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Med classes Urology- Quiz 1 Flashcards

1
Q

What is erectile dysfunction (ED) caused by and how is it treated ?

A
  1. Caused by: vascular disease, DM, meds, depression, prostate surgery complication, psychologic
  2. Therapy: penile implant, intrapenile injections, intraurethral suppositories (Aloprostil), PDE-5 inhibitors (first line choice d/t safety, efficacy, ease of use)
  3. Patho: Flaccidity–> Sex stim–> production of NO–> increased CCMP–> relaxation of smooth muscle in corpus cavernosum–> increased blood flow–> erection
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2
Q

Phosphodiesterase-5 Inhibitors
(PDE-5)

A

-They “FIL” it up
1. Are all equally effective in treating ED/ have similar side effect profiles
2. Sildenafil, Tadalafil, Vardenafil, Avanafil
2. Sildenafil and Tadalafil are also approved to treat pulm HTN at different doses
3. All PDE5 inhibitors interact with nitrates, alpha blockers, and have the potential to cause low blood pressure when combined with BP meds
4. All PDE5 inhibitors interact with CYP3A4 inhibitors

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3
Q

PDE-5
MOA and FDA indication

A

MOA: Sexual stimulation triggers the relaxation of smooth muscle in the corpus cavernosum, leading to increased blood flow. This process is mediated by nitric oxide (NO), which activates the production of cyclic GMP (Guanosine monophosphate). cGMP then promotes smooth muscle relaxation by lowering intracellular calcium levels (Ca++).

FDA indication: First line treatment for ED
(Sildenafil and Tadalafil approved for pulm HTN)
(Tadalafil approved for BPH)

-fil

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4
Q

What do PDE-5 meds do?

A

They inhibit PDE-5 which inhibits
the isoenzyme responsible for breaking down of cGMP in the corpus cavernosum—the result is to increase the flow of blood into the corpus
cavernosum—THESE AGENTS HAVE NO EFFECT IN THE ABSENCE OF SEXUAL STIMULATION

-fil

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5
Q

Prototype drug- Sildenafil (Viagra)

A
  1. Take on empty stomach at least 1 hour before sex: dosed once a day
  2. Metabolized by CYP3A4
  3. Reduce dose when hepatic or renal disease is present
  4. Use caution with CV disease and in those at risk for CV disease

PDE-5

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6
Q

PDE-5 inhibitors: Sildenafil
ADE

A

ADE: (generally mild)—headache, flushing, dyspepsia, nasal stuffiness,
disturbances in perception of blues and greens, sudden transient hearing loss [from vasodilation], priapism (medical emergency; treated with aspiration, phenylephrine injection, if not surgical shunt)

-fil

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7
Q

PDE-5 inhibitors: Sildenafil
Drug interactions

A

(known to potentiate hypotensive effects of NO)

  1. Can potentiate hypotension [if on other agents that can lower BP—alpha blockers, vasodilators]
  2. Start at low dose and titrate up as needed for effect
  3. Reduce dose of these agents if patient on CYP3A4 inhibitors—Biaxin, Ritonavir and other protease inhibitors

-fil

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8
Q

PDE-5 inhibitors: Sildenafil
Contraindications

A
  1. Contraindicated with nitrates, isosorbide
  2. Use with caution in CV disease or those with increased risk of CV disease
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9
Q

Sildenafil (Viagra)

Route
Onset/half life
Food/med interaction

A
  1. Route: PO
  2. Onset of action: 60 minutes
  3. Half life: 3-4 hours
  4. Food interaction: can interact with food (high fat meal delays absorption)
  5. Small potential for hypotension with concurrent use of alpha blockers
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10
Q

What is Alprostadil?

A
  1. A synthetic prostaglandin E1
    (PGE-1)
    -“PROST”= prostaglandin
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11
Q

Alprostadil:
MOA/ FDA indication

A
  1. MOA: In the penile tissues, PGE1 allows relaxation of the smooth muscle of corpus cavernosum (smooth muscle relaxes, exact physiological mechanism unknown)
  2. FDA indication: first-line therapy for ED, so this may be used for patients who are not a candidate for oral therapy (in contrast to oral agents, acts locally and systemic absorption is minimal so may reduce adverse effects)
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12
Q

Alprostadil: Action

A
  1. Route: intra-uretheral suppository or injection
  2. Onset of action: Suppository is 5-10 minutes and injections is 2-25 minutes
  3. Lasts 30-60 minutes

-prost PROSTaglandin

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13
Q

Alprostadil:
ADE

A
  1. Rare d/t local effects: hypotension,
    headache; local effects—penile pain, urethral pain, testicular pain
  2. Priapism may occur (medical emergency)
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14
Q

What is BPH?

A
  1. Nonmalignant growth of the prostate—occurs with age
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15
Q

What are the three categories of drugs approved to treat BPH?

A
  1. Alpha Blockers
  2. 5 Alpha Reductase Inhibitors
  3. PDE-5 Inhibitors
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16
Q

What are alpha blockers?

A

-It’s a “SIN” to be unable to pee
1. Block Alpha1A & Alpha1B receptors in the prostate& cause smooth muscles in the gland to relax, which leads to improved urine outflow
2.SELECTIVE agents only block ALPHA1B and have no BP effect
3. Nonselective decrease peripheral vascular resistance and lower BP
3. Meds: Terazosin, Doxazosin, Alfuzosin, Prazosin, Tamulosin, and Silodosin
4. Begin working in 7-10 days

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17
Q

Hard to identify prototype drug for alpha blockers–
Terazosin (Hytrin) and Tamulosin (Flomax)

A
  1. Terazosin (Hytrin) = NONSELECTIVE
  2. Tamulosin (Flomax) = SELECTIVE
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18
Q

Terazosin (Hytrin)

A
  1. FDA approved for BPH
  2. NONSELECTIVE
  3. May be taken w/o regard to food
  4. Liver metabolism but not CYP450 system

Alpha blocker -sin

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19
Q

Tamulosin (Flomax)

A
  1. FDA approved to treat BPH
  2. SELECTIVE
  3. Take WITH food (helps absorption)
  4. Metabolized by CYP450 system

Alpha blocker -sin

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20
Q

Alpha Blockers:
Onset of action and half life

A
  1. Onset of action: Peak effects seen in 1-4 hours
  2. Half life: 8-22 hours

Alpha blocker -sin

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21
Q

Alpha Blockers:
ADE

A
  1. ADE: dizziness, fatigue, nasal congestion, HA, drowsiness
    and orthostatic hypotension [effects are less withselective agents]; nonselective agents given at night
  2. Alpha blockade can effect ejaculatory ducts and impair smooth muscle contractions (aka ejaculation can be inhibited or retrograde ejaculation can occur) but do NOT have effect on male sexual function

Alpha blocker -sin

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22
Q

Alpha Blockers:
Drug interactions

A
  1. Drugs that inhibit CYP3A4 and CYP2D6—Verapamil, Diltiazem
    may increase the drug levels
  2. Drugs that induce CYP450—Tegretol, Dilantin and St. John’s Wort
    may decrease the plasma concentrations of the
    aforementioned agents
  3. Use caution when giving
    other drugs that can prolong QTc

Alpha blocker -sin

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23
Q

What are 5 Alpha Reductase Inhibitors?

A

-It is a wild “RIDE” waiting a year for these to work
1. 2 agents in this class that work very slowly (9-12 MONTHS) to reduce the size of the prostate gland
2. Agents: Finasteride/ Dutasteride
3. PROSTATE MUST BE ENLARGED FOR THESE MEDS TO WORK
4. ALL drugs in this category are TERATOGENIC FOR WOMEN (child bearing age age or pregnant should not handle or ingest may lead to birth defects of male fetus genitals)

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24
Q

5 Alpha Reductase Inhibitors:
MOA/ FDA indication

A
  1. MOA: Inhibits 5 alpha reductase—which converts testosterone to dihydrotestosterone[DHT], the more
    potent, active compound that stimulates prostate growth. By decreasing DHT the gland shrinks and urine outflow improves.
  2. Usually used in combination with alpha blockers
  3. FDA indication: BPH

-Ride

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25
Q

Finasteride (Proscar) Prototype

A
  1. Prototype drug for this class
  2. Used in small doses for Alopecia
  3. Food doesn’t affect absorption
  4. Rare drug interactions
  5. Half life: 6-12 hours

5 alpha reductase inhibitor -Ride

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26
Q

5 Alpha Reductase Inhibitors:
ADE

A
  1. Decreased ejaculate, decreased libido, ED, gynecomastia
  2. SEXUAL SIDE EFFECTS
  3. NOT ideal to use concurrently with Testosterone (inhibits conversion of testosterone to to its active form DHT

5 alpha reductase inhibitor -Ride

27
Q

BPH effect on the urethra

A
  1. As the prostate enlarges, it can obstruct urethra–> As a result, men can present with urgency, postvoid dribbling or overflow incontinence
  2. Women can have urethral obstruction—from a cystocele, stricture or meatal stenosis
  3. Conservative therapy includes bladder retraining and prompted voiding, which can be used if none of the following are present–> Hydronephrosis, large PVR, recurrent UTI or hematuria
28
Q

Urethral Outflow Obstruction
Treatment

A
  1. Alpha blockers decrease tone in prostatic capsule and urethra—really helpful in BPH
  2. 5 alpha reductase inhibitor also added
  3. last resort, intermittent or indwelling catheter
29
Q

Detrusor Underactivity

A
  1. If prolonged outflow obstruction, a
    neurogenic type situation can
    develop–> this patient has a
    large PVR and overflow leakage
  2. Goals: drain urine from the
    bladder; decrease incontinence; prevent hydronephrosis & urosepsis
  3. Trial of indwelling/intermittent catheterization to decompress bladder; left in for 2 weeks; then removed to see if voiding recurs normally. If not, catheter can be reinserted for 4 weeks & a voiding trial reattempted. Valsalva’s to induce bladder contractions.
  4. Bethanechol- a cholinergic agonist (helps bladder to contract and empty)
30
Q

Evaluation of an ED should include testing for what?
NEED TO CHECK WHAT ELSE THEY’RE LOOKING FOR HERE

A
  1. Testosterone deficiency
  2. Testosterone deficiency can be part of male hypogonadism and lead to osteoporosis—in addition to sexual issues.
  3. Prefer topical agents as opposed to oral as levels stay steadier in blood
31
Q

Urinary Incontinence
What is it?
Secondary effects

A
  1. Involuntary loss of urine that leads to hygienic or social problems
  2. UI is associated with pressure ulcers, skin irritation and falls
  3. UI can lead to anxiety, depression,
    embarrassment and isolation
  4. Prevalence increases with age, more common in women until age 80 where equals out
32
Q

Lower Urinary Tract A/P

A

Consists of:
1. Detrusor (Bladder): muscular storage/ contractile organ; smooth muscles that accommodates large volumes at low intravesical pressure
2. Internal sphincter: smooth muscle in urethra
3. External sphincter: striated muscle

33
Q

Continence

A
  1. Is maintained by urethra
  2. Autonomic and somatic systems coordinate micturition (voiding)
  3. PNS, SNS, and somatic nerves are also involved (complicated process)
34
Q

PNS (cholinergic), SNS (adrenergic), and somatic nerves contribution to voiding

A
  1. PNS facilitates bladder emptying, SNS supports urine retention, & somatic nerves provide voluntary control.
  2. If brain lesion in the pons–> Pons coordinates bladder contraction with sphincter relaxation aka will have voiding issues
35
Q

Bladder emptying

A
  1. Bladder filling is controlled by inhibiting contractions and maintaining sphincter tone, while emptying requires parasympathetic activation and sphincter relaxation.
36
Q

Types of urinary incontinence

A
  1. Functional Incontinence: Lower urinary tract function intact; Outside influences cause incontinence
  2. All other causes of UI are from problems in bladder, urethral outlet or both.
37
Q

Detrusor overactivity

A
  1. Usual mechanism= urge incontinence
  2. Most common cause of geriatric UI
  3. Inhibition of bladder contractions is impaired and bladder contracts
    on its own, leading to leakage
  4. Patient feels urge to void and doesn’t make it to the toilet
  5. May be associated with nocturia
38
Q

Detrusor Overactivity definitions

A
  1. Detrusor hyperreflexia: overactivity because of a neuro lesion
  2. Detrusor instability: Overactivity with no neuro lesion present
  3. Local bladder pathology can also cause involuntary contractions
39
Q

2 subsets of bladder overactivity

A
  1. Overactivity with normal
    contraction: Bladder can empty most of its contents
  2. Detrusor hyperactivity with impaired contractility: Bladder can’t empty and >100 cc of urine remains after contraction
40
Q

Detrusor Underactivity

A
  1. Bladder contractions so diminished that overflow incontinence ensues
  2. Bladder contracts [if at all] only when patient tries to void
  3. Uncommon in geriatrics
  4. It can be: Neurogenic in
    origin, Secondary to nerve damage from DM, ETOH or vertebral disease, or From long standing obstruction
41
Q

Outlet Incontinence (AKA Stress Incontinence)

A
  1. Common in women (DUH)
  2. Patient has involuntary loss of
    urine with physical activity/ coughing
  3. Leakage is small/ rare when
    patient is recumbent
  4. Usually from weakening of supporting structures of pelvic floor
  5. Uncommon in men (Except after
    transurethral surgery or XRT that damages sphincter)
42
Q

Outlet Obstruction

A
  1. Common cause of UI in old men
  2. Can lead to: urinary retention, distention, overflow incontinence
  3. Post-void dribbling or urge
    incontinence d/t detrusor
    overactivity
    4: Causes BPH, Alpha agonists, Tumors, Strictures, Spinal cord
    lesions
43
Q

Mixed Incontinence

A
  1. Combination of aforementioned types of incontinence
  2. Aka “you have ticks AND fleas” (very bothersome symptoms)
44
Q

Treatment of UI

A
  1. Goal: relieve most bothersome aspects
  2. Stepped management strategy: Lifestyle–> behavioral–> drugs–> surgery
45
Q

Detrusor Overactivity
Non-Pharmacological Treatment

A
  1. Prompted voiding should be tried or bladder training
  2. Patient voids at a time interval
    less than incontinent interval and resists urge to void in between
  3. Once incontinence improves, interval between scheduled voiding is increased by ½ hour increments until 3-4 hour interval is reached
  4. For demented patient, prompted
    voiding CAN be tried
46
Q

What medication class is used to treat Detrusor Overactivity?

A
  1. Anticholinergics/ smooth muscle relaxants used to decrease
    involuntary contractions of the bladder and increase volume needed to elicit involuntary contractions
  2. Systemic side effects—xerostomia (dry mouth), confusion, constipation, urinary retention (HAH)
47
Q

Detrusor Overactivity Drugs
(Anticholinergic properties)

A
  1. Propantheline
  2. Dicyclomine
  3. Tricyclic antidepressants
  4. Ditropan (Oxybutynin)
48
Q

Detrusor Overactivity Antimuscarinic

A
  1. Tolterodine- Detrol, Detrol LA
  2. Oxybutynin- Ditropan XL
  3. Hyoscyamine- Levbid
  4. Hyoscyamine- Symax
  5. Oxybutynin patch- Oxytrol Patch
  6. Oxybutynin gel- Gelnique
  7. Solifenacin- Vesicare
  8. Trospium chloride- Sanctura, Sanctura XR
  9. Darifenacin- Enablex
  10. Fesoterodine- Toviaz
49
Q

Oxybutynin (Ditropan)

A

Protoype for antimuscarinics
4 formulations:
-Immediate release
-Extended release (ER)
-Topical patch
-Topical gel (Gel)
-Pros: Generic (low cost), can take twice daily , quick onset
Cons: Dry mouth, constipation, possible AMS, P450 interactions, XL can be wide titration range, topical patch can cause skin irritation but only need twice a week patch

50
Q

Antimuscarinic Meds
ADE

A

-Side effects (less frequent with ER and topical): Dry mouth, Blurry vision, Constipation, Possibly cognitive, (Monitor PVR if UI worsens)

51
Q

WTF is the difference between anticholinergic and antimuscarinics?

A

-All antimuscarinics are anticholinergics, but NOT all anticholinergics are antimuscarinics. Antimuscarinics specifically target muscarinic receptors, making them more selective for certain conditions like overactive bladder

52
Q

What do antimuscarinic meds do?

A

-Inhibit acetylcholine at muscarinic receptors, reducing activity of PNS
-Used to calm overactive bladder

53
Q

Fesoterodine (Toviaz):
MOA
ADE

A

Quaternary Amine
(Does not cross BBB and therefore less likely to have CNS effects)

  1. Atropine like agent that is used to treat overactive bladder (has fewest cholinergic effects)
  2. Increases bladder capacity
  3. For those on drugs that may increase cholinergic neurotransmitters [agents
    for dementia]—this is one of the drugs of choice in those individuals
54
Q

B 3 Agonist:
Mirabergon (Myrbetriq)

A
  1. Used for OAB in patients that have failed other agents or have a CI to the use of the anticholinergics
  2. Activates beta-3 adrenergic receptors, particularly in the bladder, to promote bladder relaxation and treat OAB by increasing bladder capacity and reducing urgency.
  3. This class of medication offers a more targeted mechanism with fewer side effects than traditional antimuscarinic drugs.
  4. Can increase BP [this effect is more marked at lower doses]
  5. It increases digoxin levels; can decrease Metoprolol levels; can inhibit CYP2D6
55
Q

Other treatments for overactive bladder

A
  1. Botulinum toxin
  2. Sacral Nerve Stimulation
  3. Perc Tibial Nerve Stimulation
56
Q

Stress Incontenence Non surgical treatment

A

-The outlet is incompetent
-Weight loss, Kegel exercises, Use of vaginal cones, Biofeedback, Adjusting fluid intake, Voiding frequently

57
Q

Stress Incontinence: Medications

A

-Both off label:
-Oral or topical estrogen
-Alpha adrenergic agonists (Pseudoephrine)
-Slides don’t say this but when googled chat says Cymbalta IS FDA approved for stress incontinence

58
Q

Stress Incontinence: Surgery

A
  1. Women= Surgery
  2. Post prostatectomy= pelvic exercises, silicone injections, protective garments, catheters, artificial sphincter replacement (high chance of re-operation), and new info on sling operations
59
Q

Pediatric Enuresis:
Education for family

A
  1. Is a common condition that reflects a delay in the normal development of night-time continence.
  2. Is unintentional and cannot be resolved through punitive measures or “consequences” for bedwetting.
  3. Encouraging motivational strategies that target behaviors within the child’s control can help improve enuresis, esp with consistent support, time, and guidance.
60
Q

Pediatric Enuresis:
Clinician Assessment

A
  1. Perform a thorough history and physical examination to confirm the diagnosis of enuresis, differentiate between monosymptomatic and non-monosymptomatic enuresis.
  2. Identify or rule out comorbidities. Particular attention should be given to conditions such as constipation, developmental/ psychiatric disorders, and upper airway obstruction.
  3. Lower urinary tract symptoms (LUTS) may not be evident unless clinicians specifically ask about them. When LUTS are present, they should be addressed first or concurrently with treatment for enuresis. Referral to urology when symptoms are severe, numerous, or atypical.
  4. Work with patients and families to determine whether treatment is necessary or desired. Consider the impact of enuresis on the child’s self-esteem, and family factors such
    as motivation, support, and available resources. Children who are not bothered by it and whose self-esteem is intact, and families who are okay waiting for bedwetting to stop, should be reassured that waiting is recommended course of action.
  5. Patients experiencing distress related to their enuresis
    may respond well to active treatment, such as an enuresis alarm and/or the intermittent use of desmopressin. If these two active therapies fail, and when further treatment is desired, refer to an expert in enuresis.
61
Q

Enuresis Common causes

A
  1. Constipation
  2. Developmental delay/psych issues
  3. Upper airway obstruction (OSA)
  4. Rarely: can be a sign of DM or DI, renal disease, hyperthyroidism, infections, seizure disorders, and cardiac arrhythmias
  5. Child maltreatment, trauma, and psychosocial stressors, including bullying, may also precipitate enuresis, and should be considered.
62
Q

Pediatric enuresis treatment

A
  1. Behavioral therapy
  2. Alarm therapy
  3. Desmopressin (Intermittent)
  4. Antispasmodics
  5. Mirabegron
  6. NO LONGER USE tricyclic antidepressants (CV issues)
    7.Rarely= neuromodulators
63
Q

Testosterone therapy overview

A
  1. In patients with male hypogonadism (s/s of testosterone deficiency plus low serum levels), testosterone therapy helps to increase libido, muscle strength, fat-free mass, and bone density.
  2. testosterone therapy can be considered for some patients with age-related low testosterone levels plus sexual dysfunction
  3. Symptoms associated with age-related low testosterone (low energy, reduced vitality, lessened physical functioning, reduced cognition) are NOT indications for testosterone.
  4. Risks may include prostate disorders, sleep apnea, VTE, CV
  5. Discontinuation of testosterone therapy should be considered after six to 12 months if T levels become normal and symptoms not resolved.
64
Q

Testosterone Replacement

A

-T is the most important androgen in humans
-Used mainly for primary or secondary hypogondaism or for transgender men
-Is ineffective orally d/t inactivation by first- pass metabolism (patch, topical, nasal gel, or implant)

No evidence suggests to take it just for aging or performance improving

  • Effects in women: Masculinization
    -Effects in me: Priapism, impotence, gynecomastia, increased libido
    -Potential for misuse= controlled substance
    -

Pharm (20 decks)

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