Prostate cancer is a common condition with up to 30,000 men diagnosed and 9,000 deaths per year in the UK. Diagnosis involves PSA measurement, digital rectal examination, and imaging for staging. Pathology shows 95% adenocarcinoma, often multifocal and graded using the Gleason system. Treatment options include watchful waiting, radiotherapy, surgery, and hormonal therapy. Active surveillance is recommended for low-risk men, with treatment decisions made based on disease progression and individual factors.

Sheehan’s syndrome is a condition that arises from pituitary ischaemia, which is caused by blood loss during or after childbirth. The syndrome is characterized by symptoms that indicate global hypopituitarism, including agalactorrhoea (lack of prolactin), amenorrhoea (lack of FSH and LH), cold intolerance and constipation (lack of thyroid hormones), and weight loss (lack of steroid hormones).

Malignancy is an uncommon cause of hypopituitarism.

While pituitary adenoma is a frequent cause of hypopituitarism, it is unlikely to be the cause of this patient’s symptoms, given that they occurred after childbirth. Pituitary adenoma may also present with symptoms related to mass effect, such as headache and bilateral hemianopia.

Understanding Hypopituitarism: Causes, Symptoms, and Management

Hypopituitarism is a medical condition that occurs when the pituitary gland fails to produce enough hormones. This can be caused by various factors such as compression of the gland by non-secretory pituitary macroadenoma, pituitary apoplexy, Sheehan’s syndrome, hypothalamic tumors, trauma, iatrogenic irradiation, and infiltrative diseases like hemochromatosis and sarcoidosis. The symptoms of hypopituitarism depend on which hormones are deficient. For instance, low ACTH can cause tiredness and postural hypotension, while low FSH/LH can lead to amenorrhea, infertility, and loss of libido. Low TSH can cause constipation and feeling cold, while low GH can result in short stature if it occurs during childhood. Low prolactin can cause problems with lactation.

To diagnose hypopituitarism, hormone profile testing and imaging are usually conducted. Treatment involves addressing the underlying cause, such as surgical removal of pituitary macroadenoma, and replacement of deficient hormones. It is important to manage hypopituitarism promptly to prevent complications and improve the patient’s quality of life.

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.

Renal tumours typically have a yellow or brown hue, but TCCs stand out as they have a pink appearance. If a TCC is detected in the renal pelvis, a nephroureterectomy is necessary.

Renal Lesions: Types, Features, and Treatments

Renal lesions refer to abnormal growths or masses that develop in the kidneys. There are different types of renal lesions, each with its own disease-specific features and treatment options. Renal cell carcinoma is the most common renal tumor, accounting for 85% of cases. It often presents with haematuria and may cause hypertension and polycythaemia as paraneoplastic features. Treatment usually involves radical or partial nephrectomy.

Nephroblastoma, also known as Wilms tumor, is a rare childhood tumor that accounts for 80% of all genitourinary malignancies in those under the age of 15 years. It often presents with a mass and hypertension. Diagnostic workup includes ultrasound and CT scanning, and treatment involves surgical resection combined with chemotherapy. Neuroblastoma is the most common extracranial tumor of childhood, with up to 80% occurring in those under 4 years of age. It is a tumor of neural crest origin and may be diagnosed using MIBG scanning. Treatment involves surgical resection, radiotherapy, and chemotherapy.

Transitional cell carcinoma accounts for 90% of lower urinary tract tumors but only 10% of renal tumors. It often presents with painless haematuria and may be caused by occupational exposure to industrial dyes and rubber chemicals. Diagnosis and staging are done with CT IVU, and treatment involves radical nephroureterectomy. Angiomyolipoma is a hamartoma type lesion that occurs sporadically in 80% of cases and in those with tuberous sclerosis in the remaining cases. It is composed of blood vessels, smooth muscle, and fat and may cause massive bleeding in 10% of cases. Surgical resection is required for lesions larger than 4 cm and causing symptoms.

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.

If a young child with a history of fever and sore throat develops hematuria and proteinuria, it could be either acute post-streptococcal glomerulonephritis or IgA nephropathy. However, post-streptococcal glomerulonephritis usually presents 2 to 4 weeks after a group A streptococcus infection, while IgA nephropathy presents at the same time as the upper respiratory tract infection. This child has IgA nephropathy, also known as Berger disease (First Aid 2017, p564-566).

1. Acute post-streptococcal glomerulonephritis is associated with glomerular hypertrophy.
2. IgA nephropathy involves the proliferation of mesangial cells.
3. Immune complex deposits in mesangial cells are present in IgA nephropathy but can only be visualized with electron microscopy.
4. Thickening of the glomerular basement membrane is characteristic of diabetic nephropathy and membranous nephropathy, both types of nephrotic syndrome.
5. Diabetic nephropathy is associated with an expansion of the mesangial matrix.

Understanding IgA Nephropathy

IgA nephropathy, also known as Berger’s disease, is the most common cause of glomerulonephritis worldwide. It typically presents as macroscopic haematuria in young people following an upper respiratory tract infection. The condition is thought to be caused by mesangial deposition of IgA immune complexes, and there is considerable pathological overlap with Henoch-Schonlein purpura (HSP). Histology shows mesangial hypercellularity and positive immunofluorescence for IgA and C3.

Differentiating between IgA nephropathy and post-streptococcal glomerulonephritis is important. Post-streptococcal glomerulonephritis is associated with low complement levels and the main symptom is proteinuria, although haematuria can occur. There is typically an interval between URTI and the onset of renal problems in post-streptococcal glomerulonephritis.

Management of IgA nephropathy depends on the severity of the condition. If there is isolated hematuria, no or minimal proteinuria, and a normal glomerular filtration rate (GFR), no treatment is needed other than follow-up to check renal function. If there is persistent proteinuria and a normal or only slightly reduced GFR, initial treatment is with ACE inhibitors. If there is active disease or failure to respond to ACE inhibitors, immunosuppression with corticosteroids may be necessary.

The prognosis for IgA nephropathy varies. 25% of patients develop ESRF. Markers of good prognosis include frank haematuria, while markers of poor prognosis include male gender, proteinuria (especially > 2 g/day), hypertension, smoking, hyperlipidaemia, and ACE genotype DD.

Overall, understanding IgA nephropathy is important for proper diagnosis and management of the condition. Proper management can help improve outcomes and prevent progression to ESRF.

GnRH agonists used in the treatment of prostate cancer can paradoxically lead to lower LH levels in the long term. This is because chronic use of these agonists can result in overstimulation of GnRH receptors, which in turn disrupts endogenous hormonal feedback systems. While initially stimulating the production of LH/FSH and subsequent androgen production, chronic use of GnRH agonists can cause negative feedback to suppress the release of gonadotropins, resulting in a significant decrease in serum testosterone levels. This mechanism can be thought of as switching on to switch off. It is important to note that inhibiting the 5 alpha-reductase enzyme and relaxing prostatic smooth muscle are not mechanisms of action for GnRH agonists, but rather for other medications used in the treatment of prostate conditions.

Prostate cancer management varies depending on the stage of the disease and the patient’s life expectancy and preferences. For localized prostate cancer (T1/T2), treatment options include active monitoring, watchful waiting, radical prostatectomy, and radiotherapy (external beam and brachytherapy). For localized advanced prostate cancer (T3/T4), options include hormonal therapy, radical prostatectomy, and radiotherapy. Patients may develop proctitis and are at increased risk of bladder, colon, and rectal cancer following radiotherapy for prostate cancer.

In cases of metastatic prostate cancer, reducing androgen levels is a key aim of treatment. A combination of approaches is often used, including anti-androgen therapy, synthetic GnRH agonist or antagonists, bicalutamide, cyproterone acetate, abiraterone, and bilateral orchidectomy. GnRH agonists, such as Goserelin (Zoladex), initially cause a rise in testosterone levels before falling to castration levels. To prevent a rise in testosterone, anti-androgens are often used to cover the initial therapy. GnRH antagonists, such as degarelix, are being evaluated to suppress testosterone while avoiding the flare phenomenon. Chemotherapy with docetaxel is also an option for the treatment of hormone-relapsed metastatic prostate cancer in patients who have no or mild symptoms after androgen deprivation therapy has failed, and before chemotherapy is indicated.

The histological examination of IgA nephropathy reveals an increase in mesangial cells, accompanied by positive immunofluorescence for IgA and C3.

Understanding IgA Nephropathy

IgA nephropathy, also known as Berger’s disease, is the most common cause of glomerulonephritis worldwide. It typically presents as macroscopic haematuria in young people following an upper respiratory tract infection. The condition is thought to be caused by mesangial deposition of IgA immune complexes, and there is considerable pathological overlap with Henoch-Schonlein purpura (HSP). Histology shows mesangial hypercellularity and positive immunofluorescence for IgA and C3.

Differentiating between IgA nephropathy and post-streptococcal glomerulonephritis is important. Post-streptococcal glomerulonephritis is associated with low complement levels and the main symptom is proteinuria, although haematuria can occur. There is typically an interval between URTI and the onset of renal problems in post-streptococcal glomerulonephritis.

Management of IgA nephropathy depends on the severity of the condition. If there is isolated hematuria, no or minimal proteinuria, and a normal glomerular filtration rate (GFR), no treatment is needed other than follow-up to check renal function. If there is persistent proteinuria and a normal or only slightly reduced GFR, initial treatment is with ACE inhibitors. If there is active disease or failure to respond to ACE inhibitors, immunosuppression with corticosteroids may be necessary.

The prognosis for IgA nephropathy varies. 25% of patients develop ESRF. Markers of good prognosis include frank haematuria, while markers of poor prognosis include male gender, proteinuria (especially > 2 g/day), hypertension, smoking, hyperlipidaemia, and ACE genotype DD.

Overall, understanding IgA nephropathy is important for proper diagnosis and management of the condition. Proper management can help improve outcomes and prevent progression to ESRF.

A man presented with symptoms of acute urinary retention and a history of poor urine flow and straining to void, suggesting bladder outlet obstruction possibly due to an enlarged prostate. While prostatic adenocarcinoma is common in men over 50, it is unlikely to cause urinary symptoms. However, patients should still be screened for it to allow for early intervention if necessary. The man’s increased levels of free PSA indicate BPH rather than prostatic adenocarcinoma, as the latter would result in decreased free PSA and increased bound-PSA levels.

The lateral and middle lobes of the prostate are closest to the urethra and their hyperplasia can compress it, leading to urinary and voiding symptoms. If the urethra is completely compressed, acute urinary retention and bladder outlet obstruction can occur. The anterior lobe is rarely enlarged in BPH and is not positioned to obstruct the urethra, while the posterior lobe is mostly involved in prostatic adenocarcinoma but does not typically cause urinary symptoms due to its distance from the urethra.

Benign prostatic hyperplasia (BPH) is a common condition that affects older men, with around 50% of 50-year-old men showing evidence of BPH and 30% experiencing symptoms. The risk of BPH increases with age, with around 80% of 80-year-old men having evidence of the condition. Ethnicity also plays a role, with black men having a higher risk than white or Asian men. BPH typically presents with lower urinary tract symptoms (LUTS), which can be categorised into obstructive (voiding) symptoms and irritative (storage) symptoms. Complications of BPH can include urinary tract infections, retention, and obstructive uropathy.

Assessment of BPH may involve dipstick urine testing, U&Es, and PSA testing if obstructive symptoms are present or if the patient is concerned about prostate cancer. A urinary frequency-volume chart and the International Prostate Symptom Score (IPSS) can also be used to assess the severity of LUTS and their impact on quality of life. Management options for BPH include watchful waiting, alpha-1 antagonists, 5 alpha-reductase inhibitors, combination therapy, and surgery. Alpha-1 antagonists are considered first-line for moderate-to-severe voiding symptoms and can improve symptoms in around 70% of men, but may cause adverse effects such as dizziness and dry mouth. 5 alpha-reductase inhibitors may slow disease progression and reduce prostate volume, but can cause adverse effects such as erectile dysfunction and reduced libido. Combination therapy may be used for bothersome moderate-to-severe voiding symptoms and prostatic enlargement. Antimuscarinic drugs may be tried for persistent storage symptoms. Surgery, such as transurethral resection of the prostate (TURP), may also be an option.

The patient’s painless hematuria and fatigue, combined with a history of smoking and occupation in a dye factory, suggest a diagnosis of transitional cell carcinoma of the bladder. This is supported by the observation of an abnormal growth in the bladder during ureteroscopy (First Aid 2017, p219 & p569).

1. Arsenic is a carcinogen that raises the risk of angiosarcoma of the liver, squamous cell carcinoma of the skin, and lung cancer.
2. Aromatic amines, such as 2-naphthylamine and benzidine, are carcinogens that increase the risk of transitional cell carcinoma of the bladder. They are commonly used in dye manufacturing.
3. Aflatoxins from Aspergillus increase the risk of hepatocellular carcinoma. Aflatoxins are frequently found in crops like peanuts and maize.
4. Nitrosamines in smoked foods are linked to an increased risk of stomach cancer.
5.

Risk Factors for Bladder Cancer

Bladder cancer is a type of cancer that affects the bladder, and there are different types of bladder cancer. The risk factors for urothelial (transitional cell) carcinoma of the bladder include smoking, which is the most important risk factor in western countries. Exposure to aniline dyes, such as working in the printing and textile industry, and rubber manufacture are also risk factors. Cyclophosphamide, a chemotherapy drug, is also a risk factor for this type of bladder cancer. On the other hand, the risk factors for squamous cell carcinoma of the bladder include schistosomiasis and smoking. It is important to be aware of these risk factors and take steps to reduce your risk of developing bladder cancer.