Urology Flashcards

1
Q

voiding vs storage LUTS

A

voiding - hesitancy, poor stream, terminal dribbling

storage - nocturia, urgency, frequency

NB normal frequency = 4-7 times per day

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2
Q

phimosis vs paraphimosis

A

phimosis = foreskin cannot be retracted

paraphimosis = can’t be pulled back up

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3
Q

Peyronie’s disease

A

due to inflammation and fibrosis of the tunica cavernosum - segments of scar tissue builds up under the skin of the penis so that it bends

is likely caued by minor injury to the penis

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4
Q

what sort of cancer is penile carcinoma

A

squamous cell carcinoma

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5
Q

benign prostate hyperplasia vs benign prostate enlargement

A

BPH - biopsy (although not routine) shows signs of hyperplastic changes

BPE describes enlargement of the prostate via BPH

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6
Q

5 causes of voiding LUTS

A

BPH/BPE - most common
drugs with antimuscurinic action - TCAs, sedating antihistamines, oxybutynin
diabetic autonomic neuropathy and neurogenic bladder
urethral stricture + phimosis
prostate/bladder/rectum cancer

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7
Q

causes of overactive bladder

A
-	Weak pelvic muscles
o	E.g. due to pregnancy + childbirth 
o	This can cause the bladder to sag out of its normal position
-	Nerve damage – brain telling the bladder to contract when it shouldn’t 
o	Pelvic or back surgery
o	Herniated disc
o	Radiation
o	PD
o	MS
o	Stroke 
-	Medications, alcohol and caffeine
-	Infection – can irritate the nerves 
-	Excess weight
o	Being overweight places extra pressure on your bladder. This can lead to urge incontinence.
-	Oestrogen deficiency after menopause
-	Often idiopathic
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8
Q

drugs that can cause nocturnal polyuria

A

CCBs
diuretics
SSRIs

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9
Q

drugs that can cause stress incontinence

A

increase urine production - alcohol, caffeine, diuretics
relax bladder outlet and urethra - alpha blocker
Can cause urinary retention, which may result in overflow incontinence (for example sympathomimetics [such as pseudoephedrine], drugs with an antimuscarinic action [such as TCAs, sedative antihistamines, and some antipsychotics], and opioid analgesics).
Reduce awareness of the need to urinate (for example benzodiazepines and z-drugs [such as zopiclone and zolpidem]).

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10
Q

other asking about storage + voiding symptoms, what are some other important questions to ask in a urological history

A

dysuria
haematuria
suprapubic pain or discomfort
fluid intake and types of fluid

PMH:
history of pelvic surgery or pelvic radiotherapy 
history of spinal surgery or trauma 
PD or diabetes 
previous urethral surgery
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11
Q

examination for someone with LUTS

A
  • Palpate the abdomen
    o Palpable bladder suggests retention of urine
    o If acute (or acute on chronic) will be painful while chronic retention is painless
    o Can also check for abdominal distension and suprapubic dullness on percussion
  • Examine the external genitalia
    o A phimosis (foreskin cannot be retracted) may result in bladder outflow obstruction, as may a carcinoma of the penis.
    o If the foreskin looks normal and is retractile examine the urethral meatus. Is it in a normal position? Is there any meatal stenosis?
    o Palpate the penis for thickening in the urethra which may indicate the presence of a urethral stricture
  • Ask the patient to turn onto his left side and examine the spine
    o Scars from spinal surgery, hairy naevus or post-natal dimple (spina bifida occulta) may suggest a neurological cause
    o Assess saddle sensation, anocutaneous reflex and anal tone
    o Abnormalities may again suggest a neurological cause for the patients LUTS
  • Assess saddle sensation
    o Anocutaneous reflex and anal tone. Abnormalities may again suggest a neurological cause for the patients LUTS
    o May also chose to do an examination of the perineum and/or LLs to evaluate their motor and sensory function
  • Perform a rectal examination
    o Look for abnormal masses
    o Faecal impaction
    o Feel for the prostate
     should feel two “lobes” with a depression, the median sulcus between them
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12
Q

example investigations for someone with LUTS

A

U+Es + eGFR - assess overall renal function
urine dipstick
- exclude UTI + check for haematuria (microscopic haematuria associated with malignancy in 7%)
IPSS
frequency volume chart for at least 3 days
urine flow test
abdominal US to check for residual urine after micturition
serum PSA
imaging of the urinary tract if history of stones or haematuria

2 week appointment if suspecting prostate cancer

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13
Q

IPSS

A

international prostate symptom severity score

made of up 7 symptom questions e.g. incopmlete empyting, urgency, weak stream, nocturia

each Q can be scored 0-5 with an overal score of 0-35

allows for a baseline assessment to allow assessment of subsequent symptom change

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14
Q

urine flow test

A

patient drinks 500-1000ml of fluid and is asked to wait until they need to void
2-3 tests should be done and max value used (Qmax)
at least 150ml should be passed for the test to be valid
measurement of the urinary flow rate allows an estimate of the probaility of bladder outflow obstruction to be made

If the Qmax rate is <10ml/sec the patient has a 90% chance of having bladder outflow obstruction

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15
Q

normal urinary flow rate

A

around 15-20ml/second although some sources says lower than this

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16
Q

normal PSA

A

<4nmol/ml (or 4 nanograms/ml) but increases with age, urinary tract infection, prostatic inflammation

upper limit varies according to age and race

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17
Q

when should you delay doing a PSA test

A

 An active urinary infection (PSA may remain raised for many months).
 Ejaculation in the previous 48 hours.
 Vigorous exercise in the previous 48 hours.
 A prostate biopsy in the previous 6 weeks

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18
Q

management of voiding symptoms

A

PATIENT EDUCATION + reassurance - can offer active surveillance
CONSERVATIVE MANAGEMENT
pelvic floor muscle training + bladder training
advise not excessively limit fluid intake (->UTIs)
limit caffeine, artifical sweeteners, fizzy drinks
use of containment products like pads, waterproof pants, external sheath
MEDICAL
of moderate to severe voiding symptoms then alpha blocker then reassess with IPSS
if enlarged prostate then 5 alpha reductase inhibitor
if voiding symptoms + enlarged prostate then both
if mixed picture with storage symptoms and voiding symptoms that persist after treatment with an alpha-blocker alone, consider adding an antimuscarinic (anticholinergic) drug
SURGICAL
TURP, TUEVAP, HoLEP, TUIP, open prostatectomy

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19
Q

alpha blockers for voiding symptoms

A

tamsulosin
alfluzosin
doxazosin
trazosin

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20
Q

5 alpha reductase inhibitors for enlarged prostate

A

finasteride

dutasteride

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21
Q

antimuscurinics for mixed picture of storage and voiding symptoms that persist despite treatment with an alpha blocker alone

A

oxybutynin
tolterodine
darifenacin

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22
Q

why shouldn’t you offer oxbutynin to older frail men

A

due to the risk of impairment of daily functioning, chronic confusion, or acute delirium

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23
Q

what is TURP

A

Uses a wire loop with electrical current flowing in one direction to excise tissue via the resectoscope

done under spinal or Ga

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24
Q

what is TUEVAP

A

transurthreal electro-vaporization of the prosate

Instead of using an electrical current loop as is done in the TURP procedure, TUEVAP uses a roller ball to heat the prostate so that it is reduced to vapor

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25
Q

what is HoLEP

A

Holmium laser enucleation of the prostate

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26
Q

what is TUIP

A

Transurethral incision of the prostate

A less invasive and safer procedure than TURP

A combined visual and surgical instrument (resectoscope) is inserted – then grooves are cut to open the urinary channel

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27
Q

open prostastectomy

A

 Done if the prostate is very large – involves a lower abdominal incision
 Is different to a radical prostatectomy because it just removes the obstruction part of the prostate

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28
Q

what sort of cancer is prostate cancer and where does it occur

A

adenocarcinoma - 95%
cancers of glandular cells

usually develops in the outer zone of the prostate where it seldom causes symptoms

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29
Q

risk factors for prostate cancer

A

age
black
FHx
obesity

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30
Q

investigations for prostate cancer

A

DRE - hard and nodular (if this is the case then refer) - although a normal DRE does not exclude prostate cancer

PSA - if >3nanograms/ml then refer for 2 week appointment

once referred, will get a TRUS biopsy (transrectal US guided) - this takes 10-12 cores of prostatic tissue thorugh the rectum

NICE recommends that for men with a negative TRUS biopsy, multiparametric MRI (mpMRI) is considered to determine whether a further biopsy is required (false negative rates can be as high as 45%)

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31
Q

a decision aid to help men decide whether or not to have a PSA test

A

SWOP - an online decision aid developed by the department of urology in the netherlands

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32
Q

managemnet of prostate cancer

A

perform risk stratisifcation based on Gleason score, TNM and PSA

low risk - active surveillance or watchful waiting for those with older men, or those with significant comorbidities or those that are likely to die from other causes. or radical prosatectomy or radical radiotherapy (external-beam radiotherapy or brachytherapy)

intermediate risk - radical prostatecomty or radical radiotherapy with 6 months of androgen deprivation therapy (before, during or after radiotherapy) can be offered
other treatments can be considered like watchful waiting, active surveillance, high dose brachytherapy in combination with EBR

high risk - basically same as above

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33
Q

active surveillance vs watchful waiting for prostate cancer

A

Watchful waiting = followed up in primary care – regular clinical assessments and repeat PSA (not DRE or prostate biopsies)

Active surveillance = same at watchful waiting but repeat prostate biopsy as well (and some other things involved – see NICE guidelines)
Active surveillance is the preferred option for men with low prognostic risk who are suitable for radical treatment in the event of disease progression – good for men who do not wish to have immediate radical prostatectomy or radical radiotherapy

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34
Q

types of androgen deprivation therapy

A
  • Androgen withdrawal — surgery (bilateral orchidectomy) or medical, with LHRH agonists (such as goserelin, leuprorelin, triptorelin), or antagonists (such as degarelix).
  • Androgen blockade — with drugs that bind to and block the hormone receptors of cancer cells (for example, cyproterone acetate), thus preventing androgens from stimulating cancer growth
  • Hormone therapy can be used as neoadjuvant therapy (before radical treatment), concurrent therapy given at the same time as radiotherapy or adjuvant therapy
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35
Q

SE of androgen deprivation therapy

A
erectile dysfunction
loss of libido
breast swelling
hot flushes
osteoporosis
36
Q

risks of radical prostacteomy

A

urinary incontinence
erectile dysfunction
incomplete resection of the tuomur

Approximately 20% of men develop biochemical or clinical recurrence of prostate cancer

37
Q

how can radical prostacectomy be performed

A

open
laparascopic
robot-assisted

38
Q

risks of external beam radiotherapy

A

EBRT short-term include bowel and bladder problems. Long-term complications include erectile dysfunction and urinary problems.

There is a small increased risk of colorectal cancer after EBRT

39
Q

TNM staging of prostate cancer

A
  • T1 - clinically inapparent tumour that is not palpable
    o ABC criteria for this (don’t learn)
  • T2 – tumour that is palpable and confined within the prostate
    o A – tumour involves half of one lobe or less
    o B – tumour involves more than half of one lobe, but not both
    o C – involves both
  • T3 – tumour extends through the prostatic capsule
    o A – extracapsular extension (unilateral or bilateral)
    o B – tumour invades seminal vesicle(s)
  • T4 – tumour is fixed or invades adjacent structures other than seminal vesicles: bladder neck, external sphincter, rectum, levator muscles, and/or pelvic wall
  • NX – regional LNs cannot be assessed
  • N0 – no regional LN metastasis
  • N1 – regional LN metastasis
  • M0 – no distant mets
  • M1a – non-regional lymph nodes
  • M1b – bone(s)
  • M1c – other site(s)
40
Q

gleason scoring

A
  • The commonest and second most common tumour patterns are analysed and graded from 1 to 5.
  • The Gleason score is the sum of these two grades and can range from 2 to 10.
  • The tumour grade is classified into either of three risk categories on the basis of the Gleason score:
    o Low: 6 or less.
    o Intermediate: 7.
    o High: 8–10
41
Q

what is risk stratisification of prostate cancer based on - 3 things

A

TNM
gleason
PSA

e.g. intermediate risk:
PSA 10-20 nanograms/ml or gleason score 7 or clinical stage T2b

42
Q

complications of prostate cancer

A
  • Local invasion
    o Prostate cancer can be locally invasive and spread to the seminal vesicles, base of the bladder, urethral sphincter, or side wall of the pelvis.
  • Distant metastases
    o Metastasizing prostate cancer most commonly spreads to the bones, where it can cause pain, pathological fractures, or spinal cord compression.
  • Lower urinary tract symptoms (LUTS)
    o Early prostate cancer does not usually cause LUTS.
    o By the time prostate cancer causes LUTS, it may be advanced and incurable
43
Q

most common type of bladder cancer

A

over 90% are urothelial carcinoma - previously termed transitional cell carcinoma

44
Q

presentation of bladder cancer

A

painless haematuria = primary presenting symptom - macroscopic is more common than microscopic. episodes are typically intermittent

recurrent UTIs

there may also be voiding symptoms in advanced disease

45
Q

risk factors for bladder cancer

A
smoking
aromatic amines (rubber industry)
polycyclic aromatic hydrocarcbons used in aluminium, coal and roofing industries
chronic cystitis
shcistomiasis (increased risk of squamous cell carcinoma) 
pelvic radiaiton 
age
systemic chemo
male
FHx

NB carcinogens such as nitrosamines are excreted in the urine - thus exposing them to cells of the tract

46
Q

investigations for bladder cancer

A

cystoscopy with biopsy is diagnostic - high grade tumours may be flat and more difficult to see
blue light cystoscopy can be performed to assist finding a tumour - a dye is washed into the bladder one hour before the op which is absorbed by the cancer and glows pink under blue light
CT urogram - images urinary tract with contrast during the excretory phase and can highlight tumours and/or obstruction
urine microscopy/cytology
dip for haematuria

MRI or lymphangiography may show pelvic nodes

47
Q

an alternative to blue light cystoscopy

A

narrow band imaging

48
Q

TNM staging on bladder cancer

A
  • TX – primary tumour cannot be assessed
  • T0 – no evidence of primary tumour
  • Ta – non-invasive papillary carcinoma
  • Tis – carcinoma in situ – flat tumour
  • T1 – invades lamina propria
  • T2 – invades muscularis propria
    o a = superficial
    o b = deep
  • T3 – invades perivesical tissue
    o a = microscopically
    o b = macroscopically
  • T4 – invades any of the following: prostatic stroma, seminal vesicles, uterus, vagina, pelvic wall, abdominal wall
    o T4a: tumour invades prostatic stroma, uterus, or vagina
    o T4b: tumour invades pelvic wall or abdominal wall
  • N0: no regional lymph node metastasis
  • N1: metastasis in a single lymph node in the true pelvis (hypogastric, obturator, external iliac, or presacral)
  • N2: metastasis in multiple regional lymph nodes in the true pelvis (hypogastric, obturator, external iliac, or presacral)
  • N3: metastasis in a common iliac lymph node
  • M0: no distant metastasis
  • M1a: non regional lymph nodes
  • M1b: other distant metastasis
49
Q

management of bladder cancer - Tis (carcinoma in situ), Ta (non-invasive papillary carcinoma), T1 (invades lamina propria)

A

low risk

  • diathermy via transurethral resection of bladder tumour (TURBT)
  • AND a single dose of mitomycin chemo follwing this
  • then maintenance with mitomycin C, doxorubicin and cisplatin

intermediate risk
- same but at least 6 doses of mitomycin

high risk
- offer the choice of intravesical BCG or radical cystectomy to people with high-risk non-muscle-invasive bladder cancer

50
Q

management of bladder cancer - T2-3 (muscle invasive)

A

o Radical cystectomy is gold standard - then form a urostoma
o Radiotherapy gives worse 5-year survival rates but preserves the bladder -External beam radiotherapy alone should only be considered as a therapeutic option when the patient is unfit for cystectomy
o Neoadjuvant chemotherapy with CMV (cisplatin, methotrexate and vinblastine) has improved survival compared to cystectomy or radiotherapy alone
o Post-op chemotherapy is toxic but effective

51
Q

management of bladder cancer - T4

A

usually palliative chemo/radiotherapy

Chronic catheterization and urinary diversion may help to relieve pain

52
Q

management of metastatic bladder

A

o Is chemosensitive – cisplatin-based treatment is the mainstay

53
Q

complications of TURBT

A
urine infection 
bladder perforation 
requirement for a prolonged (7-10 day) period of catheterisation 
dysuria
LUTS
54
Q

risk factors for testicular cancer

A

cryptorchidism
FHx or previous personal history
white
Klinefelter syndrome - 47XXY (small testicles and infertility)

55
Q

types of testicular cancer

A

divided into germ cell tumours (95%) and non-germ cell tumours (5%)

germ cell tumours include;
seminomas
non-seminomas - embryonal carcinoma, teratocarcinoma, choriocarcinoma, yolk sac tumours, teratoma

non-germ cell tumours include
leydig tumour
gonadoblastoma
other rarer ones

56
Q

presentation of testicular cancer

A
  • Painless testicular mass
  • Irregular, fixed, firm, does not transilluminate

uncommon:
o Gynaecomastia from beta human chorionic gonadotrophin (beta-hCG) production
o Metastasis - seminomas metastasise to para-aortic nodes and produce back pain; teratomas undergo blood-borne spread to the liver, lung, bone and brain

57
Q

investigations for testicular cancer

A

palpate the abdomen for masses - either para-aortic masses or hepatomegaly
check for supraclavicular lymphadenopathy
testicular US
serum tumour markers
CT of abdomen and chest for staging

A trans-scrotal percutaneous biopsy SHOULD NOT BE PERFORMED, as it might cause seeding of the cancer. Diagnosis is made through tumour marker and imaging alone

(tissue histology can follow an inguinal orchidectomy)

58
Q

serum tumour markers for testicular cancer

A

B-HCG - elevated in 60% of NSGCTs and 15% of seminomas
AFP
LDH - can be a surrogate marker for tumour volume

59
Q

staging of testicular cancer

A

Marsden staging

  • Stage 1, confined to testis
  • Stage 2, infra-diaphragmatic lymph node involvement
  • Stage 3, supra- and infra-diaphragmatic lymph node involvement
  • Stage 4, extralymphatic spread
60
Q

treatment of testicular cancer

A

where possible: radical orchidectomy - it removes the testes along with the spermatic cord - is performed via an inguinal approach
a testicular prosthesis should be offered to all

THEN
for NSGCTS:
- if low risk then can enter surveiallance and have CT at 3 and 12 months
- if high risk or those with vascular invasion then will require adjuvant chemo (bleomycin, etoposide, cisplatin)
for seminomas:
- same - if low risk then surveillance, for higher risk then consdier chemo with carboplatin
- for metastatic seminoma then require chemotherapy or radiotherapy

Where appropriate, sperm storage should be offered to men who may require chemotherapy or radiotherapy

61
Q

features of penile cancer

A

usually affects the glands but may involve the shaft
early cases present with a painless ulcer, nodule, or warty outgrowth on the penis that may involve the forekin

advanced disease presents with a fungating mass - usually ulcerated

Inguinal lymphadenopathy may be present
Nodes are often reactive rather than being metastatic and Abx should be given prior to further assessment

62
Q

investigations for penile cancers

A
  • Biopsy lesion to confirm the diagnosis
    o T2 lesions invade the corpus spongiosum/ cavernosa, T3 invade the urethra, and T4 invade beyond the penis
  • Pelvic and abdominal CT scanning provide further evidence of nodular involvement in cases with positive inguinal nodes
63
Q

treatment of penile cancer

A

Treatment

  • If confined to glans, treatment involved either partial amputation or radiotherapy
  • Superficial lesions can be treated by excision of the gland followed by glans reconstruction
  • More advanced carcinomas require total penectomy
  • Inguinal and iliac lymph node dissections are considered
64
Q

types of renal cancer

A

renal cell carcinoma - 85%
transitional cell carcinoma (urothelial tumours)
nephroblastoma in children (wilm’s tumour) squamous cell carcinoma

65
Q

pathophysiology of RCC

A

adenocarcinoma of the renal cortex
arises predominantly from the PCT
microscopically are mostly composed of polyhedral clear cells with dark staining nuclei and cytoplasm rich with lipid and glycogen granules

66
Q

presentation of renal cancer

A

haematuria = most common
flank pain
flank mass
non-specific symptoms like lethargy or weight loss
is relatively common to be picked up incidentally on abdominal imaging

Paraneoplastic syndromes caused by ectopic secretion of hormones by RCC can lead to uncommon presentations include polycythaemia due to erythropoietin, hypercalcaemia due to parathyroid hormone, hypertension due to renin, or pyrexia of unknown origin

67
Q

investigaitons for renal cancer

A
  • BP
    Raised from increased renin secretion
  • FBC
    Erythrocytosis from excess EPO production
  • LFTs
    Elevated liver enzymes may be indicative of metastatic lesions
  • U+Es
    Bony mets?
  • Urinalysis for haematuria
  • Ultrasound
  • CT imaging of the abdomen and pelvis pre and post IV contrast is the gold standard
  • An additional CT or MRI once confirmed cancer for tumour staging
    Or can do CXR – classical cannon ball secondaries may be seen – however CT is more sensitive
  • There is a role for biopsy of renal lesions, particularly small renal masses when surveillance or minimally invasive ablative therapies are being considered
    ‘biopsy is rarely indicated – but may be considered after MDT discussion if there is significant doubt over the diagnosis
  • Bone scan
    Only recommended if patient presents with localising bone pain and/or elevated ALP
68
Q

staging of renal cell carcinoma

A

stage 1 - tumour ≤7cm and confined to renal capsule
stage 2 - tumour >7cm or invading the renal capsule (but confined to Gerota’s fascia)
stage 3 - tumour extending into the renal vein, vena cava or spread to 1 local LN
stage 4 - tumour extending beyound Gerota’s fascia, >1 local LN, involvmenet of ipsilateral adrenal gland or perinephric fat, or distant met

69
Q

management for localised renal cell carcinoma

A

partial nephrectomy is considered first line whenever possible for patients with a localsied tumour <7cm
for larger tumours - radical nephrectomy - open or laparscopic (spare adrenals if possible)

if not suitable for surgery then percutaneous radiofrequency or laparscopic/percutaneous cryotherapy
renal artery embolisation for haemorrhaging disease
some will have a good response to biological therapy, especially angiogenesis targeted therapies; sunitinib, bevacizumab, sorafenib

70
Q

treatment of metastatic kidney disease

A
  • Chemotherapy generally ineffective in RCC
  • Nephrectomy combined with immunotherapy is often recommended
    o Such as IFN alpha or IL-2 agents
  • Biological agents that can be used in combination for metastatic disease include Sunitinib (a tyrosine kinase inhibitor) and Pazopanib (also a tyrosine kinase inhibitor)
    o These are angiogenesis targeted agents
  • Metastasectomy (surgical resection of solitary metastases) is recommended where the disease is resectable and the patient is otherwise well
71
Q

points where stones cause obstruction

A

vesico ureteric juntcion (VUJ) - most common site
mid-ureter where it crosses the iliac vessels
pelvic ureteric junction (PUJ) where it enters the bladder

72
Q

composition of renal stones

A
  • 80% are composed of calcium salts (calcium oxalate (60%), calcium phosphate, or both)
  • The rest are composed of struvite (2-15%), uric acid (10%), cystine (1-2%) or other substances (1%)

NB staghorn calculi are usually composed of struvite

73
Q

risk factors for renal stones

A

Dehydration
Urine pH
o High pH predisposes to calcium phosphate stones
o Low pH predisposes to uric acid stones
Men
FHx
Obesity
Diet
o Excessive dietary intake of oxalate, urate, sodium, and animal protein are associated with increased stone formation
Drugs — treatment with calcium or vitamin D supplements, protease inhibitors (for example indinavir), or diuretics (for example furosemide) may increase the risk of stone formation

74
Q

presentation of renal/ureteric stones

A

abrupt onset of severe unilateral pain originating in the loin and radiating to the groin
pain typically lasts minutes to hours and occurs in spasms, with intervals of no pain or dull ache - pain is often described by patients as constant compared to biliary colic which is episodic
often accompanied by nausea, vomiting and haematuria
restless and cannot lie still

May complain of dysuria, urinary frequency, and straining — when the stone reaches the vesico-ureteric junction (due to the stone irritating the detrusor muscle)

may be pyrexial

75
Q

investigaitons for urinary tract stones

A

examine the abdomen - can sometimes reveal tenderness over the affected loin
FBC + CRP - infection
U + E - renal functino
PT and INR if intervention is planned
urine dip - haematuria + nitrates (absence of haematuria does not rule out)
midstream urine for micrscopy, urine culture + sensitivies if infection
CT KUB - gold standard
US - to assess for hydronephrosis and any bladder distension
X ray KUB still used in some centres for initial assessment and can be useful in watching the passage of radio-opaque stones

The European Association of Urology’s guidelines on urolithiasis recommend stone analysis for all first-time stone formers - encourgage patient to urinate through a tea strainer

76
Q

differentials for urinary tract stones

A
  • Biliary colic
  • Dissection of an aortic aneurysm
  • Pyelonephritis – very high temp and pain is unlikely to radiate to the groin
  • Acute pancreatitis
  • Acute appendicitis
  • Perforated peptic ulcer
77
Q

investigations for overactive bladder

A
  • Frequency volume chart
  • Symptom assessment tool e.g. ICIQ
  • Fluid intake
  • Exclude UTI
  • Exclude malignancy – red flags such as haematuria + weight loss
  • Dipstick
  • Urodynamics
    o To determine whether detrusor overactivity is causing the symptoms
  • Uncomplicated OAB can be treated without further investigation (i.e. without infection for example)
78
Q

management for overactive bladder

A
  • Lifestyle modifications
    o E.g. reduce caffeine, stop smoking, drink plenty of non-irritating fluids (highly concentrated urine is irritating to the bladder and can actually cause you to urinate more)
  • Bladder training
    o Try to slowly increase the interval between urinations – e.g. wait a few minutes when you have to urinate
    o To try and resist the urge, take a seat and take deep breaths in and out and try imagining yourself somewhere peaceful
    o Once you can maintain your new schedule without accident for one-two weeks then try increasing the time further
  • Medications
    o Anticholinergics – oxybutynin, Solifenacin, tolterodine, darifenacin – these are first line
    o Beta-3 adrenergic – mirabegron (Myrbetriq)
     NICE: mirabegron is only recommended as an option by NICE when antimuscarinic drugs are contraindicated or ineffective or have unacceptable SEs
    o Offer intravaginal oestrogen to treat OAB symptoms in postmenopausal women with vaginal atrophy
    o Explain that substantial benefits may not be seen for at least 4 weeks and that symptoms may continue to improve over time
  • Botox
    o Botox is done via injection of botox A via a cystoscope
  • Sacral nerve stimulation
    o ‘offer percutaneous sacral nerve stimulation after they have not responded to non-surgical management including botox (or they are not prepared to accept the risks of needling catheterisation associated with botox)
  • Surgery e.g. augmentation cystoplasty
    o This increases the size of the bladder by using some bowel wall – only done in severe cases
79
Q

some criteria for inpatient admission with renal stones

A

person is in shock or has signs of systemic infection
person is at increased risk of AKI e.g. if solitary kidney, pre-exisiting CKD
pregnant
uncontrollable pain from analgesia
large stone >5mm
uncertainty about the diagnosis

80
Q

management of urinary tract stone if hospital admission is not required

A

analgesia e.g. 75mg IM diclofenac or if less severe/for ongoing relief then NSAIDs. codeine can be added
antiemetic if required like IM metoclopramide
advise a normal fluid intake to maintain colourless urine
explain that the majority of stones will pass spontaneously but may take 1-3 weeks
use a tea strainer if possible
seek urgent medical assistance if they develop fever or rigors or pain worsens

arrange urgent referral to urology within 7 days of onste so that diagnostic investigatios can be done to confirm diagnosis

81
Q

medication to help with stone expulsion - medical expulsive therapy (MET)

A

alpha blocker e.g. tamsulosin or a CCB e.g. nifedipine can be use

82
Q

stone options for those that have been admitted/ where they do not pass spontaneously /unremitting colic

A

stent insertion via cystoscopy with a JJ stent - done as a tempory holding measure as it prevents the ureter contracting + thus reducing pain, buying time until a more definitive measure can be done

nephrostomy - patients with evidence of obstruction nephropathy or significant infection

extracorpeal shock wave lithotripsy (ESWL) - <2cm - radiological via X ray or US

flexible uretero-renoscopy - scope is passed up ureter and fragmented through laser lithotripsy

percutaneous nephrolithotomy - for large stones >2cm or staghorn

open surgery if other methods failed

83
Q

how may urinary tract stones will not pass spontaneously

A

1 in 5

84
Q

advise to reduce recurrent stones

A

o Increase oral fluids
o Reduce dietary salt intake
o Reduce intake of oxalate-rich foods for calcium stones (e.g. spinach, nuts, rhubarb, tea)
o Reduce intake of urate- rich foods for uric acid stones (e.g. kidney, liver, sardines)
o Limit dietary protein

85
Q

causes of acute urinary retention

A

local compression - BPH, urethral stricture, bladder neck stenosis, pelvic mass, claculi, bladder cancer, faecal impaction
infection and inflammation - UTI, prostatits
medication - anticholinergics, alcohol, opioids, antidepressants
neuro - cauda equina, MS, autonomic dysfunctino, CVA

86
Q

investigations for acute urinary retention

A
abdo exam 
genitourinary exam - phimosis + meatal stenosis 
PR - check anal tone, prostate size
neuro exam 
urinalysis - infection
blood tests - FBC, U+E, glucose, PSA
US for post residual urine + hydronephrosis
CT for pelvic, abdominal, retroperitoneal masses causing bladder neck compression
MRI /CT brain
MRI spine 
cystoscopy
urodynamic studies
87
Q

management of acute urinary retention

A
  • Immediate catheterisation to decompress the bladder
  • An alpha-blocker should be offered before removal of the catheter
  • Then TWOC
  • Treat underlying cause