Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endocrine and Reproduction Systems > Male Reproduction > Flashcards

Male Reproduction Flashcards

1
Q

Embryogenesis vs fetal development

A

First 8 weeks vs the rest of the weeks leading to birth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Difference between male and female at the genetic level? The gonadal level?

A

Genetic level: male = XY (note that without it, neither testicular nor masculine development occurs), female = XX
Gonadal level: Males = 2 testis. Females = 2 ovaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is in the Y chromosome?

A

Sex determining region of the Y chromosome (SRY) gene. This encodes the testis determining factor (TDF), which is a gene specific transcription factor that initiates the conversion of primitive gonad into the testis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is needed for completely “man-ness”

A
  1. Y chromosome
  2. Sox9 transcription factor
  3. SF-1
  4. Androgen receptor, which is actually sex linked.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is special about gonadal tissue up until week 7?

A 
Both male and female genitalia are identical. Can turn into oogonia or spermatogonia (testes have formed here).
Coelomic epithelium (happens at week 7...first differentiation): turns into GRANULOSA cells in female and SERTOLI cells in males.
Mesenchymal cells (week 8/9): Turns into THECA cells in females and LEYDIG cells in males
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What do leydig cells secrete? sertoli cells?

A

Leydig: Androgens
Sertoli: ANTIMULLERIAN HORMONE (ser = serious, since this is legit crucial for male development)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the 2 ducts present up until week 7.

A

Wolffian duct: male INTERNAL genital tract

Mullerian Duct: female INTRERNAL genital tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What happens at week 9 of male development?

A

Testis:

  1. Secrets testosteoreon to foster wolffian duct developement. Makes seminal vescicles, vas deferens, epididymis
  2. Sertoli cells in testes Secretes anti mullerian hormone (AMH), which triggers mullerian duct regression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What happens at week 9 of female development?

A

Ovaries don’t do crap. XX gonad changes into 2 ovaries. Female development is default. Wolffian duct regresses in the absence of T. in absence of Anti mullerian hormone, mullerian duct takes over.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are female internal genital components?

A

Fallopian tubes, uterus, upper vagina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How could genetic male develop both male and female gentalia?

A

You would need the XY chromosome set, and the Y chromosome would need to be defective of sertoli cells, or at the very least anti-mullerian hormone (secreted from said sertoli cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Where do the mullerian and wollffian duct emanate from?

A

Primitive urogeneital sinus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does external male genitalia form in week 10?

A

T is still secreted locally, but is also secreted into circulatory system and is converted to dihydrotestosterone (DHT), which is a more potent tetsosterone, with 5-alpha-reductase. DHT then acts at pluripotent genital tubercle/urethra folds/urogenital sinus/genital swelling into PROSTATE, scrotum, penis, urethra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What happens if DHT is not present at week 10?

A

Female external genitalia is default.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the 3 hormones secreted from the testes? Are testis only important at puberty?

A

Testosterone, anti-mullerian hormone, DHT. So testis are important waaaaay before puberty…actually, they are important starting in utero.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Caper’s gland =

A

bulbourethra gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the 2 functions of testis?

A
  1. Produce sperm

2. Produce androgens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Where is mature spermatozoa stored? What happens at ejaculation?

A

Spermatozoa are stored in epididymus. At ejaculation, spermatozoa move up vas deferens, combines with seminal fluid from seminal vesicles and prostate gland, and this makes semen. The semen enters urethra and exits penis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Where is the bulbourethral gland? What is its job? What helps spermatozoa travel in pathway?

A
  1. Located below prostate gland
  2. Secretes mucus pre-ejaculation which neutralizes and lubes urethra for sperm passage.
  3. Smooth muscle contraction along the tract from the epididimus to the urethra
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What happens when male is sexually excited?

A

SNS triggers closure of neck of bladder (urinary sphincter). Makes it so micuration (peeing) and ejaculation cannot happen at same time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Why is male reproductve system symetrical?

A

2 wolffian ducts at embryogenesis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Job of seminal vesicles

A

Secretes fluid rich in fructos and prostaglandins and citrate, and nutrients. Feeds ejaculated sperm. Prostaglandins react with cervical mucus to allow for better sperm motility. Also produces peristaltic contractions in female reproductive tract to propel sperm up the tract. It’s 60% of semen volume.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Prostate gland job

A

30% of semen volume. Secretes milky alkaline fluid. Has calcium, acid phosphatase, and PSA (prostate specific androgen) which helps mark for prostate cancer (check at age 50 and up). The milky fluid also helps with sperm motility and helps neutralize acidic environment of female vagina, prolonging sperm survival.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Bulbourethral glands job

A

Upon sexual arousal, but BEFORE ejaculation, produces clean, salty viscous secretion called pre-ejaculate. Neutralizes traces of acidic urine and lubes urethra for sperm passage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What causes prostate growth? What issues could occur?

A

DHT (dihydrotestosterone). Never stops. BPH = benign prostate hyperplasia, which occurs when growth is too much…too many cells. Prostate cancer = malignannt form. Most common cancer in men in US.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Where is the prostate gland? Why does that matter?

A
  1. right up against and below the bladder, and completely surrounds urethra. Sits are bottom part of rectum.
  2. As gland enlarges, it constricts urethra. Causes frequent/slow/painful urination. Also, at age 50, digital rectal exam can be done to look at the size of the rectum gland.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Why are testis situated away from the scortum 1-2 degrees below core body temp?

A

Lower bp is crucial fro optimal spermatogenensis. If too cold, smooth muscle lining wall of scrotum, innervated by sns, will contract to draw testis closer to body.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Where is sperm produced?

A

Seminiferous tubules. Drains into epididymus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

where do leydig cells reside?

A

In the last 20% of the testes, which is connective tissue inrerstitum. Leygid cells sit on seminiferous tubules. note that sperm in seminiferus tubules has spermatozoa throughout the sertoli cells in sequence of development. Note that sertoli cells completely surround the developing sperm cells, which is why they are critical to their development.

30
Q

Explain th epoint of the tight junctions in semiiferous tubuels.

A

Blood sperm barrier. Separates blood and area above basement membrane from the developing sperm below it. Otherwise, spermatogenesis would be contaminated. Also prevents sperm with flagella to get into the circulatory system (would otherwise set off immune response)

31
Q

Why do seminiferous tubules contract (note that they have actin filaments that allow them to do this)?

A

Pushes mature spermatozoa into lumen so they can swim to epididymus.

32
Q

Where are androgens made?

A

Leydig cells outside the seminiferus tubules. All within the testis.

33
Q

What two drugs do the testes make? What are they eventually all converted to?

A

DHEA (converted to T with 3b-HSD) and androstenedione (converted to T with 17B-HSD).

34
Q

How do you convert T to the more potent form, dihydrotestosterone (DHT)? Which cells express this enzyme? What tissues have receptors for this? Where is most of DHT produced? Wher does most of T and DHT originate from in males?

A

5-a-reductase, expressed by leydig cells. Prostate is an example of a target tissue for DHT Most DHT is made outside of the body. Most of D and DHT originate from the testis in males.

35
Q

What is the obligate precursor of estrogen? Which androgen is converted to estrone with aromatase (CYP19)? Which androgen is converted to estradiole with the same enzyme? How do you convert Estrone to estadiol?

A
  1. Androgens.
  2. Androstenedione
  3. T
  4. 17B-HSD
36
Q

Where is the highest level of CYP19 expression? How do you identify a successful androgen to estrogen conversion?

A
  1. Ovaries

2. “A” ring becomes aromatic (hence aromatase)

37
Q

Where do you find aromatase (CYP19) in males? WHat enzyme is present in the testis and not in the andrenal gland?

A
  1. Leydig cells, brain, pit, bone, adipose (predominant source of estrodaiol)
  2. 17B-HSD, which is mandatory to make testosterone. So the bulk of testosterone its made in the testes
38
Q

What 3 hormones are secreted from sertoli cells? What other things do they secrete?

A
  1. Inhibin (negatively feeds back FSH production and release at pit)
  2. Activin (Stimulates FSH production and release at pit)
  3. Anti-mulherian hormone (triggers mullherian duct regression)
    All 3 are formed by ssame overall protein
    Note that they also make a bunch of mitogenic and insulin growth factors. They stay put, not entering blood stream
39
Q

Describe the major hormones of testes regulation

A

FSH and LH (the main gonadotropal hormones). They have same alpha and different beta subunit. Hypothalamus releases GnRH from ant pit in PULSES and this causes FSH and LH release.

40
Q

What controls GnRH? What does it do?

A

Hypothalamus….gets bombarded by hormones, neruotransmitters, and neuropeptides. Releases GnRH in pulses (8-10 daily) from ant pit. Used to trigger LH and FSH release.

41
Q

What id job of LH? Why is the T involved inportant?

A

Acts on leydig cells to create T. Does so by catalyzing rate limiting step. T that is created acts on sertoli cells (autocrine function) to help with spermatogenesis.

42
Q

Where does FSH act?

A

Acts on sertoli cells to stimulate spermatogenesis.

43
Q

What happens in situations of high T?

A

Negative feedback, which kills GnRH production at hypothalm and LH at anterior pit.

44
Q

What is inhibin? Where does it come from? What about inhibin? (hypothalamic pit gonadal axis)

A

Sertoli cells releases inhibin (only made in sertoli cells) in order to possibly inhibit hypothalmus from releasing GnRH that leads to FSH production. Activin does the exact opposite.

45
Q

Describe gonadotropin secretion over a given lifetime.

A

Increase at midway of gestation, drop at birth, transient rise and fall at year 1, GnRH, LH, FSH all stay low in childhood even tho T, E2, and Inhibin are also low at this point (GnRH pulse gen is likely dormant here). GnRH kicks back up at puberty, and body is more receptive to the hormones. Increase in E2 in females and T in males. Increase in hGH in both. In adults, females, pulses of LH outway pulses of FSH (menstrual cycle). At older ages, gonandal responsiveness wanes. In females, there’s a drop in E2, but the the dropoff is slower in males. THe dropoff means there is no FSH or LH negative feedback, so FSH grossly runs wild. T profile follows the same exact pattern. At 17-20, T is at max and plateaus for 30-40 years. T levels start to decrease 100 nm/dl at the end of this every 10 years.

46
Q

Testes fun facts

A
  1. 1 spermatagonia yields 64 spermatazoa
  2. 100-200 mil sperm a day is made. same amount is ejaculated during sex
  3. takes 60-70 days to develop a spermatazoa.
47
Q

At puberty, what happens to spermatagonia?

A

2 divisions, leading to one resting spermatagonia (serves as future sperm generator) and 3 active spermatagonia, which turns into type B spermatagonia and later primary spermatocyte. Tight junction is formed by sertoli cells to separate these guys from the resting spermatagonia. Primary spermatocyte takes over and enters prophase of miosis, dividing for 3 weeks. Resulting daughter cells undergo a second division becoming haploid. The haploids have 22 chromosomes and either an X or y chromosom on top of that. In the final stage (spermiogenesis), their cytoplasms shrink drastically., flagella and acromiun head form. This haploid is now termed a spermatazoa.

48
Q

Describe the sperm flagella.

A

End piece: helps propel
principla piece: flagellar motion
Middle piece: mitochondria for atp that drives principal piece
Head piece with chromosomes and acrosome cap. It ill only release contents if it reaches female egg. Helps sperm penetrate the ova.

49
Q

What is essential for spermatogenesis?

A
  1. FSH is not the sole contributor. You need LH. Males with a deficiency in either are sterile
  2. LH cells stimulate leydig cells to make T and E2, and when combined with FSH, sertoli cells are stimulated to make androgen receptor and keeps concentration of hormones high in testes. E2 and T and all 3 kinds of sperm all express estrogen receptors.
50
Q

How does T travel?

A

Bound to Sex Human Binding Globulin (SHBG) (for E2 in females too), up until it hits destination where it’s released directly into the cell. SHBG is 2/3, albumin is the last 1/3. Protects sterod form being broken down in the liver, and extends halflife of the steroid.

51
Q

What happens to T upon entering the cell?

A

T is converted to DHT with 5-a-reductase rapidly since it binds more tightly to androgen receptor inside the cell. Cells with CYP19 convert the T to E2 instead to bind to estrogen receptor.

52
Q

What happens to DHT upon binding to androgen receptor?

A

COnformation change occurs, and androgen receptor and DHT enter nucleus as a homerdimer onto ARE of DNA. Coactivators binds to it and gene expression runs through.

53
Q

What happens to adutls with too much DHT?

A

Balding (andro genetic atropesia).

54
Q

Which hormone controls larnyx, and thus deep voice development? Muscle mass by stimulating protein synth to increase size of protein fiber? Heart disease more in men than in woman?

A

T

55
Q

What gland is entirely dependent on DHT? Why is this problematic? Who’s more likely to get prostate cancer?

A

Prostate. If cells become malignant, DHT doesn’t know. It keeps secreting, helping both healthy and malignant prostate cells.
*Males greater than 50 are 97% of prostate cancer cases.

56
Q

What does prostate gland initially need for growth and survival? How is this exploited for treatment?

A

Androgens. Treat with androgen ablation therapy (worst case…normally, surgery would suffice) (block androgen receptors)

57
Q

List treatment options for prostate cancer.

A
  1. Remove testes (orchidectomy)
  2. Drugs that inhibit hypothalmus-pit-gonadal access. usually GnRH agonists/antagonists (sometimes) to distort natural pulse of hypothalamus. Pit responds by killing FSH and LH production entirely.
  3. E2 treatment. Just like T, it too can negatively feedback hypothalamus and pit, suppressing GnRH and thus FSH and LH. This treatment works well since E2 does not bind to the androgen receptor.
  4. Glucocortical steroids can be used, inhibitng Pit,m killing FSH and LH.
  5. CYP17 inhibitors can block T production from both adrenal glands and testes.
  6. T to DHT conversion can be blocked with 5-a-reductase inhibitors.
  7. Androgen receptor antagonists can be use. Very powerful. T and DHT can’t bind in this case.
58
Q

Describe hypothalamic-pit disorders

A

Primary defect in one of these glands, automatically leading gonadotropin secretion block secretion, and thus male hypogonandism. Examples: adenomas of hypothalmus or pit, severe head trauma, radiation, infections, infarctions. There could also be GnRH receptor mutations, LH and FSH mutations in BETA subunit. Cushings and fastings/critical illness (all scenarios where cortisl levels are expected to spike…remember the cortisol neg feedback? Turns out LH is effected since tit too comes out the pit!) can also screw up gonadotropin secretion.

59
Q

Describe how secondary gonadotropin deficiency can lower gonadotropin secretions.

A

Cushings syndrome. elevated cortisol levels usually kill CRH in hypothalamus and acth production in pit. However, in cushing’s disease, the excess of cortisol blocks both acth and LH productions since they are both in the pit. This is the rationale for treating prostate cancer patients.

60
Q

Describe primary gonadal abnormalities that lead to hypogonandism.

A

Chromosomal defect leads to screw up in gonadotropin production

61
Q

Describe how 47xx male syndrome (klinefelter’s syndrome…1/500 males) screws up gonandotropin hormone secretion

A

Issue is inheritance of extra X chromosome (meiotic maternal fusion, nondisjuntion of paternal sperm, or mitotic nondisjuntion). Purely random, not genetically passed on. Characteristics aren’t seen till puberty, but signs include: weak masculinityvariable degrees of feminization, weak development of testis/genetalia, weak muscle tone, ADHD, elevated gonadotropin but low T and High E2, weak facial hair, abnormal breast development (gynecomastia), and zero to weak sperm development due to fibrotic seminiferous cells. Note that 90% of these patients are sterile and 2/3 of these patient go undetected. Note that this disease is treatable if found before puberty.

62
Q

How does 46xx male syndrome (1/20000 males) affect gonadotropin secretion?

A

Y to X trasnlocation occured, with the portion of the y translocating to the X always having the SRY gene, which is why you see an xx male. Note that if y chromosome lacks sry gene, you get xy female. You would also see pseudohermatophedic phenotypes. Testicular inflamation, mumps and zika virus, drugs, radiation…may have defects in 17-b-HSD which is responsible for making adrogens. May also have cryptyorchidism (failure of one or more of the testis to descend into the scrotum)

63
Q

Describe cryptorchidism

A

Descent of testis. Entrirely t regulated. In male babies born with this, the testes descend later. But if they fail to descend and it does not correct itself, person is infertile since the temps are too high for spermatogenesis. Primary risk for testicular cancer and inguninal hernia.

64
Q

Describe defects in androgen action

A

Testis develop normally and can synth T but there is a defect in ability for T to hit target tissue. Androgen resistence, or androgen receptor mutations (reifenstein’s syndrom). Could even be defective mutation of 5-a-reductase (converts T to DHT). Remember, AR gene is linked to X chrome, so you only need one allel to see this issue. Patients with thsi issue would not be able to act on wolffian duct since it’s receptor is wrecked…could be weak or nonexistent. DHT also would not be able to act on pluripotent tubercle, so no external male genitalia (patient default external is female.) Severity of phenotype depends on severity of mutation.

65
Q

What happens in the case of In the case of defective 5-a-reductase?

A

T can still act on Mullerian and wolffian ducts. However, you can’t make DHT, so DHT can’t act on pluripotent tubercle. Severity of phenotype depends on severity of mutation.

66
Q

What is the WORST case scenario for androgen resistance?

A

Defect that completely knocks out androgen receptor since neither DHT or T can act as a result. In mice, neither mullerian or wolffian ducts develope. No fallopian tubes present. However, externa geitalia looks more female.

67
Q

What happens in complete androgen resistence?

A

Male pseudo hermaphroditism. Complete AR knock out. Genetic man has xy and 2 testis but external genitalia and secondary gonadal characteristics are all female. Even feminine behavior.

68
Q

Why would patietn with complete androgen resistance have secondary female characteristics?

A

Estrogen is still present even though T is not. Nothing is wrong with E2 receptor. The two testis can still make T, but no T receptor. But T can still be converted to E2. Make no mistake, E2 is not high in this patient. it’s just uncontested.

69
Q

Partial androgen resistance characteristics.

A

Ambiguous genitalia. Aka reifenstein’s syndrom. there would be a broad spectrum of secondary female characteristics.

70
Q

5-a-reductase deficiency characteristics

A

Autosomal genes. No DHT, so phenotype of genitalia is ambiguous. spectrumof secondary characteristics. This can be treated to a degree if detected early

Endocrine and Reproduction Systems (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions