male reproductive system Flashcards

1
Q

what is the biosynthetic precursor of steroids?

A

cholesterol

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2
Q

what hormonesa re needed for male reproductive function?

A

estrogen and progesterone

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3
Q

why are estrogen and progesteron needed within a male?

A

sustain spermiogenesis = production of mature and motile spermatozoa

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4
Q

what is the main parts of the male reproductive tract/

A

testes is the site of sperm production
epididmysis is where the sperm pass through on their way to the vas deferens
the prosate semi vesicles and rhe bulbourethal gland are the three accessory glands within the male - they give the fluid in the ejaculation

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5
Q

what happens in the anterior cutaway of the male reproductive tract?

A

the prostate gland adds secretions

- little bit of the fluid goes through the ves deferens but majority of ejaculate comes from the 3 accessory glands

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6
Q

what causes an erection?

A

tissue within the penis becoming filled with blood

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7
Q

what are the male reproductive tract functions?

A

 Testis – sperm production, steroid hormone production
 Epididymis – sperm collection and maturation
 Ductus deferens – transport and storage
 Accessory glands – contributions to seminal fluid
 Urethra – transport

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8
Q

what is the testicular anatomy?

A

Seminiferous tubles is where the sperm are produced and from here, they pas through some tubes to get to the efferent ducts into the epididmyus.
As a male you have about 600 m of tubes, so there is a lot fo tubes concentrated into one space.

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9
Q

what do blue dots show on a histological section of a testes seminiferous tubules?

A

The larger round dots = resident epithelial cells of the tubules – nurse cell provide an environment where sperm production can occur.
Smaller dots are more conc in the center of the tubules – nuclei are smaller. These are moving upwards through the nurse cell environment and conc near the top side of the inner suface of the cell. From here they are extruded and transported.

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10
Q

where is sperm produced?

A

the sperm from precursor as they mature move towards the lumen.
produced in the seminiferous tubule.

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11
Q

where does steroid production start?

A

beginning of the step from cholestreol to androgen is in the leydig cell.
they need to be then transprotted to the sertoli cell

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12
Q

where are androgens produced?

A

mostly in LEYDIG CELLS

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13
Q

why is DHT important?

A

if men have mutations it impeded the function of alpha 5 reductase, so you will get developmental abnormalties.
dht is needed for maturation of testerone (more active then testerone itself)

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14
Q

what are the common properties of the receptors superfamily for steroid hormones?

A
  • they are a protein which has TWO binding sites, one for the steroid and one for the DNA
  • binding to the steroid ligand produces a compled that acts on DNA
  • this alters the gene expressed
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15
Q

what is the androgen receptor?

A
  • androgens are defined as compunds which interact with the androgen receptor.
  • all major cell populations of testis, epididymis and accessory glands express androgen receptor.
  • the receptors are also found in tissues where secondary sexual characterstics appear
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16
Q

what is a target tissue for androgens, estrogen and progesterone?

A

the brain

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17
Q

what is more likely to lead to male pattern baldness?

A

having a higher endogenous androgen level

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18
Q

what happens in the HPG axis?

A
  • GnRH arises in the hypothalmus and is transported down small blood vessels to the anterior pituiatry
  • the anterior pituitary produced two important polypeptide hormones LH and FSH.
  • these control sperm production and maturation
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19
Q

what is LH and FSH?

A
LH = luteninsing hormone
FSH = follicle stimulating hormone
20
Q

where do polypeptide hormones need receptors?

A

on the membrane so they can signal as they are macromolecules.

21
Q

are steroid hormones lipid soluble?

A

yes

this means they can pass across cell membranes and reach the cytoplasm

22
Q

what does the sertoli cell produce?

A

androgen binding protein

ABP

23
Q

what does ABP do?

A

has the steroid isnt very water soluble
so it binds to the steroid hormone and is released as a complex to get from one organ to another.
it helps to impive the capacity of the system to transport the steroid which isnt very water soluble

24
Q

what does ABP bind to?

A

T and DHT and concentrates them in the luminal fluid of the seminiferous tubule

25
Q

what does the binding of ABP stimulate?

A
  • spematogenesis in the seminiferous tubule
  • sperm maturation in the epididymis
  • accessory gland secretions
  • myoid cell contractile actibity to propel sperm along the tract
26
Q

how is feedback controlled in male?

A

much easier in male then female
- the feedback of testosteron is both at the anterior pituitary and the hypothalamus. thus means there is a system in place so you cannot overproduce.

27
Q

how is feedback controlled within the female?

A

in female there is a specific time window in menstrual cycle where estrogen stimulates positive feedback - short time period.
there is also a pulsatile release of GnRH within a female where in a male there is just a constant frequency

28
Q

what happens during spermatogenesis?

A
  1. sperm move from the base of the cell upwards this then leads to them undergoing two miotic divisions.
  2. after this they begin to acquire characterstics which allow us to recognise them as sperm
  3. sperm exit from the inner suface tail first
  4. they grow a tail from the lumen
  5. later stages you get maturation which is androgen dependent
29
Q

when do sperm become motile?

A

when sperm are released into the lumen they are not yet motile.
they gain the ability to swim in the epididymis (DHT dependent)

30
Q

what is the volume of an ejaculation?

A

1.5-5mL

31
Q

what is the sperm count within an ejaculation?

A

40-250 million per mL

32
Q

what is the sperm motility 1 hour and 3 hours after ejaculation?

A

1 hour = 70%

3 hours = 60%

33
Q

what is the leukocyte count of an ejaculation?

A

0-2000 per mL if there are lots then this needs to be addressed

34
Q

what is the pH of semen/

A

7.2-7.8 - slightly alkali of neutral as vagina is acidic so accessory glands need to protect the sperm

35
Q

what is the fructose content of sperm?

A

150-600mg per 100mL - metabolic substrate for the motility

36
Q

what are the contributions of accessory glands within the compostion of the ejaculate/

A
  • Epididymis & Ductus deferens (sperm-rich fraction):5 % of the ejaculate volume
  • Prostatic secretion: 13-33% of the ejaculate volume
  • Seminal vesicle secretion: 46 – 80% of the ejaculate volume
  • Bulbo-urethral gland secretion: 5% of the ejaculate
37
Q

what is an erection?

A

erectile tissues become engorged with blood, arterioles dilated as a result of parasympathetic nervous system activity.

38
Q

what are the erectile tissues?

A

corpus cavernosum and corpus spongiosum

39
Q

what is erectile dysfunction`?

A

unable to always get an erection when needed / wanted?

40
Q

what are the pathological bases which may cause erectile dysfunction?

A

psychogenic
neurogenic
vascular
endocrine

41
Q

what else may cause erectile dysfunction?

A

many drugs including tricyclics and SSRIs ; antihypertensives including beta blockers and calcium antagonists

42
Q

how can you manage erectile dysfunction?

A
  • PGE1 – alprostadil
  • PDE5 inhibitors – eg sildenafil
  • Look up what can be prescribed on NHS
43
Q

what are the risk factors of prostate cancer?

A
  • age
  • ethinicity
  • family history
44
Q

what are the symptoms of prostate cancer?

A
  • Urgent and frequent urination
  • Nocturnal enuresis (involuntary urination)
  • Difficulty starting or emptying the bladder
  • Urine flow weak, interrupted or difficult to control
  • Back or pelvic pain
45
Q

what is the pharmacological management of prostate cancer?

A
  • Gonadorelin (GnRH) agonists and antagonists. Block so you don’t get the gondatropins so you won’t get the steroids oR agonist= high levels the receptor will downregulate and the pituitary gland becomes deaf to action of the gondatropins
  • Androgen antagonist – cyproterone acetate could be affected provided the tumour retains normal androgen state of the prostate but tumours mutate and they can become independent to normal control.
  • 5-a-reductase inhibitors – dutasteride & finasteride. More subtle option as you still have testerone acting but you are blocking DHT which is the more active progesterone
46
Q

what is the new way of have contraception for a male?

A

exogenous testosterone

  • decrease LH and FSH and therefore decreases fertility
  • needs to be given in HIGH doses
  • this causes loss of sperm production
  • this may lead to hypogonadotropic hypogonadism
  • but you produce that much sperm it might not affect them all