(a) A 36-year-old cyclist suffered pelvic injury while riding into a pothole on the road. Following this incident, he has severe…

The case combines pelvic trauma, perineal anatomy, trace-element biochemistry and endocrine signalling.

Urethral injury. The most likely injured structure is the bulbous (spongy) urethra in the bulb of the penis, lying in the superficial perineal pouch. A pelvic or perineal impact can distract the urethra at the bulb; rupture disrupts urethral continuity and allows urine or contrast to leak into the superficial perineal pouch, explaining urinary retention and a retrograde urethrogram with contrast limited to that pouch. Although pelvic fractures often injure the membranous urethra, the contrast pattern here localises the lesion to the bulbous urethra.

Parts of the urethra. The principal structure, the male urethra, has prostatic, membranous and spongy parts. The prostatic part traverses the prostate from the bladder to the apex of the prostate; the short membranous part crosses the urogenital diaphragm/perineal membrane; the spongy or penile part runs through the corpus spongiosum from the urogenital diaphragm to the external urethral orifice and includes the bulbous, pendulous/penile and fossa navicularis portions.

Superficial perineal pouch. In a labelled diagram, both pouches are bounded above by the perineal membrane and below by Colles fascia. The male pouch contains the bulb of the penis, crura of the penis, ischiocavernosus, bulbospongiosus and superficial transverse perineal muscles, with superficial external pudendal vessels and the dorsal nerve of the penis. The female pouch contains the bulbs and crura of the clitoris, ischiocavernosus, bulbospongiosus and superficial transverse perineal muscles, greater vestibular (Bartholin) glands, and superficial external pudendal vessels and perineal nerves. The key difference is penile bulb and crura in males versus clitoral bulbs and crura, and greater vestibular glands, in females.

Selenium. Dietary sources include Brazil nuts, seafood, organ meats, eggs, meat and cereals grown on selenium-rich soil; soil selenium determines cereal selenium, and Brazil nuts are the richest single food. Biochemically, selenium is incorporated as selenocysteine into selenoproteins: glutathione peroxidases and thioredoxin reductases protect against oxidative stress; iodothyronine deiodinases regulate thyroid hormone activation and inactivation; selenoprotein P transports selenium in plasma. Deficiency causes Keshan disease, a congestive cardiomyopathy with dyspnoea, oedema and heart failure; Kashin-Beck disease, an osteochondrosis with joint pain, deformity and short stature; and myxoedematous cretinism, with hypothyroidism and developmental delay.

RFLP applications. RFLP, using restriction enzymes and DNA probes, detects restriction-site changes linked to disease alleles. It is used in prenatal diagnosis of genetic disorders such as sickle-cell disease or thalassaemia, DNA fingerprinting for forensic identification or paternity testing, and carrier detection for autosomal recessive conditions such as thalassaemia or cystic fibrosis.

Second messengers. Hormones acting through GPCRs use second messengers. Glucagon and β-adrenergic hormones activate Gs, adenylyl cyclase, cAMP and PKA, causing hepatic glycogenolysis and lipolysis; cAMP can also activate EPAC and ion channels. α1-adrenergic, GnRH and vasopressin V1 receptors activate Gq, phospholipase C, IP3 and DAG; IP3 releases Ca2+ from the endoplasmic reticulum, Ca2+ activates calmodulin, and DAG activates PKC, producing smooth-muscle contraction or secretion. Insulin uses a receptor tyrosine kinase: dimerisation, autophosphorylation, IRS, PI3K/Akt and MAPK increase GLUT4 glucose uptake, glycogenesis and protein synthesis.

Posterior pituitary hormones. The posterior pituitary does not synthesize these hormones; it stores and releases hypothalamic neurohormones. ADH and oxytocin are synthesised in supraoptic and paraventricular hypothalamic neurons, transported down the hypothalamohypophyseal tract, stored in Herring bodies and secreted into capillaries. ADH is released by hyperosmolarity or hypovolaemia and increases water reabsorption in collecting ducts via aquaporin-2, with vasoconstriction at high levels; oxytocin is released by cervical stretch or suckling and stimulates uterine contraction and milk ejection.

Thus the clinical picture localises the lesion to the bulbous urethra, while the biochemical and endocrine parts show how trace elements and second messengers integrate metabolic and reproductive control.