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SF4 - Test 3 > 2 - Male Reproductive System > Flashcards

2 - Male Reproductive System Flashcards

1
Q

Where does Spermatogenesis (sperm production) occur?

When does this process begin?

What occurs in Leydig Cells?

A

Spermatogenesis ocurs within the seminiferous tubules

Begins at puberty

Steroid Hormon Synthesis occurs in the Leydig Cells

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2
Q

What is the major hormone produced in the testes?

Where is estradiol made in males?

A

Major hormone produced by the testes in testosterone

Majority of estradiol in males in made in adipose tissue from testosterone

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3
Q

What is the source of bioavailable testosterone?

A

Albumin-bound testosterone readily dissociates from albumin

and is taken up by tissues along with free testosterone

These two sources of testosterone are bioavailable

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4
Q

What receptor regulates androgen synthesis?

What type of receptor is it? What pathways does it activate?

What gene transcription is increased?

A

LH Receptor

G protein-coupled receptor; Activates Adenylyl Cyclase/cAMP signaling

Genes of steroidgenesis: StAR, Side Chain Cleavage Enzyme (P450scc), 17a-Hydroxylase, proteins/enzymes of cholesterol synthesis

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5
Q

What are the two possibilities of testosterone metabolism?

How is DHT formed?

How is estradiol formed?

A

Testosterone can be converted to other biologically active steroids or to excretory metabolites

In androgen-sensitive tissues testosterone can be converted to DHT by 5a-reductase

In some tissues, testosteron is metabolized via Aromatase Enzyme to form estradiol

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6
Q

What can be useful in treating benign postatic hyperplasia or prostate cancer?

What tissues does the aromatization of testosterone occur?

Where does inactivation of testosterone occur?

A

5a-Reductase Inhibitors

In some tissues testosterone is metabolize via aromatase to form estradiol

Tissues: Some CNS nuclei, Leydig/Sertoli Cells, Adipose Tissue

Inactivation of testosterone occurs primarily in liver; conjugated with sulfate/glucuronic for excretion in urine

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7
Q

How does plasma testosterone profile change during lifepsan of normal man?

Neonatal

Puberty

Remainder of life

A
  • Leydig cells differentiate from mesenchymal cells (8-9 wks gestation);
    • primary stimulus hCG
    • Mid-gestation, fetal pituitary gonadotropins affect secretion
  • Testosterone LOW during childhood
  • At puberty, LH promotes androgen biosynthesis in Leydig Cells
  • General age related decline during 40s-50s
    • Age related increase of Steroid Hormone Binding Globulin (SHBG) decreases bioavailable fractio nof testosterone
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8
Q

What type of receptor is the andorgen receptor?

How does affinity compare between testosterone and DHT?

How does DNA binding begin?

A

The androgen receptor is a ligand-activated transcription factor

Androgen receptor binds testosterone and DHT but has greatest affinity for DHT (androstenedione/DHEA have weak effects due to low affinity)

Androgen receptor does not bind to DNA unless hormone is bound to its appropriate binding site on receptor

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9
Q

Androgen Actions at Stages of Development:

Fetus

Puberty

Adult

Protein effects?

Erythropoietin?

A
  • Fetus:
    • Adrogens promote differentiation of male reporductive tract and external genitals
  • Puberty:
    • Androgens promote growth and maturation of reproductive structures
    • Development of male secondary sexual characteristics
    • Enlargement of larynx and thickening of vocal cords (deeper voice)
  • Adult
    • Functional integrity of the reproductive system and regulate spermatogenesis
    • Promote growth of hair and sebaceous glands in both genders + male hair pattern
    • Behavioral effects (aggression / libido)
  • Androgens promote protein anabolism
  • Stimulates erythropoietin; increased hematocrit
    *
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10
Q

How do androgens effect bone growth?

A

Androgens promote bone growth and formation; actions of testosterone may involve its conversion to estradiol

Stimulates GH release

Stimulate pubertal growth spurt

Promotes closure of epiphyseal plate

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11
Q

What are the purpose of Sertoli Cells?

A

Sertoli cells line the basal lamina of the seminiferous tubules; main fx are to transfer nutriets to developing germ cells and creat environent conducive for germ cell differentiation into mature spermatozoa

Nourish, clean up debris, lubricate/move sperms along

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12
Q

What is formed by the tight junction between adjacent Sertoli Cells?

A

These tight junctions between adjacent Sertoli Cells divide the seminiferous tubules into two functional compartments–basal (early sperm) and adluminal (later, mature sperm)

They also form a blood-testis barrier that limits exchange of materials between interstitial fluid and the lumen of the seminiferous tubules–may help prevent auto-antibodies against sperm

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13
Q

What substances are secreted by Sertoli Cells?

A
  • Androgen Binding Protein
  • TGB-B glycoproteins:
    • Anti-Muerian Hormone (AMH)
    • Inhibits
    • Activins
  • Estradiol (E2)
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14
Q

Androgen Binding Protein (ABP)

Secreted?

Action?

Stimulation?

Clinical use?

A
  • Secreted by Sertoli Cells
  • Keeps testosterone levels elevated in the seminiferous tubules and epididymis ( [T]Tubule = 100 x [T]Circulation )
  • Stimulated by: FSH / Testosterone
  • Clinical: [ABP] = Method to assess Sertoli Cell function
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15
Q

Anti-Mullerian Hormone (AMH)

Family?

Action?

Mechanism?

A
  • Family - TGF-B family of growth factors
  • Action - Promotes regression of mullerian ducts in male embryo
  • Mechanism
    • Receptor: Transmembrane Serine-Threonin Kinase (RI / RII)
    • AMH binds RII, RII recruits RI and phosphorylates
    • RI phosphorylates Smad3
    • Smad4 complexes w/Smad3
    • Complex translocates nucleus to regulate genes that promote apoptosis
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16
Q

Inhibins and Activins

Synthesis?

Family?

Actions of Inhibin

A
  • Synthesis: Secretory product of Sertoli Cells
  • Family: TGF-B glycoproteins
  • Actions:
    • Inhibin B = Principle circulating inhibin in males; feedback regulation of FSH secretion
      • ​FSH and Testosterone stimulate Inhibin B
      • Inhibin B blocks GnRH-stimulated FSH release
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17
Q

Estradiol (E2)

Formation?

A

Estradio is formed by aromatization of androgens in response to FSH stimulation

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18
Q

What are the three distinct phases of Spermatogenesis?

A
  1. Mitosis to increase number of spermatogonia
  2. Meiosis to provide haploid spermatids
  3. Spermiogenesis to transform immature spermatids to mature spermatoza
19
Q

What two things does normal spermatogenesis in adults require?

What is the role of GnRH and FSH?

A
  1. Functional Sertoli Cells
  2. Intact Hypothalamic-Pituitary-Gonadal Axis
    - - -

GnRH is delivered in pulsatile fashion; required for appropriate FSH / LH secretion

*FSH action on sertoli cells is necessery for maintenance of normal levels of sperm production

20
Q

In males, what are the only cells to express FSH receptors?

What are the actions of FSH on such cells?

A
  • Sertoli Cells are only cells to express FSH receptors (males)
  • FSH actions on Sertoli Cells:
    • Promotes proliferation / differentiation of Sertoli Cells in immature testes
    • FSH maintains Sertoli Cell function (in absence testicular size decreases and spermatogenesis reduced)
    • Spermatogonia appear to be principle target of FSH action
      • ​Growth Factors / Anti-Apoptic Factors
    • Synthesis / Release of Androgen-Binding Protein
    • Stimulates Inhibin release
21
Q

What type of receptors regulate the actions of FSH on Sertoli Cells?

A

Mediated by G protein-coupled receptors that activate cAMP signaling pathway

22
Q

What is the role of LH in spermatogenesis?

A

LH is required for spermatogenesis

Sertoli Cells do NOT have LH receptors; however it INDIRECTLY affects spermatogenesis by stimulating release of testosterone from Leydig Cells

23
Q

How does testosterone affect spermatogenesis?

A

Testosterone acts as local regulator of spermatogenesis

Low levels of testosteron will result in decreased sperm production

  1. Activates Sertoli Cells to promote spermatogenesis
  2. Tends to work synergistically with FSH

Estradiol also plays role in spermatogenesis

24
Q

Summary of Endocrine Regulation on Spermatogenesis:

Pituitary Gonadotropins: FSH and LH

Testosterone

A
  • FSH - Direct stimulation of Sertoli Cells
  • LH - Indirect via increasing testosterone synthesis by Leydig Cells
  • Testosterone
    • Activates Sertoli Cells
    • Basis for Estradiol
    • Stimulates synthesis of Androgen-Binding Protein
25
Q

What forms the blood-epididymis barrier?

What function to spermatozoa gain while at the epididymis?

Why are the sperm covered with special substances?

What role does testosterone play in this section?

A

The tight epithelium of the epididymis forms the blood-epididymis barrier

Gain unidirectional motility

Spermatazoa coated with substance to block acrosomal reaction (decapacitation)

Testosterone (either blood borne, or entering lumen as T-ABP) plays role in regulation of function

26
Q

What are the gonadotropins?

What type of cell secretes them?

What stimulates their secretion?

What is special about the delivery of said stimulus?

What will occur if this delivery varies? (clinical)

A
  • Gonadotropins - Ant. Pituitary hormones that regulate gametogenesis/steroidogenesis
    • Follicle Stimulating Hormone (FSH)
    • Luteinizing Hormone (LH)
  • FSH / LH secreted by Gonadotropes @ Ant. Pituitary
  • FSH / LH stimulated by GnRH; which is released in secretory bursts–modulated by CNS neurons
  • Continuous exposure of gonadotropes to GnRH will suppress secretory activity (can be clinically manipulated w/”functional castration” to treat prostate cancers)
27
Q

How does the Hypothalamic-Pituitary-Gonadal (HPG) Acid change with age?

Fetal

Neonatal

A
  • Fetal Development
    • Established during 1st trimester
    • Peaks at mid-gestation, declines toward birth due to placental estrogens
    • Low levels of gonadotropin at birth
  • Fetal
    • Short after birth, HPG becomes active again
    • Males - Testosterone secretion begins after rise in LH
    • Females - Estradiol levels fluctuate
    • Elevated levels of gonadotropin for first few months; gradully decline as CNS inhibits HPG axis
28
Q

How does the Hypothalamic-Pituitary-Gonadal (HPG) Acid change with age?

Childhood

Late Prepubertal

Puberty

A
  • Childhood
    • CNS inhibits GnRH pulse generator
    • HPG axis remains quiescent during childhood
  • Late prepubertal
    • Gradual disinhibition of GnRH pulse generation
    • First detectable = Sleep associated surge in LH release
  • Puberty
    • Levels of gonadotropins stay elevated during day
    • Adult pattern of HPG activity is established
29
Q

What are the major events associated with puberty?

What can affect the timing of puberty?

A
  • Establishment of adult HPG activity pattern
  • Maturation of reproductive system and development of secondary sexual characteristics
  • Growth spurt
  • Development of gametes capable of fertilization
  • Timing of Puberty
    • Affected by genetics, ethnicity, environmental cues (nutrition, weight gain)
    • Leptin connects nutrition to change timing
30
Q

What are the negative feedback effects of testosterone?

A

Testosterone inhibits the hypothalamic pulse generator

Causes reduction of GnRH pulse frequency, lowers ratio of LH / FSH in pituitary secretions

31
Q

What are the feedback regulation mechanisms of Inhibin in males?

A
  • Inhibin secreted by Sertoli Cells
  • FSH / Testosterone increase production of Inhibin
  • Inhibin INHIBITS FSH release
  • Little effect on LH release
32
Q

Explain the physiology of the penis with regards to the erectile response?

Flaccid State

A

Tissue organized into a single corpus spongiosum, and two corpora cavernosa

Corpus Cavernosa surrounded by Tunica Albuginea; blood flow is supplied by helicine arteries

In FLACCID STATE blood flow is minimal because these vessels are constricted

33
Q

Explain the physiology of the penis with regards to the erectile response?

Erection State

A
  • Erectile State mediated by tactile (lower motor neuron reflex) or psychic (mediated over corticospinal pathways) stimuli
  • Arterial flow increased into cavernous spaces; parasympathetics relax smooth muscle of helicine arteries
  • Venous efflux reduced due to compression of subtunical venous plexus against wall of tunica albuginea
34
Q

Explain the physiology of the penis with regards to the erectile response?

Where is the response a reflex mechanism of? Nerve?

What is effect of parasympathetics? What do they release?

A
  • Reflex mechanism integrated in sacral portion of spinal cord (S2-S4)
    • Afferent tactile stimuli transmitted via pudendal nerve
  • Efferent Parasympathetic Fibers (cavernous nerve) to helicine arteries are vasodilatory
    • ​Release Nitric Oxide (NO) / Vasoactive Intestinal Peptide (VIP)
    • Cause relaxation of helicine arteries and smooth muscle fibers in sinusoids
35
Q

Explain the physiology of the penis with regards to the erectile response?

What does NO bind to? Action?

What can be a treatment for erectile dysfunction?

What can be a cause of erectile dysfunction?

A

NO binds to and activates soluble form of guanylyl cyclase, rise in cGMP leads to smooth muscle relaxation/dilation

cGMP-phosphodiesterase Inhibitors (Viagra) can be used to treat erectile dysfunction

Alterations in NO formation can result in impaired smooth muscle relaxation and ED

36
Q

What is the role of urethral and bulbourethral glands during sexual stimulation?

What mediates this?

A

Increased mucus secretion

Mediated by parasympathetic nerves

37
Q

Explain emission during sexual intercourse

What mediates emission? Nerve? Neurotransmitter?

What prevents retrograde ejaculation?

A

Emission is movement of semen into proximal part of urethra

Emission is mediated by Sympathetic Neurons in upper lumbar region (L1-L2); signals reach via hypogastric nerve; Norepinephrine acts on a1-adrenrgic receptors

Sympathetic Signals promote constriction of urethral sphincter to prevent retrograde ejaculation into bladder

38
Q

Explain the ejaculatory response.

Initiation?

Efferent signals? Nerve? Key muscles?

Male orgasm?

A
  • Filling the urethra with semen elicits sensory signals that are transmitted to the sacral portion of the spinal cord by pudendal nerve
  • Efferent Signals, transmitted by somatic efferent fibers in pudendal nerve, trigger contraction of striated musculature of perineum
    • ​Especially bulbocavernous muscle
  • Wavelike Contractions propel semen
  • Awareness of these contractions = male orgasm
39
Q

What are three clinical manifestations of testicular dysfunction?

A

Infertility

Decreased Libido

Poor development of Secondary Sexual Characteristics

40
Q

Clinical: Gynecomastia

A

Estrogens have a stimulatory effect on growth/differentiation of breast tissue; testosterone inhibits this

Males - Exposure to excessive estrogen (or estrogen-like) compounds can decrease testosterone production

Other Causes: Prolactin, anti-androgens, medicinal (spirolactone, ketoconazole, cimetididne) and marijuana

41
Q

Primary Hypogonadism - Primary Testicular Failure

Clinical - Klinefelter Syndrome

Common Karyotype

Internal Structure Dysfunction

Phenotype

Hormonal Lab Findings

A
  • Most common cause of hypogonadism
  • Caused by Excessive X Chromosome
    • ​Most common = XXY
  • Testes small/firm
  • Seminiferous Tubules = fibrotic/hylanized
    • ​Usually infertile
  • Degress of Leydig Function = Variable
  • Phenotype
    • Male, but signs of androgen deficiency / Estrogen Excess; Gyneocomastia common
  • Lab Findings
    • ​High FSH / LH
    • Low Testosterone
    • High Estradiol
42
Q

Primary Hypogonadism - Primary Testicular Failure

Orchitis

Irradiation

A

Inflammation of testes; usually secondary to mumps

Seminiferous Tubule destruction

Leydig Cells usually not affected

Seminiferous tubules more sensitive to radiation; Leydig Cells more resistant

43
Q

Secondary Hypogonadism - Impaired Gonadotropin Secretion

Hypopituitarism

Kallmann Syndrome

A

May result from destruction of pituitary by tumor, trauma, surgery, irradiation

Deficient production of GnRH by hypothalamus

Second most common reproductive disorder in mlales

Testes = Arrested spermatogenesis, low gonadotropins, androgen deficiency appears at puberty, often associated with defective sense of smell

44
Q
A

SF4 - Test 3 (12 decks)

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