GU Flashcards

1
Q

All anti-spasmodics may cause confusion.* What does the CNS effects of antimuscarinics depend on?

A

CNS penetration PLUS M1 receptor binding

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2
Q

Where are M3 receptors and what is the effect of blocking them?

A

Bladder smooth muscle, salivary gland, eye, gut

AAG = DEC bowel/bladder contractility, dry eyes/mouth, and blurred vision

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3
Q

What are the 3 nonselective muscarinic AAG? What are common themes for their ADRs?

A
  1. tolterodine
  2. fesoterodine
  3. trospium

ADRs: xerostomia, constipation, fatigue/dizziness

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4
Q

What are the two ‘primarily’ M3 selective AAGs? Common theme of ADRs?

A
  1. oxybutynin
  2. solifenacin

ADRs: xerostomia, constipation

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5
Q

What is the M3 selective AAG?

A
  1. darifenacin
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6
Q

What is the MOA of nonselective muscarinic agents?

A

AAG M2 and M3 receptors on detrusor smooth muscle

INC bladder capacity, DEC uninhibited contractions, delay desire to void –> DEC IVS

Caution: pt w/urinary retention and closed angle glaucoma**

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7
Q

What are the CYP isoenzymes related to Tolterodine and Fesoterodine?

A

2D6 and 3A4 substrate

Tolterodine - QT issues

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8
Q

Why do we avoid using Oxybutynin?

A

Xerostomia

  • rarely used bc of this intolerance**
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9
Q

What is the MOA of oxybutynin and solifenacin?

A

AAG primarily M3 receptor –> INC bladder capacity, DEC uninhibited contractions, delay desire to void –> DEC IVS

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10
Q

What must you remember about an elderly patient on a urinary antimuscarinic?

A

All products are on Beers List

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11
Q

What is Mirabegron used for and what is the MOA? What is the most concerning ADR?

A

OAB

MOA: B3 agonist
- relax bladder and INC storage capacity

ADR: HTN*

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12
Q

What drug interactions should you be aware of with Mirabegron?

A

Inhibits 2D6 and digoxin excretion

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13
Q

Tell me about the three different alpha receptors (r/t BPH) - location and results of AAG.

A

a1A

  • prostate, bladder neck
  • AAG = bladder neck / prostate relaxation

a1B

  • peripheral vasculature
  • AAG = orthostasis, syncope

a1D

  • SC, bladder, nasal passages
  • AAG = may help BPH sxs?
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14
Q

What two drugs are ‘a-blockers’ and what are the two MOA?

A

“-zosins”: terazosin, doxazosin

MOA:

  1. AAG a1A in bladder neck, prostate, urethra = relax smooth muscle = relieve OVS
  2. AAG a1B in vascular smooth muscle = relax vascular tone = postural hypotension / syncope (limited by dose titration*)
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15
Q

What are three clinical indications for a-blockers?

A
  1. BPH - not used d/t uroselective agents
  2. HTN - minimal use except “endocrine” HTN
  3. medical expulsive therapy for nephrolithiasis
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16
Q

What is the main C.I. with alpha blockers? What are two other interactions?

A

** C.I. with vasodilators - overlapping vasodilation**

  • additive hypotension w/other anti-HTN
  • avoid decongestants - may lead to acute urinary retention
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17
Q

5 ADRs related to alpha blockers?

A
  1. postural hypotension / dizziness *
  2. retrograde ejaculation *
  3. floppy iris syndrome
  4. drowsiness, fatigue
  5. nasal congestion / rhinitis
18
Q

What are the three “uroselective” a-blockers? And MOA?

A
  1. alfuzosin
  2. tamsulosin
  3. silodosin

MOA: a1A AAG = smooth muscle relaxation

19
Q

What is a clinical pearl regarding tamsulosin?

A

Nonsulfonylarylamine

20
Q

What are the clinical indications for uroselective a-blockers?

A

Men: BPH

Women: improve sxs d/t bladder outlet obstruction (not FDA approved)

Both: off-label to pass kidney stones

21
Q

What ADRs are r/t uroselective a-blockers?

A
  1. less postural hypotension / dizziness
  2. more retrograde ejaculation (silodosin&raquo_space; tamsulosin > alfuzosin)
  3. floppy iris syndrome (MC w/tamsulosin)
  4. QT issues (alfuzosin)
22
Q

What two drugs work as 5a-reductase inhibitors?

A
  1. finasteride
  2. dutasteride

Inhibits conversion of testosterone to dehydrotestosterone

23
Q

What are the clinical pearls with 5a-reductase inhibitors?

A
  • shrinks prostate
  • 6-12 mo for max effect
  • may use w/a-blockers

** DEC [PSA] ~ 50% –> dec overall risk of prostate cancer

24
Q

What are the clinical indications of 5a-reductase inhibitors?

A
  • both agents = BPH

- Finasteride = male-pattern baldness

25
Q

What is the precaution regarding 5a-reductase inhibitors?

A
  • preg women should not handle (can be absorbed through skin)

** abnormalities of external male genitalia reported (cat X)

26
Q

What are two ADRs related to 5a-reductase inhibitors?

A
  1. ED and ejaculation disturbances

2. Rare reports of high-grade prostate CA (both) and male breast cancer (finasteride)

27
Q

What other condition should pop into your mind with an ED patient?

A

CAD

** ED is a “vascular equivalent” - occurs 2-5yrs before CAD [potential window to create lifestyle changes to prevent CAD] **

28
Q

Describe the general treatment plan for ED?

A
  1. Lifestyle
  2. PDE5 inhibitors
  3. Intraurethral or intracavernosal alprostadil
  4. Implant or vacuum device
29
Q

What is the MOA of PDE5 inhibitors? What are some examples of these meds?

A

Inhibits PDE5 to prevent breakdown of cGMP –> potentiates relaxation of smooth muscle –> engorgement

Avanafil, Sildenafil, Vardenafil, Tadalafil

30
Q

What are the 3 main clinical indications for PDE5i?

A
  1. ED
    - all PRN, Tadalafil approved for daily use to inc spontaneity
  2. BPH
    - Tadalafil - consider if BPH & ED
  3. Pulmonary Arterial* HTN
    - Sildenafil, Tadalafil
31
Q

What drug is C.I. in someone on a PDE5i?

A

Nitrates** - catastrophic hypotension possible

32
Q

What are the class ADRs related to PDE5i?

A
  1. VD = HA, facial flushing, nasal congestion, dyspepsia
  2. Priapism*
  3. Nonarteric ischemic optic neuropathy
    - blood flow blocked to optic nerve = sudden vision loss
33
Q

What are two unique ADRs with PDE5i?

A
  1. Sildenafil - cyanopsia

2. Tadalafil - backache and myalgias

34
Q

What are the clinical indications for Flibanserin?

A

Tx PREmenopausal women w/FSIAD (female sexual interest / arousal disorder) not caused by another medical/psych condition

35
Q

What are the clinical pearls regarding Flibanserin?

A
  • not approved for men or POSTmenopausal women*
  • may take 8wk for max effect*
  • dose at night to dec r/o hypotension, syncope, CNS depression
36
Q

Describe the Pk of Flibanserin?

A

2C19 and 3A4 substrate

  • mod/strong inhibitors C.I.
  • single dose of fluconazole for vaginitis is Bad!**

Pgp inhibitor

37
Q

Flibanserin is on the REMS program. What must the prescribe counsel patient on and why?

A

** Must counsel patient on risk of alcohol consumption **

EtOH C.I. d/t severe hypotension and syncope

38
Q

Besides Flibanserin, what is the other medication indicated for PREmenopausal FSIAD?

A

Bremelanotide

  • SQ injection 45min before anticipated sex
39
Q

What is the main drug interaction to be aware of with Bremelanotide?

A

May slow gastric emptying and alter rate of absorption of PO drugs

Be thoughtful with GLP-1s, opioids, lubiprostone

40
Q

Who is Bremelanotide C.I. in?

A

Women with CVD or uncontrolled HTN

Transient INC BP and DEC HR after each dose

41
Q

List some ADRs related to Bremelanotide?

A
  • Nausea (esp w/first dose)
  • flushing
  • injection-site rxn
  • HA
  • hyperpigmentation* rare, but may not be reversible