Male Reproduction -- Wright

What structures within the testes are responsible for sperm production?

Seminiferous tubules

Which cells in the seminiferous tubules support sperm development?

Sertoli cells

Which cells in the testes produce testosterone?

Leydig (interstitial) cells

WHat is the role of the epididymis in male reproduction?

Maturation and storage of sperm.

What is the correct order of sperm development from stem cell to mature sperm?

Spermatogonia → primary spermatocytes → secondary spermatocytes → spermatids → spermatozoa

Which stage of spermatogenesis is diploid but post-meiotic DNA replication?

Primary spermatocyte

Which step introduces genetic diversity in sperm?

Meiosis I (crossing over in primary spermatocytes).

Where does spermatogenesis occur?

Seminiferous tubules

What is the function of the acrosome in sperm?

contains enzymes for penetrating the egg

What structure provides motility to sperm?

the flagellum (tail).

What organelle provides ATP for sperm motility?

Mitochondria in the midpiece.

What is a normal sperm morphology important for?

Fertility and successful egg penetration.

Where do sperm mature and gain motility?

Epididymis.

What is capacitation?

Physiological changes in sperm within the female tract that enable fertilization.

What is the acrosomal reaction?

Release of enzymes from the acrosome to penetrate the egg's zona pellucida.

Where are sperm stored prior to ejaculation?

Epididymis and vas deferens.

Which hormone from the hypothalamus controls testosterone secretion?

GnRH (Gonadotropin-releasing hormone).

Which pituitary hormones regulate male reproduction?

LH (stimulates Leydig cells for testosterone) and FSH (stimulates Sertoli cells for spermatogenesis).

What feedback effect does testosterone have on the hypothalamus and pituitary?

Negative feedback on GnRH and LH secretion

What is the role of inhibin in male reproduction?

Released from Sertoli cells, inhibits FSH secretion.

During development, what role does testosterone play in sex determination?

Drives differentiation of male internal and external genitalia.

Which derivative of testosterone is essential for development of external male genitalia?

Dihydrotestosterone (DHT).

What is the role of testosterone in puberty?

A: Development of secondary sexual characteristics (voice, muscle mass, hair growth)

How does testosterone affect spermatogenesis?

Maintains Sertoli cell function and sperm production.

Which nervous system branch controls erection?

Parasympathetic nervous system.

Which nervous system branch controls ejaculation?

Sympathetic nervous system.

Which neurotransmitter mediates penile erection via smooth muscle relaxation?

Nitric oxide (NO)

What is the mechanism of PDE-5 inhibitors in erectile dysfunction?

Inhibit breakdown of cGMP, enhancing NO-mediated vasodilation.

Which muscle controls urine release from the bladder?

External urethral sphincter (voluntary control).

What is BPH (benign prostatic hyperplasia)?

Noncancerous enlargement of the prostate gland causing urinary symptoms.

Which drug classes are used to treat BPH?

α1-blockers (relax smooth muscle) and 5α-reductase inhibitors (reduce prostate size).

How can BPH cause bladder outflow obstruction?

Enlarged prostate compresses the urethra.

What is the first hemodynamic event in penile erection?

Relaxation of penile arterioles → increased blood flow.

What role do cavernosal smooth muscles play in erection?

Relax to allow engorgement of erectile tissue.

What are the two phases of ejaculation?

Emission (sperm into urethra, sympathetic) and expulsion (ejection via somatic reflexes).

What are common causes of erectile dysfunction?

Vascular disease, diabetes, neuropathy, psychological factors, medications.

A 68-year-old male presents with difficulty initiating urination, weak stream, and nocturia. His PSA is within normal limits. On physical exam, he has an enlarged prostate. His blood pressure today is 108/68 mmHg.

Which is the best initial pharmacologic option for symptom relief?

A. Finasteride

B. Tamsulosin

C. Testosterone gel

D. Dutasteride

B. Tamsulosin

Rationale:

Tamsulosin is an α1-adrenergic antagonist that relaxes smooth muscle in the bladder neck and prostate, improving urinary flow.

Finasteride/Dutasteride (5-α reductase inhibitors) shrink the prostate but take months to work.

Testosterone would worsen BPH.

His blood pressure is normal, so a selective α1-blocker (tamsulosin) is preferred to minimize orthostatic hypotension.

A 55-year-old man with type 2 diabetes reports inability to achieve an erection. He is prescribed sildenafil.

Which is the mechanism of action of sildenafil?

A. Enhances breakdown of cAMP in smooth muscle

B. Inhibits phosphodiesterase-5, increasing cGMP levels

C. Stimulates nitric oxide synthase directly

D. Blocks alpha-1 receptors in penile vasculature

B. Inhibits phosphodiesterase-5, increasing cGMP levels

Rationale:

PDE-5 inhibitors (sildenafil, tadalafil) prevent cGMP breakdown, prolonging smooth muscle relaxation and increasing penile blood flow.

They do not directly release NO or block adrenergic receptors.

A 22-year-old man is undergoing evaluation for infertility. Labs show:

Low sperm count

Low inhibin B

Normal testosterone

Normal LH levels

Which is the most likely site of dysfunction?

A. Leydig cells

B. Sertoli cells

C. Hypothalamus

D. Adrenal glands

B. Sertoli cells

Rationale:

Sertoli cells are responsible for spermatogenesis and produce inhibin B, which provides negative feedback to FSH.

Low inhibin B + low sperm count suggest Sertoli cell dysfunction, despite normal testosterone (Leydig function intact).

A newborn male presents with ambiguous genitalia. Genetic testing reveals a 46,XY karyotype. Labs show elevated testosterone but decreased dihydrotestosterone (DHT).

What is the most likely enzyme deficiency?

A. 5-α reductase

B. Aromatase

C. 17α-hydroxylase

D. 21-hydroxylase

A. 5-α reductase

Rationale:

5-α reductase converts testosterone → DHT, required for external male genitalia development.

Aromatase converts androgens → estrogens.

17α/21-hydroxylase deficiencies affect adrenal steroid synthesis, not specifically DHT.

A 70-year-old man with hypertension and BPH reports worsening erectile dysfunction after starting a new medication. Which of the following is the most likely culprit?

A. Hydrochlorothiazide

B. Tamsulosin

C. Sildenafil

D. Finasteride

D. Finasteride

Rationale:

Finasteride (5-α reductase inhibitor) reduces DHT, which can decrease libido and cause ED.

Hydrochlorothiazide may rarely cause ED but less commonly than finasteride.

Tamsulosin improves urinary flow and usually does not cause ED.

Sildenafil improves ED

A 25-year-old male has low testosterone, low LH, and low FSH levels. Which condition best explains his presentation?

A. Primary hypogonadism

B. Secondary hypogonadism (pituitary)

C. Sertoli cell-only syndrome

D. Leydig cell tumor

B. Secondary hypogonadism (pituitary)

Rationale:

Low testosterone + low gonadotropins (LH/FSH) = secondary hypogonadism due to hypothalamic or pituitary dysfunction.

Primary hypogonadism = low testosterone but elevated LH/FSH.

Sertoli cell-only = low sperm, low inhibin, but usually normal testosterone.

Leydig cell tumors ↑ testosterone, not ↓.

A male patient undergoing infertility evaluation has normal testosterone and LH but elevated FSH. Which dysfunction is most likely present?

A. Impaired Leydig cell function

B. Impaired Sertoli cell function

C. Hypothalamic tumor

D. Increased aromatase activity

B. Impaired Sertoli cell function

Rationale:

Sertoli cells secrete inhibin B, which suppresses FSH.

If Sertoli function is impaired → ↓ inhibin B → ↑ FSH despite normal testosterone.

A 30-year-old bodybuilder is taking high-dose testosterone injections. Which lab finding is most likely?

A. High FSH, high LH, low inhibin B

B. Low FSH, low LH, low inhibin B

C. High FSH, low LH, high inhibin B

D. Normal FSH, normal LH, normal inhibin B

B. Low FSH, low LH, low inhibin B

Rationale:

Exogenous testosterone → negative feedback on hypothalamus/pituitary → suppresses GnRH, LH, and FSH.

Without FSH, Sertoli activity ↓ → low inhibin B → impaired spermatogenesis.

Which enzyme is responsible for converting testosterone to estradiol in adipose tissue?

A. 5-α reductase

B. Aromatase

C. 21-hydroxylase

D. 17α-hydroxylase

B. Aromatase

Rationale:

Aromatase converts testosterone → estradiol.

5-α reductase → testosterone → DHT.

21/17α-hydroxylase are adrenal enzymes for cortisol/aldosterone synthesis.

A 17-year-old boy has delayed puberty. He has low testosterone, low LH/FSH, and anosmia. What is the underlying defect?

A. Mutation in androgen receptor

B. Failure of GnRH-secreting neurons to migrate

C. Excess aromatase activity

D. Leydig cell destruction

B. Failure of GnRH-secreting neurons to migrate

Rationale:

Kallmann syndrome: defective migration of GnRH neurons → ↓ GnRH → ↓ LH/FSH → ↓ testosterone, delayed puberty, anosmia.

Not an androgen receptor issue (that would have high LH/testosterone).

A 46,XY infant is born with ambiguous genitalia but normal male internal reproductive organs. Which hormone is most directly responsible for this finding?

A. Lack of testosterone during development

B. Lack of DHT during development

C. Excess estradiol during development

D. Lack of inhibin during development

B. Lack of DHT during development

Rationale:

Testosterone = internal male structures (Wolffian ducts).

DHT = external genitalia, prostate.

Deficiency in 5-α reductase (→ ↓ DHT) = ambiguous external genitalia but normal internal male organs.

A 40-year-old male with pituitary adenoma secreting LH would be expected to have which hormonal profile?

A. ↑ LH, ↑ testosterone, ↓ FSH

B. ↑ LH, ↑ testosterone, ↑ FSH

C. ↑ LH, ↑ testosterone, ↓ GnRH

D. ↓ LH, ↓ testosterone, ↑ GnRH

C. ↑ LH, ↑ testosterone, ↓ GnRH

Rationale:

Pituitary adenoma producing LH = ↑ testosterone from Leydig cells.

Negative feedback decreases hypothalamic GnRH.

FSH may not be directly affected.

A man with BPH is prescribed finasteride. What is the main mechanism by which it works?

A. Blocks testosterone receptors in prostate tissue

B. Inhibits aromatase, reducing estrogen

C. Inhibits 5-α reductase, reducing DHT

D. Blocks α1 receptors, relaxing smooth muscle

C. Inhibits 5-α reductase, reducing DHT

Rationale:

Finasteride reduces DHT production, shrinking prostate size.

Does not act as an α-blocker (tamsulosin does that).

T/F: Leydig cells are found within the seminiferous tubules where they help sperm mature.

False

Rationale: Sertoli cells help sperm to mature; Leydigs are in between the tubules and produce testosterone.

Sperm production begins when?

At birth

Spermatagonia develop from primordial germ cells shortly after birth but then the process halts until puberty.

What is not found in mature sperm?

Endoplasmic Reticulum

Rationale: The ER is converted into the acrosome which helps the sperm penetrate the egg.

For sperm to be successful, semen must...

-- Make the environment of the vagina conducive to fertilization.

--Keep sperm immobile until needed.

-- Provide nutrition

Testosterone surges before puberty are necessary for...

-- Correct expression of the male genotype

-- Proper development of male sex organs

-- Descent of testes into scrotum for viable sperm

Which hormone specifically feedsback to inhibit FSH produtcion

inhibin

T/F: The anterior pituitary secretion of FSH and LH is controlled by the hypothalamus using antagonistic tropic factors.

False, only positive simulation via GnRH