SEXUAL HEALTH + GUM TO DO Flashcards

1
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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2
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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3
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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4
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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5
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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6
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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7
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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8
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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9
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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10
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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11
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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12
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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13
Q

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

A
  • Painful erections
  • Dyspareunia
  • Urinary Sx
  • Soreness
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14
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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15
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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16
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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17
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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18
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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19
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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20
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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21
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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22
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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23
Q

SYPHILIS
What is the causative organism?

A

Treponema pallidum – spirochete (spiral-shaped) bacteria

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24
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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25
Q

HIV
What are high risk groups for HIV?

A

MSM,
IVDU,
commercial sex workers

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26
Q

HIV
When is HIV classified as AIDS?

A

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

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27
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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28
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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29
Q

BALANITIS
what are the causes?

A

candidiasis
dermatitis
bacterial
anaerobic
lichen planus
lichen sclerosis

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30
Q

BALANITIS
what are the acute causes?

A

candidiasis
dermatitis
bacterial
anaerobic

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31
Q

BALANITIS
what are the chronic causes?

A

lichen sclerosis
plasma cell of balanitis of Zoon

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32
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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33
Q

LYMPHOGRANULOMA VENEREUM
what is it?

A

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

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34
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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35
Q

LYMPHOGRANULOMA VENEREUM
what are the investigations?

A

swab PCR to detect chlamydia trachomatis

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36
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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37
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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38
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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39
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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40
Q

CHANCROID
what are the investigations?

A

clinical diagnosis
diagnosis can be confirmed using culture or PCR

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41
Q

CHANCROID
what is the management?

A

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

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42
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.
43
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.
44
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.

45
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.
46
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.
47
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).
48
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.
49
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.

50
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.

51
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.
52
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).
53
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).
54
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.
55
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
56
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.
57
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.
58
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.
59
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.
60
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.
61
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.
62
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.
63
Q

COILS
What are the contraindications to the coils?

A
  • PID or infection,
  • immunosuppression,
  • pregnancy,
  • unexplained bleeding,
  • pelvic cancer,
  • uterine cavity distortion (fibroids).
64
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.
65
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.
66
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.
67
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).
68
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.
69
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

70
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

71
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

72
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

73
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

74
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

75
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.
76
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

77
Q

FEMALE INFERTILITY
What are some risk factors of infertility?

A
  • Extremes of weight
  • Increasing age
  • Smoking
  • Alcohol/drug use
78
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
79
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)
80
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
81
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
82
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

83
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
84
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

85
Q

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

A

Klinefelter’s,
Y chromosome deletions

86
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

87
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)
88
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
89
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
90
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.
91
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
92
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
93
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
94
Q

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

A
  • Younger age.
  • Lower BMI.
  • PCOS.
  • Higher antral follicle count.
95
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.
96
Q

ASSISTED CONCEPTION
How do you manage ovarian hyperstimulation syndrome?

A
  • PO fluids
  • Monitor urine output
  • LMWH
  • Paracentesis for ascites
  • IV colloids
97
Q

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

A

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

98
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

99
Q

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

A

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

100
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).

101
Q

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

A

Steroid abuse,
vasectomy

102
Q

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

A

Testicular cancer

103
Q

MALE INFERTILITY
How would you manage hormonal causes of infertility?

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