GU Flashcards
All anti-spasmodics may cause confusion.* What does the CNS effects of antimuscarinics depend on?
CNS penetration PLUS M1 receptor binding
Where are M3 receptors and what is the effect of blocking them?
Bladder smooth muscle, salivary gland, eye, gut
AAG = DEC bowel/bladder contractility, dry eyes/mouth, and blurred vision
What are the 3 nonselective muscarinic AAG? What are common themes for their ADRs?
- tolterodine
- fesoterodine
- trospium
ADRs: xerostomia, constipation, fatigue/dizziness
What are the two ‘primarily’ M3 selective AAGs? Common theme of ADRs?
- oxybutynin
- solifenacin
ADRs: xerostomia, constipation
What is the M3 selective AAG?
- darifenacin
What is the MOA of nonselective muscarinic agents?
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**
What are the CYP isoenzymes related to Tolterodine and Fesoterodine?
2D6 and 3A4 substrate
Tolterodine - QT issues
Why do we avoid using Oxybutynin?
Xerostomia
- rarely used bc of this intolerance**
What is the MOA of oxybutynin and solifenacin?
AAG primarily M3 receptor –> INC bladder capacity, DEC uninhibited contractions, delay desire to void –> DEC IVS
What must you remember about an elderly patient on a urinary antimuscarinic?
All products are on Beers List
What is Mirabegron used for and what is the MOA? What is the most concerning ADR?
OAB
MOA: B3 agonist
- relax bladder and INC storage capacity
ADR: HTN*
What drug interactions should you be aware of with Mirabegron?
Inhibits 2D6 and digoxin excretion
Tell me about the three different alpha receptors (r/t BPH) - location and results of AAG.
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?
What two drugs are ‘a-blockers’ and what are the two MOA?
“-zosins”: terazosin, doxazosin
MOA:
- AAG a1A in bladder neck, prostate, urethra = relax smooth muscle = relieve OVS
- AAG a1B in vascular smooth muscle = relax vascular tone = postural hypotension / syncope (limited by dose titration*)
What are three clinical indications for a-blockers?
- BPH - not used d/t uroselective agents
- HTN - minimal use except “endocrine” HTN
- medical expulsive therapy for nephrolithiasis
What is the main C.I. with alpha blockers? What are two other interactions?
** C.I. with vasodilators - overlapping vasodilation**
- additive hypotension w/other anti-HTN
- avoid decongestants - may lead to acute urinary retention
5 ADRs related to alpha blockers?
- postural hypotension / dizziness *
- retrograde ejaculation *
- floppy iris syndrome
- drowsiness, fatigue
- nasal congestion / rhinitis
What are the three “uroselective” a-blockers? And MOA?
- alfuzosin
- tamsulosin
- silodosin
MOA: a1A AAG = smooth muscle relaxation
What is a clinical pearl regarding tamsulosin?
Nonsulfonylarylamine
What are the clinical indications for uroselective a-blockers?
Men: BPH
Women: improve sxs d/t bladder outlet obstruction (not FDA approved)
Both: off-label to pass kidney stones
What ADRs are r/t uroselective a-blockers?
- less postural hypotension / dizziness
- more retrograde ejaculation (silodosin»_space; tamsulosin > alfuzosin)
- floppy iris syndrome (MC w/tamsulosin)
- QT issues (alfuzosin)
What two drugs work as 5a-reductase inhibitors?
- finasteride
- dutasteride
Inhibits conversion of testosterone to dehydrotestosterone
What are the clinical pearls with 5a-reductase inhibitors?
- shrinks prostate
- 6-12 mo for max effect
- may use w/a-blockers
** DEC [PSA] ~ 50% –> dec overall risk of prostate cancer
What are the clinical indications of 5a-reductase inhibitors?
- both agents = BPH
- Finasteride = male-pattern baldness
