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28 Cards in this Set

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  • Back
Leydig cells produce what hormone? This hormone has what effect on germ cels?
LH binds LH receptors on Leydig cells that convert cAMP to testosterone (via cholesterol and pregnenolone)
In the seminiferous tubules, what is testosterone bound to?
Bound to ABG.
What can happen to testosterone in periphery?
Can be converted to DHT via 5a-reductase.

Can be converted to estradiol via aromatase (c19 --> c18)
What do Sertoli cells do?
1) Form tight junctions that are called blood-testes barrier.

2) Sertoli cells respond to FSH and are support cells for maturation of spermatogonia.

3) Also secretes inhibin, a feedback regulator

4) FSH --> ABP and aromatase (to estradiol) synthesis.
At what level of the HPA axis does inhibin work?
Inhibin acts by negative feedback on anterior pituitary and hypothalamus.
Hormones from Leydig cells inhibit where?
Estradiol from testosterone negatively feedbacks on A.P.

Testosterone itself negatively feedbacks on Hypothalamus.
What are the layers of testes from skin to testes?
Skin --> Dartos --> Tunica vaginalis --> Tunica albuginea --> Tunica vascularis --> Seminiferous tubules.
What is the relevance of the blood-testes barrier?
Keeps spermatogonia from being exposed to immune system. Pass barrier as primary spermatocytes...then they can be exposed.
Will you see more primary spermatocytes or secondary spermatocytes in histological stains?
You will RARELY see secondary spermatocytes. MAJORITY will be primary because MOST TIME DURING SPERMIOGENESIS is spent in PRIMARY phase.
How long is spermiogenesis
64 days.
What is the energy source added to sperm in the seminal vesicle?
FRUCTOSE
What are two things mentioned about cystic fibrosis patients in terms of infertility?
No fructose added to sperm and ABSENCE of seminiferous tubules.
What is the minimum requirements for a normal semen analysis?
10-20 million/mL.

40% motility (must have FORWARD motility)

40-60% show normal morphology.

Semen must coagulate first, then liquefy.

Approximately 2-5 mL.
What is Kallman's syndrome?
Migration problems of GnRH neurons from olfactory placode.

Patients have difficulty smelling.

Patients will have not have GnRH release.
What effect does hyperprolactemia have on GnRH secretions?
Prolaction DOWNREGULATES GnRH secretions.
Do ANDROGEN or ESTROGEN excess cause problems with testicular development?
YES!

Estrogen negatively feedbacks at Anterior Pituitary

Androgen feedbacks at hypothalamus. BOTH BAD!

Increases in testosterone can also lead to precocious puberty and premature secondary sex characteristics (increase in DHT too)
How many twists do you need to cause hemorrhagic infarct in torsion of testes?
2.5 twists for 12 hours.
Cryptorchidism can lead to what two abnormalities?
Infertility (germ cells not at ideal temperature) AND neoplasms
What are some causes of testicular damage?
Toxins, drugs, alcohol use. Diabetes.
What are causes of post-testicular infertility?
Ductal obstruction secondary to STD (gonorrhea/chlam). Epididimytis.

Ejaculatory dysfunction (neuropathy, prostatectomy with nerve damage)
What are the TWO TYPES of testicular cancer?
Seminomas and NON-seminomas
What is the morphology of a seminoma?

Hallmark histological feature?
Homogenous, tan colored mass.

NO NECROSIS/HEMORRHAGE

Fried eggs. Retraction of cell.
What is the morphology of a NON-seminoma?
Necrosis and hemorrhage.

Combination of solid and cystic.
What are the TWO tumor markers you test for in a NON-seminona.
AFP (produced by yolk sac tumors) and hCG produced by CHORIOcarcinoma.

NON-seminiferous tumors included yolk sac (AFP) and CHORIOcarcinoma (hCG) and embryonal carcinoma, and IMMATURE and MATURE carcinomas
What is the difference between a mature and immature carcinoma?
Mature teratoma shows cells that have differentiated into other tissue types.

Immature teratomas have immature cell types, no differentiation.
Metastases above/below the diaphragm make up the cutoff between what two stages of germ cell tumors?
II and III.
Do testes atrophy? Do Leydig cells decrease in number with age?
Yes! yes!
What is cortical adrenal hyperplasia?
1) ACTH drives production of cortisol.

2) There is a key enzyme that has been MUTATED (21-hydroxylase). 17a-OH-progesterone build-up can be converted INSTEAD to Androstenedione --> Testosterone.

Leads to precocious puberty, premature development of male characteristics.

SIMILAR SYMPTOMS with thyroid dysfunction.