NSAIDs are commonly used drugs that have anti-inflammatory properties. They work by inhibiting the enzymes COX-1 and COX-2, which are responsible for synthesizing prostanoids such as prostaglandins and thromboxanes.

Prostaglandins play a crucial role in the kidney by causing vasodilation of the afferent arterioles in the glomeruli. This increases blood flow into the glomerulus and leads to an increase in the glomerular filtration rate (GFR).

When NSAIDs inhibit the COX enzymes, they reduce the levels of prostaglandins in the body. This results in a loss of vasodilation in the afferent arterioles, which leads to reduced renal perfusion and a decrease in GFR.

The Impact of NSAIDs on Kidney Function

NSAIDs are commonly used anti-inflammatory drugs that work by inhibiting the enzymes COX-1 and COX-2, which are responsible for the synthesis of prostanoids such as prostaglandins and thromboxanes. In the kidneys, prostaglandins play a crucial role in vasodilating the afferent arterioles of the glomeruli, allowing for increased blood flow and a higher glomerular filtration rate (GFR).

However, when NSAIDs inhibit the COX enzymes, the levels of prostaglandins decrease, leading to a reduction in afferent arteriole vasodilation and subsequently, a decrease in renal perfusion and GFR. This can have negative consequences for kidney function, particularly in individuals with pre-existing kidney disease or those taking high doses of NSAIDs for prolonged periods of time.

It is important for healthcare providers to consider the potential impact of NSAIDs on kidney function and to monitor patients accordingly, especially those at higher risk for kidney damage. Alternative treatments or lower doses of NSAIDs may be recommended to minimize the risk of kidney injury.

The correct answer is the zona glomerulosa. This patient is experiencing symptoms of hyperaldosteronism, which is likely caused by an adenoma in the zona glomerulosa, as indicated by the mass seen on CT scan (also known as Conn’s syndrome). The adenoma stimulates the production of aldosterone, leading to hypertension and hypokalemia.

The adrenal medulla produces catecholamines, such as adrenaline and noradrenaline.

The juxtaglomerular apparatus is located in the kidney and produces renin in response to decreased renal perfusion.

The zona fasciculata is the middle layer of the adrenal cortex and is responsible for producing glucocorticoids, such as cortisol.

The zona reticularis is the innermost layer of the adrenal cortex and produces androgens, such as dehydroepiandrosterone (DHEA).

The renin-angiotensin-aldosterone system is a complex system that regulates blood pressure and fluid balance in the body. The adrenal cortex is divided into three zones, each producing different hormones. The zona glomerulosa produces mineralocorticoids, mainly aldosterone, which helps regulate sodium and potassium levels in the body. Renin is an enzyme released by the renal juxtaglomerular cells in response to reduced renal perfusion, hyponatremia, and sympathetic nerve stimulation. It hydrolyses angiotensinogen to form angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme in the lungs. Angiotensin II has various actions, including causing vasoconstriction, stimulating thirst, and increasing proximal tubule Na+/H+ activity. It also stimulates aldosterone and ADH release, which causes retention of Na+ in exchange for K+/H+ in the distal tubule.

Where is the osmolarity highest in the nephrons of the kidneys, and why is this relevant to the effectiveness of mannitol as an osmotic diuretic?

The Loop of Henle and its Role in Renal Physiology

The Loop of Henle is a crucial component of the renal system, located in the juxtamedullary nephrons and running deep into the medulla. Approximately 60 litres of water containing 9000 mmol sodium enters the descending limb of the loop of Henle in 24 hours. The osmolarity of fluid changes and is greatest at the tip of the papilla. The thin ascending limb is impermeable to water, but highly permeable to sodium and chloride ions. This loss means that at the beginning of the thick ascending limb the fluid is hypo osmotic compared with adjacent interstitial fluid. In the thick ascending limb, the reabsorption of sodium and chloride ions occurs by both facilitated and passive diffusion pathways. The loops of Henle are co-located with vasa recta, which have similar solute compositions to the surrounding extracellular fluid, preventing the diffusion and subsequent removal of this hypertonic fluid. The energy-dependent reabsorption of sodium and chloride in the thick ascending limb helps to maintain this osmotic gradient. Overall, the Loop of Henle plays a crucial role in regulating the concentration of solutes in the renal system.

Hyperkalaemia can be identified on an ECG by tall tented T waves, small or absent P waves, and broad bizarre QRS complexes. In severe cases, the QRS complexes may form a sinusoidal wave pattern, and asystole may occur. On the other hand, hypokalaemia can be detected by ST segment depression, prominent U waves, small or inverted T waves, a prolonged PR interval (which can also be present in hyperkalaemia), and a long QT interval.

Hyperkalaemia is a condition where there is an excess of potassium in the blood. The levels of potassium in the plasma are regulated by various factors such as aldosterone, insulin levels, and acid-base balance. When there is metabolic acidosis, hyperkalaemia can occur as hydrogen and potassium ions compete with each other for exchange with sodium ions across cell membranes and in the distal tubule. The ECG changes that can be seen in hyperkalaemia include tall-tented T waves, small P waves, widened QRS leading to a sinusoidal pattern, and asystole.

There are several causes of hyperkalaemia, including acute kidney injury, drugs such as potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor blockers, spironolactone, ciclosporin, and heparin, metabolic acidosis, Addison’s disease, rhabdomyolysis, and massive blood transfusion. Foods that are high in potassium include salt substitutes, bananas, oranges, kiwi fruit, avocado, spinach, and tomatoes.

It is important to note that beta-blockers can interfere with potassium transport into cells and potentially cause hyperkalaemia in renal failure patients. In contrast, beta-agonists such as Salbutamol are sometimes used as emergency treatment. Additionally, both unfractionated and low-molecular weight heparin can cause hyperkalaemia by inhibiting aldosterone secretion.

The level with L2 is where the renal arteries typically branch off from the aorta.

Anatomy of the Renal Arteries

The renal arteries are blood vessels that supply the kidneys with oxygenated blood. They are direct branches off the aorta and enter the kidney at the hilum. The right renal artery is longer than the left renal artery. The renal vein, artery, and pelvis also enter the kidney at the hilum.

The right renal artery is related to the inferior vena cava, right renal vein, head of the pancreas, and descending part of the duodenum. On the other hand, the left renal artery is related to the left renal vein and tail of the pancreas.

In some cases, there may be accessory arteries, mainly on the left side. These arteries usually pierce the upper or lower part of the kidney instead of entering at the hilum.

Before reaching the hilum, each renal artery divides into four or five segmental branches that supply each pyramid and cortex. These segmental branches then divide within the sinus into lobar arteries. Each vessel also gives off small inferior suprarenal branches to the suprarenal gland, ureter, and surrounding tissue and muscles.

Autosomal dominant polycystic kidney disease (ADPKD) is a commonly inherited kidney disease that affects 1 in 1,000 Caucasians. The disease is caused by mutations in two genes, PKD1 and PKD2, which produce polycystin-1 and polycystin-2 respectively. ADPKD type 1 accounts for 85% of cases, while ADPKD type 2 accounts for 15% of cases. ADPKD type 1 is caused by a mutation in the PKD1 gene on chromosome 16, while ADPKD type 2 is caused by a mutation in the PKD2 gene on chromosome 4. ADPKD type 1 tends to present with renal failure earlier than ADPKD type 2.

To screen for ADPKD in relatives of affected individuals, an abdominal ultrasound is recommended. The diagnostic criteria for ultrasound include the presence of two cysts, either unilateral or bilateral, if the individual is under 30 years old. If the individual is between 30-59 years old, two cysts in both kidneys are required for diagnosis. If the individual is over 60 years old, four cysts in both kidneys are necessary for diagnosis.

For some patients with ADPKD, tolvaptan, a vasopressin receptor 2 antagonist, may be an option to slow the progression of cyst development and renal insufficiency. However, NICE recommends tolvaptan only for adults with ADPKD who have chronic kidney disease stage 2 or 3 at the start of treatment, evidence of rapidly progressing disease, and if the company provides it with the agreed discount in the patient access scheme.

Testicular cancer in young men may manifest as a hydrocele, which is the accumulation of fluid around the testicle. Therefore, it is important to investigate all cases of hydrocele to rule out cancer. On the other hand, epididymitis, which is usually caused by a bacterial infection, is unlikely to be a presenting feature of testicular cancer. If a male patient presents with frank haematuria, urgent investigation is necessary to rule out bladder cancer. A chancre, which is a painless genital ulcer commonly seen in the primary stage of syphilis, is not a presenting feature of testicular cancer.

Testicular cancer is a common type of cancer that affects men between the ages of 20 and 30. The majority of cases (95%) are germ-cell tumors, which can be further classified as seminomas or non-seminomas. Non-germ cell tumors, such as Leydig cell tumors and sarcomas, are less common. Risk factors for testicular cancer include infertility, cryptorchidism, family history, Klinefelter’s syndrome, and mumps orchitis. Symptoms may include a painless lump, pain, hydrocele, and gynaecomastia.

Tumour markers can be used to diagnose testicular cancer. For germ cell tumors, hCG may be elevated in seminomas, while AFP and/or beta-hCG are elevated in non-seminomas. LDH may also be elevated in germ cell tumors. Ultrasound is the first-line diagnostic tool.

Treatment for testicular cancer depends on the type and stage of the tumor. Orchidectomy, chemotherapy, and radiotherapy may be used. Prognosis is generally excellent, with a 5-year survival rate of around 95% for Stage I seminomas and 85% for Stage I teratomas.

Hyponatremia is a common side effect of SSRIs, including Sertraline, which can cause SIADH. However, medications such as Statins, Levothyroxine, and Metformin are not typically linked to hyponatremia.

SIADH is a condition where the body retains too much water, leading to low sodium levels in the blood. This can be caused by various factors such as malignancy (particularly small cell lung cancer), neurological conditions like stroke or meningitis, infections like tuberculosis or pneumonia, certain drugs like sulfonylureas and SSRIs, and other factors like positive end-expiratory pressure and porphyrias. Treatment involves slowly correcting the sodium levels, restricting fluid intake, and using medications like demeclocycline or ADH receptor antagonists. It is important to correct the sodium levels slowly to avoid complications like central pontine myelinolysis.

Aquaporin channels are inserted into the apical membrane of the distal tubule and collecting ducts as a result of ADH (vasopressin).

The Loop of Henle and its Role in Renal Physiology

The Loop of Henle is a crucial component of the renal system, located in the juxtamedullary nephrons and running deep into the medulla. Approximately 60 litres of water containing 9000 mmol sodium enters the descending limb of the loop of Henle in 24 hours. The osmolarity of fluid changes and is greatest at the tip of the papilla. The thin ascending limb is impermeable to water, but highly permeable to sodium and chloride ions. This loss means that at the beginning of the thick ascending limb the fluid is hypo osmotic compared with adjacent interstitial fluid. In the thick ascending limb, the reabsorption of sodium and chloride ions occurs by both facilitated and passive diffusion pathways. The loops of Henle are co-located with vasa recta, which have similar solute compositions to the surrounding extracellular fluid, preventing the diffusion and subsequent removal of this hypertonic fluid. The energy-dependent reabsorption of sodium and chloride in the thick ascending limb helps to maintain this osmotic gradient. Overall, the Loop of Henle plays a crucial role in regulating the concentration of solutes in the renal system.

The correct answer is the zona fasciculata of the adrenal cortex.

This patient’s symptoms suggest that they may have Cushing’s syndrome, which is caused by excess cortisol production. Cortisol is normally produced in the zona fasciculata of the adrenal cortex.

The adrenal medulla produces catecholamines like adrenaline and noradrenaline.

The juxtaglomerular apparatus is located in the kidney and produces renin in response to reduced renal perfusion.

The zona glomerulosa is the outer layer of the adrenal cortex and produces mineralocorticoids like aldosterone.

The zona reticularis is the innermost layer of the adrenal cortex and produces androgens like DHEA.

The renin-angiotensin-aldosterone system is a complex system that regulates blood pressure and fluid balance in the body. The adrenal cortex is divided into three zones, each producing different hormones. The zona glomerulosa produces mineralocorticoids, mainly aldosterone, which helps regulate sodium and potassium levels in the body. Renin is an enzyme released by the renal juxtaglomerular cells in response to reduced renal perfusion, hyponatremia, and sympathetic nerve stimulation. It hydrolyses angiotensinogen to form angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme in the lungs. Angiotensin II has various actions, including causing vasoconstriction, stimulating thirst, and increasing proximal tubule Na+/H+ activity. It also stimulates aldosterone and ADH release, which causes retention of Na+ in exchange for K+/H+ in the distal tubule.

Post-streptococcal glomerulonephritis is a condition that typically occurs 7-14 days after an infection caused by group A beta-haemolytic Streptococcus, usually Streptococcus pyogenes. It is more common in young children and is caused by the deposition of immune complexes (IgG, IgM, and C3) in the glomeruli. Symptoms include headache, malaise, visible haematuria, proteinuria, oedema, hypertension, and oliguria. Blood tests may show a raised anti-streptolysin O titre and low C3, which confirms a recent streptococcal infection.

It is important to note that IgA nephropathy and post-streptococcal glomerulonephritis are often confused as they both can cause renal disease following an upper respiratory tract infection. Renal biopsy features of post-streptococcal glomerulonephritis include acute, diffuse proliferative glomerulonephritis with endothelial proliferation and neutrophils. Electron microscopy may show subepithelial ‘humps’ caused by lumpy immune complex deposits, while immunofluorescence may show a granular or ‘starry sky’ appearance.

Despite its severity, post-streptococcal glomerulonephritis carries a good prognosis.

Understanding Anion Gap in Metabolic Acidosis

Metabolic acidosis is a condition where the body produces too much acid or loses too much bicarbonate. Anion gap is a useful tool in diagnosing metabolic acidosis. It is calculated by subtracting the sum of bicarbonate and chloride from the sum of sodium and potassium. A normal anion gap is between 8-14 mmol/L.

There are two types of metabolic acidosis: normal anion gap and raised anion gap. Normal anion gap or hyperchloraemic metabolic acidosis can be caused by gastrointestinal bicarbonate loss, renal tubular acidosis, drugs like acetazolamide, ammonium chloride injection, and Addison’s disease. On the other hand, raised anion gap metabolic acidosis can be caused by lactate due to shock or hypoxia, ketones in diabetic ketoacidosis or alcohol, urate in renal failure, acid poisoning from salicylates or methanol, and 5-oxoproline from chronic paracetamol use.

Understanding anion gap in metabolic acidosis is crucial in identifying the underlying cause of the condition. It helps healthcare professionals in providing appropriate treatment and management to patients.

The vesicouterine venous plexus is responsible for draining the bladder in females, while the vesicoprostatic venous plexus serves the same function in males by connecting the prostatic venous plexus and vesical plexuses. The pampiniform plexus is responsible for draining the ovaries in females. It is important to note that the terms vesicorectal and vesicovaginal plexuses are not accurate anatomical structures, but rather refer to fistulas that may form between the bladder and nearby structures.

Bladder Anatomy and Innervation

The bladder is a three-sided pyramid-shaped organ located in the pelvic cavity. Its apex points towards the symphysis pubis, while the base lies anterior to the rectum or vagina. The bladder’s inferior aspect is retroperitoneal, while the superior aspect is covered by peritoneum. The trigone, the least mobile part of the bladder, contains the ureteric orifices and internal urethral orifice. The bladder’s blood supply comes from the superior and inferior vesical arteries, while venous drainage occurs through the vesicoprostatic or vesicouterine venous plexus. Lymphatic drainage occurs mainly to the external iliac and internal iliac nodes, with the obturator nodes also playing a role. The bladder is innervated by parasympathetic nerve fibers from the pelvic splanchnic nerves and sympathetic nerve fibers from L1 and L2 via the hypogastric nerve plexuses. The parasympathetic fibers cause detrusor muscle contraction, while the sympathetic fibers innervate the trigone muscle. The external urethral sphincter is under conscious control, and voiding occurs when the rate of neuronal firing to the detrusor muscle increases.

Hyperkalaemia is present in the patient.

Although all the options are used in treating hyperkalaemia, they have distinct roles. Calcium gluconate is the only option used to stabilise the cardiac membrane.

Hyperkalaemia is a condition where there is an excess of potassium in the blood. The levels of potassium in the plasma are regulated by various factors such as aldosterone, insulin levels, and acid-base balance. When there is metabolic acidosis, hyperkalaemia can occur as hydrogen and potassium ions compete with each other for exchange with sodium ions across cell membranes and in the distal tubule. The ECG changes that can be seen in hyperkalaemia include tall-tented T waves, small P waves, widened QRS leading to a sinusoidal pattern, and asystole.

There are several causes of hyperkalaemia, including acute kidney injury, drugs such as potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor blockers, spironolactone, ciclosporin, and heparin, metabolic acidosis, Addison’s disease, rhabdomyolysis, and massive blood transfusion. Foods that are high in potassium include salt substitutes, bananas, oranges, kiwi fruit, avocado, spinach, and tomatoes.

It is important to note that beta-blockers can interfere with potassium transport into cells and potentially cause hyperkalaemia in renal failure patients. In contrast, beta-agonists such as Salbutamol are sometimes used as emergency treatment. Additionally, both unfractionated and low-molecular weight heparin can cause hyperkalaemia by inhibiting aldosterone secretion.

Diabetes insipidus is a medical condition that can be caused by either a decreased secretion of antidiuretic hormone (ADH) from the pituitary gland (cranial DI) or an insensitivity to ADH (nephrogenic DI). Cranial DI can be caused by various factors such as head injury, pituitary surgery, and infiltrative diseases like sarcoidosis. On the other hand, nephrogenic DI can be caused by genetic factors, electrolyte imbalances, and certain medications like lithium and demeclocycline. The common symptoms of DI are excessive urination and thirst. Diagnosis is made through a water deprivation test and checking the osmolality of the urine. Treatment options include thiazides and a low salt/protein diet for nephrogenic DI, while central DI can be treated with desmopressin.

The patient’s autosomal dominant polycystic kidney disease type 1 is not caused by a gene on chromosomes 13, 18, or 21. It is important to note that nondisjunction of these chromosomes can lead to other genetic disorders such as Patau syndrome, Edward’s syndrome, and Down’s syndrome. The chance of the patient passing on the autosomal dominant polycystic kidney disease type 1 to her children would depend on the inheritance pattern of the specific gene mutation causing the disease.

Autosomal dominant polycystic kidney disease (ADPKD) is a commonly inherited kidney disease that affects 1 in 1,000 Caucasians. The disease is caused by mutations in two genes, PKD1 and PKD2, which produce polycystin-1 and polycystin-2 respectively. ADPKD type 1 accounts for 85% of cases, while ADPKD type 2 accounts for 15% of cases. ADPKD type 1 is caused by a mutation in the PKD1 gene on chromosome 16, while ADPKD type 2 is caused by a mutation in the PKD2 gene on chromosome 4. ADPKD type 1 tends to present with renal failure earlier than ADPKD type 2.

To screen for ADPKD in relatives of affected individuals, an abdominal ultrasound is recommended. The diagnostic criteria for ultrasound include the presence of two cysts, either unilateral or bilateral, if the individual is under 30 years old. If the individual is between 30-59 years old, two cysts in both kidneys are required for diagnosis. If the individual is over 60 years old, four cysts in both kidneys are necessary for diagnosis.

For some patients with ADPKD, tolvaptan, a vasopressin receptor 2 antagonist, may be an option to slow the progression of cyst development and renal insufficiency. However, NICE recommends tolvaptan only for adults with ADPKD who have chronic kidney disease stage 2 or 3 at the start of treatment, evidence of rapidly progressing disease, and if the company provides it with the agreed discount in the patient access scheme.

Hyperacute transplant rejection is a type II hypersensitivity reaction, which is characterized by a cytotoxic response caused by pre-existing antibodies to the ABO or HLA antigens. This reaction leads to widespread thrombosis and ischaemia/necrosis within the transplanted organ, necessitating its surgical removal.

In contrast, type I hypersensitivity is an immediate IgE-mediated reaction that occurs within minutes, while type III hypersensitivity is an IgM-mediated reaction that involves the formation of circulating immune complexes. Type IV hypersensitivity is a cell-mediated response that takes weeks to develop and is seen in chronic graft rejections. Finally, type V hypersensitivity is an autoimmune reaction that involves the binding of auto-antibodies to cell surface receptors, either preventing the intended ligand binding or mimicking its effects.

The HLA system, also known as the major histocompatibility complex (MHC), is located on chromosome 6 and is responsible for human leucocyte antigens. Class 1 antigens include A, B, and C, while class 2 antigens include DP, DQ, and DR. When matching for a renal transplant, the importance of HLA antigens is ranked as DR > B > A.

Graft survival rates for renal transplants are high, with a 90% survival rate at one year and a 60% survival rate at ten years for cadaveric transplants. Living-donor transplants have even higher survival rates, with a 95% survival rate at one year and a 70% survival rate at ten years. However, postoperative problems can occur, such as acute tubular necrosis of the graft, vascular thrombosis, urine leakage, and urinary tract infections.

Hyperacute rejection can occur within minutes to hours after a transplant and is caused by pre-existing antibodies against ABO or HLA antigens. This type of rejection is an example of a type II hypersensitivity reaction and leads to widespread thrombosis of graft vessels, resulting in ischemia and necrosis of the transplanted organ. Unfortunately, there is no treatment available for hyperacute rejection, and the graft must be removed.

Acute graft failure, which occurs within six months of a transplant, is usually due to mismatched HLA and is caused by cell-mediated cytotoxic T cells. This type of failure is usually asymptomatic and is detected by a rising creatinine, pyuria, and proteinuria. Other causes of acute graft failure include cytomegalovirus infection, but it may be reversible with steroids and immunosuppressants.

Chronic graft failure, which occurs after six months of a transplant, is caused by both antibody and cell-mediated mechanisms that lead to fibrosis of the transplanted kidney, known as chronic allograft nephropathy. The recurrence of the original renal disease, such as MCGN, IgA, or FSGS, can also cause chronic graft failure.

The normal value for renal plasma flow is 660ml/min, which is calculated by dividing the amount of PAH in urine per unit time by the difference in PAH concentration in the renal artery or vein.

The Loop of Henle and its Role in Renal Physiology

The Loop of Henle is a crucial component of the renal system, located in the juxtamedullary nephrons and running deep into the medulla. Approximately 60 litres of water containing 9000 mmol sodium enters the descending limb of the loop of Henle in 24 hours. The osmolarity of fluid changes and is greatest at the tip of the papilla. The thin ascending limb is impermeable to water, but highly permeable to sodium and chloride ions. This loss means that at the beginning of the thick ascending limb the fluid is hypo osmotic compared with adjacent interstitial fluid. In the thick ascending limb, the reabsorption of sodium and chloride ions occurs by both facilitated and passive diffusion pathways. The loops of Henle are co-located with vasa recta, which have similar solute compositions to the surrounding extracellular fluid, preventing the diffusion and subsequent removal of this hypertonic fluid. The energy-dependent reabsorption of sodium and chloride in the thick ascending limb helps to maintain this osmotic gradient. Overall, the Loop of Henle plays a crucial role in regulating the concentration of solutes in the renal system.

The risk of urinary tract infection is higher in individuals with posterior urethral valves.

Posterior urethral valves are a frequent cause of blockage in the lower urinary tract in males. They can be detected during prenatal ultrasound screenings. Due to the high pressure required for bladder emptying during fetal development, the child may experience damage to the renal parenchyma, resulting in renal impairment in 70% of boys upon diagnosis. Treatment involves the use of a bladder catheter, and endoscopic valvotomy is the preferred definitive treatment. Cystoscopic and renal follow-up is necessary.

The superior and inferior hypogastric plexuses are responsible for providing sympathetic innervation to the bladder, which helps maintain detrusor capacity by preventing parasympathetic contraction of the bladder.

Bladder Anatomy and Innervation

The bladder is a three-sided pyramid-shaped organ located in the pelvic cavity. Its apex points towards the symphysis pubis, while the base lies anterior to the rectum or vagina. The bladder’s inferior aspect is retroperitoneal, while the superior aspect is covered by peritoneum. The trigone, the least mobile part of the bladder, contains the ureteric orifices and internal urethral orifice. The bladder’s blood supply comes from the superior and inferior vesical arteries, while venous drainage occurs through the vesicoprostatic or vesicouterine venous plexus. Lymphatic drainage occurs mainly to the external iliac and internal iliac nodes, with the obturator nodes also playing a role. The bladder is innervated by parasympathetic nerve fibers from the pelvic splanchnic nerves and sympathetic nerve fibers from L1 and L2 via the hypogastric nerve plexuses. The parasympathetic fibers cause detrusor muscle contraction, while the sympathetic fibers innervate the trigone muscle. The external urethral sphincter is under conscious control, and voiding occurs when the rate of neuronal firing to the detrusor muscle increases.