Repro Physl 4 Flashcards

1
Q

What happens to the vascular in response to sexual excitation?

A

Dilation of the small arteries and engorgement of vascular compartments

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2
Q

What does the engorgement of the vascular compartments do?

A

Causes passive compression of adjacent veins

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3
Q

What causes the contraction in the erect state?

A

Noradrenaline

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4
Q

What causes the relaxation in an erect state?

A

Acetylcholine from parasympathetic nerves

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5
Q

What is the dominant input to the small arteries that supply the penile tissue at rest?

A

Sympathetic

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6
Q

What is the main transmitter being released by sympathetic nerves onto the penile arteries at rest?

A

Norepinephrine from sympathetic nerves

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7
Q

What is the effect of sexual arousal on the inputs to the penis?

A
  • Sympathetic input is inhibited during erection

* Neurons that release nitric oxide increase

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8
Q

What causes the net vasodilation in the net vasodilation in an erection?

A

The decrease of sympathetic stimulation and the release of NO

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9
Q

What are the four primary stimulus for an erection?

A
  • Mechanoreceptors in the head of a penis
  • Increased afferent neural firing
  • Spinal reflex in lower spinal cord
  • Controls efferent neural outflow
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10
Q

What is ejaculation controlled by?

A

Its a spinal reflex controlled by afferent pathways from penile mechanoreceptors

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11
Q

What are the two phases of ejaculation?

A
  • Emission

* Ejaculation

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12
Q

What occurs in emission?

A

Sympathetically mediated contraction of the epididymis, vas deferens, ejaculatory ducts, prostate and seminal vesicles

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13
Q

What occurs in ejaculation?

A

Semen is expelled from the urethra by a rapid contraction of urethral smooth muscle and skeletal muscle at the base of the penis

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14
Q

What part of the NS is emission mediated from?

A

The sympathetic NS which is opposite from erection which inhibits the sympathetic input

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15
Q

What are some treatment options for ED?

A
  • Increasing Nitric Oxide through PDE5 inhibitors

* Prostaglandins

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16
Q

How does NO act in ED?

A

It elicits the release of cGMP which decreases calcium levels which promotes smooth muscle relaxation of the blood vessels which increases blood flow to the penile tissue

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17
Q

What is cGMP which is activated by NO broken down by?

A

PDE5

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18
Q

How do PDE5 inhibitors work?

A

They inhibit PDE5 which inhibits the breakdown of cGMP which can go on to decrease calcium and increase muscle relaxation

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19
Q

How can Prostaglandins help with ED?

A

PGE1 binds to the prostaglandin receptor and through an AC pathway will decrease intracellular calcium and increase vasodilation

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20
Q

What does the prostate convert testosterone to?

A

DHT by 5 alpha-reductase

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21
Q

What converts testosterone to estradiol (estrogen) and by what?

A

Brain, liver, and adipose tissue by aromatase

22
Q

What happens if there is decreased testicular function/testosterone synthesis?

A
  • Accessory organs decrease in size
  • Glands reduce secretion rates
  • Smooth muscle activity ducts is decreases
  • Sex drive, erection and ejaculation impaired
  • Mitigated by testosterone treatment
23
Q

What are the first signs of puberty in males due to?

A

Secretion of adrenal androgens under the influence of ACTH

24
Q

What do the adrenal androgens support during puberty?

A

The development of pubic and axillary hair

25
Q

Why don’t the testes produce a lot of testosterone before puberty?

A

There is strong suppression of GnRH and gonadotropin release

26
Q

What is a theory to what puberty occurs?

A

Kisspeptin neurons in the hypothalamus is upstream of the GnRH containing neurons is activated which leads to an increased GnRH and reduced sensitivity to negative feedback

27
Q

What are the secondary sex characteristics of males dependant on?

A

Testosterone and DHT

28
Q

What do the secondary sex characteristics do?

A
  • Include growth of the larynx, thick secretion of skin and oil glands
  • Masculine fat distribution
29
Q

How do androgens stimulate bone growth?

A

By stimulating GH secretion

30
Q

Why can androgens be considered anabolic steroids?

A

Because they have a stimulatory effect for protein synthesis in muscle

31
Q

Why do males have an increased hematocrit?

A

Because androgens stimulate erythropoietin from the kidneys

32
Q

What are the positives to anabolic steroid use?

A

Increased muscle mass and athletic performance

33
Q

What are the negative effects of anabolic steroids?

A
  • Overstimulation of the prostate
  • Aggression
  • Decreased GnRH, LH and FSH
34
Q

Why don’t anabolic steroid increase sperm production?

A

Because they cannot cross the blood-testis barrier and access the Sertoli cells

35
Q

What is Hypogonadism?

A

The reduction of testosterone release from the testes

36
Q

What is Primary hypogonadism related to?

A

Testicular failure

37
Q

What is Secondary hypogonadism related to?

A

Failure to supply testes with gonadotrophic stimulus. So this is a problem with either the pituitary or the hypothalamus

38
Q

What are the gonadotropin levels in primary hypogonadism?

A

There is sufficient gonadotropin levels

39
Q

What are the gonadotropin levels in secondary hypogonadism?

A

There is low gonadotropin levels. So low LH, FSH and testosterone

40
Q

What is the most common genetic cause of primary hypogonadism?

A

Klinefelter’s syndrome

41
Q

What is the genotype of Klinefelter syndrome?

A

XXY

42
Q

What is the appearance of people with Klinefelters syndrome?

A

They have small poorly developed testes and long arm span

43
Q

How are Leydig and Sertoli cells affected by Klinefleter’s syndrome?

A

There is insufficient Leydig and Sertoli cell function so no sperm production or development of seminiferous tubules

44
Q

How are secondary sex characteristics affected by Klinefelters?

A

There is absence of them and an increased breast size

45
Q

Why is there high LH and FSH in Klinefelter’s primary hypogonadism?

A

Because there is a loss of inhibin and negative feedback that would’ve acted on the hypothalamus and anterior pituitary

46
Q

How are LH and FSH affected by secondary hypogonadism?

A

Their production is decreased

47
Q

How does Hyperprolactinemia cause secondary hypogonadism?

A

Pituitary cells release prolactin and excessive production can cause high levels of prolactin which has strong negative feedback effect on gonadotropin release from the anterior pituitary

48
Q

How does Hypopituitarism cause secondary hypogonadism?

A

A loss of anterior pituitary gland function

49
Q

What would happen if the testes are removed after puberty?

A

They would still have secondary sex characteristics but they would have atrophy of androgen-sensitive tissue

50
Q

Why is there a testosterone in andropause?

A

Because of the deterioration of testosterone levels