Genitourinary D+M Flashcards

1
Q

Causes of enlarged kidney

A

Bilaterally enlarged, ballotable kidneys can occur in polycystic kidney disease or amyloidosis.

A unilaterally enlarged, ballotable kidney can be caused by a renal tumour.

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2
Q

urolithiasis

A

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

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3
Q

Urolithiasis risk factors

A
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
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4
Q

Urolithiasis presentation

A

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

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5
Q

Urolithiasis investigations

A

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

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6
Q

Urolithiasis management

A
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
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7
Q

Urolithiasis complications and prevention

A

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)

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8
Q

Male lower UTI and risk factors

A

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
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9
Q

Lower UTI presentation

A
Dysuria
Frequency
Urgency
Change in urine appearance or odor
Nocturia
Suprapubic discomfort 
Delirium
Reduced functional ability
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10
Q

Lower UTI investigations

A

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

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11
Q

Male lower UTI management

A

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

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12
Q

Female lower UTI management

A

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)

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13
Q

Pyelonephritis

A

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

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14
Q

Pyelonephritis acute and chronic risk factors

A
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
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15
Q

Acute pyelonephritis presentation

A

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

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16
Q

Acute pyelonephritis investigations

A

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

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17
Q

acute Pyelonephritis management and complications

A

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
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18
Q

Chronic pyelonephritis presentation and investigations

A
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

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19
Q

Chronic pyelonephritis management and complications

A

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

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20
Q

balanitis and cause

A

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.

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21
Q

balanitis risk factors

A
Diabetes 
Oral antibiotics
Poor hygiene in uncircumcised males
Immunosuppression
Chemical or physical irritation of glans
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22
Q

Balanitis presentation

A

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

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23
Q

Balanitis investigations and complications

A

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

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24
Q

Balanitis management

A

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

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25
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
26
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
27
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
28
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)
29
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
30
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
31
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.
32
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
33
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)
34
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
35
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
36
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
37
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
38
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
39
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
40
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
41
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 ```
42
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 ```
43
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
44
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
45
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
46
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
47
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
48
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
49
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
50
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
51
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
52
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
53
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
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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 ```
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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
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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 ```
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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.
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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
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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
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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
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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
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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
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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
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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 ```
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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 ```
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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 ```
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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
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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
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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
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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 ```
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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
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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 ```
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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
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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
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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
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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
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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%
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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
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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) ```
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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 ```
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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 ```
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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
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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
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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
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investigations for dysuria
``` Physical examinations Urine dipstick, microscopy and culture Pregnancy test STI screening USS of urinary tract KUB Urodynamic studies Urine cytology Cystoscopy ```
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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 ```
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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
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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)
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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 ```
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oliguria management
Treat underlying cause Fluid resus and catheterisation Correct electrolyte imbalances Surgery if secondary to obstructive cause
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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 ```
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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)
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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
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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
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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
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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
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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 ) ```
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renal cancer risk factors
``` Smoking Obesity HTN Long term dialysis Von hippel-lindau disease ```
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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!!**
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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
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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 ```
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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 ```
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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 ```
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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 ```
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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 ```
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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
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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
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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
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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 ```
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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 ```
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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
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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
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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
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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
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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 ```
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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
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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
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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
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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
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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
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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 ```
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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
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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
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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
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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 ```
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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
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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
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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
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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
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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
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Uracus
Remnant of connection between navel and bladder in embryological period Origin of discharge (urine) from umbilicus in later life
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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
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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
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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
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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
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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)
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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
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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
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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
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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 ```
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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
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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
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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
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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)
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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
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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)
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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
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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
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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 ```
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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
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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
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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
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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 ```
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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)
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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. ```
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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 ```
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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
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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
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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
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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
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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
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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
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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
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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 ```
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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 ```
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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
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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
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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
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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
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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 ```
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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
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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
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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
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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 ```
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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
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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
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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
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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
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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
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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
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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
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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
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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)
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HIV risk factors
Men who have sex with men Migrants from high HIV incidence countries IV drug users
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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)
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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
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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
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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
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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 ```
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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 ```
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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
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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)
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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 ```
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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 ```
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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 ```
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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 ```
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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 ```
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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
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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
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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
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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
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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 ```
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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)
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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 ```
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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
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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
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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
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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
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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 ```
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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
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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 ```
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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 ```
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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) ```
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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)
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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
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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
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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.
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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
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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. ```
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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.
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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)
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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”
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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
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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
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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
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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
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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