Prostatic Carcinoma (CaP)

Etiology

  • Notknown

+ Risk factors: 

  • Increased incidence in persons of African descent
  • Family history:
  • High dietary fat increases risk by 2x
  • Cigarette smoking


Epidemiology

  •  Most prevalent cancer in males
  •  Third leading cause of male cancer deaths (following lung and colon)
  •  Lifetime risk of a 50 yrs old man for CaP is 50%, and risk of death from CaP is 3%
  •  75% diagnosed between ages of 60 and 85 and mean age at diagnosis is 72

Pathology

Aadenocarcinoma

  • >95%
  • often multifocal


+ Urothelial carcinoma (4.5%)

  • associated with TCC of bladder
  • does NOT follow TNM staging below
  • not hormone-responsive

+ Endometrial (rare)

  • carcinoma of the utricle

 

Clinical Features

+ Usually asymptomatic

+ Most commonly detected by DRE, elevated PSA, or as an incidental finding on TURP

  • DRE: hard irregular nodule or diffuse dense induration involving one or both lobes
  • PSA: see Prostate Specific Antigen, U24

+ Locally advanced disease:

  • storage and voiding LUTS, erectile dysfunction (all uncommon without spread)
  • suspect with LUTS, incontinence ± back pain

+ Metastatic disease:

  • bony metastasis to axial skeleton is very common (osteoblastic)
  • visceral metastasis is less common with liver, lung and adrenal metastases occurring most frequently
  • leg pain and edema with nodal metastasis obstructing lymphatic and venous drainage

Methods of Spread

  • local invasion
  •  lymphatic spread to regional nodes: obturator > iliac > presacral/para-aortic
  •  hematogenous dissemination occurs early

Investigations

  •  DRE
  •  PSA elevated in the majority of patients with CaP
  •  transrectal ultrasound (TRUS) -7 size and local staging
  •  TRUS-guided needle biopsy
  •  bone scan may be omitted in untreated CaP with PSA <10 ng/ml
  •  CT scanning to assess metastases



Treatment

+ Tl/T2 (localized, low-risk)

  • if adequate life expectancy or no other significant co-morbidities, consider active surveillance vs definitive local treatment (RP, brachytherapy or EBRT)
  • no difference in cure rate between definitive treatment modalities
  • in older population- watchful waiting+ palliative treatment (see below) for symptomatic progression (cancer death rate up to 10%)

+ Tl/T2 (intermediate or high-risk)

  • definitive therapy over active surveillance

+ T3, T4

  • EBRT + androgen deprivation therapy or RP + adjuvant EBRT

+ N >0 or M >0 (see Common Medications, U43)

  • requires hormonal therapy/palliative radiotherapy for metastases; may consider combined androgen blockade
  • bilateral orchiectomy – removes 90% of testosterone
  • GnRH agonists [e.g. leuprolide (Lupron’” or Eligard’”), goserelin (Zoladex’”)]
  • estrogens [e.g. diethylstilbestrol (DES)]
  • antiandrogens [bicalutamide (Casodex’”)]
  • local irradiation of painful secondaries or half-body irradiation
  • in hormone-refractory metastatic prostate cancer, chemotherapy with docetaxel or regiments that include cabazitaxel or sipuleucel-T may improve survival

Management For Dysuria

INTRODUCTION

Description: Dysuria is the painful passage of urine (symptom, not diagnosis).

Prevalence: Common in women, 10% to 20% per year. One third of women during their lifetime.

Predominant Age: Any.

Genetics: No genetic pattern.

ETIOLOGY AND PATHOGENESIS

Causes: Infection and inflammation in the urethra and suburethral tissues. Most urinary tract infections in women ascend from contamination of the vulva and meatus acquired via instrumentation, trauma, or sexual intercourse. (A history of intercourse within the proceeding 24 to 48 hours is present in up to 75% of patients with acute urinary tract infection.) Coliform organisms, especially Escherichia coli, are the most common organisms responsible for asymptomatic bacteriuria, cystitis, and pyelonephritis. Ninety percent of first infections and 80% of recurrent infections are caused by E. coli, with between 10% and 20% resulting from Staphylococcus saprophyticus. Infection with other pathogens such as Klebsiella species (5%) and Proteus species (2%) account for most of the remaining infections. Infection with Neisseria gonorrhoeae, Chlamydia trachomatis, Mycoplasma, and Ureaplasma should all be considered when urethritis is suspected. Chemical irritation, allergic reactions, or vulvitis may all produce symptoms of dysuria.

Risk Factors: Sexual activity, instrumentation, more virulent pathogens, altered host defenses, infrequent or incomplete voiding, foreign body or stone, obstruction, or biochemical changes in the urine (diabetes, hemoglobinopathies, pregnancy) estrogen deficiency, diaphragm use, spermicides.

CLINICAL CHARACTERISTICS

Signs and Symptoms

  • Painful urination
  • Frequency, urgency, nocturia (commonly associated, indicate irritation of the bladder wall)
  • Pelvic pressure (if cystitis is present)
  • Pyuria (more than five white blood cells per high-power field in a centrifuged specimen, most prominent in first one third of voided specimen)

DIAGNOSTIC APPROACH

Differential Diagnosis

  • Cystitis
  • Traumatic trigonitis
  • Urethral syndrome
  • Interstitial cystitis
  • Bladder tumors or stones
  • Vulvitis and vaginitis (may give rise to external dysuria as in herpetic vulvitis)
  • Urethral diverticulum
  • Infection in the Skene’s glands
  • Detrusor instability

Associated Conditions: Dyspareunia, cystitis.

Workup and Evaluation

Laboratory: Nonpregnant women with a first episode of dysuria suggestive of urinary tract infection do not need laboratory confirmation of the diagnosis; they may be treated empirically. (Recent data suggest that this may be an acceptable strategy for women with fewer than three episodes per year, who lack fever or flank pain, and have not been treated recently for the same symptoms.) For others, urinalysis and culture should be performed. For uncentrifuged urine samples, the presence of more than one white blood cell per high-power field is 90% accurate for detecting infection. Gram stain of urine samples or sediments may help to establish the diagnosis or suggest a possible pathogen.

Imaging: No imaging indicated.

Special Tests: A sterile swab inserted into the urethra may be used to obtain material for culture and Gram stain to establish the diagnosis.

Diagnostic Procedures: History and physical examination, urinalysis. (Gentle pressure beneath the urethra or bladder trigone will often reproduce the patient’s symptoms when significant urethritis is present.)

Pathologic Findings

Pyuria (hematuria may be present as well).

MANAGEMENT AND THERAPY

Nonpharmacologic

  • General Measures: Fluids, frequent voiding, and antipyretics. Urinary acidification (with ascorbic acid, ammonium chloride, or acidic fruit juices) and urinary analgesics (phenazopyridine [Pyridium]) may also be added based on the needs of the individual patient.
  • Specific Measures: Antibiotic therapy when infection is suspected.
  • Diet: Increased fluids and reduction of caffeine.
  • Activity: No restriction.
  • Patient Education: Reassurance; American College of Obstetricians and Gynecologists Patient Education Pamphlet AP050 (Urinary Tract Infections).

Drug(s) of Choice

(Nonpregnant Patients)

Single-dose therapy: amoxicillin 3 g, ampicillin 3.5 g, a fi rst-generation cephalosporin 2 g, nitrofurantoin 200 mg, sulfi soxazole 2 g, trimethoprim 400 mg, trimethoprim/ sulfamethoxazole (320/1600 mg). Three- to seven-day therapy: amoxicillin 500 mg every 8 hours, a first-generation cephalosporin 500 mg every 8 hours, ciprofloxacin 250 mg every 12 hours, nitrofurantoin 100 mg every 12 hours, norfloxacin 400 mg every 12 hours, ofloxacin 200 mg every 12 hours, sulfisoxazole 500 mg every 6 hours, tetracycline 500 mg every 6 hours, trimethoprim/sulfamethoxazole 160/800 mg every 12 hours, trimethoprim 100 (200) mg every 12 hours.

  • Contraindications: Known or suspected hypersen – sitivity.
  • Precautions: Urinary analgesics (phenazopyridine [Pyridium]) should be used for no longer than 48 hours and may stain some types of contact lenses.
  • Interactions: See individual medications.

Renal Cell Cancer in Management

  • Renal Cell Cancer or Hypernephroma is a serious pathological condition of the kidney. Renal cell cancer originates from small renal tubules of the kidney. Kidney tubule functions as a filtering apparatus of the body. The survival rate of the advanced renal cell carcinoma or cancer is usually five years. Renal cell carcinoma is often resistant to radiation and chemotherapy treatment. In this article, we will discuss in detail about the various causes, symptoms, and treatment options for Renal Cell Cancer.

How Do We Define Renal Cell Cancer Or Hypernephroma?

  • Renal Cell Cancer is also known by the name of Hypernephroma.
  • Cancer of Proximal Convoluted Tubule
  • The cancer of the kidneys stems from the lining of proximal convoluted tubule.

Renal Filter

  • Renal symptoms are caused by abnormalities of electrolytes, metabolites and water retention.
  • Capillaries surround the tubule. Capillaries are integrated with proximal tubule. The excessive electrolytes, metabolites and water are filtered in proximal convoluted tubule from capillary blood.
  • Most of the electrolytes and water are reabsorbed into blood.
  • Excessive water and unwanted metabolites are discharged as urine.

Common Cancer

  • Renal Cell Cancer or Hypernephroma is one of the commonest forms of cancer of the kidneys and constitutes for more than 75% of cases of kidney cancer.

Fatal Cancer Growth

  • Renal Cell Cancer or Hypernephroma is also termed to be one of the most lethal tumors of the Genitourinary System.

Non-Metastasize Cancer

  • Non-metastasize cancer is treated by removal of kidney.
  • Survival rate is over 5 years in over 65% of the cases.

Treatment Resistant

  • Renal Cell Cancer is resistant to chemotherapy and radiation treatment, thus metastatic spread is often difficult to treat.
  • Incidental Asymptomatic Renal Cell Tumor.
  • The disease is asymptomatic during initial stage and diagnosis is delayed until cancer is spread in distant organ.

Causes Of Renal Cell Cancer Or Hypernephroma

Age Factor

  • It is usually known to occur in adults in the age range of 50-70.

Hereditary Factor

  • The exact cause of Renal Cell Cancer/Hypernephroma is unknown.
  • Family history of Renal Cell Cancer/Hypernephroma
  • Hereditary is one of the causes not yet eliminated.
  • NSAIDs (Non-Steroidal Anti-Inflammatory Drugs)
  • Long-term use of NSAIDs is associated with cancer of the kidney.

Occupational Hazards

  • Exposure to chemicals- asbestos, cadmium, lead, chlorinated solvents and petrochemicals.

Dialysis

  • Several years of dialysis may be triggering the cancerous activities of the renal cells.
    Risk Factors Of Renal Cell Cancer Or Hypernephroma
  • Hypertension
  • Horseshoe Shaped Kidney
  • Polycystic Renal Disease
  • Tobacco abuse and Obesity.

Symptoms Of Renal Cell Cancer Or Hypernephroma

Nonspecific Symptoms of Renal Cell Cancer Or Hypernephroma

  • Weakness and fatigue
  • Loss of weight
  • Loss of appetite
  • Specific Symptoms of Renal Cell Cancer Or Hypernephroma

Pain

  • Moderate to severe flank pain often radiates to lower back
  • Severe abdominal pain, intensity becomes severe following abdominal examination.

Abdominal Mass

  • Abdominal mass is felt during examination on right or left side of the umbilicus.

Urine Discoloration

  • Urine may be dark brown or red because of bleeding from cancer in to renal tubule.
  • Increased Erythropoietin Secretion
  • Deep vein thrombosis
  • Polycythemia
  • Decreased Erythropoietin Secretion

Pale skin

  • Anemia
  • Increased Angiotensin Secretion

Vision problems

  • Hypertension
  • Night sweating
  • Diagnosis Of Renal Cell Cancer Or Hypernephroma

Urine Examination

  • Hematuria
  • Proteinuria
  • Frank Blood in urine
  • Bacteria in urine

Blood Examination

  • Complete Blood Cell Count (CBC)-
  • White Blood Cell Count- Elevated, if renal cell cancer is associated with kidney or bladder infection.
  • Red Blood Cell Count- Elevated, secondary to increased erythropoietin secretions.
  • Platelet Count- Elevated, secondary to increased secretion of erythropoietin hormone.
  • Hemoglobin
  • Decreased hemoglobin results in anemia secondary to decreased secretion of erythropoietin in few cases.
  • Erythrocyte Sedimentation Rate (ESR)-
  • ESR is elevated.

Kidney Function Test

  • Blood urea nitrogen- Elevated
  • Creatinine- Elevated
  • Liver Enzyme Test- (Elevated If Cancer is Metastasized in Liver)
  • Aspartate Aminotransferase (AST)- Elevated
  • Alanine Aminotransferase (ALT)- Elevated

Hydronephrosis

Dilation of the renal pelvis and calyces caused by the backward pressure of trapped urine.

Etiology

Mechanical:

+ Congenital

+ Acquired:

  • Intrinsic: trauma, inflammation and bleeding, calculi, urologic neoplasms, BPH, urethral stricture, phimosis
  • Extrinsic: trauma, neoplasms (uterine fibroid; colorectal, uterine, and cervical malignancies; lymphoma), aortic aneurysm

+ Functional:

  • Neurogenic: neurogenic bladder, diabetic neuropathy, spinal cord disease
  • Pharmacologic: anticholinergics, a-adrenergic agonists
  • Hormonal: pregnancy can cause hydronephrosis due to hormonal effects on ureteral tone and mechanical pressure

Investigations

  • Focused history, inquiring about pain (flank, lower abdomen, testes, labia), urine output, medication use, pregnancy, trauma, fever, history ofUTis, calculi and pelvic inflammatory disease (PID)
  • CBC, electrolytes, Cr, BUN, urine R&M, C&S
  • Imaging studies (ultrasound is >90% sensitive and specific for hydronephrosis)

Treatment

    • Treatment depends on cause, and aims to relieve the cause of obstruction/stasis
    • Urgent treatment is required if associated with infection, acute renal failure, or severe pain

  • Percutaneous nephrostomy tube or ureteral stenting to relieve pressure

Gonnococcal Urethritis in Men

Urethritis is a well-defined clinical syndrome manifested by dysuria, a urethral discharge, or both.

_ The major single specific etiology of acute urethritis is Neisseria gonorrhoeae, producing gonococcal urethritis (GCU). Urethritis of all other etiologies is called nongonococcal urethritis (NGU).

_ N. gonorrhoeae is a gram-negative, kidneyshaped diplococcus with flattened opposed margins. The urethra is the most common site of infection in all men.

CLINICAL

_ Symptoms of GCU: urethral discharge and dysuria are the most common symptoms. There is complaint of urethral itching. Prostatic involvement can cause frequency, urgency, and nocturia. It can involve the epididymis through spreading down the vas deferens, causing acute epididymitis.

_ Incubation period: 3 to 10 days. Without treatment, urethritis persists for 3 to 7 wk, with 95% of men becoming asymptomatic after 3 mo. GCU is asymptomatic in up to 60% of contacts.

_ Signs of GCU: yellow-brown discharge, meatal edema, urethral tenderness to palpation.

LABORATORY TESTS

  • Nucleic acid amplification tests (NAATs)
  • Calcium alginate or rayon swab on a metal shaft (not cotton-tipped swabs, which are bactericidal) of the urethra should be performed anywhere from 2 to 4 hr after voiding to prevent bacterial washout with voiding
  • Concomitant serologic testing for syphilis on all patients.
  • Concomitant Chlamydia testing on all patients.

MANAGEMENT

  • Ceftriaxone 250 mg IM × 1 dose plus azithromycin 1 g orally single dose. Doxycycline 100 mg orally twice/day for 7 days can be substituted for azithromycin in cases of allergy to azithromycin.

_ Alternative regimens

  • Cefixime 400 mg PO × 1 dose plus azithromycin 1 g orally single dose.

Renal Vein Thrombosis Management

DEFINITION
Renal vein thrombosis is the thrombotic occlusion of one or both renal veins.

EPIDEMIOLOGY & DEMOGRAPHICS
• Incidence unknown; probably an underdiagnosed condition
• May occur at any age with no gender preference
• Epidemiology tied to the underlying cause.


PHYSICAL FINDINGS & CLINICAL PRESENTATION
Acute bilateral renal vein thrombosis:
• Back and bilateral flank pain
• Acute renal failure
Acute unilateral renal vein thrombosis:
• Flank pain
• Decline in renal function
• Hematuria
• Increase in the amount of proteinuria if associated with nephrotic syndrome
Chronic unilateral renal vein thrombosis:
• May be silent
• Pulmonary emboli and hemolysis
• Back pain
• Deep vein thrombosis in lower extremities
• Edema
• Glycosuria
• Hyperchloremic acidosis
• Left varicocele (if the left renal vein is thrombosed)
• Dilated abdominal veins

DIFFERENTIAL DIAGNOSIS
The diagnosis of renal vein thrombosis does not include any differential consideration. The differential diagnosis is that of proteinuria. Renal vein thrombosis should be considered if proteinuria worsens or if renal function worsens
in a patient with glomerulonephritis. Renal vein thrombosis should also be considered in patients with pulmonary emboli and no lowerextremity deep vein thrombosis.

TREATMENT

• Anticoagulation in acute renal vein thrombosis to prevent pulmonary emboli and in attempt to improve renal function and decrease proteinuria
• Thrombolytic therapy or surgical thrombectomy has also been reported to be effective
• The value of anticoagulation in chronic renal vein thrombosis is dubious except in nephrotic patients with membranous glomerulonephritis with profound hypoalbuminemia where prolonged prophylactic anticoagulation
may be of benefit even if renal vein thrombosis has not been documented.