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Reproductive Block > Pharm - Male > Flashcards

Pharm - Male Flashcards

1
Q

Short acting selective alpha 1 blockers

A

Prazosin, Alfuzosin

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2
Q

Long acting selective alpha 1 blockers

A

Terazosin, Doxazosin

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3
Q

alpha 1 alpha pertially selective blockers

A

Tamsulosin, Silodosin

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4
Q

PDE-5 Inhibitors (for BPH)

A

Tadalafil

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5
Q

5 alpha reductase inhibitors

A

Finasteride, Dutasteride

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6
Q

Type of alpha receptor in prostate

A

alpha-1a

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7
Q

Type of alpha receptor in the bladder detrusor muscle

A

alpha-1d

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8
Q

Prazosin PKPD

A

demethylation; conjugation; fecal elimination (2-4hr half life)

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9
Q

Alfuzosin PKPD

A

3A4; fecal/renal elimination; (10hr half life)

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10
Q

Terazosin PKPD

A

Hepatic-fecal/renal elimination; 12hr half life

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11
Q

Doxazosin PKPD

A

3A4>2D6; fecal elimination; 5-22hrs

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12
Q

Tamsulosin PKPD

A

3A4/2D6; renal/fecal elimination; 5-15hrs half life; bioavailability decreased by food

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13
Q

Silodosin PKPD

A

3A4; glucuronide conjugaiton; fecal/urine elimination; 13hr half life

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14
Q

Prazosin Dosing requirements

A

needs dosing every 12hrs with dose titration; making it a less attractive drug to use due to that and short half life.

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15
Q

Alpha 1 blocker SE

A

GI (xerostemia), CNS (dizziness, somnolence), retrograde ejaculation, floppy iris syndrome

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16
Q

Tadalafil MOA

A

PDE5 inhibtor which causes smooth muscle relaxation

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17
Q

Tadalafil PKPD

A

3A4; fecal elimination

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18
Q

Tadalafil AE

A

non-arteritic ischemic optic neuropathy; retinal artery occlusion; hearing loss

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19
Q

Tadalafil contraindications

A

concurrent organic nitrates - profound hypotension exacerbated by alcohol consumption

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20
Q

Finasteride: Dutasteride

A

F - type 2 5 alpha reductase enzyme; D - type 1&2; competitive long binding time, slow reversal; extensive 3A4 metabolism; pregnancy category X

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21
Q

Finasteride: Dutasteride AE

A

well tolerated; ejaculatory dysfunction, decreased libido, gynecomastia; decreases PSA levels (can be issue if using to monitor prostate cancer)

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22
Q

Beta sitosterols

A

herbal therapy used OTC for BPH - shows improved urinary symptoms and flow but no reduction in prostate size

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23
Q

Saw Palmetto

A

herbal therapy used OTC for BPH; no proven benefit.

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24
Q

Alprostadil MOA

A

mimics PGE1 which activated adenylate cyclase to increase intracellular cAMP

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25
Q

Alprostadil drug delivery

A

either urethral suppository or intra-cavernosal injection - limits systemic effects, rapid onset

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26
Q

PDE5 inhibitors PKPD

A

hepatic metabolism (3A4, 2C), primarily fecal elimination

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27
Q

PDE5 inhibitors adverse effects

A

Most commonly HA; rarely non-arteritic ischemic optic neuropathy, hearing loss, angina, MI, tachycardia

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28
Q

PDE5 inhibitors drug interaction

A

Nitrates (contra), alpha blockers, drugs affecting CYP activity

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29
Q

Vardenafil interactions

A

more than 70 drugs leading to increased risk of QT prolongation

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30
Q

Role of hormone replacement in ED

A

little effect alone; may improve response to PDE5 inhibitors

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31
Q

Yohimbine MOA

A

alpha 2 receptor inhibitor, causing decreased intracellular Ca2+ and increased smooth muscle relaxation; also antagonizes NANC nerves, increasing release of NO

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32
Q

Yohimbine effectiveness

A

little increase over placebo

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33
Q

Yohimbine PKPD

A

rapid absorption, short half life,, crosses BBB (AE of CNS)

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34
Q

Yohimbine Interaction

A

MAOI effect at high levels (interaction with tyramine and caffeine); worsens renal function in those with kidney issues (contraindicated)

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35
Q

Serum testicular cancer markers

A

alpha fetoprotein (AFP), lactate dehydrogenase (LDH), beta-human chorionic gonadotropic (B-HCG)

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36
Q

Primary cheomtherapy for testicular cancer

A

Etoposide/Cisplatin, Bleomycin/Etoposide/Cisplatin, Estoposide/Mesna/Ifosfamide/Cisplatin

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37
Q

Second-Line or metastatic for testicular cancer

A

Vinblastine/Mesna/Ifosfamide/Cisplatin, Paclitaxel/Mesna/Ifosfamide/Cisplatin

38
Q

High dose regimens for testicular cancer

A

Paclitaxel/Ifosfamide/Mesna followed by Carboplatin/Etoposide then stem cells; Carboplatin/Etoposide then stem cells

39
Q

Mechanism of resistance to cisplatin

A

decreased influx, increased efflux, sequestration, increased DNA repair, increased tolerance to DNA lesion, defective apoptotic response

40
Q

Bleomycin MOA

A

binds DNA in presence of iron with ferrous oxide mediated DNA stand breakage

41
Q

Cisplatin MOA

A

nuclear and mitochondrial DNA damage and redox stress

42
Q

Carboplatin MOA

A

slower reaction with nuclear DNA, less potent than cisplatin - give bigger dose than Cisplatin

43
Q

Etoposide MOA

A

stabilizes DNA and topoisomerase II complexes resulting in strand breakage

44
Q

Ifosfamide MOA

A

metabolically activated alkylating agent producing intra and inter strand DNA cross links

45
Q

Paclitaxel MOA

A

promotes microtubule assembly and stabilizes their formation by inhibiting depolymerization

46
Q

Vinblastine MOA

A

binds to low affinity sites on tubulin, resulting in splitting of the microtubules into spiral aggregates or protofilaments; this leads to the disintegration of the microtubule

47
Q

Mesna MOA

A

forms acrolein-mesna thioether complexes which are inactive and eliminated in the urine without causing hemorrhagic cystitis.

48
Q

Bleomycin Toxicity

A

late developing skin toxicity

49
Q

Cisplatin toxicity

A

renally eliminated; active accumulation in renal cells; inhibits breakdown of lipids to generate metabolic energy, ototoxic, neurotoxic

50
Q

Carboplatin toxicity

A

less nausea, neurotoxicity, ototoxicity and nephrotoxicity than cisplatin

51
Q

Etoposide toxicity

A

n/v, stomatitis, diarrhea, hepatic toxicity after high dose treatment

52
Q

Ifosfamide toxicity

A

neurotoxic (coma, seizures, ataxia from release of chloroacetaldehyde)

53
Q

Paclitaxel toxicity

A

(fligastim protectant) peripheral neuropathy (esp. bad in DM neuropathy)

54
Q

Mesna toxicity

A

most commonly dysgeusia, soft stools, HA

55
Q

Bleomycin dose limiting toxicity

A

pulmonary fibrosis, intersitial pneumonitis

56
Q

Cisplatin dose limiting toxicity

A

renal toxicity (amifostine protectant)

57
Q

Carboplatin dose limiting toxicity

A

thrombocytopenia

58
Q

Etoposide dose limiting toxicity

A

leukopenia

59
Q

Ifosfamide dose limiting toxicity

A

myelosuppression

60
Q

Paclitaxel dose limiting toxicity

A

bone marrow suppression

61
Q

Vinblastine dose limiting toxicity

A

neuropathy

62
Q

Cisplatin mechanism of toxicity

A

CDDP causes redox/ER stress which leds to interruption of inracellular energy production leading to renal epithelial cell death; it also depletes the antioxidant system in the Cochlea causing ototoxicity

63
Q

Bleomycin mechanism of toxicity

A

stimulate the production of ROS, chemokines, and cytokines; these pro-inflammatory and pro-fibrotic mediators in the initiation and maintenance of fibrosis

64
Q

Androgen receptor blockers

A

Bicalutamide, Enzalutamide, Flutamide, Nilutamide

65
Q

Targeted Alkylator

A

Estramustine

66
Q

GnRH Agonists

A

Goserelin, Histrelin, Leuprolide, Triptorelin

67
Q

GnRH Antagonist

A

Degarelix

68
Q

17-alpha inhibitor

A

Abiraterone

69
Q

Immunotherapy for prostate cancer

A

Sipuleucel-T

70
Q

First line therapy for prostate cancer

A

medical or surgical castration plus a pure anti-androgen

71
Q

GnRH agonist AE

A

transient hyperandrogenic state; then hypoadrenergic state leading to edema, HTN, decreased libido, gynecomastia, decreased bone mineral density; teratogens

72
Q

Histrelin AE

A

seizures, suicidal ideation

73
Q

Leuprolide AE

A

MI, CHF

74
Q

Degarelix

A

reversible GnRH antagoinst given subq; causes castrate levels within 3 days

75
Q

Degarelix AE

A

hot sweats, weight gain, HTN, elevated hepatic enzymes, QT prolongation

76
Q

Estramustine MOA

A

binds EBP on prostate CA, inhibiting microtubules, promoting dis-assembly and G2/M arrest, producing DNA strand breakage

77
Q

Estramustine AE

A

GI upset, gynecomastia, mastalgia, impotence, edema, thromboembolism, MI, PE and stroke, elevated LFTs, hyperbilirubinemia

78
Q

Bicalutamide receptor specificity

A

antagonist and some agonist activity with prostate>central; only one with CYP inhibition 3A4>2C9, 2D6

79
Q

Flutamide receptor specificity

A

prostate only

80
Q

Flutamide AE

A

hepatotoxicity, liver failure (BBW), blood dyscrasias

81
Q

Nilutamide AE

A

respiratory insufficiency (BBW), interstitial pneumonitis, increased time to accomodate transition from light to dark, HF/HTN

82
Q

Enzalutamide AE

A

CNS issues (dizziness, insomnia, seizures)

83
Q

General Androgen Receptor Blocks AE

A

GI toxicity, hot flashes, aches and pains; all teratogens (except Nilutamide)

84
Q

Sipuleucel-T MOA

A

autologous cellular immunotherapy designed to stimulate T-cell immunity against prostatic acid phosphatase (PAP) using patient’s APC

85
Q

Sipuleucel-T AE

A

mild infusion reactions, fevers, chills, dyspnea, n/v, parasthesias, citrate toxicity and fatigue

86
Q

Difference in 17alpha hydroxylase inhibitor (Abiraterone) and Ketoconazole

A

Ketoconazole causes a hypo-aldosterone and hypo cortisol state in addition to its hypo-androgenic state, while 17alpha inhibitor causes a hyper-mineralocorticoid effect

87
Q

Abiraterone AE

A

hyper-mineralocorticoid state (decrease effects by giving corticosteroids also), elevated hepatic enzymes, Cat X drugs

88
Q

ER-alpha in the prostate

A

activation mediates aberrant proliferation, inflammation, and malignancy

89
Q

ER-beta in the prostate

A

activation mediates a protective, antiproliferative, anti-inflammatory effect; may reduce aromatase expression and local estrogens

90
Q

Chemotherapeutics for prostate cancer

A

Docetaxel and Carbazitaxel with corticosteoids and anithistamines to preempt edema and injection reactions; Mitoxantrone + prednisone used for palliation of severe pain from hormone refractory disease

Reproductive Block (4 decks)

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