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Urology In-Service/Board Review > CRAM > Flashcards

CRAM Flashcards

1
Q

Dietary recommendations: Ca++ stones and high urinary Ca++

A

Limit Na+
Maintain normal Ca++ (1-2g/day)

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2
Q

Dietary recommendations: Ca++Oxalate stones + high urinary oxalate

A

Limit oxalate
Maintain normal Ca++ (1-2g/day)

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3
Q

Dietary recommendations: Ca++ stones + low urinary citrate

A

Limit non-dairy animal protein and increase fruits and veggies

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4
Q

Dietary recommendations: Uric acid or Ca++ stones and high urinary uric acid

A

Limit non-dairy animal protein

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5
Q

Dietary recommendations: Cystine stones

A

Limit Na+ and protein intake

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6
Q

Medical therapy:
Recurrent stones + high urinary Ca++

A

Thiazide diuretic

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7
Q

Medical therapy:
Recurrent Ca++ stones + low urinary citrate

A

Potassium citrate

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8
Q

Medical therapy:
Recurrent CaOx stones + hyperuricosuria + normal urinary Ca++

A

Offer urinary allopurinol

If uric acid stones, DON’T offer allopurinol as first-line therapy

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9
Q

Medical therapy:
Recurrent Ca++ stones without other lab abnormalities

A

Empiric thiazide diuretics and/or K-cit

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10
Q

Medical therapy:
Uric acid and cystine stones

A

K-cit to raise urinary pH (these stones form in acidic urine)

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11
Q

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

A

Offer cysteine-binding thiol drugs (alpha-mercaptopropionylglycine = Thiola = tiopropin), which is better tolerated than D-Penicillinamine

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12
Q

Medical therapy:
Residual/recurrent struvite stones after surgery exhausted

A

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

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13
Q

Renacidin = citric acid glucono-delta-lactone magnesium carbonate

A

Used for dissolution treatment of residual struvite stones/fragments

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14
Q

Urease-producing organisms

A

Proteus, klebsiella, staph aureus, pseudomonas, providentia, ureaplasma

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15
Q

Enteric/acquired hyperoxaluria is a/w:

A

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

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16
Q

Crohn’s stone formation

A

low urine volume (dehydration) + low urine pH and hypocitraturia (metabolic acidosis) + hyperoxaluria (over absorption of intestinal oxalate –> CaOx stones

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17
Q

Isolated hypomagnesemia

A

Suggests IBD –> refer to GI

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18
Q

PO Reloxaliase

A

Recombinant oxalate decarboxylase enzyme derived from B. subtilis and expressed in E. Coli

Degredes oxalate within GI tract –> decreased oxalate absorption and urinary excretion

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19
Q

Lumasiran = Oxlumo

A

siRNA
decreases glycolate oxidase, which decreases glyoxylate’s conversion to oxalate

Approved for Tx of type 1 primary hyperoxaluria

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20
Q

CF is a/w which urinary abnormalities?

A

Hyperoxaluria, hypocitraturia (prone to stones)

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21
Q

Prevent stones: Roux-En-Y

A

Dietary Ca++ at mealtime
Decrease high oxalate foods
Metabolic acidosis –>decreased urinary citrate –> K-Cit

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22
Q

Stones: Colon resection and end ileostomy

A

Fluid and bicarbonate loss
Concentrated urine with low pH
Increased risk of uric acid stone formation

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23
Q

Lesch-Nyhan Syndrome

A

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

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24
Q

Pregnancy and stones

A

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

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25
Q

Ammonium acid urate stones

A

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)

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26
Q

Keto(genic) diet affect on stones

A

Excess meat (purine) consumption
Hyperuricosuria, increased urinary sulfate + urea nitrogen
Hypercalciuria
Hypocitraturia
Decreased urine pH
Uric acid + calcium nephrolithiasis

Treat with dietary changes +/- allopurinol

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27
Q

Topiramate and stones

A

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

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28
Q

Vitamin C effect on urine

A

10-20% is metabolized into oxalic acid and excreted into urine

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29
Q

Most common risk factor for Ca++ stones

A

Hypercalciuria

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30
Q

Absorptive hypercalciuria pathophysiology

A

Increased GI Ca++ absorption
Normal or increased serum Ca++
Decreased serum PTH and decreased vitamin D

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31
Q

Absorptive hypercalciuria management options

A

Avoid excess dietary Calcium
Decrease salt and animal protein in diet
Thiazides +/- K-Cit

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32
Q

Renal calcium leak hypercalciuria pathophysiology and management

A

Increased calcium loss into urine
Normal or decreased serum Calcium
Increased serum PTH

Management: Thiazides +/- K-Cit

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33
Q

Renal phosphate leak hypercalciuria pathophys and management

A

Increased phosphate loss in urine, decreased serum phos
Increases vitamin D, which increased GI calcium absorption

treat with PO orthophosphates

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34
Q

Resorptive hypercalciuria pathophys and management

A

HyperPTH leads to increased Ca++ resorption from bone + increased GI Ca++ absorption –> increased serum Ca++

Tx with parathyroidectomy

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35
Q

Drug-induced renal calculi: TIME

A

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

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36
Q

Stones form due to metabolic effect of the drug

A

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

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37
Q

Type 1 RTA

A

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
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38
Q

Type II Proximal RTA

A

Proximal tubule can’t reabsorb HCO3

Increased urine calcium but stable citrate, so not increased stone formation risk

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39
Q

What is a thiazide challenge?

A

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)

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40
Q

Medullary sponge kidney + hypercalciuria treatment

A

Thiazide to arrect stone development

They still need metabolic evaluation

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41
Q

Radiolucent Stones

A

Ammonium acid urate
Indinavir
Uric acid
Xanthine
Triamterene

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42
Q

Citrate mechanism

A

Binds Ca++ in urine and intestines
Raises urine pH
Decreases spontaneous nucleation of CaOX

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43
Q

Medical treatment of nonobstructing uric acid stones (HU 300-500) with acidic urine (pH <5.5)

A

Try to dissolve stones by raising pH with K-Cit

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44
Q

Uric acid or cysteine stone formers whose urine remains pH <6.5 despite K-Cit…

A

Can try adding acetazolamide (CAI) to further raise pH

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45
Q

Recurrent CaOx stone former sand high urinary oxalate refractory to diet changes

A

Treat with pyridoxine (vit B6)
Increases conversion of glyoxylate to glycine and decreases conversion to oxalate by LDH

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46
Q

What should Cr level be in an adequately collected 24 hr urine study?

A

About 1 gram

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47
Q

Improved dusting efficiency

A

Longer pulse width/duration
Lower peak power (lower energy and higher frequency)

48
Q

Improved fragmentation efficiency

A

Shorter pulse width/duration
Higher peak power (low frequency, higer energy)

49
Q

Physiologic changes with ureteral stent placement

A

Hyperplasia and inflammation of urothelium
Smooth muscle hypertrophy
Decreased ureteral contractility
Increased VUR
Increased intrapelvic pressure

50
Q

Physiology of complete ureteral obstruction

A

Increased glomerular perfusion pressure via preglomerular vasodilation (BL and UL)

Efferent arteriolar constriction (BL only)

51
Q

Pathophysiology of unilateral renal obstruction

A

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.

52
Q

Physiology: PCT

A

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)

53
Q

Physiology: Descending Thin Loop of Henle

A

Descending = downhill = ‘easy’ for water to exit through the wall of the loop –> filtrate becomes hypertonic

54
Q

Physiology: Ascending Thick Loop of Henle

A

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

55
Q

Physiology: Distal Convoluted Tubule

A

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)

56
Q

Physiology: Collecting Duct

A

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)

57
Q

Parathyroid hormone

A

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

58
Q

Primary hyperparathyroidism

A

Most common type
Inappropriate PTH secretion by parathyroid gland
= absorptive hypercalcemia

59
Q

Secondary hyperparathyroidism

A

Appropriate PTH secretion
Occurs in response to hypocalcemia
Most commonly due to vitamin D deficiency

60
Q

Angiotensin II maintains GFR during hypovolemia by…

A

Causing vasoconstriction of the efferent arteriole

61
Q

ATN effects on urine

A

Renal tubular cells can no longer resorb sodium or water or excrete urea
Urine will have increased Na, decreased urea, decreased Osm

62
Q

Urinary concentration is primarily the result of…

A

…hypertonic medullary interstitial fluid

63
Q

Cisplatin is nephrotoxic because of…

A

…a direct toxic effect on renal tubular cells

64
Q

IgA nephropathy vs. post-strep glomerulonephritis

A

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

65
Q

Sensitivity, specificity, PPV, NPV

A
66
Q

Spot Urine Na+ meaning

A

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

67
Q

Sacral neuromodulation is FDA approved for:

A

Non-obstructive retention
UUI
Urgency/frequency syndrome
Chronic fecal incontinence
Interstitial cystitis

68
Q

Botox mechanism of action

A

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

69
Q

On clinical evaluation, a patient has global polyuria as defined as >40 ml/kg urine in 24 hours. Testing and ddx?

A

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

70
Q

NLUTD: Unknown Risk
- Stratification
- Further workup
- Goal

A

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

71
Q

NLUTD: Medium Risk
- Stratification
- Surveillance

A

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

72
Q

NLUTD: High Risk
- Stratification
- Surveillance

A

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

73
Q

How is normal micturition initiated?

A

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)

74
Q

Detrusor Leak Point Pressure Numbers

A

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

75
Q

DLPP and VLPP are determined by the resistance of EUS to fluid leak

A

Interventions that don’t affect the resistance of EUS will not affect either LPP

76
Q

Open bladder neck at rest without prior prostatectomy

A

Multiple System Atrophy
Progressive degeneration of neurons in multiple areas of the brain
Incomplete emptying, ED, “hot crossed buns sign” on MRI

77
Q

Primary Bladder Neck Obstruction

A

Level of obstruction on VUDS is clearly the bladder neck itself
Reduce bladder neck with TUIP vs. TURP

78
Q

Uroflow curve without pressure data: flattened bell

A

A/w adequate detrusor function with fixed obstruction

79
Q

Uroflow curve without pressure data: saw tooth

A

A/w DU or DESD

80
Q

“Poor compliance” on UDS

A

<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

81
Q

Spina Bifida and NGLUTD

A

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

82
Q

Higher chance of paternity with SB at which lesion level?

A

L5 or sacral level

83
Q

Spinal shock

A

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

84
Q

Guarding reflex

A

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

85
Q

Lesions above the pons (brainstem still functioning, CVA or Parkinson’s): bladder/ sphincter

A

Detrusor Overactivity: Yes (Parkinson’s with impaired contractility)
DESD: No
DISD: No
Autonomic Dysreflexia: No
Intact Bladder Sensation: Yes
Detrusor Areflexia: No

86
Q

Neurologic Insult Pons to T6-8: bladder/sphincter

A

Detrusor Overactivity: Yes
DESD: Yes
DISD: Yes
Autonomic Dysreflexia: Yes
Intact Bladder Sensation: Yes
Detrusor Areflexia: No

87
Q

Neurologic Insult T6-8 to S2: bladder/sphincter

A

Detrusor Overactivity: Yes
DESD: Yes
DISD: No
Autonomic Dysreflexia: No
Intact Bladder Sensation: No
Detrusor Areflexia: No

88
Q

Neurologic Insult Injury below S2: bladder/sphincter

A

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

89
Q

Neurologic Insult MS: bladder/sphincter

A

Detrusor Overactivity: Yes
DESD: Maybe
DISD: No
Autonomic Dysreflexia: No
Intact Bladder Sensation: Yes
Detrusor Areflexia: No

90
Q

Neurologic Insult Multiple System Atrophy: bladder/sphincter

A

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

91
Q

Lesions above the pons (brainstem still functioning like CVA or Parkinson’s)

A

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

92
Q

Lesions involving brain stem + cord above T6 (including C-spine)

A

After spinal shock:

Detrusor overactivity + detrusor external sphincter dyssynergia (DESD) + Smooth muscle sphincter dyssynergia (DISD) + autonomic dysreflexia

93
Q

Autonomic dysreflexia

A

Afferent stimuli below T6 (bladder distention) in patient with injury above T6 –> massive reflex sympathetic discharge –> vasoconstriction, HTN, reflex bradycardia, flushing, HA, diaphoresis

94
Q

Complete lesion between T6 and S2

A

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

95
Q

Detrusor External Sphincter Dyssynergia

A

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

96
Q

Cauda Equina (Horse’s Tail): L2-S5 spinal nerve bundle

A

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

97
Q

Lesions at or distal to sacral cord

A

Detrusor areflexia and denervation potentials on EMG

Below S2: (after spinal shock) persistent detrusor areflexia +/- decreased compliance +/- open smooth sphincter +/- residual resting sphincter

98
Q

The cremasteric artery is a branch of the…

A

…inferior epigastric artery (from external iliac)

99
Q

The vasal artery is a branch of the…

A

…superior vesical artery (a branch of the anterior trunk of the internal iliac)

100
Q

Inferior hypogastric plexus injury (after LAR or APR or TAH)

A

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

101
Q

SCI in T11 - L2 may damage sympathetic supply to bladder and impair tonic outlet resistance…

A

Crede maneuver may allow patient to overcome remaining outlet resistance and void

102
Q

Quinolones side effects

A

(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

103
Q

Painful necrotic penile ulcer + painful inguinal LAD

A

Gram-negative coccobacilli (haemophilus ducreyi)
Chancroid
Tx with Azithromycin (1g PO)

104
Q

Gonorrhea treatment

A

Single dose IM ceftriaxone

105
Q

Chlamydia treatment

A

10 days PO doxycycline

106
Q

Non-gonoccocal urethritis

A

think chlamydia or ureaplasma
treat with two weeks PO doxycycline vs. single dose azithromycin

107
Q

Alpha-blocker most likely to cause retrograde ejaculation?
Least likely?

A

Most = Silodosin
Least = Alfuzosin

108
Q

Prostatitis is characterized into 4 syndromes

A

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

109
Q

Male urethral blood supply

A

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)

110
Q

How is baseline flaccidity maintained?

A

Tonic contraction of penile vascular smooth muscle via norepinephrine release from postganglionic sympathetic nerves

111
Q

How is an erection achieved?

A

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

112
Q

Detumescence?

A

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

113
Q

After complete suprasacral SCI, reflexogenic (but not psychogenic) erections are generally preserved

A

Sacral SCI eliminates reflexogenic erections but may not eliminate psychogenic

114
Q

Painless, slowly growing ulcers without lymphadenopathy

A

Granuloma inguinale (klebsiella granulomatosis)

Azithromycin 1g PO weekly for 3 weeks
Doxycycline for 3 weeks

Treat partners within 60 days

115
Q

NLUTD: Low Risk
- Stratification
- Further workup
- Surveillance

A

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)

Urology In-Service/Board Review (12 decks)

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