Assessment Questions

Test and refresh your knowledge with these assessment questions:

1.Which form of cryptorchidism is more likely to lead to no sperm production?

Answer:

Azoospermia, where there is no sperm present in semen, is more likely to occur in bilateral cryptorchidism.

2.What causes a hydrocele to occur?

Answer:

Fluid is thought to occur as a result of the patent processus vaginalis in infants permitting peritoneal fluid to pass into the scrotum and surround the testicle; when excess fluid cannot drain the hydrocele forms.

3.What is the theory behind how a varicocele impairs fertility?

Answer:

The pooling of warm, refluxed blood in the veins is thought to raise scrotal temperature which in turn reduces testosterone synthesis by Leydig cells and reduces Sertoli cell secretory function. The result is reduced testosterone production and therefore reduced sperm production, leading to possible infertility. Varicoceles are also associated with spermatozoa DNA damage, and impaired testis and spermatozoa maturation which can lead to infertility as the sperm do not mature.

4.Why will deficit secretion or action of GnRH lead to hypogonadism?

Answer:

Deficit secretion or action of GnRH results in insufficient, or absent, production of FSH and LH via the hypothalamic–pituitary–gonadal axis. This leads to impaired gonadal maturation as FSH stimulates rapid reproduction of immature Sertoli cells and spermatogonia and LH stimulates Leydig cells to produce testosterone. Without this intensive stimulation of Sertoli cells and raised intragonadal testosterone levels, spermatogenesis is inhibited or not initiated at all.

5.What is the most common cause of epididymitis?

Answer:

Bacterial infection is the main cause; bacteria ascend the urinary tract, translocating into the vas deferens and making their way to the epididymis. Bacterial colonisation begins at the tail of the epididymis, spreading to its body and head, resulting in suppurative inflammation with fibrin covering. Pus may collect within the epididymal duct, causing it to rupture, creating sperm granulomas.

6.What is the most common cause of testicular torsion and what may it lead to?

Answer:

Twisting of the testis on the spermatic cord, obstructing the blood flow to the testis. It largely occurs as a result of an abnormality in the tunica vaginalis which permits the testis to move, resulting in axial rotation in the spermatic cord above. Disruption in blood flow occurs as the arteries contained within the spermatic cord are compressed.

7.Explain the pathophysiology behind how anterior urethral strictures form.

Answer:

The anterior urethral mucosa is surrounded by the corpus spongiosum along its length. When there are fibrotic changes in the corpus spongiosum, this impacts upon the extent and severity of the stricture in the underlying urethra as the fibrotic changes progressively result in scar formation (spongiofibrosis) whereby spongiol tissue is replaced by dense scar tissue that lacks elasticity and contains fibroblasts, forming the urethral stricture.

8.What are the main causes of erectile dysfunction?

Answer:

·    Neural: Neurological disorders can impair the regulation of penile erection when neurotransmitters and neural structures within both the spinal and supraspinal pathway are involved. Cavernous nerve injury can also be a cause.

·    Vascular: Impaired blood flow to the corpus cavernosum (e.g. from arterial disease, hypercholesterolaemia and hypertension). Reduced bioavailability of NO can impair the necessary blood flow to achieve an erection.

·    Hormonal: It is thought that a threshold level of testosterone is necessary for an erection to occur; consequently, hypogonadism can lead to ED as a result of insufficient testosterone.

·    Psychogenic: Depression, performance anxiety, and low libido can cause ED secondary to inhibition of the spinal erection centre and/or excessive levels of peripheral catecholamines.

9.Describe the three types of ejaculatory dysfunction and how they could impair fertility.

Answer:

i.    Premature: There are two forms of premature ejaculatory dysfunction, both of which can lead to ejaculation before sexual penetration occurs, preventing fertilisation of the ovum:

o primary: this lifelong form is thought to have a genetic predisposition that predisposes to impairment of inhibitory serotonergic pathways that regulate ejaculation

o secondary: this form occurs following having had normal ejaculatory experiences and can be psychogenic or have organic causes (prostatitis, hyperthyroidism, or be secondary to weaning from medication)

ii.   Delayed: This form of ED results in a delay in orgasmic response and subsequent ejaculation despite sufficient sexual stimulation and is associated with low androgen levels. When there are low levels of testosterone, subsequent reduction in NO can lead to penile flaccidity which can reduce ejaculatory volume but also lead to a loss of psychogenic libido. Additionally, delayed ejaculation may also occur secondary to the threshold for ejaculation not being met or delayed, also exacerbated by a loss of psychogenic libido. This can result in no ejaculation occurring, inhibiting the fertilisation of the ovum.

iii.  Retrograde: When semen is directed to exit the body through the urethra but is misdirected into the bladder, preventing fertilisation of the ovum. This can occur as a result of failure of contraction of the internal urethral sphincter secondary to neural impairment or from contraction of the external urethral sphincter, preventing external urethral outflow.

10.What is benign prostatic hyperplasia and how does it occur?

Answer:

BPH occurs when there is hyperproliferative of epithelial and stromal cells in the transition zone of the prostate gland. This is thought to occur as a result of excess testosterone which is converted to dihydrotestosterone in the prostate gland, triggering cell proliferation and differentiation. It can also occur as a result of inflammation as cytokine release in inflammation may promote the presence of growth factors that trigger cell proliferation in the prostate. It is thought that chronic inflammation and these hormonal changes result in hyperplasia and fibrotic changes to prostatic tissue.

11.Explain the difference between phimosis and paraphimosis.

Answer:

Phimosis is when there is an inability to retract the foreskin over the glans penis whereas paraphimosis occurs when the foreskin becomes trapped behind the corona of the glans penis, compromising arterial supply to the gland and preventing venous and lymphatic return.

12.What is the link between zinc and prostate cancer?

Answer:

The prostate gland uses zinc to make citrate which is an important component of semen. This process uses significant amounts of energy. This is reliant on a transport protein (ZIP1) to bring zinc into the cell and the gene to create this transport protein is suppressed in prostate cancer. Cancerous prostate cells are found to be devoid of zinc and therefore use the energy not used to generate citrate to proliferate. Introducing zinc into cancerous prostate cells is known to eliminate them as it induces apoptosis in abnormal cells.

13.From what cells does testicular cancer originate?

Answer:

Neoplasms in testicular cancer are derived from gonocytes that have failed to differentiate into spermatogonia.