Genitourinary Diseases Flashcards
What is Benign Prostatic Hyperplasia ?
Non-cancerous enlargement of the prostate
Age dependent condition: affects 50% of men aged 50 and above; by the age of 85, 90% of men are affected
What is the pathophysiology of BPH?
Glandular cell hyperplasia causes an increase in cell number - theorised in 2 ways
1. As men age, they decrease in serum testosterone (a major circulating androgen) levels. BPH is associated with an increase in estrogen which may enlarge the prostate. 2. Dihydrotestosterone (DHT), the principal androgen in prostate tissue, increases as testosterone decreases causing the prostate to enlarge
What are the clinical manifestations of BPH?
• Obstructive symptoms: weak urinary stream, prolonged voiding, incomplete emptying, post-urinary dribble and abdominal straining
• Irritative symptoms: urgency to urinate, nocturia, bladder pain, and incontinence
*Urinary obstruction causes bladder and/or kidney infection, acute urinary retention, haematuria and renal insufficiency
What is the diagnosis of BPH?
- Based on history, physical exam, clinical manifestations
- A prostate-specific antigen blood test measures a protein produced by both cancerous and non-cancerous tissue in the prostate
- Urinalysis: detect and rule out other pathogens as the presence of WBC or haematuria in the presence of infection/ inflammation
- A digital rectal exam (DRE): examines external surface and size of prostate
- Transrectal US can also determine size of prostate
What is the treatment of BPH?
Pharmacological treatment is primarily administered to relieve symptoms (.e.g decrease urinary outflow resistance, reduce long-term complications):
• α1A-adrenoceptor antagonists (Prazosin, tamsulosin)
○ Block α1A-adrenoceptors on the smooth muscle decreasing muscle contractility (greater selectivity for bladder and prostate α1 receptors)
○ Adverse effects: abnormal ejaculation
• 5α-reductase inhibitors (dutasteride, finasteride)
○ Prevents conversion of testosterone to DHT
○ Adverse effects: may cause impaired libido - impotence)
• fixed-dose combination (dutasteride and tamsulosin)
Other options:
• TURP - transurethral prostatectomy: surgical option to dilate for greater flow
What is pyelonephritis ? What are the classifications?
infection and inflammation of one or both upper urinary tracts
• Acute pyelonephritis is an acute infection
• Chronic pyelonephritis are episodes of acute pyelonephritis leading to a shrunken and fibrotic kidney
• Females are more affected and the severity increases with age
What is Acute Pyelonephritis?
- Medullary infiltration of WBC with oedema, inflammation and contaminated urine
- ROS damage tubular cells
- In severe infections, abscesses formation can occur extending from the medulla to the cortex
- After the acute phase, the kidney heals with scar tissue deposition and atrophy of the tubules
- Common cause is Escherichia coli (E. coli)
Clinical Manifestations:
Rapid onset of fever, chills and flank pain with UTI symptoms (painful and frequent urination) prior to the onset of systemic signs. Not all individuals will exhibit classic symptoms:
• older people (small increases in body temperature)
• toddlers (very high fever)
Diagnosis:
• Through clinical manifestations and lab tests
• Urinalysis: bacteriuria, blood and urine culture. A positive result is usually the same pathogen in blood and urine
Treatment:
• Antibiotic therapy (usually fluoroquinolones for 2 weeks) - patients who do not require hospitalisation
*Post-treatment: follow up culture to ensure infection has been cleared and a CT scan: any scarring is present
What is Chronic Pyelonephritis?
- Persistent infection of one or both kidneys with inflammation and scarring
- Likely to occur in individuals with pathologic conditions (renal stones/calculi)
- Prevents elimination of bacteria leading to inflammation = tubular destruction atrophy fibrosis and scarring leading to chronic renal failure
Clinical Manifestations:
• (Similar to end-stage renal failure) dysuria, flank pain and frequency of urination
• Uraemia (elevated Search Blood Urea Nitrogen and creatinine levels), anorexia, fatigue, nausea and vomiting
Diagnosis:
• Urinalysis: presence of WBC
• Definitive diagnosis is through an ultrasound or CT scan, which shows a small kidney
Treatment: Usually addresses the underlying cause such as relieving obstruction (renal stones) and the symptoms of recurrent infections with antibiotic therapy
What is glomerulonephritis?
inflammation of the glomerulus
Can be caused by immunological abnormalities (auto-immune), effects of drugs, diabetes mellitus and some viruses (hepatitis B and C, human immunodeficiency virus (HIV))
What are the classifications of glomerulonephritis?
- Acute glomerulonephritis
- IgA nephropathy
- Crescentic glomerulonephritis
- Chronic glomerulonephritis
What is acute glomerulonephritis?
• Causes glomerular damage and inflammation (inflammatory cytokines, ROS, proteases attack epithelial cells) = deposition of IgG and C3 = alterations in membrane permeability = proteinuria and haematuria
• Affects primarily children but can affect persons of any age
• Typically following a Group A post-streptococcal infection (pharynx) but may occur after infections by other pathogens: virus-related (mumps, measles, chickenpox)
Clinical Manifestations: Prolonged infection causes severe renal diseases. Signs and symptoms occur 10-21 days after infection:
• Proteinuria, haematuria, decreasing GFR: thickening of the glomerular membrane = oliguria, elevated BUN, oedema (eye, feet, ankles) = Na+ and water retention, hypertension and back pain
- In children, there is no specific treatment and patients can recover without significant loss of renal function or recurrence of the disease. Adults tend to recover more slowly (20% show proteinuria and decreased GFR 12 months after presentation)
- Antibacterial agents are used to eliminate the streptococcal infection and antihypertensive agents can help with treating any hypertension
What is IgA Nephropathy/ Berger’s Disease?
- Most common form of acute glomerulonephritis in developed countries; occurs in adults aged 20-30 years
- Abnormal IgA binding to glomerular mesangial cells = stimulates proliferation, release of ROS and proteases = glomerulosclerosis
- Common sign is haematuria occurring 24-48 hours following a respiratory or gastrointestinal viral infection
- Treatment: Steroids to suppress the immune response and ACE inhibitors
What is Crescentic Glomerulonephritis?
- Sub-acute or rapidly progressive; Idiopathic and mostly affects adults aged 50-60 years
- Cellular proliferation in the Bowman space
- Linked to proliferative glomerular disease
- Antibody formation against the glomerular basement membrane, pulmonary capillaries proliferation of epithelial cells, and fibrin depositions in Bowman’s space = decrease in renal blood flow and GFR
- Clinical Manifestations: haematuria, proteinuria, oedema and hypertension
- Treatment: plasma exchange combined with steroids, anti-viral therapy (hepatitis C), anticoagulants (heparin and warfarin), dialysis or transplantation
What is Chronic Glomerulonephritis
complex disease causing chronic renal failure
• Pathologic changes in the glomerulus, through the proliferation of cells in the connective tissue = tubular dilation and atrophy and tubulointerstitial injury
• Primary cause often difficult to establish; DM is an example of secondary injury
What is the pathophysiology of Glomerulonephritis?
- Acute glomerular injury is caused by antibodies against the glomerular basement membrane = deposition of Ag/Ab complexes = release of neuraminidase.
- Glomerular damage releases inflammatory mediators, lysosomal enzymes and ROS = alters membrane permeability = proteinuria and haematuria
