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Reproductive System I > Male Reproductive Physiology Lecture (Dr. Lopez) > Flashcards

Male Reproductive Physiology Lecture (Dr. Lopez) Flashcards

1
Q

Before getting started: Sex vs. gender; Definitions

A

β€’ SEX: refers to a person’s biological status (male, female, or intersex)
– Indicators of biological sex includes: sex chromosomes, gonads, internal reproductive organs, & external genitalia

β€’ GENDER: refers to the attitudes, feelings, & behaviors that a given culture associates with a person’s biological sex
– Gender-normative: Behavior that is compaRble with cultural expectaRons
– Gender nonconformity: refers to the attitudes, feelings, and behaviors that a given culture associates with a person’s biological sex

β€’ GENDER IDENTITY: refers to β€œone’s sense of oneself as male, female, or transgender” (American Psychological AssociaRon, 2006)
– When one’s gender identity & biological sex are not congruent, the individual may identify as transsexual or as another transgender category (cf. Gainor, 2000)

  • GENDER EXPRESSION: β€œβ€¦way in which a person acts to communicate gender within a given culture…”
  • SEXUAL ORIENTATION: refers to the sex of those to whom one is sexually and romantically attracted
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2
Q

Before getting started: Sex; some definitions cont

A

β€’ GENETIC SEX: determined by the sex chromosome (XX – female; XY – male)
– During the first 5 weeks of gestational life, the gonads are bipotenRal (neither male or female)
– Gestational weeks 6 – 7 the testes begin to develop in genetic males
– Gestational week 9 the ovaries begin to develop in geneRc females

β€’ GONADAL SEX: testes or ovaries

β€’ PHENOTYPIC SEX: Physical characteristics of the internal genital tract & the external genitalia
– Determined by the hormonal output of the gonads

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3
Q

Puberty in males & females is initiated by the pulsatile secretion of GnRH, which drive the pulsatile secretion of FSH & LH

A

β€’ PUBERTY:
– One of the earliest event is the appearance of large
nocturnal pulses of LH during REM sleep

– Pulsatile secretion of FSH & LH stimulates secretion of gonadal steroid hormones, Testosterone, & Estradiol
β€’ INCREASE Circulating levels of the sex steroid hormones are then responsible for the appearance of the secondary sex characteristics at puberty

– If a GnRH analogue is administered in INTERMITTENT PULSES to replicate the normal pulsatile secretion, PUBERTY is INITIATED & reproductive function is established

– If a LONG-ACTING GnRH analogue is administered, PUBERTY is NOT INITIATED

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4
Q

Puberty in males & females is initiated by the pulsatile secretion of GnRH, which drive the pulsatile secretion of FSH & LH CONT

A

– The CNS & nutritional status may alter the onset of puberty
β€’ Extreme STRESS or CALORIC DEPRIVATION in girls DELAYS the Onset of Puberty

β€’ MELATONIN may be a natural INHIBITOR of GnRH Release
– Secreted by the Pineal Gland
– May be a Natural INHIBITOR of GnRH release
Β» Melatonin levels are HIGHEST during Childhood & DECLINE in Adulthood
β€’ DECLINE might release an INHIBITION of GnRH secretion

Β» Removal of the Pineal gland precipitates EARLY Puberty

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5
Q

Anatomy of the Male Reproductive Tract

A
  • TESTES: two main functions are SPERMATOGENESIS & SECRETION of TESTOSTERONE
  • SCROTUM: its lower temperature is essential for spermatogenesis (1 Β° or 2 Β°C below body temperature )
  • EPIDIDYMIS: primary location for the maturation & storage of sperm

β€’ VAS DEFERENS:
– Provides another storage area for sperm (AMPULLA)
– Secretes fluid rich in CITRATE & FRUCTOSE

  • SEMINAL VESICLES: Secretes fluid rich in CITRATE, FRUCTOSE, PROSTAGLANDINS, & FIBRINOGEN
  • PROSTATE GLAND: Secretes MILKY AQUEOUS SOLUTION. rich in Citrate, Calcium & Enzymes
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6
Q

Anatomy of the Male Reproductive Tract CONT

A

β€’ The SEMINIFEROUS TUBULE: Epithelium formed by the SERTOLI Cells, with interspersed germ cells
– SPERMATOGONIA: most IMMATURE germ cells, located near the PERIPHERY of the tubule

– SPERMATOZOA: MATURE Germ cells, located near the LUMEN of the Tubule

β€’ LEYDIG CELLS: interstitial cells that lie BETWEEN the Tubules

*** Adult testis: 80% SEMINIFEROUS TUBULES & 20% CONNECTIVE TISSUE interdispersed with Leydig cells!

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7
Q

General functions of Sertoli & Leydig cells

A

1) SERTOLI CELLS:
– Provide nutrients to the
differentiating sperm

– Form Tight junctions with each other, creating a barrier between testes & bloodstream
β€’ BLOOD-TESTIS BARRIER: imparts selective Permeability
a) Admits certain substances to cross (e.g. testosterone) but prohibits noxious substances

– Secrete an Aqueous Fluid into the lumen of the seminiferous tubules
a) Helps to TRANSPORT Sperm through the tubules into the epididymis

2) LEYDIG CELLS:
– Synthesis & Secretion of Testosterone

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8
Q

Testes secrete several Male Sex Hormones

A
  • Androgens secreted by the testes include: Testosterone, Dihydrotestosterone, & Androstenedione
  • Testosterone is the MOST ABUNDANT
  • However, in Target Tissues, much of the testosterone is eventually converted into the MORE ACTIVE hormone Dihydrotestosterone
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9
Q

Leydig cells & Steroidogenesis

A

β€’ In the testis, the main steroidogenic cells are the LEYDIG Cells

β€’ Two distinct populations of Leydig cells that arise during development: FETAL & ADULT Leydig cells
– FETAL Leydig cells are responsible for MASCULINIZING the Male Urogenital tract & INDUCING testis descent
a) These cells ATROPHY shortly after BIRTH & DO NOT contribute to the Adult Leydig cell population

– ADULT Leydig cells derive from undifferentiated precursors present after birth & become FULLY Steroidogenic AT Puberty

– The differentiation of BOTH Leydig cell populations is Controlled by Locally PRODUCED Paracrine Factors & by Endocrine Hormones

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10
Q

Leydig cells & Steroidogenesis CONT

A

1) Leydig cells Synthesize CHOLESTEROL DE NOVO
– They can also acquire cholesterol from the circulation, through Low-Density Lipoprotein (LDL) receptors &, to a lesser extent, through High-Density Lipoprotein (HDL) receptors

2) Leydig cells STORE Cholesterol as CHOLESTEROL ESTERASE
– FREE cholesterol is generated within the Testis, particularly in Leydig cells, by a Cholesterol Hormone-Sensitive Lipase (HSL)
a) HSL converts CHOLESTEROL ESTERS to FREE Cholesterol for androgen production

– Cholesterol is then transferred within the mitochondrial membranes via the Steroidogenic Acute Regulatory Protein (StAR)

3) In Leydig cells, Cholesterol is converted to PREGNENOLONE

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11
Q

Testosterone (T)

A
  • MAJOR Androgenic Hormone
  • Synthesized & Secreted by the Leydig cells of the Testes

β€’ The Testes LACK 21 Ξ²-HYDROXYLASE & 11 Ξ²-HYDROXYLASE
– NO Glucocorticoids or MineralocorRcoids are synthesized

β€’ The Testes have an additional enzyme: 17Ξ²-HYDROXYLSTEROID DEHYDROGENASE
– Converts ANDROSTENEDIONE to TESTOSTERONE
– End product of steroid synthesis in the testes is Testosterone NOT dehydroepiandrosterone (DHEA) & androstenedione, like in the Adrenal Gland

β€’ In the Lumen of Seminiferous Tubules, Testosterone is concentrated by binding to ANDROGEN BINDING PROTEIN (ABP)

β€’ Testosterone is NOT ACTIVE in all androgenic Target Tissues
– In some Tissues, Dihydrotestosterone (DHT) is the ACTIVE Androgen (E.g.
Prostate Gland in the adult & external genitalia of the male fetus, skin, liver)
– 5Ξ±-REDUCTASE, in Peripheral Tissue, converts Testosterone to Dihydrotestosterone

β€’ Most of the circulating Testosterone is bound to Plasma Proteins & Albumin
– SEX HORMONE BINDING GLOBULIN (SHBG)

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12
Q

Production of Estrogen in the Male

A
  • In addition to Testosterone, small amounts of Estrogens are formed in the male
  • Exact source of Estrogen is UNKNOWN

β€’ In the fluid of the Seminiferous tubules, the [Estrogens] is quite HIGH
– The source of this estrogen might be the Sertoli cells & might be the product of the CONVERSION of Testosterone to Estradiol, mediated by AROMATASE

– Potential IMPORTANT role in Spermatogenesis
a) Human Sperm cells express at least one isoform of the ESTROGEN RECEPTOR (ER)

β€’ Much larger amounts of Estrogens are formed from Testosterone & Androstanediol in other Tissues of the body, especially the liver
– Accounts for as much as 80% of total male estrogen PRODUCTION!!!!!!!!

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13
Q

Biosynthetic Pathway o Androgens

A

1) MITOCHONDRIAL PATHWAY FOR TESTOSTERONE SYNTHESIS: Cytochrome P450 side-chain cleavage (P450SCC) enzyme removes the side-chain (carbons 22 to 27) from the carbon at position 20 of cholesterol
2) RATE LIMITING STEP IN SYNTHESIS OF TESTOSTERONE: Conversion of CHOLESTEROL to PREGNOLONE

*****An important RATE LIMITING step is mediated by the Steroidogenic Acute Regulatory Protein (StAR)
Β­ - Transfers CHOLESTEROL from Inner to Outer Mitochondrial membrane

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14
Q

Synthesis and Secretion of Testosterone occurs in Leydig Cells

A

β€’ Leydig cell is the PRIMARY Endocrine cell of the Testis
– Located in the PERITUBULAR Compartment

β€’ Testosterone diffuses BOTH into the Neighboring Seminiferous Tubules & into the Peritubular Capillary network to be carried into the Peripheral circulation
– In Seminiferous Tubules, Testosterone is concentrated by binding to ANDROGEN BINDING PROTEIN (ABP)

– T is carried in the Peripheral Circulation by SEX HORMONE BINDING GLOBULIN (SHBG) & ALBUMIN

β€’ The Leydig cell makes limited amounts of DHT & ESTRADIOL-17Ξ², but considerably MORE of these two steroids is made by PERIPHERAL CONVERSION

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15
Q

LH stimulates the conversion of Cholesterol to Pregnenolone & regulates the OVERALL RATE of Testosterone synthesis by the Leydig cell

A

LH promotes pregnenolone synthesis in two ways:
Β­1) INCREASES AFFINITY of P450SCC enzyme for Cholesterol
Β­
2) Long-term action in which it stimulates Synthesis of P450SCC enzyme

***Note: Cholesterol side-chain cleavage enzyme is commonly referred to as P450scc. Another name for this enzyme is CHOLESTEROL DESMOLASE!!!!

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16
Q

Testosterone production

A

β€’ Production begins in FETUS at 14-15 weeks’ gestation

β€’ After production, Androgens diffuse to target cells &
bind to Androgen Receptors (AR)
– AR are found in Prostate, Testis (Sertoli, Leydig & myoid cells) Epididymis, Seminal Vesicles

– Non-reproductive Tissue where AR can be found include: Neurons in CNS, Anterior Pituitary, Thyroid Skin, Adrenal Cortex, Liver, Kidney Tubules, Bladder, Cardiac & Striated Muscle, Bone, Vasculature

– There are also AR in female, in ovary (Interstitial & Granulosa cells), Mammary glands, Uterus

β€’ Androgen receptor COMPLEX is a Nuclear Receptor which DIRECTS protein synthesis

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17
Q

Dihydrotestosterone (DHT) production

A
  • DHT also binds to androgen receptors, however with GREATER AFFINITY
  • Plays important role in causing CHANGES at Puberty
  • Deficiency of 5Ξ±-REDUCTASE results in AMBIGUOUS External Genitalia
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18
Q

Fates of Testosterone

A

β€’ As Testosterone enters the Peripheral Circulation, it quickly reaches equilibrium with serum proteins
– ~ 60% of circulaRng T is bound to SEX HORMONE BINDING GLOBULIN (SHBG)

– ~ 38% of circulating Testosterone is bound to ALBUMIN

– ~ 2% remains as FREE Testosterone, which is the MOST IMPORTANT biologically form

β€’ Testosterone and its metabolites are EXCRETED PRIMARILY in the Urine
– ~ 50% of excreted androgens are found as Urinary 17- KETOSTEROIDS

– Remainder being CONJUGATED Androgens or DIOL or TRIOL derivatives

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19
Q

Tissues producing Androgens

A

1) Adrenal
a) Cholesterol β€”> Androstenedione

2) Peripheral Tissues:
a) Testosterone –(5Alpha REDUCTASE)—–> DHT

b) Testosterone —– (AROMATASE) β€”-> Estradiol

3) Testis:
a) Cholesterol β€”> Androstenedione

b) Testosterone –(5Alpha REDUCTASE)—–> DHT
c) Testosterone —– (AROMATASE) β€”-> Estradiol

20
Q

Testosterone actions during Fetal Development

A

β€’ Present at 2nd month of embryonic life
– Presence or Absence of Testosterone determines
development of genital organs & characteristics
β€’ + Testosterone β€”-> Penis, Scrotum

β€’ - Testosterone —–> Clitoris and Vagina

β€’ Fetal Actions:
– Fetal differentiation of the Internal Male Genital tract
(epididymis, vas deferens, & seminal vesicles)

– Causes DESCENT of Testes into Scrotum during last 2-3 months of pregnancy
β€’ CRYPTORCHIDISM: lack of descent!!!!!!!!!

21
Q

Testosterone actons at Puberty

A 
β€’  Testosterone is responsible for:
–  Increased muscle mass
–  Pubertal growth spurt
–  Closure of the Epiphyseal Plates
–  Growth of the Penis & Seminal Vesicles 
–  Deepening of the voice
–  Spermatogenesis
–  Libido
22
Q

Specific actions of DHT

A
  • Fetal differentiation of the EXTERNAL Male Genitalia (i.e. penis, scrotum, & prostate)
  • Male HAIR Distribution & Male Pattern BALDNESS
  • SEBACEOUS Gland Activity
  • Growth of the PROSTATE

*** Because the growth of the prostate gland & male pattern baldness depend on DHT rather than testosterone, 5Ξ±-REDUCTASE INHIBITORS can be used as treatment for BENIGN PROSTATE HYPERTROPHY & HAIR LOSS in Males

23
Q

Summary of the Androgenic & Anabolic actions of Androgens

A

1) ANDROGENIC:
– Regulation of differentiation of Male Internal & External genitalia in fetus

– Stimulation of Growth, Development of SECONDARY sexual characteristics at Puberty

– Maintenance of reproductive tract & production of Semen

– Initiation & Maintenance of SPERMATOGENESIS

2) ANABOLIC:
– Stimulation of ERYTHROPOIETIN Synthesis (stimulates Red Blood Cell production)

– Stimulation of Sebaceous Gland secretion

– Control of Protein Anabolic effects (nitrogen retention)

– Stimulation of Linear Body Growth, bone growth & Closure of the Epiphyses

– Stimulation of ANDROGEN BINDING PROTEIN (ABP) synthesis

– Maintenance of secretions of sex glands

– Regulation of behavioral effects, including LIBIDO

24
Q

Intracellular Mechanism of Action of Testosterone

A

β€’ LEYDIG CELL: LH receptor
– LH receptor pathway is coupled to cAMP-PKA pathway resulting in Steroidogenesis &
Testosterone production
– Testosterone diffuses into Seminiferous Tubules & Peripheral Circulation

β€’ SERTOLI CELL: Stimulated by Testosterone & FSH
– FSH receptor is coupled to cAMP-PKA pathway and is involved in protein synthesis & production of INHIBIN which Inhibits FSH release

25
Q

What about Sertoli cells & testosterone?

A
  • FSH stimulates the Sertoli cells to secrete ANDROGEN BINDING PROTEIN (ABP) into the Lumen of the Seminiferous Tubules
  • Binding of Testosterone in the lumen provides a LOCAL Testosterone supply for the developing Spermatogonia
26
Q

Sertoli cells have supportive, exocrine & endocrine functions

A

1) SUPPORTIVE FUNCTION:
β€’ Maintaining BLOOD-TESTIS Barrier
β€’ Phagocytosis
β€’ Transfer of nutrients from blood to Sperm (transferrin, Fe, lactate) β€’ Receptors for hormones & Paracrines

2) EXOCRINE FUNCTION:
β€’ Production of fluid
β€’ Production of ABP
β€’ Determination of release of Sperm from Seminiferous Tubule

3) ENDOCRINE FUNCTION:
β€’ Expression of testosterone, ABP and FSH receptors
β€’ Production of AntimΓΌllerian Hormone
β€’ Aromatization of Testosterone to Estradiol-17Ξ²
β€’ Production of INHIBIN to Regulate FSH levels

27
Q

Spermatogenesis

A
  • Occurs along the Seminiferous Tubules
  • The Seminiferous Tubules are lined by a COMPLEX Stratified Epithelium containing two distinct populations of cells, SPERMATOGENIC CELLS, that develop into SPERMATOZOA, & SERTOLI CELLS which have a Supportive & Nutrient Function
  • Entire process takes ~ 74 days
  • Process is staggered to allow a group of cells to enter Maturation ~ every 16 days!!!!!!!
28
Q

Sertoli cells & Spermatogenesis

A

β€’ Sertoli Cells are the epithelial supporting cells of the Seminiferous Tubules
– Are tall SIMPLE COLUMNAR CELLS, which span from the Basement Membrane to the Lumen

– They surround the proliferating and differentiating germ cells forming pockets around these cells, providing NUTRIENTS, & PHAGOCYTOSIS-ING excess Spermatid cytoplasm

– Are connected to each other by CONTINUOUS Tight Junctions that SEAL the tubule into TWO Compartments:

1) The BASAL (close to the basal lamina)
2) ADLUMINAL (towards the lumen)
* *****BLOOD-TESTIS Barrier: large molecules CANNOT pass between the Basal and Adluminal compartment

29
Q

Spermatogenesis

A

3 Phases:

1) Mitotic divisions
2) Meiotic divisions
3) Spermiogenesis

30
Q

Steps in Spermatogenesis

A

1) MITOTIC DIVISION (Spermatocytogenesis):
– PROLIFERATIVE phase

– AT PUBERTY, Mitotic cycles Increase & Spermatogonia or stem cells divide to produce DAUGHTER Spermatogonia

– AFTER the Last Division, the Resulting cells are called PRIMARY SPERMATOCYTES

2) MEIOSIS (Production of the HAPLOID Gamete):
– Primary spermatocytes undergo TWO Meiotic Divisions

– The FIRST Division produces TWO Secondary Spermatocytes, each with a HAPLOID Number of DUPLICATED chromosomes

– Secondary Spermatocytes enter SECOND Meiotic division, producing TWO Spermatids, each with a HAPLOID Number of UNDUPLICATED Chromosomes

3) SPERMIOGENESIS (Maturation):
– Spermatids Undergo Spermiogenesis & Mature into Spermatozoa

– Nuclear & cytoplasmic changes to produce MATURE Spermatozoa

– Ends in Testis with RELEASE of Spermatozoa from Sertoli Cells

31
Q

Hormonal factors that Stimulate Spermatogenesis

A

β€’ LUTEINIZING HORMONE (LH)
– Secreted by Anterior Pituitary
– Stimulates the Leydig cells to Secrete Testosterone

β€’ TESTOSTERONE
– Secreted by Leydig Cells
– Essential for growth & division of the Testicular Germinal Cells, which is beginning of sperm formation

β€’ FOLLICLE STIMUALTING HORMONE (FSH)
– Secreted by Anterior Pituitary
– Stimulates the Sertoli Cells to Nurse & form Sperm.
– Without this stimulation Spermatogenesis will NOT occur

β€’ ESTROGENS
– Formed from the testosterone by the Sertoli cells when they are stimulated by FSH
– Might be also essential for Spermatogenesis

β€’ GROWTH HORMONE (GH)
– Necessary for controlling background Metabolic Functions of the Testes
– Promotes early division of the Sperm themselves
– Without it, as seen in PITUITARY DWARFS, Spermatogenesis is severely DEFICIENT or ABSENT rendering them INFERTILE

***Leydig Cells are located in the INTERSTITIAL!!!!!

32
Q

Sperm maturation- Epidydymis

A
  • Sperm spend an average of a month in the Epididymis undergoing further maturation after release from the Rete Testis
  • Sperm are WEAKLY Motile upon entering the epidydymis, but strongly motile upon exiting
  • DECAPACITATION occurs here which involves adding molecules to the membranes of sperm to prevent the Acrosomal reaction before contact with an egg
  • Function DEPENDENT on Testosterone-ABP!!!!!!!!!!!
  • Can act as STORAGE site for mature sperm for Several months
33
Q

Function of the Seminal Vesicles

A

β€’ Secretes a Mucoid Material containing: fructose, citric acid, & other nutrient substances, as well as prostaglandins & fibrinogen

– Adds considerable nutrient value for the ejaculated sperm
a) Each Seminal Vesicle empties its contents into the Ejaculatory Duct shortly after the Vas Deferens empties its Sperm, which adds greatly to the BULK of the ejaculated semen & adds to the nutrients available for the ejaculated sperm

– PROSTAGLANDINS aid in fertilization
a) React with the Female Cervical MUCUS to make it more Receptive to Sperm Movement (make cervical mucus LESS Thick)

b) Cause Backward, Reverse Peristaltic Contractions in the Uterus and Fallopian Tubes to move the Ejaculated Sperm Toward the Ovaries

34
Q

Function of the Prostate Gland

A

β€’ Secretes a THIN, Milky fluid that contains Ca2+, citrate ion, phosphate ion, a clotting enzyme, & a Profibrinolysin
– Secreted during emission

β€’ PH Adjustment:
– The slightly ALKALINE Prostatic fluid helps Neutralize the
Acidity of the other Seminal Fluids during ejaculation & thus ENHANCES the Motility and Fertility of the Sperm

35
Q

Semen

A

β€’ Composed of fluid & sperm from the Vas Deference (~10%), fluid from the Seminal Vesicles (~60%), fluid from Prostate (~30%), & Small Fluid amounts from the Mucous Glands (BULBOURETHRAL Gland)

β€’ pH = 7.5 final
– Alkaline Prostatic fluid NEUTRALIZES the mild acidity of the other Semen components

  • Sperm can live for many weeks in the Male Genital ducts, however, once they are Ejaculated in the semen, their maximal life span is only 24 to 48 hours AT BODY Temperature
  • Each Ejaculation contains approximately 2-6 ml, 20-200 million sperm (
36
Q

The male sexual response: The Male Reproducetive Tract conveys Sperm

A

β€’ Once Spermatozoa emerge from the efferent ductules, they leave the Gonad & enter the Extratesticular portion of the male reproductive tract [Epididymis (head, body, and tail), Vas Deferens, Ejaculatory Duct, Prostatic Urethra, Membranous Urethra, & Penile Urethra]

β€’ Two MAIN Differences from the Female tract:
– There is a CONTINUOUS Lumen from the Seminiferous Tubule to the END of the Male Tract (i.e., the Tip of the penile urethra).

– The Male Tract connects to the Distal Urinary Tract (i.e., Male urethra)

37
Q

The Male Sexual response: Erection

A

β€’ Erection is a Neuromuscular event

β€’ 3 erectile bodies in the penis: 2 Corpora Cavernosa & 1 Corpus Spongiosum
– Penile Urethra runs through the CORPUS SPONGIOSUM

– The 3 bodies are composed of Erectile Tissue β€”an anastomosing network of potential Cavernous Vascular spaces lined with continuous Endothelia within a Loose Connective Tissue support

β€’ During the Flaccid state, blood flow to the Erectile Tissue is MINIMAL due to VASOCONSTRICTION of vasculature

38
Q

The male sexual response: Erection

A

β€’ During Erection, PARASYMPATHETIC nerves innervating the vascular SM of the helicine arteries that supply blood to the cavernous spaces release NO
– NO activates Guanylyl Cyclase, increasing cGMP, which decreases intracellular Ca 2+ & causes relaxation of the vascular SM

– Vasodilation allows blood to flow into the spaces, causing Engorgement & Erection

– The engorged Tissue presses the veins against a noncompliant outer fascia, thereby REDUCING
Venous Drainage

– Somatic stimulation INCREASES contracton of muscles at the base of the Penis, further promoting Erection

39
Q

The male sexual response: Emission

A

β€’ EMISSION is the movement of Semen from the Epididymis, Vas Deferens, Seminal Vesicles, & Prostate to the Ejaculatory Ducts:

1) Under SYMPATHETIC control (adrenergic transmitter)

2) Causes sequential PERISTALTIC Contraction of SM of Vas Deferens, closing the Internal Sphincter of the Bladder
a) This PREVENTS RETROGRADE Ejaculation of the semen into the bladder
* *** Destruction of this Sphincter by prostatectomy often results in Retrograde Ejaculation

b) Also mediated Sympathetic Adrenergic stimulation
3) Emission normally precedes ejaculaRon but also conRnues during ejaculaRon

40
Q

The male sexual response: Ejaculation

A

β€’ Ejaculation is the Propulsion of Semen out of the male Urethra

β€’ Caused by the RHYTHMIC Contraction of the Bulbospongiosus & the Ischiocavernous Muscles (striated muscles), which surround the base of the penis
– These Striated muscles are Innervated by SOMATIC motor nerves

– Contraction causes the Semen to exit Rapidly &
outwardly through the Urethra

41
Q

Capacitation of the Spermatozoa

A

β€’ Sperm are mature when they leave the epididymis, but their activity is held in check by secretions from the genital duct epithelia:

1) When they are first expelled in the semen, they are unable of performing their duties in Fertilizing the ovum
2) The CHANGES that occur when they come in contact with the Fluids of the Female Tract allow for CAPACITATION of the Sperm

3) Changes include:
β€’ Uterine & Fallopian tubes WASH AWAY Inhibitory factors

  • LOSS of Cholesterol that had built-up on the Acrosome, which now make the HEAD of the Sperm WEAKER
  • Membrane of the sperm is much more Permeable to Ca2+; Increases the Motility of the Sperm
42
Q

Sperm Acrosome Reaction

A

β€’ Stored in the acrosomal head of the sperm are large quantities of HYALURONIDASE & PROTEOLYTIC Enzymes
– HYALURONIDASE Depolymerizes the Hyaluronic Ccid polymers in the intercellular cement that HOLD the ovarian Granulosa cells Together

– The PROTEOLYTIC Enzymes digest proteins in the structural elements of Tissue cells that ADHERE to the Ovum

43
Q

Gonadal dysfunction in the male

A

β€’ Testosterone deficiency effects depend upon the age of onset:
– 2nd to 3rd MONTH OF GESTATION: results in varying degrees of ambiguity in the male genitalia & male Pseudohermaphrodism

– 3rd TRIMESTER OF PREGNANCY: leads to problems in tesRcular descent (Cryptorchidism) along with Micropenis

– PUBERTY: leads to poor Secondary Sexual Development & overall Eunuchoid features
a) EUNUCHOIDISM: persistence of Prepubertal characteristics, and osen by the presence of characteristics typical of the opposite sex

– POST-PUBERTY: leads to decreased Libido, Erectile Dysfunction, Decrease Facial & Body Hair growth, Low Energy, & Infertility

44
Q

Male Hypogonadism

A
  • Usually caused by geneotic inability to produce GnRH, resulting in LOW Testosterone levels & is thus associated with Infantile Sex Organs
  • Gonadal failure/sex steroid synthesis failure can lead to HYPOGONADISM

β€’ KALLMAN’S SYNDROME: A Genetic disorder, occurs when the hypothalamic neurons that are responsible for releasing Gonadotropin-Releasing Hormone (GnRH neurons) FAIL to Migrate into the hypothalamus during Embryonic Development
– Characterized by Delayed or Absent puberty & an impaired sense of smell!!!!!!!!!!!!!!!!!!!
– A form of HYPOGONADOTROPIC HYPOGONADISM!!!!!

β€’ KLINEFELTER SYNDROME (also called Seminiferous Tubular DYSGENESIS): Men with an EXTRA X chromosome
– Affected persons are phenotypically male because of the presence of the Y chromosome, & they appear normal at birth

– At puberty, increased levels of gonadotropins fail to induce normal tesRcular growth & spermatogenesis

– Androgen production is usually low (but this is highly variable among parents), whereas the levels of Gonadotropins are elevated, thereby indicaRng primary hypogonadism

– Seminiferous Tubules are largely destroyed, resulting in Infertility

Primary Hypogonadis:
**KLEINEFELTER’S Syndrome!!!!

Secondary Hypogonadism:
** TUMOR or KALLMAN’S Syndrome!!!!!!!

45
Q

Pathologies

A
  • β€œMale-pattern baldness”: caused by DHT; treated by 5-ALPHA REDUCTASE INHIBITOR
  • Benign Prostatic Hypertrophy: caused by DHT; treated with 5-ALPHA REDUCTASE INHIBITOR
  • Cancer of the PROSTATE: treated with Androgen Receptor ANTAGONIST, Radiotherapy, Radical Prostatectomy
  • Tumors of TESTIS (interstitial cell tumors): produce large amounts of Testosterone
  • Germinal Epithelial Tumors: produce NO hormones
46
Q

Andropause

A
  • As men age, gonadal sensitivity to LH Decreases & Androgen production DROPS
  • As this occurs, serum LH and FSH levels rise (FSH > LH)

β€’ Testosterone in aging: Decrease slowly aser age 40
– Decreased: bone formation, muscle mass, growth of facial hair, appetite, libido

β€’ Although sperm production typically begins to Decline after age 50 years, many men can maintain reproductive function & Spermatogenesis throughout life

β€’ Loss of Sexual Activity
– typically about 68-70 yrs of age

Reproductive System I (18 decks)

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