Urology Flashcards
What is benign prostatic enlargement?
Increase in size of prostate without presence of malignancy
How common is benign prostatic enlargement?
24% men 40-64 40% men over 60 More common over 60 Ususual before 45 Affects Afro-Caribbean's more severely than white men, probably due to high levels of testosterone
What can increase your risk of having benign prostatic enlargement?
Age - increases with age
Castration is protective - androgens don’t cause BPH but are a requirement for BPH, not seen in those with castration prior to puberty or genetic disease that inhibits androgen action or production
What occurs in benign prostatic enlargement?
Benign nodular or diffuse proliferation of musculofibrous and glandular layers of prostate
Inner (transitional) zone enlarges in contrast to peripheral layer expansion seen in prostate carcinoma
As prostate gets bigger, it may squeeze or partly block the urethra (narrows urethra)
Often causes problems with urinating
What are lower urinary tract symptoms?
Nocturia (> 30% voided volume at night) Frequency Urgency Post-micturition dribbling Poor stream/flow Hesitancy Overflow incontinence Haematuria Bladder stones Delay in intiation of micturition Incomplete bladder emptying
What symptoms may suggest BPE?
LUTS
Abdominal exam reveals enlarged bladder
Acute urinary retention
May cause bladder to become occluded leading to anuria - results in acute urinary retention leading to UTIs, bladder stones or kidney damage
What could be a differential diagnosis for BPE?
Bladder tumour Bladder stones Trauma Prostate cancer Chronic prostatitis UTI
How is BPE diagnosed?
Digital rectal exam - feel enlarged, smooth
Serum electrolytes and renal ultrasound - to exclude renal damage caused by obstruction
Transrectal USS - to see size of prostate
Serum PSA
Biopsy and endoscopy
Mid-stream urine sample - excludes infection
Flow rates and residual volume - max flow rate < 10ml per second suggestive of bladder outflow obstruction
Frequency volume chart
How is BPE treated?
If symptoms minimal watchful waiting
Lifestyle - avoid caffeine and alcohol to reduce urgency and nocturia, relax when voiding, void twice in a row to aid emptying
Medications
- Alpha-1 antagonist eg tamsulosin (relaxes smooth muscle)
- 5-alpha reductase inhibitor eg finasteride
Surgery
- Usually for those who failed to respond to adequate trial of medial therapy/large prostate
Required if acute urinary retention, failed voiding trials, recurrent gross haematuria, renal insufficiency due to obstruction
What are the indications for surgery in BPE?
RUSHES Retention UTIs Stones Haematuria Elevates creatinine due to BOO Symptoms deterioration
What are the complications of BPE?
Bladder calculi
UTI
Haematuria
Acute retention
What are the symptoms and signs of acute urinary retention?
Painful 600ml-1L residual vol Normal U&Es Pain relieved by catheterisation Precipitation retention Spontaneous retention Bladder outflow surgery
What are the symptoms and signs of chronic urinary retention?
More difficult to define
Incomplete bladder emptying
Increased risk of infections and stones
Can be low pressure with detrusor failure
Can be high pressure - risk of interactive obstructive uropathy
What is bladder cancer?
Type of transitional cell carcinoma
How common is bladder cancer?
Most common TTC - 50% 4th most common cancer in men 8th most common cancer in women Incidence peaks in 8th decade Most commonly occurs after age 40
What are the risk factors for getting bladder cancer?
Smoking
Occupational exposure to carcinogens - beta-napthylamine, benzidine, azo dyes, workers in petroleum, chemical, cable and rubber industries particularly at risk
Exposure to drugs eg phentacetin and cyclophosphamide
Chronic inflammation of urinary tract eg schistomiasis or indwelling catheter
> 40 years
Male
FHx
How does bladder cancer spread?
Local - pelvic structure
Lymphatic - iliac and para-aortic nodes
Haematogenous - to liver and lungs
How does bladder cancer present?
Painless haematuria - pain may result due to clot retention
Any patient over 40 with haematuria should be assumed to have a urothelial tumour until proven otherwise
Recent UTIs
Voiding irritability
What could be a differential diagnosis of bladder cancer?
Haemorrhagic cystitis
Renal cancer
UTI
Urethral trauma
How is bladder cancer diagnosed?
Cytoscopy (bladder endoscopy) with biopsy - diagnostic
Urine microscopy/cytology - sterile pyuria (pus in urine)
CT urogram (staging and is diagnostic)
Urinary tumour markers
MRI/lymphangiography may show involved pelvic nodes
CT/MRI pelvis
How is bladder cancer treated?
Depends on staging
Non-muscle invasive bladder cancer
- Surgical resection
- +/- chemo - mitomycin, doxorubicin, cisplatin to reduce recurrence
Localised muscle invasive disease
- Radical cystectomy - post-op chemo - M-VAC (methotrexate, vinblastine, adriamycin, cisplatin)
- Radical radiotherapy is not fit for surgery
- Chemo - CMV cisplatin, methotrexate, vinblastine
Metastatic bladder cancer
- Palliative chemotherapy and radiotherapy
What is chronic kidney disease?
Long standing, usually progressive, impairment in renal function (haematuria, proteinuria, or anatomical abnormality) for more than 3 months
GFR < 60ml/min/1.73m2 for more than 3 months with/without evidence of kidney damage
How common is CKD?
Between 6-11% of people defined as having CKD
Risk of CKD increases with age - incidence rising as we are living longer
More common in women
How is CKD classified?
Renal damage - proteinuria, haematuria or evidence of abnormal anatomy or systemic disease
Intervening early in CKD can reduce progression to end-stage renal failure and so screening recommended to at risk patients
GFR 60-89 mild
45-59 mild-moderate
30-44 moderate-severe
15-29 severe
< 15 kidney failure
What can cause CKD?
DM - type 2 more than type 1 Hypertension Atherosclerotic renal vascular disease Polycystic kidney disease Tuberous sclerosis Primary glomerulonephritis eg IgA nephropathy SLE Amyloidosis Hypertensive nephrosclerosis Small and medium sized vessel vasculitis FHx of stage 5 CKD or hereditary kidney disease Hypercalcaemia Neoplasma Myeloma Idiopathic - 20%
What can increase your risk of CKD?
DM Hypertension Old age CVD eg IHD, PVD Renal stones or benign prostatic hyperplasia Recurrent UTIs SLE Proteinuria AKI Smoking African, Afro-Caribbean, Asian origin Chronic use of NSAIDs
What occurs in CKD?
Tends to progress to ESRF although rate of progression may be slow
Speed of decline tends to depend on underlying nephropathy and on BP control
Each kidney has roughly 1 million nephrons
Many nephrons fail, scarred, burden of filtration falls to fewer functioning nephrons
Functioning nephrons increased flow per nephron (hyperfiltration), as blood flow has not changed, and adapt with glomerular hypertrophy and reduced arteriolar resistance
Increased flow, increased pressure, and increased shear stress set in motion a cycle of raised intraglomerular capillary pressure and strain which acclerated remnant nephron failure
Increased flow and strain may be detected as new/increasing proteinuria
What role does angiotensin II play in CKD?
Produced locally, modulates intraglomerular capillary pressure and GFR - vasoconstriction of post-glomerular arterioles
Increases pore sizes and impairs selective function of basement membrane for macromolecules resulting in increased proteinuria
Prognosis of CKD correlates with - hypertension, proteinuria, degree of scarring in interstitium on histology
Therapy aimed at inhibit angiotensin II and reducing proteinuria mainly with ACEi or ARBs
How does CKD present?
Often completely asymptomatic at first due to reserve
Serum urea and creatinine used as surrogates of accumulating metabolites (uraemic toxins)
Symptoms common when serum urea concentration exceeds 40mmol/l but many patients develop uraemic symptoms at lower levels of serum urea
Malaise
Anorexia and weight loss
Insomnia
Nocturia and polyuria due to impaired concentrating ability
Itching
Nausea, vomiting, diarrhoea
Symptoms due to salt and water retention - peripheral or pulmonary oedema
Amenorrhoea in women and erectile dysfunction in men
Increased risk of peptic ulceration, acute pancreatitis, hyperuricaemia and incidence of malignancy
What could be a differential diagnosis of CKD?
AKI - differentiate on history, duration of symptoms, previous urinalysis or measurement of serum creatinine
Normochromic anaemia, small kidneys on USS and presence of renal osteodystrophy favour CKD
How is CKD diagonsed?
ECG for high K signs
Urinalysis
- Haematuria (glomerulonephritis)
- Proteinuria
- Mid-stream urine sample
- Albumin to creatinine ratio or protein to creatinine ratio
Urine microscopy
- WCC - bacterial UTI
- Eosinophilia - allergic tubulointerstitial nephritis/cholesterol emboli
- Granular casts - active renal disease
- RBCs - glomerulonephritis
Serum biochem
- Urea, electrolytes, bicarbonate, creatinine
- Low eGFR
- Raised alkaline phosphatase
- Raised PTH if CKD stage 3 or more
Bloods
- Raised phosphate
- Low Ca
- Hb low - normochromic normocytic anaemia
- Raised viscosity - myeloma/vasculitis
- Fragmented RBC indicate intravascular haemolysis
Immunology
- Auto-antibody screening for SLE, scleroderma, Goodpastures
- Hep B, C, HIV and streptococcal antigen tests
Imaging
- USS to check renal size and exclude hydronephrosis - kidneys small
- CT - detect stones, retroperitoneal fibrosis and other causes of urinary obstruction and may be cortical scarring
Biopsy and histology to diagnose condition causing renal failure
How is CKD treated?
Identify and treat reversible causes - obstruction, stop nephrotoxic drugs, stop smoking, weight loss, tighten glucose control in diabetes
Limit progression and complications
- BP, bone disease (vit D, avoid phosphate), CVD
Symptom control
- Anaemia - iron/folate/folic acid, acidosis (sodium bicarb), oedema (furosemide)
Renal replacement therapy - transplant, dialysis
Why do you get anaemia in CKD?
Reduced EPO production by diseased kidney
Normochromic normocytic anaemia
Why do you get bone disease in CKD?
Bone pain
Renal osteodystrophy - osteomalacia, osteoporosis, hyperparathyroidism
Renal phosphate retention, impaired 1,25-dihydroxyvitamin D production leads to fall in serum Ca2+ thus compensatory increase in PTH which can result in skeletal decalcification leading to bone disease
What are the neurological complications of CKD?
Autonomic dysfunction presents as postural hypotension and disturbed GI motiligy
Polyneuropathy resulting in peripheral paraesthesiae and weakness
In advanced uraemia depressed cerebral function, myoclonic twitching and seizures
What are the CVD risks of CKD?
MI, cardiac failure, sudden cardiac death, stroke
Occurs due to increased frequency of hypertension, hyperlipidaemia, vascular calcification
Pericarditis and pericardial effusion occur in severe anaemia
Pericardial friction rub
Flow murmurs
Why can you get skin disease in CKD?
Pruritus due to nitrogenous waste products of urea - may be scratch marks
Brown discolouration of nails
What is cystitis?
Urinary infection of bladder
How common is cystitis?
Much more common in women
Can occur in children
Most common cause E coli
What can increase your risk of cystitis?
Urinary obstruction resulting in urinary stasis
Previous damage to bladder epithelium
Bladder stones
Poor bladder emptying
How does cystitis present?
Dysuria Frequency Urgency Suprapubic pain Haematuria Offensive smelling/cloudy urine Abdominal/loin tenderness
How is cystitis diagnosed?
Microscopy and sensitivity of sterile mid-stream urine
Dipstick analysis - positive leucocytes, blood and nitrites
How is cystitis treated?
Antibiotics
- First line - trimethoprim or cefalexin
- Second line - ciprofloxacin, co-amoxiclav
How common is prostate cancer?
Most adenocarcinomas arising in peripheral zone of prostate gland
Commonest male malignancy
Most slow growing but some can be aggressive
Most common site of metastases is bone and lymph nodes
Malignant change becomes more common with age
7% of all cancers in men and is 6th most common in world
Incidence increases with age
By age of 80, 80% men have malignant foci within gland but most appear to be dormant
More common in black people due to higher testosterone
What can cause prostate cancer?
Hormonal factors eg increased testosterone
What can increase your risk of prostate cancer?
FHx- 3/more affected relatives or 2 relatives with early onset
Genetic - HOXB12 predisposition gene, BRCA2 confers 5-7 times higher risk
Increasing age
Black
If one first-degree relative has prostate cancer then risk doubled
What is the pathology of prostate cancer?
Most adenocarcinomas arising in peripheral prostate
Spread may be
- Local - seminal vesicles, bladder, rectum
- Via lymph
- Haematogenously - bone (sclerotic bony lesions) or less common - brain, liver and lung
Androgen receptors on prostate are responsible for cancerous growth
How does prostate cancer present?
LUTS if local disease
Weight loss, bone pain, anaemia suggests metastasis
What could be a differential diagnosis of prostate cancer?
BPH, prostatitis, bladder tumours
How is prostate cancer diagnosed?
DRE - hard, irregular prostate
Raised PSA - if metastases then will be > 16ng/ml
Trans-rectal ultrasound and biopsy
- Diagnostic
- Histological diagnosis essential before treatment
- Gleason score used
- Urine biomarkers eg PCA3 or gene fusion protein
- Endorectal coli MRI - to locally stage tumour
How is prostate cancer treated?
Disease confined to prostate
- Radical prostatectomy if < 70
- Radio and hormone therapy alternative
- Brachytherapy - implantation of radioactive material targeted at tumour
- Hormone therapy temporarily delays tumour progression
- Active surveillance if > 70 and low risk
Metastatic disease
- Endocrine therapy (most hormone-sensitive malignancy, binding at androgen receptor stimulates tumour growth, androgen deprivation (orchidectomy, LHRH agonists, androgen receptor blockers))
Symptomatic
- Analgesia, treat hypercalcaemia, radiotherapy for bone metastaes/spinal cord compression
What is prostatitis?
Infection and inflammation of prostate gland
Can be acute or chronic
How common is prostatitis?
Common in men of all ages
Most common UTI in men < 50
Usually presents > 35
Associated with LUTS
What can cause acute prostatitis?
Steptococcus faecalis
E coli
Chlamydia
What can cause chronic prostatitis?
Bacterial eg streptococcus faecalis, E coli, chlamydia
Non-bacterial eg elevated pressure, pelvis floor myalgia
What can increase your risk of getting prostatitis?
STI UTI Indwelling catheter Post-biopsy Increasing age
How does acute prostatitis present?
Systemically unwell Fever, rigors, malaise Pain on ejaculation Significant voiding LTUS eg poor intermittent stream, hesitancy, incomplete emptying, post-micturition dribbling, straining, dysuria Plevic pain
How does chronic prostatitis present?
Acute symptoms > 3 months
Recurrent UTIs
Pelvic pain
What could be a differential diagnosis of prostatitis?
Cystitis BPH Calculi Bladder neoplasia Prostatic abscess
How is prostatitis diagnosed?
DRE - tender/hot to tough, hard from calcification
Urine dipstick - positive for leukocytes and nitrites
Mid-stream urine microscopy and sensitivity
Blood cultures
STI screen - for chlamydia in particular
Trans-urethral USS
How is acute prostatitis treated?
IV gentamycin and IV co-amoxiclav or IV tazocin or IV carbapenem
2-4 weeks on a quinolone eg ciprofloxacin once well
Second line- trimethoprim
TRUSS guided abscess drainage if necessary
How is chronic prostatitis treated?
4-6 weeks of quinolone
Don’t tend to respond as well to antibiotics
+/- alpha-blockers eg tamsulosin
NSAIDs
What is a possible complication of prostatis?
Urinary retention
What is pyelonephritis?
Infection of renal parenchyma and soft tissues of renal pelvis and upper ureter
Majority caused by UPEC - uropathogenic E coli
Main organisms KEEPS
How common is pyelonephritis?
Predominantly affects women under 35
Associated with significant sepsis and systemic upset
Unusual in men
Mainly caused by UPEX typically with P pilli on surface to all ureteral ascent
What can increase your risk of pyelonephritis?
Structural renal abnormalities Calculi (stones) Catheterisation Pregnancy Diabetes Immunocompromised
What is the pathology of pyelonephritis?
Infection mostly due to bacteria from own patient’s bowel flora
Most common via the ascending transurethral route by can be via bloodstream/lymphatics
E coli adhesive factors
- P pilli to allow urethral ascent
- Aerobactin for Fe acquisition
- Haemolysin - for pore formation
How does pyelonephritis present?
Triad of - loin pain, fever, pyuria May have severe headache Significant bacteriuria Malaise, nausea, vomiting Oligouria (small amounts of urine) if it causes AKI
What is a differential diagnosis for pyelonephritis?
Diverticulitis Abdominal aortic aneurysm Kidney stones Cystitis Prostatitis
How is pyelonephritis diagnosed?
Tender loin on examination
Urine dipstick
- Detects nitrites (bacteria break down nitrates to produce nitrites)
- Detect leukocyte elastase
- Foul smelling urine
- Dipstick positive for nitrites, leukocytes and protein
Mid-stream urine microscopy, culture and sensitivity
Bloods - FBC (elevated WCC), CRP/ESR raised in acute infection
Urgent ultrasound - detection of calculi, obstruction, abnormal urinary anatomy and incomplete bladder emptying
How is pyelonephritis treated?
Rest
Cranberry juice and lots of water
Analgesia
Antibiotics
- Oral ciprofloxacin or oral co-amoxiclav
- If sever IV gentamycin or IV co-amoxiclav
Surgery to drain abscesses or relieve calculi that are causing infection
What is renal cell carcinoma?
Arises from proximal convoluted tubular epithelium
AKA hypernephroma and Grawitz tumour
What is Wilms tumour?
Childhood tumour of primitive renal tubule and mesenchymal cells
AKA nephroblastoma
How common is renal cell carcinoma?
Most common renal tumour in adults 2-3% all malignancies More common in men Present after 50 years of age Rare before 40 Average age at presentation 55 Highest incidence in Czech Republic
How common is Wilms’ tumour?
Seen within first 3 years of life - chief abdominal malignancy in children
What can increase your risk of renal cell carcinoma?
Smoking
Obesity
Hypertension
Renal failure and haemodialysis
Polycystic kidneys
Von Hippel Lindau syndrome
- Autosomal dominant
- Mutation of chromosome 3 on short arm
- Loss of both copies or tumour suppressor genes
- 50% develop RCC that often bilateral and multifocal
- Renal and pancreatic cysts as well as cerebellar malignancy also arise
What is the pathology of renal cell carcinoma?
Malignant cancer of proximal convoluted tubular epithelium
Spread direct (renal vein), via lymph or haematogenous (bone, liver, lung)
25% metastases at presentation
How does renal cell carcinoma present?
Often asymptomatic and discovered incidentally
Haematuria, loin/flank pain, abdominal mass
Anorexia, malaise, weight loss
Invasion of L renal vein results in compression of left testicular vein causing a varicocele
Polycythaemia in 5%
Hypertension in 30% - renin secretion by tumour
Anaemia due to depression of erythropoietin
Fever 20%
How does Wilms’ tumour present?
Abdominal mass and less commonly haematuria
What could be a differential diagnosis for renal cell carcinoma?
Transitional cell carcinoma
Wilms’ tumour
Renal oncocytoma
Leiomyosarcoma
How is renal cell carcinoma diagnosed?
USS - to distinguish from cysts
CT chest and abdomen with contrast
- More sensitive than USS in detecting a renal mass and well show involvement of renal vein of inferior vena cava
- Using contrast demonstrates kidney function since normal kidney should see it being taken up and excreted well
MRI - tumour staging
BP - increased due to renin
Bloods - FBC (polycythaemia, anaemia due to EPO decrease), ESR raised, liver biochemistry, may be abnormal
Renal biopsy - histology to identify tumour
Bone scan - only is signs of raised serum Ca2+
How is Wilms’ tumour diagnosed?
USS, CT, MRI
How is renal cell carcinoma treated?
Localised disease - surgery
- Nephrectomy unless bilateral
- If bilateral partial nephrectomy
Ablative techniques
- Cryoablation and radiotherapy for patients with significant co-morbidity who would not tolerate surgery
- Can harm kidney function
Metastatic or locally advanced
- Interleukin-2 and interferon alpha
- Biological angio-genesis targeted therapy - sunitinib, bevacizumab, sorafenib
- Temsirolimus - found to improve survival more than interferon
- Last 2 options if patient doesn’t respond to first
How is Wilms’ tumour treatment?
Combination nephrectomy, radiotherapy, chemotherapy
What are renal stones?
Consist of crystal aggregates,s tones form in collecting ducts and may be deposited anywhere from the renal pelvis or urethra
Classically deposited at 3 narrowings (pelvicureteric junction, pelvic brim, vesicoureteric junction)
How common are renal stones?
Increasing incidence
10-15% lifetime risk
Peak age between 20-40
More common in males than females 2:1
Unusual in children
More than 50% lifetime risk of recurrence once had them
Most stones composed of calcium oxalate and phosphate
What can increase your risk of renal stones?
Anatomical abnormalities that predispose stone formation eg duplex obstruction or trauma
- Congenital - horseshoe, duplex, PUJO, spina bifida
- Acquired - obstruction, trauma, relfex
Chemical composition of urine that favours stone crystallisation
Dehydration resulting in concentrated urine
Infection
Hypercalcaemia, hyperoxalruria, hypercalciuria, hyperuricaemia, cysteine
Primary renal disease eg polycystic kidneys, renal tubular acidosis
Drugs - diuretics, antacids, acetazolamide, corticosteroids, aspirin, allopurinol, vitamin C and D
Diet - chocolate, tea, strawberries, rhubarb all increase oxalate levels
Gout
FHx
Metastable urine
How do stones form?
Solute concentration exceed saturation, often in context of trigger that starts crystallisation
Renal stone/calculi form crystals in supersaturated urine - calcium oxalate most common, calcium phosphate uncommon
Stones vary in size and may be single or multiple
Stone regularly cause obstruction leading to hydronephrosis - combination of obstruction and dilation of renal pelvis that often causes lasting damage to kidney
What are the two main causes of calcium renal stones?
Hypercalciuria causes - hyperparathyroidism resulting in hypercalcaemia, excessive dietary intake of calcium, idiopathic hypercalciruia (increased gut absorption), primary renal disease such as polycystic kidneys or medullary sponge kidney
Hyperoxaluria (increased oxalate in urine) causes - high dietary intake of oxalate rich foods (spinach, rhubarb, chocolate, tea), low dietary Ca resulting in decreased binding of oxalate so increased oxalate absorption and urinary excretion, increased intestinal resorption due to GI disease
What can cause uric acid stones?
Associated with hyperuricaemia with/wtihout gout
Dehydration
Patients with ileostomies at particular risk from dehydration and from bicarbonate loss from GI secretion resulting in production of an acidic urine thereby stimulating stone formation
What can cause infection induced stones?
Mixed infective stones composed of magnesium ammonium phosphate as well as calcium
Often large
Usually due to UTI with organisms such as proteus mirabilis that hydrolyse urea forming ammonium hydroxide
What can cause cystine stones?
Caused by cystinuria - autosomal recessive condition affecting cyseine in epithelial cells of renal tubules and GI tract
Resulting in excessive urinary excreting and formation of cysteine stones
How do renal stones present?
Most asymptomatic
Renal colic
Loin pain
If urinary tract obstructed the fluid/diuretics may make pain worse as peristaltic flow increases
Dysuria, burning when peeing, frequency, urgency
Recurrent UTIs - increased risk if voiding impaired
If urinary tract obstruction and infection present then may get acute pyelonephritis - fever, rigors, loin pain, nausea, vomiting
Bowel sounds reduced
BP low
How does renal colic present?
Rapid onset - woken from sleep
Pain that results from upper urinary tract obstruction, unilateral
Unable to get comfortable - writhing
Excruciating ureteric spasms - patient writhing in pain
Pain from loin to groin and comes and goes in waves as ureters peristalise
Associated with nausea and vomiting
Worse with fluid loading
Radiates to groin and ipsilateral testis/labia
Often cannot lie still (differentiates from peritonitis)
Spasmodic/colicky, worse with fluid loading
Classically severe 12/10
What could be a differential diagnosis for renal stones?
Vascular accident eg ruptures AAA if over 50 until proven otherwise
Bowel pathology eg diverticulitis or appendicitis
Ectopic pregnancy or ovarian cyst torsion - do uric pregnancy test
Testicular torsion - can present with loin pain and nothing else
Musculoskeletal
How are renal stones diagnosed?
Focused history and examination - vit D consumption (hypercalcaemia), recurrent UTIs, lots of rhubarb/tea
Urine dipstick for haematuria, proteinuria, glucose
Mid-stream specimen of urine sent for microbiology culture and sensitivity if +ve
Bloods
- Serum urea, electrolyte, creatinine, calcium
- FBC
KUBXR
- First line investigation
- 80% sensitive
- See stone in line of renal tract
NCCT-KUB
- Non-contrast computerised tomogrpahy
- Very rapid
- 99% sensitive for stones
- No contrast so no renal damage/allergy
Ultrasound
- Shows kidney stones and renal pelvis dilatation well but ureteric stones can be missed
- Sensitive for hydronephrosis
- V poor at visualising stones in ureter
- Useful in pregnant and younger recurrent stone formers
- Rarely used acutely
How are renal stones treated?
ABC
Strong analgesics for renal colic eg diclofenac IV, NSAIDs, opiates
Antibiotics if infection eg IV cefuroxime or gentamicin
Antiemetics
IV fluids
Observe for sepsis
Stones less than 5mm in lower ureter 90% pass spontaneously
Medical expulsive therapy
- Stone larger than 5mm with pain and not resolving
- Oral nifedipine or alpha blocker oral tamsulosin can promote expulsion and reduce analgesic requirements
If still not passing
- Extracorporeal shockwave lithotripsy - US stone fragments
- Endoscopy (uteroscopy) with YAG for larger stones
- Percutaneous nephrolithotomy key hole surgery to remove stones that are large
- Ureteric stent
How are renal stones treated?
Conservatie - small, safe location, asymptomatic, static size, comorbid
ESWL- up to 1-2cm, problems with fragment passage and clearance
Ureteroscopic
PCNL - for larger stones
Nephrectomy - if split function
How are ureteric stones treated?
Conservative - allows 2 weeks to pass Drainage if sepsis Medical expulsive therapy ESWL Ureteroscopy
How are bladder stones treated?
Conservative -asymptomatic/unfit
Endoscopic - can be accompanied by treatment of BOO
Open/laproscopic surgery - ideal for larger stones
Due to incomplete bladder emptying
How do you prevent renal stones?
Overhydration 2.5-3L/24 hr output Low salt diet Normal diary intake Healthy protein intake Reduce BMI Active lifestyle Remember to check calcium Uric acid stones - Only form in acidic urine - Deacidification of urine Cysteine stones - Excessive overhydration - Urine alkalisation - Cysteine binders - +/- genetic counselling
What is pyonephrosis?
Combination of infection and obstruction, medical emergency Can lose renal function in 24 hours Systemic sepsis leading to septic shock IV antibiotics Drainage Can kill very quickly
How common is testicular cancer?
Most common cancer in males aged 15-44 10% occur in undescended testes More than 95% arise from germ cells - Seminomas 25-40 yrs and 60 yrs - Teratomas - infancy 4% arise from non-germ cells - Leydig cell tumours - Sertoli cell tumours - Sarcomas
What can increase your risk of testicular cancer?
Undescended testes
Infant hernia
Infertility
FHx
How does testicular cancer present?
Painless lump in testicle
Testicular pain and/or abdominal pain
Hydrocele
Cough and dyspnoea - indicative of lung metastases
Back pain - indicative of para-aortic lymph node metastasis
Abdominal mass
What is a possible differential diagnosis of testicular cancer?
Testicular torsion
Lymphoma
Hydrocele
Epididymal cyst
How is testicular cancer diagnosed?
USS - to differentiate between masses in body of testes and other intrascrotal swellings
Biopsy and histology
Serum tumour markers
- Alpha fetoprotein and/or beta subunit of hCG (raised in teratomas, b-hCG in minority of those with seminomas)
CXR and CT -assess staging
How is testicular cancer treated?
Radical orchidectomy via inguinal approach
Seminomas with metastases below diaphragm only treated with radiotherapy
More widespread tumours treated with chemotherapy
Teratomas treated with chemo
Sperm storage offered
What is urethritis?
Urethral inflammation due to infectious of non-infectious cases
Primarily a sexually acquired disease
How common is urethritis?
Most common condition diagnosed and treated in men at GUM clinics
Non-gonococcal urethritis more common than gonococcal urethritis
Chlamydia most common STI in young people aged 15-24
What can cause urethrtis?
Gonococcal - Neisseria gonorrhoea
Non-gonococcal - chlamydia trachomatis (most), mycoplasma genitalium, ureaplasma urealyticum, trichomonas vaginalis
Non-infective - trauma, urethral stricture, irritation, urinary calculi
What can increase your risk of urethritis?
Sexually active, unprotected sex, male to male sex, male
How does urethritis present?
May be asymptomatic (90-95% with gonorrhoea, 50% with chlamydia) Dysuria +/- discharge, blood, pus Urethral pain Penile discomfort Skin lesions Systemic symptoms
What could be a differential diagnosis of urethritis?
Candida balantis Epididymitis Cystitis Acute prostatitis Urethral malignancy
How is urethritis diagnosed?
Nucleic acid amplification test - Female - self collected vaginal swab, endocervical swab, first void urine - Male - first void volume - High specificity and sensitivity Microscopy of gram-stained smears of genital secretions Blood cultures Urine dipstick - to exclude UTI Urethral smear
How is urethritis treated?
Chlamydia - Oral azithromycin STAT or 1-week oral doxycycline - Test for other STIs - Pregnancy - oral erythromycin for 14 days or oral azithromycin stat Gonorrhoea - IM ceftriaxone or oral azithromycin - Partner notification Patient education Contact tracing
How common is urinary tract obstruction?
Common - should be considered in anyone with renal impairment
Damage can be permanent if obstruction not treated properly
Can be partial, complete, unilateral or bilateral
What can cause urinary tract obstruction?
Luminal - stones, blood, clot, sloughed papilla, tumour
Mural - congential or acquired structure, neuromuscular dysfunction or schistomiasis
Extra-mural - abdominal or pelvic mass/tumour, retroperitoneal fibrosis, BPH, prostate cancer, pregnancy, inflammation (peritonitis/diverticulitis)
How does urinary tract obstruction present?
Acute upper tract (kidney and ureter) obstruction - loin pain radiating to groin
Chronic upper tract obstruction - flank pain, renal failure, infection and polyuria may occur due to impaired urinary concentration
Acute lower tract (bladder to urethra) obstruction - acute urinary retention with severe suprapubic pain, often preceded by symptoms of bladder outflow obstruction, distended, palpable bladder thats dull to percussion
Chronic lower tract obstruction - urinary frequency, hesitancy, poor stream, terminal dribbling, overflow incontinence, distended, palpable bladder, large prostate on rectal exam - complications of UTI, urinary retention
How is urinary tract obstruction diagnosed?
Bloods - U&Es and monitor creatinine raised
Mid-stream urinary sample - culture and sensitivity
USS - hydronephrosis then arrange CT
How is urinary tract obstruction treated?
Upper - nephrostomy, alpha-1 antagonist, 5-alpha reductase inhibitor
Lower - urethral catheter, suprapubic catheter
Surgery - transurethral resection of prostate - risk of being incontinent, impotent and erectile dysfunction
Indications for surgery
What does RUSHES stand for?
R - retention U - UTIs S - stones H - haematuria E - elevated creatinine due to bladder outflow obstruction S - symptoms deteriorated
What is nephrotic syndrome?
Triad of proteinuria > 3.5g/24 hrs, hypoalbuminaemia, oedema
Severe hypolipidaemia often present - liver goes into overdrive due to albumin loss and other protein loss increasing risk of blood clots and produces raised cholesterol
Don’t develop kidney failure but leaking huge amounts of protein but kidney function remains the same
Caused by structural and functional abnormalities of podocytes
How common is nephrotic syndrome?
Relatively rare
Diabetes most common secondary cause
Minimal change disease accounts for 10-25% of nephrotic syndrome in adults and is commonest cause of nephrotic syndrome in children
What are the primary causes of nephrotic syndrome?
Minimal change disease - commonest cause in children
Membranous nephropathy - asymptomatic proteinuria/nephrotic syndrome +/- microscopic haematuria, hypertension and renal impairment, idiopathic/secondary drugs, autoimmune, infection, neoplasia
Focal segmental glomerulosclerosis - focal scarring and only some glomeruli involved and segmental
What are the secondary causes of nephrotic syndrome?
DM Amyloidosis Infections eg Hep B/C and HIV SLE/RA Drugs - gold, penicillin, NSAIDs, ACEi Malignancy
What can increase your risk of nephrotic syndrome?
DM
What is the pathology of nephrotic syndrome?
Injury to podocyte appears to be main cause of proteinuria
Podocytes wrap around glomerular capillaries and maintain the filtration barrier - preventing large molecular weight proteins from entering urine
Damage to podocyte foot processes or loss of podocytes can cause heavy protein loss
How does nephrotic syndrome present?
Nomal-mild increase in BP Proteinuria > 3.5g/day Normal-mild decrease GFR Hypoalbuminaemia Pitting oedema of ankles, genitals, abdominal wall and sometimes face Frothy urine
What could be a differential diagnosis of nephrotic syndrome?
Congestive HF - oedema, raised JVP, in nephrotic syndrome normal/low JVP (unless renal failure and oligouria)
Cirrhosis - hypoalbuminaemia and oedema, signs of chronic liver failure eg jaundice, fever, and loss of body hair
How is nephrotic syndrome diagnosed?
Establish cause - renal biopsy
Urine dipstick shows v high protein
CXR or ultrasound for pleural effusion or ascites
Serum albumin low
BP normal/mildly increased
Renal function normal/mildly impaired
Serum creatinine, eGFR, lipids and glucose
ANA, double stranded DNA antibody, C3 and 3 indicates SLE
Antiphospholipase A2 receptor antibody indicates membranous nephropathy
HepB surface antigen, HepC antibody, HIV
How is nephrotic syndrome treated?
Reduce oedema
- Loop diuretics IV furosemide (IV as gut oedema may prevent oral absorption)
- Thiazide diuretics
- Fluid and salt restriction whilst on diuretics
Reduce proteinuria
- ACEi
- ARB
- Eat normally rather than high protein diet
Reduce risk of complications
- Prophylactic anticoagulation with warfarin, especially when albumin low
- Reduce cholesterol with statins
- Treat infections promptly and vaccinate
Treat underlying cause
What are the potential complications of nephrotic syndrome?
Increases susceptibility to infection such as cellulitis, strep infection, spontaneous bacterial peritonitis, due to low serum IgG, decreased complement activity and reduced cell function due in part to loss of immunoglobulin in urine and also to immunosuppressive treatment
Thromboembolism - DVT, PE, renal vein thrombosis, hypercoagulable state due to increased clotting factors and platelet abnormalities
Hyperlipidaemia - increased cholesterol and trigylcerides due to hepatic lipoprotein synthesis in response to low oncotic pressure due to low albumin
What causes acute nephritic syndrome?
Commonest primary cause - IgA nephropathy Bacterial infection eg MRSA, typhoid, secondary syphilis Hep B and C Schistomiasis Malaria Post-steptococcal infection IE SLE Systemic sclerosis ANCA associated vasculitis Good pastures disease
How does ANCA associated vasculitis cause acute nephritic syndrome?
Multisystem small vasculitis attacks small vessels in kidney and eye
How does Good pastures disease cause acute nephritic syndrome?
Co-existence of acute glomerulonephritis and pulmonary alveolar haemorrhage and presence of circulating antibodies directed against intrinsic antigen to the basement membrane of both kidney and lung, rapidly progressing kidney failure
What is IgA nephropathy?
Associated with tonsilitis and results in haematuria
How does acute nephritis syndrome present?
Haematuria - visible/non-visible - mild microcytic Proteinuria usually < 2g in 24 hrs Hypertension (moderate-severe increase) and oedema (periorbital, leg or sacral) caused by salt and water retention Oligouria Uraemia and symptoms of it - Anorexia - Pruritus - Lethargy and nausea Deteriorating kidney function Moderate-severe decrease in GFR
How is acute nephritic syndrome diagnosed?
Take history to determine cause
Measure eGFR proteinuria, serum urea and electrolytes and albumin - to determine current status and monitor progress
Culture - swab from throat or infected skin
Urine dipstick to detect proteinuria and haematuria
Renal biopsy if necessary
How is acute nephritic syndrome treated?
Post streptococcal infection - antibiotics, supportive
SLE - immunosuppression, steroids, cyclophosphamide, rituximab
ANCA associated vasculitis - immunosuppression, steroids, cyclophosphamide, rituximab, plasma exchange
Good pastures disease - remove antibody via plasma exchange, immunosuppression, steroids/cyclophosphamide
IgA nephropathy - BP control with ACEi/ARBs
Hypertension also treated with salt restriction, loop diuretics, and CCBs
What is an epididymal cyst?
Smooth, extratesticular, spherical cyst in head of epidiymus
How common are epididmyal cysts?
Usually develop around 40
Not uncommon
Rare in children
What do epididymal cysts look like?
Clear, milky fluid
Lies above testes
How do epididymal cysts present?
Lump
Often multiple and may be bilateral
Small cysts may remain undetected and asymptomatic
Once get large may be painful
Well defined and will transluminate since fluid filled
Testis palpable quite separately from cyst
What could be a differential diagnosis for epididymal cyst?
Spermatocele - fluid and sperm filled cyst in epididymis, only differentiated as sperm present
Hydrocele - collections of fluid surrounding entire testicle
Varicocele - dilated veins that increase with increases in abdominal pressure
How are epididymal cysts diagnosed?
Scrotal ultrasound
How are epididymal cysts treated?
Usually not necessary
Painful and symptomatic then surgical excision
What is a hydrocele?
Abnormal collection of fluid within tunica vaginalis
How common are hydroceles?
Clinically apparent scrotal hydrocele evident in 6% of term males beyond new born period
Most paediatric hydroceles congential
What the two types of hydrocele?
Primary hydrocele
- More common and larger
- Usually in younger men
- Associated with patient processus vaginalis, which typically resolves during 1st year of life
Secondary hydrocele
- Rarer and present in older boys and men
- Secondary to - testis tumour, trauma, infection, TB, testicular torsion, generalised oedema
What causes hydroceles?
Overproduction of fluid in tunica vaginalis (simple hydrocele)
Processus vaginalis fails to close, allowing peritoneal fluid to communicate freely with scrotal portion (communicating hydrocele)
How do hydroceles present?
Scrotal enlargement with non-tender, smooth, cystic swellng
Pain not feature unless hydrocele infected
Testis usually palpable but may be difficult to palpate in larger hydrocele
Lies anterior to and below testits and will transluminate
What is a differential diagnosis of hydrocele?
Testicular torsion
Strangulation hernia
How is hydrocele diagnosed?
Ultrasound
Serum alpha-fetoprotein and hCG to help exclude malignant teratomas or other germ cell tumours
How are hydroceles treated?
Resolve spontaneously
Many of infancy resolve by 2 years
Therapeutic aspiration or surgical removal
What is autosomal dominant polycystic kidney disease?
Multiple cysts develop, gradually and progressively, throughout the kidney eventually resulting in renal enlargement and kidney tissue destruction
How common is autosomal dominant polycystic kidney disease?
Commonest inherited kidney disease
Autosomal dominant inheritance with high penetrance
Usually presents in adulthood (20-30)
More common in men
How common is autosomal recessive polycystic kidney disease?
Rarer than ASPKS with prevalence 1 in 40,000
Autosomal recessive inheritance
Disease of infancy
What can cause autosomal dominant polycystic kidney disease?
Mutations in PKD1 gene on chromosome 16
Mutations in PKD2 gene on chromosome 4
What can cause autosomal recessive polycystic kidney disease?
PKHD1 mutation on long arm of chromosome 6
What can increase your risk of getting autosomal dominant polycystic kidney disease?
FHx of ADPKD, ESRF or hypertension
What can increase your risk of getting autosomal recessive kidney disease?
FHx
What is the pathology of autosomal dominant polycystic kidney disease?
PKD1 encodes polycystin 1 which is involved in cell-cell and/or cell-matrix interactions - regulates tubular and vascular development in kidneys
PKD2 encodes polycystin 2 which function as calcium ion channel
Polycystin complex occurs in cilia that are responsible for sensing flow in tubule
Disruption of polycystin pathway results in reduced cytoplasmic Ca2+, which in principle cells of collecting duct, causes defective ciliary signalling and disoriented cell division resulting in cyst formation
Progressive loss of renal function in usually attributed to mechanical compression, apoptosis of healthy tissue and reactive fibrosis
Rate of renal function decline is dependent on growth and size of cysts - patients with rapidly growing cysts of MRI low renal function more rapidly
How does autosomal dominant kidney disease presnet?
Can be clinically silent for many years - family screening essential
Symptoms present from 20 onwards
Loin pain and/or haematuria from haemorrhage into cyst, cyst infection/urinary tract stone formation
Loin of abdominal discomfort as size of kidneys increase
Excessive water and slat loss
Nocturia
Bilateral kidney enlargement
Renal colic due to clots
Hypertension
Renal stone (calculi) - mainly uric acid
Progressive renal failure
What are the extrarenal symptoms of ADPKD?
Subarachnoid haemorrhage associated with berry aneurysm rupture Polycystic liver disease Pancreatitis Male infetility Mitral valve prolapse Ovarian cysts Diverticular disease
How does ARPKD present?
Variable
May present in infancy with multiple renal cysts and congenital hepatic fibrosis
Enlarged polycystic kidneys
30% develop kidney failure
What could be a differential diagnosis of ADPKD?
Acquired and simple kidney cysts
Autosomal recessive PKD
Medullary sponge kidney
Tuberous sclerosis
What could be a differential diagnosis of ARPKD?
ADPKD
Mutlicystic dysplasia
Hydronephrosis
Renal vein thrombosis
How is ADPKD diagnosed?
Personal history FHx of ADPKD, ESRF, hypertension BP raised USS - for at risk individuals diagnostic if - 15-39 > 3 cysts (uni/bilateral) - 40-59 > 2 cysts (bilateral) - > 60 > 4 cysts (each kidney) - Exclude ADPKD if > 40 < 2 cysts - Cannot exclude ADPKD by USS if < 30 Genetic testing for PKD1 and 2
How is ARPKD diagnosed?
Diagnosed antenatally or neonatally
USS - to see cysts
CT and MRI to monitor liver disease
Genetic testing
How is ADPKD treated?
No treatment shown to slow disease progression
BP control with ACEi
Treat stones and give analgesia
Laparoscopic removal of cysts help with pain/nephrectomy
Disease progression monitored by serial progression of serum creatinine
Renal replacement therapy for ESRF
Children and sibling of patients with disease offered screening by renal USS in 20s
Counselling and support
How is ARPKD treated?
Currently none available Genetic counselling for family members Laproscopic removal of cysts to help with pain/nephrectomy BP control with ACEi Treat stones and give anaglesia Renal replacement therapy for ESRF Counselling and support
What is testicular torsion?
Twisting of spermatic cord resulting in occlusion of testicular blood vessels which can rapidly lead to ischaemia and infarct and thus the potential loss of testis (germ cells are most susceptible cell line to ischaemia)
Aim to recognise condition before cardinal symptoms fully manifest, as prompt to surgery saves testes
If surgery performed in < 6 hrs, salvage rate 90-100% if > 24 hrs 0-10%
How common is testicular torsion?
Common urological emergency among adolescent boys and young men
Typically occurs in neonates or post-pubertal boys but can occur in males of all ages - most common at 11-30 yrs
Left side more commonly affected that right
What can cause testicular torsion?
Underlying congenital malformation - belt clapper deformity where testis not fixed to scrotum completely, allowing free movement leading to twisting
What can increase your risk of testicular torsion?
Genetic factors
How does testicular torsion present?
Any boy presenting with abdominal pain - testes should be checked
Sudden onset of pain in ones testis - makes walking uncomfortable
Pain often comes on during sport/physical activity
Pain in abdomen, nausea, vomiting common
Inflammation of one testis - v tender, hot, swollen
Testis may lie high and transversely
With intermittent torsion, pain may have passed on presentation, if severe and lie is horizontal prophylactic fixing may be worse
What could be a differential diagnosis of testicular torsion?
Epididymo-orchitis - usually patient older and may be symptoms of UTI and more gradual pain onset
Tumour, trauma, acute hydrocele
Torsion of testicular or epididymal appenage - usually occurs in boys between 7-12 and causes less pain, small blue nodule under scrotum, due to surge in gonadotrophins that signal the onset of puberty
Idiopathic scrotal oedema - benign condition usually occurs between 2-10 and differentiated from torsion by absence of pain and tenderness
How is testicular torsion diagnosed?
Doppler USS may demonstrate lack of blood flow to testis
Urinalysis to exclude infection and epididymis
Do not delay surgical exploration
How is testicular torsion treated?
Surgery- expose and untwist testes - 6hr window
Orchidectomy and bilateral fixation
What is a varicocele?
Abnormal dilatation of testicular veins with pampiniform venomous plexus, caused by venous reflux
How common are varicoceles?
Left side more commonly affected
Unusual in boys under 10
Incidence increases after puberty
Associated with sub-fertility
What is the pathology of varicocele?
Angle at whcih left testicular vein enters left renal vein
Increased reflux from compression of renal vein
Lack of effective valves between testicular and renal veins
How do varicoceles present?
Often visible as distended scrotal blood vessels that feel like a bag of worms
Patient may complain of dull ache or scrotal heaviness
Scrotum hangs lower on side of varicocele
What could be a differential diagnosis of varicocele?
Secondary to other pathological processes blocking the testicular veins eg kidney tumours and other retroperitoneal tumours
How are varicoceles diagnosed?
Venography
Colour doppler ultrasound
How are varicoceles treated?
Surgery if pain, infertility or testicular atrophy
What is acute urinary retention?
Sudden onset of painful inability to pass urine usually over 500ml in the bladder
Bladder usually tender
What can cause acute urinary retention?
Prostatic obstruction Urethral stricutures Alcohol Constipation Anticholinergics Post-op Infection Neurological (spinal compression - cauda equina syndrome)
How is acute urinary retention diagnosed?
Examination - abdomen, prostate (DRE), perineal sensation (cauda equina)
Normal renal biochemistry
Renal ultrasound if abnormal renal biochemistry
PSA test - to look for BPH/prostate cancer
How is acute urinary retention treated?
Catheter relieves pain
Alpha-1 blocker eg tamsulosin which relaxes smooth muscle in bladder neck ot aid voiding
Prevent by giving 5-alpha reductase inhibitor which reduces testosterone conversion to dihydrotestosterone and thus reduces prostate size
What can cause chronic urinary retention?
Prostatic enlargement due to BPH/prostate cancer
Pelvic malignancy or rectal surgery
Diabetes
How does chronic urinary retention present?
Overflow incontinence - leaking urine during the day/wetting the bed
Loss of appetitie, constipation, distended abdomen, UTI
How is chronic urinary retention treated?
Only catheterise if pain, urinary infection or renal impairment
What is erectile dysfunction?
Neurovascular phenomenon under hormonal control
Arterial dilatation, smooth muscle relaxation, activation of corporeal veno-occlusive mechanism
Persistent inability to attain and maintain an erection sufficient to permit satisfactory sexual performance
How common is erectile dysfunction?
Common worldwide Shares risk factors with CVD Lifestyle modifications can improve Symptom not a disease Radical prostatectomy
What can cause erectile dysfunction?
Organic - Vasculogenic - Neurogenic - Hormonal - testosterone deficiency (primary testicular failure, pituitary/hypothalamic failure) - Anatomical - Drug induced Psychogenic
What can increase your risk of erectile dysfunction?
Lack of exercise Obesity Smoking Hypercholesterolaemia Metabolic syndrome - DM CVD - MI, hypertension Liver disease and alcohol Renal failure Trauma - pelvic fracture Iatrogenic - prostatectomy
What is the pathology of erectile dysfunction?
Arterial supply - internal iliac - dorsal penile artery, cavernosal artery/deep penile arteries, bulbar artery
Venous drainage - sinusoids (subtunical plexus), corpora cavernosa (cavernous sinus)
Parasympathetic erectile S2-4
Sympathetic T11-L2
Cavernous nerve - carries both fibres, passes posterolateral to prostate - risk of damage in prostatectomy
Vascular event - balance between inflow and outflow of blood
Flaccid state - sympathetic tone, arterioles constrict
Erect state - PNS, arteriolar dilatation, trabecular smooth muscle relaxation
Flaccid state - SNS, arterioles contricted
Higher control - hypothalamus, oxytocin pro-erectile pathways
Spinal reflex
Testosterone required for normal erectile function - acquired low testosterone - primary (pituitary, hypothalamus), secondary (testes), congenital syndromes (Kleinfelters, Noonans)
Peripheral control (smooth muscle mediated - arteriolar dilatation, trabecular relaxation, no release important (Ach effect on endothelium, PNS nerve ending, intracellular cuclic GMP rise)
How is erectile dysfunction diagnosed?
Psychological cause indicators
- Sudden onset, good nocturnal and early morning erections, situational, younger patient
Sexual history
- erectile dysfunction, orgasmic function, sexual desire, ejaculation, intercourse, overall satisfaction
Examination
- BP, HR, hepatosplenomegaly, genitalia, prostatic enlargement or cancer, hypogonadism (small testes, secondary sexual characteristics)
Tests
- Falling glucose, lipid profile, morning testosterone - if low, prolactin, FSH, LH
How is erectile dysfunction treated?
Treat underlying condition
If hormonal cause - testosterone replacement (contraindicated if prostate cancer Hx), monitor for hepatic or prostate disease
Psychosexual couselling
Most treated successfully but not cures
Treat reversible causes
Lifestyle and risk factor modification
Patient and partner involvement in education and counselling
First line - phosphodiesterase inhibitors (viagra) - increase arterial blood flow, vasodilatation and erection, action on NO
Second line - apomorphine SL, intracavernous injection, intraurethral alprostadil, vacuum devices
Third line - penile prosthesis implantation
What is glomerulonephritis?
Broad term referring to a group of parenchymal kidney diseases that all result in inflammation of glomeruli and nephrons
Common cause of ESRF
How common in glomerulonephritis?
Causes 25% ESRF
Can present in a number of ways
- Acute nephritis syndrome (acute glomerulonephritis)
- Nephrotic syndrome
- Asymptomatic urinary abnormalities - haematuria, proteinuria or both
- CKD
What are the possible complications of glomerulonephritis?
Damage to filtration mechanism resulting in haematuria and proteinuria
Damage to glomerulus restricts blood flow, leading to compensatory hypertension
Loss of usual filtration capacity leads to AKI
What can cause LUTS?
BPE - benign prostate enlargement (clinical diagnosis)
BPH - histological diagnosis
BOO - bladder outflow obstruction (urodynamic diagnosis)
Hydronephrosis - dilation of renal pelvis or kidney leading to damage
Obstructive uropathy - functional or anatomical obstruction of urine flow at any level of urinary tract
Supravesical obstruction - above level of bladder
Infravesical obstruction - below level of bladder
What are the storage symptoms?
Urgency
Nocturia
Frequency
Overflow incontinence
What are the voiding symptoms?
Poor intermittent stream Hesitancy Incomplete emptying Post micturition dribbling Straining Haematuria Dysuria (painful urination)
How common is renal cystic disease?
Solitary or multiple renal cysts common, especially with advancing age - 50% of those over 50 have one or more
Often asymptomatic and found incidentally on ultrasound examination
Occasionally may cause pain and/or haemturia if large, or bleeding may occur into the cyst
What are the different types of renal cystic disease?
Simple cysts - most common, benign
Polycystic when lots can be bad
Hydronephrosis - when ureter blocked and kidney dilatates and gets bigger
Dysplasia - when not formed properly
Medullary sponge - dilation of collecting ducts
Acquired cystic disease - medullary uraemic, dialysis cystic
What are congenital renal cysts?
Present at birth
Uni/bilateral
Isolated/multisystem disorder
Inherited - caused by mutation - ADPKD, PRPKD
Development - genetic mutation leads to predisposition for cyst formation, increased abnormal cell hyperproliferation -> loss of planar polarity -> cyst initiation -> fluid secretion by epithelial cells -> cysts
What are acquired renal cysts?
Develop over time No genetic mutation Uni/bilateral Isolated to kidneys Normal/small kidney size Associated with CKD Route of development not clear
What can cause simple cysts?
Develop over time
What can cause acquired cysts?
CKD
What can cause drug related cysts?
Lithium
What can cause syndromic renal disease?
Tuberous sclerosis
How common are chlamydia and gonorrhoea?
Chlamydia is most common STI
Chlamydia is more common in women and 15-25 year olds
Gonorrhoea is more common in men and less common than chlamydia
Asymptomatic carriage much more common that gonorrhoea
What causes chlamydia?
Chlamydia trachomatis
Gram negative bacterium
What causes gonorrhoea?
Neisseria gonorrhoea
Gram negative diplococcus bacterium
Where do STIs occur in adults?
Urethra Endocervical canal Rectum Pharynx Conjuntiva
Where do STIs occur in neonates?
Conjunctive
Atypical pneumonia
How do STIs present in men?
Primary site of infection urethra Dysuria and urethral discharge Incubation - CT 7-21 days - GC 2-5 days Asymptomatic - CT at least 50% more likely to be asymptomatic thus more likely to get complications since undetected and thus untreated for longer - GC 10-90% men have symptoms Transmission male to female - CT 70% - GC 60-80% Complications mainly with CT - epididymo-orchitis and reactive arthritis
How do STIs present in women?
Primary site of infection is cervix Non-specific symptoms of dysuria, menstrual irregularity and discharge Asymptomatic - CT over 70% - GC 50% Incubation - CT ill-defined - GC 50-90%
What are the possible complications of STIs in women?
Pelvic inflammatory disease
- Infection spreads up to fallopian tube leading to inflammation and scarring
- Tubular factor infertility
- Ectopic pregnancy
- Chronic pelvic pain
Neonatal transmission
- Opthalmia neonatorum - neonatal conjuntivitis
- Atypical pneumonia with CT
Fitz Hugh Curtis syndrome - peri-hepatits but no decline in liver function
How is chlamydia diagnosed?
Often diagnosed in established relationships as long asymptomatic carriage
Nucleic acid amplification tests - high specificity and sensitivity but negative test does not mean infected
Women
- Self collected vaginal swab - better since more material collected
- Endocervical swab
- First void urine - lower sensitivity
Men - first void urine
How in gonorrhoea diagnosed?
Associated with recent partner change Near patient test - Microscopy of gram-stained smears of genital secretions - looking for gram-negative diplococci - Male - sample from urethra - Female - sample from endocervix Culture on selective medium to confirm Antibiotic sensitivity testing NAAT
How is chlamydia treated?
Partner management
Test for other STIs
Oral azithromycin STAT or oral doxycycline for 7 days
Pregnant - erythromycin for 14 days or azithromycin stat
How is gonorrhoea treated?
Partner notification Test for other STIs Continuous surveillance of antibiotic sensitivity Single dose treatment preferred IM ceftriaxone with azithromycin stat
In whom is incontinence more common?
In females
What are the different types of incontinence?
Stress (sphincter weakness) incontinence Urge incontinence Nephropathic bladder problems - Spastic spinal cord injury - Flaccid spinal cord injury
What can cause stress incontinence?
Women - secondary to birth trauma
Men - post-prostatectomy
Neurogenic or congenital
What can cause urge incontinence?
Detrusor overactivity - rise in detrusor pressure on filling associated with urgency (most often in women)
Less commonly bladder hypersensitivity from local pathology eg UTI, bladder stones, tumour
What is the pathology of stress incontinence?
Caused by sphincter weakness
Small leak of urine when intra-abdominal pressure rises eg when coughing, laughing and standing up
What is urge incontinence?
Strong desire to void and unable to hold urine
What is the pathology of spastic spinal cord injury?
Reflexes work but not controlled by brain
Supra-conal (higher in spinal cord) lesion
Loss of co-ordination and completion of voiding
Features
- Reflex bladder contractions - involuntary urination
- Detrusor sphincter dysyndergia - loss of completion of voiding
- Poorly sustained bladder contraction
- Potentially unsafe - puts kidneys at risk
- Reflex bowel - involuntary defecation
What is the pathology of a flaccid spinal cord injury?
Conus lesions (lower spinal cord injury) decentralised bladder - conus destroyed or non-functional
Lost
- Reflex bladder contraction
- Guarding reflex
- Receptive relaxation
Features
- Areflexic bladder - fills until it overflows
- Stress incontinence
- Risk of poor compliance
- Potentially unsafe - puts kidneys at risk
How is stress incontinence treated?
Females - Pelvic floor exercises - Duloxetine - Surgery - sling, artificial sphincter Males - Artificial sphincter or male sling
How is urge incontinence treated?
Bladder exercises - gradually increasing the interval between voids
Behavioural therapy - controlling caffeine, alcohol and frequency volume charts
Drugs
- Anticholingeric agents - act against the cholinergic system eg oxybutynin decreases detrusor excitability
- Beta-3 agonist eg mirabegron
- Botox of bladder - stop release of Ach from the pre-synaptic terminal and thus effectively paralyses the bladder, huge side effect isurinary retention
Bladder augmentation - detrusor myectomy, cystoplasty (adding some bowel to bladder to increase SA, give increase bladder capacity and reduced detruosor overactivity, may have to self-catheterise due to muscle loss
How are nephropathic bladder problems treated?
Preventing autonomic dysreflexia
- Commonly causes over-distension of bladder
- Occurs in lesions above T6
- Overstimulation of sympathetic nervous system below levels of lesion in response to noxious stimulus
- Headache, severe hypertension, flushing
Maintain bladder safety
- Unsafe bladder is one that puts kidneys at risk
- Risk factors - raised bladder pressure, vesico-ureteric reflus, chronic infection eg residual urine/stones
Symptom control
- Harness reflexes to empty bladder into incontinence device - but may not keep bladder safe
- Suppress reflexes converting bladder to flaccid type and then empty regularly
Alpha adrenergic blockers eg oral tamsulosin or sphincterotomy
Cystoplasty
Permanent catheterisation
What is a UTI?
Inflammatory response of urothelium to bacterial invasion, usually associated with bacteriuria and pyuria
Defined as > 10^5 organsims/ml in fresh mid-stream urine
How common are UTIs?
Uropathogenic strains of E coli causes around 80% of uncomplicated UTIs
More common in women - affects 1/3 in lifetime
How are UTIs classified?
Location
- Lower vs upper tract
- Upper tract - pyelonephritis
- Lower tract - cystitis (bladder), prostatitis, epididymo-orchitis, urethritis
Clinical risk
- Uncomplicated vs complicated
- Uncomplicated - UTI in healthy non-pregnant women with normally functioning urinary tract
- Complicated - infection in patients with abnormal urinary tract eg stones, obstruction or systemic disease involving kidney (DM, sickle cell or virulent organism) - treatment failure, complications more likely eg renal papillary necrosis and renal abscess, majority of UTIs in men complicated - associated with urological abnormalities such as bladder outlet obstruction
Timing
- Single/isolated vs unresolved (persistent infection or re-infection)
- Acute vs chronic
What can increase your risk of UTIs?
Female Sex Pregnancy Menopause Decrease in host defence Urinary tract obstruction resulting in urine stasis Catheter
What are the pathogens that can cause UTIs?
KEEPS
K - klebsiella spp
E - E coli
E - enterococci
P - proteus spp
S - staphylococcus spp (coagulase negative)
Much broader range from hospitalised or catheterised patients
How do E coli cause UTIs?
Majority of UPEC have surface attachment molecules
- Fimbrae/pilli
- Afimbral attachments eg glycocalyx
- Acid polysaccharide coat that resists phagocytosis
Bacteria adhere to
- Urothelium, vaginal epithelium, vaginal mucus
Higher rates of adhesion in
- Oestrogen depletion due to loss of lactobacilli and pH change
- Seen in post-menopausal where pH rises and thus there is increased colonisation by colonic flora and a reduction in vaginal mucus secretion
- Results in increased susceptibility to UTI
Those with HLA-A3 blood group antigens tend to have recurrent UTI
How do UPEC avoid host defences?
Capsule to resist phagocytosis
Toxins - E coli release cytokines that are directly toxic
Enzyme production
- Proteus spp secrete urease
- Increases risk of stone formation
- Bacteria that secrete urease - gram negative (proteus, klebsiella, pseudomonas), gram positive (staphylococci, mycoplasma)
What are host defences against UTIs?
Antegrade flushing of urine - forward flow of urine
Tamm-Horsfall protein - has antimicrobial properties
Low urine pH and high osmolarity
Urine IgA
How do pathogens cause UTIs?
Infection of urinary tract via the ascending transurethral route - sex and urethral catheter contribute
Women most susceptible due to shorter urethra and proximity to anus and facilitates transfer of bowel organisms to bladder
E coli most common cause - arise from patients own flora
What is epididymo-orchitis?
Acute epididymo-orhcitis clinical syndrome of pain, swelling and inflammation of epididymis that can extent into the testis
Causes by extension of infection from the urethra to bladder
In whom is epididymo-orchitis most common?
Most common in males 15-30 and those over 60
What can cause epididymo-orchitis?
Under 35 - chlamydia trachomatis/neisseria gonorrhoea
Over 35s - UTI KEEPS
Mumps (viral)
Trauma
In elderly - predominantly catheter related
What can increase your risk of epididymo-orchitis?
Previous infection
Indwelling catheter
Structure/functional abnormality of urinary tract
Anal intercourse
How does epididymo-orchitis present?
Subacute onset of unilateral scrotal pain and swelling
In STD epididymo-orchitis there may be urethritis or urethral discharge
Mumps usually presents with headache, fever and uni/bilateral parotid swelling
Sweats/fever
On examination there is tenderness and palpable swelling of epididymtitis and also testicles
What could be a differential diagnosis of epididymo-orchitis?
Testicular torsion - urological emergency must be ruled out
Hydrocele
Trauma
Abscess formation
How is epididymo-orchitis diagnosed?
Nucleic acid amplification test
- Female self collected vaginal swab, endocervial swab, first void urine
- Male first void urine
- High sensitivity and specificity
- If intracellular gram-negative diplococci are present - suggestive of gonorrhoea
Mid-stream urine dipstick for UTI symptoms
US to rule out abscess
STD screening
Urethral smear and swab
How is epididymo-orchitis treated?
Chlamydia - oral doxycycline 7 days or stat azithromycin
Gonorrhoea - IM ceftriaxone and stat oral azithromycin
UTI - oral ciprofloxacin or oral ofloxacin
Antibiotics for 2-4 wks
Analgesia - NSAIDs
Scrotal support - supportive underwear
Abstain from sexual intercourse
Partner notification and testing
What is saline used for?
Used to replace fluids and try to increase blood pressure
Normal saline - physiologically similar to normal composition of ECF
Each litre of saline contains
- 150mmol Na+
- 150mmol Cl-
- 300mmol osmotically active ions
NO K+
Give an example of an alpha blocker?
Tamsulosin
Alfuzosin
Doxazocin
What are alpha blockers used for?
First line treatment for BPH where lifestyle changes insufficient
Can be used alongside 5-alpha reductase inhibitors eg finasteride or surgery
Can be used to aid passage of kidney stones
How do alpha blockers work?
Highly selective for alpha-1 adrenoceptor found mainly in smooth muscle including blood vessels and the urinary tract (bladder neck and prostate)
Stimulation induces contraction, blockade indices relaxation so thus causes vasodilatation and a fall in BP and reduced resistance to bladder outflow
What are the main adverse effects of alpha blockers?
Can cause postural hypertension, dizziness and syncope
Should not be used in existing hypotension
Combining antihypertensives can provide profound effect so omitting doses of other medications when starting can help avoid first dose hypertension
Name a 5-alpha reductase inhibitor?
Finasteride
What are 5-alpha reductase inhibitors used for?
Used for treatment of benign prostatic hyperplasia as an add on to alpha blockers
Provides less relief and takes longer for effect
How do 5-alpha reductase inhibitors work?
5-alpha reductase is an enzyme that converts testosterone to dihydrotestosterone (active form of testosterone), so blocking this conversion results in a dramatic decrease in serum dihydrotestosterone levels
Reduces prostate volume and improves symptoms of enlarged prostate and reduces the risk of cancer
What are the main adverse effects of 5-alpha reductase inhibitors?
Since treatment lowers PSA it may hide prostate cancer, there is a possible risk of sexual dysfunction
Contraindicated in women
Name a phosphodiesterase type 5 inhibitor
Sildenafil
What are phosphodiestase type 5 inhibitors used for?
Erectile dysfunction
Primary pulmonary hypertension
How do phosphodiesterase type 5 inhibitors work?
Sildenafil is selective for phosphodiesterase type 5 which is predominantly found in the smooth muscle of the corpus cavernosous of the penis and arteries of lung
Causes vasodilatation by inhibiting PDE5 which is responsible for the breakdown of cyclic GMP, thus increasing cyclic GMP concentrations which then causes arteria; smooth muscle relaxation and vasodilation and penile engorgement
What are the main adverse effects of phosphodiesterase type 5 inhibitors?
Flushing, headache, dizziness, nasal congestion and more seriously - hypotension, tachycardia and palpitations
Increased risk of MI and stroke
Avoided where vasodilatation is dangerous eg recent stroke, ACS, or other CVD and should be used with caution in hepatic and renal failure
Contraindicated with other drugs that increase NO ie nitrates since combined effect on cyclic GMP can cause severe vasodilatation and CVS collapse
Name an example of an anti-muscarinic
Oxybutynin
Tolterodine
What are anti-muscarinics used for?
To reduce urinary frequency, urgency and urge incontinence in overactive bladder
How do anti-muscarinics work?
Competitively inhibits acetylcholine, blocking the muscarinic receptors and promoting bladder relaxation to increase capacity
Reduces urgency and frequency or urination
Selective for M3 receptor which is main receptor in bladder
What are the main adverse effects of anti-muscarinics?
Dry mouth, tachycardia, constipation, blurred vision
Contraindicated in UTI, use with care in elderly as can cause drowsiness
Use with care in angle closure glaucoma as can cause rise in intraocular pressure and in patients with arrhythmias and those at risk of urinary retention
Name an example of an androgen receptor blocker
Flutamide
Bicalutamide
Cyproterone acetate
What are androgen receptor blockers used for?
Used to treat prostate cancer
How do androgen receptor blockers work?
Anti-androgens decrease the body’s response to androgens and so are beneficial in prostate cancer as cells require androgens for growth
Drug competes with circulating androgens for receptors on prostate cells and promote apoptosis and inhibit growth
Can be used as monotherapy or with surgery or chemotherapy
What are the main adverse effects of androgen receptor blockers?
Bicalutamide better tolerated
GI disturbance and possible liver injury
