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Gynae infections Flashcards

1
Q

What are the types of Chlamydia and how does it spread?

A
  • A-C cause ocular infection
  • D-K classical GU infection
  • L1-3 lymphogranuloma venerum (a/w MSM)

Transmitted through unprotected sex/fluid in eyes/skin contact of genitals/vertical transmission

Incubation period of 7-21d

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2
Q

What are the CF of chlamydia?

A

50% of men and 75% of women are asymptomatic!

  • Females: dysuria, abnormal DC, IMB/PCB, deep dyspareunia, lower abdo pain; signs may include cervicitis, contact bleeding, mucopurulent endocervical discharge, pelvic tenderness, cervical excitation
  • Males: urethritis (dysuria, DC), epididymo-orchitis (painful testes); signs may include epididymal tenderness and mucopurulent DC
  • Both: conjunctivitis, rectal discomfort/dc, pharynx (often no sx)
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3
Q

What investigations are done for chlamydia?

A
  • NAAT to see, as too small for microscopy
  • Women do a vulvovaginal self-administered swab or endocervical swab taken or can do first catch urine; for men a first catch urine or urethral swab
  • Contact trace + offer full STI screen if positive
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4
Q

How is chlamydia managed?

A
  • 7d doxycycline (1st line) or 3d azithromycin or erythromycin for 10-14d. All PO
  • Avoid SI until post-treatment or a week after azithromycin
  • If <25y then rpt test in 3m
  • Should ideally be referred to GUM
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5
Q

What are the complications of chlamydia?

A
  • Female: salpingitis, endometritis, PID
  • Men: epididymo-orchitis, fertility problems
  • Both: reactive arthritis (but more in men)
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6
Q

What are the CF of gonorrhoea?

A
  • 2-5d incubation or asymptomatic, strong affinity for MM
  • Female: altered DC (thin, increased, watery, green/yellow), dysuria, dyspareunia, lower abdo pain, rarely may cause ICB/PMB, often normal exam but may see DC/cervix bleeds/tender
  • Men: mucopurulent/purulent urethral DC, dysuria, epididymal tenderness
  • Rectum - DC/pain/discomfort
  • Pharyngeal- >90% asymptomatic
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7
Q

What Ix are done for gonorrhoea?

A
  • NAATs as test fo chlamydia at the time time plus MCS for sensitivity (esp resistant strains are an issue)
  • Endocervical/vaginal swab for NAAT in F and 1st pass urine in M
  • Endocervical /urethral swab for MCS
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8
Q

How is gonorrhoea managed?

A
  • Treat empirically whilst wait for results of culture
  • Should be treated by GUM not primary care
  • IM ceftriaxone single dose (alternatives: cefixime + azithromycin oral if pt refuses IM etc; but azithromycin has high resistance; used to use ciprofloxacin so now resistant but obv give if MCS shows sensitivity)
  • Abstain until treatment complete
  • Test of cure recommended for all
  • Offer full STI screen
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9
Q

What are the complications of gonorrhoea?

A

PID, epididymo-orchitis, prostatitis, disseminated gonococcal infection (uncommon - tenosynovitis, migratory polyarthritis, dermatitis (maculopapular/vesicular lesions), septic arthritis, endocarditis, perihepatitis [Fitz Hugh Curtis]; prob cos of haematogenous spread)

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10
Q

How might gonorrhoea affect pregnancy and neonates?

A
  • Pregnancy: perinatal mortality, spontaneous abortion, premature labour, P-PROM
  • Neonate: gonococcal conjunctivitis - treat ASAP to prevent blindness
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11
Q

What are the organisms causing chlamydia and gonorrhoea?

A

Chlamydia trachomatis: gram negative intracellular bacteria

Neisseria gonorrhoea: gram negative diplococcus

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12
Q

What do you want to ask about in a sexual history?

A
  • Explain confidentiality and that we ask everyone these questions
  • PC as normal
  • Sexual risk assessment - last intercourse, h/o unprotected sex, number + gender of contacts in the last 3-12m, ever had MSM, type of activity, condoms, relationship, sx/infection in a recent contact
  • STI + BBV - date + result of previous dates. h/o IVDU/piercings/tattoos, sex abroad, sex industry work or contact, vaccination history
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13
Q

How might chlamydia affect a pregnancy?

A
  • Preg: preterm delivery, low birth weight, higher risk of miscarriage/stillbirth - ensure treat with azith/erythro
  • Neonate: neonatal chlamydial conjunctivitis (5-12d old) or pneumonia (1-3m old); treat w oral erythromycin
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14
Q

How does HIV cause infection?

A

Enters CD4 cells - ssRNA turns into dsDNA (reverse transcriptase) + combines with host DNA (integrase) - cell divides 0 viral proteins made - immature virus pushed out of cell - virus matures, host cell destroyed

Virus is transmitted by V/A/O UPSI, sharing injecting equipment, blood products and vertical transmission (in utero, during delivery or during breastfeeding)

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15
Q

What is HIV post-exposure prophylaxis?

A

Given within 24h after a suspected exposure for 2 months of Truvada + Raltagavir

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16
Q

What are the stages of HIV infection?

A
  • Seroconversion (2-6w post-exposure): fever, malaise, myalgia, lymphadenopathy, maculopapular rash, pharyngitis
  • Asymptomatic latent phase
  • Symptomatic phase: fever, WL, diarrhoea, frequent minor opportunistic infections e.g. HZD/candida, generalised lymphadenopathy
  • AIDS-defining illnesses: P. jiroveci pneumonia, NHL, Kaposi’s sarcoma, TB
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17
Q

How is HIV diagnosed?

A
  • Rapid tests within 30m (less accurate)
  • ELISA - accurate 4-6w from exposure
  • Contact tracing
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18
Q

How is HIV managed?

A
  • Monitor CD4 count (low means low immunity), HIV viral load (aim for undetectable), FBC, U+E, LFTs, hCG if female, urinalysis
  • Combination of HAART drugs to target the enzymes of viral replication + maturation, in one tablet to improve compliance as need for rest of life
  • Non adherence leads to resistance
  • Psychological aspects
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19
Q

What is syphilis and how is it diagnosed?

A

Treponema palladium - a gram negative spirochaete (other Treponema spp cause non-STI infections)

  • Blood - VDRL, which rises in early disease. False positives in pregnancy and inflammatory diseases
  • Microscopy of chancre fluid
  • PCR of swabs
  • LP in neurosyphilis
  • Is increasing esp in MSM
  • All pregnant women are screened at booking as it crosses the placenta
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20
Q

How may syphilis affect a pregnant woman?

A
  • Pregnancy: MC, SB, pre-term labour

* Congenital syphilis: saddle nose deformity, rashes, fever, failure to thrive

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21
Q

Primary syphilis

A
  • 9-90d post-exposure
  • Papule that develops into a chancre (painless ulcer, infectious). Usually single hard and non-itchy, and heals in a few weeks, may have inguinal LN
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22
Q

Secondary syphilis

A
  • ~3m post-exposure
  • Maculopapular rash of hands + soles, alopecia in the area, fever, malaise, arthralgia, WL, headache, Condylomata lata (plaque like warts at genitals or mouth), painless lymphadenopathy, silvery/grey mucus membrane lesions
  • Possible renal/hepatic/brain issues
  • Then enters a latent phase
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23
Q

Tertiary syphilis

A
  • May occur, after many years
  • Gummatous syphilis: granulomas anywhere, non-infectious, e.g. in bone, MMs, connective tissue
  • Neurosyphilis: tabes dorsalis (ataxia, lightning pains), dementia, CN palsies/stroke, Argyll-Robertson pupils (they accommodate but do not react to light, v rare)
  • Cardiac syphilis: aortic regurgitation, aortic root dilatation, angina, calcification
24
Q

How is syphilis managed?

A

IM benzathine benzylpenicillin (doxycycline or erythromycin if not suitable)
Full STI screen + contact trace

25
Q

What are anogenital warts and how are they caused?

A

Benign epithelial or mucosal outgrowths (also called Condyloma accuminatum), 90% are caused by HPV types 6 + 11, most spread skin to skin so condoms aren’t fully protective (e.g. thighs)

26
Q

How do warts present and what else may they be?

A
  • Painless fleshy growths, hard/soft, single/multiple, occasionally cause irritation
  • May also occur in oral cavity, larynx, conjunctiva, nose
  • Turn white with acetic acid

Differentials: vestibular papillomatosis (non-viral + non-STI), molluscum contagious (viral, small firm papules with central umbilication)

27
Q

How are genital warts treated?

A
  • Usually spontaneously resolve but may treat if causing issues
  • Topical: podophyllotoxin (for small non-keratinised lesions), Imiquimod (for larger keratinised warts)
  • Physical: excision, cryotherapy, laser
28
Q

What is the issue with warts in pregnancy?

A

Pregnancy can cause them to enlarge, treat in pregnancy by physical means to avoid transmission to neonates during delivery - as rarely it can cause respiratory papillomatosis

29
Q

How does herpes virus cause infection?

A

Mostly, HSV-1 causes genital herpes + cold sores + HSV-2 causes genital herpes

Virus enters MM - travels to a ganglion - may lie dormant until primary infection then lie dormant again after this until later outbreaks

Can get asymptomatic shedding ie transmit the virus without knowing you are infected

Incubation 2-14d

30
Q

What are the CF of genital herpes?

A
  • Primary: red vesicles, v painful, can form open sores, flu-like sx, inguinal lymphadenopathy, pruritus, urinary retention from the pain. Crust and heal in about 3w
  • Secondary: often shorter + less intense outbreaks causing burning, itching, may have a trigger like stress, consider HIV if >5 infections in a year
  • Cold sores - painful lesions around mouth + nose lasting 7-10d
31
Q

How is genital herpes managed?

A
  • Primary: acyclovir, full STI screen, avoid all SI, rest + fluids
  • Secondary: OTC painkillers, petroleum jelly, ice; if regular give acyclovir as soon as symptoms occur
32
Q

What is the effect of genital herpes on pregnancy?

A
  • Small chance of vertical transmission if pre-existing so offer mother acyclovir; if new infection during T3 there isn’t time for antibodies to develop so a high chance of transmission so offer a CS
  • Neonatal herpes - skin/eyes/mouth, disseminated to internal organs or CNS
33
Q

What is Trichomonas vaginalis?

A

A protozoal STI transmitted by vaginal sex only, and can rarely be transmitted to a neonate during delivery or cause premature labour/low bw

34
Q

How does trichomonas vaginalis present?

A
  • 28d incubation period
  • Males often asymptomatic, or have urethral DC, dysuria etc, foreskin pain/itch and rarely balanoposthitis
  • Female: offensive odour, abnormal DC (thick/thin/frothy/yellow/green), pruritic/sore vulva, dyspareunia, dysuria, abnormal bleeding; O/E vulvitis/vaginitis/strawberry cervix, pH >4.5

Diagnosed from a high vaginal swab/urethral swab or 1st void urine in a man

35
Q

What is the management of trichomonas vaginalis?

A
  • Metronidazole or tinidazole for 7d, or single higher dose of metronidazole (more ADRs)
  • Test partners from past 4w (28d incubation)
  • Abstain until meds finished
  • Test of cure if not responding
36
Q

What is bacterial vaginosis and what causes it?

A

Not an STI, but an imbalance in vaginal organisms such as Gardnerella, Mycoplasmas and anaerobes as a result of reduced lactobacilli that cause the pH to increase

RF are anything that changes the pH such as a new partner, IUD, receptive oral sex, STIs, douching, scented soaps, recent Abx, smoking

37
Q

What are the CF of BV and what else could it be?

A
  • Thin white-grey fishy discharge with an increased pH
  • Usually no irritation or soreness
  • DDx: candida, TV (thin offensive dc, causes dysuria etc), other STIs
38
Q

What classical investigation findings indicate BV?

A
  • HVS - clue cells (epithelial cells with coccobacili)
  • Reduced lacotbacilli
  • No pus cells (so not STI)
  • Presence of G vaginalis isn’t an indicator as is present in non-BV
39
Q

How is bacterial vaginosis managed?

A
  • Usually oral or topical gel metronidazole for 5-7d (topical if woman prefers it), or oral clindamycin or tinidazole (these less preferred). Can also give in pregnancy
  • Adv about avoiding scented soaps etc, consider removal of IUD, reassure that it is common
40
Q

What is the effect of BV on pregnancy?

A

Can increase prematurity, miscarriage + chorioamnionitis - so deffo treat
If BF use a lower dose as it changes the taste

41
Q

What causes vulvovaginal candidadiasis?

A

Usually C albicans which is a GIT commensal

RF include immunosuppression e.g. DM/pregnancy, oestrogen e.g. COCP, hypersensitivity and increased acidity (e.g. ABx - less bacteria - more yeast)

42
Q

How does thrush present and what else may it be?

A

CF: vulval/perineal pruritus, white/curd like noninfectious DC, superficial dysuria, erythema + swelling, satellite lesions (red pustular lesions with plaques that can be scraped off)

Ddx: BV, TV, UTI, contact dermatitis, eczema; DM should be considered if recurrent

43
Q

What is the management of thrush?

A
  • Reasure that is not an STI
  • Intravaginal anti fungal with an applicator (e.g. clotrimazole or fenticonazole) +/- an oral anti fungal (fluconazole/itraconazole) +/- topical imidazole for vulval sx –> this is the OTC like canestan
  • Should go in 7-14d, if not consider underlying cause/alternative
  • In pregnancy use intravaginal + topical not oral and be careful with the applicator
44
Q

What is pelvic inflammatory disease and what causes it?

A

An infection of the upper genital tract (uterus, FT, ovaries, peritoneum) due to ascending spread of bacteria from the vagina or cervix

Causes: C trachomatis or N gonorrhoea are the main causes but others include Strep, bacteroides and anaerobes

45
Q

What are the RF for PID?

A

Age 15-24, recent change in partner, UPSI, h/o STIs/PID, instrumentation of the cevix (IUD, TOP, hysteroscopy, gynae surgery etc)

46
Q

What are the symptoms of PID?

A

Lower abdo pain (usually b/l as salpingitis), deep dyspareunia, menstrual abnormalities, PCB, dysuria, abnormal discharge (purulence, odour). Acute severe - severe pain, fever, N+V

47
Q

What are the signs of PID?

A

Systemic illness, peritonism, rigors, tender uterus/adnexae, cervical excitation on bimanual palpation, thickened fornices, cystic swellings in tubes, palpable masses, discharge, abscess (fullness in PoD)

48
Q

What Ix are done for suspected PID?

A
  • Endocervical swabs for NG+CT) and HVS for TV + BV (negative does NOT exclude PID)
  • WCC + CRP often raised, Hb normal (unless another cause for low Hb obv)
  • Full STI screen, urine dip/MSU, pregnancy test
  • TV USS
  • Laparoscopy if severe/uncertain diagnosis
49
Q

What is the management of PID?

A
  • Broad spectrum Abx, start empirically , e.g. doxy + ceftriaxone + metro (covers most likely organisms)
  • Analgesia
  • Abstain from SI until treated
  • Admit if pregnant, severe N+V, signs of peritonism/sepsis, unresponsive to oral Abx and in need of surgery
  • Laparotomy if unresolving with pelvic mass - pyosalpinx or tubo-ovarian abscess
50
Q

What are the possible complications of PID?

A
  • Recurrence (20% over 2y)
  • Infertility (10%)
  • Ectopic pregnancy as FTs are scarred
  • Tubo-ovarian abscess
  • Chronic pelvic pain
  • Fitz-Hugh Curtis syndrome
  • Chronic PID
51
Q

What is a Jarische Herkheimer reaction?

A

An inflammatory response from endotoxins released from the death of Treponema causing a flu-like illness
*If cardiac/neuro syphilis then give steroids as prophylaxis

52
Q

What is Fitz-Hugh-Curtis syndrome?

A

A complication of PID (usually Chlamydial) causing an acute peri-hepatitis due to adhesions with the liver and parietal peritoneum

Causes RUQ pain + deranged LFTs

CT may show inflammatory stranding, fluid in the right para-colic gutter, gallbladder wall thickening

53
Q

Chronic pelvic inflammatory disease

A

Hydrosalpinx + pelvic adhesions lead to chronic pain, purulent discharge, dysmenorrhoea, deep dyspareunia, infertility, parametritis (infection of pelvic cognitive tissue), fixed retroverted uterus, thickened fornices

Pelvic clearance or IVF for fertility are the treatments

54
Q

What are triple swabs?

A
  • Endocervical chlamydia NAAT swab (take from bit between internal + external Os)
  • Endocervical charcoal gonorrhoea swab
  • High vaginal charcoal swab for fungal + other bacterial infections (like TV, GBS, BV) (take from the posterior fornix)
55
Q

Disseminated gonococcal infection

A

Acute complication causing fever, asymmetrical polyarthralgias and pustules overlying small joints. It can lead to meningitis or endocarditis

56
Q

Reactive arthritis

A

A HLA-B27-associated seronegative spondyloarthropathies, develops following an infection where organism cannot be recovered from the joint (so not septic arthritis)

Usually triggered by a GI (dysenteric) or GU infection. STI form much more common in men and usually caused by Chlamydia

Classic triad of arthritis, conjunctivitis and urethritis - Reiter’s syndrome

M: symptomatic (analgesia, intra-articular steroids), sometimes methotrexate, usually gone within a year

57
Q

How might organism acquire antibiotic resistance?

A
  • Bacteria inactivate the Abx e.g. beta-lactamase producing bacteria
  • Altered target site e.g. penicillin binding protein
  • Metabolic pathways are altered so they are not the ones targeted
  • Reduced accumulation of the Abx inside the cell by an active efflux or reduced permeability

Obstetrics + gynaecology (13 decks)

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