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Physl Part 2 > Repro Physl 4 > Flashcards

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
Why don't the testes produce a lot of testosterone before puberty?
There is strong suppression of GnRH and gonadotropin release
26
What is a theory to what puberty occurs?
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
What are the secondary sex characteristics of males dependant on?
Testosterone and DHT
28
What do the secondary sex characteristics do?
* Include growth of the larynx, thick secretion of skin and oil glands * Masculine fat distribution
29
How do androgens stimulate bone growth?
By stimulating GH secretion
30
Why can androgens be considered anabolic steroids?
Because they have a stimulatory effect for protein synthesis in muscle
31
Why do males have an increased hematocrit?
Because androgens stimulate erythropoietin from the kidneys
32
What are the positives to anabolic steroid use?
Increased muscle mass and athletic performance
33
What are the negative effects of anabolic steroids?
* Overstimulation of the prostate * Aggression * Decreased GnRH, LH and FSH
34
Why don't anabolic steroid increase sperm production?
Because they cannot cross the blood-testis barrier and access the Sertoli cells
35
What is Hypogonadism?
The reduction of testosterone release from the testes
36
What is Primary hypogonadism related to?
Testicular failure
37
What is Secondary hypogonadism related to?
Failure to supply testes with gonadotrophic stimulus. So this is a problem with either the pituitary or the hypothalamus
38
What are the gonadotropin levels in primary hypogonadism?
There is sufficient gonadotropin levels
39
What are the gonadotropin levels in secondary hypogonadism?
There is low gonadotropin levels. So low LH, FSH and testosterone
40
What is the most common genetic cause of primary hypogonadism?
Klinefelter's syndrome
41
What is the genotype of Klinefelter syndrome?
XXY
42
What is the appearance of people with Klinefelters syndrome?
They have small poorly developed testes and long arm span
43
How are Leydig and Sertoli cells affected by Klinefleter's syndrome?
There is insufficient Leydig and Sertoli cell function so no sperm production or development of seminiferous tubules
44
How are secondary sex characteristics affected by Klinefelters?
There is absence of them and an increased breast size
45
Why is there high LH and FSH in Klinefelter's primary hypogonadism?
Because there is a loss of inhibin and negative feedback that would've acted on the hypothalamus and anterior pituitary
46
How are LH and FSH affected by secondary hypogonadism?
Their production is decreased
47
How does Hyperprolactinemia cause secondary hypogonadism?
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
How does Hypopituitarism cause secondary hypogonadism?
A loss of anterior pituitary gland function
49
What would happen if the testes are removed after puberty?
They would still have secondary sex characteristics but they would have atrophy of androgen-sensitive tissue
50
Why is there a testosterone in andropause?
Because of the deterioration of testosterone levels

Physl Part 2 (96 decks)

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