Genitourinary D+M Flashcards
Causes of enlarged kidney
Bilaterally enlarged, ballotable kidneys can occur in polycystic kidney disease or amyloidosis.
A unilaterally enlarged, ballotable kidney can be caused by a renal tumour.
urolithiasis
Renal calculi are formed when urine is supersaturated with salt and minerals such as calcium oxalate, uric acid and cystine.
Vary in size from gravel like to large staghorn calculi
May stay in position where they formed, or can move down urinary tract causing symptoms
Another factor leading to formation is formation of randall’s plaques. Calcium oxalate precipitates form in the basement membrane of thin loops of henle; these eventually accumulate in subepithelial space of renal papillae, leading to Randall’s plaque and eventually a calculus.
Male:female 3:1
Peak age for stones developing is 30-50 years old
Bladder calculi
Bladder calculi account for 5% urinary tract stones and usually occur because of foreign bodies, obstruction or infection.
Most common cause is urinary stasis from failure to empty, from bladder outflow obstruction
Urolithiasis risk factors
Anatomical anomalies in urinary tract - horseshoe kidney, urethral stricture etc Family history HTN Gout Hyperparathyroidism Immobilisation Dehydration Metabolic disorders - chronic metabolic acidosis, hypercalciuria, hyperuricosuria Deficiency of citrate in urine Cystinuria Drugs: diuretics like triamterene and calcium or vitamin D supplements Hot climates Higher socio-economic status
Urolithiasis presentation
Asymptomatic in many cases
Renal colic: sudden severe pain starting at loin moving to the groin with tenderness of loin or renal angle
Pain is sharp and more constant than intestinal colic, with dull pain as periods of relief
Tends to ‘writhe around in agony’
Sometimes with haematuria
If stone is high, pain can be in flank but as stone moves down pain moves anteriorly towards groin
Stones moving cause greater pain than static ones
Pain can radiate towards testis, scrotum, labia or anterior thigh
Rigors and fever
Dysuria
Urinary retention
Nausea and vomiting
Urolithiasis investigations
Abdominal exam
Stick testing of urine for haematuria, white cells and nitrites (both suggest infection) and pH (>7 suggests urea-splitting organisms, <5 suggests uric acid stones)
Midstream specimen for microscopy
Bloods: FBC, CRP, renal function, electrolytes, calcium, phosphate and urate, creatinine
Prothrombin time and INR if intervention planned
Urgent CT
USS for pregnant women, children and young people
KUB and AXR
Stone analysis: suggests for all first times, all those with recurrent stones and those who’ve had late recurrence after long time stone-free period
Urolithiasis management
Prevention advice: increase fluid intake to maintain UO at 2-3 L/day, reduce salt intake, reduce meat and animal protein, reduce oxalate intake (chocolate, rhubarb, nuts) and urate rich foods (offal, certain fish), drink cranberry juice, maintain Ca intake as normal, depending on stone can be given medications to help prevent such as thiazide diuretics for calcium stones, allopurinol for uric acid stones and calcium citrate for oxalate stones Hospitalisation for systemic features (fever), known non-functioning kidney, solitary kidney, persistent pain, dehydration, anuria, pregnancy, >60 years with concerns on clinical condition Urgent outpatient appointment: pain relieved, able to drink large volumes, no complications evident NSAIDs or paracetamol for analgesia (NSAIDs thought best first line for pain) Antiemetics and rehydration therapy PRN Majority of stones pass spontaneously within 1-3 weeks; those who have not passed stone in that time or have continuing symptoms need monitoring weekly for progression CCB (nifedipine) or alpha-blockers (tamsulosin) given for medical expulsive therapy >3 weeks to facilitate stone passage Shockwave lithotripsy (SWL) is noninvasive procedure to break up stones Surgery for stones that will not pass or there are signs of obstruction. Includes ESWL, PCNL, ureteroscopy and open surgery
Urolithiasis complications and prevention
Complete obstruction can cause irreversible kidney damage if >48 hours
Symptomatic >4 weeks there is 20% risk of complications like deterioration of renal function, sepsis and ureteric stricture
Infection
Pyelonephritis
prevention:
Increase oral fluid intake and reduce calcium intake
Correct metabolic abnormalities
Treat infections UTI promptly
Urinary alkalinisation eg sodium bicarbonate 5-10g/24hour PO in water (for cystine and urate stones)
Male lower UTI and risk factors
Infection of any part of the urinary tract
Usually caused by bacteria (80% E coli)
UTI less common in men than women but higher in elderly men
Risk factors: BPH and other obstruction to urinary flow (strictures, stones etc) Catheterisation Previous UTI Immunocompromised state
Lower UTI presentation
Dysuria Frequency Urgency Change in urine appearance or odor Nocturia Suprapubic discomfort Delirium Reduced functional ability
Lower UTI investigations
male:
Urine culture and sensitivity (DIAGNOSTIC)
Urine dipstick or microscopy
female:
Urine dipstick (nitrites and leukocytes and RBC high or normal)
Urine culture for pregnancy, >65 years, persistent symptoms, recurrent UTI, catheterised, VH or NVH
Male lower UTI management
Hospitalisation for nausea and vomiting, confusion, tachypnea, tachycardia, hypotension
Empirical antibiotic treatments: trimethoprim or nitrofurantoin (CAN COLOUR URINE RED) 7 days (3 days for women) for non-catheterised or pivmecillinam 2nd line or cefalexin
Follow up in 48 hours; if not improving review sensitivity and use narrow spectrum AB where possible
Refer to urology if needed: ongoing symptoms despite treatment, underlying causes suspected or recurrent episodes (>2 in last 6 months)
Consider trial of daily antibiotics prophylaxis - trimethoprim 100mg at night or nitrofurantoin at night first line
Female lower UTI management
Simple lower UTI:
Self care: analgesia and hydration
Antibiotics (delayed script for mild cases non-pregnancy) nitrofurantoin (CAN COLOUR URINE RED) 50mg QDS 3 days (7 days in men)
Persistent haematuria after treatment must be followed up for underlying causes
Refer unknown causes of recurrent UTI, if catheterised or malignancy suspected
Hygiene, topical vaginal oestrogen and antibiotic prophylaxis can be considered
Pregnancy:
Asymptomatic or suspected UTI treated promptly with 7 day course antibiotics and followed up - first line nitrofurantoin (50mg QDS 3 days - CAN COLOUR URINE RED)
Amoxicillin, cephalexin can be 2nd line if symptoms don’t improve within 48 hours of 1st line
Consider ‘back up’ prescription that can only be taken in 48 hours if symptoms do not improve
Urgent specialist advice for recurrent UTI, catheter associated, atypical pathogens or underlying cause suspected
Antenatal services following treatment of UTI must be followed up
During term of pregnancy CANNOT be prescribed nitrofurantoin as causes neonatal haemolysis
Trimethoprim CI in pregnancy (teratogenic risk)
Pyelonephritis
Infection within renal pelvis usually accompanied by infection within renal parenchyma
Source of infection is often ascending infection from the bladder
Causative organisms are same for lower UTI: e coli, klebsiella, proteus, enterococcus etc
Repeated attacks of acute pyelonephritis can lead to chronic pyelonephritis, involving destruction and scarring of renal tissue due to repeated inflammation
Acute:
Occurs at any age
1% boys and 3% girls have had by age 7
Highest incidence in women ages 15-29, followed by infants and elderly
chronic:
Scarring of kidneys occurring after recurrent or persistent infections
Pyelonephritis acute and chronic risk factors
acute: Structural renal abnormalities, including vesicoureteric reflux Calculi and catheterisation Stents or drainage procedures Pregnancy Diabetes Primary biliary cirrhosis Immunocompromised Neuropathic bladder Prostate enlargement
chronic: Structural abnormalities, obstruction or calculi VUR Intrarenal reflux in neonates Diabetes Factors predisposing recurrent UTI
Acute pyelonephritis presentation
Rapid onset over day or two
Uni or bilateral loin pain, suprapubic pain or back pain
Fever variable can produce rigors
Malaise
Nausea and vomiting
Anorexia
Occasionally diarrhoea
Accompanying lower UTI features: frequency, dysuria, gross haematuria or hesitancy
Pain on firm palpation of one/both kidneys
Moderate suprapubic tenderness without guarding
Presentation in children can be less specific
Acute pyelonephritis investigations
Urinalysis: urine often cloudy with odor, +ve for blood, protein, leukocyte esterase and nitrite
MSU sent for microscopy and culture
Catheter specimen
Bloods: FBC, CRP, WCC, SR, plasma viscosity and cultures
Contrast enhanced CT (CECT) and KUB gold standard!
Children first line is urine samples
DMSA scan for detailed renal cortical views
MRI
Renal biopsy to exclude papillary necrosis
acute Pyelonephritis management and complications
Fluid intake and analgesia
Hospitalisation for severe condition or comorbidities
Antibiotics whilst awaiting culture and sensitivity (1st line ciprofloxacin or co-amoxiclav, trimethoprim if sensitivity confirmed)
Surgery rare needed to drain renal or perinephric abscesses or to relieve obstructions like stones
Complications: Sepsis Perinephric abscess Renal abscess Acute papillary necrosis Pregnancy tends to be more complex: can cause preterm labour, consider prophylaxis antibiotics if >3 x infection within a year Impaired renal function
Chronic pyelonephritis presentation and investigations
Often asymptomatic Fever Malaise Loin pain Nausea and vomiting Dysuria HTN Failure to thrive Features of CKD
investigations:
Urine microscopy, culture and sensitivity
Renal USS
Intravenous pyelogram (IVP) small kidneys, ureteric and calyceal dilatation with cortical scarring
Micturating cystourethrogram MCUG
USS and KUB
Technetium scan for renal scars most sensitive
Renal biopsy
Chronic pyelonephritis management and complications
BP controlled to slow progression of CKD ideally with ACEi
Supervening UTI may need long courses antibiotics
Severe underlying VUR in children may need antibiotic prophylaxis until puberty or resolution
Calculi removal
Surgical reimplantation of ureters in severe cases
Dialysis or renal transplant in severe cases
Monitored for development of hyperlipidaemia, HTN, diabetes and deteriorating renal function
Complications:
Progressive renal scarring with reflux nephropathy and CKD
Secondary HTN
Pyonephrosis
Focal glomerulosclerosis
Urea splitting organisms can lead to staghorn calculi
balanitis and cause
Inflammation of glans penis
If foreskin also inflamed it is termed balanoposthitis, although commonly still called balanitis
More common in men than boys
Cause:
Intertrigo
Infection with candida is cause of less than 20% cases, often signifies underlying dermatosis
Bacterial cases may be polymicrobial (candida, staph or strep especially group B, anaerobes etc)
Fixed drug eruption (particularly sulfonamides and tetracycline)
Circinate balanitis (associated with reactive arthritis)
Zoon’s balanitis (plasma cell infiltration); a benign, idiopathic condition presenting as a solitary, smooth, shiny, red-orange plaque of the glans and prepuce of a middle-aged to older man
Queyrat’s erythroplasia (penile Bowen’s disease - carcinoma in situ)
Psoriasis
Lichen planus
Leukoplakia
Seborrhoeic dermatitis
Pemphigus
Pemphigoid
Irritation or contact dermatitis: wet nappies, poor hygiene, smegma, soap, condoms.
Trauma: zippers, accidental or inappropriate foreskin retraction by a child/parent.
Stevens-Johnson syndrome.
Severe oedema due to right heart failure.
Morbid obesity.
balanitis risk factors
Diabetes Oral antibiotics Poor hygiene in uncircumcised males Immunosuppression Chemical or physical irritation of glans
Balanitis presentation
Sore, inflamed and swollen glans/foreskin
Non-retractile foreskin/phimosis
Penile ulceration
Penile plaques
Satellite lesions
May be purulent and/or foul smelling discharge (most common with strep or anaerobic infections)
Dysuria
Interference with urinary flow in severe cases
Obscuration of glans/external urethral meatus
Impotence or pain during coitus
Regional lymphadenopathy
Balanitis investigations and complications
blood/urine testing for glucose if diabetes possible
Swab of discharge for microscopy, gram staining, culture and sensitivity
Refer to GUM clinic is STI suspected
Bacterial infection suspected: swab and await results/consider GUM referral
Complication:
Difficulty retracting foreskin can develop especially if recurring or chronic
Balanitis management
Daily cleansing with warm water and gentle drying. Saline baths (4 tbs salt in bath)
STI screening and treatment of patient and partners PRN
If dermatological cause; treat cause with advice from GUM/dermatology referral. Biopsy may be needed for referral
Contact irritant causes = Avoid triggers (latex condoms etc.) usually resolves over period of days with irritant removal
Topical hydrocortisone 1% therapy recommended (ONCE DAILY UP TO 14 DAYS). Systemic for severe inflammation affecting penile shaft or marked genital oedema
No improvement = stop hydrocortisone and take subpreputial swab to exclude or confirm fungal or bacterial infection - manage according to results
Candidal infection suspected = clotrimazole cream 1% or miconazole 2% apply twice daily until symptoms settle
Nystatin if resistance suspected
Topical imidazole with 1% hydrocortisone if marked inflammation
Bacterial = flucloxacillin or erythromycin. Anaerobic = metronidazole 400mg 2x daily for one week or co-amoxiclav.
Consider hospital for IV antimicrobials for gross inflammation or systemic illness
Surgery considered for circumcision if recurrent or pathological phimosis present
Prognosis:
Depends on underlying cause and presence of risk factors
More likely to recur in diabetes, poor genital hygiene, phimosis, contact irritants if re exposed
Prostatitis
Inflammation of prostate gland and can result in various clinical syndromes
Acute symptoms of bacterial prostatitis more likely to drive patients to consult GP or A+E
Prostate pain syndrome PPS sometimes used to describe men with chronic prostatic pain with no identifiable infective cause
If prostate can’t be identified as source of pain, the term pelvic chronic pain syndrome CPPS sometimes used
2-10% adult men experience symptoms compatible with chronic prostatitis at some point
Chronic is much more common than acute (chronic defined as >3 months symptoms)
Bacterial is most common form in <35 years
HIV predisposes to prostate cancer, also suggested that chronic prostatitis may be associated with benign prostatic hyperplasia and prostate cancer
Causes:
Bacterial: usually gram negative organisms, especially E coli, enterobacter, serratia, pseudomonas and proteus species. STIs can also cause. Rarer causes include mycobacterium tuberculosis
Non-bacterial (more common): elevated prostatic pressures. Pelvic floor myalgia. Emotional disorders
Causes of prostatitis and risk factors
Bacterial: usually gram negative organisms, especially E coli, enterobacter, serratia, pseudomonas and proteus species. STIs can also cause. Rarer causes include mycobacterium tuberculosis
Non-bacterial (more common): elevated prostatic pressures. Pelvic floor myalgia. Emotional disorders
Risk factors:
STI
UTI
Indwelling catheters
Acute bacterial prostatitis can occur after sclerotherapy for rectal prolapse
Follow manipulation of gland eg post-biopsy
Increasing age
Prostatitis presentation
Fever, malaise, arthralgia, myalgia
Urinary frequency, urgency, dysuria, nocturia, hesitancy and incomplete voiding
Low back pain, low abdominal pain, perineal pain and pain in urethra. Chronic pelvic pain common finding of chronic prostatitis
Pain on ejaculation common especially with CPPS. also significant association with premature ejaculation
Urethral discharge
Examination:
Acute bacterial:
Nodular gland, boggy or possibly normal
Tender on palpation
Feels hot to touch
Inguinal lymphadenopathy and urethral discharge
Features of UTI and systemic infection - tachycardia, dehydration
Chronic bacterial and nonbacterial:
Glands feel normal or can be hard from calcification
Prostatitis investigations
Bloods: FBC, U+E, creatinine and cultures if toxic or septic
Acute bacterial diagnosis made on urine culture
Urine microscopy for white blood cells and bacterial count as well as oval fat bodies and lipid laden macrophages
Do NOT use prostatic massage in acute prostatitis (painful and may spread infection)
Suspicion of cancer = check PSA (can be elevated by prostatitis anyway)
chronic nonbacterial prostatitis overview
Impairs quality of life and diagnostic index needed to aid diagnosis research outcome
National institutes of health funded chronic prostatitis collaborative research network has developed index of symptoms and quality of life impact in men with chronic prostatitis
Cause is unknown but thought to be unidentified infection, immune reaction, pelvic SNS dysfunction, interstitial cystitis, prostatic cysts and calculi. Mechanical problems causing retention of prostatic fluid
Contains 13 items scored in three discrete domains:
Pain
Urinary symptoms
Quality of life impact
Diagnostic criteria includes:
Symptoms suggestive of prostatitis (pelvic discomfort/pain) lasting >3 months
Negative cultures of urine and prostatic fluid
Inflammatory type, leukocytes present in prostatic fluid, vice versa non-inflammatory type
Management of acute prostatitis
Hospitalisation for acute symptoms or oral AB intolerance (septic shock, fluid resus)
Analgesia
Urine retention = catheterisation (may need suprapubic)
Avoid repeated PR exam (spread infection)
If sexually transmitted; GUM clinic may be referred to
FIRST LINE fluoroquinolones (CIPROFLOXACIN or OFLOXACIN) for four weeks (review at 14 days) SIDE EFFECTS: convulsion risk, tendon damage, Aortic aneurysm and dissection risk
Severely ill pts may need parenteral aminoglycosides (gentamicin) in addition
Second line = levofloxacin 500BD 14 days then review or co-trimoxazole 960mg BD for 14 days then review
Referral for inadequate AB response, immunocompromised, pre-existing urological conditions, acute urinary retention
Following recovery all need referral for investigation of urinary tract, to exclude structural abnormalities
Management of chronic prostatitis
Chronic infectious prostatitis:
Referral made for all chronic cases
Antibiotics while awaiting referral (quinolone for 4-6 weeks, repeated PRN)
Analgesia and stool softeners
Where calculi serve as focal point for infection, transurethral resection of prostate (TURP) or total prostatectomy may be needed
Chronic nonbacterial prostatitis:
Simple analgesia (paracetamol or NSAIDs)
Antibiotics for infection but avoid repeating
Prazosin or other alpha blocker may be of value. Give for 3-6 months if beneficial ad less highly selective blockers preferred
Stress management for suspected strong psychological component
MDT approach (urologist, pain specialist, nurse, physiotherapist, GP, CBT specialist, sexual health specialist etc)
Emerging therapies: thermotherapy, bioflavonoids, bee pollen etc.
epididymitis and orchitis
Inflammation of the epididymis
Acute epididymo-orchitis is clinical syndrome consisting of pain, swelling, inflammation of the epididymis, with (Epididymo-orchitis) or without (epididymitis) testes inflammation
Orchitis (infection limited to tesis) is much less common
Chronic epididymitis refers to epididymal pain and inflammation (usually without scrotal swelling) lasting for more than 6 months
Acute epididymitis commonly present in aged 15-30 and >60 years
Prepubertal epididymitis thought to be post viral infectious phenomenon
epididymitis cause
Under 35 YO, most likely STI eg chlamydia or gonorrhea
In men over 35 YO, most often due to gram negative enteric organism causing UTI eg E coli, pseudomonas spp. Specific risk factors include recent instrumentation or catheterisation
Mumps
Extrapulmonary TB (40-45% cases in UK)
12-19% men with Behcets disease will develop EO. noninfective and thought to be part of more severe disease process
Also reported as adverse side effect of amiodarone (dose dependent)
cause of acute orchitis
Viral: mumps is most common. Coxsackievirus A, varicella and echoviral infections are rarer
Bacterial and pyogenic: E coli, klebsiella, pseudomonas, staph and strep species (rare causes)
Granulomatous: syphilis, TB, leprosy (rare causes)
Trauma
Epididymitis risk factors
Previous gonorrhoea infections
Instrumentation and indwelling catheters for acute epididymitis
Structural or functional abnormalities of urinary tract common risk factors for gram negative enteric organisms
Anal sex (enteric pathogens)
Strenuous exertion with full bladder
Epididymitis presentation
Unilateral scrotal pain (bilateral sometimes)
Relatively acute onset swelling of scrotum
In sexually transmitted cases of epididymo-orchitis may be urethritis or urethral discharge
History suggestive of UTI or bacteriuria
Mumps: headache, fever, uni or bilateral parotid swelling.
Symptoms of TB infection: subacute/chronic scrotal swelling, systemic symptoms of TB, scrotal sinus or thickened scrotal skin
Tenderness to palpation on affected side
Palpable swelling
Urethral discharge
Secondary hydrocele
Erythema or oedema of scrotum on affected side and pyrexia
Lifting testis over symphysis may ease pain
Epididymitis-orchitis investigations
Exclude STI with screening
Gram stained urethral smear microscopy
Gram stained prep of first passed urine (FPU) for microscopy
Urethral swabs for STI
Microscopy and culture of midstream urine for bacteria including nitrate and leukocyte esterase test
HIV if suspected
Doppler USS for blood flow to differentiate between torsion
management of epididymitis-orchitis
Possible torsion: urgent urology opinion
Possible STI: refer to GU clinic for full screening, treatment and contact tracing. Advise against unprotected sex until treatment and follow up
Rest, analgesia (NSAIDs) and scrotal support. Abstain from intercourse until resolved and followed up especially with STI
Empirical therapy to all patients with epididymo-orchitis before culture/NAAT results. Antibiotic given should be chosen determined by immediate tests as well as history
For sexually transmitted: ceftriaxone 250mg IM single dose + doxycycline 1–mg orally 2x daily 10-14 days
Enteric organisms: ofloxacin 200mg oral 2x daily 14 days
Severe symptoms: IV antibiotics
All cases of cephalosporin/tetracycline allergy given ofloxacin 200 mg oral 2xdaily 14 days
Surgical: scrotal exploration if torsion or tumour cannot be ruled out
Follow up:
No improvement after 3 days reassess patient diagnosis and treatment
Two week follow up to assess compliance, partner notification and symptom improvement
Swelling and tenderness can persist but should be significantly improved, with little improvement, consider USS or surgical assessment
urethritis
Urethral inflammation
Can be result of infectious or noninfectious causes
Primarily a sexually acquired disease
Can affect both sexes
Chlamydia most common in those aged 15-24 (most common STI in UK)
Gonorrhoea also common cause
Classification of male urethritis:
Gonococcal - caused by neisseria gonorrhoeae
Non-gonococcal urethritis (NGU) - caused by number of organisms as well as non infective agents
Persistent or recurrent urethritis - 10-20% cases treated for NGU
urethritis presentation
Asymptomatic (90-95% men with gonorrhoea, 50% patients with chlamydial infections)
Urethral discharge with/without blood, more noticeable in morning after holding urine overnight (more common in gonococcal infection)
Urethral pruritus, dysuria or penile discomfort
Skin lesions in herpes simplex virus
Systemic symptoms if other organs involved: conjunctivitis or arthritis
Haematuria or lymphadenopathy can be present
urethritis risk factors
Sexually active Male Unprotected vaginall sex Male with male sex or bisexual More common in cities Age <35-40 years Recent partner change
urethritis diagnosis
Mucopurulent or purulent discharge from urethral meatus
Gram stain of urethral smear showing >5 PMN cells per high power field (highly sensitive test)
First pass urine FPU positive for >10 PMN per high power field.
Urethritis in women: Urine sample to screen for bacteria High vaginal swab (HVS) Cystoscopy USS for pelvic inflammation caused by STIs Sexual health swabs/screen
urethritis complications
Epididymitis and/or orchitis
Prostatitis
Systemic dissemination of gonorrhoea - eg,
conjunctivitis, skin lesions.
Reactive arthritis
Pelvic inflammatory disease (PID) - infection of
female partners with the organisms that cause
urethritis can cause PID and subsequent
complications
HIV transmission is increased
urethritis management
Explain likely causes, advise partner notification, explain subsequent consequences of inadequate treatment and emphasise complications and importance of abstaining from sex (inclduing oral) for seven days after treatment (if azithromycin used) or on completion (if doxycycline used) and until symptoms resolve and partners also completed treatment
Patients should also be offered HIV, hepatitis B and syphilis testing (associated diseases)
Must be treated as early as possible and presumed chlamydial infection (most common cause)
NGU:
Doxycycline 100mg 2xdaily 7 days
Or azithromycin 1g stat then 500g OD for next 2 days (patients advised to abstain from sex for 14 days after start of treatment or until symptoms resolve to limit trasmission of resistant organisms)
Or if known to be M genitalium positive: azithromycin 500mg stat then 250mg daily for four days
Ofloxacin 200mg BD or 400mg OD for 7 days
Gonococcal urethritis:
Confirmed and uncomplicated = ceftriaxone 500mg IM + azithromycin 1g stat oral
Empirical treatment - specialist service encouraged
Doxycycline 100mg BD 7 days or azithromycin 1g single dose for presumed chlamydial cases
Testicular torsion
Torsion of the spermatic cord, causing occlusion of blood flow to the testes
Unless prompt action taken, ischaemia rapidly occurs resulting in loss of testis
Urological emergency
Typically occurs in neonates or post-pubertal boys but can occur at all ages
Left side more commonly affected than right
Bilateral cases are rare
Testicular torsion presentation
Acute swelling of scrotum and retracted upwards
Assume torsion in young boys until proven otherwise
Severe sudden onset pain in testis
Lower abdominal pain
Often comes on during sport or activity
Nausea and vomiting
Often history of brief pain similar to this that resolves itself (torsion that spontaneously resolves - indicates intermittent torsion/de-torsion)
Can present with mild less acute symptoms
Pain can ease and may indicate necrosis
Erythema of scrotal skin
Lifting testis over symphysis increases pain
Testicular torsion investigations and complications
USS most important with colour doppler
Do not delay surgical intervention with high suspicion
Complications:
Infarction and atrophy, infection and cosmetic deformity
Subfertility and infertility (although provided other functions normally will not impact fertility
Testicular torsion management
Immediate referral to emergency urology or surgical team
Give analgesia and ensure NBM
Extent of torsion has major influence on immediate salvage rate and later atrophy. Duration <6 hours has good salvation rate, >24 hours necrosis is likely
Benign prostatic hyperplasia
Increased size of prostate gland without malignancy present
Can put pressure on urethra causing difficulty passing urine
Does not increase cancer likelihood, can increase UTI likelihood
Common with increasing age
Seems likely to be from failure of apoptosis and some drugs can also induce the process
Unusual before 45
More severe in afro-american men often
BPH presentation and investigations
Urinary frequency Urgency Hesitancy Incomplete emptying Push or strain during micturition
Investigations:
Examination: check for palpable bladder
PR exam assess prostate size: should be below two fingers breadth. Firm but not hard and smooth (normally)
Urine dipstick and MSU microscopy and culture
Bloods: FBC, U+E and creatinine, LFTs
PSA elevated with large benign cases
USS or KUB of urinary tract
Management of BPH
Watch and wait if symptoms are minimal
Trial medications: alpha adrenergic antagonists (tamsulosin, alfuzosin) or alpha blockers (doxazosin) reduce tone in muscle of bladder (relieve mod-severe voiding symptoms)
Tamsulosin important to advise patient of risk of intraoperative floppy iris syndrome (causes billow out of iris during cataract surgery)
For those with enlarged prostate, raised PSA and elderly should use 5 alpha reductase inhibitor eg finasteride or dutasteride (HIGHLY teratogenic - women should not touch), can also use in combination with alpha blocker
If unsuccessful surgery can be used: transurethral resection TURP is standard technique. Risk of bleeding is high
urinary retention
Inability to voluntarily pass urine
May be secondary to urethral blockage, drug treatments (antimuscarinics, tricyclic antidepressants), conditions reducing detrusor contractions or interfering with relaxation of urethra, neurogenic causes or can occur postpartum or postoperatively
Acute retention is a medical emergency with abrupt development of inability to pass urine over period of hours
Chronic retention is gradual over months or years developing an inability to empty the bladder completely, characterised by residual volume greater than 1L or associated with presence of distended or palpable bladder
Urinary retention is more common in men and more common cause is BPH
causes of acute urinary retention
Obstructive
BPH, prostate cancer, glynae mass, bladder stones, faecal impaction, vaginal prolapse
Infectious/inflammation
UTI, prostatic abscess, acute vulvovaginitis
Neurologic
Cauda equina syndrome, cord compression, transverse myelitis, spinal cord trauma, MS
Medications
Tricyclic antidepressants, antipsychotics, opioids, diphenhydramine, ephedrine, NSAIDs, drugs with anticholinergic activity
presentation and investigations of acute urinary retention
Severe abdominal pain
Unable to pass urine for hours
Sensation of needing to void
On examination may have distended bladder with suprapubic dullness to percussion
History of haematuria - think of clot retention
Investigation: Bladder USS Post void 300ml + of urine 150ml + may also be significant Bloods: infection markers and eGFR renal function
acute Urinary retention management
Catheter insertion if patient is safe to go home, give all appropriate info
Trial without catheter usually occurs in 2 weeks time
Assess and investigate any underlying causes and treat PRN
If patient drains 1000ml + needs referral for admission to urology team
chronic urinary retention and presentation
Not immediately life threatening but can lead to hydronephrosis and renal impairment over time
presentation: Symptoms usually develop slowly and may not be noticed Urinary frequency Urgency Hesitancy Poor stream Incomplete voiding sensation Increasing lower abdo discomfort Acute retention Lethargy Pruritus Recurrent infections HTN due to CKD
chronic urinary retention investigations
BP for HTN
Abdominal and GU exam: palpable non-tender bladder
PR exam for evidence of prostatomegaly or carcinoma
Examine external genitalia in children for urethral abnormalities might be causing obstruction
Neurological exam to exclude cord compression and neuro conditions
Urinalysis
MSU
Bloods: U+E, FBC, glucose
PSA
Voiding diary
Secondary care investigations: USS, MRI, CT, cystometry etc.
chronic Urinary retention management
Intermittent bladder catheterisation offered before an indwelling catheter
Catheter may be long term solution where persistent retention causes incontinence, infection, renal dysfunction and surgery is not an option
Consider surgery on bladder with no renal impairment
Monitoring kidney function and urine output throughout life
Ureteric trauma
Relatively uncommon but very severe as can result in serious complications due to diagnosis often being delayed
Often associated with micro or macroscopic haematuria (absent in about 25% cases)
causes:
Iatrogenic from laparoscopic procedures (most commonly gyanae procedures)
Traumatic: uncommon <1% urological trauma, direct trauma from penetrating injury
Ureteric trauma presentation and diagnosis
Classic clinical signs and symptoms may also be absent, but pts may present with abdominal/flank pain, renal failure and/or urine leaking from vagina
Diagnosis:
Often based on high index of clinical suspicion
CT with contrast
Immediate diagnosis and correction will give good prognosis
Ureteric trauma management and complications
Ureteric stents may be needed for obstruction
Percutaneous nephrostomy if surgery not sufficient
Complications:
Haematoma
Abscess and intra-abdominal sepsis
Urinoma (urine collections usually found in retroperitoneal space)
Strictures and obstructive nephropathy or renal failure
Ureterovaginal fistula
Renal injury
Account for 10% abdominal trauma
Risk of injury increases in preexisting congenital or acquired renal pathologies
Majority of isolated renal trauma is minor (95-98%) due to favourable anatomical position of the kidneys protected by ribs and retroperitoneal position
Causes:
Blunt force from motor vehicle collisions, falls and personal collisions are most common cause (85%) from deceleration injuries from collision of kidney with vertebrae or ribs
Iatrogenic from surgery, percutaneous renal biopsy, nephrostomy, extracorporeal shock wave lithotripsy (ESWL)
Serious injuries associated with blunt and penetrating trauma associated with multiorgan injuries in 80% cases
Spectrum of renal injuries and presentation
Contusion/haematoma
Laceration
Haemorrhage
Avulsion of renal pedicle leading to devascularization of kidney
Pseudoaneurysm
AV fistula
Renal artery thrombosis, transection or dissection
Presentation:
Tend to present with VH or NVH
Flank and/or abdominal pain
Hypotension and shock in severe cases
Renal injury investigations, management and complications
Imaging reserved for hemodynamically stable pt usually while unstable pt taken directly to surgery
CT main line of imaging
Management:
Depends on trauma and complications present
Complications: Urinoma most common complication Delayed bleeding within 1-2 weeks injury Urinary fistula Perinephric abscess HTN from renal artery injury Hydronephrosis Pyelonephritis
acute kidney injury
Abrupt loss of kidney function
Can occur in those with or without preexisting renal disease
Causes:
Prerenal:
Majority of AKI due to prerenal state (90% cases)
Volume depletion (haemorrhage, vomiting, diarrhoea)
Oedematous states: cardiac failure, cirrhosis, nephrotic syndrome
Hypotension
Cardiovascular: cardiac failure and arrhythmias
Renal hypoperfusion: NSAID or selective COX-2 inhibitors, ACEi, angiotensin-II receptor antagonists (AIIRAs), AAA, renal artery stenosis, hepatorenal syndrome
Intrinsic: Glomerular disease Tubular injury Acute interstitial nephritis Vascular disease: vasculitis, renal artery stenosis etc Eclampsia
Postrenal: Calculus Blood clot Papillary necrosis Urethral stricture Prostatic hypertrophy or malignancy Bladder tumour Radiation fibrosis Pelvic malignancy Retroperitoneal fibrosis
risk factors for acute kidney injury
Pt having iodinated contrast agent: CKD Diabetes Heart failure >75 YO Increasing volume of contrast agent Intra-arterial administration of contrast agent
Pt having surgery: Emergency surgery particularly with sepsis or hypovolaemia Intraperitoneal surgery CKD (with eGFR <60 in adults) Diabetes HF >65YO Nephrotoxic medication
presentation of AKI
Depends on underlying cause
Decreasing urine volume (oliguria or anuria)
And rise in serum creatinine
Associated with one of the following: creatinine 26umol/L or more within 48 hours, 50% or greater increase in serum creatinine within 7 days or a fall in urine output to less than 0.5ml/kg/hour for more than 6 hours
Nausea and vomiting
Dehydration
Confusion
Hypertension
Dehydration with postural hypotension
Fluid overload with raised JVP, peripheral or pulmonary oedema
AKI NICE criteria and investigations
Creatinine 26umol/L or more within 48 hours
50% or greater increase in serum creatinine within 7 days
Fall urine output to less than 0.5ml/kg/hour for more than 6 hours
In children or young people a fall in eGFR of 25% or more in preceding seven days
Stages of AKI:
Investigations:
Detected and monitored by serum creatinine readings which acutely rise
Urine output
eGFR
Management:
No specific management - largely supportive
Monitor UO and fluid intake
AKI from prerenal cause often responds to fluid replacement and temporary withdrawal of drugs affecting kidney function
Stop nephrotoxic drugs where possible
Monitor creatinine, Na, K, Ca, phosphate, glucose
Identify and treat infection
Urgent relief of urinary tract obstruction
Refer to nephrologist for specific treatment of intrinsic renal disease
AKI management and prevention
No specific management - largely supportive
Monitor UO and fluid intake
AKI from prerenal cause often responds to fluid replacement and temporary withdrawal of drugs affecting kidney function
Stop nephrotoxic drugs where possible
Monitor creatinine, Na, K, Ca, phosphate, glucose
Identify and treat infection
Urgent relief of urinary tract obstruction
Refer to nephrologist for specific treatment of intrinsic renal disease
Prevention:
Best ‘treatment’ for AKI
Close monitoring of UO and creatinine levels for early detection
Avoid nephrotoxic drugs
All acutely ill pts in hospital should be closely monitored for signs of AKI developing
At risk pt who need iodinated contrast agents should be offered IV volume expansion with saline
CKD and risk factors
Abnormal kidney function and/or structure
Definition is based on presence of kidney damage (albuminuria) or decreased function (GFR) <60ml/minute per 1.73m2 for three months of more
Often associated with old age, diabetes, HTN, obesity and CVD
Risk factors: CVD AKI HTN Diabetes Smoking Proteinuria African, african-carribean or asian family origin Chronic NSAID use Untreated urinary outflow tract obstruction
other evidence of CKD
Persistent microalbuminuria
Persistent haematuria without other explanation
Structural abnormalities of kidney seen on USS or other radiological tests eg polycystic kidney disease, reflux nephropathy
Biopsy proven chronic glomerulonephritis
presentation of CKD
Usually asymptomatic Specific symptoms usually only develop in severe CKD Anorexia Nausea and vomiting Fatigue Weakness Pruritus Lethargy Peripheral oedema Dyspnoea Insomnia Muscle cramps Pulmonary oedema Nocturia Polyuria Headache Sexual dysfunction Hiccups Pericarditis Coma and seizures
CKD investigation
eGFR
Albumin:creatinine ratio (ACR) - Increased ACR and decreased GFR associated with risk of adverse outcomes
Urine testing: haematuria and proteinuria suggest glomerulonephritis which may progress rapidly
Renal USS
staging of CKD and management
I: 90+
Normal: eGFR >90ml/minute/1.73m2 with other evidence of CKD
Observation and control of BP
II: 60-89
Mild impairment: eGFR 60-89 with other evidence of CKD
Observation, control BP and CVD risk factors
IIIa: 45-59
moderate impairment: eGFR 45-59
Observation, control BP and CVD risk factors
IIIb: 30-44
moderate impairment: eGFR 30-44
Observation, control BP and CVD risk factors
IV: 15-29
severe impairment: eGFR 15-29
Planning for end-stage kidney disease
V: <15
established renal failure (ERF): eGFR <15 or on dialysis
Transplant or dialysis
renal replacement therapy
Most pts with CKD stage 4-5 or rapid progressing stage 3 need nephrologist referral, ideally a year before they might need renal replacement therapy
Three choice available for end stage kidney disease: conservative care and symptom control, dialysis (peritoneal or haemodialysis) and kidney transplant
Dialysis usually begins when GFR <10 ml/min or 15 if diabetic
Peritoneal considered first choice for children <2 years or people with residual renal function and adults without significant comorbidities
haemodialysis and peritoneal dialysis
Blood filtered outside of the body via machine
To prep will need one time minor surgery to create vascular access to sustain high flow rate (fuse artery to vein creating fistula or grafting a synthetic tube)
In emergency - can use catheter via jugular veins for temporary access
Blood flows through machine (acts as capillaries using dialysate fluid to osmotically remove waste and add bicarbonate for pH, medications, anticoagulants and erythropoietin) based on patients needs
Normally performed as four hour treatments 3x weekly
Complications: blood infection, thrombosis, internal bleeding
Peritoneal dialysis:
Catheter introduces dialysate fluid into the abdomen, and peritoneum acts as natural filtering surface
Can be done automatically at night for longer periods of time
Less effective than haemodialysis but is better tolerated and can be done for longer
kidney transplantation
Provides best long term outcome for end stage kidney disease
Can come from cadaver or live donor
All pts should be considered for transplant but comorbidities affect survival likelihood
Need follow up after discharge 2-3 times weekly initially
To prevent rejection will receive induction with depleting or non-depleting monoclonal/polyclonal antibodies directed against T cells
Immunosuppression maintained in long term for effective transplant
Followed up for life including annual screening for cancers, drug toxicity and CVD
CI for transplant: cancer, active infection, uncontrolled IHD, acquired immunodeficiency, active viral hepatitis, extensive peripheral vascular disease and mental incapacity
Prognosis shows 10 year survival between 71-89%
Haematuria
Blood in the urine Non-visible haematuria (NVH) is microscopic/dipstick positive. Can be symptomatic NVH (s-NVH) symptoms including voiding lower urinary tract symptoms. Or can be asymptomatic NVH (a-NVH) Visible haematuria (VH) Intermittent Persistent: suspect cancers Painful: renal or ureteric stones Painless: renal Ca/bladder cancer Urological and non-urological causes
Significant haematuria defined as:
Single episode of VH
Any single episode of s-NVH in absence of UTI or other transient cause
Persistent a-NVH in absence of UTI or other transient cause. Persistence is defined as 2 out of 3 dipstick positive for NVH
timing:
Early stream: indicates urethral bleeding
End stream: indicates bladder
Continuous indicates ureter or kidneys
causes of Haematuria
Malignancy of kidney, ureter or bladder BPH Bilirubinuria Urinary calculi UTI Anticoagulation therapy Glomerulonephritis: IgA nephropathy Polycystic kidney disease Schistosomiasis False positive: myoglobin eg extreme exercise (MbU) *Red urine can be caused by food or medications such as beetroot, rhubarb, black pudding, rifampicin, senna laxatives, pyridium (urinary analgesic) *Urine contamination during menstruation (NOT haematuria)
Haematuria investigations
Exclude transient causes eg exercise induced, myoglobinuria, menstruation Exclude UTI Plasma creatinine and eGFR Measure proteinuria Urine send for protein:creatinine ratio 24 hour urine sample for protein Measure BP FBC Urine red cell morphology (dysmorphic suggest renal origin) Cytological examination of urine USS renal tract Cystoscopy (GOLD STANDARD) IV urography Renal angiography, CT scan or renal biopsy
Haematuria management
Indications for referral: All children with haematuria All patients with VH: consider nephrology referral is glomerulonephritis suspected All patients with s-NVH All patients with a-NVH >40 years
Management:
VH, sNVH, aNVH >40 years old, refer to urologist for imaging and cystoscopy
NVH with eGFR <60, PU, high BP or family history of renal disease referral to nephrologist
Those with unknown diagnosis need repeated investigations whenever gross haematuria occurs or after 4-6 months. Occult cancer will become evidence within one year usually
Monitoring for those who don’t need referral: voiding LUTS, VH. significant or increasing proteinuria, progressive renal impairment, hypertension and if meet criteria; refer as appropriate
Frank haematuria: Hospitalisation 3 way catheter insertion VBG; check Hb, G+S Resus if unstable
2WW criteria for pelvic related cancers
Bladder or renal cancer: VH and unexplained haematuria with/without UTI or persists or recurs after successful treatment of UTI in patients >45 years
Bladder cancer: NVH and unexplained haematuria with dyuria or raised WCC in patients aged 60+
Endometrial cancer: VH with low haemoglobin levels or thrombocytosis or hyperglycaemia or unexplained vagainal discharge in women >55 years. Consider direct access USS
Prostate cancer: VH in men. Consider prostate specific antigen (PSA) est and PR exam.
Consider non-urgent referral for bladder cancer in ages >60 with recurrent or persistent unexplained UTI
dysuria
Pain on micturition
Lower UTI: urethritis - cystitis (dysuria is common in adult women)
STI: vaginitis - balanitis
Causes:
Abdominal causes can be appendicitis, ectopic pregnancy (irritation of nearby structures)
Urinary tract causes: UTI (urethritis eg chlamydia), kidney stones, malignancy, interstitial cystitis
Genital causes: trauma or foreign body, herpes simplex, vaginitis (vaginal candidiasis, atrophic vaginitis, bacterial vaginosis etc), prostatitis, epididymo-orchitis, epididymitis
Other: spondyloarthropathy or compression from pelvic mass
Irritants: drugs (NSAIDs), chemicals (soaps, contraceptives), mechanical (poorly fitted contraceptives), radiation or chemical exposure
dysuria presentation and history taking
Lower urinary tract symptoms:
Voiding symptoms: poor flow, hesitancy, post-micturition dribbling
Storage symptoms: frequency, nocturia, urgency, urge incontinence
History taking:
Pain: onset, duration, abdominal, radiation of pain (lion or back suggests UTI pathology)
Other symptoms: fever, malaise (pyelonephritis), haematuria (infection, stones, neoplasms, renal disease), urethral or vaginal discharge (genital tract infection), odour (bacterial), pruritus (genital candidiasis), frequency and urgency (bladder irritation), urine volume and flow (obstruction)
Possible pregnancy?
Past history of UTI, GU disease, pelvic surgery, irradiation, medications
Recent sexual history: method of contraception
Occupation: exposure to dyes and solvents risk factors for bladder cancer
investigations for dysuria
Physical examinations Urine dipstick, microscopy and culture Pregnancy test STI screening USS of urinary tract KUB Urodynamic studies Urine cytology Cystoscopy
frequency (urinary symptoms)
Vesical storage symptoms:
Frequency = frequent/more than usual (4-7/day) but usually total volume is normal or less than
Nocturia: most often due to too much drinking before bed or BPH (men >50)
Urgency = has no warning or little control
Causes of increased frequency: UTI Benign Prostatic Hyperplasia, prostatitis Urinary stone Pregnancy Diuretics Anxiety Urinary incontinence
polyuria overview
Excessive urine output >3L/d Common causes: Polydipsia Osmotic diuresis (hyperglycaemia, glycosuria) Diabetes insipidus Diuretics CKD
Polyuria vs frequency:
Important to differentiate between the two
In polyuria = total amount is increased
In frequency = number of episodes increases
Urinary frequency and polyuria can exist singular or co-exist
oliguria
Urine output <0.5 mL/kg/hour in children
<400mL/day adults
<0.1mL/kg/hr infants
Pathological causes:
Pre-renal: perfusion disorder (e.g. dehydration, vascular collapse or low CO) (70% cases)
Renal: renal parenchymal disease
Post-renal: urinary obstruction (most commonly blocked catheter)
oliguria history and investigations
Excessive fluid loss (diarrhoea, vomiting)
Drugs: NSAIDs, gentamicin
Gross haematuria and oedema (children) indicates glomerular disease or postinfectious glomerulonephritis
Symptoms of urinary tract obstruction: complete failure to pass urine (ANURIA) is medical emergency needs USS urgently
Investigations: Midstream specimen of urine (MSU) dipstick CRP Renal function and electrolytes Creatinine FBC ABG Renal USS with doppler Kidney biopsy PRN
oliguria management
Treat underlying cause
Fluid resus and catheterisation
Correct electrolyte imbalances
Surgery if secondary to obstructive cause
Prophylaxis of recurrent UTI
Nitrofurantoin immediate release 50-100mg OD at night or 100mg following exposure to trigger Trimethoprim 100mg OD at night or 200mg one dose following exposure to trigger Methenamine hippurate (HIPREX) broad spectrum cover
bladder carcinoma
90% are transitional cell carcinomas, 10% SCC
¾ cases are male
5 year survival rate is 55%
Majority of cases occur over aged 60
Uses TNM staging
Arise from endothelial lining (urothelium)
Bladder carcinoma risk factors
Increasing age
Smoking (50% cases caused by)
Occupational exposure to aromatic amines, polycyclic aromatic hydrocarbons and chlorinated hydrocarbons and dyes, paints, solvents etc
Radiation of pelvis
Squamous cell tumours causing chronic inflammation from stones or indwelling catheters
Presentation of bladder cancer
Most commonly haematuria (painless, usually visible)
Changes to pattern of urination (frequency, urgency)
If advanced: pelvic pain, general bone pain, weight loss, leg swelling
Metastatic disease: usually to lymph nodes, lung, liver, bone and CNS
Bladder cancer investigations and 2WW criteria
Urinalysis: if a patient presents with haematuria and infection, always follow up again once infection is treated to see if the haematuria is cleared also. Always send to the lab for NVH especially in males. MALES with haematuria is ALWAYS a RED FLAG
Abdominal exam
Bloods: FBC, eGFR, U+Es
Urine cytology
CT/MRI: T staging of tumour, node and metastases
Cystoscopy
White light-guided TURBT (specialist only)
Biopsy of prostatic urethra
2WW criteria:
In patients >45 YO
With unexplained VH without UTI
VH persisting of recurs after successful UTI treatment
>60YO with unexplained NVH and either dysuria or raised WCC on FBC
Management bladder cancer
Not invading the muscle
Transurethral Resection of a Bladder Tumour (TURBT)
Chemo into bladder after surgery (use barrier contraception afterwards)
Weekly treatments for 6 weeks with BCG vaccine squirted into the bladder via catheter, then every six months for 3 years.
Muscle-invasive bladder cancer
Radical cystectomy with ileal conduit
Radiotherapy (as neoadjuvant, primary treatment or palliative)
IV chemotherapy as neoadjuvant or palliative
Monitoring:
Follow up on completion of treatment
Those with low risk non invasive with no recurrence within 12 months discharged to primary care
Those with intermediate risk non invasive offered cystoscopy follow up at 3, 9 and 18 months and annually after
Those with high risk non invasive offered cystoscopy follow up every 3 months for first 2 years, then 6 months for two years then annually
renal cancer
60% cases are male
5 year survival rate is 55%
Types: Clear cell 75-90% Papillary 10% Chromophobe 5% Collecting duct carcinoma 1% Wilms tumour (children <5 years )
renal cancer risk factors
Smoking Obesity HTN Long term dialysis Von hippel-lindau disease
Renal carcinomas presentation and 2WW criteria
Often asymptomatic
Similar presentation to bladder cancer: Most commonly haematuria (painless, usually visible) Changes to pattern of urination (frequency, urgency)
May also present with back/flank pain at earlier stage
May have renal failure
Cannonball metastases in lungs are common
Vague loin pain
Non-specific symptoms of cancer (weight loss, fatigue, anorexia, night sweats)
Paraneoplastic features: polycythaemia (RCC secretes unregulated erythropoietin), hypercalcaemia (RCC secretes hormone mimics PTH) and stauffer syndrome (abnormal liver function tests demonstrate obstructive jaundice without any localised metastases)
2WW criteria:
45+ YO with VH persisting or recurring after UTI treatment
Unexplained haematuria without UTI
always review haematuria AFTER UTI treatment!!
Renal cancer investigations and management
Urine analysis Abdominal exam Bloods: FBC, U+E, eGFR Cystoscopy Urine cytology
Management:
Surgery (partial nephrectomy first line)
Radiotherapy and chemotherapy depending on disease stage
Prostate cancer and risk factors
Most common male cancer
Currently has no screening program
Tends to be more slow growing
Staging used is TNM
Risk factors: Increasing age Family history Black ethnicity Tall Use of anabolic steroids
Prostate cancer presentation and 2WW criteria
Frequency of urination Nocturia (>2 times per night raises suspicion) Hesitancy Straining or long time to wee Weak flow Haematuria in urine or semen Erectile dysfunction General cancer signs (weight loss, night sweats, fatigue, bone pain)
HOW TO DIFFERENTIATE FROM BPH
BPH will have bilateral smooth enlargement
Cancer will be lumpy, unilateral and craggy/one lobe will feel different to another in size and texture
2WW criteria: Any DRE suspicious texture/feel Erectile dysfunction VH Nocturia: urinary frequency: urgency or retention PSA high for age range
Prostate cancer investigations and grading
PSA: non-specific but good for monitoring
DRE: Cancer will be lumpy, unilateral and craggy/one lobe will feel different to another in size and texture
Prostate biopsy for definitive diagnosis
Gleason grading system: specific to prostate cancer, helps determine what treatment most appropriate. Higher grade = worse prognosis Gleason grading system: Well differentiated Moderately differentiated Moderately differentiated Poorly differentiated Anaplastic
Prostate cancer management and complications
Watch and wait in early stages
Radiotherapy directed at prostate
Brachytherapy: radioactive seeds implanted in prostate for continuous targeted delivery
Hormonal treatment: antiandrogen therapy to stop growth
Surgery - total prostatectomy
Complications of radial treatment: Erectile dysfunction Urinary incontinence Radiation induced enteropathy - GI symptoms like PR bleeding, pain, incontinence) Urethral strictures
testicular cancer and presentation
Peak age 30-35 YO
Most common male cancer between ages 16-24
5 year survival almost 100% very good prognosis
Seminome 50% cases, teratoma 50% cases, rarely other types.
Presentation:
Lump or enlargement in either testicle (usually non-tender), hard without fluctuance or transillumination, irregular
Feeling of heaviness in scrotum
Dull ache in abdomen or groin
Sudden collection of fluid in scrotum
Pain or discomfort in testicle or scrotum
Back pain
Metastases: Lymphatics Lungs Liver Brain
Testicular cancer investigations and 2WW criteria
Testicular examination
USS
Tumour markers: alpha-fetoprotein raised in teratomas, beta-hCG raised in both but more commonly teratomas, lactate dehydrogenase
2WW criteria:
Non painful testicular enlargement or change in shape
Consider direct USS in men with unexplained or persistent testicular problems
Testicular cancer management
Orchiectomy with testicular prosthesis
Chemotherapy or radiotherapy based on staging
Monitoring post treatment with tumour markers and imaging
Prognosis is good unless metastatic, slightly better for seminomas
Wilms tumour
Undifferentiated mesodermal tumors of intermediate cell mass (primitive renal tubules and mesenchymal cells)
Most common intra abdominal tumour of children
1 in 10,000 children affected, only 3% adults affected
10% cases associated with overgrowth syndromes: excessive prenatal and postnatal somatic growth and edwards syndrome (trisomy 18)
Hereditary wilms is uncommon, all are autosomal dominant caused by mutations in at least three genes
Staged I-V
Wilms tumour presentation
Usually in first five years of life 95% unilateral Asymptomatic abdominal mass Abdominal pain Haematuria UTI HTN Fever (uncommon) Advanced disease: respiratory symptoms from lung metastases
Wilms disease screening and investigations
Recommended for high risk children (family or associated conditions)
Surveillance by clinical geneticist carried out by renal USS every 3-4 months
Continue until 5 years old aside from beckwith-wiedemann syndrome, simpson-golabi-behmel syndrome and some familial wilms tumour pedigrees when should continue to 7 years old
Investigations: Bloods: FBC, eGFR, U+Es Urinalysis Genetic studies USS Renal angiography CT/MRI Renal biopsy Chest CT for metastases
Wilms disease management
Nephrectomy and chemotherapy can be curative
Routine postoperative radiotherapy to flank beneficial in stage III
With massive, unresectable uni/bilateral tumors can consider preoperative chemotherapy
>90% survival rate long term, 75% with metastatic disease
Urinary incontinence
Involuntary leakage of urine
Affects women more commonly
3.5 million people in the UK
Results from failure to store urine during filling phase due to:
Dysfunction of bladder smooth muscle (detrusor)
Dysfunction of urethral sphincter
Anatomical abnormalities like ectopic ureter or vesicovaginal fistula
Urinary incontinence types
Stress incontinence: urine leakage at times of increased intravesical pressure. Eg coughing, sneezing, lifting. Results from incompetence of urethral sphincter and bladder neck mechanism. Usually related to pregnancy and childbirth
Urge incontinence: urine leakage occurs in association with strong desire to void. Leaks from the bladder before the patient is able to reach the toilet. Usual cause is overactivity of detrusor muscle (unknown etiology in women)
Insensible urine leakage: continuous urinary incontinence, patient is sometimes unaware
Other forms of incontinence:
Functional incontinence: patient is unable to reach the toilet in time due to poor mobility or unfamiliar surroundings etc.
Mixed incontinence: involuntary leakage associated with urgency and exertion, effort, sneezing or coughing
Overactive bladder syndrome: urgency that occurs with/without urge incontinence and usually with frequency and nocturia. Can be called wet or dry depending on if urgency is associated with incontinence or not. Usually caused by detrusor overactivity
Overflow incontinence: usually from chronic bladder outflow obstruction. Often from prostatic disease in men
Insensible urine leakage can be due to:
Overflow incontinence from chronic retention (BPH in men)
Fistulation commonly between bladder and vagina
Gross sphincter disturbance resulting from surgery or neurological disease
urinary incontinence risk factors
Women: pregnancy, vaginal delivery, oral oestrogen therapy, menopause, hysterectomy (stress incontinence)
UTIs
Neurological disease or cognitive impairment
Obstruction
Stool impaction (elderly)
Diabetes
Obesity
Urinary incontinence assessment and red flags
Urine dipstick MSU microscopy Urinary flow rates Urodynamic studies History to establish type of incontinence
Red flags: Pain Haematuria Recurrent UTI Significant voiding Obstructive symptoms Previous history of pelvic surgery.radiotherapy
Abdominal including DRE to confirm stress UI (after coughing), R/O cytocele, rectocele…
Red flags: New neurological deficit Haematuria urethral , bladder or pelvic mass Suspected fistula
Urinary incontinence management
Pads or collecting devices temporarily while investigations and management plans put in place
Mixed incontinence: pelvic floor exercises first line both sexes.
Antimuscarinic - Annual review of those on long term meds
Overflow incontinence: relieve obstruction, intermittent self catheterisation
Stress incontinence
Most common urinary complaint for women
1 in 10 women will experience at some point
Occurs when intravesical pressure exceeds closing pressure on urethra
Cause:
Childbirth most common causative factor, leads to denervation of pelvic floor usually in parturition
Oestrogen deficiency at time of menopause leads to weakening of pelvic support and thinning of urothelium
Occasionally weakness of bladder neck can occur congenitally or through trauma from radical pelvic surgery or irradiation
stress incontinence Ix and Mx
MSU to exclude UTI and DM
frequency/volume chart shows frequency and functional bladder capacity - in SUI is urodynamic studies to assess detrusor and sphincter
Management:
Pelvic floor muscle exercises: 3 months trial as first line (8 contractions 3x daily)
Duloxetine 2nd line in those who do not want surgery
Surgical intervention
Overactive bladder/urge incontinence management
Bladder retraining: first line. Pelvic muscle training, scheduled voiding intervals with stepped increases and suppression of urge with distraction or relaxation techniques
Lifestyle: reduce caffeine, modify fluid intake
Medications can work alongside: anticholinergics eg oxybutynin, intravaginal oestrogens in postmenopausal women
Pelvic floor exercises
Botulinum toxin A injection
Sacral nerve stimulation
Surgery last resort
urolithiasis stone types
Calcium: 75% urinary calculi, usually combined with oxalate or phosphate. Sharp stones may cause symptoms even when small
Triple phosphate stones (struvite stones): 15%, compounds of magnesium, ammonium and calcium phosphate. Commonly with a background of chronic urinary infection and may grow rapidly. Staghorn calculi (fill the calyceal system) are a form of struvite
Uric acid stones: 5%, as a consequence of high uric acid in urine. Are radiolucent
Cystine stone: 1-2%, difficult to treat due to extremely hard consistency
Cryptorchidism (hidden testicle)
Absence of testis in the scrotum
Most common birth defect in boys
Affects 1-6% males
Higher incidence in premature babies
Unilateral is 4x more likely than bilateral
Cause is multifactorial (genetic, maternal, environmental)
Most often occurs as isolated disorder with no obvious cause
Normal physiology:
Normal testicular development in utero begins along the mesodermal ridge of post. Abdominal wall
By 28 weeks the right and left testes reach respective inguinal canal and by weeks 28-40, each testis has usually reached the scrotum
Classifications: Testicular agenesis (anorchia) uncommon Retractile testis Ascending testis syndrome Testicular maldescent
retractile testes
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 physical activity
This is normal and will descend when relaxed and warm or can be manipulated back into the scrotum
Does not require any treatment but does need close follow up until puberty as they can become ascendant
Have increased risk of ascending or acquired cryptorchidism
Ascending testis syndrome
A previously normal or retractile testis can become high with shortened spermatic cord, preventing testis from staying in the scrotum
Rare condition, occurs more commonly on the left side
Usually diagnosed in those aged 8-10 years
Maldescended testes
Usually unilateral
Scrotum may be underdeveloped
Is due to anatomical abnormality or hormonal lack/resistance
Most undescended testis will migrate to the lower scrotum within the first 3 months of life, presumably due to testosterone surge
Less than 1% remain undescended by 1 year of age
Descent can be arrested: incomplete but along normal path (pubic tubercle, inguinal canal or abdomen). Testis is often small and abnormal with short spermatic cord, may have associated inguinal hernia
Descent can be ectopic: deviates from normal path. Most often in superficial inguinal pouch. Testis and spermatic cord usually normal
Cryptorchidism investigations and associated symptoms
Physical examination (70% are palpable), should take place while sat cross-legged. Perform a visual exam. Inhibit cremasteric reflex with one hand above pubic symphysis before touching scrotum. Try to manipulate the testis into scrotum. Retractile testis can usually be moved into the scrotum and will remain there until retracted with cremasteric reflex (touching inner thigh). Look at femoral, penile and perineal regions for ectopic testes. Diagnostic laparoscopy Abdominal and pelvic USS if intersexuality suspected
Syndromes associated with: Prader- willi syndrome Kallmann’s syndrome Laurence-moon syndrome Intersexuality or congenital adrenal hyperplasia Prune belly syndrome
Cryptorchidism management
No treatment only follow ups until 1YO (or if retractile - until puberty)
If unilateral undescended at 3 months, refer to paediatrician surgeon before 6 months
If undescended at 1 YO treatment should be initiated and completed by 12-18 months of age
Treatment with hCG or GnRH (success best with lower descended testis) but is not usually recommended anymore as side effects may include decreased sperm count
Orchiopexy surgery before 10-11 years (should NOT be performed before 6 months of age)
Orchidofuniculolysis (mobilisation of testis and cord)
If testis is removed, can implant prosthesis
Cryptorchidism complications and prevention
Increased risk of testicular torsion and trauma
Lower fertility rate (but same paternity rate) in unilateral
Lower fertility and paternal rate in those with bilateral
3 fold increase of testicular cancer
Prevention:
National screening program - should physically examine boys within 72 hours of birth and at 6-8 week check ups
Hypospadias
Affects 1/250 male births
Opening of urethra (the meatus) is on the underside (ventral) part of the penis, anywhere from the glans to the perineum
Often seen with ‘hooked’ foreskin and chordee (ventral curvature of penile shaft)
Associated with undescended testes, inguinal hernia and hydrocele
types:
- glandular
- coronal
- mid shaft
- penoscrotal
- scrotal
- perineal
Hypospadias diagnosis and management
Full clinical examination to establish hypospadias and type and detect any associated abnormalities
Management:
No treated for very mild hypospadias
Surgery if severely deformed, interferes with voiding or predicted to interfere with sexual function
Repair is performed between 6-18 months of age
Circumcision should be AVOIDED as this is used for construction of new urethra
Epispadias overview
Urethra opens onto dorsal surface of penis anywhere from glans, penile shaft or most commonly the penopubic region
Incomplete urethral sphincter mechanism results in high risk incontinence
Also associated with dorsal chordee (causing upward curvature of penis) and with incomplete foreskin dorsally
Rare congenital disorder
Part of the exstrophy-epispadias complex
Vesical exstrophy - protrusion of urinary bladder through defect in the abdominal wall
Managed by surgery only to reconstruct and repair
Uracus
Remnant of connection between navel and bladder in embryological period
Origin of discharge (urine) from umbilicus in later life
Phimosis
Condition in which contracted foreskin (prepuce) has tight and narrow orifice and cannot be retracted over the glans of the penis
Very important to distinguish between the two types to form management plan
Majority of boys will have retractable foreskin by age 10 and nearly all by 17 (1% will have phimosis)
This is often the result of chronic infection caused by poor hygiene
Usually occurs in uncircumcised males but can occur in circumcised males where excess skin becomes sclerotic
In older diabetic patients often results from chronic balanoposthitis (inflammation of the glans penis and prepuce)
Female condition is uncommon and poorly recognised - clitoral phimosis may present in 22% females, may contribute to dyspareunia and occasionally caused by lichen sclerosus
Types of phimosis and complications
Physiological phimosis: conservative management methods. Present at birth however with penile growth, erection and accumulation of epithelial debris (smegma) under foreskin, separation occurs enabling foreskin to be retracted
Pathological phimosis: surgical intervention needed. Presence of pathology prevents the prepuce from being retracted over glans of penis in any circumstance
complications:
risk of penile carcinoma
Common issues affecting the foreskin and risk factors for phimosis
Smegma: dead or desquamated epithelial cells have been trapped under foreskin. This is common finding in children known to cause balanitis leading to phimosis
Paraphimosis
Adhesions: penile skin adhered to glans of the penis
Risk factors:
Poor hygiene and enthusiastic attempts to correct the congenital phimosis increase the risk of developing pathological phimosis
Balanitis or balanoposthitis both increase the risk of developing a scared preputial orifice
Recurrent UTI
Physiological phimosis
Typical scenario is concern over foreskin not retracting and may be ballooning during micturition
Requires reassurance
Risk factors: recurrent UTIs, balanitis or balanoposthitis
Management: conservative as much as possible, gentle retraction and good hygiene during bathing. Corticosteroid cream and antibiotics effective for underlying balanitis and softening phimosis
If congenital - avoid forcible retraction as much as possible as this can result in scar formation and acquired phimosis
Pathological phimosis
Prevalent in older men
Usually pathological and any associated infections must be treated
Secondary to infection or inflammation can cause: pain, dysuria, bleeding or pus from orifice
Management: surgery - circumcision, plastic surgery (dorsal incision, partial circumcision, release of adhesions, division of short frenulum or meatoplasty)
Paraphimosis
Urologic emergency occurring in uncircumcised males
Foreskin becomes trapped behind the corona and forms a tight band of constricting tissue
Often iatrogenically induced
Can be prevented by returning the prepuce to cover glans penis following penile manipulation
Management often begins with reduction of oedema, followed by variety of options, including mechanical compression, medications, puncture technique and dorsal slit
Prevention and early intervention are key elements in management of paraphimosis
Paraphimosis investigations
Pink colour to glans indicates good blood supply while dark, dusky or blakc implies ischaemia or necrosis
If urinary catheter is in place this may aid reducing paraphimosis
After reduction, indication for catheter should be reviewed and replaced if necessary
PARA - pulled back, attached behind glans, cannot be Reduced Again
Paraphimosis management
Urgent referral to urology for severe cases
Course of topical steroids or preputioplasty
Paraphimosis that is reduced with minimal intervention by emergency department physician still needs outpatient urology follow up in anticipation of recurrences and evaluation for possible circumcision
Nephritic syndrome
acute nephritic syndrome - group of symptoms with kidney inflammation, not specific diagnosis
features of nephritic syndrome: VH/NVH (red cell casts) Oliguria (<300/day) Proteinuria <3.5g/day Fluid retention HTN cola/smoky urine mod-severe eGFR
causes: IgA nephropathy mesangiocapillary GN post strep infection vasculitis (granulomatosis with polyangiitis or microscopic polyangiitis) anti-GBM disease SLE Cryoglobulinaemia
Nephrotic syndrome
group of symptoms without specifying underlying cause:
Peripheral oedema Proteinuria >3g/24 hours Serum albumin <25g/L Hypercholesterolaemia frothy looking urine hypoalbuminaemia from loss in urine oedema from loss of albumin hyperlipidemia fatty casts in urine (proteinuria >3.5g/day)
causes:
minimal change disease no.1 cause in children
focal segmental glomerulosclerosis most common cause in adults
Glomerulonephritis
Umbrella term for Inflammation of glomeruli and nephrons of the kidney
Damage to glomerulus restricts blood flow leading to compensatory high BP
Damage to filtration mechanism allows protein and blood to enter urine (PU-HU)
Loss of usual filtration capacity leads to AKI
Two main syndromes:
Nephrotic syndrome: normal/mild HTN, proteinuria >3.5g/day with normal-mild eGFR (AKI), likely hyperlipidaemia also.
Nephritic syndrome: moderate/severe HTN, haematuria, moderate-severe eGFR (AKI)
classification:
Can also be split into proliferative and non-proliferative:
Non-proliferative: characterised by lack of glomerular cell proliferation and typically presents with nephrotic syndrome (e.g. minimal change GN or FSGS)
Proliferative: characterised by increased numbers of cells in glomerulus and typically presents with nephritic syndrome (E.g. IgA nephropathy, post-infectious GN etc)
Etiology:
Primary: no known underlying disease
Secondary to autoimmune diseases (SLE, DM), infections (strep, viral), malignancy
Both can cause either nephrotic or nephritic syndromes
Glomerulonephritis investigations
Bloods: autoantibodies Anti-neutrophil cytoplasmic antibody (ANCA), antistreptolysin O titer (ASOT), U+Es, eGFR
Urine microscopy and sensitivities, casts and ACR (albumin:creatinine ratio) or PCR (protein: creatinine ratio)
USS: renal vein thrombosis
CXR: cavities in Wegener’s granulomatosis malignancy
Biopsy definitive diagnosis
Underlying cause Ix: BG, throat culture/swab, hep B/C antibodies, HIV screen
renal biopsy reports
Light microscopy:
What element is affected (mesangial cells, capillaries, basement membrane, endothelium)
How much of the kidney is involved (focal/diffuse)
How much of glomerulus is involved (segmental/global)
Immunofluorescence:
Deposition of Igs, complement, immune complexes or pauci-immune
Electron microscopy:
Fusion of foot processes (podocytes)
Glomerulonephritis general management and types of GN
types:
Minimal change disease
Focal segmental glomerulosclerosis
Membranous nephropathy
Mesangiocapillary glomerulonephritis (MCGN)
Mesangial proliferative nephritis
Diffuse proliferative glomerulonephritis
Focal segmental proliferative glomerulonephritis
Crescentic glomerulonephritis
Most are treated with immunosuppression (steroids)
Or Blood pressure control by blocking renin-angiotensin system (ACEi or ARBs)
Control of BP and inhibition of renin-angiotensin axis
Specific treatment depends on histological diagnosis, severity, progression and comorbidities
Membranous glomerulonephritis
Most common type of GN overall
Bimodal peak in 20s and 60s
Histology shows IgG and complement deposits on basement membrane
Majority (70%) cases are idiopathic
Can be secondary to malignancy, rheumatoid disorders and drugs (NSAIDs)
Minimal change disease overview
Nephrotic syndrome - most common nephrotic syndrome in children
Mainly presents in children 2-4 YO
Non specific presentation
Glomerular podocyte foot process damage causing selective proteinuria: normal renal function, normal BP, normal complement levels. Causes hypoalbuminemia (loss of albumin) and hyperlipidaemia
Have increased risk of infections: UTI, pneumococcal peritonitis (primary peritonitis)
Associated with atopy in children
Diagnosis:
Electron microscopy shows widespread fusion of epithelial cell foot processes
Mangenent:
Course of High dose prednisolone, relapse is frequent
Relapsing disease: prednisolone and cyclophosphamide or ciclosporin
Disease DOES NOT progress to end stage CKD
Diffuse proliferative GN/post streptococcal GN overview
Eg post strep infection GN (PSGN)
Common in less developed world, more common in children (or under 30 years)
Presents with strep pharyngitis or tonsillitis then 1-3 weeks later shows
Skin infection (impetigo, cellulitis, erysipelas) then 3-6 weeks later
Strep antigen deposits in glomerular - immune complex forms causing inflammation (nephritis)
Presents with HU, oedema, high BP, oliguria
Diagnosis:
Evidence of strep infection (increased ASOT, increased anti DNAse B, increased C3)
Treatment:
Supportive, antibiotics to clear nephritogenic bacteria
Almost all children recover without treatment
Alport syndrome, Goodpasture syndrome and rapidly progressive GN
Alport syndrome:
Genetic disorder X linked
Defect in IV collagen found in ears, eyes and kidneys
Glomerulonephritis
Haematuria, PU = end stage kidney disease
Hearing loss and eye problems
Goodpasture syndrome:
anti-GBM antibodies attack glomerulus and pulmonary basement membranes
Causes GN and pulmonary haemorrhage
Patients may present with acute kidney failure and haemoptysis
Rapidly progressive GN: Histology shows crescentic GN Presents with very acute illness with sick patients Responds well to treatment Often secondary to goodpasture syndrome
IgA nephropathy/ Berger’s disease overview
Most common cause of primary glomerulonephritis
Peak presentation in 20s YO
Histology shows IA deposits and glomerular mesangial proliferation from IgA immune complexes depositing in the mesangium, causing glomerular injury
Have high serum IgA, varied severity
Non-specific URTI, 1-2 days later presents with episodic haematuria (VH or NVH)
URTI leads to deposition of IgA in the glomerulus
Henoch-schonlein purpura (HSP) is disease with same pathology but more widespread: affects the kidneys, skin, connective tissue, GIT, scrotum and joints
Diagnostic:
Light microscopy: Mesangial proliferation
Electron microscopy: Immune deposits in mesangium
Immunofluorescence: Immune complexes IgA
Management:
Prevent further damage as cannot reverse damage already done
Control BP; lifestyle changes (salt and cholesterol)
Antihypertensives (ACEi, ARB)
Steroids - prednisolone to prevent immune complex formations
Hydronephrosis
Urine filled dilation of renal pelvis and/or calyces as result of obstruction
Does not generally cause long term problems if treated promptly
Increases chance of UTI
If left untreated can cause kidney scarring leading to failure
Can be found in babies on antenatal USS - mostly nothing to worry about and does not affect pregnancy outcome as 4 out of 5 cases resolve spontaneously before birth, remaining are treated with antibiotics to prevent kidney infections or need surgery
Bilateral hydronephrosis
Bladder outflow obstruction (BPH, urethral strictures and valves, phimosis causing retention)
Malignant invasion of bladder trigone (bladder or prostate carcinoma)
External compression from malignant pelvic LAP
Retroperitoneal fibrosis
Schistosomiasis
Unilateral hydronephrosis
Pelvi-ureteric obstruction (congenital PUJ stenosis, pressure from aberrant vessels crossing PUJ, stones and tumours in renal pelvis occluding opening) Ureteric obstruction (stones, tumours, ureterocele, schistosomiasis) Reflux
Presentation of hydronephrosis
Sudden or severe pain in back or flank or dull ache that is intermittent
Can get worse with drinking fluids
UTI symptoms, burning or stinging when urinating
Fatigue, malaise
Haematuria
Less frequently with weaker stream of urine (oliguria)
Diagnosis and management of hydronephrosis
Diagnosis:
USS
Management: Depends on underlying cause Pregnant women and babies may not need treatment Adults: 1st line is drainage by catheter into bladder or kidneys Remove kidney stones Treat enlarged prostate Surgery to stent strictures etc. Remove tumours/treat cancers etc.
Genital warts and presentation
Spread through sexual contact
Caused by HPV types 6 and 11
Generally only cause mild irritation but can cause great psychological stress
Important to educate patient and emphasize HPV types that cause warts are NOT associated with neoplasia
Presentation: Generally painless May have broad base or be pedunculated May have pink, red, white, grey or brown May bleed or itch May be small or coalesce into larger lesions called condylomata acuminata
Genital warts management
May resolve spontaneously, remain or increase in size
Refer to STI screening at GUM clinic
95% associated with low risk HPV, coinfection with HPV 16 or 18 increase risk for anogenital cancers
Soft non-keratinised:
Podophyllotoxin cream or solution self application used BD for 3 days
Imiquimod 5% cream for keratinised and non-keratinised external lesions applied 3x weekly until they resolve or up to 4 months
Keratinised:
Surgical removal or cryotherapy
No treatments are entirely curative and all have high recurrence rates
HPV
Hundreds of viral strains
Different types result in different conditions
HPV 6 and 11 responsible for genital warts
Types 16 and 18 have increased risk of anogenital cancers and some head and neck cancers
Heparan Sulfate receptor needed to invade and replicate in cells while suppressing immune response, can then begin to present as warts
90% cases spontaneously self resolve
HPV prevention and cervical screening
Prevention:
Vaccine given to prevent HPV very effective given to school children not yet exposed to HPV (both sexes) - now protects against types 16, 18, 6 and 11
Cervical screening:
All women between ages of 25-64
Checks for presence of abnormal cells on cervix
If abnormal cells detected, lab test sample for HPV
If HPV detected, offered colposcopy to check for presence of precancerous cells
Herpes
Highly contagious, spread through direct contact
Most contagious through viral lesions but can spread through asymptomatic shedding (found in mucous and saliva)
Virus penetrates epidermis/epithelium and replicates within cell, can travel up through CNS neurons and stay latent there until they are released back down neurons again to invest skin and latent cycle repeats
Classic triggers are stress, fatigue, local trauma, exposure to sunlight or alterations of the immune system
After primary infection virus remains latent, can move ‘silently’ through most of the population
If later reactivates, invades the skin and causes outbreak of lesions
HSV2 typically causes genital lesions but HSV1 can also cause
HSV1 tends to cause infection above waist, HSV2 below but both can cause both
Lesions may itch, tingle and later burn and become painful for 12-24 hours
May appear like blisters that pop, ooze or bleed
Usually resolves in around 7-10 days
Can be found on penile shaft, glans penis
Labia in women
Herpes primary infection and recurrent infection
Often asymptomatic
Symptoms start 3-7 days after contact with infected person
Constitutional symptoms; low grade fever, myalgias and LAD
Pain, burning, itching or tingling may last several hours
Grouped vesicles appear and ulcerate or crust within 48 hours
Lesions last 2-6 weeks and heal without scarring
Recurrent infection:
Alteration of immune system ie stress, fatigue, local trauma, exposure to sunlight
Prodromal symptoms include fatigue, burning or itching of skin lasting lasting 12-24 hours
Cluster of lesions evolve within 24 hours
Vesicles rupture forming crusts in 1-2 days
Herpes investigations and management
Diagnosis clinical
Tests not usually needed: can use viral swab from base of ulcer if needed
Management:
Refer to GUM clinic for diagnosis, treatment and screening for other STIs
Oral antivirals commenced within 5 days (prodromal period): aciclovir 400mg TDS for 5 days or 200mg 5x dailys, valaciclovir 500mg BD for 5 days or famciclovir 250mg TDS (side effects nausea and vomiting, TDS regimens usually more suitable for patients)
Simple analgesia and topical lidocaine for pain relief
Saline baths may help
Counselling and patient education as to asymptomatic shedding, relationships and importance of letting medical staff know about herpes infection if you are pregnant
Chlamydia
Most commonly reported curable bacterial STI in UK and most common preventable cause of infertility worldwide
Most cases (70%) <25 YO
Caused by chlamydia trachomatis
Affects the urethra in men, endocervix or urethra (or both) in women
At least 70% women and 50% men are asymptomatic
Termed uncomplicated when infection has not ascended to upper genital tract
Termed complicated when spread to upper genital tract causing pelvic inflammatory disease PID in women and epididymo-orchitis in men
Infection primarily spread through penetrative sex, but can occur via autoinoculation or splash from genital fluids
Risk factors for sexually transmitted infections
<25 YO New sexual partner More than one sexual partner in last year Lack of consistent condom use Social deprivation Infection with other STIs
Chylamidia presentation
Sexually active women: 70% asymptomatic Increase VD, often yellow and thick Post coital or intermenstrual bleeding Purulent VD Cervical discharge Dysuria Deep dyspareunia Pelvic pain and tenderness Cervical motion tenderness Inflamed or friable cervix (may bleed on contact) Cobblestone cervix appearance (inflammation)
Sexually active men: Dysuria Mucoid or mucopurulent urethral discharge Urethral discomfort/urethritis Epididymo-orchitis Reactive arthritis Epididymal tenderness
Rectal chlamydia:
Anal discharge and anorectal discomfort
Usually asymptomatic
Lymphogranuloma venereum LGV: Tenesmus Anorectal discharge (often bloody) and discomfort Diarrhoea or altered bowel habit
Chylamidia investigations
Endocervical or vulvovaginal swab first line for women
First catch urine FCU second line or first line men (hold bladder at least 1 hour before being tested, capture first 20mL)
Urethral swab 2nd line men
Rectal swabs for LGV
HIV +ve men who have sex with men should have rectal swabs for LGV
NAAT for asymptomatic screening in those with high risk
Asymptomatic people who should be tested include:
Sexual partners of those with proven or suspected chlamydial infection
All sexually active people <25YO, annually or more frequently if they have changed partner
All people with concerns about sexual exposure (if exposure was within last 2 weeks and test is negative must be retested two weeks after)
People <25 YO who have been treated for chlamydia in previous 3 months
People who have had two or more sexual partners in previous 12 months
All women seeking termination of pregnancy
All men and women attending GUM clinics
National screening program:
Those aged 15-24
Encourages testing annually or with each partner change
Recommends retesting around 3 months after treatment
Chlyamidia management
Referral to GUM clinic for management and partner notification or refer urgently if no response to treatment, or suspected PID
Doxycycline 100mg twice daily for 7 days (CI in allergy or pregnancy - calcium deposits in bone and teeth)
2nd line azithromycin 1g orally one day then 500mg orally once daily for two days (caution in cardiac disease due to long QT association) or erythromycin 500mg twice daily 10-14 days
With strong suspicion, do not wait for lab conformation to start treatment
Advise sexual contact including oral should be avoided until treatment is completed
Provide leaflets and written information for patient education and on safe sex practices
Strongly suggest STI screening for them and any other partners including gonorrhea, hep B, HIV, syphilis
Offer repeat testing to <25 YO at high risk of re-infection
Child safeguarding/protection if abuse suspected
Re-test for cure in pregnant women
Chylamidia prognosis and complications
Untreated infection may persist or resolve spontaneously
Up to 50% resolve within 12 months diagnosis
PID including endometritis and salpingitis occurs in 16% women and increases risk of tubal infertility, UTIs, ectopic pregnancy, chronic pelvic pain
Epididymo-orchitis in men
Septic arthritis
Reactive arthritis, eye and urethra all affected - Reiter’s syndrome (can’t see, can’t pee, can’t climb a tree)
Adult conjunctivitis or trachomatis (leading cause of blindness in developed world) from autoinoculation or splash from genital fluids
Sexually acquired reactive arthritis SARA more common in men
In pregnancy associated with: increased risk of premature delivery, low birth weight, intrapartum pyrexia, late postpartum endometriosis, infections of eyes, lungs, nasopharynx and genitals in neonates
Gonorrhoea
STI caused by N. gonorrhoeae
Uncomplicated is localised and primarily affects mucous membranes of urethral, endocervix, rectum, pharynx, conjunctiva
Disseminated gonorrhoea is uncommon. May present as petechial or pustular acral skin lesions, asymmetrical arthralgia, tenosynovitis or septic arthritis
Transmitted via direct inoculation of secretions from one mucous membrane to another
Infection of the eye most commonly results from autoinoculation
Gonococcal infection among infants usually results from exposure to infected cervical exudates at birth
Highest transmission in age group 15-20
Gonorrhoea presentation
men
Usually symptomatic (95%)
Mucopurulent or purulent urethral discharge in more than 80%
Rectal infection usually asymptomatic but may cause discharge, acute proctitis, perianal or anal pain or discomfort, tenesmus or rectal bleeding
Pharyngeal infection often asymptomatic but can cause tonsillitis or pharyngitis
Prostatitis
Epididymitis or orchitis
women Asymptomatic in 50% women Symptoms usually develop within 10 days Increased or altered VD Lower abdominal pain Dysuria Intermenstrual bleed or menorrhagia Pain with intercourse indicates spread to endocervix Pharyngeal infection asymptomatic 90% cases but may cause tonsillitis or pharyngitis In most women no abnormal findings are present but may show Mucopurulent endocervical discharge Easily induced endocervical bleeding Pelvic or abdominal tenderness
gonorrhoea investigation
NAAT urine sample, no earlier than 3 days after sexual contact with infected person gold standard
Vulvovaginal swab
FPU in men
Cultures taken for all those NAAT positive
gonorrhoea management
Refer to GUM clinic for management, partner tracing (from last 3 months) and treatment
NAAT and swabs taken before prescribing, use culture for antibiotics choice
Offer STI screening and HIV
Advise abstaining from sex until they and partners have completed treatments (If azithromycin used this is 7 days after treatment is given)
1st line: ceftriaxone 1g IM single dose! (if antimicrobial susceptibility unknown) generally CI in penicillin allergy
If susceptibility to antimicrobials is known - Ciprofloxacin 500mg oral single dose for uncomplicated or pharyngeal gonorrhoea in primary care
Follow up one week to verify success and test of cure (TOC) with NAAT (asymptomatic) or culture (symptoms persisting), report all failures of treatment to public health england
Can give single IM ceftriaxone 1g injection in primary care if needed for uncomplicated anogenital gonorrhoea
Pregnancy - ceftriaxone 1 g IM single dose DO NOT prescribe fluoroquinolone for pregnant or breastfeeding women
Provide patient education and leaflets, advise follow up and need for partner tracing and treatment
Prognosis:
Usually resolve spontaneously
If untreated can result in complications (epididymitis or orchitis, prostatitis, urethral stricture, infertility, gland infections, PID, peritoneal spread, miscarriage, congential infections
Trichomoniasis
STI caused by trichomonas vaginalis
Flagellated protozoan: single cell organisms
Transmission almost only via sexual intercourse and can still be passed on if asymptomatic
Most common in ages between 20-24 in women
Frequently coinfected with other STIs
Trichomoniasis presentation
only 30% are symptomatic Men: urethritis urethral discharge urinary frequency
female: frothy, yellow discharge vulval itching, soreness or ulceration dysuria offensive fishy odour cervicitis dysparenuria
Trichomoniasis management, complications and prevention
GUM clinic referral for diagnosis, testing, treatment and other STI screening and partner contacting from last 4 weeks
Oral metronidazole 400-500mg BD for 5-7 days OR 2g single dose (not in pregnancy or breastfeeding, must avoid alcohol)
Treat current partners proceeding 4 week period
Abstain from sex until they and all partners are treated
Complications:
Infection of bartholin’s skin or skene’s glands
LAD (rare)
Pregnancy women more likely to give birth preterm or low birth weight
Increases risk of other STI contraction from genital inflammation
Prevention:
Latex condoms (still possible to transmit)
Only way to prevent is through abstaining from sex
STI screening regularly
Restricting number of sexual partners at a time
Syphilis
Caused by bacteria treponema pallidum (obligate parasite, cannot survive outside host)
Associated with high risk behaviours
Long term partner notification needed
Contacts should be offered full sexual health screening
Transmitted via bodily fluids, needlestick injury, direct contact with skin lesions, congenital (mum to baby during birth)
Untreated condition passess through several stages:
Early syphilis:
Primary (early localised)
Secondary
Early latent
Late syphilis: occurs after 2 years infection
Late latent
Tertiary syphilis
Syphilis presentation early phases
Primary syphilis -
Appear up to 3 months post exposure
Resolves over 3-10 weeks
If had blood transfusion may not show primary stage at all as it is the result of the bacteria entering through the skin - does not happen in transfusion -
Chancre: solitary and painless ulcer with clean base and defined margins
Usually located on genitals and may go unnoticed if not visible, can be on hands if direct contact used
May be multiple or purulent (must check HIV coinfection if this is the case)
LAD may also be present
Secondary syphilis -
Appear 1-2 months after chancre appearance
Resolve over 3-12 weeks
MOST INFECTIOUS STAGE -
Non-pruritic maculopapular generalised rash, can be localised to palms or soles
Condylomata lata - grey or white moist warty lesion on oral or genital mucosa or perianal area (painless)
Oral or genital mucosa may develop oval, shallow ulcers with raised silver borders known as ‘snail track’ ulcers
General systemic features: fever, malaise, headache, organomegaly, hair loss
In early neurosyphilis meningitis, hearing loss, visual changes, ischaemia, thrombosis or infection may occur (consider HIV coinfection with this)
Latent syphilis -
Early latent occurs less than 2 years after initial infection
Late latent occurs more than 2 years after initial infection
Usually asymptomatic
Syphilis presentation late phases
Tertiary syphilis -
15-40 years after initial infection
Type IV hypersensitivity reaction causing symptoms due to bacteria sitting in tissue capillaries
Granulomatous lesions called Gumma, occur anywhere on skin and bone
Non-tender, dusky red or brown plaques appear punched out with necrotic centres
CVsyphilis caused by vasculitis and chronic inflammation leading to aortic regurgitation, aneurysms, HF or angina
Neurosyphilis causes inflammation of spinal cord, nerve roots, general paresis, personality changes, dementia and seizures
Can cause tabes dorsalis (wasting of back of spinal cord) causing loss of sensation of vibration and proprioception
Can also loose light sensitivity (but NOT accommodation reflex) of the eye
Congenital syphilis overview
infection occurs via placenta or childbirth early disease (first 2 years) shows stillborn, dying in womb, or maculopapular rash, optic neuritis, snuffles, hepatosplenomegaly, damage to liver and spleen
late disease shows saddle nose, saber shins, hutchinson teeth, hearing loss
Syphilis investigations
Swabs from primary lesions (PCR testing)
Serological tests detect treponemal IgG and IgM in blood: false negative if taken too soon after exposure, false positives from viral infections, malignancy, drugs use and pregnancy
T pallidum particle agglutination TPPA
Congenital - looks at both mother and baby RPR ratio, long bone XRs and hearing scans also good
Syphilis management and prevention
Refer to GUM clinic for diagnosis, treatment, contact tracing for last several years
1st line treatment not available in primary care (GUM clinic): for primary, secondary and early latent syphilis give benzathine penicillin 2.4 mega units IM injection single dose (doxycycline allergy)
First line late latent syphilis give benzathine penicillin 2.4 mega units weekly for 3 weeks
Tertiary stage treated with specialist
Advise avoiding sexual contact of any kind until diagnosis excluded or successful treatment is completed
Prevention:
Treatment of asymptomatic contacts
Screening of all pregnancy women
HIV
RNA retrovirus
HIV 1 predominant strain
HIV 2 predominant outside of west africa
Transmitted through sexual contact, mother to child in pregnancy, birth or breastfeeding, by inoculation from needlestick injury, blood products, bodily fluids or human bites breaking the skin
Heterozygous mutations in CD4 proteins can cause resistance to HIV reducing infection and spread
Homozygous mutations can actually create HIV immunity
HIV pathophysiology
Pathophysiology:
Immune cells (T, monocytes, macrophages) have CD4 receptors
HIV binds to these, then travel inside lymphoid tissue
Virus replicates infecting more CD4 +ve cells, as it replicates it very commonly mutates and creates mini strains within the host which can act differently
Function of immune cells is impaired and numbers depleted
Leads to immune dysfunction or acquired immunodeficiency syndrome (AIDS)
HIV risk factors
Men who have sex with men
Migrants from high HIV incidence countries
IV drug users
Stages of HIV and presentations
Stage 1 - acute primary infection (seroconversion)
20-60% patients develop symptoms between 1-6 weeks after infection
Commonly see glandular fever type illness: fever, malaise, muscle pains, pharyngitis, headaches, diarrhoea, LAD or rash
Some patients remain asymptomatic
Viral levels and antigen levels are elevated but antibodies will be low
Stage 2 -asymptomatic
Viral levels low but replication slowly continues
CD4 levels normal
Can continue for many years
Stage 3 - symptomatic
Nonspecific constitutional symptoms like fever, night sweats, diarrhoea, weight loss
Opportunistic infections such as oral candida, herpes, tinea infections or hair leukoplakia (below) can occur
AIDS - LATE STAGE HIV
CD4 count very low
Opportunistic infections and diseases such as pneumocystis pneumonia and Kaposi’s sarcoma which presents with dark purple or brown intradermal skin lesions that look like bruises (below)
HIV investigations
HIV screening offered to all patients as part of routine antenatal care, STI screening, new patients registering with GP who travelled from area of high prevalence, RFs such as IV drug users, sex workers, anyone reporting high risk behaviours, unusually severe, recurrent or prolonged unexplained symptoms or those presenting with HIV indicating condition
HIV antibodies or antigen tests
Viral load and CD4 count
Tests should be performed between becoming infected and antibodies appearing
HIV antibodies usually appear 4-6 weeks after infection but can take up to 12 weeks
Management and progression of HIV
Antiretroviral treatments now help fewer patients progress to AIDS - those on antiretrovirals have LESS CHANCE of passing it on to others but not impossible
Abacavir, emtricitabine, lamivudine, tenofovir, zidovudine (All Elephants Like To Zing) - nucleotide reverse transcriptase inhibitors
Nevirapine, delavirdine, efavirenz - non-nucleoside reverse transcriptase inhibitors
Raltegravir and bictegravir - integrase inhibitors
Must be initiated and monitored in secondary care
Can have significant side effects, aims to reduce viral loads by limiting viral replication
Given in combination to avoid drug resistance
Progression:
No cure, aim to extend life and maintain QoL while reducing transmission
Monitored with CD4 and viral load
Normal CD4 >500 cells/microlitre, once below 200 is opportunistic for infections and cancers to arise
Viral loads reflects rate of viral replication, when load is suppressed through treatment CD4 recovers and risk of HIV related illness declines
varicocele
Scrotal swelling consisting of collection of dilated veins of pampiniform plexus in the spermatic cord
May be caused by incompetent or absent valves in the testicular (spermatic) vein or rarely may be secondary to tumour or other pathology obstructing the spermatic vein
Generally become noticeable at puberty due to testicular growth and increased blood flow
Occur in about 15% adolescent boys and men
Varicocele pathology
Increased hydrostatic pressure in left renal vein and incompetent or congenitally absent valves are typically primary causes
Clinically detectable varicoceles can be associated with abnormal gonadotropin levels, impaired spermatogenesis, histological changes to sperm and infertility
Thermal damage secondary to impaired countercurrent mechanism normally keeping intrascrotal temperatures 1-2 degrees C may be contributing factor
Other possible causes include reduced venous out-flow or impaired arterial inflow
About 90% occur on the left side because of the difference in drainage routes of right and left spermatic veins
anatomy: Varicocele drains into spermatic vein within inguinal canal on each side Left internal spermatic vein then drains into the left renal vein at a right angle and increased pressure in vertical column of blood can lead to dilation of pampiniform plexus Left inguinal spermatic vein is also 8-10cm longer resulting in increased hydrostatic pressure The right internal spermatic vein drains at an oblique angle into the IVC giving more protection/decreased pressure Bilateral varicoceles (10% cases) may occur from cross circulation from left to right pampiniform plexus
Varicocele presentation
Usually painless scrotal swelling on left side (can be bilateral swelling if both involved)
Right sided alone is very rare and must be referred to urologist
Pain is uncommon, but can have heavy or dragging sensation in scrotum
Characteristically presents as a ‘bad of worms’ within spermatic cord above the testis on left side of scrotum
Scrotum on affected side can hang lower
Dilation and tortuosity of veins increased on standing and decreases when supine
Performing valsalva manoeuvre while standing increases dilation
May be cough impulse
Small testis - larger varicoceles associated with testicular growth arrest in adolescents
Older than 12 years - rare in pre-pubertal boys
Infertility
Varicocele grading and risk factors
Grading:
Subclinical - detected only with doppler USS
Grade I - small, palpable only with valsalva manoeuvre
Grade II - moderate, palpable without valsalva
Grade III - visible through scrotal skin
Risk factors:
Tall and heavy with lower BMI than age-matched controls
Family history especially first degree
Varicocele diagnosis
Clinical: Examine all adolescents in supine and standing positions and assess if testicular growth has occurred. Examine once annually through puberty if testes are symmetrical and refer to urologist if any asymmetry (left smaller than right) or impaired growth
USS with colour flow doppler imaging if diagnostic uncertainty, or thick scrotal skin or increased amount of scrotal tissue making exam difficult
Varicocele management
Dependent on grade/severity
For adolescents with subclinical or grade I - no treatment needed, advice and reassurance
Grade II or II and symmetrical testes - observe with annual examinations
Grade II or III asymmetrical testes - refer to urologist for possible surgery
For men with subclinical or grade I - no treatment needed, offer fertility screening if this is concern
Grade II or III asymptomatic and normal semen parameters - observe with semen analysis every 1-2 years
Grade II or III symptomatic or abnormal semen parameters - refer to urologist for possible surgery
varicocele general advice
Reassure does not often need treatment and is unlikely to cause symptoms or long term complications
Explain any associated discomfort may be initially managed with supportive underwear and simple analgesia
Although associated with fertility problems, nearly two thirds of men with condition have no difficulty with fertility
For men with fertility problems explain evidence does not support use of varicocele ablation to improve pregnancy rates
If surgery being considered, explain urologist will discuss risks and benefits of available procedures
varicocele when to refer and complications
Urgent referral to urology if: painful, does not drain while supine, solitary right sided varicocele
Refer routinely if there is pain or discomfort
Refer adolescents to urologist if: concerns about reduced ipsilateral testicular volume, if concerned about cosmetic appearance or symptoms and cannot be reassured in primary care
Refer to urologist if uncertain of nature of scrotal swelling
Refer with solitary right side varicocele
Complications:
Consider semen analysis in adults and evaluation of serum FSH and testosterone levels to assess testicular function. Abnormal sperm production with elevated FSH shows impaired spermatogenesis
Hydrocele
Abnormal collection of serous fluid between parietal and visceral layers of membrane (tunica vaginalis) that surrounds the testis or along spermatic cord
Affects 1-3% male neonates when results from entrapment of fluid after closure of processus vaginalis
Congenital simple hydrocele typically spontaneously resolves within first year of life
More prevalent in premature infants and those whose testes descend relatively late
Causes in older boys and men include minor trauma, infection, epididymitis, testicular torsion, varicocele operation and testicular tumour
Hydrocele classifications
Simple - accumulation of fluid within tunica vaginalis
Abdominal-scrotal hydrocele - rare, simple cases enlarged through inguinal canal resulting in abdominal component
Hydrocele of spermatic cord - when processus vaginalis closes segmentally, trapping fluid anywhere along spermatic cord
Communicating hydrocele - persistence of processus vaginalis allows peritoneal fluid to freely communicate with scrotal portion of processus. By definition, these are congenital but many manifest for first time in older boys and men when precipitated by increased intra abdominal pressures, continuous peritoneal ambulatory dialysis or fluid overload
Hydrocele presentation and diagnosis
Scrotal enlargement with non-tender, smooth cystic swelling
Pain is not a feature unless there is infection or underlying cause
Testis usually palpable but may be difficult to feel is hydrocele is large
A hydrocele lies anterior to and below the testis and will transilluminate *NOTE some prepubertal tumour such as tetatomas may also transilluminate**
Diagnosis:
Exam - transillumination
USS for uncertain diagnosis or underlying cause
Hydrocele management
Congenital:
For infant/toddler with hydrocele since birth: reassure parents it’s likely to resolve spontaneously by age 2
Progression to hernia is rare and does NOT result in incarceration
Refer to paediatric surgeon if: underlying pathology, concomitant inguinal hernia suspected, hydrocele is localised to spermatic cord, palpable abdominal mass, simple non communicating hydrocele either is not decreasing in size or is still present after age 2
Non-congenital:
Admit or refer depending on suspected underlying cause
If man is 20-40 years of age or testis cannot be palpated, arrange urgent USS scan of scrotum
Reassurance and scrotal support for idiopathic hydroceles
Refer men or boys with large, uncomfortable hydroceles for outpatient appointment with urologist or paediatric surgeon
Aspiration and sclerotherapy is alternative for people unfit for or choose not to have surgery
Erectile dysfunction
Persistent inability to attain and maintain an erection sufficient to permit satisfactory sexual performance
Very common disorder, can occur at any age but prevalence increases with increasing age, this is due to increase comorbidities, chronic diseases and age related changes
Can be classified according to cause: organic, psychogenic and mixed, however EAU guidelines suggest primary organic or primary psychogenic used instead as most cases of erectile dysfunction are of mixed etiology
Causes:
It is often a symptom, not a disease
May have organic or psychogenic cause
Can be caused by drugs
causes of erectile dysfunction
Organic causes:
vasculogenic (most common cause): CVD, DM, hyperlipidaemia, smoking, major pelvic surgery
Neurogenic (central): degenerative disorders, stroke, spinal cord trauma or diseases, CNS tumours
Neurogenic (peripheral): DM, chronic renal failure
Anatomical or structural: penile or prostate cancer, congenital curvature of penis, phimosis
Psychogenic causes:
General: lack of arousability and disorders of sexual intimacy
Situational: due to partner or performance related issues, stress, psychiatric illness depression, anxiety, schizophrenia)
Drugs: Antihypertensives Diuretics Antidepressants Antiarrhythmics Antipsychotics Hormones and hormone modifiers Histamine antagonists Recreational - alcohol, cocaine etc
Risk factors for ED
Same as CVD risk factors
Obesity
Diabetes
Dyslipidemia
Metabolic syndrome
HTN
Endothelial dysfunction
Lifestyle factors: smoking, alcohol intake, recreational drugs
also some evidence for association between ED and psoriasis, non-alcoholic fatty liver disease
also some evidence that long cycling can cause ED (>3 hours a week) possibly due to saddle contact
ED and CVD link
Link between ED and CVD probably involves endothelial dysfunction and small vessel atherosclerosis, resulting in disorders of penile and coronary circulation
Penile arteries are smaller than coronary so will cause a more significant reduction of blood flow compared to coronary
Both share the same risk factors and ED is also an independent marker of increase CVD risk
In men with preexisting CVD, assessing CV risk of sexual activity is also very important (low, mod or high risk)
ED investigations
History and clinical diagnosis Fasting glucose, HbA1c, lipid profiles BP and BMI to calculate QRISK score Morning testosterone sample PSA if indicated FSH, LH and prolactin profile if testosterone is low
ED management lifestyle
Identify and manage reversible RFs (drug review and lifestyle review)
Ensure underlying conditions (diabetes, HTN etc) are well controlled
If taking medications that may cause ED, consider changing for other drugs if possible if link can be demonstrated within 2 weeks of taking the medication
Lose weight, smoking cessation, reducing alcohol consumption (modifying CVD RFs)
Men who cycle >3 hour/week should trial not cycling to see if this improves their ED
Assess response after 6-8 weeks
ED medications
1st line PDE-5 inhibitors (VIAGRA/sildenafil, tadalafil, vardenafil and avanafil), has NO CI
Choice dependent on frequency of sex, personal preference and cost
Viagra can be bought OTC 50mg
Tadalafil available in 2.5mg and 5mg to be taken OD for men who anticipate frequent use (>twice weekly)
Common adverse effects include back pain, dyspepsia, flushing, migraines, myalgia, nasal congestion, dizziness, nausea and vomiting
They are NOT erection initiators, still need sexual stimulation but help facilitate and maintain erection
Time taken to work depends on brand (15min-1 hour before sexual activity)
Can be eligible for prescription or may need private script (NHS qualify: have diabetes, MS, parkinons, poliomyelitis, prostate cancer, severe pelvic injury, single gene neuro disease, spina bifida, spinal cord injury, are receiving renal dialysis for renal failure, have had recent pelvic surgery, prostatectomy or kidney transplant or were receiving ED medication before 1998)
One treatment per week recommended but if more considered then can be prescribed on NHS
ED secondary care management and when to refer
Vacuum erection devices: 1st line in older men with infrequent intercourse and comorbidities CI for medications
2nd line: alprostadil comes as cream or intraurethral application, can be useful following spinal cord injury or major pelvic surgery
Penile prosthesis: 3rd line for organic cause ED who fail to respond to medications or who prefer permanent solution
When to refer:
Hospitalisation for priapism - persistent erection
Referral to urology for young men who have always had difficulty with ED, have history of trauma or abnormal testicles on examination
Does not respond to medications
Refer to endocrinology for hypogonadism
To cardiology for severe CVD that CIs sexual activity with ED medications
To mental health services for psychogenic underlying cause of ED or with severe mental distress
Vaginal discharge
Can be physiological or pathological
Most common cause is normal physiological, bacterial vaginosis and candida infections
STIs and non-infective causes should also be considered
Can be infective but not STI related also: BV, candidiasis etc.
Normal physiological discharge:
Should be white or clear
Non-offensive
Varies with menstrual cycle
Vaginal discharge causes
Non-infective causes of VD:
Physiological: newborns may have small amounts, sometimes mixed with a little blood from high maternal oestrogen. Should disappear by 2 weeks of age
Varying stages of menstrual cycle (low oestrogen = thick and sticky mucus, with rising oestrogen becomes clearer, wetter and more stretchy, after ovulation increases thickness and stickiness once again)
Menopause: normal amount of VD decreases as oestrogen levels fall
Cervical polyps and ectopy
Foreign bodies eg retained tampon
Vulval dermatitis
Erosive lichen planus
Genital tract malignancy eg cancer of cervix, uterus or ovaries
Fistulae
Non-sexually transmitted infection:
Bacterial vaginosis most commonly seen in sexually active women
Candidal infections - caused by overgrowth of candida albicans
STI:
Chlamydia trachomatis
Neisseria gonorrhoeae
Trichomonas vaginalis - particularly common in young women attending genitourinary medicine (GUM) clinic and often found in association with gonorrhoeae infection
Sexual history taking
Full clinical sexual history
Nature of discharge - colour, smell, consistency, amount, frequency, onset, duration (heavy, pus-like, clumpy, blood tinged, foul smelling, itching etc)
Associated symptoms - itching, superficial dyspareunia or dysuria, abdominal pain, deep dyspareunia, abnormal bleeding, pyrexia
Risk of STI - how many sexual partners current and previous, barrier protections used? When was last sex without barrier protection, how many times etc. have they ever been tested, when was last test? Have they ever had positive tests? What types of sex do they have (vaginal, oral, digital or anal)
Current contraceptive methods or medications
common VD presentations and indications
bloody/brown, abnormal vaginal bleeding or pelvic pain - irregular menstrual cycles, cervical or endometrial cancer
thick cloudy or yellow VD, bleeding between periods, urinary incontinence, pelvic pain, pain and itching while urinating can indicate chlamydia or gonorrhoea
Frothy, yellow or greenish with bad BAD smell bleeding between periods, urinary incontinence, pelvic pain, pain and itching while urinating can indicate trichomoniasis
white, cheesy thick VD with swelling, pain around vulva, itching, painful sex can indicate candidiasis infection
white, grey, yellow with FISHY odour with itching, burning, redness and swelling of vagina or vulva can indicate bacterial vaginosis
Bacterial vaginosis, risk factors and presentation
Most common cause of VD in women of childbearing age
Commonly asymptomatic
More common in women with pelvic inflammatory disease PID
Risk factors: IUD Smoking Vaginal douching Perfumed gels or vaginal deodorants Bubble baths Washing underwear with strong detergents Presentation: Thin, profuse and fishy smelling discharge Without itch or soreness
In pregnancy:
Associated with poor perinatal outcomes, particularly preterm birth
Routine screening for asymptomatic BV during pregnancy not recommended
Bacterial vaginosis diagnosis and management
Increased vaginal pH >4.5 from anaerobic overgrowth
Positive amine test (release of amine odour when discharge mixed with 10% KOH)
Management:
Metronidazole and clindamycin oral or vaginally
Pregnant or breastfeeding women may use metronidazole 400mg twice daily for 5-7 days or intravaginal therapies. 2g stat dose NOT recommended
Testing and treatment of male partners not indicated but should be considered with female sexual partners
Recurrent BV treated with metronidazole vaginal gel
Offer STI testing if co infection suspected
Candidiasis overview
Thick, typically curd like VD White coloured Non-offensive smelling Associated with vulval itch and soreness May cause mild dyspareunia and dysuria
In pregnancy:
Common (30-40%) often asymptomatic
No evidence of harm for foetus
Management:
Vaginal or oral azole antifungals
Avoid oral in pregnancy
With vulval symptoms, topical antifungals may be used in addition for symptoms
No need for routine screening or treatment of sexual partners
Latex contraceptives may be weakened by vaginal antifungal treatments !!
Recurrent cases can be treated with 150mg fluconazole every 3 days followed by 150mg once a week for six months
vaginal foreign bodies
Foul smelling serosanguinous VD
Diagnosis confirmed with examination
Must be removed or may require lavage if too small or not located
Short course antibiotics may be needed if object was there for long enough to cause secondary infection
changes to VD in pregnancy
Increased production most commonly
Change in consistency
VD following miscarriage, abortion or delivery:
Patients should be fully investigated and empirically treated while waiting for swab results
BV associated with endometriosis and PID following abortion but retained products of conception should be considered in ALL women, particularly with heavy growth of coliforms
female GU history of presenting complaint
Pain: onset, nature, duration, radiation, exacerbation, relieving factors, severity
Have they had any previous investigations or treatment?
Any dysmenorrhoea?
Any dyspareunia (pain during or after sexual intercourse)
Determine effects of pain on life and work
Discuss ideas, concern and expectations
Dysparenunia history taking
Superficial (vaginal or episiotomy scar) or deep (uterine, cervical or adnexal)
Is there radiation
Does it prevent full penetration
Is libido and foreplay adequate
Pain with deep penetration may relate to ovaries
Is there dryness or atrophy
Any rash?
Intermittent or recurrent or always present?
Severity?
Evidence of mood disorder?
Relationship to menses? Are they postmenopausal
Urinary symptoms and vaginal discharge or abnormal vaginal bleeding history taking
If pain is urinary, discuss micturition Is there urethral discharge Frequency Nocturia Urgency Stress incontinence Is there restriction to daily activities and plans because of this? Are symptoms intermittent/recurrent or always present?
Vaginal discharge:
Colour, blood?
Odour?
Consistency?
Is it intermittent, consistent, recurrent?
Use of gels, douches, vaginal deodorants or perfumed bath additives
Any localised tenderness?
Abnormal vaginal bleeding: Any clotting or flooding? Is there intermenstrual or postcoital bleeding? Periodicity Relationship to menses Possibility of pregnancy
Menstrual history taking
Age at menarche (usually 12 YO, affected by weight)
If concern about abnormal puberty - ask about secondary sexual characteristics and thelarche (onset of breast development)
Are they sexually active, if so when last active?
Are they on contraception or trying for baby
Pattern of menstrual cycle: First day of last normal period Days of bleeding Length of cycle Blood loss heavy (no of tampons or pads, where clots present) Form of contraception used Any discharge other than menses
Primary and secondary amenorrhoea history taking
Primary amenorrhoea:
Look for presence of secondary sexual characteristics
Consider imperforate hymen (rare)
Features suggesting genetic abnormality eg turner syndrome
Features of hyperandrogenism
Secondary amenorrhoea:
Physiological: pregnancy, lactation
Psychological: mood swings
BMI: anorexia nervosa
Extrinsic hormonal causes: drugs (COC and POP)
Intrinsic hormonal causes: hypothalamic, pituitary, thyroid, adrenal disorders
Ovarian factors: PCOS, ovarian tumours, infection, primary ovarian failure
Normal menstrual cycle and abnormal bleeding patterns
Normal menstrual cycle:
21-35 days (av. 28) long
Blood loss 50-200mls (av 70mls)
Passage of large clots suggests excessive bleeding
Abnormal bleeding patterns:
Polymenorrhea - too frequently
Oligomenorrhea - usually infrequent or scanty (common around puberty
Menorrhagia - heavy periods
Menometrorrhagia - prolonged, excessive and irregular uterine bleeding
Intermenstrual bleeding - between periods, can be caused by breakthrough bleeding on pill, diseases of uterus and cervix, mucosal disorders or postcoital bleeding (usually local cervical or uterine disease)
Postmenopausal bleeding - occuring >12 months after amenorrhoea of menopause
Dysfunctional uterine bleeding - abnormal bleeding that cannot be ascribed to pelvic pathology. Regular pattern suggests ovulation occurring, irregular suggests anovulatory cycles
Sexual history symptoms to screen for, occupational, foreign travel and family history
Other symptoms: Loin pain Urinary incontinence Urethral discharge Systemic symptoms of AKI or CKD (anorexia, vomiting, fatigue, pruritus, peripheral oedema) or consider abnormal BP or urinalysis, renal function or serum biochem problems
Occupational history:
Exposure to carcinogens may indicate bladder cancers
Foreign travel:
Egypt or africa can result in exposure to schistosomiasis
Dehydration during time in hot climate may lead to development of kidney stones
Family history:
CKD or polycystic kidney disease
past medical and medication history for sexual history taking
Past medical history:
Neuro diseases (parkinson’s or MS) can cause abnormal bladder function
Previous kidney disease, HTN, diabetes, gout or back injury may be relevant
Previous surgery may indicate urinary incontinence
Ureteric injury may occur following abdo or gynae operations
Medication history:
Full current and past medical history
Prolonged analgesic may cause CKD
Dosages of some drugs may need to be adjusted or stopped in CKD
Male urethral discharge
Most commonly presents as urethritis
Risk factors: 20-40 YO, sexually active, vaginal unprotected sex, recent change of sexual partner, male with male sex or bisexual
Common differentials: candidal balanitis, epididymo-orchitis, acute prostatitis, cystitis
FPU preferred sampling type in men
Treatment recommended before testing results arrive
UKMEC and categories
UK medical eligibility criteria (UKMEC):
Offers guidance of contraception of who can use safely
For each personal characteristics or medical conditions a category of 1-4 is given
Categories:
Condition with no restriction for use of methods
Condition where advantages of using method generally outweighs risks
Condition where risks outweigh the benefits - must have clinical judgement or referral to specialist contraceptive provider
Condition with unacceptable health risk is method is used
COC
Oestrogen and progesterone 20-40 micrograms oestrogen
First line options are monophasic prep containing 30 mcg oestrogen plus either norethisterone or levonorgestrel (loestrin, rigevidon, microgynon)
Mode of action: acts on HPG axis to suppress FSH and mid cycle LH surge to inhibit development of follicles and ovulation
Also thicken cervical mucus and inhibits blastocyst implantation by reducing endometrial receptivity
CI (UKMEC 4) in women with current breast cancer, breastfeeding or <6 weeks postpartum and women >35 YO and smoking 15+ cigarettes/day
Should only be used after consultation with expert (UKMEC 3) in women with history of breast cancer, no evidence of recurrence for 5 years, women taking liver enzyme inducing drugs (rifampicin) and women with BMI >35
Must enquire about migraines, CVD risk factors, past and current medical condition, family history
increased DVT risk
increased MI risk, possible increased stroke risk
small increased risk of breast and cervical cancer
Combined vaginal ring
Pros:
Convenient
Lasts 3 weeks - remove for one week
Does not become less effective with vomiting or diarrhea
Appears to be at least as effective as COCs at pregnancy prevention
Cons:
Side effects: headaches, vaginal infections and discharge
Foreign body sensations or discomfort with intercourse
May break during use or be expelled
Delay returning to normal fertility up to few months once stopped
Incorrect insertion
Initiation:
Advise insertion on day 1-5 menstrual cycle (no additional contraception needed)
If inserted at any other time barrier method needed for first 7 days
If pregnancy cannot be excluded but wishes to start without delay - advise pregnancy test to be taken 3 weeks after last unprotected sex
Combined transdermal patch
Evra patch UK only available
203 mcg progesterone and 33.9 mcg oestrogen into systemic circulation over 24 hours for 7 days
Mode of action:
Ovulation inhibited same method as COC pill
Pros:
Convenient - only applied once weekly
Not affected by vomiting or diarrhoea
As effective as COC at pregnancy prevention
Cons:
Can be seen
May detach and become less effective
Less effective in women >90kg
Risks and adverse effects: skin irritation, nausea and vomiting, irregular bleeding
Delay in return to normal fertility up to few months
Initiation
Starting on day 1-5 no additional contraception needed
Started at any other time need contraception for 7 days
If pregnancy cant be excluded but still wants contraception - advice pregnancy test at least 3 weeks after last unprotected sex
POP
Particularly used when COC is contraindicated (breastfeeding moths or women with RFs
Mode of action: ovulation inhibited to varying degrees, about 60% with levonorgestrel and 97% desogestrel
Transport to ovum delayed
Cervical mucus more viscous and impenetrable to sperm and endometrium becomes unsuitable for implantation
brands: norgeston, noriday, cerazette etc.
How to take:
Take daily at same time for 28 days no break
Starting on days 1-5 no additional contraception needed
If started another time needs contraception for 48 hours after starting pill
If pregnancy can’t be excluded but wish to start without delay - assess need for emergency contraception, advise pregnancy test at least 3 weeks since last UPS
Pros: Reliable Easily reversible Avoids CVD risks of oestrogen Wider range of patients can use Can be used during breastfeeding Can be used up to age of 55
Cons:
Menstrual irregularity - amenorrhoea and breakthrough bleeding
Must be taken at same time each day
Increased risk of functional ovarian cysts and small increased risk of breast cancer
When pregnancy does occur, increased risk of ectopic
Progesterone only injection
Long acting synthetic progesterone released into systemic circulation via IM or subcut injection
Mode of action: suppress ovulation, decreased suitability for implantation and increases mucus viscosity
three forms in UK:
- Depo-provera
- sayana press
- noristerat
Pros:
Effective and convenient (only every 12-13 weeks)
Can be used while breastfeeding
Amenorrhoea common (good for menorrhagia or dysmenorrhoea)
Self administration may be option for sayana press in future
Cons:
Not quickly reversible - fertility can take up to one year to return
Loss of bone density - osteoporosis risk which recovers after stopping
possible increased breast cancer risk
CI for those under 18
should be reviewed in 2 years
Administration:
Usually given first injection up to and including day 5 after start of menstrual bleeding no other contraception needed
If not possible, advise barrier contraception for 7 days
Progesterone only implant
Progesterone only subdermal implant is long acting reversible contraceptive
Progesterone containing rod slowly releases into systemic circulation following insertion into upper arm
Mode of action: inhibit ovulation, thickens cervical mucus and prevents implantation
brands: nexplanon
Pros:
Highly effective
Long action duration
Reversible - no fertility delay
Convenient - 3 years long
Reduced menstrual problems like dysmenorrhoea
Cons:
Irregular bleeding common in first year
Changes in weight, mood, libido
Initiation:
Ideally insert up to day 5 of menstrual cycle, no additional contraception needed
If not possible, use protection for 7 days
IUD assessments
Exclude pregnancy
UKMEC 4 criteria CI in women with current breast cancer (IUS only), PID, unexplained vaginal bleeding
UKMEC 3 caution in women with uterine fibroids with distortion of uterine cavity or history of breast cancer and no evidence of recurrence in last 5 years (IUS only)
Assess STI risk and screen as necessary
Do not insert with unexplained vaginal bleeding until diagnosed or use alternate method of contraception
IUD copper coil
Safe and effective reversible contraception
Most effective barriers are T shaped
Mode of action: prevent fertilisation with Cu effect on ova and sperm, reduced sperm penetration due to Cu affect on cervical mucus, endometrial inflammation reaction gives anti-implantation effect
Pros: Highly effective and convenient Effective as soon as fitted Can be used as emergency contraception No hormones involved Effective for up to 10 years Possibly reduces risk of endometrial cancer
Cons: Insertion can be unpleasant Spotting or bleeding common Pelvic pain Increased blood loss and painful periods Displacement or expulsion risk Uterine perforation Ectopic pregnancy more likely if to be become pregnant
Initiation:
Insert Cu IUD at any time in menstrual cycle if reasonably certain they are not pregnant
Effective immediately no extra contraception needed
If unprotected sex occured before insertion and there is risk of pregnancy, Cu IUD can safely be put in up to 5 days after episode or within 5 days earliest expected time of ovulation
Levonorgestrel IUS
Two systems available the Mirena and Jaydess, both T shaped
Mirena effective for 5 years or until contraception no longer needed, Jaydess for 3 years
Mirena also now licensed for idiopathic menorrhagia and endometrial protection with HRT
Mode of action - mainly reducing endometrial growth and preventing implantation. There is endometrial atrophy within one month of insertion
Progestogenic effects on cervical mucus reduce penetration by sperm
Ovulation usually not inhibited
Pros:
Very effective, convenient and reversible
Reduces blood loss and dysmenorrhoea
May reduce risk of PID
Does not significantly affect bone density
Cons:
Insertion may be unpleasant
Menstrual irregularities
Typical progestogenic side effects (acne, breast tenderness, headache, mood swings)
Dysfunctional ovarian cysts which usually resolve spontaneously
Ectopic pregnancy if to become pregnant
Expulsion or perforation
Initiation:
LNG-IUS insertion on day 1 to 7 of menstrual cycle no extra contraception needed
Inserted at any other time assuming not pregnant use barrier method for 7 days
Sterilisation assessment
Assess mental capacity
Level of understanding of advantages and disadvantages
Risk of later regret (often in those younger than 30, without children, decisions during pregnancy or reaction to end of relationships or partners wishes)
Cultural, religious, psychological and psychosexual beliefs
Also assess partners suitability for sterilisation eg if other partner is CI for sterilisation
Perform scrotal examination
Perform a bimanual exam on women
Vasectomy
Interruption of vas deferens via minimally invasive approach
Vas deferens exposed and isolated, lumen occluded and VD then divided. Part of VD may or may not excised
Various methods of occlusion used: coagulation, ligation with clips, insertion of intra VD devices, irrigation etc.
Conformation of success needs post op semen analysis confirming azoospermia
FSRH guidelines advise testing 12 weeks post-vasectomy and no further tests needed if successful
Advise carrying on normal contraception during 12 WW
Pros: Less likely to fail and less likely to have post op complications than female Permanent solution Less invasive than female Convenient long term
Cons: Bleeding into scrotum and haematoma risk Infection Epididymitis Sperm granuloma Persistent pain in genital area Contraceptive failure 1 in 2000 Regret - not easily reversible
Tubal occlusion
Can be performed laparoscopically, hysteroscopically or as open procedure
Aim to use clips to mechanically occlude fallopian tubes or tubal cannulation and placing intrafallopian implants
Mini-laparotomy is rarely used - small incisions made above pubis at level of pubic hairline. Forceps used to pull tubes, divide and tied
Usual to remove small piece of tubes for histology to prove fallopian tube was identified correctly, cut ends tied back to assure separation
Pros: Sterile immediately after procedure Periods unaffected Very effective Convenient Permanent
Cons: If laparoscopy may need to be converted to open procedure Increased risk of ectopic pregnancy Increased risk of hysterectomy Regret - not easily reversible Does not protect against STIs
Natural fertility awareness based methods
Basal body temperature, cervical mucus, urine hormone level methods (preferential) as well as calendar and palpating cervix
Devices and dipsticks can help keep track of cycle and fertile times
Not recommended as limited evidence of efficacy compared to more effective methods
Not covered by UKMEC
Lactational amenorrhoea method also used: for breastfeeding mothers. For LAM to be effective, woman must be fully breastfeeding, have amenorrhoea and baby must be less than 6 months old
Factors that could affect fertility to make FAM difficult:
Conditions affecting ovaries or menstrual bleeding (stroke, serious liver disease, hyerthyroid, hypothyroid, cervical cancer)
Breastfeeding, postpartum or recent termination
Lithium, tricyclic antidepressants and some antibiotics
Irregular menstrual cycle
Any infections in last 3 months - VD makes methods depending on secretions difficult
Pros:
No side effects
Complies with religious practices of some patients
Cons:
Considerable commitment from both partners needed
Unreliable with unpredictable cycles
Less effective than other methods
Barrier methods assessment
Cervical cap or diaphragm:
Vaginal examination for initial fitting
Advise those using teratogenic drugs (lithium and phenytoin) to consider alternatives
Not suitable for those <6 weeks postpartum or 6 weeks following second trimester termination
Advise women to wait 6 weeks after delivery before using to allow uterus to return to prepregnancy size
May need different sizings
May not be suitable for those with poor vaginal tone, shallow pubic ledge, abnormality of vagina, cannot touch genital area with comfort or cervix in position that makes it difficult to fit, higher failure rates seen in those with learning difficulties
Male condom
Barrier method
Pros:
Readily available
Protects against STIs and may protect women against cervical cancers
Some qualify for free
Cons: Relatively expensive unless free Need to plan prior May reduce sensitivity Can break or slip off Relatively los efficacy
always check in date
use new one every time
teach how to put on
Female condom
Female condom (femidom) Barrier method of contraception
Pros: No known side effects Helps prevent STIs and possibly reduces cervical carcinoma Inserted prior to intercourse No fitting needed
Cons:
Needs careful insertion
Can be pushed into vagina or bypassed
May be uncomfortable or noisy, or interfere with sensation
Not as effective as some of other methods of contraception above
How to use:
Check condom for relevant safety markings and use by date
Use new condom every time
Should be inserted before penetration or genital contact
Find a comfortable position, hold the closed end of the female condom and squeeze the inner ring between thumb and middle finger.
Keeping index finger on inner ring facilitates insertion
Use other hand to separate labia and put squeezed ring into vagina and push up as far as can go
Place index or middle finger or both inside open end of femidom until inner ring felt, then push back into vagina as far as it can go
Ring will be lying behind pubic bone which can be felt by inserting finger in vagina and curving forward slightly
Following insertion, outer ring should rest closely against vulva
After intercourse, remove by twisting outer ring to keep semen inside and pull condom gently out
Wrap and dispose in bin
Good idea to guide penis into femidom so it does not enter between vagina and condom
Normal for condom to move during intercourse but will remain effective if penis stays inside it
Diaphragm and caps
Physical barrier preventing entrance of sperm into cervix
Pros:
Compared to timing of condoms, insertion allows more spontaneity
No serious side effects and no hormonal effects
Cons: Women need to be well motivated and careful with use Not as effective methods Spermicides can cause local reaction Little evidence of protection from STIs UTIs increased risk with diaphragms
Spermicide
Should always be used in conjunction with diaphragms and cervical caps
Not suitable with condoms
Gygel vaginal cream contains nonoxynol-9 which disrupts sperm cell membranes
Pros:
Easy to use
Easy to obtain OTC
Cons:
Not as effective as other methods, should not be used alone
Lose effectiveness after about 1 hour
Some people find them messy to use
May irritate genital mucosa
Do not protect against STIs
Should NOT be used in women at increased STI risk (increase risk of HIV transmission)
HIV typical drug regimens
Involves three drugs ‘triple therapy’
Comprises of two NRTIs with a third either integrase inhibitor or NNRTIs or boosted protease
Drug interactions are common as many are P450 enzyme inhibitors/inducers
Particularly Ritonavir is very potent inhibitor - boosting other medication blood concentration
Adherence to therapy is crucial. MDT approach often used to utilise all specialities (sexual health, pharmacy etc) to ensure newly diagnosed patients know how to take the medications
HIV pre-exposure prophylaxis
to reduce risk of transmission in high risk individuals
Used to prevent HIV infection
Two NRTIs (emtricitabine and tenofovir) taken in one of several regimens ensuring enough drug in the blood to counter any potential HIV infection
Regimen 1: 1 tablet with both drugs OD
Regimen 2: 4 tablets per week (sunday, tuesday, thursday, saturday)
Regimen 3: 2 tablets 2-24 hours before intercourse and then one tablet per day for following 2 days
Post-exposure HIV prophylaxis
Can prescribe for those who have potentially been exposed to HIV
Typically use truvada (emtricitabine and tenofovir) PLUS raltegravir for 28 days
Truvada is one tablet taken OD, raltegravir 400mg taken BD
Should be prescribed within 72 hours of potential exposure
stages of contraceptive metabolism
Absorption - oral ethinylestradiol EE and progesterones absorbed
metabolised in liver, excreted into bile and small intestines
In large intestine active EE is reabsorbed via enterohepatic circulation
Active EE excreted from urine
conjugated metabolites not split in bowel are excreted in faeces
Contraceptive efficacy and drugs interactions
ABSORPTION - drugs causing vomiting or diarrhoea may affect absorption like prep sachets, as well as PPIs, H2RAs
LIVER ENZYME INDUCTION - p450 induction INCREASES metabolism of hormones DECREASING effectiveness. includes anti epileptics (carbamazepine, eslicarbazepine, fosphenytoin etc), antibacterials (rifabutin, rifampicin), antiretrovirals (efavirenz, nevirapine), antidepressants (st Johns wart)
LIVER ENZYME INHIBITION - decreases hormone metabolism and INCREASES effects potentially leading to toxicity or increased side effects antibacterials (erythromycin), antifungals (fluconazole, itraconazole, ketoconazole), antiretrovirals (atazanavir), immunosuppressants (tacrolimus), NSAIDs (etoricoxib), statins (atorvastatin, rosuvastatin), vasodilators (sitaxentan sodium)
Degree of absorption oral ethinylestradiol in enterohepatic circulation varies in individuals may be affected by lamotrigine - antiepileptic - and griseofulvin - antifungal - but this is unknown currently
anti epileptics and hormonal contraceptive pill
COC moderately reduced lamotrigine exposure which can lead to decreased seizure control and increased exposure with risk of toxicity in hormone free week
Desogestrel might increase levels and adverse effects
EE may slightly reduce sodium valproate levels
Evidence to suggest starting pill shortly after taking emergency contraceptive may reduce ECs effectiveness
immunosuppressants:
tacrolimus may increase hormonal exposure theoretically and can monitor serum tacrolimus levels
Ciclosporin may be increased by hormones
Emergency contraceptive predicted to increase everolimus and sirolimus concentrations
Dopaminergics:
selegiline potentially increased by hormones, increased toxicity risk. advised to avoid concurrent use.
also increase levels of melatonin
Possible adverse effects and consider monitoring for concurrent contraceptive pill use with drug interactions
Antihypertensives: hormone can increase BP and antagonise antihypertensive therapy (monitor BP regularly)
Antidiabetics: esotrogens may antagonise hypoglycaemic effects but unusually seriously disturbed
Anxiolytics and hypnotics: hormones may reduce lorazepam, diazepam and temazepam
thyroid hormone: may increase need for higher doses in thyroid hormones for hypothyroidism - monitor TFTs
antifungals: may increase levels of voriconazole
bronchodilators: slightly reduce clearance of theophylline - may need to reduce dosage if adverse effects occur
muscle relaxants: increase tizanidine levels and side effects
K sparing diuretics and aldosterone antagonists: additive hyperkalaemia or hypotension risk with drospirenone and K+ sparing diuretics
retinoids: maybe additive hormonal side effects on isotretinoin. This is also highly teratogenic so highly effective contraception methods (IUD, implants etc)
Triptans: slightly increased levels of frovatriptan, naratriptan and zolmitriptan but not thought to be clinically significant
Advise for women going onto hormonal contraceptives about drug interactions
Must be made aware of potential drug interactions
Reassure efficacy of IUD and IUS and injection are NOT affected by any drug interactions
if on antibiotics - more broad spectrum are better and do not require special precautions
advise women starting enzyme inducing drugs of interactions and offer reliable contraception method (IUD/IUS/injections) not affected by these
Short term enzyme inducing drugs use (<2 months) can be managed more flexibly than longer term use eg use barrier contraception alongside normal contraception while on these drugs
Teratogenic drugs: it is essential that women on these should always be advised to use highly effective contraception methods (IUD/IUS/implant) both during treatment and recommended timeframe after discontinuation - pregnancy prevention plan should be in place to ensure no risk of conception
enzyme inducing drugs and which contraceptions can be used/must be avoided during and 4 weeks after treatments
Avoid and find alternative:
COC, POP, IMP (progesterone only implant), UPA emergency contraceptive
potential interaction:
LNG emergency contraceptive
no interactions:
progesterone only injection, IUS and IUD
examples of drugs:
anti epileptics: carbamazepine, phenytoin, primidone, eslicarbazepine etc
antibiotics: rifabutin, rifampicin
antiretrovirals
antidepressants: St johns wart
Cystitis
A lower UTI (infection of the bladder)
Bacteria can enter form GIT ascending through the urethra into the bladder (retrograde)
Or via the bloodstream especially if immunosuppressed
Or direct spread of infection due to insertion or urinary catheter or surgery
Causes:
Most common cause if E. coli
Others include staphylococcus species
Risk factors include: Female (urethra is shorter and closer to anus) Post menopause: absence of oestrogen Sexual intercourse (females) History of UTI Catheterisation Diabetes
cystitis presentation and investigations
Presentation: Dysuria Frequency Urgency Cloudy appearance or bad odour Haematuria Nocturia Suprapubic discomfort or tenderness Elderly or underlying cognitive impairment: Delirium Lethargy Reduced appetite Confusion
Investigations:
Diagnosis based on clinical history and positive urine dipstick
Urine dipstick/urinalysis
Urine microscopy culture and sensitivity
Bladder scan/post void residual volume if suspected retention
Renal tract USS for persistent symptoms or underlying cause suspected
cystitis management
drink plenty of fluids
OTC: cystopurin
Non-pregnant women:
First line nitrofurantoin or trimethoprim for 3 days; can be extended to 7 days if needed
Second line (no improvement within 48 hours or first line unsuitable) then nitrofurantoin, pivmecillinam or fosfomycin single dose sachet
Pregnant women or UTI in men
First line nitrofurantoin for 7 days but avoid near term
Second line (no improvement within 48 hours or first line unsuitable), amoxicillin (if culture result available) or cefalexin
Catheterised women:
First line nitrofurantoin or trimethoprim for 7 days; don’t treat asymptomatic bacteriuria and check for blockage and consider changing the catheter if it has been in place for >7 days
Complications:
Pyelonephritis
Renal and perirenal abscesses
Impaired renal function or renal failure
Urosepsis
Pregnancy may be associated with preterm delivery and low birthweight
Urinary stones
Polycystic kidney disease (PKD)
Genetic condition in which the kidneys become filled with cysts causing enlargement and malfunction
Cysts develop in cortex and medulla of both kidneys
The cysts fill over time and get so large that they impeded blood vessels or tubular systems leading to decreased filtration and hypoxia of kidney tissue
Poorly perfused vessels activate renin-angiotensin system inducing HTN
Large cysts may cause urinary stasis from blocking nephrons leading to increased risk of infection and urolithiasis (stones)
Two types:
Autosomal dominant (ADPKD):
Most common inherited renal disease, begins with random mutation in the functional gene but with no functional prevention (acts recessive).
Classified as PKD1 (more severe, early onset), PKD2 or PKD 3. Symptoms manifest in adulthood
Cysts can occur on the liver, seminal vesicles, vasculature (associated with higher risk of aortic root dilatation and berry aneurysms) and pancreas
Loin pain
HTN
Enlarged kidneys
Haematuria
Kidney stones or infection
Autosomal recessive (ARPKD):
More likely to present in childhood, mutation is present on multiple genes.
Likely several months old with organomegaly
Can have renal failure even prior to birth (less fetal urine) therefore developing oligohydramnios (low amniotic fluid) which can cause potter’s sequence and pulmonary hypoplasia leading to respiratory insufficiency
Also causes congenital hepatic fibrosis and portal HTN
Bile duct problems can occur
PKD investigations and management
Urinalysis: haematuria
Bloods: polycythaemia secondary to increased erythropoietin
USS: GOLD STANDARD
CT
ARPKD can be detected in prenatal USS seen with bilateral large kidneys, cysts and oligohydramnios
Management: General: Manage infections Simple analgesia for pains (NSAIDs) Laparoscopic surgery to drain cysts Transplant or dialysis for severe disease
ADPKD:
Avoid contact sports
Reduced salt intake
Treat associated HTN (target 130/80 with ACEi)
ARPKD:
Monitor closely
liver/renal transplant
Liver bypass
renal vasculitis and presentation
ANCA glomerulonephritis AKA microscopic polyarteritis and granulomatosis with polyangiitis
An autoimmune disease that causes the WBCs to attack the glomeruli causing swelling and damage
Vasculitis with kidney involvement affects 20-30 people per million per year
Can vary with severity, some may rapidly decline and require dialysis within days while others can be unaffected
Glomeruli become inflamed, swollen and can burst (glomerulonephritis)
Causes include immunological, WNB and antibodies are damaging kidneys
Triggers can include operations, flu, bacterial infection
Presentation: Haematuria Spider naevi Nosebleeds Bleeding in lungs and haemoptysis Skin rashes Fatigue Dyspnea Loss of appetite Increased blood creatinine
renal vasculitis investigation and management
Investigations:
Bloods: creatinine, eGFR, ANCA (anti-neutrophil cytoplasmic antibodies)
Kidney biopsy
Urinalysis (nitrites for infection, glucose, blood or protein)
Management:
Steroids (prednisolone) and cyclophosphamide/azathioprine to reduce immune activity, high dose for 3-6 months then tapered off (potentially for whole life)
Careful monitoring of kidney function and for steroid side effects or withdrawal complications
If kidney function is very low (creatinine >500umol/l) may also use plasma exchange
Relapses may occur and will be picked up in urine tests
Dialysis or renal transplant for end stage disease
infertility
1 in 7 couples will struggle to conceive naturally
Investigation and referral for infertility should be initiated after the couple has been trying to conceive without success for 12 months (<6 months if >35yo)
Aetiology: Sperm problems (30%) Ovulation problems (25%) Tubal problems (15%) Uterine problems (10%) Idiopathic (20%) 40% of infertile couples have a mix of male and female causes
infertility investigations
BMI (low - anovulation, high - PCOS) STI screening (chlamydia) Semen analysis Female hormonal testing Rubella immunity in mother Pelvic USS (PCOS) Hysterosalpingogram - fallopian tube patency Laparoscopy and dye test - patency of fallopian tubes, adhesions, endometriosis and shape of uterus
infertility management general advice
Women to take 400mcg folic acid daily Healthy BMI Avoid smoking and excessive alcohol Reduce stress Aim for intercourse every 2-3 days Avoid timing intercourse (not necessary to time with ovulation or recommended as it can lead to increased stress and pressure)
infertility anovulation management
Weight loss for PCOS if this is the cause
Clomifene may be used to stimulate ovulation
Letrozole may be used instead to stimulate ovulation (aromatase inhibitor with anti-oestrogen effects)
Gonadotropins may be used to stimulate ovulation in women resistant to clomifene
Ovarian drilling - PCOS
Metformin may be used for insulin sensitivity and obesity (usually PCOS associated)
infertility tubal or uterine factors management
Tubal factors:
Tubal cannulation during a hysterosalpingogram
Laparoscopy to remove adhesions or endometriosis
IVF
Uterine factors:
Surgery to correct polyps, adhesions or structural abnormalities
infertility sperm issue management
Surgical sperm retrieval (blockage preventing ejaculation): needle and syringe to collect sperm from the epididymis through the scrotum
Surgical correction of obstruction
Intrauterine insemination (collect high quality sperm and inject directly into uterus)
Intracytoplasmic sperm injection (ICSI): inject sperm directly into the cytoplasm of an egg to make an embryo which is then injected into the female’s uterus
Donor insemination
female hormone testing
Serum LH, FSH on days 2-5 of cycle: high FSH suggests poor ovarian reserves. High LH may suggest PCOS.
Serum progesterone on days 21 of the cycle (or 7 days before end of the cycle if not a 28 day cycle): high progesterone may indicate ovulation has occurred and corpus luteum has formed
Anti-mullerian hormone: release by granulosa cells, high = good ovarian reserve
Thyroid function tests
Prolactin (hyperprolactinemia - anovulation, galactorrhoea, amenorrhea)
Clomifene is an anti-oestrogen (a selective oestrogen receptor modulator). It is given on days 2 to 6 of the menstrual cycle. It stops the negative feedback of oestrogen on the hypothalamus, resulting in a greater release of GnRH and subsequently FSH and LH.
Ovarian drilling involves laparoscopic surgery. The surgeon punctures multiple holes in the ovaries using diathermy or laser therapy. This can improve the woman’s hormonal profile and result in regular ovulation and fertility.
female sexual dysfunction
Background:
Female sexual dysfunction is estimated to affect up to 40% of all women and among postmenopausal women is thought to affect up to 87%
Pathology:
Involves hormonal, neurological, vascular, psychological and emotional aspects
Dysfunction may be triggered or maintained by any of these factors or multiple of them and is highly dependent on physical-psychological feedback causing mixing of original pathologies
Menopause reduces blood flow, causes clitoral shrinking, reduced sensitivity and discomfort from associated vaginal/urogenital atrophy
female sexual dysfunction cause and risk factors
Aetiology:
Female orgasmic disorder - lifelong may suggest unfamiliarity or discomfort with self-stimulation or sexual communication with a partner. Delayed or less intense may be a natural process of ageing due to decreased genital blood flow, atrophy and reduction in sensitivity
Risk factors: Thyroid disorders Diabetes Addison's disease PCOS Obesity and metabolic syndrome Pregnancy - assisted vaginal delivery and postpartum hormonal changes CVD Pelvic surgery History of sexual abuse, depression, anxiety, OCD Weaker pelvic floor Menopause Medications - antihistamines, anticonvulsants, metronidazole, antihypertensives, anticholinergics, oral contraceptives, alcohol, analgesics, opiates, drug dependency etc.
female sexual dysfunction presentation
Sexual interest/arousal disorder: reduced or absent sexual interest, responsiveness, erotic thoughts and sexual pleasure
Female orgasmic disorder: absence, infrequency, reduction, delay of orgasm
Genito-pelvic pain/penetration disorder: difficulty in vaginal penetration, marked vulvovaginal or pelvic pain during penetration, fear or anxiety about pain, tightening or tensing of pelvic floor muscles in attempted penetration
Persistent genital arousal disorder: persistence of genital arousal in absence of sexual arousal. Can last hours, days or occur constantly arising through non-sexual stimuli. Does not remit after orgasm and is usually distressing, confusing, intrusive and unwanted. May be associated with shame or embarrassment.
female sexual dysfunction investigations and management
History - CVD, smoking, alcohol, sexual health history, endo or neurological disease, fitness, exercise, diet, menstrual and contraceptive history, Obs and gynae history, psychological impact and history
Bloods - FBC, lipid profile, renal and liver FTs, TFTs, FSH and LH, oestrogens
Pelvic/transvaginal USS
Questionnaires to assess dysfunction (female sexual function index)
Management:
Lifestyle advice - general fitness, diet, smoking and alcohol cessation
Relationship counselling
CBT
Pelvic floor exercises
Medical devices such as eros clitoral therapy device
Oestrogens - particularly in postmenopausal women (tibolone is synhetic oestrogen)
Testosterone, prostaglandins, vasoactive peptide (none are licensed in UK)
sexual assault
Background:
Around 1 in 50 women and 1 in 200 men experience some kind of sexual assault in the year 2011
Risk of sexual violence for women during their lifetime is 1 in 3 and lifetime risk of rape or attempted rape is 1 in 5
Majority of victims know their assailant and domestic violence is strongly linked
Pathology:
Rape - penetration of the vagina, anus or mouth by penis without consent. Both men and women can be raped
Assault by penetration - penetration of the vagina or anus with an object/body part without consent
Sexual assault - rape or assault by penetration including attempts are “serious”; indecent exposure or unwanted touching are “less serious”
sexual assault at risk groups and presentation
Those at risk:
Women at at greater risk than men
People in vulnerable position: survivors of childhood/adolescence abuse, adolescents, young women (16-24), disabled, those with substance abuse, homeless, sex workers, prisoners and those in detention centres, institutions or in areas of military conflict
Presentation:
Many never report incidence to the police
May seek healthcare without reason for presentation - non-genital injuries and emergency contraceptive request for example
sexual assault investigation and management
Investigation/diagnosis:
History - could you have said no? Where did it happen, when, who did it?
If they wish to report it to the police - refer to sexual assault referral centre (SARC) for evidence collection and specialist management
Early evidence kit - most fragile evidence from the mouth is lost within 24 hours, mouth rinse and urine sample can be taken and stored without immediate decision of needing to go to the police
Management:
Emergency contraceptive PRN
STI screening and management
Psychological effects of depression, PTSD may need therapy referral
EllaOne EC overview
action: Delays ovulation for 5 days or more
Side effects: No long-term side effects
Pros: No procedure needed
Can be taken up to 5 days after unprotected sex
Cons: Less effective than the emergency contraceptive IUD
May affect the next period
Vomiting and headaches
Caution: Use with caution in those with severe asthma
CI: Less than 21 days following giving birth
Less than 5 days following a miscarriage or abortion
Leveonrgestrel EC overview
action: Inhibits ovulation and causes luteal dysfunction
side effects: No long-term side effects
Pros: No procedure needed
Cons: Can only be taken up to 3 days after unprotected sex
May affect the next period
Less effective than other emergency contraceptive methods
Vomiting and headaches
Caution: Use with caution in those with a BMI of more than 26 or a weight of more than 70 kg
CI: Less than 21 days following giving birth
Less than 5 days following a miscarriage or abortion
Cu-IUD EC overview
action: Plastic and copper coil
An inhibitory effect on both fertilisation and implantation
Pros: Non-hormonal
Can be used as regular contraception for up to 10 years
Can be inserted up to 5 days following unprotected sex
Cons: An uncomfortable procedure needed to fit the IUD
Period type pain and bleeding are common a few days following fitting
Small risk of infection, perforation and expulsion
CI: Less than 28 days following giving birth
Less than 5 days following a miscarriage or abortion
Active sexually transmitted infection
