UROLOGY PHARM Flashcards

1
Q

ALPHA-1 BLOCKER DRUGS

A
Tamsulosin (Flomax)
Terazosin (Hytrin)
Doxazosin (Cardura)
Alfuzosin (Uroxatrol)
Silodosin (Rapaflo)
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2
Q

Combo 5-alpha reductase inhibitor-alpha-1 blocker

A

Dutasteride-Tamsulosin (Jalyn)

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3
Q

more effective than 5-alpha reductase inhibitors for short & long term symptom management

A

alpha-1 blockers

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4
Q

MOA OF ALPHA-1 BLOCKERS

A

relaxes smooth muscle in bladder neck, prostatic capsule, and prostatic urethra

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5
Q

where are alpha-1 receptors located

A

in the base of the bladder and in the prostate

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6
Q

which 2 alpha-1 blockers were more effective than finasteride (proscar)

A

doxazosin

terazosin

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7
Q

which alpha-1 blocker has equal efficacy with finasteride

A

Tamsulosin (Flomax)

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8
Q

MOST COMMON SE OF ALPHA-1 BLOCKERS

A

DIZZINESS

ORTHOSTATIC HYPOTENSION

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9
Q

which alpha-1 blockers cause more BP lowering effects than others

A

Doxazosin (Cardura) & Terazosin (Hytrin)

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10
Q

which alpha-1 blockers have less BP effects

A

Tamsulosin (Flomax)
Silodosin (Rapaflo)
Alfuzosin (Uroxatrol)

TSA! = less BP effects

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11
Q

how to start patients on alpha-1 blockers

A

generally start a small dose at bedtime and titrate up slowly over several weeks

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12
Q

⦁ ***Alpha-1 blockers = can cause severe hypotension if used with

A

PDE-5 inhibitors

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13
Q

***Alpha-1 blockers = can cause severe __________ if used with PDE-5 inhibitors

A

hypotension

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14
Q

SE OF ALPHA-1 BLOCKERS

A
  • dizziness & hypotension….also

⦁ Asthenia (muscle weakness)
⦁ nasal congestion
⦁ problems with ejaculation

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15
Q

which alpha-1 blocker has the most problems with ejaculation

A

Tamsulosin (Flomax)

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16
Q

alpha-1 blockers problems with ejaculation

A
  • can decrease volume of ejaculate by 90%
    • 35% of patients may have no ejaculate
    • up to 28% have retrograde ejaculation in Silodosin (Rapaflo)
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17
Q

which alpha-1 blocker causes retrograde ejaculation

A

Silodosin (rapaflo)

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18
Q

5-alpha reductase inhibitor drugs (5-ARI)

A

Finasteride (Proscar)

Dutasteride (Avodart)

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19
Q

he only agents that provide LONG TERM DECREASE IN PROSTATE SIZE and decreased need for prostatic surgery

A

5- ARIs

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20
Q

5-ARI MOA

A
  • competitive inhibitor of both tissue & hepatic 5-alpha reductase
  • 5- alpha reductase converts testosterone to dihydrotestosterone
  • by inhibiting 5-alpha-reductase = blocks conversion of testosterone to dihydrotestosterone = suppresses serum dihydrotestosterone levels
    ⦁ serum dihydrotestosterone decreases by 70%
    ⦁ serum testosterone increases by 10%
  • This decreases prostate size
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21
Q

EFFICACY OF 5-ARIs

A
  • may take up to a year to notice reduction in symptoms
    ⦁ reduction in obstructive symptoms = 23%
    ⦁ reduction in non-obstructive symptoms = 18%
  • increase in maximum urinary flow rate
  • reduction in mean prostatic volume by about 18%
  • decreased need for surgery
  • decreased development of acute urinary retention
  • the larger the prostate volume, the more effective the medication
  • Dutasteride (Avodart) may be more potent than Finasteride (Proscar)
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22
Q

the larger the prostate volume, the more _____________________ (5-ARI)

A

effective the medication is

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23
Q

which 5-ARI is more potent than the other

A
  • Dutasteride (Avodart) may be more potent than Finasteride (Proscar)
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24
Q

MAJOR SE OF 5-ARIs

A

⦁ decreased libido
⦁ ejaculatory or erectile problems (ED)
- may only have these SE for the first year of therapy

⦁ decreases serum PSA by 50%

- in the first 24 months of therapy = multiply PSA by 2 when interpreting results
- after 24 months of therapy = multiply PSA by 2.5 when interpreting results
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25
Q

what classes/meds are used for treatment of BPH

A

⦁ Alpha-1 blockers
⦁ 5 alpha-reductase inhibitors
⦁ Combo = Dutasteride-Tamsulosin (Jalyn)
⦁ Tadalafil (Cialis) = 5PDE-inhibitor

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26
Q

PDE5-INHIBITORS SHOULD NOT BE USED WITH

A

nitrates
alpha-1 blockers

  • can cause severe hypotension
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27
Q

MOA of Cialis (PDE5-inhbiitor) for BPH

A

Cialis blocks PDE5 in the prostate in bladder

  • the mechanism of how cialis reduces BPH symptoms is not completely understood
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28
Q

takes ____________ to note symptom improvement with Cialis when used for BPH

A

2-4 weeks

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29
Q

PDE-5 INHIBITORS (phosphodiesterase inhibitors)

A

Tadalafil (Cialis)
Vardenafil (Levitra)
Sildenafil (Viagra)
Avanafil (Stendra)

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30
Q

prostaglandin injectable

A

Alprostadil (Caverject), Muse (pellets) = vasodilator

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31
Q

drug classes/meds used for ED

A

PDE-5 inhbiitors & prostaglandin injectables (alprostadil)

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32
Q

MOA OF ALPROSTADIL (prostaglandin injectable)

A
  • causes vasodilation by directly acting on vascular & smooth muscle. Relaxes trabecular smooth muscle by dilation of cavernosal arteries when injected along the penile shaft –> allows blood flow to the penis and entrapment of blood flow through veno-occlusive mechanism
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33
Q

onset/duration of action of alprostadil

A
  • Onset = 5-20 minutes

- Duration = < 1 hour

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34
Q

CONTRAINDICATIONS TO PROSTAGLANDIN INJECTABLES (alprostadil)

A

⦁ conditions that predispose the patient to priapism (painful erection > 4 hrs)
⦁ anatomic or fibrotic conditions of the penis
⦁ For the pellets (Muse) = urethral stricture or perineal pain

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35
Q

SE OF PROSTAGLANDIN INJECTABLES

A

⦁ syncope
⦁ priapism
⦁ may cause BP lowering

36
Q

MOA OF PDE-5 INHIBITORS

A
  • For an erection to occur, nitric oxide (NO) is released in the corpus cavernosum during sexual stimulation
  • Nitric Oxide (NO) then activates the enzyme guanylate cyclase –> results in increased levels of cGMP (cyclic guanosine monophosphate) –> produces smooth muscle relaxation and inflow of blood to the corpus cavernosum (erection)
  • PDE-5 degrades cGMP in the corpus cavernosum, so PDE-5 inhibitors enhance the effect of NO by inhibiting PDE-5 from degrading cGMP = leads to maintained erection
37
Q

PDE-5 inhibitors Do not directly cause penile erections

A

they increase the potential for this, but still needs the stimulus like they normally would…still need to be aroused

38
Q

CONTRAINDICATIONS TO PDE-5 INHIBITORS

A

⦁ men taking nitrates

⦁ caution with alpha-1 blockers due to risk for severe hypotension

39
Q

ADVERSE REACTIONS OF PDE-5 INHIBITORS

A

⦁ severe hypotension (with nitrates or alpha-1 blockers)
⦁ common = flushing, headaches, dyspepsia
⦁ visual effects = transient blue vision with sildenafil (viagra), may increase risk for nonarteritic ischemic optic neuropathy
⦁ Hearing loss
⦁ Priapism

40
Q

which PDE-5 inhibitor can cause transient blue vision

A

sildenafil (Viagra)

41
Q

common adverse reactions with PDE-5 inhibitors

A
  • flushing
  • headaches
  • dyspepsia
42
Q

DRUG INTERACTIONS with PDE-5 inhibitors

A
  • CYP3A4 inhibitors may increase the serum concentration of PDE-5 inhibitors
43
Q

ADMINISTRATION

A
  • in general = take 1 hour before sex
  • Vardenafil (Levitra) & Avanafil (Stendra) = have a quicker onset of action (30 minutes)
  • Food & Alcohol delay the onset of action in Sildenafil (Viagra) & Vardenafil (Levitra)
  • Daily dose Tadalafil (Cialis) is available
  • average duration of action = 8-12 hours
  • Tadalafil (Cialis) average duration of action = 36 hours

For Levitra & Viagra = have to wait 24 hours before taking Nitrates
For Cialis = have to wait 48 hours before taking Nitrates

44
Q

which PDE-5 inhibitors have a shorter onset of action of 30 minutes rather than 1 hour

A

Vardenafil (Levitra) & Avanafil (Stendra)

45
Q

which PDE-5 inhibitor has a daily dose available

A

Tadalafil (Cialis)

46
Q

which PDE-5 inhibitors have a delayed onset of action with food & alcohol

A

Sildenafil (Viagra) & Vardenafil (Levitra)

47
Q

which PDE-5 inhibitor has a duration of action of 36 hours (instead of 8-12 hours)

A

Tadalafil (Cialis)

48
Q

For Levitra & Viagra = have to wait ______ before taking Nitrates
For Cialis = have to wait _______before taking Nitrates

A

24 hours

48 hours

49
Q

which PDE inhibitors have SE of visual abnormalities

A

Viagra & levitra

50
Q

which PDE inhibitor has SE of myalgias / back pain

A

cialis

51
Q

primary vs secondary hypogonadism

A

⦁ Primary hypogonadism = testes fail to produce testosterone

⦁ Secondary hypogonadism = pituitary or hypothalamus malfunction

treat with testosterone

52
Q

MOA of testosterone replacements

A
  • direct action by binding to androgen receptor
  • acts on tissues that express the enzyme 5-alpha reductase
    ⦁ converts to dihydrotestosterone, which binds more readily to the androgen receptor than testosterone
  • can act as an estrogen after converting to estradiol via an aromatase and bind to the estrogen receptor
53
Q

symptoms that are treated with testosterone replacement

A
decreased libido
decreased AM erections
loss of body hair
low bone density
gynecomastia
small testes
decreased muscle mass
- need 3-6 months of therapy to note improvement in symptoms
- need 2 years for improvement of BMD (bone mineral density)
54
Q

⦁ do NOT use testosterone replacement to treat impaired

A

impaired spermatogenesis

- testosterone therapy suppresses pituitary gonadotropin secretion and leads to more impairment of spermatogenesis
55
Q

PRIOR TO STARTING TESTOSTERONE THERAPY

  • need to screen for…….
  • and make sure __________ is being treated if present
A

PRIOR TO STARTING TESTOSTERONE THERAPY

  • screen for prostate cancer in men > 50 or men > 40 who have any risk factors
  • screen for erythrocytosis
  • if sleep apnea is present, make sure it is being treated!
56
Q

REDUCES SERUM PSA

INCREASES SERUM PSA

A

5-ARI

testosterone replacement

57
Q

SIDE EFFECTS OF TESTOSTERONE REPLACEMENT

A

⦁ polycythemia (which is why screen for erythrocytosis)
⦁ worsening of BPH
⦁ acne
⦁ increase in PSA (unlike 5-ARI)
⦁ oral & prolonged IM doses = associated with multitude of liver issues (jaundice, hepatitis, elevated LFTs)
⦁ increased risk of prostate cancer (screen for prostate cancer >50/> 40 with risk factors)
⦁ decreased spermatogenesis (so don’t use for impaired spermatogenesis!)
⦁ fluid retention
⦁ worsening of sleep apnea (so need to have treatment for sleep apnea prior to tx)
⦁ possible increased risk of cardiovascular events

58
Q

CONTRAINDICATIONS TO TESTOSTERONE THERAPY

A

⦁ known prostate cancer
⦁ known breast cancer (can be converted to estradiol)
⦁ severe lower urinary tract symptoms
⦁ HCT > 50% (because of polycythemia)
⦁ untreated severe sleep apnea (because it worsens sleep apnea)
⦁ PSA > 4.0 or PSA > 3.0 with any prostate cancer risk factors (increases prostate CA risk)

59
Q

hepatic SE (jaundice, hepatitis, elevated LFTs)

A

testosterone (oral & prolonged IM doses)

60
Q

LABS - prior to initiating testosterone therapy

A
  • serum testosterone
  • hematocrit
  • PSA
61
Q

good 1st choice of testosterone therapy

A

transdermal gel

⦁ well tolerated
⦁ achieves normal testosterone levels in most
⦁ the testosterone patch is another option
⦁ educate patients about the transfer of gel onto others

62
Q

testosterone gels

A
  • AndroGel = comes in pumps or packets
  • Testim = tubes
  • Fortesta = pump - apply to front & inner thighs
  • Axiron = pump - apply to each underarm
63
Q

testosterone patch

A

androderm

  • worn on the arm or torso
  • can cause significant skin irritation - 1/3 of men discontinue patch due to this SE
64
Q

IM testosterone

A

⦁ Testosterone enanthate (Delatestry)
⦁ Testosterone cypionate (Depo-Testosterone)

  • Gluteal injections once weekly (50-100mg) or once every 2 weeks (100-200mg)
65
Q

MONITORING WITH TESTOSTERONE THERAPY

A
  • serum testosterone
  • serum LH if primary hypogonadism
  • bone density
  • PSA & DRE
  • HCT

⦁ check serum testosterone - 2-3 months after starting or changing dose

⦁ if primary hypogonadism, check for normalization of serum LH (with primary hypogonadism in which testes aren’t responding, LH would by really high)

⦁ check Bone density - recheck every 2 years until normalizes or stabilizes

⦁ check PSA & DRE - 3-6 months after starting treatment, then yearly
- problematic if prostate nodule present, if PSA increases > 1.4 in a year, or PSA velocity > 0.4 per year x 2+ years

⦁ check HCT - 3-6 months after starting therapy, then yearly
- D/C if HCT >/= 54

66
Q

urinary tract analgesic drugs

A

⦁ Phenazopyridine (Pyridium)
⦁ Pentosan (Elmiron)

OTC = Azo-Gesic, Baridium

67
Q

INDICATIONS OF URINARY TRACT ANALGESIC DRUGS

A

Symptomatic relief of urinary burning, itching, frequency and urgency associated with UTI or post urologic procedures

68
Q

do not urinary tract analgesic drugs if

A

GFR < 50

69
Q

turns urine bright orange, turns skin/sclera yellow

A

phenazopyridine (pyridium)

urinary tract analgesics

70
Q

urinary tract analgesic considerations

A
  • don’t use for more than 2 days
  • can turn skin and/or sclera YELLOW
  • turns urine bright orange
  • Only used for symptom relief….does NOT treat the infection
71
Q

adverse reactions to urinary tract analgesics

A
  • headache
  • dizziness
  • stomach cramps
72
Q

INDICATIONS FOR PENTOSAN

A

cystitis

73
Q

low molecular weight heparinoid

A

pentosan - so can cause significant blood thinning

74
Q

MOA of Pentosan

A

drug adheres to the bladder wall mucosa and acts as a buffer to protect the tissues from irritating substances in the urine

75
Q

SE OF PENTOSAN

A

o CNS
⦁ headache
⦁ dizziness

o Derm
⦁ Alopecia
⦁ rash

o GI
⦁	rectal hemorrhage
⦁	diarrhea
⦁	nausea
⦁	abdominal pain
⦁	dyspepsia

o Hepatic
⦁ LFT abnormalities

76
Q

MUSCARINIC ANTAGONISTS/ANTISPASMODIC DRUGS

A
⦁	Oxybutynin (Ditropan) (Ditropan XL) (Oxytrol transdermal patch)
⦁	Tolterodine (Detrol) (Detrol LA)
⦁	Trospium (Sanctura), (Trospium XR)
⦁	Solifenacin (Vesicare)
⦁	Darifenacin hydrobromide (Enablex)
⦁	Fesoterodine (Toviaz)
77
Q

indications for muscarinic antagonists/antispasmodic drugs

A

for treatment of urgency / urgency predominant mixed or overactive bladder symptoms

78
Q

do NOT use muscarinic antagonists/antispasmodic drugs in patients with

A

dementia

79
Q

CONTRAINDICATIONS FOR muscarinic antagonists/antispasmodic drugs

A

gastric retention
angle closure glaucoma
dementia

80
Q

MOA OF MUSCARINIC ANTAGONISTS/ANTISPASMODIC DRUGS (oxybutynin / Detrol)

A
  • increases bladder capacity

- blocks basal release of acetylcholine during bladder filling, resulting in decreased urgency

81
Q

FACTS ABOUT MUSCARINIC ANTAGONISTS/ANTISPASMODIC DRUGS

A

**Extended release = have lower rates of adverse effects than immediate release agents

  • start with lowest available dose; evaluate response in 4-6 weeks
  • on average, takes at least 4 weeks to peak efficacy
  • reduce starting dose in age 60 or older
  • may respond to one agent and not another, so okay to try others in the same class***
82
Q

ADVERSE EFFECTS OF MUSCARINIC ANTAGONISTS/ANTISPASMODIC DRUGS

A
(high discontinuation rate due to SE)
⦁	dry mouth
⦁	constipation
⦁	blurred vision to near objects
⦁	tachycardia
⦁	drowsiness
⦁	decreased cognitive function
⦁	dizziness

CONSIDERATIONS FOR PRESCRIBING

  • hepatic metabolism at CYP450 - many interactions - except for Trospium
  • renal failure
  • hepatic failure
  • cognitive impairment
  • combinations to avoid
  • adverse effects to avoid

*Generally prescribe extended release (less SE) or transdermal formulations

83
Q

AVOID MUSCARINIC ANTAGONISTS/ANTISPASMODIC DRUGS WITH THESE DRUGS

A
  • 1st generation antihistamines, muscle relaxants, some antipsychotics, TCAs, ipratropium, Spiriva, Cholinesterase inhibitors, Trospirum & ETOH within 2 hrs of each other, Mirabegron, Metoprolol & Darifenacin, Grapefruit juice with any…
84
Q

COMMON ANTIBIOTICS FOR UTIs

A
Ciprofloxacin
Trimethoprim/sulfamethoxazole (Bactrim/Septra)
Nitrofurantion (Macrodantin)
Amoxicillin
Ampicillin
85
Q

CIPRO

  • class
  • MOA
  • pregnancy category
  • BBW
  • indications
A
Class = fluoroquinolone
MOA = inhibits DNA topoisomerase
Pregnancy category = C
Black box warnings (2) = tendon rupture; may exacerbate myasthenia gravis
Adjust dose based on renal function
Urologic indications
⦁	Cystitis
⦁	UTI
⦁	Prostatitis
86
Q

BACTRIM

A
Class = Sulfonamides
MOA = inhibits folic acid synthesis - avoid in pregnancy!
Pregnancy category = X
- 2nd best coverage for MRSA after Vanco
- oral tx for MRSA