Urinary diseases Flashcards
How does a UTI present?
Dysuria (pain on micturition), frequency and smelly urine.
- If very young = unwell, failure to thrive
- Very old = incontinence, off their feet
What is a UTI?
Urinary tract infection
What are the bacteriostatic properties of a normal urinary tract?
- Free flow of urine through normal anatomy - assume drinking enough fluids.
- Low pH, high osmolarity, and high ammonia content of normal urine
- Prostatic secretions are bacteriostatic
- anti-bacterial antibodies
Is a normal renal tract sterile?
Urinary tract sterile except for terminal urethra which contains perineal and gut flora.
Why do we want a Mid Stream Specimen of urine?
Urethra flora diminished but always present.
Patients void and stop mid stream, discarding urine then collects next volume.
How can we tell contamination is from real infection?
MSSU - microbiology for culture under set conditions.
Can count the number of bacteria - 10 to power 5 = usually infection. (99% accuracy)
10 to power 3-4 = infections sometimes ( if symptoms) more likely.
Less than 10 to 3 = usually no infection.
What are the main micro-organisms that cause UTI?
Gut flora - especially E.coli
Viral infection rare.
What is the route of infection?
Almost always ascending: Infection in kidneys usually infection has spread up from bladder. Upper UTI = more serious.
What is:
- Urethritis
- Cystitis
- Ureteritis
- Acute/chronic pyelonephritis?
- Inflammation of urethra
- Inflammation of bladder
- Inflammation of ureter
- Inflammation of kidney / If recurrent to prolonged chronic inflammation.
What are the predisposing factors to UTI?
- Stasis of urine
- Pushing bacteria up urethra from below
- Generalised predisposition to infection
What can cause stasis of urine?
- Obstruction, congenital or acquired
2. Loss of feeling of full bladder - spinal cord/brain injury
What can cause pushing bacteria up urethra from below?
- sexual activity in females
2. Catheterisation (other urological procedures)
What are the consequences of obstruction?
- Proximal dilatation
- slowed urine flow - cannot flush out bacteria - infection
- Slowed urine flow - sediments form calculous (stone) formation - obstruction
- Triad - infection - calculi - obstruction.
What are the common causes of obstruction in adults?
Men - benign prostatic hyperplasia of prostate - functional and anatomical obstruction.
Women - uterine prolapse
Both sexes - tumours and calculi.
What can causes obstruction in children?
Numerous renal tract abnormalities
Most important example = vesicoureteric reflux.
What is vesicoureteric reflux?
Decreased angulation - bladder - ureter reflux.
How does sexual activity in females cause UTI?
Tends to move lower urethral flora up the tract (back wall of urethra is just in front of vagina)
- Short urethra
- Lack of prostatic bacteriostatic secretion
- Closeness of urethral orifice to rectum
- pregnancy - pressure on ureters and bladder.
What are some of the generalised predisposition to infection that cause UTI’s?
Glucose in urine - diabetes
Poor function of WBC
What are the complications of UTI?
- Acute
- Chronic
- Severe sepsis and septic shock (bacteria get into blood)
- Chronic damage to kidneys if repeated infections - lead to hypertension, chronic renal failure
- Calculi - obstruction - hydroneophrosis.
What is contained in the filter barrier of the glomerulus?
Membrane:
Endothelial cell cytoplasm, basal lamina (connective tissue) and podocyte.
What are mesangial cells>
“tree like” group of cells which support capillaries
What is Glomerulonephritis?
Disease of glomerulus
Inflammatory or non-inflammatory
Primary or secondary.
Causes of Glomerulonephritis
Immunoglobulin depostition
Some are diseases with no immunoglobulin deposition e.g. diabetic glomerular disease.
What are the 4 common presentations of Glomerulonephritis?
- Haematuria (blood in urine)
- Heavy proteinuria (nephrotic syndrome)
- Slowly increasing proteinuria
- Acute renal failure
What are the main causes of Haematuria?
UTI
UT stone
UT tumour
Glomerulonephritis
Causes of IgA glomerulonephritis? (GN)
Unknown - could be excess antibody produced?
What happens in IgA GN?
Mesangium becomes clogged with antibody. Red blood cells then escape into urine. Causes proliferation and production of more matrix.
What is prognosis of IgA nephropathy?
Usually self-limiting, i.e. return to normal
Small percent go onto chronic renal failure.
What happens in Membranous glomerulonephritis?
Thickened glomerular basement membrane
IgG stuck in membrane - between basal lamina dn podocyte.
IgG too big to be filtered into urine. But activates complement which punches holes in filter.
What does the leaky filter cause?
Albumin to be filtered into urine - nephrotic syndrome
Prognosis of Membranous GN?
1/4 chronic renal failure within 10 years.
Diabetic nephropathy prognosis
Inevitable decline if established or continued poor diabetic control.
What is Crescentic GN?
Granulomatosis with polyangiitis - form of vasculitis (inflammation in vessels)
Antiglomerular basement membrane disease.
Wegener’s prognosis
Fatal if left untreated.
When thinking of what could be the cause of symptoms and presentation what should we think about?
Surgical sieve
Infection Inflammation Iatrogenic Neoplasia Trauma Degenerative Congenital Genetic/Hereditary Vascular Endocrine Failure Idiopathic
Nature of renal diseases what are we looking for?
Infection - pyelonephritis
Inflammation - glomerulonephritis
Iatrogenic - nephrotoxicity, PCNL
Neoplasia - renal tumours, collecting system tumours
Trauma - blunt
Vascular - atherosclerosis, hypertension, diabetes
Hereditary - polycystic kidney disease, nephrotic syndrome
Presentation of renal diseases
Pain Pyrexia Haematuria Proteinuria Pyuria (leukocytes) Mass on palpation Renal failure
Define proteinuria
Urinary protein excretion > 150mg/day
How many types of haematuria are there?
3 - microscopic, macroscopic and dip stick
What is the definition of microscopic haematuria?
> 3 or equal to 3 red blood cells per high power field.
Define the following:
- Oliguria
- Anuria
- Polyuria
- Nocturia
- Nocturnal polyuria
- Urine output < 0.5 ml/kg/hour
- Absolute anuria = no urine output; relative = <100ml/24hr
- Urine output > 3l/24hr
- Waking up at night are than 1 occasion to pee
- Nocturnal urine output > 1/3 of total urine output in 24 hr (frequency volume chart)
Acute kidney injury:
What is the RIFLE staging criteria?
- Risk - increase in serum creatinine level (1.5x) or decrease in GFR by 25%. UO <0.5ml for 6 hr
- Injury - increase in serum creatinine level (2x) or decrease in GFR by 50%. UO<0.5ml for 12 hr
- Failure - Increase serum creatinine level (3x), decrease in GFR by 75% or UO < 0.3 for 24hr or Anuria for 12 hr
- Loss - persistent ARF or complete loss of kidney function > 4 weeks
- End stage kidney disease - completely loss of kidney function > 3 months
Chronic renal failure:
Presentation
Asymptomatic (found on blood and urine testing) Tiredness Anemia Oedema High Blood pressure Bone pain due to renal bone disease Pruritus (in advanced and all below) Nausea/vomiting Dyspnoea Pericarditis Neuropathy Coma
Presentation of ureteric diseases
Pain (renal colic 10/10) Pyrexia Haematuria Palpable mass Renal failure (only if bilateral obstruction or single functioning kidney)
What are the different natures of ureteric disease?
- Infection - ureterirtis
- Trauma/Iatrogenic - hysterectomy or inadvertently cut.
- Neoplasia - TCC of ureter or bladder obstructing VUJ, prostate cancer. (transitional cell carcinoma)
- Hereditary - PUJ obstruction, VUJ reflux
- Obstruction
- intra-luminal (stone, blood clot)
- intra-mural (scar tissue, TCC)
- Extra-luminal (pelvic mass, lymph nodes)
Natures of bladder disease
- Infection - cystitis
- Inflammation - interstitial cystitis, colonic diverticulitis
- Iatrogenic/trauma - Bladder rupture, bladder injury from hysterectomy
- Neoplasia - TCC of bladder, SCC of bladder
- Idiopathic - overactive bladder syndrome
- Degenerative - Chronic urinary retention
- Neurological - neurogenic bladder dysfunction
Presentation of bladder disease
Pain (suprapubic)
Pyrexia
Haematuria
LUTS:
- storage - frequency, nocturne, urgency, urge
- Voiding - poor flow, intermittency, terminal dribbling - underachieve bladder
- Incontinence - stress, urge, mixed,overflow
Nature of bladder outflow tract diseases
Infection/inflammation - prostates, balanitis
Iatrogenic/trauma - pelvic floor damage, urethral injury
Neoplasia - prostate cancer, penile cancer
Idiopathic - chronic pelvic pain syndrome
OBSTRUCTION - primary bladder neck obstruction, benign prostatic enlargement, urethral stricture, metal stenosis.
Presentation of bladder outflow tract diseases
Pain Pyrexia Haematuria Lower urinary tract symptoms Recurrent UTIs Acute urinary retention Chronic urinary retention
Define acute urinary retention
Painful inability to void with a palpable and percusible bladder.
- BPO
Define Chronic urinary retention
Painless, palpable and permissible bladder after voiding.
- detrusor under activity
What types of organisms can be seen in a UTI?
E.coli Staph saprophyticus Klebsiella proteus Pseudomonas Staph aureus
Complications of UTI
Infective sepsis Renal failure Bladder malignancy Acute urinary retention Bladder/renal stones frank haematuria
Treatment for UTI
Appropriate oral antibiotic therapy
Treat complications and cause.
Investigations for UTI
Urine dipstick
Urine microscopy
Culture and sensitivity
How do we assess for kidney disease?
Filtration (excretory) function - remove
Filtration (barrier) function - retain
Anatomy - structural abnormality
How do we measure excretory Renal function?
Isotope GFR used if someone is donating a kidney.
Used all the time is serum creatinine to measure eGFR.
What is the problem with using creatinine?
generated from breakdown of muscle and not everyone has same muscle mass - depends on age, ethnicity, gender, weight.
Also It will not be raised above normal range until 60% of total kidney function is lost.
How do we assess kidney filtering function?
Urinalysis - dipstick for blood and protein.
PCR - protein creatinine ratio
Definition of CDK
Chronic kidney disease - presence of kidney damage (abnormal blood, urine, or x-ray) or GFR<60 this is present for > 3 months.
Causes of CDK
Diabetes Genetic disorders - Polycystic kidney disease Glomerulonephritis Systemic disease - high BP Reno vascular disease
Symptoms of CKD
Risk factors present Fatigue Peripheral oedema Nausea and vomiting Anorexia Pruritis (itch and cramps)
What to look for in 1. History and 2. Examination
- Previous renal disease, sam history, systemic diseases, drug exposure, pre/post renal factors, uraemia symptoms
- Vital signs, VOLUME STATUS, obstruction
What tests should be carried out for CKD?
Blood tests - FBC, U&Es
Urine tests - dip, PCR and ACR (24hr collection)
Histology - Renal biopsy (specifically in glomerulus)
Radiology - US, CT
How can you slow rate of renal decline?
BP control
Control proteinuria (particularly ACE inhibitors)
Treat underlying cause
Complications of CDK
Acidosis - bicarb Anaemia - EPO and iron Bone disease - diet and phosphate binders CV risk - BP - aspirin, exercise Electrolytes - diet and consider drug Fluid overload - salt and fluid restriction Gout - optimise plus/minus meds. Hypertension - weight, diet, drugs
Glomerulonephritis features
Haematuria - cola coloured, nephritic > nephrotic, dysmorphic RBC.
Proteinuria - Persistent, proteinuria of more than 1 gram.
Hypertension
Renal insufficiency
What is a nephritic state?
Active urine sediment: haematuria, dysmorphic RBCs, cellular casts
hypertension
renal impairment
What presentation occurs with nephrotic syndrome?
Oedema Proteinuria > 3.5 g/day Hypoalbuminemia Hyperlipidemia Can be caused by primary or secondary glomerular diseases.
Causes of glomerulonephritis
Autoimmune, infection, malignancy, drugs
Treatment for post-infective glomerulonephritis
Antibiotics for infection
Loop diuretics such as frusemide for oedema
Vasodilator drugs for hypertension (amlodipine)
IgA nephropathy (most common) presentation
Microscopic haematuria and proteinuria
Nephrotic syndrome
IgA crescentic glomerulonephritis
Treatment for crescentic GN
High dose steroids, cyclophosphamide, plasma exchange, B cell therapy.
Anti - GBM disease presentation and treatment
Nephritis + lung haemorrhage.
Treatment - aggressive immunosuppression: steroid, plasma exchange, cyclophosphamide
Proliferative GN summary
Nephritic syndrome
Blood on dipstick
Rapid decline in renal function can be seen
Early diagnosis and treatment needed.
What shows with proliferative GN?
Excessive numbers of cells in glomeruli. Infiltrating leucocytes.
What shows in Non-proliferative GN?
Glomeruli look normal and have areas of scaring. Normal number of cells.
Nephrotic syndrome-management
General measures:
treat oedema, hypertension, reduce risk of thrombosis, reduced risk of infection.
What is minimal change nephrotic syndrome?
Commonest form in children
sudden onset of oedema - days
complete loss of proteinuria with steroids
2/3 patients relapse
Treatment for minimal change disease
Prednisolone 1mg/kg for up to 16 weeks.
Many relapses treated with cyclophosphamide, cyclosporin
What is focal and segmental glomerulonephritis?
Not a single disease, rather a syndrome with multiple causes
presents with nephrotic syndrome.
Pathology reveals focal and segmental sclerosis with distinctive patterns
Treatment for focal and segmental glomerulosclerosis
General measures
Trail of steroids
Alternative - cyclosporin
Membranous nephropathy what is it?
Commonest cause in adults.
Serological markers
Summary of non-proliferative GN
Present with nephrotic syndrome.
Renal biopsy is key investigation
General measures important
Specific treatment as appropriate.
Where is a transplanted kidney placed?
Iliac fossa and anastomosed to iliac vessels.
What would be indications for native nephrectomy?
Size (polycystic kidneys) and infection (chronic pyelonephritis)
What are possible surgical complications of transplant?
Vascular complications:
Bleeding:
- usually anastomotic sites
- perirenal haematoma can be arterial or venous
Arterial thrombosis
Venous thrombosis
Lymphocele
Uteric
- Urine leak
Infections
What is the protocol for immunosiuppresions for people after surgery?
Induction - Depleting agent e.g. (Basiliximab)
Maintenance - Calcineurin inhibitors (tacrolimus) + Anti-proliefratives (mycophenolate) + corticosteroids
Steroid free is possible
Others: CNI-free using Costimulatory signal blocker (belatacept)
What are the side effects of
- Corticosteroids
- Tacrolimus
- Cyclosporin
- Belatacept
- Mycophenolate mofetil
- Hypertension, hyperglycaemia, infections, bone loss, GI bleeding.
- Hyperglycaemia, AKI, tremor
- Hirsutism (men body hair on women), Hypertension, AKI, gout
- Infections, malignancy
- Cytopenia, GI upset.
What are the types of kidney donors?
- Deceased donors
- Donation after brain death/ DBD
- Donation after cardiac death / DCD
* both standard / extended criteria - Living Donors
- Living related donor
- Living unrelated donors
Spousal, altruistic, paired/pooled
What is the standard brain death criteria?
What is the Extended criteria?
Standard:
- Coma, unresponsive to stimuli
- Apnoea off ventilator
- Absence of cephalic reflexes
- Body temp above 34
- Absence of drug intoxication
Extended:
- Donor aged over 60yr
- Donar aged 50-59 and history of hypertension, death from cerebrovascular accident or terminal creatinine of over 132.
Complications after renal transplantation
Rejection:
- cell mediated
- Humoral (Ab mediated)
Infective:
- bacterial
- fungal
- viral
Cardiovascular:
- underlying renal disease
- CRF (chronic renal failure)
- Hypertension
- Hyperlipidaemia
- PT diabetes
Malignancy:
- skin
- lymphoma
- Solid cancers
What is Cytomegalovirus?
What tissue invasive disease can come with it?
Most important transplant-related infection:
- Affects around 8% of transplant recipients, despite prophylaxis therapy.
- High mortality and morbidity if untreated
- Recipient affected via:
Transmission from donor tissue
Reactivation of latent virus
Tissue invasive disease: Pneumonitis hepatitis Retinitis Gastroenteritis Colitis Nephritis
What is acute rejection?
Hyper acute rejection - pre-existing alloreactivity to donor.
Acute rejection:
- T cell mediated (TCMR) Lymphocytic infiltrate.
- Acute antibody mediated rejection (ABMR)
Microvascular inflammation
Donor specific antibodies
Positive C4d
What is the definition of acute renal failure?
Increase in SCreatinine by > 26.5 within 48hr or more than 1.5 times baseline.
Urine volume <0.5 ml/kg/h for 6 hours
What are the different stages of acute renal failure?
AKI 1 = serum creatinine = 1.5-1.9 times baseline or more than 26.5 increase.
Urine output = <0.5 ml/kg/h for 6-12 hours.
AKI 2 = serum creatinine = 2.0-2.9 times baseline
Urine output <0.5 for > 12 hours.
AKI 3 = serum creatinine = 3 times baseline or increase to 354 and above.
Urine output < 0.3 for > 24hr or anuria for > 12 hours
Incidence of Acute renal injury
Hospital admissions = 1 in 5
ITU admissions = more than half.
What are the immediately dangerous consequences of AKI?
Dependent on cause to an extent at least in the first few hours.
Acidosis (cause cardiac arrest) Electrolyte imbalance Intoxication TOXINS (cause resp arrest) Overload (cardiac arrest) Uraemic complications
Outcomes of AKI even if “not that bad”
Short term (in hospital) - Death, dialysis, length of stay
Intermediate / Long term (post-discharge)
- Death, CKD, Dialysis, CKD released CV events.
Causes of Acute renal injury
Pre-renal
- Blood flow to kidney:
Sepsis, hypotension, hypovolaemia, haemorrhage, Cardiac failure
Renal
- Damage to renal parenchyma:
Acute tubular necrosis, glomerulonephritis, toxin-related, acute interstitial nephritis, intra renal vascular obstruction.
Post-renal
- obstruction to urine exit:
Kidney stones, tumours, Intraluminal (clot) , Intramural (malignancy), Extramural (Malignancy)
What is the most common cause of AKI?
Poor perfusion leading to established tubule damage.
What is Radiocontrats nephropathy?
AKI following administered iodine as contrast agent.
Common contributor to hospital acquired AKI.
Usually resolved after 72hr
May lead to permanent loss of function.
Risk factors for RCN
Diabetes mellitus Renovascular disease Impaired renal function Paraprotein High volume of radio contrast
What renal failure can be seen in myeloma?
Cast nephropahy "myeloma kidney" Light chain nephropathy Amyloidosis Hypercalcaemia Hyperuricaemia
Investigations for AKI
History Examination (fluid status) Drugs Insults Renal function Urine dipstick, PCR, ACR FBC, U&E, Bicarb USS Blood gas
Prevention of AKI
Avoid dehydration Avoid nephrotoxic drugs Review clinical status in those in risk and act on findings: Sepsis Toxins Optimise BP and vol status Prevent harm
Management of AKI
- Maintain fluid balance
- Optimise blood pressure - give fluid/vasopressors
- Stop nephrotoxic drugs (NSAIDS, ahminoglycosides)
How do we spot hyperkalaemia on ECG?
Peaked T waves
P wave widens and flattens
PR segment lengthens
P waves eventually disappear
How to treat hyperkalamia?
Stabilise (myocardium) - calcium glutinate Shift (K intracellularly) - salbutamol - insulin-dextrose Remove - diuresis - dialysis - anion exchange resins
What is Benign prostatic hyperplasia?
Characterised by fibromuscular and glandular hyperplasia. Predominately affects transition zone. LUTS caused by bladder outlet obstruction due to BPH.
How common is BPH?
Part of waging process in men:
50% of men at 60
90% of men at 85
Assessment of LUTS
Frequency volume charts.
Symptom scoring system: Voiding (obstruction): - Hesitancy - Poor stream - Terminal dribbling - Incomplete emptying
Storage (Irritative)
- Frequency
- Nocturia
- Urgency +/- urge incontinence
What physical examination take place for BPH?
Abdomen:
- palpable bladder?
Penis:
- External urethral metal stricture?
- Phimosis?
Digital rectal examination:
- assess prostate size
- Suspicious nodules or firmness
Urinalysis:
- Blood?
- Signs of UTI
What investigations could you do for BPH?
MSSU Flow rate study Bloods: - PSA - Urea and creatinine (if chronic retention) Ultrasound renal
Treatment for uncomplicated Benign prostatic obstruction
Watchful waiting
Medical therapy:
- alpha bockers (smooth muscle relaxation)
- 5 alpha reductase inhibitors (reduce prostate size and reduces risk of progression)
Surgical
- TURP (prostate size <100cc)
- Open retropubic or transvesical prostatectomy
Complications of Bladder outflow obstruction
Progression of LUTS Acute/chronic urinary retention Urinary incontinence UTI Bladder stone Renal failure
Treatment for complicated BOO
Medical therapy:
Surgery.
Long term urethral or suprapubic cathertirisation.
Define acute urinary retention
Painful inability to void with a palpable and perusable bladder.
- What is treatment for AUR?
2. Complications?
- Catheterisation.
2. UTI, post-decompression haematuria, pathological diuresis, renal failure.
Define chronic urinary retention
Painless, palpable and percussible bladder after voiding. Main cause is detrusor under activity.
Treatment for CUR?
Catheterisation.
Manage with IV fluids.
What are the types of Urinary tract Obstruction?
Upper tract (supra-vesical)
- PUJ
- ureter
- VUJ
Lower tract (bladder outflow obstruction)
- Bladder neck
- prostate
- urethra
- urethral meatus
- foreskin
Causes of upper tract obstruction
Pelvic-ureteric junction:
Intrinsic:
- stone, Ureteric tumour (TCC), Blood clot, fungal ball.
Extrinsic:
-Lymph nodes (tumour), Abdominal mass (tumour)
Ureter:
Intrinsic:
- Stone, Ureteric tumour, scar tissue, blood clot, fungal ball.
Extrinsic:
-Lymph nodes (tumour), Iatrogenic, abdominal/ pelvic mass (tumour)
Visio-ureteric junction (VUJ):
Intrinsic:
- Stone, bladder tumour, ureteric tumour
Extrinsic:
- cervical tumour, prostate cancer
Presentation of upper tract obstruction
Symptoms:
- pain, frank haematuria, symptoms of complications.
Signs:
- palpable mass, microscopic haematuria, signs of complications
Complications:
- infection and sepsis, renal failure
What is used for emergency treatment of obstruction?
Percutaneous nephrostomy insertion (usually under LA with US guidance) or retrograde stent insertion (silicone, polyurethane, nickel titanium)
Chronic retention:
High pressure and low pressure presentation
High pressure: Painless Incontinent Raised cr Bilateral hydro-nephrosis
Low pressure: Painless Dry Normal cr Normal kidneys
Complications of chronic retention
Decompression haematuria
Post obstructive diuresis.
Presentation of Lower tract obstruction
Acute/chronic urinary retention Recurrent UTI and sepsis Frank haematuria Bladder stones Renal failure
What is the relative incidence of stone types
Calcium oxalate - 45% Calcium oxalate and phosphate - 25% Triple phosphate (infective) - 20% Calcium phosphate - 3% Uric acid - 5% Cystine - 3%
Symptoms and signs of stones
Renal pain (fixed in loin) Ureteric colic (radiating to groin) Dysuria/haematuria/testicular or vulva pain Urinary infection Loin tenderness Pyrexia
Investigations for stones
Blood tests - FBP, U&E, Creatinine Calcium, Albumin, Urate Parathormone Urine analysis and culture 24hr urine collections KUB US IVU (IV urogram) CT KUB
What are the techniques for surgical treatment?
Open surgery
Endoscopic surgery
ESWL
- Advantages and disadvantages of open surgery
2. What are the indications for open surgery?
+ Single procedure with least recurrence rate
- Large scar, long hospital stay, general wound complications
2. Non functioning infected kidney with large stones necessitating nephrectomy. Technical reasons cannot be managed by PCNL or ESWL.
Indications for Percutaneous nephrolithotomy
Large stone burden Associated PUJ stenosis Infundibular stricture Calyceal diverticulum Morbid obesity or skeletal deformity ESWL resistant stones e.g. Cystine
Contraindications for PCNL
Uncorrected coagulopathy
Active UTI
Obesity or unusual body habits unsuitable for X-ray tables
Relative contraindications include small kidneys and sever perirenal fibrosis.
Complications of PCNL
Local complications - AV fistula
UT injury - Pelvic tera, Ureteral tear, Stricture of PUJ
What is E.S.W.L?
When is it used?
Extracorporeal Shock Wave Lithotripsy
- Shock waves crush stones and smaller pieces pass out of body in urine.
Commonly used for renal and ureteric calculi as first line treatment. Day case. Repeated as often as required.
Indications for open ureterolithotomy
Not suitable for laparoscopic approach.
Failed ESWL or ureteroscopy.
Severe obstruction, uncontrollable pain, persistant haematuria.
What are bladder stones?
Suprapubic / groin/ penile pain. Dysuria, frequency, haematuria UTI Usually secondary to outflow obstruction Most treated endoscopically
Prostate cancer: How common is it?
- Commonest cancer diagnosed in men
- 75% of new cases are aged > 65yrs
- 11,300 deaths / year
- 800 million/year
Causes and risk factors of prostate cancer
Age
Race/ethnicity
Geography
Family history - first degree relative 2x risk.
Diagnosis of prostate cancer
80% newly diagnosed prostate cancers are localised.
Mostly asymptomatic
Diagnosed through opportunistic PSA testing
Diagnostic triad of PSA, digital rectal examination and TRUS-guided prostate biopsies
Presenting symptoms of localised prostate cancer
Locally invasive disease: Haeamaturia Perineal and suprapubic pain Impotence Incontinence Loin pain or anuria resulting from obstruction of the ureters Symptoms of renal failure Haemospermia Rectal symptoms including tenesmus
Metastatic prostate cancer presenting symptoms
Distant:
Bone pain, paraplegia secondary to spinal cord compression, lymph node enlargement, lymphedema, loin pain.
Widespread:
Lethargy
Weight loss and cachexia
Why do we not screen for prostate cancer?
Leads to over-diagnosis and over treatment of harmless cancers.
