Genitourinary Flashcards
Define urinary tract stones
Calculi form that cause symptoms by blocking and abrasing structures.
Types of urinary tract stones
Renal.
Bladder.
How do urinary tract stones clinically present?
Many asymptomatic.
Haematuria possible.
Renal colic: Sudden, severe pain in the loin -> groin.
More painful if the stone is moving. They tend to writhe around in agony rather than lie still.
Urinary tract stones - bladder - note
5% of UT stones.
Pathophysiology of urinary tract stones - renal
Formed when the urine is super saturated with salt and minerals (calcium oxalate, calcium phosphate, magnesium ammonium phosphate (struvite), uric acid and cystine).
Additionally, calcium oxalate precipitates form in the basement membrane of loops of henle -> (Randall’s plaque) in the renal papillae -> Develops into a stone.
Renal colic: Caused by the stones in the kidney, renal pelvis or ureter causing dilatation, stretching and spasm of the ureter.
Pathophysiology of urinary tract stones - bladder
Most commonly, urinary stasis due to failure of optimal emptying -> Precipitation.
Consider in women with UTI.
Cause of urinary tract stones - renal
Calcium: Hypercalcaemia. Excessive dietary calcium.
Excessive bone resorption (long term immobilisation).
Uric acid: Hyperuricaemia (possibly with gout)
Cystine stones: Cystinuria (autosomal recessive)
Cause of urinary tract stones - bladder
Usually occur because of foreign bodies, obstruction or infection.
Epidemiology of urinary tract stones - renal
Common.
10% lifetime incidence.
Diagnostic test for urinary tract stones
Midstream urine culture.
CT is gold standard.
Chemical analysis of passed stones to determine composition.
Treatment of urinary tract stones
NSAIDs (diclofenac) for pain.
Allow stones to pass spontaneously.
Complications of urinary tract stones
Irreversible renal damage.
Long term blockage -> Sepsis.
Sequelae of urinary tract stones
Recurrence.
Define acute kidney injury
Rapid deterioration of renal function.
Define chronic kidney disease
Longterm,
usually progressive impairment of kidney function (>3 months of evidence of kidney damage).
How does acute kidney injury clinically present?
Oliguria common.
Anuria possible.
Nausea, vomiting.
How does chronic kidney disease clinically present?
Anaemia: Pallor, lethargy.
CNS: Confusion, coma (severe)
CVS: Hypertension
Renal: Nocturia, polyuria, haematuria(?)
Renal osteodystrophy: Osteomalacia, bone pain, hyperparathyroidism
Skin: Pruritus
Pathophysiology of acute kidney injury
Prerenal: Impaired perfusion of the kidneys.
Kidneys require adequate perfusion to maintain glomerular filtration
Renal: Damage to kidney apparatus impairs ability to function
Postrenal: Urinary outflow obstructed
Pathophysiology of chronic kidney disease
Anaemia: Reduced erythropoietin production and increased blood loss.
Bone disease: Renal phosphate retention and impaired production of 1,25 - dihydroxyvitamin D -> Fall in serum calcium concentration -> Compensatory release of PTH -> Sustained skeletal decalcification.
Neuro: Peripheral paraesthesiae and weakness.
Advanced uraemia -> depressed cerebral function, myotonic twitching and fits.
Median nerve compression caused by amyloidosis.
CVS: Increased frequency of hypertension, dyslipidaemia and vascular calcification
Cause of acute kidney injury
Prerenal: Volume depletion (vomiting/diarrhoea), hypotension, cardiac failure
Renal: Glomerular disease, tubular injury, nephritis (NSAIDs), vascular disease
Postrenal: Calculus, urethral stricture
Cause of chronic kidney disease
Various.
Congenital: Polycystic kidney disease, tuberous sclerosis
Renal: Glomerular disease, urinary tract obstruction
CVS: Hypertension, arteriopathic renal disease
Epidemiology of acute kidney injury
15% of adults admitted to hospital develop AKI.
More common in elderly.
Epidemiology of chronic kidney disease
Common (varying severity).
Increases with age.
Diagnostic test for acute kidney injury
Serial serum creatinine readings: Acute rise.
Diagnostic test for chronic kidney disease
Bloods: Normochromic, normocytic anaemia. Serum calcium, phosphate and uric acid.
GFR: Assess renal function
Renal ultrasound: Check for damage.
Dipstick: Haematuria, proteinuria
Treatment of acute kidney injury
Conservative.
Treat underlying cause.
Treatment of chronic kidney disease
Renoprotection: Maintain blood pressure at less than 120/80 mmHg (antihypertensive)
Bone: Vitamin D supplements, bisphosphonates
Complications of acute kidney injury
Volume overload.
Metabolic acidosis.
Complications of chronic kidney disease
Hypertension,
renal osteodystrophy,
uraemic encephalopathy,
dialysis amyloid deposition.
Define nephritic syndrome
Inflammation of the kidney.
Define nephrotic syndrome
Oedema and loss of protein due to increased glomerular permeability.
Define minimal change disease
Loss of podocyte foot processes,
vacuolation
and appearance of microvilli in the glomerulus.
How does nephritic syndrome clinically present?
Haematuria,
proteinuria (slight),
hypertension,
low urine volume,
uraemia,
can occur 1-3 weeks after strep infection
How does nephrotic syndrome clinically present?
Proteinurea,
hypoalbuminaemia,
oedema,
hyperlipidemia.
How does minimal change disease clinically present?
Presents as nephrotic syndrome.
Proteinurea,
hypoalbuminaemia,
oedema,
hyperlipidemia.
Nephritic syndrome - note
Loss of a lot of blood
Nephrotic syndrome - note
Loss of a lot of protein
Minimal change disease - note
Named since minimal change can be seen under a light microscope.
Pathophysiology of nephritic syndrome
Inflammation
-> Podocytes develop large pores,
which allows blood to flow into the urine.
Red cell casts; characteristic.
Low renal function -> Low urine volume
Pathophysiology of nephrotic syndrome
Gaps in podocytes allow proteins to leak into urine.
Albumin lost
- > hypoalbuminemia
- > decreased intravascular oncotic pressure
- > fluid moves into surrounding tissue causing oedema.
Additionally, hypoalbuminema
- > liver compensation
- > (s/e) increased lipid production
- > hyperlipidemia.
Pathophysiology of minimal change disease
Three hallmarks:
Diffuse loss of podocyte foot processes,
Vacuolation
and Appearance of microvilli.
Podocyte losses may account for proteinuria.
Considered idiopathic.
Causes of nephritic syndrome
Inflammation of the glomerulus.
Streptococcus, viral infection, parasitic infection ->
antigen becomes trapped in the glomerulus.
Any of above.
Causes of nephrotic syndrome
Primary renal disease: Minimal change disease
Secondary: Diabetes, toxins, SLE.
Cause of minimal change disease
Unknown
Epidemiology of nephrotic syndrome
Mainly adults.
Twice as common in men.
Epidemiology of minimal change disease
Accounts for 80% of all nephrotic syndrome in children, and 20% in adults.
Peak incidence 2-3 years.
Diagnostic test for nephritic syndrome
Urine dipstick
Diagnostic test for nephrotic syndrome
Urine dipstick
Diagnostic test for minimal change disease
Light microscope - no change
Electron microscope of biopsy - abnormal podocytes.
Treatment of nephritic syndrome
Treat underlying disease.
Allow spontaneous recovery.
Treatment of nephrotic syndrome
Treat underlying disease.
Treatment of minimal change disease
Supportive care (reduce oedema).
Prednisolone (can halt process).
Complications of nephritic syndrome
Depends on underlying disease.
Generally; AKI,
decreased resistance to infection.
Complications of nephrotic syndrome
Depends on underlying disease
Complications of minimal change disease
Nephrotic syndrome.
Define polycystic kidney disease
Multiple renal cysts
Define epididymal cyst
Extratesticular, spherical cysts in the head of the epididymis.
Types of polycystic kidney disease
Autosomal Dominant
Autosomal Recessive
How does autosomal dominant polycystic kidney disease clinically present?
Presents at any age after 20s.
Acute loin pain (cyst haemorrhage),
abdominal discomfort,
hypertension.
How does autosomal recessive polycystic kidney disease clinically present?
Highly variable.
Presents at any age.
Consistently; renal enlargement.
Less commonly; liver disease.
How does an epididymal cyst clinically present?
Lump.
Often multiple and bilateral.
Often asymptomatic.
Pathophysiology of autosomal dominant polycystic kidney disease
PKD1 codes polycystin, an integral membrane protein which regulates tubular and vascular development in kidneys and other organs.
Cysts develop throughout both kidneys
- > Increase in size with age
- > Renal enlargement
- > progressive destruction of renal tissue.
Pathophysiology of autosomal recessive polycystic kidney disease
Dilatation and elongation of renal collecting ducts
-> bilaterally enlarged and cystic kidneys.
At birth, the interstitium and the rest of the tubules are normal,
but can later develop interstitial fibrosis and tubular atropy ->
End stage kidney disease.
Cause of autosomal dominant polycystic kidney disease
Autosomal dominant.
PKD1 gene most common.
Possibly PKD2.
Cause of autosomal recessive polycystic kidney disease
Autosomal recessive.
Fibrocystin gene, responsible for tubulogenesis.
Cause of an epididymal cyst
Possibly obstruction of the epididymis.
Epidemiology of autosomal dominant polycystic kidney disease
Most common cause of inherited serious renal disease.
1/1000 individuals.
Epidemiology of autosomal recessive polycystic kidney disease
10/100,000 births.
Epidemiology of epididymal cyst
Onset at age 40.
Diagnostic test for autosomal dominant polycystic kidney disease
Examination.
Ultrasound.
Diagnostic test for autosomal recessive polycystic kidney disease
Ultrasound.
Diagnostic test for epididymal cyst
Ultrasound.
Transilluminate.
Treatment of autosomal dominant polycystic kidney disease
Control blood pressure.
Many eventually require renal replacement.
Treatment of autosomal recessive polycystic kidney disease
Nephrectomy may be necessary.
Fluid overload can be managed with diuretics and continuous renal replacement therapy.
Treatment of an epididymal cyst
Not usually necessary.
Surgical excision.
Complications of autosomal dominant polycystic kidney disease
Subarachnoid haemorrhage:
polycystin involved in the production of berry aneurysms.
Complications of autosomal recessive polycystic kidney disease
Infant death if congenital.
Define Hydrocele
Abnormal collection of fluid within the remnants of the processus vaginalis.
Define Varicocele
Abnormal dilatation of the testicular veins in the pampiniform plexus.
Types of Hydrocele
Simple
Communicating
Non-communicating
How does simple hydrocele clinically present?
Scrotal enlargement with a non-tender, smooth cystic swelling.
Anterior to and below the testis transilluminate.
How does communicating hydrocele clinically present?
As simple hydrocele.
Vacillates in size and is usually related to ambulation.
How does varicocele clinically present?
Usually asymptomatic.
Scrotum feels like ‘a bag of worms’.
Side affected hangs lower.
Pathophysiology of simple hydrocele
Accumulation of fluid within tunica vaginalis.
Usually disappears in the first 2 years of life.
Pathophysiology of communicating hydrocele
Persistence of the processus vaginalis allows peritoneal fluid to communicate freely with the scrotal portion of the processus.
Pathophysiology of varicocele
Heat generated by varicocele affects sperm quality.
Proteins required for healthy sperm are reduced.
Causes of simple hydrocele
Congenital.
Trauma, testicular torsion.
Also possibly due to generalised oedema from other cause.
Cause of communicating hydrocele
Congenital.
Can present in older males as a result of intra-abdominal pressure or fluid overload.
Cause of non-communicating hydrocele
Imbalance between secretion and reabsorption of fluid.
Also secondary to trauma, torsion.
Cause of varicocele
Venous reflux.
More common on the left, due to the angle of the left testicular vein entering the left renal vein.
Can be due to problems with the valves causing backflow of blood.
This causes swelling due to excessive pressure.
Epidemiology of hydrocele
1-2% of male neonates.
Epidemiology of varicocele
Incidence increases after puberty.
Diagnostic test for hydrocele
Ultrasound.
Transilluminate.
Diagnostic test for varicocele
Observation.
More accurate: Ultrasound.
Treatment of hydrocele
Observation for first 2 years.
Surgical removal.
Treatment of varicocele
If symptomatic: Surgery.
Avoid if possible; surgery can cause testicular damage.
Complications of hydrocele
Infection.
Depending on underlying pathology; infertility or testicular atrophy due to trauma.
Complications of varicocele
Left untreated - can cause infertility.
Define testicular torsion
Torsion of the spermatic cord.
Define benign prostatic hyperplasia
Increase in the size of the prostate gland without malignancy.
How does testicular torsion clinically present?
Acute swelling of the scrotum.
Sudden severe pain in one testis.
Often follows sport or physical activity.
How does benign prostatic hyperplasia clinically present?
Frequent urination,
incomplete emptying,
intermittent stream,
weak stream,
urgency,
nocturia
and straining (I-PSS grading).
Pathophysiology of testicular torsion
Occlusion of the testicular blood vessels.
Pathophysiology of benign prostatic hyperplasia
Glandular epithelial cells and stromal cells undergo hyperplasia.
Usually the median lobe is affected.
Cause of testicular torsion
Trauma.
RF: High insertion of the tunica vaginalis.
Cause of benign prostatic hyperplasia
Not fully known.
Assumed relationship to androgens, possibly promoting cell proliferation in the prostate.
Epidemiology of testicular torsion
1/4000 males under 25.
Epidemiology of benign prostatic hyperplasia
Affects QOL of 40% of men in 50s,
and 90% of men in 90s.
Diagnostic test for testicular torsion
Examination is often sufficient.
Diagnostic test for benign prostatic hyperplasia
History.
Ultrasound.
DRE.
Treatment of testicular torsion
Reduce manually (twist).
Verify by doppler ultrasound.
Treatment of benign prostatic hyperplasia
Watchful waiting.
Alpha blockers (doxazosin) to those with severe voiding problems.
5-alpha reductase inhibitor (finasteride)
Surgery: Large prostate/failure to respond.
Transurethral resection of the prostate.
Complications of testicular torsion
Infarction of the affected testicle followed by atrophy
Complications of benign prostatic hyperplasia
Recurrent UTI.
Bladder calculi.
Define bladder carcinoma
Cancer of the bladder.
Define renal carcinoma
Cancer of the kidney.
Types of renal carcinoma
Renal cell carcinoma
Transitional cell carcinoma
How does bladder carcinoma clinically present?
Painless haematuria.
Advanced disease may have voiding symptoms.
Classic cancer symptoms.
How does renal carcinoma clinically present?
Haematuria,
abdominal mass,
lethargy,
anorexia,
weight loss,
abdo pain.
Renal cell carcinoma - note
Arises from the renal tubule
Transitional cell carcinoma - note
Arises from the renal pelvis
Pathophysiology of bladder cancer
Arises from the transitional cells of the mucosal urothelium.
Can invade the muscle to cause voiding symptoms. Has a high propensity for metastasis.
Pathophysiology of renal cell carcinoma
Can secrete PTH (hypercalcaemia),
ACTH (Cushings like syndome),
EPO (polycythaemia),
renin (HTN).
Common metastases:
Lymphoma, lung, breast, skin
Pathophysiology of transitional cell carcinoma
Common metastases:
Lymphoma, lung, breast, skin.
Cause of bladder carcinoma
Genetic (no specific gene).
Strong link with smoking.
Aromatic amines and polycyclic aromatic hydrocarbons (working in a dye factory) are renally excreted.
Also associated with increasing age.
Cause of renal carcinoma
RF: Regular NSAID use,
obesity,
FH
Epidemiology of bladder carcinoma
Smokers and dye factory workers.
Diagnostic tests for bladder carcinoma
Cystoscopy: Examine for signs of tumour
Biopsy: Determine cell type, confirm diagnosis
Urine cytology: Rule out infection
Diagnostic tests for renal carcinoma
IVU: Dye stains kidney -> passes into ureters.
Blurs the outline.
Ultrasonography: Solid or cystic
CT: Preoperative staging
Treatment of bladder carcinoma
Non-invasive: Transurethral resection
Invasive: Cystectomy (with orthotopic bladder substitute).
Chemotherapy (cisplatin).
Treatment of renal carcinoma
Surgical.
Radio/Chemo.
Complications of bladder carcinoma
Urinary retention.
UTI.
Recurrence.
Metastasis.
Define prostatic carcinoma
Cancer of the prostate
Define testicular carcinoma
Cancer of the testicle
Types of testicular carcinoma
Seminoma
Teratomas
How does prostatic carcinoma clinically present?
Serum PSA elevated.
Bladder outflow obstruction (I-PSS grading).
Occasionally; presents with metastases (usually to bone).
How does testicular carcinoma clinically present?
Classic cancer symptoms.
Painless lump in the testicle.
Possible mestastasis to the lung.
Pathophysiology of prostatic carcinoma
Adenocarcinoma.
Androgen driven.
Mostly affects the lateral lobes (in constrast to BPH).
Can spread through lymphatics, haematogenously, local invasion.
Pathophysiology of seminoma - type of testicular carcinoma
96% arise from germ cells.
Pathophysiology of teratomas - type of testicular carcinoma
Composed of tissue not normally present at the site (teeth and stuff).
Cause of prostatic carcinoma
Genetic (no specific gene).
Can develop from benign prostatic hyperplasia.
Cause of testicular carcinoma
Unknown.
RF: Undescended testes, FH.
Epidemiology of prostatic carcinoma
Most common cancer in men.
Epidemiology of testicular carcinoma
Most common cancer in young men.
Diagnostic tests for prostatic carcinoma
DRE: hard irregular gland.
Ultrasound.
Serum PSA: raised (markedly if metastasis).
Diagnostic test for seminoma - type of testicular carcinoma
Ultrasound.
CXR/CT: Tumour staging; check metastases.
Serum conc. Of beta-hCG: Raised.
Diagnostic test for teratomas - type of testicular carcinoma
No markers.
CXR/CT: Tumour staging; check metastases.
Treatment of prostatic carcinoma
Microscopic: Watchful waiting
Confined to gland: Prostatectomy or radiotherapy
Metastatic: Androgen suppression (surgical/chemical castration).
Treatment of seminoma - type of testicular carcinoma
Surgery: Orchidectomy (offer sperm banking).
Metastasis: Radiotherapy (Chemo if advanced).
Treatment of teratomas - type of testicular carcinoma
Surgery: Orchidectomy (offer sperm banking)
Metastasis: Chemotherapy.
Complications of prostatic carcinoma
Metastasis and death.
Complications of testicular carcinoma
Metastasis and death.
Define Pyelonephritis
Infection within the renal pelvis.
Define Cystitis
Infection causing inflammation of the bladder.
Define Prostatitis
Bacterial infection of the prostate gland.
Types of Pyelonephritis
Acute.
Chronic.
How does acute pyelonephritis clinically present?
Rapid, loin, suprapubic or back pain.
Fever, malaise, nausea, anorexia.
Possibly lower UTI, with frequent dysuria, haematuria or hesitancy.
How does chronic pyelonephritis clinically present?
As acute pyelonephritis.
Failure to thrive.
Possibly hypertension.
How does cystitis clinically present?
Frequent urination, urgency, dysuria.
Abdominal tenderness, swollen bladder, confusion (elderly).
How does prostatitis clinically present?
Macroscopic haematuria, fever, dysuria, pyrexia.
Sharp pelvic/penile/anal pain.
Pathophysiology of acute pyelonephritis
Often, infection will rise from the bladder to the renal pelvis.
Haematogenous spread also possible.
Local infection will cause inflammation and damage.
Pathophysiology of chronic pyelonephritis
Chronic infection can cause characteristic scarring of the kidney.
Pathophysiology of cystitis
Infection of urine stored in the bladder.
Can be ‘washed out’ with frequent fluids.
Cause of acute pyelonephritis
Infection by UTI organisms (Escherischia coli, Klebsiella, Proteus, Enterococcus).
RF: Calculi, catheterisation, pregnancy, diabetes
Cause of chronic pyelonephritis
As acute pyelonephritis.
Infection by UTI organisms (Escherischia coli, Klebsiella, Proteus, Enterococcus).
RF: Calculi, catheterisation, pregnancy, diabetes
Cause of cystitis
Can be caused from incomplete emptying.
Cause of prostatitis
Usually gram negative organisms; Escherichia coli, Enterobacter, Serratia.
Sometimes STI: Neisseria gonorrhoeaeand
Chlamydia trachomatis.
Epidemiology of acute pyelonephritis
Can occur at any age.
Generally more frequent in females, except in neonates.
Epidemiology of chronic pyelonephritis
4/100,000 asymptomatic adults.
Epidemiology of cystitis
Very common.
Epidemiology of prostatitis
15% of men experience symptoms at some point in life.
Diagnostic test for acute pyelonephritis
Urine dipstick.
Urine is cloudy with an offensive smell.
Midstream culture.
Diagnostic test for chronic pyelonephritis
Urine dipstick.
Midstream culture.
Diagnostic test for cystitis
History.
Midstream culture.
Diagnostic test for prostatitis
DRE: Gland can feel nodular, ‘boggy’, tender and hot.
Treatment of acute pyelonephritis
Support.
Antibiotics, empirically.
Ciprofloxacin / co-amoxiclav first line.
Treatment of chronic pyelonephritis
Blood pressure control to slow progression of renal failure.
Antibiotics, empirically.
Treatment of cystitis
Often resolves without treatment.
Fluids and possibly antibiotics.
Treatment of prostatitis
Antibiotics, empirically.
Quinolones, first line.
Complications of acute pyelonephritis
Septicaemia,
renal abscess.
Complications of chronic pyelonephritis
Septicaemia,
progressive renal scarring,
secondary hypertension.
Complications of prostatitis
Chronic infection.
Define Urethritis
Urethral inflammation.
Define Epididymo-orchitis
Pain,
swelling
and inflammation of the epididymis.
Types of urethritis
Gonococcal.
Non-gonococcal.
How does gonococcal urethritis clinically present?
May be asymptomatic.
Usually is asymptomatic in women.
Urethral discharge, more noticeable after holding urine overnight.
Dysuria.
How does non-gonococcal urethritis clinically present?
As gonococcal urethritis, no discharge.
How does epididymo-orchitis clinically present?
Unilateral scrotal pain and swelling.
In STI: urethral discharge also.
Tenderness to palpation on affected side.
Palpable swelling.
Pathophysiology of epididymo-orchitis
Most common route of infection is infection spreading from the urethra.
Second is from the bladder.
Cause of gonococcal urethritis
Neisseria gonorrhoeae.
As a result of STI.
Cause of non-gonococcal urethritis
Number of organisms.
Chlamydia trachomatis,
Mycoplasma genitalium most commonly.
Cause of epididymo-orchitis
In men under 35, most commonly STI.
Over 35, gram negative enteric organisms.
Can also be viral.
Epidemiology of non-gonococcal urethritis
Most common condition diagnosed and treated in men in genitourinary.
Epidemiology of epididymo-orchitis
25/10,000 (likely dropped now).
Diagnostic test for urethritis
Urethral smear.
Screen for STIs.
Diagnostic test for epididymo-orchitis
Culture urethral smear.
Treatment of gonococcal urethritis
Antibiotics, empirically.
Quinolones, first line.
Treatment of non-gonococcal urethritis
Antibiotics.
Specifically ceftriaxone.
Treatment of epididymo-orchitis
Check for torsion.
STI advice.
Empirical antibiotics if appropriate.
Complications of gonococcal urethritis
Epididymitis,
prostatitis,
gonococcal arthritis.
Complications of non-gonococcal urethritis
Epididymitis,
prostatitis.
Complications of epididymo-orchitis
Reactive hydrocele,
abscess formation.
Sequelae of gonococcal urethritis
If untreated, can remit spontaneously.
Sequelae of non-gonococcal urethritis
10-20% become recurrent.
