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Urology Flashcards

1
Q

Define Symptomatic non-visible haematuria (s-NVH)

A

microscopic haematuria or dipstick-positive haematuria with associated symptoms

including lower urinary tract symptoms (LUTS): hesitancy, frequency, urgency, dysuria

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2
Q

What are the common causes of haematuria

A 
UTI, 
bladder tumours, 
urinary tract stones, 
urethritis, 
benign prostatic hypertrophy (BPH)
prostate cancer.
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3
Q

How can you classify causes of haematuria

A

Infection: cystitis, tuberculosis, prostatitis, urethritis, schistosomiasis, infective endocarditis.

Tumour: renal carcinoma, Wilms’ tumour, carcinoma of the bladder, prostate cancer, urethral cancer or endometrial cancer.

Trauma: renal tract trauma due to accidents, catheter or foreign body, prolonged severe exercise, rapid emptying of an overdistended bladder (eg, after catheterisation for acute retention).

Inflammation: glomerulonephritis, Henoch-Schönlein purpura, IgA nephropathy, Goodpasture’s syndrome, polyarteritis, post-irradiation.

Structural: calculi (renal, bladder, ureteric), simple cysts, polycystic renal disease, congenital vascular anomalies

Haematological: sickle cell disease, coagulation disorders, anticoagulation therapy.

Surgery: invasive procedures to the prostate or bladder.

Toxins: sulfonamides, cyclophosphamide, non-steroidal anti-inflammatory drugs

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4
Q

What questions are important to ask in a haematuria history

A

LUTS symptoms - dysuria, freq, hesitancy, urgency
where - in urine/on wiping
pain - intermittent, constant, loin to groin
TURP in past?
DH - anticoag
smoking
jobs - carcinogens

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5
Q

How would you investigate haematuria?

A 
urine dip - ?UTI 
eGFR, U+E, FBC, ?PSA
MSU
USS KUB, flexible cystoscopy
TURB
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6
Q

What kinds of bladder cancer are there? What percentage of each kind?

A

transitional - 90%

squamous 10%

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7
Q

What are hte risk factors for bladder cancer?

A 
Transitional:
Smoking
Exposure to aniline dyes in the printing and textile industry: examples are 2-naphthylamine and benzidine
Rubber manufacture
Cyclophosphamide
squamous:
Schistosomiasis
Calmette-Guérin (BCG) treatment
Smoking
recurrent UTI
bladder stones
long term catheter
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8
Q

What are the criteria for a 2 week wait bladder cancer referral?

A

Aged 45 and over and have:
Unexplained visible haematuria without urinary tract infection or
Visible haematuria that persists or recurs after successful treatment of urinary tract infection

Aged 60 and over
and have unexplained non-visible haematuria
and either dysuria or a raised white cell count on a blood test

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9
Q

What are the symptoms of bladder cancer?

A

painless haematura

voiding problems

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10
Q

What can cause a false positive for blood on a dipstick?

A

menses
exercise
myoglobin-

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11
Q

What investigations need to be done to stage bladder cancer?

A

CT with contrast enhancement

For patients with confirmed muscle-invasive bladder cancer, CT of the chest, abdomen and pelvis is the optimal form of staging, including CT urography for complete examination of the upper urinary tracts

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12
Q

What is the difference between papillary and non-papillary bladder cancer

A

a non-invasive, papillary tumour protruding from the mucosal surface is less aggressive

a solid, non-papillary tumour that invades the bladder wall has a high propensity for metastasis.

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13
Q

What is considered when deciding on the management of bladder cancer

A

whether it invades the muscle layer or not
staging TNM
PS

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14
Q

What is the treatment of low risk non-invasive bladder cancer

A

TURBT = transurethral resection of bladder tumour
ensuring that detrusor muscle is obtained

give a single dose of intravesical mitomycin C

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15
Q

What is the treatment of intermediate risk non-invasive bladder cancer

A

TURBT

at least 6 doses of intravesical mitomycin C

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16
Q

What is the treatment of high risk non-invasive bladder cancer

A

TURBT

radical cystectomy
or
intravesical BCG

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17
Q

What is the treatment for muscle invasive bladder cancer

A

neoadjuvant chemotherapy using a cisplatin combination regimen

radical cystectomy or radical radiotherapy

or palliative chemo/radio

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18
Q

What happen to the urine after a radical cystectomy?

A

ileal conduit
- to form urostomy
ureters plumbed into part of ileum

bladder reconstruction

  • continent cutaneous diversion (catheterisable stoma to pouch of bowel containing urine)
  • orthoptic neobladder (segment of the small intestine forms reservoir for urine. The ureters and urethra are attached to the neobladder, allowing voiding)
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19
Q

What are the risks of radical cystectomy

A

bowel obstruction,
obstruction of the ureter,
pyelonephritis
infection of the wound.
damage to the S2,3,4 outlet causing complete erectile dysfunction
Orthotopic bladders have a risk of urinary incontinence.

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20
Q

What are the risk factors for prostate cancer

A

age
family history
ethnicity - black>white>asian
FH - breast, ovarian, prostate (BRCA2)

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21
Q

Explain the screening of prostate cancer

A

no formal screening program
instead NHS Prostate Cancer Risk Management Programme
patients can ask for a PSA, but there needs to be informed consent

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22
Q

What are the problems with screening for prostate cancer

A

Most men with prostate cancer detected by PSA testing have tumours that will not cause health problems (over-diagnosed)
but almost all undergo early treatment (over-treated)
treatment leads to reduced quality of life
not cost effective

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23
Q

What is PSA

A

serine protease enzyme produced by normal and malignant prostate epithelial cells
liquefies semen

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24
Q

What can cause a raised PSA

A 
Acute urinary retention.
Benign prostatic hyperplasia.
Old age.
Prostatitis.
Prostate cancer.
Transurethral resection of the prostate.
Urinary catheterisation.`
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25
Q

Why is PSA raised in prostate cancer

A

disordered glands

more PSA leaks into semen

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26
Q

What are the symptoms of prostate cancer

A

bladder outlet obstruction: hesitancy, urinary retention
haematuria, haematospermia
pain: back, perineal or testicular
erectile dysfunction

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27
Q

Why is prostate cancer often asymptomatic

A

cancers tend to develop in the periphery of the prostate

therefore don’t cause obstructive symptoms early on.

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28
Q

What would prostate cancer feel like on DRE

A

asymmetrical, hard, nodular enlargement with loss of median sulcus, lack of mobility

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29
Q

What investigations are done in suspected prostate cancer

A

DRE
PSA, U+E, eGFR
TRUS biopsy

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30
Q

How is the TRUS biopsy carried out

A

trans rectal USS

take biopsy of 12 cores

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31
Q

What is the Gleason grade and how is it calculated

A

the two most common types of glandular growth patterns within the tumour biopsy are graded.
A grade from the scale is given to each of these two patterns.
The two grades are added together to get the total Gleason score.
For example, if the grade given to the most common growth pattern is 3 and the grade given to the second most common growth pattern is 4, the total Gleason score is 7 (3 + 4).

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32
Q

Above what Gleason grade is a prostate cancer high risk?

A

> =4+3

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33
Q

What investigations need to be done for prostate cancer to be staged

A

DRE
PSA
MRI pelvis
bone scan

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34
Q

What are the treatment options for localised prostate cancer (T1/T2)

A

conservative: active monitoring & watchful waiting
radical prostatectomy
radiotherapy: external beam and brachytherapy

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35
Q

What is the difference between active monitoring and watchful waiting in prostate cancer?

A

You have active surveillance if the doctor aims to cure your cancer if it starts to grow.

You have watchful waiting if the doctor aims to control your cancer if it starts to grow.

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36
Q

What does active monitorting of prostate cancer involve?

A

In year one of active surveillance you have:
PSA levels – every 3 to 4 months
DRE every 6 to 12 months
biopsy after 12 months

In year 2 to year 4 you have:
PSA levels – every 3 to 6 months
DRE every 6 to 12 months

In year 5 and afterwards you have:
PSA levels – every 6 months
DRE – every 12 months

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37
Q

What does watchful waiting of prostate cancer involve?

A

PSA every year

investigation if symptoms appear

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38
Q

Who is watchful waiting of prostate cancer suitable for?

A

locally advanced or advanced cancer with no symptoms

localised cancer but multiple comorbidities

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39
Q

What is the difference between locally advanced and advanced prostate cancer?

A

Locally advanced = spread to nearby tissues.

Advanced = spread to distant lymph nodes or other sites

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40
Q

What are the treatment options for Localised advanced prostate cancer (T3/T4)

A

hormonal therapy with LHRH analogues eg. goserelin, leuprorelin, and triptorelin
radical prostatectomy
radiotherapy: external beam and brachytherapy

+adjuvant chemo

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41
Q

How do hormone treatments for prostate cancer work?

A

LHRH analogues eg goserelin, leuprorelin, and triptorelin

LHRH stimulates pituitary gland to make LH, leading to an initial increase in testosterone. therefore need to give antiandrogen cover for first two weeks

prolonged exposure then leads to down regulation of the LHRH receptors at the pituitary, so there is eventual androgen deprivation as the testes no longer produce testosterone

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42
Q

What are the treatment options for metastatic prostate cancer?

A

Bilateral orchidectomy

continuous LHRH agonist treatment + docataxel chemo

single dose radiotherapy

bisphosphonates for mets

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43
Q

What indicates high risk prostate cancer

A

PSA >20mg/ml
Gleason score 8-10
stage >=T2c

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44
Q

Define urolithiasis

A

formation of stone in the urinary tract

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45
Q

define renal colic

A

intermittent severe loin to groin pain caused by presence of renal stones

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46
Q

What are renal stones made out of

A

calcium phosphate
calcium oxalate
uric acid
struvite

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47
Q

What is the most common material for renal stones to be made of

A

calcium oxalate

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48
Q

Which renal stones are radio lucent

A

uric acid

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49
Q

Which are the most common sites for renal stones

A

ureteropelvic junction
as the ureter crosses the iliac vessels
vesicoureteric junction

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50
Q

Describe the pathophysiology of renal colic

A

obstruction of ureter
tension in wall of ureter leads to prostaglandin release
causes vasodilation and smooth muscle spasm

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51
Q

What are the risk factors of renal colic

A 
dehydration
prev stone
obesity
diet - oxalate, urate, animal protein
drugs -  calcium or vitamin D supplements, protease inhibitors, diuretics
PMH - parathyroid, RTA, gout
kidney malformations - horseshoe, strictures, 
family history
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52
Q

What are the signs and symptoms of renal colic

A 
loin to groin
extreme pain
sudden onset, comes and goes
fever, UTI sx if infection
cannot keep still
N+V
tender renal angle/loin
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53
Q

What is the differential diagnosis for renal stones

A

urinary: pyelonephritis
abdo: biliary colic, peritonitis, appendicitis
gynae: ectopic pregnancy, ovarian cyst, PID
vascular: AAA dissection

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54
Q

What investigations should be done in renal stones

A

urine dip
FBC U+E CRP, bone profile, clotting, urate
MSU - microscopy, culture and specificity
CT KUB without contrast

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55
Q

What is the immediate management of renal stones

A

IM diclofenac for pain relief
anti emetics
fluids if dehydrated

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56
Q

What are the signs of an emergency case of renal stones

A

any sign of concurrent infection

increased risk AKI: solitary or transplanted kidney, CKD, bilateral stones

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57
Q

What is the management of an emergency case of renal stones

A

nephrostomy
ureteric catheter
ureteric stent

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58
Q

What are the indications for conservative management of renal stones

A

<5mm stone

no obstruction present

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59
Q

Who is extracorporeal shockwave lithotripsy suitable for as a treatment of renal stones

A

stone <2cm

not pregnant

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60
Q

Who is ureteroscopy suitable for as a treatment of renal stones

A

stone <2cm

pregnant

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61
Q

Who is percutaneous nephrolithotomy suitable for as a treatment of renal stones

A

stones >2cm
Complex renal calculi
staghorn calculi

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62
Q

Describe extracorporeal shockwave lithotripsy

A

shock waves are directed over the stone to break it apart.

The stone particles will then pass spontaneously.

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63
Q

How can renal stone recurrence be prevented?

A

Increase fluid intake
Reduce salt intake.
Maintain a healthy weight.

For people with calcium stones, avoid:
Oxalate-rich products, such as rhubarb, spinach, cocoa, tea leaves, nuts, soy products, strawberries, and wheat bran.
Animal protein — limit intake to 0.8–1.0 g/kg body weight.
Sodium — do not exceed 3 g daily.
The use of calcium supplements, but they should not restrict dietary calcium intake.

For people with uric acid stones, avoid:
Urate-rich products, such as liver, kidney, calf thymus, poultry skin, and certain fish (herring with skin, sardines, anchovies, and sprats).

64
Q

What are the causes of painless scrotal swelling

A 
inguinal hernia
hydrocoele
varicocoele
epedidymal cyst
testicular cancer
65
Q

What are the causes of painful scrotal swelling

A

testicular torsion!!!
epididymoorchitis
torted hyatid of Morgani
Trauma causing haematocoele

66
Q

What are the clinical features of an inguinal hernia causing scrotal swelling

A

cannot get above it
May enlarge with Valsalva-type manoeuvres,
may disappear on lying down (if reducible).
not possible to palpate the spermatic cord or inguinal ring
there is a positive cough impulse.

67
Q

What is the difference between direct and indirect inguinal hernias

A

Indirect: a protrusion through the internal inguinal ring passes along the inguinal canal through the abdominal wall, running laterally to the inferior epigastric vessels. Failure of closure of processus vaginalis.

Direct: the hernia protrudes directly through a weakness in the posterior wall of the inguinal canal, running medially to the inferior epigastric vessels.

68
Q

What are the risks associated with an inguinal hernia

A

incarceration
strangulation
bowel obstruction

69
Q

What is the management of inguinal hernias in adults and children

A

features of strangulation or obstruction, admit immediately for surgical reduction

infant or young boy, refer urgently to a paediatric surgeon (preferably to be seen within 2 weeks).

For men or older boys:
Refer urgently for surgical repair if the hernia is irreducible, or only partially reducible.
Refer all others routinely for surgical repair, unless they have minimally symptomatic inguinal hernias and significant comorbidity, and do not want to have surgery.

70
Q

What are the clinical features of a hydrocoele

A

acute or chronic
Painless and non-tender.
Will transilluminate.
fluctuant, ovoid swelling enveloping the testis or located above the testis along the spermatic cord

71
Q

What is a hydrocele of the spermatic cord

A

the processus vaginalis closes segmentally, trapping fluid along the spermatic cord.

72
Q

What is a communicating hydrocele

A

persistence of the processus vaginalis allows peritoneal fluid to freely communicate with the scrotal portion of the processus.

73
Q

What is a hydrocoele

A

abnormal collection of serous fluid between the parietal and visceral layers of the membrane tunica vaginalis surrounding the testis, or along the spermatic cord.

74
Q

When does a hydrocoele in an infant normally spontaneously resolve by?

A

within the first 1–2 years of life

75
Q

When is surgical management considered for a hydrocoele

A

persistent hydrocoele beyond 2 years of age

76
Q

What causes testicular torsion

A

torsion of the spermatic cord causing loss of arterial supply and venous drainage of the testis

77
Q

What are the risk factors of testicular torsion

A

Testicular tumour.
Testicles with horizontal lie.
History of undescended testis.
Spermatic cord with long intra-scrotal portion.

78
Q

What are the features of testicular torsion

A

Sudden onset
Severe unilateral pain
N+V
most commonly occurs in neonates or around puberty.
There may be a history of previous episodes of severe, self-limiting pain.

The cremasteric reflex is almost always absent. The testis is often elevated in the scrotum, and may have a transverse lie.
Neonatal cases of testicular torsion may present with scrotal swelling and discoloration (similar to scrotal haematoma).

79
Q

What is the management of testicular torsion

A

urgent admission
operation within three hours
Bilateral orchiopexy is required immediately following detorsion to prevent further episodes of torsion
A baby born with testicular torsion should have the affected testis removed (because it is always non-viable) and orchidopexy of the other side (because bilateral torsion is common).

80
Q

What is a torted hyatid of Morgani

A

The appendix testis and appendix epididymis are remnants of the Mullerian ducts which can become torted. They sit on a stalk on the outside of the testicle.

81
Q

What are the features of a torted hyatid of Morgani

A

Onset is sudden, or gradual over a few days.
Typically painful and tender over the head of the testis or epididymis,
not associated with nausea and vomiting.
Early on, a nodule can be palpated at the upper end of testis or epididymis. Later, there is more generalized scrotal oedema.
usually the testis is mobile and of normal size
the cremasteric reflex is still present.
An infarcted appendage may be seen through the skin (the ‘blue dot sign’).

82
Q

What is epididymo-orchitis

A

infection of the epididymis and testicle

83
Q

What causes epidiymo-orchitis in pre-pubertal boys?

A

non-infective and self-limiting, caused by reflux of urine into the ejaculatory ducts

Can also be caused by enteric organisms, such as Escherichia coli or Enterococcus faecalis that cause urinary tract infections, and may be associated with anatomical abnormalities of the urinary tract.
Can also be caused by mumps

84
Q

What causes epidiymo-orchitis in sexually active men?

A

In sexually active males aged 14-35 years, it is usually caused by Chlamydia trachomatis or Neisseria gonorrhoeae

In men 35 years of age or older, it is usually caused by enteric organisms (Escherichia coli or Enterococcus faecalis) that cause urinary tract infections, and may be associated with anatomical abnormalities of the urinary tract.

In men who have penetrative anal intercourse, it may be caused by enteric organisms that cause urinary tract infections.

Can also be caused by mumps or TB

85
Q

What are the features of epididymo-orchitis

A

gradual onset over hours or days
Usually painful and tender - may be relieved by elevation of testis
There is palpable swelling of the epididymis and/or testis.

There may be urethral discharge,
dysuria
parotid swelling (mumps orchitis usually occurs 4–8 days after parotitis),
or vomiting.

There may be erythema or oedema of scrotum on the affected side, or a hydrocele.

86
Q

What are the features of epidiymo-orchitis caused by TB?

A

scrotum is painless and non-tender
the epididymis is hard with an irregular surface,
the spermatic cord is thickened,
the vas deferens feels hard and irregular (like a string of beads).

87
Q

What is the management of epididymo-orchitis in an adult?

A

If due to STI:
ceftriaxone 500 mg IM,
plus doxycycline 100 mg orally twice daily for 10–14 days.
If gonorrhoea is considered likely, azithromycin should be added to ceftriaxone and doxycycline.
Refer to a sexual health specialist for follow up and contact tracing.
Advise the man or adolescent boy not to have any sexual contact during treatment and until his sexual partners have been traced and treated.

If due to an enteric organism (for example, Escherichia coli):
Treat without waiting for test results with ofloxacin 200 mg by PO BD for 14 days, or levofloxacin 500 mg PO OD for 10 days.
If a quinolone is contraindicated, treat with co-amoxiclav 500/125 mg three times daily for 10 days.

88
Q

What is a varicoele and what causes it?

A

collection of dilated veins of the pampiniform plexus in the spermatic cord leading to scrotal swelling
It may be caused by incompetent or absent valves in the testicular (spermatic) vein or may be secondary to a tumour or other pathological process obstructing the spermatic vein.

89
Q

How are varicocoele’s graded?

A 
Sub-clinical — detected only by Doppler ultrasound.
Grade I (small) — palpable only with Valsalva manoeuvre.
Grade II (moderate) — palpable without Valsalva manoeuvre. 
Grade III (large) — visible through the scrotal skin.
90
Q

Which side do most varicocoeles occur on? Why?

A

The left side

A varicocele drains into the spermatic vein within the inguinal canal on each side.

The right internal spermatic vein drains at an oblique angle into the inferior vena cava

The left internal spermatic vein drains vertically into the left renal vein at a right angle and is 8–10 cm longer
resulting in increased hydrostatic pressure, leading to dilation of the pampiniform plexus.

91
Q

What are some of the complications of varicoceles? Why?

A

abnormal gonadotrophin levels,
impaired spermatogenesis,
histological changes to sperm
infertility.

impaired countercurrent mechanism leading to thermal damage (intrascrotal temperatures normally 1–2°C lower than normal body temperature)

92
Q

What are the clinical features of a varicocoele?

A

painless scrotal swelling (on the left)
‘bag of worms’ within the spermatic cord above the testis
The scrotum on the side of the varicocele may be seen to hang lower than on the normal side.
Dilation and tortuosity of the veins is increased on standing and is decreased no lying down - cannot usually be palpated lying down.
Performing the Valsalva manoeuvre whilst standing increases dilation.
There may be a cough impulse.
smaller testis on affected side

93
Q

How is a varicoceole managed in an adolescent?

A

Subclinical or grade I varicocele — no treatment is necessary.

Grade II or III varicocele and symmetrical testes — observe with annual examinations.

Grade II or III and asymmetrical testes - The primary indication for surgery is testicular growth arrest.

94
Q

How is a varicoceole managed in a man?

A

Sub-clinical or grade I varicocele — no treatment is necessary.
Offer semen analysis if fertility is a concern.

Grade II or III asymptomatic varicocele and normal semen parameters — observe with semen analysis every 1–2 years.

Grade II or III symptomatic varicocele, or with abnormal semen parameters — refer to a urologist for possible surgery.

95
Q

What investigations might be done in a man with a suspected varicocele

A

Serum FSH and LH levels and response to luteinising hormone-releasing hormone (LHRH) - Testicular injury can be assessed by a supranormal LH and FSH response to LHRH

sperm count

colour doppler - only if clinical examination inconclusive

CT to diagnose obstructing tumour

96
Q

What are the indications for surgical treatment of a varicocele

A

Pain.
Infertility (controversial)
To prevent testicular atrophy.

97
Q

What does surgical treatment of a varicocele involve?

A

ligation of veins to prevent abnormal blood flow.

98
Q

What is an epididymal cyst?

A

benign, usually small, non-painful cystic swellings of the epididymis,
may be multiple and are frequently bilateral.
If the cyst contains spermatozoa, it may be referred to as a spermatocele.

99
Q

What are the features of an epididymal cyst?

A

Occur in middle-aged men
Onset is chronic.
painless, non-tender, soft, fluctuant, smooth, round nodule in the epididymis.
the testis is palpable separately from the cyst
It is usually small, but can become large.
Does not usually transilluminate.

100
Q

How is an epididymal cyst managed?

A

If confident of the diagnosis:
Reassure the man that epididymal cysts/spermatoceles are common, harmless, rarely cause any symptoms, and rarely need treatment.
If the man has bothersome symptoms, offer referral for a routine outpatient appointment with a urologist.

If there is diagnostic uncertainty, refer for ultrasound.

101
Q

What are undescended testes

A

the incomplete descent of one or both testes and absence from the scrotum
The testis or testes usually remain in the abdomen or inguinal canal

102
Q

Define true undescended testes

A

testes lie along the normal path of descent in the abdomen or inguinal region and have never previously been present in the scrotum.
The testis is often small and abnormal with a short spermatic cord

103
Q

Define ectopic testes

A

testes lie outside of the normal path of descent, for example in the femoral region, perineum, or penile shaft.

104
Q

Describe normal testicular descent

A

Normal testicular development in utero begins along the mesodermal ridge of the posterior abdominal wall. By 28 weeks, the right and left testes reach their respective inguinal canals
by 28-40 weeks, each testis has usually reached the scrotum.

105
Q

What are ascending testes

A

when testes have previously been present in the scrotum but have come to lie permanently outside it.

This may occur with spontaneous involution of connecting structures, such as a shortened spermatic cord that prevents the testis from staying in the scrotum.

106
Q

What are some risk factors for undescended testes

A

A first degree relative with a history of undescended testes.
Low birth weight.
Small for gestational age.
Preterm delivery.
Having another genital abnormality (for example hypospadias).

107
Q

When are boys screened for undescended testes?

A

At each baby check!

Within 72 hours of birth.
At 6–8 weeks of age.
A further examination should be carried out at 3 months of age if testes have previously been found to be undescended.

108
Q

What are retractile testes?

How are they managed?

A

Prepubertal boys can have an exaggerated cremasteric reflex, so the testis may retract out of the scrotum in the cold, on examination, on excitement or on physical activity.

It is normal and will descend when relaxed and warm, or it can be manipulated back into the scrotum.
Retractile testes do not need any treatment but do need close follow-up until puberty, as they can become ascendant.

109
Q

How should a boy be examined for undescended testis?

A

lying down in a warm room.
Ensure your hands are warm and the person relaxed, if possible.

Examine for a testis in the inguinal region
An undescended testis may be felt as a ‘pop’ under the examiner’s fingers.

If the testis is not present in the scrotum or inguinal region, examine for an ectopic testis in the femoral, penile, and perineal regions.

Check for ambiguity of the external genitalia, and for abnormalities such as hypospadias and any syndromic features.

110
Q

How can an undescended testis be distinguished from an retractile testis on examination?

A

Try to move the testis down from the inguinal region into the scrotum and hold it there for one minute to fatigue the cremaster muscle, then release.

An undescended testis will return to its original position as soon as it is released

A retractile testis can be brought to the base of the scrotum and remain there by itself and will usually stay in the scrotum for a short time until the cremasteric reflex retracts it into the groin.

111
Q

How should undescended testes be managed in an child if there is a suggestion of a disorder of sexual development or there is bilateral undescended testes?

A

If there is a suggestion of a disorder of sexual development (for example ambiguous genitalia or hypospadias), urgently refer to a senior paediatrician within 24 hours (ideally within a tertiary children’s unit with a specialist disorders of sexual development service) as the child may need urgent endocrine or genetic investigation.

If undescended testes are bilateral at birth:
Urgently refer to a senior paediatrician within 24 hours (ideally within a tertiary children’s unit with a specialist disorders of sexual development service) as the child may need urgent endocrine or genetic investigation.

112
Q

How should unilateral undescended testes be managed in an child at birth?

A

arrange review at 6–8 weeks of age.

113
Q

How should unilateral undescended testes be managed in an child at 6-8w?

A

re-examine at 3 months of age.

114
Q

How should unilateral undescended testes be managed in an child at 3m?

A

If one or both are retractile, annual follow up is needed throughout childhood as there is a significant risk of ascending testes.

If the testis is still undescended, refer the child to be seen by an appropriate paediatric surgeon, ideally before 6 months of age.

115
Q

What is the treatmetn for undescended testes?

A

palpable: inguinal orchidopexy
impalpable: laparoscopy + 1/2 stage orchidopexy

116
Q

What investigations can be done to locate an undescended non-palpable testis?

A

EUA may reveal the previously non-palpable testis.

laparoscopy

117
Q

What are the complications of undescended testes?

A

Impaired fertility
Testicular cancer
- risk may be reduced if orchidopexy is performed before puberty
Testicular torsion

118
Q

What is the cause of impaired fertility in undescended testes?

A

Undescended testes are 2–3 °C warmer in the abdomen than in the scrotum, which may result in impaired spermatogenesis.

119
Q

What is acute urinary retention

A

a sudden inability to pass urine

120
Q

Give some categories of teh causes of acute urinary retention

A 
structural
infectious/inflammatory
drugs
neuro
post-operative
121
Q

Give someo structural causes of acute urinary retention

A

In men - benign prostatic hyperplasia (BPH), meatal stenosis, paraphimosis, penile constricting bands, phimosis, prostate cancer.

In women - prolapse (cystocele, rectocele, uterine), pelvic mass (gynaecological malignancy, uterine fibroid, ovarian cyst), retroverted gravid uterus. Postpartum - c section, instrumental

In both - bladder calculi, bladder cancer, faecal impaction, gastrointestinal or retroperitoneal malignancy, urethral strictures, foreign bodies, stones.

122
Q

Give some infectious or inflammatory causes of acute urinary retention

A

In men - balanitis, prostatitis and prostatic abscess.

In women - acute vulvovaginitis, vaginal lichen planus and lichen sclerosis, vaginal pemphigus.

In both - bilharzia, cystitis, herpes simplex virus (particularly primary infection), peri-urethral abscess, varicella-zoster virus.

123
Q

Give some drugs that can cause acute urinary retention

A 
Anticholinergics (eg, antipsychotic drugs, antidepressant agents, anticholinergic respiratory agents).
Opioids and anaesthetics.
Alpha-adrenoceptor agonists.
Benzodiazepines.
Non-steroidal anti-inflammatory drugs.
Detrusor relaxants.
Calcium-channel blockers.
Antihistamines.
Alcohol.
124
Q

Give some neurological causes of acute urinary retention

A

Autonomic or peripheral nerve (eg, autonomic neuropathy, diabetes mellitus, Guillain-Barré syndrome, pernicious anaemia, poliomyelitis, radical pelvic surgery, spinal cord trauma, tabes dorsalis).

Brain (eg, cardiovascular disease (CVD), multiple sclerosis (MS), neoplasm, normal pressure hydrocephalus, Parkinson’s disease).

Spinal cord (eg, invertebral disc disease, meningomyelocele, MS, spina bifida occulta, spinal cord haematoma or abscess, spinal cord trauma, spinal stenosis, spinovascular disease, transverse myelitis, tumours, cauda equina).

125
Q

Give some post-operative causes of acute urinary retention

A

Pain.
Traumatic instrumentation.
Bladder overdistension.
Drugs (particularly opioids).
Iatrogenic - for example: Suburethral sling procedures for stress incontinence.
Decreased mobility and increased bed rest.

126
Q

What questions is it important to ask when taking a history in acute urinary retention

A

any LUTS?
any precipitants - alcohol, surgery, UTI, constipation
any neuro probs?
current meds

127
Q

What should be examined, and what for, in acute urinary retention

A

abdomen - tender, enlarged bladder. dullness to percussion well above symphysis pubis

GU - phimsis, meatal stenosis, urethral discharge, vulval inflam, prolapse, pelvic mass

PR - tone, prostate, faecal impaction

neuro - power, reflexes

128
Q

What investigations should be done in acute urinary retention

A 
urine dip, MSU
FBC, U+E, PSA, CRP
USS bladder
CT abdomen pelcis
cystoscopy
129
Q

How should acute urinary retention be managed

A

immediate: insertion of indwelling catheter for complete bladder decompression
During this polyuric state large volumes of salt and water are lost, with the risk of patients developing hypovolaemia, dehydration, and electrolyte imbalances.
Consequently, daily monitoring of U+Es is required to monitor patients,

long term:
alpha blocker (alfuzosin) and TWOC
intermittent catheterisation
long term indwelling catheter
130
Q

What are some complications of acute urinary retention

A

UTI
AKI
post obstructive diuresis
post retention haematuria

131
Q

What are the symptoms of acute urinary retention

A

uncomfortable
unable to pass urine
painful bladder!

132
Q

What is the most common cause of acute urinary retention

A

BPH

133
Q

What is chronic urinary retention

A

a bladder that does not empty completely or does not empty at all. most commonly due to bladder outlet obstruction

134
Q

What commonly causes bladder outlet obstruction in chronic urinary retention

A

BPH
prostatic carcinoma
sphincter dysfunction - antispasmodics etc
iatrogenic - colposuspension
congenital
urethral strictures - due to trauma or infection (TB, gonorrheoa)

135
Q

What are the symptoms of chronic urinary retention

A

LUTS!

Nocturia
Urinary urgency.
Urinary frequency.
Urinary incontinence.
New-onset enuresis

Urinary hesitancy.
Poor urinary stream.

Post-micturition dribbling.
.A sensation of incomplete voiding after micturition.
‘Double’ or recurrent voiding of urine (returning to micturition due to a sensation of ‘needing to go again’).

also:
Increasing lower abdominal discomfort
Acute urinary retention.
Lethargy, pruritus, recurrent infections, hypertension due to chronic kidney disease

136
Q

What are the signs of chronic urinary retention

A

abdo = palpable bladder, non tender. ?enlarged kidneys
PR - prostate

also check genitalia and neuro

137
Q

What investigaitons should be done in chronic urianry retention

A

Urine dip, MSU
U+E, FBC, glucose, PSA
USS - transrectal!
urodynamic studies

138
Q

How is chronic urinary retention managed

A

intermittent catheterisation
or indwelling catheter

Stop any precipitating/aggravating medication.

General lifestyle advice such as:
Regulating fluid intake and avoiding evening drinking.
Reducing alcohol intake.
Reducing tea and coffee intake.
Preparation enabling access to toileting facilities.

Use of bladder retraining and regular voiding. Bladder training is less effective than surgery for bladder outlet obstruction.

surgery if appropriate

139
Q

What are the complications of chronic urinary retentions

A

Acute (on chronic) retention of urine.
Hypertrophy of detrusor muscle and formation of bladder diverticula.
Hydronephrosis due to chronic back pressure on kidneys, ultimately resulting in acute kidney injury or chronic kidney disease.
Urinary incontinence due to overflow.

140
Q

State the LUTS symptoms to do with storage

A 
urgency
frequency
nocturia
incontinence
feeling the need to urinate again after voiding
141
Q

State the LUTS symptoms to do with voiding

A 
hesitancy
weak or intermittent stream
splitting 
spraying
straining
intermittency
terminal dribbling
142
Q

State the LUTS symptoms post micturition

A

post voiding dribble

incomplete emptying

143
Q

What are the causes of voiding LUTS

A 
BPH
antimuscarinic drugs
diabetic autonomic neuropathy
urethral stricture
phimosis
prostate cancer
bladder cancer
144
Q

What examination need to be done for LUTS

A

abdominal - ?distended bladder
external genitalia - discharge, phimosis, meatal stenosis
DRE - size, consistency, nodules on prostate
neuro motor and sensory of lower limbs

urinary frequency-volume chart for 3 days
IPSS - international prostate symptom score

145
Q

What are the groups of causes of male infertiltiy

A 
primary spermatogenic failure
genetic
obstructive azoospermia
varicocoele
hypogonadism
undescended testes
drugs
ejaculation problems or erectide dysfunction
lifestyle
146
Q

What are the causes of primary spermatogenic failure

A

Congenital:
Anorchia (absence of testes).
Testicular dysgenesis/cryptorchidism.
Genetic abnormalities (karyotype, Y-chromosome deletions).

Acquired:
Trauma.
Testicular torsion.
Post-inflammatory forms, especially mumps orchitis.
Exogenous factors (medications, cytotoxic or anabolic drugs, irradiation, or heat).
Systemic diseases (liver cirrhosis, renal failure).
Testicular tumour.
Varicocele.
Surgery that may compromise vascularisation of the testes and lead to testicular atrophy.

Idiopathic (unknown aetiology and pathogenesis).

147
Q

What is obstructive azoospermia

A

absence of both spermatozoa and spermatogenic cells in semen and post-ejaculate urine due to bilateral obstruction of the seminal ducts

148
Q

what can cause obstrucitve azoospermia

A

Ejaculatory duct obstruction:
Congenital — prostatic cysts (Mullerian cysts).
Acquired — after infection or surgery (such as bladder neck surgery).

Vas deferens obstruction:
Congenital — absence of the vas deferens.
Acquired — after vasectomy or surgery (such as hernia, scrotal surgery).

Epididymal obstruction:
Congenital — idiopathic epididymal obstruction.
Acquired — after infection (such as epididymitis) or surgery (such as epididymal cysts).

149
Q

What can cause hypogonadism in a male

A

Primary (hypergonadotropic) hypogonadism due to testicular failure.

Secondary (hypogonadotropic) hypogonadism caused by insufficient gonadotropin-releasing hormone (GnRH) and/or gonadotropin (follicle stimulating hormone [FSH] and luteinizing hormone [LH]) secretion.

Androgen insensitivity (end-organ resistance).

150
Q

Which drugs can cause infertility in a male

A

Sulfasalazine - reversible on withdrawal of therapy or by switching to mesalazine
Androgens and anabolic steroids — can lead to reduction in the volume of the testes and azoospermia or oligospermia because of suppression of gonadotropins
Chemotherapy with cytotoxic drug

151
Q

What questions need to be asked in a history of male infertility

A 
any prev children
freq/difficulties in intercourse
mumps
STIs
torsion
trauma
urogenital surgery
ED, ejaculatory dysfunction
systemic disease
DH
occupation
lifestyle - stress, obesity, smoking, recreational drugs, alcohol
152
Q

What should be examined when investigating a man for infertility

A

penis - position of the urethral meatus, for structural abnormalities.
scrotum - lumps (cancer, varicocele, or hernia); small, soft testes (which may indicate hypogonadism); or undescended testes.
secondary sexual characteristics - hypogonadism
gynaecomastia - hypogonadism.

153
Q

What investigations should be done in a male with infertlity

A

semen analysis

chlamydia

154
Q

Define erectile dysfunction

A

the persistent inability to attain and maintain an erection sufficient to permit satisfactory sexual performance.
organic and/or psychogenic cause

155
Q

Name some organic causes of ED

A

Vasculogenic — cardiovascular disease (CVD), hypertension, hyperlipidaemia, diabetes mellitus, smoking, major pelvic surgery (radical prostatectomy), radiotherapy (pelvis or retroperitoneum).

Neurogenic (central) — degenerative disorders (such as multiple sclerosis, Parkinson’s disease, and multiple atrophy), stroke, spinal cord trauma or diseases, central nervous system tumours.

Neurogenic (peripheral) — diabetes mellitus, chronic renal failure, polyneuropathy, major surgery of the pelvis or retroperitoneum, urethral surgery (for example urethral stricture and urethroplasty).

Anatomical or structural — Peyronie’s disease, penile cancer, congenital curvature of the penis, micropenis, hypospadias, epispadias, phimosis.

Hormonal — hypogonadism, hyperprolactinaemia, hyperthyroidism, hypothyroidism, Cushing’s disease, panhypopituitarism and multiple endocrine disorders, hypopituitarism following traumatic brain injury (erectile dysfunction is estimated to occur in 15–25% of survivors of traumatic head injury and is often unrecognized)

156
Q

Name some psychogenic causes of ED

A

Generalized — for example due to lack of arousability and disorders of sexual intimacy.

Situational — for example due to partner-or performance-related issues, stress, and psychiatric illness (including depression, anxiety, and schizophrenia).

157
Q

Name some drugs that can cause ED

A

Antihypertensives — beta-blockers, verapamil, methyldopa, and clonidine.
Diuretics — spironolactone and thiazides.
Antidepressants — tricyclics, monoamine oxidase inhibitors, selective serotonin reuptake inhibitors.
Antiarrhythmic drugs — digoxin, amiodarone.
Antipsychotics — chlorpromazine, haloperidol.
Hormones and hormone-modifying drugs — antiandrogens (flutamide, cyproterone acetate), luteinising hormone releasing hormone agonists (leuproelin, goserelin), corticosteroids, 5-alpha reductase inhibitors (for example finasteride).
Histamine (H2)-antagonists — cimetidine, ranitidine.
Recreational drugs — alcohol, heroin, cocaine, marijuana, methadone, synthetic drugs, anabolic steroids.

Finals (32 decks)

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