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My Phase 3a Revision > WOMEN'S HEALTH - SEXUAL HEALTH + GUM > Flashcards

WOMEN'S HEALTH - SEXUAL HEALTH + GUM Flashcards

1
Q

STI SCREENING
What asymptomatic screening would you do in females?

A
  • Self-taken vulvo-vaginal swabs for gonorrhoea + chlamydia (NAAT)
  • bloods for HIV + other STIs like syphilis
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2
Q

STI SCREENING
What asymptomatic screening would you do in heterosexual males?

A

First-void urine sample for NAAT,
?bloods

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3
Q

STI SCREENING
What asymptomatic screening would you do in homosexual males?

A
  • First-void urine sample for NAAT
  • pharyngeal + rectal swab,
  • bloods for HIV, hep B
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4
Q

STI SCREENING
What symptomatic screening would you do in GUM for females?

A

Double/triple swabs
- NAAT endocervical swabs
- High vaginal charcoal swabs (HVS) for BV, TV, candida, GBS
- Endocervical charcoal swab for triple (gonorrhoea)
Bloods for HIV, syphilis, Hep B
Urinalysis if dysuria for pus cells

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5
Q

STI SCREENING
What symptomatic screening would you do in GUM for men?

A
  • Urethral swabs + first-void urine NAAT.
  • Bloods for HIV, syphilis, hep B
  • Rectal + pharyngeal MC&S for MSM
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6
Q

GUM
What is the purpose of contact tracing?

A
  • Prevent re-infection of index patient
  • Identify + treat asymptomatic infected individuals as a public health measure
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7
Q

GUM
What are some risk factors for STIs?

A
  • <25y
  • Multiple sexual partners
  • Lack of barrier methods
  • Poor socioeconomic status
  • Having other STIs
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8
Q

CHLAMYDIA
What is chlamydia?

A
  • Most common STI in UK (approx 1 in 10 young women have it)
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9
Q

CHLAMYDIA
What is it caused by?

A

Chlamydia trachomatis – obligate intracellular gram -ve cocc

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10
Q

CHLAMYDIA
What is the incubation period?

A

7–21days

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11
Q

CHLAMYDIA
What is the clinical presentation of chlamydia most of the time?

A

Asymptomatic in 70% F + 50% M

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12
Q

CHLAMYDIA
What is the clinical presentation of chlamydia in women?

A
  • Cervicitis (abnormal PV discharge, PCB, IMB),
  • dysuria,
  • dyspareunia
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13
Q

CHLAMYDIA
What is the clinical presentation of chlamydia in men?

A

Urethral discharge,
dysuria,
urethritis

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14
Q

CHLAMYDIA
What are some differentials of chlamydia?

A
  • Gonorrhoea
  • Prostatitis
  • Trichomonas vaginalis
  • UTI, BV
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15
Q

CHLAMYDIA
What findings may there be on clinical examination in chlamydia?

A
  • Pelvic/abdo tenderness
  • Cervical excitation
  • Cervicitis
  • White/purulent discharge
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16
Q

CHLAMYDIA
What swabs would be taken for chlamydia?

A

Nucleic acid amplification tests (NAAT)
- M = first-void urine sample or urethral swab
- F = endocervical, vulvo-vaginal swab (self-taken) or first-void urine
- MSM = pharyngeal/rectal swab if indicated
Charcoal swab (HVS or endocervical) for MC&S to screen for other conditions

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17
Q

CHLAMYDIA
Who is chlamydia screening aimed at?

A
  • M/F 15–24, relies heavily on opportunistic testing
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18
Q

CHLAMYDIA
What is the chlamydia screening programme aim?
What is the process?

A
  • Aims to screen every sexually active pt annually or on changing sexual partner
  • +ve tests are retested 3m after treatment to ensure haven’t re-contracted
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19
Q

CHLAMYDIA
Generic GUM STI testing Tests for which conditions?

A

Chlamydia, gonorrhoea, syphilis + HIV.

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20
Q

CHLAMYDIA
What are some generic complications of chlamydia?

A
  • Reactive arthritis,
  • epididymitis,
  • PID,
  • endometriosis,
  • increased incidence of ectopic pregnancy,
  • most common preventable cause of infertility
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21
Q

CHLAMYDIA
What are some pregnancy-related complications?

A
  • Preterm delivery,
  • PROM,
  • low birth weight
  • neonatal infection
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22
Q

CHLAMYDIA
How would you manage chlamydia?

A
  • Test for other STIs, contraceptive advice, ?safeguarding if child.
  • Doxycycline 100mg BD for 7d (C/I pregnancy or breastfeeding).
  • 1g azithromycin stat dose in pregnancy (erythromycin or amoxicillin safe too)
  • Referral to GUM for partner notification + contact tracing.
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23
Q

CHLAMYDIA
What is the process of contact tracing for chlamydia?

A
  • Men with urethral Sx – all contacts since + in 4w prior to onset
  • A-Sx M/F = all partners from last 6m or most recent sexual partner
  • Contacts of confirmed chlamydia offer treatment prior to results of investigations then treat test
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24
Q

GONORRHOEA
What is gonorrhoea?

A
  • STI that affects any mucous membrane surface with columnar epithelium (endocervix, urethra, conjunctiva, rectum, pharynx).
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25
Q

GONORRHOEA
What is it caused by?

A

Neisseria gonorrhoea –gram -ve diplococcus

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26
Q

GONORRHOEA
What is the incubation period and how does it spread?

A

2–5d, spreads via contact with infected mucous secretions, often if co-existing STI

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27
Q

GONORRHOEA
What is the clinical presentation of gonorrhoea most of the time?

A

Asymptomatic 90% F, 50% M

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28
Q

GONORRHOEA
What is the clinical presentation of gonorrhoea in women?

A

Cervicitis (PV discharge, PCB, IMB, dyspareunia)

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29
Q

GONORRHOEA
What is the clinical presentation of gonorrhoea in men?

A

Urethral discharge,
dysuria,
testicular pain/swelling (epididymo-orchitis)

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30
Q

GONORRHOEA
What is the clinical presentation of gonorrhoea in rectal + pharyngeal infection?

A

Asymptomatic but sometimes peri-anal pain

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31
Q

GONORRHOEA
What is the clinical presentation of gonorrhoea discharge?

A

Odourless purulent, can be green/yellow

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32
Q

GONORRHOEA
How would you investigate for gonorrhoea?

A

NAAT testing
- M = first-void urine or urethral swab
- W = endocervical, vulvo-vaginal or first-void urine
- Pharyngeal/rectal swab in MSM or clinical indication
Charcoal swab (endocervical or HVS) MC&S

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33
Q

GONORRHOEA
What is the importance of a charcoal swab MC&S in gonorrhoea?

A
  • To screen for other STIs.
  • Reduces antibiotic resistance by matching to sensitivities
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34
Q

GONORRHOEA
What are the local complications of gonorrhoea?

A
  • Urethral strictures
  • Epididymo-orchitis + salpingitis (can lead to infertility)
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35
Q

GONORRHOEA
What are the systemic complications of gonorrhoea?

A
  • PID
  • Gonococcal arthritis (most common cause of septic arthritis in young adults)
  • Disseminated gonococcal infection as triad (tenosynovitis, migratory polyarthritis, dermatitis lesions can be maculopapular or vesicular)
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36
Q

GONORRHOEA
What complication of gonorrhoea may present in neonates?

A
  • Ophthalmia neonatorum (gonococcal conjunctivitis) –medical emergency associated with sepsis, eye perforation + blindness.
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37
Q

GONORRHOEA
What is the management of gonorrhoea?

A
  • 1g single dose IM ceftriaxone (add PO ciprofloxacin 500mg but only if sensitive as high antibiotic resistance)
  • Follow-up test of cure with NAAT testing or cultures
  • Contact tracing, partner notification, contraceptive advice, ?safeguarding
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38
Q

BACTERIAL VAGINOSIS
What is the pathophysiology of BV?

A
  • Loss of lactobacilli which are the main component of healthy vaginal flora
  • These bacteria produce lactic acid to keep vaginal pH low (3.5–4.5)
  • The acidic environment prevents other bacteria overgrowing so pH rises > alkaline environment > anaerobes overgrow
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39
Q

BACTERIAL VAGINOSIS
What are the causative organisms of BV?

A
  • Gardnerella vaginalis (#1), mycoplasma hominis, prevotella spp.
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40
Q

BACTERIAL VAGINOSIS
Is BV an STI?

A

No but can increase risk of STIs, may co-exist with other infections like candidiasis, chlamydia + gonorrhoea.

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41
Q

BACTERIAL VAGINOSIS
What are the risk factors of bacterial vaginosis?

A
  • Multiple sexual partners
  • Excessive vaginal cleaning
  • Recent Abx
  • Smoking
  • IUD
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42
Q

BACTERIAL VAGINOSIS
What causes BV to occur less frequently?

A

Less frequent if COCP or effective condom usage

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43
Q

BACTERIAL VAGINOSIS
What is the clinical presentation of BV?
What symptoms would suggest an alternative or co-existing diagnosis?

A
  • Fishy-smelling watery grey or white PV discharge
  • Commonest cause of abnormal vaginal discharge in younger women
  • Itching, irritation + pain are not common.
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44
Q

BACTERIAL VAGINOSIS
What investigations may you do?

A
  • Speculum (not necessary if classic Sx + low STI risk) to visualise discharge + HVS to exclude other causes.
  • ?NAAT to screen for STIs
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45
Q

BACTERIAL VAGINOSIS
What diagnostic criteria is used in BV?

A

Amsel’s (3/4)
- Thin, white discharge (can present asymptomatically)
- Vaginal pH using swab + pH paper >4.5
- Clue cells on cervical swab MC&S (endocervical or self-taken vaginal)
- Positive whiff test (add potassium hydroxide to get very strong fishy odour)

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46
Q

BACTERIAL VAGINOSIS
What are clue cells?

A
  • Cervical epithelial cells that have bacteria stuck inside them.
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47
Q

BACTERIAL VAGINOSIS
What are the complications of BV?

A
  • Pregnancy related – miscarriage, preterm delivery, PROM, chorioamnionitis, LBW
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48
Q

BACTERIAL VAGINOSIS
What is the management of BV?

A
  • Asymptomatic usually resolves without Tx
  • PO metronidazole 5–7d to target anaerobic bacteria (avoid alcohol as can cause N+V + flushing)
  • Topical metronidazole or clindamycin are alternatives
  • Advice about avoiding excessive vaginal cleaning
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49
Q

TRICHOMONAS VAGINALIS
What is TV?

A
  • STI spread through sexual activity + lives in uretha of men + women as well as vagina in women
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50
Q

TRICHOMONAS VAGINALIS
What can it increase the risk of?

A

Contracting HIV by damaging vaginal mucosa
BV,
cervical cancer,
PID
pregnancy-related complications.

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51
Q

TRICHOMONAS VAGINALIS
What causes TV?
What is the structure of this organism?

A
  • Protozoan parasite, single-celled organism with flagella – trichomonas vaginalis
  • 4 flagella at front, 1 on back making it highly motile, attach to tissues + cause damage
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52
Q

TRICHOMONAS VAGINALIS
What is the clinical presentation of TV?

A
  • PV discharge classically offensive, frothy + yellow/green.
  • Vulvovaginitis, itching, dysuria + dyspareunia.
  • May cause urethritis + balanitis in men
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53
Q

TRICHOMONAS VAGINALIS
What might clinical examination of TV show?

A
  • Speculum = strawberry cervix (colpitis macularis) due to cervicitis + tiny haemorrhages on surface of cervix due to infection
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54
Q

TRICHOMONAS VAGINALIS
What investigations would you do for TV?

A
  • Vaginal pH >4.5
  • Charcoal swab for MC&S (HVS, urethral swab or first-catch urine).
  • Microscopy shows motile trophozoites + wet microscopy shows polymorphonuclear leukocytes
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55
Q

TRICHOMONAS VAGINALIS
What is the management of TV?

A
  • Referral to GUM for Dx, Tx + contact tracing
  • PO metronidazole 5–7d (or stat 2g dose)
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56
Q

SYPHILIS
How does syphilis infect?

A
  • Gets in through skin or mucous membranes, replicates + then disseminates
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57
Q

SYPHILIS
What is the incubation period?

A

About 3 weeks

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58
Q

SYPHILIS
What is the causative organism?

A

Treponema pallidum – spirochete (spiral-shaped) bacteria

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59
Q

SYPHILIS
What are the modes of transmission of syphilis?

A
  • Oral, vaginal + anal sex with direct contact with infected area
  • Vertical transmission
  • IVDU, blood transfusions + other transplants (rare due to screening)
  • Biggest RF = MSM
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60
Q

SYPHILIS
What are the 3 stages of syphilis infection?

A
  • Primary
  • Secondary
  • Tertiary
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61
Q

SYPHILIS
Explain what primary syphilis is.

A
  • Involves painless ulcer (chancre) at the original site of infection.
  • Often genitals but may not be visible (cervix)
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62
Q

SYPHILIS
Explain what secondary syphilis is.
How is it further subdivided?

A
  • Systemic Sx once chancre healed, particularly of mucous membranes, Sx often resolve after 6–12w + then becomes latent (asymptomatic but still infected)
  • Early latent is <2y since initial infection, late latent is >2y
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63
Q

SYPHILIS
Explain what tertiary syphilis is.

A
  • Occurs many years after the initial infection + can affect many organs, particularly with development of gummas + CV/neuro complications
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64
Q

SYPHILIS
What is the clinical presentation of primary syphilis?

A
  • Painless genital chancre, resolves over 3–8w with clear base + serum, rounded edges
  • Local lymphadenopathy
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65
Q

SYPHILIS
What is the clinical presentation of secondary syphilis?

A
  • Systemic (low grade fever, lymphadenopathy).
  • Maculopapular rash (trunk, soles + palms).
  • Condylomata lata (grey wart-like lesions around genitals + anus).
  • Alopecia
  • Buccal ‘snail track ulcers’
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66
Q

SYPHILIS
What is the clinical presentation of tertiary syphilis?

A
  • Gummas (granulomatous lesions that can affect skin, organs + bones)
  • Aortic aneurysms
  • Neurosyphilis – tabes dorsalis (locomotor ataxia), paralysis, dementia, Argyll-Robertson (prositutes) pupil
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67
Q

SYPHILIS
What is an Argyll-Robertson pupil?

A

“Accommodates but does not react”
- Constricted pupil that accommodates when focusing on near object but does not react to light, often irregularly (small) shaped

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68
Q

SYPHILIS
What investigations would you do for syphilis?

A
  • Treponemal tests (enzyme immunoassay or haemagglutination assay)
  • Samples from site of infection tested with dark field microscopy or PCR
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69
Q

SYPHILIS
How would you manage syphilis?

A
  • Specialist GUM (full STI screening, contact tracing, contraceptive information).
  • Single dose IM benzathine benzylpenicillin or PO doxycycline if allergic
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70
Q

SYPHILIS
What is a potential adverse effect of treating syphilis?

A
  • Jarisch-Herxheimer reaction within a few hours of treatment
  • Fever, rash + tachycardia thought to be due to release of endotoxins following bacterial death
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71
Q

GENITAL HERPES
What causes genital herpes?

A
  • Herpes simplex virus (HSV) causes both cold sores + genital herpes
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72
Q

GENITAL HERPES
What happens after initial infection?

A

Virus becomes latent in associated sensory nerve ganglia, commonly trigeminal nerve ganglion in cold sores (initial contraction in childhood, reactivates in stress) or sacral nerve ganglia in genital herpes

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73
Q

GENITAL HERPES
How does herpes spread?

A
  • Direct contact with affected mucous membranes or viral shedding in mucous secretions, can be shed even when no Sx (more common in first 12m).
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74
Q

GENITAL HERPES
What causes herpes?

A

HSV-1 mostly cold sores
- If genital, due to oro-genital sex (oral > genital)
HSV-2 mostly genital herpes
- STI but can cause lesions in mouth

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75
Q

GENITAL HERPES
What is the clinical course of genital herpes?

A
  • Can be asymptomatic or develop Sx when latent virus reactivated
  • Initial infection usually appears within 2w + lasts for 3w being more severe than recurrent episodes which resolve quicker.
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76
Q

GENITAL HERPES
What is the clinical presentation of genital herpes?

A
  • Multiple painful ulcers or blistering lesions affecting genital area
  • Neuropathic type pain (tingling, burning, shooting)
  • Flu Sx (fatigue, headaches, fever, myalgia)
  • Dysuria
  • Inguinal lymphadenopathy
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77
Q

GENITAL HERPES
What other specific symptoms may be seen in genital herpes?

A
  • Aphthous ulcers (small painful oral sores)
  • Herpes keratitis (inflammation of the cornea = blue)
  • Herpetic whitlow (painful skin lesion on finger/thumb)
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78
Q

GENITAL HERPES
What is the investigation for genital herpes?

A
  • Viral PCR swab from a lesion
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79
Q

GENITAL HERPES
What is the main complication of genital herpes in pregnancy?
Does the foetus have any immunity?

A
  • Neonatal HSV infection as high morbidity + mortality.
  • After initial infection woman will produce IgG that cross placenta to give foetus passive immunity + protect during labour + delivery
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80
Q

GENITAL HERPES
What is the management or primary genital herpes contracted before 28w gestation?

A
  • Aciclovir during infection
  • Prophylactic aciclovir from 36w gestation onwards to reduce risk of genital lesions during labour + delivery
  • Asymptomatic at delivery can have vaginal if >6w from initial infection, if Sx then c-section
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81
Q

GENITAL HERPES
What is the management of primary genital herpes after 28w gestation?

A
  • Aciclovir during infection + immediate prophylactic aciclovir
  • C-section in all cases
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82
Q

GENITAL HERPES
What is the management of recurrent genital herpes in pregnancy?

A
  • Occurs if woman known to have genital herpes before pregnancy
  • Low risk of neonatal infection even if lesions at delivery
  • Prophylactic aciclovir from 36w to reduce risk of Sx at delivery
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83
Q

GENITAL HERPES
What is the management of genital herpes?

A
  • Specialist GUM Mx
  • Conservative (paracetamol, topical lidocaine 2% instillagel, clean with warm saltwater, topical vaseline, PO fluids, loose clothing, avoid sex).
  • Aciclovir may be used
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84
Q

GENITAL WARTS
How is genital warts spread?

A
  • Sex, sharing sex toys or potentially oral.
  • Can be transmitted even if asymptomatic
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85
Q

GENITAL WARTS
What causes genital warts?

A
  • Human papilloma virus 6 + 11
  • Can stay in skin + warts can develop again
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86
Q

GENITAL WARTS
What is the clinical presentation of genital warts?

A
  • 2-5mm fleshy, slightly pigmented warts around vagina, penis or anus
  • Itching or bleeding from genitals or anus
  • Abnormal urine stream
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87
Q

GENITAL WARTS
What are the investigations for genital warts?

A
  • Clinical diagnosis (may use magnifying glass or colposcope)
  • Application of acetic acid/vinegar produces acetowhite changes of surface
  • Biopsy if atypical
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88
Q

GENITAL WARTS
What are the potential complications of genital warts?
How are these managed?

A
  • May increase in number, size or recur during pregnancy
  • Cryotherapy offered, usually can give birth vaginally
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89
Q

GENITAL WARTS
How is genital warts managed?

A
  • Prophylaxis with HPV vaccine for 12–13y (may be given to MSM, trans men/women + sex workers)
  • Topical podophyllotoxin cream/lotion or cryotherapy.
  • GUM contact tracing, contraceptive advice
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90
Q

CANDIDIASIS
What is candidiasis?
How does it cause an infection?

A
  • Thrush – vaginal infection with a yeast of the Candida family
  • May colonise without causing Sx then progresses to infection with the right environment (during pregnancy/after Tx with Abx that alter vaginal flora)
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91
Q

CANDIDIASIS
What causes candidiasis?

A
  • Candida albicans (#1)
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92
Q

CANDIDIASIS
What are some risk factors?

A

Increased oestrogen (pregnancy, during menstrual years)
poorly controlled DM,
immunosuppression,
broad spectrum Abx

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93
Q

CANDIDIASIS
What is the clinical presentation of candidiasis?

A
  • Thick, white discharge that does not smell (cottage cheese)
  • Vaginal + vulval itching, irritation or discomfort
  • Severe infection > erythema, fissures, oedema, dysuria, dyspareunia
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94
Q

CANDIDIASIS
What are the investigations for candidiasis?

A
  • Tx often started empirically on clinical presentation
  • Vaginal pH <4.5
  • Charcoal swab MC&S to confirm
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95
Q

CANDIDIASIS
What is the management of candidiasis?

A
  • Anti-fungal cream/pessary (clotrimazole) or PO anti-fungal tablets (fluconazole)
  • Canesten duo is standard OTC Tx with single fluconazole tablet + cream
  • Recurrent infections with induction + maintenance regime of PO/PV anti-fungals
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96
Q

CANDIDIASIS
What treatment should be used in pregnancy?

A

Clotrimazole in pregnancy as fluconazole can cause congenital abnormalities

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97
Q

CANDIDIASIS
What advice should be given to patients using anti-fungal creams + pessaries?

A
  • Can damage latex condoms + prevent spermicides from working so alternative contraception needed for 5d after
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98
Q

LICHEN SCLEROSUS
What is lichen sclerosus?

A
  • Chronic inflammation dermatosis where elastic tissue becomes collagen
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99
Q

LICHEN SCLEROSUS
What is meant by lichen?

A

Lichen refers to a flat eruption that spreads.

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100
Q

LICHEN SCLEROSUS
Where does it affect in women?

A

Labia, perineum + perianal skin

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101
Q

LICHEN SCLEROSUS
Where does it affect in men?

A

Glans penis + foreskin

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102
Q

LICHEN SCLEROSUS
What causes lichen sclerosus?

A
  • Thought to be autoimmune as associated with other autoimmune conditions (T1DM, alopecia, hypothyroidism, vitiligo)
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103
Q

LICHEN SCLEROSUS
What is the clinical presentation of lichen sclerosus in women?

A
  • 45–60y with vulval itching + skin changes
  • Soreness/pain (worse at night), skin tightness + superficial dyspareunia
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104
Q

LICHEN SCLEROSUS
What is the clinical presentation of lichen sclerosus in men?

A
  • Painful erections
  • Dyspareunia
  • Urinary Sx
  • Soreness
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105
Q

LICHEN SCLEROSUS
What phenomenon can occur in lichen sclerosus?

A
  • Koebner phenomenon where signs + Sx worse with friction to skin
  • Can be worse with tight, rubbing underwear, scratching + incontinence
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106
Q

LICHEN SCLEROSUS
What are the investigations for lichen sclerosus?

A
  • Porcelain-white in colour, shiny, tight, thin, slightly raised, ± papules or plaques
  • Hyperkeratosis if chronic scratching
  • Affects vulva + perianal areas but not perineum giving hourglass/8 shape
  • Biopsy if ?malignancy
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107
Q

LICHEN SCLEROSUS
What are the complications with lichen sclerosus?

A
  • 5% risk of developing squamous cell carcinoma of the vulva.
  • May be pain + discomfort, sexual dysfunction, bleeding + narrowing of vaginal or urethral openings
108
Q

LICHEN SCLEROSUS
What is the management of lichen sclerosus?

A
  • Cannot be cured by symptoms controlled
  • Potent topical steroids like clobetasol propionate 0.05% (Dermovate) giving long-term control + reduces risk of malignancy
  • Topical emollients
109
Q

HIV
What is HIV?
What is the pathophysiology of HIV?

A
  • RNA retrovirus that encodes reverse transcriptase
  • Binds to GP120 envelope glycoprotein to CD4 receptors which migrate to lymphoid tissue where virus replicates + produces billions of new virions
  • Reverse transcriptase makes single strand RNA > double stranded DNA + viral DNA is integrated to host cell’s DNA with enzyme integrase + core viral proteins synthesised + cleaved by viral protease
  • These then released + in turn infect new CD4 cells
110
Q

HIV
What is the aetiology of HIV?

A
  • HIV-1 is most common type
  • HIV-2 is rare outside West Africa
111
Q

HIV
What are high risk groups for HIV?

A

MSM,
IVDU,
commercial sex workers

112
Q

HIV
How is HIV transmitted?

A
  • Unprotected anal, vaginal or oral sex (co-existing STIs can enhance transmission)
  • Vertical transmission (pregnancy, breastfeeding)
  • Mucous membranes, blood or open wound exposure to blood or bodily fluids (IVDU, needle-sticks, blood splashed in eye)
113
Q

HIV
What is the clinical presentation of HIV?

A
  • Initial seroconversion 2–6w post infection (flu Sx with fever, malaise, myalgia, maculopapular rash)
  • Clinical latency with progressive CD4 loss (poor immunity but no Sx).
  • Early Sx HIV (rise in viral load + fall in CD4 count) where fever, night sweats, diarrhoea + opportunistic infections (HSV, herpes zoster) > AIDS-related complex
114
Q

HIV
When is HIV classified as AIDS?

A

AIDS = Sx of immune deficiency and a CD4 count of <200

115
Q

HIV
What are AIDS-defining illnesses?
Give some examples

A
  • All associated with end-stage HIV infection where CD4 count dropped to a level that allows opportunistic diseases to occur.
  • Kaposi’s sarcoma, pneumocystis jiroveci pneumonia, cytomegalovirus, candidiasis (oesophageal or bronchial), lymphomas, TB
116
Q

HIV
What tests can be used to investigation HIV?

A
  • Serum/salivary HIV enzyme-linked immunosorbent assay (ELISA)
  • Rapid point of care screening blood test for HIV antibodies
  • PCR testing
117
Q

HIV
Explain the process of HIV ELISA

A

Can take 3m for HIV Ab detection so confirmatory assay after 3m.

118
Q

HIV
Explain the process of rapid point of care tests.

A

Immunoassay kit provides rapid result but needs serological confirmation, repeat within 3m of exposure if initially negative.

119
Q

HIV
Explain the process of PCR testing

A

P24 antigen tests directly for viral antigen in blood + can give +ve earlier in infection compared to antibody test, HIV RNA levels tests directly for number of viral copies in blood giving a viral load

120
Q

HIV
How can HIV infection be monitored?

A
  • Monitoring CD4 count
  • Monitoring viral load
121
Q

HIV
Explain the process of monitoring CD4 count.

A

i) Destroyed by virus so lower = increased risk of opportunistic infection
(<200 cells/mm^3 = AIDS, 500–1200 normal range)

122
Q

HIV
Explain the process of monitoring viral load.

A

Undetectable refers to viral load below labs recordable range (usually 50–100 copies/ml), may be in hundreds of thousands if untreated.
Undetectable = untransmissable

123
Q

HIV
What are the considerations with HIV and pregnancy?

A
  • Normal vaginal delivery if viral load <50 copies/ml
  • Consider c-section if >50, but mandatory in >400
  • IV zidovudine 4h before c-section
  • Neonatal PO zidovudine if maternal viral load <50 if not triple ART both for 4–6w
  • No breastfeeding
124
Q

HIV
What is the generic management for HIV?
What is the standard therapy?
What is the aim of therapy?

A
  • Specialist HIV, infectious diseases + GUM clinics
  • Highly active anti-retrovirus therapy (HAART) with 2 NRTIs + third agent
  • Goal to achieve normal CD4 count + undetectable viral load
125
Q

HIV
What are the 4 main groups of HIV treatment?

A
  • Nucleoside reverse transcriptase inhibitors (NRTIs)
  • Protease inhibitors (PIs)
  • Integrase inhibitors (IIs)
  • Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
126
Q

HIV
What are some examples of and the mechanism of action of…

i) NRTIs?
ii) PIs?
iii) IIs?
iv) NNRTIs?

A

i) Zidovudine, tenofovir, emtricitabine – inhibits synthesis of DNA by reverse transcriptase
ii) Indinavir (end –navir) – acts competitively on HIV enzyme involved in production of functional viral proteins
iii) Raltegravir (end –gravir) – inhibits insertion of HIV DNA to genome
iv) Nevirapine – binds directly to + inhibits reverse transcriptase

127
Q

HIV
What is the role of post-exposure prophylaxis (PEP) in HIV?

A
  • Given within 72h of exposure to HIV+ (sooner = better)
  • ART therapy = Truvada (emtricitabine + tenofovir) + raltegravir for 28d
  • HIV test done immediately + 3m after, should abstain for 3m
128
Q

HIV
What additional management can be given to HIV +ve patients?

A
  • Education about safe sex + condoms, less partners, regular tests.
  • Prophylactic co-trimoxazole if CD4 <200 to protect from PCP
  • Monitor blood lipids + CVD RFs as increased risk
  • Yearly smears for women
  • Vaccines up to date but avoid live vaccinations
  • Can conceive safely via techniques like sperm washing + IVF
129
Q

BALANITIS
what is balanitis?

A

Balanitis is inflammation of the glans penis and sometimes extends to the underside of the foreskin which is known as balanoposthitis

130
Q

BALANITIS
what are the causes?

A

candidiasis
dermatitis
bacterial
anaerobic
lichen planus
lichen sclerosis

131
Q

BALANITIS
what are the acute causes?

A

candidiasis
dermatitis
bacterial
anaerobic

132
Q

BALANITIS
what are the chronic causes?

A

lichen sclerosis
plasma cell of balanitis of Zoon

133
Q

BALANITIS
what is the clinical presentation?

A
  • red, swollen, itchy and sore penis
  • pain when peeing
  • thick discharge from under foreskin
  • unpleasant smell
  • difficulty pulling back foreskin
134
Q

BALANITIS
what are the investigations?

A
  • mostly clinical diagnosis
  • if infective a swab can be taken for microscopy
135
Q

BALANITIS
what is the general management for balanitis?

A
  • gentle saline washes
  • ensuring to wash foreskin properly
  • 1% hydrocortisone for short period
136
Q

BALANITIS
what is the treatment for fungal (candidiasis) infection?

A

topical clotrimazole for 2 weeks

137
Q

BALANITIS
what is the treatment for bacterial infection?

A

flucloxacillin or clarithromycin if penicillin allergic

138
Q

BALANITIS
what is the treatment for anaerobic balanitis?

A

saline washing
oral metronidazole

139
Q

BALANTITIS
what is the specific treatment for balanitis caused by dermatitis?

A

mild topical corticosteroids (hydrocortisone)

140
Q

BALANTITIS
what is the specific treatment for balanitis caused by lichen sclerosus?

A

strong topical corticosteroids (clobetasol)

141
Q

LYMPHOGRANULOMA VENEREUM
what is it?

A

STI caused by serovars L1, L2 or L3 or chlamydia trachomatis

142
Q

LYMPHOGRANULOMA VENEREUM
what are the clinical features?

A

Painless genital ulcer
Appears 3-12 days after infection
May not be noticeable e.g. if occurs inside the vagina
Inguinal lymphadenopathy
Proctitis, rectal pain, rectal discharge (in rectal infections)
Systemic symptoms such as fever and malaise

143
Q

LYMPHOGRANULOMA VENEREUM
what are the investigations?

A

swab PCR to detect chlamydia trachomatis

144
Q

LYMPHOGRANULOMA VENEREUM
what is the management?

A

Treatment is with antibiotics. Common regimes include:

Oral doxycycline 100 mg twice daily for 21 days
Oral tetracycline 2 g daily for 21 days
Oral erythromycin 500 mg four times daily for 21 days

145
Q

CHANCROID
what is it?

A

Chancroid is an infection of the genital skin caused by Haemophilus ducreyi.

It typically produces a painful, potentially necrotic genital lesion.

Associated symptoms include painful lymphadenopathy and bleeding on contact.

146
Q

CHANCROID
what are the causes?

A

Haemophilus ducreyi

Given its relatively high incidence in topical areas and Greenland, it is important to inquire in the history about recent travel.

147
Q

CHANCROID
what are the clinical features?

A

A painful genital lesion which may bleed on contact
Associated symptoms include painful lymphadenopathy

148
Q

CHANCROID
what are the investigations?

A

clinical diagnosis
diagnosis can be confirmed using culture or PCR

149
Q

CHANCROID
what is the management?

A

The infection is treated using antibiotics (typically Ceftriaxone, Azithromycin or Ciprofloxacin)

150
Q

CONTRACEPTION
What is the UKMEC?

A

UK Medical Eligibility Criteria to do with safe contraception use.
- UKMEC1 = no restriction in use (minimal risk).
- UKMEC2 = benefits generally outweigh the risks.
- UKMEC3 = risks generally outweigh the benefits.
- UKMEC4 = unacceptable risk, C/I.

151
Q

CONTRACEPTION
What methods of contraception are most effective and why?

A
  • Abstinence is only 100% effective method.
  • Long-acting methods as not dependent on user to take regular action.
  • Effectiveness is expressed as perfect use + typical use as it can be user dependent.
152
Q

CONTRACEPTION
What are the least–most effective contraceptive methods (perfect/typical use)?

A
  • NFP (≥95%, 76%)
  • Condoms (98%, 82%)
  • COCP/POP (>99%, 91%)
  • PO-injection (>99%, 94%)
  • PO-implant, coils + sterilisation (>99% both)
153
Q

CONTRACEPTION
What contraception should be avoided in…
i) breast cancer?
ii) cervical/endometrial cancer?
iii) Wilson’s disease?

A

i) Any hormonal contraception (use IUD or barrier methods).
ii) Avoid IUS.
iii) Avoid copper coil.

154
Q

CONTRACEPTION
What advice should be given about contraception for perimenopausal women?

A
  • Require contraception for 2y if <50y/o or 1 y if >50.
  • HRT does not prevent pregnancy.
  • COCP can be used up to age 50 + can treat perimenopausal Sx.
  • Injection stopped before 50 due to risk of osteoporosis.
155
Q

CONTRACEPTION
What advice should be given about contraception in under 20s?

A
  • COCP + POP unaffected by age.
  • Implant good choice of long-acting reversible contraception (UKMEC1).
  • Injection UKMEC2 due to concerns about reduced BMD.
  • Coils UKMEC2 as higher rate of expulsion.
156
Q

CONTRACEPTION
What advice should be given about contraception after childbirth?

A
  • Fertility not considered to return until 21d postnatally.
  • Lactational amenorrhoea is >98% effective for up to 6m after if women fully breastfeeding + amenorrhoeic.
  • POP + implant considered safe in breastfeeding + can start any time after birth.
157
Q

CONTRACEPTION
What is the natural rhythm method?

A
  • Woman monitors her menstrual cycle + only has sex when less fertile.
  • Requires 3–12m of cycles to predict fertile time, partner commitment.
  • 6d prior to ovulation (sperm live for 6d) to 2d after (ovum life) is fertile window.
158
Q

BARRIER CONTRACEPTION
What is barrier contraception?

A
  • Provide a physical barrier to semen entering the uterus.
  • Only method that protect against STIs (but not 100%).
159
Q

BARRIER CONTRACEPTION
What are condoms? What are some limitations?

A
  • Latex barrier around the penis, using oil-based lubricants can damage latex + make them more likely to tear.
  • Polyurethane condoms can be used in latex allergy.
160
Q

BARRIER CONTRACEPTION
What are diaphragms + cervical caps?

A
  • Silicone cups that fit over the cervix + prevent semen entering the uterus.
  • Woman fits them before having sex + leaves in place for at least 6h after sex.
  • Should be used with spermicide gel to further reduce risk of pregnancy.
  • 95% perfect use but little protection to STIs.
161
Q

BARRIER CONTRACEPTION
What are dental dams? What STIs spread via oral sex?

A
  • Used during oral sex to provide barrier between mouth + vulva and the vagina or anus to prevent infections that spread via oral sex.
  • Chlamydia, gonorrhoea, HS1+2, HPV, E. coli, pubic lice, syphilis.
162
Q

COCP
What is the COCP?

A
  • Pill containing supraphysiological level of oestrogen (ethinylestradiol) AND progesterone (of varying types).
163
Q

COCP
What is the mechanism of action of the COCP?

A
  • Inhibits ovulation (primary mechanism).
  • –ve feedback on hypothalamus/pituitary so suppression of GnRH/LH/FSH so anovulation.
  • Progesterone thickens cervical mucus, inhibits proliferation of endometrium, reducing chance of successful implantation.
164
Q

COCP
What is a withdrawal bleed? What is breakthrough bleeding?

A
  • Endometrial lining is maintained in a stable state so when the pill is stopped, the lining breaks down + sheds causing a withdrawal bleed.
  • This is not a menstrual period as it’s not part of the natural menstrual cycle.
  • Unscheduled bleeding (spotting) may occur in extended use without a pill-free period.
165
Q

COCP
What is the difference between monophasic and multiphasic pills?

A
  • Monophasic contain the same amount of hormone in each pill, everyday formulations like microgynon, pack contains 7 inactive pills.
  • Multiphasic pills have varying amounts of hormones to match the normal cyclical changes more closely.
166
Q

COCP
What pill is recommended…
i) as first line?
ii) in PMS?
iii) in acne + hirsutism?

A

i) Pills with levonorgestrel or noresthisterone (microgynon or Leostrin) as lower VTE risk.
ii) Pills containing drospirenone as anti-mineralocorticoid + anti-androgen activity can help Sx (esp. w/ continuous use).
ii) Pills containing cyproterone acetate (co-cyprindiol) as anti-androgen effects but the oestrogenic effects give it higher VTE risk so usually stopped after 3m when Sx reduced.

167
Q

COCP
What regimes are used for the COCP?

A
  • 21d on 7d off.
  • Tricycling 63d on (three packs), 7d off.
  • Continuous use without a pill-free period.
168
Q

COCP
What are the benefits of the COCP?

A
  • Effective contraception, rapid return of fertility after stopping.
  • Improvement in PMS, menorrhagia + dysmenorrhoea (acne in some).
  • Reduced risk of endometrial, ovarian, colon cancer + benign ovarian cysts.
169
Q

COCP
What are some side effects + risks with the COCP?

A
  • Unscheduled bleeding common in first 3m.
  • Breast pain + tenderness.
  • Mood changes + depression.
  • Headaches, HTN, VTE.
  • Small raise in risk of breast + cervical cancer (risk normalises after 10y taking pill).
  • Small raise in risk of MI + stroke.
170
Q

COCP
What are the UKMEC4 criteria for the COCP?

A
  • Uncontrolled HTN.
  • Migraine with aura.
  • > 35 smoking >15/day.
  • Major surgery with prolonged immobility (stop 4w before major surgery)
  • Hx of stroke, IHD, AF, VTE.
  • Active breast cancer.
  • Liver cirrhosis or tumours.
  • SLE + antiphospholipid syndrome.
  • Breastfeeding before 6w postpartum (UKMEC2 after).
171
Q

COCP
What are the UKMEC3 criteria for the COCP?

A
  • > 35 smoking <15/day.
  • BMI >35kg/m^2.
  • Controlled HTN.
  • VTE FHx in 1st degree relatives.
  • Immobility.
  • Known carrier of BRCA1/2.
172
Q

COCP
What are the important starting instructions for the COCP?
Rules for switching from POP to COCP?

A
  • Start on day 1 = immediate protection.
  • Start after day 5 = extra contraception for first 7d.
  • Can switch from traditional POP at any time but 7d extra contraception.
  • Can switch from desogestrel with no additional contraception as it inhibits ovulation.
173
Q

COCP
What is a missed pill? What are the missed pill rules for one pill?

A
  • When the pill is >24h, D+V is managed as missed pill.
  • Take missed pill ASAP even if means 2 pills on same day, no extra protection required as long as back on track.
174
Q

COCP
What are the missed pill rules for >1 pill?
What are the rules regarded unprotected sexual intercourse (UPSI)?

A

Take most recent missed pill ASAP even if means 2 pills on same day, extra contraception for 7d.
- Day 1–7 + UPSI = emergency contraception.
Day 8–14 + UPSI = ok.
Day 15–21 + UPSI = next pack back-to-back so skip pill free period.

175
Q

POP
What is the POP?

A
  • Pill containing only progesterone, taken continuously with fewer contraindications + risks compared with the COCP.
176
Q

POP
What different types of POP are there and what are their mechanisms?

A

Traditional POP (norgeston) –
- Thickens cervical mucus.
- Alters endometrium so less accepting of implantation.
- Reduced ciliary action in fallopian tube.
Desogestrel POP (Cerazette) –
- Inhibits ovulation (main mechanism) + above.

177
Q

POP
What are the instructions for starting the POP and why?
How do you switch between POPs?

A
  • Start day 1–5 = immediate protection.
  • Other times = 48h additional contraception to allow cervical mucus to thicken enough to prevent entry of sperm.
  • Can switch between POPs with no extra contraception.
178
Q

POP
What are the rules regarding switching from COCP to POP?

A
  • Best time to change is days 1–7 of the hormone-free period after finishing the COCP pack as no additional contraception required.
  • Any other time requires 48h contraception.
179
Q

POP
What is the UKMEC4 criteria for POP?

A
  • Active breast cancer.
180
Q

POP
What is the main complaint/side effect of the POP?
What are some other side effects of the POP?

A
  • Unscheduled bleeding common in first 3m (if persists exclude other causes like STIs, pregnancy, cancer).
  • Changes to bleeding schedule one of primary adverse effects (40% regular bleeding, 40% irregular, prolonged or troublesome + 20% amenorrhoeic).
  • Breast tenderness, headaches + acne.
181
Q

POP
What are some risks of the POP?

A
  • Increased risk of ovarian cysts, small risk of ectopic pregnancy with traditional POP due to reduced ciliary action, minimal increased risk of breast cancer (returns to normal 10y after stopping).
182
Q

POP
What classes as a missed pill for POP?

A
  • > 3h in traditional POP is a missed pill.
  • > 12h for desogestrel-POP is a missed pill.
183
Q

PROGESTERONE INJECTION
What is the progesterone only injection? What types are there (long and short acting)?

A
  • Depot medroxyprogesterone acetate.
  • Depo-Provera = IM.
  • Sayana press = s/c (can be self-injected).
  • Noristerat is alternative that contains noresthisterone + works for 8w so used as short-term interim contraception (e.g. after vasectomy).
184
Q

PROGESTERONE INJECTION
What is the mechanism of action of the progesterone injection?

A
  • Inhibits ovulation by inhibiting FSH secretion by the pituitary gland + prevents development of follicles in the ovary.
  • Thickens cervical mucus + alters endometrium to make it less favourable for implantation.
185
Q

PROGESTERONE INJECTION
What are the instructions for the progesterone injection?

A
  • Day 1–5 = immediate protection.
  • > day 5 = 7d of contraception.
  • Injections every 12–13w, any longer = less effective.
186
Q

PROGESTERONE INJECTION
What is the main side effect of the progesterone injection?

A

Changes to bleeding schedule main issue
- Bleeding often more irregular, heavier + last longer.
- Usually temporary, >1y of regular use most become amenorrhoeic.
- Exclude other causes of bleeding.
- Can use COCP for 3m if problematic bleeding.
- Short course (5d) of mefenamic acid can halt bleeding.

187
Q

PROGESTERONE INJECTION
What are 3 unique side effects to the progesterone injection?

A
  • Weight gain
  • Reduced BMD (oestrogen maintains BMD + mostly produced by follicles in ovaries)
    – Makes depot unsuitable for those >45
  • Takes 12m for fertility to return after stopping
188
Q

PROGESTERONE INJECTION
What are some general side effects of the progesterone injection?

A
  • Acne.
  • Reduced libido.
  • Mood issues (depression).
  • Headaches.
  • Alopecia.
  • Skin reactions at injection sites.
  • Small rise in breast/cervical cancer risk.
189
Q

PROGESTERONE INJECTION
What are the UKMEC3 + 4 criteria for progesterone injection?

A
  • UKMEC4 = active breast cancer.
  • UKMEC3 = IHD + stroke, unexplained vaginal bleeding, severe liver cirrhosis + liver cancer.
190
Q

PROGESTERONE IMPLANT
What is the progesterone implant?

A
  • Small flexible plastic rod placed in upper arm beneath skin + above s/c fat that slowly releases progesterone into circulation.
191
Q

PROGESTERONE IMPLANT
What is the mechanism of action for the progesterone implant?

A
  • Inhibits ovulation.
  • Thickens cervical mucus.
  • Alters endometrium to make it less accepting to implantation.
192
Q

PROGESTERONE IMPLANT
What are the instructions for the progesterone implant?

A
  • Day 1–5 = immediate protection.
  • > Day 5 = 7d contraception.
  • Lasts 3y then needs replacing.
193
Q

PROGESTERONE IMPLANT
What are the pros of progesterone implant?

A
  • Effective + reliable.
  • Can improve dysmenorrhoea + can make periods lighter or stop altogether.
  • No weight gain, effect on BMD, no VTE risk, no restrictions for obese patients.
194
Q

PROGESTERONE IMPLANT
What are the side effects of the progesterone implant?

A
  • Problematic bleeding (20% amenorrhoeic, 25% frequent/prolonged bleeding, 33% infrequent, rest normal, can use COCP for 3m if problematic bleeding + no C/Is).
  • Can worsen acne, no STI protection.
195
Q

PROGESTERONE IMPLANT
What are the risks with the progesterone implant?

A
  • Can be bent/fractured or impalpable/deeply implanted needing extra contraception until located (USS/XR), may need specialist removal.
  • Very rarely can enter vessels + migrate through body to lungs.
196
Q

PROGESTERONE IMPLANT
What is the UKMEC4 criteria for the progesterone implant?

A
  • Active breast cancer.
197
Q

COILS
What are the coils?

A
  • Device inserted into uterus to provide contraception offering long-acting reversible contraception.
198
Q

COILS
What are the instructions for insertion/removal of a coil?

A
  • Screen for STIs before insertion.
  • Women seen 3–6w after insertion to check the threads.
  • Abstain from sex or use extra contraception for 7d before coil removed.
199
Q

COILS
What are the risks of coil insertion?

A
  • Insertion risks (bleeding, pain on insertion [use NSAIDs],
  • vasovagal reactions,
  • uterine perforation,
  • PID + expulsion rate highest in first 3m.
200
Q

COILS
What are the contraindications to the coils?

A
  • PID or infection,
  • immunosuppression,
  • pregnancy,
  • unexplained bleeding,
  • pelvic cancer,
  • uterine cavity distortion (fibroids).
201
Q

COILS
What is the copper IUD and its mechanism?

A
  • Licensed for 5–10y after insertion depending on device + can be used as emergency contraception.
  • Copper toxic to ovum + sperm, alters endometrium making it less favourable to implantation.
202
Q

COILS
What are the benefits of the IUD?

A
  • Reliable contraception.
  • Insert at any time in cycle + immediate protection.
  • No hormones so safe in VTE risk of Hx or cancer.
  • May reduce risk of endometrial + cervical cancer.
203
Q

COILS
What are the drawbacks of the IUD?

A
  • Procedure with risks for insertion/removal.
  • Can cause HMB/IMB which often settles.
  • Some women have pelvic pain.
  • No STI protection.
  • Increased risk of ectopic pregnancies.
  • Occasionally falls out.
204
Q

COILS
What types of levonorgestrel intrauterine system (LNG-IUS) coil are there?

A
  • Mirena effective for 5y in contraception, 4y for HRT + licensed for menorrhagia.
  • Levosert effective for 5y + licensed for menorrhagia
205
Q

COILS
What is the mechanism of action for the IUS?

A
  • Progesterone component thickens cervical mucus.
  • Alters endometrium making less hospitable + inhibits ovulation in small # of women.
206
Q

COILS
What are the benefits of the IUS?

A
  • Can make periods lighter or stop.
  • May improve dysmenorrhoea or pelvic pain related to endometriosis.
  • No effect on BMD, VTE, no restrictions in obese pts.
207
Q

COILS
What are the drawbacks of the IUS?

A
  • Procedure with risks for insertion/removal.
  • Can cause spotting or irregular bleeding.
  • Some women experience pelvic pain.
  • No STI protection.
  • Increased risk of ectopic pregnancies.
  • Occasionally falls out.
  • Increased incidence of ovarian cysts.
  • Systemic absorption can lead to progesterone Sx (acne, headaches, breast tenderness).
208
Q

COILS
What problematic bleeding can occur with the IUS?

A
  • Irregular bleeding can occur particularly in first 6m.
  • Exclude causes (STI, pregnancy, cervical smears up to date).
  • COCP in addition for 3m can settle the bleeding.
209
Q

COILS
What incidental finding might there be on a cervical smear in a woman with a coil?

A
  • Actinomyces-like organisms (ALO).
  • No treatment unless Sx (pelvic pain, abnormal bleeding) ?removal.
210
Q

EMERGENCY CONTRACEPTION
What 3 types of contraception can be used as emergency contraception?

A
  • Copper IUD
  • PO Ulipristal acetate (ellaOne)
  • PO levonorgestrel (levonelle)
211
Q

EMERGENCY CONTRACEPTION
For the copper IUD, answer the following…
i) effectiveness?
ii) time frame?
iii) mechanism?
iv) extra notes?

A

i) 99% regardless of time in cycle
ii) <120h of UPSI or 120h after earliest estimated date of ovulation
iii) Toxic to sperm + ovum so inhibits fertilisation + implantation.
iv) Keep in until at least next period

212
Q

EMERGENCY CONTRACEPTION
For the copper IUD, what are the pros and cons?

A

Pros
- Choice not affected by BMI, enzyme-inducing drugs or malabsorption.
- Can leave in as long-term contraceptive
Cons
- PID (especially if STIs)
- Normal risks with coil insertion

213
Q

EMERGENCY CONTRACEPTION
For Ulipristal acetate, answer the following…
i) dose?
ii) effectiveness?
iii) time frame?
iv) mechanism?
v) extra notes?
vi) side effects?

A

i) Single 30mg dose
ii) Second most effective but decreases with time
iii) <120h
iv) Selective progesterone receptor modulator that inhibits ovulation
v) Vomiting within 3h then repeat dose
vi) Spotting + changes to next menstrual period, abdo/pelvic/back pain, mood changes, headaches, dizziness, breast tenderness

214
Q

EMERGENCY CONTRACEPTION
For Ulipristal acetate, what are the pros and cons?

A

Pros
- More effective than levonorgestrel
- Can be used >1 in one cycle
Cons
- Avoid breastfeeding for 1w (express but discard)
- Avoid in severe asthma
- Wait 5d before starting COCP or POP with 7 or 2d extra contraception needed

215
Q

EMERGENCY CONTRACEPTION
For levonorgestrel, answer the following…
i) dose?
ii) effectiveness?
iii) time frame?
iv) mechanism?
v) side effects?

A

i) Single 1.5mg dose (3mg if BMI >26kg/m^2)
ii) Least effective of group 84%
iii) <72h
iv) Stops ovulation + inhibits implantation
v) Spotting + changes to next menstrual period, diarrhoea, breast tenderness, dizziness, depressed mood

216
Q

EMERGENCY CONTRACEPTION
For Levonorgestrel, what are the pros and cons?

A

Pros
- Safe during breastfeeding (Avoid for 8h to avoid infant exposure though).
- COCP/POP can start instantly but with extra contraception for 7/2d
- Use more than once in a menstrual cycle
Cons
- Less effective

217
Q

STERILISATION
What is sterilisation?
Is it offered on the NHS?

A
  • Permanent surgical interventions to prevent conception but does not protect against STIs.
  • Yes but the NHS does not provide reversal, these are private and have a low success rate.
218
Q

STERILISATION
What is the process of female tubal occlusion?

A
  • Laparoscopic under GA
  • Occlusion of tubes using “Filshie clips” or fallopian tubes can be tied + cut/removed altogether either as elective or during c-section.
  • Prevents ovum travelling along fallopian tube to the uterus + so sperm and ovum will not meet.
219
Q

STERILISATION
How effective is female sterilisation?
What advice is needed after?

A
  • 99% effective (1 in 200 failure rate).
  • Alternative contraception until next menstrual period as ovum may have already reached uterus during that cycle.
220
Q

STERILISATION
What is the process of male vasectomy?

A
  • Cutting the vas deferens, preventing sperm travelling from the testes to join the ejaculated fluid so prevents sperm being released into the vagina.
  • Relatively quick, less invasive and under LA.
221
Q

STERILISATION
How effective is male sterilisation?
What advice is needed after?

A
  • 99% effective (1 in 2000 failure rate).
  • Alternative contraception required for 2m after.
  • Test semen to confirm absence of sperm before it can be relied upon contraception, usually 12w after to allow clearance.
222
Q

FEMALE INFERTILITY
What is infertility?

A
  • Failure to conceive after 1 year of regular (2–3/7) unprotected sex.
223
Q

FEMALE INFERTILITY
When should you refer a female to specialist services?

A

After >1y or…
- Female >35
- Menstrual disorder
- Previous abdo/pelvic surgery
- Previous PID/STI
- Abnormal pelvic exam

224
Q

FEMALE INFERTILITY
What causes infertility in general?

A
  • 40% factors in both partners
  • 30% male factors
  • Unexplained, ovulatory disorders, tubal damage.
  • Less commonly uterine/peritoneal disorders.
225
Q

FEMALE INFERTILITY
In terms of causes of female infertility, what are disorders of ovulation?

A

PCOS
POI,
pituitary tumours,
hyperprolactinaemia,
Turner syndrome,
Sheehan’s,
previous radio/chemo

226
Q

FEMALE INFERTILITY
What are some risk factors of infertility?

A
  • Extremes of weight
  • Increasing age
  • Smoking
  • Alcohol/drug use
227
Q

FEMALE INFERTILITY
What are some first line investigations for female infertility?

A
  • STI screens (particularly chlamydia).
  • Ovulatory tests (mid-luteal progesterone levels, ovarian reserve testing)
  • TFTs + prolactin if clinical suspicion
  • Pelvic USS for PCOS or structural abnormalities
  • Karyotyping
228
Q

FEMALE INFERTILITY
In the ovulatory tests, what are you looking for in mid-luteal progesterone?
When would you test?
What results do you expect?

A
  • Indication of ovulation
  • 7d before end of cycle (usually day 21)
  • <16 = anovulation, >30 is ovular
229
Q

FEMALE INFERTILITY
What are the ovarian reserve tests?

A
  • Serum FSH + LH on days 2–5 (high = poor ovarian reserve)
  • Anti-mullerian hormone (released by granulosa cells in growing follicles so falls as eggs depleted)
  • Antral follicle count on USS (Few suggest poor ovarian reserve)
230
Q

FEMALE INFERTILITY
What further investigations can you do to assess for infertility?

A
  • Hysterosalpingogram – no anaesthetic required, use in those with no risk factors.
  • Laparoscopy + dye test (gold standard) –use in those with risk factors
231
Q

FEMALE INFERTILITY
What pre-conception advice would you give?

A
  • Intercourse 2–3 a week, regular smear tests, check rubella status.
  • Take 0.4mg folic acid (or 5mg if high risk).
  • Healthy BMI, no alcohol, drugs or smoking, control any co-morbidities.
232
Q

FEMALE INFERTILITY
How would you manage anovulation?

A
  • Weight loss
  • Clomiphene (selective oestrogen receptor modulator on days 2–6 to inhibit oestrogen + cause more GnRH + so FSH + LH release) or letrozole (aromatase inhibitor) to stimulate ovulation.
  • Gonadotrophins to stimulate ovulation if resistant to clomiphene
  • Ovarian drilling may be used in PCOS
233
Q

FEMALE INFERTILITY
How would you manage tubal disease?

A
  • Laparoscopy/tomy adhesiolysis + ablation or resection of endometriosis
  • Tubal catheterisation during HSG or selective salphingography
234
Q

FEMALE INFERTILITY
How would you manage uterine factors?
What is the ultimate management, especially if unexplained?

A
  • Surgery to correct polyps, adhesions or structural deformities
  • IVF
235
Q

MALE INFERTILITY
When should you refer a male to specialist services?

A

After >1y or…
- Previous genital pathology or urogenital surgery
- Previous STI
- Systemic illness
- Abnormal genital exam

236
Q

MALE INFERTILITY
What are the 5 main categories of male infertility?

A
  • Pre-testicular causes
  • Testicular causes
  • Post-testicular causes
  • Genetic/congenital causes of defective/absent sperm production
  • Azoospermia or teratozoospermia
237
Q

MALE INFERTILITY
In terms of male infertility, what are the pre-testicular causes?

A

Pituitary/hypothalamus pathology,
suppression due to stress,
chronic conditions,
hyperprolactinaemia,
Kallmann’s

238
Q

MALE INFERTILITY
In terms of male infertility, what are the genetic/congenital causes?

A

Klinefelter’s,
Y chromosome deletions

239
Q

MALE INFERTILITY
What initial investigation would you do for male infertility?
What results are considered normal?
What do you do if it’s abnormal?

A

Semen analysis
- Count >15m/ml
- Motility >40%
- Morphology >4%
- Total >39 million
- Repeat in 3m if abnormal

240
Q

MALE INFERTILITY
What other investigations can you do for male infertility?

A
  • FSH (increases in testicular failure)
  • Vasogram (inject dye to vas deferens + XR for obstruction), USS.
  • Testicular biopsy in azoospermia only if cryopreservation facilities.
  • CF screen, karyotyping (Klinefelters)
241
Q

MALE INFERTILITY
What pre-conception advice would you give to men?

A
  • Optimise weight
  • No alcohol/drugs/smoking
  • Control any co-morbidities
  • Avoid extreme heat near genitals
  • Looser fitting underwear
  • Avoid harmful chemicals in occupation
  • Zinc supplements
242
Q

MALE INFERTILITY
When managing male infertility, what are some management options?

A
  • Intrauterine insemination, IUI (collect + separate high-quality sperm + inject into uterus)
  • Intracytoplasmic sperm injection, ICSI (inject sperm directly into cytoplasm of egg + inject into uterus)
  • Surgical correction of an obstruction in the vas
243
Q

MALE INFERTILITY
How would you manage azoospermia?

A
  • Surgical sperm recovery or donor insemination
244
Q

ASSISTED CONCEPTION
What are the various methods for assisted conception?

A
  • Ovulation induction
  • Stimulated intrauterine insemination, IUI
  • Donor insemination, egg or embryo
  • Host surrogacy (same-sex or if uterine pathology)
  • IVF (ICSI, surgical sperm recovery, embryo freezing, assisted hatching)
245
Q

ASSISTED CONCEPTION
What counts as one cycle of IVF?

A
  • Ovarian stimulation + collection of oocytes.
  • May have several embryos + may be frozen.
246
Q

ASSISTED CONCEPTION
What is the treatment cycle in IVF?

A
  • Suppression of natural menstrual cycle
  • Ovarian stimulation to promote follicles developing.
  • Oocyte collection with a needle under TVS
  • Oocyte insemination (or ICSI especially if male factor infertility)
  • Embryo culture (2-5d until blastocyst)
  • Embryo transfer of highest quality embryos (usually 1, or 2 if >35y), may have cryopreservation
  • Pregnancy test performed around day 16 after egg collection
  • USS performed in early pregnancy (7w) to check for foetal heartbeat
247
Q

ASSISTED CONCEPTION
What is used to suppress the natural menstrual cycle?
How are the ovaries stimulated to promote follicles developing?
What should be given until 8–10w gestation and why?

A
  • GnRH agonist like goserelin or GnRH antagonist like cetrorelix.
  • FSH initially then hCG 36h before collection
  • Progesterone via vaginal suppositories to mimic corpus luteum, placenta takes over after.
248
Q

ASSISTED CONCEPTION
What factors affect the success of IVF?

A
  • Age is biggest factor
  • Cause of infertility
  • Previous pregnancies (increase likelihood)
  • Duration of infertility
  • # of previous attempts
  • Medical conditions + environmental factors
249
Q

ASSISTED CONCEPTION
What are the risks and complication with IVF?

A
  • Multiple pregnancy
  • Miscarriage + ectopics
  • Ovarian hyperstimulation syndrome
  • Bleeding + infection at egg collection
  • Failure
250
Q

ASSISTED CONCEPTION
What is the clinical presentation of ovarian hyperstimulation syndrome?

A
  • Mild = abdo pain + vomiting
  • Mod = N+V + ascites on USS
  • Severe = ascites, oliguria
  • Critical = anuria, VTE, ARDS
251
Q

ASSISTED CONCEPTION
What are the risk factors for ovarian hyperstimulation syndrome?

A
  • Younger age.
  • Lower BMI.
  • PCOS.
  • Higher antral follicle count.
252
Q

ASSISTED CONCEPTION
What investigations would you do in ovarian hyperstimulation syndrome and what would they show?
How could you identify someone at risk?

A
  • Activation of RAAS > high renin
  • Haematocrit raised as less fluid in intravascular space
  • USS + serum oestrogen (high = risk) – monitor these to identify those at risk.
253
Q

ASSISTED CONCEPTION
How do you manage ovarian hyperstimulation syndrome?

A
  • PO fluids
  • Monitor urine output
  • LMWH
  • Paracentesis for ascites
  • IV colloids
254
Q

POP
What are the missed pill rules for the POP?

A
  • Take pill ASAP but only 1 pill (even if >1 missed),
  • continue with next pill as usual (even if it means taking 2 on same day),
  • contraception for 48h.
255
Q

POP
What are the rules about UPSI in for the POP?

A

Sex since missing pill or within 48h of restarting = emergency contraception.

256
Q

PROGESTERONE IMPLANT
Which one is used in the UK and what age range?

A

Nexplanon used in UK, 68mg of etonogestrel, licensed 18–40y/o.

257
Q

COILS
What might non-visible threads indicate?

A
  • ?expulsion,
  • ?pregnancy,
  • ?uterine perforation
    > USS or XR, hysteroscopy/laparoscopy as last line.
258
Q

COILS
Can coils be used after birth?

A

Can be inserted either within 48h of birth or >4w after birth (UKMEC1) but not between (UKMEC3).

259
Q

COILS
What are the starting instructions for IUS?

A
  • Up to day 7 = immediate protection.
  • > Day 7 = extra contraception for 7d
260
Q

FEMALE INFERTILITY
How many couples does it affect?
How common is conception?

A
  • 1 in 7 couples struggle to conceive naturally.
  • 80% of couples <40 conceive within a year + 50% of those remaining will within 2.
261
Q

FEMALE INFERTILITY
In terms of causes of female infertility, what are the tubal/uterine/cervical factors?

A

PID,
sterilisation,
Asherman’s,
fibroids,
polyps,
endometriosis,
uterine deformity

262
Q

MALE INFERTILITY
In terms of male infertility, what are the testicular causes?

A

Damage from mumps, undescended testes, trauma, cancer, radio/chemo

263
Q

MALE INFERTILITY
In terms of male infertility, what are the post-testicular causes?

A

Retrograde ejaculation,
scarring from epididymitis (chlamydia),
absence of vas deferens (may be associated with cystic fibrosis, even carriers),
damage to testicle or vas (trauma, surgery, cancer).

264
Q

MALE INFERTILITY
In terms of male infertility, what are the azoospermia causes?

A

Steroid abuse,
vasectomy

265
Q

MALE INFERTILITY
In terms of male infertility, what are the teratozoospermia causes?

A

Testicular cancer

266
Q

MALE INFERTILITY
How would you manage hormonal causes of infertility?

A
  • Gonadotrophins if hypogonadotrophic hypogonadism, bromocriptine if hyperprolactinaemia + sexual dysfunction
267
Q

ASSISTED CONCEPTION
What is ovarian hyperstimulation syndrome?
What is it associated with?

A
  • Increased vascular endothelial growth factor (VEGF) from granulosa cells increases vascular permeability so fluid leaks from intravascular>extravascular space (oedema, ascites + hypovolaemia).
  • Gonadotrophins to mature follicles.

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