CRAM Flashcards
Dietary recommendations: Ca++ stones and high urinary Ca++
Limit Na+
Maintain normal Ca++ (1-2g/day)
Dietary recommendations: Ca++Oxalate stones + high urinary oxalate
Limit oxalate
Maintain normal Ca++ (1-2g/day)
Dietary recommendations: Ca++ stones + low urinary citrate
Limit non-dairy animal protein and increase fruits and veggies
Dietary recommendations: Uric acid or Ca++ stones and high urinary uric acid
Limit non-dairy animal protein
Dietary recommendations: Cystine stones
Limit Na+ and protein intake
Medical therapy:
Recurrent stones + high urinary Ca++
Thiazide diuretic
Medical therapy:
Recurrent Ca++ stones + low urinary citrate
Potassium citrate
Medical therapy:
Recurrent CaOx stones + hyperuricosuria + normal urinary Ca++
Offer urinary allopurinol
If uric acid stones, DON’T offer allopurinol as first-line therapy
Medical therapy:
Recurrent Ca++ stones without other lab abnormalities
Empiric thiazide diuretics and/or K-cit
Medical therapy:
Uric acid and cystine stones
K-cit to raise urinary pH (these stones form in acidic urine)
Medical therapy:
Cystine stones refractory to dietary changes (adequate hydration, limit salt to 2-3 g daily) and urinary alkalinization (pH >7) or large recurrent stone burdens
Offer cysteine-binding thiol drugs (alpha-mercaptopropionylglycine = Thiola = tiopropin), which is better tolerated than D-Penicillinamine
Medical therapy:
Residual/recurrent struvite stones after surgery exhausted
Offer acetohydroxamic acid (AHA = Lithostat; urease inhibitor)
q3month CBC to monitor for hemolytic anemia
This drug decreases stone growth rate, doesn’t change stone recurrence
Renacidin = citric acid glucono-delta-lactone magnesium carbonate
Used for dissolution treatment of residual struvite stones/fragments
Urease-producing organisms
Proteus, klebsiella, staph aureus, pseudomonas, providentia, ureaplasma
Enteric/acquired hyperoxaluria is a/w:
IBD and short-gut syndrome
Unabsorbed fat binds to Ca++ –> oxalate goes unbound until it is reabsorbed in the colon –> high oxalate in the blood and then urine –> treat with Ca++ supplementation to bind oxalate in the gut
Crohn’s stone formation
low urine volume (dehydration) + low urine pH and hypocitraturia (metabolic acidosis) + hyperoxaluria (over absorption of intestinal oxalate –> CaOx stones
Isolated hypomagnesemia
Suggests IBD –> refer to GI
PO Reloxaliase
Recombinant oxalate decarboxylase enzyme derived from B. subtilis and expressed in E. Coli
Degredes oxalate within GI tract –> decreased oxalate absorption and urinary excretion
Lumasiran = Oxlumo
siRNA
decreases glycolate oxidase, which decreases glyoxylate’s conversion to oxalate
Approved for Tx of type 1 primary hyperoxaluria
CF is a/w which urinary abnormalities?
Hyperoxaluria, hypocitraturia (prone to stones)
Prevent stones: Roux-En-Y
Dietary Ca++ at mealtime
Decrease high oxalate foods
Metabolic acidosis –>decreased urinary citrate –> K-Cit
Stones: Colon resection and end ileostomy
Fluid and bicarbonate loss
Concentrated urine with low pH
Increased risk of uric acid stone formation
Lesch-Nyhan Syndrome
Absence of HGPRT
Neuro dysfunction, behavioral disturbances, uric acid overproduction with hyperuricosuria and hyperuricemia
A/w uric acid stones
Patients can get xanthine oxidase stones while on allopurinol –> decrease (don’t stop) allopurinol and start K-cit
Pregnancy and stones
Placental production of VitD –> increases calcium absorption and decreases serum PTH –> physiologic hypercalciuria
BUT
Urine citrate and GAG also increased so stone formation risk is unchanged
Ammonium acid urate stones
Rare, a/w chronic diarrhea and heavy laxative use/abuse, decreased urinary Na+ excretion,
pH >6.3, and ileal or large volume colon resection
Radiolucent stones, can be mistaken for uric acid stones
AAU stones no NOT dissolve with alkalinization
Idiopathic (endemic) bladder stones are also AAU (kids with cereal based diets)
Keto(genic) diet affect on stones
Excess meat (purine) consumption
Hyperuricosuria, increased urinary sulfate + urea nitrogen
Hypercalciuria
Hypocitraturia
Decreased urine pH
Uric acid + calcium nephrolithiasis
Treat with dietary changes +/- allopurinol
Topiramate and stones
Topiramate creates a chronic intracellular acidosis
Urinary milieu similar to distal RTA with hyperchloremic acidosis, HIGH urine pH, SEVERE hypocitraturia and hypercalciuria
Treat with cessation of topiramate or K-cit
Vitamin C effect on urine
10-20% is metabolized into oxalic acid and excreted into urine
Most common risk factor for Ca++ stones
Hypercalciuria
Absorptive hypercalciuria pathophysiology
Increased GI Ca++ absorption
Normal or increased serum Ca++
Decreased serum PTH and decreased vitamin D
Absorptive hypercalciuria management options
Avoid excess dietary Calcium
Decrease salt and animal protein in diet
Thiazides +/- K-Cit
Renal calcium leak hypercalciuria pathophysiology and management
Increased calcium loss into urine
Normal or decreased serum Calcium
Increased serum PTH
Management: Thiazides +/- K-Cit
Renal phosphate leak hypercalciuria pathophys and management
Increased phosphate loss in urine, decreased serum phos
Increases vitamin D, which increased GI calcium absorption
treat with PO orthophosphates
Resorptive hypercalciuria pathophys and management
HyperPTH leads to increased Ca++ resorption from bone + increased GI Ca++ absorption –> increased serum Ca++
Tx with parathyroidectomy
Drug-induced renal calculi: TIME
Triamterene: K sparing diuretic for edema and HTN
Indinavir: protease inhibitor for HIV (non-dense stone on CT)
Magnesium trisilicate: antacid for GERD
Ephedrine +/- guaifenesin: stimulant/expectorant
Stones form due to metabolic effect of the drug
Furosemide: increases urinae Ca++ excretion, causes stones in low birth weight infants
Acetazolamide and other carbonic anhydrase inhibitors
Topiramate: severe hypocitraturia and high urinary pH –> 2% of chronic users get CaPhos stones
Zonisamide: sulfonamide anticonvulsant –> 4% of long term users get CaPhos stones
Laxative abuse: ammonium acid urate stones
Vitamin C supplements - metabolized into oxalate
Vitamin D supplements: increase Ca++ absorption
Type 1 RTA
Distal tubule can’t excrete H+ (in the form of ammonium)
Leads to systemic acidosis (decreased serum CO2) and alkaline urine (pH >5.5)
Increased urinary calcium
Decreased urinary citrate
3/4 of these patients get CaPhos stones
Treat with K-Cit + bicarb to address systemic acidosis
- Type I RTA can be drug-induced (ifosfamide for NSGCT pr penile cancer)
Anion gap is not elevated in RTA
Type 1 distal RTA is a/w nephrocalcinosis
Type II Proximal RTA
Proximal tubule can’t reabsorb HCO3
Increased urine calcium but stable citrate, so not increased stone formation risk
What is a thiazide challenge?
Give two weeks of a thiazide
Recheck serum Ca++, PTH, urine calcium
Used to differentiate renal hypercalciuria (thiazide corrects primary problem of renal calcium leak so urinary Ca++ goes to normal) and true hyperparathyroidism (thiazide blocks appropriate renal response of Ca++ excretion leading to worsening hypercalcemia –> tx with parathyroidectomy)
Medullary sponge kidney + hypercalciuria treatment
Thiazide to arrect stone development
They still need metabolic evaluation
Radiolucent Stones
Ammonium acid urate
Indinavir
Uric acid
Xanthine
Triamterene
Citrate mechanism
Binds Ca++ in urine and intestines
Raises urine pH
Decreases spontaneous nucleation of CaOX
Medical treatment of nonobstructing uric acid stones (HU 300-500) with acidic urine (pH <5.5)
Try to dissolve stones by raising pH with K-Cit
Uric acid or cysteine stone formers whose urine remains pH <6.5 despite K-Cit…
Can try adding acetazolamide (CAI) to further raise pH
Recurrent CaOx stone former sand high urinary oxalate refractory to diet changes
Treat with pyridoxine (vit B6)
Increases conversion of glyoxylate to glycine and decreases conversion to oxalate by LDH
What should Cr level be in an adequately collected 24 hr urine study?
About 1 gram
Improved dusting efficiency
Longer pulse width/duration
Lower peak power (lower energy and higher frequency)
Improved fragmentation efficiency
Shorter pulse width/duration
Higher peak power (low frequency, higer energy)
Physiologic changes with ureteral stent placement
Hyperplasia and inflammation of urothelium
Smooth muscle hypertrophy
Decreased ureteral contractility
Increased VUR
Increased intrapelvic pressure
Physiology of complete ureteral obstruction
Increased glomerular perfusion pressure via preglomerular vasodilation (BL and UL)
Efferent arteriolar constriction (BL only)
Pathophysiology of unilateral renal obstruction
Acute phase (1-2 hours):
Increased renal blood flow (decreased afferent arteriolar resistance)
Little change in GFR
- Mediated by increased NO and PGE2
Mid phase (2-5 hours):
Renal blood flow decreases (increased afferent arteriolar resistance)
GFR decreases (increased proximal tubular hydraulic pressure, increased afferent arteriolar resistance)
Late Phase (24 hours):
Renal blood flow decreased (increased afferent arteriolar resistance)
GFR still decreased (now decreased proximal tubular hydraulic pressure, increased afferent arteriolar resistance)
- Mediated by decreased NO
In solitary kidney, GFR immediately goes down. Late phase mediated by ANP.
Physiology: PCT
2/3 of glomerular ultrafiltrate is reabsorbed in PCT (all AAs and glucose) in isosmotic fashion coupled to Na+ active transport
PCT is responsible for ammoniagenesis (formation of ammonia from glutamine)
Physiology: Descending Thin Loop of Henle
Descending = downhill = ‘easy’ for water to exit through the wall of the loop –> filtrate becomes hypertonic
Physiology: Ascending Thick Loop of Henle
Thick LoH = ascending = water impermeable
Reabsorption of Na+ via 2Cl-K-Na triporter is blocked by loop diuretics here
The medullary thick ascending loop of Henle is most ischemia-sensitive part of kidney and may be damaged with prolonged ischemia during partial nephrectomy
Physiology: Distal Convoluted Tubule
Thiazides block Na-Cl cotransporter in early distal tubule
- Promotes net calcium reabsorption Directly in Distal tubule and indirectly by way of extracellular volume depletion in proximal tubule –> decreased urine Ca++
PTH and Vitamin D stimulate calcium reabsorption in distal tubule
Renin promoters: Decreased BP (JG cells in glomerular afferent arteriole), Decreased Na+ delivery (Macula densa in DCT – abuts JG cells), increased sympathetic tone (Beta1 receptors)
Physiology: Collecting Duct
Principal cells facilitate NaCl reabsorption and Intercalated cells facilitate acid secretion
ADH increases the water permeability of distal tubule and collecting duct
- Blocked in kidney by lithium and release blocked in brain by alcohol
DDAVP works in collecting duct to absorb water
Aldosterone increases open Na+ channels and regulates Na+-K+ exchange in the collecting duct
- Amiloride blocks epithelial sodium channels in DCT and collecting duct –> reduces Na+ reabsorption and K+ secretion (K-sparing)
Parathyroid hormone
Secreted by chief cells in parathyroid in response to hypocalcemia or ectopically by peripheral malignancies (SCC of lung)
Primary role is in kidney: decreases phos reabsorption in proximal tubule and increases calcium reabsorption in ALoH, DCT and collecting duct
PTH activates enzyme 1 hydroxylase in proximal tubule –> increases vitamin D metabolism –> Increases gut absorption of Calcium
Primary hyperparathyroidism
Most common type
Inappropriate PTH secretion by parathyroid gland
= absorptive hypercalcemia
Secondary hyperparathyroidism
Appropriate PTH secretion
Occurs in response to hypocalcemia
Most commonly due to vitamin D deficiency
Angiotensin II maintains GFR during hypovolemia by…
Causing vasoconstriction of the efferent arteriole
ATN effects on urine
Renal tubular cells can no longer resorb sodium or water or excrete urea
Urine will have increased Na, decreased urea, decreased Osm
Urinary concentration is primarily the result of…
…hypertonic medullary interstitial fluid
Cisplatin is nephrotoxic because of…
…a direct toxic effect on renal tubular cells
IgA nephropathy vs. post-strep glomerulonephritis
In IgA, will have URI with renal/UA abnormalities simultaneously –> get renal biopsy
In post-strep, the renal/UA changes will be a few weeks after URI.
Path from biopsy:
IgA = crescent shaped glomeruli + mesangial proliferation
Post-strep GN = cellular proliferation
Sensitivity, specificity, PPV, NPV
Spot Urine Na+ meaning
Prerenal failure: UNa+ is <25 mEq/L because the nephron can still reabsorb Na+ and does so to increase intravascular volume
Intrinsic renal failure: UNa+ is >40 mEq/L because the nephron is no longer reabsorbing Na+ effectively
Sacral neuromodulation is FDA approved for:
Non-obstructive retention
UUI
Urgency/frequency syndrome
Chronic fecal incontinence
Interstitial cystitis
Botox mechanism of action
Decreased acetylcholine release from postsynaptic efferent nerves at presynaptic junction at bladder (by cleaving SNARE proteins (SNAP25) that otherwise allow ACh to be released into the synapse
On clinical evaluation, a patient has global polyuria as defined as >40 ml/kg urine in 24 hours. Testing and ddx?
Overnight water deprivation test
If >800 mOsm/kg –> primary polydipsia, tx with behavioral modifications
If <800 mOsm/kg –> Diabetes Insipidus, do renal concentrating capacity test
NLUTD: Unknown Risk
- Stratification
- Further workup
- Goal
Lesion in suprasacral SC (SCI, MS, transverse myelitis, spinal dysraphism) or any lesion with any GU complications or change in LUTS
Further workup: upper tract imaging + renal fxn + UDS
- Don’t perform cystoscopy
Goal: Determine medium vs. high risk
NLUTD: Medium Risk
- Stratification
- Surveillance
Imaging and renal function are normal, BUT PVR is elevated and/or UDS demonstrated retention, BOO, or DO with incomplete emptying
Surveillance: Annual H+P, renal function, annual vs. biannual upper tract imaging
- Don’t perform surveillance cysto
UDS: Repeat PRN if new symptoms/abnormalities arise
NLUTD: High Risk
- Stratification
- Surveillance
Abnormal/unstable imaging (hydro, scarring, parenchymal loss, staghorn, large/increased stone) and/or renal function and/or UDS demonstrates poor compliance, increasing storage Pdet with DO, DSD, or VUR
Surveillance: Annual H+P, renal function, annual upper tract imaging
- Don’t perform surveillance cysto
UDS: Repeat when clinically indicated and PRN if new symptoms/abnormalities arise
How is normal micturition initiated?
Relaxation of the striated (external) sphincter
Onuf’s nucleus (anterior horn S2-S4) contains the pudendal motor neurons that innervate the EUS
Onuf is the gatekeeper of micturition and needs to be inhibited in order to allow for micturition to proceed
(Sympa-gastrics, Para-pelvic, Soma-dendal)
Detrusor Leak Point Pressure Numbers
Note: This metric is only used for patients with neurogenic lower urinary tract dysfunction
DLPP is most reliable predictor of upper tract deterioration in NLUTD
DLPP >40 is predictive of future upper tract deterioration
DLPP >15 indicates impaired compliance
DLPP and VLPP are determined by the resistance of EUS to fluid leak
Interventions that don’t affect the resistance of EUS will not affect either LPP
Open bladder neck at rest without prior prostatectomy
Multiple System Atrophy
Progressive degeneration of neurons in multiple areas of the brain
Incomplete emptying, ED, “hot crossed buns sign” on MRI
Primary Bladder Neck Obstruction
Level of obstruction on VUDS is clearly the bladder neck itself
Reduce bladder neck with TUIP vs. TURP
Uroflow curve without pressure data: flattened bell
A/w adequate detrusor function with fixed obstruction
Uroflow curve without pressure data: saw tooth
A/w DU or DESD
“Poor compliance” on UDS
<10-15 cc/cm H2O is a reasonable rough definition
Practically, absolute storage pressure > 40 cm H2O is more relevant as this has been a/w deterioration of upper tracts
Spina Bifida and NGLUTD
Highly a/w NGB in children and highly a/w upper tract damage (especially with DESD on initial UDS) if not managed appropriately
Unlike SCI, in lumbosacral SB, neural function and UDS findings cannot be predicted by the level of the lesion
If SB patient develops new hydro, perform UDS
If findings concerning, get spinal MRI to rule out tethered cord or other changes prior to bladder augmentation
Higher chance of paternity with SB at which lesion level?
L5 or sacral level
Spinal shock
Bladder acontractility, areflexia, synergic internal and external sphincters, absent guarding reflex, absent somatic control of the external sphincter
Resolution: return of bulbocavernosus reflex or return of DTRs below the SCI
Guarding reflex
Ability of the striated sphincter (EUS) to contract during bladder filling
- External sphincter activity at the time of DO is part of the normal guarding reflex
Lesions above the pons (brainstem still functioning, CVA or Parkinson’s): bladder/ sphincter
Detrusor Overactivity: Yes (Parkinson’s with impaired contractility)
DESD: No
DISD: No
Autonomic Dysreflexia: No
Intact Bladder Sensation: Yes
Detrusor Areflexia: No
Neurologic Insult Pons to T6-8: bladder/sphincter
Detrusor Overactivity: Yes
DESD: Yes
DISD: Yes
Autonomic Dysreflexia: Yes
Intact Bladder Sensation: Yes
Detrusor Areflexia: No
Neurologic Insult T6-8 to S2: bladder/sphincter
Detrusor Overactivity: Yes
DESD: Yes
DISD: No
Autonomic Dysreflexia: No
Intact Bladder Sensation: No
Detrusor Areflexia: No
Neurologic Insult Injury below S2: bladder/sphincter
Detrusor Overactivity: No
DESD: No (may have fixed EUS tone at rest)
DISD: No (may have open or contracted IS)
Autonomic Dysreflexia: No
Intact Bladder Sensation: No
Detrusor Areflexia: Yes
Neurologic Insult MS: bladder/sphincter
Detrusor Overactivity: Yes
DESD: Maybe
DISD: No
Autonomic Dysreflexia: No
Intact Bladder Sensation: Yes
Detrusor Areflexia: No
Neurologic Insult Multiple System Atrophy: bladder/sphincter
Detrusor Overactivity: Yes
DESD: No (may have EUS denervation)
DISD: No (may have open bladder neck at rest)
Autonomic Dysreflexia: No
Intact Bladder Sensation: Yes
Detrusor Areflexia: No
Lesions above the pons (brainstem still functioning like CVA or Parkinson’s)
DO with synergistic/coordinated activity of internal and external sphincters
The sphincters will relax appropriately during involuntary bladder contractions
Supra-pontine insults should NOT cause detrusor sphincter dyssynergia
Sphincter bradykinesia can occur with Parkinson’s –> slow relaxation of EUS at start of void
Lesions involving brain stem + cord above T6 (including C-spine)
After spinal shock:
Detrusor overactivity + detrusor external sphincter dyssynergia (DESD) + Smooth muscle sphincter dyssynergia (DISD) + autonomic dysreflexia
Autonomic dysreflexia
Afferent stimuli below T6 (bladder distention) in patient with injury above T6 –> massive reflex sympathetic discharge –> vasoconstriction, HTN, reflex bradycardia, flushing, HA, diaphoresis
Complete lesion between T6 and S2
After spinal shock:
Absent sensation + DO + DESD + smooth muscle sphincter synergy
DESD arises because the normal pathways for supraspinal centers to inhibit external sphincter contraction during voiding has been disrupted
Intact sacral nerve arcs (can be assessed by presence of bulbocavernosus reflex) are required for DESD
Detrusor External Sphincter Dyssynergia
Involuntary rise in EMG activity (EUS contraction) during an involuntary DO contraction, narrowing of the membranous urethra, which can lead to incomplete bladder emptying and risk to upper tracts
Further neurological evaluation is warranted (i.e. MS)
Sacral nerve arcs must be present to have DESD, intact bulbocavernosus reflex indicates the presence of sacral nerve arcs (only 70% of women have this reflex, 30% do not)
Sphincterotomy is a historical option for a patient with DESD (new hydro or on UDS) and inability/refusal to CIC.
Actual DESD is only possible in the setting of a spinal cord lesion; a patient may have pelvic floor dysfunction with symptoms that sound like DESD - the most likely UDS finding for such a patient is a low peak flow rate –> try PFPT or SNM
Cauda Equina (Horse’s Tail): L2-S5 spinal nerve bundle
STARTS at L1 vertebra, typically a/w spinal pathology (disc herniation) in the L4-S2 region injury
Typically presents with lumbar spinal pain a/w bladder and bowel incontinence
Nerve compression –> impairment of parasympathetic motor and sensory fibers to the bladder and pelvic floor (bulbocavernosus reflex absent) +/- impairment of pudendal nerve fibers innervating the external sphincter
- UDS shows detrusor areflexia, normal compliance +/- denervation potentials from external sphincter
- NSGY emergency to decompress nerve
Lesions at or distal to sacral cord
Detrusor areflexia and denervation potentials on EMG
Below S2: (after spinal shock) persistent detrusor areflexia +/- decreased compliance +/- open smooth sphincter +/- residual resting sphincter
The cremasteric artery is a branch of the…
…inferior epigastric artery (from external iliac)
The vasal artery is a branch of the…
…superior vesical artery (a branch of the anterior trunk of the internal iliac)
Inferior hypogastric plexus injury (after LAR or APR or TAH)
Denervation of bladder +/- sphincter mechanisms –> areflexia (pelvic nerve damage) + fixed external sphincter tone (pudendal nerve innervation of external sphincter is disrupted) –> increased outlet resistance –> areflexic poorly compliant bladder –> UDS shows decreased compliance, incompetent bladder neck, fixed EUS, detrusor underactivity
SCI in T11 - L2 may damage sympathetic supply to bladder and impair tonic outlet resistance…
Crede maneuver may allow patient to overcome remaining outlet resistance and void
Quinolones side effects
(ciprofloxacin, levofloxacin, etc)
Inhibit DNA gyrase
May cause false positive on opiate screen
Risk of tendon rupture
Affect metabolism of theophylline (tx asthma/COPD), caffeine
Painful necrotic penile ulcer + painful inguinal LAD
Gram-negative coccobacilli (haemophilus ducreyi)
Chancroid
Tx with Azithromycin (1g PO)
Gonorrhea treatment
Single dose IM ceftriaxone
Chlamydia treatment
10 days PO doxycycline
Non-gonoccocal urethritis
think chlamydia or ureaplasma
treat with two weeks PO doxycycline vs. single dose azithromycin
Alpha-blocker most likely to cause retrograde ejaculation?
Least likely?
Most = Silodosin
Least = Alfuzosin
Prostatitis is characterized into 4 syndromes
Category I: ABP, MC due to E. Coli
II: Chronic bacterial prostatitis - rUTI due to same organism, mc E. Coli, enterococcus or another gram -
III: Chronic prostatitis/pelvic pain syndrome. Type A = inflammatory with WBCs, Type B = non-inflammatory, no WBCs
IV: Asymptomatic inflammatory prostatitis - incidental Dx on TRUS Bx for elevated PSA
Male urethral blood supply
Internal iliac –> internal pudendal –> branches into (from ventral to dorsal) BCD
B = bulbourethral (artery of bulb of penis)
C = cavernosal (deep artery of penis)
D = dorsal penile arteries (also supplies most of blood flow to glans penis)
How is baseline flaccidity maintained?
Tonic contraction of penile vascular smooth muscle via norepinephrine release from postganglionic sympathetic nerves
How is an erection achieved?
Parasympathetic stimulation
Release of NO from non-adrenergic, non-cholinergic nerves
NOx binds guanylyl cyclase
Increases cGMP (cGMP is broken down by PDE5)
+ protein kinase
Opens K+ channels and closes Ca++ channels
Decreases intracellular Ca++
Ca++ dissociates from Calmodulin
Relaxation of penile arterial smooth muscle and increased arterial blood flow
PGE1 also increases conversion of ATP to cAMP by adenylate cyclase
Decreases intracellular Ca++
Ca++ dissociates from Calmodulin
Relaxation of penile arterial smooth muscle
Detumescence?
PDE5 breaks down cGMP so smooth muscle relaxation is reversed + PIP3 pathway
increased intracellular Ca++
cavernosal SM contraction
increased intracorporeal pressure
slow decrease in pressure as reopening of venous channels occurs with resumption of baseline arterial flow
Rapid decrease in intracorporal pressure
Flaccidity
After complete suprasacral SCI, reflexogenic (but not psychogenic) erections are generally preserved
Sacral SCI eliminates reflexogenic erections but may not eliminate psychogenic
Painless, slowly growing ulcers without lymphadenopathy
Granuloma inguinale (klebsiella granulomatosis)
Azithromycin 1g PO weekly for 3 weeks
Doxycycline for 3 weeks
Treat partners within 60 days
NLUTD: Low Risk
- Stratification
- Further workup
- Surveillance
Lesion is suprapontine (CVA, Parkinson’s, brain tumor, TBI, CP) or distal to cord (disk disease, s/p pelvic surgery, DM)
Spontaneously voiding with low PVR
No rUTIs
No bladder stones
Normal/stable renal function and upper tract imaging
Synergistic voiding on UDS
Further workup and surveillance not indicated
Reevaluate ID new problems arise (autonomic dysreflexia, UTIs, stones, upper urinary tract or renal function deterioration)
Best intravesical therapy for NMIBC
BCG
Most commonly used agents are BCG, mitomycin, and gemcitabine.
Other options include: sequential gemcitabine/docetaxel, epirubicin, valrubicin, docetaxel, or sequential gemcitabine/mitomycin.
If feasible, the dose of BCG may be split (1/3 or 1/2 dose) so that multiple patients may be treated with a single vial in the event of a shortage.
3-4 weeks after TURBT w/ or w/o maintenance; weekly instillations x 6 weeks
MAX 2 consecutive cycles
Withhold if traumatic catheterization, bacteriuria, persistent gross hematuria, persistent severe local symptoms, or systemic symptoms.
Immunotherapy agents for prostate CA
Sipuleucel-T: dendritic cell vaccine: adverse effects: chills, fever, fatigue, nausea, headache
Ipilimumab: Monoclonal antibody (CTLA-6): Fatigue, diarrhea, pruritus, rash, colitis, severe immune mediated adverse reactions
Tasquinimod: Novel small molecule inhibitor: GI disroders, fatigue, MSK pain
Prostvac-VF: Recomibinant viral vaccine targeting PSA; Injection site reactions, fatigue
Classification of ED
Campbell Table 69.4 PSYCHOGENIC Sudden onset Complete immediate loss Situational dysfunction Waking erections present
ORGANIC
Gradual onset
Incremental progression
Global dysfunction
Types of URINARY RETENTION
EAU 2021
Acute retention of urine is defined as a painful, palpable or percussible bladder, when the patient is
unable to pass any urine
Chronic retention of urine is defined as a non-painful bladder, which remains palpable or percussible after
the patient has passed urine. Such patients may be incontinent
Management of Post-RP incontinence
Urodynamics Imaging of urinary tract Urethrocystoscopy (if indicated) ⬇️ IF STRESS UI: - Due to sphincteric incompetence - If initial therapy fails: AUS, male sling
IF MIXED UI:
- Treat major component first
- If with coexisting BOO:
- Alpha-blockers
- Correct anatomic BOO
- Antimuscarinics/beta-3 agonists
IF URGENCY UI:
- Due to detrusor OA (during filling)
- if with coexisiting DU (during voiding)
- Intermittent catheterization
- Antimuscarinics/beta-3 agonists
Trauma: URETHRA
- Bulbar: most common affected by blunt - compressed against pubic symphysis
Iatrogenic anterior urethra: STC or IFC
Partial blunt anterior urethra: STC or IFC
Complete blunt anterior urethra: immediate urethroplasty (if surgical expertise available), otherwise suprapubic diversion with delayed urethroplasty
PFUI with hemodynamic instability: IFC or STC
PFUI male: early endoscopic realignment when feasible
DO NOT repeat endoscopic treatments after failed re-alignment for male PFUI
Partial posterior urethra: STC or IFC
DO NOT perform immediate urethroplasty (<48h) in male PFUIs
Male PFUIs with complete disruption, stable, short gap, soft perineum, lithotomy possible: Early urethroplasty (2-6 weeks)
Complete posterior urethral disruption: SP diversion and at wait at least 3 months before urethroplasty
Female PFUIs: Early repair (within 7 days) (NOT delayed repair or early realignment)
Anterior urethral injury: immediate repair
Penetrating stable patients
Penile fracture
with IFC or STC x 2-3 weeks then RUG
Anterior urethral trauma: STC or IFC
Iatrogenic
Blunt: partial or complete
Penetrating UNSTABLE
IFC or STC x
1-2 weeks for partial
3 weeks for complete
Then RUG
Male posterior urethral injury:
RUG/urethroscopy – PARTIAL injury
Early endoscopic realignment - STC if failed
If short flimsy non-obliterative stricture: DVIU
Otherwise: delayed urethroplasty (>3 months)
Male posterior urethral injury:
RUG/urethroscopy – COMPLETE injury + BLADDER NECK and/or PROSTATE injury
EARLY REPAIR
Male posterior urethral injury:
RUG/urethroscopy – COMPLETE injury, no bladder or prostate
Surgery for associated injuries – YES – early endoscopic realignment – if failed, STC
Assess 2days-6 weeks
IF short distraction defect, soft perineum, lithotomy possible – early urethroplasty
IF not: delayed urethroplasty (> 3 months)
IMMEDIATE INTRAVESICAL
• A single instillation of chemotherapy is administered within 24 hours of surgery (ideally within 6 hours).
• Gemcitabine (preferred) (category 1)1 and mitomycin (category 1)2 are the most commonly used agents in the United States for intravesical
chemotherapy. Thiotepa does not appear to be effective.3
• Immediate postoperative intravesical chemotherapy reduces the 5-year recurrence rate by approximately 35% and has a number needed to
treat to prevent a recurrence of 7. However, it does not reduce the risk of progression or the risk of cancer mortality.3
• It is not effective in patients with an elevated EORTC recurrence risk score (≥5). This includes patients with ≥8 tumors and those with
≥1 recurrence per year.
• Contraindications include: bladder perforation, known drug allergy
INDUCTION INTRAVESICAL
• Treatment option for NMIBC.
• The most commonly used agents are BCG, mitomycin, and gemcitabine.
• In the event of a BCG shortage, BCG should be prioritized for induction of high-risk patients (eg, high-grade T1 and CIS). Preferable
alternatives to BCG include mitomycin or gemcitabine.
Other options include: sequential gemcitabine/docetaxel, epirubicin, valrubicin, docetaxel, or sequential gemcitabine/mitomycin.
If feasible, the dose of BCG may be split (1/3 or 1/2 dose) so that multiple patients may be treated with a single vial in the event of a shortage.
• Initiated 3–4 weeks after TURBT with or without maintenance.
• Weekly instillations during induction are given for approximately 6 weeks.
• Maximum of 2 consecutive cycle inductions without complete response.
• Withhold if traumatic catheterization, bacteriuria, persistent gross hematuria, persistent severe local symptoms, or systemic symptoms.
MAINTENANCE INTRAVESICAL
• Although there is no standard regimen for maintenance BCG, many NCCN Member Institutions follow the SWOG regimen consisting of a 6-week induction course of BCG followed by maintenance with 3 weekly instillations at months 3, 6, 12, 18, 24, 30, and 36.4 • In the event of a BCG shortage, BCG should be prioritized for high-risk patients (eg, high-grade T1 and CIS), especially in the early maintenance period (ie, 3 and 6 months post-induction). If feasible, the dose of BCG may be split (1/3 or 1/2 dose) so that multiple patients may be treated with a single vial in the event of a shortage. • Ideally maintenance should be given for 1 year for intermediate-risk and 3 years for high-risk NMIBC. • BCG would be withheld if traumatic catheterization, bacteriuria, persistent gross hematuria, persistent severe local symptoms, or systemic symptoms. • Dose reduction is encouraged if there are substantial local symptoms during maintenance therapy. 4 • Data suggest the benefit of maintenance BCG therapy through a decreased rate of recurrence for NMIBC
CAH
- Low cortisol production caused by a metabolic enzymatic abnormality in the cholesterol-steroid biosynthesis pathway
- ACTH production by the pituitary gland is increased, resulting in hyperplasia of the adrenal cortex and overproduction of adrenal androgens
Deficiency of aldosterone in the salt-wasting form results in renal sodium losses (HYPONATREMIA), hypovolemia, and HYPERKALEMIA. Cortisol deficiency results in poor cardiac contractility with decreases in vascular tone
Low-dose dexamethasone test
Patient’s failure to suppress cortisol levels after an overnight low-dose dexamethasone administration is indicative of CUSHING syndrome.
This test does not delineate the cause of hypercortisolism, but simply suggests its presence.
Common tumors Pediatric
Neuroblastoma: most common extracranial solid tumor of childhood
Wilms Tumor: most common primary malignant tumor of childhood; most common form of renal cancer in children younger than 15 years
Congenital mesoblastic nephroma: most common renal tumor on antenatal ultrasound and in infants
Rhabdomyosarcoma: most common soft tissue sarcoma in children AND most common pediatric solid tumor
Most common histopath of renal tumors:
Adult: renal cell carcinoma
Pediatric: Wilms tumor
Prostate cancer drugs: SIDE EFFECTS
Bicalutamide: gynecomastia, mastodynia, liver toxicitiy
Flutamide: GI toxicity, diarrhea
Nilutamide: delayed adaptation to darkness after brightness
Enzalutamide: seizures, fatigue, hypertension
Apalutamide: hypothyroidism, rash, fracture
GnRH agonists (Leuprolide): FLARE, increases bone turnover
Abarelix: severe allergic reactions (vs. degarelix, none)
Abiraterone: HYPOKALEMIA, liver toxicity, hypertension, edema
Docetaxel and cabazitaxel: febrile neutropenia
Sipuleucel-T: chills, fever, headache
Pembrolizumab: fatigue
Cyproterone acetate: severe cardio complications, hypogonadal state
Aminogluthetimide: anorexia, nausea, lethargy
Ketoconazole: gynecomastia, hepatic dysfunction
Most common tumors in the kidney
MOST COMMON MALIGNANT:
Clear cell RCC accounts for 70% to 80% of all RCCs, representing the garden variety of RCC
2nd most common: Papillary RCC
MOST COMMON BENIGN:
Renal cyst disease
MOST COMMON BENIGN ENHANCING RENAL MASS:
Oncocytoma
BONE HEALTH
DENOSUMAB 120 mg SC (Xgeva); 60 mg q6 months if M0: (preferred) is given subcutaneously every 4 weeks. Although renal monitoring is not required, denosumab is not recommended in patients with creatinine clearance <30 mL/min.
- SE: hypocalcemia (2x more than zoledronic)
Zoledronic acid 5 mg IV annually for M0; every 3 to 4 weeks or every 12 weeks for metastatic; not recommended for creatinine clearance <30 mL/min.
Alendronate 70 mg PO
ONJ: RFs: tooth extractions, poor dental hygiene, or a dental appliance.
referred
for dental evaluation before starting either zoledronic acid or denosumab.
ED post-RP
EAU 2021
1st LINE: PDE5 inhibitors - alternative: topical/intraurethral alprostadil if not suitable for vasoactive therapy
2nd line: ICIs
3rd line: Penile implants
Systemic therapy for bladder CA
DDMVAC: 3-4 cycles
GC: 4 cycles
Radical cystectomy interval
12 weeks after TURBT
NAC should not be delayed by more than 8 weeks
Indications for ACTIVE STONE REMOVAL URETER
Low likelihood of spontaneous passage
Persistent pain despite adequate medication
Persistent obstruction
Renal insufficiency
Nerve-sparing RPLND Testicular Tumors
RIGHT SIDED nerve sparing: post-ganglionic sympathetic fibers posterior to vena cava
LEFT SIDED nerve sparing:
post ganglionic fibers ANTEROLATERAL aspect of spine - thoracolumbar sympathetic outflow (T12-L2)
Apalutamide vs. darolutamide
Darolutamide DOES NOT CROSS THE BBB – does not cause seizures
PIRADS percent detection of CA
PIRADS
3: 40% detection
4: 70%
5: 90%
Apalutamide and Darolutamide for M0CRPC EFFECT ON OUTCOMES:
Increases metastasis-free survival, by 3 months
Questions to ask when a man presents with inability to conceive? (BD)
Normal potency, libido, ejaculation?
History of surgery, chemotherapy, radiation, heat exposure?
History of mumps, EtOH, tobacco, viral illness, environmental toxins, chronic illness?
(Previous children)
What are the key components of sexual history? (BD)
Personal: Gender identity, sexual orientation, age of sexual partner(s), relationship status, relationship duration, frequency of sexual activity
Sexual dysfunction: Severity, onset, rate of decline, nocturnal erections, ability to sustain erection, exacerbating or alleviating factors, previous treatments, degree of distress, goals of treatment
Social: Job, stress level, life changes, health changes associated with sexual dysfunction timing
Nitroglycerin and PDE5i (BD)
Serum half-life is relevant if a patient developed chest pain after a PDE5i is taken.
Nitroglycerin must be withheld for:
24 hours with sildenafil and vardenafil
48 hours for tadalafil
12 hours for avanafil
PDE Metabolism (BD) + Drug Interactions
CYP4A4 system
Dose reduction when taking CYP450 inhibitors (ketoconazole, erythromycin, ritonavir, indinavir, grapefruit juice)
Dose should be increased (or these meds may increase the metabolism): rifampin, phenobarbitol, phenytoin, carbamazepine
Men with severe hepatic or renal dysfunction (GFR <30 mL/min) should start at the lowest dose
What is Bimix and why might it be used versus the others? (BD)
Bimix is papaverine (non-specific PDE inhibitor not used in monotherapy, metabolized by the liver and can rarely result in liver enzyme elevation) and phentolamine (alpha adrenergic receptor inhibitor not effective as a monotherapy, inhibits detumescence).
90% efficacy with NO penile pain
Alprostadil (only FDA approved medication) activates adenylate cyclase and increases intracellular cAMP but causes pain 37% of the time
DO NOT GIVE ICI WITH MAOIs
What is the differential diagnosis of an enlarging “boil” in the perineum/scrotum?
Fournier’s Gangrene
Furuncles and abscesses
Cellulitis
Balanitis or Balanoposthitis
Post-operative infections
Hidradenitis Suppurativa
Sexually Transmitted Infections -Certain sexually transmitted infections can present with cutaneous manifestations including: lymphogranuloma venereum, chancroid, granuloma inguinale, syphilis, herpes simplex, human papilloma virus, and molluscum contagiosum.
Intertrigo - A candidal infection of skin folds where the macerated skin becomes red and inflamed
Epididymo-orchitis
Non-infectious genital ulcers -Examples include fixed drug eruption and Behcet’s disease (inflammatory disorder that can result in oral and genital ulcerations, ocular disease, and skin lesions).
What questions should you ask if you are told a patient has hyperkalemia?
What are the vitals? Hyperkalemia can result in abnormalities in cardiac conduction which can predispose towards deadly arrhythmias.
What were some of the specifics of her operation? Long operations, especially those performed in flank position, can result in rhabdomyolysis and liberation of intracellular potassium.
What is her baseline renal function? There are two main mechanisms by which the body maintains potassium hemostasis: renal excretion and cellular shifts of potassium. Risk of hyperkalemia is inversely related to glomerular filtration rate, and increase perceptibly once the GFR is < 30 mL/min.
Was there a blood transfusion? Acute hemolytic transfusion reactions can occur due to use of incompatible red blood cells or large volume of incompatible plasma.
These reactions are rare but can cause release of large amount of intracellular potassium, which can cause hyperkalemia, especially in the setting of impaired renal function.
Differential diagnosis of hyperkalemia
Causes
Metabolic Acidosis
Mineral acidosis (NH4Cl or HCl) can directly result in potassium movement into extracellular fluid to maintain electroneutrality.
Acute or Chronic Renal
Renal failure is a significant risk factor for the development of hyperkalemia and can occur whether acute or chronic. Decreased renal function results in impairment of potassium excretion
Decompensated Heart failure
can exacerbate hyperkalemia due to decreased renal perfusion
Medications
Renin angiotensin aldosterone system (RAAS) inhibitors
angiotenisin-concerning enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), aldosterone receptor antagonists
Calcineurein inhibitors
decrease aldosterone synthesis and the activity of the sodium-potassium ATPase pump
Nonsteroidal anti-inflammatory drugs
decrease prostaglandin-mediated renin release, renal blood flow, and glomerular filtration
Heparin
blocks the biosynthesis of aldosterone in the adrenal gland
Ketoconazole
Interferes with biosynthesis of adrenal steroids and can cause aldosterone deficiency
Potassium-sparing diuretics
spironolactone, eplerenone, amiloride, triamterene
Trimethoprim
blocks luminal sodium channels
Pentamide
blocks luminal sodium channels
Nonselective beta blockers
(i.e. propranolol, carvedilol, labetalol, nadolol)
High potassium diet
Tissue Injury
rhabdomyolysis, hemolysis, tumor lysis
Insulin Deficiency: insulin promotes potassium entry into cells
Diabetic Ketoacidosis or Hyperosmolar Hyperglycemic State
Although patients generally have a potassium deficit in these conditions, some patients may develop hyperkalemia. The increased serum osmolality can result in water shift from intracellular into extracellular space, which results in potassium also following out of the cells by solvent drag and redistribution11
Hyperkalemic Periodic Paralysis
Exercise
potassium increases during exercise, but rarely important clinically
Use of jejunum as urinary diversion
Reduced aldosterone secretion
hyporeninemic aldosteronism (e.g. diabetic nephropathy, medications), primary adrenal insufficiency, severe illness, congenital hypoaldosteronism, pseudohypoaldosteronism type 2
Aldosterone resistance
medications, pseudohypoaldosteronism type 1, reduced sodium delivery to distal tubule, defects in the sodium resorptive capacity of distal tubule (i.e. obstructive uropathy)
‘Pseudohyperkalemia’
Spurious elevations in measured serum potassium levels can occur with hemolysis during venipuncture (fist clenching during phlebotomy, application of tourniquets, use of small-bore needles) or handling/processing of blood, thrombocytosis, familial pseudohyperkalemia, or polyctemia14
A 68-year-old man with a history of muscle-invasive bladder cancer treated by radical cystectomy and urinary diversion 6 years ago presents to your office complaining of weakness, fatigue, and weight loss.
What are your first questions?
What are the patient’s vitals?
Weakness and fatigue should first prompt a consideration of infection and fluid status.
What was the patient’s pathology, treatment, and disease status?
In a patient with advanced bladder cancer, disease recurrence should also be considered as a possibility.
What type of urinary diversion did the patient have?
Urinary diversions are associated with metabolic abnormalities. The typical pattern of metabolic abnormality seen is dependent on the segment of bowel used for urinary diversion, and is typically more severe with continent vs. incontinent urinary diversions, as well as with the length of bowel resected. When ileum and colon are used, the typical pattern of electrolyte abnormality is hyperchloremic metabolic acidosis, with the possibility of hypokalemia. Less commonly, when jejunum is used, this can result in hyponatremic, hyperkalemic, hypochloremic metabolic acidosis. When stomach is used, this can result in a hypochrloremic, metabolic alkalosis with the possibility of hypokalemia.
How is he emptying his urinary diversion?
If he has a continent urinary diversion, then there is a greater contact time between the urine and intestinal mucosa.
What is the patient’s baseline and current renal function?
Patients with poor renal function are less capable of compensating for an increased acid load and more likely to exhibit metabolic acidosis.
What is the patient’s baseline liver function? Patients with poor liver function can experience sequelae of elevated ammonia levels.
What medications is the patient taking?
How are the patient’s bowel movements? Chronic diarrhea and steatorrhea can occur after urinary diversion.
A 68-year-old man with a history of muscle-invasive bladder cancer treated by radical cystectomy and urinary diversion 6 years ago presents to your office complaining of weakness, fatigue, and weight loss.
What is the differential diagnosis?
Metabolic Acidosis: Most urinary diversions can lead to electrolyte abnormalities. The most common bowel segments used are ileum and colon are generally lead to a hypercholeremic, hypokalemic, metabolic acidosis
Hypokalemia: Signs of hypokalemia include fatigue, constipation, weakness, muscle spasms
Renal Failure: Following urinary diversion, patients have multiple sources of developing renal failure including age, utero-enteric anastomosis stricture, recurrent infections, nephrolithiasis, and reabsorption of creatinine through the intestinal epithelium (pseudoazotemia)
Urinary tract infection: Common occurrence following urinary diversion
Hyperammonemic encephalopathy: In urinary diversions, ammonia is re-absorbed through the bowel wall. Patients with normal liver function can typically deal with the increased ammonia load, however infections with urea-splitting bacteria, urinary tract obstruction, and poor liver function can lead to hyperammonemic encephalopathy and even coma
Chronic Diarrhea: Following urinary diversion, patients may experience chologenic (bile acid) diarrhea due to loss of bile acids. Normally, the ileum will resorb most conjugated bile acids, however resection of longer segments can produce a malabsorption of bile acids and these enter the colon with resultant loss of bile acids, water, and sodium.4 Depletion of bile acids can also result in malabsorption of fatty acids and the development of steatorrhea
Disease recurrence: Metastatic disease can produce the constitutional symptoms the patient is complaining of
What kind of stones do diabetic get more often than the general population?
Uric acid stones are over-represented among diabetic patients compared to the general population. Low urine pH in patients with type 2 DM and insulin resistance is thought to be the result of both impaired renal ammonium excretion and increased net acid excretion, leading to reduced urinary buffering capacity and acidic urine.
Uric acid stone formation has been linked to the metabolic syndrome, sharing a number of features including hypertension, obesity, hypertriglyceridemia and hyperglycemia.
When performing 24 hour urinalysis, it is important to note that in the setting of low urine pH (<5.5), uric acid can precipitate out in the collection jug and may not be properly measured. Rechecking uric acid levels after the urine has been adequately alkalinized may reveal a significant increase in uric acid levels due to resolublization.
Cystine Stones
Cystinuria is an autosomal recessive disorder which leads to defective renal proximal tubule and intestinal epithelium transport of the four dibasic amino acids: cystine, ornithine, lysine and arginine (COLA).
Cystinurics excrete abnormally high levels of all four, but only cystine (cysteine-cysteine) is poorly soluble and uniquely forms stones.
Cystine is a dimeric amino acid formed by two oxidized cysteine monomers linked ay a disulfide bond (cysteine-cysteine).
Cystine solubility is highly pH dependent and increases exponentially with increasing urinary pH.
Sodium enhances cystine excretion and methionine is a precursor in cystine synthesis.
Therefore, dietary management for cystinurics includes high fluid consumption, sodium restriction, and low methionine diet which most practically means decreased animal protein intake.
Medical management is primarily urinary alkalinization with an oral agent such as potassium citrate or sodium bicarbonate.
Thiol therapy is given to select patients and works by forming a cysteine-drug complex, which is 50 times more soluble than cystine (cysteine-cysteine).
Bacteria that raise concern for struvite stones
Urine culture should be obtained in patients with recurrent urinary tract infections or in those with a urinalysis suspicious for infection. Infection with a urease-splitting organism should raise concern for struvite (magnesium ammonium phosphate) stones.
Common Urease-Producing Bacteria
Gram Negative Bacteria Gram Positive Bacteria
Proteus mirabilis Corynebacterium sp
Klebsiella Pneumoniae Staphylococcus aureus
Pseudomonas sp Staphylococcus epidermidis
Indications for 24 hour urine evaluation
Recurrent calcium stone former
Family history of stone disease
Intestinal or malabsorptive disease
Pathologic skeletal fracture
Osteoporosis
Gout
Young age of onset of stone disease
Uric acid nephrolithiasis
Cystine stones
Patient-specific risk factors (Solitary kidney, chronic kidney disease, vocation, infirm health)
Side effects of Thiazides
↑’s calcium reabsorption in distal renal tubule (direct mxn) and through extracellular volume depletion in the proximal tubule (indirect mxn)
Decreases urinary calcium
Thiazide use may be accompanied by hypokalemia, hyperglycemia, hyperuricemia, dyslipidemia and hypocitraturia, and therefore monitoring of these levels is indicated.
To prevent thiazide-induced hypokalemia and hypocitraturia, potassium supplementation is recommended. Potassium citrate has the advantage of enhancing urinary citrate and further reducing the risk of stone formation.
What does K Citrate do? What is the effect of it, and what are the side effects?
Binds to ionized calcium; inhibits calcium oxalate and calcium phosphate crystallization
↓ in urinary ionized calcium; ↑ in urinary citrate and pH
GI symptoms (nausea, heartburn, loose stools)
What does allopurinol do? What is the effect of it, and what are the side effects?
Inhibits xanthine oxidase
↓ in serum and urinary uric acid
Elevation in liver enzymes, rash (Stevens-Johnson syndrome)
What does acetohydroxamic acid do? What is the effect of it, and what are the side effects?
Inhibits urease
↓ in urine pH and urinary urea
Nausea, headache, tremor, anemia, GI symptoms, DVT
What does Alpha mercaptopropionyl glycine (thiola) do? What is the effect of it, and what are the side effects?
Disulfide exchange
↓ in urinary cystine
Hematologic abnormalities (anemia, pancytopenia), proteinuria, loss of taste, anemia, rash
Lymph node staging for bladder cancer
NX Lymph nodes cannot be assessed
N0 No lymph node metastasis
N1 Single regional lymph node metastasis in the true pelvis (hypogastric, obturator, external iliac, or presacral lymph node)
N2 Multiple regional lymph node metastasis in the true pelvis (hypogastric, obturator, external iliac, or presacral lymph node metastasis)
N3 Lymph node metastasis to the common iliac lymph nodes
Metastasis staging for bladder cancer
M0 No distant metastasis
M1 Distant metastasis
M1a Distant metastases limited to lymph nodes beyond the common iliacs
M1b Non-Lymph – node distant metastases
Checklist of data to include in a TURBT Operative Note
1 Describe number of bladder tumors
2 Describe size of bladder tumors (largest diameter and aggregate diameter)
3 Describe tumor morphology (nodular, papillary, flat, sessile)
4 Describe recurrent versus primary tumors
5 Assess for CIS (suspicious or not)
6 Assess AJCC clinical stage (cTa, cT1, cTis, cT2, cT3, cT4)
7 Report bimanual exam findings
8 Report whether resection was visually complete
9 Report whether muscle was visually resected
10 Report presence of absence of perforation
Additional items
11 Use of immediate postoperative chemotherapy (drug, dose, dwell time)
12 Diagram of tumor location(s)
Indications for second look TURBT
(i) Incomplete first TURBT
(ii) Large (> 3 cm) or highly multifocal tumor
(iii) High grade Ta tumor
(iv) pT1 tumor with or without muscle in the original specimen.
Types of Retroperitoneal Sarcomas
Liposarcoma
Leiomyosarcoma
Solitary fibrous tumor
Undifferentiated pleomorphic sarcoma Malignant peripheral nerve sheath tumors
Antihypertensives associated with ED
Beta Blockers
Thiazide Diuretics
Angiotensin Converting Enzyme Inhibitors
Spironolactone
Medications associated with ED
5-Alpha Reductase Inhibitors
Anti-androgens
LH-RH agonists/antagonists
Anti-hypertensives
-Beta Blockers
-Thiazide Diuretics
-Angiotensin Converting Enzyme Inhibitors
-Spironolactone
H2 Blockers
Psychiatric Drugs
-Selective Serotonin Reuptake Inhibitors
-Tricyclic Antidepressants
-Benzodiazepines
-Antipsychotics
Phenytoin
Miscellaneous
Digoxin
Collagenase for Peyronie’s
AUA Guideline Recommendations: May be offered in men with stable PD, curvature 30-90 degrees, and intact erectile function (Evidence Strength Grade B)
Collagenase injections are approved for the treatment dorsal or lateral plaques but not ventral plaques, due to potential risk of urethral injury.
Following dorsal penile block, a medium gauge needle (e.g. 25g) is used to repetitively puncture the plaque. At the same time, a small amount of the treating medication (usually diluted in 5-10 ml of normal saline) is injected into the plaque.
The importance of completing the full four cycles of CCH injections was emphasized in a 2021 study of 296 men which showed that 2/3 of men who fail to achieve 10 degrees or 20% curvature improvement with an initial 2 cycles achieved this with the final two cycles.
What to look for on urodynamics
bladder sensation (recorded as the bladder volume at which the patient reports first desire to void, normal desire to void, strong desire to void, urgency, and pain, if applicable)
bladder capacity (maximum cystometric capacity)
bladder compliance (measured as the change in volume over change in pressure)
detrusor overactivity (i.e. the presence of uninhibited detrusor contractions with or without leak)
stress urinary incontinence
The 8 Cs that you’re looking for on urodynamics (this is a bit much)
Filling cystometry
Contractions (involuntary bladder)
Compliance
Continence
Capacity
Conscious sensation
Pressure-flow studies
Contractility
Complete Emptying
Clinical Obstruction
NIH Classification for Types of Prostatitis
Category I—Identical to acute bacterial prostatitis
Category II—Identical to chronic bacterial prostatitis
Category III Chronic Pelvic Pain Syndrome (CPPS)—Presence of GU pain in absence of uropathogenic bacteria
Category IIIA (Inflammatory CPPS)—Excessive WBC in EPS or post-prostatic massage urine or semen
Category IIIB (Non-inflammatory CPPS)—No significant WBC
Category IV (Asymptomatic Inflammatory Prostatitis)—Significant WBC or bacteria in prostate specimens with no symptoms
When do you repair VUR?
(1) progressive renal injury
(2) documented failure of renal growth
(3) breakthrough pyelonephritis
(4) intolerance or non-compliance with antibiotic suppression
Risk factors for UTUC
Smoking
Bladder cancer (CIS, multifocality, proximity to ureteral orifice)
Lynch syndrome (especially with MSH2 mutations)
Aristolochic acid (Balkan nephropathy, Chinese and Taiwanese herbal nephropathy)
Arsenic
Analgesics
Occupational exposure (petroleum, plastic, coal, tar, dyes)
Chronic inflammation and infection
Cyclophosphamide
Staging for UTUC
Tx: tumor invasion cannot be assessed
Tis: carcinoma in situ; for UTUC generally accepted as a positive selective cytology in the absence of visible tumor. However, CIS may coexist with papillary and sessile tumors.
Ta: noninvasive on biopsy
T1: invasion of lamina propria on biopsy
T2: invasion of muscularis; however, this is typically not seen on biopsy nor on imaging thus is rarely if ever documented
T3: invasion of periureteral fat, renal parenchyma, or renal sinus fat; seen on imaging only and not on biopsy
T4: invasion of adjacent organs; seen on imaging only.
N0: no involvement of lymph nodes on imaging
N1 (or N+): involvement of lymph nodes on imaging.
Low Risk Vs High Risk UTUC
Low-risk UTUC
Unifocal disease
Tumor size <2cm
Low-grade cytology
Low-grade URS biopsy
No invasive aspect on CTU
High-risk UTUC
Hydronephrosis
Tumor size >2cm
High-grade cytology
High-grade URS biopsy
Multifocal disease
Previous radical cystectomy for bladder cancer
Variant histology
