Urology Flashcards
Ureteritis
Inflammation of ureters due to ascending infection from vesicoureteric reflux or descending kidney infections
- Intrinsic causes: calculi (urolithiasis), intraluminal blood clots, fibroepithelial polyps, inflammatory strictures, amyloidosis, tumors of ureter
- Extrinsic causes: Tumors (cervical cancer), pregnancy, endometriosis, aberrant renal vessels to lower pole of kidney
Urolithiasis
Formation of stones in collecting system of urinary tract
Nephrolithiasis
Stones in the collecting system of kidney.
- Due to urine concentration with precipitation of minerals
- Most are unilateral, usually in the calyces, renal pelvis, or bladder
- Presents with severe, abrupt flank pain, groin pain, fever, frequency, pain with urination (dysuria), and blood in the urine (hematuria)
Staghorn Calculi= large stones dilating renal pelvis, calices–> cast formation
(Struvite, cystine, uric acid stones)
Types of Stones:
- Calcium stones= most common
- Calcium oxalate= due to hypercalciuria
- Acidic urine (low pH)
- Calcium oxalate stones are hard and dark
- Urinalysis: calcium oxalate crystals are colorless tetrahedra (envelope shape), oval or dumbbell shapes; polarizable
* * seen in ethylene glycol poisoning (antifreeze) - Struvite stones= Magnesium ammonium phosphate (15% of stones)
- Due to urea-splitting bacteria (Proteus, Staphylococcus, Providencia)
- Alkaline urine (high pH)
- Triple phosphate crystals in urinalysis are colorless, rectangles or coffin lids shaped - Uric Acid stones= due to hyperuricemia (6% of stones)
- Radiolucent
- Acidic urine (low pH)
- Rhomboid crystals - Cysteine stones= due to genetic defects in cystine transport
- Autosomal recessive
- Yellow-brown radiopaque stones
- acidic urine (low pH)
- Crystals hexagonal
Hydronephrosis
Dilated renal cortex
- Most commonly caused by congenital obstruction of ureteropelvic junction in children
- Most common in males, < 6 months
- Left sided (23-30% bilateral)
Sclerosing retroperitoneal fibrosis
Ureteral obstruction due to dense fibrosis of retroperitoneal soft tissues and chronic inflammation
- Adults age 40-60
- Associated with drugs, autoimmunity
- can also be seen with Riedel thyroiditis, liver PSC, mediastinal fibrosis
Bladder exstrophy
Absence of anterior bladder wall, anterior abdominal wall
- May be associated with epispadias
- 1:3 M:F ratio
Bladder diverticula
Pouch-like evaginations of bladder wall
- Seen in males > 55 years
- Requires surgery when associated with infections, stones, perforation
Urachus
Vestigal structure connecting bladder dome to umbilicus in abdomen
- Can persist in adults, give rise to malignancies
Congenital incompetence of vesicoureteral valve
Abnormal junction between ureters, urinary bladder
- Ureters enter bladder perpendicularly (short intravesical segment–> does not prevent urine backflow during micturation
- More common in young firls
- Mostly asymptomatic, but can cause reflux pyelonephritis
Cystitis
Inflammation of the bladder.
– Clinically manifest as dysuria (pain or burning with urination), frequent urination including nocturia, urgency, hematuria and lower abdominal pain.
Bacteriuria
Bacteria colonization of urine without symptoms
Infectious cystitis
Most common UTI
Caused by:
- Fungal cystitis (candida)
- Schistosomiasis
- Viral cystitis: Adenovirus (type 11), HSV (hemorrhagic cystitis)
- Cyclophosphamide (give Mesna to reverse)
- Bacterial: e. coli, staph saprophyticus, klebsiella sp.
Interstitial cystitis
Painful bladder syndrome
- Persistent cystitis with pelvic pain and irritative voiding symptoms
• More frequently in females
• Multifactorial
• Cytoscopy: punctate hemorrhage or “Hunner ulcer”
• Diagnosis is of exclusion
• Overactive bladder is characterized by “urgency” of urination, pain is not the key feature but urine leakage
- Mucosal ulceration “Hunner ulcer” covered by fibrin and necrotic debris
• Inflammation, including mast cells, and later, a contracted bladder due to transmural fibrosis.
Malakoplakia
Malakos= Soft Plax= plaque - Papule, plaque, ulceration of GU tract - Accumulation of macrophages - 5-7th decades, females - Associated with e.coli infection
Histo: Inflammation with large macrophages, eosinophilic cytoplasm with PAS stain
Michaelis-Gutmann bodies (calcifications)
- Engorged macrophage lysosomes with bacterial fragments (lysosomal defect)–> calcium salt deposition–> Michaelis Gutman bodies
Radiation cystitis
4-6 weeks post-radiotherapy
- Edema, chronic cystitis, ulcers, fibrosis
Brunn Buds and Nests
Type of benign urothelial lesion; associated with chronic inflammation, caliculi
Buds= Normal invaginations of surface urothelium into lamina propria
Nests= similar to buds, urothelial cells have detached from surface, seen within lamina propria
Cystitis Cystica
Type of benign urothelial lesion; associated with chronic inflammation, caliculi
Cystic dilation of Brunn nests (common)
- See eosinophilic, proteinaceous material in lumen
- Can also be seen in urethra/ureter
Cytstitis glandularis
Type of benign urothelial lesion; associated with chronic inflammation, caliculi
Differs from Cystitis Cystica only in the nature of lining cells–> mucin-secreting columnar epithelial cells
Squamous metaplasia of urothelium
transformation of urothelium to squamous mucosa: reaction to chronic injury and inflammation associated with calculi (50% normal adult women, 10% men)
Nephrogenic metaplasia
Lesion caused by transformation of urothelium into renal tubules
- Small tubules clustered in lamina propria–> exophytic nodule
- Lesions may result form implants of detached renal tubular cells carried downstream
- Can produced tumor-like protrusions that obstruct the ureters
Hypospadia
Urethra opens on underside of penis
- Incomplete closure of urethral folds of urogenital sinus
Non-complicated surgical repair
Epispadia:
RARE- Urethra opens on upper side of penis
- Can commonly see entire urethra open along entire shaft
Complicated surgical repair
Phimosis
Narrowing of prepuce–> impairs retraction over glans
Paraphimosis: narrow prepuce retracted, can strangulate glans (due to infection, trauma)
- Both cured by cirumcision
Scrotal massas
Hydrocele= serous fluid collection in scrotal sac between two layers of tunica vaginalis
- Congenital: most common cause of scrotal swelling in infants, associated with inguinal hernia
- Acquired: secondary to infection, tumor, trauma; U/S or transluminate fluid–> can lead to testicular atrophy or fluid can become infected and cause periorchitis
Hematocele: accumulation of blood between tunica vaginalis layers due to trauma, hemorrhage into hydrocele, tumor, infection
Spermatocele: Cyst in efferent ducts (widened) of rete testis or epididymis
- Ressembles paratesticular nodule or fluid-filled mass
- Cyst is lined with cuboidal epithelium with spermatozoa in various degenerative stages
Varicocele: Dilation of testicular veins
- Cause infertility, oligospermia (most asymptomatic)
Scrotal inguinal hernia: protrusion of intestines into scrotum through inguinal hernia
Priapism
Painful erection unrelated to sexual excitation
- Secondary to blood outflow blockage, hematologic disorders (sickle cell, polycythemia vera, leukemia), brain, spinal cord diseases
STDs causing painful lesions
Herpes: Most common STD of the glans; manifestsed as grouped vesicles, ulcerate–> crusts
Chancroid: Haemophilus Ducreyi
- Accompanied by inflammation of inguinal lymph node
STDs causing non-painful lesions
Syphillis: Solitary, soft ulcer
Granuloma inguinale: Klebsiella
- Donovan bodies: rod-shaped bacteria within histiocytes
- Tropical disease
- Ulcers enlarge, heal very slowly
Lymphogranuloma Venereum: Chlamydia trachomatis
- Swollen groin lymph nodes
- Sinuses drain pus and serosangoinous fluid from nodes
Condylomata Acuminata: HPV genital wart
- Hyper- and parakeratosis, koilocytes
- Warts on shaft, small polyps on glans
Inflammatory disorders of Penis
Balanitis: Glans, due to poor hygeine
Balanoposthitis: glans and foreskin; bacteria, fungi
Complications: meatal stricture, phimosis, paraphimosis
Balanitis Xerotica Obliterans
Chronic inflammatory syndrome of subepithelial connective tissue
Xerotica= fibrosis
Obliterans= sclerosis
Glans= white, indurated
- Can cause strictures, phimosis
Equivalent to lichen sclerosis atrophicus of vulva
Circinate Balanitis
Circular, linear, or confluent plaque-like discolorations of glans, superficial ulcerations
Seen in Reiter syndrome
Plasma cell balanitis
Zoon balanitis
Chronic disease of unknown origin–> macular discoloration/painless papules on glans
- Infiltration of plasma cells, lymphocytes, epithelial thickening
Peyronie disease
Fibrous induration of penis with asymmetric fibrosis of penile shaft, induration and normal overlying skin
- “Penile strabismus”–> lost penile curvature, pain in erection
- Seen in young, middle-aged men (1% over 40)
- Dense fibrosis with chronic inflammation
Urethritis
Nonspecific infectious urethrits: e.coli, pseudomonas
- Associated with cystitis
- Seen in hospitalized patients (indwelling catheters)–> urgency, burning on urination, rare discharge
Urethral caruncles= polypoid inflammatory lesions of femal urethral meatus–> pain and bleeding
- Could be caused by prolapse of urethral mucosa, inflammation
- Seen in post-menopausal women (exophytic, ulcerated mass 1-2 cm in diameter)
- Treat with surgical excision
Reiter syndrome= urethritis, conjunctivitis, arthritis in weight-bearing joints
- can also see circinate balantitis, cervicitis, skin eruptions
- Effects adults with HLA-B27 haplotype
- Symptoms after chlamydia, Shigella, Salmonella, Campylobacter
- Inappropriate immune reaction- spontaneously resolves
Cryptorchidism
Bilateral in 30% of cases
Seen in 1% of infants: most common urologic condition requiring surgery
- Increases infertility, germ cell neoplasia
- Orchiopexy= surgery at age 6-12 months to correct; does not reduce neoplastic risk but improves fertility
Infertility (Male)
Klinefelter’s syndrome:
- Hyalinzed seminiferous tubules
- Prominent Leydig cells
- Results in infterility
Immature seminiferous tubules
Decreased spermatogenesis (hypospermatogenesis)
Idiopathic Germ cell maturation arrest
Germ cell aplasia (“Sertoli cells only” syndrome)
Peritubular and tubular fibrosis
Epididymitis
Clinical features: Intrascrotal pain with or without fever, and infertility
Bacterial epididymitis: young men with gonorrhea or Chlamydia and in older men and children with E. coli
Tuberculous epididymitis
Spermatic granulomas
Orchitis
Gram-negative bacterial orchitis is the most common form, often secondary to urinary tract infection
Syphilitic orchitis
Mumps orchitis unilateral
Granulomatous orchitis type IV (cell-mediated) hypersensitivity reaction and tuberculosis
Prostatitis:
Cause: coliform uropathogens, but often cannot be determined
** May cause elevated serum prostate-specific antigen (PSA)
Types of Prostatits:
- Acute Prostatitis
- Chronic Bacterial Prostatitis
- Nonbacterial Prostatitis
- Granulomatous Prostatitis
Benign Prostatic Hyperplasia
Enlargement of the prostate and urinary outflow tract obstruction: – decreased vigor of the urinary stream – increasing frequency – post urinary dripping – hydroureter, hydronephrosis – ultimately renal failure Higher among blacks than among whites Peaks in the 7th decade 10% has incidental adenocarcinoma
Treatment: Transurethral resection, suprapubic enucleation
Prostate Carcinoma
- The most frequently diagnosed cancer in men the United States: 220,000 new cases
- The second cause of death in men after lung cancer
- Elderly men
- American blacks exhibit a rate over twice as high as white Americans and have the highest prostate carcinoma death rates in the world
- Geographic variation: highest being in the United States and the Scandinavian
- Unknown etiology: “Androgen” and PIN.
Tumors of the Testis
Germ Cell Tumors (90-95%) - Germ Cells within Seminiferous Tubules Sex Cord-Gonadal Stromal Tumors (5%): - Leydig cell - Sertoli cell Metastasis to the Testis (5%) - Lymphoma - Carcinoma
Epidemiology of Renal cell carcinoma
- RCC 2–3% of all adult cancer
- Seventh most common cancer in men, ninth in women.
- Incidence approx 209,000/year and 102,000 deaths per year.
- Incidence of all stages has increased, contributing to a steadily increasing mortality rate
Risk factors of Renal cell carcinoma
- Cigarette smoking established risk factor - relative risk of about 2–3
- Obesity (BMI) is also a known risk factor
- ESRD
- Acquired renal cystic disease
- Hypertension
Presentation of renal cell carcinoma
Frequency 2:1 male:female
Usually in sixth to seventh decade of life
More presenting asymptomatic
Hematuria, flank pain, palpable mass – poor
Vena caval / atrial involvement (5-10%)
- can produce ascites, hepatic dysfunction, PE
Local extension (liver, pancreas, colon)
- Brain, ipsilateral adrenal, contralat kidney, bone, lung, pancreas
Types:
- 70-80% clear cell
- 10-15% papillary
- 3-5% chromophobe
Management of RCC by Bosniak Criteria
Category I and II:
- Further evaluation not required
Category III: Indeterminant cystic masses
- Low risk of metastatic malignancy
Category IV: Malignant cystic lesions with soft-tissue components
- High risk of metastatic malignancy
Risk of malignancy of renal mass
Rises with lesion size:
< 3 cm has rare metastases
Surgical management of RCC
Stage I – partial or radical nephrectomy
- Three years after surgery, partial vs radical nephrectomy - significantly lower risk of GFR below 45 mL/min (5 vs 36 percent)
Patients with hereditary cancer syndromes:
- Loss of renal function associated with increased risk of cardiac death and a decrease in overall survival (5yr overall survival 78 versus 85 percent for patients treated with radical and partial nephrectomy, respectively).
Stages II and III – radical nephrectomy
Radical Nephrectomy : Ligation of renal artery and vein, removal of kidney, Gerota’s fascia, and ipsilateral adrenal gland)
Laparascopic = open in experienced hands, 4 cm) upper pole lesions, non-organ confined tumor stage (T3 or greater), or solitary ipsilateral adrenal metastases identified by preoperative imaging studies
Cavoatrial invasion in 5 to 10 percent of cases – concern for thrombus migration and embolization
RCC metastases: predictors of poor prognosis
LDH > 1.5 ULN
Hemoglobin < LLN
Corrected calcium >10
Interval 2 sites of organ metastasis
Low risk= 0 : overall survival 30 months
Intermediate= 1-2 : overall 15 months
High risk= 3-5 : overall 5 months
Sites of metastases:
- Lung, Bone Brain
- Contralateral Kidney
- GI including pancreas
Cytoreductive nephrectomy (RCC)
- for resectable tumors
- patients with good performance status
- palliation of local symptoms
- oligometastatic or lung only disease
- survival benefit in surgery followed by interferon vs interferon alone
- improvement in paraneoplastic syndrome symptoms
Targeted systemic therapy for RCC
In selected groups of patients, still use IL-2 (low burden disease patients)
2 main pathways targeted:
- HIF: hypoxia inducible factor
- mTOR
First line:
- TKIs: Sunitinib, Sorafenib
- Side effects= HTN (marker of efficacy of treatment), thyroid dysfunction, renal insufficiency, thromboembolic events, decline in ejection fraction, hand/foot syndrome, hepatotoxicity, GI toxicity/taste, cytopenias - VEG-F: Bevacizumab
- Side effects: HTN, thromboembolic events, proteinuria, GI performation, RPLS (reversible posterior leukencephalopathy syndrome)
Second line: tesmirolimus (mTOR-inhibitor)
- Side effects: rash, hyperglycemia, hypertriglyceridemia, pneumonitis, anemia/cytopenias
Bladder cancer: epidemiology
- 70,980 new diagnoses in 2009, 14,330 deaths
- 4th most common cancer
- 3:1 M:F
- Rare <40
- Median age 65 - medical comorbidities
- Often multifocal
- Can involve the urothelium from the renal pelvis to the urethra
Cytogenic abnormalities:
- Deletion of chromosome 9 (9p- or 9q-), 11p, 13p, 14q, or 17p
Risk factors:
- Cigarettes
- Arsenic exposure
- Bladder caliculi, infections, TB, schistosoma
- Radiation therapy
- Cyclophosphamide, analgesics
- Occupational exposure to aromatic amines, β-naphthylamine, phenacetin, dye and others
- Infection with Schistosoma haematobium is a risk factor for squamous cell carcinoma of the bladder
Categories of bladder cancer
- Non-Invasive: most common (90%)
- prevent recurrence and progression - Invasive
- preserve bladder or prevent progression - Metastatic
- maintain quality and prolong life
Signs and symptoms of bladder cancer
- Gross or microscopic hematuria
- Irritative symptoms (Dysuria, frequency, urge incontinence, urgency)
- Obstructive symptoms
- Advanced: abdominal, pelvic pain, anorexia, edema
Treatment of non-invasive bladder cancer
TURBT: transurethral resection of bladder tumor;
- Low risk: observe
- Intermediate: chemo, BCG/maintenance
- High risk: BCG/maintenance
- Recurrence–> radical cystectomy
Chemo: Cisplatin
Surgery:
- urinary diversion: ileum connected to ureters
- Neobladder/continent diversion: patients may have to self-catheterize
Epidemiology of testicular cancer
- 2-3 new cases per 100,000 US males per year
- Marked variation in incidence among different countries/races
- 90-95% are germ cell
- Most common solid tumor in males ages 15-35
Risk factors for testicular cancer
Cryptorchidism: 7-10% of patients with testicular cancer have a history of cryptorchidism
- Abnormal germ cell morphology
- Elevated temperature
- Interference with normal blood supply
5-10% of patients with testicular cancer and a history of cryptorchidism develop cancer in the contralateral testis
Orchidopexy does not prevent development of cancer – just allows for detection
Gonadal Dysgenesis - 20-30% develop cancer (gonadoblastoma) Trauma ?? - prompts evaluation Hormones - DES/OCP probably do not increase risk Atrophy (nonspecific vs. mumps orchitis) - Speculative
Symptoms of testicular cancer
Painless swelling / mass
30-40% dull / aching sensation
10% present with metastatic symptoms
Gynecomastia:
- 5% germ cell
- 30-50% Sertoli/Leydig
1-2% have bilateral disease at diagnosis
More common on the right
Workup for testicular cancer
Exam
U/S
CXR +/- Chest CT
Abdominal CT
- Can identify small nodal deposits <2 cm
- MRI and PET scan no advantage over CT
Serum markers: AFP, BHCG and LDH
- Elevation after orchiectomy represents metastatic disease
- Conversely normalization does not rule out metastatic disease
** Fertility preservation – Sperm Bank
Risk stratification
Seminoma: good/moderate risk
Non-seminoma: good/moderate or poor risk
Poor risk seminoma:
- May have metastases, mediastinal primary tumor
- AFP > 10,000, HCG> 50,000, LDH > 10x upper limit of normal
Isochromosome 12p
Patients with testicular cancer (80-90%) will gain short arm of chromosome 12p
- Not 100% specific, but highly diagnostic
Alpha-Fetoprotein
Expressed by the early embryo (also liver and GI tract)
- Half-life: 5-7 days
- Produced by pure embryonal, teratocarcinoma, yolk sac, mixed tumors (NOT pure choriocarcinoma or seminoma)
- Falsely elevated in liver dysfunction, viral hepatitis and ETOH
- Presence of AFP in what’s thought to be pure seminoma suggests a mixed tumor
Human chorionic gonadotropin
Secretory product of the placenta
Alpha unit (LDH,FSH,TSH) and beta unit
Half-life: 24-36 hours
Produced by syncytiotrophoblastic tissue
All choriocarcinomas, 40-60% embryonal, 5-10% seminoma
Falsely elevated in hypogonadism and marijuana use
Lactate dehydrogenase
- Presents normally in smooth, cardiac and skeletal muscle, liver and brain
- Most useful in advanced seminoma or tumors where other markers are not elevated
- Many false positives
LDH correlates to tumor burden
Radical orchiectomy
Inguinal approach
- Avoid seeding the scrotum and disrupting lymphatics
- Wait 5 half lives before rechecking markers
- Biopsy not recommended due to the risk of tumor spread
Treatment of seminoma
Stage I: carboplatin
Stage II: Radiotherapy, chemotherapy (bleomycin)
- Marker positive: chemotherapy
Stage IIC, III:
- Cisplatin based chemo (4 cycles of EP or 3 cycles of BEP)
- 90% will have a complete response
- Residual retroperitoneal masses are usually fibrosis
- RPLND warranted if >3cm and well circumscribed
RPLND: retroperitoneal lymph node dissection
Stage and remove lymph nodes that drain lymph nodes
- Can cause ejaculatory dysfunction (hence sperm-banking beforehand important)
Risk factors for prostate cancer
Increased risk with first degree relative: 2.5 odds ratio)
- 2-3 first degree relatives: 2-10 fold increase
- Also increased risk with familial breast cancer history
Hereditary prostate cancer (HPC) meet at least one criteria:
- Family including prostate cancer in >3 first-degree relatives
- Family with prostate cancer in three successive generations of the maternal or paternal lineages
- Family with two first-degree relatives affected at age ≤ 55 years
Screening for Prostate cancer
- Digital rectal exam:
Various organizations recommend annual testing (digital rectal exam)
- Age varies from 35 to 50 based on risk
- Screen with 10 year life expectancy
Some are more cautious; more discussion with patient
- No uniform guidelines; testing controversial - PSA: Biggest concerns:
- Over diagnosis of clinically unimportant cancers leading to over-treatment
- PSA may not detect all cancers
**Starting at age 30, men have 1/3 chance of having cancerous foci in prostate
Interpreting PSA
Increased PSA: Prostatitis, BPH, cancer, prostatic trauma, ejaculation (rarely), NOT routine rectal exam
Decreased PSA: Antibiotics with infection, Tx prostate cancer , meds (finasteride/dutasteride)
- 20% assay variability
- No lower PSA limit eliminates cancer risk
- As a rule of thumb PSA level of 2.5 ng/dL can be considered abnormal
- Changes in PSA (velocity) better than absolute level
- With cancer, PSA > 20 ng/dL more likely mets** (high risk)
Diagnosis of Prostate cancer
ONLY through biopsy
- Trans-rectal ultrasound with local anaesthesia
- 10-12 core biopsy as lesions rarely seen on ultrasound/CT
Staging prostate cancer
T1= inapparent tumor (not palpable, visible by imaging)- detected with PSA
T2- confined to prostate (most diagnoses here)
T3- outside prostate (through capsule)
T4- invading local structures (bladder wall)
Gleason scoring
Histopathologic tumor architecture score
Gleason 1: normal glands
Gleason 2: Smaller, more numerous glands
Gleason 3: tight glands with lumen still present
Gleason 4: glands within glands
Gleason 5: Halo around nuclei, sheets of cells
Gleason > 5 = addition of primary and secondary architectural pattern
Gleason 8, 9, 10= high risk
Prostate cancer NCCN Risk Categories
- Low risk
- T1-2a, Gleason Score ≤ 6, and PSA < 10 ng/mL - Intermediate risk
- T2b-2c and/or Gleason Score 7, and/or PSA 10-20 ng/mL - High risk
- T3a or Gleason Score 8-10, or PSA > 20 ng/mL
Management of low risk prostate cancer
- Active surveillance:
- PSA, digital rectal, regular biopsies
- Die “with” rather than from prostate cancer - Radical prostatectomy
- remove prostate through 5” incision
- Nerve sparing preserves potency
- PSA should be 0 afterwards
- No rectal issues
- Cons: operation, urethral narrowing, ED, incontinence - External beam radiation therapy
- Intensity modulated radiation therapy
- Can dose to rectum, bladder
- Grade dosage to prevent radiation to external structures - Prostate brachytherapy
- Insert probe in rectum, implant radioactive seeds around prostate (spare urethra)
Treatment of Metastatic prostate cancer
Androgen deprivation therapy: ADT
- GnRH analogs: Lower LH–> decrease testosterone therapy
- Anti-androgen therapy: block testosterone production
- Surgical orchiectomy
Side effects of androgen deprivation therapy:
- Fatigue
- CV morbidity
- Loss of libido
- Cognitive decline
- Altered body composition
- Arterial stiffness
- Osteoporosis/ Skeletal fractures
- Metabolic syndrome
Clinical presentation of urolithiasis (stones)
Asymptomatic
- Many times found Incidentally
- Non-obstructing stones usually cause no pain
Symptomatic (Renal Colic)
- Symptoms are secondary to obstruction
- Intermittent flank pain, nausea, vomiting
- Hematuria
- Groin pain, lower urinary tract symptoms
- Read Cope’s Early Diagnosis of the acute abdomen
Ureteral stone emergencies
Obstructing Ureteral Stones
- May cause sepsis (fever, hypotension, tachycardia, mental status changes)
Obstructed Solitary Kidney
- s/p nephrectomy or atrophic / natural history
Bilateral Obstruction
- Simultaneous obstructing ureteral stones
*** ANURIA, fluid overload, hyperkalemia, metabolic acidosis (MAY REQUIRE EMERGENT DIALYSIS)
Treatment:
- Ureteral stent (go up urethra)
- Percutaneous nephrostomy: Go through back into kidney collecting system to drain kidney
- Extracorporal shock-wave lithotrypsy (ESWL)
- Ureteroscopy with laser lithotripsy
- Surgical excision
- Medical treatment
- Observation
ESWL= extracorporal shock-wave lithotripsy
Localize stone with fluoroscopy or U/S
- Popular with patients & urologists
- 60 – 90% success rate
- Time for fragment passage varies.
Contraindications:
- Anticoagulation
- Pregnancy
- AAA
- Distal obstruction, infection
Side effects:
- Hematoma (1 in 500)
- Steinstrasse= stone street: column of stone dust accumulating in distal ureter
Ureteroscopy with lase lithotripsy
Long, thin, flexible
- Dual deflection
- Holmium laser
- Nitinol baskets allows for active stone removal
- Usually requires stent
- Safe in pregnancy, anticoagulation
Complications:
- Ureteral stricture
- Stent encrustation (if patient doesn’t have stent removed in timely manner)
PCNL: percutaneous nephrolithiasis
Used for renal staghorn calices (large stones)
- Percutaneous Access via peripheral calyx
- Ultrasonic lithotripter breaks and suctions out stone
- Most efficient
- Most invasive
Risk: Hemorrhage: - Acute (10% transfusino rate) - Delayed (pseudoaneurysm, AV malformation) Infection Renocutaneous fistula Damage to surrounding organs Intrarenal scarring Renal loss
Surgical excision
- Open surgery rarely used today
- Laparoscopy and robotics have renewed interest
- Look for old incisions: may indicate strictures
Medical treatment: dissolution therapy
- Pure uric acid stones will dissolve with urinary alkalinization.
- Urine pH (6.5 – 7.0)
- Potassium Citrate
- Na Bicarbonate
- Calcium stones cannot be dissolved.
Observation of stones: when to observe vs intervene
Ureteral Calculi:
- <5mm can have trial of passage
- Larger ureteral stones require treatment
Renal Calculi
- May be observed if not obstructing
Staghorn Calculi
- Require treatment
- Natural history: Infection, abscess, atrophy, potential for emergent nephrectomy
Prevention of kidney stones
50% of stone patients will get recurrent stone within 5 yrs
Surgery alone does not prevent future stone formation
Identifiable abnormalities which predispose to stone formation found in over 90% of stone formers
20% of new stone formers demonstrate systemic disorder predisposing to stone formation
Correction of abnormalities may reduce recurrence rates
Metabolic evaluation in nephrolithiasis
Serum testing:
- SMA-7, Ca, Mg, PO4, PTH, uric acid (urate)
Urine testing
- 24 hr urine electrolyte testing
- UA and urine culture
Chemical stone analysis
Identifiable abnormalities in nephrolithiasis
Hypercalcuria (> 200 mg calcium excreted in 24 hrs) due to:
- Increased intestinal absorption (normal serum PTH, serum Ca but elevated urine Ca)
- Renal hypercalcuria: slight elevation in serum PTH (can develop osteoporosis over time), normal serum calcium, elevated urine calcium
- Primary hyperparathyroidism: elevated PTH, elevated serum calcium, elevated urine ca
Hyperoxaluria
- Enteric hyperoxaluria: super-absorbers of oxalate thru gut due to:
- Inflammatory bowel disease (Crohn, UC) or surgical resection of bowel
- -> intestinal fat malabsorption
- -> saponification
- -> Ca moves out with fat, Oxalate crystals get reabsorbed
Hyperuricosuria (> 600 mg uric acid excreted in 24 hrs)
Hypocitraturia: Lack of citrate (natural stone inhibitor)
Conservative managment of calcium stones
Consider before medical managment
Empiric diet and lifestyle modifications
1. Hydration: urine output > 2500 cc/day
2. Limit sodium: 2300-3300 mg/day
3. Normal calcium: 800-1200 mg/day
4. Limit oxalate (plants, plant byproducts)
5. Limit red meat (no more than 6-8 oz/day)
Thiazides for calcium stones
- Augments Ca reabsorption in distal tubule
- Reduces urinary saturation of Ca
- Retained calcium accreted in bone
- Eventual attenuation of effect in absorptive hypercalciuria
Side effects:
- Wastes K: check labs, consider adding K-citrate)
- Limited effectiveness with persistant high dietary Na
- Rash, pancreatitis, elevated LDH, impotence (contraindicated with high serum calcium)
Potassium citrate for calcium stones
Citrate= natural stone inhibitor (forms soluble complex with calcium)
Side effects:
- Dyspepsia (contraindicated in peptic ulcer disease
- Hyperkalemia (caution with K-sparing meds, ACE-I; renal insufficiency)
Urine pH and stone formation
Alkalinze patient’s urine–> prevent uric acid precipitation
- Also lower uric acid levels in patient’s blood to prevent stones
Insulin resistance and increased urine acidity
Higher incidence of uric acid stone formation in type 2 DM stone formers than non-diabetic stone forming pts (34% vs 6%).
Prevalence of DM or impaired glucose tolerance over 50% in uric acid stone formers.
MECHANISM: Insulin resistance at level of PCT leads to defective ammonia production and excessive urine acidity due to unbuffered H+
Uric acid stone prevention and dissolution
Dietary Modification:
- Increase fluids (generate 2- 3 Liters urine per day)
- Limit purine intake ( 6- 8 oz meat per day)
- Limit sodium (2300 – 3300 mg per day)
Medication
- Increase uric acid solubility
- Potassium citrate 20 – 60 meq / day
- Sodium bicarbonate 1.3 – 2.6 grams / day
- Stones dissolve 1 cm per month (depends on compliance)
- pH range 6.5 – 7.0 - Reduce uric acid concentration
- Allopurinol 100 – 300 mg /day (Inhibits enzyme xanthine oxidase)
- Use only if UUA still elevated after urine alkalinized
Struvite stone treatment
Formed due to Proteus infection (urease-producing bacteria)
- Surgical removal of all stone burden
- Correction of anatomic abnormality if possible
- Culture specific antibiotics
- IRRIGATE, IRRIGATE, IRRIGATE (if applicable)
- Long term culture specific antibiotic suppression
- Pen VK 250 mg po daily for 6 mos - Acetohydroxamic Acid (urease inhibitor)
- 80% stone growth arrest (vs 40% placebo)
- Multitude of complications: Palpitations, Edema, rash, Nausea, vomit, diarrhea, Headache, loss of taste, hallucination
Cystine nephrolithiasis
Rare stone type (1 – 3%)
Autosomal recessive inherited disorder with defective renal transport of dibasic amino acids
- Cystine
- Ornithine
- Lysine
- Argenine
* Cystine poorly soluble in urine (250 mg/ Liter)
See Hexagonal crystals, positive Nitroprusside Test
Treatment for cystine stones
- Surgical considerations: very dense (ESWL resistant)
- Increase fluids
- Low methionine diet (meat, eggs; precursor to cystine)
- Limit sodium (increases renal cystine excretion)
- Alkalinization (limited role)
- Chelating Agents
- Captopril
- D-penicillamine (Add pyridoxine to prevent Vit B6 Deficiency)
- Thiola
BPH: pathophysiology
- Mechanical Component
- Glandular proliferation - Dynamic Component
- Baseline tonicity of smooth muscle (activated by alpha receptors)
** Prostate enlargement in BPH driven by androgens= dihydrotestosterone (DHT)
BPH: clinical presentation
Obstructive symptoms:
- Decreased force of stream
- Feeling of incomplete emptying
- Intermittency (double voiding)
- Hesitancy (delay of onset of voiding)
- Need to strain to empty bladder
Irritative:
- Frequency of urination
- Urgency (strong desire to void)
- Nocturia (waking to urinate)
- Dysuria (pain during urination)
- Hematuria (blood in urine)
BPH: evaluation
- Assess symptoms: AUA symptom score:
- 7 questions: Incomplete emptying, frequency, intermittency, urgency, weak stream, straining, nocturia
- Each question has severity (1-5)
- Mild= 0-7; moderate= 8-19; severe= 20-35 - Labs: serum creatinine, PSA, urinalysis, urine culture
- Check PVR (post-void residual)
- Remaining volume after micturation
- Transabdominal U/S or catheterization - Renal ultrasound:
- Check for hydronephrosis, cortical thinning
BPH: treatment
- Observation
- Medical management
- Alpha blockers
- 5-alpha reductase inhibitors - Surgery
- Various methods of clearing bladder outlet (TURP, etc)
Indications for surgery:
- Refractory urinary retention (may require catheters.
- Recurrent UTI
- Renal Insufficiency
- Bladder calculi
- Recurrent gross hematuria from prostate
Risks:
- bleeding, bladder neck contracture
- Retrograde ejaculation (30-97%)- usually indicator of treatment effectiveness
- Tranurethral syndrome: absorption of hypotonic solution used in TURP procedure (hyponatremia)
Coude catheter
Foley catheter with 35 degree bent angle
Practical for catheterizing BPH patients
Stress urinary incontinence
More common in women Risk factors - Obesity - Parity - Route of delivery (vaginal delivery vs C-Section) Leakage with increase in intra-abdominal pressure (cough, sneeze, laugh) ALPP (Abdominal leak point pressure) - Normal ALPP is infinity - Severe SUI has low ALPP
Treatment
- Slings
- Collagen Injection
Urge incontinence
Involuntary loss of urine associated with strong sudden desire to void
Hyperactive detrusor muscle
Treatment
- Medical (anticholinergics)
- Surgery (botox injections, neurostimulator)
- Lifestyle modifications
Continuous incontinence
Continual leakage of urine
Fistulas
- Vesicovaginal (3rd world country with prolonged labor)
- Ureterovaginal (radiation, pelvic surgery)
Ectopic ureter
- Usually presents in pediatric population
Transient incontinence
Reversible, transient loss of urine
* Usually associated with mental status changes in geriatric population
D.I.A.P.P.E.R.S. Delirium infection atrophic vaginitis pharmaceuticals psychological problems excess urine output Restricted mobility Stool impaction
