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Renal II > Drugs for GU Disorders - Konorev > Flashcards

Drugs for GU Disorders - Konorev Flashcards

1
Q

Cause of epithelial tissue hyperplasia

A

androgens

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2
Q

Cause of stromal tissue hyperplasia

A

estrogens

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3
Q

aromatase

A

converts androgens to estrogens

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4
Q

Tx: dynamic prostatic pathogenic factors

A

selective alpha-1 andrenergic antagonists

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5
Q

Tx: static prostatic pathogenic factors

A

5alpha-reductase inhibitors

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6
Q

second generation alpha-1 andrenergic antagonists

A
  • terazosin
  • doxazosin
  • alfuzosin
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7
Q

third generation alpha-1 andrenergic antagonists

A
  • tamulosin

- silodosin

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8
Q

5alpha-reductase inhibitors

A
  • finasteride

- dutasteride

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9
Q

benefits of using alpha-1 and antagonisis over 5alpha-reductase inhibitors

A
  • faster acting
  • effective reduction of LUTS
  • ass’d w/ less sexual dysfxn
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10
Q

alfuzosin

A
  • second generation alpha-1 and antagonist
  • more uroselective (d/t PK not selectivity)
  • doesn’t need titration
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11
Q

AE: doxazosin

A
  • may cause orthostatic hypotension
  • first does syncope
  • dizziness
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12
Q

AE: terazosin

A
  • may cause orthostatic hypotension
  • first does syncope
  • dizziness
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13
Q

tamsulosin

A
  • alpha-1A selective (prostatic sm), some 1B activation (vasculature)
  • used in BPH pts who have significant orthostatic hypotension
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14
Q

silodosin

A
  • highly alpha-1A selective
  • no orthostatic hypotension
  • severe ejaculatory dysfxn
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15
Q

AE: alpha-1 antagonists

A
  • syncope, dizziness, hypotension (2nd gen)
  • ejaculatory dysfxn (3rd gen)
  • nasal congestion
  • flu-like s/s
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16
Q

DI: alpha-1 antagonists + PDE5 inhibitor

A

marked systemic hypotension

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17
Q

DI: alpha-1 antagonists + cimetidine, diltiazem

A

decreased alpha-1 antagonists metabolism

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18
Q

DI: alpha-1 antagonists + carbamazepine, phenytoin

A

increased metabolism

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19
Q

MOA: finasteride

A
  • selective type II reductase inhibitor

- inhibits DHT synthesis from T

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20
Q

MOA: Dutasteride

A
  • non-selective ( type I and II) reductase inhibitor

- inhibits DHT synthesis from T

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21
Q

Type I enzyme reductase locations

A

skin, hair follicles, liver

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22
Q

Type II enzyme reductase locations

A

prostate, genital tissue, scalp

-responsible for epithelial tissue enlargement in prostate

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23
Q

MOA: 5alpha-reductase inhibitors

A
  • reduce DHT formation
  • prevent AR activation
  • shrink prostate
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24
Q

negative aspects of 5alpha-reductase inhibitors

A
  • need 6-12 m to develop effect
  • more pronounced sexual dysfunction
  • “second-line” agent
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25
when to use 5ARi over A1AAs
- severe prostatic enlargement (40g or >) - andrenergic ant contraindications - pts with high PSA (>1.4 ng/ml)
26
drug classes that exacerbate BPH
- T replacement therapy - alpha-and agonists - antimuscarininc drugs
27
types of organic ED
- hormonal - neurologic - vascular
28
Oral phosphodiesterase type 5 inhibitors
- sildenafil - vardenafil - tadalafil
29
injectable or intraurethral prostaglandins
alprostadil
30
unapproved ED tx agents
- phentolamine - papaverine - trazodone
31
MOA: PDE-5 inhibitor
- stops degredation of cGMP - cGMP used to decreased the intracellular Ca2+ - decreased intracellular Ca2+ = smooth mm relaxation = erection!
32
DOA: sildenafil and vardenafil
- onset = 1 hr | - DOA = 5-6 hr
33
DOA: tadalafil
- onset = 2 hr | - DOA = 36 hr
34
AE: PDEi
- hypotension - HA - dizziness - flushing - priapism
35
unique AE: sildenafil & vardenafil
-visual defects: impaired blue-green discrimination d/t PDE6
36
unique AE: tadalafil
-lower back mm & limb pain d/t PDE11 inhibition
37
DI: PDEi
- nitrates: severe hypotension - alpha1-adrenergic ants - EtOH: orthostatic hypertension
38
MOA: Alprostadil
-acts via EP2 receptor to cause smooth mm relaxation
39
AE: Alprostadil
- pain and burning at injection site - fibrotic plaque formation - hematomas & brusin - priaprasm
40
Use of flibanserin
enhance sexual desire in women
41
MOA: flibanserin
- postsynaptic 5HT1A receptor agonist | - 5HT2A receptor antagonist
42
AE: flibanserin
- dizziness - nausea - sleepiness - syncope (espt w/ etoh use)
43
CI:flibanserin
- etoh use - liver damage - concomitant use of CYP3A4i
44
detrusor mm receptor
cholinergic M3 (ANS)
45
intrinsic sphincter mm receptor
alpha-1 AR (ANS)
46
external sphincter mm receptor
nicotinic (voluntary control)
47
stress urinary incontinence
occurs as a result of physical exertion - anything that increases intrabdominal pressure - urethral underactivity
48
urge urinary incontinence
detrusor mm overactivation, contracts during filling phase - bladder overactivity
49
drugs that aggrevate UI manifestation
- diuretics - AChEi - mAChR agonists - alpha1- adrenergic antagonistis - alpha2-adrenergic agonists - ACEi
50
nonselective mAChR antagonists used in UI
- oxybutynin (MC) | - trospium
51
M3 R selective mAChR antagonists used in UI
- darifenacin - solifenacin - tolerodine: drug of choice - festoerodine: same active metabolite as toler-
52
MOA: mAChR antagonists in UI
- relax detrusor muscle - increase bladder capacity - prevent urgency
53
AE: mAChR antagonists in UI
- dry mouth - constipation - dry eyes - tachy - cognitive impairment, confusion, memory loss - vision impairment
54
indirect anticholinergic drug
botox
55
clinical use of botox in UI
- local injection into detrusor mm | - mm paralysis lasst from 3-9 mos
56
andrenergic agonists used to tx UI
- ephedrine | - midodrine
57
MOA: midorine
- alpha-1AR selective agonist | - improve intrinsic sphincter
58
AE: midodrine
- isomnia - elevated BP - myocardial ischemia exacerbation - cardiac arrhythmias
59
MOA: impramine
tricyclic antidepressant used to tx UI - blocks NE reuptake - antimuscarinic effect - increases intrinsic sphincter tone
60
MOA: dulozetine
antidepressant used to tx UI - block NE and 5HT reuptake - increases intrinsic sphincter tone
61
MOA: estrogens
- increase urethral epi prolif - enhance local blood circulaiton - increase urogenital alpha1-andrenergic receptors - only topical use!

Renal II (7 decks)

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