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life cycles test 1 > androgen pharmacology > Flashcards

androgen pharmacology Flashcards

1
Q

general androgen half life

A

Test and its metabolites are degraded rapidly by the liver, making it difficult to sustain effective levels in the plamsa

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2
Q
  1. Identify the two principal androgens in males.
A

testosterone and DHT

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3
Q

List the inactive metabolites of Testosteron

A

androsterone and etiocholanolone

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4
Q

Where are levels of DHT highest

A

prostate, scrotum, penis, hair and skin

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5
Q

Sites of testosterone syntesis in males vs females

A

men: most in leydig cells, small amount from adrenals. Females: small amounts come from both ovary and adrenal gland

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6
Q

What stimulates testosterone synthesis

A

LH stimulates leydig cells- increases synthesis of pregnenolone from cholesterol.

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7
Q

What is the major pathway by which T is synthesized in leydig cells

A

Cholesterol > pregnenolone > > DHEA > androstenedione > T > DHT

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8
Q

Testosterone forms in the blood

A

40% is bound to sex hormone binding globulin and is not biologically active. 2% is unbound and the rest is bound to albumin. The portion bound to albumin is biologically active since it freely dissociates from albumin

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9
Q

Where is GnRH released from

A

arcuate nucleus and anterior hypothalamus

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10
Q

Is E or T more potent at inhibiting GnRH and LH release

A

Estrogen is more potent

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11
Q

Name time periods where T secretion is high in male

A

fetal phase, neonatal phase and adult phase

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12
Q
  1. Characterize the genomic mechanisms of action of androgens.
A

T or DHT binds to nuclear androgen receptor > dimerization > interacts with hormone response elements on DNA > trxn of target genes

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13
Q
  1. Characterize the non-genomic mechanisms of action of androgens.
A
  1. T or DHT binds membrane associated androgen receptor (mAR) > activates L-type Ca Channels > increased Ca > activation of PKC > activate PKA and MAPK > gene trx. 2. T or DHT binds mAR > activation of PLC > increased IP3 > release of intracellular Ca > activation of RAS/MEK/ERK pathway. 3. DHT metabolite interacts with GABA receptor > increased intracellular Cl and membrane potential. 4. T interacts with membrane bilayer phospholipids > changes flexibility and alters Na/K pump and Ca ATPase functions
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14
Q
  1. Explain the therapeutic uses of androgens
A

hypogonadism, osteoporosis, muscle wasting associated with AIDS, hormone therapy replacement in aging men.

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15
Q

compare primary, secondary and tertiary hypogonadism

A

primary: low T and normal or high LH/FSH. Secondary: defect at level of pituitary, low T and low FSH and LH, normal GnRH. Tertiary: defect at level of hypothalamus, low GnRH, Low FSH/LH.

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16
Q

Causes of tertiary hypogonadism

A

Kallmans syndrome (failure of GnRH neurons to migrate from olfactory placode) or acquired during illness or high stress.

17
Q

When should low T in older men be treated

A

If T is consistently <200mg/dl and accompanied by problematic Sx

18
Q
  1. Discuss the modifications of testosterone that increase its bioavailability
A
  1. Esterification of 17 beta hydroxyl group makes T more lipid soluble and they can be given parenterally or as a patch. 2. Alkylation of 17 alpha position slows degradation by liver making oral administration more effective. They are toxic to the liver.
19
Q

What is the structure of most anabolic steroids

A

17alpha alkylated androgens which are toxic to the liver. These include axandrolone, stanozolol, fluoxymesterone, danazol

20
Q
  1. List the formulations of testosterone available in US
A

Oral (not used for long periods due to hepatotoxicity): methyltestosterone (android, testred) and fluoxymesterone (halotestin). Parenteral: testosterone enanthate (delatestryl) and testosterone cypionate (virilon). Transdermal: testosterone ( androderm, testoderm). Gels and buccal tablets also

21
Q

Side effects of androgen therapy

A

testicular atrophy (decreased LH/FSH), gynecomastia, virilization in women, elevation of LDL, polycythemia, jaundice and hepatic carcinoma (17a-alkyl analogs), BPH, prostate cancer???

22
Q

Monitoring tests during T therapy

A

Screen for prostate cancer before therapy and while on therapy. Hematocrit should be measured before treatment and again after 3-6 months then yearly.

23
Q
  1. Explain the therapeutic uses of androgen antagonists.
A

Prostate cancer, benign prostatic hyperplasia, male baldness, hirsutism, precocious puberty in boys, acne

24
Q

List the types of anti-androgens

A
  1. Inhibitors of T secretion/synthesis: GnRH agonists or antagonists, drugs that block Cty P 450. 2. 5 alpha reductase inhibitors. 3. Androgen receptor antagonists
25
Q

List GnRH agonists and how they work

A

leuprolide, buserelin, nafarelin, histrelin, goserelin and deslorelin. Result in initial surge of GnRH followed by down-regulation of GnRH receptors and action

26
Q

List GnRH antagonists and how they work

A

cetrorelix, ganirelix, abarelix and degarelix. Block GnRH binding.

27
Q

List drugs that block Cyt P 450 and side effcts

A

Ketoconazole and abiraterone acetate. SE: hypertension and hypokalemia due to excess mineralocorticoids and adrenocorticoid insufficiency

28
Q

List 5 alpha reductase inhibitor and its uses

A

Finasteride- used for BPH and male baldness. Both are DHT driven processes

29
Q

List the androgen receptor antagonists and their affects on GnRH, FSH/LH and testosterone

A
  1. cyproterone acetate- steroid with progesterone like effects. Decreases GnRH, LH/FSH and testosterone. 2. Flutamide and bicalutamide- non-steroidal. Blocks negative feedback. Increases GnRH, LH/FSH and testosterone. Given with GnRH agonist
30
Q

Side effects of anti-androgens

A

decreased muscle strength, impotence, decreased libido, gynecomastia, osteoporosis, hot flashes/sweating, increased risk of prostate cancer (finasteride)

31
Q

List the top selling anabolic steroids through the internet

A

injectable: deca durabolin, testosterone enanthate, trenbolone, primolobone, equipoise, sustanon, and winstol. Oral: anavar, Tbol, dianabol, proviron

life cycles test 1 (19 decks)

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