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C TO REVISE - PHASE 3A > WOMENS HEALTH - SEXUAL HEALTH, BREAST AND EXTRA CONDITIONS > Flashcards

WOMENS HEALTH - SEXUAL HEALTH, BREAST AND EXTRA CONDITIONS Flashcards

1
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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2
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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3
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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4
Q

GONORRHOEA
What are the local complications of gonorrhoea?

A
  • Urethral strictures
  • Epididymo-orchitis + salpingitis (can lead to infertility)
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5
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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6
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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7
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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8
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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9
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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10
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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11
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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12
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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13
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 - accomodates but does not react
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14
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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15
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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16
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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17
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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18
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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19
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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20
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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21
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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22
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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23
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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24
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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25
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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26
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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27
Q

GONORRHOEA
What is the clinical presentation of gonorrhoea discharge?

A

Odourless purulent, can be green/yellow

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28
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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29
Q

SYPHILIS
What is the causative organism?

A

Treponema pallidum – spirochete (spiral-shaped) bacteria

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30
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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31
Q

CANDIDIASIS
What treatment should be used in pregnancy?

A

Clotrimazole in pregnancy as fluconazole can cause congenital abnormalities

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32
Q

BALANITIS
what are the causes?

A

candidiasis
dermatitis
bacterial
anaerobic
lichen planus
lichen sclerosis

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33
Q

BALANITIS
what are the acute causes?

A

candidiasis
dermatitis
bacterial
anaerobic

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34
Q

BALANITIS
what is the treatment for bacterial infection?

A

flucloxacillin or clarithromycin if penicillin allergic

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35
Q

BALANITIS
what is the treatment for anaerobic balanitis?

A

saline washing
oral metronidazole

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36
Q

LYMPHOGRANULOMA VENEREUM
what is it?

A

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

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37
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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38
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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39
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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40
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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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

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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43
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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44
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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45
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.
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46
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).
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47
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.
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48
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
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49
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.
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50
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.
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51
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.
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52
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.
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53
Q

COILS
What are the contraindications to the coils?

A
  • PID or infection,
  • immunosuppression,
  • pregnancy,
  • unexplained bleeding,
  • pelvic cancer,
  • uterine cavity distortion (fibroids).
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54
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.
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55
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.
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56
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).
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57
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

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58
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

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59
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

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60
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

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61
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

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62
Q

FEMALE INFERTILITY
What are some risk factors of infertility?

A
  • Extremes of weight
  • Increasing age
  • Smoking
  • Alcohol/drug use
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63
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
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64
Q

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

A
  • Younger age.
  • Lower BMI.
  • PCOS.
  • Higher antral follicle count.
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65
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.
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66
Q

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

A
  • Increased vascular endothelial growth factor (VEGF) from granulosa cells increases vascular permeability so fluid leaks from intravascular>extravascular space (oedema, ascites + hypovolaemia).
  • Gonadotrophins to mature follicles.
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67
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
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68
Q

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

A
  • TP53 (Li Fraumeni)
  • Peutz-Jeghers
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69
Q

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

70
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)
71
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)
72
Q

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

A
  • Same as lactational mastitis (flucloxacillin or erythromycin) but + metronidazole
73
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
74
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)
75
Q

DUCT ECTASIA
What is the management?

A

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

76
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

77
Q

BREAST CANCER
what are the complications of tamoxifen?

A

hot flushes
nausea
vaginal bleeding
rarely thrombosis and endometrial cancer

78
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

79
Q

BREAST CANCER
what are the side effects of aromatase inhibitors?

A

hot flushes
reduced bone density
joint pains

80
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
81
Q

1* AMENORRHOEA
What is primary amenorrhoea?

A

Absence of menstruation by –
- 14y if no secondary sexual characteristics (more indicative of a chromosomal abnormality)
- 16y with secondary sexual characteristics (breast buds)

82
Q

1* AMENORRHOEA
What is the difference between hypogonadotrophic hypogonadism and hypergonadotrophic hypogonadism?

A
  • Deficiency in gonadotrophins (LH + FSH) stimulating ovaries due to abnormal hypothalamus or pituitary means they do not respond by producing sex hormones (oestrogen)
  • Gonads fails to respond to stimulation of gonadotrophins meaning no negative feedback + increasing amounts of FSH/LH
83
Q

1* AMENORRHOEA
What are some causes of hypogonadotrophic hypogonadism?

A
  • Constitutional delay (temporary delay, no pathology, ?FHx)
  • Hypopituitarism
  • Kallmann’s (failure to start puberty + anosmia)
  • Excessive exercise, dieting or stress causes hypothalamic failure
  • Endo = Cushing’s, prolactinoma, thyroid
  • Damage (cancer, surgery)
84
Q

1* AMENORRHOEA
What are some causes of hypergonadotrophic hypogonadism?

A
  • Turner’s syndrome XO
  • Congenital absence of ovaries
  • Previous damage to gonads (torsion, cancer, infections like mumps)
85
Q

1* AMENORRHOEA
What are some other causes of primary amenorrhoea and how may they present?

A
  • Congenital adrenal hyperplasia (tall, deep voice, facial hair)
  • Androgen insensitivity syndrome (46XY but female phenotype)
  • Congenital malformations of genital tract (if ovaries unaffected = secondary sexual characteristics but no menses)
  • Gonadal dysgenesis (no ovaries or uterus form)
86
Q

1* AMENORRHOEA
What are some first line investigations for primary amenorrhoea?

A
  • Examination = signs of puberty, PV exam, BMI, visual fields
  • FBC + ferritin (anaemia), U+E for CKD, anti-TTG for coeliac, urinary beta-hCG crucial
87
Q

1* AMENORRHOEA
What hormonal blood tests would you do for primary amenorrhoea?

A
  • FSH + LH (low or high)
  • TFTs, prolactin (if indicated)
  • Free androgens raised in PCOS, AIS + CAH
  • Insulin-like growth factor I used for screening for GH deficiency
88
Q

2* AMENORRHOEA
What is secondary amenorrhoea?
What is oligomenorrhoea?

A
  • Previously normal menstruation ceases for >3m in a non-pregnancy woman
  • Where menses are >35d apart (up to 6m), can be ovarian normality but exclude PCOS
89
Q

2* AMENORRHOEA
What are the causes of secondary amenorrhoea?

A
  • Pregnancy (most common), breastfeeding, menopause (physiological)
  • Iatrogenic (contraception)
  • Hypothalamic/pituitary
  • Ovarian causes (PCOS, POI)
  • Thyroid, uterine pathology (Asherman’s)
  • Excessive exercise, stress or eating disorders
90
Q

2* AMENORRHOEA
What are the hypothalamic or pituitary causes of secondary amenorrhoea?

A
  • Sheehan’s syndrome = pituitary necrosis following PPH
  • Pituitary tumour like prolactinoma leading to hyperprolactinaemia which prevents GnRH
  • Trauma, radiotherapy or surgery
91
Q

2* AMENORRHOEA
How does excessive stress or eating disorders cause secondary amenorrhoea?

A
  • Hypothalamus reduces GnRH in times of stress > hypogonadotrophic hypogonadism to prevent pregnancy in adverse situations
92
Q

2* AMENORRHOEA
What hormonal tests would you do in secondary amenorrhoea?

A
  • Urine/blood beta-hCG
  • High FSH (POI)
  • Low FSH/LH (hypgonadotrophic hypogonadism)
  • High LH or LH:FSH ratio suggests PCOS
  • Free androgen raised in PCOS
  • Mid-luteal (day 21) progesterone to check ovulation happened
  • Prolactin + TFTs if indicated
93
Q

2* AMENORRHOEA
What is the management of…

i) hyperprolactinaemia?
ii) hypothalamic failure?

A

i) Bromocriptine or cabergoline (dopamine agonists)
ii) GnRH replacement

94
Q

POI
What are some causes of POI?

A
  • Majority idiopathic
  • Iatrogenic (chemo/radio, oophorectomy)
  • Autoimmune (coeliac, T1DM)
  • Genetic (FHx, Turner’s)
  • Infections (mumps, TB, CMV)
95
Q

POI
What are the complications of POI?

A
  • Higher risk of conditions due to lack of oestrogen > CVD, stroke, osteoporosis, dementia + cognitive impairment + Parkinsonism
96
Q

FGM
What is the WHO classification for the types of FGM?

A
  • 1 = partial or total clitoridectomy
  • 2 = excision
  • 3 = infibulation
  • 4 = all other non-medical harmful procedures incl. pricking, piercing, incising
97
Q

MACROSOMIA
What are the causes of macrosomia?

A
  • Constitutionally large or familial (parental height + weight)
  • Maternal diabetes, previous macrosomia, obesity or rapid weight gain
  • Overdue
  • Male baby
98
Q

INFECTIONS + PREGNANCY
What is Parvovirus?
What are the adverse effects?
What is the management?

A
  • Parvovirus B19 can give viral Sx then ‘slapped cheeks’ (erythema infectiosum)
  • Worse <20w = suppresses foetal erythropoiesis causing anaemia + foetal hydrops, death, pre-eclampsia-like (mirror) syndrome in women
  • Maternal IgM + IgG, supportive, refer to foetal medicine to monitor
99
Q

INFECTIONS + PREGNANCY
What is the management of HIV in pregnancy?

A
  • Normal vaginal delivery if viral load <50 copies/ml if. not c-section (IV zidovudine 4h before)
  • Neonatal zidovudine PO if maternal viral load <50 if not triple ART, both for 4–6w
  • Breastfeeding C/I
100
Q

THYROID + PREGNANCY
What is the management of hyperthyroidism in pregnancy?

A
  • Propylthiouracil is choice in 1st trimester (associated with maternal hepatic injury)
  • Carbimazole C/I until 2nd trimester as causes foetal abnormalities
  • If mother has stimulating antibodies, monitor foetal growth with USS
101
Q

THYROID + PREGNANCY
Is hypothyroidism in pregnancy common?
What is the prognosis of untreated hypothyroidism in pregnancy?
What is the management?

A
  • Yes
  • Early foetal loss + congenital hypothyroidism leading to impaired neurodevelopment
  • Aim for adequate replacement with levothyroxine (safe), especially in 1st trimester
102
Q

THYROID + PREGNANCY
What is post-partum thyroiditis?

A

3 stages –
- Thyrotoxicosis (3m)
- Hypothyroidism (3–6m)
- Normal thyroid function
Sx control of thyrotoxicosis, treat hypothyroidism with levothyroxine
Just need TFTs to Dx if within 12m of giving birth + Sx

103
Q

PREMATURITY
What is the prophylaxis for prematurity and how do they work?

A
  • Progesterone gel or pessary decreases activity of myometrium + prevents cervix remodelling in preparation for delivery
  • Cervical cerclage = ≥1 sutures to strengthen + keep cervix closed
  • ‘Rescue’ cerclage to halt delivery
104
Q

PREMATURITY
What are the indications for…

i) progesterone prophylaxis?
ii) cervical cerclage?
iii) ‘rescue’ cerclage?

A

i) Cervical length <25mm on TVS at 16–24w
ii) Cervical length <25mm on TVS at 16–24w, previous premature birth or cervical trauma (colposcopy, cone biopsy)
iii) Cervical dilatation without ROM at 16–27+6 with no infection, bleeding or contractions

105
Q

PREMATURITY
What is the acute management of prematurity?

A
  • Senior obs + neonate input
  • Foetal monitoring (CTG)
  • Tocolytics
  • Corticosteroids
  • IV magnesium sulfate
  • Consider delayed cord clamping or cord milking (increases circulating blood volume + Hb in baby)
106
Q

AMNIOTIC EMBOLISM
What are some risk factors for amniotic fluid embolism?
Presentation?

A
  • Increasing maternal age + ARM
  • Often around time of labour + delivery but can be postpartum
  • Sx = SOB, sweating, anxiety, seizures, haemorrhage
  • Signs = hypoxia, tachycardia + hypotension, may lead to cardiac arrest
107
Q

MATERNAL SEPSIS
What are the investigations for maternal sepsis?

A
  • Monitor Maternal Early Obstetric Warning Score (MEOWS)
  • Warning signs of sepsis (3Ts white with sugar)
108
Q

MATERNAL SEPSIS
What are the warning signs of sepsis?

A

3Ts white with sugar –
- Temp <36 or >38
- Tachycardia >90bpm
- Tachypnoea >20bpm
- WCC >12 or <4
- Hyperglycaemia >7.7mmol/L in absence of diabetes

109
Q

MATERNAL SEPSIS
What are the SEPSIS 6 components?

A

BUFALO (3 in, 3 out) –
- Blood cultures (out)
- Urine output by catheter (hourly, out)
- Fluids resus (IV, in)
- Abx (IV broad-spec, in)
- Lactate (ABG, out)
- Oxygen (high flow SpO2 >94%, in)

110
Q

PUERPERIUM
What are some drug contraindications in breastfeeding?

A
  • Abx (ciprofloxacin, tetracyclines, chloramphenicol)
  • Psych drugs (lithium, BDZs)
  • Amiodarone, aspirin
  • Carbimazole, methotrexate
  • Sulfonylureas
  • Cytotoxic drugs
111
Q

PUERPERIUM
What are the pros + cons of breast feeding?

A
  • Readily available good nutrition, cheaper, contraceptive effect, decrease childhood infections (gastroenteritis), decrease in necrotising enterocolitis
  • Feed more often, uncomfortable + pain (mastitis)
112
Q

SHEEHAN’S SYNDROME
What is Sheehan’s syndrome?

A
  • Drop in circulating blood volume leads to avascular necrosis of the pituitary gland
  • Ischaemia + infarction of anterior pituitary cells as supplied by hypothalamo-hypophysial portal system which is susceptible to rapid drops in BP after PPH
113
Q

SHEEHAN’S SYNDROME
How does Sheehan’s syndrome present?
What is the management?

A
  • Reduced lactation (lack of prolactin)
  • Amenorrhoea (lack of LH + FSH > HRT)
  • Hypothyroidism (lack of TSH > levothyroxine)
  • Adrenal insufficiency (lack of ACTH > hydrocortisone)
114
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
115
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

116
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

117
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)
118
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
119
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
120
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
121
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
122
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

123
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
124
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
125
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
126
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

127
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
128
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
129
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
130
Q

PREGNANCY PHYSIOLOGY
In terms of haematology in pregnancy, what…

i) increases?
ii) decreases?

A

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

131
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
132
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
133
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)
134
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)
135
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
136
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
137
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
138
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
139
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
140
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)
141
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
142
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
143
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)
144
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

145
Q

REPRODUCTION
When do actual organs begin to develop?

A
  • 6w foetal heart forms + starts to beat
  • 8w all major organs start development
146
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
147
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
148
Q

REPRODUCTION
What are the main hormones produced by the placenta?

A
  • hCG (maintain corpus luteum)
  • Oestrogen
  • Progesterone
  • Human placenta lactogen
149
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
150
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
151
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
152
Q

MENSTRUAL CYCLE
what are the roles of FSH and LH?

A

FSH - enables production of oestrogen
LH - enables production of progesterone

153
Q

MENSTRUAL CYCLE
what are the stages of the ovarian cycle?

A

follicular phase
luteal phase

154
Q

MENSTRUAL CYCLE
what happens during the follicular phase?

A
  • rising levels of FSH stimulates developing follicles to produce oestrogen
  • oestrogen inhibits FSH leading to one dominant follicle
  • follicle starts developing LH receptors
  • egg completes first meiotic division
  • oestrogen levels cause positive feedback leading to LH surge
155
Q

MENSTRUAL CYCLE
what causes the LH surge at the end of the follicular phase?

A

oestrogen levels cause positive feedback leading to LH surge

156
Q

MENSTRUAL CYCLE
what happens during the luteal phase?

A
  • follicle becomes corpus luteum (lifespan of 14 days)
  • corpus luteum secretes progesterone which peaks 7 days after ovulation unless maintained by pregnancy
  • falling progesterone causes menstrual bleeding
157
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
158
Q

MENSTRUAL CYCLE
What happens if the egg is fertilised?

A
  • Syncytiotrophoblast of embryo secretes human chorionic gonadotropin (hCG) which maintains corpus luteum
159
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
160
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)
161
Q

MENSTRUAL CYCLE
What happens during the menstrual phase?

A
  • falling levels of progesterone cause shedding of endometrium
  • spasm of spiral arteries
  • ischaemic necrosis
  • generalised inflammation
162
Q

MENSTRUAL CYCLE
What happens in the proliferative phase?

A
  • endometrium grows under influence of oestrogen
  • oestrogen causes hyperplasia of the endometrium
  • early development of glands and spiral arterioles
163
Q

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

A
  • after ovulation progesterone predominates
  • changes from focusing on growth to preparing for implantation
  • development of complex glands, increased spiral arterioles
  • endometrial cells produce and store glycogen
164
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
165
Q

CONTRACPETION
What is the method of action for COCP?

A

Inhibits ovulation

166
Q

CONTRACEPTION
what is the method of action for POP (excluding desogestrel)?

A

Thickens cerivcal mucus

167
Q

CONTRACEPTION
What is the method of action for desogestrel POP?

A

Primary = inhibits ovulation
Also thickens cervical mucus

168
Q

CONTRACEPTION
What is the method of action for injectable contraceptives (e.g. depo)?

A

Primary = inhibits ovulation
Also thickens cervical mucus

169
Q

CONTRACEPTION
What is the method of action for IUD?

A

Decreases sperm motility and survival

170
Q

CONTRACEPTION
What is the method of action for IUS?

A

Primary = prevents endometrial proliferation
Also thickens cervical mucus

171
Q

EMERGENCY CONTRACEPTION
What is the method of action for levonogestrel?

A

Inhibits ovulation

172
Q

EMERGENCY CONTRACEPTION
What is the method of action for ulipristal acetate?

A

Inhibits ovulation

C TO REVISE - PHASE 3A (11 decks)

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