Appearance
15.1 — Male Reproductive Anatomy
The testes sit outside the body, in a thin-walled sac with no protection at all, in the most exposed position they could possibly occupy. That arrangement is a genuine design problem, and the reason for it is temperature.
Sperm production requires about 2 to 4 °C below core body temperature. Everything about male reproductive anatomy follows from getting the testes out of the abdomen and keeping them there at the right temperature — including the hernia weakness of Chapter 3.6.
The testes
Each testis is about 4 to 5 centimetres long and weighs 15 to 25 grams.
And the left usually hangs lower than the right — in around 70 percent of men. The explanation is that the left testicular vein drains into the left renal vein at a right angle, while the right drains directly into the vena cava, so the left has slightly higher venous pressure and a longer cord.
That same drainage difference explains why varicoceles are far commoner on the left — around 85 to 90 percent — and why a right-sided varicocele appearing suddenly in an adult warrants investigation, because it can indicate something obstructing the vena cava.
Internally, each testis is divided into 200 to 300 lobules containing seminiferous tubules — tightly coiled tubes where sperm are made. Uncoiled, the tubules of both testes would run for around 500 metres.
Between the tubules sit the Leydig cells, which produce testosterone (Chapter 12.6).
Inside the tubules are the Sertoli cells, which support developing sperm and form the blood–testis barrier — tight junctions sealing the developing sperm off from the bloodstream.
And that barrier exists for an immunological reason. Sperm first appear at puberty, long after the immune system has established what counts as self (Chapter 13.2). So sperm carry surface molecules the immune system has never seen and would attack.
Which produces a real clinical consequence: a testicular injury or a vasectomy can breach the barrier, and some men develop anti-sperm antibodies afterwards — a recognised cause of infertility after vasectomy reversal.
Keeping cool
Three mechanisms, all working on the same problem.
Position — outside the body cavity, in the scrotum.
The cremaster muscle — which raises and lowers the testes with temperature. In the cold they are drawn close to the body; in heat they hang lower. The cremasteric reflex — stroking the inner thigh causes the testis to rise — is used clinically and is absent in testicular torsion.
The pampiniform plexus — a network of veins wrapped around the testicular artery, forming a countercurrent heat exchanger (Chapter 14.2). Warm arterial blood arriving is cooled by the returning venous blood before it reaches the testis.
And this explains why several things reduce fertility: prolonged hot baths and saunas, laptops on the lap, tight underwear to a modest degree, and — most significantly — varicocele, where the dilated veins impair the heat exchange and raise testicular temperature.
Undescended testis (cryptorchidism) — present in about 3 percent of full-term and 30 percent of premature male infants.
Most descend spontaneously in the first 3 to 6 months. Those that do not are brought down surgically, ideally by 12 to 18 months.
And the reason for the timing is specific. A testis kept at body temperature undergoes progressive damage to the sperm-producing cells, and the damage is largely irreversible after the first year or two. Surgery also reduces — though does not eliminate — the increased risk of testicular cancer, and it places the testis where it can be examined.
Testicular torsion
The most important emergency in this chapter, because it is time-critical and it is missed.
The testis twists on its cord, cutting off its own blood supply.
Sudden severe testicular pain, often with nausea and vomiting, frequently waking the person from sleep. The testis is high, horizontal and exquisitely tender, and the cremasteric reflex is absent.
Peak incidence is in the first year of life and at 12 to 18 years, corresponding to periods of rapid testicular growth.
And the window is narrow. Salvage rates are around 90 to 100 percent within 6 hours, around 50 percent at 12 hours, and under 10 percent beyond 24 hours.
So the rule is absolute: acute testicular pain is torsion until proven otherwise, and it is a surgical emergency. Imaging must not delay surgery — if the history is convincing, the correct action is exploration.
Two things cause preventable delay. Embarrassment — adolescent boys frequently do not tell anyone for hours. And pain referred to the abdomen, because the testis develops in the abdomen and drags its nerve supply down (Chapter 4.5), so torsion can present as abdominal pain with no complaint about the testis at all.
Which is why examining the testes is mandatory in any adolescent boy with acute abdominal pain.
The duct system
Epididymis — a single coiled tube, about 6 metres long, packed onto the back of each testis.
Sperm leaving the testis cannot swim and cannot fertilise. They acquire both capacities during the 2 to 12 days spent travelling through the epididymis, and they are stored in its tail.
Vas deferens — a muscular tube, about 45 centimetres, carrying sperm from the epididymis up through the inguinal canal into the pelvis.
Its wall is unusually thick and muscular, which is why it feels like a firm cord and why it can be located through the scrotal skin — the basis of vasectomy.
Ejaculatory ducts — formed where each vas joins the duct of a seminal vesicle, passing through the prostate to open into the urethra.
Urethra — about 20 centimetres in the male, carrying both urine and semen. The two never mix, because the bladder neck closes during ejaculation (Chapter 10.5).
The accessory glands
They contribute about 95 percent of the volume of semen. Sperm are a small fraction of it.
Seminal vesicles (about 60 to 70 percent of volume) — a thick alkaline fluid rich in fructose, which is the sperm's fuel supply, plus prostaglandins and a clotting protein.
Measuring fructose in semen is diagnostically useful: its absence suggests blockage or absence of the seminal vesicles or ducts.
Prostate (about 20 to 30 percent) — a thin milky alkaline fluid containing enzymes, zinc and prostate-specific antigen (PSA).
PSA liquefies the semen after ejaculation — semen coagulates immediately and then liquefies over 15 to 30 minutes, which appears to help retain it initially and then release the sperm.
And PSA leaks into the blood in small amounts, which is what makes it measurable as a test (Chapter 21.7).
The alkalinity of both secretions matters. Vaginal pH is around 3.5 to 4.5, which is hostile to sperm. Semen at pH 7.2 to 8.0 buffers it locally for long enough for sperm to reach the cervix.
Bulbourethral glands — a small volume of clear fluid released before ejaculation, lubricating and neutralising residual urine acidity in the urethra.
And it can contain sperm. Which is why withdrawal is a poor contraceptive method (Chapter 15.11) — around 20 percent failure in typical use.
Semen
Volume 1.5 to 5 ml per ejaculation. Sperm concentration normally above 15 million per ml, so 40 to 300 million in total.
Of which, in a normal sample, only around 4 percent or more need be of normal shape — which is a strikingly low threshold and reflects how variable sperm morphology is.
Sperm survive 3 to 5 days in the female tract, occasionally longer (Chapter 4.3).
The penis
Three cylinders of erectile tissue.
Two corpora cavernosa on the upper side, which do the work of erection.
One corpus spongiosum on the underside, containing the urethra and expanding into the glans.
And the corpus spongiosum is deliberately less rigid, so that it does not compress the urethra during erection and block ejaculation.
Each corpus cavernosum is a sponge of vascular spaces surrounded by a tough fibrous sheath — the tunica albuginea.
How erection works
It is a vascular event controlled by nerves, and the sequence is worth following because it explains every treatment.
Parasympathetic stimulation releases nitric oxide from nerve endings and endothelium (Chapter 1.8).
Nitric oxide raises cGMP, relaxing the smooth muscle of the arteries and of the spaces themselves.
Blood flows in rapidly — arterial inflow increases up to fortyfold — and the spaces fill.
And the crucial step is the venous one. As the spaces expand, they compress the veins draining them against the rigid tunica albuginea. Outflow is blocked mechanically by the expansion itself.
So erection is achieved by increasing inflow and then trapping the blood, and the trapping is what maintains rigidity.
Ejaculation is sympathetic — hence the teaching phrase "point and shoot" from Chapter 11.9. The bladder neck closes, the vas and accessory glands contract, and the pelvic floor muscles produce the rhythmic expulsion.
And this explains erectile dysfunction and its treatments.
PDE5 inhibitors — sildenafil, tadalafil — block the enzyme that destroys cGMP (Chapter 1.8), so the relaxation persists.
They do not cause erection. They amplify one that is starting, which is why they require sexual stimulation to work — a point that is frequently not explained and leads people to conclude the drug has failed.
And the nitrate contraindication is absolute (Chapter 1.8).
Erectile dysfunction affects around 50 percent of men aged 40 to 70 to some degree, and its causes divide usefully.
Vascular — much the commonest, and the reason erectile dysfunction matters medically. The penile arteries are small, around 1 to 2 millimetres, compared with the coronary arteries at 3 to 4.
So atherosclerosis narrows them first (Chapter 18.1).
Which makes erectile dysfunction an early warning of cardiovascular disease, typically preceding cardiac symptoms by three to five years. A man presenting with erectile dysfunction should have his blood pressure, lipids and glucose checked, and this is one of the more valuable and least-known facts in men's health.
Neurological — diabetes, spinal injury, multiple sclerosis, and pelvic surgery.
Hormonal — low testosterone, high prolactin (Chapter 12.2), thyroid disease.
Drugs — antihypertensives, particularly older ones; antidepressants, particularly SSRIs; antipsychotics; and alcohol.
Psychological — and the distinguishing feature is genuinely useful. Preserved spontaneous night-time and early morning erections indicate the machinery works, pointing toward a psychological or situational cause. Their absence points toward a physical one.
Priapism — a persistent erection lasting over four hours without arousal.
It is an emergency, because the trapped blood becomes deoxygenated and acidotic, and the tissue dies. Beyond about 24 to 48 hours, permanent erectile dysfunction is likely.
Causes: sickle cell disease — a common cause in affected boys and men (Chapter 2.8) — injected erectile dysfunction treatments, some antipsychotics, and trauma. Treatment is aspiration of the trapped blood, with or without injected agents to constrict the arteries.
The prostate
Position determines everything (Chapter 10.5). The urethra passes through it.
A walnut-sized gland, about 20 grams in a young man, growing steadily from about 40 onward.
Three conditions:
Benign prostatic enlargement — Chapter 10.5.
Prostatitis — inflammation, acute or chronic. Chronic prostatitis and chronic pelvic pain syndrome is common, poorly understood, and frequently managed badly with repeated courses of antibiotics for a condition that is usually not bacterial.
Prostate cancer — Chapter 19.5, and the essential points belong here.
It is the commonest cancer in men in many countries, and most men who have it die of something else.
Which is the central difficulty. Post-mortem studies find prostate cancer in around 30 percent of men over 50 and 70 percent over 80, most of whom had no symptoms and no diagnosis.
So the challenge is not finding prostate cancer — it is distinguishing the ones that matter from the ones that do not.
PSA screening is genuinely contested for exactly this reason. It detects cancers, and a substantial proportion of those cancers would never have caused harm. Treatment carries real risks of incontinence and erectile dysfunction.
The approach has improved. MRI before biopsy identifies which men need one and which do not, reducing unnecessary biopsies substantially. And active surveillance — monitoring low-risk cancers rather than treating them — has become standard, which resolves much of the overtreatment problem.
The honest position is that a man considering PSA testing should be given the actual numbers and make his own decision, rather than being screened by default or discouraged by default.
Testicular cancer
Uncommon overall, and the commonest solid cancer in men aged 15 to 35 — which is exactly why it deserves attention here.
And it is one of the great success stories in oncology. Cure rates exceed 95 percent overall, and even widely metastatic disease is cured in the majority, because these tumours are exceptionally sensitive to chemotherapy. Survival went from around 10 percent to over 90 percent following the introduction of cisplatin-based treatment in the 1970s.
Presentation: a painless lump or swelling in the testis. Occasionally an ache or heaviness.
Risk factors: undescended testis, previous testicular cancer, family history, and infertility.
Self-examination is worth teaching, and the practical version is: once a month, after a warm bath or shower when the scrotum is relaxed, roll each testis between thumb and fingers. You are feeling for a firm lump within the testis itself.
The epididymis at the back feels lumpy and is normal, and confusing it for a tumour is the commonest source of unnecessary alarm.
Any new firm painless lump in the testis needs assessment within days, and the assessment is an ultrasound, which is quick and definitive.
And sperm banking is offered before treatment, because chemotherapy and surgery can impair fertility — a step that is occasionally forgotten in the urgency and matters enormously to a young man later.
What the next page fixes
The anatomy is in place. Chapter 15.2 covers what it produces — sperm production from stem cell to mature cell, the hormonal control of it, and what determines male fertility.