Urology Flashcards
DDx for microscopic/gross hematuria
Pre-renal:
1) Coagulation disorders, anticoagulants.
2) Pseudohematuria: beets, dyes, laxatives.
Renal:
1) stones
2) Trauma
3) Tumor
4) Infection
5) Inflammation (e.g. glomerulonephritis)
6) Vascular malformation (AVM)
Post-renal:
1) stones
2) Trauma
3) tumors
4) infections (KEEPS)
Important Q’s on history for hematuria
Flank/abdominal pain vs suprapubic pain vs painless.
Dysuria, frequency, voiding changes.
Trauma hx.
Fever/chills.
Wt loss, night sweats.
Hx of stones.
RF for Ca: smoking, occupational exposures, radiation exposure.
Labs/investigations for hematuria
UA + culture (infection vs nephritis).
Urinary cytology: picks up more aggressive cancers only (if negative cannot r/o malignancy as low grade tumors don’t shed cells).
CBC, PTT/INR.
Creatinine (look for renal impairment).
List situations for when US, CT IVP (contrast), CT KUB (non-contrast) would each be first line in the context of hematuria and the pros/cons of each.
US: First line for microscopic hematuria or signs of upper UTI. Good for upper tract imaging when suspected renal tumors, stones in the kidneys or looking for hydronephrosis. However, will miss ureteral stones/tumors, small/flat bladder tumors and gives no functional info.
CT IVP (contrast): first line for pts with gross hematuria for upper imaging. Most sensitive for detecting GU pathology. C/I for contrast may include renal dysfunction, MM, contrast allergy, pregnancy.
CT KUB (non-contrast): 1st line for pts with renal colic. Helps to ID stone location and size and guides tx.
Hematuria: when to refer to uro
Gross hematuria with no obvious cause (e.g. no overt signs infection).
Microhematuria with risk factors.
Abnormal cytology results.
Symptoms of urothelial carcinoma
Main: painless gross hematuria.
Wt loss, night sweats, voiding changes.
Investigations for suspected urothelial carcinoma
CT IVP: triphasic protocol to look at arterial, venous and excretory phases. (upper tract imaging).
Cystoscopy: for lower tract imaging.
Upper and lower imaging needed as everything lined with urothelium is exposed to same risk (field defect theory).
Acute management of acute GU bleeding
ABC’s: stabilize.
Determine site of bleeding: CT IVP and cystopscopy.
CBI: manually irrigate all clots first then start CBI to prevent new clots from forming.
Surgical mgmt:
cystoscopy + fulguration.
Intravesicular therapies: aluminum, formalin, silver nitrate.
Hyperbaric oxygen or vascular embolization if unable to control bleeding.
Cystectomy and urinary diversion if severe/unable to control.
4 common risk factors for urothelial malignancy
1) SMOKING!!
2) Occupational exposure to aniline dyes (hairdressers, leather tanners, textile workers, painters, dry cleaners).
3) Medications: phenacetin (old analgesic), cyclophosphamide.
4) Chronic cystitis: catheters, infections (associated w/ squamous cell carcinoma).
Diagnosis of urothelial carcinoma
Cystoscopy and biopsy with transurethral resection of lesion and underlying detrusor muscle to stag the tumor.
Types of urothelial tumors, grading and staging.
1) urothelial carcinoma: transitional cell carcinoma.
2) Adenocarcinoma: affects dome of bladder. Assocated with urachus (remnant connection to bladder).
3) SCC: associated with chronic inflammation (neurogenic bladder, indwelling catheter, bladder stones, schistosomiasis).
Grading: low grade (70%) or high grade.
Staging: Non-muscle invasive (NMIBC) T0, T1 or muscle invasive (MIBV) T2+ (T2 once muscularis propria invaded).
Treatment of non-muscle invasive bladder cancer
Transurethral resection of lesion (TURBT) but associated with hi recurrence rate.
Follow up with intravesicular chemo.
Strong indications for intra-vesicular chemo include high grade NMIBC, lamina propria invasion (T1), CIS, multi-focal NMIBC, unable to completely resect, rapid recurrence initial resection.
Options for intra-vesicular chemo:
1) BCG: bacille Calmette Guerin. Attenutated bacillus that causes and immune response in the bladder such that cytokines are released that attack cancer cells. Decreases progression of cancer. Need maintenance tx every 3 months to keep steady state.
2) Mitomycin C: Reduces recurrence risk. Give immediately post-TURBT int he OR to kill free cancer cells.
When to give radical therapy:
1) persistent CIS after intravesicular chemo.
2) extensive superficial tumors that are not amenable to resection.
Tx of muscle invasive bladder cancer
1) Radical cystectomy + lymphadenectomy +/- systemic chemo: urinary diversion (ileal conduit or neobladder can be surgically created). Chemo with cisplatin/gemcitabine.
2) Palliative: may still require cystectomy tho if uncontrollable hematuria.
DDx for a benign solid mass in the kidney
1) Oncocytoma: capsulated area with central scarring. Treat as RCC as difficult to differentiate on imaging.
2) Angiomyolipoma: composed of blood vessels, muscle and fat. Excise/embolise if symptomatic or if >4 cm (50% hemorrhage risk!). Follow with imaging (1-2% malignancy risk).
3) Abscess
4) Adenoma: not symptomatic, small.
5) Pseudotumor: E.g. dromedary hump, hypertrophied column of Bertin, compensatory hypertrophy. DMSA scan wil have normal uptake vs tumors have decreased uptake.
DDx for a malignant renal mass
1) RCC makes up 90% of solid renal masses, 25% presents with mets.
2) Urothelial cell carcinoma: nephrourecterectomy required.
3) Metastasis: lymphoma, leukemia, lung, breast.
4) Wilm’s tumor (peds)
Histological subtypes of RCC (4)
Clear cell, papillary, chromophobe, sarcomatoid.
Typical presentation of pt with RCC.
1) Incidental finding: asymptomatic until late.
2) Classic triad: flank pain, hematuria, palpable mass (uncommon until late).
3) Paraneoplastic syndromes are common (20-30% of RCC)
What are some of the common paraneoplastic syndromes associated with RCC?
1) hematologic: anemia, polycythemia (secondary to high EPO).
2) Hypercalcemia: PTH like substance secretion.
3) High ESR.
4) HTN: increased renin.
5) Stauffer syndrome: abnormal liver enzymes, low WBC, fevers. Reversible with treatment of RCC.
Labs and imaging for suspected RCC
Labs: CBC, ESR, LE, Ca, ALP (look for bone involvement), UA.
Imaging:
CT abdo/pelvis with contrast to characterize mass, assess tumor extension, look for IVC thrombus/nodes/mets. Contralateral renal abnormalities (5% chance of cancerous lesion).
CXR for mets.
Biopsy NOT recommended.
Tx options for RCC
If localized:
1) Nephrectomy.
2) Partial nephrectomy: if small tumor (<7cm), pt w/ solitary kidney/impaired RF, bilateral tumors, hereditary syndromes (Von Hippel-Lindau Syndrome).
3) Ablation therapy: radiofrequency or cryotherapy.
4) Targeted therapies: Y kinase inhibitrs, anti-VEGF mAb, mTOR inhibitors.
Metastatic RCC: nephrectomy and chemo.
DDx flank pain
Life-threatening: AAA rupture, AA dissection, appendicitis, ectopic pregnancy, septic stone.
GI: Cholecystitis, biliary colic, acute pancreatitis, diverticulitis, PUD, IBC, gastritis, infarct.
Gyne: PID, Ovarian torsion/rupture, endometriosis.
GU: renal/ureteric calculi, renal abscess, pyelonephritis, renal vein thrombosis, acute glomerulonephritis.
Nephrolithiasis: etiology of pain + sites of obstruction
Acute obstruction of ureter by stone causes distension of ureter which causes pain.
Sites of impaction include: ureteropelvic junction, crossing of iliac and ureterovesicular junction.
Labs and imaging for renal colic
Labs: WBC, Cr, UA/urine microscopy (bacteriuria, pyuria, pH).
CT KUB (non-contrast): picks up uric acid stones. Can infer degree of obstruction by presence of hydronephrosis.
XR KUB: 85% of stones are radio-opaque but can’t pick up uric acid stones or tell degree of obstruction.
What are the 4 types of kidney stones
Calcium oxalate (most common), calcium phosphate, struvite (infection stones), uric acid stones.
Etiology of calcium oxalate stones
1) Dietary hyperoxaluria (chocolate, nuts, tea, strawberries, PB, excessive dietary Ca restriction).
2) Hypercalcuria: inherited icnreased absorption, hyperPTH.
3) Dietary hypercalciuria: if increased sodium and protein intake as well.
Etiology of calcium PO4 stones
Associated with metabolic abnormalities including:
1) Primary hyperparathyroidism.
2) Distal RTA
3) Hypercalcemia due to malignancy or sarcoid
Composition and etiology of struvite (infection) stones.
Formed from MAP (magnesium, ammonium phosphate and Ca).
Only form if urine pH >8 which occurs with urease positive bacteria such as klebsiella, Proteus, Pseudomonus, staph. Does NOT form with E coli (not urease positive).
Forms staghorn stones.
Etiology of uric acid stones
1) Persistent acidic urine (low urine volume, chronic diarrhea, excessive sweating ,dehydration).
2) Gout: hyperuricemia.
3) Excess dietary purine: meats.
4) chemotherapy for lymphoma or leukemia patients.
4 Tx options for symptomatic urinary calculi
1) Acute medical tx with analgesia, anti-emetics, warm compress.
2) Retrograde ureteric stents (double J stents).
3) Percutaneous nephrostomy tubes (drain kidney proximally).
4) Removal of stone: Spontaneous passage (if <5 mm), extracorporeal shockwave lithotripsy (ESWL) if <2 cm, ureteroscopy and basket/laser or percutaneous nephrolithotomy if >2cm or staghorn calculi (risk of bleeding, renal perforation).