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
