Urology Flashcards
At what spinal level are the kidneys?
Usually T12 - L3
right kidney is generally lower than the left due to the liver
What are the two main regions of kidney parenchyma ?
- inner medulla
2. outer cortex
Role of the renal corpuscle
= site of initial filtration
Consists of Bowman’s Capsule and Glomerulus
Role of proximal convoluted tubule
Brush border to increase luminal surface area for reabsorption of ions and solutes.
Also important for regulating pH by secreting bicarbonate
Loop of Henle - permeability of descending thin limb
impermeable to ions, but high permeability to water
Loop of Henle - permeability of ascending thin and thick limb
mostly impermeable to water, permeable to ions (passive diffusion in thin part and active transport in thick part).
What is the aim of the loop of henle
Aims to create a strong osmotic gradient for absorption of large amounts of water from the descending limb
Role of distal convoluted tubule
Regulation of potassium, sodium, calcium and pH.
Macula Densa cells involved in paracrine function (detect Na+ levels and initiate RAAS).
Role of collecting duct
Filtrate is concentrated to form urine, which feeds into the renal pelvis and then the ureters.
Electrolyte and fluid balance, regulated by aldosterone and ADH
What is the role of the kidney?
Regulating volume and composition of bodily fluids.
Regulating acid-base balance.
Excretion of metabolic breakdown products
=> Ammonia, urea, uric acid, creatinine, drugs, toxins.
Hormonal functions
=> Produces EPO
=> Vitamin D metabolism (converts to active form)
=> Secretes renin in response to reduced afferent pressure.
Renin-Angiotensin-Aldosterone System
The juxtaglomerular cells of the kidneys are stretch-receptors
Reduced stretch from a decrease in blood volume will lead to the release of renin.
Renin is involved in the cleavage of angiotensinogen to AI. AI is cleaved to AII by ACE.
What is the role of angiotensin II?
- Vasoconstriction (of afferent arteriole)
- Increase release of aldosterone
=> Enhances reabsorption of sodium and water
What is AKI?
= a rapid decline in kidney function occurring over hours or days, as measured by serum urea and creatinine.
This results in a failure to maintain fluid, electrolyte and acid-base homeostasis
Causes can be pre-renal, intrinsic or post-renal
When is AKI common?
very common in acute illness
(>15% of emergency admissions and 25% of septic patients).
Risk factors for AKI
- Age >65 years.
- Pre-existing CKD
- Male
- Cardiac failure
- Chronic liver disease
- Diabetes
- Sepsis
- Hypovolaemia
Pre-renal AKI
Reduced renal perfusion leads to a reduction in GFR
Main causes:
- Shock – hypovolaemic, cardiogenic, distributive.
- Renovascular obstruction – AAA, renal artery stenosis (and ACEis given in bilateral renal artery stenosis), renal vein thrombosis.
- Fluid overload – cardiac failure, cirrhosis, nephrotic syndrome.
If interruption in the blood supply is prolonged, there will be acute tubular necrosis (ATN).
Acute tubular necrosis in pre-renal AKI
Ischaemia leads to necrosis of the cells lining the renal tubules.
Leads to porous tubular membranes (leading to loss of concentrating power) and also blockage of the tubules by necrosed cells
Causes of hypovolaemia
Hypovolaemia can be caused by:
- haemorrhage,
- dehydration,
- third space losses (e.g. due to bowel obstruction/pancreatitis),
- burns and GI losses (vomiting and diarrhoea).
Post-renal AKI
Occurs when there is obstruction of the urinary tract
=> Leads to a backflow of urine, damage to the kidney architecture and resultant organ failure
e.g. blockage of ureter (stones, strictures, clots, malignancy) or bladder outlet obstruction
Intrinsic AKI
= Injury or damage to the renal parenchyma, by 3 potential mechanisms
- Acute tubular necrosis
- Interstitial nephritis
- Glomerular disease
Renal causes of Acute tubular necrosis
due to drugs/toxins damaging the tubular cells (rather than ischaemia, which is pre-renal).
- Drugs – aminoglycosides, cephalosporins, radiological contrast mediums, NSAIDs.
- Toxins – heavy metal poisoning, myoglobinuria, haemolytic uraemic syndrome (HUS).
Interstitial nephritis
Damage is not limited to tubular cells (as in ATN) and bypasses the basement membrane to cause damage to the interstitium
Most commonly caused by drugs (especially antibiotics, but also diuretics, NSAIDs allopurinol and PPIs).
Can be caused by infection, auto-immune mechanism or lymphoma.
Normally responds to withdrawal of the drugs and a short course of oral steroids
Myoglobinuria
Follows an episode of rhabdomyolysis (muscle breakdown from trauma, strenuous exercise or medications), releasing myoglobin which is readily filtered by the glomerulus.
Gives the classical dark urine, but in high quantities will precipitate out within the tubules to cause damage
haemolytic uraemic syndrome (HUS)
Occurs in children following diarrhoeal illness caused by verotoxin-producing E. coli O157, or following a URTI in adults.
Thrombocytopaenia, haemolysis and ATN.
Children recover within a few weeks, prognosis for adults is poor.
Treatment is supportive, including dialysis
Signs and Symptoms of AKI
Reduced urine output Nausea and vomiting Dehydration Confusion Fatigue
Signs depend on cause - look for:
- Fluid overload
- Hypotension
- Palpable abdominal mass
- Associated features of vasculitis – petechiae, skin changes, bruising, etc.
NICE criteria for diagnosis of AKI
- A rise of serum creatinine >26 micromol/L in 48 hours
- A 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days
- A fall in urine output <0.5mL/kg/hour for more than 6 consecutive hours
AKI Stage 1
Serum Creatinine
150-200% increase OR
>25 micromol/L increase in 48h
Urine Output
<0.5 mL/kg/hour for 6h
AKI Stage 2
Serum Creatinine
200-300% increase
Urine Output
<0.5 mL/kg/hour for 12h
AKI Stage 3
Serum creatinine
>300% increase OR
>350 micromol/L increase in 48h
Urine output
<0.3 mL/kg/h for 24h OR
Anuria for 12h
AKI - Bedside tests
Urine dip Urine cultures Observations – BP, RR, HR Glucose ECG
AKI - Bloods
FBC U&E LFTs Coag CRP
ABG – ?acid-base imbalance
Creatine Kinase if indicated
Immunology if indicated
AKI - imaging
USS KUB
CXR if pulmonary oedema
CT KUB if obstruction
When would test for creatinine kinase be indicated in AKI?
Creatine kinase can show rhabdomyolysis, but this would only be done if indicated in the history and symptoms/signs
Management of AKI
Treat the underlying cause
Fluid management (input and output)
Medication review
=> hold/change dose?
Seek renal specialist input if indicated
What might indicate the need for renal specialist input in AKI?
No improvement
Complicated cases
Complications of AKI
Hyperkalaemia Other electrolyte imbalances Metabolic acidosis Volume overload Uraemia CKD and ESRD
What electrolyte imbalances are associated with AKI?
Hyperkalaemia
Hyperphosphataemia
Hypermagnesaemia
Hyponatraemia
Hypocalcaemia
Indications for renal replacement therapy
Refractory pulmonary oedema
Persistent hyperkalaemia (>7)
Severe metabolic acidosis
Ureamic complications (encephalopathy, pericardial rub)
Drug overdose
What is the biggest cause of CKD?
Diabetes mellitus
Causes of CKD:
Diabetes mellitus
Interstitial diseases
Glomerular diseases
Obstructive uropathy
Hypertension
Renovascular disease
Drugs (long-term NSAIDs)
Congenital/inherited
Unknown causes
Symptoms of CKD
Often asymptomatic until very advanced
Polyuria/nocturia Restless leg syndrome Sexual dysfunction Nausea & Pruritis (early uraemia) Yellow pigmentation, encephalopathy and pericarditis (severe uraemia) Pedal oedema & pulmonary oedema.
Signs of CKD
Pallor – due to anaemia Excoriations – due to pruritis Hypertension/fluid overload signs Pericardial rub (rare) Proteinuria
What are some very late features of CKD?
Hiccups Kussmaul’s respiration (due to metabolic acidosis) Muscle twitching Drowsiness Coma Fits
Assessment of CKD
Bloods - anaemia? hyperkalaemia? Urinalysis ECG - hyperkalaemia? Renal USS Renal biopsy - if cause unclear 24-hour CrCl - for staging
What would small kidneys on USS indicate?
Chronicity of disease (not acute presentation)
What would asymmetry of kidneys on USS indicate?
renovascular or developmental disease
How is CKD diagnosed?
when any two tests three months apart show reduced eGFR and can be stages 1-5 depending on the level of reduction
CKD Stage 1
eGFR >90 but urine findings/structural abnormalities/ genetic traits suggest CKD
Pt will be asymptomatic
CKD Stage 2
eGFR 60-89
Mildly reduced eGFR and other findings (as for stage 1) point to CKD
Pt will be asymptomatic
CKD Stage 3A
“Moderate CKD”
eGFR 45-59
usually asymptomatic
CKD Stage 3B
“Moderate-severe CKD”
eGFR 30-44
Pt might be anaemic
CKD Stage 4
“Severe CKD”
eGFR 15-29
Symptoms often at eGFR <20
Electrolyte disturbances
CKD Stage 5
“End-stage renal failure (ESRF)”
eGFR <15 / dialysis
Significant complications and symptoms
Dialysis usually at eGFR <10
Management of CKD
Treat reversible causes – e.g. obstruction, nephrotoxic drugs
1st line = BP control/diabetic control
2nd line = control of complications
=> recombinant EPO
=> calcium/vitD supplementation
=> K+ restriction for hyperkalaemia
RRT in ESRD
What are the complications of CKD?
Renal anaemia
Renal bone disease
Electrolyte disturbances
Myopathy
Peripheral neuropathy
Increased risk of infection
GI – Anorexia, N+V, peptic ulcer disease.
CV – pericarditis, atherosclerosis, HTN, hyperlipidaemia.
Depression – particularly in later stages/dialysis
Renal anaemia
Lack of secretion of EPO in response to hypoxia
Severity of anaemia correlate with severity of CKD
Recombinant EPO can be given to correct it
BUT treating anaemia may not affect mortality and returning Hb to normal may carry additional risks (hypertension, thrombosis).
Renal bone disease
Kidneys normally hydroxylate vitamin D to its active form.
Low VitD levels in CKD cause:
- reduced intestinal Ca2+ absorption
- reduced renal reabsorption of Ca2+
- reduced bone protective activities
thus lead to osteoporosis, osteosclerosis and osteomalacia
hyperparathyroid bone disease can occur (due to low Ca2+)
What are the indications for renal replacement therapy?
A intractable acidosis E electrolyte disturbance (hyperkalaemia, hyponatraemia, hypercalcaemia) I intoxitants O intractable fluid overload U uraemia symptoms
Is the risk of renal disease higher in T1DM or T2DM?
Risk is equivalent
How does diabetes mellitus affect the kidneys?
- Direct glomerular damage
- Ischaemia due to arterial disease
- Ascending infection (more common in DM)
What factors of DM contribute to renal disease?
Multifactorial
the most important factors:
- extent and duration of hyperglycaemia
- hypertension.
Other:
Smoking, obesity, physical inactivity, dyslipidaemia, proteinuria, dietary factors
What are the principles of management for diabetic nephropathy?
the same as for CKD, but with additional tight glycaemic control
What are the types of polycystic kidney disease?
- Autosomal dominant (ADPKD) – more common
2. Autosomal recessive (ARPKD)
What does polycystic kidney disease consist of?
Renal and extra-renal cysts (e.g. liver)
Intracranial aneurysms
Dolichoectasias (elongated and distended arteries)
Aortic root dilatation and aneurysms
Mitral valve prolapse
Abdominal wall herniae
How do patients with polycystic kidney disease present?
= most common cause of ballotable kidneys.
systemic hypertension,
CKD
abdominal swelling due to very large kidneys bilaterally.
Cysts in the liver lead to portal hypertension and fibrosis
Management of polycystic kidney disease?
the same as for CKD, but consider screening for berry aneurysms
Chronic pyelonephritis
chronic tubulointerstitial inflammation and deep segmental cortical renal scarring
clubbing of the pelvic calyces as the papillae retract into scars
Most commonly caused by chronic vesico-ureteric reflux.
What are the 3 layers of the glomerulus?
What is the purpose of this structure?
- Fenestrated capillary endothelium
- Basement membrane
- Visceral layer – formed by podocytes.
to allow small, charged ions through, but not transport of proteins or blood
pathophysiology of Glomerulonephritis/glomerular disease
involves an immunological attack by an antibody or T cell, attacking a primary/secondary antigen in the glomerulus
The immune attack leads to pathological responses in the glomerulus:
=> thickened basement membrane
=> deposition of cells in bowman’s space
=> endothelial cell proliferation, capillary wall necrosis and sclerosis
What can cause deposition of a secondary antigen in the glomerulus?
Neoplasm, SLE, amyloid, infection, diabetes, Henoch Schonlein Purpura
Global glomerular pathology
when the whole glomerulus is diseased
Segmental glomerular pathology
Small patches of one glomerulus are damaged in a “patchy” fashion
Diffuse glomerular pathology
Affecting >50% of glomeruli
Focal glomerular pathology
Affecting <50% of glomeruli
How can glomerular damage manifest?
AKI CKD Asymptomatic haematuria Nephrotic Syndrome Nephritic Syndrome
Rapidly progressive glomerulonephritis (acute version of nephritic syndrome).
What is the triad of nephrotic syndrome?
- Proteinuria - >3.5 g in 24h
- Hypoalbuminaemia - <30g/L
=> due to protein loss in the urine.
=> In response, liver will produce albumin (but also cholesterol, resulting in hypercholesterolaemia) - Oedema
=> due to decreased capillary oncotic pressure
a NON-PROLIFERATIVE condition
Symptoms/signs of nephrotic syndrome
Fatigue – hypoalbuminaemia. Leukonychia – hypoalbuminaemia. Xanthelasma and xanthomata – dyslipidaemia. Oedema Breathlessness – pulmonary oedema Urine “frothy” in appearance - protein
Causes of nephrotic syndrome
Minimal change nephropathy
Membranous glomerulonephritis
Focal Segmental Glomerulosclerosis
Bacterial/viral infection
Diabetic nephropathy
Drugs
Neoplasm
Nephrotic Syndrome - investigations
Urine Dipstick, MSU
FBC, U&E, LFT, Ca2+, CRP, glucose
Serum and urine immunoglobulins
Autoimmune screen, Hep B&C, HIV
CXR – pleural effusion/oedema
USS kidneys (+ renal biopsy?)
Minimal change nephropathy
= most common cause of nephrotic syndrome in childhood
Characterised by minimal change on light microscopy of renal biopsy
Nephrotic Syndrome - management
Treat the cause.
Diuretics, salt/water restriction and ACEis to reduce proteinuria.
Anticoagulation if immobile due to risk of thrombosis
Nephritic Syndrome
Presents as a tetrad of:
- Haematuria and red cell casts (can be microscopic)
- Oliguria
- Proteinuria (can be <3.5 g/day)
- Hypertension
It is proliferative, with increased cell numbers as well as damage to the basement membrane
Causes of nephritic syndrome
IgA nephropathy
Goodpasture’s disease
SLE
Henoch Schonlein Purpura (HSP)
What is the main risk factor for UTI?
BEING FEMALE
- shorter urethra (closer to anal and genital regions).
- Pregnancy - hormonal changes lead to urinary stasis and thereby vesicoureteric reflux
- Post-menopause - low oestrogen levels cause decreased amounts of lactobacilli, which leads to increased pH (better conditions for E. coli colonisation)
Risk factors for UTI in males
Lack of circumcision Urologic Surgery Catheterisation Neurogenic bladder Urinary Tract obstruction (incl. caliculi) Renal Transplant Immunosuppression Penetrative anal intercourse Functional/mental impairment. Prostatic enlargement Convene
Risk factors for UTI in females
Previous UTI Urologic Surgery Catheterisation Neurogenic Bladder Urinary Tract obstruction (incl. calculi) Renal Transplant Immunosuppression Sexual intercourse Lack of urination after sex Spermicides Pregnancy Diaphragm Use Diabetes Functional/mental impairment Oestrogen deficiency Bladder prolapse
What are the two most common pathogens causing UTI?
What are some rarer causes?
- E. coli (most common - ~80%)
- Staph. saprophyticus (common in young, sexually active females)
Rarer:
- Enterococci
- Proteus
- Klebsiella
- Pseudomonas (more likely from catheterisation)
Upper UTI
Above the Vesico-ureteric junction (VUJ)
=pyelonephritis
Lower UTI
below the Vesico-ureteric junction (VUJ)
= Cystitis
Clinical Features of Lower UTI
Increased frequency, urgency and nocturia
Dysuria (typically “burning” pain).
Suprapubic pain/tenderness
Foul smelling/cloudy urine.
Strangury – painful, frequent urination of small volume, expelled only by straining despite a severe sense of urgency.
Haematuria
Eventually confusion, lethargy and fatigue – signs of urosepsis.
Lower UTI - investigations
Urine dipstick – double positive nitrites and leucocytes.
Midstream urine culture and sensitivity – confirms diagnosis if >10^5 pathogenic organisms per mL.
–
Symptomatic women - empirical treatment is started if nitrites and leucocytes are positive on dipstick.
Women should have MCS sent in certain situations, and men should have MCS sent in all suspected UTI.
What should be ruled out before starting empirical UTI treatment?
Check for vaginal discharge to rule out STI
When is renal tract imaging needed in lower UTI?
in children, persistent symptoms, recurrent UTIs, if ?pyelonephritis, if an unusual organism is grown
What is the difference between persistent UTI symptoms and recurrent UTI?
Persistent symptoms – symptoms after more than 48-72 hours of antibiotic treatment.
Recurrent UTI – within a few weeks of appropriate treatment.
What is sterile pyuria and what are the causes?
= raised WBCs in urine, but no organism grown
- Recently treated UTI
- Appendicitis
- TB
- Chlamydia
- Bladder cancer
Lower UTI - treatment
Lifestyle advice – personal hygiene, drinking plenty of fluids, urinating often.
Simple uncomplicated UTIs are treated with antibiotics:
Most commonly Trimethoprim or Nitrofurantoin (though resistance is increasing)
• 3-day course for women (100mg b.d.)
• 7-day course for men (100mg b.d.)
Symptomatic control (for pain) - NSAIDs/paracetamol
If problems with recurrent UTIs, sometimes put on prophylactic Abx but might need further investigations.
Clinical features of upper UTI
Dysuria (typically “burning” pain). Frequency Flank pain > suprapubic pain Haematuria High grade fever Nausea and vomiting
Usually acute onset and systemically unwell.
Upper UTI - investigations
Urine dip and MCS still key but additional investigations needed
Bloods -
=> FBC – raised WCC and CRP
=> U&E – renal function maintained? AKI?
Blood cultures?
Imaging
=> USS KUB - 1st line, can help identify obstruction, inflammatory changes and hydronephrosis.
=> CT
=> DMSA scan
when is CT generally avoided in investigating upper UTI?
in children or pregnant women due to radiation
What does a DMSA scan do?
allows for detailed imaging of the renal cortices and helps clarify areas of poor renal function and scarring
Upper UTI - Treatment
If severe symptoms, patients will need to be admitted to hospital and have a 7-day course of IV antibiotics (cefuroxime or ciprofloxacin).
If not severely unwell, patients can have oral Abx for 7 days (ciprofloxacin, trimethoprim or co-amoxiclav).
Drink lots of fluid to prevent dehydration.
May need imaging (USS KUB) to look for structural damage or changes
Complications of upper UTI
Sepsis
AKI > CKD
Perinephric abscess
Renal papillary necrosis
What are the possible causes of ureteric obstruction?
Stones Clots Severe constipation (more common in children) Enlargement of prostate Strictures Malignancy Pregnancy
Congenital abnormalities
=> Duplicated ureters, ureterocoele, connection abnormalities
What is the most common cause of ureteric obstruction?
Ureteric Stones
When can ureteric clots occur?
can form when large amounts of blood are passing into the urine (e.g. in renal malignancy)
When can ureteric strictures occur?
following previous injury (e.g. previous stone)
following infections (particularly recurrent).
Acute ureteric obstructions
Stones
Clots
Severe constipation
Chronic ureteric obstructions
Enlarged prostate Strictures Malignancy Pregnancy Congenital abnormalities
Luminal ureteric obstruction
Stones
Clots
TCC of renal pelvis
Bladder tumour
Mural ureteric obstruction
Ureteric stricture
Congenital pelviureteric neuromuscular dysfunction
Congenital mega-ureter
Extra-mural ureteric obstruction
Pelviureteric compression (due to external tumours, diverticulitis, AAA, retroperitoneal fibrosis)
Clinical features of ureteric obstruction
Symptoms: • Pain – “ureteric colic” • N+V • Frank haematuria • Difficulty passing urine • Recurrent UTIs
Signs: • Frequency • Oliguria • Haematuria • Hypertension • Pyrexia • Rigors
Where are the 3 sites of ureteric constriction?
What is the clinical relevance of these points?
- Pelviureteric Junction
- Pelvic Brim
- Vesicoureteric Junction
= the 3 common sites where stones can get lodged
Risk factors for urolithiasis
More common in males (3:1)
More common in affluent areas
Anatomical abnormalities
=> E.g. horseshoe kidney, ureteral stricture
HTN Gout Hyperparathyroidism Immobilisation Dehydration Metabolic disorders
What can renal/ureteric stones consist of (most to least common)?
- Calcium
- Urate
- Struvite - magnesium, ammonium, phosphate
- Cysteine
What are the risk factors for calcium stones?
Low urine volume
Hypercalciuria (e.g. primary parahyperthyroidism).
What are the risk factors for urate stones?
high levels of blood purines from diet (increased red meat) or haematological disorders
Which ureteric/renal stones are radiolucent?
urate stones
Staghorn calculi
where the the renal pelvis and calices are filled with stone to give a “stag horn” appearance
What are the risk factors for cysteine stones?
associated with familial disorders of cysteine metabolism
What is the cause of ureteric colic?
occurs due to increased peristalsis around the site of the obstruction.
the pain radiates down to the testis, scrotum, labia or anterior thigh
Investigation of Ureteric Obstruction
BLOODS – FBC, U&Es, CRP, LFTs, coag, calcium, phosphate, glucose, bicarbonate and urate levels
Urine dip - blood? infection?
(including bHCG)
Urine MCS
Abdominal exam
Imaging - AXR, renal tract USS, Non-contrast CT KUB
what is the gold-standard imaging modality for ureteric obstruction?
Non-contrast CT KUB
Causes of true frank haematuria
Malignancy of renal tract Stones Infection Nephritis Bleeding disorders (incl. over-coagulation) Trauma
Causes of apparent (i.e. not true) frank hematuria
Menstruation
Dyes
Some drugs (e.g. rifampicin)
Spontaneous passing of renal stones
~ 80% pass spontaneously (esp if <5mm or in lower ureter)
can take 1-3 weeks
Fluid resuscitation + analgesia (buscopan as antispasmodic?)
Abx if infection
Management of large renal stone (>5mm)
ESWL - sonic waves are used to break up the stone
Percutaneous nephrolithotomy (PCNL) => for complex renal calculi and staghorn calculi.
Endoscopic removal
Open surgery
When should hospital admission be considered in renal stones?
- Post-renal AKI
- Uncontrollable pain from simple analgesics
- Evidence of infection or shock.
- Stone >5mm
Complications of renal stones?
Acute obstruction – infection, post-renal AKI.
Recurrent/chronic obstruction – CKD, renal scarring
what temporary measures can be done to relieve obstruction and avoid renal damage?
- Retrograde stent insertion:
=> Placement of a stent within the ureter, allows the ureter to be kept patent and temporarily relieve the obstruction. - Nephrostomy
=> A tube placed directly through the skin on the back, into the renal pelvis and collecting system, relieving the obstruction proximally.
Renal cell carcinoma - presentation
60% of patients have haematuria
Other symptoms include mild loin discomfort and a loin mass.
Renal cell carcinoma - pathophysiology
Invades along the renal vein to the IVC and spreads via haematological route.
Forms PTH-related protein, so patients may get pathological fractures.
Renal cell carcinoma - diagnosis
Typically forms a solid mass on USS; also seen on CT scan
Bloods commonly show anaemia and may show a raised ALP and/or ESR
Renal cell carcinoma - treatment
Radical nephrectomy
No role for chemo/radiotherapy (ineffective)
Tyrosine Kinase inhibitors can be useful; as can renal artery embolisation
Renal cell carcinoma - prognosis
Classically causes cannonball lung metastases.
Even T1 disease has only 70% 5-year survival prognosis.
Average survival with mets is <2 years.
What are common causes of bladder outlet obstruction?
Benign Prostatic Hypertrophy (BPH) Bladder stones Urethral strictures Prostate cancer Tumours of the rectum, uterus, or cervix.
What are risk factors for bladder stones?
due to stasis of urine
=> such as in chronic retention, infection, obstructive uropathy of other aetiology, and catheters.
Bladder stones - presentation
Lower Urinary Tract Symptoms
Chronic irritation of bladder epithelium increases transitional cell carcinoma risk
Bladder stones - investigation
As for renal stones
Bladder stones - management
Cystoscopy
Stone drainage
Lithotripsy
Bladder cancer - presentation
Typically painless haematuria (+/- clots)
Recurrent UTI
Voiding symptoms
Pain from invasion of local structures.
Risk factors for bladder cancer
Male, smoker, age >50, aromatic amines, schistosomiasis
Bladder cancer - pathophysiology
= transitional cell carcinoma
Commonly due to prolonged carcinogen contact
Initially forms carcinoma in situ
Bladder cancer - diagnosis
Screening undertaken of those who work in at-risk industries.
Usually diagnosed visually (with biopsies) on flexi-cystoscopy.
Which industries are considered “at risk” of bladder cancer?
Rubber/plastic/dye industry workers
Bladder cancer - treatment and prognosis
Cystoscopic removal of the tumour +/- intravesical BCG
In extensive cases – radical cystectomy
Need to look for parallel primaries in the entire urinary tract. 50% change of recurrence so follow-up is life-long
Benign Prostatic Hyperplasia
Benign nodular/diffuse proliferation of the glandular layers of the prostate, leading to enlargement of the inner transitional zone
Common in middle-aged men
BPH - symptoms
Symptoms occur due to urethral compression:
Hesitancy Poor flow Terminal dribbling Frequency and nocturia UTI Retention (less common)
BPH - Complications
UTI Overflow incontinence Bladder calculi Bladder diverticulae Bilateral hydronephrosis and renal failure
BPH - treatment
Acute retention – attempt urethral catheter drainage
If symptoms are mild – “watch and wait”
Medical management with alpha-blockers or 5alpha-reductase inhibitors
If medical management fails, then Trans-urethral resection of the prostate
Prostate cancer - presentation
Most commonly raised PSA (but 20% have normal PSA)
Often asymptomatic
PR exam – hard and craggy prostate
Where does prostate cancer commonly metastasise to?
bone
iliac/para-aortic nodes.
Prostate cancer - treatment
T1/2 = active surveillance.
T 3/4 = radiotherapy or surgery
Apart from prostate cancer, what else can affect PSA levels ?
mountain biking, infection, recent intercourse (48h), cystoscopy
Gleason Grade of prostate cancer
Two areas of tissue are graded out of 5 to give a combined score out of 10.
Vital for prognosis
<7 = low risk; >7 = high risk.
what might an enlarged prostate with a deep sulcus suggest?
benign prostatic hyperplasia
what might an enlarged and very tender prostate suggest?
(acute/chronic) prostatitis
what might an enlarged prostate with a rough nodule suggest?
unilateral prostate cancer
what might a hard, asymmetrical and irregular prostate with an impalpable sulcus suggest?
prostate cancer
what are some things to comment on when examining the prostate in a PR exam?
Size – normal size? Sulcus – normal central sulcus? Symmetry – are the lobes symmetrical? Consistency – smooth/irregular? Any pain on palpation?
