Renal/GU Flashcards
describe the neural control of the lower urinary tract
Parasympathetic (cholinergic) S2-4 drives detrusor contraction Sympathetic (noradrenergic) T10-L2 contracts the sphincter and inhibits detrusor contraction
list 4 storage LUTS
frequency nocturia urgency urgency incontinence
list 7 voiding LUTS
hesitancy straining poor/intermittent stream incomplete emptying post micturition dribbling haematuria dysuria
what is the difference between BPH and BPE
benign prostatic hyperplasia is a histological finding whereas benign prostatic enlargement is found on DRE
what is BPH
increase in epithelial and stromal cell numbers in the periurethral area of the prostate. can be due to increase in cell number, decrease in apoptosis or combination of the two. it’s common - most men over 60 have some
what is BPO and what causes it
benign prostatic obstruction has a dynamic component which is the alpha 1 adrenoreceptor mediated contraction of the prostatic smooth muscle and a static component due to the volume effect of BPE
how are prostate symptoms assessed and what are the 8 points
the international prostate symptom score
what investigations for LUTS
- flow rates and residual volume
- frequency volume chart
- renal biochemistry
- imaging
- PSA????
- TRUSS (trans rectal ultrasound scan)
two reasons that flow rate might be reduced
due to obstruction in the lower urinary tract
due to detrusor underactivity
what is PVR
post void residual
100% of normal men have a PVR of <12ml
high PVR is a risk for hydronephrosis and elevated creatinine
consider detrusor underactivity as a cause of high PVR
name some complications of BPE
symptom progression
infections
stones
haematuria
acute retention
chronic retention
interactive obstructive uropathy
acute retention of urine presentation
extreme pain
600ml - 1L residual urine
normal U&E
pain is relieved by catheterisation
chronic retention of urine
more difficult to define
is basically incomplete bladder emptying
increased risk of infection and stones
can be low pressure: detrussor failure
can be high pressure if there’s obstruction
obstructive uropathy
nocturnal enuresis should alert to the risk of interactive obstructive uropathy
residual volume can be up to 4L
check U&Es and monitor daily if creatinine is raised
observe for a diuresis
check lying/standing blood pressures
treatment for prostate symptoms
watchful waiting for men with mild symptoms
the medical treatments are aimed at reducing the tone of prostatic smooth muscl or reducing the size of the prostate
alpha-adrenergic agonists (e.g. tamsulosin) improve flow
5-alpha-reductase inhibitors (e.g. finasteride) inhibit conversion of testoserone to the more active dihydrotestosterone (androgens are necessary for hyperplasia) this reduced prostate size
combination of the above are better than either singly
anti-cholinergics for overactivity
indications for prostate surgery
RUSHES
Retention
UTI
Stones
Haematuria that is refractory to 5-ARIs
Elevated creatinine due to BOO
Stmptom deterioration
what is BOO
Bladder Outflow obstruction
name a type of prostate surgery and some complications of it
TURP (trans urethral resection of prostate)
Immediate complications: sepsis, haemorrhage
Early: sepsis, haemorrhage and clot retention
Late: retrograde ejaculation, erectile dysfunction, urethral stricture, bladder neck stenosis and urinary incontinence
diagnosing AKI
you need one of the following:
rise in creatinine >26micromol/L in 48hrs
rise in creatinine >1.5x baseline within 7 days
urine output <0.5mL/kg/h for >6 consecutive hours
three types of causes of AKI
pre-renal (decreased perfusion to the kidney)
renal (intrinsic renal disease)
post renal (obstruction to urine)
four causes of pre-renal pathology with an example of each
decreased vascular volume (e.g. haemorrhage, burns or D&V)
decreased cardiac output (e.g. cardiogenic shock)
systemic vasodilation (e.g. sepsis)
renal vasoconstriction (e.g. NSAIDs, ACEi, ARB)
three examples of renal pathology and an example of each
glomerular problems (e.g. glomerulonephritis)
interstitial problems (e.g. infection, sarcoidosis)
vessel problems (e.g. vasculitis)
4 risk factors for AKI
pre-existing CKD
age
male sex
comorbidity (DM, CVD, malignancy etc)
5 most common causes of AKI
- sepsis
- major surgery
- cardiogenic shock
- other hypovolaemia
- drugs
management of hyperkalaemia
insulin + dextrose
calcium gluconate
IV fluid
salbutamol
investigation of AKI
Bloods: identify and treat hyperkalaemia
monitor fluid balance
do daily creatinine
urine dipstick to look for proteinuria and/or casts
imaging
assess current volume status
AKI management
Identify and treat cause
refer to renal for dialysis if necessary
treat sepsis
stop nephrotoxic medication
give IV fluid
what are the indications for dialysis
refractory pulmonary oedema
persistent hyperkalaemia
severe metabolic acidosis
uraemic encephalopathy or pericarditis
drug overdose
prognosis of AKI
dependent on cause it changes:
burns: 80% mortality
medical illness: 30% mortality
what is the nerve that controls the external sphincter of the bladder
pudendal nerve
S2-S4
uses acetylcholine neurotransmitter
which nerve tells us that the baldder is filling
the afferent pelvic nerve senses stretch in the detrussor muscle
it is a sensory nerve
describe the neural control of the bladder
the cortex mediates voluntary control
the pontine micturation centre and the periaqueductal grey coordinate voiding
the sacral micturation centre coordinates the micturation reflex
- if there’s no coordination between this and the pontine M centre then you will void safely when the bladder is full but you will have no conscious control over when this happens
describe what is happening during the storage phase of bladder filling
- normal adult bladder capacity is 400-500ml with first sensation at 100-200ml (mediated by pelvic nerve)
- as the volime in the bladder increases the pressure remains low due to receptive relaxation
- sympathetic stimulation (T11-L2) causes detrusor muscle relaxation
- pudendal stimulation (S2-4) causes external urethral sphincter contraction
describe what happens during the voiding phase
- voluntary control from the cortex and the PMC
- PMC sends a signal to the sacral MC and mediates:
- detrusor contraction via parasympathetic stimulation (S2-4)
- external urethral sphincter relaxation via pudendal inhibition S2-4
What is OAB
overactive bladder is defined as urgency with frequency with or without nocturia when appearing in the absence of local pathology
what is the management of OAB
- behavioural
- reduce caffeine/alcohol intake
- frequency volume chart
- anti-muscarinic agents
- decrease parasympathetic activity by blocking M2/3 receptors but give dise effects of dry mouth
- botox
- blocks nmj for ach release - se: incomplete bladder emptying and need to catheterise in 15%
stress incontinence in females
is usually secondary to birth trauma due to denervation of pelvic floor and urethral sphincter or weakening of fascial support of bladder or urethra
management on stress urinary incontinence
pelvic floor physiotherapy
surgery
stress incontinence in males: two causes and how to treat
iatrogenic following prostatectomy
neurogenic
treat with artificial sphincter or a male sling
what is the commonest cancer in men?
prostate cancer
what is the mean age at diagnosis for prostate cancer
72
what percentage of men die of prostate cancer
3%
what type of cancer is prostate cancer
adenocarcenoma
where does prostate cancer occur
it occurs in the peripheral zone of the prostate and spreads locally through the capsule
mets are to lymph nodes and bone and occasionally lung liver and brain
what is PSA
Prostate specific antigen is a serine protease thats responsible for the liquefaction of semen
it is commonly detected in small quantities in the blood
name some occasions when PSA is raised
in benign prostate enlargement, urinary tract infection and prostatitis as well as prostate cancer
how well does PSA work
70% of men with elevated PSA will not have prostate cancer
6% of men with prostate cancer will have a ‘normal’ PSA
prostate cancer diagnosis
LUTS
PSA
TRUSS
prostate biopsy is definitive diagnosis
how is prostate cancer graded
gleason grading based on histological appearance - a higher score has a worse prognosis
treatment of prostate cancer
based on how advanced the cancer is:
localised: watch and wait or curative surgery, radiotherapy
locally advanced: surgery, radiotherapy with neoadjuvant hormone therapy
metastatic: palliative care with hormone therapy
arguments against treatment for localised prostate cancer
it is a disease of the elderly
there may be competing causes of death
only 30% of men with prostate cancer die of prostate cancer
there are adverse effects of treatment
prognosis of advanced prostate cancer
median survival is 2.5 years but significant number of patients in long-term remission from androgen deprivation therapy
80% of tumours are androgen sensitive
castration leads to remission of advanced disease
there is far better palliation than in most metastatic solid tumourss
reasons for screening prostate cancer
commonest cancer in men
responsible for 10,000 deaths pa in UK
4th most common cause of cancer deaths
3% men will die of prostate cancer
reasons not to screen for prostate cancer
uncertain natural history
overtreatment
morbidity of treatment
anxiety associated with false positives
what is CKD
chronic kidney disease is abnormal kidney structure or function presnt for more than 3 months with implications for health
what is the lifetime risk of renal stones
10-15%
name 5 functions of the kidney
blood volume/fluid
generates erythropoietin for red cell production
waste/toxin/drug excretion
vitamin D metabolism
acid base regulation (excretes H+ iond and reabsorbs HCO3- ions)
what is creatinine
it is a waste product of muscle metabolism
it is purely excreted by the kidneys
there is a relationship between serum creatinine and GFR
this means that serum creatinine can be used to come up with eGFR
CKD risk factors
diabetes
dyslipidemia
left ventricular hypertrophy
age
smoking
male sex
hypertension
how is CKD classified
based on GFR category, the presence of albuminuria as a marker of kidney damage and the cause of the kidney disease
why might CKD cause anaemia
due to reduced production of erythropoietin
treat with EPO and IV iron supplements
how many people in the UK get haemodialysis and how often for how long
24,000 patients in the UK
vast majority do it 3 times a week for 4hrs a time
what is RRT
renal replacement therapy includes peritoneal dialysis, haemodialysis and kidney transplants
how many patients in the UK recieve peritoneal dialysis
6000
early complications of kidney transplantation
surgical complications
- thrombosis
- obstruction
infection
- urinary tract
- chest
rejection
- can be easily treated
- does affect long term survival of graft
what are the three most common causes of CKD in the UK
diabetes
glomerulonephritis
hypertension/renovascular disease
CKD is associated with
all cause mortality
superimposed AKI
progressing renal symptoms
cardiovascular disease
CKD patients are more likely to die of CVD than to need RRT
monitoring of renal function in CKD
GFR and albuminuria should be monitored at least annually, every 6 months if high risk and every 3 months if very high risk (based on heat map)
small fluctuations common but decrease in GFR of >25% is significant
what are the risk factors for decline of GFR
hypertension
diabetes mellitus
volume depletion
infection
NSAIDs
smoking
investigation of CKD
Blood
- U&E - compare with previous
- Hb - there may be normocytic anaemia
- glucose - to check for DM
- if there is renal bone disease there will be low Ca2+ and high PO43- with high PTH
Dipstick
- check for proteinurea and casts
Ultrasound
- check size and corticomedullary differentiation
what does glomerulonephritis mean
it is a term that encompasses a number of conditions that
- are caused by pathology in the glomerulus
- present with proteinuria, haematuria or both
- are diagnosed on renal biopsy
- cause CKD
- can progress to kidney failure
what is the difference between nephrotic and nephritic syndromes
glomerulonephritis presents on a spectrum ranging from nephrosis (proteinuria due to podicyte pathology) to nephritis (haematuria due to inflammatory damage
5 types of nephritic glomerulonephritis
IgA nephropathy
Henoch-Schonlen purpura
post-streptococcal GN
anti-glomerular basement membrane (Anti-GBM) disease
rapidly progressive GN
what is the commonest primary GN
IgA nephropathy
IgA nephropathy
- asymptomatic or presents with episodic haematuria 12-72hrs after non-specific URTI
- high BP
- proteinuria
- 20-50% progress to renal failure over 30yrs
- diagnosis is by renal biopsy showing IgA deposition
- Treatment is with ACE-i/ARBs
- corticosteroids if persistent disease
if there is oedema you should always
dipstick the urine to avoid missing renal disease
definition of nephrotic syndrome
triad of:
- proteinuria
- hypoalbuminaemia
- oedema
aetiology of nephrotic syndrome
primary renal disease or secondary to a disorder
- primary renal disease
- minimal change disease
- membranous nephropathy
- focal segmental glomerulosclerosis
- secondary causes
- DM
- Lupus nephritis
- myeloma
- amyloid
- pre-eclampsia
pathophysiology of nephrotic syndrome
filtration barrier of kidneys, made of podicytes, the GBM and endothelieal cells is damaged and proteinuria results from podicyte pathology
- minimal change disease - abnormally functioning podicytes
- membranous nephropathy - immune mediated damage
- FSGS - podicyte injury/death
presentation of nephrotic syndrome
generalised pitting oedema - can be rapid and severe
4 prinicples of management of nephrotic syndrome
reduce oedema
treat underlyign cause
reduce proteinuria
treat complications
reducing oedema in nephrotic syndrome
fluid and salt restriction
diuresis with loop diuretics like furosemide
add thiazide diuretics if oedema persists
Treating the underlying cause of nephrotic syndrome
biopsy is needed in adults to understand and treat cause
in children minimal change disease is the most common cause so treat with corticosteroids which induce remission in most. biopsy only needed if there’s no response to steroids
reducing proteinuria in nephrotic syndrome
ACEi/ARBs reduce proteinuria but may not be needed in minimal change disease
treating complications of nephrotic syndrome
thromboembolism - treat with heparin
infection - urine loss of Ig and immune mediators means they’ve increased risk of urinary, respiratory and CNS conditions. ensure pneumococcal vaccination is given
hyperlipidaemia - increased cholesterol, LDLs and triglycerides due to hepatic synthesis in response to decreased oncotic pressure
3 types of glomerulonephritis
minimal change disease
focal segmental glomerulosclerosis (FSGS)
membranous nephropathy
minimal change disease
~25% of adult nephrotic syndrome
most is idiopathic or due to drugs like NSAIDs
does not cause renal failure
diagnosis: light microscopy is normal but electron microscopy shows podicyte displacement
treatment is with prednisolone which normally causes remission - relapses managed longer term, stronger immunosupression (e.g. with cyclophosphamide)
focal segmental glomerulosclerosis
this is the commonest glomerulonephritis seen on renal biopsy
primary is idiopathic but can be secondary to HIV, heroin, lithium, lymphoma
all are at risk of progressive CKD and kidney failure
disease recurs in 30-50% of kidney transplants
diagnosis: histology shows glomeruli scarring in spots (hence focal)
treatment is ACEi/ARBs and BP control. Corticosteroids in primary disease only
membranous nephropathy
~25% of adult nephrotic syndromes
primarily idiopathic but can be secondary to: malignancy, infection (schistosomiasis, malaria, hep B/C), drugs and immunological disease (SLE, RA)
spontaneous remission in 25%
auto-antibodies present in most. there is a thickened GBM due to subepithelial immune deposits
treatment: ACEi/ARB and blood pressure control
describe the nerve supply to the penis
parasympathetic
- erectlie S2-4
- mediates arteriolar dilatation
Sympathetic
- ejaculation T11-12
- in the flaccid state the sympathetic tome constricts arterioles
Cavernous nerve carries both of these fibres and passes posterolateral to the prostate so there is risk of damage in prostatectomy
causes of low testosterone
Testosterone is required for normal erectile function
Primary
- pituitary or the hypothalamus
Secondary
- testes
- tumour, injury etc
Congenital syndromes
- kleinfelters
role of nitric oxide in erection
released by cavernous nerves and endothelium
it causes smooth muscle relaxation and dilatation of the arterioles
role of phosphodiesterase in erection
returns the penis to a flaccid state by degrading the cGMP produced by the nitric oxide in the smooth muscle cell
phosphodiesterase inhibitors stop the degradation of cGMP
sildenafil (viagra) is a phosphodiesterase inhibitor
what is the definition of erectile dysfunction
the persistend inability to attain and maintain an erection sufficient to permit satisfactory sexual performance
causes of ED
Organic
- vasculogenic
- neurogenic
- hormonal
- anatomical
- drug induced
Psychogenic
give 4 indicators that ED might be psychogenic
sudden onset
good nocturnal and early morning erections
situational ED
younger patients
risk factors for ED
Lots are in common with CVS disease
- lack of exercise
- obesity
- smoking
- hypercholesterolaemia
- metabolic syndrome
- diabetes gives 3x risk of ED
others
- renal fialure
- trauma i.e. pelvic fracture
- iatrogenic - prostatectomy
- liver disease and alcohol overuse
Physical examination of a patients with ED
BP and heart rate
prostatic enlargement (PR)
hypogonadism (small testes and secondary sexual characteristics)
check penile sensation to rule out CNS problem
in majority of patients the examination will be normal
lab testing of an ED patient
morning testosterone - if low then look at prolactin, FSH and LH
in majority of patients blood tests will be normal
treatment for ED
identify and treat the reversible causes of ED
advise on lifestyle and risk factor modification
patient partner involvement and counselling
oral phosphodiesterase inhibitors
how do oral phosphodiesterase inhibitors work and name one
they increase intracellular CGMP (which N20 creates) in smooth muscle cells of the arterioles
sildenafil (viagra)
what is the efficacy of sildenafil and what are some common adverse events
2/3 improved errections and 2/3 sumularly successful intercourse
common adverse events:
- headache
- flushing
- dyspepsia
what is a prolonged erection and what should you do
if it lasts more than 4 hours there’s risk of permanent ischaemic damage to the corpora
aspirate the corpora
if that fails then inject phenylephrenine
three classifications of UTI
asymptomaric bacteruria
uncomplicated
complicated
what is pyuria
it is the presence of leukocytes in the urine
it is associated with infection
but there can be sterile pyuria
what is an uncomplicated UTI
this is when it occurs in non-pregnant women
when is a UTI ‘complicated’
when there is some structural or functional abnormality of the urinary tract so when it is in:
pregnant
men
catheterised patients
children
the immunocompromised
when it’s recurrent
etc
what percentage of women experience a UTI in their lifetime
10-20%
there’s much higher incidences of UTI in hospitalised patients
name a UTI causing pathogen associated with:
renal stones
hospital catheterisation
deep seated infection
renal stones: Proteus
- they produce urea which boosts the pH and contributes to stone formation
hospital catheterisation: Klebsiella
deep seated infection: S.aureus
what is by far the most likely pathogen to cause a UTI
E.coli causes >50% of UTIs
what are the two types of lower urinary tract infection
cystitis (bladder) and prostatitis (prostate)
what is an upper urinary tract infection
pylonephritis = an infection of the kidney and the renal pelvis
what is the incidence of pylonephritis
3 per 1000 patients per year
4 risk factors of a UTI
increased bacterial inoculation: e.g. sexual activity, urinary or faecal incontinence
increased binding of bacteria e.g. spermicide use, lowered oestrogen
decreased urine flow: e.g. dehydration
increased bacterial growth: e.g. immunosuppression, stones etc
6 cystitis symptoms
frequency
dysuria
urgency
suprapubic pain
polyuria
haematuria
7 symptoms of pylonephritis
fever
rigor
vomiting
loin-groin tenderness
associated systitis symptoms
septic shock
prostatitis
pain in the perineum, rectum, scrotum, penis, bladder, lower back
fever
malaise
nausea
urinary symptoms
swollen or tender prostate on PR
UTI investigation
- in a non-pregnant woman with >3 symptoms or one severe symptom of cystitis then treat empiracally without further tests
- otherwise:
- dipstick
- msu culture if >105 CFU/ml then indicative of infection
- blood tests (U&E, FBC and CRP) if systemically unwell
UTI treatment in non-pregnant women
if three or more symptoms (or one severe) of cystitis then treat with a three day course of nitrofurantoin or trimethoprim
if this first line treatment fails then culture MSU and treat according to abx sensitivity
in pylonephritis treat initially with broad spectrum like co-amoxiclav until you can treat according to antibiotic sensitivity
treatment for prostatitis
ciprofloxacin cause it can penetrate the prostatic fluid
what are casts and what does it indicate if they are found in the urine?
they are microscopic cylindrical structures formed in the distal convoluted tubule and collecting ducts of nephrons, then dislodge and pass into the urine in disease states
they are indicative of damage to the kidney epithelium i.e. glomerulonephritis
catheter associated UTI pathogenesis
at risk of infection up to 24hrs post removal
forms biofilms
change and remove catheter when starting treatment
send a fresh sample, not from the bag
don’t dipstick bag as all catheters get colonised
treatment of asymptomatic bacteriuria in >65
do not treat as very common and rarely causes problems
UTI in pregnancy
this is a complicated UTI
asymptomatic bacteruria is common but should be treated as often turns into symptomatic pyelonephritis if untreated
culture rather than dipstick
sh
what is pyelonephritis
it is the infection of the renal parenchyma and soft tissues of the rena pelvis/upper ureter
associated with sepsis and systemic upset and rigors
patients are often fluid depleted and require prompt fluid resuscitation
it predominantly affects women over 35
classical triad of pyelonephritis symptoms
loin pain
fever
pyuria
investigation of pyelonephritis
abdo exam
- tender loins
- renal angle tenderness
- do a PV to rule out tubal/ovarian/appendix pathology
Bloods including cultures
US scan to rule out obstruction of upper tract
MSU
Treatment for pyelonephritis
fluid replacement - increased losses
IB Abx - broad spectrum like co-amoxiclav or gentamicin
drain the obstructed kidney
catheter
analgesia
are men or women more affected by urolithiasis
M:F is 2:1
what is the commonest age to have urolithiasis
30-50
what is the lifetime risk of recurrence of urolithiasis
>50%
where can you get stones - split into upper and lower urinary tract
you can get them anywhere from the collecting duct to the external urethral meatus
- upper urinary tract
- renal stones
- uretic stones
- lower urinary tract
- bladder stones
- prostatic and urethral stones are much rarer
why might patients get renal stones
- anatomical factors
- congenital (e.g. horseshoe kidney. spina bifida)
- acquired (obstruction, trauma, reflux)
- Urinary factors
- calcium, oxalate, urate imbalance
- dehydration
- infection
what is the nucleation theory of stone formation
stones form from crystals (Ca2+, oxalate etc) in supersaturated urine
what are the constituents of renal stones
most are made of normal urinary constituents
- 80% are calciumbased with oxalate and phosphate
- 10% are uric acid
- 10% are struvite and these are infection stones
rarely they are formed of drugs
how to prevent stones
overhydration
low salt diet
normal dairy intake
healthy protein intake
reduce BMI
active lifestyle
what are the symptoms of renal stones
asymptomatic
loin pain
renal colic
UTI symptoms like urgency frequency and dysuria
recurrent UTIs
haematuria (visible and non-visible)
what is renal colic
pain that results from upper urinary tract obstruction.
- using socrates it presents like this:
- unilateral loin pain
- rapid onset
- unable to get comfortable/writhing
- radiates to groin and ipsilateral testis/labia
- associated nausea/vomiting
- spasmodic/colicky - worse with fluid loading
- classically it’s very severe “worse than childbirth” “12/10”
how to investigate renal colic
- ABC and give analgesia/antiemetic
- BE WARY OF SEPSIS - urolithiasis can cause pyonephrosis
- focussed history and examination
- urinalysis and MSU if +ve
- Bloods
- FBC
- U&E
- Calcium
- Uric acid
- Imaging
- NCCT KUB
- KUBXR
- USS
differential diagnoses for renal colic
vascular accident - it’s a ruptured AAA in >50 until proven otherwise
bowel pathology (diverticulitis/appendicitis)
Gynae (ectopic pregnancy, ovarian (cyst) torsion)
testicular torsion
MSK
what is the gold standard diagnostic investigation for urolithiasis
NCCT-KUB
no contrast in case of allergies or impaired renal function
it’s 99% sensitive for stones and very specific
however: it doesn’t give any functional info and there’s a bit of radiation
why would you do a USS for ureteric colic?
it’s more sensitive for hydronephrosis than CT as not all acute obstructions dilate
but it is very poor at detecting stones in the ureter
useful in the pregnant an the young as there is no radiation risk
what is metabolic syndrome?
a cluster of conditions that occur together, increasing your risk of heart disease, stroke and type 2 diabetes. These conditions include increased blood pressure, high blood sugar, excess body fat around the waist, and abnormal cholesterol or triglyceride levels
what is the management of ureteric colic
- analgesia
- NSAID suppository
- opiates
- antiemetics
- admit them
- give IV fluid
- be aware that this may make the pain worse
- Observe them closely for sepsis
what is pyonephrosis
it is where there is an infection of the kidney’s collecting system and the renal pelvis fills with pus causing obstruction
this can lead to sepsis and they can lose renal function in 24hrs
they need IV abx, IV oxygen and they need drainage with a nephrostomy or a uretic stent
this is serious and can kill a patient rapidly
what are the 4 types of treatment for renal stones and what do they depend on
conservative
medical
surgical
lithotripsy
the treatment chosen depends on the site and site of the stone as well as patient factors and risks of complications
which stones are dangerous and why/
big stones - they can occlude calyces and/or the PUJ
they can acutely obstruct and cause chronic renal damage including abscesses, fistulae and xanthogranulomatous pyelonephritis (XPN)
small stones <1cm can be observed and only 1/3 will progress
treatment of renal stones
- conservative treatment if they’re small, in a safe location and asymptomatic or if the patient’s very comorbid
- drainage if there is sepsis
- lithotomy by size
- <2cm ureteroscopy
- 1-2cm ESWL
- for larger stones: PCNL
ureteric stones treatment
- conservative for 2 weeks
- the majority <4mm will pass and only 10% >7mm will pass
- drainage if there’s sepsis
- ESWL for stones <1cm
- laser ureteroscopy is suitable for any stone
what does urolithiasis mean and what is the lifetime risk
the formation of stony concretions in the bladder or urinary tract
10-15%
bladder stone treatment
conservative if they’re asymptomatic or unfit
endoscopic (can be accompanied by treatment of BOO)
Open/laperoscopic surgery (ideal for larger stones)
what is the ECG appearance of hyperkalaemia
Tall tented T-waves
Flattening of P-waves
Broad QRS complexes
what two types of PKD are there? and which is more common
- autosomal recessive polycycstic kidney disease (ARPKD)
- autosomal dominant polycystic kidney disease (ADPKD)
- by far the more common
what is the prevalence of ADPKD
1 in 400-1000 (7 million patients worldwide)
what is ADPKD mostly caused by and how does this affect disease course
85% is caused by a mutation in PKD1 on chromosome 16 and these patients reach ESRF by their 50s
can also be caused by mutation in PKD2 on chromosome 4 and this has a slower disease course
10% of these mutations are de-novo
presentation of ADPKD
try and think of 5 things
may be asymptomatic until increased size/haemorrhage of cysts
loin pain
visible haematuria
cyst infection
renal calculi
high blood pressure
progressive renal failure
extrarenal features of ADPKD
propensity to sub arachnoid hemorrhage
- so MRI screening for intracranial aneurysms is recommended if there is a family history of SAH/aneurysms
diverticular disease
ovarian cysts
diagnosis of PKD generally
generally by USS
since renal cysts are common and prevalence increases with age the diagostic criteria reflect this
- <39 years >3cysts
- 40-59 >2 cysts in each kidney
liver and pancreatic cysts are supportive of diagnosis
genetic testing is available but there are ~1500 possible mutations so is limited to diagnostic uncertainty, potentia donors
treatment for ADPKD
- water intake of 3-4L per day can limit cyst growth if their GFR is good enough
- blood pressure control
- 1st line: ACEi/ARB
- 2nd line: thiazide like diuretics
- (e.g.chlorothiazide/hydrochlorothiazide)
- 3rd line: Beta blockers
- CCBs are contraindicated
- 2/3 will need RRT which can include transplantation
what is the prevalence of ARPKD
1 in 20,000
what chromosom is the mutation for ARPKD
chromosome 6
presentation of ARPKD
presents ante-perinatally with renal cysts (salt and pepper appearance on USS)
there’s congenital hepatic fibrosis as well which causes portal hypertension
there’s very poor prognosis if neonatal respiratory distress
no specific therapy
two very important things to think about testicle examination
a testicular lump is cancer until proven otherwise
acute tender enlargement of testis is torsion until proven otherwise
what is an epididymal cyst?
it usually develops in adulthood and comntains milky spermatocele fluid. they often lie above and behind the testis
only remove if symptomatic
what is a hydrocele
- this is fluid in the tunica vaginalis
- can be primary or secondary
- primary (more common)
- resolve during 1st year of life typically
- secondary
- due to trauma, tumour or infection
- primary (more common)
- may need aspiration but many resolve on their own
varicocele
dilated veins
left side more commonly affected (lack of valves between testicular vein and the renal vein on left side whereas on right side testicular vein goes straight into the IVC)
scrotal blood vessels feel like a bag of worms
may be associated with a dull ache
90% of renal cancers are what type
renal cell carcinoma
what is the mean age at which people get RCC and are men or women affected more
mean age 55
M:F is 2:1
what are the clinical features of RCC
haematuria
loin pain
abdominal mass
anorexia
malaise
weight loss
PUO
rarely presents with varicocele when if invasion compresses left testicular vein
50% are found incidentally
what percentage of RCCs have mets at presentation?
25% have mets at presentation
investigation of suspected RCC
- increased BP from renin secretion
- RBC (there may be polycythaemia from increased EPO secretion)
- imaging
- CT and MRI are best and you may see ‘cannonball’ mets
treatment for RCC
- it is generally chemo and radio resistant
- radical nephrectomy can be curative
- for unresectable/metastatic disease then options include:
- high dose IL-2 to activate T-cells
- anti-angiogenesis agents e.g. pazopanib
the mayo prognostic risk score of RCCand what it means for prognosis
- SSIGN uses info on
- Stage
- Size
- Grade
- Necrosis
- 10yr survival:
- 96% in scores 0-1
- 19% in scores >10
Where do you get transitional cell carcinoma
TCC can occur in the bladder (50%) ureter or renal pelvis
who gets TCC
age sex and risk factords
age >40
M:F is 4:1
smokers
those with chronic cystitis
those with schistosomiasis
presentation of TCC
painless haematuria
frequency
urgency
dysuria
urinary tract obstruction
diagnosis of TCC
CT/MRI KUB
urine cytology (tumours can call sterile pyuria)
cystoscopy and biopsy
what percentage of bladder cancers are TCCs
90%
what is the UK incidence of bladder cancer
1:6000
what is M:F for bladder cancer
5:2
risk factors for bladder cancer
smoking
aromatic amines (so working in the rubber industry)
chronic cystitis
schistosomiasis infection
pelvic irradiation
treatment of TCC Tis, Ta and T1
and what is the 5 yr survival
- Tis, Ta and T1 are grades where the cancer has not yet invaded the muscle and has remained in or within the lamina propria
- this is 80% of TCCs
- trans urethral resection of bladder tumour (TURBT)
- consider regimen of intravesical BCG which produces a non-specific immune response
- 95% 5yr survival
Treating TCC T2-4
- palliative care for T4
- T2-T3
- radical cystectomy is the gold standard
- post op chemotherapy like methotrexate or doxorubicin
- they will need a urostoma
what is phimosis
when the foreskin occludes the meatus
what is paraphimosis
occurs when a tight foreskin is retracted and becomes irreplaceable preventing venous return and leading to oedema and even ischaemia of the glans
which bacteria commonly cause prostatitis
chlamydia, e.coli and s.faecalis
what is the commonest male malignancy
prostate cancer
what are the associations of prostate cancer
age (80% of men >80%)
+ve family history
high testosterone
treatment of prostate cancer
depends on prognosis
radical prostatectomy if <70yrs has excellent survival
radical radiotherapy ± hormone therapy can also be curative
hormone therapy alone can delay tumour progression but eventually leads to refractory disease
active surveillance if old and low risk
