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Endo/Repro Exam 2 > 8. Male Physio > Flashcards

8. Male Physio Flashcards

1
Q

Does the presence of chromosomes determine gonads?

A

Not entirely.

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2
Q

Initially, sexual differentiation is driven by what?

A
  1. Genetic sex is dirven by XX/XY chromosomes.
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3
Q

What is the process of sexual differentiation?

Describe using genetic sex, gonadal sex and phenotypic sex.

A
  • Genetic sex is determined by XX or XY (SRY gene) chromomes.
    • First 5 weeks of gestation: gonads are bipotential (not M/F)
    • 6-7 weeks: testes develop in genetic M
    • 9 weeks: ovaries develop in genetic F
  • Normally, genetic sex determines gonadal sex (presence of male/female gonads (testes/ovaries))
    • XY -> Testes are made up of sertoli cells and leydig cells -> male genital tract and external genitalia (phenotypic sex)
      • Sertoli cells make AMH
      • Leydig cells make testosteone.
    • XX -> ovaries -> do not make AMH or testosterone -> female genital tract and external genitalia (phenotypic sex).
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4
Q

Do the gonads appear in males of females first?

A

Appear in males slightly earlier.

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5
Q

What is phenotypic sex and what is it deteremined by?

A
  • Physical characteristics of the internal genital tract and external genitalia.
  • Phenotypic sex is determined by the homrones secreted from goands.
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6
Q

Male internal genital tract includes what?

A

1. prostate

2. seminal vesicles

3. vas deferens

4. epididymis

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7
Q

Female internal genital tract includes what?

A

1. Fallopian tubes

2. Uterus

3. Upper 1/3 of the vag

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8
Q

External genitalia in M/F.

A
  • M: scrotum and penis
  • F: clit, labia majora/minora, lower 2/3 of vagina.
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9
Q

How does gonadotropin (FSH/LH) secretion change over the lifetime?

Fetus:

Childhood:

Puberty:

Reproductive years:

Senescence:

A
  1. Secretion of FSH/LH begins at gestational week 10/12. Levels are low until puberty, with more FSH being secreted.
  2. Puberty and adult reproductive years: At puberty, secretion of GnRH, FSH and LH increases and becomes pulsatile and we begin to secrete more LH than FSH. During adulthood reproductive years, women begin periods and see cycles of FSH/LH release. Men have a steady secretion of FSH and LH.
  3. Senescence: Gonadatropic secretion increases in M/F, with FSH being secreted more than LH. In F, there is a sharp increase because menopause causes lack of negative FB.
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10
Q

What initiates puberty?

A
  • Pulsatile secretion of GnRH, causing FSH and LH to be secreted pulsitile as well. This will then cause the secretion of [gonadal steriod hormones, testosterone and estradiol].
    • -> cause secondary sex characteristics to appear
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11
Q
  • What happens if GnRH analogue is administered in intermittent pulses to replicate normal pulsatile secretion?
  • What about if a long-acting (non-pulsitile) GnRH anaglogue is given?
A

1. Puberty is initiated and reproductive function is established.

2. No puberty.

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12
Q

What can affect when puberty begins?

A
    1. CNS: melatonin, secreted from the pineal gland, is highest during childhood and decreases as we become adults. It inhibits GnRH release
    1. Stress or calories deprivation in girls
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13
Q

What happens to puberty if we remove pineal gland?

A

Puberty begins early.

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14
Q

Describe the functions of the testes and scrotum.

A
  • Testes: spermatogenesis and secrete testosterone.
  • Scrotum: keeps testes at. a lower temperature so spermatogenesis can occur.
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15
Q

Fx of the epididymis.

A

Main location for maturation and storage of sperm.

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16
Q

Function of vas deferens, seminal vesicles and prostate gland.

A
  • Vas deferens is secretes a fluid rich in citrate and fructose and stores sperm in the ampulla.
  • Seminal vesicles will then secrete a fluid rich in citrate, fructose, prostaglandins and fibrinogen giving it nutrients!
  • Prostate gland will then secrete a alkaline milky soln that. is rich in citrate, Ca2+ and enzymes during emission to neutralize.
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17
Q

How does sperm leave the testes?

A
  1. Sperm leave the testes -> epididymis, the main location for the maturation and storage of sperm. They can stay in the epididymis for several months.
  2. During sexual arousal, contractions of the smooth muscle around the ducts pushes sperm through the epididymis.
  3. At ejaculation, sperm -> vas deferens -> ejaculatory duct..
    1. Ampulla of the vas deferens -> another storage area for sperm and secretes a fluid rich in citrate and fructose, which nourishes the ejaculated sperm.
  4. The seminal vesicles secrete a fluid rich in fructose, citrate, prostaglandins, and fibrinogen. As the vas deferens empties its sperm into the ejaculatory duct, each seminal vesicle contributes its secretions, which also provides nutrients for ejaculated sperm.
  5. Prostate gland then adds its own secretion of ejaculate: basic milky aqeuous rich soln in citrate, calcium and enzymes.
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18
Q

How do the prostaglandins in seminal fluid help with fertilization?

A
    1. React with cervical mucus and make it less thicc so sperm can penetrate.
    1. Cause backward, reverse peristaltic contraction in female reproductive tract to help sperm go to ovaries
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19
Q

What makes up the adult testis?

A
    1. Seminiferous tubules (80%), which have epithelium lined by sertoli cells and germ cells, such as spermatogonia and spermatocytes.
    1. Leydig cells (20%) intersitial cells between tubules that make and secrete testosterone when LH acts on them.
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20
Q

80% of adult testis is made up of seminiferous tubules (80%), which have epithelium lined by sertoli cells and germ cells, such as spermatogonia and spermatocytes.

What are spermatogonia and spermatocytes?

A
  1. Spermatogonia: immature germ cells located at the periphery of tubule
  2. Spermatozoa: mature germ cells located near the lumen of the tubule
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21
Q

Sertoli cells have 3 important functions that support spermatogenesis. What are they?

A
    1. Provide nutrients for differentiating sperm.
    1. From tight junctions with each other, creating the blood testes barrier.
    1. Secretes aqeuous fluid into the lumen of the seminiferous tubules which helps transport sperm -> tubules -> epidiymis.
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22
Q

What is the importance of the blood-testes barrier?

A
  • A barreir between. testes and bloodstream that allows good things, like testosterone, to cross but not bad things that could damage developing sperm.
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23
Q

The TESTES make several male sex hormones (androgens), such as:

A

1. Testosterone (most adbundant)

2. DHT

3. Androgestenedione

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24
Q

Where is much of the testosterone we have eventually converted to DHT?

A

Target tissue.

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25
Q

Testosterone is made and secreted by our Leydig cells of the testes.

How does steriod synthesis result in testosterone and not other things?

A
  • Testes do not have 21B-hydroxylase or 11B-hydroxylase, thus, no glucocorticoids or mineralcorticoids are made.
  • They have 17B-hydroxysteroid DH, which converts androstendione -> T.
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26
Q

How do we concentrate testosterone in the lumen of the seminiferous tubules?

A

It is bound to ABP (androgen-binding protein).

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27
Q

Is testosterone the active hormone is all andronergic target tissue?

A
  • No. In some tissue, it is DHT (prostate gland, external genitalia of male fetus, skin and liver).
  • T-> DHT via 5-alpha reductase.
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28
Q

How does testoerone travel in blood?

A

Most bound to plasma proteins, such as sex-hormone binding globulin (SHBG) and albumin.

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29
Q

What are the main steroidogenic cells in the testis?

A

Leydig cells

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30
Q

Leydig cells make T. How?

A
    1. Make cholesterol de novo or get some from blood using LDL/HDL receptors
    1. Store cholesterol as cholesterol esters.
    1. Hormone-sensitive lipase frees up cholesterol from cholesterol esters to make androgens.
    1. Transferred within mitochondrial membrane via steriodogenic acute regulatory protein (StAR).
    1. Converted to prenenolone.
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31
Q

Do males make estrogen?

A

Yes, they make small amounts.

In the fluid in the seminiferous tubules, amount is actually high and we have more in other tissue, such as liver (80%)

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32
Q

What is the importance in males making estrogen?

A
  • Potential role in spermatogenesis (bc sperm cells have at least 1 estrogen receptor).
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33
Q

Where is estrogen in males made?

A

Sertoli cells; it is a product made when T -> estradiol via aromatase.

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34
Q

What pathway what cholesterol go through to become pregnenolone?

A

1. Mitochondrial pathway: Cytochrome P450 removes side chain from cholesterol at carbon 20.

THIS IS THE RATE-LIMITING STEP.

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35
Q

Leydig cells are the main endocrine cell of the testis, making T.

Does it make alot of DHT and estradoil-17B?

A

It makes limited amounts. More is made peripherally.

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36
Q

After Leydig cells make T, where does it go?

A
    1. Goes into seminiferous tubules, bound to ABP.
    1. Peripheral circulation, bound to SHBG and albumin.
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37
Q

Cholesterol -> Prenenolone.

What is the enzyme and what regulates the enzyme action?

A

Cholesterol desmolase (P450scc), which is regulated by LH.

LH will increase synthesis of P450scc and increase affinity for cholesterol.

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38
Q

When does testosterone production begin?

A

7-8 weeks into gestation.

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39
Q

How do androgens bind to receptors and where are the receptors located?

A
  • Androgens diffuse into cells -> bind to androgen receptors located in the nuclear receptor, which makes proteins.
  • AR are found in: prostate, testis (sertoli and leydig cells), epididymis, seminal vesicles
  • Non-reproductive tissue
  • Ovary (interstitial and granulosa cells), mammary glands and uterus.
40
Q

DHT plays in important role in ________.

What has higher affinity for androgen receptors: DHT or testosterone?

A
  • causing changes during puberty
  • DHT.
41
Q

Kenny has a deficiency in 5a-reductase.

What does this result in?

A

Ambiguous external genitalia.

42
Q

What are the two fates of testosterone?

A
  1. Goes into circulation: 60% is bound to SHBG, 38% is bound to albumin and 2% is free (biologically active).
  2. Excreted in urine as urinary 17-ketosteroids (50%) and conjugated androgens, diol or triol derivates.
43
Q
  1. Cholesterol -> androstenedione occurs where?
  2. What happens next?
A
  1. Adrenal CTX and testes
  2. Adrostenedione -> testorone in the testes then goes into peripheral tissues or stay. in testes testis,
  • Testosterone -> DHT via 5a-reductase
  • Testosterone -> estradiol via aromatase.
44
Q

Actions of testosterone during fetal development is different depending on TIMING.

What happens during:

  1. month 2 of embryonic life
  2. fetal period
  3. at the end of pregnancy (2/3 months)
A
    1. 2nd month of embryo: Presence of absence will determine the development of genitals
      * + testosterone -> penis and scrotum
      * no testosterone -> clitoris and vagina.
    1. Fetus: Differentiation of internal male genital tract
    1. Last 2/3 months of pregnancy: Causes testes to descend into scotum.
      * When dont descend -> cyptorchidism.
45
Q

Actions of testosterone during puberty.

A
    1. Increased muscle mass
    1. Growth spurt on puberty
    1. Close epiphyseal plates
    1. Causes penis and seminal vesicles to grow
    1. Deepens voice
    1. Spermatogenesis
    1. Libido
46
Q

What are the SPECIFIC actions of DHT?

WHICH IS IMP DURING PUBERTY!

A
  • 1. Differentiation into male external genitalia (penis, scrotum and prostate).
  • 2. Hair distribition and baldness.
  • 3. Growth of prostate
  • 4. Sebaceous gland activity.
47
Q

How can we treat BPH (benign prostatic hypertrophy) and hair loss in males?

A

5a-reductase inhibitor

  • bc these occur d/t DHT.
48
Q

What are the actions of androgens?

A
    1. Differentiation of M internal/external genitalia.
    1. Stimulate growth and help to develop secondary sex characteristics during puberty.
    1. Maintain reproductive tract and make semen.
    1. Initiate and maintain spermatogenesis.
49
Q

What are the anabolic actions of androgens?

A
    1. Makes RBC
    1. Stimulates secretion from sebaceous gland
    1. Controls protein anabolic effects
    1. Causes linear body growth, bone growth, closure of epiphses
    1. Makes ABP
    1. Maintains secretions of sex glands
    1. Regulates behavioral effects, like libido.
50
Q

What are the symptoms of BPH?

A
    1. Need to pee more
    1. Urgently pee
    1. Nocturia (need to pee at night)
    1. Problem initiating and maintaining urinary stream
    1. Feels like bladder is full even after peeing
    1. Dribbling of pee
51
Q

Is BPH d/t increase in concentration of DHT?

A
  • No. Ppl with BPH have the same concentration of DHT than those without.
  • HOWEVER; they may have more DHT receptors on prostate.
52
Q

Describe the intracellular mechanism of testosterone.

A
  1. LH binds to LH receptor on the Leydig cell.
  2. +Gs -> +cAMP/PKA pathway
  3. Makes enzymes that convert cholesterol -> testosterone
  4. Cholesterol -> testosterone
  5. Testosterone diffuses into sertoli cells of seminiferous tubules and lumen of semiferous tubules
    1. ​In Sertoli cell of seminiferous tubules: Testosterone has two actions:
      • Aromatoization of testosterone to estradiol-17B via aromatase
        • Estradiol can then: go back to circulation, help with protein production in Leydig cell or it can stay in seminiferous tubule.
      • Bind to ABP and go to seminiferous lumen.
  6. Sertoli cells are then stimulated by testosterone and FSH
  7. +Gs -> +cAMP/PKA pathway
  8. Makes proteins such as
    1. inhibins
    2. ABP -> goes into lumen of seminiferous tubules
    3. Aromatase
    4. Growth factors and other products
53
Q

What does inhibin do?

A

Inhibin inhibits FSH.

54
Q

What provides a supply of testosterone for developing spermatogonia?

A

Binding of testosterone to ABP in the lumen.

55
Q

What types of functions do sertoli cells have?

A

1. Supportive

2. Exocrine

3. Endocrine

56
Q

What are the supportive functions of sertoli cells?

A
    1. Maintain blood-testis barrier
    1. Phagocytosis
    1. Transfer nutrients from blood -> sperm (such as transferrin, Fe and lactate)
    1. Receptors for hormones and paracrines
57
Q

What are the exocrine functions of sertoli cells?

A

1. Makes fluid

2. Makes ABP

3. Determines when sperm is released from seminiferous tubule

58
Q

What are the endocrine functions of sertoli cells?

A

1. Expresses receptors for ABP, T and FSH

2. Makes AMH

3. Aromatization of T -> estradiol-17B

4. Makes inhibin to regulate FSH.

59
Q

Draw the hypothalamic-pituitary gonadal axis.

60
Q

Spermatogenesis occurs continuously throughout the reproductive life of the male, from ________ until ________. Spermatogenesis occurs ___________, and the process can be divided into three phases:

A

Spermatogenesis occurs continuously throughout the reproductive life of the male, from puberty -> senescence. Spermatogenesis occurs along the length of the seminiferous tubules, and the process can be divided into three phases:

  • 1. Mitotic division
  • 2. Meitotic division
  • 3. Spermiogenesis
61
Q

Seminiferous tubules are lined by epithelium that contain 2 populations of cells. What are they?

A
    1. Spermatogenic cells that develop into spermatozoa
    1. Sertoli cells, which have supportive and nutrient function
62
Q

How long does spermatogenesis take?

A
  • Entire process is 64 days. The process is staggered to allow a group of cells to enter maturation every 16 days.
63
Q

Where do the 3 phases of spermatogenesis occur?

A
    1. Mitotic division creates spermatogonia occurs in the basement membrane of seminiferous tubules.
    1. Meiosis and spermogenesis occurs near the lumen of seminiferous tubules.
64
Q

Describe what happens in mitotic division of spermatogenesis.

A

Spermatocytogenesis (mitotic division) is the proliferative phase

  • At puberty, mitosis increases and spermatogonia or stem cells divide to make -> daughter spermatogonia
  • After last division, they are called primary spermatocytes.
65
Q

Describe what happens in the meiosis division of spermatogenesis.

A

Meisosis makes our haploid gametes.

  1. Primary spermatocytes (diploid 4N) -> 2 Secondary spermatocytes (haploid 2N) via 1 division of meiosis
    • Duplicated chromosomes
  2. 2 Secondary spermatocytes (haploid 2N) -> 4 spermatids (haploid 1N) via meiosis II
    • spermatids -> immature haploid gametes
66
Q

Describe what happens in the spermiogenesis phase in spermatogenesis.

A
    1. 4 Spermatids -> 4 mature spermatozoa through the loss of the cytoplasm, nuclear changes and development of flagella.
    1. Sertoli cells in the testis release spermatozoa
67
Q

Spermiogenesis and structure of spermatozoon

slide 49

A

resideual body is phagocytozed by. sertoli cell

68
Q

What 5 hormones stimulate spermatogenesis?

A

1. LH

2. FSH

3. GH

4. Testosterone

5. Estrogen

69
Q

LH, FSH, and GH stimulate spermatogenesis.

Actions of each?

A
  1. LH
  • Secreted by AP.
  • Causes leydig cells to secrete testosterone
  1. FSH
  • Secreted by AP
  • Needed for spermiogenesis ) and causes sertoli cells to nurse and form sperm
  1. GH
    * Needed to control metabolic functions of testes and promotes early division of sperm
70
Q

What. happens if we do not have FSH or GH?

A
  • No FSH-> no spermiogenesis
  • No GH-> spermatogenesis is deficient or absent -> infertility like in dwarfs
71
Q

Testosterone and estrogen stimulate spermatogenesis.

Actions of each.

A
  1. Testosterone
  • Secreted by: Leydig cell
  • to grows and divides testicular germinal cells -> begining of sperm formation
  1. Estrogen
    * Formed from testosterone in sertoli cells when stimulated by. FSH
72
Q

What happens if we have high levels of testosterone in a. normal man?

A

? Look at. slide 53

73
Q

Describe the sperm maturation that occurs in the epididymis.

A
  1. When sperm enters the epididymis from rete testis, they are weakly motile.
  2. Spend a month in epididymis to mature.
    1. Decapcitation occurs: add molecules to the membrane of sperm to prevent acrosomal reaction before it meets with an egg.
  3. Can store mature sperm for several months and they leave strongly motile.
74
Q

We see an increase in testosterone during ________.

What happens in adulthood?

A
  • Puberty.
  • Men will see a decrease in testosterone around 40 years old, leading to a decrease in sperm production later.
75
Q

Semen is made up of what?

A
  1. Fluid and sperm from vas deferens (10%)
  2. Fluid from seminal vesicles (60%)
  3. Fluid from prostate (30%)
  4. Small amount of fluid from bulbourethral gland
76
Q

What is the pH of the semen and how does it get to such pH

A
  • pH= 7.5
  • The alkaline fluid from prostate neutralizes the acidity of other semen components.
77
Q

Sperm can live for many weeks in male genital ducts. One ejaculated in the semen, how long can it live?

A

28-48 hours at our body temperature

78
Q

What is the track of sperm?

A
    1. Spermatozoa leave seminiferous tubules of gonad via efferent ductules
    1. Epididymis
    1. Vas deferens
    1. Ejaculatory duct
    1. Prostatic urethra
    1. Membranous urethra
    1. Penile urethra
79
Q

What are the TWO main differences between the male and female reproductive tract?

A
  1. Males have a continous lumen from the seminiferous tubules -> end of tract
  2. Male tract connects to the distal urinary tract (urethra)
80
Q

An erection is a neurovascular event where the 3 erectile bodies in the penis (2 corpora cavernosa and corpus spongiosum) fill with blood due to ________

A

Vasodilation.

Thus, flaccid penises usually have minimal blood flow d/t vasconstriction.

81
Q

Describe the process of an erection.

A
    1. Parasympathetic nerves that innervate vascular SM of helicine arteries that supply blood to erectile tissue release NO.
    1. +GC: GTP->cGMP
    1. Decreases intracellular Ca2+
    1. Relaxes vascular SM and vasodilation.
    1. Increase blood flow into sinusoidal cavernous spaces
    1. Engorged tissue presses the veins and reduce drainage
    1. Somatic stimulation caues muscles around the base of penis to contract.
  • –> ERECTION
82
Q

What is emission?

A

Movement of semen from epididymis -> vas deference -> seminal vesicles and prostate -> ejaculatory ducts thats under sympathetic control.

83
Q

Emission is under sympathetic control. What to prevent semen from flowing backwards.

A

Peristaltic contraction of SM of vas deferens which closes the internal sphincter of the bladder, preventing retrograde ejaculation of semen back into the bladder.

84
Q

What. happens if we destroy internal spincter of bladder?

A

Retrograde ejaculation.

85
Q

When does emission occur?

A

Before and during ejaculation.

86
Q

What is ejaculation?

A
  • Bulbospongiosus and ischiocavernous muscles are striated muscle that surround the base of the penis and are innervated by somatic motor nerves.
  • Contraction will cause ejaculation, (sperm movement out. of the urethra)
87
Q

How do we get rid of an erection?

A

Type 5 phosphodiesterase converts cGMP-> GMP.

88
Q

What type of drug is viagra (sildenafil)?

A

Type 5 PDE inhibitor

89
Q

The effects of testosterone deficiency depends on how old we are

What happens when deficient at 2-3 months of gestation and 3rd trimester of pregnancy?

A
  1. 2-3 months: ambiguity in male genitalia and male pseudohermaphridism (intersex).
  2. 3rd trimester: cryptorchdism and micropenis
90
Q

The effects of testosterone deficiency depends on how old we are

What happens when deficient at puberty and post-puberty?

A
  • Puberty: poor secondary sexual development and eunuchoid features (prepubertal characteristics and those of opp sex).
  • Post-puberty: decreased libido, erectile dysfunction, decrease facial and body hair, low NRG and infertility.
91
Q

Klinefelters syndrome

Classification:

Cause:

Effect:

A
  • Classification: Primary hypogonadism (low T, high LH)
  • Cause: Testicular dysfunction
  • Effect: low T secretion
92
Q

Pituitary tumor

Classification:

Cause:

Effect:

A
  • Classification: Secondary hypogonadism ( low T, low or normal LH)
  • Cause: problem with pituitary
  • Effect: Decrease LH/FSH secretion
93
Q

Kallmann’s syndrome

Classification:

Cause:

Effect:

A

Classification: Tertiary hypogonadism (decrease GnRH, decrease FSH/LH, decrease T)

Cause: Hypothalamic dysfunction

Effect: decrease GnRH

94
Q

What is Klinefelter’s syndrome?

A

Male genotype 46XY with one extra X chromosome that are phenotypically male at birth.

Testicular dysfunction (destruction of seminiferous tubules) causes low T and high gonadotropins (LH/FSH) at puberty, which do no result in normal growth of testicles and spermatogenesis.

95
Q

What is Kallmann’s syndrome?

A

Hypogonadotropic hypogonadism genetic disorder that occurs when GnRH neurons do not migrate to hypothalamus during embryonic development.

Causes: delayed/absent puberty and impaired sense of smell.

96
Q

BPH is related to _____ signaling and treated with ______.

A
  • DHT signaling
  • 5a-reductase inhibitor

Endo/Repro Exam 2 (17 decks)

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