Repro Session 6 Flashcards

1
Q

Are STIs acute or chronic/relapsing?

A

Both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

Papillomaviruses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A

Papillomaviruses, chlamydia, genital herpes, gonorrhoea and syphilis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

MSM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the possible sequelae of STIs?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the difference between STI and STD?

A

STI includes symptomatic and asymptomatic cases whereas STD is symptomatic only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

Maximises compliance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How are STIs managed?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A

~4%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Which are the two most common types of HPV?

A

6 and 11

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Which are the two high risk types of HPV?

A

16 and 18

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why are HPV16 and 18 considered high-risk?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How can HPV infection be diagnosed?

A

Clinically, biopsy and genome analysis/hybrid capture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the treatment for HPV infection?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

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

A

99%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the most common causative agent in chlamydia?

A

Chlamydia trrachomatis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

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

A

D-K

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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