Urology Flashcards

1
Q

HAEMATURIA

i) what are the two main types? which type has a higher risk of underlying malignancy?
ii) name four causes?
iii) what is the priority when someone presents with haematuria?
iv) what is likely happening if there is blood at the start of urinating? blood at the end? or mixed throughout? what if there are darker clots?

A

i) two main types are microscopic and macroscopic
- macroscopic has higher risk of underlying malignancy (20%)

ii) infection, trauma, stones, drugs (wafarin), gynae, pseudo (rifampicin and beetroot)
iii) need to rule out neoplasms and TCC bladder (20% of macro haematuria patients have an underlying neoplasm)

iv) blood at start > urtheral/prostatic
blood at end > blood from vladder neck
mixed > higher renal tract eg renal TB, stones, nephrotic/nephritic
- darker clots = from higher in the renal tract

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2
Q

INVESTIGATIONS FOR HAEMATURIA

i) what bloods are important?
ii) which type of CT is used for looking for cancer? what may be seen?
iii) which type of CT is used to look at renal masses?
iv) what does a cystoscopy allow visualisation of?
v) what area of the urinary tract must be imagined if there is haematuria?

A

i) FBC, U+E (obstruc renal fail), LFT (clotting problems), PSA
ii) CT urogram - contrast in the ureters and look for filling defects (any filling defect is cancer until proven otherwise)
iii) triple phase CT (nephrogenic, arterial and venous phase) to look for renal massess
iv) cystoscopy looks at urethra and bladder
v) must image upper tract if there is haematuria

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3
Q

CAUSES OF HAEMATURIA

i) what neoplasm may be the cause and is 80% of all abdominal tumours?
ii) name three things that can cause glomerulonephritis and therefore haematuria
iii) name three things that occur in childhood that can lead to haematuria
iv) name three things that can cause nephritic syndrome
v) name three neoplastic causes?

A

i) renal call carcinoma

ii) anti PLA2R (precursor to glom BM) - blood in urine due to leaky glom
- cancer
- hepatitis

iii) post strep glomerulonephritis (forms IgA complexes get stuck), IgA vasculitis (HSP)
iv) SLE, anti GBM (goodpasture), infective endocard, IgA nephropathy

v) transitional cell carcinoma (TCC) - bladder and urethra (multifocal)
renal cell carcinoma (unifocal)
prostate cancer

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4
Q

RENAL CELL CARCINOMA

i) what is the triad of presentations? what % of people have this triad?
ii) name three things that might be seen if a patient present with a paraneoplastic syndrome
iii) what histological subtype is this tumour? where does it arise from? what % of renal malig does it make up?
iv) does it affect M or F more? name three non familial risks
v) which two conditions can it be associated with?
vi) what is 5yr prognosis for T1, T2/3 and distant mets?

A

i) haematuria (50%), loin pain (40%), mass (30%) - <10% of people have all three
ii) paraneoplas (renin/EPO secretion) - hypercalc, HTN, fever, night sweat, polycythaemia
iii) adenocarcinoma of the renal cortex > arises from the PCT and makes up 85% of all renal malignancies

iv) M>F in 2:1 ratio over 60yrs
non fam risks - smoking, asbestos, cadmium, lead, renal disease

v) may be assoc with VHL anc phaeo
vi) T1 (90%), T2/3 (60%), distant mets (0-20%)

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5
Q

RCC STAGING

what is the extent of the tumour in T1, T2, T3 and T4?

A

T1 - tumour <7cm and limited to kidney > do partial nephrectomy

T2 - tumour >7cm and do total nephrectomy

T3 - infiltration to RV/renal sinus fat/perirenal fat/IVC

T4 - extends beyond gerotas fascia / invades adrenal

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6
Q

RCC INVESTIGATIONS AND MANAGEMENT

i) which two bloods are important?
ii) what is an US useful for? what score is used?
iii) what size can CT detect tumours at? what will MRI show?
iv) what appearance may be seen on CXR if there is lung mets?
v) do patients with complete resection benefit from adjuvant chemo? what immunotherapy may be useful for metastatic RCC?
vi) is embolisation reccomended? what will need to be done if there is a TCC?

A

i) ESR and U+E
ii) USS - contrast enhanced > detect tumours vs cysts (bosniac score)

iii) CT can detect tumours <1cm
MRI will show lymphatic and venous involvement

iv) lung mets > cannon ball mets on CXR

v) patient with complete resec dont benefit from post op chemo
- metastatic > give sunitinib (TK inhibitor)

vi) embolisation isnt recommended
- if TCC > need to do a nephoureterectomy (kidney and ureter) as TCC are multifocal and will just recur if both kidney and ureter are not removed

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7
Q

BLADDER AND UROTHELIAL TUMOURS

i) what is the most common type? what % affect the bladder? what % affect the upper tract?
ii) what imaging technique is used to look for filling defects?
iii) is it more common in F or M? at what age does incidence peak?
iv) how may it look on imaging?

A

i) most commonly TCC
95% affect bladder and 5% affect the upper tract

ii) CT urogram to look for filling defects
iii) 3M:F, incidence peaks at 65yrs
iv) may see finger like projections (papillary)

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8
Q

TCC PRESENTATION

i) what do 90% of patients present with?
ii) what should microscopic haematuria + >50yrs be investigated for?
iii) name two other symptoms that may be seen
iv) name three investigations
v) what does staging depend on?

A

i) 90% patients present with painless macroscopic haematuria
ii) investigate for bladder cancer
iii) may also see irritative bladder symptoms (chronic urine infection) annd flank pain (due to obstruction)
iv) urine micro/cytology (cancer can cause sterile pyuria - WC with no bacteria), USS and CT, cystoscopy and biopsy if cancer is suspected
v) staging dep on how far it has infiltrated the bladder wall

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9
Q

TCC MANAGEMENT

i) which chemo is given?
ii) what immunotherapy can be given? what does this do? what do both treatments cause as a SE
iii) how should high risk tumours be followed up?
iv) how should intermed and low risk tumours be followed up?
v) what is the 5 year survival for lesions not involving the bladder muscle and for those with met disease?
vi) what may be done surgically for patients that have radical cystectomy?

A

i) mitomycin C > weekly for 6 weeks

ii) immuno - BCG > upregulates host immune response to tumour, 6 week course
- both BCG and mitomycin cause cystitis

iii) high risk > cystoscopy every 3 months for 2yrs then every 6 months then annual for life
iv) intermed - cystoscopy x3 in first year then annually for 5 years. low risk discharge at 24 months

v) lesions not involving bladder muscle = 90-90% survival
met - 5% survival

vi) urostomy (ileal conduit > plug ureters in to form a stoma)

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10
Q

URINARY RETENTION

i) what is the most common cause of a bladder outflow obstruction causing retention? name three other causes
ii) what may be given to treat the most common cause?
iii) is acute retention painful or painless? is chronic retention painful or painless? why?
iv) what two investigations would you order? which two scans?

A

i) BPH is most common cause
- also caused by cauda equina, diabetes, MS, PD

ii) shrink the prostate with finasteride/tamulosin
iii) acute retention is painful and chronic retention is painless (bladder wall dilates over time but in acute the detruor muscle still works)

iv) U+E to look for renal failure, urine dip
- USS KUB - renal cortical thickness and urinary retention
CT KUB - for imaging of the entire tract

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11
Q

ACUTE URINARY RETENTION

i) where is tenderness felt? what volume will be seen in bladder scan?
ii) name four causes
iii) name a bedside and imaging? what three bloods would you want?
iv) what is the main treatment? what else can be done?
v) name two things that can be given to prevent it? what does each do?

A

i) suprapubic tenderness
- >600ml on bladder scan but not more than 1L

ii) prostatic obstruction, urethral strictures, anticholinergics, alcohol, constipation, post op, infection, cauda equina

iii) mid stream urine and USS to look at volume and prostate size
- blood - FBC, UE, PSA

iv) main tx is put in a catheter (if clot retention need a 3 day catheter)
- can also do a washout - pump bladder with saline then irrigate

v) prevent with finasteride (reduces prostate size and retention risk)
tamulosin (reduces risk of needing recatheter after retention)

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12
Q

CHRONIC URINARY RETENTION

i) does it present suddenly or gradually?
ii) what may the bladder capacity be? what does this mean for bladder contractility?
iii) what type of incontinence may this cause?
iv) name three causes
v) when are patients catheterised? (3)

A

i) present gradually
ii) bladder >1L - may not be able to contract again therefore may not be suitable for surgery
iii) overflow incontinence
iv) prostatic enlargement, pelvic malignancy, diabetes, MS

v) only catheterise if there is pain, infection or renal impair (urea>12)
- intermittent self catheterisation may also be appropriate

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13
Q

HIGH VS LOW PRESSURE CHRONIC RETENTION

i) how does high pressure affect pain? continence? creatinine?
ii) which pressure are hydroureters/hydronephrosis seen?
iii) what is low pressure retention caused by? is there pain?
iv) how is high pressure retention managed? (3)
v) how is low pressure retention managed?

A

i) high pressure > painless, incontinent, raised creatinine
ii) hydroneph > high pressure

iii) low pressure retention is caused by failure of the detrusor muscle
- painless with normal creatinine/ureters/kidneys

iv) IV access, IV saline, catheter, U+Es to monitor renal fail, monitor output (post obstructive diuresis)
v) not as urgent, treat the cause

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14
Q

COMPLICATIONS OF URINARY CATHETERS

i) name three
ii) what should never be used to inflate the balloon?
iii) what is post obstructive diuresis? how does it present? what does this cause in realtion of electrolytes?
iv) what is a potential mechanism of POD?

A

i) urethral trauma, UTI, bladder stone formation, bladder perforation
ii) never use saline (only use water) > can cause retained balloon fragments

iii) polyuric response initiated by the kidneys after relief of an obstruction
- presents with polyuria > deranged electrolytes and dehydration
- hypokal, hypo/hypernatremia, metab acidosis, shock and death

iv) numerous mechsn - reduction in GFR > ischaemia and loss of juxtamed nephrons
reduces response of collecting duct to ADH > nephrogenic DI

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15
Q

RENAL TRAUMA

i) name three common causes
ii) what % of abdo trauma does it occur in? what causes 90% of all renal trauma?
iii) name four signs
iv) what is the first step in management? what imaging may be done?
v) how is grade I, II, III trauma managed? (vasc injurt confined to perineph facia)
vi) how is grade IV, V managed?

A

i) blunt trauma, boxing, RTAs

ii) 8-10% of abdo trauma > renal trauma
blunt trauma causes 90% (crushes kidney against ribcage)

iii) loin/abdo bruising, loin tenderness, loin mass, macro haematuria or clots

iv) ABCDE
- do a triple phase CT (pre contrast, venous, arterial) to look where the trauma is and if there is an acute bleed

v) conservative mx as will self tamponade due to gerotas fascia (manage with bed rest and abx)
vi) embolise then if that fails > nephrectomy

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16
Q

TESTICULAR TORSION

i) name four differentials for scrotal pain?
ii) what happens in torsion? when is it most common?
iii) how does it present? what is the course of the pain? how is this different from epididymorchitis?
iv) which reflex is absent? why?
v) within how many hours may the testicle die if not managed?

A

i) testic torsion, epididymitis, orchitis, torsion of hydatid morgagni

ii) twisting of the spermatic cord & artery > ischaemia to testicle
- most common in adolescence

iii) presents with acute onset painful testicle, N=V, lower abdo pain
- pain crescendos (if epidid - wax and wane)

iv) cremaster reflex is absent as the cremaster muscle is already contracted
v) 4-6 hours

17
Q

OTHER TESTICULAR PATHOLOGIES

i) what is hydatid of morgagni? what sign is seen?
ii) how is epididymoorchitis treated? what is the most common cause <30yrs and >50yrs?
iii) what is paraphimosis? what can it cause? how is it treated?

A

i) torsion of the testicular appendage (remnant of mullerian duct) - blue dot sign

ii) give abx (ciprofloxin)
<30yrs - chlamidyia
>50yrs - ecoli

iii) foreskin retracted behind glans > common in catheterised patients
- can cause glans ischaemia
- tx with manual reduction, dundee method (local anaes) or surgical release

18
Q

RENAL/URETERIC STONES PATHOPHYSIOLOGY

i) are they more common in males or females? what are 80% of stones made from? name three other things they can be made from
ii) what causes each stone type?
iii) what are the three most common areas for stones to develop?
iv) what is the most common presenting feature? name three other features
v) which two bedside tests should be done? what is gold standard imaging?

A

i) males
- 80% of stones are calcium (oxalate and phosphate or mixed)
- urate > high levels of purine in blood (diet) or myeloprolif diease
- struvite
- cystine > inherited defects that affect absorption of cysteine and reduce citrate (anti stone)

iii) PUJ, VUJ and pelvic brim where iliacs cross ureter
iv) pain (colic) is most common feature, N+V, 90% present with non visible haematuria

v) bloods > FBC etc with calcium, urate, phosphate and urine dip for micro haematuria/infection
- gold standard imaging is non contrast CT KUB

19
Q

RENAL/URETERIC STONE TREATMENT

i) name three criterias for in patient admin
ii) name two ways it can be surgically managed?
iii) what size stone will likely pass spontaneously?
iv) what can be done if not passing? (3) when may these be contraindicated
v) name three complications

A

i) post obstructive AKI, uncontrolled pain, infected stone, large stone >5mm
ii) stent insertion via cystoscopy or nephrostomy to relive obstruc proximally
iii) <5mm

iv) shock wave lithotripsy (extetnal sonic waves to break it up)
- dont use if pregnant or stone is very big (used for small stones)
ureteroscopy (collect with basket - may break up with laser)
perc nephrolithotomy - direct access to kidney to remove stone

v) infection, post renal AKI, recurrent stones > scar and lose kidney function

20
Q

URINARY INCONTINENCE

i) what is stress incontinence? name three times it may happen? what is it usually due to?
ii) what is urge incontinence? what causes it? what drug class can cause it
iii) what is overflow incontinence? what is it a complication of? which fibres are damaged? what is the most common cause?
iv) what is continous incontinence? name two causes
v) name two non surgical and two surgical treatments

A

i) urine leak when intra abdo pressure exceeds uretheral pressure eg when cough, strain, laugh
- usually due to weak pelvic floor muscles (can be constipation, obesity, pelvic surgery)

ii) overactive bladder (detrusor hyperactiv) > uninhibited bladder contraction > rise in intravesical pressure > urine leak
- caused by neurogenic causes eg previous stroke, infection, cholinesterase inhibitors

iii) complication of chronic urinary retention > stretching of bladder wall > damage to efferent fibres of sacral plexus and loss of bladder sensation
- bladder over fills > dribbling of urine
- prostatic hyperplasia is most common cause

iv) constant leakage of urine
- anatomical abnorms eg ectopic ureter or bladder fistula
- can also be due to severe overflow incontinence

v) non sx - lifestyle advice eg weight loss, reduce caffiene, smoking cessation, pelvic floor muscle training
anti muscarinics trialled in urge UTI to inhibit detrusor contraction
sx - botox injections for urge UTI, tension free vaginal tape stress UTI

21
Q

BENIGN PROSTATIC HYPERPLASIA

i) what is it? how is it characterised histologically? name three risk factors
ii) what type of symptoms are seen? (2)
iii) which examination is done? why? name three other investigations that can be done
iv) will PSA be raised?

A

i) enlargement of the prostate
- charac by non cancerous hyperplasia of glandular epithelium and stromal tissue in the prostate > inc in size
- RF = age, family history, black/african, obese

ii) see lower UTI symptoms
- voiding symptoms (hesistancy, weak stream, incomplete empty, dribbling
- storage symptoms (inc urine frequency, nocturnia, urge incontinence)

iii) rectal exam to distinguish between BPH and prostatic cancer (firm, smooth and symmetrical)
- urine freq and volume chart, urine dip, post void bladder scan to assess for chronic retention

iv) PSA may be marginally elevated

22
Q

BENIGN PROSTATIC HYPERPLASIA

i) what is it? how is it characterised histologically? name three risk factors
ii) what type of symptoms are seen? (2)
iii) which examination is done? why? name three other investigations that can be done
iv) will PSA be raised?

A

i) enlargement of the prostate
- charac by non cancerous hyperplasia of glandular epithelium and stromal tissue in the prostate > inc in size
- RF = age, family history, black/african, obese

ii) see lower UTI symptoms
- voiding symptoms (hesistancy, weak stream, incomplete empty, dribbling
- storage symptoms (inc urine frequency, nocturnia, urge incontinence)

iii) rectal exam to distinguish between BPH and prostatic cancer (firm, smooth and symmetrical)
- urine freq and volume chart, urine dip, post void bladder scan to assess for chronic retention

iv) PSA may be marginally elevated

23
Q

BPH TREATMENT

i) which drug can be trialled if symptomatic? how does this work?
ii) what should be given if this doesnt work?
iii) name two surgical procedures that can be done and how they work
iv) what is the main complication of BPH? name two others
v) what is TURP syndrome?

A

i) alpha adrenoreceptor antagonist (alpha blocker eg tamulosin) > relax prostatic smooth muscle via block of alpha adrenoRs
ii) still symptomatic post adreno antag > give 5alpha reductase inhibitors such as finasteride (prevent conversion of testos to DHT > decerase in prostatic volume) - may take 6 months to see benefits of 5a inhibitors

iii) refractory to medical management or develop significant sequale of BPH > surgery
- TURP - trans urethral resection of prostate > endoscopic removal of obstructive prostate tissue using a diathermy loop to increase urethral lumen size
- HoLEP prodecure involves laser to hear and dissect sections of prostate into the bladder > good outcomes and low post op complications
- can also do photoselective vaporisation, transurethral microwave therapy

iv) Main complication is high pressure retention > chronic or acute on chronic urinary retention > post renal kidney injury
- reccurent UTIs
- significant haematuria

v) TURP syndrome > hypo osmolar irrigation is used during procedure which can cause fluid overload and hponatremia (confusion, nausea, agitation, visual change)

24
Q

PROSTATE CANCER

i) what subtype are the majority? where do they mostly arise from?
ii) which subtype are most common? which one is less common? which is more aggressive?
iii) name three RF? what is the grading system used? what is this based on?
iv) how does localised disease present? (3) how does adv loc disease present? (3)
v) how does metastatic disease present?

A

i) majority (95%) are adenocarcinomas with 75% arising from the peripheral zone

ii) adenocarcinomas > acinar (orig in glandular cells that line postate) = most common
- ductal (orig in cells that line ducts of prostate) = grows and mets faster than acinar
iii) RFs - age, ethnicity (black african or carribean), FH, genetic predis BRCA2/1
- graded using Gleason grading system - score of 1-5 (how much cells form glands)

iv) loc disease > lower UT symptoms eg weak urinary stream, increased frequency and urgency
- advanced loc disease - heamaturia, dysuria, incontinence, haematospermia, suprapubic pain, loin pain

v) met disease > bone pain, lethargy, anorexia, unexplained weight loss

25
Q

PROSATE CANCER INVESTIGATIONS AND TX

i) what is commonly found on DRE? what is PSA? how is it implicated in prostate cancer
ii) name two types of biopsy that may be used in diagnosis? what imaging may be done alongside this?
iii) what is risk strat based on? (3) how is low risk, intermed and high risk, metastatic treated?
iv) what is castrate resistant? how may these patients be treated?
v) how can it be surgically managed? which two types of RT may be given?
vi) when is chemotherapy used? name two drugs that may be given

A

i) Digital rectal exam - asymmetry, nodularity or fixed irregular mass
- PSA = serum protein produced by malignant and normal cells > can be elevated in PC but also in BPH, prostatitis, exercise, ejaculation (low specificity)
- free:total PSA ratio

ii) biopsy of prostatic tissue
* transperineal biopsy > sample tissue transperineal - day case under GA (good access to anterior prostate and low risk of infection)
* trans rectal US biopsy - under local anaes > generate 12 cores taken bilaterally in equal distrib from base to apex (assoc with 1-2% risk of sepsis)
- Imaging - multi parametric MRI - ident abnormal areas of prostate > target for biopsy

iii) risk strat based on PSA, gleason score, TNM staging
- low risk > active surveillance (monitor 3 monthly PSA, 6 monthly DRE and rebiopsy 1-3yrs), radical treatment if signs of progression
- intermed and high risk > radical options
- metastatic > chemo and anti hormonal agents
* castrate resistant = evidence of hormone relapsed disease (disease even when testos levels are very low) > consider for chemo such as docetaxel (may offer corticosteroids third line after androgen deprivation therapy)

v) Surgical management
* radical prostatectomy > remove prostate, seminal vesicles and surround tissue, pelvic LNs (open or laparo) > SEs are erectile dysfunc, stress incontinence, bladder neck stenosis
- RT > external beam or brachytherapy
- brachytherapy = transperineal implantation of radioactive seeds directly to prostate
- ext beam = focused RT to prostate and limits damage to surrounding tissues
vi) Chemotherapy only in metastatic disease
- docetaxel, cabazitaxel

26
Q

TESTICULAR CANCER PATHPHYS AND PRESENTATION

i) which type is malignant and which is benign?
ii) what are the two subtypes of germ cell tumours? which are usually loc and which are usually met?
iii) name two types of non germ cell tumours?
iv) name four risk factors?
v) what may be felt OE? name three weight met disease can present

A

i) Germ cell (usually malig) or non germ cell (usually benign)

ii) germ cell > seminomas and non seminomatous
- seminomas remain localised until late and have good prognosis
- Non seminomatous = yolk sac, choriocarcinoma, embryonal carcinoma and teratoma > met early and and have worse prognosis them seminomas

iii) non germ cell - leydig cell tumour or sertoli cell tumours
iv) RF = undesc testes (crptochidism) 4-10x increased risk, previous tesicular malignancy, positive FH or kleinfelter syndrome

v) unilateral painless testicular lump
- OE mass is irregular, firm, fixed
- mets = weight loss, back pain from RP mass, dyspnoea (lung mass) (lymph drains to para aortic nodes therefore may not get loc lymphadenopathy)

27
Q

TESTICULAR CANCER TREATMENT

i) which two things are commonly found alongside prostate cancer? what effect do they have and what can be done to mitigate
ii) which surgical approach is taken? why is this approach used?
iii) which staging system is used?
iii) which type of tumours are more aggressive? what treatment do these need?
iv) how are seminomas treated? what is their risk of relapse?

A

i) sperm abrnomalities and leydig cell dusfunction are commonly found and tx can impair fertility therefore do pre treatment fertlilty assessmnt (semen analysis and cryopreservation)

ii) Surgery
* inguinal radical orchidectomy
* inguinal approach for limited lymphatic disrup and risk of seeding

iii) NSGCTs
* more aggresive > stage I req orchiectomy then given a risk score
* low risk can have surivellance but high risk need adjuvant chemo then surviellance (CT at 3 and 12 months)
* met disease is also risk scored > intermed have chemo, poor prognosis have intensified chemo

iv) Seminomas
* stage I > orchidectomy and surveillance
* high risk of relapse and often consudered for chemo
* met disease > stage IIA = RT or chemo but higher stage need primary chemo then treated similar to met NSGCT

28
Q

EPIDIDYMITIS

i) what is it? what ages does it commonly occur? what other condition does it classically occur with?
ii) what is it usually caused by? how the cause be further categorised?
iii) name two RF for each cause?
iv) what may be felt on examination? name three other associated symptoms? does it commonly present bilaterally?

A

i) Inflammation of the epidiymis
- bimodal age distribution - 15-30yrs then >60yrs
- classically occurs with orchitis - epididym-orchitis but most cases are just epididymitis (sole orchitis is rare)

II) usually caused by local extension of infection from lower urinary tract eg bladder urethra via enteric (UTI) or non enteric (STI) organisms
* males <35yrs most likely to be STI > n gonnorhoea and c trachomatis (anal = ecoli)
* >35yrs enteric organism (usually due to bladder outflow obstruc from prostatic enlarge) more likely cause = ecoli, proteus spp, klebsiella pneum, psuedomonas

iii) RF dep on mechanism of disease - non enteric (STI) are MSM, multiple sexual partners
enteric - recent instrumentation/catherisation, bladder outlet obstruc, immunocompromised

iv) unilateral scrotal pain assoc with swelling
- fever and rigors may be present
* assoc with dysuria, storage lower UT symptoms or uretheral discharge
- epidid (and testes) will be very tender on palpation > assoc hydrocele (fluid around testicle)
- bilateral presentation is rare

29
Q

EPDIDYMITIS

i) which reflex is in tact and which sign will be positive?
ii) what bedside test should be done? what should be done if a non enteric cause is suspected? which imaging may be done
iii) name two reasons why outpatient treatment may not be possible? name three things that can be done to treat?
iv) what advice should be offered? does the patient need routine follow up?
v) name three complications

A

i) cresmasteric reflex is in tact and prehns sign positive (pain relived by scrotal elevation - poor specificity)

ii) urine dipstick for infection
- low threshold for sending for MC&S
- non enteric suspected > first void urine sent for nucleic acid amplification to assess for N.gonnorhea, C tachomatis and M genitalium
- further STI screening if history indicates
- bloods - FBC, CRP for infection, blood cultures
- dx is uaully clinical but can do US with doppler to confirm (increased blood flow) and rule out complications eg testicular abscess

iii) systemic infection or uncontrolled pain
- give antiobiotics and anaglesia and best rest with scrotal support
- Abx are definitive treatment - depends on enteric or non enteric (STI) organism

iv) abstain from sexual activity until abx course is complete and symptoms resolve
- dont need routine follow up

v) reactive hydrocele formation, abscess formation and testicular infection