UROLOGY ICM/PATH

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UROLOGY ICM/PATH by Mind Map: UROLOGY ICM/PATH

1. Pediatric Urology

1.1. What is Pediatric Urology?

1.1.1. Surgical subspecialty focused on disorders of the pediatric genitourinary tract

1.1.1.1. *Congenital anomalies of the bladder, kidney, ureters -->Reflux, obstruction, neurogenic bowel and bladder *Congenital anomalies of the penis, urethra, testicles -->Hypospadias, undescended testicles, chordee *Pediatric cancers of the bladder, kidney, testicle, prostate -->Rhabdomyosarcoma *Disorders of the sexual differentiation -->CAH, Mixed Gonadal Dysgenesis, Androgen Insensitivity *Pediatric Urolithiasis *Voiding dysfunction -->Nocturnal enuresis, incontinence

1.1.2. Common Problems in Pediatric Urology

1.1.2.1. Antenatal Hydronephrosis

1.1.2.1.1. Antenatal Hydronephrosis

1.1.2.2. Ureteropelvic junction obstruction (UPJ)

1.1.2.2.1. Indications for surgery: Symptomatic Hypertension Decreased function with delayed drainage Worsening US or Renal Scan

1.1.2.2.2. Need at least a US (or CT) and Renal Scan before surgery

1.1.2.3. Vesicoureteral Reflux (VUR)

1.1.2.3.1. Workup: RBUS and VCUG *Indications for prophylactic antibiotics -->High grade 3-5 VUR, severe hydro, duplicated systems -->Voiding Dysfunction -->~5% reduction in UTI risk *Indications for surgery: -->Breakthrough febrile UTI -->Renal Scarring

1.1.2.4. Hydroceles

1.1.2.4.1. Patent processus normal at birth may resolve over time

1.1.2.4.2. If fluctuating and not improving after 1 year can consider correction

1.1.2.4.3. If any bowel contents felt or identified in groin needs urgent correction

1.1.2.5. Hypospadias

1.1.2.5.1. Buried Penis: DO NOT CIRCUMCISE

1.1.2.5.2. Hypospadias: DO NOT CIRCUMCISE

1.1.2.5.3. Any concern: DO NOT CIRCUMCISE

1.1.2.6. Undescended Testicles

1.1.2.6.1. If not descended by 6 months, unlikely to descend

1.1.2.6.2. Earlier intervention seems to reduce testicular cancer risk and increases fertility potential

1.1.2.6.3. No imaging needed, unless obese or bilateral undescended (US best)

1.1.2.7. (Acute Scrotum) Testicular Torsion

1.1.2.7.1. Acute scrotum is testicular torsion until proven otherwise

1.1.2.7.2. Torsion = OR for exploration, possible salvage and contralateral fixation

1.1.2.7.3. Epididymitis (pediatric) – almost always chemical: ibuprofen, scrotal support

1.2. How to think about Pediatric Urological Disorders

1.2.1. Take home points for each common urologic conditions: Pediatric urology usually just comes down to plumbing

1.2.1.1. The 3 studies of Pediatric Urology: *Renal Bladder US -->Anatomy of the kidneys and bladder *Voiding Cystourethrogram -->Function, appearance of bladder, reflux, urethra *Mag 3 renal scan -->Measure function and drainage, check for obstruction

2. References

2.1. Prostate Cancer Visual MD http://www.thevisualmd.com/center.php?idg=8188

2.2. Prostate Cancer http://www.youtube.com/watch?v=1AiY_G-l6Ic

2.3. Prostate Cancer Treatment Options- Dr. Troy Gianduzzo http://www.youtube.com/watch?v=k8i9gu3K1lY

2.4. Nutrition Facts and Prostate Cancer http://www.youtube.com/watch?v=DEAcUyv4LZ4

2.5. Prostatectomy Using the da Vinci http://www.youtube.com/watch?v=6At3zIwwk7Q

3. Nephrolithasis

3.1. Epidemiology

3.1.1. 16-24 cases per 10,000

3.1.2. Prevalence: 7% in males, 3 % in females

3.1.3. Males have a 3-4 fold increased risk of stones. Infectious stones are more common in females

3.1.4. Age: peak incidence – 20-40years

3.1.5. 10% of all first time stone formers will have a recurrence in 1year and 50% in 10 years

3.2. Pathogensis

3.2.1. Genetics

3.2.1.1. Idiopathic hypercalciuria: autosomal dominant

3.2.1.2. Cystinuria: autosomal recessive

3.2.1.3. Primary hyperoxaluria: autosomal recessive

3.2.1.4. Lesh-Nyhan syndrome, familial renal tubular acidosis

3.2.2. Diet

3.2.2.1. High protein and sodium intake- hypercalciuria

3.2.2.2. High purine diets- hyperuricosuria

3.2.2.3. Pyridoxine deficiency- hyperoxaluria

3.2.2.4. Dehydration

3.2.2.5. Vitamin C excess

3.2.3. Geographical/Seasonal Factors

3.2.3.1. Southern US

3.2.3.2. Summer

3.3. Stone Composition

3.3.1. Calcium oxalate 36-70%

3.3.1.1. Calcium Stone Etiology

3.3.1.1.1. Hypercalciuria

3.3.1.1.2. Hypocitraturia

3.3.1.1.3. Hyperuricosuria

3.3.1.1.4. Hyperoxaluria

3.3.2. Calcium phosphate 6-20%

3.3.3. Mixed calcium oxalate and phosphate 11-31%

3.3.4. Magnesium ammonium phosphate (Struvite) 6-20%

3.3.5. Uric acid: 6-17%

3.3.6. Cystine: 05-3%

3.3.7. Miscellaneous: Xanthine, silicates, triamterene, etc

3.3.8. Cholesterol does NOT form kidney stones

3.4. Presentation: Clinical Features

3.4.1. Pain: colicky flank pain, can radiate

3.4.2. Can be due to ureteral obstruction: at sites of ureteral narrowing:

3.4.2.1. Uretero-pelvic junction (UPJ)

3.4.2.2. Level of iliac vessels

3.4.2.3. Uretero-vesical junction (UVJ)

3.4.3. Nausea and vomiting

3.4.4. Irritative voiding symptoms

3.4.5. Flank tenderness

3.4.6. Hematuria

3.5. Diagnosis

3.5.1. What will a patient with Nephrolithasis have on urinalysis?

3.5.1.1. Microhematuria: present in about 90% of patients

3.5.1.2. Crystalluria: cystine

3.5.1.3. UTI on urine culture

3.5.1.4. Leukocytosis

3.6. Diagnostic Test

3.6.1. Radiology

3.6.1.1. Non-contrast CT: 97% sensitivity and 96% specificity IVP: Useful for treatment planning for calyceal anatomy Renal ultrasound: Pregnant females KUB

3.6.2. Metabolic WorkUp

3.6.2.1. Indications

3.6.2.1.1. Recurrent urolithiasis

3.6.2.1.2. Bilateral stones

3.6.2.1.3. Large stone burden

3.6.2.1.4. Children

3.6.2.1.5. Risk factors

3.7. Treament

3.7.1. Tx of Acute Renal Colic

3.7.1.1. Analgesia: ketorolac, demerol

3.7.1.2. Hydration: >80% of ureteral stones <4mm pass spontaneously

3.7.1.3. Alpha adrenergic antagonist: tamsulosin

3.7.1.4. Urgent referral to a urologist

3.7.1.4.1. Persistent pain Stone unlikely to pass spontaneously Solitary kidney High grade obstruction UTI, signs of sepsis Urinary extravasation

3.7.2. Summary of Tx options for Urinary Calculi

3.7.2.1. Conservative Management

3.7.2.1.1. hydration, pain control : <4mm

3.7.2.1.2. Relieve obstruction (Percutaneous or Endoscopic)

3.7.2.1.3. Alkalinization

3.7.2.2. ESWL – Extra-corporal shock wave lithotripsy

3.7.2.2.1. Kidney <2 cm with good drainage

3.7.2.3. PCNL – Percutaneous nephrolithotomy

3.7.2.3.1. Kidney >2 cm

3.7.2.4. Ureteroscopy (laser, EHL, basket)

3.7.2.4.1. Distal > mid > upper

3.7.3. ESWL

3.7.3.1. Factors Affecting SWL

3.7.3.1.1. Stone Composition

3.7.3.1.2. Stone size

3.7.3.1.3. Patient size

3.7.3.2. Contraindication of SWL

3.7.3.2.1. Pregnancy

3.7.3.2.2. Uncorrected coagulopathy

3.7.3.2.3. UTI

3.7.3.2.4. Uncontrolled hypertension

3.7.3.2.5. Distal obstruction

3.7.4. Ureteroscopy

3.7.4.1. Indications

3.7.4.1.1. Distal ureteral stones that have failed conservative treatment

3.7.4.1.2. Ureteral stones>1cm

3.7.4.1.3. Some Renal stones not amenable to ESWL

3.7.4.2. Flexible Ureteroscope

3.7.4.3. Holminum Laser Lithotripsy

3.7.4.4. PCNL

3.7.4.4.1. Indications

3.7.5. Percutaneous Renal Access

3.7.6. Prevention

3.7.6.1. General measures

3.7.6.1.1. Can reduce 5 year recurrence by 60%

3.7.6.1.2. Increase fluid intake to maintain urine output >2 lts./day

3.7.6.1.3. Low animal protein diet (1g/kg/d)

3.7.6.1.4. Low sodium diet (2-3g/day)

3.7.6.1.5. Calcium restriction not normally required

3.8. Complications

3.8.1. Hemorrhage, Obstruction, and Infection

3.9. Summary

3.9.1. Low urine output is the most common cause for renal stones

3.9.2. Noncontrast CT is the best initial diagnostic test

3.9.3. Clinicians should assess the need for urgent intervention and the likelihood of spontaneous passage

3.9.4. Urologic intervention must be individualized.

3.9.5. Open surgery is rarely required

4. Prostate Cancer

4.1. Prostate Anatomy

4.1.1. Normal prostate Anatomy

4.1.1.1. The prostate normally produces fluid important to the survival of sperm. After the reproductive years, it is the source of significant morbidity and mortality to men through BPH and prostate cancer. It is strategically located near the nerves for sexual function (nervi erigentes), external urinary sphincter, rectum, bladder, and the ureters.

4.1.2. Prostate and Bladder Proximity

4.1.2.1. Seen in this schematic view, the prostate encircles the urethra just below the bladder. The nervi erigentes course posterolateral to the prostate and lateral to the urethra. These parasympathetic nerves cause release of nitric oxide in the corpora cavernosa which is responsible for male erections.

4.2. Prostate Screening

4.2.1. Note: The prevalence of prostate cancer increases with age.

4.2.1.1. Additionally, the prevalence of BPH increases with age as well; however, it is a gradual increases in prevalence.

4.2.2. Prostate Specific Antigen

4.2.2.1. Serine protease related to the kallekrein family

4.2.2.2. Normal function is to liquefy the ejaculate

4.2.2.3. First developed by forensic pathologists for use in sexual assault cases

4.2.2.4. Almost completely specific to prostate tissue

4.2.2.5. Details about PSA Screening

4.2.2.5.1. The characterization of serum prostate specific antigen (PSA) has been undoubtedly the most significant advance in prostate cancer in many years. PSA was first isolated and characterized by forensic pathologists for use in sexual assault cases. It is a serine protease, related to the kallekrein family, which is produced by the epithelial cells in the prostate. Its normal function appears to be to liquefy the ejaculate. This enzyme is only produced by prostate tissue.

4.2.2.5.2. It is unique amongst tumor markers in that it is elevated in 90% of cases of localized disease and the serum level is zero in men that have had their prostate removed. While it is entirely specific to the prostate and produced by no other organ or tissue, it is not specific for specific prostatic conditions. For example, with low level elevations of 4-10 (normal <4ng/ml), the most common cause is benign prostate enlargement. Most importantly, in men that have undergone ablative treatment of the prostate such as radiation therapy or radical prostatectomy, PSA levels should be very low to undetectable if the prostate cancer has been eradicated.

4.2.3. ACS Guidelines for Prostate Cancer Screening

4.2.3.1. 50 years of age discuss screening

4.2.3.1.1. Pt should make informed decision

4.2.3.1.2. Annual PSA and DRE

4.2.3.2. 45(40) years of age and high risk

4.2.3.2.1. African American

4.2.3.2.2. Positive family history

4.2.4. Note: The incidence of Prostate Cancer is rising.

4.2.4.1. More people are getting diagnosed with Prostate Cancer because they are living longer. And less people are dying from Prostate Cancer.

4.2.5. Hereditary Prostate Cancer Risk Stratification

4.2.5.1. 9 % of all cancers

4.2.5.1.1. Higher proportion of cases < 55 y/o

4.2.5.2. First degree relative 2.4

4.2.5.2.1. Father or Brother

4.2.5.3. Second degree relative 2.1

4.2.5.3.1. Grandfather or Uncle

4.2.5.4. 2 affected relatives 4.9

4.2.5.5. 3 affected relatives 10.9

4.2.5.6. No clinical difference

4.2.6. Note: Some PSA levels are based on age and race.

4.2.6.1. Figure 1-8. Age- and race-specific prostate-specific antigen (PSA) levels. The 95th percentile of PSA levels seen in men without prostate cancer (95% specificity) and the PSA range required to maintain the detection of 95% of prostate cancers (95% sensitivity) have been used to establish `normal´ age-specific reference ranges among black and white men. PSA increases with age, primarily because of increases in prostate size, and age-adjustment of PSA are ways of accounting for this size increase with age.

4.2.6.2. It has been suggested that use of an age-adjusted PSA rather than a single PSA cutoff for all ages may lead to increased cancer detection in younger men more likely to benefit from treatment and minimize unnecessary evaluations in older men who are less likely to benefit from treatment. It has been shown that PSA levels are higher in black men without prostate cancer than in white men without prostate cancer of the same age. It has not definitely been shown, however, that use of age- or race-specific reference ranges has an advantage in detecting curable cancer over the use of a single cut-point of 4.0 ng/mL. Currently, the data suggest that a cut-point of 4.0 ng/mL­using the Tandem assay (Hybritech, San Diego, CA)­is an effective threshold for maximizing prostate cancer detection and minimizing unnecessary biopsies in men between the ages of 50 and 70 years. The optimal PSA threshold, ie, the cutoff that will result in detection of clinically significant cancers in those men who are most likely to benefit from treatment, is not known.

4.2.6.3. For younger men, a greater index of suspicion is warranted at PSA levels below 4.0 ng/mL because the relative risk of cancer is increased even at PSA levels between 2.0 and 4.0 ng/mL: these men have the most to gain from early diagnosis and treatment of prostate cancer. A greater suspicion of prostate cancer at lower PSA levels is especially important in the setting of known risk factors of family history and black race. The use of higher PSA thresholds among older men, who are less likely to benefit from prostate cancer treatment, should take into consideration the overall health and life expectancy of the individual.

4.2.6.4. For younger men, a greater index of suspicion is warranted at PSA levels below 4.0 ng/mL because the relative risk of cancer is increased even at PSA levels between 2.0 and 4.0 ng/mL: these men have the most to gain from early diagnosis and treatment of prostate cancer. A greater suspicion of prostate cancer at lower PSA levels is especially important in the setting of known risk factors of family history and black race. The use of higher PSA thresholds among older men, who are less likely to benefit from prostate cancer treatment, should take into consideration the overall health and life expectancy of the individual.

4.3. Diagnosis of Prostate Cancer

4.3.1. Clinical Staging with Digital Rectal Exam

4.3.2. When to biopsy a Prostate

4.3.2.1. Elevated PSA (>4.0)

4.3.2.1.1. Age Specific (>2.5)

4.3.2.1.2. PSA Density (>.15 ng/cc)

4.3.2.1.3. PSA Velocity (>.75 ng/yr)

4.3.2.1.4. Low % Free PSA (<15%) (4-10 range)

4.3.2.2. Palpable nodule

4.3.3. Grading of Prostate Cancer (Gleason's Score)

4.3.3.1. Chance of Death from Observed Localized Prostate Cancer

4.3.3.1.1. One of the most confusing issues in prostate cancer is regarding its biologic significance. Prostate cancer invariably progresses in every patient how, the rate that it progresses is highly variable and in some cases very slow. The old adage that men usually die with prostate cancer and not from it is frequently correct, particularly in older men with well differentiated tumors. However, younger healthier men, particularly those with Gleason’s score 7 and higher, are very likely to suffer morbidity and or mortality if their disease cannot be eradicated. In general, urologists select those patients with estimated life expectancies of at least 10 years for treatment based upon these principals.

4.3.4. TNM Staging System

4.3.5. Staging Evaluation

4.3.5.1. CT Scan PSA >10, GS >7 Bone Scan PSA >20, GS >7

4.3.6. Patterns of Metastasis

4.3.6.1. Bone

4.3.6.2. Lymph Nodes

4.3.7. Prostate Cancer Under Hormonal Control

4.4. Treatment of Prostate Cancer

4.4.1. Options (The Benefits)

4.4.1.1. Watchful Waiting

4.4.1.1.1. No immediate risks

4.4.1.2. Prostatectomy - Retropubic, Perineal, Laparoscopic

4.4.1.2.1. Best chance for long term cure

4.4.1.3. Radiotherapy External beam, Brachytherapy, Proton beam

4.4.1.3.1. Similar to surgery at 10 years

4.4.1.4. Hormonal Blockade – Orchiectomy, LHRH agonist, Antiandrogens

4.4.1.4.1. 95% initially respond

4.4.1.5. Thermal Therapy - Cryotherapy, High Intensity Focused U/S

4.4.1.5.1. Minimally invasive

4.4.2. Options (The Risks)

4.4.2.1. Watchful Waiting

4.4.2.1.1. Disease progression

4.4.2.2. Prostatectomy - Retropubic, Perineal, Laparoscopic

4.4.2.2.1. Impotence, incontinence, bleeding, infection

4.4.2.3. Radiotherapy External beam, Brachytherapy, Proton beam

4.4.2.3.1. Rectal and urinary frequency

4.4.2.4. Hormonal Blockade – Orchiectomy, LHRH agonist, Antiandrogens

4.4.2.4.1. Hot flashes, water retention, fatigue, metabolic syndrome

4.4.2.5. Thermal Therapy - Cryotherapy, High Intensity Focused U/S

4.4.2.5.1. Long term data not available

4.4.3. Treatment Options Risk vs Benefits Analysis

4.4.3.1. Provide Information

4.4.3.2. Help patient make choice

4.4.3.3. Individualize treatment to patient

4.4.3.3.1. Nomagrams

4.4.3.4. Support patient’s decision

4.5. Prostate and Testis Pathology

4.5.1. Prostate

4.5.1.1. Acute Bacterial Prostatitis

4.5.1.1.1. May present with fever, chills, pain, and obstructive symptoms

4.5.1.1.2. DRE: swollen, tender prostate

4.5.1.1.3. E. coli accounts to 80% of cases

4.5.1.1.4. Diagnosis confirmed by culture of midstream urine or prostatic secretions

4.5.1.1.5. Biopsy contraindicated

4.5.1.1.6. Histological findings: Neutrophil and lymphocyte infiltrate Microscopic absceses Destruction of acinar epithelium Stromal hemorrhage and edema

4.5.1.2. Chronic Prostatitis

4.5.1.2.1. Chronic “nonbacterial” prostatitis is more common than acute bacterial prostatitis

4.5.1.2.2. Chlamydia trachomatis and Ureaplasma urealyticum are common etiologic agents

4.5.1.2.3. Often relatively mild symptoms, relapsing

4.5.1.3. Granulomatous Prostatitis

4.5.1.3.1. History of UTI is common

4.5.1.3.2. May be nodular, suspicious for carcinoma on DRE

4.5.1.3.3. Granulomas with or without necrosis

4.5.1.3.4. Epithelial degeneration with inflammatory infiltrate of macrophages, multinucleated giant cells, neutrophils, lymphocytes, and plasma cells

4.5.1.3.5. Etiology

4.5.1.4. Prostate Cancer

4.5.1.4.1. Adenocarcinoma

4.5.1.4.2. Prostatic Intraepithelial Neoplasia

4.5.1.4.3. Epidemiology (yr 2008)

4.5.1.4.4. Risk Factors

4.5.1.4.5. Screening

4.5.2. Testis

4.5.2.1. Testis anatomy

4.5.2.1.1. Paired, 12-19 g, 4.5 x 3.0 x 2.5 cm

4.5.2.1.2. Covered by fibrous capsule (tunica albuginea) within the tunica vaginalis, both mesothelium lined

4.5.2.1.3. Epididymis connects testis to vas deferens

4.5.2.2. Testis Histology

4.5.2.2.1. Parenchyma composed of tubules with germ cells/spermatocytes, Sertoli cells (elongate cells in the tubules)

4.5.2.2.2. Leydig cells in the interstitium (endocrine features: round cells with round nuclei, coarse chromatin, relatively abundant cytoplasm)

4.5.2.3. Testis Cancer

4.5.2.3.1. Germ Cell Tumor

4.5.2.3.2. Leydig Cell Tumors

4.5.2.3.3. Sertoli Cell Tumors

4.5.2.4. Testicular Dysgenesis Syndrome

4.5.2.4.1. Recently much interest in the association between increasing rates of male infertility, cryptorchidism, and testicular germ cell tumors.

4.5.2.4.2. Epidemiologic evidence suggests that in utero exposure to endocrine-disrupting chemicals (phthalates) may be responsible.

4.5.2.5. Cryptochidism

4.5.2.5.1. Failure of one or both testes to descend into the scrotum

4.5.2.5.2. Bilateral in 18% of cases

4.5.2.5.3. Orchiopexy does not decrease GCT risk

4.5.2.5.4. Histologically interstitial fibrosis, tubular sclerosis, and Leydig cell prominence are seen