Final Exam (Lecture 58) - Male Reproduction Flashcards

1
Q

What is the difference between musculovascular and fibroelastic penises?

A

Musculovascular:
- Enlarges in length and diameter during tumescence

Fibroelastic:
- Sigmoidal shaped that extends only in length during tumescence

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2
Q

What is the urethral process, what is its function, and why can it be problematic?

A

Urethral process is an extension of the urethra that extends beyond the length of the penis in the ram and buck

Mechanism to propel sperm deeper into the female reproductive tract

Can be problematic because it is a site for uroliths to get trapped

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3
Q

What are the corpus cavernosum and spongiosum?

A

1) Corpus cavernosum:
- Erectile tissue of the penis

2) Corpus spongiosum:
- Spongy area that surrounds the urethra and prevents occlusion of the urethra during tumescence

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4
Q

Describe the biochemical and vascular basis for tumescence and detumescence.

A

The flaccid penis becomes tumescent via the corpus cavernosum.
- Nitric oxide (released by the parasympathetic system) causes helicine artery dilation allowing blood to
move through loosened inter-endothelial junctions

  - The NO causes the vasodilation by relaxing the vascular smooth muscle (VSM) of the helicine (central)
     arteries in the corpus cavernosum

  - The blood fills the corpus cavernosum causing turgor pressure that causes tumescence 

  - NO is released by NANC (non-adrenergic/non-cholinergic) neurons and activates guanylate cyclase which
    converts GTP to cGMP
         - cGMP inactivates myosin light chain kinase (MLCK) in VSM cells
         - Phosphodiesterase 5 (PDE5) recycles cGMP to GMP, thus halting tumescence by returning the VSM to
           the contracted state (restoration of sympathetic tone via norepinephrine)
         - VSM relaxation allows for the extravasation of blood from the helicine artery into corpus cavernosum
         - Blood cells "trickle" between the endothelial cells and the VSM cells
         - Upon VSM contraction, veins drain the blood from the corpus cavernosum as part of detumescence
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5
Q

Describe the autonomic components of tumescence, detumescence, and ejaculation.

A

Tumescence:
- parasympathetic

Detumescence:
- sympathetic

Ejaculation:
- sympathetic

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6
Q

Name the hypothalamic peptide that is the central regulator of male reproductive physiology.

A

GnRH

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7
Q

What are the two anterior pituitary hormones that regulate male reproductive physiology, and what are their functions?

A

Prolactin and LH

Prolactin:
- Stimulates the synthesis of LH receptors on the Leydig cells

LH:
- Released into systemic circulation and reaches the Leydig cells that have an abundance of LH receptors
- Activation of the LH receptors leads to the synthesis of testosterone by the Leydig cells

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8
Q

What is the negative regulator of male reproductive physiologic hormones, where does it come from, and how does it work?

A

Inhibin
- Produced by Sertoli cells
- Travels to the brain where it prevents the release of FSH and GnRH
- Inhibin activates its receptor that promotes the synthesis of proteins that trap FSH in the AP cells or GnRH
in the hypothalamus

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9
Q

Why does testosterone interact with an intracellular receptor while the other hormones (LH, FSH, GnRH, prolactin, and inhibin) interact with receptors that extend outside of the cell?

A

Testosterone is lipid-soluble, so it can cross biologic membranes and interact with its intracellular receptor.

The other hormones are not lipid-soluble so they cannot freely cross biologic membranes and must interact with receptors on the outside of the cell.

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10
Q

What is the os penis and the bulbus glandis?

A

Os penis:
- Penis bone (baculum)
- Helps to maintain tumescence in species in which coitus is protracted (dogs, cats, non-human primates)

Bulbus glandis:
- Tissue that enlarges during coitus
- Helps to maintain the interaction with the female (the “tie”)

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11
Q

Why is cancer a side effect of anabolic steroids that mimic testosterone?

A

Anabolic steroids up regulate specific gene expression of genes that encode for proteins that promote cell growth, cell division, and hyperplasia.

Excessive cell growth/division = cancer

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