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Flashcards in Repro Session 6 Deck (98):
1

Are STIs acute or chronic/relapsing?

Both

2

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

Papillomaviruses

3

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

Papillomaviruses, chlamydia, genital herpes, gonorrhoea and syphilis

4

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

MSM

5

Who are the at risk groups of STDs?

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

6

Why has the incidence of STIs increased?

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

7

What are the possible sequelae of STIs?

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

8

What is the difference between STI and STD?

STI includes symptomatic and asymptomatic cases whereas STD is symptomatic only

9

How are genital tract infections identified?

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

10

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

Maximises compliance

11

How are STIs managed?

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

12

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

~4%

13

Which are the two most common types of HPV?

6 and 11

14

How does an infection with HPV6 or 11 present?

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

15

Which are the two high risk types of HPV?

16 and 18

16

Why are HPV16 and 18 considered high-risk?

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

17

How can HPV infection be diagnosed?

Clinically, biopsy and genome analysis/hybrid capture

18

What is the treatment for HPV infection?

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

19

What screening methods are in place for HPV?

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

20

What vaccines are available for HPV infection?

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

21

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

99%

22

What is the most common causative agent in chlamydia?

Chlamydia trrachomatis

23

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

D-K

24

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

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

25

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

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

26

When does peri hepatitis arise in chlamydia trachomatis infection?

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

27

How can chlamydia trachomatis infection lead to conjunctivitis?

Contact between secretions of genitalia and eye

28

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

Pneumonia

29

How is diagnosis of chlamydia trachomatis made?

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

30

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

It will contain urethral cells

31

What are the treatment options for chlamydia trachomatis infection?

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

32

Who is chlamydia trachomatis screening targeted at?

Sexually active

33

How is chlamydia trachomatis screening conducted?

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

34

What is associated with HSV2 infection?

Genital herpes

35

Which strain of HSV is associated with cold sores?

HSV1

36

What are the S/S of primary genital herpes?

Extensive painful genital ulceration, dysuria, inguinal lymphadenopathy and fever

37

How does recurrent genital herpes present differently to primary infection?

Primary symptoms diminish and reappear but are usually less severe

38

Where does latent HSV infection remain?

Dorsal root ganglia

39

How is HSV diagnosed?

PCR of vesicle fluid or swab from ulcer base

40

What is the treatment for HSV?

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

41

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

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

42

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

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

43

What can be seen if gonococci like infection becomes disseminated?

Bacteraemia, skin lesions, and gonococcal arthritis

44

How is Neisseria gonorrhoea infection diagnosed?

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

45

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

Fastidious and needs special media

46

What is the gold standard treatment for Neisseria gonorrhoea infection?

Single IM dose of ceftriaxone

47

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

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

48

What is treponema pallidum?

Aetiological spirochaete agent of syphilis

49

How is treponema pallidum imaged?

Needs dark-field microscopy that reveals spiral-shaped bacteria

50

Who is mostly affected by treponema pallidum?

Mostly men, esp MSM. Can be congenital

51

How does primary treponema pallidum infection present?

Indicated painless ulcer (chancre)

52

How does secondary treponema pallidum infection present?

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

53

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

Years

54

What is seen in tertiary treponema pallidum infection?

Neurosyphilis, cardiovascular syphilis, gummas

55

How is treponema pallidum infection diagnosed?

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

56

What is the treatment for treponema pallidum infection?

Penicillin

57

How is efficacy of treatment for treponema pallidum assessed?

Follow serological measures

58

How does lymphogranuloma venereum present?

Rapidly healing papule --> inguinal bubo

59

How does Haemophilus duareyi present?

Chancroid-painful genital ulcers

60

How does Klebsiella granulomatis present?

Genital nodules become ulcers known as granuloma inguinale

61

What is trichomonas vaginalis?

Flagellated protozoan that causes vaginal discharge

62

What are the S/S of trichomonas vaginalis infection?

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

63

How is trichomonas vaginalis infection diagnosed?

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

64

What is the treatment for trichomonas vaginalis infection?

Metronidazole

65

What are the causative agents of vulvovaginal candidiasis?

Candida albicans and other candida species from GI or genital flora

66

What are risk factors for developing vulvovaginal candidiasis?

Abx, OCP, pregnancy, obesity, steroids, diabetes

67

What are the S/S of vulvovaginal candidiasis?

Profuse, white, itchy curd-like discharge

68

How is vulvovaginal candidiasis diagnosed?

High vaginal smear +/- culture

69

How is vulvovaginal candidiasis treated?

Topical azoles, nystatin or oral Fluconazole if necessary

70

What is the pathogenesis of bacterial vaginosis?

Perturbed normal flora causes scanty but offensive fishy discharge

71

What are the causative agents of bacterial vaginosis?

Gardnella, anaerobes, mycoplasmas

72

How is bacterial vaginosis diagnosed?

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

73

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

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

74

What is the treatment for bacterial vaginosis?

Metronidazole

75

Are pubic and human body lice the same?

No

76

What is PID the result of?

Infection ascending from the endocervix

77

How does endometriosis lead to PID?

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

78

How does salpingitis lead to PID?

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

79

How does tubo-ovarian abscess form?

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

80

What are the sequelae of PID?

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

81

What makes a tubo-ovarian abscess complex?

Tube and ovary are indistinguishable in the mass

82

What is Reiter's syndrome?

Reactive arthritis leads to urethritis, conjunctivitis and arthritis

83

What is Fitz-Hugh-Curtis syndrome?

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

84

Why is inflammation from PID uncommon in the upper abdomen?

Omentum usually localises infection

85

What is the aetiology of PID?

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

86

In what group is peak incidence of PID seen?

Sexually active women aged 20-30 y.o.

87

What are the risk factors for developing PID?

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

88

What is the typical history of PID?

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

89

What is found O/E in PID?

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

90

What are the differentials for PID?

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

91

What investigations are performed in suspected PID?

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

92

What is the gold standard investigation for PID?

Laparoscopy

93

How is PID managed?

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

94

Why is PID management initiated STAT?

To minimise infertility risk

95

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

Will not be penetrated

96

What advice is given to a pt with PID?

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

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

Risk of complications increases with repeat episodes

98

What are the indications for IV treatment in PID?

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