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Pharmacology of androgens and anti-androgens Flashcards

1
Q

what secretes androgens

A

testes and adrenal cortex

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2
Q

what is the primary synthesiser of androgens

A

testes

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3
Q

where is testosterone sythesised

A

leydig cells of the testes
from cholesterol
also secrete it

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4
Q

some types of androgens include

A

testosterone
DHT
androstendione

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5
Q

do females have androgens

A

adrenal cortex and ovary do secrete some androgens. Adipose tissue does secrete some androgens as well. Thus females do have some levels of androgens albeit much lower than in males

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6
Q

what enzyme allows testosterone conversion to DHT

A

5-alpha-reductase

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7
Q

what is the hypothalamic pituitary gonadal axis

A

controls the testes

  • secretes GnRH into portal vessels i in pulsatile manner
  • GnRH acts on gonadotrophs in ant pituitary to release FSH/LH
  • LH acts at leydig cells
  • FSH acts at sertoli cells
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8
Q

what is the effect of LH in men

A

LH stimulates the Leydig cells to synthesise and secrete testosterone which has both anabolic effects (growth) and androgenic effects (virulisation, development of male characteristics).

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9
Q

effect of sertoli cells (SC) in men

A
  • FSH acts on SC to maintain their number
  • testosterone acts on SC to initate and maintain spermatogenesis
  • SC release AMH = regression of mullerian ducts in utero
  • SC release inhibit B which acts on ant pituitary to reduce fsh release
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10
Q

effects of testosterone

A
  • on SC to initiate and maintain spermatogenesis
  • reduces secretion of GnRH from hypothalamus
  • inhibit LH secretion from ant pituitary
  • (embryo) stimulates growth of wolffian duct. Inducing differentiation of epididymis, vas deferens, seminal vesicles and ejaculatory duct
  • Induces the male secondary sexual characteristics and opposes the action of oestrogen on breast growth
  • provokes boisterous play, enhance sex drive and aggression
  • induces bone growth and cessation once adequate bone growth reach
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11
Q

effects of DHT

A

DHT causes the male external genitalia to develop, this involves enlargement of penis and prostate at puberty
- facial hair, acne and temporal hairline recession

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12
Q

what happens when testosterone and DHT are absent

A

external genitalia develop in their female form

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13
Q

why may a male have testosterone and DHT yet still produce female genitalia

A

The tissues that the androgens are acting on require the testosterone receptors to respond, otherwise testicular feminisation will occur (genetic males appear female).

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14
Q

other effects of both DHT and testosterone

A
  • Height (males on average are taller)
  • Muscularity
  • Bone growth (stronger bone growth, heavier skull, larger hands and feet)
  • Deep voice (growth of larynx)
  • Pubic hair (often continuous with abdominal and chest hair)
  • prominant subcutaneous veins (due to lack of subcutaneous fat)
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15
Q

unwanted effects of androgens

A
  • hypertension and oedema (calcium, sodium and water retaining actions)
  • cholestatic jaundice (anabolic steroids may cuase liver cancer
  • supression of Gonadorophin (-ve feedback loop) (cause testicular regression and reduced spermatogenesis)
  • gynacomastia (conversion of testosterone to oestrogen by aromatase)
  • virulisation, hirsuitism, male pattern baldness, acne
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16
Q

what is virulisation

A

Virulisation is the development of male physical characteristics (e.g. deep voice, body hair, muscle bulk in a female or precociously in a boy due to excess production of androgens.
However virulisation can also simply refer to changes that make a male body different from a female body

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17
Q

why may an individual have high androgens for a prolonged period of time

A
  • drug induced

- taken recreationally - may arise pathologically due to endocrine tumours.

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18
Q

how do anabolic steroids work

A

Anabolic steroids are structurally and functionally similar to testosterone and have androgenic and virulising properties. They are essentially synthetic androgens`

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19
Q

what may abuse/excessive use of anabolic steroids result in

A

similar to unwanted effects of excess testosterone

  • testicular regression
  • decreased spermatogenesis
  • Hepatotoxicity with cholestasis, hepatitis or hepatocellular tumours
  • Increased LDL and decreased HDL levels leading to vascular disease
  • Changes in libido, increased aggression
  • Weight gain and acne
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20
Q

examples of anabolic steroids

A

Stanozolol

nandrolone

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21
Q

mechanism of action of testosterone

A
  • testosterone reaches target cell and diffuses through
  • binds to nuclear receptor in cytosol (ligand activated transcription factor)
  • on binding, complex travels to nucleus and causes changes in gene expression
  • causes effects of testosterone
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22
Q

difference between testosterone and DHT

A

testosterone is converted to DHT by 5a-reductase
is more potent than testosterone
binds to same receptor

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23
Q

action of DHT

A

causes changes in transcription of target cells resulting in development of male external genitalia and sexual maturation at puberty

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24
Q

use of 5a-reductase inhibitors

A

DHT is important in adult prostate and hair follicles
In prostate cancer we give 5-alpha-reductase inhibitors to block production of DHT, that is the principle androgen of the prostate
DHT also promotes hair loss, so male pattern baldness may be treated with 5-alpha-reductase inhibitors.

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25
what are the two types of 5a-reductase
Type I 5α-reductase is found on the scalp and skin | Type II 5α-reductase is found on the genital skin and in the prostate
26
what happens when a female has raised testosterone during puberty
clitoris becomes enlarged | called 'penis at 12' syndrome
27
what happens if a male has a deficiency in 5a-reductase
testes will still develop but without the prostate and the external genitalia will resemble that of females
28
what is male pseudohermaphroditism
pseudohermaphroditism in which the gonads are male and the karyotype is XY but with genital anomalies
29
what may cause female pseudohermaphroditism
LH levels & testosterone levels increase at puberty. May be enough substrate to be converted to DHT so they develop male external genitals. Females may then adopt the normal male role post-puberty.
30
what may be an effect of inadequate metabolism of DHT
Inadequate metabolism of DHT, can lead to high levels of DHT resulting in prostatic hyperplasia. This may be associated with acne and hirsuitism (growth of hair).
31
what happens when there is a mutation in an androgen receptor gene
mutated receptor protein -> reduced sensitivity to androgens.
32
male presentation of
As a result a male XY foetus has female external genitalia but a short vaginal length, but retained testes but no female internal genitalia. -no internal male architecture. - feel female as have never been exposed to testosterone (bc are insensitive) The testes may later be surgically removed and the patient put on oestrogen therapy at puberty.
33
male presentation of mild AIS
may have appear as having a male-type external genitalia, they may be given high dosage testosterone that then helps to improve their secondary sexual characteristics. - patient can then assign themselves to the gender that they feel more comfortable in
34
what is congenital adrenal hyperplasia (CAH)
rare inherited autosomal recessive disorders characterized by a deficiency of one of the enzymes needed to make specific hormones
35
what happens when there is a lack of 21hyroxylase
causes the progesterone to be shunted to DHEA and androstenedione - lack of cortisol = high ACTH. adrenal cortex stimulated to take up more cholesterol - excess production of androstenedione and testosterone leading to excess secretion of male hormones
36
what is the role of 21-hyroxylase in androgens
convert progesterone to aldosterone and 17-OH progesterone.
37
presentation of CAH in XX females
Ambigous genitalia and severe acne
38
presentation of CAH in XY males
Premature puberty (deep voice, enlarges penis, small testes, pubic and axillary hair appear early)
39
treatment of excess androgens in CAH
androgen antagonists Cyproterone danazol
40
why may we give GnRH agonist analogues in prostate + breast +endometriosis
cause an initial surge of LH/FSH but then stay bound to their receptors on gonadotrophs causing desensitisation. Thus they down-regulate gonadotrophin release. In the long-term therefore they decrease testosterone levels.
41
uses of androgens as drugs
- androgen deficiency, delayed puberty - cryptorchidism - Initiate spermatogenesis - Androgen-insensitivity syndrome
42
uses of anti-androgens as drugs
- Precocious puberty, premature sexual development | - Premature baldness
43
what is cryptorchidism
An undescended testicle happens when one or both of a child's testicles do not drop down into the scrotum before birth. Failure of testes to descend can potentially lead to testicular tumour formation and infertility.
44
what is danazol
an androgen derivative but not converted to oestrogen - decreases LH/FSH in men and women - has antioestrogenic and antiprogestogenic effects - useful for gynaecomastia, mastalgia (breast pain) and benign fibrocystic disease
45
how do hypogonadal syndromes present in males
delayed puberty (15-17yrs)
46
what is primary hypogonadism
testes failing to produce adequate testosterone in response to LH
47
what is secondary hypogonadism
a deficiency of pituitary hormones (FSH/LH) or pituitary dysfunction so inadequate testosterone
48
cause of primary hypogonadism
chromosomal abnormalities (e.g. Kinefelter's Syndrome, 47XXY). Leads to low levels of testosterone resulting in low –ve feedback to hypothalamus/pituitary leading to high FSH/LH levels
49
treatment of hypogonadism
- give testosterone and growth hormone | - following this, puberty may take 2 years to complete
50
risk of continuous administration of testosterone
premature closure of the epiphyses of long bones. Hence it is regarded as better to give testosterone for 4-6 months then stop and assess to avoid reducing the child's final height.
51
cause of secondary hypogonadism
caused by a deficiency at the hypothalamic/pituitary level, so there will be low levels of GnRH and also low levels of FSH/LH (e.g. Kallman's syndrome).
52
treatment of secondary hypogonadism
give gonadorelin (synthetic GnRH) or give LH and FSH. It may take months for their effects on spermatogenesis to develop in post-pubertal patients.
53
what are secondary sexual characteristics
Secondary sex characteristics are features that appear during puberty in humans
54
treatments for abnormalities of of secondary sexual characteristics
androgen antagonists | eg Cyprotenerone acetate inhibits peripheral androgen receptors
55
use of androgen agonists to treat secondary sexual characteristics
treat precocious puberty in boys, to suppress the intial surge effects of goserelin and buserelin. Also can be used to treat acne, hirsutism (excessive hair growth) and virilisation in women, because these are caused by high levels of androgens. Therefore if we block these androgen receptors we stop this occurring.
56
what is benign prostatic hypertrophy
enlargement of the prostate in older men, this pushes on the urethra decreasing its diameter resulting in urinary obstruction
57
treatment for benign prostate hypertrophy
5α-reductase blocker, this inhibits conversion of testosterone to DHT, therefore causes shrinkage of the prostate. Finasteride is better to use here as it inhibits type II 5α-reductase. Dutasteride is less good bc inhibits both type I and II 5α-reductase.
58
risk of an enlarged prostate
can lead to prostate cancer
59
drugs that may be useful in prostate cancer
- Cyproterone acetate - GnRH agonist analogues - 5α-reductase inhibitors - GnRH antagonist analogues - Oestrogens - Anti-androgens
60
use of Cyproterone acetate in prostate cancer
Inhibits peripheral androgen receptors, this can therefore stop the effects of testosterone and DHT on prostatic cells and be used to prevent prostatic hyperplasia or prostatic cancer
61
use of GnRH agonist analogues in prostate cancer
suppress Leydig cell function due to desensitising GnRH receptors, leading to down-regulating of LH/FSH. This can be used to treat and manage prostatic cancer as we are reducing the androgens from stimulating the cancerous cells
62
use of GnRH antagonist analogues in prostate cancer
blocking release of LH/FSH, causing regression of Leydig cells reducing testosterone
63
use of oestrogens in prostate cancer
competes (competitive antagonist) with testosterone and DHT for their receptor and thus blocks their action. It is useful for prostatic cancer
64
use of 5α-reductase inhibitors in prostate cancer
stop production of DHT, that suppress prostate cancer cells. They also inhibit androgen-dependent prostatic cancers.
65
treatment of erectile dysfunction
exogenous androgens may produce clinical improvements in the signs of hypogonadism, but they may not improve sexual function. Therefore other drugs are needed
66
use of PDE5 inhibitors in erectile dysfunction
NO released during sexual stimulation, NO activates guanylate cyclase that converts GTP to cGMP. - > cGMP then causes relaxation of smooth muscle lining of blood vessels allowing them to dilate and allow inflow of blood - > Sildenafil inhibits PDE5 so cGMP is around for longer
67
mechanism of PDE5
potent and highly selective inhibitor of PDE5 and prolongs cGMP mediated smooth muscle relaxation leading to erection. By PDE5 being inhibited it stops the breakdown of cGMP so cGMP effects are prolonged and erection is sustained. Arousal/stimulation is important in its mode of action, because stimulation is needed to get the cycle going, i.e. to get cGMP to be made in the first place

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