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Phase 3a Tera Pyo Edition > Gynaecology > Flashcards

Gynaecology Flashcards

1
Q

Explain the Hypothalamic-Pituitary-Gonadal axis in women

A
  • Hypothalamus releases GnRH (gonadotrophin releasing hormone)
  • GnRH stimulates anterior pituitary to release LH and FSH
  • LH and FSH stimulate follicle development in ovaries, causing theca granulosa cells to secrete oestrogen, which negatively feeds back to Hypothalamus and AP, reducing LH and FSH levels.
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2
Q

What is oestrogen and what does it stimulate

A

Steroid sex hormone (17-beta oestradiol is main active version).

  • Breast tissue development
  • Growth and development of female sex organs (vulva, vagina, uterus) at puberty
  • Blood vessel development in uterus
  • Development of endometrium
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3
Q

What is progesterone and what does it stimulate

A

Steroid sex hormone produced by corpus luteum after ovulation. In pregnancy, it is produced by placenta from 10 weeks gestation onwards. Acts on tissues previously stimulated by oestrogen.

  • Thickens and maintains endometrium
  • Thickens cervical mucus
  • Increases body temperature
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4
Q

What age does puberty occur in girls, how long does it last and in what sequence do changes occur? Also why does low weight delay puberty.

What staging is used

A
  • 8-14 years
  • 4 years
  • Growth spurt/breast buds, pubic hair, menarche
  • Aromatase found in adipose tissue helps create oestrogen. More aromatase (fat) = earlier puberty. Low birth weight, chronic disease/ED, athletic hence can cause delays
  • Tanner staging (under 10, no pubic hair or breasts = 1)
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5
Q

What are the 2 phases of menstrual cycle

A

Follicular phase (start of menstruation -> ovulation) - first 14 days
Luteal phase (ovulation -> start of menstruation) - final 14 days

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6
Q

What are ovarian follicles

A

oocytes are cells that have potential to develop into eggs. These are surrounded by granulosa cells, forming follicles.

Primary follicles are always maturing into primary and secondary follicles. When they reach secondary, they grow FSH receptors, which when stimulated, cause granulosa cells to secrete oestradiol (oestrogen).

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7
Q

Describe the follicular phase

A

Low oestrogen and progesterone causes endometrium shedding and bleeding.

FSH stimulates secondary follicles, causing them to grow, and for surrounding granulosa cells to secrete oestrogen. This reduces LH and FSH production (negative feedback). Rising oestrogen also causes cervical mucus to become more permeable, allowing sperm to penetrate cervix around ovulation.

One follicle will develop more than the rest (dominant follicle) LH spike causes dominant follicle to release an ovum. Ovulation occurs 14 days before end of cycle.

Overall: FSH stimulates oestrogen, which spikes ~day 12. There is an LH spike right before ovulation causing an ovum to release.

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8
Q

Describe luteal phase

A

The follicle that released the ovum collapses, becoming the corpus luteum. This secretes progesterone, maintaining the endometrial lining. It also causes the cervical mucus to become thick.

If pregnancy: the syncytiotrophoblast of the embryo secretes Human Chorionic Gonadotrophin (HCG), maintaining the corpus luteum.

Without fertilisation the corpus luteum degenerates and stops producing oestrogen and progesterone. This fall causes breakdown of the endometrium and menstruation. The stromal cells in the endometrium release prostaglandins, causing uterus contractions. The fall in Oestrogen and Progesterone causes an increase in LH and FSH, restarting the cycle.

Menstruation marks day 1 of the menstrual cycle.

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9
Q

What is amenorrhoea? Give primary and secondary causes

A

Failure to establish menstruation at 15 with normal sexual development and 13 without.

Primary
- Gonadal dysgenesis (e.g. Turners)
- Hypogonadotrophic hypogonadism (deficiency of LH and FSH), Hypergonadotrophic hypogonadism (lack of response to LH and FSH by gonads)
- Pregnancy

Secondary - 3-6 months amenorrhoea when previously normal
- Hypothalamic (secondary stress, excessive exercise)
- PCOS
- Thyroid disease
- Hyperprolactinaemia

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10
Q

What is atrophic vaginitis?

A

Inflammation and thinning of vulvovaginal tissue due to a decline in oestrogen levels. Most commonly in post-menopausal women.

Oestrogen normally makes epithelium of vagina thick and lubricated. Absence causes it to become thin and dry, making it prone to inflammation and infections, due to alteration of pH and microflora.

Lack of oestrogen can also reduce healthy connective tissue in pelvis, causing pelvic organ prolapse and stress incontinence.

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11
Q

Presentation of atrophic vaginitis

A
  • Thin/Pale vaginal mucosa
  • Vaginal dryness/itchiness
  • Pain during sex and post-coital bleeding
  • Discharge, loss of pubic hair and pH>4.5
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12
Q

Investigations and management of atrophic vaginitis

A

Clinical exam including speculum.
Discharge should be infection screened.
- Transvaginal USS and Endometrial biopsy necessary to exclude endometrial cancer.
- pH >4.5

Non hormonal:
- Moisturisers and lubricants
Hormonal:
- Systemic HRT (Estriol cream/ estradiol tablets)

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13
Q

What is bacterial vaginosis

A

Overgrowth of anaerobic organisms (e.g. Gardnerella vaginalis). Leads to a fall in lactobacilli which produce lactic acid, so vaginal pH rises.

Very commonly sexually active women (NOT sexually transmitted infection).

Presents as grey-whiteish watery discharge and fishy offensive smell.

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14
Q

Criteria for BV diagnosis

A

Amsel’s criteria (3/4 must be present)
- Thin, white, homogenous discharge
- Clue cells (stippled vaginal epithelial cells) on microscopy
- Vaginal pH >4.5
- Positive whiff test (adding potassium hydroxide causes fishy odour)

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15
Q

Management of BV

A

Not needed if asymptomatic

  • Oral metronidazole 5-7 days (could have single oral, 2g metronidazole dose if issues adhering)
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16
Q

What is trichomonas vaginalis and how does it present

A

Flagellated protozoa parasite (STI)

  • Vaginal discharge (offensive, yellow/green, frothy)
  • Vulvovaginitis
  • Strawberry cervix
  • pH>4.5
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17
Q

Investigations and management of trichomonas vaginalis

A
  • Microscopy of a wet mount shows motile trophozoites
  • Oral metronidazole 5-7 days/ 2g dose one off
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18
Q

Risk factors for urinary incontinence

A
  • Advancing age
  • Pregnancy/childbirth
  • High BMI
  • Hysterectomy
  • Family history
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19
Q

Types of urinary incontinence

A

Overactive bladder (urge incontinence)
- Caused by detrusor overactivity (Urge to urinate quickly followed by uncontrollable leakage)

Stress incontinence (Leaking small amounts when coughing or laughing)

Overflow incontinence (bladder outlet obstruction e.g. prostate)

Mixed (both stress and urge)

Functional incontinence (not enough time to get to bathroom / physical conditions)

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20
Q

Investigating incontinence

A
  • Bladder diaries/3 days
  • Vaginal examination to exclude pelvic organ prolapse and ability to initiate voluntary contraction of pelvic floor muscles
  • Urine dipstick and culture
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21
Q

Management of incontinence

A
  • Bladder retraining (6 weeks)
  • Enuresis alarm (alarm wakes you up when it senses wetness, trains brain to wake before wetting)
  • Bladder stabilising drugs (oxybutinin first line - avoid in frail old women)

If stress incontinence
- Pelvic floor muscle training (8 contractions, 3x a day for 3 months)
- Duloxetine (SSRI/SNRI)

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22
Q

What is menopause? With stages

A

Cessation of menstruation, average age 51. Clinically diagnosed after 12 months of amenorrhoea.

Peri-menopause - First clinical signs of menopause appear (Vasomotor symptoms/irregular menstrual cycles). Ends 12 months after last period, leading into menopause. (usually start around 40s)

Post menopause - >12 months after last period.

Premature menopause - Menopause before 40 as a result of premature ovarian insufficiency

Early menopause - Ovaries stop functioning between 40-45 years.

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23
Q

Clinical features of perimenopause/menopause

A
  • Hot flushes/night sweats (vasomotor)
  • Emotional instability and/or depession
  • Irregular, heavier/lighter periods
  • Joint pain
  • Vaginal dryness/atrophy, sex pain/bleeding
  • Reduced libido
  • Urinary incontinence, recurrent UTI, dysuria
  • Weight gain
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24
Q

Long term consequences of menopause

A
  • Osteoporosis/ fragility fractures - most commonly Colle’s fracture (distal radius), neck of femur and vertebrae.
  • Cardiovascular disease
  • Urogenital atrophy - causing frequency, urgency, nocturia, incontinence and recurrent UTIs. Vaginal dryness/atrophy symptoms
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25
Q

Investigations of menopause

A
  • Clinical diagnosis >45 years old

Do Serum FSH if:
- <40 years with suspected premature menopause
- 40-45 if alterations to menstrual cycle

High FSH (>30), Low oestradiol.

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26
Q

Management of menopause

A

Lifestyle
- Education
- Regular exercise, weight loss, stress reduction (to aid against hot flushes)
- Sleep hygiene
- Contraceptive use until 2 years after last period if <50. 1 year after last period if >50. (Copper IUD)

HRT

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27
Q

What is vaginal candidiasis

A

Fungal infection AKA Thrush. 80% caused by candida albicans, a dimorphic fungus made of spherical yeast cells.

Characterised by an itchy, red vulva, cottage cheese discharge, fissuring and satellite lesions

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28
Q

Describe oral candidiasis

A

Creamy white/yellow spotty plaque adhered to oral mucosa. May be bleeding and redness under this. Most commonly found on buccal mucosa, tongue and palate.

Can also present atrophic with a burning pain or under dentures (denture stomatosis - negative test on mucosa but positive on dentures)

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29
Q

Risk factors for candidiasis

A
  • Pregnancy
  • Diabetes
  • Antibiotics use
  • Immunocompromise/suppression
  • Increased oestrogen levels (e.g. combined oral contraceptive)
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30
Q

Management of candidiasis

A

Single dose
- Oral fluconazole 150mg first line
- Clotrimazole 500mg intravaginal second line

If recurrent,
- High vaginal swab for microscopy and culture
- Induction-maintenance regime (oral fluconazole every 3 days for 9 days, followed by weekly fluconazole for 6 months)

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31
Q

What is adenomyosis, how does it present how is it investigated and treated

A

The presence of endometrial tissue in the myometrium (Inside uterus, as opposed to outside in the case of endometriosis), causing dysmenorrhoea (painful), menorrhagia (heavy) and an enlarged, boggy uterus.

Investigated with a transvaginal USS

Tranexamic acid to manage menorrhagia.

Hysterectomy may be needed

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32
Q

What is cervical cancer

A

Cancer of the cervix, mostly affecting younger women (<45).

90% are Squamous cell and 10% are adenocarcinomas. Caused by HPV 16,18 and 33.

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33
Q

Risk factors for cervical cancer

A
  • Smoking
  • HIV
  • High parity (lots of kids)
  • COCP
  • Early first intercourse
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34
Q

How does HPV cause cervical cancer (mechanisms)

A

HPV 16 and 18, which code genes E6 and E7

E6 inhibits p53 tumour suppressor gene

E7 inhibits inhibits RB (retinoblastoma) suppressor gene

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35
Q

How does cervical cancer screening work?

A

Smear tests offered between 25-64

25-49: 3 yearly screening
50-64: 5 yearly screening

Cannot be offered to women over 64. In pregnancy it is delayed to 3 months post partum.

Women with low sexual history have very low risk

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36
Q

How is cervical cancer staged

A

FIGO Staging

IA - Confined to cervix, less than 7mm wide, only visible by microscopy. (A1 <3mm deep, A2 3-5mm deep)
IB - Confined to cervix, but visible. Less than 7mm wide. B1 <4cm diameter, B2 >4cm

II - Extended beyond cervix to pelvic wall. A - lower third of vagina, B - pelvic side wall

III - If causes hydronephresis or non functioning kidney.

IV - Extension beyond pelvis, or involving bladder or rectum.
A - Involvement of bladder/rectum
B - Involvement of distant sites outside pelvis

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37
Q

Management of cervical cancer (Surgical, and what chemotherapy used)

A

IA - Hysterectomy + lymph node clearance if A2. Cone biopsy if wanting to maintain fertility.

IB, II, III, IV - Radiotherapy and chemotherapy. Cisplatin most used.

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38
Q

What is CIN

A

Cervical Intraepithelial Neoplasia

Pre-invasive disease. Dysplastic but not malignant. 1/3 of women with CIN II or III develop cervical cancer in 10 years.

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39
Q

What to do if cervical cancer suspected but not confirmed?

A

2 week urgent referral to colposcopy and biopsy + gynaecology assessment

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40
Q

What is androgen insensitivity syndrome?

A

X linked recessive condition due to end organ resistance to testosterone, causing typically male children (46XY) to have a female phenotype.

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41
Q

How does androgen insensitivity syndrome present

A

Primary amenorrhoea
- Little/no axillary/pubic hair
- Undescended testes causing groin swelling
- Breast development may occur

Buccal smear or chromosomal analysis used to reveal genotype, testosterone may be high after puberty.

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42
Q

Management of androgen insensitivity

A

Bilateral orchidectomy and oestrogen (raise child female)

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43
Q

What is endometriosis?

A

Growth of ectopic endometrial tissue outside of the uterine cavity. Affects 10% of women of reproductive age

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44
Q

Clinical features of endometriosis

A
  • Chronic pelvic pain
  • Secondary dysmenorrhoea (pain starts days before bleeding)
  • Dyspareunia
  • Subfertility
  • Urinary symptoms (dysuria, urgency, haematuria) and dyschezia (painful bowel movements)
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45
Q

Examination features of endometriosis

A
  • Fixed and retroverted uterus
  • Ovarian enlargement
  • Tender blue nodules in posterior vaginal fornix
  • Visible vaginal endometriotic lesions
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46
Q

Investigations of endometriosis

A

Laparoscopy gold standard

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47
Q

Management of endometriosis

A

NSAID and/or paracetamol first line for symptomatic relief

COCP can be tried if that doesnt work

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48
Q

What is the most common gynaecological malignancy in the developed world

A

Endometrial carcinoma

90% of which are adenocarcinomas

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49
Q

Pathophysiology of the endometrium/ endometrial cancer

A

Endometrium builds in response to oestrogen in menstrual cycle. Serves to provide an optimal environment for blastocyst implantation. In absence of progesterone the blood vessels constrict and the endometrial lining undergoes ischaemia and death, causing it to shed during menstruation.

In endometrial cancer, there is normally a chronic, unopposed exposure to oestrogen.

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50
Q

Endogenous and exogenous sources of unopposed oestrogen

A

Endogenous
- Chronic anovulation (e.g. PCOS)
- Aromatisation of androgens
- Granulosa cell tumours

Exogenous unopposed oestrogen
- HRT
- Selective oestrogen receptor modulators (tamoxifen)

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51
Q

Risk factors and protective factors for endometrial cancer

A
  • > 50
  • Early menarche/late menopause
  • PCOS
  • Obesity
  • Nulliparity
  • Lynch syndrome/HNPCC
  • Cowden syndrome

Protective factors
- Multiparirty
- Smoking
- Progestin use

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52
Q

How does endometrial cancer present

A

Postmenopausal vaginal bleeding!

  • Inteermenstrual bleeding
  • Abdominal/pelvic pain
  • Anaemia, weight loss, dyspareunia

On examination:
- Enlarged uterus
- Fixed uterus with a mass

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53
Q

Investigation of post menopausal bleeding/ suspected endometrial cancer

A

ALL post menopausal bleeding should be sent via 2 week pathway

Transvaginal Ultrasound and Pipelle biopsy used to diagnose

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54
Q

FIGO staging of endometrial cancer

A

I - Confined to uterus
II - Cervical invasion
III - Ovarian, vaginal or adnexal (fallopian tubes) invasion or lymph nodes
IV - bladder, rectal, extra pelvic spread

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55
Q

Management of endometrial cancer

A

I and II - Total hysterectomy with bilateral salpingo-oopherectomy.

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56
Q

How is endometrial hyperplasia different to cancer and how is it managed

A

Proliferation of endometrium more than normal but not malignant.

Simple - expansion of glands. Atypia if architecture change

Complex - Crowding and budding of glands.

Diagnosed with biopsy but treated with progestin-based therapy.

Complex may need hysterectomy

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57
Q

What is PCOS

A

Ovarian condition causing metabolic issues. Causes insulin resistance and compensatory hyperinsulinaemia and high LH levels.

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58
Q

Features of PCOS

A
  • Oligomenorrhoea, amenorrhoea (reduced/absent periods)
  • Obesity
  • Hyperandrogenism (hirsutism (abnormal hair growth on face/body, acne vulgaris)
  • Male pattern baldness
  • Acanthosis nigricans
  • Sub/infertility
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59
Q

Investigations of PCOS

A

Pelvic USS - see cysts

Also helpful to look for FSH, LH, testosterone (total/free) and prolactin

Check for impaired glucose tolerance

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60
Q

Diagnostic criteria for PCOS

A

Rotterdam criteria
Two out of the 3:
- Oligo or anovulation
- Clinical/biochemical hyperandrogenism (hirsutism, acne, elevated test)
- PCO by USS - 12 or more follicles in one or both ovaries, and increased ovarian volume

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61
Q

Management of PCOS

A
  • Weight reduction
  • COCP to regulate periods and acne
  • Clomifene to manage infertility (encourages ovulation)
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62
Q

What are fibroids

A

Uterine fibroids, leiomyomas, are benign smooth muscle tumours of the uterus. Most common pelvic tumour in women. More in black women (50%). Develop in response to oestrogen

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63
Q

Features of uterine fibroids

A
  • Possibly asymptomatic
  • Menorrhagia
  • Bulk related symptoms (lower abdominal pain, cramping)
  • Urinary symptoms if severe
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64
Q

Diagnosis and management of Uterine fibroids

A

Transvaginal ultrasound

  • Asymptomatic - just monitor.
  • Shrink/remove fibroids - GnRH agonists (leuprorelin) short term - shrink fibroids especially before surgery (menopause side effects - decrease oestrogen)
  • GnRH antagonists (linzagolix) (cause menopausal symptoms and loss of BMD)
  • Surgery - myomectomy, uterine artery embolisation
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65
Q

What is ovarian torsion and what are some risk factors

A

Sudden onset deep colicky abdominal pain caused by torsion of the ovary. May present with vomiting, distress, fever.

Risk factors:
- Ovarian mass (90%)
- Reproductive age
- Pregnancy
- Ovarian hyperstimulation syndrome

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66
Q

Investigation and management of Ovarian torsion

A

Whirlpool sign or free fluid on USS

Laparoscopy is both diagnostic and therapeutic

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67
Q

What is pelvic inflammatory disease

A

PID is an ascending infection from the endocervix, affecting the uterus, fallopian tubes, ovaries and surrounding peritoneum.

Caused mostly by chlamydia trachomatis, but also N gonorrhoeae, M genitalium, M hominis

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68
Q

Clinical features of PID

A
  • Lower abdo pain
  • Fever
  • Deep dyspareunia
  • Dysuria and menstrual irregularities
  • Vaginal/cervical discharge
  • Cervical excitation
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69
Q

Investigations of PID

A
  • Pregnancy test to exclude ectopic pregnancy
  • High vaginal swab
  • Chlamydia and gonorrhoea
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70
Q

Management of PID

A

Low threshold for treatment

1 - stat IM ceftriaxone + followed by 14 days of oral doxycycline + oral metronidazole
2 - Oral ofloxacin + oral metronidazole

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71
Q

Complications of PID

A
  • Perihepatitis (Fitz-Hugh Curtis Sydrome) - RUQ Pain, may be confused with cholecystitis. (Ascending infection causes inflammation of liver capsule without involving liver)
  • Infertility
  • Chronic pelvic pain
  • Ectopic pregnancy
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72
Q

What is urogenital prolapse

A

Occurs most after giving birth or menopause. Occurs when pelvic floor muscles weaken and the uterus, bladder, urethra and rectum prolapse through the vagina.

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73
Q

Classify pelvic organ prolapse by its compartments

A
  • Anterior: cystocele (bladder)/urethrocele (urehtral herniation
  • Middle: Uterine, and vaginal vault prolapse (post hyterectomy)
  • Posterior: Rectocele (rectal) and enterocele (small bowel - pouch of Douglas)
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74
Q

Main symptoms of urogenital prolapse

A
  • Pelvic pressure (heaviness, dragging, bearing down. Pain worsens throughout day, back discomfort)
  • Vaginal bulging/mass (visible bulging or patient may feel something coming out when straining)
  • Urinary symptoms (Stress incontinence, urgency/frequency, urine retention)
  • Defecatory dysfunction (constipation, straining, incomplete evacuation. Splinting or need for manual support of vaginal wall during defecation)
  • Sexual dysfunction (discomfort and pain)
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75
Q

Examination structure in urogenital prolapse

A
  • Pelvic exam with patient in lithotomy (on back with legs flexed at 90 up) position, and during valsalva
  • ID involved compartments using Pelvic Organ Prolapse Quantification exam system (POP-Q)
  • Bimanual examination looking for masses, tenderness, cervical motion tenderness
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76
Q

management of urogenital prolapse

A

No treatment for mild
- Weight loss
- Pelvic floor exercises
- Ring pessary or surgery

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77
Q

Risk factors for urogenital prolapse

A
  • Increasing age
  • Multiparity w vaginal delivery
  • Obesity
  • Spina bifida
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78
Q

What is lichen sclerosus

A

Inflammatory condition affecting genitalia - more common in elderly women. Leads to atrophy of the epidermidis, forming white plaques. Thought to be autoimmune.

In women affects labia, perineum and perianal skin. In men, affects foreskin and glans penis.

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79
Q

Clinical features of lichen sclerosus

A

White, shiny, tight, thin and raised plaques. Very itchy. (porcelain)

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80
Q

Diagnosis of lichen sclerosus

A

Diagnosis made on clinical grounds, but biopsy may be used if
- Woman fails to respond to treatment
- Clinical suspicion of VIN (vulvar intraepithelial neoplasia) or cancer

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81
Q

Management of lichen sclerosus

A

High potency topical corticosteroids (clobetasol propionate 0.05% ointment)

Second line:
- Topical calcineurin inhibitors
- Topical retinoids

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82
Q

What is vulval intraepithelial neoplasia, what type of cancer does it predispose to

A

Precancerous skin lesion of the vulva. May result in squamous skin cancer if untreated. Average age >50

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83
Q

Risk factors for VIN

A

HPV 16 and 18
Smoking
HSV 2
Lichen sclerosus

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84
Q

Features of VIN

A

Itching and burning
Raised well defined skin lesions

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85
Q

Investigations of VIN

A

Punch biopsy (precancerous cells)
HPV testing

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86
Q

Management of VIN (pharmacological)

A

Imiquimod
5- fluorouracil

Surgical management if they dont work

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87
Q

What is ovarian cancer, what are its most common sites of metastasis

A

Highest mortality of any gynaecological cancer. Range of cells and peak incidence at 60.

Associated with BRCA1 and 2.

Diaphragm, right liver edge and omentum are common metastasis sites

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88
Q

Most common ovarian cancer types. What is found microscopically on the ovary?

A

Epithelial ovarian tumours (90%)
- May be benign, intermediate or malignant. Serous cystadenocarinoma is the most common subtype. Characterised by psamomma bodies (round microscopic calcium collections)

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89
Q

What is the tumour marker for ovarian cancer? What are 2 other investigations you could do? What calculation helps calculate risk?

A

CA 125 - antigen is elevated in peritoneal irritation, so not specific. Can be raised in endometriosis, adenomyosis, liver disease and pregnancy.

  • USS Abdomen and pelvis
  • Diagnostic laparoscopy and biopsy
  • RMI (risk of malignancy index) calculation.
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90
Q

NICE referral guide for ovarian cancer

A

2 week wait if:
- Ascites
- Pelvic mass, not due to fibroids
- Abdominal mass

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91
Q

What is the most common type of ovarian cyst.

What is a corpus luteum cyst, and how can this lead to pathology.

A

Ovarian cysts are really common, can be physiological (follicular most common, due to non rupture of dominant follicle). Corpus luteum cyst (occurs during mentrual cycle. If pregnancy doesnt occur this should break down, if not can fill with blood or fluid to form cyst).

Can also be benign germ cell tumours, or benign epithelial tumours

92
Q

How can these cysts rupture, and what is a ruptured ovarian cyst

A

Can occur spontaneously or in response to physical activity such as vigorous exercise, intercourse, or trauma.

Common emergency characterised by sudden severe lower abdo pain.

93
Q

Presentation of ruptured ovarian cyst

A
  • Severe unilateral sharp lower abdo/pelvic pain, radiates to back or thigh.
  • Rebound tenderness, guarding and rigidity
  • Haemodynamic instability, caused by intraperitoneal bleeding. (Tachycardia, hypotension, pallor, diaphoresis, syncope)
  • Fever
  • Nausea and Vomiting
94
Q

Investigation and management of ovarian cyst

A
  • USS to confirm diagnosis and assess bleeding
  • Conservative with pain control/observation if mild.
  • Laparoscopic surgery if severe.
95
Q

What cancers are caused by BRCA 1 and 2. What chromosomes are they found on?

A

BRCA1 - Breast/ovarian (Chromosome 17)
BRCA2 - Breast, Prostate, Ovarian (C13)

Autosomal dominant

96
Q

What is the most common type of breast cancer

A

Invasive ductal carcinomas, usually arising from Ductal Carcinomas in Situ (DCIS)

97
Q

Risk factors for breast cancer

A
  • BRCA1&2 (40% lifetime risk of breast/ovarian)
  • FH
  • Nulliparity, 1st pregnancy > 30yrs
  • Early menarche, late menopause
  • Not breastfeeding
  • Ionising radiation
  • COCP Use (1.023x/year risk increase)
98
Q

What oncogene is overexpressed in breast cancer

A

HER2 receptor - enables cell growth, survival and proliferation

99
Q

Classification of breast cancer

A

In situ - Non invasive (into basement membrane)
Invasive - Penetrate basement membrane

Ductal - From walls of ducts into the lumen. In situ can become invasive
Lobular - Grow from ducts of walls into lumen

100
Q

What is Paget’s disease

A

Eczema-ish (itchy, red, crusty, discharging) nipple associated with people with breast cancer. 90% invasive carcinoma

101
Q

Breast changes in breast cancer

A

Breast lump
- Painless, fixed, hard

Skin
- Tethering
- Oedematous
- Thickened and dimpled (peau d’orange)

Nipple
- Inverted
- Dilated veins
- Discharge
- Pagets (itchy, red, crusty)

102
Q

How is breast cancer screened for?

A

Mammogram every 3 years between 50-70

103
Q

Other investigations for breast cancer

A

USS if under 40
Fine needle aspiration and core biopsy

Receptor status (check for progesterone and oestrogen receptors (PR+ and ER+), these enable treatment options.

Triple negative (HER2-, PR-, ER-) is bad for prognosis

104
Q

When should breast cancer be referred via 2 week wait pathway?

A
  • Aged 30+ with unexplained lump
  • 50+ with nipple changes: discharge, retraction, etc.

GP Should refer for triple assessment
- History/Examination
- Imaging (biopsy or USS)
- Histology

105
Q

Pre surgical management of breast cancer

A

If axillary lymphadenopathy, axillary node clearance.
If not palpable, pre-operative USS. If nothing found, sentinal node biopsy.

106
Q

Surgical management of breast cancer

A

Mastectomy
- Multifocal tumour
- Central tumour
- Large lesion in small breast
- DCIS >4cm

Wide local excision
- Solitary lesion
- Peripheral tumour
- Small lesion in large breast
- DCIS<4cm

107
Q

Common metastasis sites for breast cancer

A
  • Bone
  • Lung
  • Liver
  • Brain
108
Q

Pharmacological management of breast cancer

A

HER2 positive - herceptin

ER/PR positive
- Tamoxifen (Oestrogen receptor blocker)
- Post menopausal, Anastrazole (aromatase inhibitor - prevents androgens being converted to oestrogen)

109
Q

Paget’s disease vs eczema of the nipple

A

Pagets affects nipple first then areolar (opposite in eczema)

110
Q

What is mastitis

A

Inflammation of the breast tissue, typically associated with breast feeding. Usually caused by bacterial infection, blocked milk ducts, or both.

111
Q

Presentation of mastitis

A
  • Hot, painful, tender breast
  • Flu like symptoms (fever, chills, fatigue)
  • Skin changes such as dimpling or puckering
  • Lymphadenopathy of the axilla
112
Q

Management and complication of mastitis

A
  • Continue breastfeeding/pumping + analgesia
  • Antibiotics if lasts longer than 12-24 hours of milk clearance (oral flucloxacillin 10-14 days)

May develop breast abscess if untreated

113
Q

What is a breast abscess

A

Complication of infectious mastitis, most commonly due to Staph aureus. Can be caused in lactating women by blocked duct or milk stasis

114
Q

Presentation of a breast abscess

A

Painful, erythematous, swelling in one quadrant of the breast with systemic fever and malaise.
+- Nipple discharge and retraction, and lymphadenopathy

115
Q

Investigations/management of breast abscess

A
  • Breast USS
  • Needle aspirate (diagnostic <5cm and therapeutic) and culture
  • Larger abscesses may need surgical incision and drainage with washout.

Flucloxacillin or doxy if MRSA. If very unwell, IV Vancomycin

Express breast milk as normal.

116
Q

What is a fibroadenoma, where do they normally occur and what can cause them

A

Benign breast tumour occuring in younger women arising from the terminal duct lobular unit. Comprised of stromal tissue and epithelial connective tissue cells.

They are smooth, painless, mobile,
firm and well circumscribed and 2-3 cm across (giant fibroadenomas (1%) can be up to 5cm).

Most commonly seen in menses, pregnancy or COCP. No increase in cancer risk. Upper right quadrant of breast.

117
Q

Features differentiating a cancerous breast lump from a fibroadenoma

What is a Phyllodes tumour

A

Breast cancer involves nipple and skin changes, and is associated with discharge and pain.

Phyllodes tumour is similar but presents older (40-50) and are fast growing. (have a leaf-like appearance on microscopy)

118
Q

How are fibroadenomas investigated

A

Urgent 2 week referral for any breast lump in 30+.

USS in <35. Mammogram if >35.

Core biopsy can be used - epithelial cells in a honeycomb pattern.

119
Q

Treatment of fibroadenoma

A

If asymptomatic and small, leave.

Can be surgically removed if >3cm. Phyllodes tumour should be widely excised.

120
Q

What are breast cysts

A

Benign, individual fluid filled lumps. Most common breast lump. Can be painful and fluctuate in size over cycle. 30-50y

Smooth, well circumscribed, mobile and possibly fluctuant.

121
Q

What are fibrocystic breast changes

A

Normal - not disease related. Stroma, ducts and lobules respond to female sex hormones and become fibrous and cystic (irregular, hard, fluid-filled). Changes fluctuate with cycle. Common in women of menstruating age

122
Q

How do fibrocystic breast changes present

A

One or both breasts:
- Lumpiness
- Pain/tenderness
- Fluctuation of breast size

Symptoms fluctuate in line with cycle, start 10 days before and end as menstruation begins

123
Q

How to manage fibrocystic breast changes

A

Exclude cancer.
- Wear supportive bra
- NSAIDs
- Avoiding caffeine
- Apply heat to area
- Hormonal treatments

124
Q

What are breast cysts and how should they be managed

A

Fluid filled benign lumps most common in women 30-50. Smooth, well circumscribed, mobile, can be fluctuant.

Need investigation and aspiration can resolve. Slightly increases risk of Breast cancer.

125
Q

How does fat necrosis cause a breast lump

A

Degeneration and scarring of fat tissue. Usually triggered by local trauma, radiotherapy or surgery, with an inflammatory response causing fibrosis and necrosis of fat tissue.

126
Q

How does fat necrosis present

A
  • Painless
  • Firm
  • Irregular
  • Fixed in local structures
  • May cause nipple inversion or skin dimpling.

Investigated as expected. Resolves with time, surgical if symptoms

127
Q

What is galactocele

A

Benign lump that occurs in lactating women that stop breastfeeding. Breast milk filled cysts in the lactiferous ducts, preventing the gland from draining milk. Firm, mobile, painless lumps, usually beneath the areola.

Usually resolve without treatment but can be needle drained

128
Q

What is intraductal papilloma

A

A warty lesion that grows in a duct in the breast. Proliferation of epithelial cells. Usually presents with tenderness/pain and nipple discharge (clear or blood stained).

Normal investigations but ductography may also be used. Shows an area that does not fill with contrast (filling defect)

Require surgical excision (microdochectomy) and examination to ensure non cancerous

129
Q

What is ductal ectasia

A

AKA Periductal mastitis. Dilation and thickening of subareolar ducts. Ducts inflame, leading to discharge that can be white, grey or green.

Most often occurs in perimenopausal women and smoking is a significant risk factor.

130
Q

How does mammary duct ectasia present

A

Nipple discharge
Tenderness/pain
Nipple retraction/inversion
A breast lump (pressure may produce discharge)

Can also have periareolar or subareolar infections which may be recurrent.

131
Q

Investigations of duct ectasia

A

Clinical history + examination
Imaging (USS, mammogram)
Histology (fine needle aspiration/biopsy)

Microcalcifications show on mammogram (not specific)

132
Q

Treatment of duct ectasia

A

If troublesome, microdochectomy if young, or total duct excision if older.

133
Q

What is a hydatidiform mole?

A

Complete - 2 sperm cells fertilise an ovum with no genetic material, causing a tumour growth with no fetal material.

Partial - 2 sperm cells fertilise a normal ovum - giving it 3 sets of chormosomes. Some fetal material may form.

Both types of tumour that act like pregnancies and grow in the uterus.

134
Q

Presentation of molar pregnancy/hydatidiform mole

A

Act like normal pregnancy, with some key differences
- More severe morning sickness
- Vaginal bleeding
- Increased enlargement of the uterus
- Abnormally high hCG
- Thyrotoxicosis (hCG mimics TSH, stimulating thyroid)

134
Q

How are hydatidiform moles investigated and managed

A

Ultrasound shows a “snowstorm” appearance.

Confirmation through histology after evacuation of the uterus to remove and investigate mole.

135
Q

What is prolactin. What is it suppressed by

A

A hormone produced in the anterior pituitary that causes breast milk production. It is counteracted by dopamine, so dopamine antagonists (e.g. antipsychotics) can cause raised prolactin and galactorrhoea.

Dopamine agonists (bromocriptine, cabergoline) can suppress prolactin secretion

136
Q

How does milk production happen in pregnancy

A

Oestrogen and progesterone inhibit prolactin secretion. Prolactin stimulates breast milk secretion and oxytocin stimulates its ejection.

In pregnancy higher oestrogen and progesterone inhibit breast milk production but shortly after birth, oestrogen and progesterone drop and oxytocin increases.

137
Q

Causes of raised prolactin

A
  • Prolactinoma (pituitary tumour secreting prolactin)
  • Primary Hypothyroidism (TRH sitmulating prolactin) and PCOS
  • Medications (antipsychotics)
  • Acromegaly
  • Idiopathic
138
Q

Drug causes of raised prolactin

A

Dopamine antagonists:

Antiemetics - Metaclopramide, domperidone
Antipsychotics - Haloperidol, chorpromazine, rispiridone etc

139
Q

Raised prolactin suppresses what hormone, and in turn causes what?

A

Suppresses GnRH by the hypothalamus, causing reduced LH and FSH.

  • Menstrual irregularities and amenorrhoea
  • Reduced libido
  • Erectile dysfunction and gynaecomastia in men
140
Q

What is a prolactinoma and what gene can it be caused by

A

An anterior pituitary adenoma of the lactotrophs causing excess prolactin release.

Can be caused by MEN-1 gene (autosomal dominant)

141
Q

How does prolactin cause increased fracture risk

A

Prolactin negatively feedsback onto GnRH causing decreased testosterone and oestrogen. As oestrogen usually inhibits osteoclasts, the risk of fracture is increased.

142
Q

How can pituitary adenomas be classified by size? What can larger tumours cause?

A

Microadenomas - <1cm
Macroadenomas - >1cm

Macros cause:
- Headaches
- Bitemporal hemianopia (pressing on optic chiasm)

143
Q

Causes of non milk nipple discharge

A

Duct papilloma
Mammary duct ectasia
Pus from an abscess

144
Q

Signs of excess prolactin in men and women

A

Women:
Amenorrhoea
Infertility
Osteoporosis
Galactorrhoea
Vaginal dryness

Men:
Impotence
Loss of libido
Galactorrhoea

145
Q

Treatment of Prolactinoma

A

Dopamine agonist - Cabergoline (dopamine inhibits prolactin), or bromocriptine

  • Sight saving - shrinks adenoma. If micro, only needs a couple small doses a week
146
Q

Investigations for prolactinoma

A

Serum prolactin - high
TRH - low (TRH normally releases prolactin)
MRI Gold imaging

TRH Stimulation test can someties be done - will show TRH administration has no effect on already high prolactin levels

147
Q

What guidelines are used to indicate whether a person is eligible for different types of contraception

A

The FSRH UKMEC (Faculty of Sexual and Reproductive Healthcare UK Medical Eligibility) Guidelines 2016.

1: No restriction
2: Benefits outweigh risks
3: Risks generally outweigh benefits
4: Unacceptable - Contraindicated

148
Q

What are the 3 most effective contraceptions

A
  • Surgery (sterilisation/vasectomy)
  • Coils (Copper coil/Mirena coil)
  • Progesterone only implant

> 99% Under both typical and perfect use

149
Q

What are some specific risk factors to keep an eye out for when prescribing contraception

A

Any hormonal contraception - Breast cancer
Any coil - Cervical/endometrial cancer
Copper coil - Wilsons disease

150
Q

What are some COCP contraindications (UKMEC 4)

A
  • Uncontrolled HTN (>160/100)
  • Migraine with aura
  • History of VTE or vascular disease/stroke
  • > 35y AND smoking >15 cigs
  • Major surgery with immobility
  • Liver cirrhosis
  • SLE/antiphospholipid syndrome
  • Heart disease/ AFib
151
Q

What are some contraception considerations in over 50s

A
  • After the last period keep contraception for 2 years if under 50 and 1 year if over 50
  • COCP can be used up to 50
  • Progesterone injection should be stopped <50y due to osteoporosis risk
152
Q

What does MEN 1 cause and whats its pattern of inheritance

A

Autosomal dominant

  • Parathyroid adenoma
  • Pituitary prolactinoma or acromegaly
  • Pancreatic endocrine tumours
153
Q

What does MEN2a cause

A
  • Medullary thyroid cancer
  • Pheochromocytoma
  • Primary hyperparathyroidism
154
Q

What does MEN2b cause

A
  • Medullary thyroid cancer
  • Phaeochromocytoma
  • Mucosal neuromas
155
Q

What is the most common STI and which one is fastest increasing?

A

Chlamydia is most common (especially in 15-24 yo) and gonorrhoea is the fastest increasing, with a big concern about antibiotic resistance

156
Q

WHat is chlamydia

A

The most prevalent STI in the UK, caused by Chlamydia trachomatis, an obligate intracellular pathogen. Affects ~1/10 young women and has a 7-21 day incubation period.

157
Q

Risk factors for chlamydia

A

Young
Sexually active
Multiple partners

158
Q

Clinical features of chlamydia

A

Largely asymptomatic (50% men, 75% women)

Women:
- Cervicitis (pain, discharge, bleeding)
- Dysuria
- Painful sex +- postcoital bleeding

Men:
- Urethral discharge/discomfort
- Dysuria
- Epididymo-orchitis
- Reactive arthritis

159
Q

What might examination for chlamydia show

A

Pelvic/abdominal tenderness
Cervical motion tenderness
Inflamed cervix
Purulent discharge

160
Q

What screening is used for chlamydia

A

National Chlamydia Screening Program

Every sexually active person under 25yo screened annually for chlamydia. Positive tests are retested in 3 months, to ensure they havent been reinfected.

Limitation: Opportunistic testing (opt in)

161
Q

When attending a GUM clinic, what is screened for at minimum

A
  • Chlamydia
  • Gonorrhoea
  • Syphilis
  • HIV
162
Q

What STIs can be investigated with a charcoal swab

A
  • Bacterial vaginosis
  • Candidiasis
  • Gonorrhoea (endocervical swab)
  • Trichomonas (posterior fornix swab)
  • Group B Strep
163
Q

What STIs are tested for using NAAT. How are samples collected in men and women

A

Nucleic acid amplification test

Chlamydia and gonorrhoea

In women, a self vulvovaginal (1), endocervical (2) swab or first catch urine (3) are used.

In men, can be done with first catch urine or urethral swab

164
Q

Where else can NAAT swabs be done to check for chlamydia

A

Rectal and pharyngeal NAAT swabs (anal and oral sex)

165
Q

What is the mangement of chlamydia

A

First line:
- Doxycycline 100mg 2xday for 7 days
- Azithromycin 1g orally (mycoplasma genitalium is resistant so less preferred)

166
Q

How is chlamydia managed in pregnancy

A

Doxycycline is inappropriate in pregnancy (fetal tooth/bone development, maternal hepatotoxicity) and breastfeeding

Use:
- Azithromycin 1g STAT
- Erythromycin or amoxicillin could be used.

Test of cure not routinely recommended, but recommended for rectal cases, in pregnancy, and where symptoms persist.

167
Q

Non medical management of Chlamydia

A

Referral to GUM clinic, with partner notification and abstinence.

Men: All contacts since 4 weeks before symptom onset
Women and asymptomatic men: All contacts from last 6 months

168
Q

Complications of chlamydia in and out of pregnancy

A

Out:
- Pelvic inflammatory disease
- Infertility
- Ectopic pregnancy
- Epididymo-orchitis
- Conjunctivitis
- Lymphogranuloma venereum

In:
- Preterm delivery
- Permature ROM
- Low birth weight
- Postpartum endometritis

169
Q

What is a complication of maternal chlamydia to the neonate, and what is an important differential to investigate

A

Pneumonia is possible

Main one is conjunctivitis (can be spread hand-to-eye)
- Presents with chronic erythema, irritation, discharge, unilateral and lasting >2 weeks.

170
Q

What is lymphogranuloma venereum

A

Urethritis and PID affecting lymphoid tissue caused by Chlamydia trachomatis serovars L1, L2, L3.

(Normal chlamydia caused by serovars D-K)

Most commonly occurs in MSM

171
Q

What are the 3 stages of lymphogranuolma venereum

A

Stage 1: Painless ulcer - penis in men, vaginal wall in women, or rectum after anal sex.

Stage 2: Lymphadenitis (painful swelling in the lymph nodes) Usually affects inguinal or femoral lymph nodes

Stage 3: Proctocolitis (anus, rectum, colon): Anal pain, change in bowel habit, tenesmus (feeling to empty bowels when already empty), discharge

172
Q

How is LGV treated

A

Doxycycline 100mg 2x/day for 21 days.

173
Q

What is gonorrhoea

A

Fastest increasing STI (maybe due to antibiotic resistance). Neisseria gonorrhoea (gram neg diplococcus).

Infects mucous membranes with columnar epithelium (endocervix in women, and urethra, rectum, conjunctiva and pharynx)

174
Q

How does gonorrhoea present

A

More likely than chlamydia to be symptomatic (90% men, 50% women)

Females:
- Odourless purulent discharge (green/yellow)
- Dysuria
- Pelvic pain

Men:
- Same discharge
- Dysuria
- Epididymo-orchitis (test. swelling/pain)

Can cause rectal (anal discharge, itching, painful poo) and pharyngeal (sore throat, difficulty swallowing) infection but usually asymptomatic.

175
Q

How do prostatitis and conjunctivitis present in chlamydia

A

Prostatitis:
- Perineal pain, urinary symptoms, prostate tenderness
- Conjunctivitis: Erythema and purulent discharge

176
Q

Investigations for gonorrhoea

A

NAAT used to detect RNA/DNA of gonococcal infection. Endocervical, vulvovaginal or urethral swab, or first catch urine. + Rectal/pharyngeal swabs in MSM

Endocervical charcoal swab MUST be taken for MCS before Abx, due to high rates of antibiotic resistance

177
Q

Management of gonorrhoea

Management in pregnancy

A
  • Single IM Ceftriaxone 1g if sensitivities not known
  • Single oral ciprofloxacin 500mg if sensitivities known

Test of cure NEEDED due to high resistance.
- 72 hours after treatment for culture
- 7 days after for RNA NAAT
- 14 days after for DNA NAAT

In pregnancy,
- IM Ceftriaxone 500mg + Oral azithromycin 1g orally

178
Q

Main complications of gonorrhoea

A

Women:
- PID

Men:
- Epididymo-orchitis
- Prostatitis

Both:
Disseminated gonococcal infection (infection spreads to skin and joints)
- Arthritis (migratory polyarthritis)
- Skin lesions (pustular or maculopapular)
- Tenosynovitis
- Fever/Chills

179
Q

Other complications of gonorrhoea

A
  • Chronic pelvic pain
  • Infertility
  • Conjunctivitis
  • Septic arthritis
  • Endocarditis

Gonococcal conjunctivitis in neonate (called ophthalmia neonatorum)
- Medical emergency, associated with sepsis, perforation of eye, blindness
- Can be passed on during vaginal birth (similar to conjunctivitis and pneumonia in the child)

180
Q

What is syphilis

A

STI caused by spriochete (spiral shape bacteria) called Treponema pallidum. Usually enters through a break in skin or mucous membranes, and has a up to 90 day incubation period

181
Q

Modes of transmission of syphilis

A
  • Oral, vaginal, anal sex
  • Vertical transmission
  • IV drug use
  • Blood transfusion
182
Q

Stages of syphilis

A

Primary - painless ulcer (chancre) at original site of infection and local non tender lymphadenopathy

Secondary (6wk - 6months) - Systemic symptoms
- Symmetrical rash on trunk, palms, soles
- Buccal “snail track” ulcers
- condylomata lata (painless warty lesions on the genitalia)
- 3-12 weeks to latent stage

Latent - Symptoms disappear and patient asymptomatic. Early latent in first 2 years, late latent after that.

Tertiary syphilis - many years later, with the development of gummas (granulomatous lesions of skin and bones)

Neurosyphilis is when infection affects CNS

183
Q

Primary stage of syphilis

A

Painless genital ulcer (chancre) (resolves over 3-8 weeks)
Local lymphadenopathy

184
Q

Secondary stage of syphilis

A

Secondary (6wk - 6months) - Systemic symptoms
- Symmetrical maculopapular rash on trunk, palms, soles, face
- Buccal “snail track” ulcers
- condylomata lata (painless warty lesions on the genitalia)
- Alopecia
- Lymphadenopathy
- Oral lesions

185
Q

Tertiary stage of syphilis

A

Late latent/tertiary - >2 years since infection
- Granulomatous lesions “gummas” affect skin, organs and bones
- Aortic aneurysm
- Neurosyphilis

Late stage involves brain, nerves, eyes, heart, blood vessels, liver, bones, joints.

186
Q

Signs of neurosyphilis

A
  • Tabes dorsalis (demyelination of the spinal cord posterior columns)
  • Ocular syphilis (blurred vision, eye pain, redness, inflammation)
  • Argyll-Robertson pupil - Constricted pupil that accommodates to close objects but doesnt react to light. Often irregularly shaped.
  • Paralysis, altered behaviour, dementia, sensory impairment
187
Q

How is syphilis diagnosed

A

Treponemal specific
- T pallidum particle agglutination assay (TPPA) and enzyme immunoassay (TPEIA). Positive results confirm exposure, but not current/past.

Non treponemal specific
- Rapid Plasma Reagin (RPR) and Venereal Disease Research Laboratory (VDRL) - Can show active disease and monitor disease progression. Sensitive but not specific, as they only assess the quantity of antibodies produced in response to syphilis.

Samples from infection sites can be tested to confirm T.pallidum with
- Dark field microscopy
- Polymerase Chain Reaction

188
Q

Causes of false positive non-treponemal tests

A
  • Pregnancy
  • SLE, anti-phospholipid syndrome
  • TB
  • Leprosy
  • Malaria
  • HIV
189
Q

Management of Syphilis

A

IM Benzathine benzylpenicillin 1.8g. 2-3 doses, 1 week apart.
- Doxycycline is an alternative
- In pregnancy: Erythromycin

Follow up at GUM clinic every 3 months, avoid sexual contact, contact tracing and partner notification. Test for HIV and full sexual health screen

190
Q

What ADR is sometimes seen after syphilis treatment

A

Jarisch-Herxheimer - fever, rash, tachycardia. Differs to anaphylaxis as NO wheeze or hypotension.

No treatment required

191
Q

How can congenital syphilis present

A

Bunted upper incisors (Hutchinsons teeth) and mulberry molars
Rhagades (scars at angle of mouth)
Keratitis
Saber shins
Saddle nose
Deafness

192
Q

What is chancroid

A

Sexually transmitted bacterial infection Haemophilus ducreyi

Presents with unilateral painful ulcers and painful inguinal lymphadenopathy.

Ulcers are sharply defined, ragged with an undetermined border

193
Q

Where does chancroid most commonly present

A

Males
- Foreskin but also shaft, glans, meatus

Females
- Labia majora, but also labia minora, thighs, perineum, cervix

194
Q

Investigations and management of chancroid

A

Clinical diagnosis

Managed with antibiotics (single IM ceftriaxone 250mg)

Alternatives;
- Single IM azithromycin 1g
- Oral ezythromycin 500mg 4xday/7days

195
Q

What is balanitis

A

Inflammation of the glans penis and sometimes the underside of the foreskin. Most commonly infective (bacterial/candidal)

Treated with simple hygiene, improper cleaning and presence of tight foreskin makes balanitis worse.

196
Q

Common causes of balanitis

A

Candidiasis (post intercourse + itching and white discharge)
Dermatitis (contact, allergic) (itchy, painful, clear discharge)
Dermatitis (eczema, psoriasis) (Very itchy, no discharge, inflammatory skin changes elsewhere)
Bacterial (Group B strep or staphylococcus, painful and itchy with yellow discharge)

197
Q

How is balanitis investigated and treated

A

Investigated clinically or with swab (bacteria or candida albicans)

Treated with;
- Gentle saline washes, including under foreskin, 1% hydrocortisone if severe and not fixing.
- Topical clotrimazole if candida
- Oral fluclox (or clarithromycin if allergic) if bacterial
- Anaerobic treated with metronidazole

198
Q

What is genital herpes

A

Ulcers/lesions affecting the genital area caused by Herpes Simplex Virus.

HSV1 usually causes cold sores, and HSV2 normally causes herpes, but there is overlap.

The virus becomes latent in nearby sensory nerve ganglia (cold sores = trigeminal nerve ganglia, genital herpes = sacral nerve ganglia)

199
Q

How is HSV transmitted

A

Direct contact
Viral shedding in mucous secretions (inactive virus can still be shed and passed on)

200
Q

Presentation of genital herpes

A

Usually present within 2 weeks of infection
- Ulcers/blistering lesions
- Neuropathic pain (shooting, tingling, burning)
- Flu like symptoms
- Pain on urination
- Inguinal lymphadenopathy
Symptoms start 3 weeks in primary infection, subsequent episodes milder and dont last as long

HSV can also cause aphthous mouth ulcers, herpes keratitis, and herpetic whitlow (painful lesion on finger or thumb)

201
Q

How is genital herpes diagnosed and managed

A

Clinical, but can do viral swab

Aciclovir to treat + saline bathing, analgesia and topical agents

202
Q

Considerations of genital herpes in pregnancy

A
  • If first episode is <28 weeks, offer antiviral therapy, and again from 36 weeks till birth
  • If first episode is on or after 28 weeks, advise antiviral treatment until birth
  • If episode is within 6 weeks of due date, elective C section
  • If first episode earlier, normal vaginal birth.
203
Q

What is neonatal HSV

A

If acquired by mother in 3rd trimester there is an increased risk.

Can cause neonatal fever, seizures, sepsis.

204
Q

What is group B Streptococcus and what are the risk factors

A

Infants may be exposed to GBS in labour (GBS found naturally in womans GI tract and vagina)
- Prematurity
- Prolonged ROM
- Previous sibling GBS
- Maternal pyrexia

205
Q

Management of GBS

A
  • Not universally screened for and maternal request not valid for screening
  • If GBS in previous pregnancy, risk is 50%. Should be offered intrapartum Abx prophylaxis OR testing in late pregnancy
  • IAP (Intrapartum Antibiotic Prophylaxis) offered to women in preterm labour and those with previous baby with GBS.
  • Treated with benzylpenicillin
  • Also given if pyrexia during labour
206
Q

What neonatal infections does group B strep cause

A
  • Pneumonia
  • Sepsis
  • Meningitis
  • Septic arthritis
207
Q

What organisms can cause neonatal sepsis

A
  • Group B strep
  • E coli
  • Listeria
  • Klebsiella
  • Staph aureus
208
Q

Risk factors for neonatal sepsis

A
  • Vaginal GBS colonisation
  • GBS Sepsis in previous child
  • Maternal sepsis, chorioamnionitis, fever >38
  • Prematurity/low birth weight
  • PROM
209
Q

Clinical features of neonatal sepsis

A

Non specific, low treatment threshold
- Respiratory distress/apnoea
- Fever/Tachycardia
- Jaundice
- Seziures
- Poor feeding
- Vomiting
- Hypoglycaemia

210
Q

Red flags for neonatal sepsis

A
  • Confirmed or suspected sepsis in mother
  • Signs of shock
  • Seizures
  • Term baby needing medical ventilation
  • Respiratory distress >4hours post birth
211
Q

Management of neonatal sepsis

A

If 2 or more risk factors or clinical features, or more than 1 red flag: TREAT
- Benzylpenicillin or gentamicin first line
- Monitor CRP at 24 hours and check blood cultures at 36 (2 bottles)
- Check CRP again at 5 days
- Maintain O2, fluid/electrolytes, prevent hypoglycaemia and acidosis

212
Q

Possible investigations in neonatal sepsis

A
  • Blood cultures (2 bottles)
  • Lumbar puncture (especially if meningitis suspected)
  • Blood gases and FBC
  • CRP for monitoring
213
Q

What are genital warts caused by

A

HPV 6 and 11

(remember 16, 18, 33 cause cervical cancer)

214
Q

Features of genital warts

A

Small (2-5mm) fleshy protuberances which are slightly pigmented that may bleed or itch

215
Q

How are genital warts treated

A

Topical podophyllum or cryotherapy, depending on location.
- Multiple, non-keratinised warts: Topical treatment
- Solitary, keratinised warts: cryotherapy
- imiquimod second line, recurrence also common

216
Q

What is HIV

A

An RNA retrovirus that targets CD4 T helper cells. AIDS (Acquired Immunodeficiency Syndrome) occurs when the disease progresses, causing person to be immunocompromised.

This leads to opportunistic, AIDS defining illnesses

HIV 1 most common, HIV 2 occurs in West Africa

217
Q

How is HIV transmitted

A
  • Unprotected anal, vaginal, oral sex
  • Vertical transmission (birth, pregnancy, breastfeeding)
  • Mucous membrane, blood or wound exposure to blood or bodily fluids (Needle stick, blood splashed in eye)
218
Q

What are some AIDS defining illnesses

A
  • Kaposi sarcoma
  • Pneumocystis jirovecii pneumonia (PCP)
  • Lymphomas
  • TB
  • Candidiasis
  • Cytomegalovirus
219
Q

Investigations in HIV

A

1st
HIV antibody test (false negative for 3 months post exposure)
P24 antigen testing

If negative, repeat in 3 months

Confirmatory
- Repeat P24 or use Western blot (p24, gp120, gp41)

220
Q

How does HIV present

A

Acute (CD4>500)
- Flu like symptoms

Chronic/latent (CD4 500-200)
- Fever
- Persistent lymphadenopathy
- Opportunistic infections like EBV causing hairy leukoplakia or oral candidiasis
- TB can reactivate

AIDS defining
- Persistent fever, fatigue, weight loss, diarrhoea, visual loss

221
Q

Management of HIV

A

Antiretrovirals, aiming to increase CD4 count and reduce viral load

  • 2 nucleoside reverse transcriptase inhibitors (NRTI) + protease inhibitor or non nucleoside reverse transcriptase inhibitor
  • E.g. Tenofovir and emtricitabine and bictegravir
222
Q

How should birth be managed in a woman with HIV? What can be given if viral load is high or unknown during labour

A

Viral load
<50copies/ml - Normal delivery
>50 copies - consider C section
Over 400 - Pre-labour C section

Give IV zidovudine if viral load high or unknown during labour

223
Q

What is mycoplasma genitalium

A

Non-gonococcal urethritis STI

Presents similarly to chlamydia, often co-infected. Urethritis is a key feature.

Increasing antibiotic resistance, especially to azithromycin.

224
Q

How is mycoplasma investigated

A

NAAT
- First urine sample for men
- Vaginal swabs for women

Macrolide resistance and test of cure needed.

225
Q

Management of mycoplasma genitalum

A

Doxycyline 100mg 2xday/7days

2nd:
Azithromycin 1g stat then 500mg 1xday/2days

226
Q

Possible complications of mycoplasma

A
  • Urethritis
  • Epididymitis
  • Cervicitis
  • PID
  • Reactive arthritis
  • Preterm delivery in pregnancy

Phase 3a Tera Pyo Edition (9 decks)

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