genito-urinary Flashcards
BPE definition
benign prostatic enlargement
clinical diagnosis
BPH definition
benign prostatic hyperplasia
histological diagnosis
BOO definition
bladder outflow obstruction
urodynamic diagnosis
LUTS definition
constellation of symptoms
neither gender nor disease specific
hydronephrosis definition
dilation of renal pelvis of the kidney
obstructive uropathy definition
functional or anatomical obstruction of urine flow at any level of the urinary tract
supravesical obstruction definition
above the level of the bladder
infravesical obstruction definition
below the level of the bladder
LUTS: storage symptoms
urgency
nocturia
frequency
overflow incontinence
LUTS: voiding symptoms
poor intermittent stream hesitancy incomplete emptying post micturition straining haematuria dysuria
PSA
PSA is a glycoprotein that is expressed by normal and neoplastic prostate tissue
In the semen
small amounts in bloodstream normally
PSA is raised in…
BPH prostate cancer perineal trauma BMI <25 taller men recent ejaculation black africans prostatitis UTI
flow rates and residual volume
how much urine being passed, how long for and flow rate
max flow rate is more useful if >150ml is voided
frequency volume chart
measure volume voided and time, over a minimum of 3 days
polyuric= >40ml/kg/24 hours
noturic >30% voided at night
acute urine retention
sudden onset of painful inability to pass urine usually with over 500ml in the bladder
bladder usually tender
acute urine retention: causes
prostatic obstruction urethral strictures anticholinergics alcohol constipation infection spinal compression- cauda equina syndrome
acute urine retention: investigations
normal renal biochemistry
renal ultrasound
PSA tests
acute urine retention: treatment
catheter
alpha-1 blocker: relaxes smooth muscle in bladder neck to aid voiding
chronic urine retention
more insidious and may be painless- over catheterise if there is pain
more difficult to define
incomplete bladder emptying
chronic urine retention: causes
prostatic enlargement due to BPH/prostate cancer
pelvic malignancy
diabetes
chronic urine retention: presentation
overflow incontinence
loss of appetite
constipation
distended abdomen
urinary tract obstruction
common and should be considered if they have a renal impairment
damage can be permanent
partial, complete, unilateral or bilateral
urinary tract obstruction: luminal causes
stones
blood clot
sloughed papilla
tumour
urinary tract obstruction: mural causes
congenital or acquired stricture
neuromuscular dysfunction
schistomiasis
urinary tract obstruction: extra mural causes
abdominal or pelvic mass retroperitoneal fibrosis BPH prostate cancer pregnancy inflammation
acute upper urinary tract obstruction: presentation
loin pain radiating to groin
chronic upper urinary tract obstruction: presentation
flank pain
renal failure
infection
polyuria
acute lower urinary tract obstruction: presentation
acute urinary retention with severe suprapubic pain
distended, palpable bladder- dull to percussion
chronic lower urinary tract obstruction: presentation
urine frequency, hesitancy, poor stream, terminal dribbling
UTI/urinary retention/large prostate possible
urinary tract obstruction: investigations
bloods
mid stream urinary sample- culture and sensitivity
ultrasound
upper urinary tract obstruction: treatment
nephrostomy- artificial opening between kidney and skin, urinary diversion from upper tract
alpha 1 antagonist
5 alpha reductase inhibitor
lower urinary tract obstruction: suprapubic catheter
less risk of urethral damage
required general anaesthetic for insertion
small risk of bowel injury during insertion
less likely to be colonised by bacteria than urethral
lower urinary tract obstruction: surgery
transurethral resection of prostate
<14% impotent
1% incontinent
10% ED
indications for surgery with LUTS
RUSHES
Retention UTIs Stones Haematuria Elevated creatinine due to bladder outflow obstruction Symptoms deterioration
BPE: benign prostatic enlargement
increase in size of prostate without presence of malignancy
BPE: epidemiology
common
24% men 40-64 y/o
40% >60
BPE: risk factors
increased age
testosterone
BPE: pathophysiology
increase in epithelial stromal cell numbers in periurethral area of the prostate
benign nodular musculofibrous and glandular layers of the prostate
transitional zone enlarges- partially blocking the urethra
BPE: presentation
LUTS
abdominal pain
acute urinary retention
BPE: LUTS
nocturia frequency urgency post-micturition dribbling poor steam haematuria bladder stones
BPE: differential diagnosis
bladder tumour bladder stones trauma prostate cancer chronic prostatitis UTI
BPE: investigations
digital rectal exam serum electrolytes transrectal ultrasound biopsy mid-stream urine sample
BPE: lifestyle treatments
avoid caffeine and alcohol
relax when voiding
void twice in a row to aid emptying
BPE: alpha 1 antagonists
oral tamsulosin
relax smooth muscle in the bladder neck and prostate
increases urinary flow rate and improve obstructive symptoms
SE= drowsiness, ejaculatory failure and dizziness- avoid in postural hypertension
BPE: 5 alpha reductase inhibitors
oral finasteride
block conversion of testosterone to dihydrotestosterone (responsible for prostate growth)
SE= impotence and decreased libido
BPE: surgical treatment
for those with large prostate or fail to respond to medical therapy
TURP or TUIP
BPE: transurethral resection of prostate
gold standard option, especially for larger prostates
BPE: transurethral incision of prostate
less destructive than TURP and less risk to sexual function
better option for smaller prostates
BPE: complications if untreated
bladder calculi
UTI
haematuria
acute retention
AKI definition
an abrupt sustained rise in serum urea and creatine due to a rapid decline in GFR leasing to a failure to maintain fluid, electrolyte and acid-base homeostasis
AKI classification: RIFLE classifications
old system to define AKI
an increase in serum creatinine or decrease in urine output
AKI classification: RIFLE stands for..
Risk Injury Failure Loss End stage renal disease
AKI KDIGO classification: criteria for diagnosing
used currently
rise in creatinine 26 micromol/L in 48 hours
ride in creatinine >1.5x baseline
urine output <0.5ml/kg/hr for over 6 hours
AKI epidemiology
common in elderly
25% of patients with sepsis and 50% of those with septic shock
AKI: associated with..
diarrhoea haematuria haemoptysis hypotension urine retention
AKI aetiology: pre renal
40-70% renal hyperfusion hypovolaemia hypotension low CO
AKI aetiology: intrinsic
10-50%
renal parenchyma damage
acute tubular necrosis
AKI aetiology: intrinsic, vascular
renal artery/vein thrombosis
cholesterol emboli
vasculitis
malignant hypertension
AKI aetiology: intrinsic, glomerular
glomerulonephritis
autoimmune
drugs
infection
AKI aetiology: intrinsic, interstitial
drugs
infiltration- lymphoma, infection, tumour lysis syndrome
AKI aetiology: post renal
10-25%
urinary tract obstruction at ureter, bladder or prostate
AKI aetiology: post renal, luminal
stones
clots
sloughed papillae
AKI aetiology: post renal, mural
malignancy
BPH
strictures
AKI risk factors
age >75 heart failure chronic liver disease sepsis poor fluid intake past history of AKI diabetes prostate cancer nephrotoxic drugs
AKI presentation
depends on cause and severity palpable bladder/kidneys small urine volume irregular heartbeat from hyperkalaemia uraemia symptoms (fatigue, weakness, confusion, seizures) Thirst oedema
AKI differential diagnosis
abdominal aortic aneurysm alcohol toxicity alcoholic/diabetic ketoacidosis chronic renal failure dehydration heart failure
AKI investigations: dipstick
can suggest infection (leukocytes and nitrates) and glomerular disease (blood and protein)
AKI investigations: blood count
anaemia and high ESR suggests myeloma or vasculitis as cause
AKI investigations: ultrasound
renal size (small= CKD) obstruction and hydronephrosis cysts and masses
AKI investigations: CT-KUB
kidneys, ureters and bladder
looks for obstructing masses or calculi
retroperitoneal fibrosis
AKI treatment: pre renal underlying cause
correct volume depletion
treat sepsis
AKI treatment: intrinsic cause
refer early to nephrology if concern over tubulointerstitial glomerular pathology
AKI treatment: post renal underlying cause
catheterise and consider CT-KUB
obstruction and hydronephrosis- cystoscopy or nephrostomy insertion
AKI treatment: nephrotoxic drugs to stop
NSAIDs
ACE inhibitor
gentamicin
amphotericin
AKI treatment: indications for dialysis
symptomatic uraemia including pericarditis or tamponade hyperkalaemia pulmonary oedema severe acids high potassium
AKI treatment: complications of renal replacement therapy
cardiovascular disease
infection
amyloid accumulates in long term
malignancy is common
stress incontinence
caused by sphincter weakness
urine leaks with increased intra-abdominal pressure rises
more common in females
stress incontinence: causes
neurogenic or congenital
different for males and females
male stress incontinence: causes
post-prostatectomy
male stress incontinence: treatment
artificial sphincter
male sling
female stress incontinence: causes
secondary to birth trauma
degradation of pelvic floor and urethral sphincter
female stress incontinence: treatment
pelvic floor exercises
duloxetine
surgery= sling or artificial sphincter
urge incontinence
strong desire to void and unable to hold urine
urge incontinence: causes
detrusor overactivity- rise in detrusor pressure on filling (more common in women)
can be bladder hypersensitivity from UTI, bladder stones or tumours
urge incontinence treatment: bladder exercises
gradually increase the interval between voids
urge incontinence treatment: behavioural therapy
controlling caffeine and alcohol
frequency volume charts
urge incontinence treatment: anticholinergic agents
oxybutynin
act against cholinergic system (parasymp)
decreases detrusor excitability
urge incontinence treatment: botox of bladder
stop release of Ach from pre-synaptic terminal- paralyses bladder
huge side effect= urinary retention
urge incontinence treatment: bladder augmentation
detrusor myecotmy
cystoplasty= adding bowel to bladder to increase surface area
voiding problems: obstructive
BPE, urethral stricture, prolapse/mass
if BPE give alpha blockers, maybe 5 alpha reductase inhibitors
if that fails then TURP
voiding problems: non-obstructive
detrusor underactivity
long term catheterisation to empty
neuropathic bladder dysfunction: spastic spinal cord injury
reflexes work but not controlled by brain
supra-conal lesion
neuropathic bladder dysfunction: spastic spinal cord injury losses
loss of co-ordination and completion of voiding
neuropathic bladder dysfunction: spastic spinal cord injury features
reflex bladder contractions
detrusor sphincter dyssynergia (loss of complete voiding)
poorly sustained bladder contraction
unsafe- bladders at risk
neuropathic bladder dysfunction: flaccid spinal cord injury
conus lesion
decentralised bladder
neuropathic bladder dysfunction: flaccid spinal cord injury losses
reflex contraction
guarding reflex
receptive relaxation
neuropathic bladder dysfunction: flaccid spinal cord injury features
areflexic bladder
stress incontinence
risk of poor compliance
unsafe- kidneys at risk
neuropathic bladder dysfunction treatment
alpha adrenergic blockers
sphincterotomy
cystoplasty
permanent catheterisation
neuropathic bladder dysfunction treatment: prevent autonomic dysreflexia
commonly causes by over-distension or bladder
occurs in lesions above T6
overstimulation of symp nervous system below lesion (due to noxious stimulus)
neuropathic bladder dysfunction treatment: maintain bladder safety
an unsafe bladder is one that puts kidneys at risk
risks= raised bladder pressure, vesico-ureteric reflux, chronic infection
neuropathic bladder dysfunction treatment: symptom control
harness reflexes to empty bladder into incontinence device
suppress reflexes converting bladder to flaccid type, then empty regularly
bladder problems in MS
caused by neurogenic detrusor overactivity overactive bladder syndrome urinary urgency frequency incomplete bladder emptying
prostate tumours
most common male malignancy
majority are adenocarcinomas in peripheral zone and slow growing
prostate tumours: epidemiology
6th most common in world
incidence increases with age
by 80 y/o, 80% have malignant foci but most seem to lie dormant
prostate tumours: aetiology
hormonal factors- increased testosterone
prostate tumours: risk factors
family history (3 or more affected relatives)
genetic (BRCA2 confers a 5/7x higher risk)
increasing age
being black- higher testosterone
prostate tumours: pathophysiology
androgen receptors on prostate are responsible for growth
local spread= seminal vesicles, bladder and rectum
spread via lymph
haematogenous spread= bone or brain, liver and lung
prostate tumours: presentation
LUTS if local disease suggestions of metastasis: weight loss bone pain anaemia
prostate tumours: differential diagnosis
BPH
prostatitis
bladder tumours
prostate tumours: investigations
hard and irregular prostate on digital exam
raised PSA
trans-rectal ultrasound
urine biomarkers
prostate tumours: treating disease confined to prostate
radical prostatectomy if <70 y/o
radiotherapy and hormone therapy
brachytherapy
surveillance if >70 y/o and low risk
metastatic prostate tumours: endocrine therapy
prostate cancer is hormone sensitive
binding androgen receptor stimulates tumour growth
choice of androgen deprivation or receptor blockers (bicalutamide)
metastatic prostate tumours: androgen deprivation
orchidectomy- removal of testes
LHRH agonists- stimulate and inhibit pituitary gonadotrophin (testosterone)
prostate tumours: symptom treatment
analgesia
treat hypercalcaemia
radiotherapy for bone metastases/spinal cord compression
renal cell carcinoma
aka hypernephroma
arises from proximal convoluted tubular epithelium
renal cell carcinoma: epidemiology
most common renal tumour in adults
more common in males
more common in >50 y/o
25% have metastases on presentation
renal cell carcinoma: risk factors and aetiology
smoking obesity hypertension renal failure and haemodialysis von hippel lindau syndrome
renal cell carcinoma: von hippel lindau syndrome
autosomal dominant on chromosome 3 short arm
loss of both copies of tumour suppressor gene
renal cell carcinoma: pathophysiology
malignant cancer of proximal convoluted tubular epithelium
spread may be direct (renal vein), via lymph or haematogenous (bone, liver, lung)
renal cell carcinoma: presentation
asymptomatic and discovered incidentally haematuria anorexia hypertension in 30% (renin secretion by tumour) fever in around 20%
renal cell carcinoma: differential diagnosis
transitional cell carcinoma
wilms’ tumour
renal oncocytoma
renal cell carcinoma: investigations
ultrasound CT abdo MRI BP bloods renal biopsy bone scan
renal cell carcinoma: CT imaging
more sensitive than ultrasound in detecting small renal mass
shows involvement of the renal vein or IVC
using contrast demonstrates kidney function
renal cell carcinoma: blood test
FBC- detect polycythaemia and anaemia- EPO decrease
ESR can be raised
liver biochemistry may be abnormal
renal cell carcinoma: treating localised
nephrectomy- remove kidneys (unless bilateral then partial nephrectomy)
renal cell carcinoma: ablative techniques of treatment
such as cryoablation and radiotherapy are used in patients with significant comorbidities who wouldn’t tolerate surgery
can harm kidney function
renal cell carcinoma: treating metastatic or locally advanced
interleukin-2 and interferon alpha: cause remission in 20%
if no response:
-biological angiogenesis targeted therapy (sunitinib, sorafenib)
-temisorlimus: improves survival more than interferon
Wilms’ tumour: pathology
childhood tumour of primitive renal tubules and mesenchymal cells
Wilms’ tumour: epidemiology
seen w/i first 3 years of life
chief abdo malignancy in children
Wilms’ tumour: presentation
abdominal mass
less common= haematuria
Wilms’ tumour: investigations
diagnosis is established by ultrasound, CT and MRI
Wilms’ tumour: treatment
combination of nephrectomy, radiotherapy and chemo
bladder cancer
transitional cell carcinoma
calyces, renal pelvis, ureter, bladder and urethra are all lined by transitional epithelium so all susceptible
but bladder is most common
bladder cancer: epidemiology
50% of TCC
4th most common cancer in men, 8th in women
mainly occurs >40 y/o, peaks >80 y/o
bladder cancer: risk factors
smoking chronic inflammation of urinary tract increased age male family history paraplegia exposure to drugs- phenacetin occupational exposure- benzidine
bladder cancer: pathophysiology
> 90% TCCm 5% squamous cell carcinoma, <1% adenocarcimona
tumour spread:
local= to pelvic structures
lymphatic= iliac and para-aortic nodes
haematogenous= liver and lungs
bladder cancer: presentation
painless haematuria is most common symptom
recurrent UTIs
voiding irritability
bladder cancer: differential diagnosis
haemorrhagic cystitis
renal cancer
UTI
urethral trauma
bladder cancer: investigations
cystoscopy with biopsy urine microscopy CT urogram urinary tumour markers MRI
non muscle invasive bladder cancer: treatment
surgical resection
possible chemo to reduce recurrence- mitomycin, doxorubicin and cisplatin
localised muscle invasive bladder cancer: treatment
radical cystectomy- bladder removal
post-op chemo- methotrexate, vinblastine, adriamycin and cisplatin (M-VAC)
radical radiotherapy if not fit for surgery
metastatic bladder cancer: treatment
palliative chemo and radiotherapy
testicular tumours: epidemiology
most common cancer in males 15-44 y/o
10% occur in undescended testes
96% from germ cells
testicular tumours: germ cell origin
seminomas: 25-40 y/o and >60y/o
teratomas: infancy
testicular tumours: non-germ cell origin
leydig cell tumours
sertoli cell tumours
sarcomas
testicular tumours: risk factors
undescended testes
infant hernia
infertility
family history
testicular tumours: presentation
painless lump in testicle testicular pain abdo pain cough and dyspnoea abdo mass
testicular tumours: differential diagnosis
testicular torsion
lymphoma
hydrocele
epididymal cyst
testicular tumours: investigations
ultrasound
biopsy
CXR and CT for staging
serum tumour markers
testicular tumours: serum tumour markers
alpha-fetoprotein and/or beta subunit of human chorionic gonadotropin:
- raised in teratomas
- B-hCG in minority with seminomas
- AFP not elevated in pure seminomas
testicular tumours: treatment
radical orchidectomy via inguinal approach
seminomas with mets below diaphragm treated with radiotherapy only
widespread tumours and teratomas= treated with chemo
sperm storage offered
kidney physiology: GFR
volume of fluid filtered from glomeruli into bowman’s space per unit time
normally 120ml/min
each kidney receives 20% of CO
kidney physiology: proximal convoluted tubule
sugars, amino acid and bicarb are reabsorbed here
absorbs 70% of Na+ and the water that follows
most vulnerable to damage
kidney physiology: faconi syndrome
rare damage resulting in: -glycosuria -acidosis -phosphate wasting resulting in osteomalacia -aminoaciduria
kidney physiology: loop of henle
reabsorbs 25% of sodium and water that follows
sodium, potassium, chloride transporters are more active in ascending loop
loop diuretics work here
kidney physiology: Distal convoluted tubule
5% sodium reabsorbed here and water follows
thiazide diuretics work here
kidney physiology: BP control
juxtaglomerular apparatus is solute sensing organ
high conc. of solutes then GFR low so releases renin
kidney physiology: collecting tubule and salts
most salt has been reabsorbed
tightly regulated by aldosterone
secreted potassium and hydrogen into urine
water absorbed via aquaporin 2 channels (controlled by ADH)
kidney physiology: aldosterone and Na+ reabsorption
hyperaldosteronism- lots of Na+ reabsorption, negative lumen, so K+ and H+ rush in and results in hyperkalaemic alkalosis
kidney physiology: potassium control
potassium freely filtered and mostly reabsorbed in proximal tubule/loop of henle
governed by distal delivery of sodium and aldosterone
kidney physiology: K+ modifying renal meds and hypokalaemia
loop diuretics
thiazide diuretics
kidney physiology: K+ modifying renal meds and hyperkalaemia
spironolactone (aldosterone antagonist)
ACE inhibitors
angiotensin receptor blockers
kidney physiology: diuretics
not nephrotoxic but cause hypovolaemia, which in itself is nephrotoxic
thiazide and loop are powerful together and result in profound diuresis
kidney physiology: water
water conc. detected through osmoreception in hypothalamus
too conc. then ADH released and cause an increase in aquaporin in collecting duct- more water absorbed
kidney physiology: erythropoietin
renal cortex= oxygen sensor- blood flow and oxygen requirement (GFR) are matched
EPO is hormone that produced haemoglobin and is produced in response to tissue hypoxia
kidney physiology: vitamin D
vitamin D hydroxylation occurs here
25-hydroxy vitamin D to 1,25-dihydroxy vitamin D (calcitriol) (active vitamin D)
chronic kidney disease
longstanding, usually progressive impairment in renal function, for more than 3 months
GFR <60ml/min/1.73m2
chronic kidney disease: epidemiology
6-11% can be defined as having CKD
more common in females
chronic kidney disease: classification
proteinuria, haematuria or evidence of abnormal anatomy or systemic disease
chronic kidney disease: aetiology
diabetes M (type 2>1) hypertension atherosclerotic renal vascular disease polycystic kidney disease amyloidosis family history idiopathic=20% cases
chronic kidney disease: risk factors
diabetes M hypertension old age females>males proteinuria AKI smoking african/asian chronic NSAIDs usage
chronic kidney disease pathophysiology
nephrons are failed and scarred so burden of filtration falls to fewer nephrons
these experience increased flow (hyperfiltration) as blood flow is unchanged so undergo glomerular hypertrophy
it’s a vicious cycle and accelerates remnant nephron failure
chronic kidney disease: presentation
early stages are asymptomatic symptoms common when serum urea conc. exceeds 40mmol/L: -malaise -anorexia -insomnia -polyuria -itching -nausea/vomiting -oedema
chronic kidney disease investigations: anaemia
normochromic normocytic
due to reduced erythropoietin produced by kidneys
chronic kidney disease investigations: bone disease
bone pain
renal osteodystrophy- osteoporosis, osteomalacia
renal phosphate retention and impaired 1,25-dihydroxy vitamin D production
chronic kidney disease investigations: neurological
occurs in all patients with sever CKD
autonomic dysfunction presents as postural hypotension and disturbed GI motility
in advance uraemia there is depressed cerebral function, twitching and seizures
chronic kidney disease investigations: CVD
MI, cardiac failure and stroke
due to increased frequency of hypertension, hyperlipidaemia and vascular calcification
chronic kidney disease complications: skin disease
pruritus due to nitrogenous waste products of urea
brown discolouration of nails
chronic kidney disease: differential diagnosis
AKI
differentiation depends on history, duration of symptoms and measurements of serum creatinine
chronic kidney disease investigations: urinalysis
haematuria- indicates glomerulonephritis
proteinuria- suggestive of glomerular disease or infection
mid stream sample sent for microscopy
chronic kidney disease investigations: serum biochemistry
urea, electrolytes, bicard and reatine
low eGFR
raised alkaline phosphatase
raise PTH if CKD stage 3+
chronic kidney disease investigations: bloods
raised phosphate low Ca2+ Hb low raised viscosity fragmented red cells indicate intravascular haemolysis
chronic kidney disease investigations:urine microscopy
white cells- bacterial UTI
eosinophilia- allergic tubulointerstitial nephritis
granular casts- active renal disease
red cells- glomerulonephritis
chronic kidney disease investigations: imaging
ultrasound to check renal size and to check for obstructions
CT to detect stones, retroperitoneal fibrosis and other causes of obstruction
chronic kidney disease treatment: aims
aimed at underlying cause
slow the deterioration of kidney function
reduce CVS risk
treat complications
chronic kidney disease treatment: treat reversible causes
relieve obstruction stop nephrotoxic drugs stop smoking become healthy weight tight glucose control in diabetes
chronic kidney disease treatment: control BP
target= <130/80
ACE inhibitors- ramipril
diuretic- oral bendroflumethiazide, prevents hyperkalaemia and reduce BP
chronic kidney disease treatment: limit bone disease
check PTH and treat if raised
restrict diet
give phosphate binders to decrease gut absorption and avoidance of phosphate food
vitamin D and calcium supplements
chronic kidney disease treatment: limit CVD complications
lower cholesterol with statins
give aspirin
chronic kidney disease treatment: controlling symptoms
anaemia- iron/folate/folic acid
acidosis- treat with sodium carbonate
oedema- furosemide
chronic kidney disease treatment: RRT
renal replacement therapy: haemofiltration haemodialysis peritoneal dialysis replacement
chronic kidney disease treatment: indications for dialysis
symptomatic uraemia-pericarditis or tamponade hyperkalaemia not controlled pulmonary oedema severe acids high potassium metabolic acidosis