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Y3 Surgery > urology > Flashcards

urology Flashcards

1
Q

What may cause pseudohaematuria?

A
  • drugs like rifampicin or methylodopa
  • hyperbilirubinurea
  • myoglobinurea
  • beetroot and rubarb
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2
Q

What may cause haematuria? (give at least 5)

A
  • infection: bladder, prostate, kidney
  • malignancy: bladder, kidney, ureter, prostate
  • renal calculi
  • trauma, recent surgery
  • radiation cystitis
  • schistomiasis
  • BPH
  • antiplatelet or anti coag drugs (investigate as normal)
  • glomerular nephritis
  • recent transrectal biopsy of prostate
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3
Q

What are important features to ask about in haematuria presentation?

A
  • timing in stream (total suggests bladder is source, early suggest lower tract and late suggests severe bladder irritation)
  • clots vs diluted
  • other syptoms: fevers, rigors, suprapubic or flank pain, weight loss, trauma
  • drug history
  • smoking status (++ risk urological malignancy)
  • occupation (industrial carcinogens ++ bladder ca)
  • travel: schistomiasis
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4
Q

How is haematuria initially managed/ investigated?

A
  • urinalysis: ? infection
  • bloods: u&e, fbc, clotting, psa
  • urinary protein levels if renal function off
  • urgent refferal if: age>45 and unexplained w/out UTI or visible that persists after UTI treatment OR age >60 w/ unexplained non visible and dysuria or raised WCC
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5
Q

What specialist investigations may be requested for haematuria?

A
  • flexible cystoscopy
  • urine cytology in some places
  • US KUB: for non visible haematuria
  • CT urogram: usually for visible haematuria
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6
Q

Where do RCCs tend to arise from and where do they spread to?

A
  • arise from PCT and appear most often in upper poles of kidneys
  • spread directly to perinephris tissues, adrenal gland or into renal vein (may cause tumour thrombosis), IVC, lymphatic system (pre aeortic or hilar nodes) and to bone, liver, brain and lung via the blood.
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7
Q

Give 5 risk factors for RCC

A
  • SMOKING (biggest)
  • industrial exposure to cadmium or aromatic hydrocarbons
  • dialysis (30x increase)
  • hypertension
  • obesity
  • APCKD
  • horseshoe kidneys
  • some other rarer genetic disorders
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8
Q

Describe the clinical features of RCC

A
  • haematuria (usually visible, may be invisible, is most common PC)
  • flank pain
  • flank mass
  • lethargy, weight loss, pyrexia of unknown origin
  • left varicocele if impinging left testicular vein
  • paraneoplastic syndrome
  • hypertension
  • features of mets such as haemoptysis or #
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9
Q

What paraneoplastic syndromes may RCC cause?

A
  • EPO secretion-> polycythaemia
  • PTH-> hypercalcaemia
  • Renin-> hypertension
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10
Q

How is suspected RCC investigated?

A
  • USS usually already one
  • CT abdo pelvis with contrast
  • CXR for mets
  • Biopsy to stage
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11
Q

How can RCC be managed? (if small, large, unfit for surg and metastatic)

A
  • SMALL-> partial nephrectomy
  • LARGE-> radial nephrectomy
  • not fit for surg-> percutaneous radiofrequency ablation, laparoscopic cyrotherappy, renal artery embolisation
  • If old person + slow growing tumour+ unfit for surg-> surveillance
  • METASTATIC-> immunotherapy (sunitinib) + nephrectomy +/- metastatectomy
  • CHEMO CONSIDERED INEFFECTIVE
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12
Q

What is involved in a radical nephrectomy?

A

Remove the kidney, perinephric fat and local lymph nodes

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13
Q

How does an upper tract TCC usually present?

A
  • haematuria (visible or invisible)
  • post renal AKI +/- hydronephrosis
  • loin pain
  • palpable mass
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14
Q

What suggests a TCC is higher risk?

A
  • hydronephrosis
  • infiltrative features
  • high grade
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15
Q

How is TCC managed? (if high and low risk)

A
  • radical nephroureterectomy with bladder cuff excision

- lower risk TCCs can be managed more conservatively

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16
Q

What age and gender tends to get bladder cancer and what is the prognosis like usually?

A
  • usually males >80

- most are superficial so have good prognosis

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17
Q

How are bladder cancers classified?

A
  • non muscle invasive (papillary (Ta), into LP or subepithelial (T1))
  • muscle invasive (T2)
  • locally advanced (into perivesible tissues (T3) or adjacent structures (T4))
  • metastatic
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18
Q

How do bladder cancers tend to present

A
  • haematuria usually
  • may be recurrent UTIs, LUTS, ureteric obstruction
  • weightloss, PUO or mets if more advanced
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19
Q

How bladder cancers investigated?

A
  • flexible cystoscopy then rigid cystoscopy if they find something
  • when doing rigid cystoscopy do TURBT and histology
  • CT staging before TURBT if lesion is invasive
  • urine cystology is rarely used
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20
Q

How is non muscle invasive bladder cancer managed?

A

TURBT resection, higher risk disease may require adjuvant intravesicle chemo with BCG or mitomycin C or they can be offered radical cystectomy.
Theyll need cytology and cystoscopy follow up due to high recurrence rates

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21
Q

How is muscle invasive and locally advanced or metastatic bladder cancer managed?

A
  • muscle invasive= radical cystectomy + neoadjuvant chemo (cisplatin) + regular CT follow up
  • locally advanced or mets= chemo (cisplatin) + symptom management, usually palliative
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22
Q

What are the two options of urinary diversion following radical cystectomy?

A
  • ileal conduit: urine drains into urostomy (ureters attach to small piece of bowel which is made into a stoma)
  • bladder reconstruction: segment of small bowel used to form neobladder, urine drains from this out through urethra or catheter. Needs routine bloods, B12 and folate annually due to ileal resection.
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23
Q

What is the most common histological type of prostate cancer and from which part of the prostate do they most commonly arise?

A
  • adenocarcinoma
  • from peripheral zone
  • can be acinar (most common) or ductal (grow and metastasise faster
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24
Q

Give 3 risk factors for prostate cancer

A
  • old age
  • black african or caribbean
  • fhx (significant if in 1st degree relative younger than 60)
  • BRCA1 or 2 genes
  • obesity, diabetes, smoking, exercise less significant
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25
Q

What is PSA and what is its use?

A

A protease normally produced by the prostate to make semen more liquid.
Youre unlikley to have prostate can cancer if its low (85% NPV) but there are lots of causes of high PSA so isnt very specific (30% PPV). It can also be used for disease progression monitoring

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26
Q

Other than prostate cancer, what may cause PSA to be elevated?

A
  • BPH
  • Prostatitis
  • vigerous exercise
  • DRE
  • ejaculation
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27
Q

How should suspected prostate cancer be investigated?

A
  • DRE and PSA initially
  • transperineal biopsy: under general, lower infection risk, better access to anterior prostate
  • transrectal US guided biopsy: under local, 12 cores are taken, 1-2% sepsis risk
  • repeat biopsy if suspicious DRE or persistently elevated PSA
  • gleason score is given based off histology
  • Multi parametric MRI may be used to target biopsies better
  • CT CAP and bone scan done for men with intermediate and high risk disease
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28
Q

What does the gleason scale take account for?

A

most common glandular growth pattern plus the highest grade (most differentiation) seen- higher gleason = worse prognosis

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29
Q

What is taken into account when assessing risk of prostate cancer?

A
  • PSA
  • gleason score
  • clinical stage (TNM)
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30
Q

How are low risk prostate cancers managed?

A
  • active surveillance (3 monthly PSAs, 6 monthly DRE and 1-3 yrly biopsies)
  • or watchful waiting (symptom and QoL guided care, used in elderly with low LE, can be offered for any stage/ risk prostate cancer)
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31
Q

How are intermediate and high risk and metastatic prostate cancers managed?

A
  • radical prostatectomy (prostate, seminal vesicles, surrounding tissues and pelvic lymph node removal)
  • if metastatic: chemo and chemical castration (LHRH agonists or GnRH agonists to surpress testosterone) or orchiectomy for surgical castration, new hormone therapies also available for metastatic
  • external beam and brachytherapy becoming curative for localised disease
  • intermediate risk sometimes managed with active surveillance
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32
Q

What are side effects/ risks of radical prostatectomy?

A

erectile dysfunction, stress incontinence and bladder neck stenosis

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33
Q

What types of testicular cancer are there and how common are they?

A
  • 95% are germ cell tumours
  • 5% non germ cell (leydig or sertoli, good prognosis)
  • 50% germ cell tumours are seminomas
  • 50% germ cell are non seminomas (yolk sac, choriocarcinoma, teratoma, usually malignant)
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34
Q

Give 3 risk factors for testicular cancer

A
  • cryptoorchidism
  • Fhx
  • kleinfelter syndrome
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35
Q

What are the clinical features of testicular cancer

A
  • unilateral painless, irregular, firm, fixed lump which doesnt transilluminate
  • weightloss, back pain or dyspnoea
  • lymphatic drainage is to para- aortic nodes so rarely presents with lymphadenopathy
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36
Q

How should suspected testicular cancer be investigated?

A
  • beta HCG
  • AFP
  • LDH as surrogate marker for tumour volume
  • Scrotal USS for initial assessment
  • CT CAP with contrast for staging
  • transcrotal percutaneous biopsy is NOT done as may cause seeding of the cancer
  • Staging is with royal marsden classification
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37
Q

What are the use of beta HCG and AFP?

A
  • beta HCG rasied in 60% NSGCT and 15% seminomas

- AFP raised in some NSGCT

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38
Q

How is testicular cancer managed? (stage 1 seminomas, higher stage seminomas, stage 1 and metastatic NSGCT)

A
  • stage 1 seminomas-> orchidectomy
  • inguinal radial orchidectomy for higher stage seminomas
  • stage 1 NSGCT-> orchidectomy, if low risk the surveillance if high risk them adjuvant chemo
  • metastatic NSGCT-> chemotherapy
  • pre treatment fetility assessment and cryopreservation is offered usually
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39
Q

What is the prognosis like for testicular cancer?

A

very good even when metastatic

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40
Q

Describe what histological type penile cancer is and how it spreads

A
  • squamous cell carcinoma
  • spreads locally into corpus cavernosa and to inguinal nodes
  • distant mets are uncommon
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41
Q

What type of renal stones can you get?

A
  • calcium oxalate (30%)
  • mixed calcium (35%)
  • calcium phosphate (10%)
  • struvite
  • cystine
  • urate
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42
Q

When do urate, struvite and cysteine stones tend to occur?

A 
Urate= high levels of purine (lots of red meat or haemotological disorders)
Struvite= from recurrent infections (tend to be soft and cause staghorn calculi)
Cysteine= hypocystinuria (less cysteine absorbtion from bowel and kidney= less citrate which is a stone absorber)
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43
Q

Where are the 3 natural narrowings in the urinary system that stones tend to get stuck

A
  • pelviureteric junction
  • where the iliac vessels cross the ureter
  • vesicoureteric junction
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44
Q

Describe the features of renal colic?

A
  • sudden onset, severe, colicky pain radiation from loin to groin
  • often associated N+V
  • haematuria in 90%, usually invisible
  • flank tenderness and signs of dehydration
45
Q

Give 3 differentials for renal colic

A
  • pyelonephritis (pain less sudden more constant)
  • ruptured AAA (central- back pain)
  • biliary pathology (usually epigastric but could be right flank)
  • lower lobe pneumonia
  • MKS related pain
46
Q

How should ureteric colic be investigated?

A
  • urine dip: expect haematuria but may have concurrent infection so do urine dip
  • routine bloods: FBC, CRP, U&E, urate and calcium levels
  • NON CONTRAST CT KUB is gold standard for diagnosis
  • plain film AXR can be used but urate stones are radiolucent
  • USS KUB can be used to asses for hydronephrosis but can only detect ureteric stones, not renal
47
Q

How are ureteric stones initially managed?

A
  • Often dehydrated secondary to reduced oral intake + vomiting -> IV fluids
  • analgesia with NO2, IM/IV morphine and/ or rectal diclofenac (most effective)
  • IV abx and urgent urology referal if sepsis or evidence of infecton
  • stones <5mm will pass spontaneously
  • JJ stent if evidence of significant infection or obstructive nephropathy
  • definitive management
48
Q

Describe what a JJ stent is

A

a stent placed within ureter via a cystoscopy to keep the ureter patent and so avoid post renal AKI

49
Q

What are the 3 definitive management options for renal calculi? when is each used?

A
  • extra corporeal shock wave lithotripsy (stones <2cm), not if pregnant or near boney landmark
  • percutaneous nephrolithotomy (for renal stones and staghorn calculi only-
    stones fragmented by lithotripsy via nephroscope)
  • flexible urtero renoscopy- pass a scope up the ureter and fragment through laser lithotripsy and remove the fragments (>2cm ureteric stones)
50
Q

Give 3 complications of renal calculi

A
  • infection
  • post renal AKI
  • renal scarring and loss of function from recurrent stones leading to CKD
51
Q

How do bladder stones form?

A

Due to urinary stasis in bladder so secondary to chronic urinary retention or infections

52
Q

How do bladder stones tend to present?

A

Lower urinary tract symptoms- pain at end or urinary often reffered to tip of penis, frequency, incomplete emptying, haematuria

53
Q

How are bladder stones managed?

A
  • cystoscopy

- allow to drain or fragment with lithotripsy

54
Q

How should recurrent stones be managed? (think about specifics for each type)

A
  • stay hydrated and collect stones for analysis
  • oxalate stone formers should avoid high purine and oxalate foods (nutes, rubarb, red meat, sesame)
  • calcium stone formers need PTH checked and avoid excess dietary salt
  • urate stone formers should avoid high purine food (red meat and shellfish), may need allopurinol
  • cysteine formers may need genetic testing
55
Q

How should non obstructive stones be managed?

A
  • active monitoring
  • can break up with extra corporeal shockwave lithotripsy
  • some removed with percutaneous nephrolithotomy
56
Q

give 3 risk factors for pyelonephritis

A
  • female age 15-29
  • reduced antegrade flow- obstruction (BPH, stone), neurogenic bladder
  • retrograde asent of bacteria- female, indwellling catheter, JJ stent, vesico ureteric reflux
  • diabetes, steroid use, untreated HIV
  • factors increasing bacterial colonisation: renal calculi, sexual intercourse, oestrogen depletion
57
Q

Describe the clinical features of pyelonephritis

A
  • Unilateral loin pain (1-2 days gradual onset, constant)
  • fever and n+v often associated
  • coexisting lower UTI and its features
  • visible or invisible haematuria
  • many are septic
  • costovertebral angle tenderness +/- suprapubic tenderness
58
Q

Give 3 differentials for pyelonephritis

A
  • renal colic
  • ruptured AAA
  • ectopic pregnancy
  • acute cholecystitis
  • PID
  • lower lobe pneumonia
  • diverticulitis
59
Q

How should suspected pyelonephritis be investigated?

A
  • urinalysis
  • pregnancy test
  • urine culture
  • routine bloods
  • renal US or CT KUB if suspect obstruction also
60
Q

How should pyelonephritis be managed

A
  • A-E
  • Iv abx (intially coamox then go off sensitivities)
  • sepsis 6
  • analgesia and anti emetics
  • admit if: complicated, clinically unstable, significant dehydration, comorbidities such as renal transplant, diabetes or immunocompromised
  • severe non responding cases need catheters and HDU monitoring as can go downhill quick
61
Q

What are the most common causative organisms of prostatitis

A

E. coli

then chlamydia and gonorrhoea

62
Q

Give 3 risk factors for prostatitis

A

indewelling catheters
phimosis or urethral stricture
recent surgery, cystoscopy or TRUPB
immunocompromised

63
Q

Describe the clinical features of prostatitis

A

Deep perineal and/ or suprapubic pain
LUTS (dysuria, frequency, incomplete emptying etc)
systemic infection
uretheral discharge (rare)
chronic= pelvic pain (usually perineal) for 3 months alongside LUTS

64
Q

How should prostatitis be investigated?

A
  • urine culture
  • STI screen and routine bloods if in hospital setting
  • if fails to respond to abx, transrectal prostate USS or CT may be needed to rule out abscess
65
Q

How are acute and chronic prostatitis managed?

A
  • 4 weeks trimethoprim or cipro
  • paracetamol and NSAIDs for analgesia
  • admit if severely ill
  • if chronic: specialist referal for 4-6 weeks of alpha blockers (doxazosin or tamulosin) and 6 weeks of abx, if this no work then chronic pain referral
66
Q

What are the most common causative organisms of epididmytis and orchitis?

A
  • epididmytis: age 15-30= gonnorrhoea, age >60= e.coli
  • orchitis: very rare, occurs as a complication of mumps, tends to be bilateral + fever, and starts 4-8 days after parotid swelling, can lead to infertility
67
Q

Describe the clinical features of epididmo- orchitis

A
  • unilateral scrotal pain and swelling
  • fevers and rigors can also be present
  • dysuria, storage LUTS, urethral dischrage may be present due to underlyin cause
  • affected testicle is usually red, hot, swollen and tender, there may be an associated hydrocele also
68
Q

Give 3 differentials for epidido-orchitis

A
  • torsion (more sudden onset and severe, no LUTS)
  • trauma
  • abscess
  • hydrocele
  • epidydmal cyst
  • testicular tumour (not painful)
69
Q

How should suspected epidido- orchitis be investigated?

A
  • urine dip and low threshold for urine cultures
  • NAAT testing of urine for gonnorrohea and chlamydia
  • USS to confirm diagnosis and rule out abscesses if any uncertainty but not required
70
Q

How is epididmytis managed?

A
  • Doxy for 10 days and single dose IM ceftriaxone if <35
  • ofloxacin for 14 days if >35
  • pain relief
  • abstain from sex until abx completed and symptoms resolve
71
Q

Give 3 risk factors for testicular torsion

A
  • age 12-25
  • bell clapper deformity (horizontal lie to testis)
  • cryptoorchidism
72
Q

Describe the clinical features of testicular torsion

A
  • severe, sudden onset unilateral testicular pain
  • N+V
  • referred abdopain
  • testis will have high position, horisontal lie, swelling and severe tenderness O/e
73
Q

Give 3 differentials for testicular torsion

A
  • epididmyitis
  • trauma
  • incarcerated inguinal hernia
  • renal colic
  • hydrocele
74
Q

How is testicular torsion managed?

A
  • diagnosis is clinical but can do doppler USS if unsure
  • infarct within 4-6 hrs, so need urgent surgical exploration
  • if testis viable-> bilateral orchidoplexy (untwist and fix testis to scrotum to prevent recurrence)
  • if not viable-> orchiectomy and prosthesis insertion
75
Q

Give 4 voiding LUTS

A
  • hesitancy to micturition
  • poor flow
  • terminal dribbling
  • feeling of incomplete emptying
76
Q

Give 4 storage LUTS

A
  • increased frequency
  • nocturia
  • increased sense of urgency to urinate
  • urge incontinence
77
Q

How may LUTS be investigated?

A
  • DRE
  • urine dip stick
  • post void bladder scan
  • flow rate
  • urine frequency and volume chart
  • PSA and routine bloods
  • cystoscopy and urodynamic studies and USS or CT scan
78
Q

How can you distinguish between bladder outflow obstruction (BOO) and overactive bladder syndrome (OAB)?

A
  • low residual volume in OAB, high flow rate, no voiding symptoms
  • high residual volume and low flow rate in BOO
79
Q

What kind of LUTS will pts with OAB syndrome experience?

A
  • storage luts (increased freq, nocturia, urgency)

- storage and voiding (dripping, low flow, hesitancy, incomplete emptying) will be experienced by BOO

80
Q

How can BOO due to BPH be managed?

A

1st line- tamulosin (alpha blocker, relaxes prostatic smooth muscle, works within days)
2nd line- 5a reductase inhibitor (finasterine- prevents testosterone creation so shrinks prostate over months)
3rd line- TURP

81
Q

Give 1 complication of BPH

A

post renal AKI secondary to high pressure retention

82
Q

How should over active bladder syndrome be managed?

A
  • bladder training for 6 weeks
  • then antimuscarinics like oxybutynin
  • then try botulin toxin a injections and percutaneous sacral nerve stimulation
83
Q

What usually causes LUTS in women?

A
  • UTI most common
  • menopause, detrusor muscle weakness, urethral stricture, maligancy, neurological disease such as MS or spinal cord injury
84
Q

What is the most common cause of urge, stress and overflow incontinence in women?

A

Urge- in elderly and due to overactive bladder, may also be neurogenic or infection
Stress- pelvic floor weakness postpartum, in constipation, elderly, obesity and after pelvic surgery
Overflow- (IN MEN) usually due to chronic retention whereby progressive stretching leads to loss of bladder sensation, neurogenic bladders and spinal cord injuries are more likely causes in women

85
Q

How should urge incontinence be managed?

A
  • bladder training 6 weeks
  • antimuscarinics (oxybutynin)
  • botulinum toxin a injections
  • augmentation cystoplasty
  • percutaneous sacral nerve stimulation
86
Q

How should stress of mixed incontinence be managed?

A
  • pelvic floor exercises for 3 months
  • then duloxetine (stronger urethral contractions)
  • then tension free vaginal tape
  • intramural bulking agent
  • artificial urinary sphincter
87
Q

What causes acute urinary retention? (6)

A
  • BPH
  • stricture
  • infection
  • constipation
  • severe pain
  • antimuscarinic drugs
  • nerve damage
  • MND
88
Q

How should acute urinary retention be managed?

A
  • USS KUB for hydronephrosis assesment
  • immediate catheterisation
  • treat cause
  • if large volume retention (>1L), monitor for post obstructive diuresis
  • if high pressure retention (hydronephrosis), keep catheter in place until definitive management arranged (eg. TURP) due to risk of AKI with further episodes
  • if no renal impairment, TWOC and if they void within 24 hrs with minimal residual volume then its successful, if not put in long term catheter
89
Q

What is post obstructive diuresis?

A

rapid loss of medullary concentration gradient due to catheterisation, over diuresis in attempt to restore gradient leads to worsening of the AKI

90
Q

What can cause erectile dysfunction?

A
  • Vascular: atherosclerosis (50%)
  • trauma, surgery and radiotherapy to the pelvis
  • Neuro: parkinsons, stroke, MS, tumours, spine injury, disc prolapse, peripheral neuropathy
  • hormonal: hypogonadism, hyperprolactinaemia, thyroid disease, cushings disease
  • drugs: antihypertensives, betablockers, diuretics, antidepressants, antihistamines
  • Psychosexual: performance anxiety, situational factors, alcoholism, depression
91
Q

describe the clinical features of erectile dysfunction due to psychogenic cause?

A
  • early onset
  • early collapse or refection
  • premature or inability to ejactulate
  • problems or change in relationship
  • young age
  • self stimulated and waking erections still present
92
Q

How does erectile dysfunction due to organic causes present?

A
  • gradual onset
  • normal ejaculation
  • normal libido
  • operations, CVS risk factors, smoking, alcohol etc
93
Q

How is erectile dysfunction of organic cause investigated?

A
  • HbA1c, testosterone, lipid profile, FSH and LH, prolactin
  • noctural penile tumescence and rigidity studies, duplex USS of cavernous arteries, IV vasoactive drug injections, arteriograph and neurology studies may be requested by specialist
94
Q

How is erectile dysfunction managed

A
  • if psych cause: short term phosphodiesterase type 5 inhibitors (sildenafil) prescriptions are effective
  • otherwise treat cause
  • vaccum devices, intraurethral and topical prostaglandins and penile prosthesis are used where it cannot be cured
95
Q

What may cause high flow priaprism (unwanted painful erection lasting >4hrs)

A
  • unregulated cavernous sinus arterial inflow
  • penile, perineal or spinal trauma
  • can be triggered by sexual stimulation
96
Q

What may cause low flow priaprism?

A
  • ischaemic
  • caused by blockage to venous system
  • drugs/ meds
  • sickle cell, leukaemia or thalassaemia
97
Q

How can you distinguish between high and low flow priaprism?

A
  • corporeal blood gas
  • high flow = high pOe
  • low flow= low pO2
98
Q

How is priaprism managed?

A
  • corporeal aspiration
  • if unsucessful, intracavernosal sympathiomimetic agent injection
  • if this also fails, insert surgical shunt between cavernosa and glands (commonly leads to ED)
  • 90% lasting >24 hrs lose ability to have intercourse again
99
Q

What is paraphimosis?

A

inability to pull retracted foreskin back over the glans, results in impaired venous return, odema and ischaemia, infarction and potential infection

100
Q

How is paraphimosis managed?

A
  • urological emergency
  • penile block with anaesthetic (no adrenaline)
  • manual pressure applied to glans to reduce odema, then apply force to reduce the glans into the prepuce
  • dextrose soaked gauze and/ or ice can also be used to reduce the odema
  • dundee technique- needle punctures into the glans then squeeze area to allow drainage before manual reduction
  • a dorsal slit or emergency circumscision is used if manual techniques fail
101
Q

What is peyronies disease?

A
  • fiberous plaques forming in the tunica albugeniea
  • leads to penile angulation or hourglass deformity with distal flaccidity
  • usually only affects erect penis
  • thought to occur due to one off or repeated vascular trauma causing leakage and inflammation
102
Q

Describe the clinical features of indirect inguinalsacal hernias?

A
  • swelling is soft and reducible
  • ilicited/ moves on coughing
  • doesnt transilluminate
103
Q

Describe the clinical features of hydrocele

A
  • soft, fluid filled lump
  • transilluminates
  • cough impulse negative, non reducible
  • painless
104
Q

Describe the clinical features of epidydmal cyst

A
  • behind body of testis and is attached to it
  • transilluminates
  • painless
105
Q

Describe the clinical features of testicular cancer lumps

A
  • firm
  • nodular
  • non mobile
  • painles
  • doesnt transilluminate
106
Q

What is fornieres gangrene? what is the most common cause

A

a form of necrotising fasciitis affecting the perineum. usually caused by group a strep, c. perfringes and e coli

107
Q

Give 3 risk factors for fornieres gangrene?

A
  • diabetes
  • excess alcohol
  • poor nurtitional status
  • steroid use
  • haematological emergencies
  • recent trauma to the region
108
Q

Describe the clinical features of fornieres gangrene

A

severe pain
pyrexia
non specific rapid deterioration and sepsis
crepitus, skin necrosis and haemorrhagic bullae appear later

109
Q

how is fornieres gangrene managed?

A
  • urgent surgical debridgement
  • partial or total orchiectomy
  • depending on size of expansion, wound is left open usually
  • broad spectrum IV abx, HDU bed, A-E resus and close monitoring
  • often further debridements and skin grafts are needed

Y3 Surgery (7 decks)

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