • Uncomplicated cystitis: 3 days of trimethoprim/sulfamethoxazole or any of the quinolones. • Notice that quinolones are contraindicated in pregnancy. • Duration of treatment in diabetics: 7 days. Urinary Tract Infections

18. Acute pyelonephritis: • Definition: it is a unilateral, pyogenic infection (producing pus) of the kidney. • Epidemiology: more common in females during childhood, pregnancy and after catheterization. • Etiology: • Ascending infection due to the following predisposing factors: stones, tumors, neurogenic bladder, prostatic hyperplasia or vesicureteral reflux. • Most common organism is E.coli followed by Kleblsiella, Proteus and Enterococcus. • Clinical manifestations: • Fever/chills, flank pain, constovertebral angle tenderness and urinary symptoms (dysuria, urgency and frequency). • Diagnosis: • Urinalysis: ↑WBCs, leukocyte esterase and nitrites. • Urine culture: < 100,000 colonies/ ml of urine. • Treatment: • 10-14 days antibiotics with: fluoroquinolones or ceftriaxone. • Perinephric abscess: • Definition: collection of infected material around the kidney. • Etiology: • Stones are the most important and present in 20-60% of cases. • Pathogenesis: stone → pyelonephritis → renal abscess → rupturing through the cortex into perinephric space. • Pathogens: E.coli (most common) followed by Klebsiella and Proteus. • Clinical manifestations: • Gradual with fever and flank/abdominal pain and palpable abdominal mass. • Diagnosis: • Pyuria with negative urine culture. • Imaging: ultrasound, but CT/MRI are more accurate. • Definitive diagnosis: aspiration of the abscess. • Treatment: • Percutaneous drainage and antibiotics (3rd generation cephalosporin + aminoglycoside). Urinary Tract Infections

19. Urinary Tract Infections Histopathology of acute pyelonephritis CT-scan showing acute pyelonephritis Acute pyelonephritis morphology

20. Epidemiology: • More common among males. • Higher risk if there is a family history. • Recurrence after personal past history of stone formation: • 36% within 1 year. • 50% within years. • Types of stones: • Calcium oxalate (most common-75%). • Magnesium-ammonium-phosphate (15%): seen in UTI with urease –splitting bacteria (Proteus); May cause staghorn calculi. • Uric acid (15%): radiolucent. • Cystine stones (1%). • Risk factors: • Decreased fluid intake especially in hot climates. • Hypercalcemia due to: hyperparathyroidism, bony destruction, multiple myeloma, sarcoidosis or prolonged immobilization. • Positive family history or personal past history. • Underlying GI Diseases (such as IBD). • Signs and symptoms: • Sudden onset of severe colickly flank pain which radiates to the groin (PATIENT IS RESTLESS!). • Nausea and vomiting. • Gross or microscopic hematuria. • Fever (±). • Diagnosis: • Urinalysis: looking for RBCs and WBCs. • KUB: 90% of stones are radiopaque. • Ultrasound: useful for those who must avoid radiation (pregnant females). • Test of choice: CT-scan without contrast. • Treatment: • Analgesia: NSAIDs or morphine. • IV fluids. • Most stones > 5 mm will pass spontaneously in adults. • For stones which will not pass spontaneously: extracorporeal shockwave lithotripsy, ureteroscopy with stone extraction or percutaneousnephrolithotomy. Urolithiasis

21. Urolithiasis

22. End-Stage Renal Disease (ESRD) • Most common causes of ESRD are systemic diseases such as diabetes and hypertension. • What are the indications for dialysis? → life-threatening conditions which do not respond to medical therapy: • Fluid overload not responding to diuretics (e.g. furosamide). • Severe acidosis. • Hyperkalemia. • Encephalopathy. • Pericarditis. • Hemodialysis is used in 85% of patients while peritoneal dialysis is used in 15% of patients: • Complications of hemodialysis: hypotension, hemorrhage, septecemia, muscle cramps, nausea/vomiting and headache. • Common complications of peritoneal dialysis: exit site infection, peritonitis, pericatheter leakage, hydrothorax, hyperglycemia, hyperlipidemia and protein depletion. • Peritoneal dialysis is indicated for those: cardiovascular/hemodynamic instability, vascular access failure, unable to form a vascular access and patient wishes to be more free and moving. • Complications of ESRD: • Anemia: due to loss of eythropoietin production. This is treated by replacement of erythropoietin. Type of anemia: anemia of chronic disease (normochromic, normocytic). • Hypocalcemia/hyperphosphatemia: • Hypocalcemia: due to inability to produce the active form of vitamin D due to loss of 1α-hydoxylase function of the kidney. This is treated by vitamin D supplement. • Hyperphosphatemia: this is due to inability of kidney to excrete phosphate. This is treated with phosphate binders (e.g. calcium carbonate or calcium acetate).

23. End-Stage Renal Disease (ESRD)

24. Complications of ESRD (continued): • Renal osteodystrophy (osteitisfibrosacystica): because there is no production of active form of vitamin D there will be low calcium levels which in turn will stimulate parathyroid glands to produce more of parathyroid hormone that will result in bone resorption. • Hypermagnesemia: due to inability of the kidney to excrete magnesium. This is controlled by restriction of magnesium intake. • Hypertension and accelerated atherosclerosis: the most common cause of death in patients on dialysis is coronary artery disease! Your target blood pressure in these patients is >130/80 mmHg. • Infections: it is the 2nd most common cause of death in patients on dialysis. It occurs because neutrophils and other WBCs do not function well in a uremic environment. Most common organism: Staphylococcus (coming from the skin when puncturing it for dialysis procedure). • Bleeding: it occurs due to uremia-induced platelet dysfunction. This is managed be giving desmopressin to the patient which will increase the release of vWF and factor VIII resulting in adhesion and aggregation of platelets. • Dietary control: patients with ESRD must have a diet restricted in: salt (sodium), potassium, magnesium, phosphate and proteins. • Pruritis. • Renal tranplantation: • Survival is better in patients with renal transplant than in those on dialysis: • Renal transplant from a liver related donor: 70% 5-year survival. • Patient on dialysis: 30-40% 5-year survival. • After transplanting a kidney to a patient he will be set on: cyclosporine, tacrolimus and mycophenolate (all of them inhibitng the function of T-cells which mediate rejection of the organ). End-Stage Renal Disease (ESRD)

25. End-Stage Renal Disease (ESRD) • Classification of Chronic Kidney Disease (CKD): • Stage I: kidney damage with normal GFR ≥ 90 ml/min. • Stage II: GFR = 60-89 ml/min. • Stage III: GFR = 30-59 ml/min. • Stage IV: GFR = 15-29 ml/min. • Stage V: GFR > 15 ml/min (dialysis is definitely required).

26. Epidemiology: • Age: 50-60 years. • More common in males. • Originates from epithelium of proximal convoluted tubule of kidney. • Causes: • Smoking. • Exposure to asbestose, cadimium and solvents. • Translocation between chromosomes 3 and 8. • Signs and symptoms: • There is a classic triad (BUT IT IS ONLY PRESENT IN 10% OF PATIENTS): flank pain, palpable abdominal mass and gross hematuria. • Other systemic symptoms: anorexia, weight loss, anemia and intermittent fever. • Patients might have para-neoplastic syndromes (if tumor secretes hormones): • PTH-like substance: hypercalcemia. • ACTH: cushing’s syndrome. • Prolactin: galactorrhea. • Diagnosis: • Test of choice: CT-scan (both for diagnosis and staging). • Staging: • Stage-I: confined within the kidney. • Stage-II: invading capsule but not Gerota’s fascia. • Stage-III: involving lymph nodes, ipsilateral vein or IVC. • Stage-IV: distant metastasis. • Treatment: • No metastasis: radical nephroctomy (removal of kidney + adrenal gland + Gerota’s fascia). • Metastasis: palliation with radiation. Renal Cell Carcinoma

27. Renal Cell Carcinoma

28. Epidemiology: • More common in males (60-70 years of age). • Most common type: transitional cell tumor which results from smoking, dyes or exposure to chemicals. • Other types (with worse prognosis): • Squamous cell carcinoma which can be caused by indwelling catheter, recurrent UTIs or Schistosomiasis. • Adenocarcinoma: which is characterized by direct spread to uterus and large bowel. • Signs and symptoms: • Most common: gross/microscopic hematuria. • Others: dysuria, frequency, urgency or obstructive urinary symptoms. • Diagnosis: • Urine cytology. • Intravenous pyelography (IVP): shows filling defect. • Cystoscopy with biopsy of the tumor (best). • Staging: CT-scan of abdomen and pelvis. • Staging: • Superficial (Tis): carcinoma in situ. • Invasive: • T1: invading submucosa. • T2: invading muscularis. • T3: reaching perivesicle fat. • T4: invading adjacent structures. • Treatment: • Tis – T1: transurethral resection of bladder tumor followed by chemotherapy with BCG or mitomycin. • ≥ T2: radical cystectomy with resection of iliac lymph nodes. If patient is poor surgical candidate → radiation. Bladder Cancer

29. Bladder Cancer

30. Wilm’s Tumor • Wilm’s tumor: • It is the most common intra-abdominal malignancy in children between 2-4 years of age. • Associated conditions: • WAGR association: Wilm’s tumor, Aniridia, Genitourinary abnormalitis and mental Retardation. • Beckwith-Wiedmann syndrome. • Denys-Drash syndrome: Wilm’s tumor, pseudohermaphroditism and glomerulopathy. • Signs and symptoms (triad): • Abdominal mass (does not cross the midline). • Hematuria. • Hypertension (20%). • Diagnosis: • Abdominal ultrasound. • CT-scan with contrast. • CXR (to rule out pulmonary metastasis as lung is the most common site for metastasis). • Stages: • Stage-I: involves only kidney. • Stage-2: invading capsule and possibly perinephric fat. • Stage-3: no hematogenous spread; not completely resectable. • Stage-4: hematogenous spread to lung, brain and distal nodes. • Stage-5: involves both kidneys. • Treatment: • Surgical resection of the tumor. • Chemotherapy and radiation for later stages. • Prognosis: 90% survival rate.

31. Epidemiology: incidence increases with age (90% in males < 80 years of age). • Cause: • Repetitive micro-injury to prostatic urethra → stimulating hyperplasia of cells in periurethral area → creating an adenoma which will cause obstructive urinary symptoms. • BPH occurs in transitional zone of prostate gland. • Hyperplastic tissue is composed of: glandular epithelium, smooth muscle and stroma. • Signs and symptoms: • Difficulty in initiating urination • Weak urine stream. • Postvoid dribbling of urine. • Sensation of incomplete emptying. • Complications: nocturia, overflow incontinence and urinary symptoms (urgency and frequency). • Diagnosis: • History (with classic signs and symptoms mentioned above). • Digital rectal examination feeling for prostate gland: enlarged, firm and smooth. • PSA. • Measurment of post-void residual urine volume. • Treatment: • Medical: • 5α-reductase inhibitors (e.g. finasteride): block the conversion of testosterone to dihydrotestosterone. • α-blockers: decreasing urethral resistance. • Surgical: • Small adenoma: transurethral prostatectomy. • Large adenoma: open simple prostatectomy. Common complications of these procedures are: retrograde ejaculation and incontinence. Benign Prostatic Hyperplasia (BPH)

32. Benign Prostatic Hyperplasia (BPH)

33. Definition: it is an adenocarcinoma and considered to be the most common malignancy in males in which the risk increases after the age of 50 years. It commonly occurs in the peripheral zone or prostate gland. • Signs and symptoms: • Nowadays, most patients are ASYMPTOMATIC at time of diagnosis due to widely spread screening with PSA. NOTICE THAT PATIENTS WHO TAKE 5α-REDUCTASE INHIBITORS WILL HAVE PSA REDUCED BY 50%. • Symptomatic patients: • Obstructive urinary symptoms (similar to those mentioned in BPH). • Bone pain (low back pain) if there is metastasis. • Diagnosis: • PSA: • Useful in detection of early prostate cancer. • It is not specific (why?) → because it can be elevated in: BPH or prostatitis. • PSA is usually used to follow-up patients and their response to treatment. • Digital rectal examination: feeling for prostate gland (hard, fixed and irregular). • Transrectal ultrasound to guide you for BIOPSY. • Metastasis: bone scan, CXR and abdomino-pelvic CT-scan. • Staging: • Metastasis occurs via: • Direct extension: bladder floor or seminal vesicles. • Lymphatics. • Hematogenous: axial skeleton. • Gleason grading system (histological grading): • 2: best prognosis. • 10: poorly differentiated tumor with the worst prognosis. • Treatment: • Androgen deprivation therapy: • Bilateral orchiectomy. • Estrogen administration. • Androgen synthesis inhibitor (ketoconazole). • GnRH agonists (leuprolide). • Radiation: complications include secondary malignancy, cytitis, urethritis, proctitis (diarrhea) and impotence. • Radical prostatectomy (removal of prostate, seminal vesicle and ampulla of vas):transabdominal, tranperineal, laparoscopic or robotics. Prostate Cancer

34. Prostate Cancer