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Semester 4 > Repro Session 6 > Flashcards

Repro Session 6 Flashcards

1
Q

Are STIs acute or chronic/relapsing?

A

Both

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2
Q

What accounts for most STD cases in the UK but has a decreasing incidence due to vaccination programmes?

A

Papillomaviruses

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3
Q

What are the 5 most common causes of STDs in the UK?

A

Papillomaviruses, chlamydia, genital herpes, gonorrhoea and syphilis

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4
Q

Which population group are gonorrhoea and syphilis cases becoming more frequent in?

A

MSM

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5
Q

Who are the at risk groups of STDs?

A

Young people, certain ethnic groups, high number of partners, certain sexual orientations, unsafe sexual activity, young age at first sexual intercourse and low SES groups

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6
Q

Why has the incidence of STIs increased?

A

Changing sexual and social behaviour, increased density and mobility of populations, better social acceptance of GUM attendance and anonymity, awareness campaigns and improved diagnostic and screening programmes

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7
Q

What are the possible sequelae of STIs?

A

PID and infertility, cancer, disseminated infection, transmission to foetus/neonate

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8
Q

What is the difference between STI and STD?

A

STI includes symptomatic and asymptomatic cases whereas STD is symptomatic only

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9
Q

How are genital tract infections identified?

A

Pt presents to GP/GUM with symptoms. Clinician notices non-genital STI indications. Contact tracing/screening of asymptomatic cases

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10
Q

Why is a single dose or short course of Abx favoured in STI management?

A

Maximises compliance

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11
Q

How are STIs managed?

A

Abx, screen, +/- empiric Tx for other STIs, contact tracing and pt education

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12
Q

What proportion of young adults are infected with HPV at some point in their life?

A

~4%

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13
Q

Which are the two most common types of HPV?

A

6 and 11

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14
Q

How does an infection with HPV6 or 11 present?

A

Benign, painless verrucous epithelial or mucosal outgrowths on external genitals or perianal skin

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15
Q

Which are the two high risk types of HPV?

A

16 and 18

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16
Q

Why are HPV16 and 18 considered high-risk?

A

> 70% of cervical cancers are associated and is associated with anogenital cancer

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17
Q

How can HPV infection be diagnosed?

A

Clinically, biopsy and genome analysis/hybrid capture

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18
Q

What is the treatment for HPV infection?

A

Most spontaneously resolve but otherwise topical podophyllin, cryotherapy, intralesional interferon or surgery

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19
Q

What screening methods are in place for HPV?

A

Cervical Pap smear cytology or colposcopy with acetowhite test for abnormal cells. Cervical swab and hybrid capture

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20
Q

What vaccines are available for HPV infection?

A

Gardasil to protect against HPV6, 11, 16 and 18 given in 2 doses to girls aged 12-13

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21
Q

How effective is the HPV vaccine against HPV16 and 18 cervical abnormalities in an uninflected population?

A

99%

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22
Q

What is the most common causative agent in chlamydia?

A

Chlamydia trrachomatis

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23
Q

Which serotypes of chlamydia trachomatis cause non-specific genital chlamydial infections?

A

D-K

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24
Q

What are the male S/S of chlamydia trachomatis infection?

A

Urethritis, epipdidymitis, prostatitis, proctitis causing pain in perineal/scrotal/urethral areas

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25
Q

What are the female S/S of chlamydia trachomatis infection?

A

Urethritis, cervicitis, salpingitis, peri hepatitis, but majority asymptomatic

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26
Q

When does peri hepatitis arise in chlamydia trachomatis infection?

A

Chronic infection causes PID and subsequent adhesions between the liver and abdominal wall

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27
Q

How can chlamydia trachomatis infection lead to conjunctivitis?

A

Contact between secretions of genitalia and eye

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28
Q

Other than conjunctivitis, what can chlamydia trachomatis infection in the mother lead to in the neonate?

A

Pneumonia

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29
Q

How is diagnosis of chlamydia trachomatis made?

A

NAAT of endocervical/urethral swabs/first void urine/conjunctival swab

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30
Q

Why can first void urine be used to detect chlamydia trachomatis infection?

A

It will contain urethral cells

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31
Q

What are the treatment options for chlamydia trachomatis infection?

A

Single large dose of azithromycin, 1-2 wk course of doxycycline or erythromycin for children

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32
Q

Who is chlamydia trachomatis screening targeted at?

A

Sexually active

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33
Q

How is chlamydia trachomatis screening conducted?

A

Urine sample or cervical swab and NAAT +/- test for Neisseria gonorrhoea

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34
Q

What is associated with HSV2 infection?

A

Genital herpes

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35
Q

Which strain of HSV is associated with cold sores?

A

HSV1

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36
Q

What are the S/S of primary genital herpes?

A

Extensive painful genital ulceration, dysuria, inguinal lymphadenopathy and fever

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37
Q

How does recurrent genital herpes present differently to primary infection?

A

Primary symptoms diminish and reappear but are usually less severe

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38
Q

Where does latent HSV infection remain?

A

Dorsal root ganglia

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39
Q

How is HSV diagnosed?

A

PCR of vesicle fluid or swab from ulcer base

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40
Q

What is the treatment for HSV?

A

Aciclovir for severe primary infection and prophylaxis and advise barrier contraception use

41
Q

What are the male S/S of Neisseria gonorrhoea infection?

A

Urethritis, epididymitis, prostatitis, proctitis, pharyngitis, purulent penile discharge

42
Q

What are the female S/S of Neisseria gonorrhoea infection?

A

Often asymptomatic but may have endocervitis, urethritis, PID, infertility

43
Q

What can be seen if gonococci like infection becomes disseminated?

A

Bacteraemia, skin lesions, and gonococcal arthritis

44
Q

How is Neisseria gonorrhoea infection diagnosed?

A

Clinically preferred but can use NAAT of cervical, urethral, throat or rectal swab if indicated

45
Q

Why is gram stain not routinely used for diagnosis of Neisseria gonorrhoea?

A

Fastidious and needs special media

46
Q

What is the gold standard treatment for Neisseria gonorrhoea infection?

A

Single IM dose of ceftriaxone

47
Q

Why is secondary treatment with azithromycin used in Neisseria gonorrhoea treatment?

A

For chlamydia as often co-infected and to prevent cephalosporin resistance

48
Q

What is treponema pallidum?

A

Aetiological spirochaete agent of syphilis

49
Q

How is treponema pallidum imaged?

A

Needs dark-field microscopy that reveals spiral-shaped bacteria

50
Q

Who is mostly affected by treponema pallidum?

A

Mostly men, esp MSM. Can be congenital

51
Q

How does primary treponema pallidum infection present?

A

Indicated painless ulcer (chancre)

52
Q

How does secondary treponema pallidum infection present?

A

6-8 wks after primary disease, fever, rash, lymphadenopathy and mucosal lesions develop

53
Q

How long can the latent period of treponema pallidum infection last?

A

Years

54
Q

What is seen in tertiary treponema pallidum infection?

A

Neurosyphilis, cardiovascular syphilis, gummas

55
Q

How is treponema pallidum infection diagnosed?

A

Intitial screening with EIA antibodies with +ves undoing more specific tests (cross-reacting antigen or particle agglutination) to establish timing

56
Q

What is the treatment for treponema pallidum infection?

A

Penicillin

57
Q

How is efficacy of treatment for treponema pallidum assessed?

A

Follow serological measures

58
Q

How does lymphogranuloma venereum present?

A

Rapidly healing papule –> inguinal bubo

59
Q

How does Haemophilus duareyi present?

A

Chancroid-painful genital ulcers

60
Q

How does Klebsiella granulomatis present?

A

Genital nodules become ulcers known as granuloma inguinale

61
Q

What is trichomonas vaginalis?

A

Flagellated protozoan that causes vaginal discharge

62
Q

What are the S/S of trichomonas vaginalis infection?

A

Thin, frothy and offensive discharge from vagina with vaginal inflammation and dysuria

63
Q

How is trichomonas vaginalis infection diagnosed?

A

Mainly clinical as discharge not candida and Tx same as for bacterial vaginosis so differentiation not needed. Vaginal wet preparation +/- culture enhancement

64
Q

What is the treatment for trichomonas vaginalis infection?

A

Metronidazole

65
Q

What are the causative agents of vulvovaginal candidiasis?

A

Candida albicans and other candida species from GI or genital flora

66
Q

What are risk factors for developing vulvovaginal candidiasis?

A

Abx, OCP, pregnancy, obesity, steroids, diabetes

67
Q

What are the S/S of vulvovaginal candidiasis?

A

Profuse, white, itchy curd-like discharge

68
Q

How is vulvovaginal candidiasis diagnosed?

A

High vaginal smear +/- culture

69
Q

How is vulvovaginal candidiasis treated?

A

Topical azoles, nystatin or oral Fluconazole if necessary

70
Q

What is the pathogenesis of bacterial vaginosis?

A

Perturbed normal flora causes scanty but offensive fishy discharge

71
Q

What are the causative agents of bacterial vaginosis?

A

Gardnella, anaerobes, mycoplasmas

72
Q

How is bacterial vaginosis diagnosed?

A

Clinically by vaginal pH>5 or KOH whiff test. Laboratory by HVS gram stain

73
Q

What may be visible on HVS gram stain from bacterial vaginosis?

A

Clue cells (epithelial and gram variable coccobacilli), reduced lactobacilli

74
Q

What is the treatment for bacterial vaginosis?

A

Metronidazole

75
Q

Are pubic and human body lice the same?

A

No

76
Q

What is PID the result of?

A

Infection ascending from the endocervix

77
Q

How does endometriosis lead to PID?

A

Inflammation and infection can be obstetric of non-obstetric. Non-obstetric –> PID

78
Q

How does salpingitis lead to PID?

A

Infection causes inflammation and damages epithelium whose cilia cannot recover fully. Decilliation allows exudate to accumulate creating adhesions between mucosal folds

79
Q

How does tubo-ovarian abscess form?

A

Pus exudes from fimbriae allowing an adhesion to form with the ovary

80
Q

What are the sequelae of PID?

A

Ectopic pregnancy, infertility, chronic pelvic pain, Fitz-Hugh-Curtis syndrome, Reiter’s syndrome

81
Q

What makes a tubo-ovarian abscess complex?

A

Tube and ovary are indistinguishable in the mass

82
Q

What is Reiter’s syndrome?

A

Reactive arthritis leads to urethritis, conjunctivitis and arthritis

83
Q

What is Fitz-Hugh-Curtis syndrome?

A

RUQ pain due to adhesions between abdominal wall and liver capsule (peri hepatitis)

84
Q

Why is inflammation from PID uncommon in the upper abdomen?

A

Omentum usually localises infection

85
Q

What is the aetiology of PID?

A

Often polymicrobial with endogenous vaginal flora, STIs and bacterial vaginosis microbes

86
Q

In what group is peak incidence of PID seen?

A

Sexually active women aged 20-30 y.o.

87
Q

What are the risk factors for developing PID?

A

Same as STIs and recent implant, recent removal of IUCD and recent termination of pregnancy

88
Q

What is the typical history of PID?

A

Pyrexia, lower abdo pain, deep dyspareunia, abnormal discharge, abnormal vaginal bleeding, sexual Hx, previous STI, contraceptive Hx

89
Q

What is found O/E in PID?

A

Fever, bilateral lower abdominal tenderness, bimanual examination shows adnexal tenderness and cervical motion tenderness, speculum examination shows cervicitis +/- purulent discharge

90
Q

What are the differentials for PID?

A

Ectopic pregnancy, endometriosis, ovarian cyst complications, IBS, appendicitis, UTI, functional pain

91
Q

What investigations are performed in suspected PID?

A

Pregnancy test, endocervical and HVS, WBC, CRP, STI screening, laparoscopy

92
Q

What is the gold standard investigation for PID?

A

Laparoscopy

93
Q

How is PID managed?

A

IM ceftriaxone, PO doxycycline, PO metronidazole or IV if severe disease

94
Q

Why is PID management initiated STAT?

A

To minimise infertility risk

95
Q

Why are Abx not useful in PID when tubo-ovarian abscess is present?

A

Will not be penetrated

96
Q

What advice is given to a pt with PID?

A

Avoid unprotected sex until F/U for themselves and partner complete. Contact tracing, full STI screen, single dose azithromycin for partner, complete Abx course and use barrier contraception

97
Q

Why must pts be advised to complete Abx courses and use barrier contraception in PID?

A

Risk of complications increases with repeat episodes

98
Q

What are the indications for IV treatment in PID?

A

Severe disease with no response to oral Tx, pyrexia, signs of tubo-ovarian abscess or pelvic peritonitis

Semester 4 (33 decks)

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