urology Flashcards
urinary tract calculi, definition, overview. epidaemiology
crystal aggregates- solutes precipitate out of the urine and form crystals. form and can be deposited anywhere.
classic sites- pelviuteric junction, pelvic brim. vesicouteral junction.
peak age is 20-40- male predominance
risk factors for pelvic stones
diet- chocolate, tea, rhubarb, strawberries, spinach, nuts
vitamin D levels (varies calcium and oxalate levels)
dehydration
certain medications (diuretics, antacids, acetazolamide, steds, theophylline)
renal tubule acidosis
urinary tract abnormalities
stents, catheters
family history
hypomagnaesia
types of stone
calcium oxalate> Ca binds to -ve oxalate. (acidic urine predisposes) - most common stone
calcium phospoate> Ca binds phosphate (alkaline urine)
magnesium ammonium phosphate / struvite > caused by UTI (dirty white colour) (bacteria have caused ammonia, which makes it more alkaline)
urate crystals- hyperuricaemia -> smooth brown and RADIOLUCENT
Cyctine- rare- renal tube defect causing leakage. semi opaque.
signs and symptoms of renal stones
Ix for stones
larger stones that cant pass- asymptomatic until haematuriea/ recurrent UTI
v painful renal colic
loin to groin
N+V+Fever
Ix: urine dipstic- +ve blood, nitrates, leucocites
24hr calcium, oxalate, urate, citrate
Gold standard CT KUB,
USS useful in pregnant, or follow up of known stone.
management of stones
is < 5mm it will probably pass- no need to admit–>
if bigger: analgesia( para, codiene) IV fluids, abx. A-adrenic blockers + calcium channel blockers.
extracorporeal shockwave lithotripsy.
last line- perc nephrolithomy/ stent.
only operate if sig infection or obstruction.
nephrostomy -> bypass obstruction.
hpertension is risk factor of kidney that has been damaged by obtruction/ infection.
urinary retention, classification, pathophys, S+S.
Acute- painful
chronic is the painless inability to pass urine.
High pressure chronic- high detrusor muscle pressure at micturition- bladder outflow obstruction–> B/L hydronephrosis + renal issues
low pressure chronic- no impaired kidney function. reduced/ absent detrusor/ compatent valves.
S+S:
overflow- nocturnal emesis (sphincter tone reduction)
weak stream, hesitancy
pain
abdo swelling- with the ability to palpate below the mass.
investigation and management of urinary retention
PR- check prostate/ constipation
bladder scan- post void
urine dip
bloods
US renal tract (bladder vol, hydronephrosis)
Mx:
analgesia if acute
catheterise- acute + chronic (if over 3-500) (long term for high pressure, short term for low pressure) TWOC low pressure and acute in >72 hrs.
if large volume comes out- then monitor for post-obstructive diuresis (loss of kidney conc grad- loads of dilute urine- need IV fluids)
laxative if constipation
Acute retention- Tamsulosin (alpha-1 antag)
common causes of acute and chronic urinary retention.
complications of urinary retention
BPH, Urethral strictures, prostate cancer, constipation, penvic prolapse, pelvic masses.
peripheral neuropathies/ central neuropahties.
UTI can cause urethral sphincter to close. , pain can caue people to enter retention. medications (anti-muscarinic)
chronic kidney injury can occur if it backs up, causing HTN and other issues. stones can also form.
prostate cancer overview, risk factors
most are adenocarcinomas arising from epithelial cells in the acini/ ducts of the gland. usually arizes in the periferal zone of the prostate, usually lots of round acinar structures.
Asymptomatic premalignant lesion –> prostatic intraepithelial neoplasia (PIN)
PIN is not inevitable to go to adenocarcinoma.
Risk factors: Age, afro-carribean, BRCA, Lynch syndrome.
prostate cancer epidaemiology and signs and symptoms
1 in 3 will develop it.
simalar to BPH, can also include haematuria, errectile dysfunction.
back pain from bony mets which are, unusually, OSTEOSCLEROTIC
prostate cancer Ix + RX
PSA test BEFORE DRE
DRE- ca prostate feels hard, asymmetrical, irregular, loose central sulcus.
MRI- will show lesion –>
TRUS (trans rectal ultrasound guided biopsy) - GOLD STANDARD- biopsy 12 areas.
Rx: difficult decisions as most will not be a problem
Curative: radical prostatectomy- rejoin urethra to bladder. – ED + incontinance comon.
radical radiotherapy/ brachytherapy (radioactive pods put into prostate)
if not significant enough- active surveilance (low psa <10, gleason 3+3, smol proportion of 12 biopsy contain cancer)
non surgical management of prostate cancer.
androgen depravation - surgical castration, anti androgens or LH-RH agonists
goserelin- GnrH agonist initially causes flare, but then causes upregulatoin of LH receptors and so long term reduciton in symptom effects
discuss gleason scoring for prostate cancer
tumor given 2 scores according to apperance (the 1st and 2nd most common cell scores)
2 scores are added up
3 + 3 is good
7 is intermediate
8+ is aggrressive worse prognosis.
bladder cancer overview (types) and risk factors
urothelial carcinomas –> transitional cell carcinoma (TCC).
more rare are squamous cell carcinoma (related to schistosoma infection)
RF:
Smoking
male
65-69
exposure to certain industrial dyes and solvents (rubber textiles, plastics)
discuss the staging of bladder cancers and what constitutes low risk and high risk bladder cancer.
TNM- as bladder is hollow- depth into muscle penetration is important in the T stage
Ta/1 - superficial tumors
Muscle invasive tumors T2,3,4.
Carcinoma in situ (CIS)
Low risk (Ta/1) 80% of cancers. dont invade detrusor. - frond like papillary growths. very high chance of recurrance
CIS- Flat and hard to identify. high chance of progression to invasive muscle cancer. - diagnosis with this is worse than low risk. TP53 and RB1 associated.
high risk 20%- muscle invasive, solid, always high grade. Tp53, RB1 mutations. poor prognosis
types of germ cell tumors in testicular cancer and the charicteristics of each, treatments for each also.
Non-seminomatous tumor origins.
Yolk sac tumour
Choriocarcinoma
Teratoma
Embryonal carcinoma
Seminoma in combination with one or more of the above.
investigation of testicular lumps
how is testicular cancer staged
benign prostatic hyperplasia summary
overgrowth of prostatic tissue in the transition zone of the gland.
large nodules form
generally due to hormonal imbalance (osestrogen levels increace with age)
progressive bladder outflow obstruction.
detrusor needs to hypertrophy (can be visible as traberculations)
eventually detrusor decompensates relaxes and becomes a big fatty sack (chronic retention)
can lead to hydronephrosis + kidney injury + obstructive nephropathy.
vicious cycle in oestrogen release- causes increaced androgen receptor expression in prostate–> increaced androgens in prostate –> increaced growth of stromal and epithelial cells –> increaced androgen levels etc etc
