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ESA 4 > Reproductive System Week 6 > Flashcards

Reproductive System Week 6 Flashcards

1
Q

What is the difference between an STI and an STD?

A

STI includes both asymptomatic and symptomatic cases

STD includes symptomatic cases only

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2
Q

Give an example of a type of infection where sexual activity is a possible mode of transmission

A

BBV

Intestinal pathogens e.g. salmonella, shigella, giardia, entamoeba

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3
Q

Describe some common STDs, the causative organism and their approximate incidence in the UK in 2015

A

Genital warts and cancer - Papillomaviruses - 68,310(warts) (decreased by 7%) - vaccine
Urethritis, LGV - Chlamydia trachomatis - 200,288 (decreased by 4%) - screening and public health campaign
Genital herpes - Herpes simplex - 31,777
Gonorrhoea - Neisseria gonorrhoeae - 41,193 (increased by 11%)
Syphilis - Treponema pallidum - 5,288 (increased by 20%)
Non-specific GI - 42,262 (decreased by 10%)
Other (chancroid/LGV, HIV, Molluscum contagiosum, scabies, pediculosis pubis, trichomoniasis - 44,976
Total STI - 434,456 (decreased by 3%)

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4
Q

Describe the at-risk groups for an STI/STD

A

Young
Certain ethnic groups
Low socioeconomic status groups
Aspects of sexual behaviour e.g. age at first sexual intercourse, number of partners, sexual orientation, unsafe sexual activity

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5
Q

Describe some reasons why there has been an increased incidence of STIs between 1995 and 1999

A

Increased transmission - changing sexual and social behaviour, incresing density and mobility of populations
Acceptability of GUM services - increased attendance
Greater public, medical and national awareness (campaigns)
Development in diagnostic methods - screening programs

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6
Q

Why will data from GUM services underestimate the true incidence of STIs ?

A

patients may be seen in a variety of other settings - GP, family planning clinics
Many infections are asymptomatic - e.g. thought that only 10% chlamydia cases may attend GUM services

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7
Q

What factors affect the burden of STIs?

A

Acute and chronic/relapsing infections
Stigma - impact of diagnosis and tracing contacts
Consequent pathology - PID and infertility, reproductive tract cancers
Disseminated infections
Transmission to foetus/neonate

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8
Q

How are STIs diagnosed?

A

Patient presents with genital lesions/problems to GP or GUM clinic - ulcers, vesicles, warts, urethral discharge or pain, vaginal discharge
Clinician notes non-genital clinical features suggestive of STI - disseminated disease
Detection of asymptomatic cases (contact tracing/screening)

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9
Q

Describe the management of STIS

A

Treatment preferably single dose/short course
Co-infections common - screen and consider empiric treatment for other STIs
Consensus UK national guidelines
Contact tracing - patient and public health management
Sexual health education, advice on contraception and detailed instruction on the practice and need for safer sex

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10
Q

Describe Human papillomaviruses, their diagnosis, treatment, screening and vaccines

A

> 100 types
DNA virus
Most common viral STI (4% young adults in lifetime)
Clinical consequences:
cutaneous, mucosal and anogenital warts (M=F) - benign, painless, verrucous epithelial or mucosal outgrowths (mainly HPV6 and 11) - vast majority of infected individuals fail to develop warts
cervical cancer (most common cancer in women 15-34) and anogenital cancer (high risk oncogenic - HPV16 and HPV18 - >70% cervical cancers)

diagnosis - clinical, biospy and genome analysis, hybrid capture

treatment - none - spontaeous resolution (70% 1 yr, 90% 2 yrs)
topical podophyllin, cryotherapy, intralesional interferon, imiquimod, surgery

screening - cervical pap smear cytology
colposcopy and acetowhite test
cervical swab - HPV hybrid capture (40% of 20-24 yr olds positive)

Vaccine - cervarix (HPV 16 and 18) - initally used in UK
gardasil (HPV 6,11,16 and 18) from 2011
offered to girls 12-13 (2 doses)
99% effective in preventing HPV 16 and 18 - related cervical abnormalities in those not already infected

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11
Q

Describe Chlamydia trachomatis, its clinical consequences in females and males, diagnosis, treatment and screening

A

Obligate intracellular bacterium - dont grow on routine lab media
Infective form is elementary body which develops within host cell into reticulate body
reticulate body replicates eventually revertine back to elementary bodies which leave cell to infect other cells
Non-specific genital chlamydial infections - serotypes D-K
Makes up nearly half of all STIs diagnosed- 50% diagnosed in GUM, 50% from screening

Clinical consequences:
Males - urethritis, epididymitis, reiters syndrome(urethritis, conjunctivitis and arthritis), prostatitis, proctitis
Females - organism infects and replicates within epithelium of cervix and urethra - majority asymptomatic, important cause of mucopurulent cervicitis, urethritis (dysuria and frequency), ascending infection with UGT involvement can result in clinical or subclinical PID presenting as endometritis or salpingitis (PID leads to tubal damage, infertility and ectopic pregnancy), rarely perihepatitis
Both - oral inoculation - conjunctivitis
Neonatal infection - cervical infection in pregnancy - inclusion conjunctivitis - may progress to neonatal pneumonia if untreated
Many cases asymptomatic - especially in women

Diagnosis:
>200 000 cases diagnosed each year (nearly half of all STIs)
Endocervical(after pus removed from cervix)/urethral swab and urethral swabs - NAAT
1st void urine (urine less sensitive than endocervical swab) - NAAT
Neonatal infection - conjunctival swab (after pus removal, invert eyelid, scrape conjunctiva surface) - NAAT - Pneumonia serology WCC may show eosinophilia
Immunofluorescence - specimen fixed - stained with monoclonal antibody tagged with fluorescein - UV microscope - observer error, time consuming so only small no. of specimens - quality of specimen can be assessed
EIA - large number of specimens processed with ease - kits vary in sensitivity and specificity but some good - relatively cheap
PCR - high sensitivity and specificity - specimen may contain inhibitors that interfere, kits may yield significant false positives and negatives - EIA or PCR debate for population screening

Treatment:
tetracyclines (Doxycycline) or macrolides (azithromycin)
erythromycin in children
conjunctivitis - more widespread infection - systemic antibiotics

Screening:
sexually-active under 25s
urine (Mand F) or swab (F)
Nucleic acid amplification test (NAAT) - dual testing with N. gonorrhoeae available

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12
Q

Describe Herpes simplex virus, its diagnosis, treatment and prevention

A

Primary genital herpes - extensive painful genital ulceration, dysuria, inguinal lymphadenopathy, fever
Usually associated with HSV 2 (HSV 1 causes cold sores)
Recurrent infection is asymptomatic to moderate (latent infection in dorsal root ganglia (as in chickenpox))
Diagnosis: PCR of vesicle fluid and/or ulcer base
Treatment: aciclovir (primary and severe disease)
Prevention: aciclovir prophylaxis for frequent recurrences
Barrier contraception - reduce risk of transmission

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13
Q

Describe Neisseria gonorrhoeae, its diagnosis, treatment and prevention

A

Gram negative intracellular diplococcus
Likes to multiply inside white cells

Clinical consequences:
Males - urethritis (purulent discharge), epididymitis, prostatitis, proctitis (MSM) and pharyngitis (MSM)
Females - asymptomatic, endocervicitis, urethritis, PID (may lead to infertility)
Disseminated gonococcal infection - bacteraemia, skin and joint lesions (can cause septic arthritis and reactive arthritis)

Diagnosis:
Swab urethra, throat or rectum 
Urine NAAT
Gram stain
Fastidious - requires special media

Treatment:
Ceftriaxone (IM) (cephalosporin) - still some resistant strains
All patients tested and treated for chlamydia with azithromycin which may help prevent resistance to cephalosporin

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14
Q

Describe syphilis, its diagnosis, treatment and prevention

A

Treponema pallidum (spirochaete)
Most cases men and MSM
Multistage disease, able to stick around for years
Primary stage - indurated, painless chancre (ulcer) - gradually heals
Secondary stage - 6 to 8 weeks later - fever, rash (anywhere), lymphadenopathy, mucosal lesions (mouth) - might not relate to the chancre
Latent stage - asymptomatic for years
Tertiary stage - neurosyphilis (GPI tabes dorsalis - general paralysis of the insane), cardiovascular syphilis, gummas
Congenital syphilis - screen pregnant women

Diagnosis: organism cannot be grown - dark field microscopy required
Screening with ELISA –> +ves RPR, TPPA, serologic pattern interpreted (possibility of disease, stage, response to treatment )

Treatment: penicillin + test of cure follow up

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15
Q

What are some other causes of inguinal lymphadenopathy?

A

Lymphogranuloma venereum - C.trachoma serotypes L1,2,3
Rapidly healing papule than inguinal bubo (abscess)
Clusters in Europe (MSM)

Chancroid (Haemophilus decreyi) - painful genital ulcers

Granuloma inguinali /donovanosis (klebsiella granulomatis) - genital nodules –> ulcers

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16
Q

What is trichomoniasis?

A

STI caused by a flagellated protozoan called trichomonas vaginalis
Causes thin, frothy, offensive discharge
Irritation, dysuria, vaginal inflammation

Diagnosis: vaginal wet preparation with or without culture enhancement

Treatment: metronidazole

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17
Q

Describe vulvovaginal candidiasis, its diagnosis, treatment and risk factors

A

Candida albicans and other candida - may be part of normal GI and genital flora

Risk factors: antibiotics, oral contraceptives, pregnancy, steroids, diabetes, obesity

Profuse, white, itchy, curd-like discharge

Diagnosis - high vaginal smear (with or without culture)

Treatment - topical azoles (pessary or cream) or nystatin, or oral fluconazole

Not necessarily sexual

18
Q

What kinds of lice can spread sexually?

A

Scabies

Pediculosis pubis - distinct from body lice - crab louse (phthirus pubis)

19
Q

Describe bacterial vaginosis, its diagnosis and treatment

A

Perturbed normal flora - Gardnerella, mycoplasma, anaerobes
Scanty but offensive fishy discharge - not itchy - creamy

Diagnosis:
Vaginal pH >5, KOH whiff test
Lab - HVS gram stained smear
'Clue' cells - epithelial cells studded with coccobacilli
Reduced lactobacilli
Absence of pus cells

Treatment: metronidazole

20
Q

Describe the organism mycobacterium chlamydiae

A

Obligate intracellular bacteria
Dont grow on media

Infective form - elementary body - develops in the host cell into the reticulate body - replicates eventually reverting back to elementary bodies –> leave to infect other cells

21
Q

Describe the chlamydia infection in females

A

Commonly asymptomatic
Replicates within epithelium of cervix and urethra
Mucopurulent cervicitis, acute urethral syndrome (dysuria and frequency - common in young sexually active women)

Ascending infection can occur - can result in clinical or subclinical PID - endometritis or salpingitis - can lead to tubal damage, infertility and ectopic pregnancy
perihepatitis is a rare complication - gonorrhoea also causes this

Ocular infections common

Cervical infection in pregnant women - source of infection in the neonate - neonatal conjunctivitis common - untreated may progress to neonatal pneumonia

Diagnosis - endocervical swab - remove any pus before collecting - urine not as good for diagnosis (not as sensitive) but more useful for screening as easier for individuals, doesnt require staff member and is more acceptable

22
Q

Describe the chlamydia infection in males

A

Usually presents as urethritis

Complications - acute epididymitis
- Reiters syndrome - reactive arthritis resulting from infection - urethritis and conjunctivitis in the classical triad of symptoms - predominantly occurs in males

Diagnosis - urethral swab or first catch urine

23
Q

Describe the chlamydia infection in neonates

A

Commonly from infected mother
Conjunctivitis common
May progress to pneumonia if untreated

Eye swab – Remove any pus. Invert eyelid and scrape conjunctiva surface to obtain cellular material
Pneumonia – Serology is useful. A differential on a WCC (white cell count) may show eosinophilia.

24
Q

Describe the methods employed for chlamydia detection

A

Immunofluorescence
Specimens may be fixed to a slide and stained with a monoclonal antibody that is tagged with fluorescein.
Slides are examined under an ultraviolet microscope
drawbacks are that results are subject to observer error and the method is time consuming and therefore only suitable for small numbers of specimens
One advantage is that the quality of the specimen in terms of cells can be assessed using this technique.

Enzyme Immunoassays (EIA) 
Such tests allow large numbers of specimens to be processed with relative ease.  Commercial kits may vary in their sensitivity and specificity, but some kits have good sensitivity/specificity.  The tests are relatively cheap.
Molecular Methods (PCR, polymerase chain reaction)
Molecular methods offer high sensitivity and specificity, however clinical specimens may contain inhibitors that will interfere with the assay, and commercial kits may yield significant false positives and negatives.  
Studies are currently underway to ascertain whether EIA or molecular methods should be used for population screening.
25
Q

Describe the treatment of chlamydia infections

A 
Chlamydia trachomatis contain relatively little peptidoglycan, the target for β lactam antibiotics.  The mainstay of treatment is the macrolides (erythromycin/clarithromycin/azithromycin) and tetracyclines (doxycycline).  
As conjunctivitis (both neonatal and adult) is part of a more widespread infection, this should always be treated with systemic antibiotics.
26
Q

Describe the gonorrhoea infection in females

A

The gonococcus primarily infects the cervix and urethra. This may lead to an acute cervicitis with vaginal discharge and “urethral syndrome” where the urethra is infected

Complications: Pelvic Inflammatory Disease: occasionally with tubo-ovarian abscess
Bartholins abscess
Disseminated gonococcal infection: a rare complication that affects women more than men. The common symptoms are pain on the joints, tenosynovitis and rash.
Perihepatitis

Diagnosis - Endocervical swab, urethral swab, rectal and pharyngeal swab

27
Q

Describe the gonorrhoea infection in males

A

Gonococal urethritis
Complications: Epididymitis
Disseminated gonoccocal infection

Diagnosis - urethral, rectal and pharyngeal swabs

28
Q

Describe the methods employed to diagnose gonorrhoea

A

Neisseria gonorrhoeae is a fragile organism and does not survive transportation well. Ideally specimens should be taken and plated directly on to media at the bedside (as occurs in GUM clinics).
Gram stain – the characteristic appearance of gram-negative diplococci allows a presumptive diagnosis to be made on the basis of the gram stain in some patients.
Culture/Sensitivities
Culture is far more sensitive than microscopy. Organisms that resemble Neisseria on culture must be confirmed as Neisseria gonorrhoeae on the basis of biochemical tests in order to distinguish them from other species. Sensitivity testing is important, as antibiotic resistance patterns are valuable in guiding future management guidelines.

29
Q

Describe the treatment of gonorrhoea

A

Neisseria gonorrhoeae may vary in its sensitivity. Initial therapy is usually guided by severity of symptoms and local knowledge of sensitivity patterns. Penicillin resistance is common

30
Q

Describe HPV

A

Genital warts caused by HPV are the commonest STI diagnosed at genitourinary medicine (GUM) clinics throughout the United Kingdom: First episode, recurrent and re-registered cases accounted for 22% (131 140 of 590 909) of all diagnoses in GUM clinics in 1999. More than 100 HPV types have been described, however, the vast majority of infected individuals fail to develop warts. Apart from being unsightly and difficult to treat, the main concern with this virus is the strong association of certain high risk types with cervical carcinoma.

31
Q

What is pelvic inflammatory disease ?

A

The result of infection ascending from the
endocervix, causing endometritis, salpingitis,
parametritis, oophoritis, tubo-ovarian abscess
and/or pelvic peritonitis

32
Q

Describe the pathophysiology behind PID

A

Ascending infection from the endocervix and
vagina
Infection causes inflammation
Inflammation causes damage
– Thus damaged tubal epithelium
– Thus adhesions form
Some tubal epithelium recovers but normally not total recovery –> infertility and ectopic pregnancy

33
Q

Describe some complications of PID

A

Ectopic pregnancy
Infertility
Chronic pelvic pain
Fitz-Hugh-Curtis Syndrome – RUQ pain and peri-hepatitis following Chlamydial PID (10-15%)
Reiters syndrome - cant see, cant pee, cant bend at the knee

34
Q

Describe the aetiology of PID

A

Often polymicrobial
Sexually transmitted infections:
– C. trachomatis
– N. gonorrhoea
Others:
– Gardnerella vaginalis, mycoplasma, anaerobes (BV)
- Actinomycetaceae - found in many body cavities (mouth/bowel/fallopian tubes) - IUD copper - long-term (8 years or more) - over time may damage womb lining allowing bacteria to penetrate the deep tissue (very rare)

35
Q

Describe the epidemiology of PID

A

Underestimated (asymptomatic)
Sexually active women – Peak 20-30 years old
Incidence rate in primary care approximately 280 per 100,000py

36
Q

What are the risk factors for PID?

A 
As for STIs
– Young age
– Lack of use of barrier contraception
– Multiple sexual partners
– Low socioeconomic class

IUCD - putting it in and removing it

37
Q

What are the clinical features of PID?

A 
History 
• Pyrexia 
• Pain
– Lower abdominal pain
– Deep dyspareunia (pain having sex)
• Abnormal vaginal/cervical discharge 
• Abnormal vaginal bleeding - friable, post coital, intermenstrual
• Sexual history & prior STI 
• Contraceptive history
Examination 
• Fever (usually>38)
• Lower abdominal tenderness which is usually bilateral 
• Bimanual examination (abscess)
– adnexal tenderness (tubes, ovaries)
– Cervical motion tenderness
• Speculum examination
– Purulent cervical discharge 
– Cervicitis (red and inflamed)
38
Q

What is the differential diagnosis of PID?

A

Gynaecological:
Ectopic pregnancy
Endometriosis - menstrual cycle pain
Ovarian cyst complications - torsion - short term

Gastro- intestinal:
IBS
Appendicitis
Vomiting and nausea (only 50% of PID patients) - do they have an appendix?

Urinary
UTI - dipstick, frequency, dysuria

Other
Functional pain - Ongoing chronic pain in lower pelvis

39
Q

Describe the investigations for PID

A 
Urinary and/or serum pregnancy test 
Endocervical and High vaginal swabs
– Presence of NG/CT supports diagnosis
– Absence of NG/CT does not exclude diagnosis - Large number not caused by
Blood tests
– WBC and CRP 
Screening for other STIs including HIV
Diagnostic laproscopy gold standard - benefit of adhesion lysis and drain abscesses if there - negatives - cost, risk of damaging, might not see any inflammation from outside of tubes etc
40
Q

Describe the management of PID

A

Low threshold for empirical treatment - analgesia, rest, management of sepsis
– Delayed treatment increases longterm sequelae
Severe disease requires IV antibiotics and admission for observation and possible surgical intervention
– Pyrexia >38, signs of tubo-ovarian abscess, signs
of pelvic peritonitis
– Increased risk of longterm sequelae

Contact tracing essential, full screen for woman

Outpatient treatment
IM Ceftriaxone 500mg STAT + PO Doxycycline 100mg BD + PO Metronidazole 400mg BD
Inpatient treatment
IV Ceftriaxone 500mg STAT + IV/PO Doxycycline 100mg BD + IV Metronidazole 400mg BD —–>
PO Doxycycline 100mg BD + PO Metronidazole 400mg BD

Treats all potential causative agents

Laparoscopy/laparotomy may be considered if
– No response to therapy
– Clinically severe disease
– Presence of a tubo-ovarian abscess
Ultrasound guided aspiration of pelvic collections is less invasive

41
Q

What should you tell a patient with PID?

A

What the diagnosis is
What treatment they are having
– Possible side effects
– Importance of completing antibiotics
What complications they are at risk of
– Risk of these increases with repeat episodes
How to reduce the risk of further episodes
Contact tracing
– Empirical treatment of partners
– Avoid unprotected sex until antibiotic course complete in self and partner

ESA 4 (28 decks)

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