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YOU BETTER WERK > Sexual + Reproductive Health > Flashcards

Sexual + Reproductive Health Flashcards

1
Q

What proportion of couples experience infertility?

A

15%

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2
Q

What is the definition of infertility?

A
  • failure to achieve pregnancy within 12 months of regular unprotected intercourse in women aged <35 - or within 6 months in a women aged > 35
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3
Q

Clinical factors which increase risk of subfertility

A
  • oligomenorrhoea - amenorrhoea - known or suspected peritoneal disease - severe endometriosis - multiple surgeries - loss of an ovary - previous chemotherapy or radiotherapy
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4
Q

Which hormone should be tested for if ovulation is uncertain?

A
  • serum progesterone should be performed mid-luteal phase (seven days before next expected menses)
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5
Q

What history would confirm ovulatory cycles?

A
  • history of regular cycle intervals of between 21-35 days with consistent characteristics and moliminal symptoms - in these patients serum progesterone is not required to confirm ovulation
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6
Q

Which investigations should be undertaken for women with oligo/amenorrhoea?

A
  • FSH - LH - oestradiol (E2) - TSH - prolactin
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7
Q

Which blood tests should be ordered in suspected PCOS?

A
  • free testosterone, free androgen index, DHEAs - need to rule out non-classical congenital adrenal hyperplasia with 17-hydroxyprogesterone concentration - in cases of severe hyoerandrogenism consider excluding Cushing’s disease
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8
Q

Ovarian reserve testing

A
  • quantity and quality are both important factors! - oocyte number peaks at 20 weeks gestation, this declines throughout reproductive life resulting in menopause - routine markers: day 2-4 FSH, E2, AMH and assessment of antral follicle count on TV ultrasound - provides information r.e. predicted response to assisted reproductive treatment - does not predict spontaneous conception!
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9
Q

Day 2-4 (basal) FSH as measure for ovarian reserve

A
  • indirect marker of ovarian reserve - based on feedback inhibition of pituitary FSH secretion - if diminished ovarian reserve ovarian steroidogenesis will be insufficient to suppress early follicular FSH - measurement of E2 increases FSH sensitivity - E2 will be raised with low ovarian reserve due to increased FSH but causes pituitary FSH suppression meaning FSH falls within normal range
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10
Q

Where is AMH produced?

A
  • by granulosa cells of the pre-antral and antral follicles - hence reflexes the size of primordial follicle pool - serum AMH concentration is inversely related to age - can be tested on any day of cycle
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11
Q

Antral follicle count on US as measure for ovarian reserve

A
  • total number of follicles in both ovaries with mean withdth of 2-10mm on USS - assessment in early follicular phase avoids underestimation of follicular number
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12
Q

Which USS features are suggesting of andemomysos?

A
  • venetian blind shadowing - globular uterine appearance - loss of junctional zone definition - “question mark sign”
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13
Q

What are the recommended preliminary fertility investigations?

A
  • day 2-4 FSH, LH, oestradiol - AMH - TSH - transvaginal USS with AFC and anatomy and to check for deep infiltrating endometriosis - blood group and antibody screen - rubella and varicella igG - hep b/c/HIV/syphilis serology=
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14
Q

How long should women defer contraception for after rubella or varicella immunisation?

A

28 days

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15
Q

What is the most important determinant for women considering oocyte cyropreservation?

A

AGE! Infertility is most common in >35 year age group - frozen eggs have survival rates of >84% compared to IVF

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16
Q

How long should women defer contraception for after rubella or varicella immunisation?

A

28 days

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17
Q

What is the most important determinant for women considering oocyte cyropreservation?

A

AGE! Infertility is most common in >35 year age group - frozen eggs have survival rates of >84% compared to IVF

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18
Q

Which forms of contraception are first line options 0-6 week post partum (breast feeding or not)?

A

Implanon and POP

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19
Q

Which form of contraception is generally recommended to be avoided in smokers?

A

COCP - contraindicated in women > 35 who are smoking > 15 cigarettes/day (cat 4) - however still increased risk if smoking <15/day or have quit smoking for <1 year (cat 3) - if have quit for > 1 year (cat 2) - women < 35 and smoking (cat 2)

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20
Q

What are the categories for contraception in patients with previous VTE?

A

Copper IUD = cat 1 Mirena/implanon/depot/POP = cat 2 COCP = cat 4

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21
Q

When is the COPC contraindicated in patients with HTN?

A
  • sustained BP > 160/ > 100 = cat 4 - BP 140-159/90-99 OR even if hypertension is well managed COPC is still cat 3
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22
Q

What are the categories for contraception in patients with previous VTE?

A

Copper IUD = cat 1 Mirena/implanon/depot/POP = cat 2 COCP = cat 4

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23
Q

What category is the COCP in patients with migraine with aura?

A

CAT 4!

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24
Q

What are the categories in patients with a history of breast cancer?

A

Copper IUD = cat 1 Current breast cancer = any hormonal contraception is cat 4 Past breast cancer = any hormonal contraception is cat 3

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25
Q

Which contraception is contraindicated in patients with family history of breast cancer?

A

Nil, all methods cat 1 Unless known BRCA carrier > copper IUD cat 1 > progesterone contraception cat 2 > COCP cat 3

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26
Q

What are the WHO classes of anovulation?

A
  1. Hypogonadotropic anovulation 2. Normogonadotropic anovulation 3. Hypergonadoropic anovulation
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27
Q

How common is idiopathic male infertility?

A

30-40% of male infertility cases

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28
Q

What are the WHO classes of anovulation?

A
  1. Hypogonadotropic anovulation 2. Normogonadotropic anovulation 3. Hypergonadoropic anovulation
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29
Q

Causes of hypergonadoropic anovulation

A
  • premature ovarian insufficiency HIGH: FSH, E2, ?LH
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30
Q

Causes of normogonadotropic anovulation

A
  • PCOS - congenital adrenal hyperplasia NORMAL: FSH, LH, E2
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31
Q

What are the classes of male infertility by mechanism?

A
  • Pre-testicular - Testicular - Post-testicular
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32
Q

What is Kallmann syndrome?

A

Hypogonadortophic hypogonadism - results fro failure of hypothalamic-pituitary axis to stimulate normal gonadal function

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33
Q

What is Kallmann syndrome?

A

Hypogonadortophic hypogonadism

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34
Q

Testicular causes of male infertility

A
  • varicocele - cryptorchidism (undescended teste) - testicular cancer - radiation - chemotherapy/pharmacological - genertic azoospermia or oligospermia - Y-chromosome microdeletions - Klinefelter syndrome - infection/injury/trauma - primary cilia dyskinesia - sertoli cell only syndrome - anti-sperm antibodies
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35
Q

What is Klinefelter’s syndrome?

A

47 XXY - additional copy of the X chromosome - features: infertility, small and poorly functioning testicles

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36
Q

Post-testicular causes of male infertility

A
  • coital - retrograde ejaculation - congenital abscence of vas deferens - obstruction - vasectomy or iatrogenic damage to vas deferens - Young’s syndrome - nerve or spinal cord injury - systemic disease
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37
Q

Describe the baseline endocrine evaluation of suspected male infertility

A
  • FSH - morning testosterone levels
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38
Q

What further investigation should be done if low morning testosterone?

A
  • repeat morning testosterone level - free testosterone - LH - prolactin
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39
Q

What is the role of endogenous testosterone in patients experiencing infertility?

A
  • exogenous testosterone is contraindicated - even if hypogonadism is identified! - spermatogenesis requires level of intra-testicular testosterone and exogenous testosterone inhibits the production of LH which feeds back to suppress the endogenous testicular testosterone function
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40
Q

Key features on physical examination in male fertility

A
  • secondary sexual characteristics: hair distribution, muscle mass, adiposity - gynaecomastia - abdomen/inguinal: scars from previous surgery - penis: position of meautus - scrotum: testicular size, consistency, location, presence of masses - epididymus: induration, cyst, engorgement - vas deferentia: agenesis, atresia - present of varicoele
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41
Q

Semen analysis

A
  • the most important test - adequate collection of sample is paramount - 2-3 days of abstinence prior may be optimal - collection should be straight into sterile container - need to be analysed within one hour - if normal = single sample is preferable - if abnormal = repeat analysis after 1-3 months if mild/mod derangement or in 2-4 weeks if severe derangement (oligospermia or azoospermia)
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42
Q

Investigation of leukocytes in semen analysis

A
  • urine culture - urine PCR for chlamydia and gonorrhoea - semen culture - causes: infections of male accessory glands (urethritis, prostatitis, orchitis, epididmyitis) are potentially treatable causes of infertility
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43
Q

When is scrotal US indicated?

A
  • indicated in patients with infertility and risk factors for testicular cancer - low threshold for US is appropriate - consider if first degree relative has hx of testicular cancer
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44
Q

What hormone profile would you expect in hypogonadotrophic hypogonadism?

A

FSH: low LH: low Testosterone: low Prolactin: normal/high

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45
Q

What hormone profile would you expect in abnormal spermatogenesis?

A

FSH: high or normal LH: normal Testosterone: low Prolactin: normal

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46
Q

What hormone profile would you expect in testicular failure?

A

FSH: high LH: high Testosterone: low Prolactin: normal (similar to hypergonadotrophic anovulation in women)

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47
Q

What hormone profile would you expect in prolactinoma?

A

FSH: normal or low LH: normal or low Testosterone: low Prolactin: high

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48
Q

What is a normal sperm concentration and sperm count?

A

Sperm concentration > 15 million/ml Sperm count > 39 million

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49
Q

What is normal morphology or total motility for a semen analysis?

A

Normal morphology > 4% Total motility > 40%

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50
Q

What is a normal leukocyte count for a semen analysis?

A

<1.0 x 10`6/mL

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51
Q

Lifestyle recommendations for possible male infertility

A
  • alcohol: up to 3-4 units/day unlikely to affect sperm quality but excessive consumption is detrimental - smoking: associated with decreased semen quality - obesity: BMI >30 likely to reduce fertility - scrotal temperature: exposure to elevated temps is associated with reduced semen quality - drugs: testosterone, opioids, psychotrophic agents, cannabis - occupations involving radiation/head, vibration and pesticides may reduce fertility - frequency of intercourse: vaginal intercourse timed around ovulation or every 2-3 days
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52
Q

Specialist testing for male infertility

A
  • post-ejaculatory urine analysis - TRUS - testicular FNA - Anti sperm antibodies - genetic testing
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53
Q

Karyotyping in male infertility

A
  • indicated in severe oligospermia (<5million/L) - most common abnormality is Klinefelter syndrome (47, XXY), responsible for 2/3 of male infertility
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54
Q

What is the median age of menopause in Australia?

A

51

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55
Q

Which contraceptions are generally not recommended in women > 50?

A
  • combined OCP - vaginal ring - depot injection
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56
Q

What are the UKMEC categories for contraception use?

A

MEC 1 = no restriction for use MEC 2 = advantages out weight theoretical/proven risk MEC 3 = risks outweigh the advantages, provision requires expert clinical judgement and or referral to specialist MEC 4 = represents unacceptable health risk

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57
Q

Levonorgestrel IUD and perimenopause

A
  • notable contraindications: current or present breast cancer (MEC 4 and 3) - if inserted in patients >45 can leave for 7 years in those who continue to bleed until menopause if amenorrhoeic - also licensed (not PBS though) as part of HRT to protect endometrium in women using oestrogen for vasomotor symptoms - always r/o other causes of inter-menstrual/abnormal bleeding!
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58
Q

Copper intrauterine device

A
  • highly effective contraception without hormonal side effects or risks - also provide emergency contraception within five days of unprotected intercourse - not PBS listed and are associated with heavier menstrual bleeding - any copper IUD inserted > 40 can be retained until menopause (off label use) - complications: perforation, infection, failure, expulsion
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59
Q

Implanon in perimenopause

A
  • can be used until menopause - contraindicated in breast cancer - not linked to reduction in BMD - be wary to have low threshold to investigate symptoms of troublesome bleeding in patients >40 - nil indication to extend implant use in perimenopause women - amenorrhea cannot be used as indicator of menopause in implanon in situ!
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60
Q

COCP and perimenopause

A
  • can be used by medically eligible women in their 40s (MEC 2) but not generally recommended > 50 - baseline risk of VTE, AMI and stroke are significantly higher in older women - should choose lowest hormone dose
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61
Q

High risk conditions + COCP

A

Multiple vascular risk factors = MEC 3 > 35 and smoking = MEC 3/4 BMI 30-34 = MEC 2 BMI > 35 = MEC 3 Controlled HTN = MEC 3 BP 140-159/90-99 = MEC 3 BP >160/>100 = MEC 4 Hx of IHD/stroke/TIA = MEC 4 FHx of VTE < 45 = MEC 3 FHx of VTE >45 = MEC 2 Breast cancer = previous MEC 3, current MEC 4 Diabetes = MEC 2

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62
Q

Which COPC have lowest VTE/AMI/stroke risk?

A

20mcg ethinyl oestradiol + levornogestrel 100mcg - however there is a higher risk of breakthrough bleeding

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63
Q

POP in perimenopause

A
  • more effective in women > 40 than in younger women - 3 hour window to be taken every day - works to thickening cervical mucus
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64
Q

Advice on ceasing LNG-IUD, POP and implant in women > 50

A
  • amenorrhoeic for > 12 months - check 2 x FSH levels at least 6 weeks apart - if both > 30 advice that contraception is only required for a further 12 months OR - continue until aged > 55
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65
Q

Advice on ceasing Cu-IUD or barrier methods in women > 50

A
  • stop method after 12 months of amenorrhoea
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66
Q

Advice on ceasing depot in women > 50

A
  • generally not recommended in women > 50 - either switch to non-hormonal method until amenorrhoea for 24 months (2 years) OR - switch to alternative progesterone only method and check FSH x 2 when amenorrhoeic for 12 months
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67
Q

Advice on ceasing COCP

A
  • generally not recommended in women > 50 - switch to non-horomonal method until amenorrhoea for 12 months OR - switch to POP, LNG-IUG or implant and repeat FSH when amenorrhoeic for 12 months
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68
Q

Emergency contraception options

A
  • 1.5mg levonorgestrel up to 72 hours after unprotected sex, but effective up to 96 hours - ulpristal acetate has superior efficacy and licensed up to 120 hours after unprotected sex - both are available without prescription - Cu-IUD can also provide effective emergency contraception
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69
Q

What is ulipristal acetate?

A
  • selective progesterone receptor modulatory - partial agonist - used for emergency contraception - taken as a single dose of 30mg as soon as possible after unprotected intercourse - has efficacy for up to 5 days later (120 hours) compared to the 72 hours from the levonorgestrel ECP - action is to prevent or delay ovulation and it does this more effectively than levonorgestrel
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70
Q

At what stage during the cycle do emergency contraceptions affect ovulation?

A
  • after LH surge neither levonorgestrel or ulipristal acetate have any effect on ovulation
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71
Q

Common side effects of ulipristal acetate?

A
  • headache, nausea, abdominal pain, dsymenorrhea - generally mild - safety comparable to lebvonorgestrel - delay breastfeeding for 1 week after ulipritsal
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72
Q

Starting contraception after ulipristal acetate?

A
  • shouldn’t start hormonal contraceptive for at least 5 days (OR unit next period to simplify) - hence need to either use barrier methods or abstain - all patients should be encouraged to repeat pregnancy test 3 weeks after starting the new contraceptive
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73
Q

Breastfeeding and contraception

A
  • no need to cover with emergency contraception up to 3 weeks postpartum - “lactational amenorrhoea”: fully breastfedding day and night with no long intervals between feeds day or night (>4 hrs during the day or > 6 hrs during night) and < 6 months post partum
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74
Q

Advice to give patients r.e. emergency contraceptions

A
  • take a soon as possible, if vomiting within 3 hours take another one - no ECP is 100% effective (risk of pregnancy for UA 0.9% if within 24 hours and 2.3% with levonorgestrel) - period may come early or late - take a pregnancy test if period is > 7 days late - either start OCP 5 days after UA or immediately if levornogestrel - opportunistic STI screen should be offered
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75
Q

What are the 3 main recommendations when caring for a victum of sexual assault?

A
  1. Offer first-line support to women and men who are survivors of sexual assault by any perpetrator 2. Consider and ask about post trauma responses by assessing for mental health problems – acute stress, PTSD depression, alcohol and drug use problems, suicidality or self-harm and offering appropriate support and treatment 3. Offer emergency contraception if within 72 hours of assault and offer all women sexually transmitted infection investigation, prophylaxis and treatment as appropriate
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76
Q

Management of sexual assault

A
  • baseline STI screening: HIV, hepB, syphilis, chlamydia, gonorrhoea, trichomonas - azithromycin 1g PO - offer hep B vaccination if required - treated for gonorrhoea, syphilis and HIV if at high risk
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77
Q

Review program post sexual assault

A
  • review in 2-3 days: assess injury healing if evident - 2 weeks: test results, pregnancy testing, coping - 3 months: follow up serology for HIV, hep B and syphilis - 6 months: follow up for hep C if high risk
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78
Q

What is the most commonly communicable disease in Australia?

A

Chlamydia - greatest risk <30 - frequently asymptomatic

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79
Q

What are the common presentations of chlamydia?

A

Men: 50% asymptomatic, dysuria, urethral discharge, testicular pain, ano-rectal symptoms Females: 75% asymptomatic, dysuria, vaginal discharge, pelvic pain, intermenstrual bleeding, post coital bleeding

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80
Q

Complications of chlamydia

A

Men: epidymo-orchitis, reactive arthritis (arthralgia, rash on soles, balanitis, psoriatic rash) Females: PID, infertility, ectopic pregnancy, reactive arthritis

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81
Q

Diagnosis of chlamydia in males

A
  • NAAT: first pass urine - consider pharyngeal and ano-rectal swabs if MSM
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82
Q

Diagnosis of chlamydia in females

A
  • NAAT: endocervical test (best test if examined) - NAAT: self collected swab if not examined - NAAT: first pass urine (not as sensitive as self collected swabs)
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83
Q

Clinical indications for chlamydia testing

A
  • < 30 and sexually active - partner change in last 12 months - history of STI in last 12 months - sexual partner with STI - increased risk of STI complication (TOP, IUD insertion) - signs and symptoms of STD - requesting STI screening
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84
Q

Empirical treatment of chlamydia

A
  • doxycycline 100mg BD for 7 days OR - azithromycin 1g PO STAT If urethritis symptoms use doxycycline while awaiting test results. Treat patient and partner/s without waiting for results
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85
Q

Advice after diagnosis and treatment of chlamydia

A
  • no sexual contact for 7 days after treatment - no sex with partners from the last 6 months until partners have been tested and treated - contact tracing back to 6 months prior
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86
Q

Treatment of chlamydia in pregnant women

A

Azithromycin 1g PO STAT

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87
Q

Is a clearance confirmation required for patients treated for chlamydia?

A

NO Unless pregnant or diagnosed with rectal chlamydia - in these circumstances repeat NAAT in 4 weeks

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88
Q

Genital warts

A
  • HPV - skin to skin transmission - generally caused by HPB 6 and 11 - long latency period hence doesn’t imply infidelity - Men: warty growths, may be itchy, rarely malignant - Women: warty growths, cervical lesions, cervical cancer - nil specific diagnostic test, clinical diagnosis
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89
Q

Treatment of genital warts

A
  • podophyllotoxin 0.15% cream of 0,5% paint BD for 3 days and then 4 days off, repeated weakly for 4-6 cycles until resolution - cream best perianal area, introital area or under foreskin OR Imiquimod 5% topically 3 times per week at bed time (wash after 6-10 hours) until resolution (up to 16 weeks)
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90
Q

What is the most common STI in MSM?

A

Gonorrhoea

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91
Q

What is the most common STI in patients returning from high prevalence areas overseas?

A

Gonorrhoea

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92
Q

What is the most common STI in young heterosexual First Nations people living remote or very remote?

A

Gonorrhoea

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93
Q

Cause and clinical presentation of gonorrhoea

A

Cause: neisseria gonorrhoeae (GNB) Men: urethral discharge, dysuria, conjunctivitis (sight threatening) Females: vaginal discharge, dyspareunia with cervicitis, conjunctivitis (sight threatening)

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94
Q

Complications of gonorrhoea

A

Men: epidymo-orchitis, disseminated disease (macular rash with necrotic pustules, septic arthritis), meningitis or endocarditis, prostatitis Females: PID, disseminated disease (macular rash with necrotic pustules, septic arthritis), meningitis or endocarditis

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95
Q

Gonorrhoea diagnosis

A
  • NAAT: first pass urine, always collect even if no discharge - MCS: urethral swab if discharge present, endocervical swab or self collected high vaginal - consider ano-rectal and pharyngeal swab if MSM
96
Q

Gonorrhoea treatment

A

Uncomplicated genital/ano-rectal disease: ceftriaxone 500mg IM plus 1g azithromycin Uncomplicated pharyngeal infection: ceftriaxone 500mg IM plus 2g azithromycin Adult gonococcal conjunctivitis: ceftriaxone 500mg IM plus 1g azithromycin

97
Q

Advice after gonorrhoea treatment

A
  • no sexual contact for 7 days after treatment - no sex with partners from last 2 months until after their have been tested and treated if necessary - contact tracing: trace back for minimum of 2 months - consider screening for other STIs
98
Q

How does treatment change for gonorrhoea in remote areas?

A

Amoxycillin 2g PO STAT + Probenacid 1g PO STAT + Azithromycin 1g PO

99
Q

Follow up after positive gonorrhoea test

A
  • treatment - repeat NAAT 2 weeks after treatment has been completed - retest patients 3 months after exposure
100
Q

Complications of herpes

A

MEN + WOMEN: neuropathic bladder, psychosexual morbidity, enhanced HIV transmission Also risk of neonatal herpes

101
Q

Diagnosis of herpes

A
  • NAAT: swab of ulcer base or de-roofed vesicle - diagnosis required visible lesions
102
Q

Management of herpes: initial episode

A

Valaciclovir 500mg BD for 5-10 days or Aciclovir 400mg TDS for 5-10 days

103
Q

Management of herpes: recurrence, episodic therapy

A

Valaciclovir 500mg BD for 3 days or Famciclovir 1g BD for 1 day

104
Q

Management of herpes: recurrence, suppressive therapy

A

Valaciclovir: 500mg daily for 6 months or Famciclovir 250mg BD for 6 months

105
Q

Causative agent of syphilis

A

Treponema pallidum

106
Q

What are the 3 stages of syphilis?

A
  1. Primary 2. Secondary 3. Tertiary
107
Q

What are the features of primary vs secondary syphilis?

A

PRIMARY - genital ulcer or chancre which is usually painless, well defined margin with indurated base, inguinal LN are usually raised, rubbery and non-tender, even untreated will usually spontaneously heal within a few weeks SECONDARY - constitutional symptoms: fever, malaise, headache, lymphadenopathy - skin is involved in 90% of cases, generalised but may just affect hands and feet - may also have neurological signs

108
Q

Complications of syphilis

A

Early latent syphilis (<2 years) - treated as infective syphilis - positive syphilis serology without signs or symptoms - if untreated patients will become asymptomatic over 12-24 months Late latent syphilis (>2 years) - no longer infectious to sexual partners but may still pass infection to unborn foetus Tertiary syphilis - may develop late symptoms months or years later in 1/3rd of cases if not treated - complications: gummas, cardiovascular or neurological disease

109
Q

Diagnosis of syphilis

A
  • Serology: screening through enzyme immunoassay, if reactive RPR and TPHA will be performed - NAAT: swab of ulcer
110
Q

What serological tests are requested to diagnose syphilis?

A
  • EIA: enzyme immunoassay - RPR: rapid plasma reagin - TPPA: treponema pallidum particle agglutination assay - TPHA: treponema pallidum haemoaglutination assay
111
Q

What tests should be considered in patients with prior treated syphilis?

A
  • EI and TPPA tests will be positive for life - only RPR is required to detect reinfection or treatment success
112
Q

When is syphilis testing indicated?

A
  • MSM: at minimum annually but up to 4 times a year - routine antenatal testing (consider repeat in late pregnancy if high risk) - routine immigration testing - sexual contact of person with syphilis - routine sexual health check - signs or symptoms of syphilis - clinically: genital ulcers, MSM with rash or symptoms, any rash affecting palms of soles of feet - consider syphilis in patients with PUO, lymphadenopathy, LFT dysfunction and alopecia
113
Q

Treatment of syphilis

A

Infectious: benzathine 1.8g IMI STAT Late latent: benzathine 1.8g IMI, weekly for 3 weeks

114
Q

What is the Jarisch-Herxheimer reaction?

A

Common reaction in patients with primary or secondary syphilis - occurs 6-12 hours after treatment - headache, malaise, fever, rigors, joint pains, lasting for several hours - alert patients to the possibility of this reaction - treat with analgesia and rest

115
Q

What is the procaine reaction

A
  • rare reaction to procaine penicillin - feeling of impending doom and hallucinations - self limiting and last 30 min
116
Q

Syphilis contact tracing

A

Primary syphilis: 3 months plus duration of symptoms Secondary syphilis: 6 months plus duration of symptoms Late latent syphilis: long term partners only Presumptively treat all sexual contacts of patients with primary or secondary syphilis regardless of serology with benzathine penicillin 1.8g IMI, stat.

117
Q

Test of cure of syphilis

A

Review all patients clinically and with repeat reactive plasma regain (RPR) testing at 3 months, then at 6 months and (if necessary) at 12 months after completing treatment.

118
Q

What type of virus if HIV?

A

Single stranded RNA virus

119
Q

What is the clinical presentation of HIV?

A

Acute infection: seen in 70% of patients, fever, rash, lymphadenopathy, pharyngitis, myalgia, diarrhoea - generally 2 weeks after exposure Asymptomatic infection: for several years following infection Immune deficiency: symptoms related to declining CD4 T cells (oral thrush, diarrhoea, weight loss, skin infections, herpes zoster)

120
Q

Complications of HIV

A

AIDS: opportunistic infections such as pneumocystis jiroveci penumonia, oesophageal candidiasis, cerebral toxoplasmosis, cancers such as Kaposi’s sarcoma

121
Q

HIV diagnosis

A
  • HIV Ag/Ab (usually reactive within 6 weeks of infection) - Western blot: confirmatory test - HIV p24 antigen: high during primary HIV illness - CD4 lymphocyte: marker of immune function, normally > 500 - HIV RNA: should be undetectable if on treatment
122
Q

What are the ovarian and uterine phases of the menstrual cycle?

A

Ovarian: follicular, ovulation, luteal Uterine: menstruation, proliferative, secretory

123
Q

How many days is a normal cycle considered to be?

A

21-35 days Median ~ 28 days

124
Q

FSH Estrogen

A

FSH: prompts production and growth of oocytes Estrogen: stimulates endometrium to thciekn to accomodate an embryo

125
Q

Fall in which hormone triggers menstruation?

A

Progesteron

126
Q

What day on average does ovulation occur?

A

Day 14

127
Q

What is day 1 of the cycle?

A

1st day of menstruation

128
Q

Follicular phase

A

DAY 1 - DAY 14 - first part of the ovarian cycle and ends with completion of antral follicles - generally lasts ~14 days but shortens with age - rise in FSH in first few days of cycle causing ovarian follicles to be stimulated - LH then further stimulates development of the follicle - oestrogen is then released causing a FSH and LH surge which usually occurs 1-2 days before ovulation - this stimulates rupture of antral follicle and release of oocyte

129
Q

Ovulation

A

DAY 14 - LH surge initiates ovulation and stimulates formation of the corpus luteum - the CL then produces and releases estrogen, progresterone, relaxin and inhibin

130
Q

Luteal phase

A

DAY 14-28 - final phase of the ovarian cycle - corresponds to the secretory phase of the endometrium - FSH asnd LH cause remaining part of the dominant follicle to turn into the corpus luteum which releases progesterone - progesterone increase induces oestrogen production - falling levels of progesterone cause menstruation and the begining of the next cycle

131
Q

Preconception counselling: hypertension

A
  • switch to pregnancy safe anti-hypertensives LABETALOL METHYLDOPA
132
Q

Preconception counselling: epilepsy

A

Review medications Sodium valproate not recommended in pregnancy Early Neurology review

133
Q

What are the folic acid recommendations in pregnancy

A
  • 400mcg for 1 month pre-conception to 12 weeks to reduce risk of neural tube defects and possibly congenital heart disease - if in a high risk group suggest 5mg folic acid
134
Q

In which groups would 5mg of folic acid be recommended?

A
  • BMI >30 - anticonvulsant therapy - pre-pregnancy diabetes - risk of malabsorption syndrome - multiple pregnancy - hyperhomoscystinaemia (MTFHR)
135
Q

What is the recommended B12 daily intake in pregnancy

A

2.6mcg/day

136
Q

What is the recommended vitamin D level and intake in pregancy?

A

Vit D > 50 = 400 IU daily Vit D 30-50 = 1000 IU daily Vit D < 30 = 2000 IU daily - low vitamin D is associated with impaired skeletal development and hypocalcaemic seizures

137
Q

Recommended dietary intake of calcium in pregnancy

A
  • 1300mg if 14-18 years old and 1000mg if > 19 - if low intake or high risk of PET need to supplement with 1000mg/day - aim: reduce incidence of hypertensive disorders and preterm labour
138
Q

How much replacement should pregnant women with known IDA take?

A
  • at least 60mg of iron daily
139
Q

What is the recommended iodine supplementation in pregnancy?

A

150mcg every day

140
Q

What is the recommended weight gain during pregnancy for a normal BMI patient?

A
  • 11.5-16kg - or 0.42 kg/week in second and third trimester
141
Q
A
141
Q

Breast cancer screening

A
  • asymptomatic low risk = mammogram every 2 years for women 50-74
  • if have a first degree relative with breast cancer may beneit from beginning scvreening between 40-49
  • cancer australia recommends annual mammograms from 40 if first degree relative <50 diganosed with breast cancer
142
Q

Management of high risk women for breast cancer

A
  • BRCA or strong family history of breast/ovarian/sarcoma cancer
  • Refer to a cancer specialist
143
Q

How often would mammograms be recommended in a women with a sister diagnosed with breast cancer @46?

A

Annually from 40

144
Q

CST: self collection eligibilty

A
  • patients > 30 who have declined cervical sample by clinician
  • patients who are overdue for cervical screening by 2 years or longer (4 years since pap or 7 more than CST)
  • have never been screened

WHO IS NOT eligible: pregnant, DES in utero exposire, symptomatic, total hysterectomy with past history of HSIL, under 30

145
Q

Management of CTS positive for HPV 16/18

A

Refer straight for colposcopy

146
Q

Management of “HPV not 16/18” detected

A
  • if unsatisfactory cytology (LBC) = repeat in 6-12 weeks
  • LBC negative = repeat in 12 months
  • pLSIL/LSIL = repeat in 12 months (if pLSIL/LSIL still present after 12 months refer for colposcopy)
  • pHSIL/HSIL = refer for colposcopy
147
Q

Management of HPV 16/18 positive CST

A

Refer for colposcopy

148
Q

Perineal tear classification

A
  • 1st: vaginal mucosa or perineal skin ONLY
  • 2nd: involving perineal muscles
  • 3A: <50% of external anal sphincter is torn
  • 3B: >50% of external anal sphincter is torn
  • 3C: external AND internal anal sphincters are torn
    4th: laceration extending through anal epitherlium (communication between vaginal and anal epithelium)
149
Q

Episiotomy evidence

A
  • aim is to increase diameter of the vaghinal outlet to facilitate passage of foetal head and ideally prevent vaginal tear
  • conflicting evidence r.e. episiotomies and prevention of obstetric anal spinchter injuries
  • some evidence may suggest an episiotomyt may increase the risk of 3rd and 4th degree tears in multis
  • routine episiotomy is not justified unless instrumental delivery is intended
  • nil indication for prophylactic episiotomy in women with hx of perineal tears
150
Q

RANZCOG episiotomy indications

A
  • high likelihood of 3rd/4th degree tear
  • soft tissue dystocia
  • requirement to accelerate delivery of compromised fetus
  • to faciliate operative vaginal delivery
  • history of female genital multilation
151
Q

Post operative management of perineal tears

A
152
Q

Dyspareunia post tear

A
  • lubrication
  • change sexual positions
  • allow women to control the initiation of intercourse
  • refer to physio, obstetrician or gynaecologist
153
Q

Complimentary and herbal therapies for hot flushes

A
  • Black cohosh: INSUFFICIENT EVIDENCE
  • Phytoestrogens: NO BETTER THAN PLACEBO, may interfere with breast cancer treatmengt
  • Wild yam: LIMITED DATA
  • Evening primrose: NO BENEFIT, may lower seizure threshold in epilepsy
154
Q

Nonhormonal treatments for vasomotor symptoms

A
  • Other than hormonal preparations, only clonidine is TGA approved for treatment of hot flushes
  • Vitamin E causes very marginal reduction in hot flushes
  • SNRI/SSRIs have been noted in very small studies to reduce hot flushes

* 75mg of SR venlafaxine is equivalent to ultra-low dose oestrogen (25 mcg) for the treatment of hot flushes *

155
Q

SNRIS

A

Venlafaxine

Desvenlafaxine

156
Q

SSRI

A

Paroxetine

Fluoxetine

Fluvoxamine

Sertraline

Citalopram

Escitalopram

157
Q

Gabapentin and hot flushes

A
  • 900m daily reduces hot flushes more effectively than placebo
  • common side effect: somnolence, may need to be taken nocte
  • high dose gabapentin appeared to be as effective a premarin
  • but higher doses = more side efffects
  • recommended to start as low dose and built up to 300mg TDS
  • side effects: rash, dizziness, sleepiness, can cause weight gain and lower limb swelling
158
Q

Clonidine for hot flushes

A
  • centrally activing alpha agonist
  • clonidine is more effective than placebo
  • has been studied in breast cancer survivors to be effective
  • start 25mcg BD and built up to 75mcg BD
  • side effects: dry mouth, dizziness, constipation, difficulty sleeping
  • cease if nil improvement after 4 weeks
159
Q

Describe the management of intermediate risk results on CST

A
  • intermediate risk = HPV not 16/18 detection
  • if cytology negative or pLSIL/LSIL should repeat in 12 months
  • however some women at this stage should be referred for colposcopy (if > 2 years overdue for screening, ATSI, women > 50)
160
Q

Which women with HPV not 16/18 should be referred straight for coloposcopy?

A

Women > 50

ATSI

If more than 2 years overdue for CST

Rest of women can have their CST repeated in 12 months –> refer for colposcopy at this stage if still positive

161
Q

What is the general time from HPV infection to development of cervical cancer?

A

10-15 years

162
Q

What proportion of cervical cancer do HPV16/18 cause?

A

more than 70%!

163
Q

What does a low risk CST mean?

A

No HPV detected

164
Q

What is co-testing r.e. cervical cancer screening?

A
  • involves HPV and liquid based cytology test concurrently
  • LBC is then performed irrespected of HPV test
  • recommended for all symptomatic patients, patients expossed to DES
  • in patients with hysterectomy with history of HSIL should have 12 monthly co-testing nutil but tests are negative on 2 consecutive occassions
  • if total hysterectomt for benign reason (menorrhagia, fibroids) no further tests are required if they had a normal screening history prior to hysterectomy

-

165
Q

Patient education r.e. CST

A

• the link between persistent HPV infection and cervical cancer, noting – HPV infections are usually cleared by the immune system in 1–2 years – if infection persists, in rare cases it can lead to development of cervical cancer after about 10–15 years • cervical screening is based on HPV testing, and that cells in the sample will only be studied for changes if HPV is detected • the sample collection procedure is similar to the previous Pap test • patients are invited to start cervical screening from the age of 25 and continue screening until they are 74 years old • screening is only required once every five years for patients who do not have HPV detected

166
Q

Investigation of ovarian masses

A
  • USS with transvaginal views
  • concerning features on USS: irregular solid tumour, ascites, at least 4 papillary structures, irregular multilocumen solid tumor > 10, very good blood flow
  • tumour markers: Ca125, HE4
  • AFP, hCG and LDH can be used to differentiate complex masses on US in women < 40 as these are elevated in germ cell tumours
167
Q

RMI for ovarian malignancy

A

Risk of malignancy index

= ultrasound findings x menopause status x Ca124

Moderate risk: 25-200

High risk = ? 200

168
Q

When would you refer a premenopausal women to a gynaecologist for review/management of ovarian cyst?

A

If > 7cm, symptomatic and complex in nature

If <5cm and simple/asymptomatic = no further investigation

5-7cm simple/asymptomatic = repeat USS in 3-4 months

169
Q

Approach to management of ovarian cysts

A
170
Q

Follow up r.e. CST for women with hysterectomy with history of cervical adenocarcinoma insitu (AIS)

A

Indefinited annual co-testing

171
Q

What is “Test of Cure” in relation to cervical cancer screening

A

Test of Cure surveillance is a co-test (HPV and LBC test) performed 12 months after treatment, and annually thereafter, until the patient receives a negative co-test on two consecutive occasions

172
Q

What is menopause?

A
  • cessation of ovulation and defined as the “final” menstrual period
  • average age in australia is 51
  • important risk factors to define in menopausal women seeking medical treatment: VTE, CVD, cancer, osteoporosis
  • women <50 should be offerred contraception for further 2 years after final period and if > 50 should be offerred a further 12 months of contraception
173
Q

Contraindications to menopausal hormone therapy

A
  • contraindications: breast/endometrial or other hormone dependent cancer, undiagnosed vaginal bleeding
  • relative contraindications: established CVD, VTE disease, active liver disease, possibly migraine with aura

Treated hypertension is NOT a contraindication

174
Q

Breast cancer and HRT

A
  • oestrogen/progesterone: increased risk, <1:1000
  • oestrogen only: decreased incidence of breast cancer
175
Q

Cardiovascular disease and HRT

A
  • no increase in CVD in young women who are peri-menopausal or post menopausal in absence of previously established CVD
  • for women who start MHT within 10 years of menopause or before the age of 60 CHD is reduced by 48%
176
Q

VTE and HRT

A
  • risk of VTE is increased by smoking, increasing age, obesity and oral MHT
  • use of transdermal MHT has not be associated with increased VTE risk and is recommended for women with VTE risk factors or previous VTE (provoked or unprovoked)
177
Q

Prescribing HRT: uterus intact

A

Uterus intact = combination MHT (progesterone for endometrial protection)

< 12 months since LMP = continuous oestrogen and cyclical progesterone

> 12 moths since LMP = continuous oestrogen and continuous progresterone

Use of continuous progresteron can cause irregular break through bleeding

178
Q

Prescribing HRT: hysterectomy

A

Oestrogen only MHT

179
Q

After commencing HRT

A

After commencing MHT women should be reviewed in 6-12 weeks to tailor treatment

  • if ongoing vasomotor symptoms may consider increasing oestrogen
  • if breast tenderness occurs can reduce oestrogen dose
  • duration: should be reviewed annually to check symptoms and for emergency of contraindications
  • can be continued long term if good symptom relief and nil contraindications
  • most women will have menopausal symptoms for up to 8 years
180
Q

Non-hormonal medications for treatment of vasomotor symptoms

A
  • SNRIs/SSRIs (s/e: nausea, drowsiness, sexual dysfunction)
  • gabapentin (s/e: dizziness, drowsiness)
  • pregabalin (s/e: dizziness, drowsiness)
  • clonidine (s/e: dry mouth, drowsiness, visual disturbance)
181
Q

Tibolone

A
  • HRT: acts as an estorgen on vagina, bone and brian
  • has progesterone and anti-estrogenic effects on breast and endometrium
  • indicated for hot flushes and prevention of post menopausal osteoporosis if alternative treatment is inappropriate
  • precautions: breast cancer, endometriosis, SLE, cardiovasclar or cerebrovascular disease

INCREASES STROKE RISK

182
Q

Management of abnormal bleeding in pre and peri-menopausal women

A
  • exclude pregnancy
  • exclude cervical pathology and screen for chlamydia
  • recommend colposcopy for post coital bleeding
  • FBC, coags and TSH if applicable
  • > low risk (no IDA, first episode): conservative monitoring
  • > increased risk (anaemia, persistent bleeding): transvaginal US to report endometrial thickness
183
Q

Breakdown of endometrial thickness and subsequent management in pre-peri menopausal bleeding

A

<12mm if pre menopausal or <5mm if peri-menopausal = conservative treatment and monitoring

>12 mm if pre menopausal or >5 if perimenpausal = referral for endometrial biopsy

184
Q

Management of post menopausal bleeding

A
  • exclude cervical pathology: CST +/- chlamydia
  • FBC if indicated
  • if on tamoxifen –> refer to gynaecologist and referal for US, will require endometrial biopsy
  • all others with post menopausal bleeding –> transvaginal US

IF endometrial thickness <4 with risk factors and peristent bleeding - refer

IF endometrial thickness >4mm of focal lesions = refer for endometrial biopsy!

185
Q

What are the risk factors for endometrial cancer?

A
  • history of chronic anovulation
  • exposure to unopposed oestrogen
  • PCOS
  • tamoxifen
  • strong family history of endometrial or colon cancer (lynch(
  • nulliparity
  • obesity: often with diabetes and HTN
  • endometrial thickness > 8mm
186
Q

HRT and post menopausal bleeding

A
  • common in the first 6 months of HRT
  • however if persists then need to evaluate futher
187
Q

Investigation of a new breast symptoms

A
  • triple test approach to diagnosis
  • imaging: mammogram + US + non-excisional biopsy

If no lump or findings consistent with hormonal change –> mammogram if due and review in 6-8 weeks immediately after period

Mass/inconclusive/nipple changes –> mammography + US

188
Q

Choice of diagnostic imaging in a new breast lesion/concern

A
  • US is more sensitivity than mammography in detection of cancer in younger women
  • often used in complementary capacity
  • if < 35: US recommended first line, mamography should be used in addition if suspicious findings or US not consistent with clinical examination
  • >35: both mammogram and US should be performed
189
Q

When to refer to a breast surgeon

A
  • if any one component of the “triple” test is positive
  • cyst aspiration is incomplete or lump remains post aspiration
  • spontaneous unliateral bloody or serous discahrge from single duct in women > 60
  • eczematoid changes of nipple which persist over 1-2 weeks and don’t response to topical treatment
  • inflammatory conditions which does resolve after 2 weeks of Abx
190
Q

CST in immunocompromise/deficient women

A
  • 3 yearly HPV testing
  • any HPV result = colposcopy
191
Q

Genital psoriasis

A
  • usually a lack of scaling due to friction
  • affects pubic area, vulva, penis, skin folds, including natal cleft, buttocks
  • doesn’t affect mucosal surfaces
  • one of the most common diseases affecting anogenital skin
  • can be generalised plaque psoriasis or rarely localised pustula psoriasis
  • in children genital psoriais is most common < 2 years old

In women, vulval psoriasis appears symmetrical. It can vary from silvery, scaly patches adjacent to the labia majora to moist, greyish plaques or glossy red plaques without scaling in the skin folds.

Treat with topical steroids

192
Q
A
193
Q

Siladenifil: MOA

A

Phosphodietserase 5 inhibiotr

  • sexual stimulation increases cyclic guanosine monophosphate (cGMP) levles causing smooth muscle relaxation and inflow of blood to corpus cavernosum and penile erection

Sildenafil inhibits break down for cGMP increasing blood flow to penis during erection

194
Q

Siladenafil pre-cautions

A
  • renal: start slow if CrCl <30
  • hepatic: start low dose in mild-mod hepatic impairment (contraindicated in severe hepatic impairment)
  • elderly: consider starting low dose, half life is increased

CONTRAINDICATED with nitrates due to profound risk of hypotension or MI

CONTRAINDICATED in pt with history of NAION (non-arteritic ansterior ischaemic optic neuropathy)

CONTRAINDICATED in patients which sex is inadvisable due to unstable cardiac disease (i.e. unstable angina)

195
Q

What are the 3 major contraindications to siladenafil

A

NITRATES

NAION (non-arteritc anterior ischaemic optic neuropathy)

UNSTABLE ANGINA/DECOMPENSATED CCF

Also: resting hypotension, recent stroke or MI

196
Q

What are the adverse effects of siladenafil?

A

common: headache, dizziness, flushing, dyspepsia, nasal congestion/rhinitis

abnormal visio: mild, transient retinal effects including blue-green colouyr tinge, light sensitivity, blurred vision

197
Q

Classification of erectile dysfunction

A
  • organic: anatomical, vasculogenic, neurogenic, ednocrinological, drug related side effects
  • psychogenic: can be generalised or situational
  • mixed

Anxiety and depression commonly accompany erectile dysfunction

198
Q

Risk factors for erectile dysfunction

A
  • advanced age
  • atherosclerosis related factors: CVD, smoking, diabetes, HTN, dyslipidaemia
  • neurological conditions: MS, parkinson’s, alzheimers, spinal cord disorder, peripheral nerve disorders (diabetic neuropathy)
  • pelvic surgery/radiation/trauma
  • endocrine: hypogonadism, hyperprolactinaemia, thyroid disorder
  • obesity and metabolic syndrome
  • penile abnormalities: Peyronie’s
  • psychological
  • medication
  • substances: alcohol and illicit drugs
199
Q

Which medications can cause erectile dysfunction?

A

Antihypertensives: diurectics, beta and alpha blockers

Psychotropic medications: SSRIs, antipsychotics, anxiolytics

Anticonvulsants and anti-Parkinson’s

Hormone affecting: anti-angrofen, steroids, chronic opioid use

200
Q

Screening in erectile dysfunction

A
  • morning testosterone (hypogonadism)
  • fasting BSL or HbA1c
  • dyslipidaemia
201
Q

Stepwise approach to erectile dysfunction

A
  1. Define problem: loss of libido vs premature ejaculation vs deformity vs loss of erectile harness
  2. History: risk factors, sexual and psychosocial hx, SHIM socre
  3. Examination: BP, BMI + waist circumference, CVD assessment, genitalia examiantion
  4. Bloods: morning testosterone, cholesterol, FBG or HbA1c
  5. Lifestyle modification: cease smoking, healthy diet, exercise, reduce ETOH, avoid drugs
  6. Treat reversible causes; i.e. low testosterone, consider alternative medications (if medication induced dysfunction), refer to therapist if psychogenic
  7. First line therapy –> phosphodiesterate type 5 inhibitor (siladenafil)
202
Q

Erectile dysfunction as a risk factor for CVD

A
  • usually preceeds coronary symptoms by 3 years and may be considered an early marker of CVD
  • depending on patients risk may need to consider stress test and or referral to cardiologist
203
Q

What is the most common drug to cause erectile dysfunction?

A

BETA-BLOCKERS!

204
Q

Gynaecomastia

A
  • results as an imablance of free oestrogen to free testosterone
  • common age groups: new borns, adolescents and odler med

CAUSES

Medications

Idiopathic

Cirrhosis

Malnutrition

Testicular or adrenal tumours: (HCG secreting tumours)

CKD

Hyperthyroidism

205
Q

Medications which cause gynaecomastia

A
  • CVD: spironolactone, digoxin, amiodarone
  • Hormonal: anti-androgens, oestrogens, GNRH, 5-alpha reductase inhibitors (finasteride, dutasteride)
  • Antimicrobials: ketoconazole, metronidazole
  • Psychoactive: haloperidol, diazepma, TCAs
  • Chemotherapy
  • Recreation: ETOH, TCH, anabolic steroids
206
Q

What are the most common testicular malignancies?

A
  • germ cell: 95%
  • sex cord stromal: 5%
207
Q

4 benign testicular cycts

A
  1. Epidiymal cysts: feel slightly seperated to testes
  2. Spermatocele: fluid filld cycts, typically connected to testes
  3. Hydatid of morgagni: small common cysts at top of testes, are moveable adn can cause pain if they twist
  4. Hydrocele: swlling in the scrotum, build up of fluid around the testes, generally painless and granduzlla increase in size. May be a sign of underlying testicular cancer in you males. In older men almost always benign.
208
Q

Investigation of tetsicular lumps

A
  • US within 1-2 days
  • refer to urologist
  • CT scan of chest/abdo/pelvis
  • serum markers: AFP, hCG, LDH
  • semen analysis and hormone profile (testosterole, FSH, LH)
209
Q

What are the 3 testicular cancer categories acording to WHO?

A
  1. Germ cell: seminoma vs non-seminoma
  2. Sex cord stromal tumours
  3. Non-specific stromal tumours
210
Q

Premature ejaculation

A
  • diagnosed on history alone
  • rx: off label SSRI use (paroxetine, sertraline, fluoxetine)
  • second line rx: CBT
211
Q

Biological causes of premature ejaculation

A
  • diabetes, thytroid disorder, other endocrine disorders
  • iatrogenic: SSRIs, antipsychotics, beta blockers
  • lifestyle: excessive ETOH
212
Q

Risk factors for testicular cancer

A
  • family history
  • congenital inguinal hernia
  • undescended testes
213
Q

Initial investigation of LUTS in men

A
  • urinealysis
  • serum creatinine + GFR
  • urine cytology should be considered in presence of haematuria
  • urinary tract USS
  • role of PSA is contraversial
214
Q

Medical therapy for BPH

A

Alpha-adrenoceptor agonists: tamsulosin
> smooth muscle relaxation of prostate and bladder neck
> prazocin is cheaper but less favourable side effect profile
> risks: retrograde ejaculation, erectile dusfunction, nasal congestion, hypotension, dizziness
> caution in med considering cataract surgery, risk of floppy iris syndrome

5-alpha reductase inhibitor: dutasteride, finasteride
> reduce prostate growth and volume
> most effective when prostate > 40ml
> common side effects: erectile dysfunction, decreased libido, decreased sperm count
> can take months to have max effectiveness

215
Q

Differential diagnosis of LUTS

A
  • benign/neoplastic conditions of lower urinary tract: UTI, prostatitis, bladder calculi, interstitial cystitis, phimosis, over active bladder syndrome, prostate cancer, bladder cancer, urethral cancer
  • neurological: parkinson’s, stroke, MS, cerebral atrophy, head injury, spinal cord or degenerative disc disease, pelvic prior surgery
  • other: polyuria from renal or cardiac dysfunction, noctural polyuria and OSA, iatrogen from medications
216
Q

Retractibilty of foreskin in kids

A

Retractability increases with age

Full retraction seen…

> in 10% of boys at 1

> 50% of boys at 10

> 99% of boys at 17

  • a non retractable foreskin is a normal variant and doesn’t require intervention
  • should never be forcibly retracted for cleaning!
217
Q

“Ballooning” in boys

A
  • some kids will notice this with non-retractable foreskins
  • ballooning will occur during urination
  • may increase risk of balanitis but usually on no-consequence
  • treat if problematic: topical steroid cream sparingingly (0.05% betamethasone TDS for 6-12 weeks)
218
Q

RCH: inflammation and balanitis

A
  • mild redness and soreness of top is common can can be managed with reassurance
  • if extensive inflammation of glans penis +/- foreskin = balanitis
  • causes: chemical, physical trauma, candida nappy rash in infants
  • treatment: warm salt water, barrier or 1% hydrocortisone cream, antifungal cream if suspect candida (clotrimazole/miconazole)
219
Q

RCH: penile infection and cellulitis

A
  • oral antibiotics: flucloxacillin
  • GAS can causes severe genital rash that is weeping and raw
220
Q

Phimosis

A
  • pathological phimosis results from scarring of the preputial ring, preventing retraction
  • obvious ring of scar tissue, foreskin not retractiable at conclusion of puberty
  • previously retractable foreskin now not retractable
  • persistent ballooning of foreskin in older children
  • causes: BXO or most commonly due to repeated forcible attempts to retract foreskin
  • treatment: steroid for 2-4 weeks if good response continue for 6-12 (0.05% betamethasone)
221
Q

Paraphimosis

A

Urological emergency

  • risk pof preputial necrosis
  • left in a retracted position, distal foreskins becomes oedematous and difficulty to retract
  • usually can be corrected without surgery: analgesia, warm firm compress bandage (coband), leave for 10-15 min, can repeat again
222
Q

Causes of priapism in children

A

Sickle cell

Leukaemia

Trauma

223
Q
A
224
Q

Indication for referral to gynacologist: Endometriosis

A
  • persistent and significant symptoms
  • symptoms not responding to first line treatments after 3 months
  • pelvic mass or nodules
  • suspicion of bladder or bowel involvement with deep endometriosis
  • refer for fertility treeatment if suspected endometriosis if unable to conceive after 6 moths of trying or is >35
225
Q

Lab investigation for hirsuitism

A

Total serum testosterone, free angdrogen idex, serum 17-hydroxyprogesterone concentration, LH, E2, progesterone , TSH

226
Q

Diagnosis of PCOS

A
  • must meet two of following criteria
    1. menstrural disturbance: secondary oligomenorrhoea or amenorrhoea
    2. clinical or biochemical hyperandrogenism
    3. polycystic appearance of ovaries

Additional features; obesity, insulin resistance, subfertility

227
Q

Metformin use in PCOS

A
  • improves glucose metabolism
  • may be considered in individuals with high risk of T2DM, subfertility, BMI > 25 with insufficienct weight loss after 6 months trial of changes
  • metformin suppresses ovarian androgen production which improved frequency of ovulation

METFORMIN IR 500mg nocte, up to 150mg daily in 2-3 doses

228
Q

Approach to heavy menstrual bleeding

A
  • exclude pregnancy, perform CST if due
  • initial examination and investigation (FBC, ferritin, coagulation profile and TSH)
  • increased endometrial cancer risk, fibroids, endometriosis –> perform US between day 5-10 of cycle if possible
  • if nil of above –> suggest contraception (LNG-IUG/COC) +/- TXA or NSAID
229
Q

Non-hormonal management of heavy menstrual bleeding

A
  • TXA 1-1.5g orally for first 3-5 days ofr cycle (Q6-8H)
  • ibuprofen/mefenamic acid/naproxen
230
Q

Male androgen deficiency

A
  • impaired testosterone production due to proven dyfunction in the hypothalamic-pituitary-testciular axis
  • male hypogonadism is androgen deficiency with impaired fertility
  • > hypergonadotrophic: primary testicular disorders
  • > hypogonadotrophic: central hypothalamic/pituitary disorder

CAUSES

  • Primary: Klinefleter (47XXY), cryotochidism, orchidectomy, orchitis, raidatyion, torsion, trauma, androgen synthesis inhibitors
  • Secondary: pituitary tumours, pituitary surgery/radiotherapy, haemochromatosis, hypophysitis, idiopathic hypogonadotrophic hypogonadism (Kallmann syndrome)

DDx for central causes: exogenous syntheic andorgen use, recent acute illness, functionally low testosterone concentrations

231
Q

Approahc to diagnosis of suspected male androgen deficiency

A
  • measure fasting morning serum total testosterone concentration
  • if low: repeat morning total testosterone with serum FSH and LH
  • if low testosterone but high LH: primary androgen deficiency
  • if low testosterone band low or normal LH and FSH: central androgen deficiency
232
Q

Precocious puberty

A
  • pubertal development is unusual in females younger than 8 and males younger than 9
  • early onset of puberty is either gonadotrophin dependent (central) or independent
  • central precocious pubert: breast development in females younger than 8 and testicular enlargement in males younger than 9 (often idiopathic but can be caused by brain lesions)
  • gonadotrophin independent early puberty is much less common: can cause feminisation of males or virilisation of females, causes include ovarian cycts, tumours, testicular stomal or germ cell tumours
  • precocious puberty more common in females and usually idiopathic however in males is more likely to be pathological
233
Q

Masculinising hormones: testosterone

A
  • aim: to reduce gender dyphoria
  • target trough testosterone level: 10-15
  • within weeks: increased clitoral size, heightened libido, oily skin, increased appetite, acne
  • within months: facial hair, body hair growth, increased muscle bulk, body fat redistribution, deeper voice (permanent), cessation of periods
  • longer term: male pattern baldness may occur, infertility, cervical/vaginal atrophy, breast tissue atrophy

Possible side effects: polycythemia, mood swings, irritability, increased risk of heart disease and dyslipidaemia

Need to monitor CVD risk and status

Practice points: check bloods Q3 monthly, consider contraception, vagifem for vaginal irritation

234
Q

Feminising hormones; oestrogens

A
  • aim for oestradiol level 300-600
  • within weeks: calmer mood, decreased libido, softer skin
  • within months: body fat redistribution, reduce muscle bulk and power, breast tenderness, swelling
  • longer term: breast growth, reduction in penis size and testicles, reduced facial/body hair, slowing of male pattern baldness, infertility (permanent)

Possible side effects

  • nausea, weight gain, DVT, PE, liver impairment, mood swings
  • if > 40 suggest transdermal oestrogens
235
Q

Anti-androgens: trans and gender non-binary health

A
  • aim: to reduce testosterone levels
  • reduce body hair growth, reduced libido and erections, reduce acne
  • possible side effects: electrolyte, renal disturbance, postural hypotension, diuresis, gynaecomastis, potential for liver impairment

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