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MY REVISION - ALL TO DO > TO DO BREAST + SEXUAL HEALTH > Flashcards

TO DO BREAST + SEXUAL HEALTH Flashcards

1
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
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2
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
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3
Q

BREAST CANCER
What are some protective factors of breast cancer?

A
  • Breastfeeding
  • Multiparity
  • Late menarche + early menopause
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4
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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5
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 nipple discharge, retraction or other change of concern in one nipple only
  • Triple assessment
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6
Q

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

A
  • CA 15-3
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7
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
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8
Q

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

A

ER-POSITIVE
- pre-menopausal = selective oestrogen receptor modulators (TAMOXIFEN)
- post-menopausal = aromatase inhibitor (ANASTROZOLE)

HER2 POSITIVE
- trastuzumab (HERCEPTIN)

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9
Q

BREAST INFECTION
What is the management of lactational mastitis?

A
  • Continue breastfeeding
  • Rx if systemically unwell with FLUCLOXACILLIN or erythromycin/clarithromycin if allergic
  • May develop abscess (lump + erythema) so need drainage
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10
Q

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

A
  • co-amoxiclav 500/125mg TDS for 10-14 days
  • erythromycin/clarithromycin + metronidazole for 10-14 days
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11
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
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12
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
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13
Q

GYNAECOMASTIA
What are some pathological causes of gynaecomastia?

A
  • Drugs (spironolactone, oestrogen, anabolic steroids, digoxin, finasteride)
  • Marijuana
  • Liver failure
  • Testicular failure or tumour (Can produce beta-hCG)
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14
Q

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

A
  • Needs biopsy, excision via mastectomy or central (nipple excising) wide local excision
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15
Q

METASTATIC BREAST CANCER
What is the management?

A
  • Bisphosphonates + denosumab, radio/chemo + Sx control
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16
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

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17
Q

BREAST CANCER
what are the complications of tamoxifen?

A

hot flushes
nausea
vaginal bleeding
rarely thrombosis and endometrial cancer

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18
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

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19
Q

BREAST CANCER
what are the side effects of aromatase inhibitors?

A

hot flushes
reduced bone density
joint pains

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20
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).

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21
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
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22
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)
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23
Q

BREAST INFECTION
what is the management of breast abscesses?

A

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

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24
Q

PAPILLOMA
what is the clinical presentation?

A
  • bloody or clear discharge from a single duct
  • typically in a premenopausal woman
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25
Q

PAPILLOMA
what is the management?

A
  • removal via vacuum assisted excision (VAE)
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26
Q

PHYLLODES TUMOUR
what is the characteristic appearance on histology?

A

leaf-like architecture

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27
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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28
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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29
Q

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

A

SYMPTOMS
- foul smelling ‘fishy’ vaginal odour
- greyish-white discharge
- 50% are asymptomatic

SIGNS
- thin, white homogenous discharge lining the vaginal walls and vestibule
- malodourous discharge
- vagina does NOT appear inflamed or irritated

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30
Q

BACTERIAL VAGINOSIS
What diagnostic criteria is used in BV?

A

Amsel’s (3/4)
- Thin, white discharge
- Vaginal pH >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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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 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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33
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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34
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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35
Q

SYPHILIS
What is the clinical presentation of primary syphilis?

A

SYMPTOMS
- single chancre (painless) on genitals
- occasionally chancre on throat, anus or intravaginally

SIGNS
- femoral lymphadenopathy (non-tender)

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36
Q

SYPHILIS
What is the clinical presentation of secondary syphilis?

A

SYMPTOMS
- fever
- headaches

SIGNS
- diffuse maculopapular rash on palms and soles
- patchy oral ulceration (snail track ulcers)
- condylomata lata (wart-like lesions at sites of skin friction)
- patchy alopecia (moth-eaten appearance)
- generalised lymphadenopathy (non-tender)

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37
Q

SYPHILIS
What is the clinical presentation of tertiary syphilis?

A

NEUROSYPHILIS
- meningovascular syphilis (stroke due to arteritis)
- argyll-robertson pupil (constricts to accommodation, but not to light)
- loss of intellect, insight, memory, spastic paraparesis
- tabes dorsalis (inflammaiton + degeneration of spinal dorsal columns)

CARDIOVASCULAR
- aortic aneurysm
- aortic regurgitation
- coronary ostia stenosis
- conduction defects

GUMMATOUS
- gumma = nodule that heals with central scarring

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38
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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39
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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40
Q

SYPHILIS
How would you manage syphilis?

A
  • Specialist GUM (full STI screening, contact tracing, contraceptive information).
  • early syphilis = Single dose IM benzathine benzylpenicillin or PO doxycycline if allergic
  • late latent/gummatous = 3 doses IM benzathine benzylpenicillin once weekly for 3 weeks
  • cardiovascular syphilis = 3 days of PO prednisolone + 3 once weekly doses IM benzathine benzylpenicillin
  • neurosyphilis = 14 days IM procaine penicillin + oral probenecid
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41
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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42
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
  • tender inguinal lymphadenopathy
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43
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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44
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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45
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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46
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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47
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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48
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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49
Q

CANDIDIASIS
What is the management of candidiasis?

A

1st line = oral fluconazole 150mg single dose
2nd line = clotrimazole 500mg intravaginal pessary single dose

  • if there are vulval symptoms, consider topical imidazole in addition to oral/intravaginal antifungal
  • if pregnant, only local treatments (creams/pessaries) may be used - oral is contraindicated
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50
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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51
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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52
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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53
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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54
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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55
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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56
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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57
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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58
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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59
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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60
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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61
Q

CHLAMYDIA
What is the clinical presentation of chlamydia in women?

A
  • Cervicitis (abnormal PV discharge, PCB, IMB),
  • dysuria,
  • dyspareunia
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62
Q

CHLAMYDIA
What is the clinical presentation of chlamydia in men?

A

Urethral discharge,
dysuria,
urethritis

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63
Q

GONORRHOEA
What is the clinical presentation of gonorrhoea in women?

A

Cervicitis (PV discharge, PCB, IMB, dyspareunia)

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64
Q

GONORRHOEA
What is the clinical presentation of gonorrhoea discharge?

A

Odourless purulent, can be green/yellow

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65
Q

BACTERIAL VAGINOSIS
What causes BV to occur less frequently?

A

Less frequent if COCP or effective condom usage

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66
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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67
Q

SYPHILIS
What is the causative organism?

A

Treponema pallidum – spirochete (spiral-shaped) bacteria

68
Q

HIV
When is HIV classified as AIDS?

A

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

69
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

70
Q

BALANITIS
what are the acute causes?

A

candidiasis
dermatitis
bacterial
anaerobic

71
Q

BALANITIS
what are the chronic causes?

A

lichen sclerosis
plasma cell of balanitis of Zoon

72
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
73
Q

BALANITIS
what is the general management for balanitis?

A
  • gentle saline washes
  • ensuring to wash foreskin properly
  • 1% hydrocortisone for short period
74
Q

BALANITIS
what is the treatment for bacterial infection?

A

flucloxacillin or clarithromycin if penicillin allergic

75
Q

BALANITIS
what is the treatment for anaerobic balanitis?

A

saline washing
oral metronidazole

76
Q

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

A

mild topical corticosteroids (hydrocortisone)

77
Q

LYMPHOGRANULOMA VENEREUM
what is it?

A

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

78
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

79
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

80
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.

81
Q

CHANCROID
what are the clinical features?

A

SYMPTOMS
- genital pain
- genital ulcer
- painful groin swelling

SIGNS
- painful ulceration
- solitary ulcers on penis or vulva
- tender unilateral inguinal lymphadenopathy

82
Q

CHANCROID
what is the management?

A
  • single dose AZITHROMYCIN
  • alternatives = ceftriaxone, erythromycin or ciprofloxacin
  • partner notification + treatment
  • abscess drainage
83
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.

84
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.
85
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.
86
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.
87
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.
88
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).
89
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.
90
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.
91
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.
92
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.

93
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.
94
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.
95
Q

POP
What is the UKMEC4 criteria for POP?

A
  • Active breast cancer.
96
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.
97
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).
98
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.
99
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.
100
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.
101
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.

102
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
103
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.
104
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.
105
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.
106
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.
107
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.
108
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.
109
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.
110
Q

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

A
  • Active breast cancer.
111
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.
112
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.
113
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.
114
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.
115
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.
116
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).
117
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

118
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

119
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

120
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

121
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

122
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

123
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

124
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

125
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
126
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)
127
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
128
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

129
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
130
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

131
Q

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

A

Klinefelter’s,
Y chromosome deletions

132
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
133
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.
134
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
135
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
136
Q

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

A
  • Younger age.
  • Lower BMI.
  • PCOS.
  • Higher antral follicle count.
137
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.
138
Q

ASSISTED CONCEPTION
How do you manage ovarian hyperstimulation syndrome?

A
  • PO fluids
  • Monitor urine output
  • LMWH
  • Paracentesis for ascites
  • IV colloids
139
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.
140
Q

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

A

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

141
Q

COILS
What are the starting instructions for IUS?

A
  • Up to day 7 = immediate protection.
  • > Day 7 = extra contraception for 7d
142
Q

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

A

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

143
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).

144
Q

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

A

Steroid abuse,
vasectomy

145
Q

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

A

Testicular cancer

146
Q

MALE INFERTILITY
How would you manage hormonal causes of infertility?

A
  • Gonadotrophins if hypogonadotrophic hypogonadism, bromocriptine if hyperprolactinaemia + sexual dysfunction
147
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.
148
Q

MENSTRUAL CYCLE
What 2 cycles exist within the menstrual cycle?

A
  • Ovarian cycle (development of follicle + ovulation)
  • Uterine cycle (functional endometrium thickens + shreds)
149
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
150
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
151
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
152
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
153
Q

MENSTRUAL CYCLE
What happens if the egg is fertilised?

A
  • Syncytiotrophoblast of embryo secretes human chorionic gonadotropin (hCG) which maintains corpus luteum
154
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
155
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
156
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
157
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)
158
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
159
Q

CANDIDIASIS
what is the management during pregnancy?

A
  • oral treatment is contraindicated
  • intravaginal pessary/cream is first line (clotrimazole)
160
Q

CANDIDIASIS
what is the management of recurrent vaginal candidiasis?

A
  • induction = oral fluconazole every 3 days for 3 doses
  • maintenance = oral fluconazole weekly for 6 months
161
Q

ERECTILE DYSFUNCTION
what normally happens during an erection?

A

sexual stimulation leads to release of nitric oxide in cavernosal smooth muscle
- this causes relaxation of vessels and increased blood flow to the cavernosa
- as they fill with blood the penis stiffens causing an erection

162
Q

ERECTILE DYSFUNCTION
what conditions can cause erectile dysfunction?

A
  • HTN
  • diabetes mellitus
  • hypercholesterolaemia
  • drug induced
  • depression
  • anxiety
  • chronic stress
163
Q

ERECTILE DYSFUNCTION
what are the investigations?

A
  • HbA1c (to assess for diabetes)
  • serum testosterone levels (to assess for hypogonadism)
  • serum TSH (assess for hypo/hyperthyroidism)
  • serum lipid profile (assess for hyperlipidaemia)
  • international index of erectile dysfunction
  • sexual inventory for men (survey to assess severity)

to consider
- penile doppler USS
- nocturnal penile tumescence testing
- neurological evaluation
- psychological assessment

164
Q

ERECTILE DYSFUNCTION
what is the management?

A

1st line
- lifestyle modification (weight loss, physical activity, reduced alcohol, smoking cessation, BP control)
- psychosexual counselling
- phosphodiesterase-5 (PDE-5) inhibitors = SILDENAFIL (viagra)
- vacuum erection device

2nd line
- intracavernous injection therapy
- surgical intervention (penile prosthesis implant)

165
Q

PUBIC LICE
what is it caused by?

A

phthirus pubis - found on pubic and perianal hairs

166
Q

PUBIC LICE
what is the management?

A
  • permethrin 5% or Malathion 0.5%

advice to prevent transmission
- decontamination of clothing + bedding by washing at 50 degrees
- avoid close body contact + sharing of clothes, bedding and personal hygiene products

MY REVISION - ALL TO DO (21 decks)

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