urology Flashcards
nervous supply of the ureters
autonomic nervous system
lymphatic drainage of ureters
left: left para aortic lymph nodes
right: right paracaval and interaortocaval lymph nodes
blood supply of ureter
upper part: gonadal and renal
middle part: common iliac and branches of abdominal aorta
distal part: superior vesicle
in which 3 locations is the ureter narrowed
pelvic ureteric junction
pelvic brim
where it enters the bladder wall
3 layers of ureter
outer: fibrous
middle: muscle
inner: epithelium
which class of organ is the bladder
when empty = pelvic organ
when distended = abdomen-pelvic organ (as rises when it fills)
3 layers of bladder
outer: loose connective tissue
middle: smooth muscle and elastic fibres
inner: transitional epithelium
blood supply and venous drainage of bladder in females
superior and inferior vesical branches of the internal iliac artery
drained by vesical plexus which drains into internal iliac vein
lymphatic drainage of bladder
internal iliac nodes then paraaortic nodes
bladder nervous supply
autonomic nervous system
describe the internal and external urethral sphincters
internal
- at neck of bladder
- thickened detrusor muscle
- smooth muscle
- involuntary control
external
- at external urethral orifice
- skeletal muscle
- voluntary control
blood supply of urethra in females
internal pudendal arteries and inferior vesicle branches of the vaginal arteries
lymphatic drainage of urethra in females
proximal urethra: internal iliac nodes
distal urethra: superficial inguinal nodes
nervous supply of urethra in females
vesical plexus and pudendal nerve
blood supply and venous drainage of bladder in males
supplied by superior and inferior vesical branches of internal iliac artery
drained by prostatic venous plexus which drains into internal iliac vein
3 lobes of prostate
left lateral
middle
right lateral
prostate blood supply and venous drainage
supplied by inferior vesical artery
drained via prostatic plexus to the vesical plexus and internal iliac vein
lymph drainage of prostate
internal and sacral nodes
prostate nervous supply
autonomic nervous system
3 parts of male urethra
prostatic
membranous
spongy
blood supply of male urethra
prostatic - inferior vesical artery
membranous - bulbourethral artery
spongy - internal pudendal
lymph drainage of male urethra
prostatic and membranous - obturator and internal iliac nodes
spongy - superficial and deep inguinal nodes
nervous supply of male urethra
prostatic plexus
what stimulates/inhibits ADH production/secretion
stimulated by
- increased plasma osmolarity
- hypovolaemia
- hypotension
- nausea
- Angiotensin II
- nicotine
inhibited by
- decreased plasma osmolarity
- hypervolaemia
- hypertension
- ANP
- ethanol
which urea transporters does ADH/vasopressin increase the numbers of
UT-A1
UT-A3
which water channels does ADH regulate the numbers of
aquaporin 2 and aquaporin 3
where is ADH produced and stored
produced in hypothalamus (neurons in supraoptic and paraventricular nuclei)
stored in posterior pituitary
treatment for central diabetes insipidus
external ADH
treatment for SIADH
non peptide inhibitors of ADH receptor (eg conivaptan, tolvaptan)
treatment for nephrogenic diabetes insipidus
thiazide diuretics and NSAIDs
symptoms for SIADH
hyperosmolar urine
hypervolaemia
hyponatraemia
what is the problem in nephrogenic diabetes insipidus
less/mutant AQP2 receptors
mutant V2 receptors
which cell in the DCT and CD becomes very important during alkalosis and why
beta intercalated cell
mediates H+ reabsorption and HCo3- secretion
mechanism of action of ADH
binds to V2 receptor
stimulates G protein signalling cascade
G protein activates adenylate cyclase which catalyses conversion of ATP into cAMP
cAMP leads to protein kinase A production which causes AQP2 production
AQP2 inserts into the apical side of the cell
ADH can also increases AQP3 numbers which insert onto basolateral side of cell
does urea concentration have an effect on ADH production
no
which part of nephron is potassium secreted
distal nephron
which compartment has the most fluid in the body
intracellular
contrast positive and negative water balance
positive water balance: have too much water - produce hypoosmotic urine
negative water balance: have too little water - produce hyperosmotic urine
describe countercurrent multiplication
water entering loop of Henle is iso-osmotic to medullary interstitium
salt is actively reabsorbed in ascending limb, increasing the osmolarity of the medullary interstitium
this causes water to be passively reabsorbed in the descending limb
new water comes in and pushes this water along, process is continual
end up with an osmotic gradient in the medullary interstitium: most osmotic at bottom of loop of Henle so most water is reabsorbed there
describe urea recycling
ADH increases number of UT-A1 and UT-A3
urea leaves collecting duct via UT-A1(apical) and UT-A3 (basolateral)
the urea is now in the medullary interstitium and can either
1) re enter nephron via UT-A2
2) enter blood via UT-B1
this maintains a concentration of urea in the medullary interstitium, which allows water to be reabsorbed
how does ADH support Na+ reabsorption
increases Na+ 2Cl- K+ symporter in thick ascending limb
increases Na+ Cl- symporter in DCT
increases Na+ channels in collecting duct
what is antidiuresis and when does it happen
concentrated urine in low volume excretion
when there is high ADH
treatment for SIADH
non peptide inhibitor of ADH
- conivaptan
- tolvaptan
normal ECF concentration of bicarbonate
24 mEq/L
what is the role of kidneys in acid base balance
excretion and secretion of H+
reabsorption of bicarbonate
production of new bicarbonate
how much of the bicarbonate freely filtered into the kidneys is reabsorbed
almsot 100%
where is most of the bicarbonate reabsorbed in the kidneys
proximal convoluted tubule
what is henderson hasselbalchs equation
[H+] = (24 x PCo2) / [HCo3-]
contrast the functions of the alpha and beta cells of the DCT and collecting duct
alpha = bicarbonate reabsorption, H+ excretion
beta = H+ reabsorption, bicarbonate excretion
(beta cells becomes. esp important during alkalosis)
what is the compensatory mechanism for respiratory alkalosis, respiratory acidosis, metabolic alkalosis, metabolic acidosis
met alkalosis: decrease ventilation, increase bicarbonate excretion
met acidosis: increase ventilation, increase bicarbonate production and reabsorption
resp alkalosis: intracellular buffering (acute), decrease bicarbonate reabsorption and production (chronic)
resp acidosis: intracellular buffering (acute), increase bicarbonate reabsorption and production (chronic)
what is an osmole
1 osmole = 1 mole of dissolved particles per litre
what is the concentration of ECF
290 mosm/L (milli osmoles per litre)
what is the normal osmolarity of plasma
285-295 mosm/L
describe central and peripheral regulation of sodium intake
central:
via lateral parabrachial nucleus
- in conditions of Na+ deprivation: increases appetite for Na+ via GABA and opioids
- in conditions of euvolemia: decreases Na+ intake via serotonin and glutamate
where is most water and Na+ reabsorbed
PCT
how to calculate GFR from RPF (renal plasma flow)
GFR = 0.2 x RPF (because approximately 20% of renal plasma enters tubular system)
what is the best way to retain sodium
filter less
what is aldosterone released in response to
angiotensin II
or
low bp
what are the effects of aldosterone
increases sodium reabsorption
increases potassium and H+ excretion
what is the effect of excess aldosterone
hypokalaemic alkalosis
what is the filling and voiding stage of urination
filling: urethral sphincter sphincter closed, detrusor muscle fills and distends without a rise in intravesical pressure
voiding: muscle contracts, upper urethral sphincter relaxes, urethra opens
describe the process of micturition
bladder fills and stretches
M3 receptors on detrusor muscle are stretched
S2- 4 parasympathetic fibres release ACh which acts on the M3 receptors, activating them and causing detrusor muscle to contract
the fibres also inhibit internal urethral sphincter, relaxing it and causing it to open
after bladder is emptied, M3 receptors are no longer stretched so are deactivated
T11- L2 sympathetic fibres release noradrenaline which acts on Beta 3 receptors, causing detrusor muscle to relax
risk factors for stress incontinence
age
obesity
smoking
pregnancy
rout of delivery
investigations for stress incontinence
stress test
urodynamics - check for urination during an increase in intra abdominal pressure (eg cough) WITHOUT detrusor muscle contractions
treatments for stress incontinence
FIRST: physio with pelvic floor examinations
if the issue is increased urethral mobility: colposuspension or mid urethral sling
if the issue is impaired urethral closing: periurethral bulking agents
causes of stress incontinence
impaired urethral closure
impaired urethral and bladder support
what is overactive bladder and what are the causes
involuntary contractions of detrusor muscle causes urinary urgency and frequency and nocturia, can be with or without urinary urge incontinence
causes: idiopathic, neurogenic, outlet obstruction (irritates the muscle so causes inappropriate contractions)
what do you need to exclude if you think the diagnosis may be overactive bladder
infection via dip stick and MC&S
prolapse for women
enlarged prostate for men
treatment for overactive bladder
lifestyle changes
bladder retraining
antimuscarinics
beta 3 agonists
botox
neuromodulation (S3)
surgical: augmentation cystoplasty and urinary diversion
what is overflow incontinence and what are the causes
chronic retention leading to over flow
- outlet obstruction (BPH or faecal impaction)
- neck of bladder stricture
- urethral stricture
- under-active detrusor muscle –> atonic bladder
- DHx (dihydrexine) alpha adrengerics, anticholinergics, sedatives
- dennervation following surgery
what is continuous incontinence and what are the causes
continuous involuntary urination
due to vesicovaginal fistula or ectopic urethra (into vagina or ureter)
what is BPH and how does it cause lower urinary tract symptoms
benign overgrowth of lateral and medial lobes of prostate due to effects of testosterone, compressing urethra and obstructing outflow
what are the lower urinary tract symptoms caused by BPH
hesitancy
poor flow
dribbling post micturition
frequency and nocturia
acute retention
what do you need to exclude before diagnosing BPH
cauda equina
bladder or prostate cancer
high pressure chronic retention
BPH investigations
urodynamics
post void reisdual volume
void diary
bloods: check PSA levels –> indicative of prostate size
USS
cystoscopy to check for cancer
BPH investigations
urodynamics
post void reisdual volume
void diary
urine dipstick
bloods: check PSA levels –> indicative of prostate size
USS
cystoscopy to check for cancer
BPH treatments
1) lifestyle changes:
lose weight, avoid constipation. reduce caffeine and fluid intake in evening
2) medication:
- alpha blockers –> alpha 1 adrenergic receptors are found on prostate stromal smooth muscle and neck of bladder. Blocking these can cause relaxation of the muscles
- 5 alpha reductase inhibitors: block the conversion of testosterone to DHT. This prevents prostate growth
3) TURP: transurethral resection of prostate
complications of untreated BPH
chronic painless retention and overflow incontinence
chronic renal failure (urine goes back up ureters and damages kidneys)
how is micturition different in adults vs infants
infants: it is a local spinal reflex
adults: higher control centre can keep external urethral sphincter closed until it is appropriate to urinate –> pudendal nerve causes contraction of the sphincter
overactive bladder risk factors
age
prolapse
IBS
bladder irritants eg caffeine, nicotine
increased BMI
what kind of cancer is the most common kidney cancer
renal cell carcinoma: adenocarcinoma
features of kidney cancer
painless visible haemturia / persistent microscopic haematuria
palpable mass
loin pain
metastatic disease symptoms eg bone pain, haemoptysis
what do renal function blood tests show for haemturia
anaemia (low rbc)
high calcium
high liver enzymes
investigations for painless visible haematuria
flexible cystoscopy
CT urogram
renal function test
investigations for painless visible haematuria
flexible cystoscopy
CT urogram
renal function test
investigation for invisible haemturia
flexible cystoscopy
US of KUB (kidney, ureter, bladder)
investigations specifically for suspected kidney cancer
CT renal triple phase
staging CT chest
bone scan if symptomatic
kidney cancer management
partial or radical nephrectomy
if tumour is small and can’t do surgery on the pt: cryosurgery (freeze it, put needle in and oblate it)
metastatic disease: receptor tyrosine kinase inhibitors
what kind of cancer is the most common bladder cancer
transitional cell carcinoma
features of bladder cancer
painless visible haematuria
persistent invisible haematuria
suprapubic pain
lower urinary tract symptoms and UTI
metastatic disease features: bone pain, lower limb swelling
investigations for bladder cancer
if visible haematuria: flexible cystoscopy, CT urogram, renal function test
if non visible: flexible cystoscopy, US KUB
also do biopsy: cystoscopy + transurethral resection of bladder lesion (but this is also treatment as you remove the cancerous tissue then send it for biopsy)
bladder cancer management
cystoscopy + transurethral resection of bladder lesion (to remove cancer and also test it as you send the tissue off as a biopsy)
if non muscle invading
- cystoscopic surveillance
- chemotherapy
- BCG (immunotherapy)
if muscle invading
- radiotherapy
- chemo therapy
- cystectomy
- palliative treatment
what kind of cancer is the most common prostate cancer
adenocarcinoma
features of prostate cancer
asymptomatic unless metastasises
investigations for prostate cancer
bloods: check for high PSA (although this isn’t specific for prostate cancer - can be high in other things too eg infection, BPH)
MRI and THEN a biopsy
transperineal prostate biopsy
bladder cancer management for a high grade and low grade cancer in a young and fit pt vs an old and unfit
young and fit:
- high grade: radical prostatectomy / Radiotherapy
- low grade: active surveillance - biopsy, PSA, MRI
old and unfit
- high grade: hormone therapy
- low grade: watchful waiting - regular PSA testing
prostate cancer treatment side effects
surgical prostatectomy carries a risk of damaging proximal urethral sphincter and also cavernous nerves
- risk of incontinence and erectile dysfunction
risk factors for prostate cancer
increasing age
westen - scandenavian - countries
African american ethnicity
why is transperineal prostate biopsy used instead of transrectal
less risk of infection
more able to sample all areas of the prostate
what are the 6 types of germ cell tumours in testicular cancer
seminoma
spermatocytic seminoma
teratoma differentiated
embryonal carcinoma group
yolk sac tumour
choriocarcinoma
(the first two are seminomatous germ cell tumours, the last 4 are non seminomatous germ cell tumorus)
what are the 5 types of sex cord/ gonadal stromal tumours in testicular cancer
leydig cell tumour
granulosa cell tumour
Sertoli cell tumour
tumours of fibroma / thecoma
mixed tumours
what are stages 1A, 1B and 1S in testicular cancer
1A: no signs of local invasion or metastases. serum tumour markers are normal after orchiectomy (testes removal)
1B: signs of local invasion but not of metastases
1S: signs of local invasion and of metastases - serum tumour markers are still abnormally high after orchiectomy
what are the 3 principal serum tumour markers in testicular cancer
AFP: alpha fetoprotein
HCG: beta subunit of human chorionic gonadotrophin
LDH: lactate dehydrogenase
what kind of cancers is alpha fetoprotein tumour marker found in
teratomatous germ cell tumour with a yolk sac component
what kind of cancers is HCG tumour marker found in
germ cell tumours containing syncitiotrophoblast cells
all choriocarcinomas
some seminomas
what kind of cancers is LDH tumour marker found in
not specific to any type
how to approach the diagnosis of testicular cancer
ultrasound
biopsy
surgery and chemo
assess serum tumour markers to stage the cancer
check surrounding structures/ lymph nodes
instruct pt how to do regular self examination
what is the difference in how you should treat seminoma germ cell tumours vs non seminoma germ cell tumours
seminoma germ cell tumours respond well to radiotherapy, non seminoma tumours do not
name some penile disorders which can make it hard for erection
tight frenulum - hard for tip to come out
phimosis - tight skin which is difficult retract
para-phimosis - skin retracts but is stuck in retracted position
how to fix para phimosis
manual pressure
dextrose soaked gauze
dundee technique
dorsal slit
what is genital lichen sclerosis and how does it present
chronic inflammatory dermatosis
- phimosis
- meatal stenosis - spraying of stream
- urethral stricture
- from white plaques with epidermal atrophy and scarring
- red cracked blistered bleeding skin
management of genital lichen sclerosis
non soap wash eg dermal
emollients
barrier cream
very strong topical steroids eg dermovate
weight loss
treatment for erectile dysfunction as a result of radical prostatectomy
PDE5 inhibitors
prostaglandin E1 injections
penile prosthesis devices
treatment for incontinence as a result of radical prostatectomy
build pelvic floor muscles
artificial urethral sphincter implants
what should the PSA level be after prostatectomy
<0.01 ng/ml (higher = relapse)
two models used to convert creatinine into GFR
MDRD - modification of diet in renal disease
CKD-EPI - CKD epidemiology collaboration
what is the Kidney failure risk equation
an equation used to predict the chance of needing a kidney transplant in 2-5 years in someone with stable CKD
takes into account age, sex, eGFR, ACR
used to improve pt understanding of their disease and to identify high risk pts
what are two precautions CKD pts should take when it comes to blood giving and receiving
shouldn’t receive any blood transfusions as could make a future transplantation be rejected
if having blood taken, don’t let them put it into antecubital fossa as this is needed for dialysis of they need that in the future, use veins on back of hand instead
is urea a good method of assessing GFR and why
no
confounded by diet, catabolic state, liver enzymes, drugs, GI bleeding
is creatinine a good method of assessing GFR and why
trend is useful in context of that particular patient
as it is confounded by age, sex, muscle mass, race
is creatinine clearance good method of assessing GFR and why
no
difficult for older people to take measurements
over estimates GFR at low GFRs
are radionuclide studies a good method of assessing GFR and why
yes
reliable but expensive
is inulin clearance a good method of assessing GFR and why
difficult/long to do
so used only in research
initial management for kidney failure
fix fluid balance
- hypovolaemia = give fluids
- hypervolameia = diuretics
fix hyperkalaemia
- drive into cells = sodium bicarbonate, insulin dextrose
- excrete = diuretics
- increase GI absorption = potassium binders
conservative management for kidney failure
(after fixing fluid and potassium balance)
EPO injections
phosphate binders
vit D supplements
how does kidney failure cause hyperparathyroidism
CKD
–> 1,25 vit D deficiency and phosphate retention
–> hypocalcaemia
–> hyperparathyroidism
how does kidney failure cause anaemia
reduced EPO production
what is the arterial blood gas in kidney failure
metabolic acidosis with respiratory compensation
how does kidney failure cause hyperkalaemia
1) acidosis: H+ ions move into cell and drive K+ out of cell
- get muscle catabolism and anorexia
2) reduced excretion of K+ in kidneys
- cardiac arrhythmias
- muscular and neural effects
- vomiting
hyperkalaemia on ECG
peaked t waves
broadened or disappearing p waves
wide QRS
asystole
heart block
what is Kussmauls respiration
in kidney failure, H+ is high
so it is converted H+ + HCO3- –> H2Co3 –> H20 + CO2
high CO2 causes increased resp rate
what causes increased CVD risk in kidney failure
reduced EPO - anaemia
reduce 1,25 vit D - hypocalcaemia, hyperparathyroidism
contrast haemodialysis and peritoneal dialysis
haemodialysis:
blood then out of your body and filtered outside via a dialyse filled with dialysate
need to go to a centre for it - 3/4 hrs 3 days a week
strict dietary restrictions
need an access point: either a arteriovenous fistula does under anaesthetic or a central venous line –> risk of bacteraemia
peritoneal dialysis:
blood is filtered inside your body - dialysate is drained in and then out
can do at home, work, travelling
2/3 hrs 7 days a week
less dietary restrictions
risk of infection
what 3 things are done to check if a kidney is able to be donated
blood type compatibility
HLA (human leukocyte antigen) typing
serum cross matching
what should pt avoid after a kidney transplant
alcohol
smoking
recreational drugs
live vaccines
NSAIDs
raw meat/fish etc
seville oranges, grapefruit, earl grey tea –> interact with immunosuppressants
why do most diuretics increase potassium excretion
they increase flow rate
this is detected int he collecting duct and stimulates K+ excretion
