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Repro > Prostate Cancer, Benign Prostatic Hyperplasia, ED > Flashcards

Prostate Cancer, Benign Prostatic Hyperplasia, ED Flashcards

1
Q

Ultimate goals of therapy for BPH?

A
  1. relax smooth muscle of prostate (ex a1 blockade)
  2. decrease stromal tissue/hyperplasia (ex 5 alpha reductase inhibitors)
  3. relax prostate vasculature (PDE-5 inhibitors – used in pulmonary HTN as well)
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2
Q

Predominate alpha receptor in prostate? main idea of alpha receptor blockade?

A

a-1a (and to a lesser extent a-1d) -

    • a-1a = lower GI tract
    • a-1d = internal sphincter of bladder?

**inhibition = prostatic/penile urethral muscle relaxation –> allows urination

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3
Q
  • Zosins (prazosin, alfuzosin, terazosin, doxazosin, tamsulosin, silodosin)
  • – MOA, Metabolism, administration, AEs, special things?
A

MOA: Alpha 1 Blockers

Metabolism: CYP – significant drug-drug interaction

Administration: Oral

AEs: GI (xerostomia, nausea), CNS (dizziness, somnolence, asthenia, HA, insomnia)

**Generally LONG T1/2, EXCEPT PRAZOSIN (only 2-4 hrs)

**

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4
Q

Advantage and disadvantage of a-1a specific agents?

** recommended, “superior” alpha blocker? why?

A

Advantage: no dose titration needed

Disadvantage: retrograde anejaculation, block dopamine/CNS transmitters

**ALFUZOSIN - achieves clinically significant improvements w/out dizziness/asthenia or ejaculatory dysfunction

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5
Q

Which BPH therapy would you need to ask about before Cataract surgery?

A

– possible AE of flaccid iris in response to intraoperative irrigation + potential for prolapse of iris toward incision

** no apparent benefit to stopping a1 blocker prior to sx!

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6
Q

PDE-5 inhibitor MOA

A

inhibit cGMP breakdown –> prolonged Ca efflux / smooth muscle relaxation / vasodilation –> erection

(Normally: NOS produces NO –> stimulates guanyl cyclase –> cGMP produced –> Ca efflux –> etc.)

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7
Q

Tadalafil

A

MOA: PDE-5 inhibitor
**Longer duration = used for BPH (t1/2 = 2-4 hr)

AEs: generally well tolerated… HA, nausea, URI possible… really rare non-arteritic ischemic optic neuropathy / retinal artery occlusion / hearing loss

Contraindication: w/ NITRATES! (^hypoTN), also exacerbated by alcohol

Metabolism: cyp3A4

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8
Q

5 alpha Reductase, and MOA of inhibitors

A

5aR-ase = T –> DHT

type I = non - genital (skin, liver, bone)
type II = UG tract

MOA: xDHT –> dec prostate proliferation/hyperplasia –> urinary evacuation

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9
Q

Finasteride, Dutasteride: MOAs, AEs,

A

5 alpha Reductase Inhibitors
Finasteride = type 2 specific
Dutasteride = type 1 and 2 (non specific) – long binding time/slow removal + Cyp3A4 metabolism

AEs: category X TERATOGEN! but not carried in semen
erectile dysfunction / dec libido / gynecomastia
decrease PSA levels (can’t use as prostate ca monitor)
Possible increased rate of prostate cancer

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10
Q

Beta-Sitosterol

Saw Palmetto

A

“Natural” products for BPH relief

B-sistosterol = symptomatic relief, but does not shrink prostate

Saw Palmetto = no found benefit

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11
Q

Alprostadil: MOA and administration

A

MOA: PGE1 mimic = activates adenylate cyclase –> inc Ca efflux –> relaxes smooth muscle

administration: intraurethral suppository or direct injection into corpus cavernosum
* *Minimal systemization + rapid onset (minutes) + durable effect (1/2-several hours)

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12
Q

Avanafil, Sildenafil, Vardenafil, (tadafil)

A

MOA: PDE-5 inhibitors (prolong cGMP)

AEs: HA…some have indigestion, etc.
rare – non-arteritic ischemic optic neuropathy / hearing loss

Contraindications: DON’T USE W/ NITRATES, or alpha-blockers, drugs interacting with CYP

*Veradenafil – interaction w/ 70+ drugs = inc risk QT prolongation

Metabolism: hepatic (cyp3A4)

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13
Q

Testosterone replacement for erectile dysfunction?

A

– 65% will benefit – levels are variable for erectile dysfunction symptoms though

– may improve PDE5 inhibitor response

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14
Q

Yohimbine: MOAs, AEs, Contraindication

A

MOA: 2 mechs! –> overall = relaxes penile smooth m.

1) alpha 2 agonist –> decreases intracellular Ca
2) NANC presynaptic inhibition –> inc NO –> guanylate cyclase/cGMP activation

*NANC = non adronergic, non cholineric nerve

AEs: crosses BBB easily –> potential anxiety, antidiuresis, dizziness, flushing, HA, HTN…

Contraindication: Renal fail – worsens

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15
Q

Drug induced ED

A

280+ drugs have ED listed as adverse effect! mechanism often unknown…don’t forget about it

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16
Q

Caution with “natural” ED remedies?

A

Many have PDE-5 inhibitor action (inc cGMP) – careful of synergistic BP effects with NO!!

17
Q

How does GnRH agonism and antagonism block FSH/LH secretion? What’s the difference in their effects, especially initially?

A

Antagonists –> decrease GnRH action –> dec FSH/LH

Agonists –> INITIAL FLARE of FSH/LH /Dz –> eventual decrease in GnRH receptors / negative feedback –> dec FSH/LH

18
Q

What is a “super androgen receptor”?

A

– AR amplification, a point mutation or a change in the coregulators of A receptors –> increases responsiveness / receptors respond at a lower [androgen]

19
Q

Goserelin, Histrelin, Leuprolide, Triptorelin: MOA, time til effect, AEs

A

MOA: GnRH agonists
— initial surge, but then 2-4 weeks until hypoandrogenic state/therapy

AEs:

    • dec bone mineral density (dec estrogen), elevated serum lipids, weight gain, DM –> increase risk of CV disease
    • dec androgens = dec libido, gynecomastia, sexual dysfunction,
    • Cat X TERATOGEN
    • injection site reaction
20
Q

Degarelix

A

MOA: reversible GnRH receptor antagonist –> reduces FSH/LH –> castrates testosterone w/in 3 days
Administration: SC injection

AEs: Hot sweats, weight gain, HTN, arthralgia, chills, fatigue, inc LFTs, QT prolongation, impotence

21
Q

Estramustine: MOA, AEs

A

MOA: conjugated drug estradiol structure binds to EMBP on prostate cancer –> delivers alkylator –> microtubule inhibitor
+
Dec testosterone levels due to estradiol negative feedback

AEs: GI upset, elevated LFTs, hyperbilirubinemia
“estrogen therapy” like AEs w/ prolonged tx = gynecomastic/mastalgia, impotence, edema, MI, PE, Stroke

22
Q

Bicalutamide, Enzalutamide, Flutamide, Nilutamide

A

Androgen receptor blockers –>
Bic-, Enz-, Nil-utamide = CENTRAL and prostate receptors
Flutamide = only prostate receptors

AEs: HTN (nilutamide), blood dyscrasias, CNS changes, GI tox,

23
Q

Androgen receptor blocker used in PCOS?

A

Flutamide

  • *Bic, Enz, and Flutamide = Teratogens
  • *
24
Q

Which androgen receptor blocker is a: male teratogen? causes respiratory insufficiency? has a BBW for interstitial pneumonitis?

A

Enzalutamide = male teratogen

Nilutamide = respiratory insufficiency

Flutamide = Interstitial pneumonitis BBW

25
Q

which androgen receptor blocker may cause increased time to accommodate transition from light to dark and may cause respiratory insufficiency?

A

Nilutamide

26
Q

SipuLEUCel - T

A

MOA: Uses pt’s APCs to create T cell response (autologous cellular immunotherapy designed to stimulate T cell immunity against Prostatic acid Phosphate)

AEs: infusion rxn, paresthesias, citrate toxicity

27
Q

Abiraterone

A

MOA: 17-hydroxylase/Cyp17 inhibitor –> dec GC and Androgen production @ adrenal cortex, but increased MCs

*MUST ADMINISTER GCs!

AEs: Hepatic dysfunction (get LFTs), teratogenic (women should not handle drug / condoms must be used during pregnancy)

28
Q

Ketoconazole vs. 17-alpha-hydroxylase inhibitor (Cyp17 inhib)

A

– Ketoconazole = less specific –> produces hypoaldosterone, hypocortisol, hypoandrogenic state

– 17-alpha-hydroxylase inhib –> HYPERmineralocorticoid, hypocortisol, hypoandrogenic state

29
Q

Could you use finasteride and dutasteride as prophylaxis for prostate cancer prevention?

A

(5 alpha reductase inhibitors)

Not recommended – thought was that it would decrease DHT levels –> dec cancer development

30
Q

Estrogen therapy in prostate cancer

A

– estrogen works as negative feed back at H-P axis

– also has osteo-protective effects

– AE: negative CV effects

**TRANSDERMAL Estrogen – similar effect to GhRH agonist, w/out CV risk!!

31
Q

estrogen and progesterone receptors in prostate cancer? ER-beta receptor effect?

A

– E-alpha and P receptors found on many prostate cancers, consistently on androgen insensitive tumors –> blockade is an area for further study!

– ER - beta = protective / tumor suppressive effect

32
Q

Conventional chemo used in prostate cancer?

A
  1. Docetaxel: taxane, used w/ prophylactic GC to prevent edema/injection reaction
  2. Carbazitaxel: “ + poor P-glycoprotein efflux pump substrate + penetrates BBB – may be useful in multidrug resistant tumors!
  3. Mitoxantrone + predinsone: palliation of severe pain in hormone refractory dz
33
Q

Why doesn’t Flutamide increase testosterone levels?

A

Doesn’t block central androgen receptors (just prostatic)

*other androgen receptor blockers bind central and prostate receptors

34
Q

which alpha 1 antagonist has a short half life (comparatively)?

A

Parazosin

35
Q

which AR antagonist is a male teratogen?

A

Enzalutamide

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