Renal/Urology Flashcards
AKI
- Diagnosis
- Causes
- Presentation
- Investigation
- Management
Diagnosis
Stage 1- 1.5-1.9x increase in Cr OR <0.5ml/kg/hr u/o for 6h
Stage 2 - 2-2.9x increase in Cr OR <0.5ml/kg/hr u/o for 12h
Stage 3 - >3x increase in Cr OR <0.3ml/kg/hr u/o for >24h OR initiation of RRT
Refer to nephrology if: renal transplant, unknown cause of AKI, inadequate response to tx, complications, stage 3 AKI, CKD stage 4 or 5, if needing RRT (see below), vasculitis, glomerulonpehiitis, myeloma
Causes
- Pre-renal - volume depletion/low BP, drugs (ACEi, aminoglycosides, NSAIDs, diuretics)
- Renal - nephritic syndromes, toxins (e.g. rhabdo (myoglobin), contrast), ATN
- Post-renal - obstruction e.g. BPH, stones
Presentation
- Oliguria
- Uraemia -> confusion, itching, pericaditis
- Acidosis
- Hyperkalaemia -> arrhythmias
Investigation
- U&Es + other routine bloods
- USS KUB
- Urinalysis - ATN/Renal cause - kidneys lose ability to hold onto Na (to preserve circulating volume) + concetrate the urine -> urine Na >40 and urine osmol <350). Pre-renal the kidneys try to help - urine Na <20 and urine osmol >500)
- (ATN is most common cause of AKI can be due to ischaemic (hypovolaemic) or toxins (e.g. meds).
- Determining between acute vs chronic kidney disease - chronic tend to have small kidneys bl on USS (except polycystic kidney disease, early diabetic nephropathy + amyloidosis) also in CKD you get hypocalcaemia/secondary hyperparathyroidism
Management
- Treat Cause
- Meds review
- Treat complications e.g. hyperkalaemia
- Consider referral for RRT: refractory hyperkalaemia, metabolic acidosis, complications of uraemia, fluid overload
CKD
- Diagnosis
- Causes
- Presentation
- Investigation
- Management
Diagnosis
- Stage 1 - eGFR >90 w/ other signs of kidney disease
- Stage 2 - eGFR 60-90 w/ other signs of kidney disease
- Stage 3a - eGFR 45-59
- Stage 3b - eGFR 30-44
- Stage 4 - eGFR 15-29
- Stage 5 - eGFR <15 or need for RRT
eGFR is adjusted for race, age, sex, Cr level
N.B. if eGFR >60 + no other signs of kidney disease then this is NOT CKD
Causes
Most common:
- Diabetic nephropathy
- HTN
Other:
- Chronic glomerulonephritis
- Chronic pyelonephritis
- Adult polycystic kidney disease
- BPH
- Myeloma
Presentation
Asymptomatic. Can -> uraemia (fatigue, weakness, anoreixa, vomtiing, metallic taste in mouth (urea), pruritis, restless legs, bone pain)
Blood gas = metabolic acidosis w/ resp compensation
Complications –> increased CVS risk, anaemia (low EPO), renal bone disease (low Ca2+ + phosphate -> PTH raised -> increased bone resorption -> osteitis fibrosa cystica), fluid overload
Investigation
- Urinalysis + ACR
- Certain patients should have regular screening: DM, HTN, >60yo, recurrent UTI, urinary obstruction, systemic illness, fam hx stage 5 CKD or PCKD
Management
- Manage cause (if HTN ACEi first line, if eGFR <45 furosemide can also help)
N.B. rise in Cr of 30% or drop in eGFR by 25% is acceptable but keep an eye on U&E
- Monitor Cr + eGFR
- Dose modifications/meds r/v
- Nephrology referral for: anaemia, bone disease (1st line: reduce dietary phosphate, 2nd: phosphate binders (stops if complexing w/ Ca + causing hypocalcaemia)
- RRT for stage 5 CKD
- General dietary advice: low protein, phosphate, sodium + potassium
Autosomal Dominant Polycystic Kidney Disease
- Inheritance
- Presentation
- Investigation
- Management
Inheritance
- Autosomal dominant
- Can be type 1 (85% of cases, presents w/ renal failure earlier) or type 2
Presentation
- HTN, recurrent UTIs, flank pain, haematuria, palpable kidneys, renal impairment, stones
- Extra-renal: liver cysts (can -> hepatomegaly), berry aneurysms (can -> subarachnoid), mitral valve prolapse, aortic root dilatation + aortic dissection, Other cysts: pancrease, spleen
Investigation
- Screening of relatives w/ abdo USS + diagnose if:
- <30 w/ 2 cysts (uni or bilateral)
- 30-59 w/ 2 cysts in both kidneys
- >60 w/ 4 cysts in both kidneys
Management
- Supportive in most
- Some may have tolvaptan (vasopressin antagonist) if CKD 2 or 3 AND evidence of rapidly progressing disease
-
Haematuria
- Causes
- Investigation/Referral Criteria
Causes
*Microscopic *
-Transient: UTI, menstruation, vigorous exercise (resolves in 3d), sexual intercourse
Persistent: cancer (bladder, renal, prostate), stones, BPH, prostatitis, urethritis, renal: IgA nephropathy, thin basement membrane disease
Spurious: rhabdo (myoglobin), foods (beetroot), drgus (rifampicin, doxorubicin)
Macroscopic
- painless macroscopic think bladder Ca
- UTI/pyelonephritis
- Stones
- Pelvic trauma
- Renal: IgA nephropathy, thin basement membrane diseases
- Iatrogenic: TRUS/TURP, traumatic catheterisation, renal biopsies, ESWL
Investigation
- In all: check ACR, U&Es, BP (if proteinuria needs renal ref), HTN could be ?nephritic syndrome)
2WW if:
- >45 AND unexplained visible haematuria (without UTI) OR visible haematuria persisting/recuring despite successful tx of UTI
- > 60 AND unexplained nonvisible haematuria AND either dysuria or raised WCC on bloods
Non-urgent ref if
- >60 w/ reucrrent or persistent unexplained UTI
Who doesn’t need referring? Age <40yo w/ normal renal function, no proteinuria + normotensive
Bladder Cancer
- Pathophysiology
- Presentation
- Investigation
- Management
Pathophysiology
Can be TCC (most common), SCC (chronic inflam eg. schisosomiasis), adenocarcinoma, sarcoma
Risk factors:
- Smoking (both TCC + SCC)
- Aniline dye exposure (eg. printing or textiles) (2-naphthylamine or benzidine dye)
- Rubber manufacuring
- Cyclophosphamide
Presentation
- Painless haematuria (micro or macroscopic)
- Recurrent UTIs or LUTs
- Sterile pyuria (rarely)
- Weight loss, lethargy, pelvic pain (if locally advanced)
Investigation
- 2ww referral for >45 + macroscopic haemturia + no UTI or >60 + microscopic haematuria w/ dysuria or raised WCC
- Cystoscopy, biopsy CT staging
Management
- Surgical eg. TURBT (if in situ/T1), radical cystectomy (w/ ileal conduit formation or bladder reconstruction (from small bowel) +/- chemotherapy
- If bladder recon w/ small bowel needs B2, folate checking annually (?def due to less absorption)
Sterile Pyuria
Causes
Investigation/Management
Causes
- Most common is actually infection: recently or partially treated UTI, UTI w/ slow-growing organism, STI
- Other: appendicitis, post-menopausal atrophic vaginitis/trigonitis, prostatitis, genitourinary TB, schistosomiasis (rare in UK), sarcoidosis
- Malig: Bladder Ca (normally w/ haematuira), Renal disease
Investigation
- MSU for miscroscopy + culture, test for chhlamydia/gonorrhoea, U&Es, ACR, BP, upper tract USS
- If persistent refer to urology for further assessment
Haemolytic Uraemic Syndrome
- Pathophysiology
- Presentation
- Investigation
- Management
Pathophysiology
Generally seen in young children –>
- AKI
- Microangioathic haemolytic anaemia
- Thrombocytopenia
Can be:
Primary (rare) - due to complement dysregulation
Secdonary (typical HUS):
- Shiga toxin producing E.Coli = most common cause (90%)
- Pneumococcal infection
- HIV
- Rare: SLE, drugs, Ca
Presentation
- Most due to E.coli shiga toxin –> bloody diarrhoea, abdo pain, fever, n+v
- Then features of HUS - anaemia, AKI, thrombocytopenia
Investigation
- FBC (anaemia w/ -ve direct coomb’s), thrombocytopenia, evidence haemolysis on film eg. schistocytes, helmet cells
- U&Es: AKI
- Stool culture: STEC infection, PCR for shigella toxin
Management
- Supportive: fluid, transfusion, dialysis +/- plasma exchange (normally only if not associated w/ diarrhoeal illness)
Renal Cell Carcinoma
Risk factors
Presentation
Investigation
Management
Risk Factors
- Smoking, von-Hippel-Lindau, tuberous sclerosis
- only slight increase in ADPKD
Presentation
- Classic triad: Haematuria, Loin pain, Abdo Mass
- pyrexia unknown origin
- Endocrine: EPO (-> polycythaemia), PTHrp (->hypercalcaemia), Renin (-> HTN), ACTH (cushing syndrome)
- Left varicocele
- Stauffer syndrome (paraneoplastic) –> cholestasis + hepatosplenomagly
Investigation
- Urinalysis, Bloods
- USS
- CT staging
- Biopsy
Management
- Confined disease - partial/total nephrectomy
- Chemo generally ineffective. Can use immunotherapy or biologic agents
- (if patient otherwise well + primary is resectable then can do resection of solitary mets)
Nephrotic vs Nephritic syndrome
- Classic Triads
- Investigations
- Causes + their management
Triads
*Nephrotic *- oedema, proteinuria, hypoalbuminaemia
- Other features: dyslipidaemia, hypercoaguability (loss of antithrombin), reduced immunity (loss of immunoglobulins)
- Presentation - peripheral oedema (aduts), facial oedema (children), frothy urine, fatigue, recurrent infections
Nephritic - HTN, AKI, haematuria
- Other: mild proteinaemia, mild oedema
- Presentation: haematuria, mild oedema, signs of uraemia (fatigue, pruritis, nausea)
- Red cell casts in urine
Investigations
- Nephrotic range of proteinuria >3.5g/day
Causes
Nephrotic
- Minimal change disease (most common in children)
most idiopathic but can be associated w/ mono, NSAIDs, hodgkins lymphoma
Present: nephrotic. renal biopsy: fusion of podocytes + effacement of foot processes
Mx: 1st: PO steroids (80% = steroid responsive),2nd= cyclophosphamide
most relapse at least once but tends to stop before adulthood - good prog
- Membranous nephropathy (most common in adults)
- Focal segmental glomerulosclerosis
Nephritic
- IgA Nephropathy (aka Berger’s disease)
most common glomerulonephritis
Present: macroscopic haematuria following URTI, young, male (renal failure is rare)
Associated conditions: Henoch-Schonlein, alcoholic cirrhosis, coeliac
Mx: if isolated haematuria then no tx just monitor. If slight reduced GFR or persistent proteinuriaa ACEi. If failure to respond to ACE: immunosupression w/ steroids
- Post-streptococcal glomerulonephritis
Present: 7-14d post group A B-haemolytic strep (normally S. Pyogenes), headache, malaise, visible haeamtura, proteinuria, HTN, oliguria, raised anti-streptolysin O (confirms recent strep), low completement
Differentiate from IgA: bigger gap between infection + onset, low complement + proteinuria in post-strep
good prog, supportive mx, resolves spon - Rapid progressive glomerulonephritis (anti-GBM or ANCA vasculitis)
What are the following?
- Alport’s Syndrome
- Goodpasture’s Syndrome
Alports Syndrome
Inheritance: X-linked dominant, problem w. collagen -> abnormal glomerular BM
Present: microscopic haematuria, progressive renal failure, B/L sensorineural deafness and eye problems: lens protrusion, retinitis pigmentosa
Diagnosis: genetic testing, renal biopsy (shows splitting of BM -> basket weave appearance)
Goodpasture’s Syndrome
Autoimmune condition affecting lungs + kidneys
Present: 10-30yo, haemoptysis, fatigue, fever, nosebleed, nephrotic syndrome
Diagnosed w/ renal biopsy, serum Ab, urinalysis
Renal Transplant
Immunosupressants
Complications
Immunosupressants
Example regime:
- Initial: ciclosporin/tacrolimus + monoclonal Ab
- Maintenance: ciclosporin/tacrolimus w/ MMF or sirolimus
- ADD steroids if >1 steroid reponsive acute rejection
Side effects:
- Ciclosporin - higher rate of rejection than tacro
- Tacrolimus - imparied glucose tolerance/DM
- Mycophenonlate mofetil - GI SEs + marrow supression
- Sirolimus: hyperlipidaemia
All patients on long-term immunosupression need monitoring for complications:
- CVS disease
- Renal failure (tacrolimus/ciclosporin are nephrotoxic also monitor for graft regection + recurrent of original disease)
- Malignancy - SCC + BCC (non melanoma skin ca)
Complications
- Post op: ATN of graft, UTI, vacular thrombosis, urine leakage, UTI
- Hyperacute Rejection (mins-hours)
Due to pre-existing Ab against ABO or HLA antigens. Type II hypersensitivity. Graft MUST be removed/no other tx
- Acute Graft Failure (<6/12)
due to mistmatched HLA, normally asymp -> rising Cr, pyuria + proteinuria. May be reversible w/ steroids + immunosupression - Chronic Graft Failure (>6/12)
*Recurrence of original disease or fibrosis of transplanted kidney *
Rhabdomyloysis
Causes
Presentation
Investigation
Management
Causes
- long-lie, crush injuries, prolonged epileptic seizure, coma, statins (esp if co-prescribed w/ clarithromycin)
Presentation
- AKI w/ disproportionately raised Creatinine + raised CK
- Dark urine (myoglobinuria), hypocalcaemia (as myoglobin binds calcium), raised phosphate (released from myocytes), raised K+, metabolic acidosis
Ix
- Raised Creatine Kinase
- AKI (w/ raised Creatinine)
Management
- IVI to maintain good u/o
- +/- urinary alkalinisation
UTI
Pathophysiology
Presentation
Investigation
Management
Pathophysiology
Causative organism: E.Coli, Klebsiella, proteus
In structural abnormality: Pseudomonas
Gram -ve organisms are nitrite +ve (e.g. E.coli) but gram +ve are nitrite -ve (eg. staph saprophyticus)
Presentation
- Dysuria, frequency, urgency, haematuria, confusion, rigors, suprapubic pain
- pyeloneph: rigors, nausea/vomiting, loin pain
Investigation
- Urine dip all <65yo
- Culture: >65yo, catheter, pregnant women, haematuria (visible or not)
Management
Uncomplicated (women)
- 3 days nitrofurantoin or trimethoprim
Complicated
- Men: 7 days nitro or trimethoprim
- Catheter: 7 days nitro or trimethoprim + consider changing catheter if been in more than 7 days (N.B. do not treat asymptomatic bacteriuria in catheterised)
- Pregnancy: 7 days - nitro in early preg, cefalexin or amoxicillin later (avoid trimethoprim throughout- esp 1st trimester)
- Asymptomatic bacteriuria in preg: 7 days abx as above (due to risk of pyeloneph) + do further culture as test of cure.
Pyelonephritis
- 10-14days broad spectrum abx (co-amox, cephalosporin or quinolone)
What are the following and their management?
Erectile Dysfunction
Priapism
Signs of Urethral Injury
Erectile Dysfunction (impotence)
- Causes: pscyhological or organic (CVS, DM, low testosterone, neuro disorders, pelvic surgery), mens (anticholinergics, antidepressants, antihypertensives etc)
- Management depends on cause:
- Psychological - therapy (then similar to organic)
- Organic: lifestyle/meds modification 1. PO phosphodiesterase inhibitors (unless taking nitrates) (eg. sildenafil) 2. Intraurethral or intracavernosal alprostadil 3. vacuum pump device 4. refer to urology (?penile prosthesis)
- If hypogonadism: testosterone supplementation
Priapism
- Persistent erection, >4h, not associated w/ sexual stimulation, painful (if not painful or any hx of trauma this suggests non-ischaemic cause)
- Can be: ischaemic (blocked outflow) or non-ischaemic (too much inflow)
- Causes: idiopathic, sickle cell, meds eg. sildenafil, antidepressants, cocaine; trauma
- Ix: cavernosal blood gas analysis (differentiates ischaemic/non); doppler USS, FBC/tox screen (?cause)
- Mx:
- Ischaemic = emergency - aspiration of blood + injection of saline flush to clear pooled blood +/- phenylephrine or surgery
- Non-ischaemic - observe initially, non emergency
Signs of Urethral injury
- perineal bruising, bood at external urethral meatus, high riding prostate on PR
- do NOT attempt catheterisation. Refer urgently to urology.
What are the following/their management?
- Balanitis
- Phimosis
- Paraphimosis
Balanitis
can have multiple causes, including pre-malignant lesions. Swab all to confirm organism. +/- biopsy if ?pre-malignant lesion (bowens disease, bowenoid papulosis or erythroplasia of Queyrat)
- Candida: rash w/ soreness/itch - tx w/ clotrimazole cream or PO fluconazole + screen partners
- Anaerobic infection: foul smelling discharge, inguinal lymphadenopathy - PO metronidazole
-
Aerobic infection -> non-specific balanitis - mx depends on sensitivities
-* Lichen sclerosus* - white patches on glans, itch, sore, splitting. Can -> phimosis + urethral stenosis + risk of malignant transformation to penile Ca. Needs biopsy to diagnose. Mx w/ strong topical steroids
-* Zoon’s *(plasma cell) balanitis: older uncircumcised men due to irritation from urine -> well-circumscribed organe-red glazed areas on glands w/ multiple pinpoint red spots - biopsy to exclude malig - mx w/ circumcision + topical steroids - Psoriasis - looks similar to elsewhere - emollients, steroids, calcitriol
- Circinate balantitis - occurs in reactive arthritis - white areas on glans that coalesce to form geographic area w/ white margin - screen for STI + tx accordingly
- Irritant/Allergic - eczematous rash - emollients/soap sub +/- hydrocortisone
Phimosis = inability to retract
Cause: physiologic (resolves w/ time); pathologic (scarring, infection, inflammation)
Pres: difficult retraction, pooling or urine, smegma, balanitis, urinary retention, painful erection
Management: topical steroids + manual retraction. If ineffective or causing problems (e.g. recurrent UTI, paraphimosis, recurrent balanitis) or pathological cause then may need circumcision
Paraphimosis = inability to replace = emergency (risk of necrosis)
Causes: not replaced post-catheter, phimosis
*Pres: erythema, pain, swelling, *
*Mx: manual reduction +/- surgery (longitudinal incision made)
Prostatitis
Pathophysiology
Presentation
Management
Pathophysiology
- UTI or STI
- Other RF: catheter, HIV, prostate biopsy, anal sex
Presentation
- Pain: around penis, testicular, lower abdo, on defaecation, perineal, painful ejaculation
- Urinary: dysuria, frequency, haematuria, acute retention
- General: myalgia, fever, gen unwell, low back pain
- (can be acute or chronic (>3m))
- PR: tender, boggy prostate (although careful exam needed as can –> sepsis + bacteraemia)
Management
Acute prostatitis, depends on suspected cause:
- Gonorrhoea - IM ceftriazone + PO azithromycin
- Chlamydia: azithromycin or doxycycline
- Urinary cause: trimethoprim, cefalexin or co-amox for 14 days
If not improving w/ abx consider ?prostatic abscess - CT to visualise
Renal Stones
- Pathophysiology
- Presentation
- Investigation
- Management
Pathophysiology
- 80% = calcium oxalate
- Struvite/staghorn related to UTIs
- RFs: dehydration, high oxalate (tea, chocolate, rhubarb), high purine (red meat or myeloproliferative disease), high cystine (hyomocystinuria), hypercalcaemia
Presentation
- Loin to groin pain (sudden onset), haematuria, n+v
- Fever –> co-existing infection
N.B. major differential is AAA
Investigation
- MSU: haematuria + culture
- Bloods: FBC (raised WCC due to inflammation), CRP, U&Es, calcium + urate (?undelrying cause), coag (if likley surgery)
- Non-contrast CT KUB
- AXR if known stones visible on x-ray
- USS to assess for hydronephrosis
Management
- Analgesia - IM or PR diclofenac
- <5mm - pass spontaneously wihin 4/52
- >5mm - unlikley to pass
- Non emergency: Shockwave lithotripsy, ureteroscopy, percutanous nephrolithotomy
- Emergency: nephrostomy or ureteric stent (if unilateral kidney, infected obstructed system, b/l obstruction)
- Prevention
- Calcium: increase fluid intake, tihazides, low salt diet
- Oxalate: low oxalate diet, cholestyramine, pyridoxine
- Uric acid: allopurinol
What are the following?
- Interstitial Cystitis
- Fourniers Gangrene
Interstitial Nephritis (aka bladder pain syndrome)
- Chronic bladder pain (months-years): varies w/ filling, suprapubic/pelvic/dyspareunia, bimanual -> pain in ant.vaginal wall over urethra + bladder neck.
- Frequency, urgency
- Cystoscopy: diffusely erythematous bladder, ulcerative patches, reduced bladder capacity (<300ml)
- Mx: symptom relief + pain management
Fourniers Gangrene - necrotising fascitis of perineum = emergency
organism: group A strep, C perfringens, E coli
RF: DM, alcohol, poor nutrition, steroid use, haem malig, trauma
Pres Early: pain out of proportion to signs, pyrexia. Later: crepitus, skin necrosis, haemorrhagic bullae, sepsis
*Mx:urgent surgical debirdement (do not delay), broad spectrum abx, HDU admission, skin grafting *
Describe the presentation + management of the following scrotal problems
- Epididymal Cysts
- Hydrocele
- Varicocele
Epididymal Cysts + Spermatoceles
- Pres: separate from body of testicle, post. to testicle, cyst = clear fluid, spermatocele = sperm
- Diagnosed w/ USS
- Mx:supportive +/- surgical removal or sclerotherapy (if large/symptomatic)
Hydrocele
Path: fluid accumulation in tunica vaginalis.
- Communicating: due to patent processus vaginalis. Common in newborns. Tend to resolve in 1st few months.
- Non-communicating: excessive fluid production within tunica vaginalis
Causes: congenitcal, epididymo-orchitis, testicular torsion, tumours
Features: soft, nontender swelling of hemiscrotum, ant/below testicle, can get above mass on exam, transilluminates, testis may be difficult to feel if large hydrocele
Diagnosis clinical but do USS if any doubt or if cannot feel underlying testis
Mx: Infantile: repair if not resolved by 1-2yrs. Adults: conservative in most, USS to r/o tumour
**Varicocele ** - abnormal enlargement of testicular veins
Pres: bag of worms, 80% left sided, subfertiligy
Diag: USS doppler
Mx conservative mostly. If pain or infertility ?for surgery
Haematocele- blood in processus vaginalis
Causes: trauma, cancer
Mx: if following trauma -> admit urology. If no tx: urgent USS
Testicular Torsion
Pathophysiology
Presentation
Investigation
Management
Main differential + distinguishing factors
Pathophysiology
- Twisting of spermatic cord -> ischaemic testis
- RF: bell clapper testis, undescednded testis
Presentation
- Commonly age 10-30yo
- Testicular or lower abdo pain, vomiting, sudden onset (+/- preceding intermittent self-resolving episodes)
- Swollen, tender testis, retracted upwards, red skin, loss of cremasteric reflex, elevating testis does NOT improve pain (Prehn’s sign - it helps w/ epididymo-orchitis)
Management
- Urgent surgical exploration
- Both testis are fixed
Differential
- Torted Hydatid of Morgagni - more in younger children, scrotum normally less erythematous w/ normal lie of testes. Blue dot sign in upper half of scrotum.
Hydatid Cysts
- What are they? How are they managed?
Pathophysiology
- Endemic in Mediterranean + Middle East
- Caused by Tapeworm parasite Echinococcus granulosus (outer fibrous capsule containing multiple small cysts, can precipitate T1 hypersensitivity reaction)
Presentation
- 90% in liver + lungs
- Mostly asymptomatic (unless large, >5cm)
- If bursts –> infection, organ dysfunction (biliary rupture (-> colic, jaundice + pruritis) , bronchial , reanl, cerebrospinal outflow obstruction)
Investigation
- USS 1st, then CT
- Serology
Management
Surgery (cyst walls must NOT be ruptured during removal)
Epididymo-Orchitis
Pathophysiology
Presentation
Investigation
Management
Pathophysiology
- STI: chlamydia or gonorrhoea (<35, sexually active)
- UTI: E.Coli (>35, low-risk sexual hx)
Presentation
- Unilateral testicular pain/swelling
- Urethral discharge
- If <20yo, severe pain, acute onset - ? torsion
Ix
- younger - screen for STI
- older: MSU/culture
Management
- Unknown organism or STI: IM ceftriaxone 500mg and doxy 100mg for 10-14d
- Enteric organism: ofloxacin or levofloxacin for 10-14d
- USS following tx - ?underlying structural abnormality
- If not improving discuss w/ micro + ix for underlying cause
Prostate Cancer
Pathophysiology
Presentation
Investigation
Management
Pathophysiology
- RF: age, obesity, afro-carribean, fam hx
- PSA optional screening. 2ww if men 50-59 w/ PSA >3 OR abnormal DRE
(PSA can also be high in: BPH, prostatitis, UTI, retention, instrumentation (not for 6/52 prior), vigorous exercise + ejaculation (not for 48h prior)
Presentation
- Asymptomatic initally
- LUTS
- Haematuria, haematospermia
- Back pain, weight loss, anorexia, testicular or perineal pain
- Craggy, enlarged, asymmetrical, nodular hard prostate w/ loss of median sulcus o/e
Investigation
- 1st: MRI (if suspected clinically localised prostate cancer)
- 2nd: TRUS biopsy if MRI suggestive of Ca (complications -> sepsis, pain, fever, haematuria, PR bleeding)
- CT and bone scan for staging (mets to bone -> sclerotic lesions)
- PSA for monitoring
Management
- Watchful waiting + surveillance (reg exam + PSA monitoring)
- Surgery - radical prostatectomy +/- clearance
- Radiotherapy
- Anti-Androgen therapy (GnRH agonists eg. goserelin w/ initial anti-androgen cover e.g. bicalutamide) or GnRH antagonists eg. degarelix OR surgical castration
- Chemo
Benign Prostatic Hypertrophy
- Pathophysiology
- Presentation
- Investigation
- Management
Pathophysiology
- driven by raised testosterone
- RF: age, ethnicity (black >white >asian)
**Presentation **
Voiding
- weaknes/intermittetn flow
- straining
- Hesitancy
- Terminal dribbling
- incomplete emptying
Storage Symptoms
- urgency/urge incontinence
- Frequency
- nocturia
Post-micturition dribbling
Complications -> UTI, retention, obstructive uropathy
Investigation
- dipstick
- U&Es (esp if suspecting chronic retention)
- PSA (if any obstructive symptoms)
- Urinary frequency-volume chart
- IPSS (international prostate symptom scre) (tx indicated if >7)
Management
- Watchful waiting
- 1st line: Alpha-1-antagonists e.g. tamsulosin (SE: dizziness, postural hypotension, dry mouth, depression) (symptomatic relief)
- 2nd: 5-alpha-reductase inhibitors e.g. finasteride (slows progression BUT takes up to 6/12 to improve symptoms) (SE: erectile dysfunction, reduced libido, gynaecomastia, ejaculation problems (low testosterone)
- Other: antimuscarinics (if mix of storage + voiding sx) or surgery (TURP)
