Lecture 2: Male reproduction and endocrine control Flashcards

1
Q

What are the types hormone glands in the testis and what do they produce?

A

Exocrine glands: Secretory product = Spermatozoa

Endocrine gland: Secretory product = Mainly Testosterone

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2
Q

Insert saggital cross section of male reproductive tract

A

now

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3
Q

Insert cross section of testis

A

now

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4
Q

What do testicular vericeoles lead to?

A

Infertility because the testicles become too hot

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5
Q

Describe the cellular structure in the testicles and the functions:

A

Seminiferous tubules, Contains;

  • > Gonocytes: Primitive germ cells that become spermatagonia (present only in early life until mini puberty)
  • > Spermatagonia (germ cells, pre sperm (mitotic)
  • > Sertoli cells: Epithelial cells, lumen of tubule and help developing pre-sperm cells (increase in numbers during mini puberty)

Leydig cells: Interstitial cells, androgen secreting

Myeloid cells: Between tubules, Help contract and move sperm

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6
Q

What compartments are the seminiferous tubules divided into?

A

Basal compartment
Adluminal compartment
Luminal compartment

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7
Q

What exists the prevents immunological attack on the testis?

A

The blood/testis barrier.

Physical barrier between semeniferous tubules and rest of testis. Created by: Tight junctions,. adherenes junctions and gap junctions between sertoli cells (injury can breach and cause issues)

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8
Q

Describe the germ cell origin of the testis:

A
  • Primordial germ cells will become either sperm or oocytes.
  • PGCs are first seen 3-4 weeks post conception.
  • PGCs are first found in the yolk sac of the extraembryonic tissues and migrate to the gonodal ridges (near the developing kidney) via the hind gut.
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9
Q

What is essential for the migration of PGCs?

A

Stem cell factor. Inadequate results in apoptotic death

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10
Q

How is pregnancy dated?

A

2 weeks post last menstural period.

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11
Q

What do germ cell tumors arise from? and where are they most commonly found?

A

PGCs

93% are found in the testis. 4% ovaries. 3% ectopic (commonly CNS) (following enteric nerves)

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12
Q

Describe the procession PGCs into primary spermatocytes:

A

AT around 3-9 months, there is a minipuberty where neonatal gonocytes become a-dark spermatognoium. These continue to develop into primary spermatocytes by 3-4 years of age. Before ten years the blood-testis barrier develops. Where the primary spermatocyte can become spermatid. Which can develop into sperm during puberty and onwards.

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13
Q

Describe the development of the testis in the fetus:

A
  • Testicle development begins around 6 weeks of gestation
  • During later fetal life and early postnatal life the testes grow slowly and the seminiferous cords are solid.
  • Embryonic leydig cells are derived from different progenitors to adults leydig cells. Adult leydig cells differentiate from stem cells at puberty.
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14
Q

Describe the testosterone production from leydig cells in the fetus and what its responsive to:

A
  • Testosterone is produced by leydig cells in adults and fetuses.
  • Initial production of testosterone (7-8 weeks of gestation) by embryonic leydig cells is not dependent on LH stimulation as occurs prior to development of the pituitary gland - hCG stimulation from placenta.
  • Approximately 14 weeks gestation production of testosterone becomes LH (pituitary) / hCG (placental) dependent.
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15
Q

Describe mini-puberty:

A
  • Occurs 2 months after birth
  • Thought to be important in;
  • > Masculinising the neonatal brain
  • > Promoting sertoli cell proliferation
  • > Promoting differentiation of gonocytes into dark AD-spermatogonia
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16
Q

Describe the stages of descent of the testicles:

A

Descent of the testis occurs in two phases:

1) The Transabdominal (10-15 weeks of gestation)
2) The Inguino-scrotal (25-35 weeks of gestation)

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17
Q

Where do the testes form in the fetus?

A

Testis form in the gonadal ridges in the lumbar region of the abdomen suspended between two ligaments the caudal and the gubernaculum

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18
Q

Describe the transabdominal phase of the testis descent:

A

Transabdominal phase:

  • As the ambryo/fetus grows the gubernaculum does not elongate and under the influence of testosterone the caudal ligament regresses
  • INSL-3 (insulin like 3) causes migration of the gubernaculum towards, and dilation of, the inguinal canal
  • INSL-3 is constitutively expressed product of the leydig cells.
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19
Q

What hormone is important in the inguino-scrotol phase?

A

Androgen is important

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20
Q

What is cryptochidism?

A
  • Failure to descend (unilateral or bilateral)
  • Maldescent
  • 1-9% term, 30% preterm
  • Most self correct, can surgically correct
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21
Q

What can cryptochordism lead to?

A

1) Infertility - due to excess temperature (hence in scrotum not abdomen)
2) Is one of the known factors for testicular cancer

Breast-fed infants are less likely to remain cryptorchid than non-breast infants.

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22
Q

Describe what testicular torsion is:

A
  • Occurs when testicle rotates, twisting the spermatic cord that brings blood to the scrotum
  • Reduced blood flow causes sudden and often severe pain and swelling
  • Can occur at any age but most common between 12-18yrs
23
Q

What are the testicular changes at puberty?

A
  • At puberty there is a sudden testicular growth by all components of the testes.
  • The seminiferous tubules develop a lumen and the germ cells (spermatogonia) begin to proliferate
  • The synthetic activity of the sertoli and leydig cells increases sharply
  • Beginning of sperm production
24
Q

Describe the stages of spermatogenesis:

A

Three phases:

1) Mitotic division
2) Meiotic division
3) Cytodifferentiation

25
Q

Insert spermatogenesis slide

A

now

26
Q

insert the testicle histology slide

A

now

27
Q

Describe spermiogenesis:

A

Spermatids form:

  • Head; heterochromatic DNA, covered in acrosome
  • Midpiece: Mitochondria
  • Tail

Excess cytoplasm of the spermatid is also lost into a body called residual body that is phagocytosed by sertoli cells after the sperm leaves.

28
Q

What does spermiogenesis require?

A

Presence of androgens

29
Q

Insert sperm diagram

A

Please

30
Q

Describe the timing of spermiogenesis:

A

~16 days between successive waves of developing spermatazoa

Thus, at any one point on a tubule, the interval between the release of successive waves of sperm into the lumen is 16 days.

(complete process of spermatogenesis takes 64 days in humans)

31
Q

Insert diagram of sperm development

A

now

32
Q

Describe the cycle of the seminiferous epithelium:

A
  • Spermatogonia division is staggered
  • It is synchronous in a cross sectional area. Called “ The cycle of the seminiferous epithelium”
  • Each segment of the tubule contains a different stage of spermatogenic development that is either ahead or behind the consecutive segments.
33
Q

What is the spermatogenic wave:

A

The synchronisation of spermatogensis along the length of the tubule is called the spermatogenic wave.

The spermatic wave is responsible is what results in constant sperm production

34
Q

What is the overall role of sertoli cells? and how are they structured:

A
  • Spatial (down tubule) and temporal organisation of spermatogenesis is controlled by sertoli cells.
  • Sertoli cells communicate with each other via their tight junctions and with spermatocytes and spermatids via gap junctions and ectoplasmic specialisation, respectively.
  • The number of sertoli cells is proportional to the sperm production capacity of the seminiferous tubule
35
Q

What are the sertoli cells important for?

A
  • Nourishing spermatogonia
  • Resorbing the excess cytoplasm - residual body
  • Producing seminiferous tubule fluid
  • Maintaining the spermatogonial stem cell niche
  • Create the blood-testis barrier (prevent antisperm antibody production)
36
Q

Are sertoli cells immune privlidged?

A

Sertoli cells are themselves immune-privilidged and can be transplanted into non-privilidged sites - they also support survival of other cells i.e islet cells

37
Q

What are the actions of the pituitary on sertoli and leydig cells:

A

Hypothalamus produces GnRH which acts on pituitary, it releases FSH and LH.

FSH acts on sertoli cells upregulating androgen receptors and androgen binding proteins leading to spermatogenesis (80% testosterone lumen of tubules, 20% enters systemic circulation) . FSH also alters sertoli gene expression to support spermatogenesis.

LH acts on leydig cells and increases testosterone release. (essential for initiation of spermatogenesis)

38
Q

What is testosterone get converted to and what is its impact?

A

Testosterone is converted to 5aDHT -> Secondary sexual characteristics i.e muscle mass, labido, hair growth, baldness, voice

39
Q

Upload the negative feedback loop for testosterone

A

yes pelase

40
Q

Describe sperm maturation and movement:

A
  • Sperm move from the seminiferous tubules to the rete testis and then into the epididymis. This movement is aided by fluid pressure from secretions of the testis and ciliated cells int he efferent ducts.
  • ~6 days
  • Sperm in the upper epididymis are not motile and cannot normally fertilise an egg.
  • The sertoli cells and the epithelium of the epididymis secrete a fluid rich in nutrients and hormones that the sperm are maintained in - important for maturation of the sperm.
41
Q

Describe the epididymis and its role in sperm maturation:

A
  • Sperm spend 10-14 days passing through the epididymis during which time they are concentrated 100 fold
  • Fluid reabsorption is mediated by stereocilia
  • Sperm gain the ability for motility and fertilisation in the epididymis
42
Q

What can go wrong in the epididymis?

A
  • Epidiymitis: Caused by bacterial infection/STI

- Can lead to testicular inflammation (epididymo-orchitis)

43
Q

Describe the vas deferns:

A

45cm long
Major site of sperm storage

3 muscular layers

  • Inner longitudinal
  • Middle circular
  • Outer longitudinal layer
44
Q

Describe the vas deferns function:

A

Contracts during ejaculation resulting in the movement of spermatozoa out of the epididymis and into the ejaculatory duct.

45
Q

Describe the vas deferns structure:

A
  • Just prior to the prostate gland the lumen becomes enlarged and folded with many crypts (called the ampuilla)
  • This allows additional sperm storage for up to a month
  • If sperm are not ejaculated by during that time they degenerate and are reabsorpbed by the body
46
Q

What are the accessory glands?

A

Glandular secretions from the seminal vesicles and prostate gland are important for sperm motility and survival in the female reproductive tract

47
Q

Describe the seminal vesicles:

A
  • Highly folded tubular/pouch like glands
  • Surrounding the secretory tissue is extensive smooth muscle
  • The excretory duct joins with the vas deferns to form the ejaculatory duct
  • Relatively unsusceptible to tumor growth
48
Q

Describe what the seminal vesicle secretes:

A
  • Secrete a slightly alkaline fluid containing:
  • > Fructose (energy source)
  • > Semenogelin, a Zn binding protein
  • > Semen clots immediately after ejaculation with semeogelin 1 (and 2) being the major constituent of the clot (fibronectin is also important)
49
Q

Describe the prostatic divisions:

A
Central zone (around urethra)
Peripheral zone (glandular)
Transition zone (glandular tissue, major site of BHP)
Anterior zone (fibromuscular zone no glands)
50
Q

Describe the penis anatomy:

A
  • Two corpus cavernosa

- One corpus spongiosum

51
Q

Describe the process of an erection:

A

Erection occurs following sexual stimulation

1) Parasympathetic nerve activity induces ACh release
2) The ACh induces NO release by endothelial cells of the corpora
3) NO induces cGMP production which in turn causes vasodilation
4) The corpora relax and engorge with blood
5) Venous outlfow is reduced increasing engorgement/erection

52
Q

Describe the role of sildenafil and ED:

A

Sildenafil;

  • Enhances erection by blocking the action of type v phosphodiesterase
  • Phosphodiesterase breaks down cGMP
  • Inhibiting phosphodiesterase increases level of cGMP (vasodilation)

Viagra is not useful if ED occurs because of parasympathetic nerve damage because there is no stimulation of NO and subsequent cGMP production

53
Q

Describe the composition of Semen:

A
  • Prostatic fluid (30%)
  • Sperm (10%)
  • Seminal vesicle fluid (60%)
  • Other secretion very minor

Normal ejaculates ~2-5mls