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Reproductive > PHARM: Urinary Incontinence or Retention > Flashcards

PHARM: Urinary Incontinence or Retention Flashcards

1
Q

What type of axons are responsible for bladder stimulation?

A

Parasympathetic postganglionic axons

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2
Q

What nerve carries the parasympathetic postganglionic axons responsible for bladder stimulation?

A

pelvic nerve

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3
Q

What is released by the parasympathetic postganglionic axons that stimulate the bladder?

A

acetylcholine and ATP (at bladder)

NO (at urethra)

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4
Q

What is the target of the parasympathetic postganglionic axons that stimulate the bladder?

A

M3 muscarinic receptors in the bladder smooth muscle (leads to SM contraction)

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5
Q

What is released by parasympathetic postganglionic axons at urethral smooth muscle?

A

NO (to relax smooth muscle for urine to flow through)

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6
Q

What type of axons are responsible for bladder relaxation?

A

Sympathetic postganglionic neurons

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7
Q

What nerve carries the sympathetic postganglionic axons responsible for bladder relaxation?

A

hypogastric nerve

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8
Q

What is released by the sympathetic postganglionic axons responsible for bladder relaxation?

A

norepinephrine

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9
Q

What is the target/action of the sympathetic postganglionic axons responsible for bladder relaxation?

A

β3 adrenergic receptors to relax bladder smooth muscle

α1 adrenergic receptors to contract urethral smooth muscle.

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10
Q

What type of nerves are responsible for contraction of the external sphincter striated muscle?

A

somatic axons (voluntary)

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11
Q

What nerve carries the somatic axons to the external sphincter striated muscle?

A

pudendal nerve

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12
Q

What is released by the somatic nerves responsible for contraction of the external sphincter striated muscle?

A

Ach

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13
Q

What is the target (receptor) of the somatic nerves responsible for contraction of the external sphincter striated muscle?

A

nicotinic cholinergic receptors

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14
Q

In the urine storage reflex, what does the distention of the bladder cause?

A

low-level vesical afferent firing

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15
Q

What is the consequent of the low-level vesical afferent firing in the urine storage reflex?

A

stimulation of the sympathetic outflow in the hypogastric nerve to the bladder outlet (the bladder base and the urethra) and the pudendal outflow to the external urethral sphincter.

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16
Q

What is the name of the “reflex” that causes urinary continence?

A

guarding reflex

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17
Q

What may lead to increase striated urethral sphincter activity (so that you do not have urine outflow in the urine storage reflex?)

A

pontine storage center

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18
Q

What nerve carries the intense bladder-afferent firing during voiding?

A

pelvic nerve

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19
Q

What is the role of the pelvic nerve during voiding reflex?

A

activates spinobulbospinal reflex pathways that pass through the pontine micturition centre

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20
Q

What does the spinobulbospinal reflex result in?

A

stimulates the parasympathetic outflow to the bladder and to the urethral smooth muscle and inhibits the sympathetic and pudendal outflow to the urethral outlet.

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21
Q

Where might the ascending afferent input from the spinal cord might pass through before reaching the pontine micturition centre?

A

periaqueductal grey (PAG)

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22
Q

Conscious bladder sensations and the mechanisms that underlie the switch from storage to voiding involve what structures?

A

cerebral circuits above the PAG.

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23
Q

What underlies urge incontinence?

A

detrusor overactivity

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24
Q

What underlies stress incontinence?

A

outlet incompetence

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25
Q

What drug class is used for urge incontinence?

A

Antimuscarinics

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26
Q

What drug class is used for stress incontinence?

A

Alpha-agonists

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27
Q

What is the first line treatment for bladder incontinence?

A

noninvasive approaches like behavioral therapy (patient education, fluid management, bladder retraining, pelvic floor exercises, biofeedback and timed bladder emptying).

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28
Q

List the anti-cholinergics used for bladder incontinence?

A 
Darifenacin
Fesoterodine
Oxybutynin
Solifenacin
Tolterodine
Trospium
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29
Q

Which anti-cholinergic can be used as a patch?

A

oxybutynin

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30
Q

What is the target of anti-cholinergics?

A

BLOCK the M2 and M3 receptors

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31
Q

What is the role of M2 receptors?

A

opposes the beta-adrenergic receptor (which works to relax the bladder so no urination occurs), leading to contraction as an indirect effect

32
Q

What is the role of M3 receptors?

A

has a direct effect in contracting the smooth muscle of the urinary bladder

33
Q

MOA: Inhibits vesicular release of excitatory Ach and axonal expression of other SNARE-complex dependent proteins in urothelium/sub-urotehlium mediating intrinsic or spinal reflexes thought to cause detrusor overactivity

A

Botulinum Toxin

34
Q

List the sympatheticomimetics used for urinary incontinence.

A

Mirabegron
Pseudoephedrine
Ephedra, Ma Huang

35
Q

What is the MOA of the sympatheticomimetics?

A

Mimics NE (activates beta-3 adrenergic receptors to relax bladder SM and activates alpha-1 adrenergic receptors to contract urothelial SM

36
Q

MOA: Creates ammonia-free urine (controls odor, dermatitis, and ulceration due to leaked out urine in patients) by acifidying urine pH

A

Methionine

37
Q

MOA: Injected into submucosal tissue of urethra or bladder neck and forms a soft, cohesive network of fibers increasing tissue bulk around the urethral lumen

A

Bovine Collagen Implant

38
Q

What are some peripheral effects of anti-cholinergics?

A

dry mouth (oral not as bad in ER), mydriasis, constipation, urinary retention, tachycardia

39
Q

What are some central effects of anti-cholinergics?

A

sedation, confusion/delirium, hallucinations, Severe cognitive impairment, sleep disruptions.

40
Q

TOXICITY: HTN (monitor), tachycardia

A

Mirabegron

41
Q

TOXICITY: HTN, A-fib, tachyarrhythmia, insomnia, anxiety, nervous, restless; MAOI interaction

A

pseudoephedrine

42
Q

TOXICITY: HTN, CHF, MI, tachyarrhythmia, insomnia, symptoms of CNS sitmulation; MAOI interaction

A

Ephedra, Ma Huang

43
Q

TOXICITY: Drowsiness, nausea, vomiting

A

Methionine

44
Q

TOXICITY: Urinary retention, hematuria, injection site rxn, worsening incontinence, erythema, urticaria, abscess formation; Interactions with immunosuppressive therapy and corticosteroids

A

Bovine collagen implant

45
Q

Which anti-cholinergic has > M3 selectivity, but is not better than others?

A

darifenacin

46
Q

Which anti-cholinergic is rapidly metabolized to 5-hydroxymethyl-tolterodine?

A

fesoterodine

47
Q

Which anti-cholinergics are available in extended release (ER) formats is to counter their otherwise short duration of clinical effect?

A

oxybutynin

tolterodine

48
Q

Which anti-cholinergic has the longest half-life (45-68 hr)?

A

solifenacin

49
Q

Which anti-cholinergic has the LEAST severe central side effects? Why?

A 
trospium
Quaternary amine (does not cross BBB)
50
Q

Which anti-cholinergic does NOT undergo hepatic metabolism because poor bioavailability?

A

trospium

51
Q

What therapy for urinary incontinence is delivered by carefully placed injections into the urothelial wall ?

A

botulinum toxin

52
Q

What drug used for urinary incontinence is a Beta-3 agonist?

A

mirabegron (increases bladder capacity by relaxing detrusor SM)

53
Q

What drug used for urinary incontinence is a direct and indirect alpha > beta agonist?

A

pseudoephedrine

54
Q

What drug used for urinary incontinence is an indirect non-selective alpha and beta agonist?

A

ephedra, ma huang

55
Q

Which drug’s half life depends on urinary pH?

A

pseudoephedrine

56
Q

How does the metabolism of mirabegron differ from the other sympatheticomimetics?

A

it is extensively CYP metabolized while the other two have minimal metabolism

57
Q

What drug for urinary incontinence must be taken with food or with milk/other liquid?

A

methionine

58
Q

What therapy is ONLY used in patients who have failed other therapies for >12 months and have incontinence due to intrinsic sphincter deficiency?

A

bovine collagen implant

59
Q

What are the contraindications for anti-muscarinic drugs?

A
  • Angle closure or narrow-angle glaucoma
  • Urinary or gastric obstruction
  • Need for mental alertness
  • Alzheimer’s type dementia (worsen already existing cholinergic effect)
60
Q

What should you monitor in a patient receiving anti-muscarinics?

A 
Urinary retention (especially in BPH)
CV effects (palpitations, tachycardia, prolonged QT)
GI effects (mild constipation to severe obstruction)
61
Q

Describe the patient profile most likely to respond to botox.

A

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 altogether.

62
Q

Other than inhibiting the afferent cholinergic impulses, what is the MOA of botox?

A

causes a phenotypic change within the urothelial tissue (integrating stretch receptors) 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

63
Q

How do opiates cause urinary retention?

A

inhibiting parasympathetic outflow and detrusor activation (via opiate receptor effects upon voiding responses arising from centers in the CNS)

64
Q

What mediates opiates’ effect on the bladder?

A

mu and delta receptors in the sacral cord

65
Q

What is the Direct Muscarinic Agonist used for urinary retention?

A

bethanechol

66
Q

What is the Ach inhibitor used for urinary retention?

A

neostigmine

67
Q

What are the opiod antagonists used for urinary retention?

A

methylnaltrexone

naltrexone

68
Q

Neostigmine inhibits Ach and augments its effects at what receptors?

A

muscarinic and nicotinic receptors

69
Q

Can bethanechol cross the BBB? Where does it act?

A

NO, urinary bladder and GI

70
Q

TOXICITY: CV (lightheadedness, syncope), GI (diarrhea, cramps), dizziness, excessive tear production, miosis, urgent desire to urinate

A

bethanechol

71
Q

TOXICITY: AV block, bradycardia, cardiac arrest, cardiac dysrhythmia, hypotension, syncope, tachycardia

A

Neostigmine

72
Q

What is the major side effect seen with opiod antagonists?

A

Reversal of analgesia may accompany reversal of detrusor relaxation

73
Q

What drug for urinary retention is NOT inactivated by cholinesterases?

A

bethanechol

74
Q

How is neostigmine inactivated?

A

inactivated by cholinesterases and hepatic microsomal enzymes

75
Q

True or false: bethanechol and neostigmine have long half-lives.

A

FALSE; Short half-lives (need administration multiple times a day)

76
Q

Do all opiods produce urinary retention?

A

no- intrathecal admin (into spine) is major

Reproductive (21 decks)

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