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Renal Week 3 > Drugs for Urinary Incontinence or Retention > Flashcards

Drugs for Urinary Incontinence or Retention Flashcards

1
Q

What does the treatment of urinary incontinence usually start with?

A

Behavioral therapy, including patient education, fluid management, bladder retraining, pelvic floor exercises, biofeedback, and timed bladder emptying

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2
Q

What things can cause urinary urgency?

A
  • Stroke
  • Alzheimer or Parkinson
  • BPH with overflow
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3
Q

What is the treatment for urinary urgency/incontinence?

A
  • anticholingerics
  • oxybutynin
  • tolterodine
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4
Q

What things can cause urinary outlet incompetence (urinary loss with cough, sneeze, laugh, etc.)?

A
  • multigravida

- estrogen deficiency

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5
Q

What is the treatment for urinary outlet incompetence?

A

focus on muscle exercise by focusing when these things happen

  • Topical estrogen
  • And then give Alpha-agonists last because of potential side effects
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6
Q

What things cause atonic bladder?

A
  • severe diabetic neuropathy

- stroke

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7
Q

What is the treatment for atonic bladder?

A

catheterization

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8
Q

What are some oral non-selective muscarinic antagonist drugs?

A
  • Darifenacin PO

- Transdermal Oxybutynin

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9
Q

How are the non-selective muscarinic antagonist drugs metabolized?

A

Extensive hepatic metabolism involving CYP3A4/2D6 (except tropsium)

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10
Q

What does parasympathetic activity in the bladder cause?

A

Parasympathetic postganglionic axons in the pelvic nerve release acetylcholine (ACh), which produces a bladder contraction by stimulating M3 muscarinic receptors in the bladder smooth muscle.

Parasympathetic postganglionic nerves also release ATP, which excites bladder smooth muscle, and nitric oxide, which relaxes urethral smooth muscle

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11
Q

What does sympathetic activity in the bladder cause during filling?

A

Sympathetic postganglionic neurons from the hypogastric nerve release noradrenaline (NA), which activates β3 adrenergic receptors to relax bladder smooth muscle/detrusor and also activates α1 adrenergic receptors in the urethra to contract urethral smooth muscle.

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12
Q

What do somatic axons in the pudendal nerve do?

A

Also release Ach, which produces a contraction of the external sphincter striated muscle by activating nicotinic cholinergic receptors.

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13
Q

What is a benefit over a muscarinic antagonist like trospium for urinary incontinence?

A

it doesnt pass the BBB so less side effects

dry mouth common

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14
Q

T or F. Although M3 receptor specificity is more selective for darifenacin (muscarinic antagonist), clinical studies have not recorded a substantially better profile for this drug in clinical use, as compared to the other, non-selective, drugs like oxybutynin and tolterodine

A

T.

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15
Q

The half lives of muscarinic antagonists vary from short to long.

A

The reason for oxybutynin and tolterodine being available in extended release (ER) formats is to counter their otherwise short duration of clinical effect.


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16
Q

T or F. ER delivery reduces risk of dry mouth without any apparent loss of efficacy

A

T.

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17
Q

What are some AEs with muscarinic antagonists?

A
  • palpitations, tachycardia, prolonged QT

- mild constipation

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18
Q

What are some contraindications to muscarinic antagonists?

A
  • angle closure or narrow-angle glaucoma
  • urinary and gastric obstruction
  • Alzheimer’s
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19
Q

What else can be used in urinary incontinence?

A

botulinum toxin (botox)- Delivered by carefully placed injections into the urothelial wall

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20
Q

How long does botox help with urinary incontinence after injection?

A

several months

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21
Q

Note about botox use

A

The botox is more effective in patients who responded to anticholinergic drugs but couldn’t tolerate the adverse effects, as opposed to those patients who were unresponsive to the anticholinergics.

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22
Q

How does the botulinum toxin work?

A

It inhibits vesicular release of excitatory neurotransmitters and axonal expression of other SNARE-complex-dependent proteins in the urothelium /suburothelium mediating intrinsic or spinal reflexes thought to cause detrusor overactivity

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23
Q

What else does the botulinum toxin do?

A

It also causes a phenotypic change within the urothelial tissue to ablate the excitatory effect of local chemical mediators that signal via the cholinergic system to make the bladder hyper-responsive in the first instance.

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24
Q

What is mirabegron?

A

daily PO drug that promote sympathetic activity in the bladder (B3) and the urethra (a1)

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25
Q

How is mirabegron metabolized?

A

extensive hepatic metabolism (3A4 over 2D6)

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26
Q

What are some other sympathetic stimulating drugs in the bladder?

A
  • Pseudoephredine
  • Ephedra (ma-huang)

both used ‘off-label’

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27
Q 
How are Pseudoephredine
and Ephedra (ma-huang) metabolized?
A

eliminated predominantly unchanged in urine (dose reduction may be needed with renal dysfunction)

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28
Q

As of sympathetic stimulators in the bladder/urethra?

A
  • HTN
  • tachycardia
  • anxiety, restlessness, nervousness, insomnia
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29
Q

What are some ancillary drugs for urinary incontinence?

A
  • methionine

- bovine collagen

30
Q

How does methionine work?

A

creates ammonia-free urine by acidifying urine pH to control oder, dermatitis and ulceration in incontinent adults

31
Q

How should methionine be taken?

A

take with food or with milk or other liquids

32
Q

AEs of methionine?

A

drowsiness

N/V

33
Q

What is bovine collagen used for?

A

incontinence due to intrinsic sphincter deficiency?

34
Q

How is bovine collagen given?

A

injected into submucosal tissue of urethra and/or bladder neck

35
Q

When should BC be given?

A

for patients failing other therapies for 12+ months

36
Q

What are some potential DD interactions of BC?

A
  • immunosuppressive therapy

- corticosteroids

37
Q

AEs of BC?

A
  • urinary retention or worsening incontinence
  • hematuria
  • injection site reaction
  • urticaria
  • abscess formation
  • erythema
38
Q

What drugs are used for urinary retention?

A

PO drugs taken several times daily

  • Bethanechol
  • Neostigmine
39
Q

What is the MOA of Bethanechol?

A

cholinesterase-resistance muscarinic agnostic with peripheral but NOT central actions

40
Q

What are the AEs of Bethanechol?

A
  • lightheadedness, syncope
  • diarrhea
  • excessive tear production, miosis
  • urinary urgency
41
Q

What is the MOA of Neostigmine?

A

acetylcholinesterase inhibitor that augments Ach at both muscarinic and nicotinic receptors

42
Q

What are the AEs of Neostigmine?

A
  • AV block, beady-arrhythmia
  • cardiac arrest
  • hypotension, syncope
43
Q

What do opiates do to the UT?

A

opiate analgesics not only produce GI stasis and urinary retention, but also modulate urinary bladder function via opiate receptor effects upon voiding responses arising from centers in the CNS.

Judicious use of cholinomimetics or opiate antagonists are used to mange the clinical problem.


44
Q

How do opiates promote urinary retention?

A

mediated by mu and delta receptor in sacral cord inhibiting parasympathetic outflow and hence detrusor activation (causes retention)

45
Q

T or F. Dertrusor relaxation is readily reversed with opiate antagonists

A

T, although reversal of analgesia is also likely

46
Q

Anatomical distribution of receptor subtype.

A

Alpha-1a predominates in the lower GU tract, whereas alpha-1d predominate in the detrussor muscle of the urinary bladder.

So, alpha-1 blockers cause relaxation of the smooth muscle in the prostatic and penile urethra, thereby permitting easier urination.


47
Q

How are a1 blockers given?

A

PO 1x daily

They generally have a long duration of action, which makes for less frequent dosing and therefore better compliance; prazosin (and alfuzosin) is the exception

48
Q

Metabolism of a1-blockers?

A

extensive CYP metbaolism (DD interactions)

49
Q

What are the common AEs of a1-blockers?

A
  • orthostatic hypotension
  • syncope, headache, etc.
  • nausea
  • asthenia
  • insomina
50
Q

What are the long-acting selective a1-blockers?

A
  • Terazosin

- Doxazosin

51
Q

What are the partially selective a1-blockers?

A
  • Tamsulosin (Flomax) (less effect on BP if hypotension is too intense)
  • Silodosin
52
Q

AEs of partially selective a1-blockers?

A
  • diminished effects on CV function

- increased sexual (ejacualtion) dysfunction

53
Q

Prazosin

A

This drug shows great variability from patient to patient, so dose titration is a necessary procedure.

54
Q

How does erection occur?

A

NO produced by the enzyme NOS is released from endothelial cells and cavernous nerves and stimulates guanylyl cyclase, resulting in increased levels of cGMP in the urethra.

Subsequent phosphorylation of cellular membrane proteins via protein kinase G results in an efflux of calcium, which leads to smooth-muscle relaxation, vasodilatation of the penile arteries and penile sinus, and erection.

55
Q

What do PDE5 inhibitors do?

A

decrease the breakdown of cGMP by inhibition of PDE5, resulting in the prolonged high levels of cGMP necessary for erections or for smooth flow of urine from the urinary bladder.

56
Q

What is a PDE5 inhibitor used to treat BPH?

A

Tadalafil

57
Q

How is Tadalafil given?

A

PO daily

58
Q

metabolism of Tadalafil?

A

3A4

59
Q

AEs of Tadalafil?

A

well-tolerated, AEs uncommon, but:

  • nasopharyngitis, URTIs
  • vision and hearing loss
60
Q

When is Tadalafil contraindicated?

A

concurrent organic nitrates and alcohol- causes profound hypotension

61
Q

What does 5-alpha-reductase do?

A

catalyzes the conversion of testosterone to dihydrotestosterone.

Although both testosterone and dihydrotestosterone act via the androgen receptor, dihydrotestosterone binds with higher affinity and activates gene expression more efficiently.

62
Q

What do dihydroestrogen promote?

A

As a result, acting via dihydrotestosterone and in tissues expressing 5-alpha-reductase, dihydrotestosterone is able to cause proliferation in tissues that would otherwise not be affected by circulating levels of testosterone.

63
Q

What are the two forms of 5-alpha-reductase?

A

type I, which is found predominantly in non-genital skin, liver and bone, and type II, which is found predominantly in urogenital tissue in men and genital skin in men and women.

64
Q

What is the effect of 5-alpha-reductase inhibitors?

A

reduce the dihydrotestosterone-driven proliferation of the prostate, and in doing so, provide relief for urinary evacuation by reducing the prostate from pressing on and contricting urine flow along the urethra.


takes longer to act than 1a-antagonists

65
Q

What drug inhibitors type 2 5-a-reductase?

A

Finasteride

66
Q

What drug inhibitors type 1 and 2 5-a-reductase?

A

Dutasteride

67
Q

How are 5-a-reductase inhibitors given?

A

PO daily (metabolized 3A4)

68
Q

AEs of 5-a-reductase inhibitors?

A
  • ejaculation and erectile dysfunction,

- decreased libido and gynecomastia

69
Q

What labs do 5-a-reductase inhibitors affect?

A

decrease PSA levels (problem if monitoring for prostate cancer)

70
Q

What are some natural products used for BPH?

A
  • Beta-sitosterols

- Saw Palmetto

71
Q

T or F. Beta-sitosterols improved urinary symptom scores and flow measures BUT did not significantly reduce prostate size compared to placebo

A

T.

72
Q

Is Saw Palmetto effective?

A

No evidence of benefit from the product.

Renal Week 3 (16 decks)

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