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MY REVISION - ALL PHASES > WOMENS HEALTH - SEXUAL HEALTH/GUM/PHYSIOLOGY/BREAST > Flashcards

WOMENS HEALTH - SEXUAL HEALTH/GUM/PHYSIOLOGY/BREAST 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 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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3
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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4
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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5
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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6
Q

CHLAMYDIA
What is chlamydia?

A
  • Most common STI in UK (approx 1 in 10 young women have it)
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7
Q

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

A

Asymptomatic in 70% F + 50% M

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8
Q

CHLAMYDIA
What are some differentials of chlamydia?

A
  • Gonorrhoea
  • Prostatitis
  • Trichomonas vaginalis
  • UTI, BV
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9
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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10
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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11
Q

CHLAMYDIA
Who is chlamydia screening aimed at?

A
  • M/F 15–24, relies heavily on opportunistic testing
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12
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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13
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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14
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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15
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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16
Q

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

A

Asymptomatic 90% F, 50% M

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17
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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18
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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19
Q

GONORRHOEA
What are the local complications of gonorrhoea?

A
  • Urethral strictures
  • Epididymo-orchitis + salpingitis (can lead to infertility)
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20
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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21
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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22
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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23
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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24
Q

BACTERIAL VAGINOSIS
What are the causative organisms of BV?

A
  • Gardnerella vaginalis (#1), mycoplasma hominis, prevotella spp.
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25
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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26
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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27
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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28
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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29
Q

BACTERIAL VAGINOSIS
What are clue cells?

A
  • Cervical epithelial cells that have bacteria stuck inside them.
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30
Q

BACTERIAL VAGINOSIS
What are the complications of BV?

A
  • Pregnancy related – miscarriage, preterm delivery, PROM, chorioamnionitis, LBW
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31
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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32
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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33
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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34
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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35
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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36
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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37
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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38
Q

SYPHILIS
How does syphilis infect?

A
  • Gets in through skin or mucous membranes, replicates + then disseminates
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39
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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40
Q

SYPHILIS
What are the 3 stages of syphilis infection?

A
  • Primary
  • Secondary
  • Tertiary
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41
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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42
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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43
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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44
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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45
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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46
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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47
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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48
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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49
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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50
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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51
Q

GENITAL HERPES
What causes genital herpes?

A
  • Herpes simplex virus (HSV) causes both cold sores + genital herpes
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52
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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53
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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54
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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55
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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56
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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57
Q

GENITAL HERPES
What is the investigation for genital herpes?

A
  • Viral PCR swab from a lesion
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58
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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59
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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60
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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61
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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62
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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63
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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64
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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65
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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66
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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67
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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68
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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69
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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70
Q

CANDIDIASIS
What causes candidiasis?

A
  • Candida albicans (#1)
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71
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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72
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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73
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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74
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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75
Q

LICHEN SCLEROSUS
What is lichen sclerosus?

A
  • Chronic inflammation dermatosis where elastic tissue becomes collagen
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76
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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77
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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78
Q

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

A
  • Painful erections
  • Dyspareunia
  • Urinary Sx
  • Soreness
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79
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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80
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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81
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
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82
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
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83
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
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84
Q

HIV
What is the aetiology of HIV?

A
  • HIV-1 is most common type
  • HIV-2 is rare outside West Africa
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85
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)
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86
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
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87
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
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88
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
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89
Q

HIV
Explain the process of HIV ELISA

A

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

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90
Q

HIV
How can HIV infection be monitored?

A
  • Monitoring CD4 count
  • Monitoring viral load
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91
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)

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92
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
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93
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
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94
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)
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95
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

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96
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
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97
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
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98
Q

CHLAMYDIA
What is the clinical presentation of chlamydia in women?

A
  • Cervicitis (abnormal PV discharge, PCB, IMB),
  • dysuria,
  • dyspareunia
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99
Q

CHLAMYDIA
What is the clinical presentation of chlamydia in men?

A

Urethral discharge,
dysuria,
urethritis

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100
Q

CHLAMYDIA
What is it caused by?

A

Chlamydia trachomatis – obligate intracellular gram -ve cocc

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101
Q

CHLAMYDIA
What is the incubation period?

A

7–21days

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102
Q

CHLAMYDIA
Generic GUM STI testing Tests for which conditions?

A

Chlamydia, gonorrhoea, syphilis + HIV.

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103
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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104
Q

CHLAMYDIA
What are some pregnancy-related complications?

A
  • Preterm delivery,
  • PROM,
  • low birth weight
  • neonatal infection
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105
Q

GONORRHOEA
What is it caused by?

A

Neisseria gonorrhoea –gram -ve diplococcus

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106
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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107
Q

GONORRHOEA
What is the clinical presentation of gonorrhoea in women?

A

Cervicitis (PV discharge, PCB, IMB, dyspareunia)

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108
Q

GONORRHOEA
What is the clinical presentation of gonorrhoea in men?

A

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

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109
Q

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

A

Asymptomatic but sometimes peri-anal pain

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110
Q

GONORRHOEA
What is the clinical presentation of gonorrhoea discharge?

A

Odourless purulent, can be green/yellow

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111
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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112
Q

BACTERIAL VAGINOSIS
What causes BV to occur less frequently?

A

Less frequent if COCP or effective condom usage

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113
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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113
Q
A
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114
Q

SYPHILIS
What is the incubation period?

A

About 3 weeks

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115
Q

SYPHILIS
What is the causative organism?

A

Treponema pallidum – spirochete (spiral-shaped) bacteria

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116
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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117
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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118
Q

CANDIDIASIS
What treatment should be used in pregnancy?

A

Clotrimazole in pregnancy as fluconazole can cause congenital abnormalities

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119
Q

LICHEN SCLEROSUS
What is meant by lichen?

A

Lichen refers to a flat eruption that spreads.

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120
Q

LICHEN SCLEROSUS
Where does it affect in women?

A

Labia, perineum + perianal skin

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121
Q

LICHEN SCLEROSUS
Where does it affect in men?

A

Glans penis + foreskin

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122
Q

HIV
What are high risk groups for HIV?

A

MSM,
IVDU,
commercial sex workers

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123
Q

HIV
When is HIV classified as AIDS?

A

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

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124
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.

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125
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

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126
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

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127
Q

BALANITIS
what are the causes?

A

candidiasis
dermatitis
bacterial
anaerobic
lichen planus
lichen sclerosis

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128
Q

BALANITIS
what are the acute causes?

A

candidiasis
dermatitis
bacterial
anaerobic

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129
Q

BALANITIS
what are the chronic causes?

A

lichen sclerosis
plasma cell of balanitis of Zoon

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130
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
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131
Q

BALANITIS
what are the investigations?

A
  • mostly clinical diagnosis
  • if infective a swab can be taken for microscopy
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132
Q

BALANITIS
what is the general management for balanitis?

A
  • gentle saline washes
  • ensuring to wash foreskin properly
  • 1% hydrocortisone for short period
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133
Q

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

A

topical clotrimazole for 2 weeks

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134
Q

BALANITIS
what is the treatment for bacterial infection?

A

flucloxacillin or clarithromycin if penicillin allergic

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135
Q

BALANITIS
what is the treatment for anaerobic balanitis?

A

saline washing
oral metronidazole

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136
Q

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

A

mild topical corticosteroids (hydrocortisone)

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137
Q

LYMPHOGRANULOMA VENEREUM
what is it?

A

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

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138
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

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139
Q

LYMPHOGRANULOMA VENEREUM
what are the investigations?

A

swab PCR to detect chlamydia trachomatis

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140
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

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141
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.

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142
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.

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143
Q

CHANCROID
what are the clinical features?

A

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

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144
Q

CHANCROID
what are the investigations?

A

clinical diagnosis
diagnosis can be confirmed using culture or PCR

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145
Q

CHANCROID
what is the management?

A

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

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146
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.

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147
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.
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148
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)
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149
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.

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150
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.
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151
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.
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152
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.
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153
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.
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154
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%).
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155
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.
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156
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.
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157
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.
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158
Q

COCP
What is the COCP?

A
  • Pill containing supraphysiological level of oestrogen (ethinylestradiol) AND progesterone (of varying types).
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159
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.
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160
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.
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161
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.
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162
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.

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163
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.
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164
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.
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165
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.
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166
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).
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167
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.
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168
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.
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169
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.
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170
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.

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171
Q

POP
What is the POP?

A
  • Pill containing only progesterone, taken continuously with fewer contraindications + risks compared with the COCP.
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172
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.

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173
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.
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174
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.
175
Q

POP
What is the UKMEC4 criteria for POP?

A
  • Active breast cancer.
176
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.
177
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).
178
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.
179
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).
180
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.
181
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.
182
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.

183
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
184
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.
185
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.
186
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.
187
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.
188
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.
189
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.
190
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.
191
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.
192
Q

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

A
  • Active breast cancer.
193
Q

COILS
What are the coils?

A
  • Device inserted into uterus to provide contraception offering long-acting reversible contraception.
194
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.
195
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.
196
Q

COILS
What are the contraindications to the coils?

A
  • PID or infection,
  • immunosuppression,
  • pregnancy,
  • unexplained bleeding,
  • pelvic cancer,
  • uterine cavity distortion (fibroids).
197
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.
198
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.
199
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.
200
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
201
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.
202
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.
203
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).
204
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.
205
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.
206
Q

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

A
  • Copper IUD
  • PO Ulipristal acetate (ellaOne)
  • PO levonorgestrel (levonelle)
207
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

208
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

209
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

210
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

211
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

212
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

213
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.
214
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.
215
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.
216
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.
217
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.
218
Q

FEMALE INFERTILITY
What is infertility?

A
  • Failure to conceive after 1 year of regular (2–3/7) unprotected sex.
219
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

220
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.
221
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

222
Q

FEMALE INFERTILITY
What are some risk factors of infertility?

A
  • Extremes of weight
  • Increasing age
  • Smoking
  • Alcohol/drug use
223
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
224
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
225
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)
226
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
227
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.
228
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
229
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
230
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
231
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

232
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
233
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

234
Q

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

A

Klinefelter’s,
Y chromosome deletions

235
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

236
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)
237
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
238
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
239
Q

MALE INFERTILITY
How would you manage azoospermia?

A
  • Surgical sperm recovery or donor insemination
240
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)
241
Q

ASSISTED CONCEPTION
What counts as one cycle of IVF?

A
  • Ovarian stimulation + collection of oocytes.
  • May have several embryos + may be frozen.
242
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
243
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.
244
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
245
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
246
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
247
Q

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

A
  • Younger age.
  • Lower BMI.
  • PCOS.
  • Higher antral follicle count.
248
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.
249
Q

ASSISTED CONCEPTION
How do you manage ovarian hyperstimulation syndrome?

A
  • PO fluids
  • Monitor urine output
  • LMWH
  • Paracentesis for ascites
  • IV colloids
250
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.
251
Q

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

A

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

252
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.

253
Q

COILS
What might non-visible threads indicate?

A
  • ?expulsion,
  • ?pregnancy,
  • ?uterine perforation
    > USS or XR, hysteroscopy/laparoscopy as last line.
254
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).

255
Q

COILS
What are the starting instructions for IUS?

A
  • Up to day 7 = immediate protection.
  • > Day 7 = extra contraception for 7d
256
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.
257
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

258
Q

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

A

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

259
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).

260
Q

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

A

Steroid abuse,
vasectomy

261
Q

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

A

Testicular cancer

262
Q

MALE INFERTILITY
How would you manage hormonal causes of infertility?

A
  • Gonadotrophins if hypogonadotrophic hypogonadism, bromocriptine if hyperprolactinaemia + sexual dysfunction
263
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.
264
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

265
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
266
Q

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

A

First-void urine sample for NAAT,
?bloods

267
Q

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

A

strong topical corticosteroids (clobetasol)

268
Q

NEWBORN SCREENING
What types of newborn screening are there?

A
  • Newborn infant physical examination (NIPE)
  • Newborn blood spot conditions
  • Newborn hearing screen
269
Q

NEWBORN SCREENING
When is the NIPE done?
What for?

A
  • First within 72h of birth + Second by GP at 6–8w
  • Screens for problems with hips, eyes, heart + genitalia
270
Q

NEWBORN SCREENING
What is the process of the newborn blood spot conditions screen (Guthrie/heel-prick)?

A
  • Screening on day 5–9
  • Residual blood spots stored for 5 years (part of consent process) for research
271
Q

NEWBORN SCREENING
What conditions does the newborn blood spot screen for?

A

3 genetic –
- Sickle cell disease
- Cystic fibrosis
- Congenital hypothyroidism
6 inherited metabolic –
- Phenylketonuria
- Medium-chain acyl-CoA dehydrogenase deficiency
- Maple syrup urine disease
- Isovaleric acidaemia
- Glutaric aciduria type 1
- Homocystinuria

272
Q

NEWBORN SCREENING
What is the rough incidence of…

i) sickle cell disease?
ii) cystic fibrosis?
iii) congenital hypothyroidism?
iv) phenylketonuria?
v) MCADD?
vi) MSUD?
vii) IVA?
viii) GA1?
ix) homocystinuria?

A

i) 1 in 2000
ii) 1 in 2500
iii) 1 in 3000
iv) 1 in 10,000
v) 1 in 10,000
vi) 1 in 150,000
vii) 1 in 150,000
viii) 1 in 300,000
ix) 1 in 300,000

273
Q

NEWBORN SCREENING
What specifically is tested for in…

i) cystic fibrosis?
ii) congenital hypothyroidism?
iii) phenylketonuria?

A

i) Immunoreactive trypsinogen
ii) TSH
iii) Phenylalanine

274
Q

NEWBORN SCREENING
What is phenylketonuria?
What are the features of phenylketonuria?
What is the management?

A
  • AR defect in phenylalanine hydroxylase (C12)
  • LDs, seizures, ‘musty’ odour to urine + sweat, (fair hair, blue eyes)
  • Phenylalanine restricted diet
275
Q

NEWBORN SCREENING
What is the management of MCADD?

A
  • Avoid long periods with no food
  • High sugar drinks when ill
276
Q

NEWBORN SCREENING
What does MSUD, IVA and GA1 have in common?
What are their differences?
What is the management?

A
  • Issues with processing amino acids
  • MSUD = leucine, isolecine + valine
  • IVA1 = leucine
  • GA1 = lysine, hydroxylysine + tryptophan
  • Limit high protein foods
277
Q

NEWBORN SCREENING
What is homocystinuria?
How does it present?
What is the management?

A
  • Cystathionine synthetase deficiency
  • Developmental delay, MSK like Marfan, fair complexion, brittle hair, dislocation of lens
  • Pyridoxine (vitamin B6)
278
Q

NEWBORN SCREENING
What is the newborn hearing screening?
Why is it done?

A
  • All babies screened within 4w of birth ideally (up to 3m)
  • Early identification crucial for developing speech, language + social skills
279
Q

NEWBORN SCREENING
What does the newborn hearing screen involve?
What is the outcome?

A
  • Automated otoacoustic emission (AOAE) test with some babies needing automated auditory brainstem response (AABR) test
  • Refer to audiology within 4w if no clear response with one or both ears
280
Q

PREGNANCY PHYSIOLOGY
What hormones increase in regards to the anterior pituitary gland?

A
  • ACTH = rise in steroid hormones (cortisol, aldosterone) = improves autoimmune conditions (RA) but susceptible to DM + infections
  • Prolactin = suppresses FSH + LH
  • Melanocyte stimulating hormone = increased skin pigmentation (linea nigra + melasma = brown pigmentation)
281
Q

PREGNANCY PHYSIOLOGY
What other hormones rise in pregnancy?

A
  • T3/T4
  • HCG = doubles every 48h until plateau at 8–12w then gradual fall
  • Progesterone
  • Oestrogen
282
Q

PREGNANCY PHYSIOLOGY
What changes occur to the uterus in pregnancy?

A
  • Increase from 100g–1.1kg
  • Hyperplasia + hypertrophy of myometrium
  • Decidual spiral arteries remodelled for wide bore low resistance
283
Q

PREGNANCY PHYSIOLOGY
What changes occur to the cervix in pregnancy?

A
  • Increased oestrogen = ?cervical ectropion + increased discharge
  • Before delivery, prostaglandins break down collagen in cervix = dilate + efface
  • Chadwick’s sign = early pooled deoxygenated blood > blue tinge
284
Q

PREGNANCY PHYSIOLOGY
What changes occur to the vagina in pregnancy?

A
  • Oestrogen > hypertrophy of vaginal muscles + increased PV discharge
  • Makes bacterial + candida infection more common
285
Q

PREGNANCY PHYSIOLOGY
What changes occur to the breasts?

A
  • Increased size with increased gestation
  • Fat deposition around gland tissue
286
Q

PREGNANCY PHYSIOLOGY
In terms of the cardiovascular system in pregnancy, what…

i) increases?
ii) decreases?

A

i) Blood volume, plasma volume, CO (as increased SV + HR)
ii) Peripheral vascular resistance (can cause flushing + hot sweats) + BP in early-mid pregnancy but returns to normal by term

287
Q

PREGNANCY PHYSIOLOGY
What changes can occur to the vascular system?

A
  • Varicose veins due to peripheral vasodilation + obstruction of IVC by uterus
288
Q

PREGNANCY PHYSIOLOGY
What CVS anatomical changes are there?

A
  • Diaphragmatic elevation > heart displaced upwards/left so apex moved laterally
  • Increased ventricular muscle mass + increased LV/LA size
  • Altered QRS (LAD), ECG changes (inverted T waves) + flow (ES) murmurs
289
Q

PREGNANCY PHYSIOLOGY
In terms of the respiratory system, what are the mechanical changes?

A
  • Increased subcostal angle, pulmonary blood flow + tidal volume
  • Decreased vital capacity + functional residual capacity
  • Progesterone causes trachea-bronchial smooth muscle relaxation
290
Q

PREGNANCY PHYSIOLOGY
In terms of the respiratory system, what are the biochemical changes?

A
  • Increased oxygen consumption (20%) + RR
  • Compensated resp alkalosis may occur as increased pO2 + reduced pCO2 (facilitates foetal CO2 excretion), renal HCO3- excretion to prevent this
  • Increased 2,3 DPG to promote maternal Hb to release oxygen
291
Q

PREGNANCY PHYSIOLOGY
In terms of the renal system, what…

i) increases?
ii) decreases?

A

i) Blood flow to kidneys (so GFR), aldosterone (Na + water reabsorption + Retention), protein excretion
ii) Serum creatinine, urate + albumin

292
Q

PREGNANCY PHYSIOLOGY
What can happen in terms of the urinary system?
What is a consequence of this?
What else contributes?

A
  • Dilatation of ureters + collecting system > physiological hydronephrosis (more R)
  • Increased risk of UTIs
  • Decreased ureter tone/peristalsis = urinary stasis
293
Q

PREGNANCY PHYSIOLOGY
What 4 forces/pressures govern fluid retention in pregnancy?

A
  • Capillary (hydrostatic) pressure of blood in vessel = draws fluid OUT
  • Interstitial fluid colloid oncotic pressure of proteins in interstitial fluid = draws fluid OUT
  • Interstitial fluid pressure of tissues surrounding vessel = draws fluid IN
  • Plasma colloid oncotic pressure (albumin) = draws fluid IN
294
Q

PREGNANCY PHYSIOLOGY
Why does pregnancy cause dilutional anaemia?
What is the purpose of this?

A
  • Increased RBC production = higher iron, folate + B12 requirements
  • Increased ECF + plasma volume MORE than RBC volume leading to lower red cell conc (haematocrit) + lower Hb conc
  • Facilitates placental perfusion
295
Q

PREGNANCY PHYSIOLOGY
What happens in terms of clotting in pregnancy?

A
  • Clotting factors (fibrinogen, VII, VIII + X) increase
  • Plasminogen activator inhibitor increases (plasmin usually breaks clots down)
  • Hypercoaguable state
296
Q

PREGNANCY PHYSIOLOGY
In terms of haematology in pregnancy, what…

i) increases?
ii) decreases?

A

i) WBCs, ESR, d-dimers, ALP
ii) Platelets, albumin

297
Q

PREGNANCY PHYSIOLOGY
What are the metabolic changes are there in pregnancy?

A
  • Early = post-prandial glucose plasma peak lower due to fat deposition + glycogen storage
  • Late = higher for longer + maternal insulin resistance (via hPL) for foetal glucose sparing
  • Maternal insulin rises during most of pregnancy
298
Q

PREGNANCY PHYSIOLOGY
What are the changes to the skin and hair in pregnancy?

A
  • Linea nigra + melasma
  • Striae gravidarum
  • General pruritus (?OC)
  • Spider naevi + palmar erythema
  • PP hair loss normal, improves within 6m
299
Q

PREGNANCY PHYSIOLOGY
What facilitates blastocyst implantation in pregnancy?

A
  • Increased GFs, proteolytic enzymes + inflammatory mediators
  • Not rejected as change in self/non-self pattern recognition molecules (HLA + MHC proteins)
300
Q

PREGNANCY PHYSIOLOGY
In pregnancy, what changes to the humoral and cell-mediated immunity?

A
  • Humoral = unchanged, plenty of circulating Th2 cells to fight infections (antibodies)
  • Cell-mediated = reduced as progesterone down regulates production of Th1 cells (phagocytes, cytotoxic T lymphocytes)
301
Q

PREGNANCY PHYSIOLOGY
What is the impact of dampening Th1 production?
What are the implications?

A
  • Shift to increased Th2 production (bias) to protect foetus
  • Pre-eclampsia, IUGR + miscarriage do not have a Th2 bias
302
Q

REPRODUCTION
What are the different stages in follicular genesis and what stage in the cell cycle are they?

A
  • Primordial follicles = diploid, arrested at prophase I
  • Primary follicle = diploid, undergoing meiosis I
  • Secondary follicle = haploid, once meiosis I complete
  • Antral (Graafian) follicle = haploid, frozen in metaphase II
303
Q

REPRODUCTION
What are the structures of…

i) primordial follicles?
ii) primary follicles?

A

i) Each contain primary oocyte (germ cells) that eventually form mature ovum
ii) Primary oocyte > zona pellucida > cuboidal granulosa cells, zona pellucida secreted from granulosa cells

304
Q

REPRODUCTION
What happens when follicles reach the secondary follicle stage?

A
  • Granulosa cells express FSH receptors = oestrogen production to grow
  • Theca cells express LH receptors = steroidogenesis
305
Q

REPRODUCTION
How is a dominant follicle chosen?

A
  • Fluid-filled chamber (antrum) starts to develop causing rapid growth
  • Rising LH leads to rising oestrogen
  • Dominant follicle with lots of FSH receptors outgrows the others
306
Q

REPRODUCTION
What happens at ovulation?

A
  • LH surge = smooth muscle of theca externa contracts
  • Follicle bursts + secretes enzymes puncturing hole in ovary
  • Fimbriae of fallopian tubes sweeps oocyte up, surrounded by zona pellucida
  • Leftover follicle > corpus luteum
307
Q

REPRODUCTION
How does fertilisation occur?

A
  • Sperm enters fallopian tube + attempts to penetrate through corona radiata + zona pellucida via acrosome reaction
  • Fusion of sperm + egg = zygote
308
Q

REPRODUCTION
What happens immediately after fertilisation?

A
  • Cell rapidly divides > mass of cells (morula) travels to uterus
  • Fluid filled cavity (blastocele) expands to form blastocyst (>80 cells) with outer layer (trophoblast) + inner layer (embryoblast)
309
Q

REPRODUCTION
When does the blastocyst reach the uterus?
What happens?

A
  • 8–10d after ovulation
  • Trophoblast cells undergo adhesion to stroma of endometrium
  • Outer layer of trophoblast (syncytiotrophoblast) forms projections into the stroma
310
Q

REPRODUCTION
Once the blastocyst has implanted, what happens to the stroma?
What signifies blastocyst implantation?

A
  • Cells of stroma convert into decidua to provide nutrients (decidual reaction)
  • Syncytiotrophoblast produces hCG to maintain corpus luteum
311
Q

REPRODUCTION
What happens to the embryoblast after implantation?

A
  • Divides into yolk sac + amniotic cavity on opposing sides with embryonic disc between
  • Chorion surrounds this complex with inner cytotrophoblast + outer syncytiotrophoblast which is embedded in endometrium
312
Q

REPRODUCTION
How does the chorion develop over time?

A
  • Chorionic cavity forms around the yolk sac, embryonic disc + amniotic sac + these structures suspended from the chorion by the connecting stalk (eventually umbilical cord)
313
Q

REPRODUCTION
When does the embryonic disc develop further?
What does it develop into?

A
  • 5w
  • Foetal pole with 3 layers = ectoderm (outer), mesoderm (mid), endoderm (inner)
314
Q

REPRODUCTION
What tissues does the…

i) ectoderm
ii) mesoderm
iii) endoderm

produce?

A

i) Skin, hair, nails, teeth, CNS
ii) Heart, muscle, bone, connective tissue, kidneys, blood
iii) GI tract, lungs, liver, pancreas, thyroid, reproductive

315
Q

REPRODUCTION
When do actual organs begin to develop?

A
  • 6w foetal heart forms + starts to beat
  • 8w all major organs start development
316
Q

REPRODUCTION
How does the placenta develop?

A
  • Syncytiotrophoblast forms chorionic villi with foetal blood vessels
  • Those nearest connecting stalk most vascular, cells proliferate + become placenta at about 10w
317
Q

REPRODUCTION
How is nutrient diffusion facilitated in terms of how the placenta develops?

A
  • Spiral arteries reduce their vascular resistance (narrow bore high resistance > wide bore low)
  • Makes them more fragile so blood flows out causing pools of blood (lacunae) at 20w surrounding chorionic villi for diffusion
318
Q

REPRODUCTION
What role does the placenta play in immunity?

A
  • IgG crosses placenta to give foetus immunity
  • Primary immune deficiency hypogammaglobulinaemia can occur in babies whose mothers did not have high enough IgG during pregnancy
319
Q

REPRODUCTION
What role does the placenta play in respiration?

A
  • Oxygen source for foetus, foetal Hb has higher affinity for oxygen so extracts it from maternal blood
  • CO2, H+, HCO3- + lactic acid exchanged to maintain acid-base balance
320
Q

REPRODUCTION
What role does the placenta play in nutrition and excretion?

A
  • Main source = glucose, can transfer vitamins + minerals as well as alcohol + meds
  • Similar function to kidneys, filters foetal waste (urea + creatinine)
321
Q

REPRODUCTION
What are the main hormones produced by the placenta?

A
  • hCG (maintain corpus luteum)
  • Oestrogen
  • Progesterone
  • Human placenta lactogen
322
Q

REPRODUCTION
What is the role of oestrogen in pregnancy?

A
  • Softening tissue > more flexible, allows muscles + ligaments of uterus and pelvis to expand + cervix become soft
  • Enlarges + prepares breasts + nipples for breast feeding
  • E3 declines with foetal distress, E2 increases endometrial progesterone receptors
323
Q

REPRODUCTION
What is the role of progesterone in pregnancy?

A
  • Produced by corpus luteum until 10w
  • Initially prepares endometrium for implantation by proliferation, vascularisation + decidual reaction
  • Later, maintains pregnancy by preventing contraction
  • Relaxation elsewhere > heartburn, constipation, hypotension
324
Q

REPRODUCTION
What is the role of human placental lactogen in pregnancy?

A
  • Diabetogenic as raises blood glucose levels to help increase nutrient supply + helps convert mammary glands into milk secreting tissue
325
Q

MENSTRUAL CYCLE
When is the last menstrual period?

A
  • 1st day of last period (cycle runs from 1st day of last to 1st day of next
326
Q

MENSTRUAL CYCLE
What 2 cycles exist within the menstrual cycle?

A
  • Ovarian cycle (development of follicle + ovulation)
  • Uterine cycle (functional endometrium thickens + shreds)
327
Q

MENSTRUAL CYCLE
What happens in the menstrual phase?

A
  • Old endometrial lining from previous cycle shed marking day 1 (lasts 5d)
328
Q

MENSTRUAL CYCLE
What happens in the follicular phase?

A
  • Independently primordial follicles mature into primary + secondary follicles with FSH receptors
  • Low oestrogen + progesterone = pulses of GnRH > LH + FSH release
  • FSH leads to follicular development + recruitment
329
Q

MENSTRUAL CYCLE
What happens as secondary follicles grow during follicular phase?

A
  • Theca cells develop LH receptors + secrete androgens
  • Granulosa cells develop FSH receptors + secrete aromatase
  • Leads to increased oestrogen > -ve feedback on pituitary to reduce LH + FSH leading to some follicles to regress
330
Q

MENSTRUAL CYCLE
What occurs during ovulation?

A
  • Follicle (dominant) with most FSH receptors continues developing
  • Secretes further oestrogen which at a threshold causes spike in LH (+ slight rise in FSH) causing release of ovum on day 14
331
Q

MENSTRUAL CYCLE
What occurs during the luteal phase?

A
  • Dominant follicle > corpus luteum + luteinised granulosa cells converts cholesterol into progesterone for 10d to facilitate implantation + reduce FSH/LH + oestrogen
  • Also secretes inhibin to reduce FSH
332
Q

MENSTRUAL CYCLE
What happens if the egg is fertilised?

A
  • Syncytiotrophoblast of embryo secretes human chorionic gonadotropin (hCG) which maintains corpus luteum
333
Q

MENSTRUAL CYCLE
What happens if the egg is not fertilised?

A
  • hCG absence > corpus luteum degenerates into corpus albicans
  • Fall in progesterone + oestrogen causes endometrium to breakdown + menstruation occurs
  • FSH + LH levels rise
  • Stromal cells of endometrium release prostaglandins to encourage endometrium breakdown + uterine contraction
334
Q

MENSTRUAL CYCLE
What happens in the early secretory phase of the menstrual cycle?

A
  • Progesterone mediated + signals ovulation occurred to make endometrium receptive, cause spiral arteries to grow longer + uterine glands to secrete more mucus
335
Q

MENSTRUAL CYCLE
What happens in the late secretory phase of the menstrual cycle?

A
  • Cervical mucus thickens + less hospitable for sperm
  • Decrease in oestrogen + progesterone > spiral arteries collapse + constrict + functional layer prepares to shred
336
Q

MENSTRUAL CYCLE
What are the stages of the menstrual cycle?

A
  • Menstruation (Days 1-5)
  • Proliferation (Days 6-14)
  • Ovulation (Day 14)
  • Secretion (Days 16-28)
337
Q

MENSTRUAL CYCLE
What happens in the proliferative phase?

A
  • High oestrogen > thickening of endometrium, growth of endometrial glands + emergence of spiral arteries from stratum basalis to feed the functional endometrium
  • Consistency of cervical mucus changes to make more hospitable for sperm
338
Q

NON-INVASIVE DUCTAL CARCINOMA IN SITU (DCIS)
What is the pathology?

A
  • Epithelial lining of breast ducts thickens as cells proliferate, often with central necrosis
  • Microcalcification on mammography, unifocal lesion in one area of breast
339
Q

BREAST CANCER
What are the 2 most common histological types of invasive breast cancer?

A
  • Invasive ductal carcinoma (70%) = invaded basement membrane, grows as little hard nots in breast
  • Lobular carcinoma (10%) = harder to feel, less likely to be visible on mammography, more diffuse so difficult to excise
340
Q

BREAST CANCER
What are some other types of breast cancer?

A
  • Inflammatory breast cancer (presents like mastitis, no Abx response)
  • Medullary cancers (younger)
  • Colloid/mucoid cancers (elderly)
  • Breast sarcomas, phyllodes tumour + lymphoma rare
341
Q

PAGET’S DISEASE OF THE NIPPLE
What is Paget’s disease of the nipple?

A
  • Eczematous change of nipple (affects nipple primarily and then spreads to areola)
  • Suspect if nipple eczema unresolved with 2w of steroid or anti-fungal cream
342
Q

PAGET’S DISEASE OF THE NIPPLE
What causes Paget’s disease of the nipple?

A
  • Infiltration of tumours cells through the ducts onto nipple surface where they infiltrate the epidermis
343
Q

BREAST CANCER
What is the epidemiology of breast cancer?

A
  • 1 in 8 women will develop breast cancer in their lifetime
  • Most common cancer in women + second most common cause of death
344
Q

BREAST CANCER
What are some modifiable risk factors of breast cancer?

A
  • Weight
  • Exercise
  • Smoking
  • Alcohol consumption
  • HRT for >5 years
  • OCP
  • post-menopausal obesity
  • first child birth >35
345
Q

BREAST CANCER
What are some non-modifiable risk factors of breast cancer?

A
  • Female (99%)
  • Breast density
  • Age of menarche + menopause
  • BRCA1/2 status + FHx
  • Increasing age
  • Nulliparous
  • Not breastfeeding
  • HRT use >5y
346
Q

BREAST CANCER
What are some protective factors of breast cancer?

A
  • Breastfeeding
  • Multiparity
  • Late menarche + early menopause
347
Q

BREAST CANCER
What are the 2 main genes involved in breast cancer and how do they act?

A
  • BRCA1 = mutation of C17, 60-80% lifetime risk, stronger incidence
  • BRCA2 = mutation of C13, 45% lifetime risk
  • Tumour suppression genes that act as inhibitors of cellular growth
348
Q

BREAST CANCER
What are some other genetic mutations associated with breast cancer?

A
  • TP53 (Li Fraumeni)
  • Peutz-Jeghers
349
Q

BREAST CANCER
What is the classic clinical presentation of breast cancer?

A
  • Normal appearing breast with palpable painless lump
  • Pain + tenderness uncommon
  • Visually = nipple inversion, bloody nipple discharge
350
Q

BREAST CANCER
What are some clinical signs of breast cancer?

A
  • Hard, irregular, painless, fixed lesions tethered to skin or chest wall
  • Indrawn nipple, peau d’orange (skin tethering), oedema or erythema
  • Palpable axillary nodes (axillary > supraclavicular > infraclavicular > neck)
351
Q

BREAST CANCER
What warrants an urgent 2ww cancer referral?
What happens under the 2ww referal?

A
  • ≥30 with unexplained breast lump ± pain
  • ≥50 with discharge, retraction or other change of concern
  • Triple assessment
352
Q

BREAST CANCER
What is the triple assessment?
What happens at end?

A
  • Clinical assessment (Hx + Examination)
  • Imaging (<35 USS as dense tissue, >35 USS + mammography)
  • Biopsy (histology + cytology) with core needle biopsy (or fine needle aspiration)
  • Each scored /5 (1=ok, 5=malignant), aim for score concordance (repeat test if one really high)
  • Pt discussed + reviewed in breast MDT
353
Q

BREAST CANCER
What imaging choices are there for investigating breast cancer and what would influence your choice?

A
  • Mammography, high resolution USS (good at Dx + targeting biopsy)
  • MRI (good assessment of implants, dense breasts or high-risk screening)
354
Q

BREAST CANCER
If someone has breast cancer, what would you like to check now?

A
  • Oestrogen receptor (ER)
  • Human epidermal growth factor 2 (HER2)
  • Progesterone
  • Ki67 status
  • Nottingham Prognostic index = grade, size + nodal status to predict survival
355
Q

BREAST CANCER
What staging is used in breast cancer?

A
  • CT CAP for TNM staging
  • T1 = confined to breast, mobile
  • T2 = confined to breast + LN in ipsilateral axilla
  • T3 = fixed to muscle, locally advanced disease
  • T4 = fixed to chest wall, metastatic
356
Q

BREAST CANCER
What tumour marker can be used to monitor response to breast cancer treatment and disease recurrence?

A
  • CA 15-3
357
Q

BREAST CANCER SCREENING
What is the NHS breast screening programme?

A
  • Women 50–70 invited every 3 years for dual-view mammography
  • it improves stage at diagnosis so 5 year survival risen from 80% to 95%
358
Q

BREAST CANCER
What are the pros of breast cancer screening?

A
  • Earlier detection,
  • Reduces morbidity + mortality,
  • Detects asymptomatic cancers before present,
  • Not overly invasive
359
Q

BREAST CANCER
What are some reasons that a woman may be recalled for further views, USS or biopsy?

A
  • Mass (well or poorly defined, rough edges, spiculated = carcinoma)
  • Microcalcification (associated with DCIS)
  • Parenchymal deformity
  • Asymmetrical density
  • Clinical or technical recall
360
Q

BREAST CANCER
What is the high risk screening for breast cancer?

A

BRCA1/2 screening –
- 30–40 annual MRI
- 40–50 annual MRI + mammograms
- 50–60 annual mammogram (+ MRI if dense breasts)
- 60–70 triennial mammograms (+ MRI if dense breasts)

361
Q

BREAST CANCER
What is the management of BRCA1/2 women?

A
  • Genetic pedigree to identify at risk
  • Additional screening, lifestyle advice
  • ?Prophylactic tamoxifen or aromatase inhibitors
  • ?Risk reducing salpingo-oopherectomy or mastectomy
362
Q

BREAST CANCER
What are some complications of breast cancer?

A
  • Locally advanced (rare), try shrink with radio, chemo, or hormone therapy to try operate, salvage surgery + stage for mets
  • Metastatic breast cancer (2Ls 2Bs) = Lungs, Liver, Bones, Brain
363
Q

METASTATIC BREAST CANCER
How may metastatic breast cancer present?

A
  • Bony pain or #
364
Q

BREAST CANCER
What is breast conservation treatment?

A
  • Lumpectomy or wide local excision where remaining breast tissue gets localised radiotherapy
365
Q

BREAST CANCER
What is mastectomy?

A
  • Uni or bilateral removal of breast
366
Q

BREAST CANCER
What is full axillary clearance?

A
  • Removal of all glands
367
Q

BREAST CANCER
What is limited axillary surgery?
What are the benefits?

A
  • Clinically normal glands but removal of targeted ‘hot’ node by sentinel LN biopsy or blindly removes 4–6 nodes
  • Day surgery, no significant complications, no drains, no effect on mortality but may need full clearance if +ve
368
Q

BREAST CANCER
What adjuvant endocrine therapy may be given to women?

A
  • All ER+ve women need endocrine therapy as increases survival
  • Bisphosphonates to reduce rate of bone mets in ER+ve
  • Trastuzumab (Herceptin) used in HER2+ve + chemo
369
Q

BREAST CANCER
What endocrine therapy is given if…

i) pre-menopausal?
ii) post-menopausal?

A

i) Tamoxifen –inhibits oestrogen receptor on breast cancer cells
ii) Anastrozole (aromatase inhibitors) – inhibits aromatase which converts androgens > oestrogen

370
Q

BREAST CANCER
What other adjuvant treatment may be offered?

A
  • Radiotherapy = always after WLE, sometimes after mastectomy if high risk (cons = skin viability risk, fibrosis, fat necrosis, loss of elasticity)
  • Chemotherapy = high/risk or aggressive disease (HER2+ve, ER-ve, node+ve)
371
Q

BREAST CANCER
Reconstruction surgery can either be primary (immediately) or delayed.
What are the pros and cons of primary reconstruction?

A
  • Increased skin preservation options, reduced psychological trauma
  • May delay chemo/radiotherapy if complications, radiotherapy may ruin results (fibrosis)
372
Q

BREAST CANCER
Reconstruction surgery can either be primary (immediately) or delayed.
What are the pros and cons of delayed reconstruction?

A
  • Minimal risks of delay in adjuvant therapies, healthy tissue used to recreate breast
  • Limited skin preservation options, psychological impact (no breast)
373
Q

BREAST CANCER
What are some options for breast mound recreation?

A
  • Implant based (implant alone or implant augmented latissimus dorsi)
  • Autologous (own tissues) such as TRAM flap, lat dorsi
  • Lat dorsi uses muscle ± skin ± fat but C/I if chronic back pain or physical hobby
374
Q

BREAST CANCER
What are some risks with breast mound recreation?

A
  • Capsule formation
  • Shape changes with age, gravity
  • Rupture
  • Infection
375
Q

BENIGN BREAST DISEASE
What are 3 main causes of benign breast lumps?

A
  • Nodularity
  • Fibroadenoma
  • Breast cyst
376
Q

BENIGN BREAST DISEASE
What is nodularity?
What is the management?

A
  • Normal variation, some ladies have lumpy breasts, often cyclical (more prominent pre-menstrual)
  • Re-examine after period as nodularity should lessen or disappear
377
Q

FIBROADENOMA
What is a fibroadenoma?

A
  • Benign tumours of stromal/epithelial breast duct tissue
378
Q

BREAST CYSTS
What are breast cysts?

A
  • fluid filled lumps
  • Abnormal response of part of the breast to hormonal stimulation, commonly seen in 40–60 year olds
379
Q

NIPPLE DISCHARGE
What are some causes of nipple discharge?

A
  • Duct ectasia
  • Duct papilloma
  • Galactorrhoea
  • Infection
380
Q

NIPPLE DISCHARGE
What are some features of surgically significant nipple discharge?

A
  • Persistent
  • Unilateral + unifocal
  • Spontaneous
  • Bloody or clear
381
Q

NIPPLE DISCHARGE
What are some differentials of bloody nipple discharge?

A
  • Duct papilloma
  • Duct ectasia
  • Occasionally invasive/in-situ Ca
382
Q

DUCT ECTASIA
What is duct ectasia?

A
  • Ducts become dilated + fill with debris, prone to secondary infections
383
Q

PAPILLOMA
What is duct papilloma?
How does it present?

A
  • Benign warty growth behind nipple
384
Q

BENIGN BREAST DISEASE
What is galactorrhoea?
How does breast infection nipple discharge present?

A
  • Milky (physiological or iatrogenic)
  • Purulent
385
Q

BREAST INFECTION
What are the 2 types of breast infection (mastitis)?

A
  • Lactational (usually peripheral in breast)
  • Non-lactational (associated with duct ectasia + so central)
386
Q

BREAST INFECTION
What is the management of lactational mastitis?

A
  • Continue breastfeeding
  • Rx if systemically unwell with flucloxacillin or erythromycin if allergic
  • May develop abscess (lump + erythema) so need drainage
387
Q

BREAST INFECTION
What is the management of non-lactational mastitis?

A
  • Same as lactational mastitis (flucloxacillin or erythromycin) but + metronidazole
388
Q

BREAST INFECTION
What is the most common cause of mastitis?
What is there a caution with?

A
  • S. Aureus then anaerobes (esp. non-lactational)
  • Repeated incision in non-lactational abscess as can develop mammary fistula which is difficult to treat
389
Q

BREAST PAIN
What is mastalgia?
What are the two types?

A
  • Breast pain
  • Cyclical = worse prior to and better after period
  • Non-cyclical (responds well to NSAIDs)
390
Q

BREAST PAIN
What is the management of cyclical mastalgia?

A
  • Supportive bra, reassurance, PO/topical analgesia
  • Danazol (weak androgen) but SEs = breast shrinkage, acne, weight gain
  • Tamoxifen (risk of endometrial cancer)
  • Goserelin
391
Q

GYNAECOMASTIA
What is gynaecomastia?
What is a differential?

A
  • > 2cm lump of breast tissue behind male nipple
  • Pseudo-gynaecomastia (deposition of fat in overweight men)
392
Q

GYNAECOMASTIA
What are the two broad causes of gynaecomastia?

A
  • Physiological = oestrogen + testosterone imbalance (puberty)
  • Pathological
393
Q

GYNAECOMASTIA
What are some pathological causes of gynaecomastia?

A
  • Drugs (spironolactone, oestrogen, anabolic steroids)
  • Marijuana
  • Liver failure
  • Testicular failure or tumour (Can produce beta-hCG)
394
Q

GYNAECOMASTIA
What is the management of gynaecomastia?

A
  • Older men >50 exclude breast cancer by biopsy
  • Remove or reverse cause/drug
  • Reassure teenagers
395
Q

BENIGN BREAST DISEASE
When investigating breast disease, what are features of a benign disease?

A
  • Breast exam = soft + mobile mass
  • Mammography = rounded mass, smooth edged, well-defined margins, low score
396
Q

NON-INVASIVE DUCTAL CARCINOMA IN SITU (DCIS)
How is it detected?

A
  • Asymptomatic on screening
  • Epithelial lining of breast ducts thickens as cells proliferate, often with central necrosis
397
Q

NON-INVASIVE DUCTAL CARCINOMA IN SITU (DCIS)
What is the pre-malignant form of breast cancer?

A
  • Non-invasive ductal carcinoma in situ (DCIS)
398
Q

BREAST CANCER SCREENING
What is the process of mammography?

A

Breast pressed between 2 plates to flatten + improve resolution
- Cranio-caudal (CC) + medio-lateral oblique (MLO) views
- Graded 1 (normal) to 5 (likely malignant)

399
Q

PAGET’S DISEASE OF THE NIPPLE
What is the management?

A
  • Needs biopsy, excision via mastectomy or central (nipple excising) wide local excision
400
Q

BREAST CANCER
What are the cons of breast cancer screening?

A
  • ?Overdiagnosis (frail women Dx with small low-grade cancers),
  • Anxiety if recalled,
  • Low dose XR > small amount of malignancies
401
Q

METASTATIC BREAST CANCER
What is the management?

A
  • Bisphosphonates + denosumab, radio/chemo + Sx control
402
Q

BREAST CANCER
What are the indications for breast conservation treatment?

A
  • Small tumour relative to breast (<25%),
  • DCIS,
  • no previous radiotherapy,
  • not underneath nipple,
  • pt choice
403
Q

BREAST CANCER
What factors affect the outcome of breast conservation treatment?

A
  • Tumour size relative to breast,
  • position of tumour in breast (lateral more favourable),
  • radiotherapy fibrosis
404
Q

BREAST CANCER
What are the indications for a mastectomy?

A
  • Large tumour relative to breast size,
  • > 1 cancer in same breast, tumour under nipple,
  • immediate or delayed reconstruction,
  • pt choice
405
Q

BREAST CANCER
What are the indications + benefits of full axillary clearance?

A
  • Glands clinically involved,
  • good control,
  • no need for further surgery or axillary radiotherapy
406
Q

BREAST CANCER
What are the risks of full axillary clearance?

A
  • 10% lymphoedema,
  • high complication rate (seromas, arm stiffness, drains, axillary numbness),
  • extends surgical time
407
Q

FIBROADENOMA
What is the epidemiology?

A

most common 20-40yrs
responds to oestrogen so become less common after menopause

408
Q

FIBROADENOMA
What is the rule with fibroadenomas?

A
  • 1/3 shrink, 1/3 same, 1/3 enlarge
409
Q

FIBROADENOMA
How does it present?

A
  • Painless
  • Smooth
  • Round
  • Well circumscribed (well-defined borders)
  • Firm
  • Mobile (moves freely under the skin and above the chest wall)
  • Usually up to 3cm diameter
410
Q

FIBROADENOMA
What is the management?

A

reassurance + only remove if large

411
Q

BREAST CYSTS
What are features of a benign cyst?

A
  • Smooth
  • Well-circumscribed
  • Mobile
  • Possibly fluctuant
  • Dx confirmed on aspiration
412
Q

BREAST CYSTS
How is it managed?

A
  • aspiration
413
Q

DUCT ECTASIA
What is the management?

A

Expectant management
If symptoms persist then operation to remove affected ducts may be offered

414
Q

DUCT ECTASIA
How does it present?

A
  • Yellow, green, thick + occasionally bloody nipple discharge
  • lump behind the nipple
  • inverted nipple
  • pain (not common)
415
Q

BREAST CANCER
what is tamoxifen?

A

tamoxifen inhibits the oestrogen receptor on breast cancer cells
It increases survival by 15-25% in woman with ER+ cancer
give for 10 years in higher risk women

416
Q

BREAST CANCER
what are the complications of tamoxifen?

A

hot flushes
nausea
vaginal bleeding
rarely thrombosis and endometrial cancer

417
Q

BREAST CANCER
what are aromatase inhibitors?

A

letrozole
Inhibit aromatase enzyme responsible for the conversion of androgens to oestogen in post-menopausal woman
slightly better anticancer efficacy than tamoxifen

418
Q

BREAST CANCER
what are the side effects of aromatase inhibitors?

A

hot flushes
reduced bone density
joint pains

419
Q

BREAST CANCER
what is Her-2?

A

HER2-positive breast cancer is a breast cancer that tests positive for a protein called human epidermal growth factor receptor 2 (HER2), which promotes the growth of cancer cells

long known as a marker for poor prognosis

420
Q

BREAST CANCER
how is HER-2 breast cancer managed?

A

Currently 1 year of 3 weekly adjuvant Trastuzumab given alongside chemotherapy (usually FEC-T).

421
Q

BBREAST CANCER
how can you find impalpable cancers?

A

wire localisation

422
Q

BREAST CANCER
what are the problems with radiotherapy?

A
  • high rates of capsule formation with implants
  • skin viability risk
  • wound healing
  • loss of elasticity
  • fat necrosis
  • implant extrusion
423
Q

PAGET’S DISEASE OF THE NIPPLE
what are the signs and symptoms?

A
  • rash like eczema or psoriasis on nipple
  • ulcerations/scabs/bleeding
  • itching/burning
  • lump
  • signs and symptoms of breast cancer
424
Q

PAGET’S DISEASE OF THE NIPPLE
what are the risk factors?

A
  • old age
  • FHx of breast cancer
  • Previous breast cancer
  • overweight
  • excess alcohol
  • smoking
  • risk factors for breast cancer
425
Q

PAGET’S DISEASE OF THE NIPPLE
what are the risk factors?

A
  • old age
  • FHx of breast cancer
  • Previous breast cancer
  • overweight
  • excess alcohol
  • smoking
  • risk factors for breast cancer
426
Q

PAGET’S DISEASE OF THE NIPPLE
what are the investigations?

A

clinical examination
mammogram/USS
biopsy

427
Q

BREAST IMPLANTS
what are the different types?

A

saline - silicone shells filled with saline (some are pre-filled and others are filled during operation)

silicone gel - silicone shell filled with silicone gel. Feel more like real breasts but more risky if leak

428
Q

BREAST IMPLANTS
what is the problem with using radiotherapy on breast implants?

A

there is a high rate of capsule formation

429
Q

BREAST IMPLANTS
what are the complications?

A
  • capsule formation
  • infection
  • rupture and shape changes with age
  • can hamper sensitivity of mammograms
  • breast implant associated anaplastic large cell lymphoma (BIA-ALCL)
430
Q

BREAST INFECTION
what are the signs and symptoms of breast infections?

A
  • fever
  • decreased milk outflow
  • breast warmth
  • breast tenderness
  • breast firmness
  • breast swelling
  • flu-like symptoms
  • nipple discharge
  • nipple inversion
431
Q

BREAST INFECTION
what is a breast abscess?

A

a localised area of infection with a walled off collection of pus

432
Q

BREAST INFECTION
what is the management of breast abscesses?

A

aspiration + antibiotics + supportive care
surgical intervention only if aspiration and antibiotics repeatedly fail

433
Q

PAPILLOMA
what is the clinical presentation?

A
  • bloody or clear discharge from a single duct
434
Q

PAPILLOMA
what are the investigations?

A
  • USS
  • mammogram
  • biopsy
435
Q

PAPILLOMA
what is the management?

A
  • removal via vacuum assisted excision (VAE)
436
Q

PAPILLOMA
what are they associated with?

A

atypical hyperplasia - this increases the risk of developing breast cancer

MY REVISION - ALL PHASES (36 decks)

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