Male Reproductive System (McCumbee and Richardson) Flashcards

1
Q

Kartagener Syndrome

A

Pts. have immotile cilia and are infertile

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2
Q

Spermatogonial proliferation

A

Spermatogonia divide mitotically to renew stem cells and expand the differentiating spermatogonia

*Differentiating spermatogonia undergo incomplete cytokinesis leaving intracellular bridges for the transport of molecules b/w cells

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3
Q

Spermatogonial meiosis

A

During prophase, homologous chromosomes pair and are held together by the synaptonemal complex which facilitates recombination; remnant of this is the chiasmata

First division => Homologous pairs separate (2C); is now a secondary spermatocyte

Second division => Sister chromatids separate (1C); are now four haploid spermatids

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4
Q

Spermiogenesis (Spermy-spermy-grow-grow)

A
  1. Chromatin is inactivated via condensation by protamines; replaces the Histones in chromatin
  2. Excess cytoplasm is collected into the residual body and digested by Sertoli cells
  3. Acrosome cap is formed and contains hyaluronidase, acrosin, neuraminidase, and acid phosphates
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5
Q

Phases of acrosomal cap formation

A
  1. Golgi- Pro-acrosomal granules bud from the Golgi complex and fuse to the anterior membrane
  2. Cap & Acrosomal- Vesicle spreads over surface
  3. Maturation- Assumes characteristic shape
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6
Q

Flagellum Formation

A

Part of spermy-spermy-grow-grow that involves the migration of centrioles near the membrane and are arranged in a 9+2 arrangement

*Occurs @ same time as acrosomal cap formation

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7
Q

Factors that impair spermy-spermy-grow-grow

A

Irradiation

Excess steroid hormones

Elevated temperature

Vitamin A deficiency

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8
Q

Ducts

A

Intratesticular: Tubuli recti and rete testis

Extratesticular: Efferent ducts, epididymis, vas deferens, urethra

*Sperm gain motility during storage in the epididymis

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9
Q

Sperm cycle stages

A

One cycle= Amount off time to make it thru all 6 stages
*16 days

Maturation of Sperm= 4 cycles X 16 days = 64 days

*Are developed asynchronously along the tubule to release sperm continuously

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10
Q

Structure of Sperm

A

Head- Contains haploid nucleus and acrosomal cap

Mid-piece- Contains axoneme, mitochondrial sheath, and outer dense fibers

Principal piece- Contains axoneme, outer dense fibers, and fibrous sheath

End piece- Contains ONLY axoneme

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11
Q

Bioavailable testosterone

A

Free testosterone+ Testosterone-albumin

-Is only weakly bound to albumin

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12
Q

LH Receptor

A

Stimulation causes increased cAMP

=> Increased StAR, Increased P450cc, and Increased 17a-hyrdoxylase

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13
Q

5a-reductase inhibitors

A

Used to treat prostatic cancer

*Enzyme normally forms the metabolically hyperactive dihydrotestosterone

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14
Q

Aromatase in males

A

Primarily found in adipose, CNS nuclei, and some Leydig/Sertoli cells

*Converts testosterone to estradiol

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15
Q

Primary stimulus for Leydig cell development

A

hCG

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16
Q

Testosterone/Sperm production in male lifespan

A

Neonate- High

Childhood- Random surge but normally low

Adolescence- Increasing

Adult- Highest

Elder- Steady decrease
*Also a steady increase in SHBG

17
Q

Androgen actions in the adult

A
  • Promote vocal cord thickening (deeper voice)
  • Promote EPO secretion (increased Hcrt)
  • Promote bone growth and resorption (also closure of epiphyseal plate)
  • Promote hair growth
  • Promote protein anabolism
18
Q

Blood-testis barrier

A

Formed by tight jnxns b/w Sertoli cells; prevents the development of autoantibodies against sperm

*Are connected to developing germ cells via gap jnxns

19
Q

ABP

A

Secreted by Sertoli cells when stimulated by FSH or testosterone; helps to keep testosterone levels elevated in the seminiferous tubules

20
Q

AMH receptor mechanism

A

Two threonine kinase receptors will dimerize after AMH binding and phosphorylate Smad 3

=> NLS is activated and Smad3 combines w/ Smad4 when it enters the nucleus and activates transcription of genes promoting apoptosis

21
Q

Inhibin B

A

Blocks GnRH stimulated release of FSH @ the gonadotrope (adenohypophysis)

  • Production is stimulated by FSH and testosterone to provide negative feedback
  • Has NO EFFECT on LH release
22
Q

Endocrine regulation of spermatogenesis

A

Pituitary: FSH => Increased Sertoli fnxn (growth factors for sperm, ABP, Inhibins)
LH => Produce testosterone to assist Sertoli fnxn

  • Testosterone will activate genes, produce some estradiol, and promote ABP production
  • Intact hypothalamic-pituitary-gonadal system required for all of this
23
Q

Events in epididymis

A

Sperm become motile and are decapacitated

*Spend a month here

24
Q

GnRH secretion

A

Must be in a pulsatile fashion to promote spermy-spermy-grow-grow

*Continuous release results in a fnxnal castration

25
Q

HPG axis control

A

Pre-pubescent: Under CNS inhibition

Puberty: Increased LH surges @ night
Decreased negative feedback inhibition of testosterone
Increased GnRH pulses and increased sensitivity
=>Increased FSH and LH

26
Q

Helicine Arteries

A

Supply the cavernous spaces of the penis; are constricted in the flaccid state

27
Q

Erectile Response

A

Lower tactile stimulus or psychic stimulation leads to the release of NO and VIP; occurs via the pudendal or corticospinal tract respectively

=> Dilation of helicine arteries increases blood flow and compressed the venous outflow

28
Q

Viagra action

A

Acts on PDE5 which breaks down cGMP

*cGMP is formed by guanylyl cyclase and promotes vasodilation and boners

29
Q

Emission

A

Sympathetic neurons reach the accessory glands via the hypogastric nerve and release NER on a2-drenergic receptors

=> rhythmic contractions of smooth muscle to move semen

*Also prevents retrograde movement into the bladder by closing the internal urethral sphincter

30
Q

Ejaculation

A

Filling of the urethra sends afferent signals via the pudendal nerve which responds w/ wavelike contractions of the bulbospongiosus to eject the load

31
Q

Gynecomastia

A

Estrogens stimulate the growth of the female breasts (prior to growth there is no difference); could also occur w/ exposure to excess PRL

32
Q

Kallman’s Syndrome

A

A type of tertiary hypogonadism caused by deficient production of GnRH

  • testes will have arrested spermy-spermy-grow-grow and androgen deficiencies (decreased muscles, pubic hair, high-pitched voice, infantile genitali)
  • Caused by a failure of the GnRH secreting cells to migrate from the olfactory placode => Anosmia
33
Q

TGF-B Family

A

“Transforming Growth Factor”

Includes Inhibins, activins, and AMH; all secreted by Sertoli cells

34
Q

Treatment of Klinefelter’s

A

Androgen replacement therapy can restore some secondary sexual characteristics and reverse gynecomastia but cannot induce spermatogenesis

-Due to hyalinization of the seminiferous tubules