Urgency ANS: Compelling, often sudden need to void that is difficult to defer.
Urge incontinence ANS: Leakage preceded by/associated with urgency. Common precipitants include
running water, hand washing, going out in the cold, even the sight of the garage or trying to unlock the
door when returning home. The need to "rush to the toilet" and length of time one can forestall an
urgency episode are less useful symptoms because they reflect cognition, mobility, toilet availability,
and sphincter control, as well as bladder function
Stress incontinence ANS: Leakage with effort, exertion, sneezing, or coughing. Leakage may be provoked
by minimal or no activity when there is severe sphincter damage. Leakage coincident with cough, laugh,
sneeze, or physical activity suggests failure of sphincter mechanisms. Leakage that occurs seconds after
the activity, especially if difficult to stop, suggests a cough-induced uninhibited detrusor contraction.
Mixed continence ANS: Presence of both urgency and stress UI symptoms. Patients vary in the
predominance, severity, and/or bother of urge versus stress leakage
Overactive bladder ANS: Symptom syndrome (not a specific pathologic condition) consisting of urgency,
frequency, and nocturia, with or without urge incontinence.
Frequency ANS: Complaint of needing to void too often during the day, as defined by the patient
Nocturia ANS: Complaint of waking at night one or more times to void. If these voids are associated with
UI, the term nocturnal enuresis may be used
Slow stream ANS: Perception of reduced urine flow, usually compared with previous performance
Hesitancy ANS: Difficulty in initiating voiding, resulting in a delay in the onset of voiding after the
individual feels ready to pass urine.
,Straining ANS: Muscular effort either to initiate, maintain, or improve the urinary stream
Intermittent stream ANS: Sensation that the bladder is not empty after voiding.
Post void dribbling ANS: Small amounts/drops of urine after voiding has stopped. More common in men.
UI pharmacotherapy ANS: duloxetine is effective in reducing stress UI (LOE = A)42 but is not approved
for this indication in the United States
Vaginal topical estrogen (cream, vaginal tablet, or slow-release ring) (LOE = B)46 is helpful for
uncomfortable vaginal atrophy and may decrease recurrent urinary tract infections.
Antimuscarinics ANS: established efficacy are oxybutynin, tolterodine, fesoterodine, trospium,
darifenacin, and solifenacin
Beta-3 Agonists ANS: Currently, mirabegron (Myrbetriq 25-50 mg once daily) is the only beta-3 receptor
agonist approved in the United States for treatment of urge UI (LOE = B for efficacy
Mirabegron can increase blood pressure; persons with hypertension should have periodic blood
pressure checks while on mirabegron, and mirabegron should not be used in patients with severe
uncontrolled hypertension
Desmopressin ANS: desmopressin should not be used to treat nocturia in older, especially frailer,
patients because of the risk of hyponatremia
Minimally Invasive Treatment for Refractory Urge Urinary Incontinence ANS: Botulinum toxin: Injection
in detrusor during cystoscopy: Can reduce UI with a slightly higher cure compared with antimuscarinics,
,although with a greater risk of urinary retention. Patients must be willing to do self-catheterization
because of the risk of urinary retention
Optimal dosing for specific patient groups such as older women is uncertain
Sacral nerve modulation Percutaneous implantation of a trial electrode at the S3 sacral root, which is
connected to an external stimulator. Patients responding to the trial have a permanent lead with a
pacemaker-like energy source implanted Anticipated newer MRI-compatible models will end need to
explant stimulators before imaging
Percutaneous tibial nerve stimulation66 Very small trials only66
Patients unlikely to see efficacy before 6 weeks of treatment
Limited coverage by insurance
UI surgery ANS: The most commonly used procedures are colposuspension (Burch operation) and slings
(synthetic mesh, or autologous or cadaveric fascia, placed at the proximal or midurethra).
Causes of Sexual Dysfunction in Older Men ANS: Vascular disease
Gradual onset
Vascular risk factors: diabetes mellitus, hypertension, hyperlipidemia, tobacco use
Neurologic disease (e.g., radiation therapy, spinal cord injury, autonomic dysfunction, surgical
procedures)
Gradual onset (unless postsurgical)
Neurologic risk factors: diabetes mellitus; history of pelvic injury, surgery, or irradiation; spinal injury or
surgery; Parkinson disease; multiple sclerosis; alcoholism
Loss of bulbocavernosus reflex
Medications (e.g., anticholinergics, antihypertensives, cimetidine, antidepressants)
Sudden onset
Lack of sleep-associated erections or lack of erections with masturbation
, Temporal association with a new medication
Psychogenic (e.g., relationship conflicts, performance anxiety, childhood sexual abuse, fear of sexually
transmitted diseases, "widower syndrome")
Sudden onset
Sleep-associated erections or erections with masturbation are preserved
Hypogonadism
Gradual onset
Decreased libido more than erectile dysfunction
Small testes, gynecomastia
Low serum testosterone concentration
Endocrine (e.g., hypothyroidism, hyperthyroidism, hyperprolactinemia) Rare, <5% of cases of erectile
dysfunction
Testosterone blood tests ANS: Ideally, blood should be obtained in the morning to account for circadian
rhythm and the result carefully interpreted. For example, a serum total testosterone concentration less
than 200 ng/dL in a symptomatic man strongly suggests hypogonadism that will likely respond to
treatment. A serum total testosterone concentration between 200 and 300 ng/dL in a symptomatic man
likely also represents hypogonadism, but response to treatment is less predictable.
ED lab testing ANS: Laboratory evaluations should target relevant comorbid conditions, such as diabetes
mellitus and vascular disease or disorders suggested by the physical examination. The measurement of
serum testosterone should be considered, especially in men with low libido.
An at-home therapeutic trial of a phosphodiesterase inhibitor (sildenafil or vardenafil) is considered
first-line evaluation and treatment.23 The initial dose should be low (sildenafil 25-50 mg or vardenafil 5-
10 mg) in men suspected of having neurogenic ED
Treatment of Erectile Dysfunction ANS: Sildenafil is a phosphodiesterase inhibitor that potentiates the
penile response to sexual stimulation. It improves the rigidity and duration of erection. It is taken 1 hour
before sexual activity and has little effect until sexual stimulation occurs. Vardenafil is a more potent
and specific phosphodiesterase inhibitor. A lower effective dose and better adverse-event profile (no
effect on color vision) make vardenafil a reasonable option. Tadalafil is a longer-acting